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Choc hyperkinétique et accès pernicieux palustre

1990; Elsevier BV; Volume: 9; Issue: 5 Linguagem: Inglês

10.1016/s0750-7658(05)80954-2

1769-6623

J.M. Saïssy, R. Gohard, O. Raux, Jean Kempf, Bakary Diatta,

Hemoglobinopathies and Related Disorders

Deux observations d'accès pernicieux palustre avec choc hyperkinétique sont rapportées. Dans le premier cas, l'étude hémodynamique notait: P̄a: 55 mmHg, CI: 5,21 · min−1 · m−2, Rsa: 290 dyn · s · cm−5, V̇O2: 120 ml · min−1 · m−2. L'évolution fut défavorable malgré un traitement par dopamine et dobutamine. Dans le second cas, l'étude hémodynamique révélait: P̄a: 54 mmHg, CI: 6,51 · min−1 · m−2, Rsa: 476 dyn · s · cm−5, V̇O2: 174 ml · min−1 · m−2. L'évolution fut favorable sous remplissage et dopamine. En l'absence d'étiologie infectieuse associée, l'origine plasmodiale de ces deux états de choc semble probable. La physiopathologie des formes algides de l'accès pernicieux palustre reste mystérieuse. Différents facteurs sont envisagés: cytoadhérence des érythrocytes infectés par le plasmodium, perturbations immunologiques ou existence d'une endotoxine spécifique. Two cases of cerebral malaria with hyperkinetic shock are reported. The first case concerned a 39-year-old european male who was not taking any prophylactic anti-malarial drugs. After having had headache and fever for a week, he was admitted to the intensive care unit (ICU) in coma and with jaundice. His initial systolic blood pressure was 60 mmg, with a central venous pressure (CVP) of — 3 cmH2O. Five-hundred ml of modified fluid gelatin increased the CVP without raising the blood pressure. Haemodynamic investigations revealed a cardiac index (CI) = 5.21 · min−1 · m−2, peripheral arterial resistances (Rsa) = 290 dyn · s · cm−5, oxygen consumption (V̇O2) = 120 ml · min−1 · m−2. Despite treatment with dopamine and dobutamine, the patient died 3 h after his admission, with a CI of 1.91 · min−1 · m−2. The second patient was a 14-year-old senegalese girl, admitted in circumstances similar to the first case. Initial haemodynamic investigations gave the following figures: CI 6.51 · min−1 · m−2, Rsa = 476 dyn · s · cm−5, V̇O2 = 174 ml · min−1 · m−2. Recovery was obtained with fluid replacement therapy and dopamine. In the absence of another associated infectious disease, the plasmodial origin of the septic shock would seem to be the most likely in both cases. Pathophysiological mechanisms of these algid forms of malaria remain enigmatic. Various factors are discussed: cytoadherence of erythrocytes infected with Plasmodium falciparum, immunological disturbances, or a specific endotoxin.