CEREBRAL MALARIA

Dr. Muhammad Sajjad Sabir

MCPS, FCPS (Paediatrics)

GLOBAL BURDEN OF MALARIA

GLOBALLY 300 MILLION MALARIA CASES A YEAR

1 MILLION DEATHS, 90% IN CHILDREN IN

AFRICA

MALARIA EPIDEMIOLOGY

LIFE CYCLE

WHAT IS CEREBRAL MALARIA?Sever form of malaria caused by P. falciparum Patient with malaria manifesting cerebral

dysfunction →cerebral malariamanifested by

Coma Convulsion and / or Hemoglobinuria

INCUBATION PERIOD

P. vivax and P. ovale 13~15 days

P. malariae 24~30 days

P. falciparum 7~12 days

EPIDEMIOLOGY

More Sever in children as No of parasites same in adult & child (proportionately smaller size)

Blood Gp A&B more protective than Gp O

Hb E & C more protective HbF , sickle cell trait & G6PD deficiency

lesser tendency for falciparum malaria

Malnutrition protective – immunity is low

Section of brain showing blood vessels

blocked with developing P. falciparum parasites

CLINICAL FEATURESPRODROMAL PHASE

FEBRILE PHASE

COMPLICATIONS –CEREBRAL MALARIA

CAUSES OF CNS DYSFUNCTION IN MALARIA

•HYPOGLYCEMIA•HIGH GRADE FEVER ALONE

•RENAL FAILURE•HEPATIC FAILURE

•SEPTICEMIA•SHOCK

CEREBRAL MALARIA FEATURESHigh grade fever, Seizures & SOMI -VE IMPAIRMENT OF CONSIOUSNESS –delerium

stupor,obtundation ,coma SIEZURES – focal /generalised (common in children)

MENINGISMUS NEURO-OPHTHALMOLOGIC SIGNS (gaze

deviation, oculomotor palsy, nystagmus)RETINAL HEMORRHAGE (in 15% patients) FOCAL NEUROLOGIC SIGNS (less common)(aphasia, hemiplegia, ataxia, chorea, and

tremor)

SEQUALETransient neurologic sequelae -

ataxia, hemiparesis, memory disturbance, visual field defects, cognitive impairment, and behavioral abnormalities

A postmalaria neurological syndrome characterized by acute onset of confusion, seizure, ataxia, myoclonus, tremor, and aphasia

COMPLICATIONS Severe anaemia Renal failure Pulmonary oedema Shock Spontaneous bleeding Repeated generalized convulsions

Acidemia or acidosisHypoglycemia

PROGNOSTIC FACTORSthe level of consciousness presence of other organ

dysfunctionRecurrent seizures,decerebration retinal hemorrhage, age < 3 years, heavy parasitemia, (>20%), lactic acidosis, elevated CSF lactate serum transaminase

DIFFERENTIAL DIAGNOSISPyogenic meningitis Viral encephalitis Febrile fitsSOLHepatic comaHypoglycemic comaUremia

DIAGNOSISDemonstration of asexual form of P. falciparum in peripheral blood smear, in thick and thin blood smear films stained by Giemsa stain. 

LIGHT MICROSCOPY

Thick blood film- enhanced sensitivity , low levels of parasitemia

Thin blood film.- identification of the parasite to the species level

Recommendations At least 3 smears 6 h apart should be examined before excluding cerebral malaria

Negative if anti-malarial given Upto 20% RBC’s may be infected

Thick & Thin film most specific

P. FALCIPARUM RINGS P. FACIPARUM GAMETOCYTES

Schizont stage –p vivax TROPHOZOITE P. FACIPARUM

CSF EXAMINATIONNecessary to exclude other causes of febrile

encephalopathy CSF is generally normal in cerebral

malaria Mild pleocytosis (10–50 cells/mm3) Protein rise up to 200 mg/dL Glucose - Normal

OTHER TESTS  Immuno Chromatographic Assay (ICT-

Malaria) Malaria antigen detection tests are a group of commercially available rapid diagnostic tests that allow quick diagnosis of malaria by people who are not otherwise skilled in traditional laboratory techniques

CBC Leucopenia Monocytosis Low Hb ↑sed Retics

BSR – hypoglycemia Serum electrolytes

CT Scan and MRI usually normal or show edema cortical or subcortical infarcts

EEG nonspecific abnormalities

diffuse slowing, spike wave discharges burst suppression pattern

MANAGEMENT

Neurologic emergency requiring urgent intervention.

In endemic area, treatment should be started without waiting for confirmation of the diagnosis

SPECIFIC THERAPY

TREATMENT OF MULTI ORGAN DYSFUNCTION

TREATMENT OF COMPLICATIONS

MANAGEMENT

TREATMENT OF CEREBRAL MALARIA

Severe malaria should always be treated with parenteral antimalarials

Drug of choice for cerebral malaria – Quinine Parenteral artemisinin derivatives or (widespread resistance to chloroquine)

QUININE a continuous and uniform flow of IV quinine

in dextrose solution should be maintained over a period of four hours

MONITORING Pulse Blood pressure Blood glucose QTc interval .

Quinine should be discontinued if QTc interval exceeds 25% of the basal value

IM injection carries the risk of necrosis at the injection site and the injection is very painful

never give as INTRAVENOUS push

IV quinine over 4Hrs in dextrose solution1mg diluted in 1ml of 5% dextrose

solution20mg/kg I.V stat10mg/kg I.V 8Hrly For 07 days Shift to oral when patient can take orally

10mg/kg/dose TDS for 7 days

QUININE

ARTEMETHER Injectable 3.2 mg /kg I.M stat then 1.6 mg /kg I.M BD for 2 daysCHLOROQUINE 25 mg/kg body weight divided over

three days i.e.10mg/kg on day 110mg/kg on day 2 and 5mg/kg on day 3

SUPPORTIVE MANAGEMENTHydration by administration of fluids

Oral fluids should be given if the patient is conscious and can swallow

High fever Paracetamol Brufen Tepid water sponging

MANAGEMENT OF COMPLICATIONS

INTENSIVE CARE UNIT VENTILATORY SUPPORT

Pulmonary oedema RENAL FAILURE

Care of hydrationDialysis(HEMODIALYSIS)1/3 ↓ dose of antimalarials

MANGEMENT OF COMPLICATIONSSevere anaemia

RCC transusion if Hb <6g/dlHypoglycemia

Glucose bolus I.V(50%, 25%, 10%)Repeated generalized convulsions

Diazepam Phenobarbitone

Acidemia or acidosisSoda bicarb

PROGNOSISMortality 10-30 %

Death mostly within 24 Hrs of admission

Residual neurological deficit in 10% of survivors

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