CEREBRAL MALARIA- DISCUSSION

UNIT V
MALARIA

● Malaria is a protozoan disease transmitted by the bite of infected female

Anopheles mosquitoes.
● Six species of the genus Plasmodium cause nearly all malarial infections
in humans. These are
● P. falciparum,
● P. vivax
● P. ovale (curtisi and wallikeri)
● P. malariae
● P. knowlesi
While almost all deaths are caused by falciparum malaria, P. knowlesi and
occasionally P. vivax can also cause severe illness.
Life cycle of Plasmodium
Manifestations of
● Unarousable coma/cerebral malaria
Severe falciparum
● Acidemia/ acidosis
malaria
● Severe normochromic, normocytic anemia
● Renal failure
● Pulmonary edema/ARDS
● Hypoglycemia
● Hypotension/ shock
● Bleeding/ DIC
● Convulsions
 ●
PATHOGENESIS OF Causes of Cerebral malaria and coma is not exactly
known

CEREBRAL ● Increase in cerebral anaerobic glycolysis with low

oxygen arterial content- cerebral blood flow

MALARIA ● Increased cerebral metabolic rates for lactate and

increased CSF concentrations of Lactate – indicates
impaired cerebral perfusion
● Highly metabolically active parasites and their
attachment to the cerebral vascular endothelium –
interferes with endothelial and blood brain barrier
function.
● Increase in cytokines- increased production of nitric
oxide- inhibits neurotransmitters- impairment of
consciousness.
Cerebral Malaria

● Coma is a characteristic and ominous feature of falciparum malaria - onset may be gradual or sudden following a
convulsion.
● Convulsions are usually generalized and often repeated, - 50% of children with cerebral malaria.
● More covert seizure activity is common- repetitive tonic–clonic eye movements or even hypersalivation.
● Cerebral malaria manifests as diffuse symmetric encephalopathy;
● Signs:-
○ Focal neurologic signs are unusual.
○ Signs of meningeal irritation are absent.
○ Muscle tone may be either increased or decreased.
○ Eyes may be divergent, and bruxism and a pout reflex are common, but other primitive reflexes are usually absent
○ Corneal reflexes are preserved, except in deep coma.
○ Tendon reflexes are variable
○ Plantar reflexes may be flexor or extensor; abdominal & cremasteric reflexes are absent
● . Flexor or extensor posturing may be seen.
On routine funduscopy,

● retinal hemorrhages (15%)

● discrete spots of retinal opacification (30–60%),
● papilledema (8% among children, rare among
adults),
● cotton wool spots (<5%), and
● decolorization of a retinal vessel or segment of
vessel (occasional cases).
 ● Marked agitation
● Hyperventilation (respiratory distress)
Indicators of Poor ●
●
Low core temperature (<36.5°C; <97.7°F)
Bleeding
prognosis ● Deep coma
● Repeated convulsions
● Anuria
● Shock
● Hypoglycemia (<40 mg/dL) Hyperlactatemia
(>5 mmol/L)
● Acidemia (arterial pH <7.25 or serum HCO3 <15
mmol/L)
● Elevated serum creatinine
● Elevated total bilirubin
● Elevated liver enzymes (AST/ALT 3 times)
● Elevated muscle enzymes (CPK ↑)
● Elevated urate
● Leukocytosis (>12,000/μL)
● Severe anemia (PCV <15%)
● Coagulopathy
Neurological Sequelae
● Adults rarely (<3% of cases)

● 10% of children surviving cerebral malaria have residual neurologic

● hemiplegia,
● cerebral palsy,
● cortical blindness, deafness,
● impaired cognition.
● persistent language deficit.
● deficits in learning, planning and executive functions, attention, memory, and nonverbal functioning.

● Majority of these deficits improve markedly or resolve completely within 6 months , Some persists.
● The incidence of epilepsy is increased and life expectancy decreased
Diagnosis
PFHRP2 dipstick test Plasmodium LDH test Acridine orange stain
Thick smear of P. falciparum-
A- Trophozoites
B- Gametocytes