MEDSTAR

CLINICAL GUIDE AND

SYNOPSIS
First Edition

Obstetrics and Gynecology

FOR
Prepared By REVISION
Medical Students of 2008 E.C Batch ONLY
Jimma University, Ethiopia
 MEDSTAR CLINICAL GUIDE AND SYNOPSIS I

MEDSTAR CLINICAL GUIDE AND SYNOPSIS

GYNECOLOGY AND OBSTETRICS

FIRST EDITION
FEB, 2020

JUMC 2008E.C. MEDICAL STUDENT BATCH

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 MEDSTAR CLINICAL GUIDE AND SYNOPSIS II

Preface
The first edition of MEDSATR CLINICAL GUIDE AND SYNOPSIS TO OBSTETRICS
AND GYNECOLOGY (OBGYN) is one of the three similar works, which include
similar sister documents for Internal medicine and Pediatrics. It is prepared as
a gift for our fellow medical students to be a guide through their clinical year
attachments. As its name suggest, we are hoping it will be like a star in the
sky showing directions to “med-travellers” through their journey into becoming
a qualified doctors.
The guide is mainly prepared by combining our ward experience and the
detailed science on the textbooks for the major cases in obstetrics and
gynecology. Unlike its sister documents in the other attachments, ours is
mostly case oriented, this is due to the limited number of major chief
complaints in OBGYN (it is not uncommon to find multiple major cases with
similar chief complaints). The management plans for the major cases is mainly
taken from the Jimma University OBGYN Management Guideline.
For history and physical examination in OBGYN we strongly recommend you to
read, Introduction to Obstetrics and Gynecology diagnosis, by Dr. Asheber Gaym.
You should also check the simplified format for history taking and physical
examination prepared by Jimma Medical Center OBGYN Department.

In conclusion, we would like to say, we have tried to make this guide as

readable as possible. This work is just a start, and without doubt there will be
some flaws in the document, but we are going to add more details and include
more cases in the coming edition. So in the meantime we hope these
documents might came handy as additional source for our fellow medicos in
understanding OBGYN.
We have prepared an Email address and Telegram bot link so that we could get
your feedback on the book and come up with a better second edition in
upcoming years.
Email address: [email protected]
Telegram bot link: @MedstarCommentsBot

The Contributors

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 MEDSTAR CLINICAL GUIDE AND SYNOPSIS III

ACKNOWLEDGMENT

We would like to express our sincere gratitude to the medical students who
have sacrificed their time in relentlessly committing to this book. And we are
grateful to Dr. Asfaw of Jimma University OBGYN department, for his
invaluable, comments and suggestions for some of the cases of this book.

Special thanks are due to all Jimma University medical students who have
been taking part by commenting on the cases, getting the right resources and
helping us build this book to guide you in need.

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 MEDSTAR CLINICAL GUIDE AND SYNOPSIS IV

CONTRIBUTORS

 Balkewkal Kebede (C-II)

 Abdulhafiz Hussein (C-II)
 Bemnet Gebremichael (C-II)
 Daniel Delessa (C-II)
 Bulcha Lemma (C-II)
 Bethel Ayele (C-II)
 Abubeker Nuredin (C-II)
 Amanuel Tefera (C-II)
 Abraham Gebeyehu (C-II)

Coordinator and editor: Balkewkal Kebede

Cover Page Designed: Nahom Asnake (nAx)

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 MEDSTAR CLINICAL GUIDE AND SYNOPSIS V

The whole MEDSTAR Team

OBGYN MEDSTAR Team

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 MEDSTAR CLINICAL GUIDE AND SYNOPSIS VI

CONTENTS
CHAPTER 1 .................................................................................................................................. 1
HYPERTENSIVE DISORDERS OF PREGNANCY (HDP) ................................................... 1
DEFINITION AND CLASSIFICATION .................................................................................................................1
GESTATIONAL HTN .............................................................................................................................................3
PREECLAMPSIA (PE) ...........................................................................................................................................5
RISK FACTORS OF PE .............................................................................................................. 6
ETIOPATHOGENESIS ............................................................................................................... 7
PATHOPHYSIOLOGIC CHANGES IN PE .................................................................................. 10
CLINICAL MANIFESTATIONS OF PE ...................................................................................... 12
PREDICTION AND PREVENTION OF PE ................................................................................. 13
ECLAMPSIA .........................................................................................................................................................13
CHRONIC HYPERTENSION IN PREGNANCY AND SUPERIMPOSED PE .................................................15
MANAGEMENT OF PE-E SYNDROME ..........................................................................................................16
Management of PE .............................................................................................................. 16
Antepartum management .............................................................................................. 17
Intrapartum management .............................................................................................. 21
Postpartum Management ............................................................................................... 21
MANAGEMENT OF ECLAMPSIA ........................................................................................... 22
SAMPLE HISTORY ..............................................................................................................................................23
CHAPTER 2 ................................................................................................................................ 28
ANTEPARTUM HEMORRHAGE (APH)............................................................................... 28
CLASSES OF HEMORRHAGE AND THE PHYSIOLOGIC RESPONSE .........................................................28
CAUSES OF THIRD-TRIMESTER BLEEDING..................................................................................................29
PLACENTAL ABRUPTION .................................................................................................................................30
PLACENTA PREVIA ............................................................................................................................................36
MORBIDLY ADHERENT PLACENTAS .............................................................................................................41
VASA PREVIA ......................................................................................................................................................44
SAMPLE HISTORY ..............................................................................................................................................46
CHAPTER 3 ................................................................................................................................ 49
POSTPARTUM HEMORRHAGE (PPH) ................................................................................ 49
DEFINITION AND INCIDENCE .........................................................................................................................49
NORMAL PHYSIOLOGIC MECHANISMS PREVENTING PPH ....................................................................50
CLASSIFICATION ................................................................................................................................................50
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 MEDSTAR CLINICAL GUIDE AND SYNOPSIS VII

Early PPH.............................................................................................................................. 50
Late PPH............................................................................................................................... 55
CLINICAL FEATURES OF PPH...........................................................................................................................56
COMPLICATION .................................................................................................................................................58
MANAGEMENT..................................................................................................................................................58
PREVENTION ......................................................................................................................................................61
CHAPTER 4 ................................................................................................................................ 63
PREMATURE RUPTURE OF MEMBRANE (PROM) AND PRETERM LABOR ........... 63
DEFINATIONS .....................................................................................................................................................63
PRETERM LABOR/BIRTH .................................................................................................................................63
ETIOPATHOGENESIS AND RISK FACTORS ............................................................................. 64
DIAGNOSIS: .......................................................................................................................... 66
PREMATURE RUPTURE OF MEMBRANE (PROM) .....................................................................................67
ETIOPATHOGENESIS AND RISK FACTORS ............................................................................. 68
COMPLICATIONS .................................................................................................................. 69
DIAGNOSIS AND INVESTIGATIONS....................................................................................... 69
DIFFERENTIAL DIAGNOSIS ................................................................................................... 71
MANAGEMENT .................................................................................................................... 72
Generally indications for pregnancy termination in PROM ........................................... 73
Components of conservative management: .................................................................. 74
SAMPLE HISTORY ..............................................................................................................................................75
CHAPTER 5 ................................................................................................................................ 79
MULTIFETAL GESTATION ................................................................................................... 79
DEFINITION AND INCIDENCE .........................................................................................................................79
TWIN PREGNANCY............................................................................................................................................80
Monozygotic twins............................................................................................................... 80
Genesis of Monozygotic twins ........................................................................................ 81
Zygosity and Chorionicity in MZ twins ............................................................................ 81
Dizygotic twins ..................................................................................................................... 84
ZYGOSITY AND CHORIONICITY IN DZ TWINS .............................................................................................85
SEX RATIOS IN MG ............................................................................................................................................86
PHYSIOLOGICAL CHANGES IN TWIN ............................................................................................................86
DIAGNOSIS OF MG............................................................................................................................................86
COMPLICATIONS OF MULTIFETAL PREGNANCY ......................................................................................88
Maternal complication ........................................................................................................ 88

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 MEDSTAR CLINICAL GUIDE AND SYNOPSIS VIII

Fetal complication ............................................................................................................... 88

Unique complications of MZ twins ...................................................................................... 89
MANAGEMENT IN MG.....................................................................................................................................95
1. Antenatal management................................................................................................... 95
2. Management during labor .............................................................................................. 95
CHAPTER 6 ................................................................................................................................ 97
MALPRESENTATION.............................................................................................................. 97
OVERVIEW ..........................................................................................................................................................97
BREECH PRESENTATION .................................................................................................................................99
INCIDENCE ........................................................................................................................... 99
CLASSIFICATION ................................................................................................................... 99
ETIOLOGY AND RISK FACTORS ........................................................................................... 100
DIAGNOSIS ......................................................................................................................... 101
COMPLICATIONS OF BREECH DELIVERY............................................................................. 103
MANAGEMENT .................................................................................................................. 103
FACE PRESENTATION .....................................................................................................................................106
BROW PRESENTATION ..................................................................................................................................109
COMPOUND PRESENTATION ......................................................................................................................111
SHOULDER PRESENTATION (TRANSVERSE LIE) ......................................................................................113
CHAPTER 7 .............................................................................................................................. 119
ABNORMAL UTERINE BLEEDING (AUB) ....................................................................... 119
DEFINITION AND TERMINOLOGIES ............................................................................................................119
INCIDENCE AND ETIOLOGY ..........................................................................................................................121
Age related distribution of Etiologies of AUB .................................................................... 121
COMMON DIFFERENTIAL DIAGNOSIS .......................................................................................................124
Ectopic pregnancy (EP) ...................................................................................................... 124
Adenomyosis ...................................................................................................................... 125
Endometrial polyps ............................................................................................................ 126
Endometrial hyperplasia .................................................................................................... 127
Endometrial cancer ............................................................................................................ 128
Chronic endometritis (infection) ........................................................................................ 130
RISK FACTORS ..................................................................................................................................................130
Coagulopathy ..................................................................................................................... 130
Hepatic and chronic renal failure ...................................................................................... 131
Thyroid disease .................................................................................................................. 131

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 MEDSTAR CLINICAL GUIDE AND SYNOPSIS IX

Leech infestation ................................................................................................................ 132

PATIENT EVALUATION ...................................................................................................................................133
HISTORY ............................................................................................................................. 133
PHYSICAL EXAMINATION ................................................................................................... 134
INVESTIGATION .................................................................................................................. 135
CHAPTER 8 .............................................................................................................................. 137
ABDOMINOPELVIC MASS (APM) ...................................................................................... 137
PATIENT APPROACH ......................................................................................................................................137
HISTORY: ............................................................................................................................ 137
PHYSICAL EXAMINATION ................................................................................................... 138
INVESTIGATIONS (IX’s) ....................................................................................................... 141
MANAGEMENT................................................................................................................................................142
DIFFERENTIAL DIAGNOSIS OF APM ...........................................................................................................142
1. Functional ovarian cysts ................................................................................................ 145
2. Ectopic pregnancy (EP) .................................................................................................. 146
3. PID related TOA & Hydrosalpinx .................................................................................... 147
4. Adenomyosis .................................................................................................................. 148
5. Hematometra/pyometra ............................................................................................... 149
6. Para ovarian/tubal cysts ................................................................................................ 150
CHAPTER 9 .............................................................................................................................. 152
LEIOMYOMAS ........................................................................................................................ 152
DEFINITION AND EPIDEMIOLOGY ..............................................................................................................152
FACTORS ASSOCIATED WITH LEIOMYOMA .............................................................................................153
Factors that increase incidences ........................................................................................ 153
Factors that decrease incidences ....................................................................................... 154
PATHOPHYSIOLOGY .......................................................................................................................................154
CLASSIFICATION ..............................................................................................................................................155
SECONDARY CHANGES IN MYOMA ...........................................................................................................156
CLINICAL FEATURES .......................................................................................................................................158
COMPLICATIONS .............................................................................................................................................161
MYOMAS AND PREGNANCY ........................................................................................................................162
DIFFERENTIAL DIAGNOSIS ............................................................................................................................163
MANAGEMENT................................................................................................................................................163
Drug therapy: ..................................................................................................................... 164
Surgical Management ....................................................................................................... 167

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 MEDSTAR CLINICAL GUIDE AND SYNOPSIS X

SAMPLE HISTORY ............................................................................................................................................169

CHAPTER 10 ............................................................................................................................ 173
OVARIAN TUMORS ............................................................................................................... 173
EPIDEMIOLOGY ...............................................................................................................................................173
ETIOLOGY AND RISK FACTORS ....................................................................................................................173
RISK FACTORS .................................................................................................................... 173
PROTECTIVE FACTORS ....................................................................................................... 175
CLASSIFICATION OF OVARIAN TUMORS(OVARIAN MASSES) .............................................................175
BENIGN OVARIAN MASSES ..........................................................................................................................176
CLINICAL FEATURE OF BENIGN TUMORS .................................................................................................177
BORDERLINE OVARIAN MASSES ........................................................................................ 178
MALIGNANT OVARIAN MASSES ......................................................................................... 179
EPITHELIAL OVARIAN CANCER (EOC) ........................................................................................................179
PATHOGENESIS .................................................................................................................. 180
HISTOPATHOLOGY AND PATTERN OF SPREAD .................................................................. 180
CLINICAL MANIFESTATIONS OF EOC .................................................................................. 181
DIAGNOSIS ......................................................................................................................... 183
DIFFERENTIAL DIAGNOSIS FOR EOC .................................................................................. 184
STAGING OF EOC................................................................................................................ 185
STAGES...............................................................................................................................................................185
MANAGEMENT PRINCIPLE ................................................................................................. 187
Prognostic Factors......................................................................................................... 188
MALIGNANT OVARIAN GERMCELL TUMORS ..........................................................................................189
HISTOPATHOLOGY .................................................................................................... 190
DIAGNOSIS................................................................................................................ 190
MANAGEMENT ......................................................................................................... 192
OVARIAN SEX CORD-STROMAL TUMORS (SCST)....................................................................................192
EPIDEMIOLOGY......................................................................................................... 192
CLASSIFICATION........................................................................................................ 193
DIAGNOSIS................................................................................................................ 194
MANAGEMENT ......................................................................................................... 195
OVARIAN CANCER DURING PREGNANCY .................................................................................................195
SAMPLE HISTORY ............................................................................................................................................197

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 MEDSTAR CLINICAL GUIDE AND SYNOPSIS XI

CHAPTER 11 ............................................................................................................................ 199

GESTATIONAL TROPHOBLASTIC DISEASE ................................................................. 199
EPIDEMIOLOGY AND RISK FACTORS ..........................................................................................................199
CLASSIFICATION ..............................................................................................................................................201
PATHOGENESIS ...............................................................................................................................................201
CLINICAL FEATURES .......................................................................................................................................203
NATURAL HISTORY OF GTD ..........................................................................................................................205
COMPLICATIONS .............................................................................................................................................205
INVESTIGATION ...............................................................................................................................................206
TREATMENT OF BENIGN GTD ......................................................................................................................209
Follow-up ........................................................................................................................... 210
GESTATIONAL TROPHOBLASTIC NEOPLASIA ..........................................................................................211
NON METASTATIC DISEASE................................................................................................ 211
PLACENTAL-SITE TROPHOBLASTIC TUMOR ....................................................................... 212
METASTATIC DISEASE ........................................................................................................ 212
DIAGNOSTIC EVALUATION ................................................................................................. 214
STAGING ............................................................................................................................................................215
MANAGEMENT .................................................................................................................. 216
SAMPLE HISTORY ............................................................................................................................................219
CHAPTER 12 ............................................................................................................................ 221
CERVICAL NEOPLASIA ....................................................................................................... 221
CERVICAL INTRAEPITHELIAL NEOPLASM..................................................................................................221
Classification of CIN ........................................................................................................... 221
Risk factors of CIN .............................................................................................................. 221
CIN and Human papilloma Virus (HPV) ............................................................................. 222
Diagnosis............................................................................................................................ 223
Screening for CIN & Cervical Cancer .................................................................................. 223
prevention .......................................................................................................................... 227
Outcome Of CIN ................................................................................................................. 228
CERVICAL CANCER ..........................................................................................................................................229
Risk factors......................................................................................................................... 229
Tumor genesis .................................................................................................................... 230
Patterns of spread ............................................................................................................. 231
Histologic types .................................................................................................................. 232
Clinical manifestation ........................................................................................................ 232
Investigations..................................................................................................................... 233
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Staging ............................................................................................................................... 234

General Treatment for Primary Invasive Cervical Carcinoma ........................................... 236
SAMPLE HISTORY ............................................................................................................................................237
CHAPTER 13 ............................................................................................................................ 240
ABORTION ............................................................................................................................... 240
DEFINITION AND TERMINOLOGY ...............................................................................................................240
INCIDENCE ........................................................................................................................................................240
CLASSIFICATION ..............................................................................................................................................241
SPONTANEOUS FIRST TRIMESTER ABORTION ............................................................................... 241
Etiologies And Risk Factors ................................................................................................ 241
SPONTANEOUS MIDTRIMESTER ABORTION ................................................................................. 247
INDUCED ABORTION......................................................................................................................................248
APPROACH ........................................................................................................................................................249
HISTORY ............................................................................................................................. 249
PHYSICAL EXAMINATION ................................................................................................... 250
INVESTIGATIONS ................................................................................................................ 250
MANAGEMENT................................................................................................................................................251
CHAPTER 14 ............................................................................................................................ 253
PELVIC ORGAN PROLAPSE ............................................................................................... 253
PATHOPHYSIOLOGY .......................................................................................................................................253
RISK FACTORS ..................................................................................................................................................255
DESCRIPTION AND CLASSIFICATION ..........................................................................................................256
POP GRADING/QUANTIFICATION SYSTEM ..............................................................................................257
POP-Q system .................................................................................................................... 257
baden-Walker Halfway System ......................................................................................... 259
CLINICAL MANIFESTATIONS OF POP .........................................................................................................259
SYMPTOMS ........................................................................................................................ 259
PHYSICAL EXAMINATION ................................................................................................... 260
MANAGEMENT PRINCIPLE ...........................................................................................................................261
SAMPLE HISTORY ............................................................................................................................................263
CHAPTER 15 ............................................................................................................................ 266
PELVIC PAIN ........................................................................................................................... 266
HISTORY.............................................................................................................................................................266
CLASSIFICATION ..............................................................................................................................................268

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 MEDSTAR CLINICAL GUIDE AND SYNOPSIS XIII

ACUTE PELVIC PAIN ........................................................................................................................................269

DIFFERENTIAL DIAGNOSIS OF ACUTE PELVIC PAIN ........................................................... 270
Ectopic pregnancy ......................................................................................................... 271
Torsion of Adnexa ......................................................................................................... 272
Leaking or Ruptured Ovarian Cyst ................................................................................ 272
Uterine Leiomyomas ..................................................................................................... 273
Appendicitis .................................................................................................................. 273
Acute Diverticulitis ........................................................................................................ 274
Intestinal Obstruction ................................................................................................... 274
Ureteral colic ................................................................................................................. 275
UTI ................................................................................................................................. 275
PELVIC INFLAMMATORY DISEASE (PID) ............................................................................. 276
Etiology and risk factors ................................................................................................ 276
Classification of PID....................................................................................................... 277
PHYSICAL EXAMINATION FOR ACUTE PELVIC PAIN...............................................................................279
INVESTIGATION ...............................................................................................................................................280
CYCLIC PELVIC PAIN ........................................................................................................................................281
CHRONIC PELVIC PAIN ...................................................................................................................................282
ENDOMETRIOSIS ................................................................................................................ 285
ADHESIONS ........................................................................................................................ 290
CHAPTER 16 ............................................................................................................................ 291
GENITOURINARY FISTULA (GUF) ................................................................................... 291
INCIDENCE ........................................................................................................................................................291
CLASSIFICATION ..............................................................................................................................................291
ETIOLOGY AND RISK FACTOR.......................................................................................................................294
SYMPTOMS.......................................................................................................................................................296
DIAGNOSIS ........................................................................................................................................................296
INVESTIGATIONS.............................................................................................................................................296
TREATMENT .....................................................................................................................................................297
SAMPLE HISTORY ............................................................................................................................................299
REFERENCE ............................................................................................................................ 300
APPENDIX ................................................................................................................................ 301
PREECLAMPSIA CHART ..................................................................................................................................301
APH CHART .......................................................................................................................................................302
PROM CHART ...................................................................................................................................................303

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 MEDSTAR CLINICAL GUIDE AND SYNOPSIS XV

SECTION ONE
OBSTETRICS

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 MEDSTAR CLINICAL GUIDE AND SYNOPSIS 1

CHAPTER 1

HYPERTENSIVE DISORDERS OF
PREGNANCY (HDP)
HDP are one of the most common obstetric complications, affecting
5-10% of all pregnancy.
 Along with hemorrhage and infection it forms the deadly triad
during pregnancy as a cause of maternal mortality.

DEFINITION AND CLASSIFICATION

Hypertension (HTN) is diagnosed empirically when appropriately#
taken blood pressure exceeds 140mmHg systolic or 90mmmHg of
diastolic.
 The blood pressure must be observed at least on two
occasions 4hrs apart but not more than 7days apart.
 #appropriate BP measurement include,
1) Avoiding smoking, caffeine and exercise for 30min prior to
measurement
2) Patient should sit quietly for 5min (10min, old JUSH
guideline) in a chair with feet on the floor.
3) Measurement is taken from right arm at the level of the heart
4) Using appropriate BP cuff size
 Width of the inflatable bladder of the cuff should be
about 40% of the upper arm circumference (about 12-
14cm in the average adult)
 Length of the inflatable bladder should be about 80%
of the upper arm circumference(almost long enough to
encircle the arm)

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 The standard cuff is 12X23cm, appropriate for arm

circumference up to 28cm
5) The 5th Korotkoff sound is used for diagnosis
 Generally, avoid factors that will falsely or temporarily
increase the BP, like:-
 smaller cuff size
 a loose cuff or a bladder that balloons outside the cuff
 taking stimulants within the 30min prior to
measurement
 stressful environment
 sitting with legs crossed
 On the contrary larger cuff size and taking antihypertensive
medications will decreases BP measurement.
 Read more on the steps and techniques of BP measurement on
Bates Guide to Physical Examination 12ed.

NB, we don’t necessarily need both the systolic and diastolic BP to be elevated
to diagnose HTN; elevation of one of them is enough for diagnosis

Severe HTN is when sustained elevation of SBP of ≥160mmHg or

DBP of ≥ 110mmHg is observed on two occasions for at least 4hrs
apart but not more than 7days
Proteinuria: Can be diagnosed before or during pregnancy, and it
is defined as:
 ≥0.3g protein in 24hr urine collection, or
 Protein: creatinine(P/C) ratio of ≥0.3, or
 A dipstick measurement of ≥ 1+ on two occasions
The concentration of urinary protein is influenced by contamination
with vaginal secretions, blood, bacteria, or amniotic fluid. It also
varies with urine specific gravity and pH, exercise, and posture.
 It usually appears after HTN, but it may also appear before
HTN too

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Edema: Is defined as an excessive weight gain of >1.8kg in 1wk in

the second or third trimester. It may be the first sign of the
potential development of PE
According to ACOG (2013) there are four types of hypertensive
disorders during pregnancy
1. Gestational HTN (GH)
2. Preeclampsia eclampsia syndrome (PE-E syndrome)
3. Chronic essential HTN
4. Preeclampsia-superimposed on chronic HTN

Delta HTN
Normally during the first and second trimester of pregnancy the
blood pressure declines to a nadir at 24-26wks of gestations and
then rises afterward (mainly due to the decreased systemic vascular
resistance, which is one of the physiologic changes during
pregnancy).
Some pregnant women may have more than usual increment in BP
especially after 32wks of gestation who by term has substantially
high BP, but still under 140/90mmHg. The term delta HTN is used
to describe this acute rise in BP
Some of these women will go on to have obvious PE, eclampsia or
HEELP syndrome.

GESTATIONAL HTN
 Is an elevated BP without proteinuria or signs/symptoms of
preeclampsia related end organ dysfunction that is diagnosed
for the first time after 20 weeks of pregnancy and resolves by
12 weeks postpartum
 It is the most frequent cause of HTN during pregnancy

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 The incidence ranges from 6-29% in nulliparous women and

from 2-4% in multiparous, the incidence increases in multiple
gestation.
Almost half of these women develop PE syndrome. The likelihood of
progression to PE depends on gestational age (GA) at the time of
diagnosis, with higher rates if the onset of HTN is before 35wks of
gestation. Fortunately, most cases of GH develop at or beyond
37wks of gestation.
GH is divided in to two: Mild GH and Severe GH
 Criteria for the diagnosis of mild GH
 Systolic blood pressure >140 mm Hg but <160 mm Hg and
diastolic blood pressure >90 mm Hg but <110 mm Hg
 Proteinuria of <300 mg per 24hr collection
 Platelet count of >100,000/mm3
 Normal liver enzymes
 Absent maternal symptoms
 Absent intrauterine growth restriction and oligohydramnios
by ultrasound
 Criteria for the diagnosis of severe GH (see gabbe 7th edition,
but there is some confusion about whether sever GH is
separate thing or it is just PE)
The overall pregnancy outcome of GH depends on GA at time of
diagnosis and the type of GH.
 Most cases of mild GH which develop after 37wks of gestation
usually have similar outcome as normotensive pregnancy,
other than higher rate of induction of labor.
 Women with severe GH has increased risk of maternal and
perinatal morbidities, (greater than those with mild PE),
including placental abruption, preterm delivery, and delivery
of small for gestational age baby
Some reclassify GH as transient hypertension, if evidence of PE
doesn’t develop and the BP returns to normal by 12 weeks
postpartum.
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 MEDSTAR CLINICAL GUIDE AND SYNOPSIS 5

PREECLAMPSIA (PE)
PE refers to the new onset of hypertension and proteinuria or
hypertension and significant end-organ dysfunction with or without
proteinuria after 20 weeks of gestation in a previously normotensive
woman.
Incidence:
 ranges from 2-7% in otherwise healthy nulliparous women
which is generally mild, with onset near term or during labor
(in 75% of cases)
NB, on Williams Obstetrics 25th Ed, the incidence is slightly
different, 3-10% for nulliparous and 1.4 -4% for multiparous
women
PE is categorized as, PE with severity features and PE without-
severity features
Criteria for Preeclampsia with Severity Features
Preeclampsia, with severe features, is defined when either disorder
is present in association with any of the following abnormalities:
 SBP ≥160 mm Hg or DBP ≥110 mm Hg on two occasions at
least 4 hours apart while the patient is on bed rest or once if
the patient has received prior antihypertensive therapy.
 New-onset persistent cerebral symptoms: headaches or
visual disturbances
 Impaired liver function as indicated by abnormally elevated
liver enzymes (at least twice the upper limit of normal [ULN]);
severe, persistent right upper quadrant or epigastric pain that
is unresponsive to medications and not accounted for by an
alternative diagnosis; or both
 Pulmonary edema (often develop in postpartum)
 Thrombocytopenia (platelet count <100,000/μl)

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 MEDSTAR CLINICAL GUIDE AND SYNOPSIS 6

 Progressive renal insufficiency (serum creatinine >1.1

mg/dl); some guidelines also include doubling in the patient’s
base line creatinine in absence of other renal diseases.
NB, the amount of proteinuria (≥5gm in a 24hr urine specimen or ≥3+
on dipstick), oliguria, and presence of intrauterine growth restriction
(IUGR) or fetal growth restriction (FGR) by ultrasound have been
removed as criteria for the diagnosis of severe disease.
Even though HTN is considered to be the hallmark of PE, some
patient with PE may present with signs of PE without HTN, - and it
is referred to as atypical PE.
 The criteria for atypical preeclampsia include gestational
proteinuria or FGR plus one or more of the following:
 Severity features of preeclampsia without hypertension:
hemolysis, thrombocytopenia, elevated liver enzymes,
 Early signs and symptoms of PE-E syndrome earlier than
20 weeks, (seen in patient with molar pregnancy,
hydropic degeneration of chorionic villi and
antiphospholipid antibody (APA) syndrome and
 Late postpartum PE-E syndrome (>48 hours postpartum
but less than six weeks after delivery).

RISK FACTORS OF PE
 Nulliparity, (limited sperm exposure)
 Age <20yrs or >40yrs
 Race, (higher in the Black population because of genetic
predisposition)
 Pregnancy with the aid of artificial reproductive
technology
 Use ART increase risk because:
o Increase chance that the women is >40yrs,
nulliparous or obese with PCOS
o Increase possibility of multiple gestation,
o It pregnancy with donated gametes or embryos
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 Multifetal gestation (increase risk to 13%)

 Obesity/gestational diabetes mellitus (BMI ≥35kg/m2
increase risk to 13.3%)
 PE in previous pregnancy
 In women with severe PE in previous pregnancy, around
21% will have severe PE in the subsequent pregnancy.
 The earlier PE is diagnosed in the index pregnancy, the
greater the likelihood of recurrence.
 Preexisting medical-genetic conditions
 Chronic hypertension
 Renal disease
 Type 1 DM
 Antiphospholipid antibody syndrome
 Factor V Leiden mutation
 Interpregnancy interval >7 years
 Family history of preeclampsia
 Woman born small for gestational age
 Poor outcome in previous pregnancy
 Fetal growth restriction (FGR), placental abruption (PA),
fetal death
 Paternal factors (men who fathered one preeclamptic
pregnancy were nearly twice as likely to father a preeclamptic
pregnancy with a different woman)
 Smoking, unlike its effect in many obstetric and gynecologic
abnormalities, carry a reduced risk for hypertension during
pregnancy, because it up-regulates placental adrenomedullin
expression which regulates volume homeostasis

ETIOPATHOGENESIS
 The etiology of PE remains unknown, but different theories
have tried to explain it.

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 Any satisfactory theory concerning the origins of preeclampsia

must account for the observation that gestational hypertensive
disorders are more likely to develop in women with the
following characteristics:-
 Are exposed to chorionic villi for the first time
 Are exposed to a superabundance of chorionic villi, as with
twins or hydatidiform mole
 Have preexisting conditions associated with endothelial
cell activation or inflammation, such as diabetes, obesity,
cardiovascular or renal disease, immunological disorders,
or hereditary influences
 Are genetically predisposed to hypertension developing
during pregnancy.

A fetus is not a requisite for preeclampsia to develop. And, although

chorionic villi are essential, they don’t need to be intrauterine.
Regardless of the precipitating etiologies, the cascade of events
leading to the PE syndrome is characterized by abnormalities that
result in vascular endothelial damage with resultant vasospasm,
transduction of plasma and ischemic & thrombotic sequelae.
The mechanisms that are currently considered important in
explaining the pathogenesis of PE include:
 Placental implantation with abnormal trophoblastic invasion
of uterine vessels
 Immunological maladaptive tolerance between maternal,
paternal (placental), and fetal tissues
 Maternal maladaptation to cardiovascular or inflammatory
changes of normal pregnancy
 Genetic factors including inherited predisposing genes and
epigenetic influences.

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Abnormal trophoblastic invasion

During normal implantation the uteroplacental (UP) arteries are
formed by the action of migratory interstitial and endovascular
trophoblasts in to the walls of the spiral arterioles, this transform
the UP arteries in to low resistance, low pressure and high flow
system.
These trophoblast induced changes extend all the way from
intervilious space to the origin of spiral arteries (to inner 3rd of
myometrium). These changes are effected in two stages:
 1st wave involve decidua segment of the arteries and occur in
1st trimester
 2nd wave involving the myometrium segment and occur in 2nd
trimester (after 16th week)
In pregnancies complicated with PE these changes are limited to the
decidua segment, leaving the myometrial segments as high pressure
and low flow system, resulting in limited UP blood flow(Placental
ischemia and FGR).
The pathogenesis of PE is divided into two artificial stages:-
 Asymptomatic Placental Stage
 Caused by faulty endovascular trophoblastic remodeling
 Symptomatic Maternal Stage
 Causes by the changes in stage one
 Is susceptible to modification by preexisting maternal
conditions that are manifested by endothelial cell
activation or inflammation, such as cardiovascular or
renal disease, DM, immunologic disorders… hence they
are risk factors!
The following diagram shows a model for Pathogenesis of PE

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PATHOPHYSIOLOGIC CHANGES IN PE
Hematological changes

 Thrombocytopenia
NB, once it developed thrombocytopenia usually continues to
worsen, so delivery is recommended
 Hemolysis, (Microangiopathic Hemolysis)
 HEELP syndrome

Renal changes

 Reduced renal perfusion and GFR (up to 25% below normal

pregnancy)
 Oliguria,
NB, Intensive IV fluid therapy is not indicated as a treatment
for preeclamptic women with oliguria, unless urine output is
diminished from hemorrhage or fluid loss from vomiting or
fever

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 Proteinuria, may develop late, for example, approximately 10-

15% of HEELP syndrome and 17% of patient with eclampsia
don’t have proteinuria at the time of presentation.
 Increased urine sodium level
 Increased serum creatinine and uric acid level
 AKI in patients with comorbid hemorrhage with hypovolemia
and hypotension (for example, in patient with severe placenta
abruption)
NB, PE is the most common cause of AKI in pregnancy

HEELP syndrome

Criteria to establish the diagnosis of HEELP syndrome

 Hemolysis (at least two of the following)

 Peripheral blood smear showing schistocytes, or burr
cells
 Serum Bilirubin ≥1.2mg/dl
 Low serum haptoglobin
 Severe anemia (Microangiopathic Hemolytic Anemia) unrelated
to blood loss
 Elevated liver enzymes
 ALT/AST at least twice the ULN (upper limits of the
normal)
 LDH >600U/L (>2x the ULN)
 Low platelets

Based on the platelet count HEELP syndrome is classified in to 3

classes

 Class I, platelet count < 50,000/mm3

 Class II,,,,,,,,,,,,,,,,,,,,,,,, 50,000 -100,000/mm3
 Class III,,,,,,,,,,,,,,,,,,,,,,, 100, 000-150,000/mm3
(See the rest of the pathophysiological changes on Williams 25 th,,
only few are mentioned here)
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CLINICAL MANIFESTATIONS OF PE
The clinical findings of PE can manifest as either a maternal
syndrome or a fetal syndrome
Maternal syndrome
 The maternal syndrome of PE represents a clinical spectrum
with major differences between near term PE without
demonstrable fetal effects and PE that is associated with low
birth weight and preterm delivery. Maternal manifestations
include:
 Symptoms
 Headache (severe, global type, which is unresponsive to
NSAIDs)
 Blurring of vision, or less commonly double vision and
blindness (from retinal detachment)
 Right upper quadrant or Epigastric pain
 Swelling of the face or vulva
 Vaginal bleeding
 Nausea/vomiting
 Difficulty of breathing
 Signs
 Elevated BP, (NB, BP could be normal and patient still can
have PE)
 Facial (generalized) edema
 Signs of pleural effusion and ascites
 RUQ tenderness
 Mental status change (confusion to coma, result of cerebral
edema)
 Hyperreflexia
 Laboratory findings
 Proteinuria
 MAHA, Thrombocytopenia
 Elevated serum AST/ALT, LDH, creatinine and bilirubin level
 Findings of DIC
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Fetal manifestations include: - Oligohydramnios, FGR, Abruption,

Vascular stillbirth and Preterm delivery

PREDICTION AND PREVENTION OF PE

 ACOG recommends the use of only risk factors for identifying
women considered to be at risk for PE and None of the
interventions suggested in the book (Gabby 7th ed) offer
significant benefit in preventing PE

ECLAMPSIA
 Eclampsia is defined as the development of convulsions
(generalized tonic-clonic) or unexplained coma during
pregnancy or postpartum in patients with signs and symptoms
of PE.
 In the western world, the reported incidence of eclampsia
ranges from 1 in 2000 to 1 in 3448 pregnancies.
 Eclampsia can develop antepartum, intrapartum (most of the
time) or postpartum (in around 10% of cases, mostly within
48hr of delivery)
 Late postpartum eclampsia is defined as eclampsia that occurs
after 48 hours but before 4 weeks of delivery.
 Eclampsia that occurs before the 20th week of gestation is
generally associated with molar or hydropic degeneration of
the placenta with or without a coexistent fetus
Diagnosis
 The diagnosis of eclampsia is secure in the presence of
generalized edema, hypertension, proteinuria, and
convulsions.

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 At least one of the following occur in 59-75% of cases

 Persistent occipital or frontal headache
 Blurring of vision (blindness is seen in up to 10-15% of
eclamptic patients, and it is mainly due to occipital lobe
edema)
 Photophobia
 Epigastric or right upper quadrant pain
 Altered mental status
 CT scan or MRI of the brain is not necessary for the diagnosis
and management of eclampsia. However, it is indicated for
patients with:
 Focal neurologic deficit or prolonged coma
 Atypical presentations
 Onset <20wk of gestation or >48hr postpartum
 Eclampsia refractory to adequate therapy
 Differential diagnosis for eclampsia (see Gabby 7th Ed, p692)
Maternal and fetal outcomes of eclampsia
Maternal (with incidence): - placental abruption (PA, 7-10%), DIC
(7-10%), Pulmonary edema (3-5%), AKI (5-9%) Aspiration
pneumonia (2-3%) and Cardiopulmonary arrest (2-5%)
Feta or perinatal: - Prematurity, PA, Severe FGR, Preterm delivery,
is about 50% and about 25% occur before 32wks of gestation
Prevention of eclampsia
Can be:-
 Primary: by preventing the development and /or progression
of PE,
 Secondary: by using pharmacologic agents that prevent
convulsions in women with established PE.
 Tertiary: by preventing subsequent convulsions in women
with established eclampsia

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Some of the recommended preventive therapies include:

 close monitoring (in-hospital or outpatient),
 use of antihypertensive therapy to keep maternal BP below a
certain level (< severe range or to normal values),
 timely delivery, and prophylactic use of magnesium sulfate
during labor and immediately postpartum in those considered
to have PE
 Prophylactic MgSo4 is recommended only for women who are
hospitalized with the established diagnosis of PE. MgSo4 is
associated with a significantly lower rate of recurrent seizures
and a lower rate of maternal death than that observed with
other agents, like diazepam.
NB, about 31-87% of eclampsia is considered unpreventable

CHRONIC HYPERTENSION IN PREGNANCY AND

SUPERIMPOSED PE
Chronic HTN: Is defined as an elevated BP that is present prior to
conception or is diagnosed before 20th week of gestation, or HTN
that persist for more than 12wks postpartum.
 The frequency of chronic hypertension in pregnancy is
estimated at 1% to 5%.
Women with chronic hypertension are at increased risk for
superimposed PE.

Maternal and Perinatal Risks

Maternal: increased risk for the development of superimposed PE,

PA (0.7% -2.7% in those with mild HTN and 5% -10% in those with
severe or high-risk HTN), and FGR
Perinatal: perinatal mortality (3-4x greater), premature delivery and
a growth restricted infant

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Superimposed PE

The overall rate of superimposed PE is 25% (14% to 28% in mild

HTN and 50% to 79% in severe HTN), the rate is not affected by
maternal age, race, or presence of proteinuria early in pregnancy.

Recommended criteria to diagnose preeclampsia in women with

preexisting medical conditions
Conditions Criteria
Hypertension only Proteinuria of ≥300 mg per
24hr or thrombocytopenia.
Hypertension plus proteinuria Worsening severe
(renal disease or class F hypertension plus proteinuria
diabetes) and either
 new onset of symptoms
 thrombocytopenia, or
 elevated liver enzymes

MANAGEMENT OF PE-E SYNDROME

Management of PE
Management of PE depends on the severity of PE and the GA. It can
be an expectant and definitive management.

NB, termination of pregnancy is the only cure for PE

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Antepartum management
Mild preeclampsia
Managed as outpatient
 Expectant management
o follow up
 Urine protein every other day
 BP measurement daily
 Weight measurement every other day
 Fetal movement count daily
 ANC follow up twice weekly
 CBC and liver enzymes during each ANC visit
 NST and serial fetal growth and amniotic fluid
evaluation
o The patient should be reminded to report any sign of
severity if developed during the expectant management
period.
NB, if expectant management is undertaken after 37 weeks, the
patient should understand that the only known benefit is a
possible reduction in the rate of cesarean birth.

 Indication for delivery (definitive mgt)

 GA is ≥40wks or ≤ 28wks
 37–40 weeks, if cervical status is favorable, induction is
initiated. If the cervical status is unfavorable, pre-
induction cervical ripening agents are used as needed
 Abnormal antepartum testing
 If evidence of worsening preeclampsia is seen
 Prophylactic intrapartum magnesium sulfate is indicated to
prevent convulsions.

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Severe preeclampsia
Severe preeclampsia mandates hospitalization.
 Expectant management
 Is given until development of maternal or fetal indications
for delivery or until achievement of fetal lung maturity or 34
weeks' gestation.
 Acute BP control and maintenance of BP below severe level
 IV MgSO4 is begun to prevent convulsions for the first 24-48
hours, anticonvulsant should be discontinued if no
indications for delivery develop
 Corticosteroids to accelerate fetal lung maturity
(Dexamethasone 6mg IM BID four doses) and delivery after
48 hours
 Follow up with preeclampsia chart
 Laboratory evaluation includes a platelet count, liver
enzymes, and serum creatinine.
 Fetal evaluation includes fetal heart monitoring, a BPP, and
fetal growth assessment

Antihypertensive therapy
The aim of this therapy is to keep the SBP between 140 &
160mmHg and DBP between 90 & 110mmHg.

Acute blood pressure control

 Hydralazine (peripheral vasodilator) 5–10 mg IV. The
onset of action is 10–20 minutes, and the dose can be
repeated in 20–30 minutes if necessary (maximum of 60
mg IV or 300 mg PO in 24 hours)
 Labetalol (Beta blocker) 5–20 mg by slow IV push. The
dose can be repeated in 10–20 minutes
 Nifedipine (calcium channel blocker) 5–10 mg orally. The
dose can be repeated in 20–30 minutes, as needed

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Maintenance antihypertensive therapy

 Methyldopa up to 4gm/day PO in divided doses
depending on the response
 Nifedipine 10-20mg PO every 6hrs

We normally do not use diuretics as an antihypertensive

medication in PE. Use of potent loop diuretics can further
compromise placental perfusion because it result in
redistribution of the intravascular volume, which most often is
already reduced in severe preeclampsia. Therefore, before
delivery, diuretics are not used to lower blood pressure.
NB, we use antepartum furosemide or similar drugs solely to
treat pulmonary edema.

Neuroprophylaxis—Prevention of Seizures

 Magnesium sulfate (MgSO4)

 Is the most preferred and effective anticonvulsant
prophylaxis
 Its neuroprotective effect is proposed to be through the
following mechanisms:
 reduced presynaptic release of the neurotransmitter
glutamate
 blockade of glutamatergic N-methyl D-aspartate
(NMDA) receptors
 potentiation of adenosine action
 improved calcium buffering by mitochondria, and
 blockage of calcium entry via voltage-gated channels
 Dosage
 IV loading dose of 4gm over 20–60 minutes and
10gm IM half on each buttock, followed by a
maintenance dose of 3gm/hour IV or 5gm IM in
alternate buttocks every 4 hours. If convulsion
occurs after MgSO4 is started, give 2gm MgSO4 IV.
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 Toxicity
 Is dependent on the plasma magnesium level
o Loss of deep tendon reflexes occurs at 8 to 10
mEq/L
o Respiratory paralysis at 10 to 15 mEq/L
o Cardiac arrest at 20 to 25 mEq/L
 In the event of these adverse effects MgSO4 should
be discontinued and Calcium gluconate (10 mL of
10% solution) should be given.
 Urine output is monitored, and the magnesium dose
is adjusted accordingly to prevent hypermagnesemia
(UOP <30 ml/hour → reduce MgSO4 dose to half).
 Other than preventing seizure, MgSO4 also has, (1)
inhibitory effect in uterine contraction(at higher plasma
concentration), (2) protective effect against the
development of cerebral palsy in very-low-birth weight
newborns, and (3) relieving effect on headache and
blindness

 Contraindications
o Hypermagnesemia
o Hypocalcaemia
o Skeletal muscle disorders, progressive muscle
weakness with carcinoma
o Severe renal impairment
o Myasthenia gravis and Allergies
 In absence of magnesium sulfate one may use diazepam
30mg/1000ml D5W 30 drops per minute and 10mg IV bolus if
convulsion occurs.

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 Indications for definitive management (delivery)

 The gestational age is ≥34wks
 Fetal pulmonary maturity is confirmed,
 When there is imminent risk for eclampsia (persistent
severe symptoms)
 Multi-organ dysfunction
 Severe IUGR (< 5th percentile)
 Suspected placental abruption
 Non-reassuring fetal testing

Intrapartum management

 If there are no contraindications to labor, vaginal delivery is

the preferred approach.
 Cervical ripening agents and oxytocin are used as needed.
 Prophylactic anticonvulsant
 To avoid pulmonary edema, total IV fluids should not
exceed 100 mL/hour.
 Pain control is achieved with regional anesthesia or with
intramuscular or IV narcotic analgesics.
 The use of either epidural, spinal, or combined techniques
of regional anesthesia is the method of choice during
cesarean delivery.

Postpartum Management

 Close monitoring of BP, of symptoms consistent with

severe disease, and accurate measurements of fluid
intake and urinary output.
 Magnesium sulfate should be continued for at least 24
hours.
 Antihypertensive medications are discontinued if the BP
remains below the hypertensive levels for at least 48
hours.

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 5 days of oral furosemide therapy (20 mg/day) enhances

recovery and reduces the need for antihypertensive
therapy in women with severe preeclampsia.
 If neurologic symptoms exist, brain imaging (if available)
is undertaken to rule out the presence of cerebral
pathology.

MANAGEMENT OF ECLAMPSIA
 Anticonvulsants – MgSO4 (same dosage as in severe PE)
 Alternative supplementary anticonvulsant medication
include
o Intravenous barbiturate (given slowly).
o Midazolam or lorazepam may also be given in a
small single dose, but prolonged use is avoided
because it is associated with a higher mortality
rate from aspiration pneumonia
 Acute BP control
 Supportive management to patients with loss of consciousness
 Deliver the baby after the patient is stabilized
N.B. mere presence of eclampsia is not an indication for CD.

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 SAMPLE HISTORY
Chief Compliant: Headache of 2days duration
HPP:
This is a 19yrs old primigravida lady whose LNMP was on 19-4-
12EC (reliable) making the EDD on 24-1-13EC and gestational age
of 33+2wks(on 12-12-12EC, date of clerking). Menses was regular,
coming every 28-30days and lasting for 3-4days, she usually used
2-3 tampons per day, and flow wasn’t associated with clot or any
abdominal discomfort. She used to take injectable contraception for
two years, but stopped 6month before she saw her last period.
She suspected she was pregnant after her period was delayed for
two weeks and when she started to have nausea & vomiting, which
was usually in the mornings, then she went to the local health
center, where urine pregnancy test was done and she was told that
she was pregnant, (NB. if she remembers, write the specific date the
test was done, and if ultrasound was done write the gestational age
too), and She was told to return after 3months to start her ANC
follow up. She has 4 ANC visits at () local health center.
Her first ANC visit was when she was around 4month pregnant,
(NB. for all visits write specific date if she has a card or if she
remembers correctly). On this visit history was taken, weight,
height and BP were measured, and abdominal examination was
done. Blood and urine sample were taken. She doesn’t remember
any of the specific results, but she was told that everything was
fine. She was given an injection on her arm and a red tablet to take
1 tablet per day. (Write “iron supplement” if she knows what it is)
and was told to return after 1month.

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Her 2nd, 3rd and 4th visits were on 5th, 6th, and 7th months of
pregnancy respectively (some seniors may expect you to write each
visit separately even though it is going to be pretty much a
repetition).
Similar examination and lab investigation (only urine) were done,
and all were uneventful. 2nd injection was given on the 2nd visit and
red tablet was given in all the visits.
She started to feel fetal movements at around 4-5month of
pregnancy( if she remembers ask exact date of fetal quickening) and
it has been increasing even since and it is a rolling and kicking
type. The pregnancy was wanted, planned and supported. She
hasn’t made any significant change in her diet after she became
pregnant. Her staple diet was injera made of teff with shiro wot 3
times per day, meat on holidays and fruit and vegetables at least
once per week.
Currently she is presented with a persistent global type of headache
of 2days duration, which hasn’t improved even if she started taking
medications for headache that she found in the house. Associated
with this she also has swelling on her face, both hands and both
legs, the swelling started from the leg and progress upward. After
admission she was told that she has an elevated blood pressure and
she was given medications. Now the headache and the swelling over
her face and her hands have disappeared, otherwise:-
Danger signs
She has no history of blurring of vision, ABM or LOC
She has no history of epigastric pain, or right upper quadrant pain.
She has no history of vaginal bleeding, or vaginal discharge, high
grade fever
She has no history of excessive vomiting
She has no history of cough, or shortness of breath
She has no history of urinary frequency, decreased urine output or
pain during urination

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She has no history of passage of liquor or pushing down pain

Risk factors
She has no previous history of hypertension, diabetes mellitus.
She has no history of use of artificial reproductive technology
She has no history of bleeding disorders
She has no family history of similar complaints
DDx (for the headache)
She has no history of neck stiffness or fever (meningitis)
She has no history of eye pain or redness of the eye (glaucoma)
She has no history of sleep disturbance, or worsening of headache
at awakening or during bending, coughing or straining (brain
tumor)
She has no history of head trauma, vomiting or abnormal body
movement (Subarachnoid hemorrhage, which is usually referred by
the patient as “the worst headache ever”, with sudden onset,
thunderclap headache)
She has no history of fever, pain in the jaw or tongue during
chewing or ringing sensation in the ears (Temporal Arteritis)

Physical examination
Vital signs: BP=> 165/105mmHg, Pulse, RR, temp, Weight, height
and BMI… normal
Abdominal examination
 Inspection
 The abdomen is symmetrically distended and moves with
respiration (sometimes the abdomen might appear
asymmetrical in pregnant ladies, more on the right
side(because of the sigmoid colon on the left side, which
occupy the space))
 The umbilicus is flat
 There is midline hyperpigmentation (linea nigra) and
purplish marks in the lower abdomen (striae gravida)
 There is no scar or distended veins over the abdomen
 Hernia sites are free
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 Palpation
 Superficial palpation: There is no tenderness, rigidity, or
superficial mass
 Deep palpation: No organomegaly or deep mass
 Obstetric palpation
o Fundal palpation:
 The fundus is 6 fingers above the level of the
umbilicus: - 32 weeks
 The fundus is occupied by a soft bulky,
irregular, non-ballotable mass: -breech

o Lateral palpation
 The longitudinal axis of the fetus is in line with
the mother’s longitudinal axis, -longitudinal lie
 There is a regular or smooth surfaced, hard
mass on the right side of the abdomen, -the
back
o Pelvic palpation
 The occiput (hard ballotable mass) is palpated
in the lower uterine pole: - cephalic
presentation
 The anterior shoulder is 5 fingers above the
symphysis pubis: - floating
 The cephalic prominence is opposite to the
side of the back: - flexed attitude.
 Percussion: No shifting dullness or fluid thrill
 Auscultation: FHB is 140bpm heard on the right side

Musculoskeletal system: Grade II bilateral pitting edema

Assessment: Early preterm pregnancy (33+2weeks) + PE with

severity feature (headache) + Primigravida
 Why early preterm? => Because of the GA determined from
reliable LNMP, if she doesn’t know her LNMP with certainly
and told you only duration of amenorrhea, (1) your diagnosis
will simply be 2nd or 3rd trimester pregnancy, and (2) you
have to include unknown LNMP on the assessment.

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Investigation
o CBC (anemia, or thrombocytopenia)
o BG (blood group, Rh)
o Urinalysis (proteinuria, bacteriuria, UTI?)
o VDRL (Venereal Disease Research Laboratory)
o PICT (Provider-Initiated Counseling and Testing)
o Liver function test
o Serum creatinine
o Serum LDH
o Abdominal Ultrasound (fetal growth and BPP)
o Coagulation profile(if thrombocytopenia or elevated
liver enzymes)

Functions of obstetric ultrasound include:-

 Diagnosis of pregnancy
 Gestational age determination
 Placental localization
 Amniotic fluid volume determination
 Fetal wellbeing assessment
 Fetal sex identification
 Confirmation of fetal viability
 Fetal weight estimation
 Diagnosis of:-
 fetal growth restriction
 congenital anomaly
 multiple gestation
 molar pregnancy
 uterine and adnexal pathology
 See details on obstetric ultrasound and other investigation in
obstetrics on Introduction to Obstetric and Gynecological
diagnosis, Asheber Gaym (M.D.)
Management plan
 See antepartum management of severe PE above

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CHAPTER 2

ANTEPARTUM HEMORRHAGE (APH)

APH or late pregnancy bleeding is vaginal bleeding during
pregnancy after 28thwks and before the delivery of the fetus (the last
fetus in case of multiple pregnancies).
Incidence: 2 – 3 % of all pregnancies

Classes of hemorrhage and the physiologic response

Normal physiologic adaptations and changes during hemorrhage
 In normal physiology when 10% of circulatory blood volume
is lost, vasoconstriction occurs in both arterial and venous
compartments in order to maintain blood pressure and
preserve blood flow to essential organs.
 As blood loss reaches 20% or more of the total blood volume,
increase in systemic vascular resistance can no longer
compensate for the lost intravascular volume and blood
pressure decreases  cardiac output falls  poor end organ
perfusion and finally cardiogenic shock will ensue.

Hemorrhage classification and physiologic response

Class Acute blood loss % lost Response
(ml)
I 1000 15 Dizziness, palpitation,
minimal BP change, narrow
pulse pressure
II 1500 20-25 Tachycardia, tachypnea,
sweating, weakness
III 2000 30-35 Significant tachycardia and
tachypnea, restlessness,
pallor and cool extremities
IV ≥2500 40 Cardiogenic shock, air
hunger, Oliguria or anuria.

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NB, it is important that you know these classes with the response,
because it will help you to estimate the blood lose in initial
assessment of the patient

CAUSES OF THIRD-TRIMESTER BLEEDING

Differential diagnosis for third trimester vaginal bleeding
1. Placental causes 2. Non-placental causes
Abruptio placentae Bloody show
Placenta previa Uterine rupture
Vasa previa Bleeding diathesis
Placenta membranacea Local Cervicitis
causes Cervical ca.
~5% Cervical polyp
Leech infestation
Vulvo-vaginal
abnormalities
Circumvallate placenta 3. Unknown/Undetermined*
causes ~25%

*Undetermined causes: is to indicate that causes of APH other than

local causes are ruled out but the local causes are not ruled out yet,
because of the need to wait 48hr after last vaginal bleeding episode
to perform speculum examination.
*Unknown causes: no identified causes after performing all the
necessary physical examination, including speculum examination
and investigations.

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Most common once are:

 Bloody show associated with cervical change
This cervical bleeding is the consequence of effacement
and dilation of the cervix, with tearing of small vessels.
 Abruptio placentae (AP)
 Placenta previa
 Vasa previa

NB, The most common cause of APH is bloody show. And the
most common cause of pathologic cause of APH is AP

PLACENTAL ABRUPTION
Placental abruption (PA), or abruptio placentae (AP), refers to the
premature separation of a normally implanted placenta from the
uterus after 20 weeks of gestation but prior to delivery of the last
fetus.
MECHANISM OF BLEEDING
 AP is commonly due to rupture of defective maternal vessels in
decidua basalis causing separation of the placenta.
 In rare cases it can be due to disruption of fetal-placental
vessels.
These factors cause bleeding which in turn results in a
decidual hematoma which promotes placental separation,
destruction of placental tissue and a loss of maternal-fetal
surface area for nutrient and gas exchange.
INCIDENCE
 The overall incidence of placental abruption is approximately
1 in 100 births.

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 About 1/3rd of all APH can be attributed to PA. And 40-60%

of abruptions occur prior to 37 weeks of gestation.

RISK FACTORS OF AP
 Increasing parity and maternal age (incidence in
primigravida ~1%, multigravida ~2.5%)
 Maternal substance use
 Cigarette smoking (40% increased risk), Cocaine abuse
(10% higher risk)
 Trauma
Blunt or penetrating trauma to the gravid abdomen has
been associated with placental abruption. After a minor
trauma, the risk for placental abruption is between 7% and
9%, whereas the risk may be as high as 13% after severe
injury.
The two most common causes of maternal trauma are motor
vehicle crashes and domestic abuse. With motor vehicle
crashes, uterine stretch, direct penetration, and placental
shearing from acceleration-deceleration forces are the primary
etiologies of trauma-related placental abruption
 Maternal diseases
 Hypertension (5 fold increased risk), Hypothyroidism,
Asthma
 Preterm premature rupture of membranes; in 2-5% ,
abruption occurs
 Rapid uterine decompression associated with multiple
gestation (3 fold higher risk) and polyhydramnios
 Uterine and placental factors
 Anomalies, Synechiae, Fibroids, Cesarean scar,
Abnormal placental formation and Chronic ischemia
 Prior abruption (risk of recurrence 5-17%, after two
consecutive abruptions risk of recurrence rises to ~25%)
 Hyperhomocysteinemia
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CLINICAL MANIFESTATION
Several factors determine the clinical manifestations of placental
abruption. These factors include:
(1) The temporal nature of the abruption (acute vs. chronic),
(2) Clinical presentation; Overt (80%) vs. concealed (20%), and
(3) Severity

An acute, overt abruption typically presents with

 vaginal bleeding,
 abdominal pain, and
 uterine contractions
As placental separation worsens, uterine tenderness, tachysystole,
fetal heart rate (FHR) patterns consistent with hypoxia, and fetal
death may occur.

The amount of vaginal bleeding correlates poorly with the extent

of placental separation and its potential for fetal compromise. In
fact, concealed abruption occurs in 10% to 20% of cases.

Chronic abruption may be insidious in its presentation and is often

associated with ischemic placental disease. Typically, these cases
present with intermittent, light vaginal bleeding and evidence of
chronic placental inflammation and dysfunction, such as
oligohydramnios, fetal growth restriction, preterm labor, premature
preterm rupture of membranes (PPROM), and PE.
With severe abruptions more than 50% of the placental surface area
separates. In these scenarios, maternal compromise in the form of
consumptive coagulopathy may result from the triggering of the
clotting cascade by hemorrhage and extensive thrombin deposition
 i.e. DIC (~10% of cases)

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DIAGNOSIS
 Placental abruption is primarily a clinical diagnosis that is
supported by radiographic, laboratory, and pathologic studies.
Clinically: Any findings of vaginal bleeding, uterine contractions,
abdominal and/or back pain, or trauma should prompt an
investigation for potential placental abruption. Port wine
discoloration of liquor and non-reassuring fetal status can also be
indicative.
Radiological (Ultrasound): for the diagnosis of placental abruption
identified less than 2% of cases.
 Early hemorrhage is typically hyperechoic or isoechoic,
 Resolving hematomas are hypoechoic within 1 week and
sonolucent within 2 weeks of the abruption.
Acute hemorrhage may be misinterpreted as a homogeneous
thickened placenta or fibroid.
There are three predominant locations for placental abruption:-
 subchorionic (between the placenta and the membranes)
 retroplacental (between the placenta and the myometrium)
 preplacental (between the placenta and the amniotic fluid)

Figure 1 A) Retroplacental abruption B) Subchorionic abruption C)

Preplacental abruption
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NB, Retroplacental hematomas are associated with a worse

prognosis for fetal survival than subchorionic hemorrhage. And
the size of the hemorrhage is predictive of fetal survival; the
greater the size, the greater the fatality.

Laboratory findings: Hypofibrinogenemia and evidence of

consumptive coagulopathy may accompany severe abruption.
Pathologic studies: Macroscopic inspection of the placenta may
demonstrate adherent clot, depression (due to missing cotyledons)
of the placental surface and bleeding into myometrium causing
Couvelaire uterus.

A B
Figure 2, A. Partial placental abruption with a dark adherent clot.
B. Couvelaire uterus from total placental abruption after CD
COMPLICATIONS OF PLACENTAL ABRUPTION
Maternal complications Fetal complications
Blood loss Intrauterine growth restriction
(IUGR)
Consumptive coagulopathy Oligohydramnios
Need for transfusion Prematurity
End organ damage Hypoxemia
Cesarean delivery Still birth
Death

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Grading of abruptio placentae:

 Grade 0: Retrospective diagnosis of abruption
 Grade 1: Vaginal bleeding
 Grade 2: Vaginal bleeding, concealed hemorrhage, uterine
tenderness, NRFHR
 Grade 3: Vaginal bleeding, shock, extensive concealed
hemorrhage, uterine tenderness, IUFD
 Grade 3 A: With no coagulopathy
 Grade 3 B: With coagulopathy

MANAGEMENT OF AP
All cases should be admitted.
 Asses hemodynamic status, then
 IV line to be opened
 Fetal wellbeing monitoring
 HCT, BGP & Rh, platelets, fibrinogen, PT, aPTT

Grade 1:
Conservative management
 Steroid in < 34 weeks of gestation
 Keep in ward till bleeding subsides
 Tocolysis in < 33 weeks of gestation
 Follow maternal V/S, bleeding, uterine contraction &
tenderness, FHB, kick count, BPP, fetal growth

Indications for delivery: Term, IUFD, malformed fetus,

NRFHR, advanced labor, excessive bleeding
Grade 2 – 3:
 Asses maternal hemodynamic status, then stabilize the
mother, then
 Maintain U.O.P > 30 ml/hr & HCT > 30%

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 Platelets (6U) transfusion if thrombocytopenia

 FFP if fibrinogen < 100mg/dl
 Delivery
 Vaginal: Amniotomy & induction with oxytocin
 C/d for uncontrolled hemorrhage & other obstetric
indications
 Hysterectomy; if uncontrolled hemorrhage occurs
 Couvelaire uterus---Uterotonic agents, hysterectomy if
unresponsive

PLACENTA PREVIA
Placenta previa is defined as the presence of placental tissue over or
adjacent to the cervical os.
Recent revised classification of placenta previa consists of two
variations:
(1) True placenta previa; in which the internal cervical os is
covered by placental tissue, and
(2) Low-lying placenta; in which the placenta lies within 2 cm of
the cervical os but does not cover it.

INCIDENCE
The overall reported incidence of placenta previa at delivery is 1 in
200 births. In the second trimester, placenta previa may occur in
up to 6% of pregnancies.
Placental migration has been used to explain this “resolution” of
placenta previa that is noted near term. Three theories have been
suggested to account for this phenomenon:
 1st theory: as the pregnancy advances, the stationary lower
placental edge relocates away from the cervical os with the
development of the lower uterine segment.

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 The lower uterine segment has been noted to increase

from 0.5 cm at 20 weeks to more than 5 cm at term.
 2nd theory: the placenta-free uterine wall has been proposed
to grow at a faster rate than the uterine wall covered by the
placenta.
 3rd theory: (trophotropism); the growth of trophoblastic
tissue away from the cervical os toward the fundus, results in
resolution of the placenta previa.
ETIOLOGY OF PP
 Exact cause is unknown
Theories include:
1) Dropping down theory
2) Persistence of chorionic activity
3) Defective decidua
4) Big surface area of placenta

RISK FACTORS
 Intrinsic maternal factors
 Increasing parity (Grand multipara 5% risk, Nulliparous
women~ 0.2% risk)
 Advanced maternal age (If age >35 , 4 fold increase risk,
if age>40, 9 fold increase risk)
 Maternal race (higher rates in Asian women)
 Extrinsic maternal factors
 Cigarette smoking (as high as 3 fold increased risk)
 Cocaine use
 Residence at higher elevation (increased placental surface
area due to decreased uteroplacental oxygenation)
 Infertility treatments
 Fetal factors
 Multiple gestations
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 Male fetus (due to larger placental size and delayed

implantation of the blastocyst)
 Prior placenta previa (8 fold increased risk)
 Prior uterine surgery and cesarean delivery.
 PP incidence increases with the numbers of cesarian
deliveries (CD). It occurs in 0.9% of women with one prior
CD, in 1.7% of women with two prior CDs, and in 3% of
those with three or more CDs.
 In patients with four or more cesarean deliveries, the risk
for placenta previa has been reported to be as high as
10%.

CLINICAL MANIFESTATION
Placenta previa typically presents as painless vaginal bleeding in
the second or third trimester.
 Between 70% and 80% of patients with placenta previa will
have at least one bleeding episode, and from those with
bleeding,
 One third of women will present before 30 weeks of
gestation,
 One third between 30 and 36 weeks, and
 One third after 36 weeks.
 About 10% to 20% of patients present with uterine
contractions before bleeding, and
 Fewer than 10% remain asymptomatic until term.

Time of bleeding in placenta previa is during:

1. Lower uterine segment formation
2. Fetal head engagement
3. Manipulation upon physical examination (eg. PV)
4. Labor

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DIAGNOSIS
Whenever there is uterine bleeding after mid-pregnancy, placenta
previa or abruption are always considered.
NB, PP should not be excluded until sonographic evaluation has
clearly proved its absence.
Radiology (ultrasound):
 Transabdominal (diagnostic accuracy of at least 95%) and
 Transvaginal (diagnostic accuracy that approaches 100%)
ultrasound provide the best means for diagnosing placenta
previa.
If a true placenta previa or low-lying placenta is diagnosed in the
second trimester, repeat sonography should be obtained in the early
third trimester at 32 weeks.

More than 90% of placenta previa cases diagnosed in the

second trimester resolve by term.

MANAGEMENT
 Admit all ladies with APH secondary to placenta previa at time
of diagnosis.
 Resuscitation based on clinical condition.
 Vaginal & rectal examinations are absolutely contraindicated.
 Monitor closely maternal & fetal conditions.
 HCT, BG & Rh, cross-match at least two units of blood
 Decide on conservative management versus immediate delivery
 Indications for immediate delivery:
o Term pregnancy, IUFD, fetal growth restriction, NRFS,
excessive bleeding, gross fetal congenital malformation
which may not be compatible with life, lady in labor.

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 Route of delivery
o depends on the type of placenta previa and presence of
other obstetric indications:
 Low lying & anterior marginal → vaginal delivery
 Partialis, totalis, & posterior marginal → c/d
 Excessive bleeding, NRFS, other indications → c/d

 In absence of any of the above indications to deliver the fetus,

conservative management is instituted till an indication comes
to picture.
 Conservative management in preterm lady includes:
 Bed rest (in hospital)-----No place for outpatient
management
 Dexamethasone 6mg IM Q 12 hours for a total of 4
doses
 Follow: Maternal V/S, vaginal bleeding, uterine
contractions, fundal height, FHB, kick count, BPP,
serial HCT.
 Deliver at 37 completed weeks of gestation after
maturity is confirmed
 Double setup examination:
 Is used in areas where U/S is not widely available/not
done by experienced people.
 It is important to decide on mode of delivery
 The procedure include:-
 Prep and client to operation room
 Everything must be ready for delivery
 Speculum examination is done gently to rule out local
causes & see the cervical status → then gentle digital
vaginal examination is done to check for presence of
placenta between fornices & presenting part, cervical
dilatation & effacement, presence of placenta through
open cervix.
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MORBIDLY ADHERENT PLACENTAS

 Morbidly adherent placenta (a.k.a accrete syndromes)
describes aberrant placentation characterized by abnormally
implanted, invasive, or adhered placenta.
Classified by the depth of trophoblastic growth, as:-
1. Placenta accrete; indicates that villi are attached to the
myometrium
2. Placenta increta; villi actually invade the myometrium, and
3. Placenta percreta; defines villi that penetrate through the
myometrium and to or through the serosa.

Figure 3. Uteroplacental relationships found with invasive

placentation
INCIDENCE
The prevalence of accrete syndromes was 3.7 per 1000 births—1
per 270

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RISK FACTORS
 Placenta previa
 Prior cesarean delivery
A classical hysterotomy incision has a higher risk for a
subsequent accrete placenta
Risk of placenta accreta with placenta previa and prior
cesarean delivery
Number of prior cesarean Placenta accrete risk (%)
deliveries

0 3
1 11
2 40
3 61
≥4 67

 Increasing parity and maternal age

 Submucosal uterine fibroids
 Curettage or endometrial ablation

CLINICAL MANIFESTATION
 In cases of first- and second-trimester accrete syndromes,
there is usually hemorrhage that is the consequence of
coexisting placenta previa. Such bleeding will typically prompt
evaluation and management.
 In some women who do not have an associated previa, accreta
may not be identified until third-stage labor when an adhered
placenta is encountered. Unfortunately, imaging modalities are
less than perfect to identify all of these placentas early.
 Hematuria can be a feature of placenta percreta with bladder
invasion.

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DIAGNOSIS
Radiographic techniques: Ultrasound is the preferred radiographic
modality for the diagnosis of placenta accreta. Findings suggestive
of placenta accreta include:
 A loss of the normal hypoechoic retroplacental myometrial
zone,
 thinning and disruption of the uterine serosa–bladder wall
interface,
 focal exophytic masses within the placenta, and numerous
intraplacental vascular lacunae

Laboratory findings: Placenta accreta has been associated with

unexplained elevations in maternal serum α-fetoprotein (MSAFP).
Pathologic studies: Placenta accreta is confirmed by the pathologic
examination of a hysterectomy specimen.

MANAGEMENT
 Because of its associated risk for massive
postpartum hemorrhage, placenta accreta accounts for
a large percentage of peripartum hysterectomies.

When performing the surgery, it is recommended that

the uterus be incised above the placental attachment
site and that the placenta be left in situ after
clamping the cord because disruption of the
implantation site may result in rapid blood loss.
 Timing of delivery depends upon clinical circumstances;
however, most authorities favor delivery at 340/7 to 356/7
weeks with or without antenatal corticosteroid
administration.
 Adequate IV access with two large-bore catheters and
ample blood product availability are mandatory.

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 In specific circumstances, uterine conservation may be

attempted. These situations include focal accreta, desired
future fertility, and fundal or posterior placentae accrete.

VASA PREVIA
 Vasa previa is defined as the presence of fetal vessels over the
cervical os.
 These fetal vessels lack protection from Wharton jelly
(velamentous cord insertion) and are prone to rupture and
compression. When the vessels rupture, the fetus is at high
risk for exsanguination.
INCIDENCE
 The overall incidence of vasa previa is 1 in 2500 deliveries;
however, data have shown a range from 1 in 2000 to 1 in 5000
deliveries.
RISK FACTORS
 Bilobed and succenturiate-lobed placentas
 Pregnancies that result from assisted reproductive technology
(ART)
 Multiple gestations
 History of second-trimester placenta previa or low-lying
placenta.

CLINICAL MANIFESTATIONS
 Most cases of vasa previa presented after rupture of
membranes with acute onset of vaginal bleeding from a
lacerated fetal vessel. If immediate intervention was not
provided, fetal bradycardia and subsequent fetal death
occurred.
 Recently, many cases of vasa previa are diagnosed antenatally
by ultrasound. In rare cases, pulsating fetal vessels may be
palpable in the membranes that overlie the cervical os.
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DIAGNOSIS
 Vasa previa is often diagnosed antenatally by ultrasound with
color and pulsed Doppler mapping. Transabdominal and
transvaginal approaches are most often used.
MANAGEMENT
 When diagnosed antenatally, vasa previa should be managed
similarly to placenta previa.
 If an intrapartum diagnosis of vasa previa is made, expeditious
delivery is needed. Immediate neonatal blood transfusion is
often required in these circumstances.

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 SAMPLE HISTORY
Chief compliant: Vaginal bleeding of 1 hour duration
HPP
This is a 30 years old G4P3 (all alive) mother whose LNMP was on
22/05/2011EC (reliable) making the EDD on 27/02/2012EC and
gestational age of 36+1 weeks (on 30/01/2012) EC, date of
clerking). Menses was regular coming every 26-28 days, lasting for
3-4 days. She used 2-3 sanitary pads per day, menses has no clots
associated and she has no abdominal discomfort. She has no
history of contraceptive use. She doesn’t remember the exact date
she felt fetal movement but claimed that she still feels the kicks and
it’s increasing through time.
She suspected she was pregnant when she missed her menses and
went to a nearby health center where the diagnosis of her
pregnancy was confirmed by a urine pregnancy test, (write the exact
date of urine pregnancy test or ultrasound if done and if she can
recall).
She had total of four ANC visits at a local health center. First visit
was at 3 month of pregnancy (write exact date if available), where
history was taken, weight, height and blood pressure was
measured, and abdominal examination was done. Blood and urine
test was done, she doesn’t remember any results, she was told
everything was fine. She was given an injection on her left upper
arm and a red round tablet to take once daily. She was appointed
after a month.

Same physical examinations and investigation (only urine

examination) were done on her 2nd, 3rd and 4th visits and they were
all uneventful. She had another injection on her left upper arm on
the 2nd visit and had a red round tablet refill in all the visits.

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The pregnancy was not planned but is wanted and supported by

her family. She hasn’t made any significant changes in her diet
after she got pregnant.

Her staple diet is Injera made of teff with shiro wot 3 times a day,
fruits and vegetables occasionally and meat on rare occasions.

Currently she presented with a sudden onset of vaginal bleeding

which was bright red, non-clotting and odorless. The blood soaked
her underwear and dress. It was not associated with abdominal
pain, gush of fluid or decreased fetal movement.

She has no history of easy fatigability, blurring of vision, ringing in

the ears or palpitation (symptoms of anemia).

Otherwise:

Danger signs
She has no history of cough, or shortness of breath
She has no history of vision disturbances, ABM or LOC
She has no history of epigastric pain, or right upper quadrant pain.
She has no history of headache
She has no history of excessive vomiting
She has no history of urinary frequency, decreased urine output or
pain during urination
She has no history of passage of liquor or pushing down pain
Risk factors
She has no history of trauma to the abdomen
She has no history of cigarette smoking or alcohol drinking
She has no history of infertility treatment
She has no history of twinning
She has no history of gynecologic operations
She has no similar previous history

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DDx
She has no history of post-coital bleeding (Cervical ca.)
She has no history of river water contact (Leech infestation)
She has no history of bleeding from other sites (Autoimmune
disorders like ITP)
She has no history of vaginal discharge, genital burning sensation
(cervicitis)

PHYSICAL EXAMINATION
V/S: BP, pulse, RR, TO, Weight, Height, BMI………normal
HEENT: Pale conjunctiva
Abdominal examination: thorough examination,
(See the Preeclampsia history in chapter 1 to know how to write
findings in obstetric palpation)
Pelvic examination (avoid Per Vaginal examinations unless
placenta previa has been ruled out)
Assessment: Late preterm pregnancy + APH secondary to R\O
Placenta previa

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CHAPTER 3

POSTPARTUM HEMORRHAGE (PPH)

DEFINITION AND INCIDENCE
 There multiple definitions to PPH from different
source/institutions. The different definitions include:-
o PPH: is defined as
1. Excessive bleeding following delivery (>500 ml in
vaginal delivery, >1000 ml in CD and twin vaginal
deliveries, >1500 ml following cesarean hysterectomy)
2. A drop in Hct > 10% from baseline
3. Bleeding that makes a patient symptomatic and/or
results in signs of hypovolemia ( best definition)
4. Blood loss of > 15% of the total estimated blood
volume
NB, hemorrhage may occur before, during, or after delivery of
the placenta
Incidence
 PPH complicates 4 to 6% of all deliveries
 World’s leading cause of maternal mortality
o Accounts for 25% of all maternal deaths worldwide &
60% in developing countries
o The worst thing about PPH is its short duration from
onset to maternal mortality if not managed

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o Major killers in maternity (enemies of Obtetritian, if u

will) and their timing till death
 PPH---2hrs
 APH--- 12hrs
 Ruptured uterus--- 1 day
 Eclampsia---- 2 days
 Obstructed labor--- 3 days
 Sepsis ---6 days
o Hence PPH is an obstetric EMERGENCY

Normal Physiologic Mechanisms Preventing PPH

 Constriction of interlacing myometrial fibers that surround the
blood vessels supplying the placental implantation site
 Formation of firm clots at mouth of vessels(placental bed)
which occurs as result of increased viscosity and
hypercoaguibility of blood

CLASSIFICATION
 PPH can be classified temporally as:-
 Primary (early) PPH
 Secondary ( late ) PPH

Early PPH

 Blood loss during the first 24hrs after delivery.

 Account for 98% PPH cases

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Etiology
 The etiologies for early PPH can easily remembered as the five
Ts-
 Tone (uterine atony)
 Trauma (genital tract laceration and Uterine rupture)
 Tissue(retained placenta and amniotic membranes
 Thrombin(coagulopathy) ,and
 Traction(uterine inversion)

1) Uterine atony (50%)

 Failure of the uterus to contract sufficiently
 Risk factors:
 excessive manipulation
 general anesthesia (halothane)
 uterine over distention (twin, polyhydramnios, big fetus)
 prolonged labor
 oxytocin induction/augmentation
 previous PPH
 precipitate labor
 grandmultiparity

2) Retained products of conception (5%-10%)

 Retained products of conception-->uterine atony-->PPH
 Diagnosis-
 when spontaneous expulsion of the tissue has not
occurred within 30 to 60 minutes of delivery
 Risk factors:
 retained placenta
 succenturate lobe
 morbid adherence
 mismanagement of third stage of labor

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3) Genital tract Laceration (20%)

 The most common lower genital tract lacerations are perineal,
vulvar, vaginal, and cervical.
 Upper genital tract lacerations are typically associated with
broad ligament and retroperitoneal hematomas.
 Risk factors:
 Episiotomy extension
 instrumental deliveries
 precipitate labor
 fetal malpresentation or macrosomia
 delivery through undilated cervix
 prior cerclage placement
 shoulder dystocia
 Inspection of placenta and fetal membranes after delivery for
completeness.
 Manual exploration of uterine cavity is both diagnostic and
therapeutic
4) Uterine rupture
 Complete nonsurgical disruption of all uterine layers
 Uterine rupture is most common in women with a scarred
uterus, including those with prior cesarean delivery and
myomectomy.
Risk of uterine rupture after CD

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 Clinical manifestations
 Fetal:
o Fetal bradycardia with or without preceding variable or
late decelerations-most common(33-70%)
o Loss of fetal station in labor
 Maternal:
o acute vaginal bleeding,
o constant abdominal pain or uterine tenderness,
o change in uterine shape,
o cessation of contractions,
o hematuria (if extension into the bladder has
occurred), and
o signs of hemodynamic instability
 Uterine inversion
 Collapse of the fundus into the uterine cavity, and it is
classified by degree and timing.
 It is classified it to:
 Three, based on timing:-
o Acute (within 24 hours of delivery)
o Subacute (>24 hours postpartum but <4 weeks)
o Chronic ( >1 month postpartum

 Four, based on degree of inversion:-

o First degree (incomplete)
o Second degree (complete)
o Third degree (prolapsed)
o Fourth degree (total)

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 The two most commonly proposed etiologies are:

1. Excessive umbilical cord traction with a fundally
attached placenta and
2. Fundal pressure in the setting of a relaxed uterus
 Risk factors include:-
 uterine over-distention
 fetal macrosomia
 rapid labor and delivery
 congenital uterine malformations
 uterine fibroids
 invasive placentation
 retained placenta
 short umbilical cord
 use of uterine-relaxing agents
 nulliparity
 manual placental extraction
 Ehlers-Danlos syndrome

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 Clinical manifestation
 Depend on by degree and timing.
o Incomplete-subtle in its clinical findings,
o Complete-brisk vaginal bleeding- inability to palpate
the fundus abdominally, and maternal hemodynamic
instability
 Coagulopathy
 Acquired
 Idiopathic thrombocytopenic purpura
 Thrombocytopenia with preeclampsia
 HELLP syndrome
 Disseminated intravascular coagulation
 Dead fetus in utero -Severe infection/sepsis
 Placental abruption
 Amniotic fluid embolus
 Severe hemorrhage
 Iatrogenic-anticoagulant administration
 Hereditary
 Von Willebrand’s disease


Late PPH
 Blood loss between 24hrs and 6wks after delivery
 Unlike primary PPH, bleeding usually is not catastrophic
Etiology

 Uterine infection
 Retained products of conception
 Placental site subinvolution
 Coagulopathy

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Uterine infection

 If the mother has fever, uterine tenderness, and/or a foul-

smelling discharge without massive bleeding, then
endometritis should be suspected.
Uterine sub-involution

 Arrest/retardation of the uterus to go back to its original

size and position
 Normally, uterine involution occurs in 4 weeks
Postpartum
 After 2 weeks postpartum, uterus should be in pelvic
cavity
 Causes:-
o Infection
o Retained placental fragments
o Abnormal healing of the thrombosed vascular sinuses
at the placental site

Clinical features of PPH

Symptoms
 Vaginal bleeding-continuous trickling of blood or copious
flow or passage of huge blood clots
 It may be concealed and accumulate in the uterus or
broad ligament, in such cases it is important to look for
symptoms of hypovolemia/anemia
o lightheadedness
o weakness
o palpitations
o diaphoresis
o restlessness, confusion
o air hunger
o syncope
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Physical examination

G/A and V/S

 Signs of shock, depend on the amount of bleeding and pre-

deliver Hb levels (see the classes of hemorrhage and the
physiologic response of the body to each class on the APH
section above)
Abdominal examination findings

 The uterus can be:-

o flabby and soft  atonic uterus
o over distended  uterus filled with blood clots
 Squeezing it leads to gush of clotted blood
pervaginum
o firmly contracted trauma
o atonic (non-contractile), tender and changing in
shapeUterine rupture
 loss of station of the fetal presenting part PV
examination is also indicative of uterine rupture
o Soft and larger than expected for the time during
PuerperiumUterine subinvolution
Pervaginal examination findings

 dark red blood atonic uterus

 bright red bloodtrauma
 Cervical laceration, paraurethral tearslower tract causes
Bimanual examination-palpation of uterine fundus in the lower
uterine segment or within the vaginauterine inversion

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COMPLICATION
PPH is a major cause of maternal morbidity, including catastrophic
sequelae:-
 Death
 Hypovolemic shock and organ failure: renal failure, stroke,
myocardial infarction, postpartum hypopituitarism (Sheehan
syndrome)
 Fluid overload (pulmonary edema, dilutional coagulopathy)
 Abdominal compartment syndrome
 Anemia
 Transfusion-related complications
 Acute respiratory distress syndrome
 Anesthesia-related complications
 Sepsis, wound infection, pneumonia
 Venous thrombosis or embolism
 Unplanned sterilization due to need for hysterectomy- control
intractable PPH
 Asherman syndrome (related to curettage if performed for
retained products of conception)

Management
Management Goal
 Restore or maintain adequate circulatory volume to prevent
hypoperfusion of vital organs
 Restore or maintain adequate tissue oxygenation
 Reverse or prevent coagulopathy
 Eliminate the obstetric cause of PPH
The first step in management of PPH is call for help. The management
is a race with time; every available practitioner should be involved

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Evaluation of persistent bleeding

 If vaginal bleeding persists after delivery of the placenta,

aggressive treatment should be initiated
 Search for the cause of bleeding and initiate definitive
management
 STEPS:
1. Compress manually the uterus and insert IV catheter
2. While doing that obtain assistance
3. Obtain blood (type and cross match)
4. Check blood for clotting to rule out coagulopathy
5. Begin fluid or blood replacement
6. Carefully explore the uterus
7. Inspect the cervix and vagina
Measures to Control Bleeding
1. Manual exploration of the uterus
 Is done if PPH occurs after:
 Vaginal delivery following previous c/d
 Intrauterine manipulation (version, extraction)
 Malpresentation
 When abnormal uterine contour has been noted prior
to delivery
 Ensure whole placenta is delivered and intact uterus.
 Uterine rupture detected by manual exploration in PPH
requires laparatomy
2. A. Bi-manual compression and massage
 Most important step in controlling atonic PPH
 Immediate bimanual compression for 20-30min
B. Uterotonic agents
 Oxytocin 20-40u/L of crystalloid at a rate of 10-
15ml/min
 Methylergonovine 0.2mg IM if mother is not
hypertensive

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3. Curettage
 It should be performed under ultrasound guidance.
 This is likely to reduce the rate of perforation, will
allow identification of placental tissue, and confirm
that this tissue has been evacuated

4. Operative Management
 The patient’s wish of childbearing should be clear
 If can’t be ascertained the operator assumes that
childbearing is to be retained
 If possible, spouse/family could be informed
 4a. Pressure occlusion of the abdominal aorta
 Immediate temporary control of pelvic bleeding
 To provide time to treat hypotension
 To identify source of bleeding
 Pressure occlusion can be maintained for several
minutes without sequelae
 4b. Uterine artery ligation
 90% of supply to the uterus is from uterine artery
 Direct ligation of uterine artery is successful (75-90%)
if bleeding is from uterus
 4c. B-Lynch Brace Suture
 An alternative to vessel ligation
 Used in cases of atony or percreta
 4d. Internal iliac artery ligation
 Most commonly used method to control severe PPH
 Exposure can be difficult (big boggy uterus or
hematoma)
 4e. Condom tamponade technique
 With aseptic precautions, a sterile rubber catheter
fitted with a condom is introduced into the uterus.
 The condom is inflated with 250-500 ml normal saline,
according to need.
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 The condom catheter is kept for 24-48 hours,

depending upon the initial intensity of blood loss, and
gradually deflated when bleeding ceased.
5. Hysterectomy
 It is the definitive method of controlling PPH
 It is the procedure of life saving
PROGNOSIS

 PPH has a recurrence rate of approximately 10% in future

pregnancies
 Maternal deaths are due to:
1) Underestimation of blood loss
2) Inadequate blood and fluid replacement
3) Delay in operative intervention

PREVENTION
Antenatal:-
 Good and early ANC
 Treatment of anemia and malnutrition
 Early detection and prompt treatment of high risk factors
Intrapartum:-
 Avoid home delivery
 keep blood grouped and cross matched
 Active management of third stage of labor(AMTSL)
 Avoid prolonged or obstructed labor
Postpartum:-
 Close observation in 4th stage of labor
 Evaluation of placenta and membranes
 Exploration of genital tract for trauma

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NB, Risk factors do not predict PPH

 Only about 10% of women with any of the risk factors develop
PPH and over two-thirds have no identifiable risk factors
Hence all pregnancies are at risk of PPH

AMTSL
 Is the main stay in prevention of PPH
 Its components are:-
1) Oxytocin 10 IU IM within one minute of delivery of the
last baby
2) Controlled cord traction (CCT) to deliver the placenta
(BrandetAndrew maneuver)
 If placenta is not delivered with CCT or cord is
severed, do manual removal of placenta.
3) Uterine massage every 15 minutes for the first 2 hours
after delivery

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CHAPTER 4

PREMATURE RUPTURE OF MEMBRANE

(PROM) AND PRETERM LABOR
DEFINATIONS
Preterm rupture of membrane: is spontaneous rupture of
membrane occurring before 37th week.
Premature rupture of membrane (PROM): is spontaneous rupture
of membrane occurring before onset of labor.
Preterm premature rupture of membrane (PPROM): is if both
occur together i.e. if spontaneous rupture of fetal membrane occurs
before 37 completed weeks and before the onset of labor.
Prolonged rupture of membrane: is any rupture of membrane for
greater than 8 hours. It becomes a risk for chorionamnionitis when
it is longer than 18 hours.
Latency Period: is the period between rupture of membrane and
onset of labor.

PRETERM LABOR/BIRTH
Classification of the time of labor onset or delivery
Very early preterm 28-32+6
Early preterm 33-33+6 weeks
Preterm Late preterm (accounts 34-36+6 weeks
for ≥70% of all preterm
births)
Early term 37-38+6 weeks
Full term 39-40+6 weeks
Term Late term 41-41+6 weeks
Post-term Post-term >42 completed weeks

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Preterm birth:
 Describes neonates who are born early i.e. born before term
(before 37 full weeks), but after fetal viability (after 28 full
weeks).
 It is with respect to gestational age, but not with respect to
size, neonates can be born before term and be small for
gestational age, appropriate for gestational age or large for
gestational age.
 It should be clearly distinguished from the concept of
prematurity. Prematurity is incomplete development of various
organ systems at birth.

ETIOPATHOGENESIS AND RISK FACTORS

The four primary processes in PATHOGENESIS of preterm labor

are:-
1. Premature activation of the maternal or fetal hypothalamic-
pituitary-adrenal axis
2. Inflammation or infection
3. Decidual hemorrhage
4. Pathological uterine distention
Etiologies of preterm births include:-
 Spontaneous unexplained preterm labor with intact
membranes
 Can be due to multifetal pregnancy, intrauterine infection,
bleeding, placental infarction, premature cervical dilation,
cervical insufficiency, hydramnios, uterine fundal
abnormalities and fetal anomalies.
 Idiopathic PPROM
 Delivery for maternal or fetal indication
 Twins and higher-order multifetal births

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Risk factors of preterm labor/birth include:-

 Prior preterm birth: is the most important risk factor
 It increases risk by threefold greater when compared with
women whose first neonate was born at term.
 The risk of recurrent preterm birth is influenced by three
factors:
o frequency of prior preterm deliveries,
o severity as measure by gestational age, and
o the order in which the prior preterm delivery
occurred (consecutively? Or every other pregnancy..)
 Infection:
 chorioamnionitis is the most common associated
condition in our setup
 Pregnancy factors:
 Threatened abortion in early pregnancy is associated
with later adverse outcomes.
 Both light and heavy bleeding are associated with
subsequent preterm labor, placental abruption and
pregnancy loss before 24 weeks.
 Birth defects may also predispose to preterm birth.
 Lifestyle factors:
 Cigarette smoking, illicit drug use
 Inadequate maternal weight gain and underweight ,
young or advanced maternal age, poverty, short stature,
vitamin C deficiency.
 Psychological factors, like depression,
 Genetic factors:
 Recurrent, familial and racial nature of preterm birth
suggests that genetics may play a causal role.

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 Interval between pregnancies:

 Intervals <18 months and >59 months were associated
with risks for both preterm and small-for-gestational age
newborns.
 Uterine condition: Like:-
 müllerian malformation
 cervical insufficiency
 uterine over distention
 Obstetric conditions:
 Preeclampsia, eclampsia, placenta Previa, fetal growth
restriction
 Other medical conditions:
 Chronic hypertension, DM, renal disease

DIAGNOSIS:
History

 Patient may complain:-

 vaginal bleeding or bloody show
 pelvic pressure, menstrual-like cramps & lower back pain
 increased vaginal discharge
o Gush of fluid rupture of membrane

Physical examination

 Uterine contraction which is regular, >2 per 30 minutes,

dilatation and effacement of cervix with at least 1 cm change
or well effaced and dilated (at least 2cm) on admission
 Sterile speculum examination is essential to assess fetal and
cervical status.
Early differentiation between true and false labor is difficult
especially before demonstrable cervical effacement and dilation.

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Uterine activity alone can be misleading because of Braxton

Hicks Contractions (irregular, non-rhythmical contraction).
Therefore, preterm labor is defined as regular contractions before
37 weeks that are associated with cervical change.

Investigation
 If there is vaginal bleeding present, an ultrasound must be
performed to rule out placenta Previa before digital
examination is performed.
 Urine specimen is sent for culture and fetal heart rate
monitoring is done.

PREMATURE RUPTURE OF MEMBRANE (PROM)

PPROM:

 What is PPROM?
 It is responsible for 25% - 33% of all of preterm births each
year.
 The risk factors for PPROM are similar to those for preterm
labor. And the pathogenesis is similar with PROM the only
difference is that it occurs before term (preterm).
PROM:
 Affects approximately 10.7% of all pregnancies
 About 94% of cases occur at term and 5% preterm.
 It is associated with considerable maternal infection and
perinatal morbidity and mortality due to sepsis and
prematurity.

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Etiopathogenesis and Risk factors

 Most PROM cases occur due to subclinical chorioamnionitis
resulting from ascending infection from lower genital tract like
STIs.
o Genital infections produce phospholipases which
stimulate production of prostaglandins which further
stimulate uterine contraction and subsequent ROM.
 The pathogenesis of PROM is poorly understood.
o But increased apoptosis or necroptosis of membrane
cellular components and greater levels of specific
proteases in membranes and amniotic fluid are related to
PROM.
Risk factors for prom
MATERNAL FETAL
 Subclinical chorioamnionitis  Polyhydramnios (uterine over
distention)
 Overt chorioamnionitis  Malpresentation
 Past history of PROM  Multiple pregnancy
 Prior history of spontaneous
preterm delivery IATROGENIC
 Collagen synthesis defect  Amniocentesis
 Cervical incompetence  External cephalic version
 Vaginal bleeding (2 and 3
nd rd  Percutaneous umbilical
trimester bleeding) blood sampling
 Cervical conization OTHERS
 Cigarette smoking  Abdominal trauma
 Low body mass index and  Idiopathic (but most cases
nutritional deficiency are often suspected to be due
to subclinical
chorioamnionitis)
 Emergency cerclage  Low socioeconomic status
 Pulmonary disease (chronic
cough)
 Straining (constipation)
 Heavy physical exercise

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COMPLICATIONS
Maternal
 Infectious complications: Chorioamnionitis, puerperal
endomyometritis, sepsis. Risk of infection increases with
prolonged PROM
 Operative deliveries: due to failed induction
 Prolonged hospitalization and financial implication
 Preterm labor
Perinatal
 Prematurity
 Fetal and neonatal sepsis
 Oligohydramnios with cord compression and fetal asphyxia
 Cord prolapse

DIAGNOSIS AND INVESTIGATIONS

 The diagnosis of PROM is made by:-
 obtaining a history of leakage of vaginal fluid,
 pooling on speculum examination, and
 positive Nitrazine and fern test
o If these tests are equivocal, an ultrasound can be
performed to examine the level of amniotic fluid.
o If the diagnosis is still unconfirmed, an amniocentesis
dye test can be performed.

 A sterile speculum examination

 is performed to evaluate the fetal membrane status and
to inspect the cervix
 this examination is a key to differentiating PROM from
hydrorrhea gravidarum, vaginitis, increased vaginal
secretions and urinary incontinence

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 The patient's cervix should also be visually inspected to

determine the degree of dilatation and effacement and
the presence of cord prolapse.
 Membrane rupture is confirmed by visualization of
amniotic fluid in the posterior fronix or by passing of
amniotic fluid from the cervical canal.
 PROM can be confirmed by the following tests and
examinations
 Pooling:
 Is the collection of amniotic fluid in the posterior
fronix
 Nitrazine test:
 This test is based on the pH difference between the
vagina and AF (normally vagina pH is 4.5 to 6.0 and
the pH of amniotic fluid is 7.1 to 7.3).
 Nitrazine test is a sterile cotton tipped swab that is
used to collect fluid from the posterior fornix and
apply it to Nitrazine (phenaphthazine) paper.
 In the presence of amniotic fluid, the Nitrazine
paper turns blue, demonstrating an alkaline pH
(7.1-7.3). False positive Nitrazine tests result from
semen, alkaline antiseptics, bacterial vaginosis and
blood.
 Ferning test:
 Fluid from the posterior fornix is placed on a slide
and allowed to air-dry.
 Amniotic fluid will form a fern-like pattern of
crystallization.
o Cervical mucus can cause ferning, but it is
usually patchy and less extensive than that
with AF.

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 Observing loss of fluid from the cervical os when patient

coughs or performs a Valsalva maneuver during
speculum examination
 If no free fluid is found, a dry pad should be placed under
the patient's perineum and observed for leakage

 If the diagnosis has not been confirmed by all the above

methods, perform:
 Ultrasound examination
o Oligohydramnios?
 Amniocentesis and inject a dilute solution of indigo
carmine dye
o Inject the dye after taking amniotic fluid for pulmonary
maturity testing, analysis for evidence of subacute
intra-amniotic infection and possible culture and
sensitivity testing.
o After 15-30 minutes, examination of the patient's
perineal pad will reveal blue dye if the membranes are
ruptured.
o This is also known as the tampon test because the dye
is usually identified by its absorption into a tampon.

DIFFERENTIAL DIAGNOSIS
 Urinary incontinence
 Leucorrhea gravidarum
 Vaginal discharge (excessive)
 Perspiration
 Ruptured cyst (like in the vagina)

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MANAGEMENT

 Management of PROM Management depends on: Gestational

age, duration of rupture of fetal membranes, fetal condition
(dead, fetal distress, congenital malformations), presence of
infection, labor and previous cesarean scar, and other
obstetric indications.
1. Gestational age greater than 34 weeks
a. Rupture of fetal membranes greater than 8hours and
no previous c/s:
o Start Ampicillin 2gm IV QID until delivery
o Start induction with oxytocin if no labor
o Caesarean delivery is indicated in
malpresentation
b. Rupture of fetal membranes greater than 8hours and
previous c/s:
o Prophylactic antibiotics (eg. Ampicillin 2gm
iv stat)
o Immediate cesarean delivery
c. Rupture of fetal membranes less than 8 hours and no
previous c/s: -
o Follow fetal and maternal condition for
spontaneous onset of labor for total of 8 hours
duration and then start induction if labor does
not start –
o Caesarean delivery is indicated immediately in
mal presentations
d. Rupture of fetal membrane less than 8hours and
previous c/s:
o Depends on mother’s preference whether she
wants observation for spontaneous onset of labor
for 8 hours or immediate delivery by cesarean.

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2. Gestational age between 28- 34 weeks and alive fetus:

a. Rupture of fetal membranes in absence of infection:
o Ampicillin 2gm IV QID for 48 hours then
amoxicillin 500 mg PO TID for 7-10 days.
o Erythromycin 500 mg IV QID for 48 hours then
500 mg PO QID for 7-10 days.
o Start dexamethasone 6 mg IM BID for four doses
or Betamethasone 12 mg IM daily for two doses.
o Follow till 34-37 weeks of GA or till an indication
for delivery comes into picture during follow up.
b. Rupture of fetal membranes in presence of infection
and no previous c/s:
o Start Ampicillin 2gm iv QID + Gentamycin 80 mg
IV TID (Ceftriaxone 1 gm IV BID alone)
o Start induction with oxytocin if no labor
o Caesarean delivery is indicated in
malpresentations
c. Rupture of membrane with fetal death or severely
malformed fetus: -
o Deliver immediately with induction if there is no
previous c/s or by cesarean if there is previous
c/s.

Generally indications for pregnancy termination in PROM

 Term PROM
 Chorioamnionitis (regardless of GA)
 Labor
 Placental abruption with significant vaginal bleeding
 IUFD
 NRFHRP
 Congenital anomalies of fetus incompatible to life
 Abnormal fetal surveillance
 Active labor with advanced cervical dilation
 Fetal malpresentation with increased risk of cord prolapse

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Components of conservative management:

 Bed rest as long as there is leakage of liquor with restriction of

efforts that increase intra-abdominal pressure
 Temperature is recorded every 4- 6 hours
 Observation for malaise, abdominal pain, uterine tenderness
and smell of liquor on sterile vulval pads
 Leucocyte count and C-reactive protein may be done every
other day
 Prophylactic antibiotics be given as in the above
 Tocolytic drugs are given if uterine activity starts
 Corticosteroid therapy is given for gestations before 34 weeks.
 Treatment with antibiotics can potentially treat or prevent
ascending infection, prevent chorioamnionitis, reduce neonatal
sepsis, and prolong the latency period.

Management of PROM with viral infection (Herpes genitalis and HIV)

 Route of delivery is abdominal by c/d if duration of rupture of
fetal membranes is less than 4 hours and active herpes
genitalis is present.

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 SAMPLE HISTORY
C/c: Gush of fluid of 4hour duration
HPP
This is a 25years old G2 P1 (alive) woman who had her LNMP on
10/05/11 EC with an EDD of 15/2/12 EC and GA of 37+1 (on
30/01/12 EC). Menses was regular and it came every 28-30 days,
lasting for 4 days and there was no associated clot and discomfort.
She never used contraception.
The pregnancy was first confirmed when she went to a local health
center for missing her menses for two weeks and got suspicious of
being pregnant. And after urine sample was taken she was told she
was pregnant. She had 6 ANC follow ups at a local hospital. Her 1 st
ANC visit was on her second month of pregnancy. Complete history
was taken and physical examination was done. Urine sample, blood
sample was taken and U/S (ultrasound) was done. She remembers
her blood type is B+ (we ask if she knows her blood type because if
she is RH negative we have to make sure she took/takes anti-D),
but she does not remember her other results. She was given an
injection on her left arm (we can ask if she knows what the injection
was for- TT (tetanus toxoid) vaccine) and she was given red tablet to
take one tablet per day (iron supplementation).
And she was told everything was on good status. Her 2nd ANC follow
up was at her third month of pregnancy. Complete physical
examination was done and she was given another injection on her
arm (second dose of TT vaccine). Her iron supplement was
continued and she was told everything was good and that there was
no problem. Her 3rd, 4th, 5th and 6th were at her 4th, 5th, 6th and 7th
months of pregnancy. Routine history taking and complete physical
examination was done and it was uneventful. On her 5th visit she
was advised on birth. And U/S was done on her 6th visit.
She doesn’t remember when she started to feel fetal movement, but
fetal movement has not decreased since first felt. She had an
increase in appetite during the pregnancy. She increased her meals
from 3 times per day to 5 times per day.

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Her staple food is injera made of ‘tef’ and ‘shiro wot’ and ‘denech
wot’. She eats vegetables and fruits. She occasionally eats meat.
She claims she gained around 5kg since she changed her diet.
The pregnancy was wanted, planned and supported.
4 hours prior to admission she felt a sudden onset of leakage of
gush of fluid while she was washing her hands and it soaked her
clothing. Its consistency is water like. The fluid was clear watery
and it was odorless, and there was no associated pushing down
pain. Associated to this she had back pain. 1 hour prior to
admission while she was on the way to the hospital she started to
have pushing down pain.
Otherwise: -
Risk factors
She has no history of fever, chills
She has no history of foul smelling vaginal discharge (besides
showing sign of infection, large amount of vaginal discharge can be
mistaken for leakage of liquor)
She has no prior history if PROM
She has no self or family history of spontaneous preterm delivery
She has no history of vaginal bleeding during pregnancy
She has no history of smoking (or alcohol consumption)
She has no history of trauma to the abdomen
She has no history of chronic cough or straining during pregnancy
She denies and serious stress (stress incontinence)
(Danger signs)
She has no history of blurring of vision
She has no history of epigastric pain or right upper quadrant pain
She has no history of abnormal body movement or loss of
consciousness

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She has no history of headache

She has no history of nausea or excessive vomiting
She has no history of swelling of the face and hand (swelling of
independent areas of the body)
She has no history of flank pain
She has no history of cough or shortness of breath
Differential diagnosis
She has no frequency, urgency (urinary incontinence)
Others
She has no history of blood transfusion
She has no personal or family history of HTN or DM
Her sero-status for RVI is negative
(Then state her economic status)

PHYSICAL EXAMINATION
Vital sign: All, patient may be febrile (?)
HEENT: Conjunctiva
Abdomen: Check for uterine tenderness, uterine size (if fundal
height less than that of expected for gestational age, it indicate
oligohydramnios)
Pelvic examination:
 External genital examination: may show ongoing AF flow
 Speculum examination: the most important examination in
PROM (see the diagnosis section above)
 Once membrane rupture has been confirmed, avoid digital
vaginal examination until labor or induction of labor (avoid in
PPROM given the risk of infection).

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INVESTIGATION
 Investigations (Tests) that confirm diagnosis
 See above in the diagnosis section
 Other investigation
 CBC with differential
 Hct and H
 Blood type and RH
 Ultrasound for fetal size and amniotic fluid index
 n preterm urinalysis, culture and sensitivity testing done
by collecting urine by catheterization
 If between 32 and 34 weeks, amniotic fluid specimen
sent for fetal lung maturity test
 Amniocentesis in all women with PPROM before 34
weeks to test for evidence of intra-amniotic infection
 High vaginal swab for culture
 Biophysical profile

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CHAPTER 5

MULTIFETAL GESTATION
DEFINITION AND INCIDENCE
Multifetal gestation (MG): is when more than one fetus
simultaneously develops in the uterus. It could be:
 Two- twins, commonest
 Three- Triplet
 Four-Quadruplets
 Five- Quintuplet, etc…
MG result from:-
 two or more fertilization events, or
 a single fertilization followed by a splitting of the zygote, or
 a combination of both
INCIDENCE
 The overall multifetal birth rate was 34.5 per 1000, with
twins representing nearly 97 percent of these births in
western countries
 The frequency of monozygotic twin births is relatively
constant worldwide, and approximately one set per 250
births (4-5% of 1000 pregnancies). It is largely
independent of race, heredity, age, and parity.
 Incidence of multiple pregnancies is approximated using:
Helen’s Formula  1: 80n-1
 Twins 1:80
 Triplets 1: 802 = 1:6400
 Quadruplets (etc.) 1:803 = 1:512,000

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TWIN PREGNANCY
 It could be monozygotic (identical/uniovular)
or dizygotic(fraternal/ biovular)
 Dizygotic is common, (2/3rd) and monozygotic-1/3rd

Monozygotic twins
 Result from division of a single fertilized ovum
 Normally they are always of same sex
 Rarely they can be discordant for phenotypic sex,
one with 45XO chromosome (Turners syndrome)
and the other with normal 46XY chromosome
 They share:-
 Same physical characteristics; color of skin, hairand
eye
 Same body fluid
 Same genetic features; blood type and
histocompatibility genes
 They are often mirror images of one another
 Sometimes identical twins can be paradoxically
antithesis of identical.
 Earliest split may be associated with simultaneous
chromosomal error, resulting in heterokaryotypic
monozygotes, for example, one with down syndrome(
Trisomy 21) the other normal
 Although they are similar in a lot of ways, they have
different fingerprints.

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Genesis of Monozygotic twins

 Genesis of monozygotic twin is poorly understood, but it is
assumed to be from:-
1. Delay in the timing of normal developmental events.
2. Delayed ovum transport (pregnancies conceived in
close temporal proximity, progestational agents & COC
pills delay tubal motility monozygotic twining)
3. Minor trauma to the blastocyst during assisted
reproductive technology (ART)
 The division of one fertilized zygote into two does not
necessarily result in equal sharing of protoplasmic material.
 Because of this the process of monozygotic twinning is
in a sense a teratogenic event, and monozygotic twins
have an increased incidence of often discordant
malformations
 About a third as often, twins arise from a single fertilized
ovum that subsequently divides into two similar structures,
each with the potential for developing into a separate
individual

Zygosity and Chorionicity in MZ twins

Zygosity: is genetic make-up of twin pregnancy.

 Normally monozygotic twins have same genetic

makeup.
Chorionictiy: is the membrane composition, it is determined by
mechanism of fertilization and in monozygotic twins by timing of
embryo division
The table below shows the variation in fetal membranes and
placentation in time correlated genesis of MZ twins

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 The percentage distribution of placental variation is shown

below.

Assessment of chorionicity

 Ultrasonography (u/c) is an effective prenatal tool for

determining amnionicity and chorionicity.
 The optimal time for performing the u/s examination is in
the first trimester after 7 weeks (sensitivity ≥98%) with
lower but acceptable accuracy in the early second trimester
(sensitivity ≥90 percent).

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 Identification of two separate placentas is a highly reliable

indicator of dichorionic twins. This indicator is generally
only useful in early pregnancy since separate placentas
often appear fused later in gestation
 The presence/absence of the inter-twin membrane should
be determined and its characteristics assessed early in
pregnancy.
 Monochorionic/monoamniotic;(MCMA)
o The intertwine membrane is absent
 Dichorionic/diamniotic;(DCDA)
o An intertwin membrane with the "twin peak" or
"lambda" sign indicates dichorionic twins.
o The twin peak or lambda sign refers to a
triangular projection of tissue that extends
between layers of the intertwin membrane from a
fused dichorionic placenta.
o It is best seen at 10 to 14 weeks, becomes less
prominent after 20 weeks of gestation, and may
disappear.
o An additional clue that twins are dichorionic is
that the intertwin membrane is thicker with
dichorionic than monochorionic twins since
the DCDA membrane consists of four layers
(i.e. two layers of both amnion and chorion)
whereas the intertwin membrane in a MCDA
pregnancy only consists of two layers of amnion.
 Monochorionic/diamniotic;(MCDA)
o An intertwin membrane with the "T" sign
indicates a monochorionic/diamniotic placenta.
This sign refers to the appearance of the thin
intertwin membrane composed of two amnions as
it takes off from the placenta at a 90 degree
angle.
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 After the first trimester, identification of fetuses of different

sex is a highly reliable means of confirming a dichorionic
pregnancy.

Dizygotic twins
 Result from separately fertilized ova
 They:-
 bear resemblance of a sibling
 may or may not have same blood type
 can have different sex, but in about 75% of cases they
have same sex
 Dizygotic twins are not in a strict sense true twins because
they result from the maturation and fertilization of two ova
during a single ovulatory cycle
Risk factors for dizygotic twins
 Use of fertility stimulating drugs or artificial
reproductive technology (ART) -
 Dizygotic twins are more common in pregnancies
conceived with in vitro fertilization (IVF) than in
naturally conceived pregnancies (≥95 percent versus
70 percent) since double embryo transfer is commonly
performed as part of IVF.
 Clomiphene citrate is associated with 5-10% increase
risk of DZ twin
 Maternal age-
 The rate of natural twinning peaks at age 37 years,
when maximal
 FSH stimulation increases the rate of multiple follicles
developing. The fall in incidence thereafter probably
reflects physiological follicle depletion.

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 Race/geographic area -
 Significant ethnic/racial variations in the prevalence of
naturally conceived dizygotic twins occur worldwide.
 In one report:
o 1.3/1000 births in Japan,
o 8/1000 births in United States and Europe,
o 50/1000 births in Nigeria, were DZ twins
 Parity – Increasing parity correlates with an increased
likelihood of dizygotic twin birth.
 Pregnancy soon after cessation of long term oral
contraception
 Due to high rebound gonadotropin secretion
 Family history –
 Dizygotic twinning appears to have a genetic
component that is expressed in women but can be
inherited from either parent.
 Maternal weight and height –
 Obese (body mass index [BMI] ≥30 kg/m2) and tall
women (≥164 cm) are at greater risk for dizygotic twin
birth than underweight (BMI <20 kg/m2) and short
women (<155 cm).
 Diet - some studies have reported that folic
acid supplementation increased the rate of twinning.
Zygosity and Chorionicity in DZ twins
 Dizygotic or "fraternal" twins occur from ovulation and
fertilization of two oocytes, which results
in dichorionic/diamniotic placentation and two separate
placentas

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SEX RATIOS IN MG
 In humans, as the number of fetuses per pregnancy rises,
the percentage of male conceptuses declines.
 Percentage of Male fetus in
 singleton pregnancy- 51.6%
 twins, it was 50.9%
 triplets, 49.5% and
 quadruplets, 46.5%
 This female predominance was explained by two
explanations.
 First, beginning in utero and extending throughout the
life cycle mortality rates are lower in females.
 Second, female zygotes have a greater tendency to
divide.

PHYSIOLOGICAL CHANGES IN TWIN

 Increased weight gain-For normal BMI (increased by
16.8-24.5 Kg)
 Increased cardiac output
 Plasma volume increased by 500ml from singleton
 Increased GFR, Tidal volume & fetoprotein
 Increase BP at least 15 mm Hg in 95 percent of women
 The uterus and its non-fetal contents may achieve a
volume of 10 L or more and weigh in excess of 20
pounds!

DIAGNOSIS OF MG

HISTORY
 Pregnancy heavier(bigger abdominal girth) than previous
pregnancies
 Personal or family history of twins

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 Early onset preeclampsia

 Pregnancy following assisted reproductive technology
 Excessive weight gain
 Exaggerated minor ailments,
 Earlier and more severe pressure in the pelvis results in,
nausea, back pain, constipation, abdominal distention,
varicosities hemorrhoids
 The hormonal change associated with pregnancy which is
more severe in MG is also responsible for the aliments
PHYSICAL EXAMINATION
 Barrel- shaped “large” abdomen
 Excessive weight gain not associated with edema or obesity
 Obstetric palpation revealing:-
 Outline or ballottement of more than one fetus
 Big for date uterus
 More than two poles
 Multiple small parts
 FHR heard by two people at different areas with rate difference
of at least 10 bpm (with different rate to the maternal pulse).
 Palpation of 1 or more fetus after delivery of one neonate

INVESTIGATIONS
 Ultrasound:
 Diagnosis of MG,
 Determination of:-
o Chorionicity
o Gestational age
o Viability,
o Fetal anomalies
o Presentation, etc…

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 Biochemical:
 Serum hcG, MSAFP & unconjugated estriol are almost
doubled.
 Radiography: rarely done these days

COMPLICATIONS OF MULTIFETAL PREGNANCY

 MG is associated with higher rates of almost every potential
complication of pregnancy, with the exceptions of post-term
pregnancy and macrosomia.
 The most serious risk is spontaneous preterm delivery, which
plays a major role in the increased perinatal mortality and
short-term and long-term morbidity observed in these infants.
 The complications are classified in to maternal and fetal.

Maternal complication
 Hyperemesis
 Abortion
 Maternal anemia
 PIH(PE)
 APH
 Dysfunctional labor
 Malpresentation
 PPH
 Postpartum Depression, etc...

Fetal complication
 Fetal-fetal hemorrhage
 Perinatal mortality(4X,12X,26X–twin,triplet, quadruplet)
 Low birth weight
 Malformations
 Discordant
 Cord accident
 Polyhydramnios

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Unique complications of MZ twins

 Cord entanglement
 Conjoined Twins
 Vascular Anastomosis
 Discordant twin
 Locked twins

Cord entanglement:

 Cord entanglement occurs in most, if not all,

monoamniotic twin pregnancies.
 Loose cord entanglements probably begin in the first
trimester, and have the potential to tighten at any time.
 Intermittent occlusion of umbilical blood vessels may be
associated with neurologic morbidity; significant
prolonged occlusion can be lethal.

Conjoined twins

Incidence

 Conjoined twins are a rare type of monoamniotic twins,

estimated to occur in 1.5 per 100,000 births worldwide.
 Females are affected more often than males.

Types

 When twins are conjoined, the fusion occurs between

same body parts. Conjoined twins are classified as:

Types of conjoined twins Fused part

Cephalopagus Head
Thoracopagus Chest
Omphalopagus Abdomen
Ischiopagus Caudal
Pygopagus Sacrum

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Prenatal diagnosis

 The diagnosis should be suspected in 1st trimester MA

twin pregnancies when the embryonic/fetal poles are
closely associated and do not change in position with
respect to each other.
 Their findings, which are not all specific to conjoined
twins, include:-
 fetal hyperextension,
 increased nuchal translucency or cystic
hygroma,
 no sign of separate movement of the twins,
 juxtaposed embryos with a single midline
cardiac motion,
 fewer limbs than expected,
 a single umbilical cord with more than three
vessels,
 both heads or breeches consistently at the same
level to each other
 Color Doppler, fetal echocardiography, and three-
dimensional ultrasound examination can confirm the
diagnosis and clarify anatomy, which is critical for
assessing prognosis and pre- and postnatal decision-
making.
 Congenital anomalies are always present in conjoined
twins. The prognosis is poor because these anomalies
often preclude survival of one or both twins, even if
surgical separation is performed.

Vascular anastomosis between fetuses

 Nearly 100 % of monochorionic twin placentas have
vascular anastomosis.

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 Most of these vascular communications are

hemodynamically balanced and of little fetal
consequence.
 The two patterns of hemodynamically significant
anastomotic circulations include acardiac twinning and
the twin-to-twin transfusion syndrome
Acardiac twin
Pathogenesis
 Large artery-to-artery placental shunts in the
embryo, often also accompanied by a vein-to-vein
shunt, result in the TRAP sequence.
 The perfusion pressure of the donor twin
overpowers that in the recipient twin, who thus
receives reverse blood flow from its twin sibling.
 The "used" arterial blood reaching the recipient twin
preferentially goes to the iliac vessels and thus
perfumes only the lower part of the body, leading to
disruption or deterioration of growth and
development of the upper body.
 In the TRAP sequence, there is usually a normally
formed donor twin who has features of heart failure
as well as a recipient twin who lacks a heart
(acardius) and various other structures like:-
o Failure of Head development
acardius acephalus
o Partially developed head with identifiable
limbsacardius myelacephalus; and
o failure of any recognizable structure to form
 acardius amorphous
 Without treatment, the donor or "pump" twin has been
reported to die in 50 to 75 percent of cases.

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Twin-to-twin transfusion syndrome (TTTS)

 TTTS results from imbalances in fetoplacental blood flow

in the shared placental circulation
 It is a potentially lethal disorder that develops in 10 to 15
percent of monochorionic twins.
 Is characterized by oligohydramnios (including
anhydramnios) in one amniotic sac and polyhydramnios
in the other sac.
Cerebral palsy, microcephaly, porencephaly, and
multicystic encephalomalacia are serious
complications associated with vascular
anastomoses in twin gestations.
 Outcomes of TTTS
o Donor twin
 small, pale, dehydrated (IUGR)
 oligohydramnios (due to oliguria)
 die from anemic heart failure
 Recipient twin
 plethoric,
 edematous,
 hypertensive, ascites,
 kernicterus (need amniocentesis for bilirubin),
 hepatomegaly,
 polyhydramnios (due to polyuria),
 die from congestive heart failure, and jaundice

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 Diagnosis
 In utero
 Two ultrasound evidences:
 1st – MCDA pregnancy is identified
 2nd - Hydramnios (SDP >8 cm) in one sac
and oligohydramnios defined by SDP <2
cm in the other twin is found
 Although growth discordance or growth
restriction may be found with TTTS, these per
se are not considered diagnostic criteria.
 postnatal
 is made based on weight discordancy between
twins of 15 or 20 percent and a hemoglobin
level difference of 5 g/dL or greater, with the
smaller twin being anemic
 Staging
TTTS is typically classified by the Quintero (1999) staging
system :-
 Stage I—discordant amniotic fluid volumes as
described in the earlier paragraph, but urine is still
visible sonographically within the bladder of the
donor twin
 Stage II—criteria of stage I, but urine is not visible
within the donor bladder
 Stage III—criteria of stage II and abnormal Doppler
studies of the umbilical artery, ductus venosus, or
umbilical vein
 Stage IV—ascites or frank hydrops in either twin
 Stage V—demise of either fetus

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 Management
 Several therapies are currently used for twin-to-twin
transfusion, including
 amnioreduction,
 septostomy,
 laser ablation of vascular anastomoses, and
 selective feticide
Discordant twin
 Restricted growth of one twin fetus usually develops late
in the second and early third trimester and is often
asymmetrical.
 The cause of birth weight inequality in twin fetuses is
often unclear
 In monochorionic twins, discordancy is usually
attributed to placental vascular anastomosis
 Dizygotic fetuses may have different genetic growth
potential
Locked twin
 Occurred only once in 817 twin gestations.
 For twins to lock, the first fetus breech & second
cephalic. With descent of the breech , the chin of first
fetus locks between the neck and chin of second,
cephalic fetus. Cesarean delivery is recommended when
the potential for locking is identified

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MANAGEMENT IN MG
1. Antenatal management
 Diet: addition 300kcal /day
 Rest
 Supplementary iron & folate
 Frequent antenatal visits
 Fetal surveillance every 3-4 weeks
 Admission not mandatory
 Tocolytics, prophylactic cerclage & steroids to decrease
preterm labor are not indicated

2. Management during labor

 Open iv line for all mother with twin gestation
 Place of delivery in a hospital
 First stage same as singleton
 Experts: obstetrician/ anesthesiologist
 Liberal episiotomy
 Avoid general anesthesia
 Avoid uterotonics after 1st baby
 Induction & augmentation are contraindicated
Mode of delivery
 Mode of delivery depends on obstetric factors, presentation
of 1st baby, chorionicity & animosity
 Vaginal delivery if no indication for CD
 Cesarean delivery: Indications:-
 1st twin non vertex,
 Twins with complications: IUGR, conjoined,
Monoamniotic twins,
 Placenta previa,
 severe preeclampsia,
 previous C/D,
 contracted pelvis,
 post-term,
 abnormal uterine contraction
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Delivery of second twins

 Immediately after delivery of first fetus assess the lie,
presentation &FHB of second fetus.
 Vaginal: longitudinal lie
 Indications of urgent delivery of second twin:
 Severe intrapartum vaginal bleeding
 Cord prolapse of second baby
 1st delivery under GA
 Occurrence of fetal distress
 Inadvertent use of Ergometrine after 1st baby

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CHAPTER 6

MALPRESENTATION
OVERVIEW
Types of pelvic shapes
 Gynecoid pelvis: Classic female pelvis (50% of women)
 Android Pelvis: Typical male pelvis (25% of women)
 Anthropoid pelvis; predisposes to occiput posterior
 Platypelloid pelvis (rare); predisposes to transverse lie
hence shoulder presentation

Figure 1. Anatomical features of parent pelvic types: (A) Inlet; (B)

Cavity; (C) Outlet
 Fetal lie
The fetal lie indicates the orientation of the fetal spine relative to
the spine of the mother. The normal fetal lie is longitudinal and
by itself does not indicate whether the pre-sentation is cephalic
or breech.
 Fetal presentation
Position of fetus overlying the pelvic inlet

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 Fetal position
Is the relationship of a definite fetal part to maternal bony pelvis.
It’s different in early and late labor.
 In early labor; Left occipitotransverse
 At delivery; Occipitoanterior are normal findings
 Fetal attitude
It’s the degree of extension and flexion of fetal head. Can be
classified as:
 Flexed: Vertex; most common, chin is pressed against the
chest.
 Military; head is straight
 Extended; Brow (increased extension) and Face (complete
extension)
 Fetal station
Is the degree of descent of the presenting part through the birth
canal
 It’s expressed in centimeter above or below the maternal
ischial spine. If at the level of the spines it is at “0 (zero)”
station, if it passed it by 2cm it is at “+2” station
DEFINATION
Malpresentation is any presentation other than a vertical
orientation, or lie, and a cephalic presentation, with the flexed fetal
vertex presenting to the pelvis.

INCIDENCE AND RISK FACTORS

Malpresentation is seen in up to 3% to 5% of singleton gestations
at term, an abnormal lie, presentation, or flexed attitude
Factors associated with malpresentation include:
1) Diminished vertical polarity of the uterine cavity
2) Increased or decreased fetal mobility,
3) Obstructed pelvic inlet,
4) Fetal malformation, and
5) Prematurity.
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Includes: - Breech, Face, Brow, Compound and Shoulder

presentations

BREECH PRESENTATION
 The most common malpresentation and the infant presenting
occupy a longitudinal axis with the cephalic pole in the uterine
fundus.

INCIDENCE
 It occurs in 3% to 4% of labors overall, although it is found in
7% of pregnancies at 32 weeks and in 25% of pregnancies of
less than 28 weeks’ duration.

CLASSIFICATION
Based on their varying relations between the lower extremities and
buttocks, breech presentation can be classified as Frank, Complete
and Incomplete breech.
Types of breech presentation
Frank Breech Complete Breech Incomplete (Footling)
Breech
Lower extremities are Both hips are flexed, Both hips & knees are
flexed at the hips and and one or both knees partially flexed or knees
extended at the knees are also flexed may even be extended
presenting part presenting part Presenting part consists
consists of the two consists of two of one or both feet
buttocks and external buttocks, external (single/double footling
genitalia only genitalia and two feet breech
Incidence ; Common Incidence; Less Incidence is about 25%
60-70% common (10%) occurs
(commonly present in mainly in multigravida
primigravida*; about → 60%
70%)
Risk of cord prolapse; Risk of cord prolapse; Risk of cord prolapse;
0.5-1% 5% 15%
Associations with Associations with Associations with
prematurity; 38% prematurity; 12% prematurity; 50%

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* The increased prevalence in primigravida is due to a tight abdominal wall, good

uterine tone and early engagement of breech
Risk of labor abnormalities:
 Incomplete (footling) breech > Complete breech > Frank breech

A. B. C.
Figure 2. A. Frank Breech B. Complete Breech C. Incomplete
(Footling) breech

ETIOLOGY AND RISK FACTORS

The following are the known factors responsible for breech
presentation. In a significant number of cases, the cause remains
obscure.
 Prematurity: It is the commonest cause of breech
presentation.
 Factors preventing spontaneous version:
a) Breech with extended legs,
b) Twins,
c) Oligohydramnios,
d) Congenital malformation of the uterus such as septate
or bicornuate uterus,
e) Short cord, relative or absolute,
f) Intrauterine death of the fetus.
 Favorable adaptation:
a) Hydrocephalus—big head can be well accommodated in
the wide fundus,
b) Placenta previa,
c) Contracted pelvis,
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d) Cornufundal attachment of the placenta—minimizes the

space of the fundus where the smaller head can be
placed comfortably.
 Undue mobility of the fetus:
a) Hydramnios
b) Multipara with lax abdominal wall.
 Fetal abnormality: Trisomies 13, 18, 21, anencephaly and
myotonic dystrophy due to alteration of fetal muscular tone
and mobility.

DIAGNOSIS
The diagnosis of breech presentation may be made by abdominal
obstetric palpation or vaginal examination and confirmed by
ultrasound.
PHYSICAL EXAMINATION:
 Leopold’s maneuver
o First maneuver, the hard, ballotable, round fetal head
occupies the fundus.
o Second maneuver, identifies the smooth surface (back)
to be on one side of the abdomen and the small irregular
parts (extremities) on the other.
o Third maneuver, if not engaged, the softer breech is
movable above the pelvic inlet.
o After engagement, the fourth maneuver shows the breech
to be beneath the symphysis.
The accuracy of this palpation varies. Thus, with
suspected breech presentation or any presentation other
than cephalic—sonographic evaluation is indicated.
 Vaginal examination
o With a frank breech, no feet are appreciated, but the fetal
ischial tuberosities, sacrum, and anus are usually
palpable. After further fetal descent, the external
genitalia may also be distinguished.

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When labor is prolonged, the fetal buttocks may become

markedly swollen, rendering digital differentiation of a face and
breech difficult. In some cases, the anus may be mistaken for
the mouth and the ischial tuberosities for the malar eminences.
With careful examination, however, the finger encounters
muscular resistance with the anus, whereas the hard, less
yielding jaws are felt through the mouth. The finger, upon
removal from the anus, may be stained with meconium. The
mouth and malar eminences form a triangular shape, whereas
the ischial tuberosities and anus lie in a straight line.

With a complete breech, the feet may be felt alongside the buttocks.
In footling presentations, one or both feet are inferior to the
buttocks.
Although physical examination is very important Ultrasonography
is most informative in the assessment of breach presentation.
 It confirms the clinical diagnosis— especially in primigravida
with engaged frank breech or with tense abdominal wall and
irritable uterus.
 It can detect fetal congenital abnormality and also congenital
anomalies of the uterus.
 Type of breech (complete or incomplete).
 It measures biparietal diameter, gestational age and
approximate weight of the fetus.
 It also localizes the placenta.
 Assessment of liquor volume (important for ECV).
 Attitude of the head—flexion or hyperextension (important for
decision making at the time of delivery).
The point of designation in a breech labor is the fetal sacrum.
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COMPLICATIONS OF BREECH DELIVERY

Maternal risk/complications Fetal risk/complications
Operative delivery High PMR* 2-4 fold increased
Prolonged labor Intracranial hemorrhage
Asphyxia
Injuries
*Perinatal mortality rate

MANAGEMENT
ANTENATAL MANAGEMENT
Identification of complicating factors associated with breech and
External Cephalic Version (ECV) can be done if not contraindicated.
And formulation of the line of management should be done, if
version fails or contraindicated.
External Cephalic Version (ECV)
 ECV should be carried out in an area that has ready access to
a facility equipped to perform emergency cesarean delivery
(ACOG, 2016a).
 Because of the risk for surgical intervention, intravenous
access is obtained, and patients abstain from eating for 6 or
more hours.
 Sonographic examination is performed to confirm nonvertex
presentation, document amnionic fluid volume adequacy,
exclude obvious fetal anomalies if not done previously, and
identify placental location and fetal spine orientation.
The success rate of version is about 60%. Successful version
reduces the risk of cesarean delivery significantly.
ECV is considered from 36 weeks onwards. While version in the early
weeks is easy but chance of reversion is more. Late version may be
difficult because of increasing size of the fetus and diminishing volume of
liquor amnii. However, the use of uterine relaxant (tocolysis) has made
the version at later weeks less difficult.

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Contraindications of ECV
 Antepartum hemorrhage (placenta previa or abruption); risk of
placental separation
 Fetal causes—hyperextension of the head, large fetus (>3.5
kg), congenital abnormalities (major), dead fetus, fetal
compromise (IUGR)
 Multiple pregnancy
 Ruptured membranes—with drainage of liquor
 Known congenital malformation of the uterus
 Abnormal cardiotocography
 Contracted pelvis
 Previous cesarean delivery—risk of scar rupture
 Obstetric complications:Severe pre-eclampsia, obesity, elderly
primigravida, bad obstetric history (BOH)
 Rhesus isoimmunization

Breech with extended legs is not a contraindication for version

Success and dangers of ECV

Successful version is likely in Dangers of version:
cases of:
Complete breech Premature onset of labor
Non-engaged breech Premature rupture of
membranes
Sacroanterior position (fetal Placental separation and
back anterior) bleeding
Adequate liquor Entanglement of the cord round
Non-obese patient the fetal part or formation of a
true knot leading to impaired
circulation
Increased chance of feto-
maternal bleed
Amniotic fluid embolism
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MANAGEMENT AT TERM/LABOR
FIRST STAGE:

The management protocol is similar to that mentioned in normal

labor. The following are the important considerations. Spontaneous
onset labor increases the chance of successful vaginal delivery.
 Vaginal examination is indicated
(a) at the onset of labor for pelvic assessment,
(b) Soon after rupture of the membranes to exclude cord
prolapse.
 An intravenous line is sited with Ringer’s solution, oral intake
is avoided, blood is sent for group and cross matching
(considering the chance of CS).
 Adequate analgesia is given, epidural is preferred.
 Fetal status and progress of labor are monitored.
 Oxytocin infusion may be used for augmentation of labor.

INDICATIONS OF CESAREAN DELIVERY (CD):

 Weight : >3500 or <1800 & >1000 gm.
 Hyperextended fetal head
 Contracted pelvis
 Footling breech
 Abnormal fetal wellbeing tests
 Cord presentation/prolapse
 Presence of any risk factors – Post term; previous CS; APH;
DM; pre eclampsia…

SECOND STAGE:
There are three methods of vaginal breech delivery:
 Spontaneous (10%): Expulsion of the fetus occurs with very
little assistance. This is not preferred.

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 Assisted breech: The delivery of the fetus is by assistance

from the beginning to the end. This method should be
employed in all cases (see below).
 Breech extraction (partial or total):When part or the entire
body of the fetus is extracted by the obstetrician. It is rarely
done these days as it produces trauma to the fetus and the
mother. Indications are:
(a) Delivery of the second twin after IPV (Internal
Podalic Version),
(b) Cord prolapse,
(c) Extended legs arrested at the cavity or at the
outlet.

FACE PRESENTATION
 Face is a rare variety of cephalic presentation where the
presenting part is the face. The attitude of the fetus shows
complete flexion of the limbs with extension of the spine. There
is complete extension of the head so that the occiput is in
contact with the back.
The fetal chin (mentum) is chosen as the point of designation
during vaginal examination.

INCIDENCE
The reported incidence of face presentation ranges from 0.14% to
0.54% and averages about 0.2%, or 1 in 500 live births overall.

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Figure 3. Face presentation

ETIOLOGY OF FACE PRESENTATION
The cause of extreme extension of the head is not clear in all the
cases. The following are the factors which are often associated.
Maternal:
1. Multiparity with pendulous abdomen,
2. Lateral obliquity of the uterus especially, if it is directed to
the side towards which the occiput lies,
3. Contracted pelvis is associated in about 40% cases. Flat
pelvis favors face presentation,
4. Pelvic tumors.
Fetal:
1. Congenital malformations (15%)
(a) The commonest one is anencephaly. The almost non-
existent neck with absence of the cranium makes it
easy to feel the facial structure even with semi-
extended head,
(b) Congenital goiter—prevalent in endemic areas,
(c) Dolichocephalic head with long anteroposterior
diameter,
(d) Congenital branchocele.
2. Twist of the cord several turns round the neck.
3. Increased tone of the extensor group of neck muscles

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DIAGNOSIS

Antenatal diagnosis is rarely made. Diagnosis is made only during

labor but in about half, the detection is made at the time of delivery.
It is more often discovered by vaginal examination.

PHYSICAL EXAMINATION:
Second Leopold’s Maneuver, if mentoanterior:
 Fetal limbs are felt anteriorly.
 Back is on the flank and is difficult to palpate.
 The chest is thrown anteriorly against the
uterine wall and is often mistaken for back
Third Leopold’s Maneuver, if mentoanterior:
 Head seems big and is not engaged.
 Cephalic prominence is to the side towards
which back lies
 Groove between the head and back is not so
prominent
FHS is distinctly audible anteriorly through the chest wall of the
fetus towards the side of limbs.

Vaginal examination
The diagnostic features are palpating the mouth with hard alveolar
margins, nose, malar eminences, supraorbital ridges and the
mentum.
Sonography/Radiography: This should be done to confirm the
diagnosis, to exclude bony congenital malformation of the fetus and
to note the size of the baby.
MANAGEMENT

VAGINAL DELIVERY
 MENTOANTERIOR

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FIRST STAGE: In uncomplicated cases, a wait and watch policy is

adopted. Labor is conducted in the usual procedure and the special
instructions, as laid down in occipitoposterior positions, are to be
followed.
SECOND STAGE: One should wait for spontaneous delivery to
occur. Perineum should be protected with liberal mediolateral
episiotomy. In case of delay, forceps delivery is done.
 MENTOPOSTERIOR

FIRST STAGE: In uncomplicated cases, vaginal delivery is allowed

with strict vigilance hoping for spontaneous anterior rotation of the
chin.
SECOND STAGE:
1. If anterior rotation of the chin occurs, spontaneous or forceps
delivery with episiotomy is all that is needed.
2. In incomplete or malrotation: Early decision for the method of
delivery is to be taken soon after full dilatation of the cervix.
The following methods may be employed to expedite the
delivery.
 Cesarean section is the preferred method and is
commonly done these days.
 Manual rotation of the chin anteriorly followed by
immediate forceps extraction is rarely done these days.
The principles and the methods are similar to those
employed in unrotated occipitoposterior position.

BROW PRESENTATION
 Brow is the rarest variety of cephalic presentation where the
presenting part is the brow and the attitude of the head is
short of that degree of extension necessary to produce face
presentation, i.e. the head lies in between full flexion and full
extension.

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INCIDENCE

The reported incidence of brow presentation varies widely, from 1 in

670 to 1 in 3433, averaging about 1 in 1500 deliveries.
Brow presentation is detected more often in early labor before
flexion occurs to a normal attitude. Less frequently, further
extension results in a face presentation.

Figure 4. Brow presentation

ETIOLOGY

The causes of persistent brow are more or less the same as those of
face presentation. The position is commonly unstable and converts
to either vertex or face presentation.

DIAGNOSIS

Antenatal diagnosis is rarely made. The findings are more or less

like those of face presentation.
PHYSICAL EXAMINATION

Leopold’s maneuver:
The cephalic prominence and the groove between it and the back
are less prominent. The head feels very big and is nonengaged.
Vaginal examination
The position is to be confirmed on vaginal examination by palpating
supraorbital ridges and anterior fontanelle.
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If the anterior fontanelle is on mother’s left, with the sagittal suture

in transverse pelvic diameter, it is left frontum transverse position.
In late labor, the landmarks may be obscured by caput formation.

Sonography:
Is confirmatory and also helps in excluding bony congenital
malformation of the fetus.
MANAGEMENT

During pregnancy:
 If the presentation is diagnosed during pregnancy and there
are no other contraindications for vaginal delivery, nothing is
to be done. Contracted pelvis and congenital malformation of
the fetus are to be excluded. Spontaneous correction into face
is likely to occur.
Elective cesarean section:
 Cases with persistent brow presentation are delivered by
elective cesarean section.
During labor:
1. In uncomplicated cases, if spontaneous correction to either
vertex or face fails to occur early in labor, cesarean section is
the best method of treatment.
2. Manual Correction to face with full dilatation of cervix is
seldom practiced nowadays.
3. Craniotomy—if the labor becomes obstructed and the baby
is dead, craniotomy is done. Rupture of the uterus should be
excluded.

COMPOUND PRESENTATION
Whenever an extremity, most commonly an upper extremity, is
found prolapsed beside the main presenting fetal part, the
situation is referred to as a compound presentation.

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INCIDENCE
 The reported incidence ranges from 1 in 377 to 1 in 1213
deliveries. The combination of an upper extremity and the
vertex is the most common.
ETIOLOGY

Conditions preventing engagement of the head can result in

slipping of either upper or lower limbs by the side of the head.
 Prematurity (commonest),contracted pelvis, pelvic tumours,
multiple pregnancy, macerated fetus, high head with
premature or early rupture of the membranes and
hydramnios are the known etiological factors.

DIAGNOSIS

The diagnosis is not difficult when the cervical os is sufficiently

dilated to feel the limb by the side of the presenting part, especially
after rupture of the membranes. Premature or early rupture of the
membranes occurs in about one-third of the cases.
Cord prolapse is to be excluded because of its frequent association;
10–15%.

MANAGEMENT

Factors to be considered are:-

1. stage of labor,
2. maturity of the fetus,
3. singleton or twins,
4. pelvic adequacy and
5. Associated cord prolapse.

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Figure 5. Compound presentation

The fetal risks in compound presentation are birth trauma and cord
prolapse.
Indication of cesarean section:
 Mature singleton fetus associated with contracted pelvis or
cord prolapse with the fetus alive should be safely delivered
by caesarean section.

Expectant Management:
 In otherwise uncomplicated cases (vertex/hand), an attitude
of wait and watch policy is preferable.
 The labor process needs to be monitored very carefully
(preferably by electronic fetal monitoring).
 Elevation of the prolapsed limb with descent of the
presenting part usually takes place spontaneously. Slight
elevation of the prolapsed limb during uterine contraction is
a favorable sign. Temptation to replace the limbs early is not
only unnecessary but carries increased maternal and fetal
risks.

SHOULDER PRESENTATION (TRANSVERSE LIE)

 When the long axis of the fetus lies perpendicularly to the
maternal spine or centralized uterine axis, it is called
transverse lie. But more commonly, the fetal axis is placed
oblique to the maternal spine and is then called oblique lie.

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 In either of the conditions, the shoulder usually presents over

the cervical opening during labor and as such both are
collectively called shoulder presentations.

INCIDENCE

 The incidence is about 1 in 200 births. It is common in

premature and macerated fetuses, 5 times more common in
multiparae than primigravidae. Transverse lie in twin
pregnancy is found in 40% of cases.

ETIOLOGY

The causes are

1. Multiparity — lax and pendulous abdomen, imperfect uterine
tone and extreme uterine obliquity are the responsible factors.
2. Prematurity — center of the gravity lies almost in the middle of
the body.
3. Twins — it is more common for the second baby than the first
one to be in transverse position.
4. Hydramnios
5. Contracted pelvis
6. Placenta praevia
7. Pelvic tumors
8. Congenital malformation of the uterus—arcuate or subseptate
and
9. Intrauterine death

DIAGNOSIS

Abdominal examination
Leopold’s Manuever
 The fundal height is less than the period of amenorrhea.
 Fundal grip—Fetal pole (breech or head) is not palpable.

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 Lateral grip—
(a) Soft, broad and irregular breech is felt to one side of the
midline and smooth, hard and globular head is felt on
the other side. The head is usually placed at a lower level
on one iliac fossa.
(b) The back is felt anteriorly across the long axis in dorso-
anterior or the irregular small parts are felt anteriorly in
dorso-posterior.
 Pelvic grip— the lower pole of the uterus is found empty. This,
however, is evident only during pregnancy but during labor, it
may be occupied by the shoulder.

Vaginal examination
 During pregnancy; the presenting part is so high that it
cannot be identified properly but one can feel some soft parts.
 During labor; Elongated bag of the membranes can be felt if it
does not rupture prematurely. The shoulder is identified by
palpating the following parts—acromion process, the scapula,
the clavicle and axilla.

MANAGEMENT

ANTENATAL:

External cephalic version should be done in all cases beyond 35

weeks provided there is no contraindication as mentioned in breech
presentation. If the lie fails to stabilize even at 36th week, the case
is to be managed as outlined in unstable lie.
If version fails or is contraindicated:
 The patient is to be admitted at 37th week, because risk of
early rupture of the membranes and cord prolapse is very
much there. Elective cesarean section is the preferred method
of delivery.

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 Vaginal delivery may be allowed in a dead or congenitally

malformed (small size) fetus. The labor may be allowed to
continue under supervision till full dilatation of the cervix,
when the baby can be delivered by internal version.

DURING LABOR:

The principles in management are as outlined below:

 EARLY LABOR:
 External cephalic version: provided there is good amount of
liquor amnii and there is no contraindication.
 External cephalic version should be tried in all cases.
 Cesarean delivery is the preferred method of delivery if
version fails or is contraindicated.
 Difficulties are faced during cesarean section as the
lower uterine segment is poorly developed. However,
the fetus can be manipulated to a polar
(cephalic/breech) presentation before entering the
uterus and a low transverse incision may be made.
Otherwise lower segment vertical incision may be
made.

 LATE LABOR:
 Baby alive — there is hardly any scope of external version
in late labor because of invariable rupture of the
membranes and drainage of liquor.
 If the baby is mature and the fetal condition is good, it
is preferable to do cesarean section in all cases.
 Internal version— in a singleton fetus, the risk of
internal version is high. Not only it might inflict injury
to the uterus (rupture uterus) but also the fetal
mortality is increased to the extent of about 50%.

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 In modern obstetric practice, internal version is

not recommended except in the case of second
twin.
 Baby dead — cesarean section even in such cases is much
safer in the hands of those who are not conversant with
destructive operations.
 If the obstetrician is conversant with destructive
operation, decapitation or evisceration is to be done.
Following destructive operation, the uterine cavity is to
be explored to exclude rupture of the uterus. Internal
version should not be done.

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SECTION TWO
GYNECOLOGY

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CHAPTER 7

ABNORMAL UTERINE BLEEDING (AUB)

DEFINITION AND TERMINOLOGIES
Abnormal uterine bleeding (AUB) is any uterine bleeding which
deviates from the normal and may present with different patterns.

 The normal menstrual cycle consists of cyclic bleeding

approximately every 28 days plus minus 7 days each lasting
3-8 days, 5 on average and with about 10-80ml of blood loss
per cycle, with an average of 50ml loss.
There are several terms used to describe different patterns of AUB:-
1. Menorrhagia (heavy menstrual bleeding (HMB)): - defined as
cyclic bleeding at normal interval, the bleeding is either
excessive in amount (>80ml) or duration (>7 days) or both. The
term menotaxis is often used to denote prolonged bleeding
(duration).
2. Metrorrhagia (intramenstural bleeding): - irregular acyclic
bleeding from the uterus or bleeding that occurs between
regular cycles. The amount of bleeding is variable.
3. Menometrorrhagia: - the term applied when the bleeding is
irregular and excessive that the menses cannot be identified. It
is a problem in both cycle length and amount.
4. Polymenorrhea: - it is a regular menstrual bleeding which
occurs too frequently, i.e. every 21 days or less.
5. Hypomenorrhea: -regular menstrual bleeding with unusually
light flow. Lasts for less than 2 days.
6. Oligomenorrhea: - regular menstrual cycle that occurs more
than 35 days apart and remains constant in that frequency.

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7. Post coital bleeding: - bleeding after or during sexual

intercourse.
8. Withdrawal bleeding: - predictable bleeding resulting from an
abrupt decline in progesterone levels.
 Postmenopausal bleeding: menopause is marked by 12
months of amenorrhea after the final menstrual period.
Postmenopausal bleeding is any vaginal bleeding that occurs
more than 12 months after the last menstrual period.

Assessing heavy menstrual bleeding (HMB) in a clinical setting is

difficult, because patient’s perception of blood loss and objective
measurement often fail to correlate.
Objective methods of assessing blood loss
 Hallberg and associates described extracting hemoglobin
from sanitary napkins using sodium hydroxide. And it is
measured spectrophotometrically.
 Hemoglobin and hematocrit evaluation can be done.
 Hemoglobin concentration below 12g/dL increases the
chance of identifying women with HMB. A normal
level, however, does not exclude HMB.
 Estimating the number and type of pads or tampons used
during menses. There is a positive correlation between
objective HMB and passing clots more than 1 inch in diameter
and changing pads more frequently than every 3 hours.
 This is done using pictorial blood assessment chart (PBAC).
With a scoring sheet, patients are asked to record daily
number of sanitary products as scores of 1 point for each
lightly stained tampon, 5 if moderately saturated, and 10 if
completely soaked. Pads are similarly given ascending scores
of 1, 5, and 20 respectively. Small clots score 1 point, whereas
large clots score 5. Points are then tallied for each day. Totals
more than 100 points per menstrual cycle correlate with
greater than 80mL objective blood loss.
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 Menstrual calendars are also use by asking the patient to

record dates and blood flow quality throughout the month.
These aids diagnosis and to document improvement during
medical treatment.

INCIDENCE AND ETIOLOGY

 AUB occurs in 10-30% of reproductive age group women and
50% of perimenopausal women.
The etiologies include anatomic change, hormonal dysfunction,
infection, system disease, medications and pregnancy
complications.

Age related distribution of Etiologies of AUB

Although it may affect females of all ages, age and reproductive
status are the most important factors affecting incidence and
etiologies of AUB. The common causes of AUB in each age groups
include:-
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 Prior to menarche:
 The vagina rather than the uterus is more frequently the
source of bleeding.
 Vulvovaginitis is often the cause, but other causes can
be dermatologic conditions, neoplasms, trauma by
accident, abuse, or foreign body.
 Urethra bleeding may also originate from urethral
prolapse or infection.
 True uterine bleeding usually results from increased
estrogen levels as a result of:
 Precocious puberty
 Accidental exogenous ingestion
 Ovarian neoplasm
 In Adolescence( 1st decade after menarche):
 Anovulation and coagulation defects are common causes
in this age group.
 Anovulation results from immature Hypothalamic-
pituitary-ovarian (HPO) axis and leads to
amenorrhea alternating with polymenorrhea.
 Pregnancy, STIs and sexual abuse are also considered.
 Benign or malignant neoplastic growths are less frequent.
 Following adolescence (20-40yrs of age):
 Bleeding related to early and late complications of
pregnancy is common in this age group.
 STIs, leiomyomas and endometrial polyps are also
common.
 Since HPO axis matures, anovulatory uterine bleeding
is encountered less often.
 Perimenopause:
 As with perimenarchal age group anovulatory uterine
bleeding from HPO axis dysfunction is common.

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 The incidence of bleeding related to pregnancy and STIs

declines.
 Risk of benign and malignant neoplastic growth
increases.
 After menopause:
 Bleeding can result from:
 Benign conditions like endometrial or vaginal
atrophy, endometrial polyps, endometrial
hyperplasia or atrophic vaginitis.
 Malignant neoplasm like:-
- Endometrial carcinoma or estrogen-
producing ovarian carcinoma.
- Ulcerative vulvar, vaginal or cervical
neoplasms
- Rarely, serosanguinous discharge from
fallopian tube cancer may be a cause.

The new FIGO classification system known by the acronym PALM-

COEIN, classifies etiologies AUB as:-
 PALM represents the structural cause of AUB including Polyp,
Adenomyosis, Leiomyoma and Malignancy and neoplasia
 COEIN represents the nonstructural causes including
Coagulopathy, Ovulatory disorder, Endometrial, Iatrogenic and Not
yet identified.

 Previously a state of abnormal uterine bleeding that occurs in

the absence of any systemic medical illness or pelvic pathology,
i.e. no pathogenic cause identified, was used to be referred to
as a dysfunctional uterine bleeding (DUB). It was a
diagnosis of exclusion and was thought to attribute to 50% of all
AUB. But we do not use this term anymore. Coagulopathy,
endometrial dysfunction and ovulatory disorders replace the
collection of disorders previously encompassed by the term
DUB.

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COMMON DIFFERENTIAL DIAGNOSIS

 Pregnancy (first rule out pregnancy in women of
reproductive age)
 Incomplete abortion
 Ectopic pregnancy
 GTD
 Myoma
 Adenomyosis
 Endometrial polyps
 Endometrial hyperplasia
 Endometrial cancer
 Cervical cancer
 Sex cord stromal tumors (ovarian tumor)
 Infections- chronic endometritis
 Systemic abnormality – coagulopathy, hepatic and
chronic renal failure
 Thyroid disease (Hypothyroidism)
 Leech infestation

Ectopic pregnancy (EP)

 EP is when the blastocyst implants anywhere other than the
endometrial lining of the uterine cavity. The commonest site is
fallopian tube 95-96% (11% fimbrial, 70% ampullary, 12%
isthmic, 2-3% interstitial and cornual), then ovarian 3%,
abdominal 1%, cervical <1% and cesarean scar <1%.

Risk factors:-
 tubal pathology and prior tubal surgery (to restore tubal
patency or tubal sterilization)
 prior ectopic pregnancies
 smoking more than one pack cigarette per day
 pelvic inflammatory disease (PID)
 prior abortion and recurrent miscarriage

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 age ≥40 years and assisted reproductive technology (ART)

 prior IUD use
Clinical manifestation:
 The classic symptom triad of EP is amenorrhea followed by
vaginal bleeding and ipsilateral abdominal pain.
 Other symptoms include pregnancy discomfort such as breast
tenderness, nausea, and urinary frequency. Vertigo and
syncope may arise from hemorrhagic hypovolemia.

Physical examination:
 Speculum and bimanual examination may reveal an adnexal
mass that is often tender, a uterus that is small for gestational
age and bleeding from the cervix.
 Patients with ruptured EP may be hypotensive, tachycardic
and unresponsive.

Adenomyosis
 It is the extension of endometrial tissue (glands and stroma)
into the uterine myometrium leading to abnormal bleeding and
pain. These rests may be scattered throughout the
myometrium (diffuse adenomyosis) or maybe form a localized
nodular collection (focal adenomyosis).
 Diagnosis is usually based on the histologic findings in
surgical specimens. On gross examination the uterus is
globally enlarged, but rarely exceeds a 12week pregnancy.
Adenomyosis, endometriosis, and uterine fibroids (myoma)
frequently coexist.

Risk factors:
 Parity and age (40s and 50s)
 Use of selective estrogen-receptor modulator like tamoxifen.

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Clinical manifestation:
 Approximately one third of women have symptoms.
 Symptomatic adenomyosis occurs most often in parous
women between age 35 and 50.
 Most common symptoms are heavy menstrual bleeding (HMB)
and dysmenorrhea. There may also be compliant of
dyspareunia (10%).

Physical examination:
 Pelvic examination may reveal a diffusely enlarged globular
uterus.
 The uterus is usually less than 14cm. The consistency of the
uterus is typically softer and boggier than the firm, rubbery
uterus containing fibroids. It should have normal motility and
no associated adnexal pathology.

Endometrial polyps
 A polyp is a mass of tissue that develops on the inside wall of
a hollow organ. Endometrial polyps are localized benign
overgrowths of endometrial gland and stroma over a vascular
core.

Risk factors:
 increasing age (commonly 40-50 years 0ld),
 obesity
 tamoxifen use
 Use of oral contraceptive pills appear to be protective.
Clinical manifestation:
 Most commonly present with abnormal vaginal bleeding, heavy
cyclic or intermenstural bleeding. Bleeding may stem from
surface epithelium breaks associated with chronic
inflammation and vascular fragility or from apical ischemic
tissue necrosis.
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Endometrial hyperplasia
 It is the abnormal proliferation of both the glandular and
stromal elements of the endometrium. If left untreated, it can
progress to endometrial carcinoma and can also coexist
alongside endometrial carcinoma.
 Types include simple hyperplasia, complex hyperplasia,
atypical simple hyperplasia and atypical complex hyperplasia.
 Patients at risk for endometrial hyperplasia, like those at risk
for endometrial carcinoma, are at risk due to unopposed
estrogen exposure.

Risk factors:
 can be memorized with the mnemonic ‘ENDOMETRIUM’
 Excess exogenous estrogen use without progesterone
 Nulliparity
 Diabetes mellitus
 Obesity
 Menstrual irregularity
 Elevated blood pressure
 Tamoxifen use
 Rectal cancer (personal history of hereditary
nonpolyposis colorectal cancer)
 Infertility history
 Unopposed estrogen
 Menopause late (>age 55).

Clinical manifestation:
 Typically present with long periods of oligomenorrhea or
amenorrhea followed by irregular or excessive uterine
bleeding.

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 Uterine bleeding in a postmenopausal woman should raise

suspicion of endometrial hyperplasia or carcinoma until
proven otherwise.

Physical examination:
 Occasionally the uterus will be enlarged from endometrial
hyperplasia. This is attributed to both the increase in the
mass of the endometrium and to the growth of the
myometrium in response to continuous estrogen stimulation.
Usually the pelvic examination is unremarkable.
 Patients may also have stigmata associated with chronic
anovulation such as abdominal obesity, acanthosis, acne or
hirsutism.

Endometrial cancer
 It is the fourth most common cancer in American women,
exceeded only by cancer of the breast, bowel and lung.
Patients usually seek medical attention early due to vaginal
bleeding and endometrial biopsy leads quickly to diagnosis.
 The primary treatment is hysterectomy with bilateral salpingo-
oophorectomy (BSO) and staging lymphadenectomy for most
women. Most are diagnosed with stage I disease.
 Endometrial adenocarcinomas are categorized based on
histology as type I (80%) which occurs in women with a history
of chronic estrogen exposure unopposed by progestin (also
known as estrogen dependent neoplasm) and type II (20%)
which is an estrogen-independent neoplasm.

Risk factors:
 Obesity
 Polycystic ovarian syndrome,
 Long term high dose unopposed menopausal estrogens,
 Early age of menarche,

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 Late age of natural menopause,

 Infertility
 Nulliparity
 Menstrual irregularities
 Older age
 Tamoxifen use
 Diabetes mellitus and chronic hypertension,
 Cancer of the breast, ovary or colon
 Family history of endometrial cancer.
 Endometrial hyperplasia is another risk factor.
 Smoking cigarette is protective of endometrial cancer.
Clinical manifestations:
 80-90% of women with endometrial cancer have either
postmenopausal bleeding or some form of abnormal vaginal
bleeding (menorrhagia, postcoital spotting or intermenstural
bleeding.
 10% of women may also present with a nonbloody vaginal
discharge.
 Pelvic pain, pelvic mass and weight loss are seen in women
who present with more advanced disease.

Physical examination:
 May reveal obesity, acanthosis, nigricans, hypertension or
stigmata of diabetes.
 Look for signs of metastatic disease, including pleural
effusion, ascites, hepatosplenomegaly, general
lymphadenopathy, and abdominal masses.
 Typically have a normal pelvic examination.
 In more advanced stages of the disease, the cervical os may be
patulous, and the cervix may be firm and expanded. The
uterus may be of normal size or enlarged. The adnexa should
be examined for evidence of extrauterine metastasis and/or
coexistent ovarian carcinoma.

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Chronic endometritis (infection)

 Is an infection of the uterine endometrium; is the infection
invades into the myometrium, it is known as endomyometritis.
Underlying infection is often due to bacterial vaginosis,
Mycoplasma species, Neisseria gonorrhea and Chlamydia
trachomatis.

Risk factors
 retained products of conception
 sexually transmitted infections (STIs)
 intrauterine foreign bodies or growths
 Instrumentation of the intrauterine cavity.
 It is seen most commonly after CD, but also after vaginal
deliveries and surgical pregnancy terminations.

Clinical manifestation:
 Chronic irregular bleeding, discharge, pelvic pain and fever.

Physical examination:
 Bimanual examination revealing uterine tenderness. Vital
sign-febrile

Coagulopathy
 Coagulopathies are infrequent causes of gynecologic bleeding.
However, in women with HMB and normal anatomy, the
incidence is significantly higher.
 Most frequently identified coagulopathies include von
Willebrand disease, thrombocytopenia and platelet
dysfunction.

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Clinical manifestation
 Easy bruising, menorrhagia, excessive bleeding after dental
extractions, bleeding complications with surgery or obstetric
delivery, recurrent hemorrhagic ovarian cysts, epistaxis,
history of spontaneous bleeding, and gastrointestinal bleeding
or a family history of bleeding disorders.

Hepatic and chronic renal failure

 Severe renal dysfunction is often accompanied by endocrine
disturbance that leads to hypoestrogenism and amenorrhea or
to normal estrogen levels but anovulation.
NB, bleeding may worsen the chronic anemia already
associated with renal failure.
 Combined oral contraceptive pills (COCs) may be
contraindicated with severe hypertension, which commonly
complicates renal disease.
 Liver dysfunction depending on its severity can lead to
menstrual abnormalities.
 The underlying mechanism for bleeding is not clear, but
as in renal failure, hypothalamus-pituitary-ovary (HPO)
axis dysfunction is suggested.
 Hemostatic dysfunction may also contribute to bleeding.
Most coagulation proteins and most of their inhibitors
are synthesized in the liver.
 Thrombocytopenia is common in women with portal
hypertension and splenomegaly.

Thyroid disease
Both hyperthyroidism and hypothyroidism can cause menstrual
disturbances ranging from amenorrhea to HMB.

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 Mostly menstrual abnormalities precede other clinical findings

of thyroid disease therefore in most women with chronic AUB,
measurement of serum thyroid-stimulating hormone (TSH)
level is recommended.
 In hyperthyroidism, hypomenorrhea and oligomenorrhea are
more frequent complaints
 In hypothyroidism, women commonly present with
anovulation, amenorrhea and anovulatory AUB.

Clinical manifestations
Symptoms:
 Tiredness, weakness, dry skin, feeling cold, hair loss, difficulty
concentrating and poor memory, weight gain with poor
appetite, dyspnea, hoarse voice, menorrhagia (later
oligomenorrhea or amenorrhea).

Signs:
 Dry coarse skin, cool peripheral extremities, puffy face, hands
and feet (myxedema), diffuse alopecia (baldness), bradycardia.

Leech infestation
 Leeches are blood sucking water (aquatic) worms and are
parasitic to man and other animals. They are usually taken
into human body when using unfiltered or contaminated water
to bathe, drink or swim.
 Leeches possess different chemicals such as proteolytic
inhibitors which plays a role in the pathogenesis of leech
infestation, causing continuous bleeding from site of
attachment.

Risk factor: use of river water for deep douching.

Clinical manifestation: itching, bleeding and if it is severe it may
result in anemia.
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PATIENT EVALUATION
The main goal of evaluation of a patient presented with AUB is:
 Exclusion of pregnancy and malignancy and
 Identification of the underlying pathology

First confirm that the bleeding is through the vagina and not from
the urethra or the rectum.

HISTORY
 Thorough menstrual history
 Age at menarche
 Date of last menstrual period
 Timing and amount of blood
 Birth control method (contraception history) (IUD can be
associated with AUB)
 History of current bleeding
 Timing of bleeding (if during sexual intercourse,
intermenstrual…)
 Quantity of bleeding (amount) (excessive bleeding is
assessed by number of pads used, passage of clots (size
and number) and duration of bleeding).
 Tissue passage (r/o abortion)
 Any passage of vesicles (r/o GTD)
 Association with sexual intercourse ( may indicate
cervical or vaginal etiology)
 Associated symptoms
 fever (r/o infection),
 fatigue, dizziness and sense of rotation (anemia due to
increased blood loss),
 pain (dysmenorrhea often accompanies AUB caused by
infection, structural abnormality, pregnancy
complication),

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 bulk symptoms (due to abdominal mass when

considering pregnancy and tumor)
 Assess risk factors
 History of use of medication
 NSAIDs
 Anticoagulants
 Oral contraception
 HRT
 Corticosteroids
 Antidepressants and antipsychotics

PHYSICAL EXAMINATION
G/A: well looking, acute sick looking (in cases like EP), or
chronically sick looking ( in cases like ovarian neoplasms)
V/S:
 Tachycardia & tachypnea (? Severe anemia)
 Febrile (?Infection)
 Hypotension (? Massive blood loss)
HEENT: pale conjunctiva (signs of anemia)
LGS: Thyroid enlargement
Abdomen:
 abdominal swelling,
 tenderness with palpation
Pelvic examination: thorough pelvic examination is important,
including taking sample for Pap smear.
I/S:
 skin pigmentation, ecchymosis, purpura
 Dry/sweaty and cold/hot skin (thyroid disorders)
 palmar pallor (sign of anemia)
 hair distribution (hirsutism)

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INVESTIGATION
 Pregnancy tests ( beta-hCG) (for all in reproductive age group)
 Complete blood count (CBC) ( assess the presence of anemia,
infections and coagulopathy)
 Thyroid stimulating hormone levels (TSH)
 Ultrasonography
 Transvaginal sonography (TVS)
 Is chosen by many as a 1st line tool to asses AUB
over endometrial biopsy (EMB), because it:
- Allows assessment of both the endometrium
and myometrium
- Offers greater patient comfort
- Allows suitable detection of post-menopausal
endometrial hyperplasia

 Saline infusion sonography (SIS) (Sonohysterography)

 Is done by installing saline into the uterine cavity
during TVS
 It permits superior detection of intracavitary lesions
 It can be used for sonography-guided Pipelle EMB.
 Limitations:(see Williams gynecology 3rd Ed)
 Endometrial biopsy –
 To r\o malignancies
 Indications for EMB in a women with AUB
 Age >45 years (ACOG, 2012), but the JUSH
guideline says age >35yrs.
 The ACOG suggest EMB in those younger than 45
years with a history of
- unopposed estrogen exposure such as seen in
obesity or polycystic ovarian syndrome (PCOS)
- failed medical management
- persistent AUB

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 Hysteroscopy – involves direct visualization of the

endometrial cavity. Usually performed with Dilation and
curettage (D&C). Particularly useful when polyp or
submucosal fibroid is suspected, because these lesions can be
confirmed and removed under direct visualization.
 Cervical cytology
 Coagulation profile- if indicated

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CHAPTER 8

ABDOMINOPELVIC MASS (APM)

WHAT IS ABDOMINOPELVIC MASS?
It is abnormal Abdominal growth/mass/swelling that took its origin
down from pelvic.

PATIENT APPROACH
HISTORY:
Detailed and Comprehensive Hx is important
 Age- very important in narrowing Ddx
 Elaboration of the c/c (swelling)
 Duration, onset and location,
 progression- rapid growth is consistent with malignancy
 Associated sx - elaborate them accordingly,
 Pelvic/abdominal pain, low back pain-eg. Inflammatory or
invasive conditions
 Vaginal bleeding- eg. Myoma, Ectopic pregnancy..
 Vaginal discharge- eg. FT cancer, TOA…
 Fever- eg. TOA, Pyometra…
 Urinary sx- urgency, incontinence, retention…
 GI sx- constipation, bloating, early satiety- eg. Ovarian masses
 Fatigue, significant weight loss (may indicate malignancy)
 Risk factors (RF)
 Family hx and previous similar self complaint
 Reproductive status- ex. infertility can be RF (eg. low malignant
potential ovarian tumors) or complication of some APM (myoma,
endometrioma, hydrosalphnix).
 Menstrual and contraception hx
 Prior hx of PID
 Prior hx of any gynecological surgery, risk for ectopic Px,
textiloma

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PHYSICAL EXAMINATION
Thorough P/E is important
 General:- wastage from cancer
 Vital Signs:- including BMI (obesity is RF for some APM)
 LGS:- important in assessing metastasis (LNs, Breast)

 Hereditary ovarian cancer may occur synchronously

with Breast cancer and/or the later may
metastasize to ovary

 HEENT:- Anemia (Pale conjunctiva)-of chronic disease in

malignancies, from AUB 20 APM
 R/S:
• Pleural effusion 20 to meig’s syndrome (Ovarian fibroma) or
pseudomeigs syndrome (eg. mature teratoma, stroma ovarii,
Myoma, Benign FT)
• Metastasis to lung (eg. Choriocarcinoma, CRC, bladder cancer)

 Findings may include:- decreased tactile fremitus,

Dullness, decreased air entry, Localized BBS on
upper border of effusion

 Abdomen:
• Inspection-shape of abdomen, location of swelling, distended
vein, any skin color change, any previous surgical scar.
• Palpation- superficial and deep
 Size- in weeks of pregnant uterus size. (...a X weeks gravid
uterus sized APM...)
 12 weeks at symphysis pubis
 20 weeks at umbilicus
 38 weeks at xiphisternum

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 Origin- APM arising from the pelvis or an abdominal mass?

It can be differentiated by identifying if one can go below the
mass in to the pelvic cavity or not.

 Lower border of AMP is unreachable. i.e. one cannot

advance fingers between the mass and pubic symphysis

 Site-Location in the Abdomen

 Shape- globular, irregular
 Consistency- soft or cystic, firm or hard
 Surface contour-smooth, or nodular
 Border-regular or irregular
 Mobility- fixation may indicate adhesions or malignancy

 a fixed mass that is hard, nodular with irregular

borders indicate malignancy.

 Tenderness - indicate inflammatory process or torsion

 Surface Temperature -comparable or not with surrounding
area.

 Ex. There is a 14 wks. gravid uterus sized APM

which occupied lower Abdomen, mostly the left
side. The mass is hard, smooth, immobile, non-
tender and globular/irregular in shape with
irregular border and comparable surface
Temperature with surrounding.

 Percussion
 Shifting dullness and fluid thrill to detect ascites
 Differentiation of a large ovarian tumor versus ascites

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 Large ovarian tumor has central dullness with

tympanicity at the flanks as opposed to ascites
with central tympanicity

 Pelvic Examination
Complete (both abnormal and normal) finding should be reported
for every Gynecologic case.
1. Examination of external genitalia- Inspection and palpation
 Discharge or bleeding from the introitus – should be noted.
 Hymen
 Unruptured - septate, annular
 Imperforate
All can result in Hemato/Pyometra
2. Speculum examination
 Look for Cervix- scarring from previous procedures or
infection and/or cervical mass may interfere with menstrual
outflow and end up with hemato/pyometra
 Submucous Myoma may deliver through cervical canal
3. Digital vaginal examination (PV)
 Appreciate Vaginal wall, esp. Bulging in posterior
fornix(Cul-de-sac) (eg. In ovarian cancer metastasis)
 Transverse Vaginal septa- hemato/pyometra
 Cervical Excitation (motion tenderness)- PID
4. Bimanual pelvic examination
 Help to differentiate whether origin of APM is uterus or
adnexa (uterine origin mass move with cervical motion while
that of adnexal will not)

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5. Rectovaginal Examination
 Appreciate the rectal wall and pouch of doglus (for
nodularity of Cul-de-sac in case of metastasis and
endometriosis)
 Inspect for blood on examining finger for possibility of
Colorectal cancer (CRC)
 I/S &MSS:-

 Lower extremities edema may result as a

complication of compressive APM (when it is
large enough to compress large Pelvic
Vessels)

INVESTIGATIONS (IX’s)
 Laboratory Ix's
 Pregnancy test - with Urine or Serum ß-hCG should be
performed in any reproductive age group women with pelvic
mass
 CBC- Anemia, leukocytosis(TOA)
 Serum Biomarkers for malignancy- their utility is limited
esp. in reproductive age group women because of low
specificity

 Mainly useful for postoperative follow-up of the

patient (assessing the degree of response to
Therapies)

 Imaging
 Ultrasonography(U/S)- TVS and/or Abdominal U/S is the
best and 1st line imaging modality for evaluation of pelvic
mass

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 MRI &/or CT- for further evaluation (Anatomical details),

staging malignancy and planning surgery

 Other Imaging modalities- depending on patient's

presentation or primary image findings. Ex. Hysteroscopy
(if bleeding), HSG(Infertility), Cystoscopy/urodynamic
study (significant urinary symptoms)

 Pathological study

 definitive Dx of type of pelvic mass can be made only with

histopathologic evaluation of tissue sample

MANAGEMENT

Will be discussed under each case

DIFFERENTIAL DIAGNOSIS OF APM

 As the female pelvis is an anatomic region which is a quite
complex and contains organ of different system, Causes of
APM can be Gynecologic or non-gynecologic.
Gynecological masses:
 Ovary:
 Benign and malignant tumors
 Organic and Functional cysts
 Endometrium (Endometriosis to Ovary)
 Metastasis to Ovary (Breast, GI...)
 Fallopian Tube:
 TOA
 Ectopic pregnancy (EP)

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 Hydrosalpinx
 Para-ovarian/tubal cysts
 FT neoplasm
 Uterus:
 Fibroids/Myoma,
 Sarcoma,
 Fibroma
 Hemato/pyometra
 Adenomyosis
Non-gynecologic masses:
 GI system:
 Appendicular mass (Abscess, mucocele)
 Diverticular abscess
 Mesenteric cyst
 Colorectal Cancer (esp. left side)
 IBD (Crohn's disease)
 Intestinal tuberculosis
 Urinary tract:
 Pelvic kidney
 Bladder tumors,
 full bladder
 Urachus Cyst
 Miscellaneous:
 LAP's (eg.mesenteric LAP)
 Peritoneal carcinomatosis
 Pelvic Musculoskeletal tumors, infections
 Previous Surgery complications
 Foreign bodies(Texitiloma)

Depending on Age and Reproductive status of the women different

types of pelvic mass may be more likely than other

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 Infants and Adolescents:

 Ovarian tumor (germ cell ca, mature cystic teratoma)
 Follicular cyst and other functional cysts
 Pregnancy and it's complications
 Hemartoma- 2⁰ to imperforated hymen
 PID and its complications
 Endometrioma
 Appendicial Abscess
 NB, risk of malignancy is higher in prepubertal than in
adolescents
 Premenopausal (reproductive age):
 Functional cysts- follicular, corpus lutem
 Pregnancy related- Pregnancy, EP, theca lutein cyst
 Inflammatory-
 PID related-TOA, Hydrosalpinx
 Appendicular/diverticular Abscess
 Ovarian tumors- benign>>malignant
 Endometrioma
 Leiomyoma (uterine fibroid)
 Adenomyosis
 Para ovarian/tubal cyst
 Postmenopausal:
 Ovarian cancer (1⁰ and metastatic)
 Fallopian tube cancer
 Sarcoma of uterus

DISCUSSION ON SOME DDX OF APM

The most common causes of APM in our setup (ward admission) -
Ovarian Tumors and Myoma- will be discussed in detail under
separate chapter.

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1. Functional ovarian cysts

Follicular cyst:

 is the most common type of ovarian cyst

 In menstruating women, a follicle containing the ovum
(unfertilized egg) will rupture during ovulation. If this does not
occur (failure in ovulation), most likely 2⁰ to disturbances in
the release of the pituitary gonadotropins, the fluid of the
incompletely developed follicle is not reabsorbed, producing an
enlarged follicular cyst.
Corpus luteum cysts:
 appear after ovulation
 following normal ovulation, the granulosa cells lining the
follicle become luteinized. In the stage of vascularization,
blood accumulates in the central cavity, producing the corpus
hemorrhagicum. Resorption of the blood then results in a
corpus luteum, which is defined as a cyst when it grows
larger than 3 cm.
Theca lutein cysts:
 Occur within the thecal layer of cells surrounding developing
oocytes
 Under the influence of excessive hCG (in case of GTD,
clomiphene therapy and rarely normal pregnancy), thecal cells
may proliferate and become cystic. This is usually bilateral
Presentation of functional cysts
 Dull aching pain within the abdomen or pelvis,
 AUB, menstrual irregularity and Dysmenorrhea.
 Fullness, heaviness, pressure, swelling, or bloating in the
abdomen.
 pressure symptoms- urinary frequency, constipation
 Nausea or vomiting or weight gain
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Complications
 Rupture of ovarian cysts
 Adnexal torsion

2. Ectopic pregnancy (EP)

It is an early complication of pregnancy in which the embryo
attaches outside the uterus. Most EP (>95%) are tubal pregnancies.
It can also occur in the cervix, ovaries, or within the abdomen.
Risk factors-
 PID,
 use of IUD (failed IUD),
 previous exposure to DES,
 intrauterine surgery (e.g. D&C),
 smoking, previous EP,
 endometriosis,
 tubal surgery, and tubal ligation.
In up to one half cases, the RF cannot be identified
Presentation-
Hx: -
 vaginal bleeding,
 acute lower abdominal pain,
 pelvic pain,
 nausea, vomiting and diarrhea
 patient may be asymptomatic (10%)
P/E: -
 adnexal mass,
 tender cervix,
 adnexal tenderness
Ix: -
 serum ß-Hcg (increased), TVS

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Complications-
Rupture of an EP leads to
 abdominal distension,
 tenderness,
 peritonism and
 hypovolemic shock

3. PID related TOA & Hydrosalpinx

Tubo-ovarian Abscess (TOA)

 It is an inflammatory mass involving the FT, ovary and,
occasionally, other adjacent pelvic organs.
 Is one of the late complications of PID.
 Most commonly in reproductive age women
Presentation:
Hx:-
 Acute lower Abdominal/Pelvic pain,
 Fever, Chills,
 Purulent Vaginal discharge,
 Abdominal swelling,
 hx of prior STD
P/E:-
 Abdominal mass,
 pelvic tenderness (lower abdomen)
 Cervical motion tenderness (CMT)
Ix's:-
 CBC (Leukocytosis, elevated ESR),
 U/S (complex mass that mimic malignancy)
Complications: -
 Sepsis if abscess ruptured- life threatening

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Hydrosalpinx
 Is a distally (at fimbriated end) blocked FT filled with serous
or clear fluid. It is usually bilateral
 Cause can be PID (major cause), endometriosis, surgery,
tubal TB, cancer of FT & Ovary
Presentation-
 Commonly Infertility, recurrent lower Abdominal or
pelvic pain, prior hx of PID, Pelvic mass

4. Adenomyosis
Is characterized by uterine enlargement caused by ectopic rest of
endometrial tissue, both glands and stroma, located deep within
myometrium
 Both-ectopic tissue should be both glands and stroma
 Deep- superficial invasion of myometrium by endometrium is
normal
Can be classified into two
1. Diffuse type -ectopic tissue rests scattered and the uterus
becomes bulky and heavier.
2. Focal type (Adenomyoma)-localized, nodular collection of
ectopic tissues
Risk factors
 Parity-90% of cases occur in parous women
 Uterine surgery
 Age-nearly 80% occur in 40s and 50s
 Tamoxifen

Presentation:
 Mostly asymptomatic,
 if symptomatic-HMB, dysmenorrhea, dyspareunia, chronic
pelvic pain and bladder irritation

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Diagnosis
TVS:-sonographic finding of diffuse Adenomyosis includes
 a globular enlarged uterus
 anterior/posterior wall thickness asymmetry
 myometrial hypoechoic cysts
 Myometrial texture heterogeneity
 Diffuse myometrial echogenicity
 Ill-defined endometrial echo
 Striated projection extending from the endometrium to
myometrium (sign of endometrial invasion to the myometria)
MRI:-provides better diagnostic capability due to the increased
soft tissue differentiation and when coexisting myoma distort
anatomy
 Exact diagnosis of adenomyosis only possible in hysterectomy
specimen.

5. Hematometra/pyometra
 collection or retention of blood (or Pus-if blood is infected) in
the uterus
 develops when the Uterus becomes distended with blood 2⁰ to
menstrual outflow obstruction from blockage or atresia of the
lower reproductive tract—the Ux, Cx or Vx
 most commonly caused by congenital abnormalities, including
imperforate hymen, transverse vaginal septum or vaginal
hypoplasia.
 Other causes are acquired, such as cervical stenosis,
intrauterine adhesions, endometrial Carcinoma, and Cervical
Carcinoma.

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Risk factors
 uterine surgery such as endometrial ablation
 cervical Surgery or procedures
 female genital mutilation(FGM)
 Abortion
 childbirth
Presentation
 cyclic, cramping pain in the midline of the pelvis or lower
abdomen and Low back pain
 urinary frequency or retention and constipation
 dysmenorrhea (pain during menstruation)
 amenorrhea (lack of menstruation)
 postmenopausal women are more likely to be
asymptomatic.
 Fever and leukocytosis (pyometra)
 May develop low blood pressure.
 firm and enlarged Ux which may become tender

Diagnosis
 often based purely on the pt's Hx of amenorrhea and cyclic
abdominal pain + palpable pelvic mass
 confirmed by ultrasound

6. Para ovarian/tubal cysts

 are epithelium-lined fluid-filled cysts in the adnexa adjacent
to the FT and ovary.
 originate from the mesothelium and are presumed to be
remnants of the Müllerian duct and Wolffian duct
 Eg. Hydatid cysts of Morgagni, or Morgagni's cysts, are
common and appear as pedunculated, often tiny, frequently
multiple cysts connected to the fimbriae of the FT. They
thus appear to be a specific variant of paratubal cysts

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Presentation
 Mostly small and asymptomatic
 Pressure sx
 Pain in the pelvis
 Infertility

SAMPLE HISTORY: for major cases (myoma and ovarian masses) is

included in the respective portions of the topics

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CHAPTER 9

LEIOMYOMAS
DEFINITION AND EPIDEMIOLOGY
 Leiomyomas, (also referred to as fibroids or simply myomas)
are benign monoclonal tumors arising from the smooth
muscle cells of the myometrium.
 They are the most common pelvic tumor in women and they
are more commonly multiple.
Epidemiology
 The incidence of myoma ranges from 20-25%, but is as
high as 70-80% in studies using histologic or
sonographic examination
 It is responsible for 27 percent of inpatient
gynecologic admission and one-third of all
hysterectomies performed are for uterine fibroids
 Typically occur in women of childbearing age.
o The prevalence is highest between 35-40 years.
o Leiomyomas have not been described in
prepubertal girls, but they are occasionally
noted in adolescents.
o Most, but not all, women have shrinkage of
leiomyomas after menopause.
o African American women are more likely to:
o be younger at the time of diagnosis
o have larger fibroids and a greater number of
fibroids
o have heavier bleeding, and more severe
anemia

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FACTORS ASSOCIATED WITH LEIOMYOMA

Factors that increase incidences

 Race: the incidence is 2x greater in black women than in
white women.
o Differences in genetic factors, diet, lifestyle,
psychosocial stress, and environmental exposures
contribute this disparity.
 Early menarche: (<10 years old)
o is associated with increase of estradiol to post-pubertal
levels which can plausibly lead to increased fibroid
growth
 Reproductive and endocrine factors:
o Leiomyoma parallels the ontogeny and life cycle
changes of the reproductive hormones estrogen and
progesterone.
 Prenatal exposure to diethylstilbestrol
 Obesity:
o production of more estrogens from increased
conversion of androgens to estrogen in adipose tissue
by aromatase
 Diet:
o Significant consumption of beef and other reds meats
or ham is associated with an increased relative risk of
fibroids.
 Alcohol:
o Consumption of alcohol, especially beer.
 Genetics:
o Studies imply a familial predisposition to leiomyoma in
some women.

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Factors that decrease incidences

 Parity:
 Hormonal contraception:
o Long-acting progestin-only contraceptives (eg, depot
medroxyprogesterone) appear to protect against
development of leiomyomas
 Smoking:
o Decreases the risk of fibroid developments possibly
through the inhibition of aromatase
 Diet:
o Consumption of green vegetables and fruit (especially
citrus fruit), dietary vitamin A from animal sources
may also be associated with decreased fibroid risk.

PATHOPHYSIOLOGY
 The cause of uterine leiomyomas is unclear.
 Fibroids are benign monoclonal tumors, with each tumor
resulting from proliferation of a single smooth muscle cell.
 Genetic predisposition, steroid hormone factors, growth
factors, and angiogenesis may all play a role in the formation
and growth of uterine fibroids.
 Fibroids are hormonally responsive to both estrogen and
progesterone but the relationship is complex.
 Evidence for the relationship include:
o Myomas contain estrogen & progesterone receptors in
higher concentration than surrounding myometrium
o Myomas may increase in size with estrogen therapy &
in pregnancy
o They are not detectable before puberty
o During menopause, the tumors usually stop growing
and may atrophy in response to naturally lower
endogenous estrogen levels.
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 Progesterone increase mitotic activity & reduce apoptosis

 There may be genetic predisposition
 mutation in chromosome 6,7,12, and 14 are associated
with the rate and direction of tumors growth

CLASSIFICATION
Uterine fibroids are classified by:

 Simply their location in the uterus

 Submucous leiomyoma
 Intramural or interstitial
 Sub serous or sub peritoneal
 Parasitic
 Intra-ligamentary
 Cervical
 The International Federation of Gynecology and Obstetrics
(FIGO), as follows
 Submucosal myomas (FIGO type 0, 1, 2)
o protrude into the uterine cavity
 Intramural myomas (FIGO type 3, 4, 5)
o are located within the uterine wall
o they may enlarge sufficiently to distort the uterine
cavity or serosal surface
 Subserosal myomas (FIGO type 6, 7)
 They may have a broad or pedunculated base and
may be intraligamentary (i.e., extending between the
folds of the broad ligament).
 Cervical myomas (FIGO type 8) – are located in the cervix
rather than the uterine corpus.

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Figure 1: FIGO Classification of myoma

SECONDARY CHANGES IN MYOMA

Benign Degeneration
 Atrophic:
 Signs and symptoms regress or disappear as tumor size
decreases at menopause or after pregnancy.
 Hyaline:
 Yellow, soft, and often gelatinous areas. These tumors are
usually asymptomatic.
 Cystic:
 Liquefaction follows extreme hyalinization, and physical
stress may cause sudden evacuation of fluid contents
into the uterus, the peritoneal cavity, or the
retroperitoneal space.

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 Calcific (Calcareous):
 Sub serous leiomyoma are most commonly affected by
circulatory deprivation, which causes precipitation of
calcium carbonate and phosphate within the tumor.
 Septic:
 Circulatory inadequacy may cause necrosis of the central
portion of the tumor followed by infection and result
acute pain, tenderness, and Fever.
 Carneous (Red)
 Venous thrombosis and congestion with interstitial
hemorrhage are responsible for the color.
 Discrepancy between growth of myoma& blood
supply results in aseptic degeneration & infarction
 The process is usually accompanied by pain but is
self-limited.
 Most common during pregnancy,
 Myxomatous (Fatty):
 uncommon and asymptomatic, it follows hyaline and
cystic degeneration.
 Metastasizing Leiomyomata
 Rarely, myomas spread beyond the uterus to distant
locations such as the Peritoneum (Leiomyomatosis
peritonealis disseminate/LPD) distant vasculature, and
lung.
 They are often asymptomatic.
 Most women with these tumors have undergone a prior
dilatation and curettage (D&C), myomectomy, or
hysterectomy, suggesting the possibility of surgically
induced vascular spread of leiomyoma cells.
Carcinomatous changes
 Very rare; mostly leiomyosarcomadenovo.

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CLINICAL FEATURES
 The majority of myomas are small and asymptomatic
 The symptoms are related to the number, size, and location of
the tumors.

Symptoms are classified into three categories:

 Abnormal uterine bleeding (AUB)
 Bulk-related symptoms, such as pelvic pressure and pain
 Reproductive dysfunction (i.e., infertility or obstetric
complications)
 AUB:- in 30% of women
 Heavy or prolonged menstrual bleeding —the most
common fibroid symptom.
 Intermenstrual bleeding and postmenopausal bleeding
should prompt investigation to exclude endometrial
pathology.
 The presence and degree of uterine bleeding is
determined, largely by the location of the fibroid (size
is of secondary importance.)
o Submucosal myomas that protrude into the
uterine cavity (eg, types 0 and 1) are most
frequently related to significant heavy menstrual
bleeding than women with myomas in other
locations (34 versus 25 percent).
 The mechanism of bleeding are:
o Interruption of the blood supply to the endometrium
o Distortion and congestion of the surrounding
vessels, particularly the veins
o Ulceration of the overlying endometrium
o increased surface area

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o Alteration of normal myometrial contractile function

in the small artery and arteriolar blood supply
underlying the endometrium.
o Inability of the overlying endometrium to respond to
the normal estrogen/progesterone menstrual
phases, which contribute to efficient sloughing of
the endometrium.
o Pressure necrosis of the overlying endometrial bed,
which exposes vascular surfaces that bleed in
excess of that normally found with endometrial
sloughing.
 Bulk-related symptoms
 Irregularly shaped and enlarged myomatous uterus
exerts pressure on the surrounding structures,
resulting in:-
o pelvic pressure or pain: it is likely to be chronic,
intermittent, dull pressure or pain
o Pain result from degeneration associated with
 vascular occlusion
 infection
 torsion of a large pedunculated tumor
 myometrial contractions to expel a
subserousmyoma from the uterine cavity
o Urinary tract or bowel symptom
 Urinary symptoms –frequency, difficulty
emptying the bladder, or, rarely, complete
urinary obstruction. It may also result in
hydronephrosis
 Bowel symptoms –constipation.
o Venous compression — Very large uteri may
compress the vena cava and lead to an increase
in thromboembolic risk

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o Painful menses —in many women appears to be

correlated with heavy menstrual flow and/or
passage of clots.
o Painful intercourse — anterior or fundal fibroids
are the most likely to be associated with deep
pain with intercourse.
o Fibroid degeneration or torsion — fibroids cause
acute pain from breaking down of the fibroid
tissue.
 Reproductive dysfunction
 Leiomyomas account for 1 to 3 % of infertility
 Fibroids, particularly those that impinge upon the
endometrium, may affect fertility by:-
o interfering with implantation over the myoma site
o rapidly distending the uterus in early pregnancy,
o impairing uterine contractility
 The location of a fibroid, and not its size, is the key
factor regarding fertility
o Leiomyomata with a submucosal or intracavitary
component were associated with lower pregnancy
rates
 the likely mechanism is inhibition to normal
implantation
o In contrast, subserosal fibroids do not impact
fertility.
o The role of intramural fibroids in infertility is
controversial
 Fibroid near a fallopian tube ostium or near the cervix
may impede fertilization.
 Spontaneous Abortion; both uterine leiomyoma and
spontaneous miscarriage are common, and an
association between these has not been shown
convincingly.
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 Prolapsed fibroid
 Infrequently, a sub mucosal leiomyoma will prolapse
through the cervix and present with a mass, bleeding,
and possible ulceration or infection.
 Endocrine effects
 Rare symptoms of fibroid tumors where fibroids can
secrete ectopic hormones include:
o Polycythemia: from autonomous production of
erythropoietin
o Hypercalcemia: from autonomous production of
parathyroid hormone-related protein
o Hyperprolactinemia
The Mnemonic: “FIBROIDS” can be used to recall clinical
symptoms of uterine leiomyomas
 F: Frequency and retention of urine, hydronephrosis
 I: Iron deficiency anemia
 B: Bleeding abnormalities (menorrhagia, metrorrhagia,
menometrorrhagia, postcoital spotting), bloating
 R: Reproductive difficulties (dysfunctional labor, premature
labor/delivery, fetal malpresentation, increased need for
cesarean delivery)
 O: Obstipation and rectal pressure
 I: Infertility (failed implantation, spontaneous abortion)
 D: Dysmenorrhea, dyspareunia
 S: Symptomless (most common)

COMPLICATIONS
 Anemia
 Urinary or bowel obstruction from large or parasitic
myomas
 Malignant transformation is rare
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 Red degeneration
 Pregnancy associated complications (see below)
 Surgical complications especially ureteric injury or
ligation in cervical myomas.

MYOMAS AND PREGNANCY

 Myoma in pregnancy: Incidence: Around 0.1 – 3.9%
Influence of pregnancy on myoma:
 1/3 of the myoma increases in size,
 1/3 remain same and
 1/3 decreases in size
o When an increase has been reported, most of
the growth takes place in the early part of
pregnancy, after which they remain static or
decrease.
 Red degeneration
Influence of myoma on pregnancy:
 Early pregnancy bleeding and abortion
 Preterm labor
 Placental abruption: placentation over a fibroid appears
to be a consistently strong risk factor for abruption.
 IUGR
 Fetal compression syndromes: Dolicocephally, head
molding, asymmetric ventricles.
 Incarceration of the uterus:
o When trapped within the pelvis with further uterine
enlargement occurring by sacculation.
o Present with abdominal pain and urinary retention.
 At delivery:
o Malpresentation, obstructed labor,
o postpartum hemorrhage
o post-myomectomy uterine rupture

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DIFFERENTIAL DIAGNOSIS
Patient with myoma can present usually with AUB (more
commonly) or abdominal mass
For mass For AUB
Pregnancy Endometrial hyperplasia
Ovarian Ca Endometrial or tubal Ca
Tubo-ovarian abscess Uterine sarcoma
Endometriosis Endometrial polyps
Adenomyosis Adenomyosis
Myometrial hypertrophy DUB
Endometrial Ca…. Endometriosis…

MANAGEMENT
 Choice of treatment depends on:
 Symptoms
 Age of patient
 Parity
 Presence of pregnancy
 Plan for future fertility
 General health of the patient
 Location of the myoma

 General treatment include:-

 Treatment of anemia
 Analgesia
 Observation

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Observation:

 Asymptomatic leiomyomas usually can be observed

and surveyed during annual pelvic examination
 Exceptions:
o Fibroids growing rapidly
o If they are pedunculated and prone to torsion
o If they are likely to complicate future pregnancy
o If there is suspicion of malignancy

 Drug therapy:
 Advantage:
o Reduces / relieves symptoms
o Correct preoperative anemia
o Option for a women at late menopausal transition
 Disadvantage:
o Recurrence of fibroids after stopping treatment
Indications for medical management of uterine leiomyoma

GnRH agonist
 Is used for 3 – 6 months
 Control bleeding and improve preoperative HCT
 Is temporarily used till surgery is planned
 Is used if menopause is anticipated

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 Shrinks myomas (40 – 60%) to allow vaginal

hysterectomy and technically easier surgery with
diminished blood loss.
Mechanism of action (MOA)
 There are two suggested MOA of GnRH agonists
a) Effect on HPO axis
 GnRH agonists stimulate receptors on pituitary
gonadotropessupraphysiological release of LH
and FSH(called Flare and typically last 1 week)
 However, with their long-term action GnRH
agonists downregulate receptors in gonadotropes-
creates desensitization to further GnRH
stimulationdecreased gonadotropin secretion
 This leads to suppression of estrogen and
progesterone levels 1 to 2 weeks after initial
GnRH agonist administration
b) Direct effect on leiomyoma
 leiomyomas themselves may contain GnRH
receptors, and agonists may directly decrease
leiomyoma size
 GnRH agonists suppress leiomyoma cell proliferation and
induce cell apoptosis by the fourth week of GnRH agonist
therapy.

Side effects of GnRH agonists

 Occur in up to 95 percent of women

 They results from the profound drop in serum estrogen
levels
 It includes vasomotor symptoms, libido changes,
vaginal epithelium dryness, accompanying
dyspareunia, and loss in trabecular bone(6 months
use will result in 6% trabecular bone loss)

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 <10% of patients terminate treatment secondary to

side effects

 To obviate the side effects:-

o These agents alone are not recommended for longer
than 6-months’ use
o Or add-back therapy is added

Add back therapy

 Typically begun 1 to3 months following GnRH

agonist initiation
 Includes: estrogen combined with a progestin or
selective estrogen-receptor modulator(SERMs)
 Advantages of SERMs include the ability to begin
them concurrently with GnRH agonist treatment
without negating the agonist effects of leiomyoma
shrinkage.

LNG-IUS:

 Advantage:
 Reduces menorrhagia
 Avoids surgery
 Prevents pregnancy
 Disadvantage:-
 No improvement of bulk symptoms
 May lose string as uterus enlarges
Androgens:

 Danazole:-
 Reduces endogenous production of ovarian estrogens

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 Surgical Management
 It is the mainstay of treatment in myomas
 It should be timed closely to planned pregnancy, if
possible, to limit the risk of tumor recurrence
 Indications for emergency surgery are presence of
complications:
o Infected myoma
o Acute torsion
o Intestinal obstruction
 It includes:-
o Hysterectomy
o Myomectomy
o Myolysis.

Hysterectomy

 In symptomatic women who have completed child

bearing
 Can be performed
o vaginally,
o abdominally, or
o laparoscopically
 Conserve ovaries unless there is indication to remove
them
 Advantage:-
o Eliminates symptoms & recurrence
o The only definitive treatment
o Malignancy can be ruled out
 Disadvantage:-
o Preclude future fertility
o Surgical complications

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Myomectomy

 Methods
o Laparoscopic in subserous& intramural myomas
o Hysterescopic in submucous myomas
 Advantage:
o Fertility is preserved(since uterus will not be
removed) or enhanced
 Disadvantage:
o Hemorrhage during surgery requiring blood
transfusion
o Persistence of menstrual symptoms
o Recurrence of fibroids: 50–60% recurrence risk with
25 % requiring surgery
o Adhesion formation
 subsequent subfertility
 difficulty of subsequent myomectomy
When to conceive after myomectomy?
 After 3 – 6 months
 If pregnancy occurs following myomectomy,
recurrence rates are diminished as pregnancy has
protective effect on myoma growth
Myomectomy during pregnancy
 Generally avoid myomectomy in pregnancy
 Indications for myomectomy during pregnancy
o Intractable pain
o to gain access to fetus
o facilitate uterine repair at cesarean delivery

 Other managements
 Endometrial Ablation
 Uterine Artery Embolization (UAE)
 Magnetic Resonance Imaging-Guided Focused
Ultrasound (MRgFUS)

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 SAMPLE HISTORY
Chief compliant: Abdominal swelling of 6 months duration.
HPI:
This is a 32 years, Para 4(no abortion) mother, whose LMP was
two weeks ago. She was relatively healthy 6 months back at w/c
time she started to experience gradual onset of lower abdominal
swelling w/c was initially small and she noticed it first while she
was taking shower but later increased gradually to attain current
size w/c is around mid-abdomen. Associated with the swelling
she also developed mild lower abdominal pain of the same
duration w/c is dull, intermittent, nonradiating with no known
aggravating or relieving factors identified.
Her menses starts at age of 14 years. It comes every 28 day, last
for 3 to 5 days and she use 1to 2 pads per day. It is dark red,
non-clotting type and has no associated pain. But since 2
months back her menses become heavy and she started to use 4
to 5 pads per day and lasts for 9 to 11 days. It becomes bright
red, clotting and painful.
Otherwise:
She has no history of cigarette smoking alcohol intake
She has no history of previous self or family history of similar
illness in the families
She has no history of use of any contraceptive or other
medications
She has no history of gynecologic surgeries and procedures
She has no history of constipation, diarrhea or blood in stool
She has no history of urgency, frequency or pain during
urination

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She has no history of pain during sexual intercourse or any

bulging of swelling through vagina
She has no history of easy fatigability, weight loss or loss of
appetite
She has no history of cough or shortness of breath
She has no history of blurring of vision, vertigo or light-
headedness
She has no history of fever, malaise or rigor
She has no history of itching, burning sensation around genitalia
or foul smelling vaginal discharge
She has no history of nausea, vomiting and absence of
menstruation
She has no history of Orthopnea, PND or lower extremity swelling
She has no history of RUQ pain or yellowish discoloration of eye
She has no history of flank pain or decreased urine output
She has no history of personal or family history of DM, HTN,
asthma, TB or renal disease
She is seronegative for RVI
Her usual diet is injera made of teff with shirowot made of Atter
&she gets 3 times per day sometimes she gets meat, fruits &
vegetables.
She was 18 years old during her marriage and first coitus; she is
sexually active

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Physical examination
G/A: well looking
V/S: (all normal), look for any distressing signs(incase of
complications)
HEENT: Pink connective and non-icteric sclera
Abdomen
 Inspection:
 Abdomen is asymmetrically distended, more on the left
side of lower quadrant.
 Flanks are not full.
 No striae gravid arum, linea nigra, scar
 Inverted Umbilicus
 no distended veins, no visible peristaltic movement, or
pulsations
 hernia sites are free
 Superficial Palpation:
 there is no superficial tenderness or mass
 Deep palpation:
 There is 24 weeks sized mobile mass, that has
irregular surface, tender, firm in consistency whose
upper border is defined but lower border cant be
reached (hand cannot pass below mass into pelvic
inlet).
 Percussion: No shifting dullness or fluid thrill
 Auscultation: Bowel sounds well heard no bruits over the
mass.

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Pelvic Examination
 Bimanual pelvic examination:
 Irregular enlarged with well-defined border firm in
consistency mobile and tender mass on upper part of
uterus.
Assessment: Abdominopelvic mass secondary to symptomatic
myoma

Investigations
 CBC
o r/o anemia/polycythemia, infection, thrombocytopenia
(important for surgical patient)
 Blood group & Rh (for all surgical patients)
 Pregnancy test
 Ultrasound:
o it is used to determine size, location, consistency,
number of mass and hydro ureter & hydro nephrosis
 RFT (BUN & Serum creatinine)
 TFT(TSH, for surgical patient)
 Hystroscophy
 KUB or IVU (if urinary symptoms are there)
 Endometrial biopsy or D&C
o is essential in the evaluation of abnormal bleeding to
exclude endometrial Ca

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CHAPTER 10

OVARIAN TUMORS
EPIDEMIOLOGY
 A woman's risk at birth of having ovarian cancer sometime in
her life is 1% to 1.5%, and that of dying from ovarian cancer is
almost 0.5%
 Each year, more than 225,000 women are diagnosed, and
140,000 women die from this disease worldwide.
 Ovarian cancer is the fifth most common cause of death from
malignancy in women.

ETIOLOGY AND RISK FACTORS

Family history of breast or ovarian cancer is the most important
identifiable risk factor
 Approximately 10% of patients have an inherited genetic
predisposition.
Most risks in the other 90% of cases are related to a pattern of
uninterrupted ovulatory cycles during the reproductive years
Uninterrupted ovulatory cycles during the reproductive years and
repeated stimulation of the ovarian surface epithelium is
hypothesized to lead to malignant transformation.

RISK FACTORS
 Nulliparity (associated with long periods of repetitive
ovulation, and patients without children have double the risk)
 Infertility (One theory suggests that pregnancy may induce
premalignant ovarian cell shedding)
 Early menarche
 Late menopause
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 White race
NB, ovarian tumors are one of the few gynecologic
abnormalities that are common in the white population (POP
too)
 Increasing age (allows accumulation of random genetic
alterations within the ovarian surface epithelium)
NB, increasing age is risk only up to mid-70s, and the risk
decreases beyond 80yrs.
 Residence in North America and Northern Europe
(developing countries and Japan have the lowest rates,
regional dietary habits may be partly responsible)
 Family history
 Of ovarian cancer in first-degree relative (mother,
daughter, or sister) triples a woman's life time risk, the
risk further increase if the number of affected family
members increase
 Of Lynch syndrome (hereditary nonpolyposis colorectal
cancer, (HNPCC))
Although this syndrome is highly associated with life time
risk of colon cancer (85 percent), it also increase risk of
gynecologic malignancies like, ovarian cancer (10 to 12%)
and endometrial cancer (40 to 60%)
 Personal history of breast cancer
 Ethnic background (European Jewish, Icelandic, Hungarian)
 Postmenopausal hormone therapy
 Pelvic inflammatory disease
 Use of coffee, tobacco, alcohol & dietary fat

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Hereditary Ovarian Cancer

More than 90 percent of inherited ovarian cancers result from
germline mutations in the BRCA1 or BRCA2 genes, Patients
with a proven mutation has a dramatically elevated risk of
developing ovarian cancer (39 to 46 percent). BRCA2 is
located on chromosome 13q12 and in general is less likely to
lead to ovarian cancer (12 to 20 percent).

PROTECTIVE FACTORS
 Parity (having at least one child is protective of the disease,
with a risk reduction of 0.3 to 0.4%)
 Breast feeding ( perhaps by prolonging amenorrhea)
 Long-term (5 year) combination oral contraceptive use
(reduces the risk by 50%. The duration of protection lasts up
to 25 years after the last use)
 Prophylactic salpingo-oophorectomy (reduces, but does not
eliminate the risk because the entire peritoneum is stillgoing
to be at risk)
 Tubal ligation and hysterectomy, (theoretically, any
gynecologic procedure that precludes irritants from reaching
the ovaries via ascension from the lower genital tract might
plausibly exert a similar protective effect)
 consumption of foods low in fat but high in fiber,
carotene, and vitamins appears protective

CLASSIFICATION OF OVARIAN TUMORS(OVARIAN

MASSES)
 Based on clinical behaviors:
1. Benign
2. Borderline (low malignant potential)
3. Malignant

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 Based on morphologic characteristics:

1. Cystic
2. Solid
3. Mixed
 Based on histological features (cell origin)
1. Epithelial ovarian tumors
2. Germ cell tumors of the ovary
3. Sex-cord stromal tumors

BENIGN OVARIAN MASSES

 Functional Cysts
 Follicular Cyst
 Corpus Luteum (Granulosa Lutein) Cysts
 Theca Lutein Cysts
 Hyperthecosis
 Polycystic Ovarian Syndrome (Stein-Leventhal Syndrome)
 Luteoma of Pregnancy
 Endometriomas, (is not a functional cyst, but it is one of the
common ovarian cyst)
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 Epithelial Tumors
 Serous Tumors
 Mucinous Tumors
 Endometrioid Lesions
 Clear Cell (Mesonephroid) Tumors
 Transitional Cell (Brenner) Tumors
 Sex Cord-Stromal Tumors
 Thecoma
 Fibroma
 Hilus Cell Tumors
 Germ Cell Tumors
 MATURE Teratomas(dermoid cysts)

CLINICAL FEATURE OF BENIGN TUMORS

 Commonly seen in late child bearing age groups and most

are asymptomatic
 Dermoid cyst & mucinous cystadenomas are common in
reproductive age group
 Dermoid cyst & serious cystadenomas are common during
pregnancy
 If symptomatic-
o Swelling (distention),
o Heaviness
o Dull aching lower abdominal pain, are seen
 Signs are usually unaffected, but if there is any, it include:-
o Cachexia (in mucinous cystadenoma)
o Pitting edema (from compression of draining lymphatic
vessels and veins from the lower limb)
o Mass (cystic/ solid, mobile (from side to side but not
from above to downwards), usually smooth surface,
non-tender )
o Positive fluid thrill

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 Presence of an abdominopelvic mass (Ovarian fibroma),

ascites (fluid thrill), right pleural effusion (reduce tactile
fremitus & chest expansion dullness in percussion) is
indicative of Meig’s syndrome.

DIFFERENTIAL DIAGNOSIS FOR BENIGN OVARIAN MASSES

 Full bladder
 Fibroid
 Functional cyst
 Encysted peritonitis
 Pregnancy with or without fibroid
 Ascites
 Mesenteric cyst
 Para-ovarian cyst
 Textiloma (can be due to a forgotten gauze)
COMPLICATIONS OF BENIGN OVARIAN TUMORS

1) Torsion of the pedicle

2) Intracystic hemorrhage
3) Infection
4) Rupture
5) Pseudomyxoma peritonei
6) malignancy

BORDERLINE OVARIAN MASSES

 10 to 15 percent of epithelial ovarian cancers have histologic
and biologic features that are intermediate between clearly
benign cysts and frankly invasive carcinomas. They are termed
as low malignant-potential (LMP) tumors or borderline tumors.

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Although LMP tumors may develop at any age, on average patients

are in their mid-40s, which is 15 years younger than women with
invasive ovarian carcinoma.
Histologically, LMP tumors are distinguished from benign cysts by
having at least two of the following:-
 nuclear atypia
 epithelial stratification
 microscopic papillary projections
 cellular pleomorphism or
 mitotic activity
Unlike invasive carcinomas, LMP tumors lack stromal invasion,
LMP tumors lack stromal invasion. However, up to 10 percent of
LMP tumors will exhibit areas of microinvasion, defined as foci,
measuring < 3 mm in diameter and forming < 5 percent of the
tumor.

CLINICAL MANIFESTATION
 Ovarian LMP tumors present similar to other adnexal masses
(see manifestation of benign masses above)

MALIGNANT OVARIAN MASSES

Include:-
1. Epithelial ovarian cancer
2. Germ cell tumors
3. Sex-cord stromal tumors

EPITHELIAL OVARIAN CANCER (EOC)

Approximately 90% of ovarian cancers are derived from tissues that
come from the coelomic epithelium or mesothelium.

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PATHOGENESIS
There are three distinct tumorigenic pathways:-
 Most carcinomas appear to originate de novo from ovarian
surface epithelial cells that are sequestered in cortical
inclusion cysts (CICs) within the ovarian stroma.
 The replicative stress and DNA damage transforms the
entrapped surface epithelial cells within CICs into any of
the histologic ovarian cancer variants
 At least 10 percent of epithelial ovarian carcinomas, invariably
high-grade serous tumors, result from an inherited
predisposition.
 Women born with a BRCA gene mutation require only
one “hit” to the other normal copy (allele) to “knock out”
the BRCA tumor-suppressor gene product. BRCA-related
serous cancers appear to have a unique molecular
pathogenesis, requiring p53 inactivation to progress.
 Accumulation of genetic alterations that leads to malignant
transformation. As such, mutation the ras family of oncogenes
(K-ras, H-ras, and N-ras) are implicated in carcinogenesis by
their inhibition of cellular apoptosis and promotion of cellular
proliferation

HISTOPATHOLOGY AND PATTERN OF SPREAD

Histologic Type Cellular Type
I. Serous Endosalpingeal
II. Mucinous Endocervical
III. Endometrioid Endometrial
IV. Clear-cell “mesonephroid” Mullerian
V. Brenner Transitional
VI. Mixed epithelial Mixed
VII. Undifferentiated Anaplastic
VIII. Unclassified Mesothelioma,

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GRADING
Ovarian tumors are classified as:
 grade 1(well-differentiated)
 grade 2 (moderately differentiated)
 grade 3 (poorly differentiated) lesions
Patterns of Spread
 Transcoelomic: The most common and earliest mode of
dissemination of ovarian epithelial cancer is by exfoliation of
cells that implant along the surfaces of the peritoneal cavity.
The cells tend to follow the circulatory path of the peritoneal
fluid, to dependent areas
 Lymphatic: to the pelvic and para-aortic lymph nodes is
common, particularly in advanced-stage disease
 Hematogenous: at the time of diagnosis is uncommon

CLINICAL MANIFESTATIONS OF EOC

 More than 80% of epithelial ovarian cancers are found in
postmenopausal women. The peak incidence of invasive
epithelial ovarian cancer is at 56 to 60 years of age
 The age-specific incidence of ovarian epithelial cancer rises
precipitously from 20 to 80 years of age and subsequently
declines. Less than 1% of epithelial ovarian cancers occur
before the age of 21 years, two thirds of ovarian malignancies
in such patients being germ cell tumors
 About 30% of ovarian neoplasms in postmenopausal women
are malignant, whereas only about 7% of ovarian epithelial
tumors in premenopausal patients are frankly malignant
Symptoms:
The majority of women with epithelial ovarian cancer have vague
and nonspecific symptoms:

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In early-stage disease,
 Irregular menses if she is premenopausal.
 If a pelvic mass is compressing the bladder or rectum, she
may report, urinary frequency or constipation
 Occasionally, she may perceive
 lower abdominal distention,
 pressure, or pain, such as dyspareunia.
 Acute symptoms, such as pain secondary to rupture or
torsion, are unusual
In advanced-stage disease,
 Patients most often have symptoms related to the presence
of ascites, omental metastases, or bowel metastases,
include:-
 abdominal distention
 bloating, constipation, nausea, anorexia, or early
satiety
 Premenopausal women may report irregular or heavy
menses, whereas vaginal bleeding may occur in
postmenopausal women
Signs:
 The most important sign of epithelial ovarian cancer is the
presence of a pelvic mass on physical examination.
 A solid, irregular, fixed pelvic mass is highly suggestive of
an ovarian malignancy. If an upper abdominal mass or
ascites is also present, the diagnosis of ovarian cancer is
almost certain.
 In patients who are at least 1 year past menopause, the
ovaries should have become atrophic and not palpable. It has
been proposed that any palpable pelvic mass in these patients
should be considered potentially malignant, a situation that
has been referred to as the postmenopausal palpable ovary
syndrome.
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DIAGNOSIS
 Hx and P/E
 Investigations
Laboratory Tests
 CBC: Of affected women, 20 to 25 percent will present
with thrombocytosis (platelet count > 400 × 109/L).
Malignant ovarian cells releasing cytokines are believed
to increase platelet production rates
 serum electrolytes: Hyponatremia, typically ranging
between 125 and130 mEq/L
 serum tumor marker:
o CA125 levels are elevated, an elevated value (false-
positive) may be associated with various common
benign indications such as PID, endometriosis,
leiomyomas, pregnancy, and even menstruation
o the human epididymal protein 4 (HE4) tumor
marker
o OVA1 is another biomarker blood test panel: women
with an identified ovarian mass when surgery is
planned Ware Scores ≥ 5.0 in premenopausal and
scores ≥ 4.4 in postmenopausal women suggest a
need or gynecologic oncologist consultation
o cancer antigen 19-9 (CA19-9) and carcinoembryonic
antigen (CEA): when a mucinous ovarian tumor is
identified
Imaging
 Transvaginal sonography: In general, malignant tumors
are multiloculated, solid or echogenic, and large (> 5 cm),
and they have thick septa with areas of nodularity .
Other features may include papillary projections or
neovascularization demonstrated by adding color Doppler
Ascites, if present is easily detected,

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 Radiographic tests (CXR): detect pulmonary effusions or

infrequently, pulmonary metastases.
 Barium enema: helpful in excluding diverticular disease
or colon cancer or in identifying ovarian cancer
involvement of the rectosigmoid.
 Computed tomography (CT): scanning has a primary
role in treatment planning or women with advanced
ovarian cancer. Preoperatively, implants in the liver,
retroperitoneum, omentum, or other intraabdominal site
are detected to thereby guide surgical cytoreduction or
demonstrate obviously unresectable disease
 Magnetic resonance (MR) imaging
 Bone scan
 Positron emission tomography (PET)

Paracentesis
 This procedure is typically avoided diagnostically as
cytologic results are usually nonspecific and abdominal wall
metastases may form at the needle entry site

DIFFERENTIAL DIAGNOSIS FOR EOC

 Benign ovarian neoplasms
 Functional cysts of the ovaries.
 Pelvic inflammatory disease (TOA?),
 Endometriosis
 Uterine leiomyomata
 Nongynecologic causes of a pelvic tumor, such as an
 Inflammatory or neoplastic colonic masses
 A pelvic kidney

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STAGING OF EOC

Steps in surgical staging of EOC

 A midline or paramedian abdominal incision is recommended to
allow adequate access to the upper abdomen
 Any free fluid, especially in the pelvic cul-de-sac, should be
submitted for cytologic evaluation
 If no free fluid is present, peritoneal washings should be
performed by instilling and recovering 50 to 100 mL of saline
from the pelvic cul-de-sac, each paracolic gutter, and beneath
each hemidiaphragm.
 A systematic exploration of all the intra-abdominal surfaces and
viscera is performed, proceeding in a clockwise fashion from the
cecum cephalad, The small intestine and its mesentery from the
Treitz ligament to the cecum should be inspected
 Any suspicious areas or adhesions on the peritoneal surfaces
should be biopsied. If there is no evidence of disease, multiple
intraperitoneal biopsies should be performed.
 The diaphragm should be sampled either by biopsy or by
scraping with a tongue depressor and obtaining a sample for
cytologic assessment
 The omentum should be resected from the transverse colon, a
procedure called an infracolic omentectomy
 The retroperitoneal spaces should be explored to evaluate the
pelvic and paraaortic lymph nodes.

STAGES

FIGO Staging of Carcinoma of the Ovary, Fallopian Tube, and

Primary Peritoneal Carcinoma Stage Characteristics

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I= Tumor confined to ovaries (or to fallopian tubes)

 IA, Tumor limited to 1 ovary (or 1 tube); capsule intact, no
tumor on surface, negative washings
 IB, Tumor involves both ovaries (or both tubes), otherwise like
IA
 IC1, Tumor limited to 1 or both ovaries (or tubes), with
surgical spill
 IC2, Tumor limited to 1 or both ovaries (or tubes), with capsule
rupture before surgery or tumor on ovarian surface
 IC3, Tumor limited to 1 or both ovaries (or tubes), with
malignant cells in ascites or peritoneal washings
II= Tumor involves 1 or both ovaries (or 1 or both tubes) a with
pelvic extension (below the pelvic brim) or primary peritoneal cancer
 IIA Extension and/or implants on uterus and/or fallopian
tubes (and/or ovaries)
 IIB Extension to other pelvic intraperitoneal tissues
III= Tumor involves 1 or both ovaries (or 1 or both tubes) a with
cytologically or histologically confirmed spread to the peritoneum
outside the pelvis and/or metastasis to retroperitoneal lymph nodes
 IIIA1 Positive retroperitoneal lymph nodes only (i) Metastasis ≤
10 mm (ii) Metastasis > 10 mm
 IIIA2 Microscopic, extrapelvic (above the brim) peritoneal
involvement ± positive retroperitoneal nodes
 IIIB Macroscopic, extrapelvic, peritoneal metastasis ≤ 2 cm ±
positive retroperitoneal nodes. Includes extension to capsule of
liver/spleen
 IIIC Macroscopic, extrapelvic, peritoneal metastasis > 2 cm ±
positive retroperitoneal nodes. Includes extension to capsule of
liver/spleen

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IV= Distant metastasis excluding peritoneal metastasis

 IVA Pleural effusion with positive cytology
 IVB Hepatic and/or splenic parenchymal metastasis,
metastasis to extra-abdominal organs (including inguinal
lymph nodes and lymph nodes outside of the abdominal
cavity)

MANAGEMENT PRINCIPLE
Early stage (stage I-II)
 Low risk (Stage IA or IB, grade 1 and 2)
 Surgery:Total abdominal hysterectomy (TAH) & bilateral
salpingo-oophorectomy(BSO)
 Adjuvant chemotherapy not recommended.

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 High-risk
Includes: stage IA or IB, grade 3; Stage IC (tumor on external
surface, ruptured capsule, ascites or positive peritoneal
washing); clear cell histology and all stage II
 Surgery: TAH, BSO & surgical staging
 Chemotherapy: adjuvant chemo is recommended.
o Regimens: carboplatin (AUC=7.5) and paclitaxel
(175/m2) chemotherapy for 3-6 cycles.

Advanced-stage Epithelial Ovarian Cancer (stage III-IV)

 Surgery:
 Primary cytoreductive surgery (debulking)
o Includes: - TAH, BSO, complete omentectomy, and
resection of any metastases from peritoneal surface
or intestine.
o The goal is residual lesion < 1.5 cm
 Secondary cytoreductive surgery
o Considered after completion of first line
chemotherapy,
 Chemotherapy.
 Neoadjuvant chemotherapy (debulking chemotherapy)
o May be considered for sub-optimally staged
(resected) stage III & IV.
o 2-3 cycles may be helpful in patients with massive
ascites and pleural effusion

Prognostic Factors
 Pathologic Factors
 High grade tumors and those with extensive invasion
have poor prognosis
 Clear cell carcinomas are associated with a prognosis
worse than that of other histologic types

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 Biologic Factors: FIGO stage and ploidy

 Low-stage cancers tend to be diploid and high-stage
tumors tend to be aneuploid.
Patients with diploid tumors have a significantly longer
median survival than those with aneuploid tumors. 30%
of epithelial ovarian tumors expressed HER-2/neu
oncogene and that this group had a poorer prognosis.
The most commonly expressed tumor suppressor gene in
ovarian cancer is p53
 Clinical Factors:
 In addition to stage, the extent of residual disease after
primary surgery, the volume of ascites, patient age, and
performance status are all independent prognostic
variables.
Ovarian cancers that undergo intraoperative rupture or spillage do
not worsen prognosis, whereas tumors found to have already
ruptured preoperatively do have a poorer prognosis.
For early stage disease, poor prognostic variables were tumor grade,
capsular penetration, surface excrescences, and malignant ascites,
but not iatrogenic rupture

MALIGNANT OVARIAN GERMCELL TUMORS

 Germ cell tumors arise from the ovary’s germinal elements and
make up one third of all ovarian neoplasms.
Three features distinguish malignant germ cell tumors from
epithelial ovarian cancers.
 typically present at a younger age, usually in their teens
or early20s
 most have stage I disease at diagnosis
 prognosis is excellent—even for those with advanced
disease—due to exquisite tumor chemosensitivity
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HISTOPATHOLOGY
Modified WHO Classification of Ovarian Germ Cell Tumors Germ
cell tumors
Germ cell tumors
 Dysgerminoma
 Yolk sac tumor (endodermal sinus tumor)
 Embryonal carcinoma
 Nongestational choriocarcinoma
 Mature teratoma
 Solid
 Cystic(dermoid cyst)
 Immature teratoma
 Mixed germ cell tumor
Monodermal teratoma and highly specialized types arising from
a mature cystic teratoma
 Thyroid tumors (struma ovarii: benign or malignant)
 Carcinoids
 Neuroectodermal tumors
 Carcinomas (squamous cell or adeno-)
 Sebaceous tumors

DIAGNOSIS
Hx:
 Subacute abdominal pain in 85% of patients and reflects rapid
growth of a large, unilateral tumor undergoing capsular
distention, hemorrhage, or necrosis
 Severe acute abdominal pain. In 10 percent of cases,
secondary to cyst rupture, torsion, or intraperitoneal
hemorrhage
 Abdominal distention In more advanced disease, ascites may
develop and cause it
 Heavy or irregular menses Because of the hormonal changes
that frequently accompany these tumors

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P/E:
 A palpable mass on pelvic examination is the most common,
premenarchal patients may require examination under
anesthesia(EUA) to adequately assess a suspected adnexal
tumor. The remainder of the physical examination searches or
signs of ascites, pleural effusion, and organomegaly

Investigations
Laboratory Testing
 Serum Tumor Markers in Malignant Ovarian Germ Cell
Tumors

Placental alkaline phosphatase (PLAP), lactate dehydrogenase

(LDH) α1-Antitrypsin (AAT) can, are rarely be detected in
association with germ cell tumors.
Imaging
 same as for EOC

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MANAGEMENT
 Surgery:
 Fertility preserving surgery is generally possible
 The minimal surgery is unilateral oophorectomy and
surgical staging
 Chemotherapy:
 Is regarded as treatment of choice to preserve fertility as
it occurs in young ladies.
 Adjuvant chemotherapy
 Completely resected Stage I-III: Stage I, II, or III
(endodermal sinus tumors, mixed cell tumors, embryonal
carcinomas, choriocarcinomas, and immature teratoma)
need adjuvant chemotherapy.
 Radiotherapy
 Sensitive but rarely used as primary therapy of germ cell
cancers

OVARIAN SEX CORD-STROMAL TUMORS (SCST)

 SCST are neoplasms that originate from the ovarian matrix.
Cells within this matrix have the potential or hormone
production, As a result, individuals with these tumors
typically present with signs and symptoms of estrogen or
androgen excess.
The overall prognosis of ovarian SCSTs is excellent—primarily due
to early-stage disease at diagnosis and curative surgery.

EPIDEMIOLOGY

 SCSTs account for 3% to 5% of ovarian malignancies. These

tumors are more than twice as likely to develop in black
women. In contrast with (EOC) or (GCT), ovarian SCSTs
typically affect women of all ages.

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 There are no proven risk factors for SCSTs. However, obesity

as a hyperestrogenic state was independently associated,
whereas parity, smoking, and oral contraceptive use were
protective.
 The etiology of SCSTs is largely unknown. However, a single,
recurrent FOXL2 gene mutation (402C> G) is present in
virtually all adult-type granulosa cell tumors.

CLASSIFICATION

Modified WHO Classification of Ovarian Sex Cord-Stromal

Tumors
Pure stromal tumors
 Fibroma/fibrosarcoma
 Thecoma
 Sclerosing stromal tumor
 Leydig cell tumor
 Steroid cell tumor
Pure sex cord tumors
 Granulosa cell tumor
 Adult type
 Juvenile type
 Sertoli cell tumor
 Sex cord tumor with annular tumbles
Mixed sex cord stromal tumors
 Sertoli-Leydig cell tumors
 Sex cord-stromal tumors, NOS

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DIAGNOSIS
Hx
 Isosexual precocious puberty is the presenting sign in more
than 80 percent of prepubertal girls ultimately diagnosed with
an ovarian SCST.
 Adolescents often report secondary amenorrhea. Abdominal
pain and distention are other common complaints in this age
group
 In adult women, heavy, irregular bleeding and
postmenopausal bleeding are the most frequent symptoms.
 mild hirsutism that rapidly progresses to frank virilization
should prompt evaluation to exclude these tumors.
 The classic presentation is a postmenopausal woman with
rapidly evolving stigmata of androgen excess and a complex
adnexal mass.

P/E:
 Abdominal tenderness or a palpable mass
Investigations
Laboratory Testing:
 Elevated circulating levels of testosterone or androstenedione
or both are strongly suggestive of an ovarian SCST in a woman
with signs and symptoms of virilization.

Clinical hyperandrogenism is more likely to be idiopathic or related

to polycystic ovarian syndrome, but serum testosterone levels > 150
g/dL or dehydroepiandrosterone sulfate (DHEAS) levels > 8000 g/L
strongly suggest the possibility of an androgen-secreting tumor.
Imaging
 CT, MRI, U/S

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MANAGEMENT
 Surgery:
 Fertility preserving surgery is possible
 Unilateral salpingo-oophorectomy and surgical staging
for young ladies, however total abdominal hysterectomy
and bilateral salpingo-oophorectomy for older ones
 Chemotherapy:
 No recommendation of chemotherapy
 Radiotherapy
 Usually for recurrence only

OVARIAN CANCER DURING PREGNANCY

 Adnexal masses occurs in 0.2-2% during pregnancy and 5%
are malignant
 Found in 1% of 20,000 deliveries, 75% are early stage. Most
are unilateral and virilization sometimes occur
Relative frequencies by histologic types
Histologic types Frequency (%)
EOC 40
Germ cell tumors 30
SCST 17
Others 13

Diagnosis
 First trimester is the best time
 Based on clinical and ultrasound

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Management
 Surgery
 The optimum time for surgery is 16-18 weeks of
gestational age
 Symptomatic, complex and solid ovarian tumors should
be operated immediately
 Never perform TAH & BSO on the basis of frozen section
diagnosis, discuss options with the patient
 If Malignant or metastatic treat as non-pregnant or one
can omit hysterectomy Progesterone replacement if before
10 weeks of gestation and pregnancy to continue
 Adjuvant chemotherapy

Prognosis
 Pregnancy doesn’t worsen ovarian cancer, 5 year survival rate
is 72-90%

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 SAMPLE HISTORY

Chief complaint: Abdominal swelling of 8 month duration

HPI
This is a 59 years old nulliparous woman who has been
amenorrheic for the past 7 years. She was relatively healthy till 8
month back at which time she started to experience abdominal
swelling, w/c was initial in lower abdomen, but increase in size
gradually to attain its current size within 5months. She also has
lower abdominal pain for past 5mo w/c is non-radiating,
intermittent and aching type, w/c has no any alleviating or
exacerbating factors, the pain increase in severity recently and has
been preventing her from doing her routine activities. Associated to
this she has history of bloating, nausea, anorexia, early satiety,
constipation, urinary frequency and urgency (11 times per day) and
unquantified but significant weight loss of the same duration.
She started seeing her menses at age of 12, it used to come every
4wk and lasted 5 days, it did not show difference in amount month
to month, and it was not associated with any lower abdominal
discomfort. She stops seeing menses at age of 52. Her mother died
of ovarian cancer 7 years back. She usually eat injera made of teff
and shiro made ater with meat, she takes coffee 3x/day, and
around 5 bottles of beer every weekend.
Otherwise she has no Hx of:
 Oral contraceptive use and Postmenopausal hormone therapy
 Gynecologic surgery and radiation to pelvic
 Talc exposure
 Breast mass
 Vaginal bleeding
 Yellowish discoloration of eyes and contact with yelloished
discolored eye(chronic liver disease)

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 Blood in stool(colonic cancer)

 Cough and SOB(plural effusion)
 Contact with chronicle coughing person(pelvic TB)
 Multiple sexual partner, vaginal discharge or itching
sensation(PID, TOA)
Gynecologic history and Past obstetric history: add to HPI if
any pertinent Hx.
Physical examination:
 Do full examination
 Refer the Approach to APM for characterization of findings in
abdominal and pelvic examination
Assessment: APM secondary to r/o ovarian tumor
Investigation:
 CBC
o r/o anemia(of chronic disease), infection,
thrombocytopenia (important for surgical patient)
 Blood group & Rh (for all surgical patients)
 Ultrasound:
o it is used to determine size, location, consistency,
number of mass and hydro ureter & hydro nephrosis
 RFT (BUN & Serum creatinine) and TFT(TSH, for surgical
patient)
 CXR
o for all surgical patients above 60yrs old
 ECG
o for all surgical patients above


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CHAPTER 11

GESTATIONAL TROPHOBLASTIC DISEASE

Gestational trophoblastic disease (GTD)

 Refers to a spectrum of interrelated but histologically distinct

tumors originating from abnormal proliferation of trophoblast
of the placenta.
Gestational trophoblastic neoplasia (GTN)
 Refers to the subset of GTD that develops malignant sequelae.
These tumors require formal staging and typically respond
favorably to chemotherapy.
 GTNs are among the rare human tumors that can be cured
even in the presence of widespread dissemination.

EPIDEMIOLOGY AND RISK FACTORS

 Estimates of the incidence of GTD vary dramatically in
different regions of the world.
 For example, in Japan it is 2 per 1,000 pregnancies, which
is about threefold higher than the incidence in Europe or
North America (about 0.6 to 1.1 per 1,000 pregnancies) .
 This variation in incidence result from differences between
reporting population-based versus hospital based data.
 In Ethiopia from various hospital based studies the magnitude
is 1.8-3 per 1000 deliveries.
 From a thorough pathologic review, the incidence of partial
mole is reported to be higher than complete mole which is:-
 Complete mole- 1 per 1,945 deliveries
 Partial mole- 1 per 695 deliveries

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RISK FACTORS

 The main risk factors for hyaditidform mole are extremes of

maternal age and a history of pervious mole.
 Other risk factors include:-
 Prior molar pregnancy: -10x increased risk after
o After 11%,
o After 223%
o So for a women with prior history of molar pregnancy
, ultrasound examination first trimester is a must
 Extreme maternal age (<15 and >35years): -
o 2x for > 35, 7.5X for > 40 years, 45 years -1% , 50
years – 17%.
o B/C ova from older women may be more susceptible
to abnormal fertilization.
o This is much greater for complete mole than partial
mole.
 Prior unsuccessful pregnancies: -
o spontaneous abortion => 2x increased risk of GTD
 Combination oral contraceptive pills use: -
o doubles the risk
 Blood type AB, A, and B impregnated by BG- O
o Those with blood group AB tend to have worse
prognosis
 Vitamin A deficiency and low dietary intake of
carotene
o are associated only with an increased risk of
complete moles
 Higher educational levels, smoking,
 Irregular menstrual cycles,
 Obstetric histories in which only male infants are
among the prior live births
o are linked with partial moles

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CLASSIFICATION

Table 1

PATHOGENESIS
 Two forms moles exist: Complete and partial moles which are
different in karyotype, in histologic features, and clinical
presentation.
Cytogenetic studies demonstrate that:-
A complete mole:-
 Are usually euploid paternal in origin, and sex chromatin
positive- 46 XX (90%) or 46 XY (10%)
 It develops when an empty ovum with an absent or inactivated
nucleus is fertilized by a haploid sperm that duplicates its own
chromosomes or by two haploid sperm
Although nuclear DNA is entirely paternal, mitochondrial DNA
remains maternal in origin.

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Photography of complete mole

A partial mole:-
 Is triploid-69 XXY (70%), 69 XXX (27%), or 69 XYY (3%).
 It arises when an ovum with active nucleus is fertilized by a
duplicated or two haploid sperm.

Table 2 Comparison Between Complete And Partial Mole

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CLINICAL FEATURES
 Patients with complete molar pregnancy are increasingly being
diagnosed earlier in pregnancy and treated before they develop
the classic clinical signs and symptoms.
 This may be because of changes in clinical practice, such as
the frequent use of serum hCG measurement and vaginal US
in early pregnancy in women with vaginal staining and even
asymptomatic women.

Symptoms
 Vaginal bleeding:
 The most common symptom causing patient to seek
treatment in 97% previously, but currently 84 % of
patients.
 It results from separation of the molar villi from
underlying decidua.
 It usually is associated with passage of grape like
vesicles.
 Pelvic pressure or pain:
 due to enlarged uterus 28% or cystic ovaries
 Nausea and vomiting:
 which is excessive and requires medical attention
(HEG due to excessively elevated β-hCG), currently 8%
 Chest pain and dyspnea:
 B/c of trophoblastic embolization in 2 % of patients
(this is one of the feared fatal complication of GTD)
 Heat and cold intolerance, palpitation, sweating:
 B/c of hyperthyroidism which was observed in 7% of
patients with complete molar gestation as a result of
thyrotrophic effect of hCG, currently rare

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 Headache, blurring of vision, ABM, and epigastric pain:

 early onset pre-eclampsia previously 27%, currently 1
in 74
 Cramping lower abdominal pain:
 b/c of uterine contraction to evacuate its content
 Absent fetal kick:
 NB, 100% of pregnant ladies feels fetal quickening by
24 weeks of gestational age, if not it needs to be
evaluated

Signs
 Acute sick looking: bleeding, in respiratory distress, in pain
 Tachycardia, tachypnea, elevated BP (pre-eclampsia) or
decreased BP (heavy bleeding)
 Pale conjunctiva, icteric sclera, dry tongue and buccal
mucosa
 Thyroid swelling
 IC/SC retraction, crackles, decreased air entry
 Active precordium, S-3 gallop, systolic murmur- high
output heart failure 2ndry to anemia
 Soft abdomen (duffy abdomen), no palpable fetal parts,
uterine size greater than gestational age (positive
discrepancy by > 2 weeks), negative fetal heart sound.
 Adnexal mass
 Warm moist skin, tremor

Patients with partial hydatidiform mole usually do not have the

dramatic clinical features characteristic of complete molar
pregnancy.
In general, these patients have the signs and symptoms of
incomplete or missed abortion, and partial mole can be diagnosed
after histologic review of the tissue obtained by curettage.

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NATURAL HISTORY OF GTD

Complete mole
 Complete moles have a potential for local invasion and
dissemination.
 After molar evacuation, local uterine invasion occurs
in 15% of patients, and metastasis occurs in 4%.
 Risk factors for developing post molar tumor are:
 hCG level >.100,000 mIU/mL
 Excessive uterine enlargement > 14 weeks
 Theca lutein cysts 6 cm in diameter
 Older patients are also at increased risk of developing
postmolar GTT
 Persistent tumor, usually nonmetastatic, develops in
approximately 2% to 4% of patients with a partial mole, and
chemotherapy is required to achieve remission

COMPLICATIONS
 Hyper emesis gravidarum (HEG): in 8% of patients
 Pre-eclampsia before 20 weeks of GA:
 it was observed in 27% of patients with a complete
hydatidiform mole
 Hyperthyroidism: in 7% of patients with a complete molar
gestation.
 Anesthesia or surgery may precipitate thyroid storm.
 Thus, if hyperthyroidism is suspected before the
induction of anesthesia for molar evacuation, β-
adrenergic blocking agents should be administered.
 Thyroid storm may be manifested by hyperthermia,
delirium, convulsions, tachyarrhythmia, high-output
heart failure, or cardiovascular collapse.

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 Theca leutin cyst:

 Prominent theca lutein ovarian cysts (6 cm in diameter)
develop in about one half of patients with a complete
mole.
 After molar evacuation, theca lutein cysts normally
regress spontaneously within 2 to 4 months. If it is
bilateral it is sign of poor prognosis.
 Anemia: Because of heavy bleeding. Currently in 5%
 Trophoblastic embolization: in 2% of patients
 Local invasion and dissemination

INVESTIGATION
1. Pelvic Ultrasonography:-
 Ultrasonography is a reliable and sensitive technique for
the diagnosis of complete molar pregnancy. Its sensitivity
is 70 to 90 %

Sonographic features suggestive of a complete mole include:

 Absence of an embryo or fetus
 Absence of amniotic fluid
 Central heterogeneous mass with numerous discrete
anechoic spaces- this has classically been described as
a “snowstorm or swiss chess pattern”
 Ovarian theca lutein cysts

Sonographic features suggestive of a partial mole include

 Placenta with one or more abnormal findings:
enlarged, cystic spaces and increased echogenicity of
chorionic villi
 Increased transverse diameter of gestational sac- due
to embryopathy of tripoidy
 Amniotic fluid is present, but the volume is reduced
 Theca lutein cysts are usually absent
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On ultrasound a partial mole is diagnosed as missed or

incomplete abortion in 15 to 60 % of cases

2. CBC: Anemia
3. hCG:
 Sometimes urine hCG is negative because of excessively
elevated hCG level.
o This is because of both the capture and tracer
antibodies used in immunoradiometric assays
become saturated, preventing the binding of the two
to create sandwich.
o So after we have collected urine specimen we have
to dilute it with normal saline in 1 to 9ratio.
 This false negative test is called hook effect.
 The minimum hCG level for a positive test
o For Urine pregnancy test
 Qualitative test: 20 to 50 milli-int. units/mL,
depending on test
o Serum pregnancy test
 Qualitative test: 5 to 10 milli-int. units/mL, depending
on test
 Quantitative test: 1 to 2 milli-int. units/mL for an
ultrasensitive test

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 Causes for false positive and false negative urine hCG test
Causes 1. Performed too soon after conception; hCG concentration
of a false- is below threshold for a positive test
negative 2. The hCG isoform measured is different from the hCG
test isoform in the sample (pertains mostly to urine tests)
3. Hook effect due to extremely high hCG concentration
(>500,000 milli-int. units/mL, these levels are most
commonly seen in gestational trophoblastic neoplasia)

Causes 1. Recent first-trimester pregnancy loss (induced or

of a false- spontaneous) in which hCG levels, though declining, are
positive still elevated
test 2. Pregnancy loss very soon after implantation ("biochemical
pregnancy")
3. hCG secretion from a tumor
4. Pituitary hCG secretion
5. Interference from human antibodies against animal
antibodies or heterophilic antibodies (serum test positive
but urine hCG will be negative)
6. Patient has received a medication containing hCG or
certain antibodies

hCG: human chorionic gonadotropin.

4. Blood group and Rh

5. Chest x-ray for those with pulmonary symptoms
6. Histopathologic examination: Two specimens
 One specimen from the content of the uterus, to confirm
GTD and determine whether it is complete or partial mole
 Another specimen from the uterine wall to know whether
it is invasive or not.
7. Metatstatic workup: RFT, LFT, TSH, serum electrolyte, chest
X-ray, CT/MRI

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TREATMENT OF BENIGN GTD

After the patient's condition has been stabilized, a decision must be
made concerning the most appropriate method.

 Suction Curettage
 Preferred method for who desire fertility & involves the
following steps:
 Oxytocin infusion be setup / made ready before
induction of anesthesia.
 Cervical dilatation
 Suction curettage/electrical is preferred.

For uterine size < 14 weeks, it is better to put one hand

on fundus and massage the uterus.

 Sharp Curettage
 To remove any residual molar tissue
 Send it separately for histopathology.
 Anti-D immune globulin
 for Rh negative give at the time of evacuation
 Prophylactic Chemotherapy
 For high-risk is recommended (one of the following
required):
o hCG level >100,000 mIU/mL
o Excessive uterine enlargement (> 14-16 weeks)
o Theca lutein cysts ≥ 6 cm in diameter
o Poor compliance for follow up.

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 Hysterectomy
 For patients who doesn’t need their fertility. Need
follow-up like other patients.
 Benefits of hysterectomy for GTD patients
o No risk of postmolar malignancy
o No risk of endometrial cancer

Follow-up

 Patient needs follow up by β-hCG weekly until levels are

normal for three consecutive weeks, then monthly until
normal for 6 months because there is risk of postmolar
malignancy.
 Effective contraception during the entire follow-up is
mandatory.
 Because of the potential risk of uterine perforation,
intrauterine devices should not be inserted until the
patient achieves a normal hCG level.
 Estrogen-progestin contraceptives are preferred
because of their lower failure rate and relatively low
incidence of irregular bleeding, since this symptom
may raise concern about recurrence.
 When follow-up is difficult as per protocol:
 Patient can be appointed at 3 months (average time
when hCG expected to be normal).
 Counsel patient on symptoms of persistence

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GESTATIONAL TROPHOBLASTIC NEOPLASIA

 This term primarily encompasses pathologic entities that
are characterized by aggressive invasion of the
endometrium and myometrium by trophoblast cells.
Histologic categories include
 Common tumors: the invasive mole and gestational
choriocarcinoma
 Rare tumors placental-site trophoblastic tumor and
epithelioid trophoblastic tumor
 Most cases follow a hydatidiform mole. Rarely, GTN
develops after a term a live birth, miscarriage, or
termination.

Non metastatic Disease

 Locally invasive GTT develops in about 15% of patients after
evacuation of a complete mole and infrequently after other
gestations.
 These patients usually present with the following
symptoms:
 Irregular vaginal bleeding
 Theca lutein cysts
 Uterine subinvolution or asymmetric enlargement
 Persistently elevated serum hCG levels.
 The trophoblastic tumor may perforate the myometrium,
causing intraperitoneal bleeding, or erode into uterine
vessels, causing vaginal hemorrhage.
 Bulky, necrotic tumor may involve the uterine wall and
serve as a nidus for infection. Patients with uterine sepsis
may have a purulent vaginal discharge and acute pelvic
pain.

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 After molar evacuation, persistent GTT may exhibit the

histologic features of either hydatidiform mole or
choriocarcinoma.
 After a nonmolar pregnancy, however, persistent GTT always
has the histologic pattern of choriocarcinoma.
 Histologically, choriocarcinoma is characterized by sheets
of anaplastic syncytiotrophoblast and cytotrophoblast
without chorionic villi.

Placental-site Trophoblastic Tumor

 Placental-site trophoblastic tumor is an uncommon but
important variant of choriocarcinoma that consists
predominantly of intermediate trophoblast.
 Relative to their mass, these tumors produce small amounts of
hCG and human placental lactogen (hPL), and they tend to
remain confined to the uterus, metastasizing late in their
course.
 In contrast to other trophoblastic tumors, placental-site
tumors are relatively insensitive to chemotherapy.

Metastatic disease
 Metastatic GTT occurs in about 4% of patients after
evacuation of a complete mole, but it is seen more often
when GTT develops after nonmolar pregnancies.
 Metastasis is usually associated with choriocarcinoma,
which has a tendency toward early vascular invasion with
widespread dissemination.
 Because trophoblastic tumors often are perfused by fragile
vessels, they are frequently hemorrhagic.
 Symptoms of metastases may result from spontaneous
bleeding at metastatic foci.
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 The most common sites of metastases are lung (80%),

vagina (30%), pelvis (20%), liver (10%), and brain (10%).
Pulmonary
 At the time of diagnosis, lung involvement is visible by chest
radiography in 80% of patients with metastatic GTT.
 Patients with pulmonary metastasis may have chest pain,
cough, hemoptysis, dyspnea, or an asymptomatic lesion
visible by chest radiography.
GTT may produce four principal pulmonary patterns:
 An alveolar or “snowstorm” pattern
 Discrete rounded densities: cannon ball apperance
 Pleural effusion
 An embolic pattern caused by pulmonary arterial
occlusion
 Because respiratory symptoms and radiographic findings
may be dramatic, the patient may be thought to have a
primary pulmonary disease.
 Pulmonary hypertension may develop in patients with GTT
secondary to pulmonary arterial occlusion by trophoblastic
emboli.
 The development of early respiratory failure requiring
intubation is associated with a poor clinical outcome.
Vaginal
 Vaginal metastases occur in 30% of the patients with
metastatic tumor. These lesions are usually highly vascular
and may bleed vigorously when biopsied.

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Hepatic
 Liver metastases occur in 10% of patients with
disseminated trophoblastic tumor.
 Hepatic involvement is encountered almost exclusively
when there is a protracted delay in diagnosis and the
patient has an extensive tumor burden.
 Epigastric or right upper quadrant pain may develop if
metastases stretch the hepatic capsule.
 Hepatic lesions may be hemorrhagic, causing hepatic
rupture and exsanguinating intraperitoneal bleeding.
Central Nervous System
 Metastatic trophoblastic disease involves the brain in 10%
of patients.
 Cerebral involvement is generally seen in patients with
advanced disease;
 Virtually all patients with brain metastasis have
concurrent pulmonary or vaginal involvement or both.
 Because cerebral lesions may hemorrhage spontaneously,
patients may develop acute focal neurologic deficits.

DIAGNOSTIC EVALUATION
 All patients with persistent GTT should undergo a careful
pretreatment evaluation, including the following:
 Measurement of the serum hCG value.
 Hepatic, thyroid, and renal function tests
 Determination of baseline peripheral white blood cell
and platelet count

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 The metastatic workup should include the following:

 Chest radiograph or computed tomography (CT) scans
 Ultrasonography or CT scan of the abdomen and pelvic
CT
 Magnetic resonance imaging (MRI) scans of the head
 In patients with choriocarcinoma or metastatic disease,
hCG levels may be measured in the cerebrospinal fluid
(CSF) to exclude cerebral involvement if the results of CT
scanning of the brain are normal.
 The ratio of plasma-to-CSF hCG tends to be lower than
60 in the presence of cerebral metastases.

STAGING
 An anatomic staging system for GTT has been adopted by
the International Federation of Gynecology and Obstetrics
Stage I: Patients have persistently elevated hCG levels and
tumor confined to the uterine corpus.
Stage II: Patients have metastases to the vagina and pelvis
both.
Stage III: Patients have pulmonary metastases with or
without uterine, vaginal, or pelvic involvement.

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Stage IV: Patients have advanced disease and involvement

of the brain, liver, kidneys, or gastrointestinal tract. These
patients are in the highest risk category because they are
most likely to be resistant to chemotherapy.

MANAGEMENT
Depends on:

 WHO’s PSI
 Disease stage
 Previous chemotherapy

 When the prognostic score is higher than 7, the patient is

categorized as high risk and requires intensive
combination chemotherapy to achieve remission.
 Malignant GTD is curable in 85 – 100% as they are Chemo
sensitive.

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Risk stratification: Approximately 80% are low risk group

Low risk
 Hysterectomy plus single agent chemotherapy: If no
need of fertility
 Chemotherapy alone
 Commonly used agents  Methotrexate (M),
Actinomycin-D (A)
 Alternatives  Etoposide (E) & 5-Flourouracil (5-FU).
 Refractory to single agent chemotherapy
 MAC regimen:
 MTX (methotrexate) 1mg/kg/d IM on day 1,3,5,7 &
leucovorin 0.1mg/kg/d IM on day 2,4,6,8.
 Actinomycin 12mcg/kg/d IV for 5 ds.
Cyclophophamide 3mg/kg/d for 5 ds Cycles repeated
Q 21ds. If resistant to this regimen EMA/CO used.

High risk: stage II, III & stage IV

 EMA/CO - preferred initial regimen.
 Etoposide 100mg/m2 iv/30’ on day 1&2.
 MTX 100mg/m2 IV push followed by 200mg/m2
iv/12hrs on day 1.
 Acatinomycin 0.5 mg IV bolus on day 1&2.
 Leucovorin 15 mg Q 12hrs for 4-doses
Cyclophosphamide 600mg IV on day 8.
 Oncovin 1mg/m2 IV on day 8.
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 Repeated every 2wks until remission (normal serum hCG

over 3 consecutive wks & negative radiographic evident
disease). Complete remission rate 78%.
Other regimens:
 EMA as effective as EMA/CO
 EMA/EP: given if relapse occur after EMA/CO and if
refractory to MAC or EMA.
 PVB/PEB: if resistant to EMA/CO or EMA/EP and it is
less toxic than EMA/EP
In patient with metastatic disease Hysterectomy may be required:-
 To control uterine hemorrhage and sepsis
 To reduce the trophoblastic tumor burden and there by limit
the need for multiple course s of chemotherapy

Duration of therapy
 After normal hCG levels are attained, at least two additional
courses of chemotherapy are administered to reduce the
risk of relapse.
Monitoring during & after chemotherapy
 Stage I-III
 Weekly serum hCG until 3- consecutive normal,
monthly until 12 consecutive normal.
 Stage IV:
 Weekly serum hCG until 3 consecutive normal,
monthly until normal for consecutive 24 months.
 CBC, organ function tests based on clinical condition of the
patient, U/S, chest X-ray, Serum electrolytes are done
Effective contraception should be used during serum hCG follow-up

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 SAMPLE HISTORY
ID: 42 years old
C/C: Vaginal bleeding of 2 days duration
HPI:
This is a gravida 4 para lll (all alive and males) mother whose LNMP
was 25/04/11 E.C which makes her EDD on 29/01/11E.C, and
gestational age 25 weeks. The cycle was regular coming every 4
weeks and she has never used contraception for 8 month before her
LMNP. She suspected she was pregnant after she missed one
menstrual cycle. Then diagnosis of pregnancy was confirmed by
urine pregnancy test. She has one ANC contact at local health
center. It was on 5thmonth of amenorrhea. Detailed history was
taken and general physical examination and laboratory tests were
done. She gave blood and urine sample. She was given TT
vaccination and she was told everything was normal and that she
should continue her follow up every 4 weeks.
She doesn’t felt any fetal quickening still now.
Currently she is presented with vaginal bleeding of 2 days duration
which is associated with passage of grape like vesicles. The bleeding
is bright red and non-clotting. It soaked 2-3pads completely per day
and her underwear is also soaked. But not associated with coitus or
deep washing. In association to this she is also complaining cramp
lower abdominal pain which does not radiate to another site and no
aggravating or relieving factors noticed by the patient. The pain is
severe enough to prevent her from her daily activities. She also
complains rapid and excessive enlargement of her abdomen
compared to her prior pregnancies. She has also history of
excessive sweating which wets her night clothes and palpitation of
the same duration. She complains tinnitus and vertigo of 1 day’s
duration. For all this complaint she was taken to local health center
where they referred her directly to our hospital for better
investigation and treatment.

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Otherwise
 She has no cough chest pain or shortness of breath
 She has no excessive form of nausea and vomiting than her
prior pregnancy
 She has no history of headache, vision disturbances,
 She has no history of epigastric pain or yellowish discoloration
of skin.
 She has no history of abnormal body movement or loss of
consciousness
 She has no history of smoking, menstrual irregularities.
 She has no previous history of similar complaint
 She has no history vaginal discharge or fever.
 She has no history of trauma to abdomen and genital area
 She has no history of bleeding from other sites
 She has no history of river water contact
 Her serostatus for RVI is negative
 She has completed her family size
She eat 4 meals per day (injera, fruits, meat, vegetables and
cereals)as the pre pregnancy time. The pregnancy was
unplanned, but wanted and supported.

Ass’t: R/o GTD + completed family size

NB: mentioning the completeness of the family size is important
for the management purposes, for example, if she has
completed her family size hysterectomy is the best treatment
option.
DDX for GTD includes
 Abortion (incomplete, missed)
 Cervicitis
 Cervical cancer
 Ectopic pregnancy
 Vaginitis
 Trauma
 Ectropion

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CHAPTER 12

CERVICAL NEOPLASIA
CERVICAL INTRAEPITHELIAL NEOPLASM
CIN, formerly called dysplasia, means disordered growth and
development of the epithelial lining of the cervix

Classification of CIN
 Based on degree of dysplasia CIN is classified in to four:-
 CIN I (Mild dysplasia), is defined as disordered growth of the
lower third of the epithelial lining.
 CIN II (moderate dysplasia), abnormal maturation of the lower
two-thirds of the epithelial lining
 CIN III (Severe dysplasia), encompasses more than two thirds
of the epithelial thickness.
 Carcinoma in situ (CIS) representing full-thickness
dysmaturity.
 According to the Bethesda system which based on cytologic
smear, it is classified in to:-
 Atypical Squamous cells of Undetermined Significance
(ASCUS)
 Atypical Squamous cells where high-grade lesions must be
excluded (ASC-H).
 Low-grade squamous intraepithelial lesion (LSIL)
encompasses cytologic changes consistent with koilocytic
atypia or CIN I
 High-grade squamous intraepithelial lesion (HSIL) denotes the
cytologic findings corresponding to CIN II and CIN III

Risk factors of CIN

 Similar with risk factor of cervical Ca (see below)
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CIN and Human papilloma Virus (HPV)

 Analyses of cervical neoplasia lesions show the presence of

HPV in more than 80% of all CIN lesions and in 99.7% of all
invasive cervical cancers.
 Based on their malignant potential, HPV subtypes are
categorized into
 Low-risk (HPV types 6, 11, 42, 43, and 44) are
associated with condylomata accuminata and low-grade
lesions (CIN I) and;
 High-risk (HPV types 16, 18, 31, 33, 35, 39, 45, 51, 52,
56, 58, 59, and 68) are associated with invasive cancer in
addition to CIN II and CIN III.
The 2 most common high-risk HPV types are HPV-16,
and HPV-18.
 Once the epithelium is acutely infected with HPV, 1 of 3
clinical scenarios ensues:
1) Asymptomatic latent infection
2) Active infection in which HPV undergoes vegetative
replication but not integration into the genome (eg,
leading to condyloma or CIN I).
3) Neoplastic transformation following integration of
oncogenic HPV DNA into the human genome
Outcomes of HPV infection:
 Resolution in more than 90% of immunocompetent women
spontaneously over a 2-year period.
 Only approximately 5% will have cytologically detectable
CIN.
This suggests that infection with HPV alone is insufficient
for the development of CIN or cervical cancer and
underscores the importance of other cofactors, such as
cigarette smoking or immunosuppression

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Diagnosis
 There are usually no symptoms or signs of CIN, and the
diagnosis is most often based on biopsy findings following an
abnormal routine cervical cytology smear.
 On cytologic examination, the dysplastic cell is characterized
by:-
 Anaplasia, an increased nuclear-tocytoplasmic ratio (ie,
the nucleus is larger),
 Hyperchromatism with changes in the nuclear chromatin
 Multinucleation, and abnormalities in differentiation.

Screening for CIN & Cervical Cancer

It is critical that women, whether vaccinated for HPV or not, follow
current cervical cancer screening guidelines.

The screening modalities include:-

 Cervical cytology screening (Pap smears)
 The American Cancer Society (ACS) updated
recommendations of 2002 states that screening with
conventional Pap testing should occur every year. If
liquid-based cytology is being used, screening can be
extended to every 2 years
 Screening begins at age 21; or within 3 years of the onset
of sexual activity
 Recommended every 3 years for women 21–29 years of
age.
 Women age 30 or older should be screened with cytology
and HPV co-testing every 5 years or cytology alone every
3 years.
 Screening should be discontinued in women older than
65 years with negative consecutive screening in the
preceding 10 years.
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 Cytology testing should be discontinued in women who

have had a total hysterectomy and do not have a prior
history of CIN 2/3 or worse
 Screening in special circumstances
o Women who are HIV positive should be screened
twice in the first year after diagnosis and annually
thereafter.( Based on 2009 ACOG guidelines,)
o Immunosuppressed women(other than those with
HIV) or those who had in utero DES exposure
should be screened annually.
 If both (cytology and HPV co-testing) results are negative,
combined screening should not be repeated for 5 years.
 If cytology and HPV testing are positive, triaging to
colposcopy is as outlined earlier.
 If cytology is normal, but HPV test is positive, repeat
cytology and HPV testing in 6–12 months is
recommended.

 Repeat cervical cytology,

 The cervical cytology smear should be repeated every 6
months until there are 2 consecutive normal smears
 HPV testing
 Primary screening modality in combination with
cervical smear testing or alone.
 HPV testing as primary screening modality should be
used only for women >30 years
 Two types of HPV tests are available for the screenin
o Hybrid capture 2
o Cervista HPV HR test, also referred as “cervista
HPV 16 &18” or HPV genotyping identifies 14
high risk serotypes.
 Positive test implies significant high risk of
development of CIN 3 or cervical cancer.
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 Visual Inspection with Acetic Acid (VIA)

 Also called cervicoscopy, consists of naked-eye
visualization of the uterine cervix after the application
of 3% to 5% acetic acid then cervix is illuminated with
a light source.
 Acetic acid dehydrates cells so that squamous cells
with relatively large or dense nuclei (eg. metaplastic
cells, dysplastic cells, cells infected with HPV) reflect
light and therefore appear white.
 Blood vessels and columnar cells are not affected by
acetic acid, but become easier to visualize against the
white background
 Visual Inspection with Lugol Iodine Schiller test.
 Lugol’s solution is an aqueous iodine preparation.
 Normal mature squamous epithelium of the cervix
contains glycogen, which combines with iodine to
produce a deep mahogany-brown color.
 Non staining, therefore, indicates abnormal squamous
(or columnar) epithelium or immature metaplastic
epithelium, and constitutes a positive Schiller test.

 Colposcopic examination.
 The colposcope is an instrument that uses illuminated
low-power magnification (5–15×) to inspect the cervix.
 After the application of 3–5% aqueous acetic acid
solution abnormalities in the appearance of the
epithelium and its capillary blood supply can be identified
by colposcopy
Indications for colposcopy are:
1. Abnormal cervical cytology smear or HPV testing;
2. Clinically abnormal or suspicious-looking cervix;
3. Unexplained intermenstrual or post coital bleeding;
4. Vulvar or vaginal neoplasia; or
5. History of in utero DES exposure
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Normal finding from colposcopy

o The original squamous epithelium, which extends from
the mucocutaneous vulvovaginal junction to the original
squamocolumnar junction.
o The columnar epithelium of the endocervical canal
o The transformation zone
 The original SCJ is the junction between the
stratified squamous epithelium of the vagina and
ectocervix, and the columnar epithelium of the
endocervical canal.
 In 2/3 of female infants, this original SCJ is located
on the ectocervix, in close to a 1/3 in the
endocervical canal, and in a very small subset out
in the vaginal fornices
 During a woman's life cycle the squamocolumnar
junction "migrates“. Following menarche, the SCJ is
generally found on the ectocervix, with further
eversion during pregnancy. In the postmenopausal
patient, the SCJ is frequently within the
endocervical canal
 If the new SCJ is visualized in its entirety, the
colposcopic examination is called satisfactory; if it
cannot be fully visualized, the examination is called
unsatisfactory.
Abnormal findings indicative of dysplasia and CIN are those of:
o Leukoplakia or hyperkeratosis
 An area of white, thickened epithelium that is appreciated
prior to the application of acetic acid and may indicate
underlying neoplasia.
o Acetowhite epithelium,
 Which is epithelium that stains white after the application
of acetic acid
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o Mosaicism or punctation
 Reflecting abnormal vascular patterns of the surface
capillaries.
 As general rule, capillary thickness and intercapillary
distances correlate with the severity of the lesion and thus
tend to be larger and coarser in higher -grade lesions.
o Atypical vessels with bizarre capillaries
 With so-called corkscrew, comma shaped, or spaghetti-like
configurations suggest early stromal invasion.

 Diagnostic conization
 Indications:-
o If colposcopy is unsatisfactory.
o If the lesion extends into the cervical canal beyond
the view afforded by the colposcope
o If there is a significant discrepancy between the
histologic and the cytologic examination,
o If adenocarcinoma in situ is suspected,
o If micro invasive carcinoma is suspected

PREVENTION
 Behavioral
 Sexual abstinence,
 delaying coitarche, and
 limiting the number of sexual partners are some of
behavioral modification.
 Condoms do not cover all potentially HPV-infected
anogenital skin. Therefore, condoms may not be completely
protective.
 HPV Vaccination
 Advisory Committee on Immunization Practices (ACIP)
recommends that all girls 11–12 years of age should be
routinely offered HPV vaccination,

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 As well as girls and women age 13–26 who have not yet
been vaccinated
 They also recommend for boys too and vaccination is
possible as early as 9 years. In case you got someone
who want to be vaccinated after 15 still you can give 3
shoots over six months.
The vaccines are:
o Cervarix (HPV2) is a bivalent vaccine against HPVs 16
and 18.
o Gardasil (HPV4) is a quadrivalent vaccine against
HPV types 6, 11, 16, and 18.
o Gardasil 9 (HPV9), a nonavalent vaccine, which
protects against all HPV types in HPV4 plus types 31,
33, 45, 52, and 58.
 They are administered in three intramuscular doses
during a 6-month period; the second dose is given 1 to 2
months after the first dose, and the third 6 months after
the first dose.
 The recent CDC guideline recommend as only two dose
(first dose-11-12 years, second dose after 6months of the
frist dose) is enough for those 9-15 years. If age is 15
and greater 3doses within six months is recommended.
 Vaccination can be given during lactation but is avoided
during pregnancy.

Outcome of CIN
CIN I CIN II CIN III
Regression to normal 60% 40% 30%
Persistence 30% 35% 48%
Progression to CIN III 10% 20% -
Progression to cancer <1% 5% 30-40%

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CERVICAL CANCER
 Worldwide, cervical cancer is common, and it ranks fourth
among all malignancies for women after breast, colorectal, and
lung cancer (WHO 2012). From this developing countries
contribute 85 percent.
 Is the second most common cause of cancer-related morbidity
and mortality among women in developing countries. The
median age at diagnosis is 49 years.

Risk factors
 Cigarette smoking:
 Both active and passive smoking increases cervical
cancer.
 Among HPV-infected women, current and former
smokers have a two- to threefold increased incidence
 plausible explanations about how smoking might
cause cervical cancer
o One is that smoking inhibits the immune
response to HPV.
o second is that carcinogenic HPV-infected cells are
exposed to smoking carcinogens that cause DNA
damage while HPV oncoproteins block apoptosis
and cell cycle arrest.
 High parity:
 Those with one or two full term pregnancy have a
twofold risk when compared with nulliparous.
 If she had seven pregnancies fourfold risk.
 Long-term combination oral contraceptive.
 Increase risk by four fold if she is HPV positive.
 Young age at first intercourse (<20years)

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 Multiple sexual partner.

 Having more than six lifetime sexual partners)
 Immunosuppression.
 Cervical cancer is one of AIDS defining illness
 Race: black and Hispanic has highest incidence.

Tumor genesis
 In general, progression from dysplasia to invasive cancer
requires several years, although times can vary widely.
 HPV is the primary etiologic in ectious agent associated with
cervical cancer. HPV 16 is more commonly associated with
squamous cell carcinoma o the cervix, whereas HPV 18 is a
risk actor or cervical adenocarcinoma
 The E6 and E7 oncoproteins produced interfere with and
accelerate degradation of p53 and pRb which are key tumor
suppressor proteins produced by the host. This is central to
host cell immortalization and transformation

Molecular pathways of cervical CA

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Patterns of spread
 Direct invasion into the cervical stroma and local invasion
 To urethra then blockage frequently develops,
resulting in hydronephrosis,
 The bladder may be invaded by direct tumor extension
through the vesicouterine ligaments
 The rectum is invaded less often because it is
separated from cervix by the posterior cul-de-sac
 Lymphatic metastasis:
 The cervix has a rich network of lymphatic’s, which follow
the course of the uterine artery
 These channels drain principally into the paracervical
and parametrial lymph nodes → obturator lymph
nodes→ the internal, external, common iliac lymph
nodes, and ultimately the paraaortic lymph nodes.
 Drainage from the posterior cervix course drains to the
rectal lymph nodes.
Lymphovascular space involvement is when the tumor invades
deeper into the stroma and enters blood capillaries and
lymphatic channels.
Distant metastasis results from hematogenous dissemination,
and the lungs, ovaries, liver, and bone are the most
frequently affected.

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Histologic types
 The two most common histologic subtypes of cervical cancer
are squamous cell (70%) and adenocarcinoma (25%).
 Squamous cell subtypes: Keratinizing, Non
keratinizing and Papillary
 Adenocarcinoma subtypes: Mucinous, Endometrioid,
Serous, Clear cell and Mesonephric.
 Mixed cervical carcinoma
 Neuroendocrine cervical tumor
 Others: Sarcoma, Lymphoma, Melanoma

Clinical manifestation

Symptoms
 Abnormal vaginal bleeding is the most common symptom
and may take the form of a blood-stained leukorrheal
discharge, scant spotting, or frank bleeding.
 A history of postcoital post douching bleeding may be
elicited on specific questioning
 Pelvic pain, radiating to the hip or thigh, is a manifestation
of advanced disease.
 Incontinence sign of fistula formation.
 Acute blood loss and anemia may occur in a bulky or
ulcerating stage I lesion.
Physical Examination
 Most women with this cancer have normal general physical
examination findings.
 With speculum examination lesions may be an exophytic or
endophytic growth; a polypoid mass, papillary tissue, or
barrel-shaped cervix; a cervical ulceration or granular mass;
or necrotic tissue.
 A watery, purulent, or bloody discharge can also be seen
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 During bimanual examination, enlarged uterus resulting

from tumor invasion and growth. Alternatively,
hematometra or pyometra may expand the endometrial
cavity following obstruction.
 The size of the cervix and the tumor measured in cm (a
normal cervix is 4×5 cm in size)
 Extend into the vagina, and disease extent can be
appreciated during anterior vaginal wall palpation or during
rectovaginal examination.
 During digital rectal examination, parametrial, uterosacral,
and pelvic sidewall involvement can be appreciated.
 Involved tissues feel thick irregular, firm, and less mobile
 A fixed mass indicates that tumor has probably extended to
the pelvic sidewalls.
 With advancing disease, enlarged supraclavicular or
inguinal lymphadenopathy suggest lymphatic tumor spread
 Lower extremity edema and low back pain, o ten radiating
down the posterior leg, may, reflect compression o the
sciatic nerve root, lymphatics, or veins.

Investigations
 When obvious tumor growth is present, a cervical biopsy is
usually sufficient for diagnosis.
 If gross disease is not present, a colposcopic examination
with cervical biopsies and endocervical curettage is
warranted
 If the diagnosis cannot be established conclusively with
colposcopy and directed biopsies, cervical conization may be
necessary.

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Investigations/procedures Used During Cervical Cancer

Evaluation
Investigations To Identify:
CBC Anemia
Urinalysis Hematuria
Laboratory Chemistry profile Electrolyte abnormality
Liver function Liver metastasis
Creatinine/BUN Renal impairment or
obstruction
Chest radiograph Lung metastasis
Intravenous pyelogram Hydronephrosis
Radiologic Nodal or CT distant organ metastasis
scan(abdominopelvic)
MR imaging Local parametrial invasion
Cystoscopy Bladder tumor invasion
Procedural Proctoscopy Rectal tumor invasion
EUA Extent of pelvic tumor
spread

Staging
Cervical cancers are staged clinically.
 Allowable components of staging include
 cold-knife conization,
 pelvic examination under anesthesia,
 cystoscopy,
 proctoscopy,
 chest radiograph, and intravenous pyelogram

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FIGO staging of cancer of the cervix uteri (2018)

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General Treatment for Primary Invasive Cervical

Carcinoma
Cancer Treatment
Stage
IA1 Simple hysterectomy preferred if childbearing completed or
Cervical conization
IA1(with Modified radical hysterectomy and pelvic
LVSI) lymphadenectomyor
Radical trachelectomy and pelvic lymphadenectomy for
selected patients desiring fertility
IA2 Radical hysterectomy and pelvic lymphadenectomyor
Radical trachelectomy and pelvic lymphadenectomy for
selected patients desiring fertility
IB1c Radical hysterectomy and pelvic lymphadenectomy or
Some IB2 radical trachelectomy and pelvic
IIA1 lymphadenectomy for selected patients desiring fertility or
Chemoradiation
Bulky IB2 Chemoradiation
IIA2
IIB to IVA Chemoradiation Or Rarely, pelvic exenteration
IVB Palliative chemotherapy and/or
Palliative radiotherapy or
Supportive care (hospice)

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 Sample history
Chief compliant: vaginal bleeding of three month duration.
HPI:
This is a 40years old Para 7(all lived) 0 abortion mother whose LMNP
was two week back. She was relatively healthy three month back at
which time she start to experience vaginal bleeding of which was
initially bright red scanty bleeding and has relationship with her
menses. The bleeding was exacerbated after sexual intercourse and
post douching and has no known relieving factor.
She also experience watery discharge which increase in amount and
sometimes become blood stained. She also has intermittent moderate
dull aching lower abdominal pain for the last two month which
radiate to her thigh and has no known relieving and exacerbating
factor. She also has loss of appetite significant but unqualified weight
loss vertigo and tinnitus since the last one month.
Her menses started when she was 13 years old and come every 24
days. It stays for 3-4 days she uses 2 pads for it. The bleeding was
black and non clotting.
She was married when she was 16years old and she claimed to be
virgin before her marriage.
She used OCP for the last four year after delivery of her last baby.
Other wise
She has no history of cigarettes smoking.
She has no history of foul smelling vaginal discharge, genital ulcer or
treatment for STD
She has no history of multiple sexual partner.

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She has no history of urinary incontinence, frequency, urgency or

dysuria.
She has no history of cough shortness of breath chest pain or blood
stained sputum.
She has no history of RUQ pain, yellowish discoloration of eye and
bleeding from other site.
She has no history of bone pain or fracture.
She has no history of pelvic trauma.
Physical examination
G/A: chronically sick looking, Look wasted and in pain
Vital sing: No vital sign derangement
HEENT: pale conjunctiva non icteric sclera.
LGS: no significant lymphadenopathy

No respiratory and cardiac finding

Abdomen: flat abdomen that moves with respiration, No scar

No distended vein.
On palpation: there is no palpable mass and organomegaly
On percussion there is no sign of fluid collection

MSS: no lower extremity edema.

Genitourinary system: no costovertabral angel tenderness. The

kidneys are not palpable.

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Pelvic examination:
External genitalia examination: Inverted triangle type of pubic hair
pattern. No discoloration of skin around vulva, no swelling, ulcer or
discharge
Speculum examination: there is cervical ulceration and necrotic
tissue are visible, Bloody discharge is also visible from cervix
Digital vaginal examination: there is irregular firm lesion on cervix
which measures around 4 cm. cervix is mobile not attached to
adjacent structure. No involvement of vagina.
Bimanual examination: the uterus is normal size and position
Digital rectal examination: no parametrial uteresacral and pelvic
side wall involvement.

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CHAPTER 13

ABORTION
DEFINITION AND TERMINOLOGY
Abortion is defined as the spontaneous or induced termination of
pregnancy before fetal viability.

 Viability lies between the lines that separate abortion from

preterm birth. It is defined by pregnancy duration and fetal
weight for statistical and legal purpose.
• Both CDC and WHO define abortion as pregnancy
termination before 20weeks of gestation or with fetus
born weighing <500g.
• In Ethiopia and the UK the age of viability is 28weeks of
gestation.
 The term miscarriage is usually for spontaneous abortion.
 The use of transvaginal sonography and precise measurement
of serum hCG concentrations are used to identify extremely
early pregnancies and makes it possible to distinguish
between a chemical and a clinical pregnancy.
o Abortion of such early pregnancies is termed as early
pregnancy loss or early pregnancy failure or wastage.

INCIDENCE
 Although the true incidence of spontaneous abortion is
unknown, approximately 15% of clinically evident pregnancies
and up to 50% of chemically evident pregnancies end in
spontaneous abortion.

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CLASSIFICATION
Based on:-
 Mechanism/onset
 Spontaneous (see further clinical classification below)
 Induced
 Gestational age at onset
 Early(<12wks) or first trimester
 Late(>12wks) or midtrimester
 Place of abortion
 Safe(health facility)
 Unsafe abortion,
 Presence or absence of infection
 Septic
 Aseptic

SPONTANEOUS FIRST TRIMESTER ABORTION

 More than 80% of spontaneous abortion occurs within the 1st
12 weeks of gestation.
Pathogenesis
 In 1st trimester losses, death of the embryo or fetus nearly
always precedes spontaneous expulsion which hemorrhage
in to the decidua basalis  necrosis of adjacent tissue that
stimulate uterine contraction and expulsion. Thus the key to
determining the cause of early miscarriage is to ascertain the
cause of fetal death.
 In contradistinction, in later pregnancy losses, the fetus
usually does not die before expulsion, and thus other
explanations are sought.

Etiologies and Risk factors

Fetal factors

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 Chromosomal abnormalities
Approximately half of first-trimester miscarriages are anembryonic,
that is, with no identifiable embryonic elements.

The remaining (embryonic miscarriages), can be further grouped as

either, those with normal chromosome (euploid abortions, in 45-
55%) or those with chromosomal anomalies (aneuploid abortions)
Chromosomal Percentage
abnormalities
Aneuploidy
Autosomal trisomy 22-32
Monosomy X (45,X) 5-20
Triploidy 6-8
Tetraploidy 2-4
Double or triple 0.7-2
trisomy
Structural anomaly 2

Almost 95 percent of chromosomal abnormalities in aneuploid

fetuses are caused by maternal gametogenesis errors. Chromosomal
abnormality decrease with advancing GA (55%, 35%, & 5% in 1st,
2nd and 3rd trimester abortuses/stillbirth respectively).
Aneuploid Abortion
 50% of embryonic abortions are aneuploid
 Monosomy X or Turner’s syndrome is the single most common
aneuploidy, comprising approximately 18% of these
gestations.
 As a group, the autosomal trisomies account for more than
half of aneuploid losses, with trisomy 13, 16, 18, 21, and 22
being the most common. Autosomal trisomies have been noted
for every chromosome except chromosome number 1.
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 Most trisomic pregnancies end in miscarriage. The exceptions

are trisomy 21, 18, and 13, which have survival to birth rates
of 22%, 5%, and 3%, respectively.
 Polyploidy, usually in the form of triploidy, is found in
approximately 20% of all miscarriages. Polyploid conceptions
typically result in an anembryonic gestation.(C)
 About 75% of aneuploid fetuses aborted before 8 week.
Chromosomal structural abnormalities infrequently cause abortion.
Maternal factors
 Age: the rate of clinical miscarriages is almost doubled when
either parent is older than 40yrs. The incidence of euploid
abortions increases dramatically after maternal age exceeds 35
yrs.
 Infections: systemic or local (GU) infections can cause
pregnancy loss. Such infections include; Chlamydia
trachomatis (in 4% of abortuses), Polymicrobial infections from
periodontal disease, HIV and Bacterial vaginosis (2nd trimester)
 Medical disorders: like DM, thyroid disorders (especially
severe iodine deficiency), celiac disease, inflammatory bowel
disease and SLE
 Uterine and cervical factors: Congenital uterine anomalies,
such as unicornuate, bicornuate, or septate uterus;
asherman’s syndrome and cervical insufficiency.
 Medications and toxic factors: IUDs, antineoplastic drugs,
anesthetic gases, alcohol, nicotine, or cocaine, lead, ethylene
oxide, and formaldehyde.
 Radiotherapy: exposure to >5rads of radiation in
abdominopelvic radiotherapy may later be at increased risk for
miscarriage.
 Surgical procedures: like early removal of the corpus luteum
or the ovaries,

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 Trauma: direct abdominal trauma, amniocentesis or chorionic

villus sampling. Generally trauma seldom cause miscarriage
 Nutrition: both extremes of malnutrition (severe dietary
deficiency and morbid obesity) are associated with
miscarriage.
 Social and behavioral factor: substance abuse
 Occupational factor: exposure to toxic chemicals.
Paternal factors
 Chromosomal abnormalities in sperm and increasing paternal
age had an increased abortion risk

Clinical classification of spontaneous abortion

 Threatened abortion
 The clinical diagnosis of threatened abortion is presumed
when bloody vaginal discharge or bleeding appears thru a
closed cervical Os during the 1st 28weeks. Bleeding is by
far the most predictive risk factor for pregnancy loss.
 Approximately 25% of pregnancies experience 1st
trimester bleeding. Bleeding must be differentiated from
an implantation bleeding
 With miscarriage bleeding usually begins 1st and crampy
lower abdominal pain follows hours to days later. The
combination of bleeding and pain predicts a poor
prognosis or pregnancy continuation.
 About 43% of these cases will subsequently miscarry.
Even if miscarriage does not occur, these pregnancies are
associated with high risk of late adverse maternal and
perinatal outcomes.
 The primary goal in evaluating a woman with early
pregnancy bleeding is prompt diagnosis of an ectopic
pregnancy. Serial quantitative serum β-hCG levels,
progesterone levels, and transvaginal sonography, alone

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or in combination, can help ascertain if the fetus is alive

and if it is within the uterus.
 Inevitable abortion
 Is characterized by bleeding with cervical dilation, often
with back or abdominal pain
 gross rupture of the membranes along with cervical
dilatation is nearly always followed by either uterine
contractions or infection, which is inevitably followed by
abortion
 the products of conception have not passed from the
uterine cavity

 Incomplete abortion
 Incomplete abortion is defined as the passage of some
but not all of the products of conception from the uterine
cavity
 Before ten weeks of gestation, the placenta and fetus are
generally passed together, but after this time, they are
passed separately.
 Bleeding and cramping usually continue until all
products of conception have been expelled
 There is dilation of the cervical Os
 Complete abortion
 All of the products of conception have passed from the
uterine cavity and the cervix is closed.
 A history of heavy bleeding, cramping, and passage of
tissue or a fetus is common
 Missed abortion
 Is defined as a pregnancy that has been retained within
the uterus after embryonic or fetal demise.
 Cramping or bleeding may be present, but often there are
no symptoms.

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 The cervix is closed, and the products of conception

remain in situ.
 It may be complicated by bleeding disorders and infection
 Recurrent abortion
 Is defined as 3 or more consecutive spontaneous
abortions
 Approximately 1 percent of fertile couples have recurrent
miscarriages; most of these are embryonic or early losses.
 The risk of spontaneous abortion is at least doubled in
women experiencing recurrent pregnancy loss.
 Possible causes:
 Parental chromosomal abnormalities
 Immunologic factors (esp, antiphospholipid
antibody syndrome)
 Anatomic factors
 bicornuate uterus, is the most common
uterine anomaly (39%) and has 40-70%
pregnancy loss rate
 septate or unicornuate uterus, seen is 14-24%
of uterine anomalies and has 34-88%
pregnancy loss rate
 uterine leiomyoma
 Endocrinologic abnormalities
 Progesterone deficiency caused by luteal phase
defect (LPD), which is associated with
inadequate endometrial development at
implantation.
 Thyroid disorders
 Microbiologic (TORCH), and thrombophilic
abnormalities. (See details on Current 11th ed).
 NB. Approximately 50% have no definitive cause

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 The prognosis after repeated losses is good, with most

couples having an approximately 60% chance of a viable
pregnancy.
 Septic abortion
 Usually occur in induced abortions that occur in an
illegal setups, especially in developing countries.
 Infection usually begins as endometritis involving the
endometrium and any retained products of conception.
 The 2 most common causes of septic abortion are
retained products of conception and bacteria that have
been introduced into the uterus via ascending infection.
 These patients present with fevers, chills, abdominal
pain, vaginal bleeding, and malodorous vaginal
discharge.
 Without treatment, endometritis may spread beyond the
uterus, leading to peritonitis, bacteremia, and sepsis.
Particularly worrisome are severe necrotizing infections
and toxic shock syndrome caused by S pyogenes.

SPONTANEOUS MIDTRIMESTER ABORTION

 The timespan that defines a midtrimester fetal loss extends
from the end of the first trimester until the fetus weighs ≥ 500
g or gestational age reaches 20 weeks (28weeks).
 Incidence and Etiology
 Abortion becomes much less common by the end of the
first trimester, overall, spontaneous loss in the second
trimester is estimated at 1.5 to 3 percent, and after 16
weeks, it is only 1 percent.
 First-trimester bleeding doubles the incidence of second-
trimester loss
 Risk factors for second-trimester abortion include race,
ethnicity, prior poor obstetrical outcomes, and extremes
of maternal age.
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 Some causes include;

 Fetal anomalies; Chromosomal or Structural
 Uterine defects; Congenital, Leiomyomas and
Incompetent cervix
 Placental causes; Abruption, previa, Defective spiral
artery transformation and Chorioamnionitis
 Maternal disorders; Autoimmune, Infections and
Metabolic

INDUCED ABORTION

 Is surgical or medical termination of a live fetus that has not

reached viability
 It can be classified in to two, (1) indicated or therapeutic and
(2) elective or voluntary.

 Indications:
 Maternal health problems like:-
 persistent cardiac decompensation
 pulmonary arterial hypertension
 advanced hypertensive vascular disease
 diabetes with end-stage organ failure
 malignancies
 maternal mental illness
 rape or incest
 significant fetal anatomic, metabolic, or mental deformity
 Age of woman less than 18 years
 Extreme poverty
Complication of abortion
 Hemorrhage, shock, anemia
 Infection
 Intrauterine synechiae (Asherman’s syndrome)
 Perforation of the uterus
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 Injury to bowl and bladder

 Fistula formation
 Rh isoimmunization
 Tetanus
 Ectopic pregnancy in later life
 Renal failure
 Death
 Psychological trauma - depression

APPROACH
HISTORY
 Age
 LNMP, hx of amenorrhea and symptoms of pregnancy like
morning sickness(nausea and vomiting)
 Vaginal bleeding, assess onset, consistency(any embryonic/
fetal(solid) part
 Cramping(lower abdominal pain), assess onset in relation to
vaginal bleeding
 Fever or chills, in case of septic abortion
 Risk factors
 Symptoms of anemia
 Sexual assault hx, in case of induce abortion
 DDx
 ectopic pregnancy in intact tube
 cervical polyps
 vaginitis
 cervical carcinoma
 gestational trophoblastic disease
 trauma
 foreign body

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PHYSICAL EXAMINATION
 G/A: well looking, distress or lethargic ( from severe anemia or
septic shock)
 V/S:
 Tachycardia, tachypnea or hypotensive (from blood loss)
 Febrile, in case of septic abortion
 HEENT: pale conjunctiva?
 Abdominal examination:
 Inspect the skin changes associated with pregnancy
 Severe unilateral tenderness in lower abdomen may
indicate ectopic pregnancy
 Determine uterine size: especially in case of midtrimester
it is important to determine size of the uterus, if it is less
than the appropriately determined GA, it may indicate
incomplete or complete loss of product of conception
 Listen to FHT
 Pelvic examination
 See if there is ongoing blood loss, or passage of amniotic
fluid
 Check the cervix (open or closed)

INVESTIGATIONS
 CBC: anemia? Or infection?
 Blood type and Rh
 Serial serum β-hCG:
 Falling or abnormally rising serum levels of β-hCG are
diagnostic of an abnormal pregnancy, either a failed
intrauterine gestation or an ectopic pregnancy.
 Ultrasound:
 Transvaginal ultrasound allows us to visualize
gestational sac (GS) as early as 4–5 weeks of gestation.
 At 5–6 weeks’ gestation, a yolk sac will be present. In
general, a GS with a mean sac diameter (MSD) of ≥8 mm
should contain a yolk sac. Similarly, a GS with an MSD
of >16 mm should also contain an embryo.

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 Pregnancies with a large GS and no embryo are typically

anembryonic gestations and are managed in a similar
manner as a missed abortion
 Fetal heart motion is expected in embryos with a crown
to rump length of >5 mm or at 6–7 weeks’ gestation.
 If a repeat ultrasound in 1 week does not show
embryonic cardiac activity, the diagnosis of embryonic
demise is made.
 Urinalysis: to identify cause
 Endocervical cultures
 Blood cultures: in septic abortion

MANAGEMENT
 Threatened abortion:
 There is no effective therapy for threatened intrauterine
pregnancy other than pelvic rest.
 Inevitable abortion:
 Awaiting spontaneous expulsion
 Oxytocin use or Suction curettage or evacuation and
curettage depending on the gestational age
 Rh D Ig for Rh negative
 Incomplete abortion:
 Uterus should be evacuated either by suction curettage
or E&C as quickly as possible depending on GA (suction
being the recommended method for GA up to 12 weeks)
 Rh Ig for Rh negative
 Prophylactic antibiotics – doxycycline 200 mg stat dose or
100mg BID for three days
 Missed abortion
 Immediate evacuation of the uterus is preferred
treatment, but treatment choice between expectant
management and immediate evacuation should depend
on the woman’s informed decision
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 Expectant management is possible for three weeks with

assessment of coagulation profile every week
 Risk of DIC is very low before 15 weeks of GA
 Nearly in 80% of cases spontaneous expulsion during
expectant management can occur in three weeks’ time.
 If immediate evacuation is decided, one has to use
protocol for induced abortion
 Septic abortion:
 Add broad spectrum antibiotics
 Induced abortion
 Medical or Surgical. See technique and procedure in
GYNEOLOGY MANAGEMENT GUIDELINE IN JUSH
Components of Post abortion care (PAC)
 Emergency treatment of incomplete abortion and potentially
life threatening complications
 Post-abortion family planning counseling and services
 Links between post-abortion emergency services and the
reproductive health care system.
 Community service provider partnership
 Counseling

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CHAPTER 14

PELVIC ORGAN PROLAPSE

POP is a bulge or protrusion of pelvic organs and their associated

vaginal segments into or through the vagina. In the United States, it
is the third most common indication for hysterectomy
 A woman has an estimated lifetime risk of 12% to undergo
surgery for prolapse or incontinence.
 50% of women older than age 50 have some degree of pelvic
organ prolapse, but fewer than 20% seek treatment.
 This may be due to a number of reasons, including lack of
symptoms, embarrassment, or misperceptions about available
treatment options.

PATHOPHYSIOLOGY

 Pelvic organ support is maintained by complex interactions

among the:-
 pelvic floor muscles
 pelvic floor connective tissue, and
 vaginal wall
 Pelvic organ prolapse results from attenuation of this
supportive structures, whether by actual tears or “breaks” or by
neuromuscular dysfunction or both.

Factors believed to be involved in pelvic organ support failure:

 Genetic predisposition,
 Loss of pelvic floor striated muscle support,
 The levator ani muscle muscles comprised of three regions
iliococcygeal, pubococcygeus and puborectalis muscle

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 When the levator ani muscle has normal tone and the vagina
has adequate depth, the upper vagina lies nearly horizontal in
the standing female.
 When the levator ani muscle loses tone, the vagina drops from
a horizontal to a semivertical position.
 This widens or opens the genital hiatus and predisposes
pelvic viscera to prolapse.
 Vaginal wall weakness, and loss of connective attachments

Vagina has three levels of support, as described by DeLancey

 Level I Support: consists of the cardinal and uterosacral

ligaments
 The uterosacral ligaments are posterior fibers that attach to
the presacral region at the level of S2 through S4.
 Defects in this support complex may lead to apical prolapse.
 Level II Support: These are the connective tissue attachments of
the lateral vagina anteriorly to the arcus tendineus fascia pelvis
and posteriorly to the arcus tendineus rectovaginalis.
 Detachment of this connective tissue from the arcus
tendineus fascia pelvis leads to lateral or paravaginal anterior
vaginal wall prolapse.
 Level III Support: The perineal body, superfcial and deep
perineal muscles.
 Damage to level III support contributes to anterior and
posterior vaginal wall prolapse,

Supports of the uterus

 Upper tier
 Endopelvic fascia covering the uterus
 Round ligament
 Broad ligament

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It is the weakest of the uterus and it maintain the uterus in

anteverted position
 Middle tier
 Condensations of endopelvic fascia
- Cardinal / Transverse cervical/ Mackenrodt’s ligament
- Utero sacral ligament
- Pubocervical ligament
- Pubourethral ligament
The strongest support of the uterus
 Inferior/ Lower tier
 Pelvic diaphragm: Levator ani muscle
 Perineal body: Fibro muscular condensation between the
vagina & the rectum

RISK FACTORS

Risk Factors Associated with Pelvic Organ Prolapse

Pregnancy
Vaginal childbirth
Menopause
Aging
Hypoestrogenism
Chronically increased intraabdominal pressure
Chronic obstructive pulmonary disease (COPD)
Constipation
Obesity
Pelvic floor trauma
Cigarette smoking
Genetic factors
Race(highest risk in white women)
Connective tissue disorders
Spina bifida

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 Vaginal childbirth is the most frequently cited risk factor. The

risk of POP increased 1.2 times with each vaginal delivery.
 In women age 20 to 59 years, the incidence of POP roughly
doubled with each decade.
 Black women more commonly have a narrow pubic arch and an
android or anthropoid pelvis. These shapes are protective against
POP compared with the gynecoid pelvis typical of most white
women.
 Being overweight (BMI 25–30 kg/m2) was associated with an
increased risk of 31 to 39%, and obesity (BMI >30 kg/m2) with
an increased risk of 40 to 75%.

DESCRIPTION AND CLASSIFICATION

Pelvic organ prolapse includes:-

Anterior compartment defects
 Urethrocele
 Cystocele
Apical defects
 Uterine prolapse
 Vaginal vault prolapse(Post hysterectomy)
Posterior compartment defects
 Enterocele
 Rectocele

 Cystocele is a herniation of the urinary bladder through the

anterior vaginal wall.
 Uterocele is generally the result of poor cardinal or uterosacral
ligament apical support, which allows downward protrusion of
the cervix and uterus toward the introitus.
 Procidentia, which involves prolapse of the uterus and vagina,
and total vaginal vault prolapse, which can occur after
hysterectomy, represent eversion of the entire vagina.

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 Rectocele is a protrusion of the rectum into the vaginal lumen

 Enterocele is a herniation of the peritoneum and small bowel
and is the only true hernia among the pelvic support disorders.

POP GRADING/QUANTIFICATION SYSTEM

POP-Q system
 This system contains a series of site specific measurements each
measured relative to the hymen which is an anatomic landmark.
 With the hymenal plane defined as zero, Points proximal to the
hymen are described with a negative number. Positions distal to
the hymen are noted using a positive number
 There are nine points; all except TVL, are measured during
patient Valsalva and should reflect maximum protrusion.

Possible Ranges of the Six Sites specific Pelvic Organ Prolapse.

Points Description Range
Aa Anterior wall 3 cm from hymen -3 cm to +3 cm
Bb Most dependent portion of rest of anterior -3 cm to +TVL
wall
C Cervix or vaginal cuff ±TVL
D Posterior fornix (if no prior hysterectomy) ±TVL or omitted
Ap Posterior wall 3 cm from hymen -3 cm to +3 cm
Bp Bp Most dependent portion of rest of -3 cm to +TVL
posterior wall

 The total vaginal length (TVL) is the greatest depth of the

vagina in centimeters when point C or D is reduced to its fullest
position.
 Genital Hiatus and Perineal Body.
 The genital hiatus is measured from the middle of the external
urethral meatus to the midline of the posterior hymenal ring.
 The perineal body is measured from the posterior margin of
the genital hiatus to the mid anal opening.

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Normal

When fully prolapsed

FIGURE 1: The anatomic landmarks used during pelvic organ prolapse

quantification (POP-Q)

The POP-Q staging system of pelvic organ support

No prolapse is demonstrated. Points Aa, Ap, Ba, and Bp are all at -

3cm, and either point C or D is between -TVL cm and
Stage 0 (TVL−2) cm
Stage I The criteria for stage 0 are not met, but the most distal portion of the
prolapse is >1 cm above the level of the hymen(i.e., its quantitation
value is < -1 cm)
Stage II The most distal portion of the prolapse is ≤1 cm proximal to or distal
to the plane of the hymen(i.e. its quantitation value is
≥ -1 cm but ≤ +1cm)
Stage III The most distal portion of the prolapse is > 1 cm below the plane of
the hymen but protrudes no further than 2 cm less than the total
vaginal length in centimeters (i.e., its quantitation value is > +1 cm.
But < [TVL−2] cm).
Stage IV Essentially, complete eversion of the total length of the lower genital
tract is demonstrated. The distal portion of the prolapse protrudes to
at least (TVL−2) cm (i.e., its quantitation value is ≥
+[TVL−2] cm).

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BADEN-WALKER HALFWAY SYSTEM

 This descriptive tool is also used to classify prolapse during
physical examination and is in widespread clinical use.

Grade 0 Normal position for each respective site

Grade 1 Descent halfway to the hymen
Grade 2 Descent to the hymen
Grade 3 Descent halfway past the hymen
Grade 4 Maximum possible descent for each site

CLINICAL MANIFESTATIONS OF POP

SYMPTOMS
 Bulge symptoms
 Sensation of vaginal bulging or protrusion
 Seeing or feeling a vaginal or perineal bulge
 Pelvic or vaginal pressure
 Heaviness in pelvis or vagina
 Urinary Symptoms
 Stress urinary and urge incontinence (SUI), urinary
frequency, urinary retention, recurrent urinary tract
infection, or Manual reduction of prolapse to start or
complete voiding.
 Bowel symptoms
 Incontinence, feeling of incomplete emptying, constipation,
urgency, digital evacuation to complete defecation.
 Sexual symptoms and pain
 Dyspareunia, decreased lubrication, decreased sensation,
decreased arousal or orgasm.
Pelvic and Back Pain
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PHYSICAL EXAMINATION
PELVIC EXAMINATION

 The vulva and perineum are examined for signs of vulvar or

vaginal atrophy, lesions, or other abnormalities.
 Sacral reflexes is using a cotton swab.
 The bulbocavernosus reflex: is elicited by tapping or stroking
lateral to the clitoris and observing contraction of the
bulbocavernosus muscle bilaterally.
 Anal wink reflex: for evaluation of anal sphincter innervation
is completed by stroking lateral to the anus and observing a
reflexive contraction of the anus.
 Intact reflexes suggest normal sacral pathways.
 Examination of prolapsed organ begins by asking a woman to
attempt Valsalva maneuver prior to placing a speculum in the
vagina.
 If unable to adequately complete a Valsalva maneuver; are asked
to cough. If the full extent of prolapse cannot be demonstrated, a
woman should be examined in a standing position.
During this assessment try to answer three questions:
(1) Does the protrusion come beyond the hymen?
(2) What is the presenting part of the prolapse (anterior,
posterior, or apical)?
(3) Does the genital hiatus significantly widen with increased
intraabdominal pressure?

 The use of a Graves speculum or Baden retractor can help to

evaluate the apical compartment of the vagina.
 The anterior and posterior compartments are best examined with
the use of a univalve or Sims' speculum.

 Rectovaginal examination may be useful in evaluating the

posterior compartment to distinguish a posterior vaginal wall
defect.
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 A clinician’s index finger is placed in the rectum and thumb

on the posterior vaginal wall.
 Small bowel may be palpated between the rectum and
vagina, confirming enterocele.
 Enterocele can only definitively be diagnosed by observing
small bowel peristalsis behind the vaginal wall.

 Bimanual examination is performed to identify other pelvic

pathology and a stress test for associated stress incontinence.
 If the POP-Q examination is performed, the genital hiatus (Gh)
and perineal body (Pb) are measured during Valsalva maneuver.
 The total vaginal length (TVL) is then measured by placing a
marked ring forceps, or a ruler, at the vaginal apex and noting
the distance to the hymen.
 A bivalve speculum is then inserted to the vaginal apex. It
displaces the anterior and posterior vaginal walls, and points C
and D are then measured with Valsalva.
 A univalve speculum is then used to displace the posterior
vaginal wall and allow for visualization of the anterior wall and
measurement of points Aa and Ba;
 Then the speculum is rotated 180 degrees to displace the
anterior wall and allow examination of the posterior wall and
Points Ap and Bp are measured.

MANAGEMENT PRINCIPLE
 Non-surgical measures:
Considered in women with:-
 Mild to moderate prolapse (stage I & II)
 Those who desire preservation of future childbearing
 Those who do not desire surgical intervention.

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Includes;-
1. Pelvic Floor Muscle Exercises
 Referred to as Kegel exercises. Aimed to tighten and
strengthen the pubococcygeus muscles.
2. Estrogen; in postmenopausal women, local estrogen therapy.
3. Weight reduction in obese patients
4. Modification of life style (avoid heavy exercise, other habits)
 Surgical measures:
 Anterior colporrhaphy for anterior prolapse
 Posterior vaginal defect repair: Colpoperineorrhaphy and
Posterior colporrhaphy
 Apical Vaginal Repair: Vaginal hysterectomy with culdoplasty;
Vaginal hysterectomy with sacrospinous fixation

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 SAMPLE HISTORY

Chief complaint: Mass protruding per vagina of 2 years and 2

month duration.

HPI
This is a 55 years old para 8,abortion 0 patient who has been
amenorrhic for the last 6 years; was relatively healthy until she
presented with protruding mass of 2 years, which begins to get
worse since 6 months back. The mass protrudes out up on
standing, coughing and lifting heavy objects and returns on
attaining supine position. The mass was soft and she was able to
push back the mass manually. It is painless and not associated
with abnormal bleeding or foul smelling discharge. She also
complains of dragging type of lower abdominal pain which doesn’t
radiate and get exacerbated when she stands and strains while
relieved upon rest. For this reason she went to a local health center
and was referred to Jimma medical center.
She also has frequent urination, urgency, leakage of urine while
coughing or sneezing and a burning sensation during urination.
Due to urinary frequency, she was forced to reduce her water intake
during work.

Her first delivery was 35years back and her last was 10 years back.
All of her children were born through spontaneous vaginal delivery
at her house attended by traditional birth attendants. Labor, lasted
less than 6 hours in all cases. All her children are alive and healthy.
None of her pregnancies had antepartum or post-partum
complications.

She works in a factory as a daily laborer(animal food product

factory). The job requires heavy lifting and lots of strenuous
activities.
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Otherwise:-
She has no history of vaginal bleeding or discharge,
She has no history of reddish discoloration of urine.
She has no history of abdominal swelling or distention.
She has no history of chronic cough,
She has no previous history of constipation.
She has no history of trauma to the pelvis or gynecological surgery
She has no history of similar illness in the family.
She has no personal and family history of chronic illness like
DM, hypertension or asthma.
She has no color change to the mass or ulceration.
She has no history of urinary retention, change in bowel habits.
She is not sexually active currently.
She came to this hospital by walking.
Pertinent physical examination:
General appearance: Stable, comfortable, well-nourished and
cooperative during physical examination.
Vital sign: BP=130/80 mm Hg from right arm, supine position.
PR=88 beats/min from radial artery.
RR=18 breaths/min
To=36.00C from axilla
Weight: 83kg height: 160cm
BMI: 32.4kg/m2
Pelvic examination
Examination of external genitalia: atrophic vulva, inverted
triangle like hair distribution. Type I clitoridectomy, No ulcers,
discolorations, pruritus or warts.
Digital vaginal examination: a soft, non-tender and reducible
mass felt bulging from the anterior vaginal wall.

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After straining a mass protruding per vagina is seen half way past
the hymen. By Baden-Walker Half Way system = stage three pelvic
organ prolapse.
No cervical motion tenderness.
Recto vaginal examination: no peristalsis felt behind the vaginal
wall
Assessment:

Differential Diagnosis
 Tumors of the urethra and bladder
 Urethral diverticulum
 Skene's and Bartholin's glands cysts or abscesses.
 Soft tumors (lipoma, leiomyoma, sarcoma)
 Cervical/endometrial tumors (pedunculated myoma or
endometrial polyps); if prolapsed through a dilated cervix.
 Elongated cervix

Investigations
 Hematocrit, Blood group & Rh, U/A
 RFT
 U/S for residual volume, kidneys, abdominal masses.
 Intravenous pyelogram (IVP)

Management
(See above)

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CHAPTER 15

PELVIC PAIN
HISTORY
Detail elaboration of the pain. We can use the mnemonic “OLD
CAARTS” to remember the contents we need to include.
 O => onset
 Sudden, indicate rupture of a cyst, an ectopic pregnancy,
obstruction or perforation of a hollow viscus
 Gradual, indicate a progressive or chronic condition
 L => location, (on history it is better to say lower abdominal
pain)
 Unilateral, usually indicate adnexal pathology in that
side and a localized etiology
 Bilateral,
 Midline (diffuse or generalized), indicates a visceral pain
from distention, stretching or spasm of abdominal
organs (which have their origin from the embryological
hind gut, like the colon or intraperitoneal portions of the
genitourinary tract)
 D => duration, (see the detail below)
 Acute or Chronic
 C => character
 Intermittent, usually associated with contraction of the
bowel or the uterus
 Continuous,
 Sharp, kind of stabbing, indicate a localized cause,
 Dull ache, diffuse pain from the viscera
 Cramp, associated with contraction of a hollow viscus,
like intestine or uterus in attempt to relive an obstruction

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 A => alleviating or aggravating factors

 Pain aggravated with motion may indicate peritonitis
(from rupture of a cyst or appendix)
 Pain relived with acquiring certain position may indicate
obstruction of a vicious organ, as in renal colic. Is the
pain relived by any medications?

 A => associated symptoms, (this should be included after

completion of the pain description)
 vaginal bleeding or discharge, amenorrhea, infertility….
=> gynecologic pathology
 dysuria, hematuria, frequency, or urgency…. => urinary
pathology
 diarrhea, constipation, or gastrointestinal bleeding…. =>
gastrointestinal (GI) disease.
 vomiting
- In the acute surgical abdomen, if vomiting occurs, it
usually follows as a response to pain and results
from vagal stimulation.
- This vomiting is typically severe and develops
without nausea. For example, vomiting has been
found in approximately 75 percent of adnexal torsion
cases
- if vomiting is noted prior to the onset of pain, a
surgical abdomen is less likely
 Fever, chills … indicate an acute inflammatory/infectious
condition
 R => radiation, to
 The shoulder, indicate hemoperitoneum, may be from
ruptured ectopic pregnancy
 The groin, from the costovertebral angle, indicate ureteral
colic
 T => timing/ temporal
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 What time of day (elation to menstrual cycle and

activities of daily living)?
 Pelvic can occur associated with
- Menses=> dysmenorrhea
- Sexual intercourse=> dyspareunia
- Urination=> dysuria
- Defecation=> dyschezia
 S => severity
 Has the patient stopped daily activity b/c of the
symptom? Or lost normal sleep?
 Does simple rest relive the pain?
 Is the pain associated any indicators systemic autonomic
response like, diaphoresis, vomiting?
See P/E and Investigations under each differentials

CLASSIFICATION
 Acute pelvic pain
 Cyclic pelvic pain
 Chronic pelvic pain
Comparison between Acute Vs Chronic pelvic pain
Acute pelvic pain Chronic pelvic pain
Duration Less than 7 days Greater than 6 months
Onset Rapid Gradual
Type Inflammatory Neuropathic
Etiology Infection, ischemia, Often it is obscure.
or chemical irritation

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Association Often associated  obvious

with autonomic reflex
 profound responses are not
autonomic present
reflex  is characterized
responses, such by neurological,
as nausea, psychological,
emesis, and behavioral
diaphoresis, alterations, like
and anxiety and
apprehension, depression
 unstable vital  vital sign
signs and derangements
obvious and obvious
abnormalities anatomic
on physical abnormalities
examination may not be there
and laboratory
assessment
Treatment Is directed against If focused on treating
the underlying the pain symptoms
condition

ACUTE PELVIC PAIN

 Acute pain is intense and characterized by sudden onset,
sharp rise, and short course.
 It can be a somatic or visceral pain
 Somatic pain arises from the parietal peritoneum,
muscle, subcutaneous tissue or the skin.it is typically
sharp and localized.it is often unilateral

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 Visceral pain arises from the visceral peritoneum or

the viscera.
 The viscera are relatively insensitive to pain.
 The first perception of visceral pain is a vague,
deep, poorly localizable sensation associated with
autonomic reflex responses; however, once the
pain becomes localized, the pain is called referred
pain.
 Referred pain is well localized and superficial. It is
appreciated within the nerve distribution or
dermatome of the spinal cord segment innervating
the involved viscus
 The pain is often diffuse and dull ache, but it can
be localized to the midline

DIFFERENTIAL DIAGNOSIS OF ACUTE PELVIC PAIN

Gynecologic Disease or Dysfunction

Complication of pregnancy
Ectopic pregnancy
Abortion, threatened or incomplete
Acute infections
Endometritis
Pelvic inflammatory disease (acute PID) or
salpingo-oophoritis
Tubo-ovarian abscess
Adnexal disorders
Hemorrhagic functional ovarian cyst
Torsion of adnexa
Rupture of functional, neoplastic, or
inflammatory ovarian cyst
Prolapsing leiomyoma

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Gastrointestinal

Gastroenteritis
Appendicitis
Bowel obstruction
Diverticulitis
Irritable bowel syndrome
Genitourinary

Cystitis
Pyelonephritis
Ureteral lithiasis
Musculoskeletal

Abdominal wall hematoma

Hernia

Ectopic pregnancy
 An ectopic pregnancy is defined as implantation of the fetus in
a site other than the uterine cavity. The fallopian tube is the
most common site of implantation (~95%)
 Implantation of the fetus in the fallopian tube produces pain
only with acute dilation of the tube. If tubal rupture occurs,
localized abdominal pain tends to be temporarily relieved and
is replaced by generalized pelvic and abdominal pain as the
hemoperitoneum develops.
 A period of amenorrhea followed by bleeding and pain compose
the classic triad of symptoms.
 A mass in the cul-de-sac may produce an urge to defecate

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Torsion of Adnexa

 Torsion (twisting) of the vascular pedicle of an ovary, fallopian

tube, paratubal cyst, or rarely just a fallopian tube results in
ischemia and rapid onset of acute pelvic pain.
 A benign cystic teratoma is the most common neoplasm to
undergo torsion.
 Ovarian carcinoma and inflammatory masses are rarely
affected by torsion (because of adhesions). It is also unusual
for a normal tube and ovary to torque, although a polycystic
ovary can undergo torsion
 The pain of torsion can be severe and constant or, if the torsion
is partial and intermittently untwists, it could be intermittent.
 The onset of the torsion and the symptoms of abdominal pain
frequently coincide with lifting, exercise, or intercourse.
 Autonomic reflex responses are usually present (e.g., nausea,
emesis, apprehension).

Leaking or Ruptured Ovarian Cyst

 Functional cysts (e.g., follicle, corpus luteum) are the most
common ovarian cysts and rupture more readily than do
benign or malignant neoplasms.
 A hemorrhagic corpus luteum cyst can develop in the luteal
phase of the menstrual cycle. Rupture of this cyst can produce
either a small amount of intraperitoneal bleeding or frank
hemorrhage resulting in significant blood loss and
hemoperitoneum.
 Nonmalignant neoplasms, most commonly cystic teratomas
(dermoid cysts) or cystadenomas, as well as inflammatory
ovarian masses, such as endometriomas, can also leak or
rupture.
 A corpus luteum cyst is the most common cyst to rupture and
lead to hemoperitoneum.
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 Symptoms of a ruptured corpus luteum cyst are similar to those

of a ruptured ectopic pregnancy.
 The onset of pain is usually sudden and is associated with
increasing generalized abdominal pain and occasionally
dizziness or syncope if a hemoperitoneum develops.

Uterine Leiomyomas
 Leiomyomas are uterine smooth muscle tumors (see the
myoma section).
 Discomfort may be present when myomas are intramural,
fundal, or encroaching on adjacent bladder, rectum, or
supporting ligaments of the uterus.
 Although rare, fibroids are more likely to cause dyspareunia
and noncyclic pelvic pain
 Acute pelvic pain can develop if the myoma undergoes
degeneration or torsion. Degeneration of myomas occur
secondary to loss of blood supply, usually attributable to rapid
growth associated with pregnancy.
 A pedunculated subserosal leiomyoma can undergo torsion
ischemic necrosis; when this situation occurs, it is associated
with pain similar to that of adnexal torsion.
 When a submucous leiomyoma becomes pedunculated, the
uterus contracts force-fully as if to expel a foreign body, and
the resulting pain is similar to that of labor. The cramping pain
is usually associated with hemorrhage.

Pelvic inflammatory disease (PID) (see below)

Appendicitis
 Is most common intestinal source of acute pelvic pain in
women
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 The symptoms and signs of appendicitis can be similar to

those of PID.
 The first symptom of appendicitis is typically diffuse abdominal
pain, especially periumbilical pain, followed by anorexia,
nausea, and vomiting. Within a matter of hours, the pain
generally shifts to the right lower quadrant. Fever, chills,
emesis, and obstipation may ensue. However, this classic
symptom pattern is often absent.

Acute Diverticulitis
 Acute diverticulitis is a condition in which there is
inflammation of a diverticulum or outpouching of the wall of
the colon, usually involving the sigmoid colon.
 Diverticulitis typically affects postmenopausal women but can
occur in women in their 30s and 40s.
 The severe, left lower quadrant pain of diverticulitis can occur
following a long history of symptoms of irritable bowel
(bloating, constipation, and diarrhea), although diverticulosis
usually is asymptomatic. Diverticulitis is less likely to lead to
perforation and peritonitis than is appendicitis.
Fever, chills, and constipation typically are present, but
anorexia and vomiting are uncommon.

Intestinal Obstruction
 The most common causes of intestinal obstruction in women
are postsurgical adhesions, hernia formation, inflammatory
bowel disease, and carcinoma of the bowel or ovary.
 Intestinal obstruction is heralded by the onset of colicky
abdominal pain followed by abdominal distention, vomiting,
constipation, and obstipation.
 Higher and more acute obstruction results in early vomiting,
whereas colonic obstruction presents with a greater degree of
abdominal distention and obstipation.

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 Vomiting first consists of gastric contents, followed by bile,

then material with feculent odor, depending on the level of
obstruction.

Ureteral colic
 Ureteral colic is a cramping lower abdominal pain that is
due to ureteral lithiasis is caused by a sudden increase in
intraluminal pressure and associated inflammation.
 The pain of lithiasis is typically severe and crampy; it can
radiate from the costovertebral angle to the groin.
Hematuria is often present

UTI
 Urinary tract infections producing acute pain include
cystitis and pyelonephritis. The most common microbes
causing urinary tract infections are E. coli followed by
Proteus, Klebsiella, and Pseudomonas.
 Cystitis is associated with dull suprapubic pain, urinary
frequency, urgency, dysuria, and occasionally hematuria.
Because urethritis can occur secondary to chlamydia or
gonorrhea and has similar symptoms, these infections must
be ruled out if appropriate.
 Pyelonephritis is associated with flank and costovertebral
angle pain, although lateralizing lower abdominal pain
occasionally is present.
 On physical examination there is pain with firm pressure
over the costovertebral angle in the case of lithiasis or
pyelonephritis. Peritoneal signs are absent. Suprapubic
tenderness may accompany cystitis.

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PELVIC INFLAMMATORY DISEASE (PID)

 Pelvic inflammatory disease (PID) comprises a spectrum of

inflammatory disorders of the upper female genital tract (above
the internal Os), including any combination of endometritis,
salpingitis, tubo-ovarian abscess, and pelvic peritonitis.
 Involvement the fallopian tube in PID is of special importance
because of subsequent complication (infertility).

Etiology and Risk factors

 Pelvic inflammatory disease is commonly caused by N.

gonorrhea, C. trachomatis, and T. vaginalis, although the
infection is usually polymicrobial.
 Upper genital tract infections are usually caused by bacteria
that ascend from the lower reproductive tract.

Risk Factors for PID

 Douching
 Single status
 Substance abuse
 Multiple sexual partners
 Lower socioeconomic status
 Recent new sexual partner(s)
 Younger age (10 to 19 years)
 Other sexually transmitted infections
 Sexual partner with urethritis or gonorrhea
 Previous diagnosis of pelvic inflammatory disease
 Endocervical testing positive for N gonorrhea or C trachomatis
 Not using mechanical and/or chemical contraceptive barriers

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Classification of PID

 Pelvic inflammatory disease can be segregated into “silent” PID

and PID. The latter can be further subdivided into acute and
chronic.
Silent PID

 Silent PID is thought to follow multiple or continuous low-

grade infection in asymptomatic women.
 Is not a clinical diagnosis. Rather, it is an ultimate diagnosis
given to women with tubal-factor infertility who lack a history
compatible with upper tract infection.
 Many of these patients have antibodies to C trachomatis
and/or N gonorrhea.
 At laparoscopy or laparotomy,
 affected women may have evidence of prior tubal
infection such as adhesions, but for the most part, the
fallopian tubes are grossly normal or they may have
hydrosalpinx
 fine adhesions between the liver capsule and anterior
abdominal wall may also reflect prior silent disease

Acute PID

 Acute gonococcal PID is manifested by the acute onset of

pelvic pain that increases with movement, fever, purulent
vaginal discharge, and sometimes nausea and vomiting.
 The pain is often associated with a menstrual period.
 Chlamydial salpingo-oophoritis is associated with more
insidious symptoms.
On physical examination:
 Direct and rebound abdominal tenderness with palpation are
usually notable

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 The most important signs of acute salpingo-oophoritis are

cervical motion tenderness and bilateral adnexal tenderness.
 Lack of a discrete mass or masses differentiates acute
salpingo-oophoritis from tubo-ovarian abscess or torsion.

The most recent diagnostic criteria presented by the CDC (2015) are
for sexually active women at risk for STDs who have pelvic or lower
abdominal pain and in whom other etiologies are excluded or
unlikely.
 PID is diagnosed if uterine tenderness, adnexal tenderness, or
cervical motion tenderness is present. One or more of the
following enhances diagnostic specificity:

1) Oral temperature > 38.3°C (101.6°F)

2) Mucopurulent cervical discharge or cervical reliability
3) Abundant WBCs on saline microscopy of cervical
secretions
4) Elevated erythrocyte sedimentation rate (ESR) or C-
reactive protein (CRP)
5) Presence of cervical N gonorrhea or C trachomatis
Thus, a diagnosis o PID is one typically based on clinical findings.

Tubo-ovarian Abscess (TOA)

 TOA, a sequela of acute salpingitis, are usually bilateral, but

unilateral abscess formation can occur.
 The symptoms and signs are similar to those of acute
salpingitis, although pain and fever have often been present
for longer than 1 week before presentation to the emergency
room.
 A ruptured tubo-ovarian abscess is a life-threatening surgical
emergency because gram-negative endotoxic shock can
develop rapidly.

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 Tubo-ovarian abscesses can be palpated on bimanual

examination as very firm, exquisitely tender, bilateral fixed
masses. The abscesses can be palpated in the pelvic cul-de-
sac.

Based on the antecedent event, PID can also be classified as:

 Post-partum
 Post abortal
 Post-operative
 Post IUCD/Instrumental
 Post STD
 Post TB

PHYSICAL EXAMINATION FOR ACUTE PELVIC PAIN

G/A: Acutely sick looking, patient lying still (peritonitis) or restless
(cramping)
V/S: tachycardia & tachypnea (severe pain), pyrexia
(infection/inflammation) or hypotension (from hypovolemia)
Abdominal examination:
 Inspection:
 Distended abdomen:- bowel obstruction, torsion or
hemoperitoneum
 Abdomen doesn’t move with respiration:- peritonitis
 Scar:- bowel obstruction, ectopic pregnancy
 Hernia sites
 Palpation
 Generalized abdominal rigidity with significant
tenderness and rebound tenderness => peritoneal
irritation (in most of the cases)
 Tenderness limited to the lower abdomen
 Percussion
 Hypertympanic=> bowel obstruction
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 Dullness=> blood or cystic fluid in the peritoneum

 Auscultation
 Hyperactive bowel sound=> early stage of bowel
obstruction
 Absent bowel sound=>

Pelvic examination
 Check the introitus and urethral orifice for discharge or
bleeding
 Cervical motion tenderness, can be seen with PID,
appendicitis, diverticulitis, and intraabdominal bleeding
 Uterine enlargement, in case of leiomyomas, pregnancy, and
adenomyosis
 A tender adnexal mass may reflect ectopic pregnancy, tubo-
ovarian abscess, or ovarian cyst with torsion, hemorrhage, or
rupture
Rectal examination can add information regarding the source
and size of pelvic masses and the possibility of colorectal
pathologies.

INVESTIGATION
 Urine or serum β-human chorionic gonadotropin (hCG)
testing is recommended in those of reproductive age without
prior hysterectomy.
 Complete blood count (CBC) can identify hemorrhage, both
uterine and intraabdominal, and can assess the possibility of
infection.
 Urinalysis, to evaluate possible urolithiasis or UTI
 ESR & CRP, shows an inflammatory state
 Microscopic evaluation and culture of vaginal discharge
 Sonography (ultrasound), transabdominal or transvaginal

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Is very important to assess most of pelvic pathologies and

identify fluid in the abdomen.
 Computed tomography (CT scan), has superior performance
in identifying GI and urinary tract causes of acute pelvic and
lower abdominal pain
 Magnetic resonance imaging (MRI), if initial sonography is
non-diagnostic
 Plain abdominal x-ray, (plain= no contrast) for bowel
obstruction
 Intravenous pyelography (IVP), for ureteral colic
 Laparoscopy, for both diagnostic and management purpose
Operative laparoscopy is the primary treatment or suspected
appendicitis, adnexal torsion, ectopic pregnancy, and ruptured
ovarian cyst associated with ongoing symptomatic
hemorrhage.
 Culdocentesis, in evaluation of suspected ruptured cyst

CYCLIC PELVIC PAIN

Cyclic pain refers to pain that occurs with a definite association to

the menstrual cycle.
Dysmenorrhea or painful menstruation, is the most common cyclic
pain phenomenon, affecting as many as 50% of menstruating
women. It is classified as primary and secondary dysmenorrhea.

Primary Secondary
dysmenorrhea dysmenorrhea
Underlying pelvic Absent Present
pathology
Onset in relation to Within 1 to 2 years of Years after menarche
menarche menarche
Onset in relation to Begins a few hours Begins 1-2wks before
menses and before or just after the menstrual flow and
duration onset of a menstrual persists until a few

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period and may last 48 days after the cessation

to 72 hours of bleeding
Mechanism Increased endometrial Diverse and not fully
prostaglandin elucidated, although
production higher most involve either
uterine tone with high- excess prostaglandin
amplitude contractions production or
causing dysmenorrhea. hypertonic uterine
contractions secondary
to cervical obstruction,
intrauterine mass, or
the presence of a
foreign body

Pain relief with NSAIDs are effective NSAIDs and hormonal

treatment contraceptives are less
likely to provide relief

Primary dysmenorrhea affects younger women but may persist into

the 40s. The pain is similar to labor, with suprapubic cramping,
and maybe accompanied by lumbosacral backache.
On examination, except suprapubic & uterine tenderness on
bimanual palpation, there is no abnormal finding.

The most common cause of secondary dysmenorrhea is

endometriosis, followed by adenomyosis and intrauterine device.

CHRONIC PELVIC PAIN

 Chronic pelvic pain remains an inclusive, general diagnosis.
 Various forms of chronic pelvic pain affect 12% to 20% of
women in the United States.
 Patients with chronic pelvic pain are frequently anxious and
depressed. Their marital, social, and occupational lives are
usually been disrupted.
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 These patients have often had poor treatment outcomes and

may have undergone multiple unsuccessful surgical
procedures for pain.
 About 12% to 19% of hysterectomies are performed for
pelvic pain.

 Approximately 60% to 80% of patients undergoing laparoscopy

for chronic pelvic pain have no intraperitoneal pathology, nor
do they have tissue distortion that correlates with the pain.

 Nongynecologic causes of pain, such as irritable bowel

syndrome, interstitial cystitis, abdominal wall or pelvic floor
myofascial syndrome, or neuropathy, are frequently over
looked but common causes of chronic pelvic pain.

 In addition to detail on the pain, history of any

musculoskeletal trauma, surgical procedure (including
cesarean delivery) and medical interventions done for similar
or other complaint are very important.

 Current and past psychological history including psychosocial

factors; history of past (or current) physical, sexual, or
emotional abuse; history of psychiatric hospitalization; suicide
attempts; and chemical dependency need to be included.

Physical examination should focus on abdomen and the

musculoskeletal system.
Abdomen
 Inspect for scars (esp. Surgicaladhesion) and hernia
 Demonstrate Carnett test, which is an evaluation of the
abdomen with muscles tensed (head raised off the table or
with straight leg raising) to differentiate abdominal wall and
visceral sources of pain. Abdominal wall pain is augmented

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and visceral pain is diminished with these maneuvers

 Perform superficial and deep palpation
 Increased bowel sound may indicate irritable or
inflammatory bowel disease.
Differential Diagnosis of Chronic Pelvic Pain

Gynecologic Genitourinary
Non-cyclic Recurrent or relapsing cystourethritis
Adhesions Urethral syndrome
Endometriosis Interstitial cystitis
Salpingo-oophoritis Ureteral diverticuli or polyps
Retained ovary Carcinoma of the bladder
syndrome
Pelvic congestion Ureteral obstruction
Ovarian neoplasms Pelvic kidney
Neurologic
Cyclic Nerve entrapment syndrome, neuroma, or
other neuropathies
Primary Trigger points
dysmenorrhea
Mittelschmerz Musculoskeletal
Secondary Low-back-pain syndrome
dysmenorrhea
Endometriosis Congenital anomalies
Scoliosis and kyphosis
Asherman's Spondylolysis
syndrome
Endometrial polyps Spondylolisthesis
Uterine leiomyomata Spinal injuries
Adenomyosis Inflammation
Pelvic congestion Tumors
syndrome
Atypical cyclic Osteoporosis
Endometriosis Degenerative changes
Adenomyosis Coccydynia
Ovarian remnant Myofascial syndrome
syndrome
Chronic functional cysts Hernia
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Gastrointestinal Systemic
Irritable bowel Fibromyalgia
syndrome
Ulcerative colitis Acute intermittent porphyria
Crohn's disease Abdominal migraine
Carcinoma Connective tissue disease including
systemic lupus erythematosus
Infection Lymphoma

ENDOMETRIOSIS
 Endometriosis is defined as the presence of endometrial
glands and stroma outside the uterine cavity.
 The annual incidence of surgically diagnosed endometriosis is
1.6 per 1000 women aged 15-49yrs.the prevalence in different
in asymptomatic women (6-11%), in patient with infertility (20-
50%) and in patient with pelvic pain (40-50%, in Novak’s
gynecology 14th ed this figure is 15_40%).

Risk factors for endometriosis

 Nulliparity
 Early menarche/late menopause
 Short menstrual cycles
 Prolonged menses
 Müllerian anomalies (increase ectopic implantation of
endometrial tissue)
Endometriosis is an estrogen dependent disorder, any factor
that increase estrogen exposure increases the risk. It is rarely
seen in postmenopausal women and nonexistent in pre-
pubertal girls.

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The definitive cause of endometriosis remains unknown, but

different theories have been suggested:
 Retrograde menstruation through the fallopian tubes (the
more favored one)
 The stem cell theory
 Aberrant lymphatic and vascular spread of endometrial tissue
 Coelomic metaplasia theory

Endometriosis may develop anywhere within the pelvis and on other

extrapelvic peritoneal surfaces. Most commonly, it develops in the
dependent areas of the pelvis like

 the anterior and posterior cul-de-sacs,

 other pelvic peritoneum,
 the ovary, and
 uterosacral ligaments are frequently involved.

Additionally, the rectovaginal septum, ureter, and bladder

and rarely, pericardium, surgical scars, and pleura may be
affected. One pathologic review revealed that endometriosis
has been identified on all organs except the spleen.

Implants may be:-

 superficial or
 deep infiltrating endometriosis (DIE), that is, infiltrative forms
that involve vital structures such as bowel, bladder, and
ureters.
o Some definitions of DIE also quantify invasion as > 5 mm
Ovarian endometriomas
 are frequent manifestations of endometriosis
 these smooth-walled, dark-brown ovarian cysts are filled with
a chocolate-appearing fluid and may be unilocular or, when
larger, multilocular

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 their pathogenesis is unclear, yet three theories include

invagination of ovarian cortex implants, coelomic metaplasia,
and secondary involvement of functional ovarian cysts by
endometrial implants located on the ovarian surface

Endometriosis produces a low-grade inflammatory reaction; over

time this results in adhesions between confluent pelvic organs.
However, the cause of the pain is not well established.

Classification

 The American Society for Reproductive Medicine allows

endometriosis to be quantified and classified in to four stages.
 With this, endometriosis on the peritoneum, ovaries,
fallopian tubes, and cul-de-sac is scored at surgery.
 At these sites, points are assigned for:-
 disease surface area,
 degree of invasion,
 morphology, and extent of associated adhesions
 Also, endometriotic lesions are morphologically categorized
as white, red, or black.
 In this system, endometriosis is classified as
 stage I (minimal, score 1-5),
 stage II (mild, score 6-15),
 stage III (moderate, score 16-40), and
 stage IV (severe, score >40)

NB, there is poor correlation with stage of disease and

pain & infertility

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Clinical manifestation

Pain:
 Is the most common symptom.
 Endometriosis associated chronic pelvic pain (dysmenorrhea,
dyspareunia and non-cyclic pain) is common.
 Less often dyschezia, dysuria and abdominal wall pain are
seen. (dysmenorrhea, dyspareunia, dyschezia and dysuria are
sometimes can be remembered as 4Ds of endometriosis)
 Vaginal, uterosacral ligament and rectovaginal septum
endometrioses are associated with deep dyspareunia.
 Dyspareunia
o may be caused by
 pressure on inflamed tissues and neural invasion,
 stretching and tearing during intercourse of pelvic
structures bound by adhesions.
o Endometriosis associated dyspareunia is suspected if pain
develops after years of pain free intercourse.
 Dysuria and dyschezia are associated with DIE to the
respective organs

Infertility:

 Endometriosis is seen in 20-30% of patients with subfertility.

 Adhesion, which is associated with impairment of normal
oocyte pick-up and transport by the fallopian tube, is the main
cause of infertility.
 Subtle defects like perturbations in follicle development,
ovulation, sperm function, embryo quality and development,
and implantation are also possible causes

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Other symptoms depend on the system/site involved.

 Rectosigmoid lesions  dyschezia, constipation diarrhea and

cyclic hematochezia
 Urinary tract lesion dysuria, hematuria, suprapubic pain
and frequency
 Abdominal wall lesions abdominal pain
 Thoracic lesions cyclic chest pain, hemoptysis and
pneumothorax associated with menses, which are sometimes
refereed as catemenial.
Physical examination

 Often no abnormal findings are seen in physical examination.

 Most common finding is tenderness when palpating the
posterior fornix.
 Other frequent findings:
 localized tenderness in the pouch of Douglas or
uterosacral ligaments,
 palpable tender nodules in the posterior cul-de-sac,
uterosacral ligaments, or rectovaginal septum,
 thickening and induration of uterosacral ligaments,
 pain with uterine movement,
 tender enlarged adnexal masses and
 fixation of adnexa or uterus in a retroverted position.

Diagnosis

 Endometriosis is a surgical diagnosis based on identification of

characteristic lesions.
 Laparoscopy is the gold standard investigation.
 Histologic and imaging studies are also required for definitive
diagnosis. Although nonspecific CA125 is elevated in
endometriosis.

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Management

Management depends on age, symptoms, stage, and the need for

fertility. It includes:
1. Expectant Management
2. Medical treatment
3. Hormonal treatment
4. Surgical treatment
5. Combination Medical and surgical treatment

ADHESIONS

 Adhesions noted at the time of laparoscopy are often in the

same general region of the abdomen as the source of the pelvic
pain; however, neither the specific location nor density of the
adhesions correlates consistently with the presence of pain
symptoms.

Symptoms
 Noncyclic abdominal pain, sometimes increased with
intercourse or activity, is a common source of pain in women
with adhesions, but there is no symptom pattern specific for
adhesions.
 Chronic pelvic pain developing from adhesions is thought to
result from restriction of bowel mobility and distention.
Furthermore, dense adhesions involving bowel can cause
partial or complete bowel obstruction.
Signs
 The abdominal wall must be carefully evaluated for myofascial
or neurological sources of pain.
 Most women with adhesions have had a prior surgical
procedure with possible injury to abdominal wall structures
that may be the cause of pain.
 Decreased mobility of pelvic organs or adnexal enlargement
can often be detected in patients with adhesions.
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CHAPTER 16

GENITOURINARY FISTULA (GUF)

A genitourinary fistula is defined as an abnormal communication
between the urinary (ureters, bladder, urethra) and the genital
(uterus, cervix, vagina) systems.

Incidence
 The true incidence of genitourinary fistula is unknown and
varies according to whether the etiology is obstetric or
gynecologic.
 In Asia and Africa, up to 100,000 new cases of obstetric
genitourinary fistula are added each year to the estimated pool
of 2 million women with unrepaired fistulas.
 For industrialized countries, most fistulas occur iatrogenically
from pelvic surgery, and the generally accepted incidence
derives from data on surgeries to correct these fistulas.
 Of genitourinary fistulas, the vesicovaginal fistula is most
common.

CLASSIFICATION
Many classification systems exist for genitourinary fistula:
Classification of Genitourinary Fistula Based on Anatomic
Communication
 Communication between the urinary tract and vagina:-
 Ureterovaginal
 Vesicovaginal
 Urethrovaginal

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 Communication between the cervix and the urinary tract

 Ureterocervical
 Vesicocervical
 Urethrocervical
 Communication between the uterus and the urinary tract
 Ureterouterine
 Vesicouterine
Vesicovaginal fistulas can also be classified by their size and
location in the vagina.
 high vaginal, when found proximally in the vagina
 low vaginal, when noted distally; or
 midvaginal, when identified centrally

Others classify vesicovaginal fistula based on the complexity and

extent of involvement
 Simple
o Size ≤ 3 cm
o Located near the cuff (supratrigonal)
o No prior radiation or malignancy
o Normal vaginal length
 Complicated
o Prior radiation therapy
o Pelvic malignancy present
o Vaginal length shortened
o Size > 3 cm
o Located distant from cuff or has trigonal involvement

In one obstetric classification system, high-risk vesicovaginal

fistulas are described by their size (> 4 to 5 cm in diameter);
involvement of urethra, ureter(s), or rectum; juxtacervical location
with an inability to visualize the superior edge; and reformation
following a failed repair.

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A surgical classification to objectively evaluate obstetric urinary

fistula repair has also been introduced:-
 Type I fistulas are those that do not involve the urethral
closure mechanism,
 Type II fistulas, .type II fistulas are divided into: (A) without
or (B) with subtotal or total urethra involvement. type IIB
fistulas are further subdivided as: (a) without or (b) with a
circumferential configuration around the urethra. and
 Type III fistulas involve the ureter and include other
exceptional fistulas.

To aid objective comparison of surgical outcomes, a more

comprehensive and standardized classification system has been
developed
 It integrates fistula distance from the external urethral
meatus, fistula size, degree of surrounding tissue fibrosis, and
extent of vaginal length reduction
 This new classification divides genitourinary fistulas into four
main types, depending on the distance of the fistula’s distal
edge from the external urinary meatus.
 Type 1: Distal edge of fistula > 3.5 cm from external
urinary meatus
 Type 2: Distal edge of fistula 2.5–3.5 cm from external
urinary meatus
 Type 3: Distal edge of fistula 1.5 to < 2.5 cm from
external urinary meatus
 Type 4: Distal edge of fistula < 1.5 cm from external
urinary meats
These four types are further sub-classified by the size of the fistula,
extent of associated scarring, vaginal length, or special
considerations.

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 By the size of the fistula

a) Size < 1.5 cm, in the largest diameter
b) Size 1.5–3 cm, in the largest diameter
c) Size > 3 cm, in the largest diameter
 By the extent of scaring/fibrosis
i. None or only mild fibrosis (around fistula and/or
vagina) and/or vaginal length > 6 cm, normal capacity
ii. Moderate or severe fibrosis (around fistula and/or
vagina) and/or reduced vaginal length and/or capacity
iii. Special consideration, e.g., postradiation, ureteric
involvement, circumferential fistula, or previous repair

ETIOLOGY AND RISK FACTOR

 Congenital genitourinary fistulas are rare, but if found, are
commonly associated with other renal or urogenital
abnormalities.
 Acquired and typically result from either obstetric trauma or
pelvic surgery.
 Obstetric Trauma: In developing countries, more than 70
percent of genitourinary fistulas arise from obstetric
trauma, specifically from prolonged or obstructed labor
or complicated cesarean delivery.

 Factors associated with fistula formation in developing

countries
 Both childbearing at a young age
 Female genital mutilation, may significantly narrow the
vaginal introitus and obstruct labor
 Prolonged obstructed labor or
 Anatomic malpresentation of the presenting fetal part
These factors can cause pressure and ischemic necrosis
of the anterior vaginal wall and bladder, subsequently
resulting in fistula formation.
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 Instrumental delivery used to deliver stillborn infants or

perform abortion, may damage the vagina
 Malnutrition and limited health care in many of these
countries can further diminish wound healing.

Fistula in developed countries

 Obstetric procedures or deliveries are unusual causes of
fistula in developed countries.
 Iatrogenic injury during pelvic surgery is responsible or 90
percent of vesicovaginal fistulas inthese nations.
 The accepted incidence of fistula formation after pelvic surgery
is 0.1 to 2 percent. In industrialized countries, hysterectomy is
the most common surgical precursor to vesicovaginal fistula,
accounting or approximately 75 percent of fistula cases.
 Other Causes include:-
o radiation therapy (6%),
o malignancy (1.8%),
o trauma (4%),
o foreign bodies, i
o infections, pelvic inflammation, and
o inflammatory bowel disease.
o Other rare causes of fistula formation include infections
such as lymphogranuloma venereum, urinary tuberculosis,
pelvic inflammation, and syphilis; inflammatory bowel
disease; and autoimmune disease.
o Additionally, conditions that inter ere with healing such as
poorly controlled diabetes mellitus, smoking, local infection,
peripheral vascular disease, and chronic corticosteroid use
are potential risks.

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SYMPTOMS
 Classically presents with unexplained continuous urinary
leakage from the vagina after a recent operation.
 Other less specific symptoms of genitourinary fistula include
fever, pain, ileus, and bladder irritability.

DIAGNOSIS
 A thorough history and physical examination identifies most
cases of vesicovaginal fistula.
 Visual assistance with an endoscopic lens and translucent
vaginal speculum can sometimes help identify a vaginal-apex
fistula, which can be more difficult to detect.

Investigations
 Measurement of the vaginal fluid’s creatinine content can
sometimes be used to confirm its origin.

o Although creatinine levels in urine vary, with mean levels

reaching 113.5 mg/dL, a value > 17 mg/dL is consistent
with urine.
o In contrast, fluid with a concentration < 5 mg/dL is
highly unlikely to be human urine.
 Retrograde bladder instillation of visually distinct solutions
such as sterile milk or dilute methylene blue or indigo carmine
can of ten indicate a fistula and aid in its localization.
 A three-swab test, commonly known as the “tampon test” is
recommended
o Two to four pieces of gauze sequentially packed into the
vaginal canal.
o A diluted solution of methylene blue or indigo carmine is
instilled into the bladder using a transurethral catheter.

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o After 15 to 30 minutes of routine activity, the gauze is

removed serially from the vagina, and each is inspected for
dye.
o The specific gauze colored with dye suggests the fistula
location-a proximal or high location in the vagina or the
innermost gauze and a low or distal fistula or the
outermost.

 Cystourethroscopy is another valuable diagnostic tool and

vaginoscopy.
 CT-scanning
 Intravenous pyelography (IVP)
o can adequately confirm integrity of the upper collecting
system and exclude ureteral involvement in a fistula
 Voiding cystourethrography (VCUG)
o can help confirm the presence, location, and number of
fistulous tracts
 Transabdominal sonography

TREATMENT
Conservative Treatment
 Approximately 12 percent of women treated by sustained
catheterization alone had fistulas that healed spontaneously.
 Fibrin sealant also colloquially called fibrin glue can be used
Surgical Treatment:
 Fundamentals of genitourinary fistula repair include accurate
fistula delineation; adequate assessment of surrounding tissue
vascularity; timely repair; multilayer, tension- free, and
watertight defect closure; and postoperative bladder drainage.

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Timing of Repair
 One principle of fistula repair dictates that, a repair be
performed in non-infected and non-inflamed tissues.
 Early surgical intervention of uncomplicated fistulas within
the first 24 to 48 hours following the inciting surgery.
 In instances of extensive and severe inflammation, we
recommend delaying operative repair or 6 weeks until the
inflammation subsides.
Route of Surgical Repair
 Vaginal: Latzko technique, classical technique
 Abdominal (Transperitoneal): This approach is used or
situations in which the fistula:
1) is located proximally in a narrow vagina,
2) lies close to the ureteral orifices
3) is complicated by a concomitant ureteric fistula
4) persists after prior repair attempts,
5) is large or complex in configuration, or
6) requires an abdominal interposition graft, described in
the next section

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 Sample history
C/c: Involuntary Leakage of urine of 05 months duration
HPI:
This is a 52 years old para 6(all alive) lady who has been amenohric
for the past 3 years, she was relatively health 5mo ago at w/c time
she started to experience involuntary leakage of urine, w/c started
2 weeks after delivering her last child by C/S(b/c it cames in upside
down) after a lobur of 2 days and is continues and small in amount
and not associated with cough, since than she has no sexual
contact and not participating in any social gathering.
Otherwise she has on Hx of
 vaginal discharge and itching sensation
 fever, pain,
 radiation therapy,
 malignancy ,
 trauma ,
 foreign bodies

Don’t forget obstetrics and gynecological Hx

See physical examination and investigation above

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REFERENCE

1. Williams Obstetrics, 24th edition and 25th edition

2. Gabbe Obstetrics, Normal and Problem Pregnancies, 7th
edition
3. Current Diagnosis and Treatment, Obstetrics And
Gynecology, 11th Edition
4. DC Dutta’s Textbook Of Obstetrics 7th Edition
5. Jimma University Specialized Hospital Obstetrics and
Gynecology Management Guideline, 2010G.C
6. Williams gynecology, 3rd edition
7. Berek and Novak’s Gynecology, 14th edition
8. Up-to date 2018

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Appendix

Preeclampsia Chart

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APH Chart

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PROM Chart

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