📋 MOCK OSCE · FCPS, MCPS, MD PAEDIATRICS ⏱ 10 min · SPLENOMEGALY (VISCERAL LEISHMANIASIS)

Splenomegaly · Visceral Leishmaniasis (Kala‑azar)

Candidate task: perform focused clinical examination (GPE + abdominal examination) on a child with splenomegaly due to visceral leishmaniasis.
Then discuss differential diagnosis, investigations, management & follow‑up.
Pre‑exam Protocol
⏤ · Wash, Warm, Introduce, Position, Expose, Approach ▾

Standard pre‑examination protocol – must be demonstrated:

🖐 Wash hands with sterilizing solution.
🔥 Warm hands and stethoscope.
👋 Introduce yourself to child & parent.
🧍 Position child: standing → sitting → supine (left side down for spleen).
👕 Exposure — shirt off, trousers rolled to expose abdomen.
➡️ Approach from the right side.
✔ CPSP marker: Pre‑exam Protocol is observed and scored.
1. Clinical Examination (≈6 min)
02 General Look (Inspection from end of bed) ▾

Key observations in visceral leishmaniasis (Kala‑azar):

  • Abdomen: massive, symmetrical or asymmetrical distension — often massive splenomegaly (may cross midline, reach pelvis).
  • Nutritional status: severe wasting, cachexia, poor muscle bulk — “slim disease” appearance.
  • Skin: pallor (anaemia), hyperpigmentation (darkening of skin — “kala-azar” = black fever), xerosis.
  • Face: pale conjunctivae, malar flush (fever), oedema (hypoalbuminaemia).
  • Behaviour: lethargy, irritable, apathetic — chronic illness.
  • Lymph nodes: generalized lymphadenopathy (especially in African variant).
⚠ Red flags: massive splenomegaly + severe pallor + weight loss + fever → visceral leishmaniasis until proven otherwise in endemic areas.
03 General Physical Exam (Hands → Face → Chest → Limbs) ▾

Systematic examination:

  • Hands: pallor (anaemia), clubbing (rare), koilonychia (iron deficiency).
  • Face: pale conjunctivae, scleral icterus (rare), hyperpigmentation (Kala-azar), oedema (hypoalbuminaemia).
  • Chest: tachypnoea (anaemia, intercurrent infection), crackles (pneumonia — common co-infection).
  • Abdomen: see next step.
  • Lower limbs: oedema (hypoalbuminaemia, nephrotic syndrome — rare), bone tenderness (rare).
  • Temperature: may be febrile (double quotidian or intermittent).
  • Lymph nodes: generalized lymphadenopathy (especially in African Kala-azar).
📏 Anthropometry: weight, height, BMI — plot growth. Chronic leishmaniasis causes growth failure.
04 Abdominal Examination — Focus on Spleen ▾

Systematic approach — splenic palpation:

  • Inspection: left upper quadrant fullness, visible mass (massive splenomegaly) — may occupy entire abdomen.
  • Auscultation: bowel sounds (normal/obstructive), splenic rub (perisplenitis – rare).
  • Palpation — start from right lower quadrant:
    • Use bimanual technique — left hand lifts the left costal margin, right hand palpates.
    • Spleen characteristics: firm, smooth, non‑tender, moves with respiration, notch may be palpable.
    • Massive splenomegaly — crosses midline, reaches iliac fossa (classic in Kala-azar).
  • Percussion: Traube's space dullness (splenic enlargement).
  • Liver: hepatomegaly (common — moderate enlargement).
  • Rectal: if indicated — check for bleeding (coagulopathy).
🔍 Key: massive, firm, smooth, non‑tender spleen crossing midline + pallor + weight loss + fever → visceral leishmaniasis.
⚠ Splenic notch may be palpable — distinguishes from other massive splenomegaly (e.g., chronic myeloid leukaemia).
05 Developmental Assessment & Associated Signs ▾

Assess for systemic and developmental effects of chronic visceral leishmaniasis:

  • Growth: stunting, underweight — chronic infection, malabsorption, anorexia.
  • Neurological: lethargy, irritability, seizures (post‑kala‑azar dermal leishmaniasis — PKDL).
  • Haematological: pancytopenia (bone marrow suppression), anaemia, thrombocytopenia, leucopenia.
  • Hepatic: hepatomegaly (moderate), jaundice (rare).
  • Renal: proteinuria, nephrotic syndrome (rare).
  • Splenic complications: rupture (trauma, spontaneous), hypersplenism (pancytopenia).
  • Immune: hypergammaglobulinaemia (polyclonal), increased risk of bacterial infections (pneumonia, tuberculosis).
  • Post‑kala‑azar dermal leishmaniasis (PKDL): maculopapular rash, hypopigmented patches — can occur months to years after treatment.
🧠 Visceral leishmaniasis causes severe growth retardation, neurocognitive impairment, and long‑term disability if untreated.

📋 Case Presentation – (fill in during exam)

This is a _____-year-old _____ child, brought with _____ (abdominal swelling / fever / weight loss). On examination, the child appears _____ (well/unwell/cachectic), with _____ (pallor / hyperpigmentation / oedema). There is a _____ (firm / smooth / non‑tender) mass in the _____ (left upper quadrant / entire abdomen), measuring approximately _____ cm below the costal margin. The spleen _____ (does / does not) cross the midline, and _____ (has / does not have) a palpable notch. The liver is _____ (palpable / not palpable), _____ cm below the costal margin. Growth parameters: weight _____ percentile, height _____ percentile. Additional findings: _____ (pallor / hyperpigmentation / fever / lymphadenopathy / oedema / skin rash).

2. Viva Discussion (≈4 min)
06 Viva · Differential, Investigations, Management, Follow‑up ▾
🔹 Differential Diagnosis
  • Visceral leishmaniasis (Kala‑azar) – massive splenomegaly, pancytopenia, fever, weight loss
  • Chronic malaria – splenomegaly, anaemia, fever (periodic), haemolysis
  • Hyperreactive malarial splenomegaly (HMS) – massive spleen, high IgM
  • Portal hypertension – cirrhosis, portal vein thrombosis (splenomegaly + varices + ascites)
  • Haematological malignancies – leukaemia, lymphoma (splenomegaly + lymphadenopathy + blast cells)
  • Haemolytic anaemias – hereditary spherocytosis, thalassaemia (splenomegaly + jaundice + reticulocytosis)
  • Infectious mononucleosis – EBV, CMV (splenomegaly + lymphadenopathy + atypical lymphocytes)
  • Storage disorders – Gaucher, Niemann-Pick (splenomegaly + bone lesions + neurological)
  • Brucellosis – fever, splenomegaly, arthralgia, animal contact
  • Tuberculosis – abdominal TB, splenic abscess (rare)
  • Schistosomiasis – hepatosplenomegaly, portal hypertension, fresh water exposure
  • HIV/AIDS – associated with visceral leishmaniasis (co‑infection)
🔹 Investigations – Diagnosis
  • Splenic aspirate / bone marrow aspirate – demonstration of Leishman‑Donovan bodies (amastigotes) – gold standard
  • Serology (rK39) – rapid immunochromatographic test (high sensitivity/specificity)
  • Direct agglutination test (DAT) – highly specific, useful in endemic areas
  • Polymerase chain reaction (PCR) – high sensitivity, species identification
  • Full blood count (FBC) – pancytopenia (anaemia, leucopenia, thrombocytopenia)
  • Quantitative buffy coat (QBC) – can detect amastigotes in peripheral blood (rare)
  • Culture (NNN medium) – promastigote growth (reference laboratory)
🔹 Investigations – Aetiology
  • Species identification – Leishmania donovani (Indian subcontinent, Africa) vs L. infantum (Mediterranean, South America)
  • HIV co‑infection – CD4 count, HIV serology (important in endemic areas)
  • Immunoglobulin levels – hypergammaglobulinaemia (polyclonal)
  • Travel & exposure history – key to identifying endemic exposure (sandfly bite)
  • Family history – similar symptoms in family members (common in outbreaks)
🔹 Investigations – Exclude Others
  • Chest X-ray – pneumonia, tuberculosis, mediastinal mass
  • Abdominal ultrasound – splenic size, structure, portal vein, biliary tree, ascites
  • Liver function tests (LFTs) – jaundice, hepatitis, biliary obstruction
  • Renal function tests (U&E, creatinine) – nephrotic syndrome (rare)
  • Blood cultures – bacteraemia (co‑infection with Salmonella, pneumococcus)
  • EBV / CMV serology – infectious mononucleosis
  • Tuberculin skin test / IGRA – tuberculosis
  • Schistosoma serology / stool O&P – schistosomiasis
  • Bone marrow biopsy – leukaemia, lymphoma, storage disorders
🔹 Investigations – Rule Out Complications
  • Severe anaemia – Hb < 5 g/dL (transfusion threshold)
  • Bleeding diathesis – PT/APTT, platelet count (DIC, hypersplenism)
  • Splenic rupture – ultrasound, haemodynamic instability, falling Hb
  • Hypersplenism – pancytopenia, reticulocyte count, marrow examination
  • Secondary infections – blood cultures, urine culture (pneumonia, tuberculosis, HIV)
  • Post‑kala‑azar dermal leishmaniasis (PKDL) – skin examination, biopsy (if rash)

🔹 Management – Across Organ Systems

Antileishmanial Therapy

First‑line (Indian subcontinent): Liposomal amphotericin B (AmBisome) — single dose 10 mg/kg IV.
First‑line (Africa, South America): Sodium stibogluconate (SSG) 20 mg/kg/day IV/IM for 28 days.
Alternative: Miltefosine (2.5 mg/kg/day PO for 28 days) — for older children.
Paromomycin (11 mg/kg/day IM for 21 days) — combination therapy.
Combination therapy: SSG + paromomycin, AmBisome + miltefosine (to reduce resistance).

Supportive Care

• Anaemia: packed RBC transfusion if Hb < 5 g/dL or symptomatic.
• Bleeding / thrombocytopenia: platelet transfusion if < 20,000 or active bleeding.
• Nutritional support: high‑calorie, high‑protein diet; micronutrients (iron, zinc, vitamin A).
• Fever management: antipyretics (paracetamol).
• Monitor for complications: ECG (for SSG — QT prolongation), renal function (amphotericin B).

Complication Management

• Splenic rupture: urgent splenectomy.
• Severe anaemia: transfusion.
• Co‑infections: treat pneumonia, tuberculosis, HIV (ART).
• PKDL: treat with liposomal amphotericin B or miltefosine.
• Relapse: treat with alternative drug (e.g., AmBisome for SSG failure).

Prevention & Control

• Vector control: insecticide‑treated nets (ITNs), indoor residual spraying (IRS).
• Sandfly repellents: DEET, permethrin‑treated clothing.
• Reservoir control: treat infected dogs (for L. infantum), culling infected animals.
• Surveillance: early diagnosis and treatment to reduce transmission.
• Vaccine: no human vaccine available.

Post‑Splenectomy

• Vaccinations: pneumococcal (PCV13, PPSV23), meningococcal, Haemophilus influenzae type b.
• Antibiotic prophylaxis: penicillin V (or amoxicillin) daily for ≥2 years.
• Parent education: fever = medical emergency, avoid travel to endemic areas.
• Monitor for sepsis: early antibiotic therapy.

Long‑term Follow‑up

• Test of cure: splenic aspirate (if available) — but response usually clinical.
• Monitor for relapse: fever, splenomegaly, pancytopenia.
• PKDL surveillance: skin examination for 2 years after treatment.
• Growth monitoring: catch‑up growth after successful treatment.
• Neurodevelopment: cognitive assessment, school performance.

📈 Prognosis

Untreated Kala‑azar
>95% mortality
Treated (uncomplicated)
~90–95% cure
HIV co‑infection
~50–70% cure
Relapse
~5–10%
Post‑kala‑azar dermal leishmaniasis (PKDL)
~5–10% (Indian subcontinent)
Post‑splenectomy sepsis
~1–5% lifetime risk
  • ✓ Good prognosis factors: early diagnosis, prompt treatment (liposomal amphotericin B).
  • ✗ Poor prognosis factors: HIV co‑infection, malnutrition, delayed treatment, severe anaemia.
  • ↗ Growth & development: catch‑up growth expected after successful treatment.

📋 Follow‑up Schedule

💡 Examiner expectation: logical differential (Kala‑azar vs other causes of massive splenomegaly), systematic investigation (diagnosis → aetiology → exclude others → complications), and a management plan covering antileishmanial therapy, supportive care, and prevention. Know the WHO classification and treatment guidelines for visceral leishmaniasis.
📚 Visit paeds.online for more CPSP resources
Mock OSCE · Splenomegaly (Visceral Leishmaniasis) · Based on Wyne‑Harris, Nelson & Pediatric Clinical Advisor