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

For therapy of severe malaria with renal failure, a 2/3 reduction in the usual intravenous dose of quinine is recommended (600 mg per 24 h instead of 600 mg per 8 h). Two patients with severe malaria and renal failure requiring dialysis have been treated. The half-life was not prolonged (15 h). Quinine proved to be nondialysable. It was shown that this dose of quinine tended to lead to a low level in blood (under 10 mg.l-1). A normal dose of quinine (2 x 15 mg/kg per day) is therefore recommended for malaria therapy, even in cases with renal failure requiring haemodialysis, in order to attain the desired plasma level (5 to 15 mg.l-1).
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PMID:Quinine dosage in severe malaria with renal failure necessitating haemodialysis. 275 74

Report of a new case of airport malaria with renal failure. The evolution of the thirty cases previously described is reviewed. Most of the time, airport malaria seems to be a severe infection.
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PMID:[The severity of airport malaria]. 305 99

Traditionally, blood rheology tests have been used in diagnosis and monitoring of infection, rheumatic diseases and malignancy, and are still of clinical value in these conditions. In the last twenty years, clinical and epidemiological studies have shown that the haematological determinants of blood flow resistance (haematocrit, fibrinogen, white cell count and altered red and white cell rigidity) are also associated with nutritional, metabolic, endocrine and vascular disorders. Decreased red cell deformability may contribute to reduced red cell survival and anaemia in burns, malaria, liver disease and kidney failure. In trauma and inflammatory disease, overt hyperviscosity is usually prevented by vasodilatation and reduction in the haematocrit. However, low-flow states may arise systemically from haemoconcentration (contracted plasma volume, Chapter 3) in severe burns, inappropriate red cell transfusion, or dehydration due to illness; systemically in circulatory shock; and locally in venous thrombosis or arterial disease. In such circumstances, the intrinsic flow resistance of blood may perpetuate flow disturbance, ischaemia and thrombosis. Conversely, optimal levels of haematocrit, fibrinogen and white cell count may be lower than normal in low-flow states. Haemodilution by colloid infusion is beneficial in burns, shock, major surgery, prevention of postoperative venous thrombosis, chronic stable claudication and possibly in acute stroke and retinal vein thrombosis. Plasma exchange may be beneficial in severe Raynaud's phenomenon. Defibrination with ancrod is effective in prevention and treatment of venous thrombosis but its role in arterial disease is unproven. The benefits of streptokinase therapy in venous thrombo-embolism and acute myocardial infarction may be partly rheological, due to fibrinogen depletion. Drugs with rheological effects may be beneficial in intermittent claudication.
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PMID:Blood rheology in general medicine and surgery. 332 67

The currently recognized toxic effects of quinine in humans are identified and the problems of management of overdosage of quinine are discussed. Quinine, available therapeutically as sulphate or hydrochloride salts, also is widely used in tonic water, and there are several case reports of allergic reactions to the drug when a patient has consumed the drug in this way. Another unintentional source of poisoning is its use as an adulterant in heroin for "street" use. This appears to be a problem in the US. Quinine, termed a "general protoplasmic poison" is toxic to many bacteria, yeasts, and trypanosomes, as well as to malarial plasmodia. Quinine has local anesthetic action but also is an irritant. The irritant effects may be responsible in part for the nausea associated with its clinical use. In addition it has a mild antipyretic effect. Several features are common to both an acute single overdose in self-poisoning and accumulation of quinine during therapy for malaria: together they are termed cinchonism. Auditory symptoms, gastrointestinal disturbances, vasodilatation, sweating, and headache occur with moderately elevated plasma quinine concentration. As these rise, increasingly severe visual disturbances and then cardiac and neurologic features occur. Mild nausea may be the only symptom, but with large overdoses profuse vomiting, abdominal pain, and diarrhea may occur. These result from a combination of the local irritant effect of quinine on the gut and the central effects of quinine on the chemoreceptor trigger zone. Vasodilatation and sweating are well recognized, and tinnitus is common. Visual symptoms usually are delayed, and blindness may not be discovered for a day or more. Aspirin-sensitive patients, and others, may develop angioedema by nonimmunological mechanisms in response to drugs, and quinine has been reported to produce pseudo-allergic reactions in aspirin-sensitive patients. Quinine also can cause drug-induced thrombocytopenia and purpura. In patients suffering with malaria due to "Plasmodium falciparum," anemia and acute intravascular hemolysis with renal failure are recognized complications. There appears to be little evidence in the literature in support of the folk tradition of quinine as an inducer of abortion. Quinine is known to cause deterioration in patients with myasthenia gravis and erythema multiforme, to stimulate insulin release in patients receiving treatment for falicparum malaria, and to be responsible at times for ataxia following moderate overdosage. Clinically, quinine poisoning is observed in 3 situations: self-poisoning; accidentally; and following use of quinine in excessive doses in the hope of achieving abortion. Treatment courses are reviewed.
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PMID:Quinine toxicity. 354 70

To receive actual information about the clinical course of falciparum malaria case history of 373 patients hospitalized in Chemin de Fer Hospital in Phnom Penh from May 1 till October 1, 1985 were evaluated. No patients were infected in Phnom Penh. We estimated that only 8.3% of patients had higher parasitaemia than 100,000 or more asexual parasites in microliter of peripheral blood which is considered as a heavy infection. Complicated malaria was found in 39 patients (10.4%). The most frequent complications were cerebral complications (80.0%), renal failure (23.3%), and liver failure (16.6%). Ten patients had multiple organ complications and they represented 25.6% of patients with complications. The 100% mortality was observed in those in coma stage III; with haemoglobinuria, epistaxis and melena. Only coma stage III as a single symptom caused the death. In other cases death resulted from multiple organ complications.
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PMID:Malaria in Kampuchea: clinical course of falciparum malaria in Chemin de Fer Hospital, Phnom Penh. 355 50

A clinical case of Black Water Fever following Plasmodium falciparum infection is reported. The patient had no previous history of malaria and had not taken anti-malarials as prophylasis. He was free from G-6-PD deficiency and abnormal haemoglobins. He had acute intravascular haemolysis, haemoglobinurea and renal failure after the third dose of quinine infusion. His life was saved by peritoneal dialysis and Artemether injection. In in vitro test, his blood haemolysed suddenly in 36 hours when incubated with quinine (10 mg per lit) at 37 degrees C in test tube while control blood took over a week for natural slow haemolysis. Thus quinine plays an important part in the cause of Black Water Fever.
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PMID:A case of black water fever treated with peritoneal dialysis and artemether (quinghaosu derivative). 366 74

Acute pharmacokinetics of intravenously infused quinine were studied in 25 patients with cerebral malaria and 13 with uncomplicated falciparum malaria. In patients with cerebral malaria receiving the standard dose of 10 mg/kg every eight hours, plasma quinine concentrations consistently exceeded 10 mg/liter, reaching a peak 60 +/- 25 hours (mean +/- 1 S.D.) after treatment was begun and then declining. Quinine total clearances (Cl) and total apparent volumes of distribution (Vd) were significantly lower than in uncomplicated malaria (Cl, 0.92 +/- 0.42 compared with 1.35 +/- 0.6 ml/min/kg, p = 0.03; Vd, 1.18 +/- 0.37 compared with 1.67 +/- 0.34 liter/kg, p = 0.0013). There was no significant difference between the two groups in elimination half-times (t/2) or renal clearances (Cu) (t/2, 18.2 +/- 9.7 compared with 16 +/- 7.0 hours; Cu, 0.21 +/- 0.16 compared with 0.21 +/- 0.08 ml/min/kg). In nine patients studied following recovery, Cl (3.09 +/- 1.18 ml/min), Vd (2.74 +/- 0.47 liter/kg), and Cu (0.53 +/- 0.22 ml/min/kg) were significantly greater (p less than or equal to 0.0004), and t/2 was significantly shorter (11.1 +/- 4.1 hours, p = 0.006) than during the acute illness. Cu accounted for approximately 20 percent of Cl in all groups. Renal failure did not alter the disposition kinetics in cerebral malaria. There was no clinical or electrocardiographic evidence of cardiotoxicity and no permanent neurotoxicity. Quinine toxicity in cerebral malaria has probably been overemphasized. The benefits of high plasma concentrations in the acute phase of this life-threatening disease appear to outweigh the risks, particularly in view of the increasing resistance of Plasmodium falciparum to quinine in Southeast Asia.
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PMID:Quinine pharmacokinetics and toxicity in cerebral and uncomplicated Falciparum malaria. 675 Oct 85

Thirty-five children with G6PD deficiency, who presented with acute intravascular haemolysis, were evaluated to define its aetiology, clinical features and ultimate outcome. All were boys with ages ranging from 6 months to 12 years. Pallor of abrupt onset and passage of cola-coloured urine were universal presenting symptoms. Incriminating factors responsible for haemolysis include hepatitis (7), malaria (4), bacterial sepsis (3) and drug intake (24), with more than one predisposing condition existing in some children. Marked elevations in serum bilirubin, coinciding with intravascular haemolysis, was a feature in all the seven children with hepatitis. Azotaemia was noted in 20 patients, of whom 14 did not have oliguria. All four children with malaria presented with protracted renal failure. Therapy focused on maintaining a high urine output in those without oliguria. A total of 15 peritoneal dialyses and five haemodialyses were required in six patients with acute renal failure, all of whom were oliguric. Supportive therapy consisted of blood transfusions and treatment of the predisposing diseases. Thirty-two children recovered completely while three died, the cause of death being severe anaemia and congestive cardiac failure, malaria with oliguric renal failure and hepatic encephalopathy, respectively.
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PMID:Acute intravascular haemolysis in glucose-6-phosphate dehydrogenase deficiency. 750 89

Falciparum malaria is the most hazardous form of malaria. Its high degree of parasitemia interferes with vital functions of most organs and is directly responsible for its high rate of mortality and morbidity. Quinine and other antimalarial drugs are relatively slow acting and not always effective due to the growing resistance developed by Plasmodium toward these drugs. Another emergency modality, which would remove the parasitic burden quickly and effectively, is thus much needed. We present a case of a 51-year-old sailor, who was admitted to the hospital because of complicated falciparum malaria. His situation deteriorated rapidly into a desparate stage, despite the various intensive treatments and quinine. He soon developed a systemic inflammatory response syndrome manifested as cerebral malaria, renal failure, acute respiratory distress syndrome and disseminated intravascular coagulation. An emergency blood exchange reversed the situation dramatically, and the patient recovered completely. It is recommended that any doctor, both in endemic and in non endemic areas, dealing with blood transfusions or infectious diseases, should be acquainted with this lifesaving modality, regardless of the controversy still surrounding this subject.
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PMID:Blood exchange [correction of exchance]-a rescue procedure for complicated falciparum malaria. 772 67

Imported malaria is increasing in Western countries, which results in considerable morbidity and mortality, the latter mainly due to delayed diagnosis and treatment. Partial exchange transfusion has been proposed as a therapy for very severe falciparum malaria, but the utility of this procedure has not been proven. We report on 12 patients with severe Plasmodium falciparum malaria, treated with exchange transfusion in 5 Belgian hospitals between 1987 and 1991. The mean parasitaemia before exchange was 17.2% (range 6-35%). An average of 3.1 l was exchanged within 3 to 7 hours. Ten of the 12 patients survived. One patient recovered initially, but died as a consequence of a cascade of complications of dialysis. Three patients developed the adult respiratory distress syndrome (ARDS), two had less serious pulmonary involvement, and five had temporary renal failure; none of the survivors had sequelae. A formula is proposed to calculate the expected reduction in parasitized erythrocytes by exchange transfusion in function of the initial parasitaemia, the initial haemoglobin level and the volume of blood exchanged. Comparison between the mathematically predicted and the observed decline in parasitaemia shows on average a 25% excess of observed over predicted efficacy per unit of blood exchanged. After introducing this correction the formula enables the clinician to estimate roughly the volume of blood that has to be exchanged in order to bring the initial parasitaemia down to a desired level.
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PMID:Twelve patients with severe malaria treated with partial exchange transfusion. Comparison between mathematically predicted and observed effect on parasitaemia. 789 99


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