Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case is reported of a 40-year-old woman presenting with cerebral malaria complicated by an adult respiratory distress syndrome (ARDS). The patient was admitted to the intensive care unit in a coma, scored 5 on the Glasgow scale. Plasmodium falciparum parasitaemia was, at the time, 50%. A continuous intravenous quinine infusion (25 mg.kg-1.day-1) was started, together with the required symptomatic treatment. Blood was transfused because of increasing anaemia (haemoglobin 60 g.l-1). After 24 h, parasitaemia was 12%, consumption of clotting factors broke out (prothrombine 43%, fibrin degradation products greater than 40 micrograms.ml-1, platelets 45 G.l-1). Hypoxaemia (PaO2 = 46 mmHg) and hypocapnia (PaCO2 = 32 mmHg) became obvious, together with bilateral diffuse alveolar infiltrates on chest X-ray. Haemodynamic data suggested non cardiogenic oedema: PEEP 20 cm H2O, cardiac output 6.15 l.min-1, mean pulmonary arterial pressure 35 mmHg, pulmonary wedged pressure 15 mmHg. The hypoxia worsened and the patient died on the 15th day after associated with high levels of parasitaemia. Several reports have suggested that it may be related to increased capillary permeability. Initial fluid overload should therefore be avoided. Parenteral quinine remains the mainstay of treatment, because of its rapid schizonticidal activity. Although exchange transfusion seems to be a valuable adjunct to chemotherapy, it requires further assessment.
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PMID:[Fatal pulmonary edema in a pernicious malaria attack]. 227 23

Thirty-four dogs suffering from severe babesiosis caused by Babesia canis rossi were included in this study to evaluate acid-base imbalances with the quantitative clinical approach proposed by Stewart. All but 3 dogs were severely anemic (hematocrit <12%). Arterial pH varied from severe acidemia to alkalemia. Most animals (31 of 34; 91%) had inappropriate hypocapnia with the partial pressure of CO2 < 10 mm Hg in 12 of 34 dogs (35%). All dogs had a negative base excess (BE; mean of - 16.5 mEq/L) and it was below the lower normal limit in 25. Hypoxemia was present in 3 dogs. Most dogs (28 of 34; 82%) were hyperlactatemic. Seventy percent of dogs (23 of 33) were hypoalbuminemic. Anion gap (AG) was widely distributed, being high in 15, low in 12, and normal in 6 of the 33 dogs. The strong ion difference (SID; difference between the sodium and chloride concentrations) was low in 20 of 33 dogs, chiefly because of hyperchloremia. Dilutional acidosis was present in 23 of 34 dogs. Hypoalbuminemic alkalosis was present in all dogs. Increase in unmeasured strong anions resulted in a negative BE in all dogs. Concurrent metabolic acidosis and respiratory alkalosis was identified in 31 of 34 dogs. A high AG metabolic acidosis was present in 15 of 33 dogs. The lack of an AG increase in the remaining dogs was attributed to concurrent hypoalbuminemia, which is common in this disease. Significant contributors to BE were the SID, free water abnormalities, and AG (all with P < .01). Mixed metabolic and respiratory acid-base imbalances are common in severe canine babesiosis, and resemble imbalances described in canine endotoxemia and human malaria.
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PMID:The mixed acid-base disturbances of severe canine babesiosis. 1159 31