Showing papers by "Greg Fegan published in 2005"
TL;DR: Risk factors for persisting neurological and cognitive impairments following cerebral malaria include multiple seizures, deep/prolonged coma, hypoglycaemia, and clinical features of intracranial hypertension.
Abstract: Background: Persisting neurological and cognitive impairments are common after cerebral malaria. Although risk factors for gross deficits on discharge have been described, few studies have examined those associated with persistent impairments. Methods: The risk factors for impairments following cerebral malaria were determined by examining hospital records of 143 children aged 6–9 years, previously admitted with cerebral malaria, who were assessed at least 20 months after discharge to detect motor, speech and language, and other cognitive (memory, attention, and non-verbal functioning) impairments. Results: The median age on admission was 30 months (IQR 19–42) and the median time from discharge to assessment was 64 months (IQR 40–78). Thirty four children (23.8%) were defined as having impairments: 14 (9.8%) in motor, 16 (11.2%) in speech and language, and 20 (14.0%) in other cognitive functions. Previous seizures (OR 5.6, 95% CI 2.0 to 16.0), deep coma on admission (OR 28.8, 95% CI 3.0 to 280), focal neurological signs observed during admission (OR 4.6, 95% CI 1.1 to 19.6), and neurological deficits on discharge (OR 4.5, 95% CI 1.4 to 13.8) were independently associated with persisting impairments. In addition, multiple seizures were associated with motor impairment, age Conclusions: Risk factors for persisting neurological and cognitive impairments following cerebral malaria include multiple seizures, deep/prolonged coma, hypoglycaemia, and clinical features of intracranial hypertension. Although there are overlaps in impaired functions and risk factors, the differences in risk factors for specific functions may suggest separate mechanisms for neuronal damage. These factors could form the basis of future preventive strategies for persisting impairments.
123 citations
TL;DR: Mortality and neurological deficits on discharge were greatest in those developing posturing after admission, although intracranial hypertension may be the primary cause.
Abstract: Abnormal motor posturing is often observed in children with cerebral malaria, but the aetiology and pathogenesis is poorly understood. This study examined the risk factors and outcome of posturing in Kenyan children with cerebral malaria. Records of children admitted to Kilifi district hospital with cerebral malaria from January, 1999 through December, 2001 were reviewed for posturing occurring on or after admission. The clinical characteristics, features of raised intracranial pressure, number of seizures and biochemical changes in patients that developed posturing was compared to patients who did not. Of the 417 children with complete records, 163 (39.1%) had posturing: 85 on admission and 78 after admission to hospital. Decorticate posturing occurred in 80, decerebrate in 61 and opisthotonic posturing in 22 patients. Posturing was associated with age ≥ 3 years (48.1 vs 35.8%, p = 0.01) and features of raised intracranial pressure on funduscopy (adjusted OR 2.1 95%CI 1.2–3.7, p = 0.009) but not other markers of severity of disease. Unlike decorticate posturing, decerebrate (adjusted OR 1.9 95%CI 1.0–3.5) and opisthotonic posturing (adjusted OR 2.9 95%CI 1.0–8.1) were, in addition, independently associated with recurrence of seizures after admission. Opisthotonus was also associated with severe metabolic acidosis (OR 4.2 95%CI 3.2–5.6, p < 0.001). Thirty one patients with posturing died. Of these, 19 (61.3%) had features suggestive of transtentorial herniation. Mortality and neurological deficits on discharge were greatest in those developing posturing after admission. Abnormal motor posturing is a common feature of cerebral malaria in children. It is associated with features of raised intracranial pressure and recurrence of seizures, although intracranial hypertension may be the primary cause.
48 citations
TL;DR: At admission to the hospital, hyperkalemia may complicate cases of acidosis due to severe malaria and is associated with high, early mortality; after admission, mild asymptomatic deficiencies in magnesium and phosphate levels were common but were not associated with any deleterious effect.
Abstract: Background. To date, information about the frequency of electrolyte disturbances among children with severe falciparum malaria is limited. Methods. We describe changes in potassium, calcium, magnesium, and phosphate levels in 56 Kenyan children ( 42 who survived and 14 who died) admitted to the hospital with clinical features of severe malaria ( impaired consciousness or deep breathing) complicated by acidosis ( base deficit, >8 mmol/ L). Results. Mild- to- moderate hypercalcemia was common at admission, particularly among children with severe anemia. Severe hyperkalemia complicated falciparum malaria in 9 children ( 16%), of whom 7 ( 78%) died, generally soon after admission. Hypokalemia, hypomagnesemia, and hypophosphatemia were uncommon ( 30% of children within 24 h. Hypocalcemia was infrequent (<5% of children) at any time point. Apart from administration of potassium, electrolyte deficiencies were not corrected and were not associated with an adverse outcome. Conclusions. At admission to the hospital, hyperkalemia may complicate cases of acidosis due to severe malaria and is associated with high, early mortality. After admission, mild asymptomatic deficiencies in magnesium and phosphate levels were common but were not associated with any deleterious effect. Thus, routine correction when serial measurement of electrolyte levels cannot be performed is unwarranted. Asymptomatic potassium deficiency developed despite provision of this electrolyte at maintenance doses. Further studies are justified but are unlikely to be a major research priority because, as these data suggest, the impact on mortality would at most be limited
39 citations