Progression of Intracranial Hemorrhage After Chemical Prophylaxis Using Low-Molecular-Weight Heparin in Patients With Traumatic Brain Injury.

INTRODUCTION: Chemical prophylaxis using low-molecular-weight heparin (LMWH) is considered a standard of care for venous thromboembolism in trauma patients. Our center performs a head computed tomography (CT) scan 24 hours after initiation with prophylactic LMWH in the setting of a known traumatic brain injury (TBI). The purpose was to determine the overall incidence of ICH progression after chemoprophylaxis in patients with a TBI. METHODS: This retrospective study was performed at a Level I trauma center, from 1/1/2014 to 12/31/2017. Study patients were drawn from the institution's trauma registry based on Abbreviated Injury Score codes. RESULTS: 778 patients met all inclusion criteria after initial chart review. The proportion of patients with an observed radiographic progression of intracranial hemorrhage after LMWH was 5.8%. 3.1% of patients had a change in clinical management. Observed radiographic progression after LMWH prophylaxis and the presence of SDH on initial CT, the bilateral absence of pupillary response in the emergency department, and a diagnosis of dementia were found to have statistically significant correlation with bleed progression after LMWH was initiated. CONCLUSION: Over a 4-year period, the use of CT to evaluate for radiographic progression of traumatic intracranial hemorrhage 24 hours after receiving LMWH resulted in a change in clinical management for 3.1% of patients. The odds of intracranial hemorrhage progression were approximately 6.5× greater in patients with subdural hemorrhage on initial CT, 3.1× greater in patients with lack of bilateral pupillary response in ED, and 4.2× greater in patients who had been diagnosed with dementia.

Evaluating a symptom-triggered gastric residual volume policy in a surgical trauma intensive care unit: Simple and safe.

BACKGROUND: Routine checking of gastric residual volumes (GRVs) during enteral feeding within surgical trauma intensive care units (STICUs) is a common practice. However, data on the necessity of this practice and its impact on nutrient delivery are limited. We aim to study the association between the replacement of a routine GRV (rGRV) policy with a triggered GRV (tGRV) policy and the safe achievement of daily nutrition goals. METHODS: We prospectively collected data on patients after we instituted a tGRV policy and compared them with a historical cohort of patients who had rGRV assessments in our STICU at a level 1 trauma center. The primary end point was achieving 80% of prescribed nutrient goals. Secondary end points included aspiration pneumonia, witnessed emesis, and glycemic control. RESULTS: A total of 145 patients accounting for 1405 STICU days were treated under the tGRV policy, and 156 patients accounting for 1694 STICU days were treated under the rGRV policy. There were no statistically significant differences between the tGRV and rGRV groups with regard to the proportion of days meeting or exceeding protein (56.7% vs 56.2%) or calorie (56.4% vs 56.0%) goals. After adjusting for in-hospital deaths, injury severity score, complications, and STICU time, the predictive margins for meeting caloric and protein goals were higher among the tGRV patients (57% vs 56%), but these differences were not statistically significant. CONCLUSION: A tGRV policy did not change protein or calorie delivery among patients or increase the risk of emesis compared with traditional monitoring methods.

A Volume-Based Feeding Protocol Improves Nutrient Delivery and Glycemic Control in a Surgical Trauma Intensive Care Unit.

BACKGROUND: Inadequate delivery of nutrition in critically ill patients has been shown to have adverse outcomes. A surgical trauma intensive care unit provides unique challenges to enteral feeds. Although volume-based feeding protocols, like Enhanced Protein-Energy Provision via the Enteral Route Feeding Protocol (PEP uP), have been successfully used in medical intensive care patients, data are sparse on its safety and efficacy in a surgical intensive care unit population. METHODS: A PEP uP protocol was recently initiated at our American College of Surgeons Level 1 verified trauma center. Medical records of 197 patients before this change (pre-PEP uP) were compared with 295 patients after this change (post-PEP uP). RESULTS: The post-PEP uP group met/exceeded energy goals (defined as 80% of target) more often (57.0% compared with 26.9%, P-value < .001), with an adjusted odds ratio (OR) of 4.98 (95% CI 3.49-7.10), and more often met/exceeded protein goals (57.4% compared with 18.6%, P-value < .001), with an adjusted OR of 11.84 (95% CI 7.94-17.64). There was no significant difference in emesis during this time. Additionally, patients in the post-PEP uP arm had less episodes of hyperglycemia (9% compared with 14.4%, P-value < .001). CONCLUSIONS: Volume-based feeding protocols like PEP uP are safe in critically ill trauma patients and are more effective at delivering energy and protein while limiting hyperglycemic episodes when compared with a traditional delivery method.

Inhibition of gamma-thrombin-induced human platelet aggregation by histone H1subtypes and H1.3 fragments.

Human platelets are differentially activated by varying concentrations of alpha-thrombin or by beta- and gamma-thrombin via three thrombin receptors, PAR-1, PAR-4 and GPIbalpha.It is likely that the development of a normal or abnormal hemostatic event in humans is dictated, in part, by the selective activation of these receptors. The ability to differentially inhibit these thrombin receptors could, therefore, have clinical significance. We have previously demonstrated that histone H1 selectively inhibits the PAR-4 receptor. In the current study we investigated whether five subtypes of the H1 molecule or fragments of the H1.3 subtype differentially inhibited the PAR-4 receptor. PAR-4 inhibition by all H1 subtypes was saturated at 1 uM with no statistical difference observed with the five H1 subtypes tested. Of the five fragments generated from the H1.3 molecule only one had significant inhibitory activity against PAR-4. The C-terminal fragment, N.1, generated by the proteolysis of the parent molecule by Asp-N endoproteinase (Aeromonas proteolytica) at the single aspartate residue, showed the same level of PAR-4 inhibition as the intact H1.3 at 1 uM concentrations. Removal of two N-terminal amino acids (Asp-Val as determined by MALDI analysis) from the N.1 fragment further enhanced its inhibitory activity. These studies may help to develop specific drugs to differentially inhibit the platelet thrombin receptors.

Injury to the conduction system: management of life-threatening arrhythmias after penetrating cardiac trauma.

BACKGROUND: Life-threatening conduction abnormalities after penetrating cardiac injuries (PCIs) are rare, and rapid identification and treatment of these arrhythmias are critical to survival. This study highlights diagnosis and management strategies for conduction abnormalities after PCI. METHODS: Patients with life-threatening arrhythmias after PCI were identified at an urban, level I trauma center registry. RESULTS: Seventy-one patients survived to reach the hospital after PCI. Of these, 3 (4%) survivors (male = 3, mean age 41.3, median injury severity score = 25) had critical conduction abnormalities after cardiorrhaphy. All patients had multichamber and atrioventricular nodal injury. After initial cardiorrhaphy and control of hemorrhage, all patients had sustained hypotension with bradycardia from complete heart block. Two patients had ventricular septal defects requiring repair. All 3 patients survived. CONCLUSIONS: Rapid recognition of injury to the cardiac conduction system after PCI as a source of sustained hypotension is essential to early restoration of cardiac function and survival.

Comparison of sea turtle thrombocyte aggregation to human platelet aggregation in whole blood.

The endangered sea turtles are living "fossils" that afford us an opportunity to study the hemostatic process as it likely existed millions of years ago. There are essentially no data about turtle thrombocyte aggregation prior to our studies. Thrombocytes are nucleated cells that serve the same hemostatic functions as the anucleated mammalian platelet. Sea turtle thrombocytes aggregate in response to collagen and beta-thrombin. Ristocetin induces an agglutination/aggregation response indicating the presence of a von Willebrand-like receptor, GPIb, found in all mammalian platelets. Samples treated with alpha-thrombin plus gamma-thrombin followed by ristocetin results in a rapid, stronger response than ristocetin alone. These responses are inhibited by the RGDS peptide that blocks fibrinogen cross-linking of mammalian platelets via the fibrinogen receptor, GPIIb/IIIa. Three platelet-like proteins, GPIb, GPIIb/IIIa and P-selection are detected in sea turtle thrombocytes by fluorescence activated cell sorting. Turtle thrombocytes do not respond to ADP, epinephrine, serotonin, thromboxane A2 mimetic, U46619, trypsin, or alpha-thrombin and gamma-thrombin added alone. Comparison of hemostasis in sea turtles to other vertebrates could provide a framework for understanding the structure/function and evolution of these pathways and their individual components.