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

In severe falciparum malaria there is a pathophysiological cascade beginning with changes in the parasitized red blood cells which induce intermediate effects, in turn contributing to dysfunction of several organs. A low serum albumin is a common but often unrecognized finding which may contribute to oedema especially in the lung and brain. The only irreversible complication in falciparum malaria is the acute respiratory distress syndrome, manifested by cyanosis and rapid breathing, basically distinct from acute pulmonary oedema caused by therapeutic overhydration. The pathophysiology of falciparum malaria may be complex but the treatment is simple. Drugs, other than antimalarials, are rarely needed. Guidelines for cholorquine or quinine dosage in severe disease are proposed; each drug is given at a dose of 5 to 10 mg/kg in 10 ml/kg of fluid as an intravenous infusion in four hours at a frequency of dosing every 12 to 24 hours. When the disease has been brought under control the treatment should be changed from the intravenous to the oral route.
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PMID:The treatment of severe falciparum malaria. 33 21

The current clinical and therapeutic aspects of cerebral malaria in non-immune adult subjects living in endemic areas of Africa were evaluated in 10 men (mean age: 40 +/- 11.4 years). On admission, 8 patients had fever, 3 were truly comatose with a Glasgow score of 7 or more. All had negative central venous pressure and only one was in a state of hyperkinetic shock. Respiratory symptoms were present in 8 cases, and jaundice was observed in 8 cases. Three patients has a haemoglobin level lower than 8 g/100 ml, and 8 had thrombocytopenia. Blood creatinine levels above 240 mumol/l and blood bilirubin levels above 50 mumol/l were found in 6 and 8 patients respectively. Plasma creatine phosphokinase was above 500 IU/l in 7 cases, and PaO2 was below 70 mmHg in 7 cases. All patients received quinine, combined with doxycycline in 6 cases. Infectious complications occurred in 5 patients, with 2 septic shocks. Two patients developed acute pulmonary oedema. Five patients died. This study shows that cerebral malaria in non-immune subjects living in endemic areas produces multivisceral deficiency similar to that observed in imported malaria. Its prognosis can be improved by loading doses of quinine and by a better prevention of nosocomial infections.
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PMID:[Cerebral malaria in non-immune subjects. Current aspects in African endemic areas]. 182 76

The current clinical and therapeutic aspects of cerebral malaria in non-immune adult subjects living in endemic areas of Africa were evaluated in 10 men (mean age: 40 + or - 11, 4 years). On admission, 8 patients had fever, 3 were truly comatose with a Glasgow score of 7 or more. All had negative central venous pressure and only one was in a state of hyperkinetic shock. Respiratory symptoms were present in 8 cases, and jaundice was observed in 8 cases. Three patients has a haemoglobin level lower than 8 g/100 ml, and 8 had thrombocytopenia. Blood creatinine levels above 240 umol/l and blood bilirubin levels above 50 umol/l were found in 6 and 8 patients respectively. Plasma creatine phosphokinase was above 500 iu/l in 7 cases, and PaO2 was above 70 mmHg in 7 cases. All patients received quinine, combined with doxycycline in 6 cases. Infectious complications occurred in 5 patients, with 2 septic shocks. Two patients developed acute pulmonary oedema. Five patients died. This study shows that cerebral malaria in non-immune subjects living in endemic areas produces multivisceral deficiency similar to that observed in imported malaria. Its prognosis can be improved by loading doses of quinine and by a better prevention of nosocomial infections.
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PMID:[Current aspects on cerebral malaria in the non-immune patient in African endemic areas]. 184 63

22 cases of adult cerebral malaria were observed between July 1987 and June 1989, either associated or not: parasitemia 5%, consciousness disorders, acute renal failure, thrombocytopenia. Two patients died (9%). Increased frequency of attacks is underlined. They are due to chloroquino-resistant parasite strains, even polychemoresistant, occurred in French speaking Tropical Africa since 1985. Therapeutic strategy is described. The necessity to use increased doses of quinine has been admitted, correlatively underlining importance of strict monitoring of the patients because, in first instance, the risk of hypoglycemia (eased by injecting too quickly high doses of quinine) and of acute pulmonary oedema (eased by too quick perfusions and/or transfusions).
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PMID:[Adult cerebral malaria. Actual experience of the Infectious Diseases Intensive Care Department at the Claude Bernard Hospital]. 236 52

Although malaria has been largely eradicated from temperate countries, it is on the increase in the tropics. Infection with Plasmodium falciparum affects a vast number of people and kills over a million annually. Severe malaria is a multisystem disease affecting particularly the central nervous system (causing coma and convulsions), the kidneys (resulting in acute tubular necrosis), and the liver (contributing to lactic acidosis and hypoglycaemia). Acute pulmonary oedema (acute respiratory distress syndrome) may occur in adults particularly in association with renal impairment. In children these symptoms are rare, whereas hypoglycaemia, lactic acidosis and severe anaemia are more common. Malaria should be suspected in any febrile patient living in or returning from the tropics, and a blood smear examined. Chloroquine has been the mainstay of antimalarial treatment for the past 40 years, but resistance in P. falciparum is now widespread throughout the tropics and has recently been recognised in P. vivax from Oceania. Sulfadoxine-pyrimethamine resistance is also common. Fortunately, quinine, and the newly introduced compounds, halofantrine and mefloquine, can be relied upon nearly everywhere. The most rapidly acting and effective of all antimalarial drugs, artemisinin and its derivatives, have come from China. They offer a genuine prospect of reducing mortality from malaria in the tropics.
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PMID:Clinical malaria in the tropics. 833 22

A 44-year-old Spanish woman travelled in Kenya without doing correct malarial prophylaxis. Upon her return to Spain, she suffered from Plasmodium falciparum malaria. She was initially treated with chloroquine for three days, but her state worsened and she was admitted to our intensive care unit. On admission, parasitaemia was 22%. She had hyperpyrexia, obtundation, hypotension, tachycardia, tachypnoea, jaundice, digestive haemorrhage, petechiae in her soles, oliguria with elevation of serum uraemia and creatinine, anaemia, thrombocytopaenia, hypoproteinaemia, hyponatraemia, hypocalcaemia, metabolic acidosis and parameters of disseminated intravascular coagulation. She was given quinine, sulfadoxine-pyrimethamine and clindamycin. An exchange transfusion was performed, during which an acute pulmonary oedema appeared, initially with high pulmonary artery wedge pressure. She required mechanical ventilation for 16 days and haemodialysis for 11 days. She remained in coma and had seizures which required diazepam, phenitoin and thiopentone. She received a total amount of 22 units of packed erythrocytes, 55 of platelets and 15 of plasma. After the first week, she had nosocomial infection due to Escherichia coli, Staphylococcus and Pseudomonas aeruginosa and was treated with the corresponding antibiotics. She cured completely. This case report gives us the possibility of discussing on frequent problems in the prevention and treatment of malaria, and on the treatment of severe, life-threatening malaria in the setting of the intensive care unit.
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PMID:[Multiple organ failure in Plasmodium falciparum malaria]. 853 25

Malaria is a major cause of maternal and fetal morbidity and mortality, and this risk is highest in the areas of unstable malaria transmission. In 1990 and 1991 the Department of Obstetrics and Gynecology of Sir Sayajirao General Hospital in central Gujarat, India, has cared for a total of 445 urban as well as rural patients with malaria in pregnancy: 232 were labor ward admissions and 213 were antenatal ward admissions. Plasmodium falciparum infection affected 97.27% of patients, both primigravidae and multigravidae. Heavy parasitemia was observed in 27.14% of primigravidae and 48.57% in secundigravidae, however, this was not statistically significant. Out of the 260 (58.42.) cases who had various degrees of anaemia, 59 (22.69) had severe anaemia with haemoglobin of less than 6.0 gm O/dl. Within this group, 71.16% women were primigravidae or secundigravidae, the rest were multigravidae. Out of the 6 patients in first trimester, the miscarriage rate was 100%. In the second trimester, out of 52 patients 74.99 pregnancies were discontinued, whereas in the third trimester, the miscarriage rate was 18.17%. This observation was statistically significant (p 0.05). 178 patients who were admitted antenatally were discharged, their pregnancy outcome was not known, and accordingly they were excluded. There were 11 patients in the first trimester, 139 in the second trimester, and 295 in the third trimester. The known pregnancy losses were 54.54% in the first trimester. 28.05% in the second trimester, and 12.88% in the third trimester. 75.59% of those with minor parasitemia and 47.36% with heavy parasitemia had a normal pregnancy outcome. The overall fetal loss was 31.08%, which was almost twice that of the miscarriage rates among the general population. Maternal deaths attributed to malaria in pregnancy were 15, with cerebral malaria accounting for 5 deaths. 46.66% of the deaths occurred in primigravidae and secundigravidae. The other causes of mortality were postpartum hemorrhage, acute pulmonary edema, and hypoglycemia.
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PMID:Maternal manifestations of malaria in pregnancy: a review. 1234 25

Malaria requiring intensive care is characterized by failure of one or more organ systems and/or development of several metabolic disorders secondary to the presence of Plasmodium faliciparum in the blood. Severe imported malaria in non-immunized adults causes multiple organ failure with variable degrees of altered mental status. Acute pulmonary edema is frequent, jaundice associated with mild disturbance of liver function is consistent, arterial hypertension due to hypovolemia is usual, and acute renal insufficiency is uncommon. Coagulation disorders are generally low-grade, acidosis is an unfavorable prognostic factor, severe hypoglycemia can occur after the beginning of quinine treatment, and anemia is an consistent but discrete symptom. In endemic areas emphasis should be placed on the complications of severe malaria in pregnant women due to the high incidence of hypoglycemia and pulmonary edema. Severe malaria can develop early in children in endemic zones. Presenting signs include cerebral malaria in older children and severe anemia in young children. Quinine is the reference treatment with a bolus of 17 mg/kg followed by a daily maintenance dose of 24 mg/kg. Use of artemether should be restricted to quinine-resistant forms. Total blood exchange transfusion is not recommended. Supportive symptomatic treatment, e.g. mechanically assisted ventilation and kidney dialysis, is required. In endemic zones over 90% of deaths involve children without access to intensive care facilities. Mortality rates associated with management of severe imported malaria in intensive care range from 10 to 30%.
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PMID:[Severe malaria in intensive care units in 2003]. 1457 63

A 57-year-old man who had been intermittently taking one 300-mg tablet of quinine sulfate orally for leg cramps experienced transient acute pulmonary edema and hypotension 30-40 minutes after ingestion on two consecutive occasions. He was not taking any concomitant drugs, and there was no alternative explanation for either event. Serial troponin T tests and electrocardiograms, obtained on admission to the hospital, followed by an outpatient echocardiogram and a coronary angiogram, were essentially normal. We compared this case with one previously published and nine previously unpublished reports of quinine-associated pulmonary edema and conclude that some cases of pulmonary edema or adult respiratory distress syndrome in patients with malaria may be caused by an adverse reaction to quinine. Although infrequent, clinicians should be aware of this potentially serious and costly adverse reaction.
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PMID:Acute pulmonary edema caused by quinine. 1546 Jan 83

Rupture of the spleen in malaria may constitute a diagnostic challenge to many clinicians particularly in non-endemic areas where experience with malaria is limited. Our aim is to increase the awareness among clinicians from non-endemic areas of serious malarial complications. We present a young American military man who was admitted to Hamad General Hospital and had 2 serious malarial complications, namely, acute pulmonary edema and rupture of the spleen. He was unusual compared with what was published previously in 4 main points: 1. The rupture of spleen occurred while the patient on mechanical ventilation and under the effect of sedation, which constituted a diagnostic challenge. 2. The 2 complications occurred in a patient with a low parasitemia. 3. The causative species for splenic rupture is Plasmodium falciparum, and 4. The first sample of peripheral blood smear for malarial parasite was negative. We treated him successfully and discharged home in a good condition.
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PMID:Rupture of spleen in a mechanically ventilated patient with falciparum malaria admitted with pulmonary edema. 1643 5


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