The impact of anemia in moderate to severe traumatic brain injury.

PURPOSE: The impact of anemia and restrictive transfusion strategies in traumatic brain injury (TBI) is unclear. The purpose of this study was to examine the outcome of varying degrees of anemia in patients who have sustained a TBI. METHODS: We performed a retrospective study of all adult patients with isolated blunt TBI admitted between January 2003 and June 2010. The impact of increasing severity of anemia (Hb ≤8, ≤9, or ≤10 g/dl measured on three consecutive draws within the first 7 days of admission) and transfusions on complications, length of stay, and mortality was examined using univariate and multivariate analysis. RESULTS: Of the 31,648 patients with blunt trauma admitted to the trauma service during the study period, 812 had an isolated TBI, among which 196 (24.1 %) met at least one of the anemia thresholds within the first 7 days [78 % male, mean age 47 ± 23 years, Injury Severity Score 16 ± 8, and head Abbreviated Injury Scale 3.3 ± 1.0]. Using a logistic regression model, anemia even as low as 8 g/dl was not associated with an increase in mortality [AOR8 = 0.8 (0.2, 3.2), p = 0.771; AOR9 = 0.8 (0.4, 1.6), p = 0.531; AOR10 = 0.6 (0.3, 1.3), p = 0.233] or complications. However, for all patients, the transfusion of packed red blood cells was associated with a significant increase in septic complications [AOR = 3.2 (1.5, 13.7), p = 0.030]. CONCLUSION: The presence of anemia in patients with TBI as low as 8 g/dl was not associated with increased mortality or complications, while the transfusion of red blood cells was associated with a significant increase in septic complications. Prospective evaluation of an optimal transfusion trigger in head-injured patients is warranted.

Alcohol exposure and outcomes in trauma patients.

OBJECTIVE: To determine the injury patterns, complications, and mortality after alcohol consumption in trauma patients. METHODS: The Trauma Registry at an American College of Surgeons (ACS) level I center was queried for all patients with a toxicology screen admitted between 1st January 2002 and 31st December 2005. Alcohol-positive (AP) patients were matched to control patients who had a completely negative screen (AN) using age, gender, mechanism, Injury Severity Score (ISS), head Abbreviated Injury Scale (AIS), chest AIS, abdominal AIS, and extremity AIS. Injuries and outcomes were compared between the groups. RESULTS: As many as 5,317 patients had toxicology data, of which 471 (8.9%) had a positive alcohol screen (AP). A total of 386 AP patients were then matched to 386 control (AN) patients. The AP group had a significantly higher mortality than the AN group overall (23 vs. 13%; p < 0.001), and by ISS stratification: ISS < 16 (6 vs. 0.4%; p < 0.001), ISS 16-25 (53 vs. 28%; p = 0.01), and ISS > 25 (90 vs. 67%; p = 0.01). AP patients had a higher incidence of admission systolic blood pressure < 90 (18 vs. 10%; p < 0.001) and Glasgow Coma Scale (GCS) score ≤ 8 (25 vs. 17%; p = 0.002). AN patients had a significantly higher incidence of hemopneumothorax (11 vs. 7%; p = 0.03), while AP patients had a higher incidence of cardiac arrest (8 vs. 3%; p = 0.004). There was no difference in intensive care unit (ICU) and hospital length of stay. CONCLUSION: In a mixed population of trauma patients, an AP screen is associated with an increased incidence of admission hypotension and depressed GCS score. In this case-matched study, alcohol exposure appeared to increase mortality after injury.

Ultrastructural and immunohistochemical characterization of autonomic neuropathy in genetically diabetic Chinese hamsters.

Selected portions of the prevertebral and paravertebral sympathetic and vagal parasympathetic nervous systems have been examined in the genetically diabetic Chinese hamster, an experimental animal model of diabetic gastrointestinal disease. The prevertebral sympathetic superior mesenteric/celiac ganglia, which provide much of the sympathetic innervation of the alimentary tract, developed large numbers of markedly dilated axons, many of which had the ultrastructural features of neuroaxonal dystrophy. Dystrophic axons, many involving presynaptic axonal elements, were increased in frequency in the prevertebral superior mesenteric/celiac ganglia, but not in the paravertebral superior cervical sympathetic ganglia, of chronically diabetic hamsters in comparison with age-matched controls. Dystrophic axons contained substance P- and gastrin-releasing peptide (gastrin-releasing peptide/bombesin)-like staining but were not labeled by antisera directed against vasoactive intestinal peptide, dynorphin-B, somatostatin, leu- and met-enkephalin and neuropeptide tyrosine. Substance P and gastrin-releasing peptide/bombesin containing subpopulations of presynaptic elements in prevertebral sympathetic ganglia are thought to participate in local reflex control of bowel motility and lesions preferentially involving these elements may contribute to bowel dysfunction. Immunohistologic techniques failed to demonstrate dystrophic axons in the superior cervical ganglia. Although morphometric studies failed to show significant axon loss in the abdominal vagus of chronically diabetic Chinese hamsters, evidence of markedly diminished numbers of axons comprising each Schwann cell unit and regenerative collections of Schwann cell processes devoid of axons are consistent with the participation of parasympathetic elements in the pathogenesis of alimentary dysfunction in this model system. These results suggest that selective subpopulations of neuropeptide containing axons are vulnerable to the diabetic condition and that these abnormalities may lead to physiologic dysfunction.

Differential susceptibility of prevertebral and paravertebral sympathetic ganglia to experimental injury.

To investigate the response of selected sympathetic ganglia to experimental injury, neonatal rat pups were treated with either 6-hydroxydopamine (6-OHDA), guanethidine, or antiserum to nerve growth factor (anti-NGF). When examined at one month of age, each of the treatments resulted in a significantly greater loss of neurons and tyrosine hydroxylase activity in paravertebral (superior cervical and stellate) versus prevertebral (superior mesenteric and celiac) sympathetic ganglia. Guanethidine treatment produced the largest differential in neuron loss and tyrosine hydroxylase activity between pre- and paravertebral ganglia. Histologically, the acute phase of guanethidine-induced injury in the superior cervical, paravertebral, ganglia was characterized by a prominent mononuclear cell infiltrate and extensive neuronal degeneration. Minimal histopathologic changes were seen in the superior mesenteric, prevertebral, ganglia of the same animals. Immunolocalization of tyrosine hydroxylase and neuropeptide Y (NPY) in guanethidine-treated animals showed a preferential loss of sympathetic innervation of the extramural mesenteric vasculature with relative sparing of the noradrenergic innervation of Auerbach's myenteric plexus. Differences in the susceptibility of sympathetic ganglia to various insults may underlie the selective and heterogeneous involvement of sympathetic ganglia in clinical and experimental situations.

Effects of chronic experimental streptozotocin-induced diabetes on the noradrenergic and peptidergic innervation of the rat alimentary tract.

Immunohistologic localization of tyrosine hydroxylase (TOH), dopamine-beta-hydroxylase (DBH) and selected neuropeptides (vasoactive intestinal polypeptide, gastrin-releasing peptide (GRP)/bombesin, substance P, Leu-enkephalin, Met-enkephalin, dynorphin B, neuropeptide Y (NPY), somatostatin) was used to investigate the innervation of the small bowel in a rat model of diabetic autonomic neuropathy. Paravascular mesenteric nerves (extrinsic) and intramural nerves of chronically (12-18 month) diabetic rats were characterized by the presence of numerous, markedly swollen dystrophic axons which stained intensely for TOH and DBH. The peptidergic complement of axons, however, showed no evidence of comparable dystrophic axonopathy.