Case report 3

Department of Pediatrics and Child Health

Case Report: Three

Submitted to: Dr. Bezaye Girma
Prepared by: Honey Godana
ID: MMR/219/10

1
Case report 3

IDENTIFICATION
This is A.S a six years old preschooler male patient from cherkos, Addis Abeba. He
is not yet enrolled to school. He was admitted to St. Paul’s Hospital Millennium
Medical College pediatric ward on nehase 29 -2013 EC and date of clerking was
meskerem 5 -2014 EC. The source of history was the patient’s mother with no
language barrier and it was reliable.
The mother’s name is T.B a 28 years old janitor who has never gone to school. She
is divorced from the patient’s father 2 years back.
The father’s name is S.T a 35 years old merchant with educational background of
grade 6. They are orthodox, Christian by religion.

Previous Admission
 Mentioned on HPI

Chief Compliant
 Worsening of Generalized body swelling of 4 days duration

History of Present Illness

 This is a 6yr old preschooler male patient who is a known renal and
hypertension patient for the past 11 months, currently on po prednisolone
2mg/kg/day (taken once per day) and po enalapril 5mg (taken twice per
day). Currently he presented with a worsening of generalized body
swelling of 4 days duration that started from his face specifically under his
eyes that worsen up on waking up in the morning and relieved during the
day. The swelling also progressed to the legs and abdomen in 2 days then
generalized to all body parts.
 Associated with the swelling the patient also experienced frothy urine,
abdominal discomfort, easy fatigability and loss of appetite.

2
Case report 3

 11 months ago, the patient experienced a generalized body swelling that

started from his face and progressed to involve his legs and abdomen over
a period of 1 week. For this complaint he was taken to “yekatit 12” hospital
where he was diagnosed to have a renal problem and hypertension and He
was started on unspecified iv medications. He was admitted there for 3
months and was referred “Tikur anbesa” hospital with no improvement. At
tikur anbesa hospital he was started on his current medications and started
to have a regular follow up every two weeks. he was adherent to his
medications but stopped taking them two months back because his
mother thought he was not improving and took him to holy water where
they stayed for 2 months with no improvement.
 The patient was exclusively breastfed until the age of 6 month and then
started on complementary feeding with “atmit” made of different cereals.
Total duration of breastfeeding was 2 years. Currently He eats 3-4 times a
day by himself. He eats up to quarter of injera per meal. His staple diet is
composed of injera and different kind of “wot” and vegetables. He eats
fruits, meat and dairy products occasionally. He usually finishes his plate.
The patient asks for food when he feels hungry.

Otherwise he has
 No hx of sore throat, and skin lesions
 No hx of reddish discoloration of urine, pain on urination, frequency,
urgency, or decreased urine output.
 No hx of poor stream, hesitancy, terminal dribbling, urinary
retention or incontinence
 No hx of abdominal pain, vomiting, diarrhea, or bloody stool
 No hx easy bruisability, joint pain or swelling
 No hx of cough or hemoptysis
 No hx malaria infection the mother is aware of
 No self or family history of similar illness in the past
 No hx of shortness of breath, orthpnea or PND
 No hx of yellowish discoloration of the eye or contact with jaundiced
person
3
Case report 3

 No medication history other than the one mentioned on HPI

 No hx of night sweats, previous TB treatment or contact with chronic
cougher

 No hx of light headedness, double vision, ringing ears, dizziness or

fainting
 No self or family history of hearing difficulty
 No hx of malar rash, photophobia, mouth ulcers or hair loss
 No hx of gum or nasal bleeding
 No hx of cold intolerance
 No hx of headache, abnormal body movement or loss of
consciousness
 No familial hx of DM, HTN and any known chronic illness
 The patients RVI status is unknown

Immunization history
The patient is vaccinated according to EPI schedule and has received the yellow
card.

Nutritional History
Mentioned on HPI
Developmental History
He is not attending school. He can skip on one leg, walk backwards and run stairs.
He is fluent in Amharic and can tell a story. He plays with his peers and he can
dress & undress himself. History of primary dentation is unknown but the patient
doesn’t have history of shedding of primary teeth and eruption of secondary
teeth. He can Copy a triangle, count up to 10 and name 4 colors.

4
Case report 3

Perinatal and Natal History

He is the first born to a Para 1 mother after 9 months of amenorrhea. The mother
had 4 ANC follow ups. She was given two tetanus vaccines and iron supplement.
She was told that all her test result were okay. The delivery was via SVD at a local
health center. The baby cried immediately after birth and there was no bluish and
yellowish discoloration of body. He was breastfed within the 1 st few hours after
delivery. Otherwise, the pregnancy as well as the delivery was uneventful.

Past Medical and Surgical History

There is no history of childhood illnesses like measles, pertussis, mumps and
chicken pox.
There are no past major medical illnesses, surgeries, or known allergies.

Personal, Family, and Social History

The patient lives in a family size of 3, in a 1 room house with 1 door and one
functional window. They have separate kitchen. They use wood and charcoal for
cooking but they always use it outside the living house. They use tap water for
drinking and house hold purposes. The toilet is far from home and they have habit
of washing hands after going to the toilet. They have a proper waste disposal and
latrine system. They don’t share room with any domestic animal; there is no
family history of asthma, diabetes mellitus, hypertension, cardiac, or renal illness.
The family’s source of income is the mother with monthly income of 1500.

Review of Systems
General: Mentioned in HPI
Head: No hx of head injury and headache.
Eyes: No hx of redness, discharge and vision defects.
Ear: No discharge, bleeding, aches, hearing loss, or ringing in the ears
Nose: No bleeding, discharge, sneezing, or stuffy nose.

5
 Case report 3

Mouth/throat: No ulcerations, gum bleeding, dental carries, difficulty of swallowing,

hoarseness.
Respiratory: mentioned in HPI
Cardiovascular: mentioned in HPI
Gastrointestinal: mentioned in HPI
Genitourinary: mentioned in HPI
Locomotors: No history of joint deformities, trauma, or limited movement
Integumentary: No rash, lump, or itching. No skin, hair, and nail changes.
Central Nervous System: No history of abnormal body movement, tremor, numbness, paralysis,
or speech defect.

Physical Examination
General Appearance
The patient is acutely sick looking. He is not on respiratory distress. No gross
dysmorphic features. He was lying on his bed He is awake but fatigued. He has no
signs of cyanosis or jaundice. He was alert and cooperative.
Vital Signs
Pulse rate: 90 beats/minute, right radial artery regular full in volume (normal for
his age)
Respiratory rate: 21 breaths/minute, deep and regular (normal for his age)
Blood Pressure: 115/60 mmHg, right arm sitting position (systolic stage 1 HTN)
Temperature: 37.2o C, right axilla afternoon (normal)
SPO2: 97% on atmospheric air
Anthropometry

Weight: 25 Kg WFA: between 1 & 2 SD, normal

Height: 110 cm HFA: between -1 & -2 SD, normal
BMI: 20.66 kg/m2 BMIFA: between 2 &3 SD, normal
MUAC: 15.5 cm, normal WFHt: 2 and 3 SD, normal

6
Case report 3

H.E.E.N.T
Head: Normal shape and size. No gross deformities, swellings or indentations. No
area of tenderness or scalp infections. Dark, non-pluckable hair.
Ears: Normally shaped and sized pinnae, normal position, no discharge, no
tenderness over the mastoid process
Eyes: periorbital edema of both eyes, pink conjunctiva, non-icteric sclera, no
discharge, no nystagmus or strabismus. No xerosis, ptosis, exophthalmos,
microphthalmos, or bitot spot
Nose: No discharge. Central septum. No tenderness over the maxillary and frontal
sinuses

Mouth and Throat: No cleft lip or palate. Tongue is not protruded. Normal size
and position of tongue. No papillary atrophy, thrush, or dryness. Moist and pink
buccal mucosa. No dental carries, no gum hypertrophy. No hyperemia or swelling
of the tonsils.

Lymphoglandular system
Lymph nodes are not palpable over the occipital, post auricular, pre auricular,
submandibular, submental, cervical, supraclavicular, axillary, epitrochlear, or
inguinal regions.
Thyroid is not enlarged.
Respiratory system:
Inspection:
 No peripheral or central cyanosis
 No clubbing
 No visible mass, deformities and scar.
 No nasal flaring, intercostal, subcostal and suprasternal retractions.
 No audible wheeze or stridor
 Chest moves with respiration symmetrically
Palpation:
 Centrally palpable trachea
 no superficial mass or tenderness
 symmetric chest expansion and
 decreased tactile fremitus on the posterior lower 1/3 of lung field
bilaterally
7
Case report 3

Percussion:
 stony dull over the posterior lower 1/3rd of lung field bilaterally
 There is resonant percussion tone over the rest of the chest wall.
 Diaphragmatic excursion is 4cm.
Auscultation:
 absent air entry over the the lower 1/3rd of the lung field bilaterally
 No wheezing, crepitation, stridor rhonchi, or pleural friction rub.
Cardiovascular system:
Arteries: Pulse is palpable over, carotid, brachial, radial, femoral, popliteal,
anterior tibialis, and dorsalis pedis bilaterally. No radio femoral delay.
Veins: There are no distended veins over the neck, the chest, abdomen, and legs.
JVP: not raised
Pericardial Examination
Inspection: There is no bulge. The precordium is quite. The apical beat is not
visible.

Palpation: The point of maximum impulse is at the 5 th intercostal space in the

midclavicular line. There is a no parasternal or apical heave. There is also no thrill
at the aortic, pulmonary, tricuspid and mitral areas.

Auscultation: S1 and S2 are well heard. There are no abnormal heart sounds or
murmurs.

Gastrointestinal system:
Inspection:
 The abdomen is distended and Flanks are full.
 It is symmetric and moves with respiration.
 The umbilicus is everted.
 There are no visible veins, peristalsis, pulsations, scars

8
Case report 3

 Hernia sites are free.

Auscultation: Normoactive bowel sounds, No bruit over the abdominal aorta,
renal arteries, or iliac arteries. No friction rub over liver or spleen.
Palpation:
 Superficial – no tenderness or superficial mass.
 Deep – Liver is not palpable below the right coastal margin
 Spleen was not palpable along the line of growth
Percussion:
 Tympanic percussion tone was appreciated centrally and dull note was
appreciated peripherally.
 No ballotable organ
 Positive shifting dullness and fluid thrill
 Total liver span: wasn’t assessed because the lower border wasn’t identified
cause of ascites

Genitourinary system:
 No suprapubic mass, no tenderness, normal male external genitalia with no
pubic hair.
Integumentary system:
Skin: No jaundice, cyanosis, hyper or hypopigmentation. There is no pallor of the
hands and feet. The skin is wet and warm.
Hair: Normal distribution, dark color, soft texture
Nails: Pale, no cyanosis, no inflammation, no spooning

Musculoskeletal system:
Look: Comparable muscle bulk, no extra digit or webbing of digit. No spine deformities.
Feel: There is no tenderness, warmth, or swelling over the joints.
There is a grade III pitting edema on the lower extremities bilaterally.
Move: There is no asymmetry and limitation in movement of limbs.

9
Case report 3

CNS:
General: He is awake, playful and oriented to time place and person.
Speech is good and well-articulated.

Cranial nerves:
CN I Can identify the odor of sanitizer via both nostrils
CN II Direct and indirect pupillary light reflexes are present. Good
visually acuity
CN III, IV &VI Patient follows finger in all directions
CN V No ptosis. Strong temporalis and masseter muscle contraction
Pain and touch sensation are intact over the forehead, cheeks
and chin
CN VII Face is symmetrical at rest and upon voluntary movements like
smiling, nasolabial folds are present bilaterally
CN VIII Able to listen to the sound rubbing fingers make.
CN IX & X Central uvula
No hoarseness of voice
CN XI No shoulder drop, patient can shrug the shoulders and turn head
against resistance
CN XII No atrophy and fasciculation of the tongue
Tongue midline upon protrusion

Motor:
 Bilaterally comparable muscle bulk, no spontaneous or induced
fasciculation.
 All 4 limbs are Normotonic.
 Power graded 5 at both upper and lower limbs, patient can move all
extremities against resistance.
Reflexes
Superficial: abdominal and corneal reflexes are intact.
plantar reflex is down going.

Deep tendon reflexes:

Biceps Triceps Supinators Patellar Ankle

Right ++ ++ ++ ++ ++
10 Left ++ ++ ++ ++ ++
Case report 3

No clonus

Sensory:
Light touch, pain and temperature sensations are intact. Deep pressure,
position sense, vibration and passive movements are well appreciated by
the patient.
Normal recognition of form, size and shape of coin as well as two-point
discrimination.

Summary
Subjective;
This is a 6 years old ore schooler male known renal and hypertension patient for
the past 11 months on medication who presented with worsening of generalized
body swelling of 4 days duration. Associated with this he has frothy urine,
abdominal pain, easy fatiguability and loss of appetite
Objective;
The patient is acutely sick looking. He is awake and looks fatigued. he was lying on
his bed. he was cooperative and playful. All his anthropometric findings are with
in normal range. His vitals are normal except for stage 1 systolic hypertension. He
has periorbital edema under both eyes, decreased tactile fremitus, stony dullness
and absent air entry on the posterior 1/3 of lung field bilaterally. He has
distended abdomen with full flanks and everted umbilicus. Positive shifting
dullness and fluid thrill. There is a grade III pitting edema on the lower extremities
bilaterally.

Differential diagnosis

11
Case report 3

The differentials here are listed and discussed from least likely to most likely
diagnosis
3- post streptococcal glomerulonephritis
2- chronic kidney disease secondary to chronic glomerulonephritis
1-Steroid resistant idiopathic nephrotic syndrome

Post streptococcal glomerulonephritis

Psgn is a disorder of the glomeruli (glomerulonephritis), or small blood vessels in
the kidneys. It is a common complication of bacterial infections, typically skin
infection by Streptococcus bacteria types 12, 4 and 1 (impetigo) but also after
streptococcal pharyngitis, for which it is also known as postinfectious or
poststreptococcal glomerulonephritis. Group A β-hemolytic streptococcal
infections are common in children and can lead to the postinfectious complication
of acute glomerulonephritis (GN). Acute poststreptococcal glomerulonephritis
(APSGN) is a classic example of the acute nephritic syndrome characterized by the
sudden onset of gross hematuria, edema, hypertension, and renal dysfunction. It
is one of the most common glomerular causes of gross hematuria in children and
is a major cause of morbidity in group A β-hemolytic streptococcal infections.
Glomerular immune complex induced by the nephritoxigenic strains of GAS lead
to complement activation and inflammation.
Poststreptococcal GN is most common in children ages 5-12 yr and uncommon
before the age of 3 yr. It commonly develops 2-3 weeks after antecedent strep
pharyngitis and 4-6 weeks after strep pyoderma.
The clinical manifestations are; edema, oliguria, hypertension, electrolyte
abnormality.
In this patient the presence of generalized body swelling and hyperattention
could be explained by post streptococcal glomerulonephritis. But the patient does
not have history of antecedent strep pharyngitis or strep pyoderma which makes

12
Case report 3

this diagnosis unlikely. Plus, psgn commonly resolves within weeks but this
patient has been symptomatic for 11 months.
This diagnosis can be ruled out by measuring serum strep aso, AHase, ASKase, and
Anti DNAase.
Chronic kidney disease secondary to chronic
glomerulonephritis
 CKD is defined as the presence of structural or functional kidney damage that
persists over a minimum of three months. Functional damage is typically
characterized by a sustained reduction of estimated glomerular filtration rate
(eGFR), a persistent elevation of urinary protein excretion, or both.
 Patient has chronic kidney disease (CKD) if either of the following criteria
are present:
1. Kidney damage for ≥ 3 mo, as defined by structural or functional
abnormalities of the kidney, with or without decreased GFR, manifested by one or
more of the following features:
• Abnormalities in the composition of the blood or urine
• Abnormalities in imaging tests
• Abnormalities on kidney biopsy
2. GFR < 60 mL/min/1.73 m2 for ≥ 3 mo, with or without the other signs of
kidney damage described above

 The etiology of pediatric CKD may be the result of congenital, acquired,

inherited, or metabolic renal disease; causes of kidney disease in children are
typically subdivided as being either nonglomerular or glomerular in origin
. The underlying cause correlates with the age at the time of
diagnosis. In children < 5 yr of age, CKD is most commonly a result of
congenital abnormalities of the kidney and urinary tract (i.e., renal hypoplasia,
dysplasia, or obstructive uropathy) and is often diagnosed with prenatal
ultrasonography. In children older than 5 yr of age, acquired or inherited forms
of glomerulonephritis predominate.
 The pathogenesis of CKD in children may be attributed to Hyperfiltration
injury which may be an important final common pathway ofglomerular
destruction, independent of the underlying cause of renal injury. Other
pathologic etiologies of chronic kidney disease include proteinuria,
hypertension, hyperphosphatemia, and hyperlipidemia. Proteinuria itself
13
Case report 3

can contribute to renal functional decline. Proteins that traverse the

glomerular capillary wall can exert a direct toxic effect on tubular cells and
recruit monocytes and macrophages, enhancing the process of glomerular
sclerosis and tubulointerstitial fibrosis.
 Glomerular forms of CKD often present with edema, hypertension,
hematuria, and proteinuria; in severe forms of glomerulonephritis,
malnutrition can be seen. As renal deterioration advances in severity,
patients can develop uremic symptoms (i.e., worsening fatigue, weakness,
nausea, vomiting, anorexia, and poor sleep patterns), as well as edema,
hypertension, and other findings of fluid overload, regardless of the cause
of CKD.
My patient presented with edema, hypertension and a frothy urine which speaks
for proteinuria. He has been diagnosed to have a kidney problem 11 months ago.
So he fulfills the definition of CKD by duration which is a structural or a functional
kidney abnormality for greater than 3 months but we need laboratory evaluations
to confirm this diagnosis. In children older than 5 yr of age, acquired or inherited
forms of glomerulonephritis predominate and my patient is six years old which
makes glomerular cause of CKD more likely.
 Laboratory findings in patient with CKD include; elevations in blood urea
nitrogen and serum creatinine in addition to hyperkalemia, hyponatremia
(secondary to either renal salt wasting versus volume overload),
hypernatremia (loss of free water), acidosis, hypocalcemia,
hyperphosphatemia, and an elevation in uric acid. A complete blood cell
count may show a normochromic, normocytic anemia. Dyslipidemia is
commonly seen. In children with glomerulonephritis, the urinalysis (UA)
shows hematuria and proteinuria Renal function can be measured or
estimated by the GFR. Inulin clearance is the gold standard to measure the
GFR, but it is no longer readily available.

14
Case report 3

Steroid resistant idiopathic Nephrotic

syndrome
 Nephrotic syndrome is the clinical manifestation of glomerular diseases
associated with heavy (nephrotic-range) proteinuria. Nephrotic-range
proteinuria is defined as proteinuria > 3.5 g/24 hr. or a urine protein:
creatinine ratio > 2. The triad of clinical findings associated with nephrotic
syndrome arising from the large urinary losses of protein are
hypoalbuminemia (≤2.5 g/dL), edema, and hyperlipidemia (cholesterol >
200 mg/dL).
 Most children with nephrotic syndrome have a form of primary or
idiopathic nephrotic syndrome. Glomerular lesions associated with
idiopathic nephrotic syndrome include minimal change disease, focal
segmental glomerulosclerosis, membranoproliferative glomerulonephritis,
C3 glomerulopathy, and membranous nephropathy. Nephrotic syndrome
may also be secondary to systemic diseases such as systemic lupus
erythematosus, Henoch-Schönlein purpura, malignancy (lymphoma and
leukemia), and infections (hepatitis, HIV, and malaria).
 The pathogenesis of nephrotic syndrome can be attributed to; effacement
of foot processes of podocytes, decreased in number and function of
podocytes and altered slit diaphragm integrity leading to protein leakiness.
The immune system also a role in the pathogenesis of this syndrome.
 Nephrotic syndrome is classically characterized by four clinical features, but
the first two are used diagnostically because the last two may not be seen
in all patients:

●Nephrotic range proteinuria

●Hypoalbuminemia
●Edema
●Hyperlipidemia
 Complications of nephrotic syndrome include increased risk of infection
due to loss of immunoglobulins in the urine, urinary loss of complement
factors and use of steroids, increased risk of thromboembolic events.
15
Case report 3

 The majority of children who present with idiopathic nephrotic syndrome

(NS) have minimal change disease (MCD), which is generally responsive to
steroid therapy. As a result, empirical steroid therapy is given to most
children who present with idiopathic NS.
 However, approximately 10 to 20 percent of patients will fail to respond to
initial steroid treatment. In many instances, steroid-resistant cases are due
to single gene variants that affect glomerular podocyte differentiation,
structure, and function. Patients with genetic forms of steroid-resistant NS
(SRNS) are usually unresponsive to immunosuppressive therapy.
 Steroid resistance is defined as inability to induce remission within 4 weeks
of daily steroid therapy

 My patient presented with a progression of edema that is typical of renal

problem especially nephrotic syndrome. His age is 6 years which goes for
idiopathic nephrotic syndrome. He also has history of frothy urine which is
caused by the increased protein in the urine which is caused by nephrotic
syndrome. As we can see from the history after he was diagnosed with
renal problem 11 month back, he has been on prednisolone for 9 months
with no improvement which speaks for steroid resistant nephrotic
syndrome. The patient has history of hypertension and also on physical
examination stage 1 systolic hypertension was detected. Even if
hypertension is not a common finding in children with NS it could be
attributed to fluid shifts, sodium retention, and medication side effects
(steroids). Others are associated with chronic and more sustained HTN such
as renal fibrosis, decreased GFR, and progression of chronic kidney disease

Investigations
16
Case report 3

 CBC; anemia in ckd

 Urine analysis
 Proteinuria
 Hematuria
 Rbc cast
 24 hr urinary protein
 Urine protein to creatinine ratio
 Renal function test
 Serum electrolytes
 Lipid profile serum albumin
 Serum complement level
 ASO titer or ANTI dnase
 Serum IGA
 Evaluation to rule out secondary forms of nephrotic
syndrome
 ANA
 Anti DS DNA
 ANCA
 Hep B and Hep C
 HIV
 Renal ultrasound; assess the size, location, and shape and presence
of obstructions. In CKD the kidney is atrophied with loss of cortical thinning
and loss of corticomedullary differentiation.
 Kidney biopsy

Final diagnosis; steroid resistant idiopathic nephrotic syndrome

Management principles
 Edema
Fluid and salt restriction
Loop diuretics
 Dyslipidemia
Low fat diet
 Infections
17
Case report 3

Antibiotics
 Thromboembolism
Heparin/warfarin
 Alternative treatment to corticosteroids
 Cyclophosphamide
 Cyclosporin
 tacrolimus

18