A resposta metabólica ao trauma cranioencefálico é autolimitada? Análise das proteínas de fase aguda e glicemia
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Data
1998-12-01
Autores
Schelp, Arthur Oscar [UNESP]
ANGELELI, APARECIDA Y.O. [UNESP]
Zanini, Marco Antonio [UNESP]
TSUJI, HISACHI [UNESP]
Burini, Roberto Carlos [UNESP]
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Editor
Academia Brasileira de Neurologia (ABNEURO)
Resumo
Nos últimos anos tem havido referências à limitação da resposta metabólica nas duas primeiras semanas após trauma cranioencefálico (TCE). Foi feita proposta de estudo a partir de experimento clínico em pacientes com trauma encefálico grave, que foram avaliados por volta de 7 dias após a lesão (M1). A segunda avaliação ocorreu 4 dias após (M2), e a terceira 3 a 4 dias após (M3). em um período de 2 anos, foram selecionados 28 pacientes do sexo masculino, com trauma encefálico grave, escala de gravidade de Glasgow entre 4 e 6. Dentre os 28 pacientes, 6 completaram o estudo proposto. Os pacientes foram acompanhados clinicamente durante toda a fase do experimento. em cada um dos momentos de análise, foram feitas análises da excreção nitrogenada e proteínas de fase aguda. da mesma forma foram feitas determinações da glicemia plasmática, N-amínico e triglicerídeos. Os resultados do estudo demonstraram não haver modificações no balanço nitrogenado, normalização da proteína-C-reativa e redução relativa da glicemia ao final do experimento. Os autores tecem considerações sobre os possíveis mecanismos envolvidos na modulação da resposta metabólica e concluem que o hipermetabolismo, a basear-se na análise da glicemia e das proteínas de fase aguda, não persiste além do 13° dia do período de recuperação pós-trauma. São feitas sugestões de estudos futuros que possam elucidar os mecanismos envolvidos na normalização do hipercatabolismo e hipermetabolismo observados nas duas primeiras semanas após TCE.
There are many reports supporting a self-limitation mechanism involved with hypermetabolic response after severe cranial injury. It was proposed a study with severe head injury patients, in three stages of the evolution. The first 7 days after admission (moment 1- M1), the second three days latter (M2) and the last 7 days after the first (M3). Among male patients with severe head injury, attended between January 1992 and December 1993 in University Hospital of Botucatu, UNESP, were selected 28 male patients, with Glasgow severity scale between 4 and 6, with pO2< 70 mm Hg, weighting 60 kg or more. Among these patients, 6 finished the study, including analysis of the excretion of N, acute phase proteins, glycemia, triglycerides and amine nitrogen. During the study there were no changes in nitrogen balance and there was a decrease in protein C-reative. Glycemia tends to fall within two weeks after injury. The authors make some considerations about possible mechanisms involved in brain modulation associated with the period of dependence of hypermetabolism and hypercatabolism after closed brain injury. There are some evidences that the brain responds to head trauma with a gobal non specific way, which tends to be reorganized beyond the first two weeks after lesion. The study does not show any influence of the type and severity of head trauma.
There are many reports supporting a self-limitation mechanism involved with hypermetabolic response after severe cranial injury. It was proposed a study with severe head injury patients, in three stages of the evolution. The first 7 days after admission (moment 1- M1), the second three days latter (M2) and the last 7 days after the first (M3). Among male patients with severe head injury, attended between January 1992 and December 1993 in University Hospital of Botucatu, UNESP, were selected 28 male patients, with Glasgow severity scale between 4 and 6, with pO2< 70 mm Hg, weighting 60 kg or more. Among these patients, 6 finished the study, including analysis of the excretion of N, acute phase proteins, glycemia, triglycerides and amine nitrogen. During the study there were no changes in nitrogen balance and there was a decrease in protein C-reative. Glycemia tends to fall within two weeks after injury. The authors make some considerations about possible mechanisms involved in brain modulation associated with the period of dependence of hypermetabolism and hypercatabolism after closed brain injury. There are some evidences that the brain responds to head trauma with a gobal non specific way, which tends to be reorganized beyond the first two weeks after lesion. The study does not show any influence of the type and severity of head trauma.
Descrição
Palavras-chave
trauma cranioencefálico, proteínas de fase aguda, metabolismo protéico, head injury, trauma, acute phase proteins, protein metabolism
Como citar
Arquivos de Neuro-Psiquiatria. Academia Brasileira de Neurologia - ABNEURO, v. 56, n. 4, p. 778-788, 1998.