Cerebral Malaria
Course Overview
Cerebral malaria is a life-threatening complication of Plasmodium falciparum infection, characterized by altered mental status, seizures, and coma. It often occurs alongside other severe malaria complications, including acute renal failure, disseminated intravascular coagulation (DIC), pulmonary edema, severe anemia, hyperparasitemia, and hypoglycemia. Prompt recognition and aggressive management are crucial to prevent mortality and long-term neurological sequelae.
Learning Objectives
By the end of this module, learners should be able to:
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Recognize the clinical features of cerebral malaria.
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Identify the appropriate investigations for diagnosis and monitoring.
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Initiate timely pharmacological interventions using parenteral and oral antimalarials.
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Monitor for complications such as hypoglycemia, renal failure, and DIC.
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Understand the supportive care measures for critically ill patients.
Pathophysiology
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Caused by Plasmodium falciparum, which leads to microvascular obstruction in the brain.
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Endothelial damage and inflammation cause cerebral edema, hypoxia, and neuronal injury.
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Other organs may be affected due to severe hemolysis, coagulopathy, and systemic inflammatory response.
Clinical Features
General Symptoms:
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Fever with chills, headache, nausea, vomiting
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Joint pains, backache, loss of appetite
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Abdominal pain and diarrhea
Severe/Cerebral Features:
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Altered mental status (confusion, disorientation)
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Reduced Glasgow Coma Scale (GCS)
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Convulsions or seizures
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Coma
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Fever or hypothermia
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Signs of other severe malaria complications: anemia, renal impairment, pulmonary edema
Investigations
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Malaria parasite identification: Blood slide microscopy or Rapid Diagnostic Test (RDT)
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Full blood count (FBC): check for anemia, thrombocytopenia
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Renal function tests (RFTs): monitor for acute kidney injury
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Liver function tests (LFTs): assess hepatic involvement
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Random blood sugar (RBS): detect hypoglycemia
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Neuroimaging (CT/MRI brain): to rule out alternative causes of altered mental status or complications
Management
A. First-line Therapy
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Intravenous/Intramuscular Artesunate:
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Dose: 2.4 mg/kg at admission (time = 0), then at 12 and 24 hours, then once daily until patient can take oral therapy
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Rationale: Rapid parasite clearance and reduced mortality compared to quinine
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B. Alternative Therapy
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Intravenous Quinine (if artesunate unavailable or hypersensitivity):
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Loading dose: 20 mg/kg in 10% dextrose at admission
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Maintenance: 10 mg/kg every 8 hours
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Infuse over 4 hours in 5% dextrose
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Switch to oral quinine as soon as patient can tolerate oral therapy
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Completion of therapy:
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Artemether/Lumefantrine orally to complete treatment once oral intake is possible
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Minimum 24 hours of parenteral therapy before switching
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C. Supportive Care
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Paracetamol: 10–20 mg/kg IV for fever
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Fluid management: careful monitoring to avoid fluid overload (risk of pulmonary edema)
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Seizure management: as needed, with anticonvulsants
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Monitoring: vital signs, urine output, neurological status
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Correction of complications:
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Hypoglycemia: administer IV glucose
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Severe anemia: consider blood transfusion
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Renal failure: supportive therapy or dialysis if indicated
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DIC: monitor coagulation and replace blood products as needed
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Key Summary Points
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Cerebral malaria is caused by Plasmodium falciparum, presenting with altered consciousness, seizures, or coma.
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It is a medical emergency requiring rapid antimalarial therapy and supportive care.
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Artesunate IV/IM is first-line treatment; quinine is reserved for contraindications or treatment failure.
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Monitor and manage complications: hypoglycemia, renal failure, anemia, DIC, pulmonary edema.
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Early recognition and aggressive intervention reduce mortality and long-term neurological deficits.
Recommended References
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WHO Guidelines for the Treatment of Malaria, 2023
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Malaria: Principles and Practice of Malaria, 3rd Edition, Warrell et al.
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Oxford Handbook of Tropical Medicine, 5th Edition
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Ministry of Health Zambia: National Guidelines for Malaria Treatment