The acute-phase response of the brain-injured patient

Abstract

The acute response to injury and infection is manifested by increased synthesis of acute-phase proteins by the liver, an increased white blood cell count, fever, a negative nitrogen balance, and altered serum mineral levels (zinc, iron, and copper). This response is thought to be partially mediated by cytokines such as interleukin-1, but has not been well studied in head-injured patients. In this study, 25 patients were studied for evidence of the acute-phase response extending from hospital admission up to 21 days postinjury. The patients were divided into two groups to determine if severity of injury influenced the response. Group 1 consisted of nine patients with admission peak 24-hour Glasgow Coma Scale (GCS) scores of 4 or less; Group 2 consisted of 16 patients with admission peak 24-hour GCS scores of 8 or greater. All patients demonstrated some evidence of the acute-phase response. Serum alpha-1 acid glycoprotein, ceruloplasmin, and C-reactive protein levels were elevated on admission and throughout the study. Serum albumin and zinc levels were depressed on admission; zinc levels gradually normalized by Day 21 in both groups, but hypoalbuminemia was observed throughout the study period. Serum copper levels were normal on admission but increased to above normal in both groups by Day 11 postinjury. Urinary urea nitrogen excretion was elevated in both groups and peaked on Day 7 for Group 1 and Day 11 for Group 2 patients. The patients with admission GCS scores equal to or less than 4 had overall higher temperatures than were seen in those with GCS scores greater than or equal to 8 (p = 0.009). All patients but one had an elevated white blood cell count on admission. It is concluded that brain-injured patients with admission GCS scores of 3 to 4 and 8 to 14 demonstrate an acute-phase response which lasts for at least 3 weeks postinjury. It is speculated that this response is at least partially mediated by increased intraventricular interleukin-1 activity.

Zaburzenia termoregulacji pochodzenia ośrodkowego — jak diagnozować i leczyć

“…Patients with CF have been found to have bradycardia, hypoidrosis, a lack of 24-hour temperature fluctuations for many days or even several weeks, and resistance to antipyretics; moreover, their body temperature is very high [7]. CF is more common in severely ill patients with diffuse white matter damage, brain oedema, hyperglycaemia, leukocytosis and hypotension [8].…”

A resposta metabólica ao trauma cranioencefálico é autolimitada? Análise das proteínas de fase aguda e glicemia

“…Apesar da proteína-C-reativa ter valor restrito para diagnóstico diferencial, sua queda após alguns dias é indício consistente de melhoria da lesão, incluindo inflamação e sepsis 21 . Young e col. 8 , estudando pacientes com trauma encefálico divididos em dois grupos, verificaram que, tanto o primeiro, constituído de 9 pacientes com Glasgow < 4 nas primeiras 24 horas, como o segundo, com 16 pacientes e Glasgow > 8, apresentavam queda significativa da proteína-C-reativa em torno do 14° dia pós-trauma. A estabilização, em níveis relativamente elevados, persistiu até pelo menos o 20° dia do período de recuperação.…”

“…As infecções respiratórias, intercorrência frequente nos pacientes com TCE, parecem não influir de maneira significativa sobre o GEB 31. É possível observar, como demonstrado, que as proteínas de fase aguda, assim como a glicemia, apresentam razóavel correlação com a evolução neurológica, tendendo à normalidade passadas duas semanas. A visualização global dos resultados confirma as impressões de Deutshman e col. 5,6,28 e Young e col. 8 , de que o trauma encefálico fechado, diferentemente das lesões que não comprometem o crânio, tem a resposta hipermetabólica restrita às primeiras duas semanas do período de recuperação, independentemente da gravidade e localização das lesões. A justificativa para esta periodicidade pode estar ligada a distintos fatores.…”

“…Dentre as alterações mais marcantes está a hiperglicemia, associada diretamente ao prognóstico do trauma 7 . No que se refere ao metabolismo protéico-energético, Young et al 8 demonstraram que as proteínas de fase aguda tendem à normalização passadas duas semanas após o TCE. A influência do tipo da lesão intracraniana é comumente associada ao prognóstico do TCE , de forma que se estabeleceu para pacientes com escore de Glasgow entre 3 a 5 , uma taxa de mortalidade de 30% a 74% e, dependendo da lesão, boa recuperação entre 6% a 52% 9 .…”

Hypermetabolism following Moderate to Severe Traumatic Acute Brain Injury: A Systematic Review

“…Although our understanding of the etiology of this phenomenon is not complete, the release of various cytokines and counter-regulatory hormones, mediated through the acute phase response, is believed to be contributory (Chiolero et al, 1989a;Young et al, 1988Young et al, , 1992. Wide variations in both the magnitude and time course of metabolic perturbations have been reported, with energy expenditures ranging from 32% (Long et al, 1979) to 200% (Haider et al, 1975) above that which would be predicted in the non-injured state.…”