Only a few reports compare the mid- and long-term outcome of the minimally invasive deltoid split (MIDS) with the classic anterior deltopectoral (DP) approach for osteosynthesis in proximal humeral fractures. This study compared the mid-term functional and the radiological results in patients with proximal humeral fractures undergoing osteosynthesis with the proximal humeral internal locking system (PHILOS™).

Background: Exsanguinating hemorrhage is the major cause of death in patients with pelvic ring disruption. Aims: The aim of this study was to document outcomes after the stabilization of pelvic ring injuries by a C-clamp and control of hemorrhage by pelvic packing. Physiological parameters were tested as prognostic factors. Setting and Design: This was a retrospective study at a level I trauma center. The study period was from January 1996 to December 2007. Materials and Methods: Fifty patients with pelvic ring disruption and hemorrhagic shock were analyzed. The pelvic rings were fixed by a C-clamp, and patients with ongoing hemorrhage underwent laparotomy and extra- and/or intra-peritoneal pelvic packing. Clinical parameters (heart rate, mean arterial pressure) and physiological parameters (lactate levels, hemoglobin, hematocrit) were documented at admission and at different time points during the initial treatment (1, 2, 3, 4, 6, 8, and 12h after admission). Results: Within 12 h of admission, 16 patients died (nonsurvivors) due to hemorrhagic shock (n=13) or head injuries (n=3). In this group, 12 patients underwent laparotomy with pelvic packing. Thirty-four patients survived the first 12 h (early survivors) after fixation by a C-clamp and additional packing in 23 patients. Four of these patients died 12.3±7.1 days later due to multiple organ failure (n=3) or severe head injury (n=1). The blood lactate level at admission was significantly higher in the group of nonsurvivors (7.2±0.8 mmol/L) compared to the early survivors (4.3±0.5 mmol/L, P<0.05). While hemoglobin values improved within the first 2 h in nonsurvivors, lactate levels continued to increase. Conclusion: Pelvic packing in addition to the C-clamp fixation effectively controls severe hemorrhage in patients with pelvic ring disruption. Early sequential measurements of blood lactate levels can be used to estimate the severity of shock and the response to the shock treatment.

BACKGROUND:Unstable pelvic ring fractures with exsanguinating hemorrhages are rare but potentially lifethreatening injuries. The aim of this retrospective study was to evaluate whether early changes in acid- base parameters predict mortality of patients with severe pelvic trauma and hemorrhagic shock.METHODS:Data for 50 patients with pelvic ring disruption and severe hemorrhage were analyzed retrospectively. In all patients, the pelvic ring was temporarily stabilized by C-clamp. Patients with ongoing bleeding underwent laparotomy with extra and/or intraperitoneal pelvic packing, as required. Base excess, lactate, and pH were measured upon admission and at 1, 2, 3, 4, 6, 8, and 12 h postadmission. Patients were categorized as early survivors (surviving the first 12 h after admission) and nonsurvivors. Statistical analysis was performed by Mann-Whitney test; significance was assumed at p < 0.05. Receiver operating characteristic curves were generated for early mortality from each acid-base variable.RESULTS:Sixteen patients (32%) were nonsurvivors due to hemorrhagic shock (n = 13) or severe traumatic brain injury (n = 3). Thirty-four patients were early survivors. Base excess, lactate, and pH significantly discriminated between early survivors and nonsurvivors. Base excess determined 1 h after admission discriminated most strongly, with an area under the receiver operating characteristic curve of 0.915 (95% confidence interval, 0.836-0.993; p < 0.001).CONCLUSION:Base excess, lactate, and pH discriminate early survivors from nonsurvivors suffering from severe pelvic trauma and hemorrhagic shock. Base excess measured 1 h after admission best predicted early mortality following pelvic trauma with concomitant hemorrhage.

Norepinephrine, regularly used to increase systemic arterial blood pressure and thus improve cerebral perfusion following severe traumatic brain injury (TBI), may activate platelets. This, in turn, could promote microthrombosis formation and induce additional brain damage.

Patients sustaining severe trauma are at high risk for the development of venous thromboembolic events (VTE). Pharmacologic VTE prophylaxis may be contraindicated early after trauma due to potential bleeding complications. The purpose of this study was to evaluate safety and feasibility of early prophylactic vena cava filter (VCF) placement and subsequent retrieval in multiple injured patients with traumatic brain injury (TBI).

To clarify the association between disturbed thyroid hormone metabolism (low T3 syndrome) and release of cytokines and markers of cell-mediated immune response.

One and a half to two million people sustain a traumatic brain injury (TBI) in the US each year, of which approx 70,000–90,000 will suffer from long-term disability with dramatic impacts on their own and their families’ lives and enormous socio-economic costs. Brain damage following traumatic injury is a result of direct (immediate mechanical disruption of brain tissue, or primary injury) and indirect (secondary or delayed) mechanisms. These secondary mechanisms involve the initiation of an acute inflammatory response, including breakdown of the blood-brain barrier (BBB), edema formation and swelling, infiltration of peripheral blood cells and activation of resident immunocompetent cells, as well as the intrathecal release of numerous immune mediators such as interleukins and chemotactic factors. An overview over the inflammatory response to trauma as observed in clinical and in experimental TBI is presented in this review. The possibly harmful/beneficial sequelae of post-traumatic inflammation in the central nervous system (CNS) are discussed using three model mediators of inflammation in the brain, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and transforming growth factor-β (TGF-β). While the former two may act as important mediators for the initiation and the support of post-traumatic inflammation, thus causing additional cell death and neurologic dysfunction, they may also pave the way for reparative processes. TGF-β, on the other hand, is a potent anti-inflammatory agent, which may also have some deleterious long-term effects in the injured brain. The implications of this duality of the post-traumatic inflammatory response for the treatment of brain-injured patients using anti-inflammatory strategies are discussed.

We present a review of the currently popular preclinical models of non-penetrating traumatic brain injury (TBI). This article focuses on animal models that cause TBI by applying mechanical energy to the head, skull or dura. It attempts to provide a compendium of the main characteristics of each of these experimental models of TBI in respect to acute and chronic histological findings and behavioral impairment in neurologic motor and cognitive function. Finally, several limitations of the described models are discussed briefly.

Glutamate contributes to secondary brain damage, resulting in cell swelling and brain edema. Under in vitro conditions, increased extracellular levels of the amino acid taurine reflect glutamate-induced osmotic cell swelling. In vivo, increases in cerebrospinal fluid (CSF) taurine could, therefore, unmask glutamate-mediated cytotoxic edema formation and possibly differentiate it from vasogenic edema. To test this hypothesis, ventricular CSF glutamate and taurine levels were measured in 28 severely brain-injured patients on days 1, 5, and 14 after trauma. Posttraumatic changes in CSF amino acids were investigated in regard to extent of tissue damage and alterations in brain edema as estimated by computerized tomography. On day 1, CSF glutamate and taurine levels were significantly increased in patients with subdural or epidural hematomas (8+/-0.8/71+/-12 microM), contusions (21+/-4.1/122+/-18 microM), and generalized brain edema (13+/-3.2/80+/-15 microM) compared to lumbar control CSF (1.3+/-0.1/12+/-1 microM; p < 0.001). CSF amino acids, however, did not reflect edema formation and resolution as estimated by computerized tomography. CSF taurine correlated positively with glutamate, eventually depicting glutamate-induced cell swelling. However, parallel neuronal release of taurine with its inhibitory function cannot be excluded. Thus, the sensitivity of taurine in unmasking cytotoxic edema formation is weakened by the inability in defining its origin and function under the conditions chosen in the present study. Overall, persisting pathologic ventricular CSF glutamate and taurine levels are highly suggestive of ongoing glial and neuronal impairment in humans following severe traumatic brain injury.

Glutamate contributes to secondary brain damage, resulting in cell swelling and brain edema. Under in vitro conditions, increased extracellular levels of the amino acid taurine reflect glutamate-induced osmotic cell swelling. In vivo, increases in cerebrospinal fluid (CSF) taurine could, therefore, unmask glutamate-mediated cytotoxic edema formation and possibly differentiate it from vasogenic edema. To test this hypothesis, ventricular CSF glutamate and taurine levels were measured in 28 severely brain-injured patients on days 1, 5, and 14 after trauma. Posttraumatic changes in CSF amino acids were investigated in regard to extent of tissue damage and alterations in brain edema as estimated by computerized tomography. On day 1, CSF glutamate and taurine levels were significantly increased in patients with subdural or epidural hematomas (8 +/- 0.8/71 +/- 12 mu M), contusions (21 +/- 4.1/122 +/- 18 mu M), and generalized brain edema (13 +/- 3.2/80 +/- 15 mu M) compared to lumbar control CSF (1.3 +/- 0.1/12 +/- 1 mu M; P < 0.001). CSF amino acids, however, did not reflect edema formation and resolution as estimated by computerized tomography. CSF taurine correlated positively with glutamate, eventually depicting glutamate-induced cell swelling. However, parallel neuronal release of taurine with its inhibitory function cannot be excluded. Thus, the sensitivity of taurine in unmasking cytotoxic edema formation is weakened by the inability in defining its origin and function under the conditions chosen in the present study. Overall, persisting pathologic ventricular CSF glutamate and taurine levels are highly suggestive of ongoing glial and neuronal impairment in humans following severe traumatic brain injury.