11/42. Diffuse lung uptake of technetium-99m sulfur colloid in malaria. Diffuse lung accumulation of colloid was seen on liver-spleen imaging in a patient during the acute stage of vivax malaria. A repeat study was performed following successful therapy and showed complete disappearance of lung uptake. Possible mechanisms for this unusual observation are discussed, with the conclusion that this phenomenon is probably related to increased reticuloendothelial system activity, due to a malaria-induced increase in the pulmonary macrophages.
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12/42. Spontaneous and quinine induced hypoglycaemia in severe falciparum malaria. Four of 21 patients with cerebral malaria developed hypoglycaemia, defined as plasma glucose concentration below 40 mg/dl (2.2 mmol/l). Two patients had spontaneous hypoglycaemia at admission and the other two developed it subsequent to quinine therapy. All recovered with continuous intravenous glucose infusion. Spontaneous hypoglycaemia in malaria has not earlier been reported from india.
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A 16-year-old Nigerian boy who had lived all his life in a malaria endemic region presented with continuing fever after what would ordinarily be accepted as adequate treatment for malaria. He went on to develop cerebral malaria, recovering only after administration of quinine.
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14/42. Subarachnoid haemorrhage in plasmodium falciparum malaria. A 41 year old man with cerebral malaria was found to have numerous bilateral retinal haemorrhages and very high parasitaemia. Despite intensive treatment his condition deteriorated and he died. autopsy showed subarachnoid haemorrhage, which has not been previously described in cerebral malaria.
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15/42. Fatal pancytopenia in falciparum malaria. Various pernicious syndromes in plasmodium falciparum infection are being reported with increasing frequency from tropical countries. A rare case of fatal pancytopenia associated with falciparum malaria is described. The patient developed fulminant aspiration bronchopneumonia which was unresponsive to antibiotic therapy and contributed to the development of adult respiratory distress syndrome. He also had severe uncontrolled gastrointestinal bleeding and possibly an intracerebral haemorrhage. Anaemia and thrombocytopenia are well known in malaria but severe leucopenia is very rare and pancytopenia has not been reported.
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16/42. Cerebral malaria in pregnancy. Three cases of cerebral malaria during pregnancy are described. One patient had intrauterine foetal death and died, one patient delivered a dead baby and the other had severe postpartum haemorrhage. Cerebral malaria worsens the outlook both for the mother and for the foetus.
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17/42. Focal neurological signs in cerebral malaria accounted for by preceding neurological damage. In 1987 at Port Moresby General Hospital, papua new guinea, two out of 103 adults with a final diagnosis of cerebral malaria had focal neurological signs noted on admission. In both cases the focal signs could be explained by documented prior neurological disease with residual focal damage. Focal neurological signs in patients presenting with malaria should prompt careful investigation to exclude other active neurological disease. Where no additional diagnosis is evident a history of past neurological damage may become apparent to explain the focal nature of the malaria presentation.
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18/42. An unusual combination of phototoxicity and stevens-johnson syndrome due to antimalarial therapy. A 12-year-old boy developed a phototoxic rash with subsequent progression to stevens-johnson syndrome due to prophylactic ingestion of antimalarials (chloroquine and sulfadoxine-pyrimethamine; Fansidar). The patient recovered from his skin symptoms after 4 weeks during which he received systemic corticosteroids and antibiotics. This unusual combination of two different patterns of adverse cutaneous drug reactions was most probably caused by the sulfonamide component of Fansidar.
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19/42. Delayed cerebellar ataxia: a new complication of falciparum malaria? Twelve cases of an unusual phenomenon of ataxia were investigated in otherwise well, conscious patients recovering from a febrile attack of presumed falciparum malaria. The ataxia occurred as the fever was subsiding, usually after an afebrile period of two to four days. The delay between onset of fever and the ataxia was three to four weeks. Peripheral blood of all the patients contained gametocytes of plasmodium falciparum, and in some cases ring stages. The ataxia was most noticeable in the legs and the clinical picture suggested selective impairment of the cerebellar system. Signs of improvement appeared in a few weeks but complete recovery took one to four months. The most likely pathogenic mechanism of the ataxia in these cases was an immune reaction triggered by the malaria parasite and affecting the cerebellum or its connections, or both.
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20/42. Malarial lung: report of a case from africa successfully treated with intermittent positive pressure ventilation. We describe the first recorded case from africa of malarial lung, acute pulmonary insufficiency in plasmodium falciparum malaria. The patient was successfully treated with intermittent positive pressure ventilation (IPPV). There was heavy parasitemia, preceding cerebral complications and rapid onset of pulmonary edema in the absence of fluid overload or cardiac failure. A further complication of polyuria from tubular dysfunction developed whilst the patient was being ventilated. IPPV may have an important place in the management of this rare and usually fatal complication of falciparum malaria.
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