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

We have described a patient with cerebral falciparum malaria who had rapidly progressive CNS deterioration, renal failure, hemolytic anemia associated with striking and varied erythrocyte morphologic changes, and thrombocytopenia. The initial diagnosis was thrombotic thrombocytopenic purpura (TTP) of unknown origin. Reexamination of the peripheral smear of this comatose patient led to correct diagnosis and effective treatment in this case of cerebral falciparum malaria--another of medicine's great mimickers.
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PMID:Cerebral falciparum malaria mimicking thrombotic thrombocytopenic purpura. 200 May 26

Over a period of 6 months in 1988, 104 patients with severe and complicated falciparum malaria were admitted to the Gonder College Hospital (GCH), Gonder, Ethiopia; 85 male (81.7%) and 19 female (18.3%). The age ranged between 14 and 70 years with a mean age of 31 years. Eighty-one patients (78.3%) had moved from a nonendemic to a malariaendemic area shortly before their illness. Altered state of consciousness, hyperparasitaemia and severe anaemia were the most frequent complications found. Fifty-three patients (51.0%) died. Non-immune status and unknown duration of symptoms were significantly associated with mortality. Among those who died, comatose state on admission, hyperparasitaemia and acute renal failure were more frequently seen. Forty-six (86.8%) had developed two or more complications and 15 (28.3%) had superimposed bacterial infections. Inadequate preventive measures and treatment facilities may be two important factors accounting for the high mortality.
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PMID:Clinical and laboratory features of severe and complicated falciparum malaria the experience from Gonder Hospital. 200 87

In endemic areas, most of the people who die from falciparum malaria are young children. Death is commonly preceded by coma (cerebral malaria). The possible role of cytoadherence in this clinical picture is considered.
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PMID:Cerebral malaria in children: clinical implications of cytoadherence. 220 28

Two cases of cerebral malaria with hyperkinetic shock are reported. The first case concerned a 39-year-old european male who was not taking any prophylactic anti-malarial drugs. After having had headache and fever for a week, he was admitted to the intensive care unit (ICU) in coma and with jaundice. His initial systolic blood pressure was 60 mmg, with a central venous pressure (CVP) of -3 cmH2O. Five-hundred ml of modified fluid gelatin increased the CVP without raising the blood pressure. Haemodynamic investigations revealed a cardiac index (CI) = 5.2 l.min-1.m-2, peripheral arterial resistances (Rsa) = 290 dyn.s.cm-5, oxygen consumption (VO2) = 120 ml.min-1.m-2. Despite treatment with dopamine and dobutamine, the patient died 3 h after his admission, with a CI of 1.9 l.min-1.m-2. The second patient was a 14-year-old senegalese girl, admitted in circumstances similar to the first case. Initial haemodynamic investigations gave the following figures: CI 6.5 l.min-1.m-2, Rsa = 476 dyn.s.cm-5, VO2 = 174 ml.min-1.m-2. Recovery was obtained with fluid replacement therapy and dopamine. In the absence of another associated infectious disease, the plasmodial origin of the septic shock would seem to be the most likely in both cases. Pathophysiological mechanisms of these algid forms of malaria remain enigmatic. Various factors are discussed: cytoadherence of erythrocytes infected with Plasmodium falciparum, immunological disturbances, or a specific endotoxin.
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PMID:[Hyperkinetic shock and cerebral malaria]. 224 Jul

A case is reported of a 40-year-old woman presenting with cerebral malaria complicated by an adult respiratory distress syndrome (ARDS). The patient was admitted to the intensive care unit in a coma, scored 5 on the Glasgow scale. Plasmodium falciparum parasitaemia was, at the time, 50%. A continuous intravenous quinine infusion (25 mg.kg-1.day-1) was started, together with the required symptomatic treatment. Blood was transfused because of increasing anaemia (haemoglobin 60 g.l-1). After 24 h, parasitaemia was 12%, consumption of clotting factors broke out (prothrombine 43%, fibrin degradation products greater than 40 micrograms.ml-1, platelets 45 G.l-1). Hypoxaemia (PaO2 = 46 mmHg) and hypocapnia (PaCO2 = 32 mmHg) became obvious, together with bilateral diffuse alveolar infiltrates on chest X-ray. Haemodynamic data suggested non cardiogenic oedema: PEEP 20 cm H2O, cardiac output 6.15 l.min-1, mean pulmonary arterial pressure 35 mmHg, pulmonary wedged pressure 15 mmHg. The hypoxia worsened and the patient died on the 15th day after associated with high levels of parasitaemia. Several reports have suggested that it may be related to increased capillary permeability. Initial fluid overload should therefore be avoided. Parenteral quinine remains the mainstay of treatment, because of its rapid schizonticidal activity. Although exchange transfusion seems to be a valuable adjunct to chemotherapy, it requires further assessment.
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PMID:[Fatal pulmonary edema in a pernicious malaria attack]. 227 23

Based on the cerebral malaria coma scale, 39 falciparum malaria autopsy cases from the Hospital for Tropical Diseases, Mahidol University, Bangkok, Thailand were divided into two groups of patients that had either cerebral malaria or non-cerebral malaria. We then studied significant pathological differences, such as parasitized erythrocyte (PRBC) sequestration, ring hemorrhages and cerebral edema, between these two groups in order to investigate the correlation between the clinical coma scale and pathological findings. Patients with a coma grade of 2 and higher were designated as having cerebral malaria, and had erythrocyte PRBC sequestration in cerebral microvessels. Ninety four percent (94%) of cerebral microvessels showed PRBC sequestration when quantitatively analyzed. On the other hand, only 13% of cerebral microvessels showed sequestration in non-cerebral malaria patients with a coma grade of 1 and lower, although some degree of PRBC sequestration was found in 50% of these patients. Our study, therefore, clearly demonstrated that the degree of the PRBC sequestration in cerebral microvessels appeared to correlate closely with the clinical coma scale.
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PMID:Human cerebral malaria in Thailand: a clinico-pathological correlation. 228 50

Seventy-five cases of childhood cerebral malaria (CM) seen within a 30-month period (January 1986 to June 1988) in the University of Calabar Teaching Hospital (UCTH), Calabar, Nigeria were prospectively studied. Fifty-five percent of the victims were aged 1-5 years while 39% were between 6 and 10 years. Eight percent of the cases were postmortem surprises, their condition having been masked by other complications of malaria. At variance with the accepted definition of CM, 20% of the patients neither convulsed nor lost consciousness. In searching for any delineating premortem features of the disease, a combination of fever, multiple seizures, coma with severe anaemia did appear impressive and also a co-existence of tonic-clonic with pure tonic seizures was highly suspicious. The need to heighten the index of suspicion and encourage extensive research into this lethal aspect of malaria is stressed.
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PMID:Preliminary observations on cerebral malaria in Nigerian children. 239 Sep 56

We tested the hypothesis that cerebral malaria is caused by blood-brain barrier inflammation and cerebral edema. In a group of 157 Thai patients with strictly defined cerebral malaria, cerebrospinal fluid (CSF) opening pressures were normal in 79% and were lower in fatal cases than in survivors (means +/- 1 SD, 144 +/- 58 and 167 +/- 51 mm CSF, respectively, P = 0.051). CSF: serum albumin ratios (X 10(3)) in 39 of them were significantly higher than in 61 British controls (medians 8.5 and 5.5, respectively, P = 0.04), but were no higher in 7 fatal cases. In a group of 12 patients this ratio was not significantly higher during coma than after full recovery (means +/- 1 SD, 9.0 +/- 6.2 and 6.7 +/- 4.2, respectively, P greater than 0.1). CSF alpha 2-macroglobulin concentrations were always normal. CSF : serum 77Br- ratios were elevated in 11/19 comatose cases but fell to normal 4 to 9 days later in 11/11 cases. Dexamethasone treatment had no significant effect on bromide partition. The percentage of an intravenously administered dose of 125I-human serum albumin detectable per ml of CSF 6 hr after intravenous injection was 2.4 +/- 1.3 X 10(-5) in 14 comatose patients and 4.4 +/- 4.0 X 10(-5) in 9 of them during convalescence (P greater than 0.1). These results demonstrate that the blood-CSF barrier is essentially intact in patients with cerebral malaria and give no support to the idea that cerebral edema is the cause of coma.
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PMID:Function of the blood-cerebrospinal fluid barrier in human cerebral malaria: rejection of the permeability hypothesis. 242 67

A recent malaria epidemic striking Antananarivo, the capital city of Madagascar, is shown from hospital records of Pediatric Service "A" of the Befelatanana General Hospital. From 1980 to 1988 malaria cases in this hospital service increased from 0.9% to 14.4% of all admissions (on average 1785 per year). The unexpected expansion is observed in 1984, 1985 and 1986 and since that time malaria has apparently maintained a stable endemic level. Malaria mortality as a proportion of general mortality in the service followed a parallel course but the case fatality rate remained constant during the whole period, in spite of the progressive increase of cerebral malaria (coma) cases. Hospitalized malaria children came mainly from Western and Southern urban and periurban areas of Antananarivo, more rarely from the central areas, the hilly zone, the North and the East of the city.
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PMID:The malaria epidemic in Antananarivo observed from Pediatric Service "A" of the Befelatanana General Hospital. 248 97

To examine the clinical and parasitologic efficacy of quinine, we studied 34 children (7 months-13 years old) with severe or moderately severe Plasmodium falciparum infections. Quinine 10 mg/kg every 8 hr for 3 days was administered, initially by intravenous infusion of quinine formate followed by oral quinine dihydrochloride when tolerated. Thirty-three of the 34 patients were clinically well and had negative malaria smears 7 days after the initiation of therapy; 1 child, who presented in coma, died 29 hr after enrollment. The mean fever clearance time was 44.1 hr, and the mean parasite clearance time was 59.6 hr. A mean peak quinine level of 9.7 ppm was attained after the second dose of quinine, and the minimum concentration was maintained at 5-7 ppm during the 2nd and 3rd hospital days. In vitro testing was conducted with parasites from 10 patients: 9 isolates were resistant to chloroquine, and inhibition of schizont development with quinine occurred at a concentration of 8-32 pmol/well.
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PMID:Intravenous quinine therapy of hospitalized children with Plasmodium falciparum malaria in Kinshasa, Zaire. 265 61


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