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Obstetrical emergencies

This document discusses several obstetric emergencies including vasa previa, cord presentation/prolapse, amniotic fluid embolism, shoulder dystocia, and obstetric shock. It defines each condition, lists risk factors and causes, and outlines signs/symptoms, diagnosis, and management approaches. Prompt recognition and treatment are emphasized as these emergencies can threaten the lives of both mother and baby if not addressed immediately.

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OBSTETRICAL EMERGENCIES Mrs. U SREEVIDYA Msc. NURSING, Associate Professor, Apollo college of nursing, CHITTOOR
DEFINITION  Obstetrical emergencies are life threatening medical conditions that occur in pregnancy or during labor or after delivery.
OBSTETRICAL EMERGENCY MEANS IMMEDIATE MANAGEMENT IS REQUIRED INCLUDING EARLY DETECTION AND PROMPT ACTION FOR BETTER OUTCOME OF PREGNANCY.
• 1. VASA PRAEVIA. • 2. PRENSENTATION AND PROLAPSE OF THE UMBILICAL CORD. • 3. SHOULDER DYSTOCIA. • 4. RUPTURE OF THE UTERUS. • 5.AMNIOTIC FLUID EMBOLISM. • 6.ACUTE INVERSION OF THE UTERUS. • 7.SHOCK IN OBSTETRICS. • 8. DIC THE IMPORTANT EMERGENCY CONDITIONS IN OBSTETRICS
VASA PRAEVIA
VASA PRAEVIA THE UNSUPPORTED UMBILICAL VESSELS, LIE BELOW THE PRESENTING PART AND RUN ACROSS THE CERVICAL OS.
VASA PREVIA INCIDENCE The actual incidence is extremely difficult to estimate, it appears that vasa previa complicates approximately 1 in 2,500 births.
 It is an abnormality of the cord that occurs when one or more blood vessels from the umbilical cord or placenta cross the cervix but it is not covered by Wharton’s jelly.  This condition can cause hypoxia to the baby due to pressure on the blood vessels.  It is a life threatening condition.
ETIOLOGY These vessels may be from either  Velamentous insertion of umbilical cord  placental lobe joined to the main disk of the placenta.  Low-lying placenta  Previous delivery by C-section.
SYMPTOMS  The baby’s blood is a darker red color due to lower oxygen levels of a fetus • Fetal distress can be seen.  Sudden onset of painless vaginal bleeding, especially in their second and third trimesters  If very dark burgundy blood is seen when the water breaks, this may be an indication of vasa previa
DIAGNOSIS Classical triad Painless vaginal bleeding Colour doppler- vessel crossing the membranes over the internal cervical os. Membrane rupture Fetal bradycardia
MANAGEMENT Antepartum  The patient should be monitored closely for preterm labor, bleeding or rupture of membranes.  Steroids should be administered at about 32 weeks.  Hospitalization at 32 weeks is reasonable .  Take patient for emergency cesarean section if membranes are ruptured.  Fetal growth ultrasounds should be performed at least every 4 weeks.  Cervical length evaluations may help in assessing the patient's risk for preterm delivery or rupture of the membranes
Intrapartum  The patient should not be allowed to labor. She should be delivered by elective cesarean at about 35 weeks.  Delaying delivery until after 36 weeks increases the risk of membrane rupture.  Care should be taken to avoid incising the fetal vessels at the time of cesarean delivery.  If vasa previa is recognized during labor in an undiagnosed patient, she should be delivered by emergency cesarean. The placenta should be examined to confirm the diagnosis.
Postpartum  Routine postpartum management as for cesarean delivery.  If the fetus is born after blood loss, transfusion of blood without delay may be life-saving.  It is important to have O negative blood or type-specific blood available immediately for neonatal transfusion
NURSINGMANAGEMENT  Assess bleeding, color, amount  Administer iv fluids.  Administer oxygen.  Strict vitals and FHS monitoring.  Prepare patient for caesarean section.  Reserve blood if (Hct >30%)
CORD PRESENTATION AND PROLAPSE
CORD PROLAPSE  There are three clinical types of abnormal descent of the umbilical cord by the side of the presenting part:  Cord presentation  Occult prolapse  Cord prolapse
 Cord presentation- When cord is slipped down below the presenting part and is felt lying in the intact bag of membranes.  Occult prolapse- the cord is placed by the side of the presenting part and is not felt by the fingers on internal examination.  Cord prolapse- the cord is lying inside the vagina or outside the vulva following rupture of the membranes **The incidence of cord prolapse is about 1 in 300 deliveries
Incidence 0.45% 0.66%(Risk ratio 2:3) 0.3% 0.9% 5% • Primigravida • Multigravida • Cephalic • Frank breech • Complete breech • Footling 10% • Shoulder • Contracted pelvis 15% 4-6times
ETIOLOGY Anything which interferes with perfect adaptation of the presenting part to the lower uterine segment, disturbing the ball valve action may favour cord prolapse.
PREDISPOSING FACTORS  MALPRESENTATION:-  Transverse lie  Breech  Compound presentation  HIGH HEAD:-  Membranes rupture but fetalhead ishigh.  PREMATURITY:-  LBW BABY <1500g.  POLYHYDRAMNIOS:-  Cord is swept down in thegush of liquor.
PREDISPOSING FACTORS CONT.. Twins or multiple pregnancy Long cord (90-100 cm) PROM CPD  Placental factor- minor degree placenta praevia  Iatrogenic- low rupture of the membranes, manual rotation of the head.  Contracted pelvis
DIAGNOSIS  OCCULT PROLAPSE  Difficult to diagnose.  Persistence of variable deceleration of fetal heart rate pattern.  CORD PRESENTATION  Feeling the pulsation of the cord through the intact membrane.
 CORD PROLAPSE  The cord is palpated directly by the fingers and its pulsation can be felt if the fetus is alive.  Cord pulsation may cease during uterine contraction, however returns after the contraction passes away.
Investigations • Cord pulsations • CTGshows variable decelerations • Cord lying outside vulva • USG – cord loops • Fundal pressure causes bradycardia • Meconium stained liquor
MANAGEMENT  Protocol is guided by:  Baby living or dead  Maturity of the baby  Degree of dilatation of the cervix
CORD PRESENTATION  Once the diagnosis is made, no attempt should be made to replace the cord.  If immediate vaginal delivery is not possible or contraindicated , caesarean section is the best method of delivery.  A rare occasion when multipara with longitudinal lie having good uterine contractions with cervix 7- 8cm dilated without fetal distress- watchful competency and delivery by forceps or breech extraction
MANAGEMENT OF CORD PROLAPSE DISCONTINUE THE VAGINAL EXAMINATION to reduce the risk of rupturing the membranes. MONITOR CONTINUOUSLY THE FHR AND FETAL WELL-BEING. LIFT PRESENTING PART OFF THE CORD INSTRUCT NOT TO PUSH POSITION PATIENT Knee chest OR Exaggerated position To minimise the cord compression.
Kneechest Position
Exaggerated Sim’s Position
CORD PROLAPSE BABYALIVE VAGINAL DELIVERY NOT POSSIBLE FIRSTAID DEFINITE- CAESAREAN SEC. CAESAREAN SECTION VAGINAL DELIVERY POSSIBLE VERTEX FORCEPS OR VENTOUSE BREECH BY EXPERT HAND BABY DEAD USG AND VAGINAL DELIVERY MANAGEMENT OFCORD PROLAPSE
CORD PROLAPSE  Living baby  Immediate take the mother for Caesarean section.  Immediate safe vaginal delivery if- head is engaged  Immediate safe vaginal delivery not possible- FirstAid  First aid  Bladder filling is done to raise the presenting part off the compressed cord.It is done by 400-750ml of NS with a foley’s catheter, the ballon is inflated and catheter is clamped.  Lift the presenting part off the cord.  Postural treatment- exaggerated and elevated sims position or trendelenburg or knee chest position.  Replace the cord into the vagina to minimize vasospasm due to irritation.
 Dead baby  Labour is allowed to proceed awaiting spontaneous delivery
AMNIOTIC FLUID EMBOLISM Definition  An amniotic fluid embolism is rare but serious condition that occur when amniotic fluid, fetal material, such as hair, enters the maternal bloodstream
INCIDENCE  Amniotic fluid embolism syndrome is rare. Most studies indicate that the incidence rate is between 1 and 12 cases per 100,000 deliveries
The body respond in 2 phases  The initial phase is one of pulmonary vasospasm causing hypoxia, hypotension, pulmonary edema and cardiovascular collapse.  The second phase sees the development of left ventricular failure, with hemorrhage and coagulation disorders and further uncontrollable hemorrhage
CAUSES A maternal age of 35 years or older Caesarean or instrumental vaginal delivery Polyhydramnios Cervical laceration or uterine rupture Placenta previa or abruption Amniocentesis Eclampsia Abdominal trauma Ruptured uterine or cervical veins Ruptured membranes
Patho Physiology
SIGNS AND SYMPTOMS  Sudden shortness of breath  Excess fluid in the lungs  Sudden low blood pressure  Sudden circulatory failure Life- threatening problems with blood clotting (disseminated intravascular coagulopathy)  Altered mental status  Nausea or vomiting  Chills  Rapid heart rate  Fetal distress  Seizures  Coma
DIAGNOSIS  Chest X-ray: May show an enlarged right atrium and ventricle and prominent proximal pulmonary artery and pulmonary edema.  Lung scan: May demonstrate some areas of reduced radioactivity in the lung field.  Central venous pressure (CVP) with an initial rise due to pulmonary hypertension and eventually a profound drop due to severe hemorrhage.  Coagulation profile: decreased platelet count, decreased fibrinogen and a fibrinogenemia, prolonged PT and PTT, and presence of fibrin degradation products.  Cardiac enzymes levels may be elevated;  Echocardiography may demonstrate acute left heart failure, acute right heart failure or severe pulmonary hypertension
MANAGEMENT  Maintain systolic blood pressure > 90 mm Hg.  Urine output > 25 ml/hr  Re-establishing uterine tone  Correct coagulation abnormalities Administer oxygen to maintain normal saturation.  Intubate if necessary.  Initiate cardiopulmonary resuscitation (CPR) if the patient arrests. If she does not respond to resuscitation, perform a cesarean delivery.
 Treat hypotension with crystalloid and blood products.  Consider pulmonary artery catheterization in patients who are haemodynamically unstable. Continuously monitor the fetus.  trauma to the uterus must be avoided during maneuvers such as insertion of a pressure catheter or rupture of membranes.  Incision of the placenta during caesarean delivery should also be avoided
NURSINGMANAGEMENT  Give immediate and vigorous treatment.  Give oxygen by face mask.  Maintain normal blood volume through administration of plasma and intravenous fluids.  Prevent development of disseminated intravascular coagulation (DIC). Serious complications can occur. (Disseminated intravascular coagulation (DIC) is a condition in which blood clots form throughout the body, blocking small blood vessels. Symptoms may include chest pain, shortness of breath, leg pain, problems speaking, or problems moving parts of the body.)  Administer whole blood and fibrinogen.  Monitor the patient’s vital signs.  Deliver the fetus as soon as possible
SHOULDER DYSTOCIA It occurs when anterior shoulder become trapped behind the symphysis pubis, while the posterior shoulder may bein the hollow of the sacrum or high above thesacral promontory. INCIDENCE:- THE INCIDENCE VARY BETWEEN 0.37%- 1.1%
RISK FACTORS OF SHOULDER DYSTOCIA FETALMACROSOMIA. OBESITY MOTHER. MATERNAL DIABETES. POSTMATURITY OF FETUS. MULTIPARITY. ANENCEPHALY. FETALASCITES.
MANAGEMENT (HELPERR) Help – obstetrician, pediatrician Episiotomy Legs – elevate Pressure - suprapubic Enter vagina – (internal rotation). Roll the woman over and try again. Remove posterior arm
McRoberts Maneuver • Hyperflexion of maternal hips Increases intrauterine pressure (1,653mmhg- 3,262mmhg) • Increases amplitude of contractions (103mmhg to 129mmhg)
Suprapubic Pressure • direct posterior or oblique suprapubic pressure
Rubin’s Maneuver • Adduction of the most accessible shoulder • Moves the fetus into an oblique position and decreases the bisacromial diameter
Woods’ Cork Screw Maneuver • Abduct posterior shoulder exerting pressure on anterior surface of posterior shoulder
Deliver posterior arm (Barnum Maneuver) • Grasp the posterior arm and sweep it across the anterior Chest to deliver
COMPLICATIONS OF SHOULDER DYSTOCIA FETALCOMPLICATION:- ASPHYXIA. BRACHIAL PLEXUS INJURY(ERB`S PALSY). HUMERUS FACTURE, CLAVICULAR FRACTURE. STERNO-MASTOID HAEMATOMA. HIGH PERINATAL MORBIDITY AND MORTALITY. MATERNAL COMPLICATION:- PPH. CERVICAL, VAGINAL AND PERINEAL TEAR. HIGH MATERNAL MORBIDITY RATE.
OBSTETRIC SHOCK  Shock is a critical condition and a life threatening medical emergency.  Shock results from acute, generalized, inadequate perfusion of tissues, below that needed to deliver the oxygen and nutrients for normal function
ETIOLOGY  Hypovolemia (Hemorrhage (occult /overt), hyperemesis, diarrhea, diabetic acidosis, peritonitis, burns.)  sepsis  Cardiogenic (cardiomyopathies, obstructive structural, obstructive non -structural, dysrhythmias).  Anaphylaxis  Distributive (Neurogenic- spinal injury, regional anesthesia
DIAGNOSIS  A high index of suspicion and physical signs of inadequate tissue perfusion and oxygenation are the basis for initiating prompt management.  Initial management does not rely on knowledge of the underlying cause.
INITIAL MANAGEMENT  MaintainABC  Airway should assured - oxygen 15 lt/min.  Breathing – ventilation should be checked and support if inadequate  Circulation- (with control of hemorrhage) – Two wide bore canulla – Restore circulatory volume  Reverse hypotention with crystalloid. – Crossmatch,  Arrange and give blood if necessary.  See for response such as , vital signs. Position of patient - Head down and left lateral tilt to avoid aortocaval compression which may further worsen the hypotension
HYPOVOLEMIC SHOCK  The normal pregnant woman can withstand blood loss of 500 ml and even up to 1000 ml during delivery without obvious danger due to physiological cardiovascular and haematological adaptations during pregnancy.  DEFINITION:- THE RESULT OF A REDUCTION IN INTRAVASCULAR VOLUME SUCHAS IN SEVERE OBSTETRIC HAEMORRHAGE.
ETIOLOGY  Antenatal – Ruptured ectopic pregancy , Incomplete abortion ,Placenta previa – Placental abruption , Uterine rupture  Post partum – Uterine atony ,Laceration to genital tract ,Chorioamnionitis – Coagulopathy , Retained placental tissue.
SIGN AND SYMPTOMS Severe symptoms, include:-  cold or clammy skin  pale skin  rapid, shallow breathing  rapid heart rate  little or no urine output  confusion  weakness  weak pulse  blue lips and fingernails  Lightheadedness  loss of consciousness Mild symptoms can include:  headache  fatigue  nausea  profuse sweating  dizziness
PRESENTING FEATURES OF HYPOVOLUMIC SHOCK ORGAN SYSTEM EARLY LATE BP NORMOTENSIVE OR HYPOTENSIVE. HYPOTENSION PULSE TACHYCARDIA. SAME. RESPIRATION NORMAL TACHYPNOEA. RENAL OLIGURIA ACUTE RENAL FAILURE SKIN COLD & CLAMMY COLD & CLAMMY. MENTAL STATUS NORMAL DISORIENTATION
MANAGEMENT  Basic shock management then treat specific cause.  Laparotomy for ectopic pregnancy  Suction evacuation for incomplete abortion  management of uterine atony  Repair of laceration  Management of uterine rupture – Stop oxytocin infusion if running  Continuous maternal and fetal monitoring
 Emergency laparotomy with rapid operative delivery  Cesarean hysterectomy may need to perform if hemorrhage is not controlled.  Management of uterine inversion. – Replacement of the uterus needs to be undertaken quickly as delay makes replacement more difficult.  Administer tocolytics to allow uterine relaxation. – Replacement under taken ( with placenta if still attached)-manually by slowly and steadily pushing upwards, with hydrostatic pressure or surgically.
CARDIOGENIC SHOCK  Cardiogenic shock in pregnancy is a life- threatening medical condition resulting from an inadequate circulation of blood.  Pregnancy puts progressive strain on the heart as progresses.  Preexisting cardiac disease places the parturient at particular risk.  Cardiac related death in pregnancy is the second most common cause of death in pregnancy
SIGN AND SYMPTOMS  Chest pain  Nausea and vomiting  Dyspnoea  Profuse sweating  Confusion/disorientation  Palpitations  Faintness/syncope  Pale, mottled, cold skin with slow capillary refill and poor peripheral pulses.  Hypotension (remember to check BP in both arms in case of aortic dissection).  Tachycardia/bradycardia.  Raised JVP/distension of neck veins.  Peripheral oedema.  Quiet heart sounds or presence of third and fourth heart sounds.  Heaves, thrills or murmurs may be present and may indicate the cause, such as valve dysfunction.  Bilateral basal pulmonary crackles or wheeze may occur.  Oliguria
MANAGEMENT  Re-establishment of circulation to the myocardium,  Minimising heart muscle damage and improving the heart’s effectiveness as a pump.  Administer Oxygen (O2) therapy to reduces the workload of the heart by reducing tissue demands for blood flow.  Administration of cardiac drugs such as Dopamine, dobutamine, epinephrine, norepinephrine,
SEPTIC SHOCK DEFINITION:- It occurs with a severe generalised infection. This is sepsis with hypotension despite adequate fluid resuscitation. To diagnose septic shock following two criteria must be met  Evidence of infection through a positive blood culture.  Refractory hypotension- hypotension despite of adequate fluid resuscitation.
ETIOLOGY  Post cesarean delivery  Prolonged rupture of membranes  Retained products of conception  rupture uterus  Intra-amniotic infusion  Water birth  Urinary tract infection  Toxic shock syndrome  Necrotizing Fasciitis
SIGN AND SYMPTOMS  Abdominal pain – Vomiting – diarrhea  Signs of sepsis – Tachycardia ,Pallor  Clamminess – Peripheral shutdown –  Systemic inflammation – Fever or hypothermia  Tachypnea  Cold peripheries  Hypotension  Confusion  Oliguria  Altered mental state
PRESENTING FEATURES OF SEPTIC SHOCK ORGEN SYSTEM EARLY LATE BP NORMOTENSIVE OR HYPOTENSIVE HYPOTENSIVE PULSE TACHYCARDIA TACHYCARDIA RESPIRATION TACHYPNO EA, PULMONAR Y EDEMA. TACHYPNOEA SKIN WARM COLD & CLAMMY. RENAL OLIGURIA ACUTE RENAL FAILURE. MENTAL STATUS NORMAL DISORIENTED
MANAGEMENTOF SEPTICSHOCK Replacement of fluid volume. Identify the sourse of infection. Infection screening should be carried out- vaginal swab, urine and blood cultures Aseptic technique should be maintain.
MANAGEMENT  Transfer to a higher level facility.  Invasive monitoring should be done  Obtain blood culture , wound swab culture and vaginal swab culture.  Start broad spectrum antibiotics.  Removal of infected tissues.
ANAPHYLYTIC SHOCK  A serious rapid onset of allergic reaction that is rapid onset and may cause death.  It is a relatively uncommon event in pregnancy but has serious implications for both mother and fetus.
ETIOLOGY cillin Pharmacological agent- pen group of drugs.  Insect stings  Foods  Latex
SIGN ANDSYMPTOMS  Cutaneous – Flushing, pruritus, urticaria , rhinitis, conjunctiva erythema, lacrimation. o Cardiovascular – Cardiovascular collapse, hypotension, vasodilation and erythema, pale clammy cool skin, diaphoresis, nausea and vomiting  Respiratory – Stridor, wheezing, dyspnea, cough, chest tightness, cyanosis.  Gastrointestinal – Nausea vomiting , abdominal pain , pelvic pain .  Central nervous system – Hypotension – collapse with or without unconsciousness, dizziness, incontinence. o Hypoxia– causes confusion
MANAGEMENT  Immediate –  Stop administration of suspected agent and call for help  Airway maintenance  Circulation – Give epinephrine IM and repeat every 5- 15min in titrated until improvement. In severe hypotension intravenous epinephrine should be given.  Rapid intravascular volume expansion with crystalloid solution.
Secondary  If hypotension persist alternative vasopressor agent should use. – Atropine if persistent bradycardia  If bronchospasm persist nebulize with salbutamol  Antihistaminic  Steroids  All patient with anaphylactic shock should referred to critical care
DISTRIBUTIVESHOCK  In distributive shock there is no loss in intravascular volume or cardiac function.  The primary defect is massive vasodilation leading to relative hypovolemia, reduced perfusion pressure, so poorer flow to the tissues.
ETIOLOGY  Spinal injuries- Neurogenic shock
SIGN ANDSYMPTOMS  Hypotension  Bradycardia  Hypothermia  Shallow breathing  Nausea vomiting  No response to stimuli  Unconscious  Blank expression of patient
MANAGEMENT  Resuscitation  Vasopressor agent and atropine may required in management because spinal injury leads bradycardia due to unopposed vagal stimulation.  Anesthesia -High spinal block  Basic ABC management –    Ventilation if needed Administer iv fluids Iv steroid such as methylprednisolone  Immobilize the patient to prevent further damage
UTERINE INVERSION  It occurs when the placenta fails to detach from the uterus as it exits, pulls on the inside surface, and turns the organ inside out.  Uterine inversion is a potentially fatal childbirth complication with a maternal survival rate of about 85%  The incidence is about 1 in 20,000 deliveries.
ETIOLOGY  The exact cause of uterus inversion is unclear.  The most likely cause is strong traction on the umbilical cord, particularly when the placenta is in a fundal location, during the third stage of labor
Causes: • uterine atony (40%) • Increase in intra abdominal pressure • Fundal attachment of placenta (75%) • Short cord • Placenta accreta • Excessive cord traction
DIAGNOSIS Prompt diagnosis is crucial and possibly lifesaving. Some of the signs of uterine inversion could include:  The uterus protrudes from the vagina.  The fundus doesn’t seem to be in its proper position when the doctor palpates (feels) the mother’s abdomen.  The mother experiences greater than normal blood loss.  The mother’s blood pressure drops (hypotension).  The mother shows signs of shock (blood loss).  Scans (such as ultrasound or MRI) may be used in some cases to confirm the diagnosis
Management • Uterine relaxant (terbutaline 0.25 mg IV followed by 2 g of MgSO4 over 10 min) • Treat hypovolaemeia • Without placenta: Repositioning
MANAGEMENT Before shock  Urgent manual replacement  After replacement, the hand should remain inside the uterus until the uterus become contracted by parentral oxytocics.  The placenta should be removed manually only after the uterus becomes contracted.  Usual treatment of shock including blood transfusion should be arranged.
Aftershock  Morphine 15mg IM , dextrose saline drip and arrangement of blood transfusion.  Push the uterus inside the vagina if possible and pack the vagina with roller gauze  Raised foot end of bed.  Replacement of uterus under general anaesthesia to be done.  Emergency hysterectomy (surgical removal of the uterus) in extreme cases where the risk of maternal death is high.
NURSING MANAGEMENT  Monitor for signs of hemorrhage and shock and treat shock  Prepare patient to reposition the uterus to the correct position via the vagina or laprotomy if unsuccessful.
RUPTUREUTERUS  The most serious complication in midwifery and obstetrics.  It is often fatal for the fetus and may also be responsible for the death of the mother.
DEFINITION  Disruption in the continuity of the all uterine layers( endometrium, myometrium and serosa) any time beyond 28 weeks of pregnancy is called rupture of uterus. INCIDENCE  The prevalence widely varies from 1 in 2000 to 1 in 200 deliveries.
TYPES OF TEAR (RUPTURE) COMPLETE INCOMPLETE
Completerupture:-  The peritoneum tears and the contents of the mother’s uterus can spill into her peritoneal cavity.  It is suggested that delivery via cesarean section (C- section) should occur within approximately 10 to 35 minutes after a complete uterine rupture occurs.  The fetal morbidity rate increases dramatically after this period
Incomplete:-  The mother’s peritoneum remains intact.  The peritoneum acts as a channel for blood vessels and nerves.  An incomplete uterine rupture is significantly less dangerous with fewer complications to the delivery process
Causes /Risk factors  Obstructed labour  Separation of previous C/S scar  Trauma due to operative manipulation  The unwise use of oxytocin  The extension of an old cervical tear.  Neglected labour  High parity
ETIOLOGY It is further divided into:  Spontaneous  Scar rupture  Iatrogenic
Spontaneous  During pregnancy-  Previous damage to the uterine walls following D& C procedure.  Manual removal of placenta  Thin uterine wall  Congenital malformation of uterus.  During labour-  Obstructive rupture due to obstructed labour  Non obstructive rupture due to weakening of walls due to repeated previous birth
 Scar rupture  Classical caesarean or hysterectomy scar.
Iatrogenic  During pregnancy-  Injudicious administration of oxytocin  Use of prostaglandin for induction of abortion or labour  Forcible external version  Fall or blow on the abdomen.  During labour  Internal podalic version.  Destructive operation.  Manual removal of placenta.  Application of forceps or breech extraction through incomplete dilated cervix.  Injudicious administration of oxytocin for augmentation of labour
SIGN ANDSYMPTOMS  Abdominal pain and tenderness  Shock  Vaginal bleeding  Undetectable fetal heart beat  Palpable fetal body parts  Cessation of contractions  Signs of intra-peritoneal bleeding  The most common sign is the sudden appearance of fetal distress during labor.  Complete laceration of uterine wall.
 Sharp pain between contractions - Contractions that slow down or become less intense  Recession of the fetal head (baby’s head moving back up into the birth canal)  Bulging under the pubic bone (baby’s head has protruded outside of the uterine scar) Sharp onset of pain at the site of the previous scar.  Uterine atony (loss of uterine muscle tone)  Maternal tachycardia (rapid heart rate) and hypotension
DIAGNOSIS  Ultrasonography is probably the safest and most useful imaging technique during pregnancy. sonographic findings associated with includes: • Extra peritoneal hematoma • intrauterine bleed • free peritoneal blood • empty uterus • gestational sac above the uterus • large uterus mass with gas  Painful bleeding.  Loss of FHS
MANAGEMENT  Principles for the treatment of uterine rupture includes:  Intensive resuscitation  Emergency laparotomy  Broad spectrum antibiotics  Adequate post operative care
 Intensive resuscitation  Correct hypovolaemia from- # Haemorrhage #Sepsis #Dehydration  Intravenous broad spectrum antibiotics #Cephalosporin + Metronidazole combination  Monitor to ensure adequate fluid and blood replacement  Blood volume expansion may worsen the bleeding from damaged vessel and so the laparotomy should not be delay, once patient condition has improved.
 Surgical options  Hysterectomy -Treatment of choice except any other compelling reasons to preserve the uterus # Total # Sub-total  Rupture repair # Occasionally one may be forced to repair # Repair with sterilization
NURSING MANAGEMENT  Monitor for the possibility of uterine rupture.  In the presence of predisposing factors, monitor maternal labor pattern closely for hyper tonicity or signs of weakening uterine muscle.  Recognize signs of impending rupture, immediately notify the physician, and call for assistance.  Assist with rapid intervention.If the client has signs of possible uterine rupture, vaginal delivery is generally not attempted. Monitor maternal blood pressure, pulse, and respirations; also monitor fetal heart tones.
 If the client has a central venous pressure catheter in place, monitor pressure to evaluate blood loss and effects of fluid and blood replacement.  Insert a urinary catheter for precise determinations of fluid balance.  Obtain blood to assess possible acidosis.  Administer oxygen, and maintain a patent airway.  Restore circulating volume using one or more IV lines.  Evaluate the cause, response to therapy, and fetal condition
Preventionofruptureuterus  Constant and careful antenatal care  Refer to hospital - mother who has obstructed labour  Detect high risk mothers and select them for hospital delivery  Previous section must always delivery in Hospital  Care during manipulation  Careful observation of the mother in labour to exclude obstructed labour  Avoid giving pitocin for previous classical c/s scar
 Conclusions: It was concluded that obstetric emergencies are more common in unbooked cases and women with low socioeconomic status with pooraccess to antenatal care.
BIBLIOGRAPHY • D.c Dutta Textbook of Obstetrics7th edition, New central book agency private limited London. • Anamma Jacob Midwifery and Gynaecological nursing 4th edition, Jaypee brothers and medical publishers, New Delhi. • Ajit virkud, Modern Obstetrics, APC Publishers Mumbai, 3rd edition 2017.
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Obstetrical emergencies

  • 1.
    OBSTETRICAL EMERGENCIES Mrs. U SREEVIDYAMsc. NURSING, Associate Professor, Apollo college of nursing, CHITTOOR
  • 2.
    DEFINITION  Obstetrical emergenciesare life threatening medical conditions that occur in pregnancy or during labor or after delivery.
  • 3.
    OBSTETRICAL EMERGENCY MEANSIMMEDIATE MANAGEMENT IS REQUIRED INCLUDING EARLY DETECTION AND PROMPT ACTION FOR BETTER OUTCOME OF PREGNANCY.
  • 4.
    • 1. VASAPRAEVIA. • 2. PRENSENTATION AND PROLAPSE OF THE UMBILICAL CORD. • 3. SHOULDER DYSTOCIA. • 4. RUPTURE OF THE UTERUS. • 5.AMNIOTIC FLUID EMBOLISM. • 6.ACUTE INVERSION OF THE UTERUS. • 7.SHOCK IN OBSTETRICS. • 8. DIC THE IMPORTANT EMERGENCY CONDITIONS IN OBSTETRICS
  • 5.
  • 6.
    VASA PRAEVIA THE UNSUPPORTED UMBILICALVESSELS, LIE BELOW THE PRESENTING PART AND RUN ACROSS THE CERVICAL OS.
  • 7.
    VASA PREVIA INCIDENCE The actualincidence is extremely difficult to estimate, it appears that vasa previa complicates approximately 1 in 2,500 births.
  • 8.
     It isan abnormality of the cord that occurs when one or more blood vessels from the umbilical cord or placenta cross the cervix but it is not covered by Wharton’s jelly.  This condition can cause hypoxia to the baby due to pressure on the blood vessels.  It is a life threatening condition.
  • 11.
    ETIOLOGY These vessels maybe from either  Velamentous insertion of umbilical cord  placental lobe joined to the main disk of the placenta.  Low-lying placenta  Previous delivery by C-section.
  • 12.
    SYMPTOMS  The baby’sblood is a darker red color due to lower oxygen levels of a fetus • Fetal distress can be seen.  Sudden onset of painless vaginal bleeding, especially in their second and third trimesters  If very dark burgundy blood is seen when the water breaks, this may be an indication of vasa previa
  • 13.
    DIAGNOSIS Classical triad Painless vaginal bleeding Colour doppler- vessel crossing themembranes over the internal cervical os. Membrane rupture Fetal bradycardia
  • 14.
    MANAGEMENT Antepartum  The patientshould be monitored closely for preterm labor, bleeding or rupture of membranes.  Steroids should be administered at about 32 weeks.  Hospitalization at 32 weeks is reasonable .  Take patient for emergency cesarean section if membranes are ruptured.  Fetal growth ultrasounds should be performed at least every 4 weeks.  Cervical length evaluations may help in assessing the patient's risk for preterm delivery or rupture of the membranes
  • 15.
    Intrapartum  The patientshould not be allowed to labor. She should be delivered by elective cesarean at about 35 weeks.  Delaying delivery until after 36 weeks increases the risk of membrane rupture.  Care should be taken to avoid incising the fetal vessels at the time of cesarean delivery.  If vasa previa is recognized during labor in an undiagnosed patient, she should be delivered by emergency cesarean. The placenta should be examined to confirm the diagnosis.
  • 16.
    Postpartum  Routine postpartummanagement as for cesarean delivery.  If the fetus is born after blood loss, transfusion of blood without delay may be life-saving.  It is important to have O negative blood or type-specific blood available immediately for neonatal transfusion
  • 17.
    NURSINGMANAGEMENT  Assess bleeding,color, amount  Administer iv fluids.  Administer oxygen.  Strict vitals and FHS monitoring.  Prepare patient for caesarean section.  Reserve blood if (Hct >30%)
  • 18.
  • 19.
    CORD PROLAPSE  Thereare three clinical types of abnormal descent of the umbilical cord by the side of the presenting part:  Cord presentation  Occult prolapse  Cord prolapse
  • 20.
     Cord presentation-When cord is slipped down below the presenting part and is felt lying in the intact bag of membranes.  Occult prolapse- the cord is placed by the side of the presenting part and is not felt by the fingers on internal examination.  Cord prolapse- the cord is lying inside the vagina or outside the vulva following rupture of the membranes **The incidence of cord prolapse is about 1 in 300 deliveries
  • 22.
    Incidence 0.45% 0.66%(Risk ratio 2:3) 0.3% 0.9% 5% •Primigravida • Multigravida • Cephalic • Frank breech • Complete breech • Footling 10% • Shoulder • Contracted pelvis 15% 4-6times
  • 23.
    ETIOLOGY Anything which interferes withperfect adaptation of the presenting part to the lower uterine segment, disturbing the ball valve action may favour cord prolapse.
  • 24.
    PREDISPOSING FACTORS  MALPRESENTATION:- Transverse lie  Breech  Compound presentation  HIGH HEAD:-  Membranes rupture but fetalhead ishigh.  PREMATURITY:-  LBW BABY <1500g.  POLYHYDRAMNIOS:-  Cord is swept down in thegush of liquor.
  • 25.
    PREDISPOSING FACTORS CONT.. Twinsor multiple pregnancy Long cord (90-100 cm) PROM CPD  Placental factor- minor degree placenta praevia  Iatrogenic- low rupture of the membranes, manual rotation of the head.  Contracted pelvis
  • 26.
    DIAGNOSIS  OCCULT PROLAPSE Difficult to diagnose.  Persistence of variable deceleration of fetal heart rate pattern.  CORD PRESENTATION  Feeling the pulsation of the cord through the intact membrane.
  • 27.
     CORD PROLAPSE The cord is palpated directly by the fingers and its pulsation can be felt if the fetus is alive.  Cord pulsation may cease during uterine contraction, however returns after the contraction passes away.
  • 28.
    Investigations • Cord pulsations •CTGshows variable decelerations • Cord lying outside vulva • USG – cord loops • Fundal pressure causes bradycardia • Meconium stained liquor
  • 29.
    MANAGEMENT  Protocol isguided by:  Baby living or dead  Maturity of the baby  Degree of dilatation of the cervix
  • 30.
    CORD PRESENTATION  Oncethe diagnosis is made, no attempt should be made to replace the cord.  If immediate vaginal delivery is not possible or contraindicated , caesarean section is the best method of delivery.  A rare occasion when multipara with longitudinal lie having good uterine contractions with cervix 7- 8cm dilated without fetal distress- watchful competency and delivery by forceps or breech extraction
  • 31.
    MANAGEMENT OF CORDPROLAPSE DISCONTINUE THE VAGINAL EXAMINATION to reduce the risk of rupturing the membranes. MONITOR CONTINUOUSLY THE FHR AND FETAL WELL-BEING. LIFT PRESENTING PART OFF THE CORD INSTRUCT NOT TO PUSH POSITION PATIENT Knee chest OR Exaggerated position To minimise the cord compression.
  • 32.
  • 33.
  • 34.
    CORD PROLAPSE BABYALIVE VAGINAL DELIVERY NOTPOSSIBLE FIRSTAID DEFINITE- CAESAREAN SEC. CAESAREAN SECTION VAGINAL DELIVERY POSSIBLE VERTEX FORCEPS OR VENTOUSE BREECH BY EXPERT HAND BABY DEAD USG AND VAGINAL DELIVERY MANAGEMENT OFCORD PROLAPSE
  • 35.
    CORD PROLAPSE  Livingbaby  Immediate take the mother for Caesarean section.  Immediate safe vaginal delivery if- head is engaged  Immediate safe vaginal delivery not possible- FirstAid  First aid  Bladder filling is done to raise the presenting part off the compressed cord.It is done by 400-750ml of NS with a foley’s catheter, the ballon is inflated and catheter is clamped.  Lift the presenting part off the cord.  Postural treatment- exaggerated and elevated sims position or trendelenburg or knee chest position.  Replace the cord into the vagina to minimize vasospasm due to irritation.
  • 36.
     Dead baby Labour is allowed to proceed awaiting spontaneous delivery
  • 38.
    AMNIOTIC FLUID EMBOLISM Definition  An amnioticfluid embolism is rare but serious condition that occur when amniotic fluid, fetal material, such as hair, enters the maternal bloodstream
  • 40.
    INCIDENCE  Amniotic fluidembolism syndrome is rare. Most studies indicate that the incidence rate is between 1 and 12 cases per 100,000 deliveries
  • 41.
    The body respondin 2 phases  The initial phase is one of pulmonary vasospasm causing hypoxia, hypotension, pulmonary edema and cardiovascular collapse.  The second phase sees the development of left ventricular failure, with hemorrhage and coagulation disorders and further uncontrollable hemorrhage
  • 43.
    CAUSES A maternal ageof 35 years or older Caesarean or instrumental vaginal delivery Polyhydramnios Cervical laceration or uterine rupture Placenta previa or abruption Amniocentesis Eclampsia Abdominal trauma Ruptured uterine or cervical veins Ruptured membranes
  • 44.
  • 46.
    SIGNS AND SYMPTOMS Sudden shortness of breath  Excess fluid in the lungs  Sudden low blood pressure  Sudden circulatory failure Life- threatening problems with blood clotting (disseminated intravascular coagulopathy)  Altered mental status  Nausea or vomiting  Chills  Rapid heart rate  Fetal distress  Seizures  Coma
  • 47.
    DIAGNOSIS  Chest X-ray:May show an enlarged right atrium and ventricle and prominent proximal pulmonary artery and pulmonary edema.  Lung scan: May demonstrate some areas of reduced radioactivity in the lung field.  Central venous pressure (CVP) with an initial rise due to pulmonary hypertension and eventually a profound drop due to severe hemorrhage.  Coagulation profile: decreased platelet count, decreased fibrinogen and a fibrinogenemia, prolonged PT and PTT, and presence of fibrin degradation products.  Cardiac enzymes levels may be elevated;  Echocardiography may demonstrate acute left heart failure, acute right heart failure or severe pulmonary hypertension
  • 48.
    MANAGEMENT  Maintain systolicblood pressure > 90 mm Hg.  Urine output > 25 ml/hr  Re-establishing uterine tone  Correct coagulation abnormalities Administer oxygen to maintain normal saturation.  Intubate if necessary.  Initiate cardiopulmonary resuscitation (CPR) if the patient arrests. If she does not respond to resuscitation, perform a cesarean delivery.
  • 49.
     Treat hypotensionwith crystalloid and blood products.  Consider pulmonary artery catheterization in patients who are haemodynamically unstable. Continuously monitor the fetus.  trauma to the uterus must be avoided during maneuvers such as insertion of a pressure catheter or rupture of membranes.  Incision of the placenta during caesarean delivery should also be avoided
  • 50.
    NURSINGMANAGEMENT  Give immediateand vigorous treatment.  Give oxygen by face mask.  Maintain normal blood volume through administration of plasma and intravenous fluids.  Prevent development of disseminated intravascular coagulation (DIC). Serious complications can occur. (Disseminated intravascular coagulation (DIC) is a condition in which blood clots form throughout the body, blocking small blood vessels. Symptoms may include chest pain, shortness of breath, leg pain, problems speaking, or problems moving parts of the body.)  Administer whole blood and fibrinogen.  Monitor the patient’s vital signs.  Deliver the fetus as soon as possible
  • 52.
    SHOULDER DYSTOCIA It occurswhen anterior shoulder become trapped behind the symphysis pubis, while the posterior shoulder may bein the hollow of the sacrum or high above thesacral promontory. INCIDENCE:- THE INCIDENCE VARY BETWEEN 0.37%- 1.1%
  • 53.
    RISK FACTORS OFSHOULDER DYSTOCIA FETALMACROSOMIA. OBESITY MOTHER. MATERNAL DIABETES. POSTMATURITY OF FETUS. MULTIPARITY. ANENCEPHALY. FETALASCITES.
  • 55.
    MANAGEMENT (HELPERR) Help –obstetrician, pediatrician Episiotomy Legs – elevate Pressure - suprapubic Enter vagina – (internal rotation). Roll the woman over and try again. Remove posterior arm
  • 56.
    McRoberts Maneuver • Hyperflexionof maternal hips Increases intrauterine pressure (1,653mmhg- 3,262mmhg) • Increases amplitude of contractions (103mmhg to 129mmhg)
  • 57.
    Suprapubic Pressure • directposterior or oblique suprapubic pressure
  • 58.
    Rubin’s Maneuver • Adductionof the most accessible shoulder • Moves the fetus into an oblique position and decreases the bisacromial diameter
  • 59.
    Woods’ Cork ScrewManeuver • Abduct posterior shoulder exerting pressure on anterior surface of posterior shoulder
  • 60.
    Deliver posterior arm (BarnumManeuver) • Grasp the posterior arm and sweep it across the anterior Chest to deliver
  • 61.
    COMPLICATIONS OF SHOULDERDYSTOCIA FETALCOMPLICATION:- ASPHYXIA. BRACHIAL PLEXUS INJURY(ERB`S PALSY). HUMERUS FACTURE, CLAVICULAR FRACTURE. STERNO-MASTOID HAEMATOMA. HIGH PERINATAL MORBIDITY AND MORTALITY. MATERNAL COMPLICATION:- PPH. CERVICAL, VAGINAL AND PERINEAL TEAR. HIGH MATERNAL MORBIDITY RATE.
  • 63.
    OBSTETRIC SHOCK  Shockis a critical condition and a life threatening medical emergency.  Shock results from acute, generalized, inadequate perfusion of tissues, below that needed to deliver the oxygen and nutrients for normal function
  • 64.
    ETIOLOGY  Hypovolemia (Hemorrhage(occult /overt), hyperemesis, diarrhea, diabetic acidosis, peritonitis, burns.)  sepsis  Cardiogenic (cardiomyopathies, obstructive structural, obstructive non -structural, dysrhythmias).  Anaphylaxis  Distributive (Neurogenic- spinal injury, regional anesthesia
  • 67.
    DIAGNOSIS  A highindex of suspicion and physical signs of inadequate tissue perfusion and oxygenation are the basis for initiating prompt management.  Initial management does not rely on knowledge of the underlying cause.
  • 68.
    INITIAL MANAGEMENT  MaintainABC Airway should assured - oxygen 15 lt/min.  Breathing – ventilation should be checked and support if inadequate  Circulation- (with control of hemorrhage) – Two wide bore canulla – Restore circulatory volume  Reverse hypotention with crystalloid. – Crossmatch,  Arrange and give blood if necessary.  See for response such as , vital signs. Position of patient - Head down and left lateral tilt to avoid aortocaval compression which may further worsen the hypotension
  • 70.
    HYPOVOLEMIC SHOCK  Thenormal pregnant woman can withstand blood loss of 500 ml and even up to 1000 ml during delivery without obvious danger due to physiological cardiovascular and haematological adaptations during pregnancy.  DEFINITION:- THE RESULT OF A REDUCTION IN INTRAVASCULAR VOLUME SUCHAS IN SEVERE OBSTETRIC HAEMORRHAGE.
  • 71.
    ETIOLOGY  Antenatal –Ruptured ectopic pregancy , Incomplete abortion ,Placenta previa – Placental abruption , Uterine rupture  Post partum – Uterine atony ,Laceration to genital tract ,Chorioamnionitis – Coagulopathy , Retained placental tissue.
  • 72.
    SIGN AND SYMPTOMS Severesymptoms, include:-  cold or clammy skin  pale skin  rapid, shallow breathing  rapid heart rate  little or no urine output  confusion  weakness  weak pulse  blue lips and fingernails  Lightheadedness  loss of consciousness Mild symptoms can include:  headache  fatigue  nausea  profuse sweating  dizziness
  • 73.
    PRESENTING FEATURES OF HYPOVOLUMICSHOCK ORGAN SYSTEM EARLY LATE BP NORMOTENSIVE OR HYPOTENSIVE. HYPOTENSION PULSE TACHYCARDIA. SAME. RESPIRATION NORMAL TACHYPNOEA. RENAL OLIGURIA ACUTE RENAL FAILURE SKIN COLD & CLAMMY COLD & CLAMMY. MENTAL STATUS NORMAL DISORIENTATION
  • 74.
    MANAGEMENT  Basic shockmanagement then treat specific cause.  Laparotomy for ectopic pregnancy  Suction evacuation for incomplete abortion  management of uterine atony  Repair of laceration  Management of uterine rupture – Stop oxytocin infusion if running  Continuous maternal and fetal monitoring
  • 75.
     Emergency laparotomywith rapid operative delivery  Cesarean hysterectomy may need to perform if hemorrhage is not controlled.  Management of uterine inversion. – Replacement of the uterus needs to be undertaken quickly as delay makes replacement more difficult.  Administer tocolytics to allow uterine relaxation. – Replacement under taken ( with placenta if still attached)-manually by slowly and steadily pushing upwards, with hydrostatic pressure or surgically.
  • 76.
    CARDIOGENIC SHOCK  Cardiogenicshock in pregnancy is a life- threatening medical condition resulting from an inadequate circulation of blood.  Pregnancy puts progressive strain on the heart as progresses.  Preexisting cardiac disease places the parturient at particular risk.  Cardiac related death in pregnancy is the second most common cause of death in pregnancy
  • 77.
    SIGN AND SYMPTOMS Chest pain  Nausea and vomiting  Dyspnoea  Profuse sweating  Confusion/disorientation  Palpitations  Faintness/syncope  Pale, mottled, cold skin with slow capillary refill and poor peripheral pulses.  Hypotension (remember to check BP in both arms in case of aortic dissection).  Tachycardia/bradycardia.  Raised JVP/distension of neck veins.  Peripheral oedema.  Quiet heart sounds or presence of third and fourth heart sounds.  Heaves, thrills or murmurs may be present and may indicate the cause, such as valve dysfunction.  Bilateral basal pulmonary crackles or wheeze may occur.  Oliguria
  • 78.
    MANAGEMENT  Re-establishment ofcirculation to the myocardium,  Minimising heart muscle damage and improving the heart’s effectiveness as a pump.  Administer Oxygen (O2) therapy to reduces the workload of the heart by reducing tissue demands for blood flow.  Administration of cardiac drugs such as Dopamine, dobutamine, epinephrine, norepinephrine,
  • 79.
    SEPTIC SHOCK DEFINITION:- It occurswith a severe generalised infection. This is sepsis with hypotension despite adequate fluid resuscitation. To diagnose septic shock following two criteria must be met  Evidence of infection through a positive blood culture.  Refractory hypotension- hypotension despite of adequate fluid resuscitation.
  • 80.
    ETIOLOGY  Post cesareandelivery  Prolonged rupture of membranes  Retained products of conception  rupture uterus  Intra-amniotic infusion  Water birth  Urinary tract infection  Toxic shock syndrome  Necrotizing Fasciitis
  • 81.
    SIGN AND SYMPTOMS Abdominal pain – Vomiting – diarrhea  Signs of sepsis – Tachycardia ,Pallor  Clamminess – Peripheral shutdown –  Systemic inflammation – Fever or hypothermia  Tachypnea  Cold peripheries  Hypotension  Confusion  Oliguria  Altered mental state
  • 82.
    PRESENTING FEATURES OFSEPTIC SHOCK ORGEN SYSTEM EARLY LATE BP NORMOTENSIVE OR HYPOTENSIVE HYPOTENSIVE PULSE TACHYCARDIA TACHYCARDIA RESPIRATION TACHYPNO EA, PULMONAR Y EDEMA. TACHYPNOEA SKIN WARM COLD & CLAMMY. RENAL OLIGURIA ACUTE RENAL FAILURE. MENTAL STATUS NORMAL DISORIENTED
  • 83.
    MANAGEMENTOF SEPTICSHOCK Replacement offluid volume. Identify the sourse of infection. Infection screening should be carried out- vaginal swab, urine and blood cultures Aseptic technique should be maintain.
  • 84.
    MANAGEMENT  Transfer toa higher level facility.  Invasive monitoring should be done  Obtain blood culture , wound swab culture and vaginal swab culture.  Start broad spectrum antibiotics.  Removal of infected tissues.
  • 85.
    ANAPHYLYTIC SHOCK  Aserious rapid onset of allergic reaction that is rapid onset and may cause death.  It is a relatively uncommon event in pregnancy but has serious implications for both mother and fetus.
  • 86.
    ETIOLOGY cillin Pharmacological agent-pen group of drugs.  Insect stings  Foods  Latex
  • 87.
    SIGN ANDSYMPTOMS  Cutaneous– Flushing, pruritus, urticaria , rhinitis, conjunctiva erythema, lacrimation. o Cardiovascular – Cardiovascular collapse, hypotension, vasodilation and erythema, pale clammy cool skin, diaphoresis, nausea and vomiting  Respiratory – Stridor, wheezing, dyspnea, cough, chest tightness, cyanosis.  Gastrointestinal – Nausea vomiting , abdominal pain , pelvic pain .  Central nervous system – Hypotension – collapse with or without unconsciousness, dizziness, incontinence. o Hypoxia– causes confusion
  • 88.
    MANAGEMENT  Immediate – Stop administration of suspected agent and call for help  Airway maintenance  Circulation – Give epinephrine IM and repeat every 5- 15min in titrated until improvement. In severe hypotension intravenous epinephrine should be given.  Rapid intravascular volume expansion with crystalloid solution.
  • 89.
    Secondary  If hypotensionpersist alternative vasopressor agent should use. – Atropine if persistent bradycardia  If bronchospasm persist nebulize with salbutamol  Antihistaminic  Steroids  All patient with anaphylactic shock should referred to critical care
  • 90.
    DISTRIBUTIVESHOCK  In distributiveshock there is no loss in intravascular volume or cardiac function.  The primary defect is massive vasodilation leading to relative hypovolemia, reduced perfusion pressure, so poorer flow to the tissues.
  • 91.
  • 92.
    SIGN ANDSYMPTOMS  Hypotension Bradycardia  Hypothermia  Shallow breathing  Nausea vomiting  No response to stimuli  Unconscious  Blank expression of patient
  • 93.
    MANAGEMENT  Resuscitation  Vasopressoragent and atropine may required in management because spinal injury leads bradycardia due to unopposed vagal stimulation.  Anesthesia -High spinal block  Basic ABC management –    Ventilation if needed Administer iv fluids Iv steroid such as methylprednisolone  Immobilize the patient to prevent further damage
  • 95.
    UTERINE INVERSION  Itoccurs when the placenta fails to detach from the uterus as it exits, pulls on the inside surface, and turns the organ inside out.  Uterine inversion is a potentially fatal childbirth complication with a maternal survival rate of about 85%  The incidence is about 1 in 20,000 deliveries.
  • 97.
    ETIOLOGY  The exactcause of uterus inversion is unclear.  The most likely cause is strong traction on the umbilical cord, particularly when the placenta is in a fundal location, during the third stage of labor
  • 98.
    Causes: • uterine atony(40%) • Increase in intra abdominal pressure • Fundal attachment of placenta (75%) • Short cord • Placenta accreta • Excessive cord traction
  • 100.
    DIAGNOSIS Prompt diagnosis iscrucial and possibly lifesaving. Some of the signs of uterine inversion could include:  The uterus protrudes from the vagina.  The fundus doesn’t seem to be in its proper position when the doctor palpates (feels) the mother’s abdomen.  The mother experiences greater than normal blood loss.  The mother’s blood pressure drops (hypotension).  The mother shows signs of shock (blood loss).  Scans (such as ultrasound or MRI) may be used in some cases to confirm the diagnosis
  • 101.
    Management • Uterine relaxant(terbutaline 0.25 mg IV followed by 2 g of MgSO4 over 10 min) • Treat hypovolaemeia • Without placenta: Repositioning
  • 102.
    MANAGEMENT Before shock  Urgentmanual replacement  After replacement, the hand should remain inside the uterus until the uterus become contracted by parentral oxytocics.  The placenta should be removed manually only after the uterus becomes contracted.  Usual treatment of shock including blood transfusion should be arranged.
  • 104.
    Aftershock  Morphine 15mgIM , dextrose saline drip and arrangement of blood transfusion.  Push the uterus inside the vagina if possible and pack the vagina with roller gauze  Raised foot end of bed.  Replacement of uterus under general anaesthesia to be done.  Emergency hysterectomy (surgical removal of the uterus) in extreme cases where the risk of maternal death is high.
  • 105.
    NURSING MANAGEMENT  Monitorfor signs of hemorrhage and shock and treat shock  Prepare patient to reposition the uterus to the correct position via the vagina or laprotomy if unsuccessful.
  • 107.
    RUPTUREUTERUS  The mostserious complication in midwifery and obstetrics.  It is often fatal for the fetus and may also be responsible for the death of the mother.
  • 108.
    DEFINITION  Disruption inthe continuity of the all uterine layers( endometrium, myometrium and serosa) any time beyond 28 weeks of pregnancy is called rupture of uterus. INCIDENCE  The prevalence widely varies from 1 in 2000 to 1 in 200 deliveries.
  • 110.
    TYPES OF TEAR(RUPTURE) COMPLETE INCOMPLETE
  • 111.
    Completerupture:-  The peritoneumtears and the contents of the mother’s uterus can spill into her peritoneal cavity.  It is suggested that delivery via cesarean section (C- section) should occur within approximately 10 to 35 minutes after a complete uterine rupture occurs.  The fetal morbidity rate increases dramatically after this period
  • 112.
    Incomplete:-  The mother’speritoneum remains intact.  The peritoneum acts as a channel for blood vessels and nerves.  An incomplete uterine rupture is significantly less dangerous with fewer complications to the delivery process
  • 113.
    Causes /Risk factors  Obstructedlabour  Separation of previous C/S scar  Trauma due to operative manipulation  The unwise use of oxytocin  The extension of an old cervical tear.  Neglected labour  High parity
  • 114.
    ETIOLOGY It is furtherdivided into:  Spontaneous  Scar rupture  Iatrogenic
  • 115.
    Spontaneous  During pregnancy- Previous damage to the uterine walls following D& C procedure.  Manual removal of placenta  Thin uterine wall  Congenital malformation of uterus.  During labour-  Obstructive rupture due to obstructed labour  Non obstructive rupture due to weakening of walls due to repeated previous birth
  • 116.
     Scar rupture Classical caesarean or hysterectomy scar.
  • 117.
    Iatrogenic  During pregnancy- Injudicious administration of oxytocin  Use of prostaglandin for induction of abortion or labour  Forcible external version  Fall or blow on the abdomen.  During labour  Internal podalic version.  Destructive operation.  Manual removal of placenta.  Application of forceps or breech extraction through incomplete dilated cervix.  Injudicious administration of oxytocin for augmentation of labour
  • 118.
    SIGN ANDSYMPTOMS  Abdominalpain and tenderness  Shock  Vaginal bleeding  Undetectable fetal heart beat  Palpable fetal body parts  Cessation of contractions  Signs of intra-peritoneal bleeding  The most common sign is the sudden appearance of fetal distress during labor.  Complete laceration of uterine wall.
  • 119.
     Sharp painbetween contractions - Contractions that slow down or become less intense  Recession of the fetal head (baby’s head moving back up into the birth canal)  Bulging under the pubic bone (baby’s head has protruded outside of the uterine scar) Sharp onset of pain at the site of the previous scar.  Uterine atony (loss of uterine muscle tone)  Maternal tachycardia (rapid heart rate) and hypotension
  • 120.
    DIAGNOSIS  Ultrasonography isprobably the safest and most useful imaging technique during pregnancy. sonographic findings associated with includes: • Extra peritoneal hematoma • intrauterine bleed • free peritoneal blood • empty uterus • gestational sac above the uterus • large uterus mass with gas  Painful bleeding.  Loss of FHS
  • 121.
    MANAGEMENT  Principles forthe treatment of uterine rupture includes:  Intensive resuscitation  Emergency laparotomy  Broad spectrum antibiotics  Adequate post operative care
  • 122.
     Intensive resuscitation Correct hypovolaemia from- # Haemorrhage #Sepsis #Dehydration  Intravenous broad spectrum antibiotics #Cephalosporin + Metronidazole combination  Monitor to ensure adequate fluid and blood replacement  Blood volume expansion may worsen the bleeding from damaged vessel and so the laparotomy should not be delay, once patient condition has improved.
  • 123.
     Surgical options Hysterectomy -Treatment of choice except any other compelling reasons to preserve the uterus # Total # Sub-total  Rupture repair # Occasionally one may be forced to repair # Repair with sterilization
  • 124.
    NURSING MANAGEMENT  Monitorfor the possibility of uterine rupture.  In the presence of predisposing factors, monitor maternal labor pattern closely for hyper tonicity or signs of weakening uterine muscle.  Recognize signs of impending rupture, immediately notify the physician, and call for assistance.  Assist with rapid intervention.If the client has signs of possible uterine rupture, vaginal delivery is generally not attempted. Monitor maternal blood pressure, pulse, and respirations; also monitor fetal heart tones.
  • 125.
     If theclient has a central venous pressure catheter in place, monitor pressure to evaluate blood loss and effects of fluid and blood replacement.  Insert a urinary catheter for precise determinations of fluid balance.  Obtain blood to assess possible acidosis.  Administer oxygen, and maintain a patent airway.  Restore circulating volume using one or more IV lines.  Evaluate the cause, response to therapy, and fetal condition
  • 126.
    Preventionofruptureuterus  Constant andcareful antenatal care  Refer to hospital - mother who has obstructed labour  Detect high risk mothers and select them for hospital delivery  Previous section must always delivery in Hospital  Care during manipulation  Careful observation of the mother in labour to exclude obstructed labour  Avoid giving pitocin for previous classical c/s scar
  • 127.
     Conclusions: Itwas concluded that obstetric emergencies are more common in unbooked cases and women with low socioeconomic status with pooraccess to antenatal care.
  • 130.
    BIBLIOGRAPHY • D.c DuttaTextbook of Obstetrics7th edition, New central book agency private limited London. • Anamma Jacob Midwifery and Gynaecological nursing 4th edition, Jaypee brothers and medical publishers, New Delhi. • Ajit virkud, Modern Obstetrics, APC Publishers Mumbai, 3rd edition 2017.