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

We have examined the possible risk factors for poor prognosis in cerebral malaria in 61 Nigerian children in an area of high malaria transmission. The level of coma, decerebrate rigidity, hypoglycaemia, and high urea levels were indicators of poor prognosis. Pyrexia, vomiting, and anaemia did not influence prognosis. Post-mortem findings suggest gross cerebral oedema and raised intracranial pressure in 4 of 7 cases with petechial haemorrhages and small focal necrosis (Durck's granuloma).
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PMID:Prognostic risk factors and post mortem findings in cerebral malaria in children. 147 13

Classification, management and prevention of seizures in children are summarized for clinicians in Papua New Guinea. Seizures are classified as febrile with or without underlying brain pathology, and afebrile, including neonatal fits, infantile spasms, myoclonic jerks, akinetic seizures, tonic clonic fits, petit mal, benign focal, and psychomotor seizures. In all cases the first step is to secure the airway, then do a fingerstick and treat hypoglycemia, and finally stop the fit if it is prolonged with paraldehyde, diazepam, phenobarbitone or phenytoin. A cause for the seizure should be sought: physical exam, especially tympanic membranes and throat, blood slide for malaria, lumbar puncture for signs of meningitis, blood culture, serum calcium, and other chemistries. Some empirical treatments to use for negative findings include: dextrose, calcium gluconate, magnesium SO4, pyridoxine, quinine and Fansidar. Hyperthermia in a febrile child can be reversed with cool sponging. The author recommends prescribing phenobarbitone to prevent subsequent simple febrile seizures if the child has 3 or more, then slowly withdrawing the drug if the child is seizure free for a year. Drug therapy for the various other types of seizures available in Papua New Guinea include sodium valproate by special order, and phenobarbitone, phenytoin, carbamazepine, nitrazepam, ethosuximide, and prednisolone. A table is provided to help select the drug for each seizure type, e.g. ethosuximide for petit mal, prednisolone for infantile spasms, and carbamazepine for various types of focal and psychomotor seizures.
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PMID:Convulsions in children. 150 14

Of 78 children with cerebral malaria who were referred to the children's emergency room, University College Hospital, Ibadan, Nigeria, between March 1987 and October 1988, 16 (20.5%) died and 62 (79.5%) survived. The survivors were assessed neurologically over 12-16 months to determine the occurrence, associations and outcome of neurological deficits in cerebral malaria. Neurological deficits occurred in 11 (17.7%) of the patients. The prominent manifestations were cortical blindness, monoparesis and speech deficits. Patients with hypoglycaemia, severe convulsions and prolonged unconsciousness were particularly prone to neurological sequelae. Five children finally recovered completely from their sequelae. These observations show that cerebral malaria is an important cause of neurological deficits in Nigerian children.
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PMID:The incidence and outcome of neurological abnormalities in childhood cerebral malaria: a long-term follow-up of 62 survivors. 156 92

To determine the incidence of hypoglycaemia in children suffering from severe falciparum malaria, 23 patients from Rourkela (Orissa), were investigated. Plasma glucose and immunoreactive insulin were estimated before and at hourly intervals during quinine infusion. No child had hypoglycaemia at the time of admission. Correlation between parasite count and prequinine plasma glucose was not significant. In the period of quinine infusion, 20 patients showed fall in plasma glucose during all the three hours (P less than 0.05, P less than 0.01, P less than 0.01 at the end of 1st, 2nd, and 3rd h respectively) but the decrease to hypoglycaemic level (plasma glucose less than or equal to 40 mg/dl) was observed in only one child. Concomitant increase in plasma insulin was noticed in 18 of these patients. Decrease in plasma glucose and increase in plasma insulin was found to correlate well (r-0.78, P less than 0.001). Hypoglycaemia was found to be an infrequent complication of severe falciparum malaria in children from the area studied. Though decrease in plasma glucose was observed after quinine infusion, it was less severe and did not reach the hypoglycaemic level.
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PMID:Incidence of hypoglycaemia in children with severe Plasmodium falciparum malaria around Rourkela, Orissa state. 160 75

Because Plasmodium berghei ANKA induces cerebral malaria and P. vinckei does not, the former has often been studied as a model for human falciparum malaria. It lacks, however, many of the systemic changes seen in the human disease. Because both of these murine models and the human disease have now been defined in terms of excess tumor necrosis factor (TNF) production, the authors have more closely examined the two murine models in this light to see which provides the better overall model for falciparum malaria. Administering TNF to malaria-infected mice did not cause cerebral symptoms nor breakdown of the blood-brain barrier, which is the hallmark of P. berghei ANKA cerebral malaria and is generally absent in human cerebral malaria. Tumor necrosis factor did, however, induce hypoglycemia and liver injury, pathology that is seen in terminal P. vinckei and falciparum malaria, but is absent in terminal P. berghei ANKA malaria. Plasma TNF and interleukin-6 (IL-6) also were found to be consistently higher in infections caused by P. vinckei than in those caused by P. berghei ANKA. The pathology of P. vinckei malaria is thus consistent with raised systemic levels of TNF and other cytokines, as is falciparum malaria. The authors therefore conclude that P. vinckei malaria, although lacking a cerebral component, is the better model for the human disease.
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PMID:Malaria mimicry with tumor necrosis factor. Contrasts between species of murine malaria and Plasmodium falciparum. 173 26

The pharmacokinetics and effectiveness of three dosage regimens of quinine were studied in a group of 59 children with severe malaria. The children were randomized to receive high-dose intravenous or intramuscular quinine (20 mg salt/kg loading, then 10 mg salt/kg every 12 hr), or low-dose intravenous quinine (10 mg salt/kg loading, then 5 mg salt/kg every 12 hr). In the group receiving the high-dose intravenous regimen, mean high and low quinine concentrations were consistently greater than 10 and 6.5 mg/l, respectively. Peak concentrations as well as the time required to achieve them were similar in the intramuscular and high-dose intravenous groups. The low-dose intravenous quinine regimen resulted in mean peak concentrations greater than 6 mg/l and mean low concentrations greater than 3.5 mg/l. All blood concentrations exceeded the 99% in vitro inhibitory concentration (EC99) of 0.89 mg/l or less of quinine for 60 isolates of Plasmodium falciparum, which were taken from children with malaria during the same period. Judged by a number of clinical criteria, the response was better in patients receiving the high-dose than the low-dose intravenous regimen. The time taken to clear parasites with both the high-dose intravenous and intramuscular regimens were significantly shorter than those obtained in the low-dose group. We have also shown for the first time that the rate of parasite clearance can be directly related to the area under the quinine concentration versus time curve. This applied to all three quinine regimens (r = 0.4252, P less than 0.02; n less than or equal to 35). Five patients, two on the low-dose regimen, two on the intramuscular regimen, and one on the high-dose regimen, developed hypoglycemia after admission, but in these cases, insulin concentrations were correspondingly low. No significant quinine toxicity was observed in any of the cases. The high-dose intravenous quinine regimen described here may be optimal for treatment of severe falciparum malaria in areas of chloroquine resistance in Africa. Our data provide no justification for reducing the dose of quinine in the treatment of severe malaria in Africa. The intramuscular regimen could provide a satisfactory alternative in areas where intravenous administration might be delayed or is impossible.
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PMID:Quinine treatment of severe falciparum malaria in African children: a randomized comparison of three regimens. 176 97

Quinine is widely used for the treatment of severe and complicated malaria, although resistant strains of Plasmodium falciparum may occur. The drug has been incriminated as a cause of hypoglycaemia in some malaria patients. To determine if quinine has untoward metabolic effects during treatment of severe and complicated malaria we have studied the effects of quinine on blood glucose and intermediary metabolites, serum insulin, C-peptide, plasma glucagon and non-esterified fatty acids in 97 children with severe malaria in Dar es Salaam. All patients responded clinically. No patient developed hypoglycaemia while on quinine therapy given as 10 mg/kg in 10 ml/kg of 5% dextrose infused over 4 h every 8 h. Endogenous insulin secretion, as reflected by C-peptide levels, increased after 4 h but insulin levels did not change significantly. Blood lactate, 3-hydroxybutyrate, plasma non-esterified fatty acids and plasma glucagon all fell appropriately during treatment. We conclude that quinine, when administered at the recommended dose and rate, does not disrupt blood glucose homeostasis, and is still the drug of choice for severe and complicated malaria in children.
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PMID:The metabolic effects of quinine in children with severe and complicated Plasmodium falciparum malaria in Dar es Salaam. 129 76

One hundred and thirteen children aged 12 years or less with cerebral malaria in Accra, Ghana were treated with chloroquine either with a low dose regime of 3.5 mg/kg 8-hourly intramuscularly, or orally by nasogastric tube, in a standard regime, both to a total of 25 mg/kg body weight. There was no obvious difference in outcome in the 2 treatment groups. The overall mortality of 5.3% (5.9% and 4.4% in the oral and intramuscular treatment groups respectively) was similar to that seen 10 years ago in this hospital. The average parasite clearance time had increased to 61 h, compared to 41 h noted 10 years ago. The incidence of hypoglycaemia (3%) was very low compared to studies in other malaria endemic areas. The reason for this is not clear but it could have contributed to the low mortality. Neurological deficits were seen on day 14 in 7.8% of patients. Parasitaemia recurred within 14 d in 22% of surviving patients, confirming the presence of RI/RII chloroquine resistance in Accra.
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PMID:Comparative trial of oral versus intramuscular chloroquine in children with cerebral malaria. 180 33

According to the literature, socio-economic factors may contribute more to geographic variations in the aetiology and prognosis of childhood coma than has previously been recognised. This prospective study involving 118 children with strictly defined coma demonstrated that the commonest causes of coma in Ibadan were cerebral malaria (55%), meningitis (13%) and encephalitis (10%). The prognosis was poor. Forty-three (36%) of 118 cases died and 75 (64%) survived, including 23 who showed neurologic deficits. Noteworthy prognostic indices of coma were the aetiology of the condition, the presence of severe anaemia, hypoglycaemia and pneumonia. The findings are discussed in the context of the socio-economic background of children in the tropics.
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PMID:Childhood coma in Ibadan. Relationship to socio-economic factors. 181 64

Paludism can occur quite easily in pregnant women in endemic zones, above all those who are primiparous or in their 2nd or 3rd terms. The onset of paludal attacks can be serious for both the mother and the child. That is to say, besides the obviously imperative therapeutic action, a prophylaxis is also a necessity. The use of antipaludial substances at our disposal has been complicated during the last few years as a result of chloroquine-resistance extension. Besides a few nuances of kinetic nature observed in pregnant women, a good knowledge of teratogenous or embryotoxic effects is necessary. But this remains fragmentary. Among the principal antipaludial medications is quinine (Q), reported to be abortifacient but in reality it is not: it is often poorly tolerated by the mother (hypoglycemia), but is not responsible for abnormalities in children, except under large doses. Chloroquine (CQ), considered to be without harmful effects, can be used in women without large restrictions, even if toxic effects have been observed in animals. The pyrimethamine-sulfanilamide (P-S) combination contains two substances which are a potential risk. Nevertheless, experiments have never showed harmful effects in pregnant women, particularly when under cover of a joint prescription of folinic acid. Proguanil is without doubt the only molecule which can be used without restriction. Two new medications, quinoline methanol, Mefloquine (MQ) and Halofantrine (HF) are contra-indicated for lack of experimentation and because of some abnormalities observed at high doses in animals. Artemisinine and amino-8-quinoline are contra-indicated, and cyclines are strongly inadvised. From the practical point of view, the present use of antipaludial medication in pregnancy should take into account the surrounding risk, namely that of paludism and of treatments. Curatively, Q remains a serious treatment in any form. In CQ-sensitive zones CQ is usable unreservedly in simple attacks. In CQ resistance zones the use of Q seems preferable to that of Fansidar proposed by certain people. MQ and HF, although contra-indicated, have already been employed without inconvenience. By way of prevention, it is important first of all to avoid all leisure stays in endemic zones. If travel is unavoidable or for indigenous people, a chemoprophylaxis, judged according to the local risk of impaludation, is desirable: CQ in sensitive zones, PG+CQ in resistant zones, P-S, as proposed by some people, is normally contra-indicated; MQ and HF are contra-indicated. Protection against nocturnal mosquito bites is still strongly applied (Mosquito net, repellents, insecticides).
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PMID:[Antimalarials and pregnancy]. 181 22


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