Linda E. Pelinka

The aim of this clinical and experimental study was to determine whether systemic neuron-specific enolase (NSE) is a useful early marker of traumatic brain injury (TBI) and whether NSE is affected by ischemia/reperfusion damage of abdominal organs. Our study included patients with and without TBI (verified by computerized tomography) admitted within 6 h after trauma and male Sprague-Dawley rats with ischemia and reperfusion of the abdominal organs liver, gut, or kidney. Thirty-eight study patients included 13 with isolated TBI and 18 patients with multiple trauma and TBI. Seven patients had multiple trauma but no TBI. Fifteen rats were anaesthetized and subjected to isolated ischemia of the liver, gut, or kidney (n = 5 each) for 1 h, followed by reperfusion for 3 h. In patients, NSE increased over 2-fold versus the upper normal limit (10 μg/L) within 6 h after trauma, regardless of whether TBI had occurred or not. In rats, NSE increased over 3-fold versus laboratory controls during ischemia of the liver and kidney (both P < 0.0005), but not of the gut. NSE increased over 2-fold after onset of reperfusion of the liver and kidney (both P < 0.05), but not of the gut and increased over 3-fold after 3 h of reperfusion of the liver, gut (both P < 0.005), and kidney (P < 0.0005). Our data show that systemic NSE increases to similar degrees with and without TBI. Therefore, NSE is not a useful early marker of TBI in multiple trauma.

This study aimed to determine whether glial fibrillary acidic protein (GFAP) is released after traumatic brain injury (TBI), whether GFAP is related to brain injury severity and outcome after TBI, and whether GFAP is released after multiple trauma without TBI. This prospective study enrolled 114 patients who had TBI with or without multiple trauma (n = 101) or multiple trauma without TBI (n = 13), as verified by computerized tomography. Daily GFAP measurement began at admission (<12 hours after trauma) and continued for the duration of intensive care (1–22 days). Documentation included categorization of computerized tomography according to Marshall classification, based on daily highest intracranial pressure (ICP), lowest cerebral perfusion pressure (CPP), lowest mean arterial pressure (MAP), and 3-month Glasgow Outcome Score (GOS). The GFAP concentration was lower for diffuse injury 2 than for diffuse injury 4 (p < 0.0005) or nonevacuated mass lesions larger than than 25 mL (p < 0.005), lower for a ICP less than 25 mm Hg than for a ICP of 25 mm Hg or more, lower for a CPP of 60 mm Hg or more than for a CPP of 60 mm Hg or less, lower for a MAP of 60 mm Hg or more than for a MAP less than 60 mm Hg (all p < 0.0005), and lower for a GOS of 1 or 2 than for a GOS of 3, 4 (p < 0.05), or 5 (p < 0.0005). After TBI, GFAP was higher in nonsurvivors (n = 39) than in survivors (n = 62) (p < 0.005). After multiple trauma without TBI, GFAP remained normal. The findings showed that GFAP is released after TBI, that GFAP is related to brain injury severity and outcome after TBI, and that GFAP is not released after multiple trauma without brain injury.

Neuron-specific enolase (NSE) is an acknowledged marker of traumatic brain injury. Several markers originally considered reliable in the setting of traumatic brain injury have been challenged after having been studied more extensively. The aim of our experimental study was to determine whether NSE is a reliable marker of traumatic brain injury early after trauma. Hemorrhagic shock was achieved by bleeding anesthetized rats to a mean arterial pressure (MAP) of 30–35 mmHg through a femoral catheter until incipient decompensation. MAP was maintained at 30–35 mmHg until 40% of shed blood had been administered as Ringer’s solution and was then increased and maintained at 40–45 mmHg for 40 min by further administration of Ringer’s solution, mimicking the phase of inadequate preclinical resuscitation. Blood samples were drawn at the end of the 40-min period of inadequate resuscitation. Femur fracture was achieved in anesthetized rats by bilateral application of forceps. Blood samples were drawn 30 and 60 min after fracture. Hemorrhagic shock caused NSE increase versus laboratory controls at the end of inadequate resuscitation (P < 0.01). Bilateral femur fracture caused NSE increase versus laboratory controls 30 min after fracture, which was significant 60 min after fracture (P < 0.01). During femur fracture, MAP remained at a level that is not associated with shock in rats. Our findings show for the first time that NSE increases after hemorrhagic shock as well as after femur fracture without hemorrhagic shock in rats. From a clinical point of view, these findings indicate that NSE cannot be considered a reliable marker of traumatic brain injury early after trauma in cases associated with hemorrhagic shock and/or femur fracture.

S100B, an acknowledged marker of brain damage, is increased post-traumatically in plasma. The aim of this study was to investigate the diagnostic value of S100B release in experimental local extracranial ischemia and reperfusion. Anesthetized rats underwent laparotomy and ligation of the afferent blood vessels to the liver, gut, or kidney to achieve local ischemia in each organ separately. After 60 min of ischemia, ligatures were removed and resuscitation was performed for 3 h. S100B was determined in plasma by immunoluminometric assay 55, 65, and 240 min after the onset of ischemia (5 min before reperfusion and 5 min and 3 h after the onset of reperfusion). During ischemia of the liver, S100B increased before ligature removal and reperfusion, reaching significance early after the onset of reperfusion and remaining almost unchanged throughout reperfusion. In contrast, S100B did not increase during ischemia of the gut or kidney before ligature removal or during early reperfusion but increased significantly to similar levels as during reperfusion of the liver 240 min after the onset of ischemia (after 3 h of reperfusion). Our findings show for the first time that S100B increases during local extracranial ischemia and reperfusion. These experimental findings support the concept that brain damage is not necessarily the cause of increased S100B. Although S100B has been an acknowledged marker of brain damage for years, our experimental clinically relevant data indicate that S100B is, in fact, not specific as a marker of brain damage in the setting of local ischemia and reperfusion of the liver, gut, and kidney because local ischemia and reperfusion of these organs cause an S100B increase per se.

S100B is an acknowledged marker of brain damage. However, trauma without brain damage also causes an increase in S100B. S100B concentrations are highest in multiple trauma patients with long bone fractures. Clinically, extensive long bone fractures are associated with haemorrhagic shock and haemorrhagic shock per se is associated with increased S100B. The aim of our experimental study was to verify the S100B increase in long bone fracture without haemorrhagic shock. and results. Bilateral femur fracture was carried out in 10 anaesthetized rats. Blood samples were drawn for immuno-luminometrical S100B measurement 5, 15, 30, 120, and 240 min after fracture. Mean arterial pressure (MAP), heart rate, and body temperature were monitored continuously. S100B increased after bilateral femur fracture and reached a peak 30-120 min after fracture (P<0.001). MAP remained at a level which is not associated with shock in rats. Heart rate and body temperature remained unchanged. Autopsy verified open bilateral femur fracture surrounded only by small zones of clotted blood. S100B is increased in bilateral femur fracture without haemorrhagic shock in rats. This finding suggests that bone marrow is a potential extracerebral source of S100B.

Objective The purpose of this study was to identify risk factors for the development of acute acalculous cholecystitis (AAC) and useful criteria to facilitate the decision to perform cholecystectomy. Methods This was a prospective study of patients with an Injury Severity Score (ISS) ≥ 12 requiring intensive care for > 4 days (n = 255), divided into three groups by ultrasound: AAC (n = 27), hydropic gallbladder (n = 37), and normal gallbladder (n = 191). Multivariate analysis was conducted for trauma scores and laboratory and intensive care unit (ICU) data and complemented by logistic regression analysis. Results Three factors sufficiently define the risk for AAC: ISS, heart rate, and units of packed red blood cells required at ICU admission. All patients who underwent cholecystectomy (n = 21) had both highly pathologic ultrasound and major clinical symptoms, and all had histologically verified AAC. There was no significant difference in daily laboratory data between patients with and without AAC. Conclusion Patients with a high ISS who are tachycardic and have required several units of packed red blood cells at ICU admission should be monitored early by ultrasound. When ultrasound is highly pathologic together with major clinical symptoms, cholecystectomy should be performed. Daily laboratory data are of no additional value regarding the decision to perform cholecystectomy.