MUHIMBILI UNIVERSITY OF HEALTH AND ALLIED SCIENCES

DEPARTMENT OF PAEDIATRICS AND CHILD HEALTH

CLINICAL NOTES OF PEDIATRIC ROTATION

AUTHOR: ELTON, MD Class of 2018.

Email: ellierolland@ gmail.com

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 INTRODUCTION
These are just summaries of different clinical case presentations in pediatrics department and some
important aspects of discussion about the particular diagnosis. They are clinical cases that one might
encounter in pediatrics department. I found this worthy during my ample time to leave behind something
that others can quickly refer especially when it is their first exposure to clinical rotation.

Contents in this document are for use among clinical students if it pleases them. It has been my pleasure
sharing moments with so many people during my stay at MUHAS and I would love to recognize their
untiring support and encouragement during my stay. I dedicate this to my beautiful classmates and
teachers.

Special thanks to my lovely friends Francis Kazoba, Humphrey Medarakini, Cornel Sizimwe, and Davis
Amani for their unconditional support when I needed them. A Special recognition to our lovely CR’s
Evelyne and Cassius for making pediatrics a smooth eight weeks of learning. Life is always beautiful, with
good people around, and I have always been grateful to Victoria for her wise advice and support in the
accomplishment of this piece of work.

How can I be so rude not to mention TAMSA and JKM for they have made me grow both academically
and spiritually.

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Table of Contents
INTRODUCTION ............................................................................................................................................. 2
HISTORY TAKING ........................................................................................................................................... 5
IMPORTANT NORMALS ............................................................................................................................... 12
NORMAL WEIGHT ................................................................................................................................... 12
NORMAL LENGTH.................................................................................................................................... 12
NORMAL HEAD CIRCUMFERENCE (OFC) ................................................................................................. 12
HEMATOLOGY ............................................................................................................................................. 13
SICKLE CELL ............................................................................................................................................. 13
ACUTE LYMPHOBLASTIC LEUKEMIA........................................................................................................ 19
ACUTE MYELOID LEUKEMIA .................................................................................................................... 21
BONE MARROW FAILURE........................................................................................................................ 21
CASE-SICKLE CELL .................................................................................................................................... 22
CASE-SICKLE CELL .................................................................................................................................... 29
INDICATIONS OF HYDROXY UREA IN SICKLE CELL DISEASE................................................................. 35
CASE-SICKLE CELL .................................................................................................................................... 35
ACUTE WATERY DIARRHEA AND SEVERE ACUTE MALNUTRITION ............................................................. 44
CASE PRESENTATION .............................................................................................................................. 44
ACUTE WATERY DIARRHOEA .................................................................................................................. 50
MANAGEMENT OF ELECTROLYTE IMBALANCES IN DIARRHEA ........................................................... 52
SEVERE ACUTE MALNUTRITION .............................................................................................................. 53
REFEEDING SYNDROME ...................................................................................................................... 53
NEPHROLOGY .............................................................................................................................................. 55
CASE- NEPHROTIC SYNDROME ............................................................................................................... 55
NEPHROTIC SYNDROME.......................................................................................................................... 62
NEPHRITIC SYNDROME ........................................................................................................................... 64
BEE STING AND NEPHROTIC SYNDROME................................................................................................ 65
HENOCH SCHONLEIN PURPURA .............................................................................................................. 65
IGA NEPHROPATHY ................................................................................................................................. 66
ACUTE GLOMERULONEPHRITIS .............................................................................................................. 67
UTI IN CHILDREN ......................................................................................................................................... 67

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NEUROLOGY ................................................................................................................................................ 69
CASE- CEREBRAL PALSY ........................................................................................................................... 69
CEREBRAL PALSY ..................................................................................................................................... 76
EPILEPSY .................................................................................................................................................. 78
FEBRILE CONVULSIONS ........................................................................................................................... 78
RESPIRATORY SYSTEM DISEASES ................................................................................................................ 79
CASE ACUTE BRONCHIOLITIS .................................................................................................................. 79
PNEUMONIA ........................................................................................................................................... 85
ASTHMA .................................................................................................................................................. 86
CASE-ASTHMA ......................................................................................................................................... 87
DISCUSSION......................................................................................................................................... 91
MENINGITIS................................................................................................................................................. 93
CASE- MENINGITIS .................................................................................................................................. 94
HIV MANIFESTATIONS IN SEVERE ACUTE MALNUTRITION ....................................................................... 103
CASE PRESENTATION ............................................................................................................................ 103
NEONATOLOGY ......................................................................................................................................... 114
CASE-NEONATAL JAUNDICE .................................................................................................................. 114
NEONATAL JAUNDICE ........................................................................................................................... 119
PREMATURITY ....................................................................................................................................... 121
LOW BIRTH WEIGHT.............................................................................................................................. 122
HYPOXIC ISCHEMIC ENCEPHALOPATHY ................................................................................................ 122
BREAST FEEDING ....................................................................................................................................... 125
KANGAROO MOTHER CARE .................................................................................................................. 126
CONGENITAL ANOMALIES......................................................................................................................... 127
DOWN SYNDROME ............................................................................................................................... 127
CASE DOWN SYNDROME .................................................................................................................. 130
DISCUSSION....................................................................................................................................... 137
OEIS MALFORMATION .......................................................................................................................... 140
SPINA BIFIDA ......................................................................................................................................... 146

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HISTORY TAKING
1. Particulars of a patient

• Name of the patient- introduce the patient by three names.

• Age of the patient- in years. For pediatric patients can be in months, weeks or years as well.

• Sex- do not ignore as some patients are trans gender or hermaphrodites. Some disease are
more prevalent in certain sex, example breast cancer is common in females.

• Residence – It’s important to know where the patient comes from because it can tell the
diagnosis also. Some diseases are common in certain areas, example Schistosomiasis is
common in lake zone.

• Religion- this is not so much important but if one asks its best to mention. It could help in
some diagnosis. Possibly not to think of pig tape worm among Muslims.

• Hospital registration number is also important and the ward the patient is residing for easy
allocation. If possible with the bed number. ( but this is not so important for you as a student
in your clinical exams presentation)

• Parity and gravidity-gravidity referring to the number of times this woman has been pregnant.
If it is her second pregnancy then you report gravid 2. Parity is the number of live births. If this
is her third pregnancy and had previous two live births you report as gravid 3 para 2. (G3P2). If
this is her third pregnancy and she had one live birth and one abortion you write (G3P1+1)
that means one live birth plus an abortion.

• Last normal menstrual period- is important to estimate the expected the date of delivery for
pregnant women. So you ask when was her last menstrual period. Example it was 3/1/2017.
To get the expected date of delivery (EDD) we use naegele’s rule by adding one year,
substracting three months and add seven days to the LNMP. So when we add one year there
we get 2018, substracting three months it becomes October and adding seven days to date it
becomes 10. So EDD is 10/oct/2018.

• Expected date of delivery.

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2. A short introduction of a patient/an opening statement- this includes mentioning the number of
days the patient has stayed in the ward, if referred where is he or she referred from and a referral
diagnosis if possible. ( In an exam setting you may not be able to see the file or see the referral letter
so its best you end up mentioning from where he or she is referred otherwise examiners will poke
your eyes). In the introduction remember mentioning if it’s a re-admission at that hospital or it’s the
first one. If it’s a re-admission remember to ask for the reason of previous admission and the
condition at discharge if possible get a look at the discharge summary at the file. Mention if there is
any chronic illness that is known of the patient. Example known patient with HIV on
regular/irregular medication for 3years now.

3. Main complains- this is what brought the patient to hospital. So ask the patient, what made you
seek health care today? It could be that the patient has pain for the past six months, but why didn’t
he come last month? So did it worsen to necessitate him or her to attend the hospital? Remember
to put complains in an order from the one which begun first to the recent one. If all complains
started at the same time then arrange them in the order of severity, beginning with the most severe
symptom.

4. History of presenting illness- this is the story of the current illness. How it started, when, anything
that gives a relief of the condition, anything that worsens the condition and whether there are
accompanying symptoms. This helps you arrive at the diagnosis. Take an example of a patient having
a swelling at the forehead. He tells you it has been there for the past two hours, grew up slowly,
painful, nothing worsens it but has been massaging it and it is fading away.

It was preceded by a fist from an angry loyal citizen that hit his forehead. There you definitely know the
diagnosis. The rule here is DONPARA

• D- DURATION

• O-ONSET

• N-NATURE OF THE CONDITION

• P-PERIODICITY

• A-AGGREVIATING FACTORS

• R-RELIEVING FACTORS

• A-ASSOCIATED SYMPTOMS

In the history of presenting illness we also ask for risk factors regarding the diagnosis you are thinking
about, complications of the disease you are suspecting, and ask for symptoms of the disease that may
mimic the disease you are suspecting to just be sure it’s not some other disease, and this is what we call
ruling out other conditions. Mention if there are any efforts the patient has done regarding his illness
along the course and if any interventions were done and lastly ask for the progress in the ward.

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5. Review of other systems- there could be coexistence of other conditions despite the illness the
patient has. If you have more than one pathologies, sometimes one is primary the others are
secondary. So you might be dealing with renal failure only to forget this patient may have
secondarily hyper parathyroidism.

6. Pre natal history, natal and post natal history follows incase it’s a pediatric case. Pre natal history
involves asking how many times the mother attended clinic while carrying this particular baby in her
womb, what was the gestation age at her first visit and ask for any drugs given during the visits and
if there was any illness like skin rash during pregnancy to just be sure she never suffered things like
rubella. Natal history involves asking for mode of delivery, time of labor, was it at term or not as
some conditions are common among pre term such as necrotizing enterocolitis, ask for the birth
weight too in the natal history and if the baby cried and sucked immediately. Postnatal events
involves the events afterwards, so ask if the baby ever got ill, jaundice or anything. These only
appear in pediatric cases and are written under separate headings, don’t include all at once as I did
in this paragraph.

7. Immunization history- this is important in pediatric cases. This can be obtained from the RCH card.
Conclude if at all they are appropriate for the child’s age. If the child missed the vaccine we conclude
it as “missed opportunity for vaccination”

8. Developmental milestones- report what the child can do and conclude if appropriate for his or her
age. Example for a 9months old baby not be able to sit unsupported is delayed milestones.

9. In obstetrics and gynecology we don’t include the parts no. 6, 7 and 8 instead follows past
gynecology and obstetrics history immediately after history of index pregnancy.

10. Past medical history- this follows review of other systems in an adult male case, otherwise it follows
after pre natal, natal, post natal, immunization and milestones history in pediatric case. For a female
adult case it follows after past gynecological history and obstetric history and if pregnant history of
index pregnancy. Past medical history includes any history of surgery, blood transfusion or any
chronic illness. Report any illness of relevance the patient suffered in the past. Example past history
of recurrent schistosomiasis could explain the bladder ca the patient has now. Any allergy to drugs
or foods should be mentioned.

11. Family and social history- here we are interested of the conditions that run in families, if there is any
social activity that is related to the patient’s illness. Example a long distance driver is at risk of HIV,
smokers have a risk of lung cancer. Alcohol is a risk to liver cirrhosis.

12. Dietary history- mention number of meals, what he eats and amount. And has it changed since he or
she became ill.

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13. Summary of the history- remember summary is the mini skirt of the history. It should be short
enough and contains important information. It should have important positives and important
negatives. If one had a history of bleeding, mentioning in the summary that so and so with history of
bleeding and symptoms of anemia not in failure, symptoms of anemia are important positives here.
One is interested to hear did this patient bleed so much? And saying not in failure is an important
negative, atleast one wants to hear has this patient gone to failure.

PHYSICAL EXAMINATION

1. GENERAL EXAMINATION- a head to toe. Report whatever you see. Example normal hair
distribution, conjunctiva pallor, conjunctiva hemorrhage, any oral lesions such as candidiasis,
ulceration, examine the hands for stigmatas of liver or heart diseases such as duptreyn
contracture, finger clubbing, mention if there is any palpable lymph nodes and finally lower
limb edema. Lymph nodes to palpate are pre and post auricular, sub mandibular, mental,
along the borders of sterno cleido mastoid, supra and infra clavicular, axillary and inguinal
nodes.

2. LOCAL EXAMINATION- in cases of local pathologies.

3. SYSTEMIC EXAMINATION. Begin with inspection, then palpation, percussion and finally
auscultate.

SYSTEMIC EXAMINATION

RESPIRATORY SYSTEM-on inspection report respiratory rate then look for the appearance of the chest
and movement. In appearance look for scars if present, shape of the chest which normally is elliptical
with antero-posterior diameter being shorter. Observe the chest movements. Are the movements
symmetrical? Then palpate for lymph nodes (though most of the times it is covered in general
examination and therefore not reported in respiratory examination), palpate for the trachea if its central
and chest expansion. Percussion is done while comparing the two sides of the chest, start with infra
clavicular then mammary and infra mammary, then percussion of the axial and finally three areas at the
back. Normal percussion is resonant. Ascultate same areas you did percussion and finish with
auscultation of the lung basis. Normal breath sounds are reported as vesicular. (more details refer
Hutchson text book)

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CARDIOVASCULAR SYSTEM- Patient should be at lying on bed inclined at 45 degrees.

We follow an inverted J and more palatable we mention it as hockey stick approach. Begin with the
radial pulse, say the rate rhythm, synchronicity, is it of good volume and whether its collapsing or not.

Then measure the blood pressure. See if there are distended neck veins, and you may need two rulers to
measure the jugular venous pressure- with one ruler at sternal angle and the other at the highest point
of jugular pulse and the rulers perpendicular to each other. Normal jugular venous pressure is 6-8 cm of
H20 from right atrium. Then inspect precordium if there is any hyper activity, locate the apex beat in
relation to mid clavicular line, palpate for heaves and thrills and finally auscultate four areas- apex,
lower left sternal border, upper left sternal edge and upper right sternal edge and these correspond to
mitral , tricuspid, pulmonary, and aortic valves. (details are in Hutchison)

PER ABDOMEN- inspect for any scars, therapeutic marks. Report if the abdomen is distended, does it
move with respiration. Palpate to see if there is any tenderness and report according to the nine
abdominal regions eg tender at hypogastric region. Palpate for the liver, spleen and kidneys( hutchson
demonstrates well). Percussion note normally is tympanic, if dull then there is fluid or something else.
Auscultate bowel sounds. Hutchson mentions just to the right of the umbilicus is best and stethoscope
should be kept for one minute. Auscultate for vascular bruits particularly renal bruits 2cm above and
2cm lateral to umbilicus. Then finish abdominal exam with digital rectal examination.

Remember to examine the gravid uterus- that is Leopold maneuver. Leopold maneuver includes fundal
palpation to know what occupies the fundus, lateral palpation to know the lie and finally pelvic grip to
know if the baby is engaged or not.

In gynecology cases remember the per vaginal digital examination and speculum.

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CENTRAL NERVOUS SYSTEM EXAMINATION

This is the most interesting per say. So begin the higher centres. Is the patient oriented to time, place
and person. Ask him whether he is aware if its day time or night to know his orientation to time as it is
difficult one to say the exact clock time like its 1245hrs. Ask him or her of where he or she is to know the
orientation to place and finally identify if can recognize people. While talking to him you must have
known the speech so report it if its slurred, normal or mute. Report memory both long and short term
memory.

You can ask him or her if he or she recalls her forexample when his or her first child was born to assess
long term memory, you can ask her your name if you introduced yourself before you begun taking
history to see if he or she remembers and that could assess short term memory. Then examine cranial
nerves

Cranial nerve examination

We know the cranial nerves and we report their functions only. Forexample

Cranial nerve 1- can smell

Cranial nerve 2- can read from a 6metre distance, has no color blindness (if at all you had ishihara plates
to test), pupils equally in size, reactive to light and measure 2-3mm, fundoscopy not done- obviously for
a medical student to not do fundoscope.

Cranial nerve 3,4 and 6- can move eyes in all directions

Cranial nerve 5- has intact facial sensations, good contraction of the temporalis and masseters.

Cranial nerve 7- it’s the facial nerve. Report if there is any facial symmetry, can blow out the cheeks?

Cranial nerve 8- can hear

Cranial nerve 9 and 10- uvula centrally located, positive gag reflex.

Cranial nerve 11- can shrug shoulders, turn neck against resistance.

Cranial nerve 12- can protrude tongue, no fasciculations, no muscle atrophy

MOTOR EXAMINATION

Mnemonic is BIG TPR.

B-Bulkiness of all groups of muscles in upper and lower limbs

I-see if there are any Involuntary movements

G-observe the GATE

T-mucle Tone

P-Power in all groups of muscle

R- Reflexes both superficial and deep tendon reflexes ie knee, ankle, elbow and wrist places you hit with
patella.

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COORDINATION

Assess coordination- finger to nose test, or heel to shin test.

SENSATION

Then test for sensation following the dermatomes.

GO THROUGH THIS LINK FOR MORE ON CNS EXAMINATIONS OR HUTCHSON-

https://googleweblight.com/i?u=https://meded.ucsd.edu/clinicalmed/neuro2.htm&hl=en-

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IMPORTANT NORMALS
NORMAL WEIGHT
The normal birth weight is above 2500grams, and the average birth weight of neonates is about 3 kg.
Birth weight below 2500mg is low birth weight. Birth weight below 1500grams is very low birth weight
and below 1000grams is extremely low birth weight.

Question: In the first few days of life an infant looses weight, you know why if one asks?

Answer: During the first few days after birth, the newborn loses extracellular fluid equivalent to about
10% of the body weight.

Question: how is the trend of gaining weight?

Answer: They gain weight at a rate of approximately 25-30 g per day for the first 3 months of life.
Thereafter, they gain about 400 g weight every month for the remaining part of the first year. An
infant usually doubles his birthweight by the age of 6 months. The birthweight triples at 1 yr and is four
times at 2 yr of age. Thus, the weight at 6 months, 1 yr and 2 yr is approximately 6, 9 and 12 kg,
respectively if he or she was born with 3kg. This will help you know if the child’s weight is appropriate
for age quickly before even using WHO charts. (in an exam setting or bedside, examiner might ask you
a 2years old child with weight of 12kg does it sound normal to you? If you know these principles you
chill and smile then answer with confidence).

The weight of a child at the age of 3 yr is approximately five times that of the birth weight. At 5 yr, the
expected weight can be calculated by multiplying the birth weight by 6, at 7 yr by 7 and at 10 yr by 10.

NORMAL LENGTH
The infant measures approximately 50 cm at birth, 60 cm at 3 months, 65 cm at 6 months, 70 cm at 9
months, 75 cm at 1 yr and 90 cm at 2 yr.

NORMAL HEAD CIRCUMFERENCE (OFC)

The head circumference increases approximately 2 cm per month for first 3 months, 1 cm per month
between 3-6 month and 0.5 cm per month for the rest of the first year of life. The head circumference
is approximately 40 cm at 3 month, 43 cm at 6 month 46-47 cm at 1 yr, 48 cm at 2 yr. By 12 yr it is 52
cm.

MILESTONES IMPORTANT TO REMEMBER- child by 3months can hold the neck, 6months can sit, by
1year can walk, 2yrs can run.

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HEMATOLOGY
SICKLE CELL
Simple explanation is that the red cells have sickle shape.

It’s a result of substitution of valine for glutamic acid at position 6 of beta globin gene. The beta globin
gene’s mutation is encoded into messenger RNA that later produces sickle hemoglobin.

PATHOPHYSIOLOGY

In sickle hemoglobin what happens is: deoxygenation of the heme moiety in a sickle hemoglobin leads
to hydrophobic interactions among adjacent sickle hemoglobin leading to formation of polymers we call
tactoids. These polymers alter the red cell shape to being sickle shaped and fragile. These sickle shaped
red cells are so fragile and don’t pass easily in vessels and get broken easily or sometimes can block
small vessels.

The other thing is that the polymerized hemoglobin molecules don’t accept oxygen. So oxygen free
molecules keep wondering about combine by themselves forming stable dimeric oxygen radicals which
later accept electron and become oxygen superoxide anions. These oxygen superoxide anions attack red
cell membrane and sickle hemoglobin too.

Once the superoxide anions attack the sickle hemoglobin they oxidize it to meta hemoglobin S. The
meta hemoglobin S aggregate to form Heinz bodies that also go to settle by the red cell membrane and
destroy the red cell membrane.

Sickle cells with deformed membranes aggregate and occlude vessels.

Macrophages always are there to eat stupid cells. So they come eat sickle cells and as they do they
produce cytokines which are the ones that bring fever in sicklers.

CLINICAL PRESENTATION

Most of the times what brings them to hospital is pain.

Sickle cell pain

It is unremitting discomfort that mostly occurs in extremities, chest or abdomen. The underlying
mechanism of pain is tissue ischemia after disruption of blood flow when a vessel is blocked.

What precipitates sickle cell pain?

Answer: infections, dehydration, acidosis, hypoxia, exposure to cold and swimming for prolonged
period.

So once a sickler comes to hospital and the complain is pain always remember the above precipitants or
things might have led him or her to that situation.

Management is usually fluids and anaelgesics.

Pain in the skeleton with or without fever must be differentiated from osteomyelitis. Osteomyelitis in
sicklers affects diaphysis of long bones while in non sicklers it’s the metaphysis.

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Children with osteomyelitis will have:

• fever and pain

• swelling of the affected area
• fewer or only one location of pain and tenderness on touch
• high white cell count and raised acute phase reactants.

If its chest pain worry of Acute chest syndrome and consider a chest x ray. If it’s abdominal pain its girdle
syndrome. Lets now see the sickle cell crisis below:

ACUTE CHEST SYNDROME

It is a life threatening pulmonary complication defined as new radiological features on chest x ray plus
any 2 of the following

• Fever
• Respiratory distress
• Hypoxia
• Cough
• Chest pain

The standard is all sickle patients with fever should do chest xray even if there are no respiratory
symptoms to identify evolving acute chest syndrome.

Radiological features- vary from involvement of a single lobe most common left lower lobe or multiple
lobes and most often both lower lobes and pleural effusion.

Etiology of acute chest syndrome

• Infection is a well known etiology yet only 30% will have positive sputum or broncho alveolar
culture and common organisms are streptococcus pneumonia, Chlamydia and mycoplasma.
• Fat emboli from infracted marrow has also been a suspect behind acute chest syndrome. They
usually have rapid onset respiratory distress, altered mental status and petechial rash may
occur.

Management of acute chest syndrome

• Give oxygen
• Antibiotics
• Blood transfusion
• Anti pain and give fluids
• Consider Bronchodilators and corticosteroids if is an asthmatic patient.

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Consider blood transfusion if there is one of the following

• Decreased oxygen saturation (<90%)

• Increased work of breathing
• Rapid change of respiratory effort with/without worsening radiography.
• Drop of Hb 2g/dl below the baseline
• Previous history of severe acute chest syndrome

SPLENIC SEQUESTRATION CRISIS

It’s the rapid enlargement of the spleen with left sided abdominal pain and decline in Hb atleast 2g/dl
below baseline. Signs of hypovolemia and profound anemia are common.

Reticulocytosis and low platelet count may be present. Parvovirus infection may be a risk factor.

Management is with isotonic fluids and/or blood transfusion. Blood transfusion should be carefully done
since the patient has no anemia but its just the red cells are sequestered in the spleen, so if you
transfuse a lot and later these red cells are released from spleen there is a risk of hyperviscosity.

Its recommended 5ml/kg of packed red blood cell. Recurrent attacks necessitate splenectomy.

APLASTIC CRISIS

It is characterized by an acute drop in hemoglobin level caused by transient arrest of erythropoiesis

(process of formation of blood cells), leading to abrupt reductions in red cell precursors in the bone
marrow and markedly reduced number of reticulocytes in peripheral blood.

Mostly it occurs following infection with human parvovirus B19 which invades proliferating erythroid
progenitors. It’s a result of chronic hemolysis with the bone failure to compensate due to arrest of
erythropoiesis. Treatment is supportive and transfusion

HYPERHEMOLYTIC CRISIS

As the name, the crisis in which there is excessive hemolysis. There is sudden excercebation of
hemolysis with worsening anemia despite ongoing reticulocyte production.

Accelerated hemolysis has been associated with acute vaso occlusive events including acute chest
syndrome and acute painful episodes. Infections and/or drug exposure maybe responsible in some
cases.

It is fatal if the cause of hemolysis is not found and transfusion is not done.

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COMPLICATIONS OF SICKLE CELL

Acute complications:

1. Infections
2. Severe anemia secondary to hyperhemolysis, aplastic crisis or splenic sequestration.
3. Vaso occlusive phenomena which are
• Priapism
• Stroke
• Dactylitis and bone infarction
• Acute chest syndrome

CHRONIC COMPLICATIONS

Pulmonary complications:

1. Pulmonary hypertension- intravascular hemolysis releases free hemoglobin that binds nitric
oxide. Depletion of nitric oxide which is a potent vasodilator leads to pulmonary hypertension.
The other reason is an enzyme arginase 1 which is normally in red cells is released following
hemolysis goes to destroy arginine which is necessary for synthesis of nitric oxide.
2. Acute chest syndrome
3. Pulmonary thrombosis pulmonary embolism since sickle cell is a hypercoagulable state.
4. Pulmonary fibrosis
5. Sleep disordered breathing

CNS complications

1. Stroke
2. Cerebral venous thrombosis
3. Seizures
4. Transient ischemic attack

Renal complications

1. Nephrotic syndrome
2. Papillary necrosis
3. Hyposthenuria
4. Gross hematuria

Hepatobilliary complications

1. Cholestasis
2. Hepatic sequestration
3. Transfusional iron overload

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Cardiac complications

1. Cardiomyopathy
2. Myocardial infarction
3. arrthymias

vascular complications

1. leg ulcers
2. proliferative retinopathy, vitreal hemorrhage

Growth and developmental delays

Skeletal complications

1. Avascular necrosis of the head of femur

2. Osteomyelitis
3. Dactylitis

Sudden change in vision in patient with SCD is an ocular emergency

MANAGEMENT

Routine health care

• Penicillin prophylaxis- pen V orally, bd, or Benzathine penicillin IM once per month

• Vaccination- pneumococcal, H.influenza -post splenectomy

• Analgesia and hydration for painful episodes, Folic Acid tabs daily.

• Education

FLUIDS IN SICKLE CELL

• Give orally if drinking well, give IV if poor oral intake.

• Give 1.5x normal maintenance (except if stroke and /or severe anaemia is suspected – give 2/3
maintenance) .

• Mantainance fluid calculation is 100ml/kg/24hrs for the first ten kg, and you add 50ml/kg/24hrs
for every rise in kg after ten kg and 20ml/kg/24hrs for every weight in kg after 20kg.

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 Examples:

1. Calculate mantainance fluid for a 5kg baby. Since 5kg is within the first 10kg then its
100ml/kg/24hrs so it will be 100x5=500mls in 24 hrs.
2. Calculate mantainance fluid for a 15kg baby. Now we have 10kg plus added 5kg after ten kg.
Formula is 100ml/kg for any weight within first ten, and every weight that adds up after ten
before 20 is we add 50ml/kg for every rise. So here mantainance fluid will be (100x10)
+(50x5)=1250mls in 24hrs.
3. If the baby’s weight is 22kg. 100mls times 10 for the first ten, add 50mls times the other ten
increase after ten then 20 times the weight after 20 which is 2…so its
(100x10)+(10x50)+(2x20)=1540mls in 24hrs.

BEFORE SPEAKING OF LEUKEMIAS UNDERSTAND THE DIAGRAM BELOW

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ACUTE LYMPHOBLASTIC LEUKEMIA
Common in children.

Abnormal proliferation of immature lymphocytes. The problem is on the line of lymphoid progenitor
cells proliferation as opposed to Acute myeloid leukemia where it is the myeloid progenitor cells

Bone marrow aspiration if has more than 25% of lymphoblasts then its ALL.

These abnormal cells become many and go to be deposited in different organs such as spleen, lymph
nodes, liver and which is why you have these organs enlarged including lymph nodes enlarge. The lymph
node at the mediastinum if they enlarge they compress superior vena cava that returns blood to the
heart as a result one gets superior vena cava syndrome. Blood from upper parts fail to return to the
heart you end with a swollen face and distended neck veins which is a presentation of superior vena
cava syndrome.

They become too many in bone marrow that they finish the space for production of other cells as a
result one will have other cell lines low. Low platelet one gets easy bruising, bleeding and petechiae.
These cells can produce cytokines which are a cause of intermittent fevers. These cells might invade the
testis and the testis enlarge.

Clinical presentation

• Hepatosplenomegally
• Lymphadenopathy
• Bone pain
• Pallor, petechiae and purpura
• Intermittent fevers
• Superior vena cava syndrome
• Testicular enlargement
• If they infiltrate the cranial nerves one ends up with cranial nerve palsy.

INVESTIGATIONS

1. Complete blood count- low number of platelets, red cells and neutrophils although total white
cell count can be raised because of a lot of abnormal immature lymphocytes in blood all
detected as white cells in our lab equipments.
2. Peripheral smear- blast cells will be seen and abnormal red blood cells appearing as tear drop
3. Serum biochemistry- raised uric acid and LDH because of increased breakdown of cells. These
abnormal cells die a lot.
4. Imaging studies as x ray which may show mediastinal adenopathy, abdominal ultrasound which
may show hepatosplenomegally or intra abdominal adenopathy or enlarged kidneys due
leukemic cells infiltrating the kidneys.

19 | P a g e
DIFFERENTIALS

Infections- CMV and EBV

Aplastic anemia

Idiopathic thrombocytopenic purpura

TREATMENT (good to know but not a frequently asked question)

There are simply three phases.

1. Induction phase- oral prednisolone +IV vincristine and daunorubicin +IM asparaginase
+intrathecal methotrexate
2. Consolidation phase- systemic chemotherapy +cranio radiotherapy plus intrathecal(drugs
injected into the csf) drugs
3. Mantainance phase- daily mecaptopurine, weekly oral methotroxate and monthly IV vincristine
plus oral prednisolone. And every 2-3months intrathecal methotroxate.

Treatment is for 2 to 3years.

Supportive treatment

To treat the conditions accompanying them

1. Tumor lysis syndrome- which is massive breakdown of the abnormal cells. Usually they have
uricaemia, hyperphosphatemia, hyperkalemia, hypocalcemia and lactic acidosis. Supportive
treatment includes alkalinization of urine and oral allopurinol for dealing with hyperuricaemia.
2. Thrombotic complications- too many cells in blood→viscous→easy clotting and forming
thrombi. Leukophoresis is indicated.
3. Infections- because of this they are covered on broad spectrum antibiotics and cotrimoxazole
prophylaxis.

Prognostic factors

1. Age. 1-9yrs with white cell count of less than 50000/ul have good prognosis than older children
with a white cell count than that.
2. White cell count
3. Poor biological features. Presence of chromosal translocations as t(9,22) is bad
4. Response to therapy where we have early and late responders
5. Absence of extramedullary involvement that is organ infiltration is good prognosis.
6. Female sex is a good prognosis.

20 | P a g e
ACUTE MYELOID LEUKEMIA
Simple just as ALL but here its abnormal proliferation of the cells in the myeloid lineage. Its not
immature lymphocytes as in ALL. It is less common as ALL

Risk factors

• Congenital/genetics
• Environmental exposure
• Ionizing radiation
• Cytotoxic chemotherapeutics

Clinically its almost same picture as ALL only that in AML CNS infiltration is earlier than in ALL. Clinically
significant coagulopathy may be present at the time of diagnosis

BONE MARROW FAILURE

Failure of bone marrow to produce adequate number of circulating blood cells.

It can be:

1. Constitutional aplastic anemia (fanconi anemia)

2. Acquired

Constitutional aplastic anemia

Fanconi anemia is a syndrome characterized by defective DNA repair characterized by a variety of

genetic mutations. Its autosomal recessive.

Hematological manifestation begin with either neutropenia or thrombocytopenia and progress to other
cytopenia.

Clinically

Symptoms depend on hematological abnormality.

Neutropenia- recurrent infections. they will come report having repeated infections usually.

Laboratory investigations

1. Full blood picture

2. Bone marrow
3. Peripheral smear

Treatment

Supportive. If anemia give blood. If low platelet give platelet.

For the case of infections treat them.

21 | P a g e
CASE-SICKLE CELL
NAME: XYXXY

Registration no. M19-XX-MM

AGE: 3yrs.
SEX: MALE
RESIDENCE: KIJICHI, DAR ES SALAAM
INFORMANT: BIOLOGICAL MOTHER
DATE OF ADMISSION: 5/12/2017
DATE OF CLERKSHIP: 5/12/2017 at 04:50pm.
INTRODUCTION
The patient is known to have sickle cell anemia diagnosed at 6months of age on regular Penicillin V
250mg and folic acid

This was a self referral from home.

MAIN COMPLAINTS

Fever for 2/52.

Joint painfor 6/7.

Cough for 3/7.

HISTORY OF PRESENTING ILLNESS

The patient was apparently well until 2 weeks ago when the child developed high grade fever of gradual
in onset with no specific periodicity slightly reduced by paracetamol however there was no any history
of excessive crying on urination, no history of convulsions, no history of headaches, vomiting or
diarrhea, also no history ear pain or discharge.

Six days ago the patient started to experience joint pain of sudden in onset involving knee joints of both
legs, throbbing in nature progressively increasing in severity currently he is unable to walk however it
was not associated with joint swelling. There is no history of trauma of the joints prior to illness.

Patient also had a history of cough for 3 days of gradual in onset, non productive in nature with no
specific periodicity, not associated with bluish discoloration, no chest pain, no history of easy fatigability,
also no lower limb swelling.

Also there was no history of significant weight loss, no night sweats also no history of tb contact.
However there was also no history of blood transfusion, no history of blood in urine, no history of
prolonged erection, no history of abnormal bleeding from the gums, no yellowish discoloration of the
body and no history of body weakness.

On the course of illness patient was treated in Dodoma general hospital, treated for malaria and given
antibiotics (ampicillin and gentamycin) but the fever did not subside.

22 | P a g e
This is his 3rd admission where by the first admission was at 6months of age where he was diagnosed
with sickle cell anemia and the 2nd admission was at Dodoma hospital with a history of abdominal pain
which was managed and resolved with medications.

PAST MEDICAL HISTORY

This is his first admission at MNH

He has no history of surgical procedures done

He is not known allergic to any food or drugs.

No history of other chronic childhood illness such as measles, DM or asthma.

PRE NATAL HISTORY

First booked the antenatal clinic at 20 weeks of gestation and made a number of 3 visits

Mother received anti malarias for prophylaxis, received hematenics, folic acid and also she was
dewormed.

Mother also received 3 doses of tetanus toxoid vaccine. She tested negative for HIV and syphilis.

There was no history of complications during pregnancy such as hypertension, diabetes mellitus or
infections such as UTI.

NATAL HISTORY

The mode of delivery was by spontaneous vaginal delivery, a healthy term baby of birth weight of 3.8kg
was born following a period of labour of 6 hours.

Spontaneous rapture of membrane was reported however the colour of liquor if meconium stained or
not is unknown.

Baby cried immediately after delivery and breast feeding was initiated within one hour after delivery.

Baby was vaccinated with BCG and OPVo within first day of life.

POST NATAL HISTORY

They were discharged after 24 hours.

Baby passed meconium by the second day of life and cord dropped by the seventh day of life.

There were no history of bluish or yellowish discoloration of the baby and also no history of fever was
reported.

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IMMUNIZATION HISTORY

RCH 1 card was not available but informant reported the child was immunized as per IVD

BCG and OPVo at birth whereas BCG scar was seen.

OPV1, OPV2 and OPV3, DPT, PCV, hepB and MR all was given as per response of the informant

Conclusion: The child was immunized appropriately according to age.

GROWTH AND DEVELOPMENTAL HISTORY

Attained neck control at 4 months, started sitting without support at 8 months, walking at 11months
and currently able to speak in full sentences.RCH1 card was not seen but she was reported to have a
good weight gain.

Conclusion: as per information obtained the child has normal growth and developmental milestones
according to age.

DIETARY HISTORY

He was exclusively breastfed for 5 months and then started on complimentary feeding whereby she was
given cow’s milk and developed persistent diarrhea hence it was stopped and re-introduced at age of
7months where he was given with unrefined maize porridge with millet, rice and vegetable oil.

Currently takes 5 meals a day whereby in the morning he takes porridge with the mentioned
ingredients, then at 10am takes tea with chapatti or buns, for lunch he takes ugali with beans and
vegetables then at 4pm he takes milk and for dinner he takes rice or ugali with beans and vegetables.
Occasionally he is given fruits such as mangoes, bananas or oranges.

Conclusion: Early weaning and inadequate breastfeeding. Currently the meal is adequate in quality and
quantity.

FAMILY AND SOCIAL HISTORY

He is the 3rd index born in the family of 3 children.

The first borne died intra uterine due to abraptio placenta. The 2nd borne is a 11 years old boy currently
studying in standard 5 and he is apparently fine.

Parents are married living together,mother is a 37 years old woman she is a business woman with a
diploma level of education.

Father is a 45years old man, he is a policeman with a form four level of education.

There is a positive family history of sickle cell on both maternal and paternal side whereas even the
mother is a known sickler.

24 | P a g e
ON EXAMINATION

General examination

No emergency signs. Patient was alert, no nasal flarring, febrile (39^c), not jaundiced, not cyanosed, no
palpable peripheral lymphadenopathy, no lower chest wall indrawing some palmer pallor, no finger
clubbing and no lower limb edema.

Anthropometric measurements

Weight-18kg

Height-100cm: weight/ height- between median and 1sd.Weight for age->1sd

MUAC-15.2cm: MUAC for age-median

OFC-50cm: OFC for age-between median and 1sd.

Conclusion: not wasted, with mild overweight.

LOCAL EXAMINATION

Normal appearance of the joints, no hyperemia on the skin, no obvious swelling, with the same
temperature as other parts of the body and mildly tenderness.

RESPIRATORY SYSTEM

RR=32breaths/min. Normal chest shape, moves bilaterally symmetrical with respiration. The chest
expansion was bilaterally symmetrical.

Trachea was centrally located, normal resonant note on percussion and normal vesicular breath sounds
with no added sounds

CARDIOVASCULAR SYSTEM

PR=104beats/min, regular, with good volume, non collapsing in character and synchronous with all
peripheral pulses.

No bulging of precordium, no hyperactivity, no heaves or thrills.

Normal s1, s2 sounds were heard with no added sounds. No basal crepitations.

PER ABDOMEN

Normal abdominal contour, moves with respiration.

No tenderness elicited on superficial palpation, no organomegally.

Normal bowel sounds were heard. And normal male uncircumcised genitalia was seen.

25 | P a g e
CENTRAL NERVOUS SYSTEM

Higher centers

She was alert, oriented place and person.

No signs of meningeal irritation.

Cranial nerves examination

Pupils are equally reactive to light,

Could move eyes in all quadrants, normal corneal reflex.

No facial asymmetry, could resist to opening her mouth, could hear normally.

Can swallow normally, uvula centrally located.

Can shrug shoulders and no fasculations of the tongue.

Motor system

Normal bulkiness of both upper and lower limbs

Normal tone and deep tendon reflexes of both upper and lower limbs

Power of 4/5 on both upper and lower limbs

SUMMARY

This is X.X.X a 3yrs old boy a known patient of sickle cell anemia on regular penicillin and folic acid who
came with complaints of fever for 2/52, joints pain6 /7 and a nonproductive cough for3/7.He has no
history of blood transfusions done and he has a positive family history of sickle cell in both maternal and
paternal side.

On examinations he was febrile, with some palmer pallor, and no signs of inflammation on local
examination.

PROVISIONAL DIAGNOSIS

1. Moderate anemia secondary to sickle cell anemia in vaso occlusive crisis

Ddx 1. Arthritis

2. Osteomyelitis

2. Septicemia with a differential of urinary tract infection (UTI) and malaria.

3. Pneumonia ddx- acute chest syndrome.

26 | P a g e
INVESTIGATIONS PLAN

1. complete blood count

WBC 16.1 k/ul Normal

NEUTROPHILS 7.22 k/ul increased

LYMPHOCYTES 7.68 k/ul increased

MONOCYTES 0.85 k/ul normal

EOSINOPHILS 0.18 k/ul normal

BASOPHILS 0.156 k/ul normal

Hb 6.85 g/dl decreased

MCV 63.4 fL decreased

MCH 19.7 pg decreased

Platelets 782 k/ul increased

Conclusion: neutrophilia sign of bacterial infection,lymphocytosis, microcytic hypochromic anemia and

thrombocytosis.

2. Urinalysis –leucocytes 1+

Protein, glucose, ketones, nitrites, WBC, RBC all were negative

3. Urine culture positive for gram negative rod( E.coli)

4. CRP- 118mg/l raised indicating acute inflammation probably due to bacterial infection.

5. Blood slide for malaria parasites – no parasites seen

6. Chest x ray- normal chest x ray with no infiltration or opacifications

7. Blood culture results were not reported.

FINAL DIAGNOSIS

Moderate anemia secondary to sickle cell anemia in vaso occlusive crisis

Septicemia

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MANAGEMENT

• Ibuprofen 100 mg 8 hourly for 3/7.

• Encourage fluid intake 3 liters orally over 24hours (1.5 *maintainace fluid).

• IV. Amoxiclav 450mg 8hourly 10/7.

• Tabs paracetamol 250mg PRN.

• Continue with penicillin 250mg BD and folic acid 5mg OD.

• Monitor vitals.

MONITORING

Patient was encouraged on hydration of about 3l of water in 24hours while monitoring his vitals and the
trend was as follows.

PARAMETER 5th Dec 6th Dec 7th Dec 8th Dec 9th Dec 10th Dec 11th Dec

TEMPERATURE 39 37.3 38.5 36.8 37.1 37.5 37

(^c)

PULSE RATE 104 102 120 144 110 112 112

(b/min)

RESPIRATORY 32 37 32 30 36 34 32
RATE (b/min)

Pain was subsiding as days progressed.

COUNSELLING

Mother were counselled on encouraging hydration to the patient also good adherence of the penicillin V
prophylaxis the patient was consuming and also adherence of life long folate so as to help reduce
frequency of crisis to the patient. Patient also should be attending regular clinic for a follow up.

PROGNOSIS

Studies show increased life expectancy, 53yrs for men and 58yrs for female and decreased mortality in
patients with sickle cell anemia in high resource countries which was attributed by early diagnosis
through newborn screening, prophylactic therapy for encapsulated bacteria, hydroxyurea therapy, bone
marrow transplant and comprehensive care education programs to caregivers.(9) With exception of
transplantation many of the interventions offer the same benefits to patients hence with appropriate
care sickle cell anemia has good prognosis.

28 | P a g e
CASE-SICKLE CELL
NAME: YYY

REG NUMBER: A00000

DATE OF BIRTH: 30/01/2011

AGE: 6 YEARS

SEX: MALE

RESIDENCE: SALASALA

DATE OF ADMISSION: 17/12/2017

DATE OF CLERKSIHP: 17/12/2017

WARD: B

INFORMANT: BIOLOGICAL MOTHER AND PATIENT.

The patient was diagnosed with Sickle cell Anaemia 2 years ago at MNH, he got a right side stroke one
year ago. Currently he is attending haematology clinic at MNH and he is on Folic acid and Hydroxyurea
medications on daily bases.

He was referred from Rabinninsia Hospital for further management.

CHIEF COMPLAINTS

1. Chest pains 1/7

2. Fever 1/7

HISTORY OF PRESENTING ILLNESS

Chest pains started a day ago, gradual on onset and generalized, associated with chest tightness and
laboured breathing. The pain was subsided by 1 paracetamol tablet. There were no joint pains
associated, no abdominal pain. The patient has no history of easy fatigability, no history of cough.

Fever started a day ago, gradual on onset, high grade with no specific periodicity. Fever was relieved by
exposing the patient and sponging him, together with Paracetamol tabs. No ear pains, swelling /
discharge, no history of abdominal pain, no history of pain during urination, no history of passing loose
stools, no history of headache or convulsions.

Last year he developed high grade fever that lead to his right side weakness in both limbs. He has history
of being transfused with blood twice (last year September, this year September) due to low blood level
counts.

29 | P a g e
PAST MEDICAL HISTORY

➢ He has no history other admissions.

➢ No known allergies to food.

➢ No known allergies to medications.

ANTENATAL HISTORY

➢ Booked at 4 months Gestation Age, made a total of 6 visits

➢ Received 2 doses of TT, was dewormed and got haematinics and SP for malaria prophylaxis. She
did not get Folic acid tabs.

➢ PMTCT-2, VDRL-non reactive.

NATAL HISTORY

➢ Labour lasted for 4 hours, Rupture of membranes was spontaneous.

➢ Delivered by SVD, term baby with birth weight of 3.5kg

➢ Baby cried and sucked immediately.

POST NATAL HISTORY

➢ Discharged after 24 hours rest in hospital

➢ Cord dropped at the 5th day.

➢ No history of bluish or yellowish discolorations reported.

SOCIAL AND DEVELOPMENTAL MILESTONES

➢ Sat alone at 5 months

➢ Began saying da, ka, ma at 6 months

➢ Walked independently at 12

.:. Essentially, he had normal developmental mile stones

IMMUNIZATION HISTORY

(RCH card number 1 was not seen)

Received all vaccines per schedule

BCG scar seen.

30 | P a g e
DIETARY HISTORY

He takes normal family food, 3 meals in a day mainly rice, stiff porridge, bananas, super get, green
vegetables and fruits.

.:. Diet is adequate in both quality and quantity.

FAMILY AND SOCIAL HISTORY

➢ Father: Amos Biseko, 41 years old, master’s degree holder (Agrometrics)

➢ Mother: Faudhia Matana 35 years old, Degree holder (Teacher)

➢ The index is the first born out of three children.

➢ 2nd born: 4 years male, in pre-unit essentially doing well.

➢ 3rd born: 7 months female, doing well.

➢ There is familiar history of sickle cell in maternal side, no history of consanguinity.

ON EXAMINATION

General Examination

Patient is alert, febrile (38˚C), jaundiced, with a boozing skull and malocclusion, he has severe palmar
pallor. No joint swelling, no finger clubbing, no lower limb oedema, no lymphadenopathy.

Ear, nose and throat examination

No ear discharge, pain or any lesion,no nasal discharge or any lesion.Tonsils not visualized. No throat
hyperaemia or any lesion.

Vitals: T = 38˚C RR = 28 breaths/minute PR = 120 beats/minute

Anthropometric measurements:

Weight = 17 kg BMI = 17 kg / 1.152m2

Length = 115 cm = 12.85 kg/m2(Below 5th percentile)

MUAC = 15.5 cm (He is underweight)

OFC = 54 cm

31 | P a g e
Systemic Examination

RS: RS = 28 breaths/minute

Normal chest contours, no chest deformity.

Trachea centrally located, generalized tenderness around the chest.

Resonant note on percussion.

Vesicular breath sounds heard.

Per Abdomen: Abdomen within normal contours, moving with respiration.

Multiple hypo-pigmented lesions measuring 5x5mm (previous chicken pox infection)

Non tender splenomegaly 6cm

Tender hepatomegaly 5 cm, with a smooth surface, liver span 8 cm.

Tympanic note heard except over the spleen and liver.

Bowel sounds heard.

CVS PR = 120 beats/minute, adequate volume, regular rhythm non-collapsing, and synchronous.

No raised Jugular venous pressure.

Visible pericardial hyper activity, no bulging, no thrill.

S1 & S2 heard with a gallop rhythm, no added sounds.

32 | P a g e
CNS Higher centres: Alert, oriented to time, place and people.

No signs of meningeal irritation.

Cranial nerves: Olfactory Not tested

Optic Intact

Occulomotor

Trochlear Intact

Abducent

Trigeminal Intact

Facial Intact

Vestibulocochlear Intact

Glossopharyngeal Intact

Vagus Intact

Accessory nerve- Weakness of the right side, can’t shrug shoulder against
resistance, can’t turn neck against resistance.

Hypoglossal. Intact

Motor:
LEFT LIMBS RIGHT LIMBS

upper lower upper lower

Bulkiness normal normal normal Normal

Power 5/5 5/5 3/5 3/5

Tone normal normal Hypotonic hypotonic

Sensory:
Normal response to both superficial and deep tendon reflexes on the left side.

Hyperreflexia on the right side with positive Babinski reflex.

Coordination: Not tested

Gait: Limping.

33 | P a g e
SUMMARY

YYY, 6 years male know with Sickle cell anaemia for two years, attending Haematology clinic at MNH, he
is on regular medications with Folic acid and Hydroxyl urea tablets. He has a history of sustaining stroke
one year ago, and has been transfused with blood several times, with a positive family history of sickle
cell anaemia.

Presented with main complaints of: - Chest pain 1/7

- Fever 1/7

He has palmar pallor, jaundice, boozing of the skull, and mild occluding teeth. He has weak CN XI, right
side hyperreflexia with reduced power and is hypotonic.

DIFFERENTIAL DIAGNOSIS

1. Sickle cell anaemia with:-

- Acute chest syndrome

- Right side hemiplegia 2˚ cerebral vascular accident.

2. Severe anaemia in failure 2˚ sickle cell anaemia

3. Malaria Ddx. Septicemia.

34 | P a g e
INDICATIONS OF HYDROXY UREA IN SICKLE CELL DISEASE
➢ Three or more moderate to severe vaso-occlusive pain episodes in a one year period. Most of
the studies conducted showed that hydroxyurea therapy was consistently associated with
overall increases in HbF (Charache S, et al 1995) and also showed that both children and adults
with SCA benefited from reductions in the frequency of VOC. (Wang WC, et al 2011).

➢ Chronic SCD-associated pain that interferes with daily activities or quality of life. Hydroxyurea
has been demonstrated to reduce acute painful episodes and is recommended for individuals
with SCD who have frequent painful episodes, including infants <9 months, older children, and
adults, as well as all very young children 9 to 24 months. (UpToDate)

➢ History of severe or recurrent acute chest syndrome. The acute chest syndrome (ACS) is a
significant cause of morbidity and mortality in patients with sickle cell disease. Patients who
survive the syndrome are more likely to suffer a recurrent episode than are people who have
never been affected. Both hydroxyurea and chronic transfusion therapy were found to decrease
the frequency of acute painful vaso-occlusive episodes and acute chest syndrome (Stettler N, et
al 2015). Hydroxyurea should be the initial therapy used in the prevention of these events.
Chronic transfusion therapy is started when the response to hydroxyurea is inadequate. In
patients who are recovering from a life-threatening acute chest syndrome, a six-month
transfusion regimen with transition to hydroxyurea therapy is often used (UpToDate)

➢ History of severe, symptomatic, chronic anaemia that interferes with daily activities or quality
of life. The anaemia and markers of hemolysis may be less severe in some individuals, including
those with concomitant alpha thalassemia, those undergoing chronic transfusion therapy, and
those receiving hydroxyurea. (Ghafuri D, et al 2017)

➢ High risk of stroke based on transcranial Dopller measurements. There is evidence of

decreased stroke rates in those children with sickle cell anaemia administered hydroxyurea
compared with no treatment (Lobo CL, et al, 2013). It was also found that children receiving
hydroxyurea had reduced transcranial Doppler (TCD) velocities. (Thornburg CD, et al 2012). In
children with SCA, hydroxyurea was found to decrease the rate of recurrent stroke compared
with no therapy (Ali SB, et al, 2011)

CASE-SICKLE CELL
PATIENT PARTICULARS:

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Patient reg no: M17-YY-XX

Name: MO-SALAH

Age: 3years and 11 Month

Sex: Male

Residence: Morogoro

Tribe: Gogo

Date of Admission: 22/11/2017

Date of Clerkship: 22/11/2017

Informant: Biological Mother of the patient

Referral from Morogoro hospital with Provisional Diagnosis of Leukemia for further management.

CHIEF COMPLAINT: Recurrent Fever for 3yrs and 7 month

Recurrent Chest pain for 3yrs and 7 month

Recurrent Joint pain for 3yrs and 7 month

Recurrent Abdominal Pain for 3yrs and 7 month

HISTORY OF PRESENTING ILLNESS

The patient presented with recurrent episodes of fever for three years and 7month now. The
episodes were acute on onset and progressive in nature with a non specific periodicity.Was associated
with yellowish colouration of the eyes that disappeared after fever episode. No changes in stool colour,
Normal urine colour and frequency of urination, No history of itching.

Each episode lasted for about 4hours following diclophenac injection, recurred every after 2 to 3 month
and was severe as compared to previous episode.

Current episode started three days ago, it was acute on onset and progressive in nature with a non
specific periodicity. Lasted for about 4hours following diclophenac injection but recurred after 3hours.

No history of convulsion/loss of consciousness, no history of neck stiffness. Have a history of ear pain
2weeks ago that was gradual on onset and persistence in nature. Was not associated with ear discharge
and subsided after two days following application of ear drop. No history of nasal discharge/painfully
swallowing.

Recurrent episodes of chest pain for 3yrs and 7month now, Acute on onset gradually increasing with
intensity with a non specific periodicity non radiating.

Associated with difficulties in breathing, wheezing, and dry cough, have a history of easy fatigability
when playing with others but denied of breathing difficulties when lying flat, syncope nor lower limb
swelling.

36 | P a g e
Each episode lasted for about 4hours following diclophenac injection, recurred every after 2 to 3 month
following fever episode.

Current episode started 7days ago the pain was more intense compare to previous episode, acute on
onset gradually increasing with intensity with a non specific periodicity non radiating. Associated with
difficulties in breathing and wheezing was relieved after 3hours by diclopenac injection, but recurred
every after 6hours. No known aggravating factors.

Recurrent Joint pain for 3yrs and 7month that was acute on onset, gradual increasing with time and non
migratory involving the joints of finger and lower limbs. First episode was associated with swelling of
thumb and toe joint of the right and left hand and leg respectively. The swelling were fluid filled,
painfully on touch, but regressed spontaneously after four days.

Each episode was associated with reduced ability to walk but was not aggravated with walking, no
history of lower limb trauma.

Each episode lasted for about half an hours following diclophenac injection, recurred every after 2 to 3
month following fever and chest pain episode.

Current episode started 3weeks ago, with acute onset and intermittent in nature non migratory,
associated with inability to walk, not aggravated with movement no history of leg trauma prior to onset
of joint pain. The episode lasted for about half an hour following diclophenac injection, recurred after 2
days. No history of muscle or back pain.

Recurrent Abdominal pain for 3yrs and 7month, the pain was acute on onset and gradually increasing
with time with a non specific periodicity.

The pain was below the umbilicus, non radiating not associated with vomiting neither
diarrhea/constipation nor of blood in stool.

Each episode lasted for about 1hour following diclophenac injection, recurred every after 2 to 3 month
following fever episode.

Current episode started one day ago, was acute on onset more intense as compared to previous episode
it persisted till the time of admission where the child was given syrup morphine and the pain subsided
after 15min. The pain was below the umbilicus, non radiating not associated with vomiting neither
diarrhea/constipation nor of blood in stool.

COURSE OF ILLNESS

37 | P a g e
This is the 9th admission, the 1st ,2nd,3rd,4th,5th,6th and 7th admissions was because of similar presentation,
the first one was 3yrs and 7month ago. Each admission was for about one week and each time the
patient was given IV fluids, diclophenac injection and other medications the mother doesn’t remember,
the symptoms subsided.

8th admission was 7month ago for a week, due to chest pain, joint pain and fever that was associated
with excessive night sweat and weight loss for one week. The patient was diagnosed with pulmonary TB
by chest X-ray, initiated with Ant TB that he used for six month, but the symptoms persisted. During this
time, the patient was also given IV diclophenac, gentamycin and folic acid.

All other episodes the child was taken to the nearby dispensary injected with diclophenac and septrine
syrup.

No history of blood transfusion but have being on hematenics for three years now. No know food/ drug
allergy.

REVIEW OF OTHER SYSTEM: As per HPI

PRE NATAL HISTORY

Booked at 20 weeks GA at Munge hospital Morogoro, made 6 visit

Received albendazole antihelmithic, haematenics, 2 doses of SP drugs for malaria prophylaxis and 2
dose of tetanus toxoid.

Was tested for HIV (negative), VDRL was reactive, both mother and the husband were treated but she
doesn’t remember for how long and with which medication.

No any other illness of complication during pregnancy.

BIRTH HISTORY

Labour lasted for 10hrs, with spontaneous rupture of membrane.

Delivered by spontaneous vertex delivery at Munge Hospital a term baby with 4kg.

A baby cried immediately after delivery and started sucking about 10min after delivery.

POST NATAL

Discharged after 24 hours, cord dropped on the 7th day.

No history of yellowish coloration, no history of bluish coloration, no history of any disease during
neonatal period.

IMMUNIZATION HISTORY

Mother had no RCH card she reported that the child received BCG, OPV-0 day 1 after birth and measles
vaccine at 9month. Other shot of vaccine the mother is not sure.

GROWTH AND DEVELOPMENTAL MILESTONE

38 | P a g e
Mother reported that, the child had delayed growth since was 4month old as compared to other sibling,
she also reported of decrease in weight for the past 4 month, from 20kg in April this year to 18kg on the
day of admission.

The child is able to dress himself with supervision, can give first and last name, play with others, can also
eat using fork.

Conclusion: the child has delayed growth as per age with normal and appropriate developmental mile
stone as per his age.

DIETARY HISTORY

Receives 3meals per day, takes tea chapatti in the morning.

Lunch: stiff porridge and meat with vegetables most of the times.

Dinner: rice or banana with meat. All the time the child doesn’t finish a plate full of food.

Conclusion: diet is adequate in quality but not quantity.

FAMILY HISTORY

Fourth born in a family of four children, 1st born is a form 4 leaver, the 2nd born is in form four and 3rd
born is in form one. All other siblings are of good healthy. Mother is the housewife, living with his
husband who is a businessman.

There is consanguinity in the family, where by the mother and father maternal side is are related.

No known history of diseases like sickle cell anemia, asthma in the family.

PHYSICAL EXAMINATION

General Examination; No danger sign

- A febrile with 37.8 degree centigrade.

- have buzzing of the skull, tinea capitis, no teeth malocclusion.

-Have bilateral tonsil enlargement and dental caries.

-Not cyanosed, not jaundiced, have some palmer pallor.

-Palpable groin lympnode bilaterally.

-No lower limb edema.

Anthropometric measurement

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Weight 18kg Height 18cm MUAC 16cm Head circumference 54cm

Interpretation;

Weight/Height -1SD (Mild wasting)

Weight/Age between median and 1SD (Normal)

Height/Age between 2SD and 3SD (not stunted)

MUAC Normal per Age

Head circumference/Age between 2SD and 3SD (macrocephaly)

Conclusion; The child is mild wasted with normal weight for age and not stunted.

Have macrocephaly which could be due to buzzing of the skull.

SYSTEMIC EXAMINATION

PER ABDOMEN

❖ Inspection: Abdomen is not distended, normal contour, moves with respiration, umbilicus
centrally located and inverted, no any visible scars, no any surgical or therapeutic mark.

❖ Palpation: Non tender, no palpable mass, no organomegally, liver span of 5.5cm, bladder not
distended.

❖ Percussion: Tympanic percussion note

❖ Auscultation: Normal bowel sounds.

Normal circumcised male genitalia.

RESPIRATORY SYSTEM:

❖ Inspection;RR-40breaths/min(tachypnoeic), and movement, no chest deformity.

❖ Palpation: bilaterally symmetrical chest movements, symmetrical chest expansion, trachea

centrally located, no tenderness.

❖ Percussion: Resonant percussion note on both sides of the chest.

❖ Auscultation: Vesicular breath sounds heard bilaterally with bilateral air entry in both sides of
the chest.

CARDIOVASCULAR SYSTEM

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 ❖ Pulse rate 112beat/min, Regular, normal volume, strong and synchronous with radial radial,
radial brachial, radial carotid, radial femoral.

❖ Inspection: No precordial hyperactivity, no precordial bulging,JVP not raised.

❖ Palpation: No palpable heave/thrill, apex beat palpable in 6th intercostals space left mid-
clavicular line.

❖ Auscultation: S1 and S2 Sounds heard, no added sounds

CENTRAL NERVOUS SYSTEM:

❖ Higher centre; Alert, interactive, appropriate speech for age, intact long term and short term
memory.

❖ Cranial nerves; Normal pupil shape and size, equally reactive to light(ii)

Can move eyes in all direction (iii, iv, vi)

Clench teeth with prominence of pterygoid (v)

Facial symmetrical, smiles, intact facial sensation (vii)

Normal balance (viii)

Can protrude tongue, No deviation no fasciculation (ix, xii)

Uvula is centrally (x)

Can slug shoulder (xi)

Conclusion: intact functions of the cranial nerve.

❖ Motor

Upper limb Lower limb

Bulkiness Normal Normal

Reflex Intact Intact

Tone Normal Normal

Power 4/5 4/5

❖ Sensation: intact in both upper and lower limb

❖ Coordination: intact pass pointing, normal heel shin test

❖ Spine: normal, no tenderness

SUMMARY

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MO SALAH 3yrs and 11month old male, presented with recurrent episodes of fever, chest pain, joint
pain and abdominal pain for 3 yrs and 7month now. Each episode occurred every after 2 to 3 month
lasting for about an hour following diclophenac injection. Had jaundice concurrent with each fever
episodes, that subsided when there was no fever. Have history of dactilitis during first episode of joint
pain when he was 4month.No known familial history of sickle cell anemia but there is consanguinity. On
examination had buzzing of the skull, dental caries, tinea capitis, some palmer pallor, tachypnoeic with
apex beat palpable at 6th intercostals space mid clavicular, other system were essentially normal.

PROVISIONAL DIAGNOSIS

2. Sickle Cell Anemia with Vaso-occlusive crisis, DDX Leukemia

3. Tonsilitis
4. Uncomplicated Malaria, DDX Urinary Tract Infections
5. Tinea capits
6. Moderate anemia

INVESTIGATION

❖ Full blood picture

Had Neutrophilia(8.3)

Normocytic normochromic anemia of 8.01g/dl Hb

Other parameters were normal

❖ Peripheral smear showed sickle red blood cell

❖ Sickling test showed sickled Hb

❖ Hb Electrophoresis showed HbSS

❖ CRP elevated(31.5) indicating acute infection

❖ Blood slide for malaria parasite was Negative

❖ Urinalysis had normal finding

❖ Blood culture normal finding

❖ Abdominal ultrasound

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Liver had normal architecture, size and echo pattern measuring 9.69cm.

Hepatic and portal veins were normal

Gall bladder and biliary track normal

Kidneys were normal.

FINAL DIAGNOSIS

Sickle Cell Anemia in Vaso occlusive crisis

MANAGEMENT

-Hydration with maintenance fluid 2100mls/24hrs

-T.Ibuprofen 100mg 8hrly for pain management

-syrup Amoxiclav 345mg bd for 3 days for tonsillitis

-T.Griseofulvin 250mg od for month for tinea capits

-T.Pen V 250mg bd for infections prophylaxis until the child reaches 6years

-T.Folic Acid 5mg od for life to prevent anemia

MONITORING

Hydration status because dehydration will cause painful crisis

Vitals( SPO2 to prevent hypoxia that will cause painfully crisis, HR and RR)

Development of any signs of infection by monitoring temperature and CRP levels.

COUNSELLING

Explaining to the mother about the nature of the diseases, the complications and the possible
precipitants for vaso occlusive crisis such as infections, dehydration, hypoxia, acidosis

Returns to the hospital early, whenever the child develops the signs of infections such as fever.

Encouraging the mother to ensure adherence to Pen V prophylaxis until the child is at least 6years old

It’s important to take folic acid for life, to prevent anemia.

The child should attend clinic every after 3 month for follow up.

PROGNOSIS

Good because the child has access to comprehensive care unit and was initiated with prophylaxis
antibiotics early and was immunized.

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ACUTE WATERY DIARRHEA AND SEVERE ACUTE MALNUTRITION
CASE PRESENTATION
NAME YYY

WARD MAKUTI A

REG NO M00-00-00

AGE 18/12 years (DOB – 15th March,2016)

SEX MALE

RESIDENCE TABATA KIMANGA

DATE OF ADMISSION 07th November, 2017

DATE OF CLERKSHIP 09th November, 2017

INFORMANT BIOLOGICAL MOTHER

INTRODUCTION

• The patient was referred from Amana hospital for further evaluation and management due to
non-responding diarrhea. This is the first admission of the child at MNH

CHIEF COMPLAINTS.

1. Poor weight gain x 8/12

2. Passing of loose stools x 2/7

3. Fever x 2/7

4. Cough x 1/7.

HISTORY OF PRESENTING ILLNESS.

• The child was presented to the hospital with the complaint of poor weight gain for 8 months in
which the last body weight of the child was 7.0kg at the age of 1 year. The mother reported that
the child was exclusively breastfed for only 3 months due to inadequate breastmilk and then
introduced to the complementary feeding in which the child was fed with porridge made of
maize flour for the next 3 months and then after the child was given variety of foods including
cassava, banana, bread and potatoes with little vegetable and fruits in a week, feeding
frequency was 4 times a day. The child’s body weight has been in the the gray zone for 4 months
and red zone for other 4 months in of RCH card 1. Mother reported no any history of chronic
illness like TB to her, no use of medications like diurects and contraceptive pills during lactation,
and the child had no history of TB contact.

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 • The child was apparently doing fine till 2 days ago when he started to suddenly pass the loose
stool yellowish in color, not mucoid, not blood contained with reported 10 episodes of loose
stools in a 24-hour period with non-specific in periodicity. No aggravating or relieving factors
reported, the passing of the loose stools was associated with general body weakness, loss of
appetite, with no history of yellowish discoloration of the eyes, no history of bruising on the
skin, no history of difficulty swallowing, no history of vomiting, no history of abdominal
distension or pain,the child had no history of easy fatigability on BF, no history of bluish
discoloration and no history lower limb swelling

• Prior to onset of passing of loose stools, mother reported no change of the last meal the child
ate, mother reported also the good hygienic practices including using clean and safe water and
foods, washing hands after defecation, after disposing child’s faecesand before preparing meal,
no same condition to any family member, no recent uses of antibiotics or herbal medications,
the child received the rotavix vaccine as per age and no cholera outbreak in the locality the
patient lives, no history of recent travel or recent hospitalization.

• The child was reported to have fever for 2 days that was low grade,sudden onset, intermittent in
nature with no aggravating condition that was relieved by paracetamol, no history of
convulsions, no history of loss of consciousness, no history of poor hearing or vision, no history
of skin rashes, no history of neck stiffness, history of normal urine volume, yellowish in color,no
history of cry of difficulty during micturition, no history of ear scratching or discharge, no history
of nasal discharge or congestion, no history of joint or muscle swelling or pain and no history of
recent head injury .The child was also reportedto have cough for 1 day that was gradual on
onset, productive in nature in which the sputum was scanty and whitish with non-specific in
periodicity, the child had no history of difficulty in breathing, no history of excessive night
sweats

• Prior to admission at MNH the child received 2 cups of ORS and paracetamol at Tabata hospital
initially and sent to Amana hospital where was directly referred to MNH, no reported
medications given at Amana Hospital.

REVIEW OF OTHER SYSTEMS

As per HPI

PAST MEDICAL HISTORY

• No history of the previous admission due to the other medical conditions

• No history of surgery or BT

• No history of the chronic illness like TB

• No history of allergy to known drugs or foods

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PRENATAL HISTORY

• Booked clinic at 6months of pregnancy at Tabata hospital and made a total of 4 visits.

• She received only Ferrous tabs, did not receive Folic acid, SP and not dewormed

• HIV and VDRL tests were done and the results were negative, received a total of 2 doses of
TT

• No any serious illness the mother had during pregnancy

NATAL HISTORY

• Period of labor was 8 hours prior to birth delivery, Spontaneous ROM

• Delivered by SVD at hospital, a term baby with the BW of 2.5kg

• The baby cried and started to suck immediately and the cord dropped on the 7th day.

POST NATAL HISTORY

• Discharged from the hospital after 24hrs rest

• No history of yellowish discoloration

• No history of bluish discoloration

GROWTH AND DEVELOPMENT HISTORY

• Controlled head at 4 months of age

• Sit with support at 4 months of age
• Sit without support at 7 months of age
• Stand without support at 9months of age
• Social smile at 6 weeks of age
• Started to say ba, ka, ma at 7 months of age

Conclusion: The child had normal developmental milestones per age

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IMMUNIZATION HISTORY

• BCG and OPVo -4th day of life

• Rotarix -6th and 10th week of life.

• OPV-6th, 10th and 14th week of life

• DPT Hib and Hep-B (Pentavalent)-6th, 10th and 14th week of life

• PCV-6th, 10th and 14th week of life

• MR-9th and 18th month of life.

Conclusion: Had BCG scar on the right shoulder and appropriate immunization per age according to
IVDP

DIETARY HISTORY

As per HPI

FAMILY AND SOCIAL HISTORY.

• The index is the second twin, the other twin is doing fine. In total the mother has two children.

• Mother is 20years old, Form 3, the housewife cohabiting with the child’s father who is 27 years
old, Form 4 leaver and a Bajaj driver.

• No family member who is alcoholic or cigarrete smoker.

• Positive history of Hypertension in maternal side.

PHYSICAL EXAMINATION

General Examination

• No emergency signs, alert,afebrile (37.2oC), wasted, pale conjunctiva, no palpable lymph nodes,
some palmer pallor, not jaundiced, no cyanosed, no finger clubbing, extremities are warm and
capillary refill is < 2seconds, no lower limb edema.

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ANTROPOMETRIC MEASURES

Weight 7kg : weight for age < -3SD (Severely underweight),

Weight for height is -3SD (Severe wasting)

Height 72cm: height for age < -3SD

MUAC=12cm: MUAC for age is -3SD to -2SD (Moderate wasting)

OFC=42 cm: OFC for age < 3rd Percentile

Conclusion: severely wasted and severely underweight.

DEHYDRATION STATUS

• Irritable

• Drinks eagerly

• Skin pinch goes back slow

• No sunken eyes

SYSTEMIC EXAMINATION

PER ABDOMEN EXAMINATION

• Normal contour and it was moving with respiration.

• No visible dilated vessels, no scars or therapeutic marks.

• Umbilicus – centrally located, inverted and retracted.

• Abdomen was soft, non-tender and spleen and kidneys were not palpable.

• Tympanic percussion note, normal bowel sounds.

• Normal male genitalia, normal perianal skin.

RESPIRATORY SYSTEM EXAMINATION.

• Respiratory rate – 25 breaths/ minute.

• Normal chest contour, symmetrical chest movement, no lower chest wall in drawing or
intercostal recessions, no visible dilated vessels.

• Trachea centrally located, bilateral chest expansion

• Resonant percussion note.

• Equal air entry and normal vesicular breaths sounds.

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CARDIOVASCULAR SYSTEM EXAMINATION.

• Pulse rate – 88 bpm, taken at radial, regular, weak, non – collapsing and synchronous with other
pulses.

• No precordial hyperactivity or bulging

• No parasternal heave or thrill.

• Apex beat was palpable at 5th intercostal space left midclavicular line.

• S1S2 heard, no murmurs.

CENTRAL NERVOUS SYSTEM EXAMINATION

• Fully conscious, Oriented to people, good speech.

• Could fix and follow. Pupils – equal in size, circular and reactive to light.

• Was able to suck the breastmilk, to chew the food

• Facial symmetry, could resist opening of her mouth

• He turned her head to voice,

• Was able to swallow with no uvula deviation, could rotate her head to either side and there was
no tongue fasciculation or asymmetry.

URL ULL LRL LLL

Muscle bulkiness Normal Normal Normal Normal

Tone Normal Normal Normal Normal

Reflex Normal Normal Normal Normal

Power 5/5 5/5 5/5 5/5

EAR, NOSE AND THROAT EXAMINATION

• No ear discharge, swelling, or scratches.

• No nasal obstruction or discharge.

• Tonsils not enlarged. No throat hyperemia or any lesion.

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SUMMARY

E.J.W, 1year8months of age, male from Tabata, brought to MNH due to non-responding diarrhea
presenting with poor weight gain for 8months, passing of loose stools, fever for 2days and cough for 1
day. The child was fed with inadequate quality and quantity of food with no h/o chronic illness, good
hygienic practice was reported with no meal change prior to diarrhea, with the history of Rotarix
vaccine, no same condition of diarrhea in the other family members. The child was alert, wasted,
afebrile, some palmar pallor, no palpable lymph nodes, no lower limb edema and presented with the
features of some dehydration. In systemic examination, the findings were essentially normal.

PROVISIONAL DIAGNOSIS

1. Acute Watery Diarrhea with some dehydration

2. Uncomplicated Malaria

3. Septicemia

4. SAM-Marasmus

DIFFERENTIAL DIAGNOSIS

• Urinary tract infection (UTI)

ACUTE WATERY DIARRHOEA

Acute watery diarrhea is the one characterized by abrupt onset of frequent, watery, loose stools without
visible blood, lasting less than two weeks. Usually, acute watery diarrhea episodes subside within 72
hours of onset. For it to be called diarrhea one must pass at least three motions in a day.

It may be accompanied by flatulence, malaise and abdominal pain. Nausea, vomiting may occur and
also fever may be present. The common causes of acute watery diarrhea in children are viral. Other
causes could be bacterial or parasitic infections.

Bacteria can cause acute food poisoning. Poor hygienic practices increase its risk. It is clinically
diagnosed, in complex cases laboratory tests may be required.

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Important points

Know the degree of dehydration

Severe dehydration if a child has two of the following

1. Unconscious/lethargic
2. Sunken eyes
3. Unable to drink or drinks poorly
4. Skin pinch returns slowly in greater or equal to 2secs. (a place to pinch the skin is on the
abdomen)

To correct severe dehydration→plan C which involves:

Give 100mls/kg of ringer lactate. for children less than 1yr give 30mls/kg for the first hr then
70mls/kg for the other five hrs, and for children above 1yr up to 5yrs (just do as above but divide
by two the time) give 30mls/kg for 30mins and 70mls/kg for the next 21/2 hrs.

Then keep assessing the condition and classify dehydration after 3-4hrs for children less than 1yr
and after 1-2hrs in children more than 1yr if no improvement give the drip rapidly.

Some dehydration if a child has two or more of the following

1. Restlessness/irritable
2. Sunken eyes
3. Drinking eagerly
4. Skin pinch goes slowly

To correct this use plan B: give 75ml/kg of ORS. Then when the child has improved give extra fluid, give
zinc suppliments, encourage the mother to continue feeding and educate the mother when to return

No dehydration- when doesn’t fit in the two categories above. Use plan A which involves 4 principles

1. Give extra fluid

2. Give zinc suppliments- children less than 6months give half a zinc tab which is 10mg, for children
above 6months give a full zinc tab which is 20mg and the time is 2weeks.
3. Encourage feeding
4. Explain to the mother when to return

Persistent diarrhea is diarrhea, with or without blood, which begins acutely and lasts for 14 days or
longer. When there is some or severe dehydration, persistent diarrhea is classified as “severe”.

To fear in diarrhea is electrolyte imbalance. They loose potassium, sodium and they loose zinc in greater
amount.

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MANAGEMENT OF ELECTROLYTE IMBALANCES IN DIARRHEA
MILD AND MODERATE HYPOKALEMIA:

Mild and moderate hypokalemia can be corrected by using ORS and slow K tabs.

Slow k tabs→one tab is 600mg which has 8meq of potassium. The child needs 4meq/kg/day.

SEVERE HYPOKALEMIA:

Severe hypokalemia we use IV Kcl. The dose is 0.3mmol/kg/hr for 3hrs. Dilution is 25 to 50 times.

1ml of 7.5% kcl has 1mmol of kcl. So if a child has 10kg will need 0.3x10=3mmol/hr. since 1ml has
1mmol of a patient then a 10kg will need 9mls of 7.5% kcl diluted 25 times (9x25=225mls) amount of
normal saline which here should be 225mls. So our patient will be given 9mls of 7.5%Kcl mixed in
225mls of normal saline.

CORRECTING HYPOMAGNESEMIA

Normal magnesium levels are 0.8-1.1mmol/l. less than 0.8 you give 5-15mg of elemental mg2+ per
kilogram body weight.

FOR HYPOCALCEMIA→ 0.3mls/kg calcium gluconate stat or 0.2mls/kg/hr IV infusion diluted in 5%

dextrose.

SEVERE ACUTE MALNUTRITION

Severe Acute Malnutrition-Marasmus is the most common form of protein-energy malnutrition and is
thought to be caused by inadequate intake of all nutrients, but especially dietary energy sources (total
calories). It is clinically diagnosed by severe visible wasting with weight for height with Z-score of <-3SD
or MUAC of <115mm.Malnutrition may cause diarrhea more severe, more frequent and more prolonged
and the vice versa is true as diarrhea for long may cause malnutrition.

52 | P a g e
SEVERE ACUTE MALNUTRITION
Can be complicated (requiring admission) or uncomplicated(treated as outpatient).

Complicated when the child has lost apetite or has a general medical condition.

HISTORY

Find out if the child has any chronic illness such as HIV, TB, chronic diarrhea. Inquire about vomiting, the
type of diet the child is eating. Dietary history is important.

MANAGEMENT (TEN IMPORTANT YOU NEED TO CORRECT)

Involves the stabilization phase and then rehabilitation.

1. Hypoglycemia
2. Hypothermia
3. Dehydration
4. Infection
5. Electrolyte abnormalities
6. Micronutrient deficiency
7. Initiate feeding- you start with F75, then F100. Introduce feeds slowly
8. Catchup feeding
9. Sensory stimulation
10. Follow up

Management of the child with SAM involves two phases; The initial stabilization phase that focuses on
restoring hemostasis and treating medical complications like hypoglycemia, hypothermia, electrolyte
imbalance heart failure and untreated infections, usually it takes 2-7 days of inpatient treatment.
Another phase is the rehabilitation phase that focuses on rebuilding the wasted tissues and may take
several weeks.

REFEEDING SYNDROME
During starvation low glucose an hence insulin is low and glucagon is high and there is increased use of
fats and protein as source of energy. If you re introduce foods rapidly after long starvation you stimulate
large amounts of insulin to be produced that shift potassium into cells and end up with hypokalemia.
There are a lot of other disturbances occur, potassium I mentioned as an easy one to understand.

The refeeding syndrome is characterized by

• Hypophosphatemia
• Hypokalemia
• Seizures
• Rhabdomyolysis
• Peripheral edema
• Congestive heart failure
• Cardiac arrhythmias

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Refeeding syndrome is a metabolic disturbance occurring as a result of aggressive nutritional
rehabilitation in severe malnourished children.

54 | P a g e
NEPHROLOGY
CASE- NEPHROTIC SYNDROME
Name of the patient: UUUU

Age: 7 years old

Sex: Female

Residence: Temeke

Date of admission: 17/11/2017

Date of clerkship: 24/11/2017

Ward: B

INTRODUCTION

The patient was referred from Temeke for further management with referral diagnosis of appendicitis
and nephrotic syndrome

The patient was admitted in the paediatric surgical ward for 1 week because of suspected appendicitis
due to complain of abdominal pain 3 days prior to admission.

After thorough investigations it was found that the patient did not have appendicitis but had UTI, so the
patient was given antibiotics, ceftriaxone and before being transferred to ward B on 24th November for
further interventions.

CHIEF COMPLAINS

1: Generalized body swelling for 2 weeks

HISTORY OF PRESENTING ILLNESS

The patient was apparently well until 2 weeks ago when she started developing body swelling. It was
gradual on onset, not painful, initially started with swelling around the eyes followed by swelling of the
whole face then 3 days later progressed to swelling of the lower limbs and the abdomen, about a week
later the patient also developed swelling of the back. The mother reported that the swelling was more
prominent in the morning or anytime the child woke up from sleep but reduced in size during daytime.
The patient reported reduced urine output compared to before the onset of the illness,there is no
history of painful micturition and did not notice any change of colour of the urine.

There is no history of easy fatiguability, no history of awareness of heart beat, no history of difficulty in
breathing on lying flat. There is no history of vomiting blood or defecating black stool, no history of
yellowish coloration of eyes or skin, no history of blood transfussion.

The mother reported that about 2 months ago the child had multiple bee stings on the head which
resulted in swollen scalp that subsided 4 days later after applying some traditional herbs.

There is also no history of use of medications prior to onset of the symptoms. The child’s HIV status is
negative

55 | P a g e
There is no history of headache, dizziness, blurred vision or loss of consciousness.

3 days prior to admission the patient also presented with abdominal pain that was sudden on onset,
aching in nature, localized on the lower part of the abdomen, not radiating to any other part of the
body. The patient reported that the pain was most of the times associated with the urge to urinate and
would get a mild relief after micturition which resulted in increased frequency of micturition. There was
no history of constipation, no history of diarrhea or vomiting.

REVIEW OF OTHER SYSTEMS

Ear, nose and throat: No history of ear pain/discharge, no history of nasal discharge, no history of sore
throat.

Musculoskeletal: No history of joint pain/swelling, no history of muscle pain, no history muscle

weakness

Respiratory system: no history of cough or chest pain.

PAST MEDICAL HISTORY

There is no history of previous admission

No known allergy to any food or drug

No history of surgery

PRENATAL HISTORY

Mother booked at 5 months pregnant, had 4 total number of antenatal visits

Received all interventions required (does not remember all the details)

She reported to have tested for HIV and was negative

No history of any complications during pregnancy

NATAL HISTORY

The mother had spontaneous rupture of membranes, does not remember the period of labor.

Delivered by spontaneous vaginal delivery to a term baby.

No any complications during delivery

POST NATAL HISTORY

The child cried and sucked immediately after birth.

No history of yellowish or bluish coloration of skin

The cord dropped after 7 days

IMMUNIZATION HISTORY

The mother reported that the child received all vaccines required

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GROWTH AND DEVELOPMENTAL HISTORY

The child sat without support by 6 months of age

Started crawling by 8 months

Walked at 1 year

Currently, the child is in standard 1, she is able to count, write and read some letters

According to the mother, the child has had good weight gain before the onset of the illness

Conclusion: normal growth and developmental history

DIETARY HISTORY

The child usually eat either bread, cassava, potato with tea or porridge in morning

In the afternoon, she eats stiff porridge with vegetables or beans and occasionally would eat meat or
fish

In the evening, she eats rice with either beans, meat or fish

The mother reported that she eats fruits occasionally (once or sometimes twice a week)

According to the mother, the child eats very well. Also the food is adequate for their family

In conclusion: the food is adequate in quantity and quality

FAMILY AND SOCIAL HISTORY

The child is the 3rd born out of 3 children, the other children are doing fine

Mother is 41, works as a food vendor, widow

The father died 2 years ago (the mother does not know the cause of death)

No familial history of similar illness or any other chronic illness such as hypertension, diabetes mellitus
or heart diseases

ON EXAMINATION:

GENERAL EXAMINATION

The child was conscious, afebrile (36.7⁰C), not cyanosed, not jaundiced, no oral thrush, not pale, no
finger clubbing, no lymphadenopathy

Had generalized edema of face, abdomen, lower limbs and back (pitting edema)

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ANTHROPOMETRIC MEASUREMENTS

Weight = 28kg

Height =124cm

MUAC =14.5cm

BMI = 18kg/m2 , above 5th percentile (normal for age)

SYSTEMIC EXAMINATION:

PER ABDOMEN

Symmetrical abdominal distension, no visible vessels

Moves with respiration

No scars or therapeutic marks

The abdomen was non-tender

No organomegally or any other mass palpable

Dull percussion note

Bowel sounds heard and were normal

Normal female external genitalia

CARDIOVASCULAR SYSTEM

Radial pulse rate: 98beats/min, normal volume, regular, synchronous with other peripheral pulses
(radial-radial, radial-carotid, radial-femoral)

No raised jugular venous pressure,

No precordial bulging or hyperactivity

No parasternal heeves/thrills

Apex beat at 5th intercostal space mid clavicular line

S1S2 heard, no murmurs

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RESPIRATORY SYSTEM

Respiratory rate: 22breaths/min

Normal chest shape

Moves with respiration

Symmetrical chest expansion

Trachea is central

Normal symmetrical vesicular breaths sounds, no added sounds

CENTRAL NERVOUS SYSTEM

Higher centers

➢ Alert

➢ Active

➢ oriented to time, place and person

➢ Good memory

➢ Normal mood

Cranial nerve

➢ Cranial nerve I:could sense smell

➢ Cranial nerve II: visual acuity 6/6, normal visual field

➢ Cranial nerve III : normal pupil size and shape, reactive to light

➢ Cranial nerve III, IV,VI: could move eyes in all quadrants

➢ Cranial nerve V: could sense the light touch in all divisions ophthalmic, maxillary and
mandibular, could clench her teeth, could resist closing of the jaw

➢ Cranial nerve VII: face is symmetrical, no mouth deviation

➢ Cranial nerve VIII: could hear

➢ Cranial nerve IXand X: uvula is central

➢ Cranial nerve XI: could shrug her shoulders

➢ Cranial nerve XII: No tongue deviation or fasciculations

Conclusion: cranial nerves were intact

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Motor function

➢ Normal muscle bulkiness of the upper limbs, could not check for bulkiness in the lower limbs
because of massive edema

➢ Normal tone in both upper and lower limbs

➢ Power 5/5 in upper limbs and 4/5 in lower limbs

➢ Normal reflexes

➢ Normal sensation in all dermatomes

SUMMARY

The patient named UUU, 7 years old female from Temeke presented with complains of generalized body
swelling for 2 weeks and abdominal pain for 3 days prior to admission. Associated with reduced urine
out and increased frequency of micturition but no history of painful micturition or blood in urine. On
examination, anasacra, not pale, not jaundiced, no finger clubbing.

PROVISIONAL DIAGNOSIS

1. Nephrotic syndrome

Differential: nephritic syndrome

2. Urinary tract infection

INVESTIGATIONS

1. Urine dipstick, to check for protein in urine

2. Urinalysis to check for amount of protein in urine, RBC cast, and signs of UTI

3. Serum albumin to check for albumin levels to confirm hypoalbuminemia

4. Lipid profile, LDL

5. Blood urea nitrogen and creatinine,

6. Full blood count to check for HB levels for anemia, white blood cells and its differentials to check
for signs of infections

7. ESBACH test for monitoring 24 hour urine protein

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RESULTS

➢ Proteinuria, 3+

➢ Total protein 55g/l (low)

➢ LDL, 7.35 (raised)

➢ Albumin 16 (low)

➢ HB, 8.79 (low), mild anemia, normochromic normocytic.

➢ Other lab investigations were essentially normal

FINAL DIAGNOSIS

Nephrotic syndrome with mild normochromic normocytic anemia

➢ Massive proteinuria, 3+

➢ Hypoalbuminemia

➢ Hypercholesterolemia, raised LDL

➢ Edema

MANAGEMENT

Non-pharmacological

➢ High protein diet, beans, meat, fish

➢ Salt restriction

➢ Fluid restriction

Pharmacological

➢ Furosemide 30mg once daily

➢ Spironolactone 60mg, 8 hourly

➢ Prednisolone 60mg once daily in 6 weeks then 1.5mg/kg/day alternate days for the next 6 weeks
and then the dose will be tapered down in the following 6 weeks

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MONITORING

➢ Weight should be monitored in the course of the treatment, whereby weight is expected to
drop as edema subsides

➢ Vitals should also be monitored, blood pressure, pulse rate, respiratory rate and temperature

➢ Side effects of medications, for instance, with the use of diuretics the patient may end up with
dehydration, also prednisolone may result in immunosuppression hence infections

➢ Urine dipstick should be performed daily to monitor protein in urine, also for detecting
remission (which free proteinuria for 3 consecutive days)

COUNSELLING

➢ Good adherence to medications

➢ The mother was counselled about the long term use of medications

➢ Salt restriction, only salt that is put in meals during cooking is enough, the patient should not be
allowed to take extra salt

➢ Early detection of new symptoms and seek medical care early

PROGNOSIS

The patient has good prognosis because of

➢ Good response to medications (in a 2 week time, the patient was already in remission and
edema subsided)

➢ No any signs of complications

NEPHROTIC SYNDROME
It is a clinical pathological condition characterized by hypoalbuminaemia, massive proteinuria,
hyperlipidemia and edema.

Its simply a problem in the kidneys, where it allows protein to be lost in urine (massive proteinuria), and
since protein is lost in urine including albumin then albumin in blood gets reduced (hypoalbuminemia),
and as proteins are lost the liver tries to compensate by producing proteins in form lipoproteins which
are proteins with lipids as a result lipid levels in blood increase→hyperlipidemia. Edema is a result of
low oncotic pressure as albumin is low in blood.

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ETIOLOGY

Can be

1. Primary/Idiopathic- where majority(80%) fall into this category

2. Secondary to other diseases such as sickle cell, malaria, alport syndrome etc

PRIMARY NEPHROTIC SYNDROME

It’s simply nephrotic syndrome in absence of systemic disease. The problem is primarily in the kidneys.
In children its usually a result of minimal change disease.

Minimal change disease is common in children less than 6years, common in males and responds to
steroid therapy. It is sometimes called steroid sensitive nephritic syndrome.

CLINICAL PRESENTATION

Insidious onset of edema. Edema in nephritic syndrome usually begins around the eyes (peri orbital
edema) and later progress to the lower limbs and later generalized with ascites, hydrothorax and
hydrocele. They may also report reduced urine output as edema increases.

They may have dyspnoea due to pleural effusion.

INVESTIGATIONS

As the definition of nephritic syndrome states investigations should be directed to confirm is there
protein in urine? Is there hypoalbuminemia? Is there hyperlipidemia?

1. Urine for protein

2. Serum albumin
3. Serum cholesterol
4. Serum creatinine and blood urea nitrogen- as kidneys are damaged we should check these
parameters
5. Complete blood count to find out if has anemia- because among the proteins lost in urine is
transferin that binds iron, so if lost they end up with iron deficiency anemia.
6. Hepatitis B surface antigen, anti nuclear antibody test and anti streptolysin 0 to find out if there
are any secondary causes.
7. Biopsy if there are any indications such as steroid resistant nephrotic syndrome, atypical age at
presentation (before 12months of age) and nephrotic syndrome with gross or microscopic
hematuria are among the indications of biopsy.

MANAGEMENT

If it’s the initial episode the patient is suffering give prednisolone 2 mg/kg per day (maximum 60 mg) in
single or divided doses for 6 weeks, followed by 1.5 mg/kg (maximum 40 mg) as a single morning dose
on alternate days for the next 6 weeks.

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TERMINOLOGIES OF IMPORTANCE

Steroid dependent- it’s when the disease relapses twice consecutively while on alternate day therapy,
or when it relapses within 2weeks after completion of 12 weeks therapy, then that patient we say has
steroid dependent nephrotic syndrome.

This means the patient completed the first 6weeks of therapy and was improving, but either during
alternate therapy the disease relapses twice consecutively, or after completion of therapy within two
weeks.

Steroid resistant- absence of remission of the disease despite being on daily prednisolone on the first
4weeks. You begin your therapy of daily prednisolone and four weeks pass and there is no improvement
that is steroid resistant.

Frequent relapsers- these have four episodes of relapse in a year, or two in initial 6months.

Infrequent relapsers- they have three or less episodes of illness in a year

COMPLICATIONS

1. Infections- among the proteins lost are immunoglobulins that fight infections.
2. Thrombotic complications due to hypercoagulability. The reasons for hypercoagulability are
immobility in patients with anasarca.
3. Pleural effusion
4. Hypotension
5. Renal insufficiency
6. Electrolyte imbalance

NEPHRITIC SYNDROME
We say it is a HOHO syndrome- the mnemonic. It’s classic presentation is:

H- hematuria

O-oedema

H-hypertension

O-oliguria

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BEE STING AND NEPHROTIC SYNDROME
Bee stings are usually followed by minor local allergic reactions and sometimes anaphylactic or delayed
hypersensitivity reactions. Bee stings may as well cause systemic manifestations of which some of the
reported systemic complications following multiple bee stings include acute renal failure (ARF),
myocarditis, myocardial infarction, centrilobular necrosis of liver, acute encephalopathy, Guillain-Barre
syndrome, vasculitis, disseminated intravascular coagulation, and thrombocytopenia.

The association between bee sting and the development of nephrotic syndrome have been described
however, no reports have revealed presence of bee venom antigens in the glomeruli to signify direct
infiltration of the kidneys.

The components of the bee venom mediate immunological disturbances, with involvement of T-
lymphocytes and their cytokine secretion, influencing the permeability of the glomerular basal
membrane with consequent development of proteinuria.

Spontaneous remission is occasionally seen in patients with nephrotic syndrome after an insect sting.
Most reported cases have good response tocorticosteroid treatment. In my case, oral prednisolone as
well as diuretics were used and the patient showed good response to medications where she attained
remission in 2 weeks time.

There are quite a number of nephrotic syndrome cases that have reported to be induced by bee sting,
whereby some of the cases had early remission and did not have relapse after follow up for some period
of time. Also there are reports of relapse in some cases.

CONCLUSION

Children with insect stings, particularly bee stings, must be closely followed up for multiple problems,
especially immune-mediated complications such as nephrotic syndrome.

Nephrotic syndrome should be diagnosed early and be treated appropriately so as to avoid

complications which may increase mortality in children. Also caution should taken with the use of
medicationsespecially steroids because of their side effects since they are usually taken for a long time.

HENOCH SCHONLEIN PURPURA

It commonly occurs in children. It is IgA mediated. It is usually preceded by upper respiratory tract
infection.

One gets upper respiratory tract infection caused by pathogens whose antigens resemble human body
antigens (molecular mimicry), and as the body makes IgA antibodies to attack the antigens it finds
attacking own body tissues. These antibodies combine with antigens and make immune complexes that
get deposited into different places. If deposited in joints the end result is joint pain. if deposited in the
kidney they get damaged end result is hematuria and proteinuria. If deposited in the GI end result is
blood in stools.

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From the above explanation you can get the clear picture of how the disease will present. The
presentation will be:

• Hematuria (microscopic mostly)

• Proteinuria and edema
• Blood in stools
• Joint pain
• Elevated IgA levels

A mother might report a child had flew or cough prior to the onset of edema and also complains of pain
in the joints and blood in stools. Most recover spontaneously though the treatment is
immunosuppresants such as corticosteroids.

IGA NEPHROPATHY
We have two types of IgA. IgA 1 found in serum and IgA 2 which is on mucosal surfaces and it is the one
referred as secretory IgA.

With IgA nephropathy the problem is IgA 1. The serine and threonine residues in this type of IgA are
usually glycosylated so that they are identified and degraded when their time of existence elapses. In
IgA nephropathy these IgA 1 are abnormally glycosylated that the body cant destroy them normally and
identifies them as foreign, and the body makes antibodies against them called anti-glycan IgG antibodies
that hunt the abnormally glycosylated IgA 1 serine and threonine residues.

The antibodies against the abnormally glycosylated IgA1 combine with the abnormally glycosylated IgA1
to make complexes that go get deposited in the kidney trigger an inflammation and damage the kidneys.

CLINICAL PRESENTATION

Gross or microscopic hematuria

It also develops following infection either upper respiratory tract or GI lining. IgA is found in high
quantity in lungs and GI so infection in these sites may be a trigger.

Patients with IgA they can report getting repeated episodes of gross hematuria following an episode of
upper respiratory tract infection that may last for 2-5days. In between these episodes they may be
getting microscopic hematuria and proteinuria.

TREATMENT

1. Control blood pressure

2. Suppress immunity- corticosteroids
3. If they have non nephritic range proteinuria (less proteinuria compared to the one of nephrotic
syndrome) and hematuria they will benefit from ACE inhibitors.

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HENOCH SCHONLEIN VS IGA NEPHROPATHY

• Both are IgA mediated.

• They all follow infection in the GI or lungs.
• IgA is elevated in both.
• Hematuria and proteinuria is a presentation in both
• Both are a result of default in immune function

The difference is that henoch schonlein purpura not only affects the kidneys but also affects the joints,
skin and GI lining.

ACUTE GLOMERULONEPHRITIS
It’s a nephritic syndrome to simplify it. It presents with HOHO symptoms as I described above in
nephritic. It commonly follows post streptococcal infection of either skin or pharynx.

The mother of a child will report the child having coca cola colored urine (hematuria), oliguria, puffy
eyes and swollen ankles (oedema) and hypertension.

Management- dietary restriction of salt and fluids, treat hypertension and give diuretics if there are
signs of heart failing. Monitor creatinine, electrolytes and blood urea nitrogen.

UTI IN CHILDREN
Older children can tell the symptoms and they will complain of

• Dysuria- pain on urination

• Lower abdominal pain
• Fever
• Frequency of micturition
• urgency

neonates cant explain the symptoms but the mother will report fever, the child is irritable( cries a lot)
and poor feeding. When you observe the child you can find has distended abdomen due to distended
bladder, the kid avoids to urinate maybe because of pain.

Predisposing factors to UTI

• Vesico ureteric reflux

• Obstructive uropathy- born with posterior urethral valves
• Catheterization
• Immunosupressed children as those with malnutrition, HIV.

Investigations- presence of nitrites and leucocyte esterase in urine dipstick done bedside shows its UTI.

Other investigations include urine culture, microscopy, CRP and creatinine plus blood urea nitrogen.

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VESICO URETERIC REFLUX

Retrograde flow of urine from bladder to kidneys.

It can be:

Primary- born with the problem in which there is incomplete closure of the vesicoureteric junction

Secondary – it could be secondary to increased pressure in the bladder leading to forceful opening of
the vesicoureteric junction. What can cause build up of pressure in the bladder? The answer could be:
obstruction beyond the bladder as in children with posterior urethral valves, or other causes could be
neurologic bladder and bowel and bladder dysfunction.

Treatment of UTI Ciprofloxacin 500mg bd for 1week

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NEUROLOGY
CASE- CEREBRAL PALSY
MR. NUMBER: MO7-RR-UU

NAME: RRRR

AGE: 1 YEAR AND 2 WEEKS

SEX: FEMALE

RESIDENCE: MWANANYAMALA

DATE OF ADMISSION: 19/12/2017

DATE OF CLERKSHIP: 19/12/2017

REFERAL FROM: MWANANYAMALA HOSPITAL

REASON FOR REFERAL: FOR FURTHER MANAGEMENT

INFORMANT: HER BIOLOGICAL MOTHER

INTRODUCTION

This is a known patient with cerebral palsy and seizure disorder attending clinic at MNH, was on syrup
Na valproate but stopped on September 2017, Mother does not remember the dose.

CHIEF COMPLAINT

Delayed developmental mile stone since birth

Recurrent startle for 1 year

Poor weight gain 5/12

Recurrent chocking 5/12

Skin lesions 1/52

Bilateral lower limb swelling 3/7

HISTORY OF PRESENTING ILLNESS

The child was born at term by assisted spontaneous vaginal delivery (Vacuum). The mother had
prolonged labor (16 hours) and was very tired. The birth weight was 3.3kg and the child did not cry after
delivery. She was resuscitated at Mwananyamala hospital, then was referred to MNH where she was
kept on ventilator machine for two weeks. The child passed meconium while in the womb and aspirated.
She had difficulty in breathing, no history of bluish coloration of the body, no history of yellowish
coloration of the body. She started crying at the age of 3 weeks. The umbilical cord dropped on day 7 of
life.

Initially she was unable to breastfeed, she was given IV fluid and started to breastfed at the age of 3
weeks.

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No history of any complication during pregnancy, No history of radiation exposure, no history of fever,
she first booked ante natal clinic at 3month of gestation age and made total of six visits. Mother
received iron, folic acid, 2 tetanus toxoid injection, malaria prophylaxis, antihelminthic, HIV tested
negative and VDRL was non reactive.

Since birth the child is unable to control the neck,cannot sit with or without support, cannot say ba or
ma, cannot stand with support, no social smile but the child recognize her mother.

At the age of 2 weeks the child started to present with startle, associated with staring look, no history of
jerking movement, no limb stiffening, no history mouth deviation, no tongue bite, no froth, no urine or
fecal incontinence. After each startle the child looks normal and lasted for one second. She had a total of
5 startle initially then was given phenobarbitone ¼ tablet. However she had some improvement after
initiation of medication. She had 2 startle per week after medication. They changed the treatment to
syrup sodium evaporate on January/2016 and there was no startle any more. However the child had one
episode of startle 1 week after she stopped taking the medication on September.

Since the age of 7 month the child failed to gain weight. The maximum weight gained was 6.6kg at 7
month of age and current the weight is 6kg.The child was exclusively breastfed for 5 months and mother
introduced complementary feeds after she noticed her child poorly gaining weight. She was given
porridge in the morning 6spoons. Porridge contained unrefined maize, blue band, sugar and artificial
milk. Afternoon ugali (four piece small in size) and vegetables with stew of meat/ fish once in a week. At
night was fed Banana and beans with vegetables. No history of loss of appetite howeverthe child did not
improve even with complementary feeding.

The child also presented with recurrent chocking during feeding which was associated with vomiting,
non projectile only contained recently eaten food, non -foul smelling, not blood stained and small in
amount. No history of diarrhoea, no history of abdominal discomfort, no history of fever, no history of
cough, no history of difficulty in breathing.

The child has skin lesion for one week now, which started on the neck, a day later it involved the face,
the limbs and genitalia, No itching, not painful but there is peeling of the skin and ulceration particularly
on the genitalia. No history of medication use prior to the onset of skin lesion and child received all
vaccine appropriate for her age.

3 days now, the child present with bilateral lower limb swelling. Which was gradual in onset and
progressive. No history of difficulty in breathing on lying flat, no history of night awakening due to air
hunger, no history of easily fatigability.

No history of convulsion, no history of loss of consciousness, no history of trauma, no history of

tuberculosis contact, No family history of epilepsy.

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REVIEW OF OTHER SYSTEM

Genital Urinary System. No history of reduced urine output, no history of dysuria, no history of
hematuria.

Ear, Nose and Throat- No history of ear pain, no history of ear discharge, no history of nasal discharge.

Musculoskeletal System- No history of joint swelling, no history of joint pain, no history of bone pain, no
history of muscle pain.

PAST MEDICAL HISTORY

This is the 3rd admission.

1stadmission at Muhimbili National Hospital due to birth asphyxia.

2ndadmission at Muhimbili National Hospital due to abscess on the occipitalwhich was treated and
subsided.

No history of Blood transfusion

No history of surgery

No history of allergy to any medication

PRE NATAL HISTORY

As per HPI

NATAL HISTORY

As per HPI

POST NATAL HISTORY

As perHPI

IMMUNIZATION HISTORY

As per HPI

BCG Scar Present

GROWTH AND DEVELOPMENT HISTORY

As per HPI

FAMILY AND SOCIAL HISTORY

Index 1st born in a family of 1 children.

Her parents they are married and live together.

Mother 21 years old, petty trader and form IIleaver.

Father 27 years old, masonry and attained university level of education.

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GENERAL EXAMINATION

No emergency signs.

Alert, a febrile (36.5oC), thin sparse hair, no bitot spot,no dryness of the cornea, not pale, not cyanosed,
not jaundiced, cortical thumb, no sign of dehydration, no palpable peripheral lymphadenopathy,
bilateral pitting lower limb edema up to the ankle joints.

Hyperpigmented and hypopigmented macules on the skin, with desquamation and ulceration in the
perineum and genitalia.

ANTHROPOMETRIC MEASUREMENT

Weight 6kg Weight Vs Height; between -3SD and -2SD

Height 6kg Height Vs Age; between -3SD and -2SD

MUAC 13cm MUAC Vs Age; - 1SD

OFC 3.8cm OFC Vs Age; < - 3SD

Conclusion: Moderate wasting, Under weight, Stunted, Microcephaly

SYSTEMIC EXAMINATION

CENTRAL NERVOUS SYSTEM

Higher centre: Alert, no active movement

Cranial nerve: pupil equally react to light,follow moving object in all direction, facial symmetry, centrally
located uvula, no difficult in swallowing, move head in eitherdirection, no tongue deviation, no
fasciculation.

Motor

Tone: Hypertonia in both upper and lower limbs

Reflex: Brisk tendon reflex

Power: 3/5

No clonus, no involuntary movement

RESPIRATORY SYSTEM

Respiratory rate; 24 bpm regular

Symmetrical chest movement, normal shape of the chest,

No surgical /traditional scar, symmetric chest expansion, Resonance note on percussion,

Vesicular breath sound heard,

No crepitation.

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CARDIOVASCULAR SYSTEM

Pulse rate 150 bpm, regular rhythm, normal volume, synchronous with other peripheral pulse, non
collapsing pulse.

Warm extremities,

No raised Jugular venous pressure,

No precordial hyperactivity,

No heaves, no thrill,

Apex beat at 4th intercostal space left mid clavicular line.

S1 and S2 heard normal intensity

No murmur.

PER ABDOMEN EXAMINATION

Normal abdominal contour, moves with respiration, no surgical/traditional scar, umbilicus inverted,

Soft abdomen, no tenderness,

Liver, spleen and both kidneys were not palpable,

Tympanic note on percussion,

Normal female genitalia.

PROVISION DIAGNOSIS

Spastic quadriplegic cerebral palsy secondary to birth asphyxia complicated to

Severe acute malnutrition (kwashiorkor type) with Flaky paint dermatoses and

Seizure disorder (Epilepsy).

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INVESTIGATION

INVESTIGATION RESULTS INTERPRETATION

Random Blood Glucose 5.9mmol/L Normal

Full Blood Count

White Blood Cells 14.5k/µL Normal

Absolute Neutrophil 5.15k/µL Normal

Absolute Lymphocyte 8.6k/µL Lymphocytosis

Absolute Eosinophil 0.051k/µL Normal

Absolute Basophil 0.164k/µL Normal

Red Blood Cells 4.52M/µL Normal

Hemoglobin 12.3g/dl Normal

Mean Cell Volume 86fl Normal

Mean Cell Hemoglobin 27.3pg Normal

Red Cell Distribution Width 16.3% Elevated

Platelet 302k/µL Normal

ALT 55U/L Normal

Creatinine 36.6µmol/L Normal

Serum Albumin 18g/L Hypoalbuminemia

Serum globulin 31g/L Normal

Serum Total Protein 47g/L Low serum protein

C-Reactive Protein 5.8mg/L Elevated

SERUM ELECTROLYTE

Sodium 134mmol/L Slightly hyponatremia

Potassium 6mmol/L Hyperkalemia

Calcium 1.96mmol/L Hypercalcemia

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Magnesium 0.75mmol/L Normal

EEG Not done

MANAGEMENT

F75 50mls 2 hourly/48hrs

IV ampicillin 300mg 8 hourly 10/7

IV gentamicin 45mg OD 10/7

T. Na valproate 50mg OD 1/12life long treatment

KMNO 0.001% BD 7/7

Physiotherapy and Occupational therapy

MONITORING

Monitor weight gain, every day before initiation of feeding.

Temperature, respiratory rate, pulse rate and oxygen saturation in room air.

DATE TEMPERATURE RESPIRATORY PULSE RATE WEIGHT(kg) SPO2

RATE

19/12/2017 36.5 30 124 6.0 99

20/12/2017 36.7 30 120 5.9 100

21/12/2017 36.5 31 120 6.0 100

22/12/2017 36.5 28 118 6.0 100

CONSELLING

The mother was counseled on the condition of the child and adherent to medication.

Also nutritional counseling was done on the important of balanced diet and breastfeeding on demand.

Keep the child well covered to prevent hypothermia

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CEREBRAL PALSY
It is the injury that occurs to the immature brain of an infant. The injury most of the time is hypoxic
injury, ie failure of the baby’s brain to get oxygen at delivery. The mother will report either having
prolonged labor, or the baby delayed crying after delivery.

Cerebral palsy by definition is a permanent disorder of movement and posture that is caused by a non-
progressive damage to the immature developing brain leading to a range of activity limitations.

It occurs in approximately 2-2.5 of 1000 live births globally.

The most common reported etiologies are: birth asphyxia, kernicterus, and neonatal infections with
prematurity or low birth weight. In addition to disordered movement or posture, children may have a
range of associated disabilities including intellectual disability, hearing and visual deficits, nutrition,
feeding and swallowing problems, respiratory infections and epilepsy. Epilepsy is the most common
comorbidity of cerebral palsy in Africa.

CLASSIFICATION OF CEREBRAL PALSY

Classification based on motor disability is as follows

1. Spastic type
2. Dyskinetic type
3. Ataxic type
4. Mixed
5. Hypotonic type

SPASTIC CEREBRAL PALSY

As its name it’s a type of cerebral palsy where the baby muscles are so spastic. There are four types
which are

❖ Spastic quadriplegic
❖ Spastic monoplegic
❖ Spastic diplegic
❖ Spastic triplegic

DYSKINETIC CEREBRAL PALSY

Usually follows neonatal jaundice. Children with this cerebral palsy a mother will report the child once
suffered jaundice in early days.

ATAXIC CP

Less common

They have difficulty in quick and precise movements

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CLASSIFICATION BASED ON FUNCTIONAL LIMITATION

This we call it Gross motor function classification

Level 1- walks without limitations

Level 2- walks with limitation

Level 3- walks indoors with support of devices

Level 4- walking ability severely limited even with assistive devices and uses wheel chair.

Level 5- has physical impairment that restricts voluntary control of movement

COMORBIDITIES IN CEREBRAL PALSY

1. Mental retardation
2. Epilepsy
3. Hearing problems
4. Speech and language problems
5. Impaired vision
6. Oromotor problems that present with drooling of saliva and feeding difficulties.
7. Behavioural difficulties.

RISK FACTORS FOR CEREBRAL PALSY

1. Low birth weight and prematurity

2. Maternal infections
3. Maternal medical conditions
4. Multiple births
5. Perinatal insults such as intraventricular hemorrhage and meningitis.

HISTORY IN CP PATIENT

❖ Assess antepartum risk factors: ask if the mother had any fever, rash during pregnancy to find
out if there was maternal infection that could have affected the fetus brain inside the womb
while still immature. Ask if the mother had anemia in pregnancy or hypertension during
pregnancy that could by any means compromise fetus brain blood supply at its immature
period.
❖ Assess intrapartum factors/ during delivery- did the child delay crying, was the child
underweight, did the labor take long.
❖ Assess if there any post delivery causes- did the child have any infections that could have harm
the brain such as meningitis, where the mother will report the child had fevers and maybe
convulsions in his or her early days. Find out if the child had jaundice.

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EPILEPSY
Seizure is a clinical expression of abnormal, excessive synchronous discharge of neurons residing
primarily in the brain cortex.

Epilepsy is when a child has at least 2 unprovoked seizures occurring more than 24 hrs apart.
Unprovoked meaning there is no a cause that can be identified. If the seizure’s cause is known for
example is due to malaria it is no longer epilepsy.

TYPES OF SEIZURE

1. FOCAL (PARTIAL) SEIZURE- only a certain part of the body is convulsing maybe only the arm.
2. GENERALIZED SEIZURE- which we commonly see. The whole body convulsing.

CAUSES OF SEIZURES

1. Structural causes
2. Metabolic causes
3. Immune
4. Infectious
5. Genetic

FEBRILE CONVULSIONS
They are defined as seizure occurring due to high fever in children between 6months and 5years. If not
in that age range we cant call it a febrile seizure.

There are of two types: simple febrile seizures and complex febrile seizures

Characteristics of a simple febrile seizure

• The seizure occurs within 24 hr of the onset of fever

• It lasts less than 15 min
• Usually single per febrile episode.
• Convulsions are generalized. There is no postictal neurological deficit.

Febrile seizures that are focal, prolonged or multiple within the first 24 hrs are defined as complex
febrile seizures.

RISK FACTORS TO DEVELOP FEBRILE CONVULSIONS

1. Fever
2. Infection- viral infections are more frequently associated followed by bacteria
3. Vaccine- some kids develop febrile seizures following administration of measles, mumps, rubella
or tetanus toxoid
4. Genetic susceptibility- ask for family history as you clerk.

Management- lower the temperature.

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RESPIRATORY SYSTEM DISEASES
CASE ACUTE BRONCHIOLITIS
PATIENT’S IDENTIFIATION

Hospital Reg No: M19-XX-RR

Name: YYYY

Age: 6 months old

Sex: Female

Residence: Gongo la mboto

Date of admission: 11th February 2018

Date of clerkship: 11th February 2018

Informant: Biological Mother

Chief complaints: Cough for 1 day

Fever for 1 day

HISTORY OF PRESENTING ILLNESS:

The mother reported that the child experienced a sudden onset of cough that was preceded by a 2 days
history of nasal congestion. The cough was dry, not specific in periodicity and was accompanied by
difficulty in breathing and decreased ability to breastfeed with no history of bluish discoloration of lips,
sweating or easy fatigability on breastfeeding.

The patient also present with fever which was of sudden onset, high grade that started at midnight and
was accompanied with sweating but no history of convulsions, vomiting, diarrhea, ear discharge, skin
rashes, crying on urination or change in urination frequency.

Review of other system:

Musculoskeletal system: No history of joint pain.

Past medical history:

This is the 2nd admission, 1st admission was at Pemba when she was 2 months old due to pneumonia
was treated and discharged.

She has no history of blood transfusion, no history of surgery, no history of any known drug or food
allergy.

Ante natal history:

Mother booked at 12 weeks Gestation age, made 4 visits, received hematinics, antihelminths, malaria
prophylaxis and 2 Tetanus toxoid doses. HIV and VDRL tests were non-reactive.

She had no any illness or problem during pregnancy.

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Natal history:

Delivered by Spontaneous vaginal delivery, a term baby weighing 3.5kg. The baby cried immediately and
started to breastfeed. Discharged 1 day after delivery.

Post natal history:

Cord dropped after 6 days. No history of yellowish or bluish discoloration of the skin. No history of any
neonatal illness.

Immunization history:

From her RCH Card no 1, the patient has received all vaccines according to her age as per IVDP.

Growth and developmental history:

Can sit without support

Can hold objects by palmar grasp

Vocalizes with coos

Conclusion: Normal developmental milestones

Dietary history:

Exclusively breastfed for 5 months.

Currently feeds on porridge made from maize flour and groundnuts, more than 3 times a day and
breastfeeds on demand.

Conclusion: Diet is adequate in quality and quantity.

Family and Social history:

The patient is the 2nd born in a family of two children.

The first born is 3 years old and is doing well.

Parents are married and live together.

Mother is 20 years old, a housewife with primary level of education.

Father is a tailor, also with a primary level of education.

She has a positive history of asthma from her paternal aunties (2 aunties).

PHYSICAL EXAMINATION

General Examination:

Emergency signs: Nasal flaring, fast breathing, audible wheezing, head nodding, SPO2 87% on
room air

Conclusion: Severe respiratory distress, was kept on Oxygen therapy 2L/min.

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The patient was alert, febrile (38.00 C), not jaundiced, not pale, not cyanosed, some palmar pallor, no
palpable peripheral lymph node, no lower limb edema.

Anthropometric measures:

Weight: 7kg Weight/age: Median

Height: 67cm Weight/height: -1SD< Z< Median

MUAC: 14.5cm Height/age: Median < Z< 1SD

HC: 45.5cm MUAC/age: Median < Z< 1SD

HC/age: 2SD< Z< 3SD

Conclusion: Good nutritional status

SYSTEMIC EXAMINATION

Respiratory system:

Respiratory rate was 44 breaths/minute, normal chest shape, no any scar or marks, moves with
respiration, had lower chest wall in drawing, no any swelling, bilateral symmetrical chest expansion.

Resonant percussion note on percussion.

Vesicular breath sounds with bilateral wheezes and crackles more on the right and left infra scapular
region were heard on auscultation.

Central Nervous system:

Higher centers

Patient was alert

Cranial Nerves

She could fix and follow, move eyes in all directions, has facial symmetry, can hear, can swallow, can
move her head in all directions.

Conclusion: Cranial nerves are intact

Motor examination:

Normal muscle bulkiness

Normal tone in all joints in both upper and lower limbs

Normal muscle power (3/5) in both upper and lower limbs

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Per abdomen:

Normal abdominal contour, moves with respiration, umbilicus was inverted, no distended veins, no any
scar or marks.

On palpation was soft, non-tender, no palpable mass, the liver and spleen were not palpable, the
kidneys were not bimanually palpable.

Tympanic percussion note and normal bowel sounds on auscultation.

Normal external female genitalia.

Cardiovascular system:

Pulse rate was 156 beats/minute, regular, good volume, synchronous with other pulses.

No precordial bulging or hyperactivity, no heaves or thrills

Apex beat at 4th intercostal space left mid clavicular line. S1 and S2 were heard with no added sounds.

Summary:

6 months old female, presenting with fever and cough foe one day. These symptoms were accompanied
with difficult breathing and decreased ability to breast feed. On examination she had severe respiratory
distress on oxygen therapy, febrile, audible wheezes and auscultated wheezes and crackles with some
palmar pallor.

Provisional diagnosis: Acute bronchiolitis

Differential diagnosis: Severe Pneumonia

INVESTIGATIONS

Complete blood count:

White blood cells – 12.0K/uL Normal

Abs Neutrophil – 6.29K/uL Normal

Neutrophils – 52.5% Normal

Abs Lymphocytes – 5.03K/uL High

Lymphocytes – 41.9% High

Abs monocytes – 0.524K/uL Normal

Monocytes – 4.38% Normal

Abs Eosinophils – 0.115K/uL Normal

Eosinophils – 0.963% Low

Abs Basophils – 0.023K/uL Normal

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Basophils – 0.193% High

Red blood cells – 3.21M/uL Normal

Hb – 11.0g/dl Normal

HCT – 32.0% Normal

MCV – 74.3fl Normal

MCH – 25.1pg Normal

MCHC – 33.7g/dl Normal

RDW – 16.9% High

Platelets – 335K/uL Normal

Final diagnosis: Acute bronchiolitis

TREATMENT:

1) Oxygen therapy 2L/min

2) Nebulized 4mls of 3% hypertonic saline solution 4 hourly for 24 hours

3) IV Ceftriaxone 560mg OD for 10 days

4) Nasal gastric tube inserted for feeding

The patient was kept on Oxygen therapy on arrival at Emergency department. She was nebulized with
salbutamol with no relief. In the ward she continued with the Oxygen therapy and was nebulized with
4mls of 3% hypertonic solution, 4 hourly. Mother encouraged to expose the baby by reducing the
amount of clothes she wore, so as to reduce her body temperature. Nasal gastric tube was kept so as to
encourage feeding where she received 130mls of porridge alternating with breast milk every 2 hours.

MONITORING AND PROGRESS IN THE WARD.

Patient was monitored for respiratory rate, Oxygen saturation and temperature throughout the night.
The oxygen saturation was ranging between 87- 90% on Oxygen but the following day it improved to
97% on Oxygen and on the 3rd day the patient was weaned from oxygen therapy with SPO2 of 96% in
room air. Her respiratory rate and temperature too, improved on the next day. On the second day post
admission the audible wheezes subsided, head nodding and nasal flaring also subsided.

On the 3rd day the patient had greatly improved with no signs of respiratory distress, she was afebrile
and could feed well without the nasal gastric tube hence it was removed. The patient continued with
antibiotic therapy and was discharged home two days later with oral Amoxicillin for 5 days.

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PROGNOSIS AND COUNSELLING

The prognosis of the patient is good. This is due to early health seeking behavior that led to early
detection and proper management of the illness. Also due to course of the illness itself that it can be
self limiting but with proper supportive management.

The mother was counseled on when to return immediately to the hospital after discharge, that is when
the child develops fever, becomes sicker, develops cough with difficult breathing or is unable to feed or
breastfeed.

DISCUSSION OF THE CASE

ACUTE BRONCHIOLITIS

Bronchiolitis is most common lower respiratory tract infection in infants, caused by virus. As in the
above case the patient is 6 months old and hence the diagnosis is more likely. The presentation is
usually preceded by nasal congestion or runny nose as how the patient in the case above presented.
Cough, fever and wheezing follow afterwards and become very severe within a short period of time as
what happened in the above case. Prompt seeking of care with proper management ensures early
recovery. The management requires close monitoring of the patient’s vital signs especially oxygen
saturation, respiratory rate and temperature as how the patient above was monitored to when she was
stable.

However its treatment has had a variable course evolving with time. In some literatures its reported
that, no medical treatment has shown to improve important clinical outcomes, such as length of
hospital stay, use of supportive care or transfer to an intensive care unit. However these patients are
still hospitalized and offered treatment most of which include supportive care with no specific
treatment to the underlying causative agent.

Currently there have been controversies on the management with saline solution. While some
literatures reported no change in improvement with use of 0.9% normal saline or 3% saline solution,
some literatures have proven that 3% saline solution is more effective. Nebulized hypertonic saline
may reduce hospital stay by 10 hours in comparison to normal saline for infants admitted with acute
bronchiolitis. In the above case the patient received nebulized hypertonic solution (3% saline solution)
and her symptoms improved and there was shortening of overall hospital stay.

There have also been the question on the use of short acting bronchodilators such as Salbutamol.
These short-acting inhaled bronchodilator therapy such as albuterol or salbutamol has not shown any
important clinical benefits in the treatment of bronchiolitis. Also epinephrine and systemic
glucocorticoids are not recommended for the treatment of children with bronchiolitis.

And regarding antibiotics, are not recommended unless there is concern about complications such as
secondary bacterial pneumonia. However antibiotics may more frequently be warranted due to
concurrent bacterial infections in infants with severe disease. All patients requiring hospitalization are
assumed to have a severe disease. As in the case above the patient had very acute symptoms that
presented with other symptoms that suggested a bacterial pneumonia co infection hence there was a
role of antibiotics early on during management.

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Oxygen should be administered in hypoxic infants with bronchiolitis, and administered via nasal cannula.
Also ensuring of hydration by encouraging breastfeeding and feeding to weaned patients. Monitoring of
vitals especially oxygen saturation, respiratory rate and temperature is also of very great importance.

PNEUMONIA
It is the inflammation of the lung parenchyma. It can be caused by virus or bacteria. Most episodes of
pneumonia are caused by bacteria.

CAUSES

1. Aspiration from the oral pharynx. During sleeping especially in elderly one can aspirate and draw
some bacteria to the airways. This can happen with people who have decreased level of
consciousness.

2. Inhalation.

3. Hematogeneous spread of bacteria from elsewhere.

4. Contiguous extension from pleural.

Clinical features of pneumonia

1. Cough
2. Fever
3. Fast breathing
4. Difficulty in breathing

Diagnostic criteria for severe pneumonia

Cough or difficulty in breathing, fever and at least one of the following

1. Lower chest wall in drawing

2. Nasal flaring
3. Grunting
4. Fast breathing (respiratory rate of 50 or more in children less than 1yr, for children 1-5yrs
respiratory rate of 40 or more)

Above features plus severe respiratory distress, inability to feed, cyanosis→very severe pneumonia

Diagnostic criteria for non severe pneumonia

Cough or difficulty in breathing plus fast breathing and fever in absence of features of severe
pneumonia.

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MANAGEMENT

Pharmacological Treatment:

Non-severe pneumonia : Amoxicillin 25 mg/kg 8 hourly for 5 days plus Paracetamol suppositories 10-
15mg/kg [if there is fever].

Severe pneumonia: Ampicillin 50 mg/kg IV/IM every 6 hourly AND Gentamicin (7.5 mg/kg IV/IM once a
day) for 5 days; then, If child responds well, complete treatment at home or in hospital with Amoxicillin
30 mg/kg 8 hourly for 7 days.

Very severe pneumonia: Ampicillin 50 mg/kg IV/IM every 6 hours And Gentamicin (7.5 mg/kg IV/IM
once a day) for 5 days; then, if child responds well, complete treatment at home or in hospital with
Amoxicillin (40 mg/kg12 hourly 10 days

Alternatively, Ceftriaxone 80 mg/kg IV or IM once daily for 10 days.

ASTHMA
Bronchial asthma is a disease characterized by an increased responsiveness of the airway to various
stimuli. It manifests by wide spread reversible narrowing of the airway. The common symptoms are
shortness of breath, wheezing, chest tightness and cough.

During an attack the muscles around the airways tighten making them narrower, lining of the airways
becomes inflamed and thick mucus is produced that blocks the airway.

Things that lead to asthmatic attacks are called triggers. Some of the triggers include viral infections,
domestic or occupational allergens (house dust mites, pollen and cockroach), exercise, stress, tobacco
smoke and drugs such as beta blockers, aspirin and NSAIDS. Triggers cause an attack in genetically
susceptible individuals.

The main investigations in the diagnosis of asthma are the lung function tests. Spirometry should be
done to determine the ratio of FEV1 to FVC which is always reduced due to reduced FEV1.

Management of asthma includes identifying the exacerbating factors, provide pharmacological

treatment to relieve the symptoms and lastly educate the parent and the patient on the nature of the
illness and the exacerbating factors and on how to avoid them.

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CASE-ASTHMA
NAME OF THE PATIENT: YYYYY

HOSPITAL REGISTRATION NUMBER: M17-BB-VV

AGE: 11Years

SEX: female

RESIDENCE: University of Dar-es-salaam

DATE OF CLERKSHIP: 9/12/2017

DATE OF ADMISSION: 9/12/2017

INFORMANT: Biological mother

She is a known asthmatic since 1 year old and has been possessing her own Sulbutamol inhaler since 5
years of age.

Referred from the dispensary of the university of Dar-es-salaam due to failure to respond to treatment

Main complaints are: cough-3/7

Difficulty in breathing-1/7

Chest tightness-1/7

History of presenting illness

The patient has been experiencing cough for the past three days that was gradual on onset, dry in
nature with no specific periodicity. No known aggravating or relieving factors. Not associated with chest
pain, fever, awareness of heart beats or easy fatigability.

Two days later the she developed difficulty in breathing that was gradual on onset and progressively
worsening, with no known aggravating or relieving factors.

It was associated with whistling sounds while breathing in air. The mother reported the child appeared
to use so much effort while breathing in air.

Along with that the child started experiencing chest tightness that was gradual on onset and
progressing. The mother reported that the child complained feeling her chest heavy and like its being
compressed. It was associated with increased effort of breathing, body weakness, and inability to feed
or drink. The child could not finish a sentence while talking due to air hunger. No history of bluish
discoloration of the skin, no history of nasal congestion, throat itching or ear discharge prior to the
present illness.

The only known triggers to her condition by the mother are weather changes, especially during cold
seasons, and dust. The mother reported that at their school the child has frequent exposure to pollen
from flowers because there are so many flowers at their school.

The child has been getting attacks irregularly and less frequently, can finish up to three months without
a single attack. The child has her own sulbutamol inhaler that she uses when she gets an attack.

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In the course of her illness she did try use her own sulbutamol inhaler but it did not give a relief and the
mother decided to rush the child to the dispensary where she was nebulized with sulbutamol and given
injection hydrocortisone and then discharged home after getting a relief. At midnight the symptoms
recurred and the mother returned the child to the same dispensary where this time she was nebulized
and given aminophylline injection but still there was no relief and was then transferred to MNH.

Review of other systems

Central Nervous System- There is no history of headache, convulsion or loss of consciousness.

Musculoskeletal system- There is no history of joint pain, swelling or back pain.

Genitourinary – There is no history of change of frequency of urination, urgency or painful urination.

Urine amount and color is normal.

Gastrointestinal- There is no history of abdominal pain, diarrhea or vomiting.

Past medical history

Has history of several previous admissions due to similar problem.

She has also been treated as an outpatient several times for asthma.

Has history of surgery at 4years of age and nasal polyps were removed.

No history of blood transfusion. No known drug or food allergy.

Pre-natal history

Booked at 12 weeks of gestation age and made 5 visits.

Received antihaelminths (mebendazole tabs), malaria prophylaxis (SP tabs) and hematenics.

No history of illness during pregnancy

Natal history

She was delivered at term by Spontaneous vaginal delivery with birth weight of 3.8kg.

Cried and sucked immediately.

Cord dropped within the first week after delivery.

Postnatal history

No history of yellowish discoloration of skin or eyes.

No bluish discoloration of the skin.

Has a history of omphalitis while 6 days of age and was treated with antibiotics.

Immunization history

RCH card 1 was not seen. The mother reported the child received all the vaccines as per the
immunization and vaccine development program. BCG scar was there.

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Developmental mile stones

Currently attending school, she is in standard six. Performing on average at school and interacts well
with peers of same age and sex.

Dietary history

She feeds regularly on ugali, rice, vegetables, beans, milk and fruits. She eats four times a day and
always finishes a plate on her own. Diet is of good quality and quantity.

Family history

The father is a lecturer at university of Dar es salaam and the mother a petty trader.

She is the last born in a family of four, and the first born has just finished university. The rest of the
siblings are studying and are fine.

There is a family history of asthma on the paternal side where the father and the paternal grandmother
are known to have asthma.

On examination

Alert, not febrile (temperature=36.8c), not jaundiced, not pale, no finger clubbing, not cyanosed , no
palpable peripheral lymphadenopathy and has no lower limb edema. Anthropometrics readings were:
weight=33kg, height=146cm: BMI=15.5 (falls between median and -1SD) normal.

Respiratory system

Tachypnoeic with respiratory rate of 33 breaths/minute. Bilateral symmetrical chest expansion, with
normal elliptical chest shape. No visible scars or traditional marks. Trachea centrally located. Resonant
note on percussion and wheezes heard on auscultation with increased duration of expiration in
comparison to inspiration. Basal crepitations were heard bilaterally.

Cardiovascular system.

Tachycardic with radial pulse rate of 127beats/min, regular, good volume, none collapsing, synchronous
with contra lateral radial, brachial and carotid pulse. Blood pressure was 110/80mmhg. Apex beat 5th
inter coastal space mid-clavicular line and the beats are regular. No heaves or thrills, S1 and S2 normally
heard. There was no added sound.

Per abdomen

Not distended, no traditional or therapeutic marks, and moves with respiration. On palpation it is soft,
non tender, no palpable mass or organ. Tympanic note heard on percussion. Bowel sounds audible.

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Central nervous system examination

Higher centers were normal- she was oriented to time place and person. Speech was normal and both
short and long term memory were intact. No hallucinations or delusions.

Cranial nerve examination- can read letters placed a meter in front, can see in all four visual fields,
pupils were reactive to light. Her eyes could follow my moving finger in all directions, facial sensory
component is intact, can chew, has no facial asymmetry, can hear, can swallow, uvula is centrally
located, can shrug shoulders and protrude the tongue.

Motor examination- normal muscle bulkiness and tone in all four limbs. Normal gate, normal deep
tendon and superficial reflexes. Power is 5/5 in all limbs.

Sensory examination- sensation was intact, both soft and pin prick sensation.

Coordination- finger to nose test AND heel to shin test were coordinated.

Provisional diagnosis- Bronchial asthma with a differential of pneumonia.

INVESTIGATIONS

Full blood picture was done and the results were WBC=12.7, NEUTROPHIL=11.8, LYMPHOCYTES=0.523,
RBC=4.93, HB=13.2g/dl, MCV=83.9, MCHC=32 and PLATELETS=227.

C reactive protein was done too and it was elevated to around 298.

MANAGEMENT

The patient was put on oxygen on arrival at Emergency department. In the ward she was nebulized with
salbutamol 4mg 6hourly for 24 hours. She was given intravenous hydrocortisone 100mg 8hourly/24hrs
and then tabs prednisolone 10mg OD for next 5days was prescribed.

MONITORING

Respiratory rate and SPO2 was monitored. The patient’s condition improved so quickly and the
respiratory rate on the next day when I saw her was 22breaths in a minute. The symptoms and signs too
were closely monitored to note any deterioration or improvement, and wheezes were reduced. She was
no longer on oxygen and could breath normally.

PROGNOSIS

The patient’s condition improved so quickly and was discharged on the day after with instruction to
attend clinic after 2weeks. She was discharged with sulbutamol inhaler to use 5mg 6hourly for one
month. Budesonide inhaler 200mcg 6hourly for 1/12. Tabs amoxicillin 625mg 8hourly for seven days.

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DISCUSSION
The literatures show asthma as one of the common chronic lung diseases and mostly affect children. The
commonest symptoms are wheezes, chest tightness, shortness of breath and cough. In this particular
case, the patient is a child 11 years of age and presented with all the typical symptoms of asthma which
are cough, chest tightness, wheezes and shortness of breath. Its not always common however to find a
similar scenario in all kinds of patients. Some may present with only one or two of the mentioned
symptoms. Wheezes and nocturnal cough are a common presentation in many patients. A study was
done to determine the prevalence of wheezes and related symptoms of asthma among school children
in Addis Ababa Ethiopia, and 27.3% were found to have nocturnal cough, 27.2% had exercise induced
wheeze and 18.2% reported to have had wheezes at least once in the last 12months. This proves
wheezes and nocturnal cough are a common presentation.

Asthma is familial, meaning there is a genetic component of it. This fact is reflected in my patient too,
as it was reported that her father and paternal grandmother are all known to have asthma. Despite the
genetics, studies have shown the environmental triggers play a very big role in the etiology. Some of
the common triggers are viral infections in young children, and exercise in older children. Other
triggers are such as weather changes, irritants such as tobacco, and environmental allergens such as
pollen and house dust mites. In this particular patient the parent has only been able to notice two
triggers which are exercise and weather changes although in this particular episode it’s the weather that
the mother suspects. There have been light rains on some days recently with changes in the day
temperature. At the child’s school there are a lot of flowers that could also be a source of triggers
through its pollens though the mother is less aware about this.

Management of asthma from the Tanzania standard treatment guidelines is based on the severity. In
this particular patient she had a severe attack which was characterized by tachypnoea, tachycardia and
unable to complete a sentence while talking.

The management of a severe attack includes putting a patient at a semi sitting position, administer
oxygen 5l/minute, sulbutamol inhalation 2-4 puffs to a maximum of 20 puffs every 20-30 minutes and
every 4hourly in 24-48 hours after being stabilized. Finally its injection hydrocortisone 5mg/kg 6 hourly
until stable then shift to tabs prednisolone 1-2mg/kg for 3-5days.

In this particular patient management begun on arrival at Emergency department. She was put in semi
sitting position, given oxygen 5l/min and treatment as per guideline was followed that is use of inhaled
bronchodilators and steroids in the management of severe asthmatic attack. The patient’s recovery was
quick and was discharged after two days stay in hospital, though her condition improved drastically
within 24 hours of stay in hospital. She was left for the next 24 hours for observation.

The patient is a student and due to this illness has not been able to participate normally in classes, so
this entails that asthma is a burden both to the patient and to the parent. The mother who brought the
child had to postpone her usual daily activities to spend two days with her child in hospital. This burden
of the disease can be avoided if parents and the patients are told about the nature of illness, and
identify possible triggers so as to avoid recurrent attacks. Counseling on drug adherence, possible side
effects of medications is also a necessary component in the management of asthma in children.

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CONCLUSION

Asthma remains to be a common disease affecting children and presents with symptoms of diffuse
airway obstruction. The diffuse airway obstruction in asthma is reversible and can resolve spontaneously
or in response to treatment. Environmental triggers are involved in the etiology of asthma in genetically
susceptible individuals. The diagnosis of asthma can be reached based on the clinical symptoms,
investigations are only done in doubtful conditions. Management targets the basic three underlying
mechanisms which are increased mucus secretion, inflammation and bronchospasms. In my patient the
clinical presentation of the illness was typical and management was as per the Tanzania standard
treatment guideline.

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MENINGITIS
Meningitis is an inflammatory disease of the leptomeninges, the tissues surrounding the brain and
spinal cord. The meninges consist of three parts: the pia, arachnoid, and dura mater. Meningitis reflects
inflammation of the arachnoid mater and the cerebrospinal fluid (CSF) in both the subarachnoid space
and in the cerebral ventricles. Meningitis is a clinical syndrome that may be self-limited or life-
threatening and may be the result of numerous infectious as well as noninfectious processes. Since the
clinical manifestations of the meningitis syndromes may be indistinguishable, it is prudent to assume
that all patients with meningitis have a bacterial infection until proved otherwise. Suspected bacterial
meningitis is a medical emergency, and immediate diagnostic steps must be taken to establish the
specific cause so that appropriate antimicrobial therapy can be initiated. The mortality rate of untreated
bacterial meningitis approaches 100 percent and, even with optimal therapy, morbidity and mortality
may occur.

Acute bacterial meningitis has two patterns of presentation. In the first, meningitis develops
progressively over one or several days and may be preceded by a febrile illness. In the second, the
course is acute and fulminant, with manifestations of sepsis and meningitis developing rapidly over
several hours. The rapidly progressive form is frequently associated with severe brain edema.

Most patients with bacterial meningitis present with fever and symptoms and signs of meningeal
inflammation (nausea, vomiting, irritability, anorexia, headache, confusion, back pain, and nuchal
rigidity). These findings are often preceded by symptoms of upper respiratory infection. However, the
clinical manifestations of bacterial meningitis are variable and nonspecific; no single sign is
pathognomonic.

On treatment of bacterial meningitis the antibiotics are used. The choice of antibiotic to be used is
governed by two principles which are, first the agent(s) used must be bactericidal against the infecting
organism and must be able to penetrate past the blood-brain barrier to reach a sufficient
concentration in the CSF. An awareness of the most likely pathogens, knowledge of local susceptibility
patterns, and assessment of the degree of urgency are necessary to devise an optimal empiric treatment
strategy. Once culture results are available, treatment should be modified to follow the guidelines for
specific pathogens. Persistent neurologic sequelae are common in children who survive an episode of
bacterial meningitis. The most common sequelae include hearing loss, seizures, intellectual disability,
and spasticity and/or paresis.

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CASE- MENINGITIS
Hospital Reg No: M19-VX-YZ

Name: MNYMX

Age: 4 month

Sex: Male

Residence: Ilala

Date of admission: 05th June, 2018

Date of clerkship: 05th June, 2018

Informant: Biological Mother

Introduction: This patient is the first twin. He was self-referral from home, came direct to Emergency
medicine department before transferred to ward B.

Chief complaints

Cough for 4 days

Difficulty in breathing for 4 days

Fever for 2 days

Vomiting for 1 day

HISTORY OF PRESENTING ILLNESS:

Mother reported her child to be doing fine until 4 days ago when he started experiencing gradual onset
of cough which was non-productive with no specific periodicity. There were no any aggravating or
relieving factors but was associated with difficulty in breathing which was more during the night with no
any abnormal whistling sound, asthma in the family, history of contact with TB patient or excessive night
sweat.

Two days later the patient started developing gradual onset of high grade fever which was progressively
increase with time with no specific periodicity. Fever was relieved temporarily with paracetamol with no
any aggravating factors. Mother reported the child to have inconsolable cries and back neck pains which
he could cries when touched at the back of the neck but there were no history of convulsion, loss of
consciousness or head trauma. Fever was associated with one episode of non-projectile vomiting which
contains recently eaten breast milk and was non – bilious with no foul smelling and there were no
history of change in bowel frequency. Mother reported the child to feed poorly since the onset of
symptoms.There were no history of skin rashes, ear or nose discharges,pain during micturition or
change in micturition frequency.

In the course of illness patient was treated in peripheral hospital with IV antibiotics with no
improvements before being referred to MNH. At emergency blood for investigations was taken, MRDT
was negative and antibiotic was initiated.

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REVIEW OF OTHER SYSTEM:

Musculoskeletal system: No history of joint pain or joint swelling.

PAST MEDICAL HISTORY:

This is second admission; first admission was when the child was 3 weeks old due to neonatal jaundice
which he was treated for 3 days before being discharged’

The child has never been transfused or operated and has no history of allergies to foods or medications.
No history chronic illness such as TB or chronic use of medications.

ANTE NATAL HISTORY:

Mother booked at 4 month of Gestation age, made 4 visits, and received haematinics, antihelminths,
malaria prophylaxis and 2 Tetanus toxoid doses. HIV test was negative and VDRL test were non-reactive.

Mother was normal tensive throughout pregnancy period with no any complications.

NATAL HISTORY:

Labor lasted for 5 hours and rupture of membrane was spontaneously. The baby was delivered by
spontaneous vaginal delivery, at 7 month weighing 1.4kg. This was the first twin, the other twin
weighing 2.0kg. Both babies cried immediately and started to breastfeed, and were discharged 3 day
after delivery.

POST NATAL HISTORY:

Cord dropped after 6 days. There were history of yellowish discoloration 3 weeks after birth which
lasted for 2 days with no history of bluish discoloration. No history of any neonatal illness.

IMMUNIZATION HISTORY:

Patient has received BCG and OPV-0 and the BCG scar is present in the right shoulder..

GROWTH AND DEVELOPMENTAL HISTORY:

Gross motor: Patient is able to control neck.

Fine motor: grasping at 4weeks,

Vision: started following objects at 6 weeks,.

Speech and hearing: He can hear sound

Social behavior: started smiling at family members at 7th weeks

Conclusion: Normal developmental milestones

DIETARY HISTORY:

The baby is on exclusive breast milk. Breastfeed up to 10 times per day but currently the child is feeding
poorly.

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FAMILY AND SOCIAL HISTORY:

This is the first born together with his second twin. The other twin is doing fine. Mother (24 years) is a
petty trader and form four leaver while father (29 years) is long distance bus driver, he is form four
leaver also. They married and living together in a rented house with 3 rooms. Mother and father both
are non-alcohol drinkers and non-smokers and there is no history of familial diseases such as asthma.

PHYSICAL EXAMINATION

General Examination:

The patient was lethargic, febrile (38.7 C), bulging anterior fontanel, normal hair color and texture, nasal
flaring, not pale, not jaundiced, not cyanosed, not dehydrated,nuchal rigidity, neck stiffness, negative
Kerning and Brudzinski sign, no finger clubbing, no skin rashes, no peripheral lymph node enlargement,
no lower limb edema.

Vital signs

Respiratory rate; 54 breath/minute

SP02; 94% at room air.

Pulse rate; 120 breaths/minute

Temperature; 38.7 0C

Anthropometric measures:

Weight: 4.3 kgWeight/age: -2 SD

Length; 55cm Weight/length: Between median and -1 SD

MUAC: 13cm Length/age: Between -2 and -1 SD

HC: 39cm MUAC/age: Between median and -1 SD

HC/age: Between median and -1 SD

Conclusion:Mild underweight, not wasted, mild stunted with normal head circumference.

Mild malnourished.

SYSTEMIC EXAMINATION

Central Nervous system:

Higher centers: Patient was lethargic

Cranial Nerves: Pupil were equally reactive to light, can moves eyes in both directions, has facial
symmetry, can hear, can swallow,

Motor examination: normal muscle bulkiness, normal tone in all joints in both upper and lower limbs, no
involuntary movements, muscle power not tested, normal superficial and deep reflexes.

Sensation and coordination were not able to be tested.

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Respiratory system:

Respiratory rate was 80 breaths/minute which was tachypnea, severe lower chest wall in drawing, no
any scar or marks, moves with respiration, no any swelling, had bilateral symmetrical chest expansion.

Resonant note on percussion.

Vesicular breath sounds on auscultation with bilateral crackles and wheezing on the inframammary and
infra-clavicular regions.

Cardiovascular system:

Pulse rate was 132 beats/minute, regular, good volume, non-collapsing synchronous with other pulses.

No engorged neck veins

No raised JVP

No precordial bulging or hyperactivity, no parasternal or apical heaves or thrills

Apex beat felt at the 4th ICS left along the mid-clavicular line.

First and second heart sounds were heard with no added sounds.

Per abdomen:

Normal abdominal contour, moves with respiration, umbilicus was inverted, no distended veins, no any
scar or marks.

On palpation was soft, non-tender, no palpable mass, the liver and spleen were not palpable, the
kidneys were not bimanually palpable.

Tympanic percussion note and normal bowel sounds on auscultation.

Normal external male genitalia.

SUMMARY:

This is a case of SS, 4 month old boy who presents with cough, difficulty in breathing and fever which
was associated with back neck pain and on examination patient had respiratory distress, bulging
anterior fontanel and nuchal rigidity.

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Provisional diagnosis:

Diagnosis Points to support Points against

1. Meningitis • High grade fever • No history of convulsion

• Neck pain and stiffness • Nohistory of skin rashes

• Vomiting • Negative Kerning and

Brudzinski sign
• Bulging anterior
fontanel

• Nuchal rigidity

• Lethargy

2. Severe pneumonia • Cough • No grunting

• Difficulty in breathing • No history of

convulsions.
• Tachypnea

• Fever

• Nasal flaring

• Severe lower chest wall

in drawing

3. Complicated Malaria • High grade fever • No history of

convulsions.
• Vomiting
• No history of jaundice
• Lethargy
• MRDT negative (EMD)
• Respiratory distress

Differential diagnosis

1. Septicemia

2. Brochiolitis

Investigations.

1. Laboratory investigations

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Full blood picture:

Parameter Value Range Interpretation

White blood cells 20.4 5 - 26

Neutrophil (Abs) 13.2 2-7 High

Neutrophils 64.7 40-80

Lymphocytes (Abs) 5.38 0.6-3.4 High

Lymphocytes 26.3 20-40

Monocytes (Abs) 1.42 0-0.9 High

Monocytes 6.94 2-10

Eosinophils (Abs) 0.223 0-0.7

Eosinophil 1.10 1-6

Basophils (Abs) 0.192 0-2

Basophils 0.941 0.02-0.1 High

Red blood cells 4.24 3 -7

Hemoglobin 11.1 11.1-22

HCT 37.7 30 -75

MCV 89.1 72-120

MCH 26.1 25-37

MCHC 29.3 29-37

RDW 22.2 11.6-14.8 High

Platelets 587 100-550 High

Blood slide for Malaria; Reveals no parasite

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CSF analysis;

Macroscopically; - Normal opening pressure, yellow/turbid in color.

Cell count; - RBCs – 10/mm3,

Biochemistry; - Glucose- 2.12 mmol/L, Protein- 1.2 g/L.

Microscopy; - no organism seen on all stains.

Culture; - No growth

C-Reactive Protein-40.3 (indicates acute phase infections)

Renal function test-Serum createnine-36.7U/L, blood urea nitrogen-3.4 U/L (normal renal function)

Serum electrolytes-Sodium-137mmol/l, Potassium 4.7mmol/l and Chloride-98mmol/l.

Blood culture- revealed no growth

HIV 1 & 2 antibodies-negative.RBG- 4.3mmol/L

2. Radiological investigations

Chest X- Ray; - Reveals infiltration in the left and right lower and middle lobes

Final diagnosis;

1) Bacterial meningitis

2) Severe pneumonia

Treatment:

Supportive therapy

• Oxygen therapy 2L per minute through nasal prongs

• Nasal gastric feeding 40mls, 2 hourly until the child is able to feed

• Nebulization with 3% normal saline alternating with salbutamol 1.25mg, 6 hourlyfor 24 hours

Medical therapy

• IV Ceftriaxone 250mg, 12 hourly for 7 days.

• IM Dexamethasone 1.5mg OD for 7 days

• IV Paracetamol 50mg PRN (when temp is above38.5 0C).

After treatment with above medications for 3 days without improvement the ceftriaxone was changed
into;

• IV Meropeneum 36mg, 8 hourly for 10 days

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MONITORING AND PROGRESS IN THE WARD.

During the first 3 days since admission the child the child had improvements on respiratory distress in
which he had no nasal flaring, mild chest wall in drawing and was having oxygen saturation of 97% in
room air. But was still lethargic with spikes of fever and was breast feeding poorly. On the fourth day
ceftriaxone was shifted to Meropeneum and on the fifth day the fever started to subside but was still
lethargic and using MGT for feeding. On day seven post admission the child started breastfeeding using
mouth although was poor so he continues using NGT. On day 10 post admission the child was having no
respiratory distress and was feeding normally using mouth and he was having normal temperature.

PROGNOSIS AND COUNSELING

The patient had good prognosis since the meningitis and severe pneumonia was treated early and
symptoms disappears after treatment.

Mother was involved in every step of management of his child and showed full cooperation, mother was
told what was child suffering from, which kind of medications the child was receiving and the prognosis
of the child also the sequaleane of meningitis which could occur late in life. On the day of discharge the
mother was counseled in the properly way of breastfeeding the child and was educated about
importance of vaccination as its very much related in the cause of meningitis also the danger signs and
was told to return to clinic after two weeks or any time when the child’s condition become worse.

DISCUSSION

Bacterial meningitis especially acute is more common in young children who had not vaccinated or
with previous treated or untreated lung infections for instance pneumonia as in our case. The
commonest organism being Streptococcus pneumonia, Haemophilusinfluenza and Neisseria
meningitidis.

Patients with meningitis usually presents with triad of fever, neck stiffness and mental status changes
but is not always that children with meningitis will presents with all features. High suspicion of bacterial
meningitis in patients with above symptoms who had predisposing features such as recent exposure to
someone with meningococcal meningitis, recent infection (pneumonia), penetrating head trauma,
CSF otorrhea or rhinorrhea and in patients with cochlear implants.

Acute bacterial meningitis is a medical emergency which require immediate diagnostic steps like taking
history, physical examination, blood tests and lumbar puncture to be done initiating treatment as soon
as possible. Ideally lumbar puncture should be done before initiating treatment but for most of the
cases received at our referral hospital, patient has been in different course of antibiotics and it’s difficult
to get the positive results of culture and sensitivity of causative organism.

So in most of our patients the treatment is empirical which has disadvantage of causing more resistance
to antibiotics and delaying in providing the appropriate medications.

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CONCLUSION

Meningitis is medical emergency which require immediate diagnosis and treatment. Lumbar puncture
should be performed in every child in whom the diagnosis of meningitis is suspected unless its
contraindicated and appropriate antibiotics should be started immediately according to sensitivity of
local strains and changed according when the culture results are available or when the patient is not
responding to initial therapy.

NEONATAL MENINGITIS

Fever plus convulsion in a neonate number one diagnosis should come to your mind is meningitis.
Neonates may have non specific clinical presentation such as excessive crying and poor feeding.

The sequence of events until a child ends with meningitis are: focal infection (example pneumonia,
UTI)→then bacteria enter the blood→sepsis→since blood goes everywhere it can send the bacteria to
the meninges too and finally meningitis.

So any neonate/ child with meningitis always find out what was the start. In the case presented above
pneumonia was a starting point and from there bacteria spread to reach the meninges.

The other way bacteria can reach the meninges is in children with spina bifida maybe, where the
meninges are exposed to the environment.

Most of the times the infection spreads hematogenously to meninges from distant foci, e.g.
pneumonia, empyema, pyoderma and osteomyelitis

Complications of meningitis in a new born could be cerebral palsy, hydrocephalus, intellectual disability
etc.

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HIV MANIFESTATIONS IN SEVERE ACUTE MALNUTRITION
Malnutrition refers to deficiencies, excesses or imbalances in a person’s intake of energy and/or
nutrients. The term malnutrition covers 2 broad groups of conditions. One is ‘under nutrition’—which
includes stunting (low height for age), wasting (low weight for height), underweight (low weight for age)
and micronutrient deficiencies or insufficiencies (a lack of important vitamins and minerals). The other is
overweight, obesity and diet-related non-communicable diseases (such as heart disease, stroke,
diabetes and cancer).

Severe acute malnutrition is defined as the presence of edema of both feet’s or severe wasting (weight
for height/length < -3sd or Mid upper circumference <115mm).

Acquired immunodeficiency syndrome (AIDS) is a term which applies to the most advanced stages of HIV
infection. It is defined by the occurrence of any of more than 20 opportunistic infections or HIV-related
cancers.

Both AIDS and SAM impairs ones immune system and makes the individual susceptible to infection thus
majority of clinical features overlap and makes it difficult to diagnose HIV infection in a child with Severe
acute malnutrition based on the clinical findings.

The case presentation below aims to identify features suggestive of HIV in children with SAM.

CASE PRESENTATION
PATIENT REGISTRATION NO; M 18-JJ-HH

NAME; MMMX

AGE; 15 MONTHS

SEX; FEMALE

RESIDENCE; MABIBO

ADMISSION; 11/ 02/ 2018

CLERKSHIP; 12/02/2018

WARD; MAKUTI B

INFORMANT; BIOLOGICAL MOTHER

A SELF REFERRAL FROM HOME AND IT IS A RE-ADMISSION WITHIN 1 MONTH OF DISCHARGE.

A newly diagnosed child with PAIDS one month ago diagnosed by DNA PCR and started on ART
(ABACAVIR, LAMIVUDINE AND LOPINAVIR/RITONAVIR). The baseline CD4+ counts and the baseline viral
load count was not measured hence not known.

This being a re-admission as a month ago the child was admitted due difficulty in breathing and poor
weight gain, during this admission, chest x ray and gastric aspirate lavage were taken for AFB staining
and they were all negative hence the child was treated as having PCP and completed a high dose of Co-
trimoxazole for 3 weeks but did not continue with the Co-trimoxazole for prophylaxis afterwards.

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Due to poor weight gain she was started on F75 then F100 then given Plumpy Nuts as the highest weight
gain before admission was 6kg.

On discharge the difficulty in breathing had subsided and she had gained weight from 6kg to 8kg. she
was discharged with plumpy nuts to continue feeding the child at home and the child could not finish
even one sachet and the mother added cow milk to the diet.

Currently the patient has lost weight to 6.3kg from 8kg on discharge one month ago. And she is now
admitted due to fever, difficulty in breathing and generalized body swelling.

MAIN COMPLAINTS

1. Fever 5/7

2. Difficulty in breathing 4/7

3. Generalized body swelling 3/7

HISTORY OF PRESENTING ILLNESS

5 days ago the patient presented with a low grade fever, gradual on onset with no specific periodicity, it
was not aggravated by anything but relieved by sponging the child. It was not associated with
convulsions, loss of consciousness, neck pain neither was it associated with ear discharge, nasal
discharge, sneezing nor associated with diarrhea, vomiting, abdominal discomfort, yellowish
discoloration of the eyes, lips or soles, no joint pain, no joint swelling, no muscle pain.

4 days ago the patient also presented with difficulty in breathing, gradual in onset, it was associated
with a dry cough with no specific periodicity and fast breathing, it was not associated with noisy
breathing, bluish discoloration of the lips, nail beds, palms and soles, excessive night sweats, easy
fatigability on exertion. No history of recent open TB contact, no history of asthma in the family.

3 days ago the child developed a generalized body swelling, gradual in onset, and it begun with the
feet’s then involved the legs then the abdomen moving towards the face with no specific periodicity, it
was not associated with crying on urination, increased urine frequency with normal color and urine
volume.

REVIEW OF OTHER SYSTEMS;

As per History of presenting illness.

PAST MEDICAL HISTORY;

- No history of any known allergy to foods or drugs

- Has a history of blood transfusion once on the previous admission, where the mother reported
that she had a low HB but doesn’t remember how much was given

- No history of surgery

- No history of chronic illness such as epilepsy, sickle cell anemia

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ANTENATAL HISTORY;

- Booked at 12 weeks of Gestational Age and made a total of 4 visits

- She only received SP for IPT but did not receive hematinic, anthelminthic and she received 2
tetanus toxoid injections during this pregnancy.

- Mother tested for HIV and she was PMTCT-1, VDRL was non-reactive

- During this pregnancy the mother had episodes of fever but no history of anemia, hypertension,
diabetes mellitus and rashes.

NATAL HISTORY;

- Labor lasted for 6 hours

- She had a spontaneous rupture of membranes and she delivered by Spontaneous vaginal
delivery, a term baby with a birth weight of 3kg

- The baby cried immediately and started sucking within one hour of birth.

POSTNATAL HISTORY;

- Discharged after 24 hours

- There was no history of yellowish discoloration, no history of bluish discoloration, no history of

fever

- The cord dropped on the seventh day of life

GROWTH AND DEVELOPMENTAL HISTORY;

- She was able to control the neck by 4 months of age.

- She started sitting with hand support by 5 months and without support by 6 months

- But at 9 months the child started crawling but due to the illness she stopped and currently she is
not crawling or standing by herself due to the illness. But she can sit without support now.

- she could follow moving objects at 6 weeks

- She could transfer objects from hand to hand by 7 months.

- She could turn to the direction of sound by 4 months

- She could say da, ba, ka by 6 months of age

- She could smile at 2 months of age

- She starts recognizing her mother from 4 months of age

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CONCLUSION; he has normal growth and development as per her age. The illness has affected her
growth and development as the child is not crawling or standing as before and she can only sit with
support. Thus the illness has caused regression of the attained milestones.

IMMUNIZATION HISTORY;

- She has received BCG, OPV0, 1, 2, 3, Pentavalent 1, 2, 3, PCV13 1, 2, 3, Rota 1, 2 as reported by

the mother.

- He has received all the vaccines at the right time with the exception of Measles at 9 month as
the child was very sick as reported by the mother.

- The growth pattern could not be assessed as the RCH card 1 the mother did not have it at the
hospital but the mother reported that the maximum weight attained by the child was 7.3kg.

DIETARY HISTORY;

- She was exclusive breastfeed for 6 months.

- She was started on mashed potatoes and banana mixed with fish/meat and vegetables, she was
fed 4 to 5 times per day and breastfeeding on demand

- Since she was 2 months the mother reports of recurrent chest infections approximately once
every month which interfered with the child’s appetites and the child was not feeding properly.

- The diet is inadequate in quality and quantity also.

FAMILY AND SOCIAL HISTORY;

- She is the 1st child living with her mother and father.

- The mother is 27 years old a house wife, HIV infected and on medication (TENOFOVIR,
LAMIVUDINE and EFAVIREN).

- The father is 30 years old a policeman and HIV infected on medication (TENOFOVIR,
LAMIVUDINE and EFAVIREN).

- Both the mother and father are non-smokers

- They live in a well-ventilated house

- They drink boiled water and they have flush toilets.

GENERAL EXAMINATION

No emergency signs.

Alert, afebrile (37.3%), tachypnoeic on oxygen, not jaundiced, not cyanosed, no angular stomatitis,
normal oral mucosa, some palmar pallor, has finger clubbing, no peripheral lymph nodes palpable,
pitting lower limb edema, facial edema.

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DEHYDRATION STATUS

Alert, no sunken eyes, drinks water normally, skin pinch goes back normally.

No signs of dehydration.

NUTRITIONAL STATUS AND ATHROPOMETRIC MEASUREMENTS

Weight = 6.3kg W/A= < -3sd

Height = 69 cm W/H = between -3sd and -2sd

MUAC = 11.5 cm

Conclusion; severe underweight, moderate wasting.

SYSTEMIC EXAMINATION

RESPIRATORY SYSTEM

- RR = 52 breath/minute, spo2 = 92%

- Normal chest contour with equal chest expansion

- Resonant percussion note

- Vesicular breath sounds heard, no added sounds

- Lower chest wall in drawing

PER ABDOMEN EXAMINATION

- normal abdominal contour and moves with respiration

- No distended veins, no any birth mark, no any traditional mark, no any surgical scar, inverted
umbilicus.

- Non tender on both superficial and deep palpation.

- Liver, spleen and kidneys were not palpable.

- Normal bowel sounds heard

- Normal external female genitalia.

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CARDIOVASCULAR SYSTEM

- PR = 155 beats/minutes, warm extremities, capillary refill < 3 seconds, normal volume, rhythm,
radial to radial and radial to brachial synchronous and non-collapsing pulse.

- No distended neck veins

- No precordial hyperactivity, no precordial bulging

- Apex beat 4th at mid clavicular left intercostal space.

- s1and s2 heard, normal and no murmurs heard.

CENTRAL NERVOUS SYSTEM

HIGHER CENTERS

- alert, oriented to her mother

CRANIAL NERVES

- she could see using both eyes

- she could moves eyes in both direction

- she can clench her teeth

- can sense prick sensation over the forehead and cheeks

- she has symmetrical facial expression

- she can swallow and the uvula is centrally located

- She can shrug her shoulder and can turn head in opposite direction against resistance.

- She has a centrally located tongue with no fasciculation’s.

MOTOR FUNCTION.

UPPER LIMBS LOWER LIMBS

RIGHT LEFT RIGHT LEFT

BULKNESS Normal Normal normal normal

TONE Normal Normal normal normal

POWER 3/5 3/5 3/5 3/5

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REFLEXES

- Normal biceps and triceps reflexes

- Normal knee jerk reflexes

- Normal ankle reflexes

- Normal plantar reflexes.

The spine was normal.

SUMMARY

YYYXX, female, 15 months, from Mabibo, a newly diagnosed child with PAIDS one month ago on ART
(ABACAVIR, LAMIVUDINE AND LOPINAVIR/RITONAVIR) and PCP that was treated and now Co-
trimoxazole prophylaxis, with the baseline CD4+ and Viral load not known. A re-admission from one
month ago due to difficulty in breathing and poor weight gain. Currently presented to us with fever 5/7,
difficulty in breathing 4/7 and generalized body swelling 3/7.

On general examination; conscious, afebrile (37.3c), tachypnoeic on oxygen, not cyanosed, no angular
stomatitis, normal oral mucosa, some palmar pallor, finger clubbing, no peripheral lymph node, pitting
lower limb edema and facial edema.

On systemic examination; respiratory rate of 52 (tachypnoeic), lower chest wall in drawing.

PROVISIONAL DIAGNOSIS

1. PAEDIATRICS AIDS STAGE IV WITH,

a. SEVERE ACUTE MALNUTRION (SAM) (below are the reasons why I thought of this
diagnosis)

- Body swelling involving the legs, abdomen and face

- Mid upper arm circumference = 11.5cm

- Poor weight gain

b. LYMPHOID INTERSTITIAL PNEUMONIA (below are the reasons why I thought of this
diagnosis)

- Difficulty in breathing

- Cough

- Finger clubbing

- Fast breathing

- Lower chest wall indrawing

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DDX; PNEUMONIA

PULMONARY TUBERCULOSIS

c. MODERATE ANAEMIA SECONDARY TO HIV INFECTION/NUTRITION

- Some palmar pallor.

INVESTIGATIONS AND RESULTS

1. Full blood picture

2. Blood for culture and sensitivity

3. Urinalysis for microscopy and culture and sensitivity

4. Viral load and CD4+ counts

5. Chest x ray

6. Gastric aspirate for AFB and gene x-pert.

7. C-reactive protein

8. Iron studies.

FULL BLOOD PICTURE RESULTS

WBC Ab Ab Ab monocytes AbEosinophils Ab Basophils

Neutrophils lymphocytes

6.67 k/ul 2.34 k/ul 3.77 k/ul 7.66 k/ul 0.005 k/ul 0.035 k/ul
Normal normal normal normal normal normal

RBC HB HCT MCV MCH MCHC RDW PLT

3.4 m/ul 8.4 g/dl 26.8% 78.9 fl 24.9 pg 31.5 g/dl 24.0% 74.7
normal LOW normal normal normal normal increased. LOW

LIPID PROFILE RESULTS

CHOLESTROL TRIGLYCERIDE LDL HDL

3.09 mmol/l normal 2.05 mmol/l HIGH 2.47 mmol/l normal 0.21 mmol/l LOW

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LIVER FUNCTION TEST

- Total protein 66 g/l normal

- Albumin 30 g/l slightly decreased.

SERUM ELECTROLYTES

K+ NA+ CL- CA+

4.1 mmol/l normal 130 mmol/l slightly 103 mmol/l normal 2.01 mmol/l normal
decreased

ECHO RESULTS

Severe pulmonary hypertension (90mmHg), dilated pulmonary artery pulmonary regurgitation grade
1, small pericardial effusion (at atrium level) = 4mm, no pleural effusion.

FINAL DIAGNOSIS

PAEDIATRICS AIDS STAGE IV WITH,

a) SEVERE ACUTE MALNUTRION (SAM)

b) LYMPHOID INTERSTITIAL PNEUMONIA

DDX; PNEUMONIA

PULMONARY TUBERCULOSIS

c) MODERATE ANAEMIA SECONDARY TO HIV INFECTION/NUTRITION

d) SEVERE PULMONARY HYPERTENSION.

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MANANGEMENT

1. F75 65mls 2 hourly for 24hours via NGT.

2. Tab co-trimoxazole 240mg once daily.

3. Tab prednisolone 10 mg once daily for 2/52

4. Oxygen therapy 2 litres/minute till the child’s saturation is above 95% at room air

5. Continue with antiretroviral drugs (ABACAVIR, LAMIVUDINE AND LOPINAVIR/RITONAVIR)

6. Intravenous Ampicillin 315mg 6 hourly 7/7

7. Intravenous Gentmycin 50 mg 7/7

8. Tablet Aldactone 6.25mg once daily

9. Tablet Enalapril 0.625mg once daily

10. Tablet Sildenafil 6.25mg 8 hourly

11. Tablet Lasix 5mg once daily

IN HOSPITAL COURSE, OUTCOME AND FOLLOW-UP

In the following four days the child was on oxygen all the time and still presenting with difficulty in
breathing, lower chest wall in drawing and some fever spikes and she was not feeding well but also the
edema was not improving.

On the fifth day the child started having improvements, with no fever spikes, breathing spontaneously
without oxygen support, subsiding edema and feeding well.

On the ninth day the child was started with F100 100mls 3hrly, the child was eating well and with a daily
increase of 10 mls with each feed until the maximum of 115 mls 3 hourly was attained. And the child is
progressing very well and on medication.

Currently she is has been discharged and she is taking plumpy nuts (Ready to use therapeutic food) 2
sachets in 24 hours. She finishes all.

PREVENTION AND COUNSELLING

• The mother is to make sure that the child takes the ART as required so as to improve the
immune function of the child which will prevent further complication of HIV infection with SAM
being included.

• The mother should encourage the child on taking the plumpy nuts as required for the time
prescribed without mixing with any other food at first then there after ensuring a balanced diet
is given to the child.

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 • Proper hygiene during food preparation at home, proper environmental sanitation with proper
use of toilet this is to reduce the risk of infections to the child due to weak immune functions.

• Psychological counselling of the mother about the illness of her child and that if she adhere to
the instructions give on medication, feeding the child will thrive very well.

• The mother should return to the hospital as soon as she sees her child not gaining weight, loss
of appetite or with other medical complications.

• Attend cardiac clinic as instructed without missing.

DISCUSSION

The case presented is a child with severe acute malnutrition, kwashiorkor type and with Pediatrics
AIDS also diagnosed one month with the use of ELISA during PITC as recommended by WHO that all
children found to have severe acute malnutrition should undergo PITC.

From the features highly associated with HIV infection in severe acute Malnourished children that is
adenopathy, oral candidiasis and severe wasting from the studies I have read none of which was
present in the child presented which might be explained by the fact that the child is already on ART
and thus the delay of this clinical manifestations.

Finger clubbing was present in the child presented which is among suggestive clinical manifestations of
HIV in a child with severe acute malnutrition as shown in different literatures.

From the case presented the child had anemia of 8.4g/dl which correlates with the study conducted in
Zimbabwe which showed that anemia of 8.3g/dl is highly indicative of HIV infection in a child with
severe acute malnutrition compared to 8.8g/dl in uninfected children with SAM.

Pitting lower limb edema and facial edema were not among the clinical features suggestive of HIV in
severe acute malnourished children in any study and the child presented also had kwashiorkor which
was not common in HIV with SAM rather Marasmus was more common in HIV with SAM.

Other clinical features that were highly indicative of HIV in children with SAM such as
Lymphadenopathy, chronic suppurative otitis media were not present in the case presented but this
does not rule out HIV infections.

CONCLUSSION

Some clinical features have been identified to be predictive of HIV seropositivity and can be useful as
indicators to prompt further investigation and/or referral in resource limited settings where HIV is highly
prevalent. This would aid in the early detection and comprehensive management of the HIV seropositive
child with SAM. As for the child I presented despite the clinical features he had, he was still diagnosed
late with the aid RDT but currently he is receiving appropriate management.

The prognosis is guarded due to the presence of a chronic illness to the child as the child may present
with complication associated with illness or the medication she is using currently.

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NEONATOLOGY
CASE-NEONATAL JAUNDICE
Hospital Reg No: M22-MM-WW

Name: Baby of XYXY

Age: 9 DAYS old

Sex: MALE

Residence: MSASANI

Date of admission: 6th JUNE 2018

Date of clerkship: 11th JUNE 2018

Informant: Biological Mother

Referral from Amana hospital; 4 days post admission before clerkship

Chief complaints: yellowish coloration of the body for 2 days

HISTORY OF PRESENTING ILLNESS

The mother reported delivering a baby at 32 week of gestation age at hospital. It was a male baby and it
weighed about 2kg,and cried immediately. She reported that the baby delayed to suck and was able
suck milk after two days

On the sixth day she noticed gradual onset of yellowish coloration of the skin first at the face, which
progressively deepened and spread to the chest. However the mother denied any change of stool color,
any change in the color of the urine or any loss of consciousness or convulsion that the baby developed.
The baby had history of high grade fever during the episode that was present all the time, slightly
decreased by exposing the baby. However no any cord smell or discharge that was reported. The baby
was put on phototherapy.

The mother booked at 3month of gestation, made a total of 5 visits and was given hematenics which
she took the whole pregnancy period, ant malarias at first and second visit, tetanus toxoid injections
thrice at first, second and third visit and ant helminths twice though she couldn’t tell at what visit she
received the second dose, the first dose was at first visit. She was screened for HIV, VDRL and Glucose
level which were all normal. Blood grouping was done and found to be group O, fathers group is not
known but the baby was found to be group B+.

No history of use of assistive devices during delivery. No family history of sickle cell and there was no
reported blood transfusion done.

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REVIEW OF OTHE SYSTEMS

CARDIOVASCULAR: No history of bluish discoloration

RESPIRATORY SYSTEM: No history of difficulty in breathing

No history of cough

No history of nasal flaring

CENTRAL NERVOUS SYSTEM: Normal anterior fontannele

Weak sucking reflex

Weak grasp reflex

Good moro reflex

MUSCULOSKELETAL SYSTEM: No history of joint pain.

PAST MEDICAL HISTORY:

unremarkable.

IMMUNIZATION HISTORY:

From her RCH Card no 1, the patient has received OPVO and BCG vaccines according to his age as per
IVDP.

GROWTH AND DEVELOPMENTAL HISTORY:

Baby has good Moro reflex

Good palm grasp reflex

Baby is in flexed posture

Conclusion: Normal developmental milestones

DIETARY HISTORY:

Currently the baby is exclusively breastfed3 hourly for 24 hours.

Conclusion: Diet is adequate in quality and quantity.

FAMILY AND SOCIAL HISTORY:

The patient is the first born in a family.

Parents are married and live together.

Mother is 26 years old, a housewife with ordinary level of education.

Father is a heavy truck driver, also with ordinary level of education.

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PHYSICAL EXAMINATION

General Examination: the baby was lying in a cub, sleepy, had yellowish coloration at the chest and face;
no Nasal flaring, not cyanosed, not pale no lower limb edema, normal fontanelles, Saturating at 90% on
room air

Anthropometric measures:

Weight: 2.2kg

Height: 43cm

HC: 40.5cm

NB; THE BABY IS BELOW 6 MONTHS

SYSTEMIC EXAMINATION

Per abdomen:

Inspection: normal abdominal contour, moves with respiration,cord not droped,dry no any smells, no
any scar or marks.

Palpation soft, non-tender, no palpable mass, the liver was 2cm below right costal margin, the kidneys
were bimanually palpable.

Tympanic percussion note

Normal bowel sounds on auscultation.

Normal external female genitalia.

Respiratory system:

Respiratory rate was 52 breaths/minute, normal chest shape, no any scar or marks, moves with
respiration, no any swelling, bilateral symmetrical chest expansion.

Resonant percussion note on percussion.

Vesicular breath sounds bilaterally; no wheezes or crackles heard on auscultation.

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Central Nervous system:

Primitive Reflexes: normal Moro reflex

Normal sucking reflex

Normal grasp reflex

Cranial Nerves; could react to light

Motor examination:

Normal muscle bulkiness

Normal tone in all joints in both upper and lower limbs

Normal muscle power (3/5) in both upper and lower limbs

Cardiovascular system:

Pulse rate was 156 beats/minute, regular, good volume, synchronous with other pulses.

No precordial bulging or hyperactivity, no heaves or thrills

Apex beat at 4th intercostal space left mid clavicular line.

S1 and S2 were heard with no added sounds.

Summary:

9 days old male, presenting with progreesive yellowish discouration of the body which was associated
with fever. On examination the baby had tinge yellowish coloration over the face and body (chest).

Provisional diagnosis: EARLY ONSET NEONATAL JAUNDICE SECONDARY TO

1. NEONATAL SEPSIS
2. ABO INCOMPATIBILITY

Differential diagnosis: CONGENITAL BILLIARY ATTRESIA

INVESTIGATIONS

Complete blood count:

White blood cells – 12.0K/uL Normal

Abs Neutrophil – 6.29K/uL Normal

Neutrophils – 52.5% Normal

Abs Lymphocytes – 5.03K/uL High

Lymphocytes – 41.9% High

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Abs monocytes – 0.524K/uL Normal

Monocytes – 4.38% Normal

Abs Eosinophils – 0.115K/uL Normal

Eosinophils – 0.963% Low

Abs Basophils – 0.023K/uL Normal

Basophils – 0.193% High

Red blood cells – 3.21M/uL Normal

Hb – 11.0g/dl Normal

HCT – 32.0% Normal

MCV – 74.3fl Normal

MCH – 25.1pg Normal

MCHC – 33.7g/dl Normal

RDW – 16.9% High

Platelets – 335K/uL Normal

C Reactive protein -6 high

Total Bil – 95.3mg/dl HIGH

Direct Bil – 22.8mg/dl HIGH

-DCT – Negative

-Blood group B +ve

FINAL DIAGNOSIS: EARLY ONSET NEONATAL JAUNDICE 2º NEONATAL SEPSIS

TREATMENT:

1) Oxygen therapy 2L/min

2) Ampiclox 220mg 12hourly for 7 days

3) Gentamycin 6mg once daily for 7 days

4) Nasal gastric tube inserted for feeding 10mls EBM 3hourly for 24 hours

5) monitoring vitals(temperature, oxygen saturation )

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DISCUSSION OF THE CASE

Neonatal jaundice is a yellowish coloration of the white part of the eyes and skin in a newborn baby due
to high bilirubin levels. Symptoms may include excess sleepiness or poor feeding. As in the case above,
the baby showed poor feeding. Other complications may include seizures, cerebral palsy, or
kernicterus, that were not present in the case presented above.

Male sex and low birth weight are among the risk factors. The baby was a male and had low birth
weight; this has been implicated as risk for developing jaundice in the studies I went through; Of babies
that are born early about 80% are affected, and shows male predominance

The baby presented with sepsis which complicated to jaundice, in some literature several cases resulted
from red blood cell breakdown, liver disease, infection, hypothyroidism, or metabolic disorders
(pathologic jaundice).

Concerns, in otherwise healthy babies, occur when levels are greater than 308μmol/L (18 mg/dL),
jaundice is noticed in the first day of life, there is a rapid rise in levels, jaundice lasts more than two
weeks, or the baby appears unwell. In those with concerning findings further investigations to
determine the underlying cause are recommended.

The need for treatment depends on bilirubin levels, the age of the child, and the underlying cause. The
baby above was kept on antibiotics and phototherapy for two days which subsided.as in the literature;
treatment included more frequent feeding, phototherapy, or exchange transfusions.

In those who are born early more aggressive treatment tends to be required. Physiologic jaundice
generally lasts less than seven days. The condition affects over half of babies in the first week of life.
Compared to the case, the baby developed jaundice in the fourth day of life.

Conclusion

Generally, neonatal jaundice is not a rare findings in our hospital. According to the guideline of
neonatal care at Muhimbili National Hospital, Rh incompatibility is the common cause of neonatal
jaundice. In the studies done in Nepal the findings showed that ABO incompatibility, Rh incompatibility
and G6PD deficiency were the most common risk factors for jaundice, followed by idiopathic jaundice.

NEONATAL JAUNDICE
Jaundice simply is yellowish coloration of skin and mucous membranes when bilirubin is high in blood.
Normally bilirubin is there but for it to cause jaundice in a new born it should be above 6mg/dl.

Jaundice can be

1. Physiological – which is normal or,

2. pathological

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PHYSIOLOGICAL JAUNDICE

Bilirubin has an advantage in a new born but when not in excess, since at birth these babies lack anti
oxidants like vitamin E, catalase and bilirubin is a potent anti oxidant.

QUESTION: How do you know it is physiological jaundice?

ANSWERS

It doesn’t appear on day 1. In a healthy baby rate of production of bilirubin is less than 5g/dl in a day, so
it’s hard for you to notice jaundice in day 1 on a healthy new born.

Secondly it disappears in 1 week in a term baby, or in 2weeks in a pre term infant. As soon as the liver
begins its function fully jaundice goes away, because the physiological jaundice is due to the fact a new
born baby’s liver can’t function to match the speed of hemolysis at first.

QUESTION: Why is there physiological jaundice?

ANSWERS

1. Low UDPGT activity at birth an enzyme that conjugates bilirubin

2. Kids are born with relatively high red cell mass. So when they are born there is massive
hemolysis.
3. Absence of intestinal flora and slow intestinal motility- In the presence of normal gut flora,
conjugated bilirubin is metabolized to stercobilins and excreted in the stool. Absence of gut
flora and slow gastrointestinal (GI) motility, both characteristic of the newborn, cause a build up
of conjugated bilirubin in the intestinal lumen, where mucosal β-glucuronidase removes the
glucuronide molecules and leaves unconjugated bilirubin to be reabsorbed back into the
blood(enterohepatic circulation).
4. increased enterohepatic circulation of bilirubin.

PATHOLOGICAL JAUNDICE

Jaundice within 24hrs. if jaundice appears on day 1 that should alarm you. It is not normal to have
bilirubin levels above 6mg/dl in day 1.

Causes could be either

1. overproduction of bilirubin
2. defect in conjugation or
3. failure to clear conjugated bilirubin- as in biliary atresia.

OVERPRODUCTION

over production could be either due to

1. hemolytic causes
2. non hemolytic causes

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hemolytic causes can be

• immune mediated- as in ABO blood group incompactibilities.

• Non immune mediated- inherited conditions as hemoglobinopathies such as sickle cell diseases,
enzymopathies as glucose 6 phosphate dhydrogenase deficiency and membranopathies as
spherocytosis.
• Bacterial or viral sepsis.

Non hemolytic causes- are such as increased entero hepatic circulation in conditions like bowel
obstruction where bilirubin cant be excreted in stool and is re absorbed.

DEFECTIVE CONJUGATION

In conditions like criggler najar syndrome, hypothyroidism in which metabolism is low.

PREMATURITY
Any baby born before 37 completed weeks of gestation.

There are a lot of reasons that lead to a woman delivering before time.

The reasons could be fetal or maternal issues that may have led to the baby to be born before time.

Fetal causes: congenital malformations, and twin pregnancy.

Maternal risk factors that can lead to pre term delivery, the ones you need to ask in history:

• Complications in pregnancy such as pre eclampsia, premature rupture of membranes. Ask the
mother and report in your history if she had hypertension in pregnancy or ruptured membranes
early where they will report seeing a gush of clear fluid per vagina before term.
• Maternal abnormalities such as cervical incompetency could be a reason. Usually such women
will report previous pregnancy loses.
• Maternal medical illnesses such as appendicitis, acute pyelonephritis. As was there fever before
delivering.
• Maternal stress
• Maternal smoking habits.

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COMPLICATIONS OF PREMATURITY

1. Respiratory complications include:

• Apnea of prematurity
• Respiratory distress syndrome
• Bronchopulmonary dysplasia
2. Cardiovascular complications include:
Low blood pressure
Patent ductus arteriosus
3. Gastro intestinal complication- necrotizing enterocolitis
4. Repeated infections
5. Intraventricular hemmorhage
6. Hypothermia
7. Hypoglycemia
8. Hematological complication- anemia of prematurity
9. Retinopathy of prematurity.
10. Feeding problems and poor weight gain

LOW BIRTH WEIGHT

Any baby born with weight below 2500grams is said to have low birth weight.

What causes a baby to be born with low birth weight?

Anything that will compromise nutrient delivery to the baby inside the mothers uterus will result to low
birth weight. Think of any factor that can compromise nutrient delivery to the child such as:

1. Maternal malnutrition
2. Maternal infections
3. Pregnancy induced hypertension that can compromise blood supply to fetus, and blood is the
one that carries nutrients.
4. Intra uterine infections- TORCHES.

COMPLICATIONS OF LOW BIRTH WEIGHT

• Feeding difficulties
• Intraventricular hemorrhage
• Temperature instability
• Respiratory problems- apnea and respiratory distress

HYPOXIC ISCHEMIC ENCEPHALOPATHY

Is simply birth asphyxia, failure to get oxygen to the brain of a baby during delivery. The result is
neonatal encephalopathy which is disturbed neurological function manifested by reduced level of
consciousness or seizures

HIE is under a broad topic of perinatal asphyxia. HIE it is specific for brain effects of perinatal asphyxia.

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PERINATAL ASPHYXIA

It is simply compromised oxygen supply to the baby either while it is still in the mother’s uterus, during
delivery or immediately after delivery.

To be professional we define it as “compromised placental or infant’s pulmonary gaseous exchange”.

Severe hypoxia leads to anerobic glycolysis and lactic acid production.

Asphyxia can occur before (anterpartum), during (intrapartum) and after delivery (post partum).

56-80% occur intrapartum.

Antepartum events contribute about 4-20% and these are such as maternal hypertension that in one
way could have compromised blood supply to the fetus and compromise oxygen supply.

Intrapartum events could be

• Fetal umbilical cord circulation is interrupted as in cord prolapsed

• Inadequate placental perfusion is in abruption placenta

SYSTEMIC EFFECTS OF PERINATAL ASPHYXIA

1. Myocardial ischemia
2. Acute respiratory distress syndrome
3. Pulmonary edema as a result of myocardial dysfunction
4. Feeding intolerance- presenting as abdominal distention, delayed gastric emptying and gaging. It
is due to transient disturbance in intestinal motor activity.
5. Necrotizing enterocolitis- in asphyxia body directs to vital organs and supply to intestine is
reduced as a result ischemia and necrotic intestines. So necrotizing enterocolitis develops due to
alteration in blood flow following perinatal asphyxia.
6. Hepatic dysfunction- transaminases are elevated several days after birth. And since the liver
makes glucose, its dysfunction can make baby’s end with hypoglycemia. Other presentations
could be cholestatic jaundice.
7. Hematological abnormality- thrombocytopenia.
8. CNS effects→HIE

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HIE SCORE (THOMPSON SCORE)

Sign 0 1 2 3

Tone Normal Hypertonia Hypotonia Flaccid

Consciousness Normal Hyperalert, stare Lethargic Comatosed

Convulsions Normal Infrequent <3 in a day Frequent >2 day

Posture Normal Fisting Strong, distal flexion Decerebrate

Moro reflex Normal Partial Absent

Sucking reflex Normal Poor Absent +/- bites

Grasp reflex Normal Poor Absent

Respiration Normal Hyperventilation Brief apnea Apnea

Fontanelle Normal Full not tense Tense

HIE is defined by a THOMPSON SCORE above 5 one hour after birth

NB: the score is derived from the nine aspects of neurological examination of infants with HIE.

Long term complications of HIE

1. Cerebral palsy
2. Epilepsy/ seizure disorder
3. Hearing impairment
4. Blindness or severe visual impairment
5. Cognitive impairment
6. Low psychomotor development

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BREAST FEEDING
Someone can annoy you in the ward in front of a mother breastfeeding with a question, do you think
the technique of this mother is correct? If you do not know the technique you will fail to answer.

Techniques of breastfeeding involves four things

1. Position of the mother-

• A mother should assume any position that is comfortable to her.
• The mothers back should be supported and should not be leaning against the child.
2. Baby’s position.
• Whole baby’s body should be supported.
• Baby’s head and trunk should lie in one line
• Baby’s body should be turned towards the mother
3. Attachment- signs of good attachment are:
• Baby’s mouth should be wide open
• All nipple and most of the areolar should be inside baby’s mouth
• Baby’s chin should touch the breast
• Lower lip of the baby should be everted.
4. Effectiveness of suckling
• The baby should suckle slowly and pose in between to swallow.
• Baby’s cheeks should be full and not hollow during suckling

Advantages of breast milk

1. Protein-has little protein compared to cow’s milk but its protein is easily digested and has
certain amino acids as taurine and cysteine responsible for neurotransmission and
neuromodulation.
2. Fats- contains polyunsaturated fats necessary for myelination of neurons. Omega 2 and omega 6
fatty acids are present necessary for prostaglandins and cholesterol synthesis required for
synthesis of steroid hormones
3. Water and electrolytes. Its 88% water.
4. Vitamins and minerals enough for the baby’s requirement.
5. Immunological advantage. Breast milk has secretory IgA
6. Decreased chances of allergy
7. Mental growth

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KANGAROO MOTHER CARE
It’s a mother to baby bonding through skin to skin contact.

Advantages

1. Temperature regulation
2. Stimulates breathing
3. Stimulates brain activity
4. Prevents infection
5. Encourages breastfeeding
6. Increases emotional bonding

Components of kangaroo mother care

1. Kangaroo positioning- baby put in between the breats.

2. Kangaroo nutrition
3. Kangaroo discharge and follow up

Who needs kangaroo mother care? →Low birth weights that are clinically stable.

Until when should the baby be given kangaroo mother care?--> until can not tolerate that is too much
sweating or refuses to stay in kangaroo mother care.

NB: during kangaroo mother care positioning the provider should be in a semi reclining position to avoid
gastric reflux in infant.

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CONGENITAL ANOMALIES
DOWN SYNDROME
Down syndrome (DS) is the most common chromosome abnormality among liveborn infants. It is the
most frequent form of intellectual disability (mental retardation) caused by a microscopically
demonstrable chromosomal aberration. Trisomy 21 is the most common chromosome abnormality
among live births (1 in 730 live births) and the most frequent form of intellectual disability caused by a
microscopically demonstrable chromosomal aberration.

Chromosomal aberrations are due to a change in the normal chromosome number or a change in the
structure of a chromosome. They may involve one, two, or more chromosomes and may involve only
part of a chromosome or the whole chromosome. Congenital anomalies, growth deficiency, and
intellectual disability are findings often present in individuals with chromosome abnormalities, although
some cytogenetic aberrations have little to no clinical effect.

Most individuals with Down syndrome have free trisomy 21 (47+21). Meiotic non disjunction error is the
cause in 95%, and the error occurs at mitosis in somatic cells in the remaining 5 percent of cases. In
approximately 90 percent of cases, the extra chromosome 21 originates from the mother. This explains,
in part, why the risk of this type of Down syndrome increases with advancing maternal age.

Trisomy 21 is the most common chromosome abnormality among live births (1 in 730 live births) and
the most frequent form of intellectual disability caused by a microscopically demonstrable chromosomal
aberration.

The risk is highest if the mother, rather than the father, is the translocation carrier. However, the
majority of translocations resulting in Down syndrome occur de novo, with only 3 to 4 percent having a
familial etiology.

DS is characterized by a variety of dysmorphic features, congenital malformations, and other health

problems and medical conditions. Not all of them are present in each affected individual.

CLINICAL FEATURES.

Up slanting palpebral fissures, epicanthic folds, and brachycephaly are nearly universal features of DS.
These features predominantly affect the head, neck and the extremities. Flat facial profile/flat nasal
bridge, Low-set small ears, Brachycephaly, Open mouth Protruding tongue, Short neck, Excessive skin
at nape of the neck, Narrow palate, Abnormal teeth.

Characteristic dysmorphic features of DS affecting the extremities include, Short broad hands,
incurved fifth finger with hypoplastic mid phalanx, Transverse palmar crease, Space between the first
and second toes (sandal gap) and Hyperflexibility of joints.

ASSOCIATED CONGENITAL AND MEDICAL COMPLICATIONS.

Down syndrome is being associated with a number of congenital anomalies or medical problems,
including Congenital heart diseases, Gastro intestinal abnormalities, Growth and development delays ,
Eye problems , Hearing loss , Endocrine disorders, Immunodeficiency disorders and Intellectual
disabilities.

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CONGENITAL HEART DISEASES.

Approximately one-half of individuals with DS have congenital heart disease.(7) In the largest
population-based study, cardiovascular abnormalities were up to (42%) infants born with DS.The
secondary lesion was most commonly an atrial septal defect (ASD) or patent ductusarteriosus (PDA).
Others are Complete atrioventricularseptal defect (CAVSD) 37%, Ventricular septal defect (VSD) 31%,
ASD 15%, Tetralogy of Fallot (TOF) 5 percent.

GASTRO INTESTINAL ANOMALIES

Children with trisomy 21 are at increased risk for gastrointestinal tract anomalies, which occur in
approximately 5% of cases. Duodenal atresia or stenosis, annular pancreas, Imperforate anus and
esophageal atresia with tracheoesophageal fistula are seen less often.

Hirschsprung disease is more common in DS than in the general population, although the risk is less than
1 percent. Among children with Hirschsprung disease, approximately 2 percent have trisomy 21.

GROWTH AND DEVELOPMENTS.

Birth weight, length, and head circumference are less in DS compared with typical infants. Newborns
with DS weigh approximately 0.18 to 0.37 kg less than their siblings. Mean length at birth is
approximately 0.5 standard deviations less than control newborns.

The cause of DS-associated growth retardation remains unknown. Low circulating levels of insulin-like
growth factor 1 (IGF-1) and diminished provoked and spontaneous secretion of growth hormone (GH)
have been reported in some patients.

EYE PROBLEMS.

Ophthalmologic disorders that require monitoring and intervention affect the majority of children with
DS. Disorders that are the most common include, Refractive errors (myopia, hyperopia, astigmatism) –
35 to 76 percent, Strabismus – 25 to 57 percent, Nystagmus – 18 to 22 percent, Cataracts occur in 5
percent of newborns.

HEARING LOSS.

Hearing impairment affects 38 to 78 percent of individuals with DS. Otitis media is a frequent problem,
affecting 50 to 70 percent of DS children, and it is often the cause of hearing loss in this population.
Monitoring for this condition is important to preserve hearing.

ENDOCRINE DISEASES.

Endocrine abnormalities in DS include thyroid dysfunction and diabetes. Thyroid disorders are common
in DS. The prevalence varies, depending in part upon the population studied and the age of testing. The
prevalence of hypothyroidism ranged from 3 to 54 percent in reports of adults with DS.

The risk of type 1 diabetes appears to be increased in DS. Data from a Dutch study in children up to 14
years of age suggest the risk of type 1 diabetes is three times greater in DS than in the general
population.

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HAEMATOLOGICAL DISORDERS.

Hematologic abnormalities affecting red blood cells, white blood cells, and platelets are common in DS,
particularly during childhood. The lifetime risk of leukemia in DS is 1 to 1.5 percent, also Approximately
65 percent of newborns with trisomy 21 have polycythemia.

ATLANTOAXIAL INSTABILITY

Atlantoaxial instability (AAI), defined as excessive mobility of the articulation of the atlas (C1) and the
axis (C2), may lead to subluxation of the cervical spine. Approximately 13 percent of individuals with DS
have asymptomatic AAI, while spinal cord compression due to the disorder affects approximately 2
percent.

IMMUNODEFICIENCY

DS is associated with a variety of immunologic impairments that are thought to be related to the
increased susceptibility to infection, autoimmune disorders, and malignancies. Chemotactic defects,
decreased immunoglobulin G4 (IgG4) levels, and quantitative and qualitative abnormalities of the T cell
and B cell systems have been inconsistently demonstrated.

INTELLECTUAL DISABILITY (MENTAL RETARDATION)

Almost all individuals with DS have cognitive impairment, although the range is wide. Most are mildly to
moderately intellectually disabled, with an intelligence quotient (IQ) in the 50 to 70 or 35 to 50 range,
respectively, although some are severely impaired with an IQ of 20 to 35.

Developmental impairment becomes apparent in the first year of life. In general, the average age of
sitting (11 months), creeping (17 months), and walking (26 months) is approximately twice the typical
age.

The sequence of language development is the same, although the rate is slower, with the average age
for the first word at 18 months. The child with DS continues to learn new skills. However, IQ declines
through the first 10 years of age, reaching a plateau in adolescence that continues into adulthood

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CASE DOWN SYNDROME
NAME: ZYZZYYYZ MR. No M23-CC-YY

AGE: 9 month

SEX: M

RESIDENCE: Morogoro

INFORMANT, Biological Mother.

Referral from, Amana Hospital to MNH for further Managements.

Chief complain:

Constipations since birth

Poor Weight gain 3/12

Recurrent episodes of Cough 3/12

HISTORY OF PRESENTING ILLNESS

Mother reports that, the child was delivered by SVD, at term GA 38 week. Cried immediately after birth,
BWT 3.2 kg. No history of bluish discoloration or Yellowish discoloration started breast feed two hours
since delivery. However the child did not pass meconium within the first twenty four hours after birth.
The attending midwife assured her that the child will pass meconium spontaneously at home. They were
discharged on second day. On third day since delivery the child passed meconium, small amount. Since
then he has been experiencing abnormal bowel habits where he could not pass stool for up to one or
two weeks, Once he get stool its little amount , hard formed stool , yellowish greenish stool.

This has been associated with episodes of abdominal distention which lead to taking a little amount of
breast and complimentary foods i.e porridge. He has a history of vomiting once, billous vomitus non
projectile vomiting.

No history of vomiting blood, no history of diarrhea, no history of blood in stool, no history of fevers
during the course of illness

However, mother reports that the child has been failing to gain weight for the past three month. He was
born with BWT 3.2 kg and he was gaining weight normally during the first six month, the maximum
weight attained was 6kg, and currently he weight is 5.2Kg

The child has a history of recurrent episodes of Cough, which was dry cough, without specific time,
associated with low grade fevers, but no history of night sweat, no history of TB contact, no history of
shortness of breath, no history of bluish discoloration. He was being attending nearby hospital and
managed as pneumonia with some improvements.

No history of convulsions or loss of consciousness, no history of blood in urine or change in urination

habit, no history of sweating during breast feeding, no history of generalized body swelling or lower
limbs swelling, no history of yellowish discoloration of eyes or skin.

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REVIEW OF OTHER SYSTEMS.

ENT- No history of ear discharge

- No history of Nasal discharge

- No history of bleeding per nose

MSS- No history of Joint swelling

- No history of skin rash.

PAST MEDICAL HISTORY.

This is the first admission at MNH, admitted at St. Francis in Morogoro due to the same complains

No history of Blood Transfusions

No known drug allergy

HIV status, tested Negative.

No history of previous Surgery.

PRE NATAL HISTORY.

First booking at 16 week, Made a total of four visit.

Blood pressure, Weight reported to be normal

No history of abnormal Per Vaginal discharge, or bleeding during pregnancy

No history of Fevers during pregnancy.

Received Malaria prophylaxis, Deworming and Iron supplements.

NATAL HISTORY.

As per HPI

POST NATAL HISTORY.

As per HPI

GROWTH AND DEVELOPMENTAL HISTORY.

Cannot support his neck until now (9month of age)

Cannot seat without support

Cannot Crawl

But, he can grasp objects, transfer from one hand to another, hold her mother’s breast

Can turn back when hearing his mother voice.

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IMMUNIZATION HISTORY.

Received all vaccines as per his age,

Waiting for Vitamin A and Measles.

FAMILY SOCIAL HISTORY.

Third born in a family of three children, First born is 17 years old , second born is 14 years , all are doing
fine. Mother 28 years education level standard VII, she is a house wife, Father 35 years a peasant. Father
provide full support in management of the child.

No history of the same illness in their family

DIETARY HISTORY.

Exclusive Breast feed for 6 months.

Current he is on complimentary feeding.

He take up to three meals per day, feeding on demands, mother reports a history of taking a little
amount of feed due to abdominal distentions.

Mother report to feed a child with porridge made up of maize floor mixed with ground nuts, sometimes
porridge made up of grinded bananas. Occasionally she could feed fish and fruits juice.

GENERAL EXAMINATIONS.

Alert, Afebrile T=37.5, Not tachypnea, No jaundice, No cyanosis, No angular chellitis

Some palm pallor, no finger clubbing.

Dysmophic features.

Wide spaced Eyes, Flat nasal bridge, Low set ears, Open protruding tongue (macroglosia), Short neck ,
Single palmer crease and he has widen space between the first and second toes ( sandal gap)

Anthropometric measurements.

Weight 5.2kg, Length 60cm, OFC 44cm, MUAC 11cm= <-3SD

Weight/ Height (length) = -2SD

Conclusion: Moderate acute malnutrition

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SYSTEMIC EXAMINATION.

P/A

Symmetrical distended abdomen, Moves with respiration, No surgical scars or therapeutic marks, no
dilated veins, normal umbilicus.

Soft non tender on superficial palpations, Liver and spleen were not palpable, Kidneys were not
bimanually ballotable.

Tympanic note on percussion all over the abdomen, Bowel sound present & exaggerated.

Normal Male genitalia, descended tests, Normal anal verge, normal anal sphincter tone, empty rectum
and gloved finger stained with normal stool color.

RS.

Normal chest shape, moves with respiration RR 42 breaths per minute, no dilated superficial veins, no
surgical marks.

Bilateral chest expansion, no palpable axillary and infraclavicular lymph node.

Vesicular breathe sound heard bilateral, no added sounds

CVS.

PR 159 bpm, regular irregular, low volume, synchronous non collapsing pulse

No precordial hyperactivity, no heave or thrill.

Apex beat, 5th ICS, MCL

S1 and S2 heard, Systolic murmurs grade III, lower left sternal border, radiating to the neck.

CNS.

Higher centers: Alert, conscious not lethargic.

Cranial nerves:

I. not assessed

II. Pupils equally reactive to light, the child can follow objects, can see his mother and cry to a strange.

III, IV and VI. The child was able to move eyes in different directions

V. Can breast feed by sucking nipples without problem.

VII. Cry without any facial asymmetry

VIII. Can hear mothers voice and turn his heard to

IX and X. Can sack milk and swallow without any problem

XI. Can turn his head

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Motor: RUL LUL RLL LLL

Power 5/5 5/5 5/5 5/5

Tone hypo hypo hypo hypo

SUMMARY.

A 9 month old boy, from Morogoro presented with history of constipations since birth and delayed
passing meconium, history of poor weight gain as well as delayed developmental milestone.

O/E he is stable, some palmer pallor, dysmorphic features suggestive of Down Syndrome. Systolic
murmurs, grade III, heard at lower left sternal border P/A symmetrical distended abdomen, DRE normal
anal tone, empty rectum, gloved finger stained with stool

PDX.

1. Down syndrome presenting with Hirschsprung Disease HD, Acyanotic Congenital heart Disease.

2. Moderate acute malnutrition , Marasmic type

3. Delayed developmental milestone

MANAGEMENT

Investigations

FBP

ABO X Matching

CRP, ESR

Serum electrolyte Na, K and Cl

Serum Cr, BUN

Liver enzyme ALT

Urinalysis

MRDT and BS for malaria parasite.

Full thickness rectal biopsy.

Imaging.

CXR

Trans thoracic ECHO

Abdominal USS

Barium Enema X rays.

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Results.

s/n Investigation Results Interpretation

1 RBC 3.35 N

2 HB 9.16 L

3 HCT 27.8 L

4 MCV 82 N

5 MCH 27.4 N

6 MCHC 33.0 N

7 PLT 25.2 L

8 WBC 3.56 L

9 Neutophils 0.16(4.61%) L

10 Lymphocyte 3.04(85.2%) H

11 Monocyte 0.156(4.38%) N

12 Easinophil 0.123(3.45%) N

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Biochemistry.

1 Creatinine 31.3 N

2 BUN 1.7 L

3 K+ 5.5 H

4 Na+ 134 L

5 Cl 106 N

6 CRP 0.5 N

7 ALT 35 N

8 FT3 2.62 N

9 FT4 0.82 N

10 TSH 0.22 L

Urinalysis: Normal

MRDT: Negative

CXR: Normal Chest X ray

Barium Enema X ray: Planned but not done yet due to financial problems, she cannot afford to pay.

Rectal Biopsy: was not done

ECHO: Isolated Large VSD.

Final Diagnosis.

1. Down syndrome presenting with Hirschsprung Disease HD, Acyanotic Congenital heart Disease.

2. Moderate acute malnutrition Marasmic type

3. Delayed developmental milestone

4. Normochromic normocytic anemia

5. Impending Megakaryoblastic Leukemia.

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TREATMENT.

IV PCM 75MG tds 3/7

IV Ampicillins 250mg BD 10/7

IV Gentamycin 37.5mg OD 10/7

Started on F75 50mls 2 hourly

Encouraging breast feed.

Monitor weight gain daily.

PROGNOSIS.

After two weeks of inpatient care, the child started to gain some weight and the plan was to discharge
through Pediatric surgery for possible surgical management of Hirschsprung disease.

COUNSELLING AND FOLLOW UP.

Mother was being informed in detail of the conditions of the patients, and she understands and was so
cooperative during the course of management.

The patients was reviewed by pediatric surgeon and transferred to Pediatric surgery wards for possible
surgical management of the Hirsch sprung disease.

DISCUSSION
Down syndrome DS, is being associated with multiple other congenital malformations and medical
problems. Generally this condition is diagnosed clinically by observing presence of dysmorphic features
from head and neck and those presenting to extremities.

The patient presented with features like: Wide spaced Eyes, Flat nasal bridge, Low set ears, Open
protruding tongue (macroglosia), Short neck , Single palmer crease and he has widen space between the
first and second toes ( sandal gap).

Also our patient presented with some associated congenital anomalies like Congenital Heart disease
CHD, Gastro intestinal malformations presented with features suggestive of Hirschsprung disease HD

Also the patient presented with a history of failure to gain weight and the delayed developmental
milestone, which are features associated with Down syndrome compared to the general population.

Endocrine abnormalities like Hypothyroidism and diabetes mellitus DM, are being associated with Down
syndrome when compared to general population. The patient presented with features of thyroxine
hormone dysfunctions, low levels of TSH and T4/T3 and he was kept on thyroxine hormone therapy,
but did not present with features suggestive of diabetic mellitus DM. Hearing and visual problems are
common in Down sysndrome DS, but was not a feature in our patient.

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Hematologic abnormalities affecting red blood cells, white blood cells, and platelets are common in
DS, particularly during childhood. The lifetime risk of leukemia in DS is 1 to 1.5 percent, also
approximately 65 percent of newborns with trisomy 21 have polycythemia. Our patient presented with
features suggestive of Impending Megakaryoblastic leukemia AMKL. The risk of hematological
malignancies are higher in DS compared to general population.

Down syndrome may presents with skeletal abnormalities. Atlantoaxial joint instability excessive
mobility of the articulation of the atlas (C1) and the axis (C2), may lead to subluxation of the cervical
spine common in DS compared to general population. This will presents with difficult in supporting
controlling neck and also may presents with lower extremities weakness. Our patient presents with
inability to support his neck as compared to his age, 9 months.

Down syndrome is also associated with Immunodeficiency, patients with DS have the risk of recurrent
infections. Our patient has a history of recurrent chest infections and was being treated as pneumonia
several time in peripheral hospitals.Hence life expectancy in DS is low when compared to general
population due to morbidities ranging from congenital anomalies and low immunity.

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CONCLUSION.

Down syndrome DS, is genetic disorder involving chromosomal abanormality in Chromosome 21

(trisomy 21). It presents with dysmorphic features as well as congenital malformations and medical
complications. Which may ranges from moderate mobidity to life threating condition.

Life expectancy in children with DS is low compared to general populations, due to increased morbidity
of medical complications. Pre natal diagnosis of DS is difficult in resource poor countries, diagnosis is
made after delivery.

Management of Down syndrome involves different specialties depending on the complications the
patient is presenting with i.e Cardiologist for CHD, Pediatric surgeons for gastrointestinal disorders
i.eHirschsprung Disease HD, ENT and ophthalmologists for hearing and visual problems and general
physician.

Counseling may begin when a prenatal diagnosis of Down syndrome (DS) is made or suspected. This
include information to patients so that they are aware of the disease their children are suffering and
involvement on the each stage of management, inform them about the prognosis of the disease.

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OEIS MALFORMATION (OPHALOCELE, BLADDER EXTROPHY, IMPERFORATED ANUS AND SPINAL
BIFIDA MALFORMATION)

Hospital reg. Number; M17-ZZ-RR

Name; Baby of MMMMM

Sex; indeterminate

Residence; Toangoma, Temeke, DSM

Religion; Muslim

Date of birth; 06th December 2017

Date of admission; 06th December 2017

Clerking day; 06th December 2017

Informant; Mother

Date of death; 08/12/2017

Chief complains

• Visible bowel

• Absence of anus and sex organs

• Swelling at the back

HISTORY OF PRESENTING ILLNESS (HPI)

Mother is 29 yrs old. This was her first pregnant. LNMP 23rd April 2017 and EDD 30th January 2018. She
booked at 3rd month of pregnancy, made three visits, was given only 10 tabs of heamatenics,
antimalaria, mebendazole, two doses of tetanus toxoid was given, VDRL negative, PMTCT-2.No obstetric
ultrasound was done prenatally. No hx of using sleeping pill,smoking cigarette or yellowish vaginal
discharge wih pain. No hx of hypertension or diabetes mellitus. No any complication during pregnancy.

Labour was for 12 hours, artificial rupture of membrane, delivered by SVD at 32 GA at Zakiem hospital.
APGAR score 7 and 10 at 1 and 5 minutes respectively. It was then noticed that the baby’s bowel was
visible outside through a thin transparent cover around a cord. Also it was noted that anus was not
patent and there was no sex organs. Mother also reported a mass at the back of achild. Mother denied
hx of a baby with these similar manifestations to be born in their family.

The patient’s bowel was covered with wet gauze, was given antibiotics and vitamin K and referred to
MNH.

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POST NATAL HX

Not passed neither meconium nor urine, no hx of difficulty in breathing, fever, abdominal distension,
yellowish or bluish discoloration of body or convulsion. Not yet started to breastfeed. No any
immunization given.

FAMILY SOCIAL HX

Mother is a housewife, std 7, Father is a pety trader, form 4 leaver. They are married, live together and
provide support during illness. No family hx of chronic illness, no hx of consanguinity.

PHYSICAL EXAMINATION

1. General examination

➢ Alert, aferbrile (T=37.1), Pink, with normal cry, reduced activity, normal breathing,
normal cranium, fontanels of normal size, neither tense nor bulging. Normal eyes, ears,
mouth, and neck .

➢ Foots are twisted medially

➢ There is a single mass at lumbarsacral region, pink coloured, ovoid, measuring 4*3 cm,
edges clearly defined, normal skin over mass, normalthermia, soft, compressable and no
deformity of surrounding structures As shown in the picture below.

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Picture1: Defect on spine

MEASUREMENTS

1. HC=28.1CM

2. WEIGHT=1.54KG

3. HEIGHT=38CM

Interpretations

1. weight/age= below 5th percentile

2. height/age=below 5th percentile

3. HC/age=below 5th percentile

Conclusion

Symmetrical intra uterine growth retardation (IUGR)/ SGA

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 2. SYSTEMIC EXAMINATION

p/A

A large defect in the anterior abdominal wall , visible bowel and part of liver through a thin transparent
membrane covering the contents (omphalocele) with widened umbilical ring with a diameter of 8cm.
Onother mass protruding at suprapubic region( Exstrophy of bladder) - anterior wall of bladder was
defective. (see pic 2)

Abdomen slightly distended and moves with respiration. Normal bowel sounds.

• External genitalia was not identified except two small ridges (see pic 2)

• Imperforate anus – there was no anal opening in the perineal region .(see pic 2)

Picture 2: omphalocele, bladder extrophy, imperforated anus, two genital ridges and talipes equinovarus

Respiratory system examination

RR=73 breath per minute, elliptical chest contour, expand symmetricallywith respiration. Resonant note
on percussion, bilateral air entry with bronchial breath sounds

CVS

Pulse rate=156, weak, regular, synchronous with branchial, femoral, popliteal and pedal artery pulse.
Normal precordium, S1 and S2 sounds heard, no murmurs.

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CNS

Reduced activity, weak cry, hypotonic, weak moro, sucking and grasp reflexes. Babinsic sign upward.

SUMMARY

Pdx Pre mature with

1. Omphalocele

3. Anal genital malformation( imperforated anus, absence of sex organs)

4. Bladder extrophy

5. Spinal bifida(myelomeningocele)

6. Talipes equinovarus

7. LBW

Investigations

The following investigations were taken and the

results available .

o FBP = was done but results didn’t come out.

o Serum electrolytes= Na+ 100, K+ 7.6, Cl· 50 ( no treatment was given as results come out
after a child died)

o Serum creatinine= not done

o Blood grouping and x-match,

o Imaging whenever possible such as plain X – ray,

o ECHO, Ultrasound if indicated= none was done

o RBG=5.1mmol/l

o CRP=0.2

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TREATMENT GIVEN

• IV fluid D10W 90ml/24 hours

• IV ampiclox 150mg bd for seven days

• IV gentamicin 5mg od for seven days

• IV metronidazole 15mg tds for seven days

MONITORING

Temperature

Blood sugar

Respiratory rate

Pulse rate

CRP

COUNSELING.

The birth of a congenitally deformed child imparts strong social stigma over the parents. Crying and guilt
feeling mother was consolidated and told that the etiology of malformation is unknown.

Parents were told that the compatibility with life is nil or minimal with OEIS complex in our setting.

Parents were informed that there is a possibility of the malformation to recur in further pregnancies, so
early ANC visit and evaluation of pregnancies with serial utrasounds would help early diagnosis and plan
for treatment.

PROGNOSIS

The defect has very poor prognosis because of the following reasons.

1. Greater association of congenital malformation

2. Late diagnosis

3. Low surgical advance at our setting(6)

DISCUSSION

OEIS has been reported in association with maternal exposure to diazepam, cigarette smoking, maternal
obesity and uterine fibroids, maternal gonococcal infection in early pregnancy and foetal alcohol
exposure throughout the pregnancy.

In the present case, there is no history of such exposure and did not have any of the risk factors. There is
no similar history of malformation in the family.

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Beside these cardinal malformations, OEIS complex has been reported to have other associated
anomalies of central nervous system, cardiovascular system, vertebrae, upper urinary tract, malrotation,
defects in vertebral column, absent appendix, lower limb abnormalities like talipes equinovalgus, single
umbilical artery

In the present case, four cardinal anomalies of OEIS were present along with the absence of external
genitalia and talipes equinovarus.

Due to electrolyte imbalance, there is a possibility that a child had upper urinary tract malformation as
well, though loss through the defect could also explain. Autopsy was important to rule out renal
malformations.

SPINA BIFIDA
Myelomeningocele- most common neural tube defect characterized by a cleft in the vertebral column
with a corresponding defect on the skin that the meninges and spinal cord are all exposed.

Spina Bifida Occulta-This anomaly consists of a midline defect of the vertebral bodies without
protrusion of the spinal cord or meninges. The skin is intact. Most individuals are asymptomatic and lack
neurologic signs,

Meningocele- its when only the meninges protrude through the defect

CLINICAL MANIFESTATION

A myelomeningocele may be located anywhere along the vertebral collumn, but the lumbosacral
region accounts for at least 75% of the cases.

The extent and degree of the neurologic deficit depend on the location of the myelomeningocele. A
lesion in the low sacral region causes bowel and bladder incontinence associated with anesthesia in
the perineal area but with no impairment of motor function.

The newborn with a defect in the mid-lumbar region typically has a saclike cystic structure covered by a
thin layer of partially epithelialized tissue . Remnants of neural tissue are visible beneath the membrane,
which may occasionally rupture and leak CSF.

An examination of the infant shows a flaccid paralysis of the lower extremities, an absence of deep
tendon reflexes, a lack of response to touch and pain, and a high incidence of postural abnormalities
of the lower extremities. Constant urinary dribbling and a relaxed anal sphincter may be evident.
Thus, a myelomeningocele in the mid-lumbar region tends to produce lower motor neuron signs due to
abnormalities and disruption of the conus medullaris. Infants with myelomeningocele typically have an
increasing neurologic deficit as the myelomeningocele goes higher into the thoracic region. However,
patients with a myelomeningocele in the upper thoracic or the cervical region usually have a very
minimal neurologic deficit and in most cases do not have.

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