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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

According to the literature, socio-economic factors may contribute more to geographic variations in the aetiology and prognosis of childhood coma than has previously been recognised. This prospective study involving 118 children with strictly defined coma demonstrated that the commonest causes of coma in Ibadan were cerebral malaria (55%), meningitis (13%) and encephalitis (10%). The prognosis was poor. Forty-three (36%) of 118 cases died and 75 (64%) survived, including 23 who showed neurologic deficits. Noteworthy prognostic indices of coma were the aetiology of the condition, the presence of severe anaemia, hypoglycaemia and pneumonia. The findings are discussed in the context of the socio-economic background of children in the tropics.
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PMID:Childhood coma in Ibadan. Relationship to socio-economic factors. 181 64

The current clinical and therapeutic aspects of cerebral malaria in non-immune adult subjects living in endemic areas of Africa were evaluated in 10 men (mean age: 40 +/- 11.4 years). On admission, 8 patients had fever, 3 were truly comatose with a Glasgow score of 7 or more. All had negative central venous pressure and only one was in a state of hyperkinetic shock. Respiratory symptoms were present in 8 cases, and jaundice was observed in 8 cases. Three patients has a haemoglobin level lower than 8 g/100 ml, and 8 had thrombocytopenia. Blood creatinine levels above 240 mumol/l and blood bilirubin levels above 50 mumol/l were found in 6 and 8 patients respectively. Plasma creatine phosphokinase was above 500 IU/l in 7 cases, and PaO2 was below 70 mmHg in 7 cases. All patients received quinine, combined with doxycycline in 6 cases. Infectious complications occurred in 5 patients, with 2 septic shocks. Two patients developed acute pulmonary oedema. Five patients died. This study shows that cerebral malaria in non-immune subjects living in endemic areas produces multivisceral deficiency similar to that observed in imported malaria. Its prognosis can be improved by loading doses of quinine and by a better prevention of nosocomial infections.
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PMID:[Cerebral malaria in non-immune subjects. Current aspects in African endemic areas]. 182 76

The current clinical and therapeutic aspects of cerebral malaria in non-immune adult subjects living in endemic areas of Africa were evaluated in 10 men (mean age: 40 + or - 11, 4 years). On admission, 8 patients had fever, 3 were truly comatose with a Glasgow score of 7 or more. All had negative central venous pressure and only one was in a state of hyperkinetic shock. Respiratory symptoms were present in 8 cases, and jaundice was observed in 8 cases. Three patients has a haemoglobin level lower than 8 g/100 ml, and 8 had thrombocytopenia. Blood creatinine levels above 240 umol/l and blood bilirubin levels above 50 umol/l were found in 6 and 8 patients respectively. Plasma creatine phosphokinase was above 500 iu/l in 7 cases, and PaO2 was above 70 mmHg in 7 cases. All patients received quinine, combined with doxycycline in 6 cases. Infectious complications occurred in 5 patients, with 2 septic shocks. Two patients developed acute pulmonary oedema. Five patients died. This study shows that cerebral malaria in non-immune subjects living in endemic areas produces multivisceral deficiency similar to that observed in imported malaria. Its prognosis can be improved by loading doses of quinine and by a better prevention of nosocomial infections.
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PMID:[Current aspects on cerebral malaria in the non-immune patient in African endemic areas]. 184 63

Severe and complicated malaria is a fatal from a human Plasmodium falciparum infection. In clinical practice cerebral malaria in children, with unrousable coma, hyperthermia, generalized convulsions, frequently hypoglycemia, is different of severe in non immunized adults resulting in multiple organ failure with degree of impaired consciousness less important. Specific treatment requires quinine with loading dose: 16.7 mg/kg then 8.3 mg/kg every 8 hours for 7 days. Symptomatic therapy, artificial ventilation in particular is indispensable. Recovery is usual in children although neurological sequelae are frequent. In adults evolution is often complicated with pulmonary edema, aggravation of coma, nosocomial infection, and sometimes late multiple organ failure.
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PMID:[Severe malaria in Black Africa]. 184 75

Characteristics of pediatric cerebral malaria, including specificity of clinical diagnosis, efficacy of antimalarial regimens, and the influence of drug resistance remain poorly defined in many parts of the world. The utility of the Glasgow coma scale and quantitative assessment of parasitaemia levels as diagnostic and prognostic indices in cerebral malaria were determined in this study. Thirty-one pediatric patients with admission diagnoses of cerebral malaria in the emergency ward at Korle Bu Hospital, Accra, Ghana were evaluated. Mean age was 4.8 years. The initial diagnosis of malaria was confirmed in 65 per cent of patients; 16 per cent ultimately received another diagnosis including pneumonia, meningitis or encephalitis. In 19 per cent the diagnoses were inconclusive. Mean initial blood parasitaemia level was 10(4.6) parasites per mm3, and mean initial Glasgow coma score was 10.4. The initial Glasgow score was a better predictor of length of stay (Pearson correlation coefficient r = 0.66) than initial parasitaemia level (r = 0.17). For most treated patients parasitaemia levels decreased a mean of 1.3 logs per day of therapy; however, in 33 per cent parasitaemia continued to rise or fluctuate. High parasitaemia levels were associated with deep levels of coma, but only when both parameters were assessed throughout the hospital stay. Both deaths in this series occurred in patients who had persistently negative blood smears for malaria parasites, but showed autopsy findings consistent with cerebral malaria.
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PMID:Pediatric cerebral malaria in Accra, Ghana. 184 87

Anti-malarial antibodies were quantified in cerebrospinal fluid (CSF) of 17 cases of cerebral malaria, 16 presumptive cases (no demonstrable parasitaemia in peripheral blood but responding to i.v. quinine therapy) of cerebral malaria, and 15 controls. A schizont-enriched Plasmodium knowlesi antigen was used in an ELISA. Anti-malarial antibodies of IgA and IgM isotypes were not detectable in most of the CSF samples analysed, although serum antibody titres were high. However, 88% of CSF from cerebral malaria and 56% of presumptive cerebral malaria cases had significant levels of IgG anti-malarial antibodies in comparison to control CSF. The antibody levels did not correlate with the severity of coma but correlated well with the duration of coma. The CSF malarial antibody titres were independent of degree of parasitaemia. The possible role of CSF anti-malarial antibodies in cerebral malaria in the light of recent demonstrations of intrathecal synthesis of immunoglobulins and deposition of immune complex in cerebral tissues is discussed.
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PMID:Human cerebral malaria: characterization of malarial antibodies in cerebrospinal fluid. 191 32

Malaria is diagnosed in 50-70 patients each year in Norway. Severe malarial infection with cerebral involvement as well as hypoglycaemia, circulatory collapse and renal failure is often difficult to diagnose since the condition is only rarely seen in Scandinavia. This report describes a 49 year old seaman, who was admitted to hospital with a clinical picture of sepsis with multiorgan involvement including cerebral affection. Subsequently, it turned out that the patient had a severe infection with Plasmodium falciparum, involving more than 50 per cent of the red blood cells. Despite being comatose for one week with repeated attacks of grand mal type, and requiring 11 days mechanical ventilation plus dialysis for 4 weeks, he recovered uneventfully and was dismissed from hospital with only minor neurological sequelae. Even severe malaria with cerebral involvement can result in full restitution if the diagnosis is made early and exchange transfusion plus treatment with relevant drugs are instituted promptly.
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PMID:[Exchange transfusion in cases of falciparum malaria]. 194 97

Two Thai girls aged 10 and 13 years from the same rural area were admitted to Paholpolpayuhasena Hospital, Kanchanaburi, Thailand during the rainy season of 1989 with cerebral malaria. After several days of conventional treatment, both developed gangrene involving the feet and toes, but the lesions healed and no other complications were seen. In the absence of convincing clinical and laboratory evidence of vasculitis or coagulopathy, it seems likely that host factors (dehydration, sluggish peripheral circulation, platelet activation, subclinical intravascular coagulation) combined with strain-specific parasite factors (tissue sequestration of mature forms, rosette formation) may predispose to peripheral microvascular occlusion sufficient to produce infarction of tissue in susceptible children. However, despite the apparently ominous appearance of such lesions in a comatose child, the prognosis seems good.
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PMID:Peripheral gangrene in nonfatal pediatric cerebral malaria: a report of two cases. 194 78

Glycaemic status on hospital admission was compared in 97 children with severe falciparum malaria (36 with cerebral malaria) and 89 children with other serious illnesses (32 in coma; 57 with acute pneumonia, not in coma). The frequency of hypoglycaemia (blood glucose below 2.2 mmol/l) did not differ significantly between malarial and control patients (5.2% vs 11.2%) nor between the comatose (11.1% vs 18.8%) and conscious (1.6% vs 7.0%) malarial and control subgroups. Compared with normoglycaemic patients, hypoglycaemic patients had appropriately low serum insulin (3.0 vs 8.2 mU/l) and C-peptide (0.13 vs 0.42 mmol/l) and high plasma non-esterified fatty acids (1.42 vs 0.83 mmol/l). Hypoglycaemia, the level of consciousness, and death were all significantly associated with the time since the last meal. Hypoglycaemia is not a specific complication of malaria but is found in severely ill fasted children, resulting from glycogen depletion and perhaps impaired hepatic gluconeogenesis. It should be sought in all severely sick children. A single bolus dose of glucose may not be enough to correct it.
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PMID:Specificity of hypoglycaemia for cerebral malaria in children. 197 69

Out of 604 Gambian children admitted with falciparum malaria to one hospital between September and December, 1988, 308 had cerebral malaria and 203 were severely anaemic (haemoglobin less than 60 g/l). 14% of those with cerebral malaria died, as did 7.8% of those with severe anaemia. 32 (12%) of children surviving cerebral malaria had residual neurological deficit. 69 other children were admitted with clinical features strongly suggestive of cerebral malaria but with negative blood films; 16 of these died and 3 had residual neurological deficits. The commonest sequelae of cerebral malaria were hemiplegia (23 cases), cortical blindness (11), aphasia (9), and ataxia (6). Factors predisposing to sequelae included prolonged coma, protracted convulsions, severe anaemia, and a biphasic clinical course characterised by recovery of consciousness followed by recurrent convulsions and coma. At follow up 1-6 months later over half these children had made a full recovery, but a quarter were left with a major residual neurological deficit. Cerebral malaria in childhood may be an important cause of neurological handicap in the tropics.
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PMID:Neurological sequelae of cerebral malaria in children. 197 27


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