Outcome in 1,000 head injury hospital admissions: the Athens head trauma registry.

BACKGROUND: The aim of this study was to establish a head trauma registry to (a) examine demographics, etiology, severity, clinical course, and outcome; (b) compare results with previous published series; (c) identify causes of bad outcomes; and (d) propose methods to improve therapy and prognosis. METHODS: The following data were collected on 1,000 consecutive victims with head injury over 14 years of age admitted during a 4-year period: demographic characteristics, cause of injury, clinical variables, neuroimaging, therapy data, and outcome in 6 months. RESULTS: Seventy-four percent were men, and mean age was 43 years. Seventy-one percent suffered injuries due to road crashes, 14% due to alcohol, and 2% due to substances. The secondary transfer rate was 49%. For severe injuries, the time intervals from incident to hospital and subsequently to neurosurgical unit were 35 minutes and 4 hours, respectively. In 65% and 72% of cases, there was no record of preresuscitation hypoxia or hypotension, respectively, whereas suspected or definite episodes of hypoxia and hypotension were 27% and 13%, respectively. Most cases were mild trauma (63%), the remaining were severe (26%) and moderate (11%) injuries. Severe systemic trauma coexisted in 18%. Cranial surgery rate was 19% and it increased to 39% in severe trauma. The 6-month overall good outcome was 71%, with lower rates in moderate (58%) and severe (24%) injuries. CONCLUSIONS: The organization of Greece's first head injury registry offered an important preliminary core data concerning brain trauma etiology, management, and long-term outcome.

Adrenal function in non-septic long-stay critically ill patients: evaluation with the low-dose (1 micro g) corticotropin stimulation test.

OBJECTIVE: To investigate the adrenal function in non-septic, long-stay critically ill patients. DESIGN: Prospective, consecutive study. SETTING: General intensive care unit in a university hospital. PATIENTS: Forty-three non-septic patients with protracted critical illness. INTERVENTIONS: A morning blood sample was first obtained to measure baseline plasma cortisol. Subsequently, 1 micro g of corticotropin (ACTH, Synacthene) was injected intravenously and 30 min later a second blood sample was drawn to determine stimulated plasma cortisol. Patients having a stimulated cortisol level of at least 18 micro g/dl were defined as responders. In 36 patients, morning interleukin-6 (IL-6) was also measured. MEASUREMENTS AND RESULTS: Baseline and stimulated plasma cortisol were 16.8+/-4.1 micro g/dl and 21.2+/-5.1 micro g/dl, respectively. Interleukin-6 was high (median 39.3 pg/ml, interquartile range 24.9-86.6 pg/ml) and correlated negatively with stimulated plasma cortisol (r=-0.40, p<0.05). Of the 43 patients studied, 31 patients (72%) were responders and 12 patients (28%) were non-responders to the ACTH stimulation test. Overall, 18 patients died and 25 patients survived to hospital discharge. Non-responders had significantly higher IL-6 levels compared to responders (106+/-73 versus 48+/-42 pg/ml, p<0.05), whereas mortality rate was comparable in the two groups (50% versus 38%, p=0.74). CONCLUSIONS: Circulating plasma IL-6 levels are high during protracted critical illness, and are partially responsible for the relative adrenal insufficiency found in a subset of severely ill patients.

Slight and short-lasting increase of serum S-100B protein in extra-cranial trauma.

OBJECTIVE: Serum S-100B protein is an established biochemical marker of traumatic brain injury. At the same time, the question of extra-cranial S-100B release has been raised. This study evaluates the post-traumatic and post-operative release kinetics of S-100B in 45 trauma victims without head injury. METHOD: Serum S-100B protein was measured on admission and every 24 hours for 4 consecutive days. RESULTS: Initial S-100B was slightly increased (median: 0.54 microg L-1) and correlated with the severity of extra-cranial trauma (p = 0.0004, Mann-Whitney test). Both severely (abdominal or chest trauma with or without bone fractures) and mildly (long bone fractures) injured showed a rapid decline of S-100B (< 0.2 microg L-1) around 72 hours post-trauma. Extra-cranial surgery caused a secondary increase of S-100B, especially in the mildly injured group (p = 0.004, Wilcoxon signed rank test). CONCLUSIONS: Extra-cranial injury results in a mild elevation of serum S-100B protein that declines rapidly (1-3 days after injury).

Myocardial ischemia in intestinal postischemic shock: the effect of hypoxemic reperfusion.

OBJECTIVE: The circulatory shock following intestinal ischemia-reperfusion injury has been attributed to hypovolemia. The purpose of the current study is to clarify the pathophysiology of this type of shock and to test the hypothesis that hypoxemic compared with normoxemic reperfusion improves hemodynamics. DESIGN: Randomized animal study. SETTING: Medical school laboratory. SUBJECTS: Twenty-one pigs. INTERVENTIONS: Pigs were subjected to 120 mins of intestinal ischemia by clamping the superior mesenteric artery. Upon declamping, the animals were randomized into two groups: a group that received hypoxemic reperfusion (HR group, n = 8) with a PaO2 = 30-35 and a control group reperfused with PaO2 = 100 mm Hg (control group, n = 13). MEASUREMENTS AND MAIN RESULTS: Measurements included mean arterial pressure, cardiac index, pulmonary artery occlusion pressure, and requirements for fluids and epinephrine. Biopsies from the terminal ileal mucosa were taken for malondialdehyde measurements at baseline, at 120 mins of ischemia, and at 30 and 60 mins of reperfusion. A piece of left ventricle was obtained after 120 mins of reperfusion for histologic studies. Five of 13 animals of the control group died in intractable shock; no animal of the HR group died (p =.11). The decrease in the mean arterial pressure during reperfusion was more pronounced in the control group (p <.008) despite the larger doses of epinephrine administered, compared with the HR group (p <.02). During reperfusion, both groups exhibited a decrease in cardiac index; this was more pronounced in the control group (p =.0007). Pulmonary artery occlusion pressure increased during reperfusion in both groups and was more pronounced in the control group (p =.04 at 60 mins). Although mixed venous blood oxygen saturation of the control animals was higher at 30 mins of reperfusion (p =.005), it declined after 60 mins and became lower than that of HR animals at the end of reperfusion (p <.02). The myocardial histopathologic injury score was higher in the control group (2.0 +/- 0.69 and 3.4 +/- 0.89 for the HR and control groups, respectively; p <.03). The concentrations of intestinal mucosa malondialdehyde were significantly higher in the control group at 60 mins of reperfusion (p <.03). CONCLUSIONS: Acute myocardial ischemia and left heart failure significantly contribute to the circulatory shock that follows intestinal ischemia/reperfusion injury and are attenuated by hypoxemic reperfusion.