Investigations 2011

Index

Chapter Growth & Development Genetics Neonatology Nutrition Respiratory Cardiology Hematology Neurology Nephrology Endocrinology GIT & hepatology

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Investigations in Pediatrics Investigations in a comparative view Growth & Development Microcephaly
Laboratory Chromosomal study(karyotyping) If chromosomal abnormality is suspected TORCH screening For mother &children Imaging

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CT or MRI Structural abnormalities of the brain or cerebral calcification

Short stature
Laboratory Chromosomal study(karyotyping) Turner syndrome Hormonal profile Pituitary ,thyroid, parathyroid & adrenal gland Growth hormone Unnecessary to subject children to assay until they have at least 6-12 months of height velocity follow up Calcium,phosphorus & alkaline phosphatase Rickets CBC Anemia in celiac or Chron’s disease. CRP Raised in Chron’s disease. Imaging CT Brain For pituitary gland lesions (e.gcraniopharyngioma) Bone age determination( x-ray wrist) To differentiate familial short stature(normal bone age) from constitutional delay of growth & puberty

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Investigations in Pediatrics Genetics Down syndrome
Laboratory
Chromosomal study(karyotyping) To determine the genetic type & risk of recurrence C.B.C If leukemia is suspected

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Imaging
Plain X-ray  Chest : pneumonia  Abdomen :anal atresia Echocardigraphy: Cardiac anomalies Abdominal ultrasonography To exclude renal & gastrointestinal anomalies

Prenatal diagnosis of down syndrome:     Triple test Ultrasongraphy Aminocentesis: low of α fetoprotein Chorionic villus sampling

neonatology Normal newborn
Biochemical screening Hypothyroidism Early diagnosis & therapy improves the prognosis Metabolic disorders ( PKU, homocystinuria, galactosemia&Marple syrup urine disease ) When milk feeding has been established between 6th& 8th day of life Cystic fibrosis Other general measures Vit K injection Heamorrhagic disease of the newborn Cord care Paint by alcohol Eye care Antibacterial eye drops

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Investigations in Pediatrics Preterm or sick infant
Laboratory
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Imaging
Chest X-ray ± abdominal X-ray Assists in the diagnosis of respiratory disorders and to confirm the position of the tracheal tube and central lines.

Haemoglobin, neutrophil count, platelet count Blood urea , creatinine, electrolytes Culture - blood ± CSF ± urine Blood glucose CRP/acute phase reactant Coagulation screen if indicated

RDS
Laboratory Blood gases & electrolytes To asses severity Imaging Chest x-ray Ground glass appearance  Diffuse reticulogranular pattern (areas of collapse) with air bronchogram (air in the major bronchi appears in contrast with the white background of collapsed alveoli as air bronchogram)  Complete calcification of both lung fields (white lung )in severe conditions

Neonatal hyperbilirubinemia
Unconjugated Serum bilirubin Increased total & indirect bilirubin Blood picture Hemolysis or septicemia Blood grouping (ABO & RH ),Coomb’s test For baby & mother to exclude hemolytic disease conjugated
Serum bilirubin Increased total & direct bilirubin AST & ALT Increased Alkaline phosphatae& gamma glutamyltranspeptidase Increased Total serum proteins & albumin

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Investigations in Pediatrics
Enzyme essay G6PD deficiency RBCs morphology & osmotic fragility test Spherocytosis CRP , ESR & cultures If septicemia is suspected Thyroid profile If not done in screening program

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Decreased Prothrombin tine Prolonged Reducing substance in urine Galactosemia CBC, CRP ,ESR , Cultures Septicemia & other bacterial infections TORCH screening specific antibodies of TORCH e.g. CMV Total IgmM antibody Level above 18-20 mg/dl is highly suggestive α 1 antitrypsin assay (NL=150-250 mg/dl) α 1 antitrypsin deficiency ferric chloride urine screening,if positive: aminogram tyrosinemia abdominal Ultrasonography choledochal cyst HIDA scan  In extrahepatic biliary atresia:no excretion of dye in the intestine  In idiopathic hepatitis : excretion of portal areas with fibrosis & bile duct proliferation Liver biopsy  In extrahepatic biliary atresia:expansion of portal areas with fibrosis & bile duct proliferation  In idiopathic hepatitis: gaint cell transformation

Neonatal seizures
Laboratory CBC, differential count & platelet count Blood culture Blood chemistry: Glucose ,calcium ,magnesium ,electrolytes & blood gases CSF analysis & culture Imaging Cranial ultrasonography For hemorrhage CT scan For hypoxic ischemic encephalopathy, hemorrhage & malformations EEG
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Investigations in Pediatrics
Specific tests for suspected cases TORCH screening ,ammonia level & amino acids in urine Normal in one third of cases

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nutrition Marasmus & KWO
Laboratory Blood picture Anemia &leucocytosis Plasma proteins Low total protein(N: 6-8 gm %) Low serum albumin Low serum alpha & beta globulins but increased gamma globlins Glucose Hypoglycemia(impaired glycogenolysis) Electrolytes K:Decreased (lost in diarrhea –low dietary intake – aldosterone effect) Na:Total Na increased (aldosterone effect) but serum Na decreased water retention (dilutionalhyponatremia) Mg: decreased Imaging Chest x-ray To exclude chest infections

Rickets
Laboratory Serum calcium Normal (N: 9-11 mg %) Or decrease in causes of tetany:  Severe cases(depletion of ca in bones)  Parathyroid exhaustion  Shock therapy with vitamin D Imaging Active rickets Epiphysis: wide Joint space (translucent non calcified area) Metaphysis :  Epiphyseal line: Frayed, irregular  Cupping (concavity) & widening
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Investigations in Pediatrics
Serum phosphorus Markedly decreased (normal 4.5-6.5mg %) Serum alkaline phosphatase High (earliest manifestation) Urine Phosphate & amino acids.

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Diaphysis:  Rafraction (decreased bone density)  Double periosteal line due to subperiostealdeposition of osteoid tissue (translucent)  Pathological fractures (green stick) Healing rickets (2 weaks of vit D therapy)  No fraying :concave continuous line of provisional calcification ,separate form the lower end of bone (osteoid tissue in between) Healed rickets  Thick dense transverse line of provisional calcification  Improved bone density

respiratory Pneumonia
Laboratory Nasopharyngeal aspirate Useful to identify viral causes. CBC and acute-phase reactants Unhelpful in differentiating between viral and bacterial causes. Imaging Chest X-ray: may confirm the diagnosis but with the exception of a classic lobar pneumonia characteristic of Streptococcus pneumoniae.  Cannot differentiate between bacterial and viral pneumonia.  Showing cavities containing fluid and air is characteristic of staphylococcal pneumonia.  Show consolidation,parapneumonic effusion (blunting of the costophrenic angle) or empyema. Ultrasound of the chest will distinguish between parapneumonic effusion and
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Investigations in Pediatrics
empyema.

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Bronchiectasis
Laboratory Imaging Sputum culture x-ray & sensitivity test honey comb or soap bubble appearance CT Others Bronchography Bronchoscopy

Empyema (purulent pleurisy)
Laboratory Thoracocentesis The collected fluid is examined (culture & sensitivity) to determine the causative organism Imaging x-ray  obliteration of costo-phernic angle by homogenous opacity raising to the axilla  pushing the mediastinum to the opposite side

Bronchiolitis
Laboratory Nasopharyngeal secretions demonstrating binding of fluorescent antibody. Blood gas analysis (In severe cases only) show lowered arterial o2 and raised co2 tension. Imaging Chest X-ray: hyperinflation of the lungs (due to small airway obstruction, air trapping and often focal atelectasis.

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Investigations in Pediatrics Bronchial asthma
-Usually the diagnosis is clear from the history and no investigations are needed. -Often response to treatment is the most helpful investigation. Laboratory IgE(total & specific to common antigens) Increased in atopic asthma Skin tests with common antigens To detect the cause Inhalation bronchial challenge tests – exercise challenge test. Pulmonary function tests. To assess the degree of airway obstruction Peak expiratory flow rate (PEFR) Most children over 5 years of age can use a peak flow meter. Asthma results in increased variability in peak flow, both diurnal variability (morning PEFR usually lower than evening PEFR) and day-to-day variability (change in PEFR over the course of a week). Imaging

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chest X-ray usually normal but may help to rule out other conditions.  Hyper inflated chest

TB
Laboratory
Skin test (Tuberculin) Principle :detection of delayed hypersensitivity induced by TB bacilli or BCG Administration :PPD(purified protein derivative)0.1 ml I.D. in the flexor surface of forearm Interpretation: after 48-72 hours( by measuring

Imaging X-ray Any lesion e.gmediatinal shadow, miliray shadows CT

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Investigations in Pediatrics
the induration not the erythema)  negative =no reaction or induration less than 5 mm Either : 1. good negative result (no TB infection) 2. false negative result  positive result =induration 10 mm or more Either : 1. TB infection 2. BCG vaccination(false positive )  Doubtful reaction =induration 6-9mm( test should be repeated) CBC Anemia ESR Elevated CRP Positive Isolation & culture of the organism Sample :sputum –gastric aspirate – stomach wash  Direct smear with Z.N stain (acid-fast organism)  Culture on lowensteinjensen medium which requires 4-6 weeks Biopsy L.N. , skin, pleura

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N.B:  Negative results due to : 1. Testing in the pre-allergic state after infection but before the development of sensitization which takes 6-8 weeks 2. Tuberculin used is inactivated or given S.C. 3. Immunosuppression: facors interfering with activation: Fulminant TB, corticosteroids therapy ,immunosuppressent,severe malnutrition ,chronic diseases with cachexia & recent viral infections or vaccinations  Recent laboratory tests: 1. New rapid culture technique in 7-10 days (bactec radiometric system) 2. ELISA: to detect specific antibodies

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Investigations in Pediatrics
3. PCR

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Cardiology Fallot tetralogy
Laboratory CBC: increase Hb&Hct (microcytosis if there is iron deficiency) Imaging & others

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CXR: -Heart: Coeur en sabot (boot-shaped)  Normal size (normal cardio-thoracic ratio)  RV hypertrophy (acute cardio-phrenic angle)-uplifted apex  Exaggerated cardiac waist (small pulmonary artery) -Chest: lung oligemia(decrease vascularity) ECG: hypertrophy of the RA &RV(mild) ECHO: for anatomical defects(pulmonary stenosis(usually infundibular, may be valvular), big VSD, overriding aorta & RVH) Catheterization (usually needed before surgery)

Transposition of the great arteries(TGA)
Laboratory Imaging & others

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CBC: increase Hb&Hct

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CXR: -Heart: Egg on side Cardiomegaly Narrow pedicle -Chest: lung plethora( PVMs) ECG: hypertrophy of the RV ECHO: for anatomical defects(aorta arises from RV, pulmonary artery arises from LV &communication either ASD, VSD or PDA)
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Investigations in Pediatrics 
Catheterization

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Ventricular septal defect (VSD)
IF SMALL  CXR: normal  ECG: normal  ECHO: diagnostic for showing the anatomical defect(defect in the interventricular septum either membranous or muscular)-showing the size ,site &direction of flow through the shunt  Catheterization: if not improved with age IF LARGE  CXR: -Heart: biventricular enlargement -Chest: lung plethora ( PVMs)  ECG: biventricular hypertrophy  ECHO: for anatomical defect(defect in the interventricular septum either membranous or muscular)  Catheterization

Atrial septal defect (ASD)
    Ostiumsecundum CXR: -Heart: RV hypertrophy -Chest: lung plethora ( PVMs) ECG: RV hypertrophy ECHO: for anatomical defect(high defect in intratrial septum) Catheterization     Ostiumprimum CXR: -Heart: biventricular enlargement -Chest: lung plethora ( PVMs) ECG: biventricular enlargement ECHO: for anatomical defect(defect in the lower intratrial septum, cleft anterior leaflet & mitral regurge) Catheterization may be needed, to assess the magnitude of the shunt & the
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Investigations in Pediatrics
degree of mitral regurgitation

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PDA&Coarctation of aorta PDA     
CXR: -Heart: LV enlargement -Chest: lung plethora ( PVMs) ECG: LV enlargement ECHO for study of anatomical defects(persistence of the ductusarteriosus) Doppler: flow across the vessels Catheterization

Coarctation of aorta
 CXR: -Heart: LV enlargement -Chest: rib notching (older children) Normal pulmonary blood flow  ECG: LV enlargement  ECHO: for anatomical defects(localized narrowing of the aorta)  Catheterization

N.B. Rib notching: enlarged intercostal arteries have eroded the underside of the ribs

Aortic stenosis&Pulmonary stenosis Aortic stenosis 
CXR: -Heart: LV enlargement -Chest: Normal pulmonary blood flow

Pulmonary stenosis
 CXR: -Heart: RV hypertrophy -Chest: normal pulmonary blood flow  ECG: RV hypertrophy, prolonged P-R interval  ECHO: for anatomical defects(if valvular(fusion of cusps), supravalvular or subvalvular)
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ECG: LV enlargement  ECHO: for anatomical defects (if valvular(fusion of cusps), supravalvular(as in William

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Investigations in Pediatrics
syndrome) or subvalvular)  Catheterization

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Catheterization

Rheumatic fever
Acute phase reactants Evidence of recent streptococcal (degree of infection inflammation)  Elevated ESR  Antistreptolysin O titer (ASOT) > More than 50 mm is 300 Todd units(normal 150) st suggestive (normal 1  Antistreptokinase nd hour=3-7 mm ,2  Antihyaluronidase hour=8-15 mm)  Throat culture( usually negative)  Elevated CRP  Leucocytosis Cardiac assessment

 CXR: cardiomegaly  ECG: tachycardia & prolonged P-R interval  ECHO: chamber enlargement & valve affection N.B. investigations are normal in isolated chorea due to long latent period

Infective endocarditis
    NB:  The 3 cultures should be obtained within 24-48 hours Laboratory Blood culture (repeated 3 times after proper skin decontamination) CBC:leukocytosis ESR & CRP Urine analysis :heamaturia Imaging  CXR, ECG & ECHO(for vegetations & anatomical defects)

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 Absence of vegetations dose not exclude infective endocarditis  TEE is more accurate (vegetations)

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hematology Iron deficiency anemia
laboratory To diagnose anemia as iron def. anemia:  CBC: o Microcytic hypochromic anemia (color index is below one) o Normal reticulocytic count (usually increases with initiation of iron therapy)  Serum iron: (normal level is 90-150 microgram/dl)  Serum ferritin:  Iron binding capacity: (normal level is 250-350/dl)  Bone marrow:hyperactive (erythroid hyperplasia), not necessary in most cases To diagnose the cause:  Stool: occult blood or parasites.  Investigations for GIT bleeding or mal-absorption.

Thalassemia
Evidence of chronic hemolytic anemia  CBC: Microcytic hypochromic anemia Increased reticulcytic count  Serum iron & serum ferritin:↑↑  Iron binding capacity:↓↓  Unconjugated hyperbirubinemia Diagnostic investigations Laboratory:  Hb-electrophoresis  Increased Hb-F (10-90%)betathalassemia major  Increased Hb-A2 (above 4%) betathalassemia minor
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 Urine analysis:↑↑urobilinogen  Blood film:target cells, anisocytosis&poikilocytosis  Stool analysis:↑↑stercobilinogen  Bone marrow: hyperactive (erythroid Imaging: hyperplasia), not necessary.  Skull x-ray: shows wide deploic space, but this finding is late & not important for diagnosis

Sickle cell anemia
Evidence of chronic hemolytic anemia as thalassemia Diagnostic investigations  Blood film: sickle-shaped red cells in the peripheral blood  Hb-electrophoresis:↑↑Hb-S In homozygous form: 90-100% & absent Hb-A In heterozygous form: 20-40% &HbA (60-80%) Diagnostic investigations  Blood film:spherocytes in the peripheral blood.  Osmotic fragility test:+ve

Hereditary Spherocytosis
Evidence of chronic hemolytic anemia as thalassemia

G6PD deficiency
To diagnose Acute Hemolytic Anemia

 CBC:
o Acute anemia with fragmented RBCs o Reticulocytosis >5% o Unconjugated bilirubin: increased

To diagnoses G6PD def. Estimation of the activity of the enzyme 3 weeks after the attack. (immediately after the attack, there is high level of reticulocytes that have relatively higher enzymatic activity that may give false normal results)

 Urine:
Hemoglobinuria

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Investigations in Pediatrics Immune Thrombocytopenic purpura (ITP) &HenochSchonleinpurpura
ITP  CBC: Thrombpcytopenia (usually below 20.000/mm2) Anemia: if present, is related to blood loss WBCs count: normal with relative lymphocytosis  Bone marrow:normal or ↑↑megakaryocytes with defective budding  Anti-platelet antibodies: in 60% of cases only Henoch-Schonlein  CBC: normal platelet count  Normal platelet function

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Aplastic anemia & Acute leukemia
Aplastic anemia  CBC: Pancytopenia (anemia, leucopenia & thrombocytopenia)  Bone marrow: hypocellular with decreased precursors of the 3 blood elements]  Chromosomal study: Increased chromosomal breakage. Acute leukemia  CBC: o Anemia and thrombocytopenia in the peripheral blood. o Leukemic lymphoblasts (ALL)  Bone marrow: o Blast cells: in acute lymphblastic leukemia (ALL) o Myeloid cells: in acute myeloid leukemia (AML)

Hemophilia A & Hemophilia B & Von Willibrand disease
Hemophilia A (classic hemophilia)  Bleeding time (BT):normal  Partial thromboplastine time (PTT):↑↑↑significant prolongation. Hemophilia B (Christmas disease)  Bleeding time (BT):normal  Partial thromboplastine time (PTT): ↑↑↑significant prolongation. Von Willibrand disease    CBC:normal platelet count. Bleeding time (BT):↑↑prolonged.(decre ased platelet adhesion) Platelet functions: www.medadteam.org

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 Specific factor VIII assay:determines the severity.  Factor IX plasma level:↓↓  

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↓↓aggregation. Partial thromboplastine time (PTT):↑↑prolonged. Reduced levels of VW protein, VW factor & factor VIII activity

Neurology Epilepsy
laboratory  Fasting blood sugar, calcium, magnesium, urea , creatinine.  CSF examination: to exclude CNS infection if the patient is febrile. imaging  EEG.  CT scan and MRI : When an intracranial organic lesion is suspected. specific  Plasma and urine aminogram or a TORCH screening: may be required if the clinical picture is suggestive (microcephaly, recurrent seizures, jaundice, hepatosplenomegaly, cataract, history of repeated abortion or still birth).

Meningitis
laboratory  Lumbar puncture and CSF examination.  Culture and sensitivity study of CSF.  Antibody and PCR:for viral infection is done to exclude viral meningitis and encephalitis. Imaging  Chest x-ray:iftuberculous meningitis is suspected.

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Encephalitis
laboratory imaging  CSF examination :typical  EEG, CT scan and MRI: CSF findings in viral a. EEG: a diffuse bilateral encephalitis include slowing of background a. Increased intracranial activity is the most pressure usual finding b. MRI :is helpful in postb. Variable pleocytosis infectious encephalitis (10-500 cells/mm3) (foci of mainly lymphocytes demyelination). c. Increased protein Herpes simplex has a level (>40 mg/dl) special predilection to d. Normal glucose level the temporal lobe. e. CSF should be also examined for bacteria, mycobacterium, fungi and viruses.  Serologic tests: Hemagglutination inhibition and complement fixation tests ELISA Others  Brain biopsy:for culture and rapid viral antigen tests. Diagnosis of herpes simplex encephalitis is best done by brain biopsy

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Investigations in Pediatrics Brain abscess & Cerebral palsy
Brain abscess  CT scan: rounded hypodense lesion. With contrast-enhanced CT, the abscess capsule shows a thin-walled regular “ring enhancement”.  MRI.

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Cerebral palsy  CT scan of the head: o Location & extent of the lesion. o Associated malformation or brain atrophy.  EEG

Hydrocephalus & Microcephaly
Hydrocephalus  CT scan of the head: o Obstructive hydrocephalus, there is dilatataion only proximal to obstruction. o Communicating hydrocephalus, all ventricles are dilated. Microcephaly  Karyotype: if a chromosomal abnormality is suspected or of the child have dysmorphicfeatures , short stature and additional congenital anomalies.  TORCH profile:for both mother and child should be done.  CT scan and MRI:may identify structural abnormalities of the brain , intracranial calcification (as in toxoplasmosis and cytomegalovirus infection) or brain atrophy.

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Investigations in Pediatrics

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Guillainbarre syndrome & Progressive motor weakness &Duchenne muscular dystrophy
Guillainbarre  CSF examination: (2 weeks after the onset of paralysis) shows increased proteins.  Electromyography:is diagnostic of peripheral nerve affection. Progressive motor weakness  With suspected brain disease:CT scan and MRI  With suspected spinal cord lesion:CT scan or MRI of the spinal cord  With suspected muscle disease:serum CPK, electromyography and muscle biopsy Duchenne  Serum creatine phosphokinase (CPK):is elevated 10-200 times higher than normal. It is elevated before muscle weakness so it can be used as a screening test.  Electromyography and muscle biopsy:(characteristic)

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Investigations in Pediatrics nephrology Nephrotic syndrome
laboratory  Urine analysis: proteinuria (urinary proteins >40 mg/m2 /h). proteinuria in minimal change nephritic syndrome is selective (mainly albumin loss)  Renal function tests and C 3 : usually normal  Serum albumin:hypoproteinemia (reduced serum albumin below 2.5 gm/dl)  Serum cholesterol: hyperlipidemia (elevated plasma cholesterol and triglycerides)

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Others  Renal biopsy :only indicated in a. Age < 1 year or >8 years b. Persistent hematuria or hypertension c. Renal failure d. Steroid resistance e. Family history of renal disease - With light microscope , the glomeruli appear normal or mild increase in mesangial cell - With electron microscope , there is alteration and fusion of epithelial cell foot processes.

Post-streptococcal glomerulonephritis
Post-streptococcal glomerulonephritis  Urine analysis: hematuria, mild proteinuria, granular and red cell casts.  Blood chemistry: Increased serum urea and creatinine. Reduced complement 3 level (important).  Cultures and serology:  Cultures from the throat and from the skin.  Antistreptococcal antibodies (ASO titer , anti- DNAase, anti  
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Chronic renal failure Renal function tests:persistent elevation of blood urea and serum creatinine levels. Acid base balance:chronic metabolic acidosis. Serum phosphate:hyperphosphatemia. Serum calcium:hypocalcemia. Serum potassium :usually high. GFR: reduced.

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Investigations in Pediatrics
hyaluronidase).

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Urinary tract infection
diagnostic
 Urine analysis: (for detection of pyuria): - Presence of > 5 WBC’s per high power field. - Numerous cells are usually present in acute infection. However , it is unreliable because false positive and false negative results are common.  Urine culture: (for detection of bacteriuria): - The only reliable test. - Presence of more than one organism in culture indicates contamination. 

Other investigations Abdominal ultrasound:with suspected pyelonephritis, pyonephrosis.  CBC and CRP:with suspected pyelonephritis.

Investigations of recurrent urinary tract infection
     Abdominal x-ray:to exclude radio-opaque urinary calculi. Abdominal ultrasound:to exclude obstructive uropathy. Intravenous pyelography (IVP) :to exclude obstructive uropathy. Evaluation of renal function:to exclude chronic renal failure. Voiding cystourethrography (important):to exclude vesico-ureteral reflux.

Chronic RF
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Chronic renal failure Renal function tests: Persistent elevation of blood urea and serum creatinine levels. Acid base balance: Chronic metabolic acidosis. Serum phosphate: hyperphosphatemia. Serum calcium: hypocalcemia. Serum potassium : Usually high. GFR: Reduced.
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Investigations in Pediatrics ENDOCRINOLOGY Primary hypothyroidism
laboratory  Serum T4 level:low (normal range: 512 microgram/dl)  TSH:high (normal range: 0.5-4 mU/L). markedly raised (above 50 mU/L)

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Imaging  Delayed bone age: Detected radiologically. Characteristic for congenital hypothyroidism.  Radioactive iodine assay: Essential for diagnosis of the cause of hypothyroidism.

Diabetes mellitus
Type 1 :  Fasting blood glucose:venous sample > 126 mg/dl.  Two hours post prandial:venous sample >200 mg/dl.  Random blood glucose sample :>200 mg/dl (with presence of symptoms of diabetes).  Acid-base balance:metabolic acidosis (low pH and bicarbonate).  Urine analysis:glycosuria and ketonuria.  Increased glycosylated Hb. Type 2: Suspected if there is family history DKA: Blood glucose (>11.1 mmol/L) Urea and electrolytes, creatinine (dehydration) Blood gas analysis (severe metabolic acidosis) Urinary glucose and ketones (both are present) Evidence of a precipitating cause, e.g. infection (blood and urine cultures performed) Cardiac monitor for T-wave changes of hypokalaemia Weight

Laboratory

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Investigations in Pediatrics GIT & HEPATOLOGY Intussusceptions
Plain x-ray: Multiple air fluid levels.

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Abdominal masses
laboratory
 Bone marrow aspiration: Neuroblastoma or lymphoma  RFT: Bilateral renal mass

Imaging  US  IVP (In cases with renal masses)  CT

Biopsy
Laparotomy: (if malignancy is suspected)

Viral hepatitis
Acute viral hepatitis
Bilirubin: May be normal in the early stages, particularly with metabolic disease. Transaminases (AST , ALT): Elevated (10-100 times normal), Alkaline phosphatase: Increased Coagulation: abnormal (PT is prolonged) Plasma ammonia: Elevated. >150mcg%

Chronic viral hepatitis Laboratory: o Liver function test: abnormal o Hepatitis markers: +ve o Igs & auto Abs: in auto immune hepatitis. Imaging: o US o Endoscopy Liver biopsy: o Portal tract infiltration with chronic inflammatory cells.
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Investigations in Pediatrics
Acid-base balance: Hypokalemia , Hyponatremia & Metabolic acidosis. EEG: acute hepatic encephalopathy CT scan: May demonstrate cerebral oedema.

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o Bridging fibrosis between adjacent porto-portal or portocentral areas.

Cholestasis
Total and direct bilirubin: Elavated AST and ALT: Elevated Alkaline phosphatase and gamma glutamyl transpeptidase: Elevated Total serum proteins and albumin: Decreased Prothrompine time: Prolonged

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