Lactato sérico como marcador prognóstico em criancas gravemente doentes / Blood lactate concentration as prognostic marker in critically ill children

OBJETIVO: Verificar a utilidade do lactato como marcador de hipoperfusão tecidual e como índice prognóstico em criancas criticamente doentes. MÉTODOS: Estudo prospectivo, longitudinal, tipo observacional de 75 pacientes admitidos na UTI pediátrica do Hospital de Clínicas (UFPR) entre novembro de 1998 e maio de 1999. De acordo com o nível de lactato na admissão, os pacientes foram divididos em grupo A (lactato > 18 mg/dl) e grupo B (lactato < 18 mg/dl). Com relacão à evolucão, em sobrevivente e óbito. No grupo A, a avaliacão clínica e a coleta de amostras de sangue arterial foram realizadas na admissão, 6, 12, 24, 48 horas e, posteriormente, a cada 24 horas. No grupo B, foram realizadas nos mesmos horários e interrompidas com 48 horas após admissão. RESULTADOS: No grupo A, foram incluídos 50 pacientes, e no Grupo B, 25. O grupo A apresentou maior freqüência de sinais clínicos de hipoperfusão (24/50). Houve diferenca estatisticamente significativa da média de lactato na admissão entre os pacientes que foram a óbito nas primeiras 24 horas de internacão (95 mg/dl) quando comparados àqueles que evoluíram a óbito após 24 horas de admissão (28 mg/dl). O nível de lactato na avaliacão de 24 horas de UTI foi o que apresentou melhor sensibilidade (55,6 por cento) e especificidade (97,2 por cento) como parâmetro preditor de óbito. CONCLUSÕES: A maioria dos pacientes com lactato > 18 mg/dl evidenciou sinais clínicos de hipoperfusão na admissão. A normalizacão ou diminuicão dos níveis de lactato a partir de 24 horas de internacão esteve significativamente relacionada com a maior probabilidade de sobrevida.

Neutrophil signaling alteration: an adverse inflammatory response after burn shock

The inflammatory response syndrome in shock-like states might frequently be accompained by an oxidative cell/tissue demage in one or more organ-systems in the body. The inflammatory response related hyperactivation of neutrophils can contribute to oxidative cell/tissue damage. Studies discussed in this review examined the role of cell sgnaling pathways in the hyperactivation of neutrophils in an early stage of burn injury shock. The studies were carried out in peripheral blood neutrophils isolated from rats with a 25 per cent body surface area scald burn. Neutrophil cell signaling responses were evaluated by measuring cytosolic [Ca2+] and protein kinase C activity, and were correlated with neutrophil superoxide production. The cytosolic [Ca2+] and protein kinase C responses were highly upregulated along with enhanced superoxide production in the early phase of burn injury. The treatment of burn-injured rats with the calcium antagonist diltiazem abrogated enhanced Ca2+ and protein kinase C signaling and superoxide generation. The signaling upregulation in neutrophils could result from potentiation of actions of burn-injury induced chemotactic mediators on the leukocytes. The neutrophil signaling upregulation leading to increased superoxide generation could thus be responsible for the oxidative cell/tissue damage. The organ-system dysfunction/failure accompanying burn shock may be initiated with the oxidative cell/tissue damage.

Hypovolemic hemorrhagic shock (an experimental study)

Com o intuito de estudar os fenomenos naturais de defesa contra as hemorragias traumaticas, foram estudados 20 camundongos examinando-se histologicamente algumas de suas grandes veias em caso de sangria, sangria+hemodiluicao e controles, apos fixacao em formol...

Plasma renin activity in shock due to aluminium phosphide poisoning.

Plasma renin activity (PRA) was estimated in 30 patients with aluminium phosphide (AIP) poisoning (study group) admitted in shock. Ten patients in shock other than due to AIP poisoning (Group II A) and 20 normal healthy subjects (Group II B) served as controls. The PRA was significantly higher in the study group and group II A as compared to normal healthy subjects (p less than 0.001). Significantly higher PRA was found in the study group as compared to Group II A (p less than 0.001). The initial higher PRA continued to rise further in the study group but it started decreasing in Group II A as the duration of shock advanced. Continuation of shock in AIP poisoning was probably due to slow release of toxic PH3 gas, which was detected by positive silver nitrate paper test. The rise in PRA was directly proportional to the dose of pesticide consumed. There was direct relationship of mortality with increased PRA. Angiotensin converting enzyme inhibitors may have a role in combating shock in AIp poisoning.