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

Malaria must be included in the differential diagnosis of all febrile patients. Malaria is classified 'complicated' or 'uncomplicated', according to clinical findings (cerebral malaria, generalized convulsions, pulmonary edema, severe anemia, hyperthermia, renal failure, haemoglobinuria, shock, spontaneous bleeding) and laboratory results (parasitemia greater than 5%, haemoglobin less than 5 g%, creatinine greater than 265 mumol/l, glucose less than 2.2 mmol/l, DIC, pH less than 7.2, bilirubin greater than 50 mumol/l). Plasmodium (P.) vivax, P. ovale and P. malariae cause uncomplicated disease as a rule, whereas P. falciparum may result in either of both. Complicated falciparum malaria is always at risk for a lethal outcome. Only microscopic evidence of malaria parasites proofs the diagnosis. The thick smear is good for screening, thin films are necessary to determine the species. Serology and cultures are not helpful in diagnosing acute malaria. Tests for drug resistance await to be applicable for emergency situations.
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PMID:[Clinical aspects and diagnosis of malaria]. 199 79

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

We studied 26 patients with severe falciparum malaria who were admitted to an ICU in Namibia. The pathophysiologic effects on various organ systems are documented and the mortality associated with organ failure is reported. Patients with three or more organ failures showed a high mortality, especially when pulmonary or renal failure occurred. Predicted mortality based on the Acute Physiology and Chronic Health Evaluation II scoring system was 34% compared to an actual mortality of 38%.
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PMID:Pathophysiology of severe forms of falciparum malaria. 218 91

During the last 15 years, at least 35 patients with severe falciparum malaria or babesiosis have recovered following treatment by exchange of up to 10 l of blood. In a patient treated in Manchester, a parasitaemia of 2.10 X 10(6) microliters (42 per cent) was virtually eliminated over eight hours by a 3.5 litre exchange blood transfusion. However, the equipment and amounts of compatible blood required for total exchange are rarely available in areas endemic for malaria and the risks of the procedure, including transfusion-related infections, are high. Partial exchange transfusion with one to two litres of blood carried out over two to seven hours, reduced Plasmodium falciparum parasitaemias of 0.33-1.48 X 10(6)/microliters (13-38 per cent) to 0.11-0.81 X 10(6) (4-17 per cent) in six Thai patients who were receiving intravenous quinine. The reduction in parasitaemia ranged from 0.13-0.67 X 10(6) microliters (9-12 per cent) within six hours. During the same period, parasitaemia in 13 patients with cerebral malaria treated with chemotherapy alone showed little reduction from initial levels of 0.20-1.74 X 10(6)/microliters (11-42 per cent). One of the patients who were treated with exchange transfusion died with intractable hypotension before the procedure could be completed and two others developed oliguric renal failure which was controlled by peritoneal dialysis. Partial exchange transfusion is a promising and practical alternative to total exchange where facilities are limited. It deserves further assessment in the rural tropics.
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PMID:Plasmodium falciparum hyperparasitaemia: use of exchange transfusion in seven patients and a review of the literature. 220 95

Seventy-two patients with severe falciparum malaria are described. Twenty-four (33.3%) were complicated by acute renal failure. Comparing patients with renal failure and those without, statistically significant differences occurred regarding presence of cerebral malaria (83% vs 46%), jaundice (92% vs 33%), and death (54% vs 17%). A significantly higher number of patients with renal failure were nonimmune visitors to malaria endemic regions. Renal failure was oliguric in 45% of cases. Dialysis was indicated in 38%, 29% died in early renal failure, and 33% recovered spontaneously. It is concluded that falciparum malaria is frequently complicated by cerebral malaria and renal failure. As nonimmune individuals are prone to develop serious complications, malaria prophylaxis and vigorous treatment of cases is mandatory.
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PMID:Acute renal failure due to falciparum malaria. 223 18

The effects of furosemide and furosemide with dopamine on renal function were studied in 23 patients with acute renal failure due to falciparum malaria whose serum creatinine ranged from 230 to 947 mumol/l. Furosemide given intravenously at the dosage of 200 mg 6 hourly for a period of 4 days did not alter the clinical course of renal failure. Intravenous administration of furosemide (200 mg 6 hourly) with dopamine (1 microgram/kg/min) for 4 days increased creatinine clearance and arrested the progress of renal failure when the serum creatinine was less than 400 mumol/l, but failed to alter the course of renal failure when the serum creatinine exceeded 600 mumol/l.
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PMID:Furosemide and dopamine in malarial acute renal failure. 265 49

Early diagnosis and differentiation of a probably mild course are the first steps in treatment of severe malaria tropica. After confirming the diagnosis by identification of Plasmodium falciparum in blood smears, causal therapy with quinine should be started immediately, followed by a 2. schizontozidal drug (chloroquine or mefloquine depending on the country of origin). To prevent the typical organ failures adjuvant therapies are as important as the causal therapy with quinine: besides continuous monitoring of vital functions and treatment according to the guidelines of intensive care, packed red cells should be given generously as well as fresh-frozen plasma in complex coagulation disturbances. Prophylactic administration of heparine is of questionable value, corticosteroids should not be given any more in cerebral malaria. Early start with renal replacement therapy (hemodialysis, hemofiltration or peritoneal-dialysis) in oligo-anuric renal failure improves the prognosis in severe malaria. In comatose patients and at signs of multi-organ failure plasma exchange by plasmapheresis and/or whole blood exchange should be performed.
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PMID:[Therapy of severe malaria]. 266 20

Severe malaria is a major cause of infant and childhood death in the tropics. Effective management relies on rapid diagnosis, prompt administration of parenteral schizonticidal antimalarial drugs, careful fluid balance, prevention of convulsions and early recognition of complications such as hypoglycemia, metabolic acidosis, anemia, pulmonary edema, renal failure, bleeding and supervening bacterial sepsis. The mortality of treated cerebral malaria remains 20%. New, more rapidly acting antimalarials and earlier referral of children with complicated infections should reduce this unacceptable death rate.
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PMID:Management of severe malarial infection. 268 Sep 36

Clinical details and present day problems encountered in 425 cases of falciparum malaria (PF) are reported. 10.11% had taken chloroquine prior to reporting to us. Parasitic count done in 23.05% cases lacked correlation with severity of disease. Pattern of fever varied markedly but 5.4% were afebrile throughout and presented only with bodyache and malaise. Apyrexial spell was noted in 5.64%. 28.70% had typical facial looks of anaemia and sallow complexion. Cerebral symptoms were noted in 3.05%. Other symptoms were severe headache 33.4%, pain abdomen 3.29%, gastroenteritis 5.64%, jaundice 2.58% and bronchitis in 7.50%. We encountered subconjunctival haemorrhages with purpura and/or urticaria in four cases, symptoms suggestive of shock lung in 3, pulmonary oedema in 2, severe anaemia (HB less than 4 g%) in seven pregnant ladies, extrapyramidal symptoms in follow up period in 5 and congenital malaria in 2 cases. 83.25% were cured with chloroquine and oxytetracycline. 8.47% (who deteriorated despite the above treatment) were treated with quinine for 6 days. 5.17% (with severe disease) were also given quinine as first line drug. 2.82% (unresponsive to chloroquine and oxytetracycline but with mild disease) were treated with pyrimethamine-sulphamezathine combination for 5 days. One case who did not respond to quinine was treated with quinidine. Recrudescence was seen in 3.67% of patients treated with chloroquine and oxytetracycline. There was no case with renal failure, haemolysis due to G6PD deficiency and black water fever. There was only one death (0.23%) in our series. Self-medication, haphazard therapy and the slogan "Fever may be malaria-take chloroquine" can lead to problems in falciparum malaria.
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PMID:Falciparum malaria--present day problems. An experience with 425 cases. 269 36

In the treatment of severe Plasmodium falciparum infection antimalarial drugs should, ideally, be given by controlled rate intravenous infusion until the patient is able to swallow tablets. In cases where infection has been acquired in a chloroquine resistant area, and where it has broken through chloroquine prophylaxis or where the geographical origin or species are uncertain, quinine is the treatment of choice. When access to parenteral quinine is likely to be delayed, parenteral quinidine is an effective alternative. A loading dose of quinine is recommended in order to achieve therapeutic plasma concentrations as quickly as possible. In the case of chloroquine sensitive P. falciparum infection, chloroquine, which can be given safely by slow intravenous infusion, may be more rapidly effective and has fewer toxic effects than quinine. There is limited experience with parenteral administration of pyrimethamine sulphonamide combinations such as Fansidar, and resistance to these drugs has developed in South East Asia and elsewhere. Mefloquine and halofantrine cannot be given parenterally. Qinghaosu derivatives are not readily available and have not been adequately tested outside China. Supportive treatment includes the prevention or early detection and treatment of complications, strict attention to fluid balance, provision of adequate nursing for unconscious patients and avoidance of harmful ancillary treatments. Anaemia is inevitable and out of proportion to detectable parasitaemia. Hypotension and shock ('algid malaria') are often attributable to secondary gram-negative septicaemia requiring appropriate antimicrobial therapy and haemodynamic resuscitation. Many patients with severe falciparum malaria are hypovolaemic on admission to hospital and require cautious fluid replacement. Failure to rehydrate these patients may lead to circulatory collapse, lactic acidosis, renal failure and severe hyponatraemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of severe malaria. 269 26


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