πŸ“‹ MOCK OSCE Β· FCPS, MCPS, MD PAEDIATRICS ⏱ 10 min Β· SPLENOMEGALY (CHRONIC MALARIA)

Splenomegaly Β· Chronic Malaria

Candidate task: perform focused clinical examination (GPE + abdominal examination) on a child with splenomegaly due to chronic malaria.
Then discuss differential diagnosis, investigations, management & follow‑up.
Pre‑exam Protocol
⏀ Β· Wash, Warm, Introduce, Position, Expose, Approach β–Ύ

Standard pre‑examination protocol – must be demonstrated:

πŸ– Wash hands with sterilizing solution.
πŸ”₯ Warm hands and stethoscope.
πŸ‘‹ Introduce yourself to child & parent.
🧍 Position child: standing β†’ sitting β†’ supine (left side down for spleen).
πŸ‘• Exposure β€” shirt off, trousers rolled to expose abdomen.
➑️ Approach from the right side.
βœ” CPSP marker: Pre‑exam Protocol is observed and scored.
1. Clinical Examination (β‰ˆ6 min)
02 General Look (Inspection from end of bed) β–Ύ

Key observations in chronic malaria:

  • Abdomen: asymmetrical bulging in left upper quadrant β€” splenomegaly. May cross midline in massive enlargement.
  • Nutritional status: may be wasted, stunted (chronic disease, malabsorption).
  • Skin: pallor (anaemia), jaundice (haemolysis), petechiae (thrombocytopenia).
  • Face: pale conjunctivae, scleral icterus, malar flush (fever).
  • Behaviour: lethargy, irritability, or apathy β€” especially during febrile episodes.
  • Respiratory: tachypnoea (anaemia, acidosis, or concurrent infection).
⚠ Red flags: pallor + jaundice + massive splenomegaly + fever in endemic area β†’ chronic malaria / hyperreactive malarial splenomegaly syndrome (HMS).
03 General Physical Exam (Hands β†’ Face β†’ Chest β†’ Limbs) β–Ύ

Systematic examination:

  • Hands: pallor (anaemia), clubbing (rare), koilonychia (iron deficiency).
  • Face: pale conjunctivae, jaundice (scleral icterus), malar flush (fever).
  • Chest: tachypnoea, crackles (pulmonary oedema in severe malaria), signs of pneumonia (co-infection).
  • Abdomen: see next step.
  • Lower limbs: oedema (nephrotic syndrome β€” quartan malaria), bone tenderness (rare).
  • Temperature: may be febrile (38–40Β°C) with periodic spikes.
  • Lymph nodes: generalized lymphadenopathy (especially in acute malaria).
πŸ“ Anthropometry: weight, height, BMI β€” plot growth. Chronic malaria causes growth failure.
04 Abdominal Examination β€” Focus on Spleen β–Ύ

Systematic approach β€” splenic palpation:

  • Inspection: left upper quadrant fullness, visible mass (massive splenomegaly).
  • Auscultation: bowel sounds (normal/obstructive), splenic rub (perisplenitis – rare).
  • Palpation β€” start from right lower quadrant:
    β€’ Use bimanual technique β€” left hand lifts the left costal margin, right hand palpates.
    β€’ Spleen characteristics: firm, smooth, non‑tender, moves with respiration, has a notch (inferior border).
    β€’ Massive splenomegaly β€” may cross midline, reach iliac fossa (chronic malaria, HMS, kala-azar).
  • Percussion: Traube's space dullness (splenic enlargement).
  • Liver: assess for hepatomegaly (concurrent liver involvement β€” common in malaria).
  • Rectal: if indicated β€” check for bleeding (coagulopathy).
πŸ” Key: firm, smooth, non‑tender spleen with a notch + pallor + fever in endemic area β†’ chronic malaria / hyperreactive malarial splenomegaly.
⚠ Splenic notch is a classical feature β€” distinguishes spleen from other masses (e.g., renal, ovarian).
05 Developmental Assessment & Associated Signs β–Ύ

Assess for systemic and developmental effects of chronic malaria:

  • Growth: stunting, underweight β€” chronic infection, malabsorption, anorexia.
  • Neurological: lethargy, irritability, seizures (cerebral malaria β€” acute), cognitive impairment (chronic).
  • Haematological: anaemia (haemolysis, bone marrow suppression), thrombocytopenia, leucopenia.
  • Hepatic: jaundice, hepatomegaly (congestive, haemolytic).
  • Renal: proteinuria, nephrotic syndrome (quartan malaria β€” P. malariae).
  • Splenic complications: rupture (trauma, spontaneous), hypersplenism (pancytopenia).
  • Immune: hypergammaglobulinaemia, increased risk of bacterial infections (pneumonia, meningitis).
🧠 Chronic malaria causes impaired neurocognitive development, school performance, and growth.

πŸ“‹ Case Presentation – (fill in during exam)

This is a _____-year-old _____ child, brought with _____ (abdominal swelling / fever / pallor). On examination, the child appears _____ (well/unwell), with _____ (pallor / jaundice / fever). 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 / jaundice / fever / lymphadenopathy / oedema).

2. Viva Discussion (β‰ˆ4 min)
06 Viva Β· Differential, Investigations, Management, Follow‑up β–Ύ
πŸ”Ή Differential Diagnosis
  • Chronic malaria – P. falciparum, P. vivax, P. malariae (quartan malaria)
  • Hyperreactive malarial splenomegaly (HMS) – massive spleen, high IgM, response to antimalarials
  • Visceral leishmaniasis (Kala-azar) – massive splenomegaly, pancytopenia, fever
  • Portal hypertension – cirrhosis, portal vein thrombosis (splenomegaly + varices)
  • Haematological malignancies – leukaemia, lymphoma (splenomegaly + lymphadenopathy)
  • Haemolytic anaemias – hereditary spherocytosis, thalassaemia (splenomegaly + jaundice)
  • Infectious mononucleosis – EBV, CMV (splenomegaly + lymphadenopathy + fever)
  • Storage disorders – Gaucher, Niemann-Pick (splenomegaly + bone lesions)
  • Brucellosis – fever, splenomegaly, arthralgia, exposure to animals
  • Tuberculosis – abdominal TB, splenic abscess (rare)
  • Schistosomiasis – hepatosplenomegaly, portal hypertension, exposure to fresh water
πŸ”Ή Investigations – Diagnosis
  • Thick & thin blood smear – identifies species, parasite density (gold standard)
  • Rapid diagnostic test (RDT) – HRP2 / pLDH (for P. falciparum)
  • Polymerase chain reaction (PCR) – species identification, low-level parasitaemia
  • Full blood count (FBC) – anaemia, thrombocytopenia, leucopenia
  • Malaria antigen detection – histidine-rich protein 2 (HRP2) / lactate dehydrogenase (pLDH)
  • Quantitative buffy coat (QBC) – fluorescent microscopy for malaria
  • Serial blood smears – if initial negative, repeat every 12–24 hours (up to 3 sets)
πŸ”Ή Investigations – Aetiology
  • Plasmodium species identification – critical for treatment (P. falciparum vs others)
  • Drug resistance testing – molecular markers (e.g., Pfcrt, Pfmdr1 for chloroquine resistance)
  • G6PD screening – before primaquine (for P. vivax / P. ovale hypnozoites)
  • Serology – anti-malarial antibodies (epidemiological, not acute diagnosis)
  • Travel & exposure history – key to identifying endemic exposure
  • Family history – haemoglobinopathies (sickle cell, thalassaemia) that modify malaria severity
πŸ”Ή Investigations – Exclude Others
  • Chest X-ray – pneumonia, tuberculosis, mediastinal mass
  • Abdominal ultrasound – splenic size, structure, portal vein, biliary tree
  • Liver function tests (LFTs) – jaundice, hepatitis, biliary obstruction
  • Renal function tests (U&E, creatinine) – nephrotic syndrome (quartan malaria)
  • Blood cultures – bacteraemia (co-infection with Salmonella, pneumococcus)
  • EBV / CMV serology – infectious mononucleosis
  • Bone marrow biopsy – leukaemia, lymphoma, kala-azar, storage disorders
  • Tuberculin skin test / IGRA – tuberculosis
  • Schistosoma serology / stool O&P – schistosomiasis
πŸ”Ή Investigations – Rule Out Complications
  • Cerebral malaria – lumbar puncture (if no contraindications), fundoscopy (retinal haemorrhages)
  • Severe anaemia – Hb < 5 g/dL (transfusion threshold)
  • Acute kidney injury – creatinine, urine output, electrolytes (blackwater fever)
  • Coagulopathy – PT/APTT, platelet count (DIC in severe malaria)
  • Metabolic acidosis – venous blood gas, lactate (poor prognosis)
  • Hypoglycaemia – blood glucose (especially in children, quinine therapy)
  • Splenic rupture – ultrasound, haemodynamic instability, falling Hb
  • Hypersplenism – pancytopenia, reticulocyte count, marrow examination

πŸ”Ή Management – Across Organ Systems

Antimalarial Therapy

Uncomplicated P. falciparum: Artemisinin-based combination therapy (ACT) – artemether-lumefantrine, artesunate-amodiaquine, dihydroartemisinin-piperaquine.
Chloroquine-sensitive: chloroquine (for P. vivax, P. ovale, P. malariae).
Primaquine – for hypnozoites (P. vivax, P. ovale) – G6PD screening required.
Severe malaria: IV artesunate (or quinine) + supportive care.

Supportive Care

β€’ Anaemia: packed RBC transfusion if Hb < 5 g/dL or symptomatic.
β€’ Hypoglycaemia: IV dextrose.
β€’ Fever: antipyretics (paracetamol).
β€’ Fluid balance: cautious IV fluids (avoid fluid overload).
β€’ Nutrition: high-calorie, high-protein diet; micronutrient supplementation (iron, zinc, vitamin A).

Complication Management

β€’ Cerebral malaria: anticonvulsants (phenobarbital, diazepam), manage ICP, maintain airway.
β€’ Acute kidney injury: haemodialysis / peritoneal dialysis if indicated.
β€’ Coagulopathy / DIC: fresh frozen plasma, platelet transfusion.
β€’ Splenic rupture: urgent surgery (splenectomy).
β€’ Blackwater fever: supportive care, stop quinine, consider exchange transfusion.

Prevention & Chemoprophylaxis

β€’ Vector control: insecticide-treated bed nets (ITNs), indoor residual spraying (IRS).
β€’ Chemoprophylaxis for travellers: atovaquone-proguanil, doxycycline, mefloquine (depending on resistance).
β€’ Intermittent preventive treatment (IPT) – in pregnancy (IPTp) and infants (IPTi).
β€’ Vaccination: RTS,S / AS01 (for children in endemic areas).

Hyposplenism / Post-splenectomy

β€’ Vaccinations: pneumococcal (PCV13, PPSV23), meningococcal (MenACWY, MenB), Haemophilus influenzae type b.
β€’ Antibiotic prophylaxis: penicillin V (or amoxicillin) daily for β‰₯2 years post-splenectomy.
β€’ Parent education: fever = medical emergency, avoid travel to endemic areas.

HMS (Hyperreactive Malarial Splenomegaly)

β€’ Prolonged antimalarial prophylaxis – chloroquine (if sensitive) or mefloquine, for β‰₯1 year.
β€’ Monitor spleen size – ultrasonography.
β€’ If no response – consider alternative diagnosis (kala-azar, lymphoma, portal hypertension).
β€’ Splenectomy – only if hypersplenism with cytopenias despite medical therapy.

πŸ“ˆ Prognosis

Uncomplicated Malaria
>95% survival
Severe Malaria (children)
~80–90% survival
Cerebral Malaria
~10–20% mortality
HMS
Good with prophylaxis
Blackwater Fever
~5–10% mortality
Post-splenectomy sepsis
~1–5% lifetime risk
  • Good prognosis factors: early diagnosis, prompt treatment, uncomplicated disease.
  • Poor prognosis factors: cerebral malaria, acidosis, AKI, hypoglycaemia, high parasite density (>10%).
  • Neurocognitive impairment – common after severe malaria in children.

πŸ“‹ Follow‑up Schedule

  • During acute treatment: daily blood smears until negative, monitor vital signs, urine output, glucose.
  • Post-treatment (day 7, 14, 28): blood smears to confirm clearance (test of cure).
  • For P. vivax / P. ovale: monitor for relapse (hypnozoites) – require primaquine.
  • HMS follow-up: monthly spleen size, Hb, IgM levels; antimalarial prophylaxis for β‰₯1 year.
  • Post-splenectomy: lifelong penicillin prophylaxis, vaccination, fever = medical emergency.
  • Growth monitoring: catch-up growth after successful treatment; micronutrient supplementation.
  • Neurodevelopmental follow-up: cognitive assessment, school performance, behavioural issues.
πŸ’‘ Examiner expectation: logical differential (chronic malaria vs HMS vs other causes of massive splenomegaly), systematic investigation (diagnosis β†’ aetiology β†’ exclude others β†’ complications), and a management plan covering antimalarial therapy, supportive care, and prevention. Know the WHO malaria classification and treatment guidelines.
Mock OSCE Β· Splenomegaly (Chronic Malaria) Β· Based on Wyne‑Harris, Nelson & Pediatric Clinical Advisor