Cerebral Malaria in Children: A Review of ... - Sudanjp.org

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SUDANESE JOURNAL OF PAEDIATRICS AND CHILD HEALTH VallO: 2010metastasis, transplant rejection, stroke, brain hypoxiaand related conditions. Indeed, platelets have beendetected during rejection episodes41InvolvementTumor necrosisof Cell Adhesion Moleculesfactor can induce or upregulatevarious cell adhesion molecules(CAM)on endothelialcells; the expression of these molecules was analyzedby immunohistochemistry.with CM showed a marked upregulationBrain vessels from miceof ICAM-1and vascular cell adhesion molecule 1(VCAM-1).42An attempt to prevent CM by intravenousinjection of anti-TNF monoclonalantibodies(MAbs)directed against LFA-1, Mac-I, ICAM-I, VCAM-I,VLA-4 and P-selectin;MAb proved to be efficient.showed that only anti-LFA-1The important role ofICAM -1 was confirmed using a SCID mouse modelin which P. falciparum-infectedto brain ICAM-Ideficient mice.43human RBC adhereand more recently using ICAM-1-An adhesion molecule CD36 also known asplatelet glycoprotein IV or IIIb, is an 88 kDamembrane protein expressed on the surface asmulti-ligandreceptor of a wide variety of cell typessuch as platelets, endothelial cells, monocytes andmacrophages. It is involved in host defense against P.falciparum. CD36 is commonly deficient, particularlyin certain ethnic groups including Africans. Its role inCM is debatable.44Obstruction to the cerebral microcirculationresultsin hypoxia and increased lactate production due toanaerobic glycolysis. The parasitic glycolysis mayalso contribute to lactate production. In patients withCM, C.S.F. lactate levels are high and significantlyhigher in fatal cases than in survivors. The adherenterythrocytes may also interfere with gas and substrateexchange throughout the brain. However, completeobstruction to blood flow is unlikely, since thesurvivors rarely have any permanent neurologicaldeficit.The mechanismof coma is not clearly known.Increased cerebral anaerobic glycolysis, interferencewith neurotransmission by sequestered andhighly metabolically active parasites has beenblamed. Cytokines induce a potent inhibitor ofneurotransmission, nitric oxide (NO), synthesisin leukocytes, smooth muscle cells, microglia andendothelium.Clinical ManifestationsCerebral malaria is an acute widespread disease ofthe brain which is accompanied by fever. In severe P.falciparum malaria the neurological dysfunction canmanifest suddenly following a generalized seizureor gradually over a period of hours.46The clinicalmanifestations however, are numerous but there arethree primary symptoms generally common to bothadults and children:(1) Impaired consciousness with non-specific fever,(2) Generalized convulsions and neurologicalsequelae and,(3) Coma that persists for24 -72% hours, initiallyarousable and then unarousable.Neurological Signs in Cerebral Malaria:Mild neck stiffness may be seen, however,neck rigidity and photophobia and signs ofraised intracranial pressure are absent. Retinalhaemorrhages occur in about 15% of cases, exudatesare rare. Pupils are normal. Papilloedema is rareand should suggest other possibilities. A variety oftransient abnormalities of eye movements, especiallydysconjugate gaze are observed. Fixed jaw closureand tooth grinding (bruxism) are common. Pouting orshowing displeasure may occur or may be elicitable,but other primitive reflexes are usually absent. Thecorneal reflexes are preserved except in a case of deepcoma. Motor abnormalities like decerebrate rigidity,decorticate rigidity and opisthotonus can occur. Deepjerks and plantar reflexes are variable. Abdominaland cremasteric reflexes can not be elicited. Thesesigns help in distinguishing CM from behaviouralproblems due to fever of other causes. Rarely, cases19
SUDANESE JOURNAL OF PAEDIATRICS AND CHILD HEALTH Vol 10: 2010of falciparum malaria may present with cerebellarataxia with unimpaired consciousness. It may evenoccur 34- weeks after an attack of falciparum malaria.It completely recovers over 12- weeks.6Management of Cerebral Malaria in ChildrenSevere malaria is a medical emergency andmay rapidly progress to death without promptand appropriate treatment. The main objective ofthe treatment of severe malaria is to prevent thepatient from dying; prevention of recrudescence,transmission or emergence of resistance andprevention of disabilities are secondary objectives.Light microscopy of well stained thick and thinfilms by a skilled microscopist has remained the«gold standard» for malaria diagnosis. However,microscopy cannot detect parasite sequestereddeep in the vascular compartment and in case ofmixed infection often one species suppresses theother, thereby making detection of the suppressedone difficult.ao Blood gases and acid base deficit,renal function profile and blood glucose are usefulpredictors of the outcomeCerebrospinal fluid analysis may have to bedone in all doubtful cases and to rule out associatedmeningitis. In malaria, C.S.F. pressure is normallyelevated, fluid is clear and WBCs are fewer than 10/Jtl; protein and lactic acid levels are elevated.d?Electroencephalogram may show non-specificabnormalities and C.T. scan of the brain is usuallynorma1.48 In addition to brain swelling, corticalinfarcts and white matter lesions can be seen on MRexaminations obtained during the course of cerebralmalaria. White matter lesions can regress witheffective treatment. The MR pattern is compatiblewith toxicity leading to intravascular engorgementand oedema and in some cases, to irreversible myelindamage.49Meticulous nursing is the most important aspectof management in patients with CM and coma.A clear airway must be maintained. In cases ofprolonged deep coma, endotracheal intubation maybe indicated. Naso-gastric aspiration is importantto prevent aspiration pneumonia. Urethral catheterhas to be inserted for monitoring urine output in anycomatose patient. All children with cerebral malariashould be admitted to an ICU if possible and childrenwith impending respiratory failure should be placedon ventilatory support.It is quite helpful to maintain strict intake/outputrecords and to monitor the vital signs every 46-hours.50 Observe for high coloured or black urine.Changes in levels of sensorium, occurrence ofconvulsions should also be observed.It is crucial to control or prevent seizures as theycan cause neuronal damage and are associated with afatal outcome. Witnessed seizures are managed withslow diazepam (0.2 mg/kg IV maximum of 10 mgor 004 mg/kg per rectum) or paraldehyde (0.1 mL/kg 1M). Because diazepam can worsen respiratorydepression, the patient's respiratory status should bemonitored carefully after diazepam administration.Patients with recurrent seizures should be treatedwith Phenobarbital or Phenytoin, as one wouldtreat a patient with status epilepticus. Phenobarbitalprophylaxis for seizures is not recommended inchildren with cerebral malaria. Large studies inAfrican children demonstrated a higher mortality ratein children who received Phenobarbital prophylaxiscompared to controls.51Hypoglycemia is common in children below 3years of age especially with hyperparasitemia orwith convulsion. It also occurs in patients treatedwith quinine. Manifestations are similar to those ofcerebral malaria so it can be easily overlooked. Bloodsugar should be Monitored every 4 to 6 hours.Exchange transfusion generally only beenjustified when peripheral parasitaemia exceeds 10%of circulating erythrocytes. The role of these blood20
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