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

Nine non-immune patients with imported falciparum malaria were examined for signs of diffuse intravascular coagulation (DIC). Although all had thrombocytopenia initially and some later had a decline in plasma fibrinogen concentrations, DIC was never detected, even in severely affected patients with coma and kidney damage. None of the patients were given heparin and all recovered without residual symptoms. Heparin administration should probably be considered only when clear-cut DIC, which possibly never occurs in falciparum malaria, has been demonstrated.
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PMID:Haemostatic defect in non-immune patients with falciparum malaria: no evidence of diffuse intravascular coagulation. 35 86

Report of a typical case of cerebral malaria with coma during 3 days, pneumopathy and renal insufficiency with failure of concentration. The delivery of a dead foetus has been started by prostaglandines.
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PMID:[Cerebral malaria with renal insufficiency in a 5 months pregnant woman. The use of prostaglandines for delivery (author's transl)]. 48 Nov 87

At least four doses of quinine followed by a single dose of mefloquine or by a single dose of sulfadoxine-pyrimethamine are two highly effective regimens for chloroquine-resistant falciparum malaria. Mefloquine alone is valuable in ambulant patients. Chloroquine-sensitive falciparum malaria can be treated with a course of chloroquine. Vivax and all other types of malaria should be treated with sequential chloroquine and primaquine. Quinine, by intravenous infusion, is the most effective drug for severe falciparum malaria. The optimum intravenous dose varies between 5 mg/kg and 10 mg/kg administered over four hours. Intravenous or oral quinine should be administered about every 12 hours and the total daily dose of quinine should rarely exceed 20 mg/kg. Intravenous fluid input should be controlled in falciparum malaria to prevent pulmonary oedema. Established renal failure is best treated by dialysis. The value of adrenocortical steroids for falciparum coma has not been established. Fresh blood transfusion may be helpful in small doses for severe anaemia and to replace clotting factors. Anticoagulants, such as heparin, should not be used in falciparum malaria.
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PMID:The treatment of malaria. 76 37

In addition to asking their patients about recent foreign travel, Canadian doctors need to be aware of what features to ask about in considering imported illnesses. Of these illnesses, malaria is one of the most common and serious. Because of its cerebral renal, pulmonary and intestinal complications, falciparum malaria must be distinguished from non-falciparum forms. Anyone with a fever who has arrived recently from an endemic area should be tested for malaria. In addition, headache, malaise, myalgias, arthralgias, low back pain, nausea, vomiting, diarrhea or cough should raise suspicion. Malaria should be remembered as a cause of coma. Persons taking any form of drug prophylaxis for malaria are not protected absolutely and those who are semi-immune can become severely ill occasionally.
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PMID:Symptoms and signs of malaria. 78 78

Coagulation and fibrinolytic studies were conducted in 18 cases of severe falciparum malaria including cases with parasitaemia above 5% and with pernicious manifestations such as coma, jaundice, anuria, pulmonary oedema, bleeding tendency, etc., irrespective of parasitaemia. Marked changes in blood coagulograms and high levels of serum fibrin degradation products appeared only in cases with very severe cerebral involvement and also in cases with very high parasitaemia alone. These investigations indicated that intravascular coagulation occurs only in patients suffering from falciparum malaira who develop cerebral manifestations and in cases with high parasitaemia.
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PMID:Studies on coagulation and fibrinolysis in cases of Falciparum malaria. 109 6

Eleven narcotic injectors from a prison in Saigon were hospitalized with falciparum malaria. Coma and intense parasitemia were common and eight patients died soon after admission. Two of three autopsied cases also had purulent pulmonary infections. No non-addicted prisoners were hospitalized for malaria. Nine more unsuspected falciparum infections were found among 29 other addicts in the prison. The clustering of malaria infections among narcotic injectors who had not been in malarious areas indicates that the malaria was transmitted by the common use of needles and syringes. Cerebral malaria in an addict may be misdiagnosed as drug intoxication. Malaria surveillance is recommended for the increasing addict population in the cities of Southeast Asia.
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PMID:Fatal falciparum malaria among narcotic injectors. 110 39

It is reported about a 56 years old woman returned from Mombaza, who was brought into hospital with high fever, jaundice and somnolence and died forty hours later in coma, anuria und hematemesis. The diagnosis of cerebral malaria resulted from autopsy. By the histological examination numerous microthrombi were observed exceptionally in certain cerebral areas, which are more vulnerable by hypoxia as other regions of the brain and other organs. The pathophysiology and the clinical importance of this correlationship are discussed.
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PMID:[A contribution to the intravascular coagulation in cerebral malaria (author's transl)]. 118 80

Seventy-nine comatose cerebral malaria patients given standard supportive treatment were randomized to receive specific antimalarial chemotherapy of intravenous quinine, intravenous artesunate, or artemisinin suppositories. Artesunate and artemisinin reduced peripheral asexual parasitaemia significantly more rapidly than quinine (90% clearance time 16 h, 18.9 h and 34.5 h respectively), but did not significantly reduce the duration of coma or mortality. The rapid lowering of peripheral parasitaemia may not ameliorate complications already present. These results demonstrate that artemisinin suppositories are as effective as artesunate and quinine given intravenously, and have economic and practical advantages for the treatment of severe malaria in areas remote from major medical centres. However, large numbers of patients will need to be studied if differences in mortality between the 3 treatment groups are to be demonstrated.
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PMID:Comparison of artemisinin suppositories with intravenous artesunate and intravenous quinine in the treatment of cerebral malaria. 128 4

Cerebral complications are important, but poorly understood pathological features of infections caused by some species of Plasmodium and Babesia. Patients dying from P. falciparum were classified as cerebral or non-cerebral cases according to the cerebral malaria coma scale. Light microscopy revealed that cerebral microvessels of cerebral malaria patients were filled with a mixture of parasitized and unparasitized erythrocytes, with 94% of the vessels showing parasitized red blood cell (PRBC) sequestration. Some degree of PRBC sequestration was also found in non-cerebral malaria patients, but the percentage of microvessels with sequestered PRBC was only 13%. Electron microscopy demonstrated knobs on the membrane of PRBC that formed focal junctions with the capillary endothelium. A number of host cell molecules such as CD36, thrombospondin (TSP) and intercellular adhesion molecule I (ICAM-1) may function as endothelial cell surface receptors for P. falciparum-infected erythrocytes. Affinity labeling of CD36 and TSP to the PRBC surface showed these molecules specifically bind to the knobs. Babesia bovis infected erythrocytes produce projections of the erythrocyte membrane that are similar to knobs. When brain tissue from B. bovis-infected cattle was examined, cerebral capillaries were packed with PRBC. Infected erythrocytes formed focal attachments with cerebral endothelial cells at the site of these knob-like projections. These findings indicate that cerebral pathology caused by B. bovis is similar to human cerebral malaria. A search for cytoadherence proteins in the endothelial cells of cattle may lead to a better understanding of the pathogenesis of cerebral babesiosis.
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PMID:A study on the pathogenesis of human cerebral malaria and cerebral babesiosis. 134 6

Cerebral malaria is still a major cause of death in patients suffering from malaria. Much of the research work in the past two decades has been done to clarify the pathophysiology of cerebral malaria which hopes to improve the management of the disease and concomitantly reduce mortality. However, the pathogenesis of cerebral malaria is still not clear. The pathophysiology of coma is believed to be brain anoxia from ischemia due to sequestration of erythrocytes containing mature parasites in cerebral capillaries and venules. Three possible mechanisms of sequestration (cytoadherence, rosette formation and decreased deformability of the infected erythrocytes) are postulated. The management of cerebral malaria includes early diagnosis and early treatment with potent antimalarial drugs, early detection and treatment of complications, correction of fluid and electrolyte imbalance and proper nursing care. In spite of these efforts, a high mortality rate (ranging 10-40%) is still encountered.
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PMID:Overview: pathophysiology and management of cerebral malaria. 136 63


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