Patrick Maluso

Inhibition of platelet function is common following even minor injury.

BACKGROUND Hemorrhage remains the leading cause of preventable death following injury. Whereas significant attention has been paid to the coagulation cascade, there are fewer studies evaluating platelet dysfunction following injury. Thrombelastogram platelet mapping (TEG-PM) allows for the measurement of maximal potential clot strength and clot strength selectively caused by arachidonic acid and adenosine disphosphate receptors on the platelet. The purpose of this study was to determine the incidence and magnitude of receptor-specific platelet dysfunction following injury in patients who are not otherwise pharmacologically anticoagulated. METHODS A retrospective study of adult trauma patients evaluated at a Level I trauma center from August 2013 to September 2014 was conducted. Platelet function was assessed using TEG-PM. Patients on any anticoagulant or antiplatelet medication were excluded. Patients were divided into those with and without radiographically evident traumatic brain injury (TBI). Demographic variables, Injury Severity Score (ISS), injury pattern, laboratory test results, and mortality were abstracted. Statistical comparisons were made using the Students t test or Mann-Whitney U-test. RESULTS The study includes 459 patients, 92% following blunt injury. Median ISS was 5. Patients with TBI (n = 102) were significantly older (median age, 54 years vs. 35 years), were more severely injured (median ISS, 10 vs. 4), had a longer stay and higher mortality (9% vs. 0.3%). Maximal potential clot strength was normal in all cohorts, but the arachidonic acid and adenosine diphosphate pathways were significantly inhibited (30% ± 26% and 58% ± 27%, respectively). There was no correlation between TEG-PM values and ISS, length of stay, or mortality. There was no difference in the TBI cohort. There were no significant differences in TEG-PM parameters in those with an ISS greater than 14. There was no significant change in TEG-PM following platelet transfusion. CONCLUSION Marked platelet inhibition is common following minor injury. Whereas the clinical significance of this finding remains unknown, the results of this study should be factored in the overall resuscitative strategy. LEVEL OF EVIDENCE Prognostic/epidemiogic study, level III.

Abdominal Compartment Hypertension and Abdominal Compartment Syndrome.

Intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) are rare but potentially morbid diagnoses. Clinical index of suspicion for these disorders should be raised following massive resuscitation, abdominal wall reconstruction/injury, and in those with space-occupying disorders in the abdomen. Gold standard for diagnosis involves measurement of bladder pressure, with a pressure greater than 12 mm Hg being consistent with IAH and greater than 25 mm Hg being consistent with ACS. Decompressive laparotomy is definitive therapy but paracentesis can be equally therapeutic in properly selected patients. Left untreated, ACS can lead to multisystem organ failure and death.

A Calculator for Mortality Following Emergency General Surgery Based on the American College of Surgeons National Surgical Quality Improvement Program Database.

BACKGROUND The complex nature of current morbidity and mortality predictor models do not lend themselves to clinical application at the bedside of patients undergoing emergency general surgery (EGS). Our aim was to develop a simplified risk calculator for prediction of early postoperative mortality after EGS. METHODS EGS cases other than appendectomy and cholecystectomy were identified within the American College of Surgeons National Surgery Quality Improvement Program database from 2005 to 2014. Seventy-five percent of the cases were selected at random for model development, whereas 25% of the cases were used for model testing. Stepwise logistic regression was performed for creation of a 30-day mortality risk calculator. Model accuracy and reproducibility was investigated using the concordance index (c statistic) and Pearson correlations. RESULTS A total of 79,835 patients met inclusion criteria. Overall, 30-day mortality was 12.6%. A simplified risk model formula was derived from five readily available preoperative variables as follows: 0.034*age + 0.8*nonindependent status + 0.88*sepsis + 1.1 (if bun ≥ 29) or 0.57 (if bun ≥18 and < 29) + 1.16 (if albumin < 2.7), or 0.61 (if albumin ≥ 2.7 and < 3.4). The risk of 30-day mortality was stratified into deciles. The risk of 30-day mortality ranged from 2% for patients in the lowest risk level to 31% for patients in the highest risk level. The c statistic was 0.83 in both the derivation and testing samples. CONCLUSION Five readily available preoperative variables can be used to predict the 30-day mortality risk for patients undergoing EGS. Further studies are needed to validate this risk calculator and to determine its bedside applicability. LEVEL OF EVIDENCE Prognostic/epidemiological study, level III.

Platelet transfusion does not improve outcomes in patients with brain injury on antiplatelet therapy

ABSTRACT Introduction: Platelet dysfunction following traumatic brain injury (TBI) is associated with worse outcomes. The efficacy of platelet transfusion to reverse antiplatelet medication (APM) remains unknown. Thrombelastography platelet mapping (TEG-PM) assesses platelet function. We hypothesize that platelet transfusion can reverse the effects of APM but does not improve outcomes following TBI. Methods: An observational study at six US trauma centres was performed. Adult patients on APM with CT evident TBI after blunt injury were enrolled. Demographics, brain CT and TEG-PM results before/after platelet transfusion, length of stay (LOS), and injury severity score (ISS) were abstracted. Results: Sixty six patients were enrolled (89% aspirin, 50% clopidogrel, 23% dual APM) with 23 patients undergoing platelet transfusion. Transfused patients had significantly higher ISS and admission CT scores. Platelet transfusion significantly reduced platelet inhibition due to aspirin (76.0 ± 30.2% to 52.7 ± 31.5%, p < 0.01), but had a non-significant impact on clopidogrel-associated inhibition (p = 0.07). Platelet transfusion was associated with longer length of stay (7.8 vs. 3.5 days, p < 0.01), but there were no differences in mortality. Conclusion: Platelet transfusion significantly decreases platelet inhibition due to aspirin but is not associated with change in outcomes in patients on APM following TBI.

Platelet dysfunction in critically ill patients.

&NA; Thrombelastography Platelet Mapping (TEG-PM) allows for measurement of maximal potential clot strength (MA) and strength from stimulation of arachidonic acid (MA-AA) and adenosine disphosphate (MA-ADP) receptors. This study was conducted to assess degree of platelet dysfunction in critically ill adult patients. A retrospective study of critically ill, adult, nontrauma patients in a medical/surgical ICU was conducted from August 2013 to September 2014. All patients who underwent TEG-PM were enrolled. Patients with intracerebral hemorrhage, following cardiac surgery, or without an APACHE II score were excluded. Patients were divided into those with and without aspirin use. Demographics, APACHE II score, and laboratory results were abstracted. Student t test was used to test significance. A total of 79 patients were enrolled (61% male). Average age and APACHE II score were 61 ± 16 years and 18 ± 9, respectively. Factor-associated coagulation measures and MA were normal in all groups but MA-AA and MA-ADP were significantly reduced irrespective of anticoagulant use. Compared to the nonanticoagulated cohort, MA-AA was significantly reduced in those on aspirin. There was no difference in mortality or length of stay in any cohort. Inhibition of the AA and ADP pathways is common in critically ill patients. Clinical correlation with propensity for bleeding and need for transfusion requires further assessment.

Damage Control Phase III: Repair of All Injuries, General Surgery

The primary goals of the third phase of damage control surgery (DC III) are to achieve definitive repair of organ injuries and to close the fascia over surgical wounds where possible. Although the optimal timing is variable and dependent on numerous patient factors, DC III is typically undertaken 24–36 h after the initial surgery. This time is needed for appropriate resuscitation, allowing the patient to reestablish proper homeostasis. The patient will thereby tolerate the longer operative time and more extensive intervention(s) that may be necessary to definitively repair the injuries sustained. Specifically, the decision to proceed with DC III should not be undertaken until the patient’s coagulopathy has been corrected and he/she is normothermic and has a normal acid-base balance. Additional considerations such as vasopressor requirements also impact on the timing and probability of success of DC III. Ideally, patients should be weaned off of vasopressors entirely or, at a minimum, their pressor requirements should be decreasing. Ongoing physiologic instability or hypothermia despite appropriate medical therapy should raise concern for a missed injury. Definitive repair should be delayed but early operative re-exploration to evaluate for missed injury may be warranted. On-demand repeat laparotomy in these cases can decrease patient mortality [1].

Rapid Response Systems and the Septic Patient

Sepsis remains the leading cause of death in the ICU. An early, aggressive strategy to identify the onset of septic shock as early as possible in order to begin therapy is associated with a significant reduction in mortality. Specifically, timely administration of appropriate antibiotics lowers mortality at least 7–12%. Unfortunately, even with timely recognition of septic shock, administration of antibiotic therapy can take several hours. A rapid response system can significantly shorten this time, particularly if a pharmacist is a core member of the team. Additionally, a rapid response system can shorten time to hemodynamic support, fluid resuscitation, and transfer to a dedicated ICU setting—all of which can further lower mortality.