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    Cerebral Malaria Discussion

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    hari.mmc2011
    This document discusses cerebral malaria, which is caused by Plasmodium falciparum infection. It outlines the signs and symptoms of cerebral malaria, including unrousable coma. It also discusses the potential causes, including impaired cerebral blood flow and increased cytokine production. Indicators of a poor prognosis are listed. The document provides details on diagnosing cerebral malaria and potential neurological sequelae in children who survive the condition.

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    Cerebral Malaria Discussion

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    hari.mmc2011
    14 views13 pages
    This document discusses cerebral malaria, which is caused by Plasmodium falciparum infection. It outlines the signs and symptoms of cerebral malaria, including unrousable coma. It also discusses the potential causes, including impaired cerebral blood flow and increased cytokine production. Indicators of a poor prognosis are listed. The document provides details on diagnosing cerebral malaria and potential neurological sequelae in children who survive the condition.

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    CEREBRAL MALARIA PPT

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    This document discusses cerebral malaria, which is caused by Plasmodium falciparum infection. It outlines the signs and symptoms of cerebral malaria, including unrousable coma. It also discusses the potential causes, including impaired cerebral blood flow and increased cytokine production. Indicators of a poor prognosis are listed. The document provides details on diagnosing cerebral malaria and potential neurological sequelae in children who survive the condition.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    14 views13 pages

    Cerebral Malaria Discussion

    Uploaded by

    hari.mmc2011
    This document discusses cerebral malaria, which is caused by Plasmodium falciparum infection. It outlines the signs and symptoms of cerebral malaria, including unrousable coma. It also discusses the potential causes, including impaired cerebral blood flow and increased cytokine production. Indicators of a poor prognosis are listed. The document provides details on diagnosing cerebral malaria and potential neurological sequelae in children who survive the condition.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    of 13

    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

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