Lydia Lam

Hyperfibrinolysis Elicited via Thromboelastography Predicts Mortality in Trauma

BACKGROUND The acute coagulopathy of trauma has been identified as a critical determinant of outcomes. Antifibrinolytic agents have recently been demonstrated to improve outcomes. This prospective study was designed to assess coagulopathy in trauma patients using thromboelastography. STUDY DESIGN Trauma patients meeting our institutions highest tier of trauma team activation criteria were prospectively enrolled during a 5-month period ending April 1, 2011. Thromboelastography was performed at admission, +1 hour, +2 hours, and +6 hours using citrated blood. Hyperfibrinolysis was defined as estimated percent lysis ≥15%. Patients were followed throughout their hospital course to collect clinical data and outcomes. RESULTS One hundred and eighteen patients were enrolled (77.1% were male, 51.7% had penetrating trauma, 7.6% had systolic blood pressure <90 mmHg, 47.5% had Injury Severity Score >16, and 23.7% had Glasgow Coma Scale score ≤8). Hyperfibrinolysis was present in 13 patients (11.0%), with a mean time to detection of 13 minutes (range 2 to 60 minutes). By the 6-hour sampling, 8 (61.5%) of the hyperfibrinolytic patients had expired from hemorrhage. Survivors at this point demonstrated correction of coagulopathy, however, 12 patients (92.3%) ultimately expired (75% hemorrhage, 25% head injury). On stepwise logistic regression, hyperfibrinolysis was a strong predictor of early (24 hours) mortality (odds ratio = 25.0; 95% CI, 2.8-221.4; p = 0.004), predicting 53% of early deaths. Compared with patients without hyperfibrinolysis, patients with hyperfibrinolysis had a greater need for massive transfusion (76.9% vs 8.7%; adjusted odds ratio = 19.1; 95% CI, 3.6-101.3; p < 0.001) and had a greater early mortality (69.2% vs 1.9%; adjusted odds ratio = 55.8; 95% CI, 7.2-432.3; p < 0.001) and in-hospital mortality (92.3% vs 9.5%; adjusted odds ratio = 55.5; 95% CI, 4.8-649.7; p = 0.001). CONCLUSIONS In this prospective analysis, hyperfibrinolysis on thromboelastography developed in approximately 10% of patients and was considerably more likely to require massive transfusion. Hyperfibrinolysis was a strong independent predictor of mortality. Additional evaluation of the role of thromboelastography-directed antifibrinolytic therapies is warranted.

Intracranial pressure monitoring in severe head injury: compliance with Brain Trauma Foundation guidelines and effect on outcomes: a prospective study

OBJECT The Brain Trauma Foundation (BTF) has established guidelines for intracranial pressure (ICP) monitoring in severe traumatic brain injury (TBI). This study assessed compliance with these guidelines and the effect on outcomes. METHODS This is a prospective, observational study including patients with severe blunt TBI (Glasgow Coma Scale score ≤ 8, head Abbreviated Injury Scale score ≥ 3) between January 2010 and December 2011. Demographics, clinical characteristics, laboratory profile, head CT scans, injury severity indices, and interventions were collected. The study population was stratified into 2 study groups: ICP monitoring and no ICP monitoring. Primary outcomes included compliance with BTF guidelines, overall in-hospital mortality, and mortality due to brain herniation. Secondary outcomes were ICU and hospital lengths of stay. Multiple regression analyses were deployed to determine the effect of ICP monitoring on outcomes. RESULTS A total of 216 patients met the BTF guideline criteria for ICP monitoring. Compliance with BTF guidelines was 46.8% (101 patients). Patients with subarachnoid hemorrhage and those who underwent craniectomy/craniotomy were significantly more likely to undergo ICP monitoring. Hypotension, coagulopathy, and increasing age were negatively associated with the placement of ICP monitoring devices. The overall in-hospital mortality was significantly higher in patients who did not undergo ICP monitoring (53.9% vs 32.7%, adjusted p = 0.019). Similarly, mortality due to brain herniation was significantly higher for the group not undergoing ICP monitoring (21.7% vs 12.9%, adjusted p = 0.046). The ICU and hospital lengths of stay were significantly longer in patients subjected to ICP monitoring. CONCLUSIONS Compliance with BTF ICP monitoring guidelines in our study sample was 46.8%. Patients managed according to the BTF ICP guidelines experienced significantly improved survival.

Impact of fibrinogen levels on outcomes after acute injury in patients requiring a massive transfusion.

BACKGROUND For critically injured patients requiring a massive transfusion, the optimal plasma fibrinogen level is unknown. The purpose of this study was to examine the impact of the fibrinogen level on mortality. We hypothesized that decreasing fibrinogen levels are associated with worse outcomes. STUDY DESIGN All patients undergoing a massive transfusion from January 2000 through December 2011 were retrospectively identified. Those with a fibrinogen level measured on admission to the surgical ICU were analyzed according to their fibrinogen level (normal [≥180 mg/dL], abnormal [≥101 to <180 mg/dL], and critical [≤100 mg/dL]). Primary outcome was death. Multivariate analysis evaluated the impact of fibrinogen on survival. RESULTS There were 260 patients who met inclusion criteria. Ninety-two patients had normal admission fibrinogen levels, 114 had abnormal levels, and 54 patients had critical levels. Patients with a critical fibrinogen level had significantly higher mortality at 24 hours compared with patients with abnormal (31.5% vs 5.3%; adj. p < 0.001) and normal fibrinogen levels (31.5% vs 4.3%; adjusted p < 0.001). Patients with a critical fibrinogen level had significantly higher in-hospital mortality compared with patients with abnormal (51.9% vs 25.4%; adjusted p = 0.013) and normal fibrinogen levels (51.9% vs 18.5%; adjusted p < 0.001). A critical fibrinogen level was the most important independent predictor of mortality (p = 0.012). CONCLUSIONS For patients undergoing a massive transfusion after injury, as the fibrinogen level increased, a stepwise improvement in survival was noted. A fibrinogen level ≤100 mg/dL was a strong independent risk factor for death. The impact of an aggressive fibrinogen replacement strategy using readily available products warrants further prospective evaluation.

Appendectomy timing: Waiting until the next morning increases the risk of surgical site infections

Objective:To investigate the association between time from admission to appendectomy (TTA) and the incidence of perforation and infectious complications. Background:Immediate appendectomy to prevent perforation has been challenged by recent studies supporting a semielective approach to acute appendicitis. Methods:Patients admitted with appendicitis from July 2003 to June 2011 were reviewed. Age, sex, admission white blood cell count, surgical approach (open vs laparoscopic), TTA, and pathology report were abstracted. Primary outcomes included perforation and surgical site infection (SSI). Logistic regression was performed both to identify independent predictors of perforation and to investigate the association between TTA and SSI. Results:Over 8 years, 4529 patients were admitted with appendicitis and 4108 (91%) patients underwent appendectomy. Perforation occurred in 23% (n = 942) of these patients. Logistic regression identified 3 independent predictors of perforation: age 55 years or older [odds ratio (95% confidence interval) OR (95% CI), 1.66 (1.21–2.29); P = 0.002], white blood cell count more than 16,000 [OR (95% CI), 1.38 (1.15–1.64); P < 0.001], and female sex [OR (95% CI), 1.20 (1.02–1.41); P = 0.02]. Delay to appendectomy was not associated with higher perforation rate. However, after controlling for age, leukocytosis, sex, laparoscopic approach, and perforation, TTA of more than 6 hours was independently associated with an increase in SSI [OR (95% CI), 1.54 (1.01–2.34); P = 0.04]. Delay of more than 6 hours resulted in a significant increase in SSI from 1.9% to 3.3% among patients with nonperforated appendicitis [OR (95% CI), 2.16 (1.03–4.52); P = 0.03], raising the incidence of SSI in nonperforated appendicitis to levels similar to those with perforation (3.3% vs 3.9%, P = 0.47). Conclusions:In this series, appendectomy delay did not increase the risk of perforation but was associated with a significantly increased risk of SSI in patients with nonperforated appendicitis. Prompt surgical intervention is warranted to avoid additional morbidity in this population.

The Incidence and Risk Factors of Post-Laparotomy Adhesive Small Bowel Obstruction

IntroductionThe purpose of this review was to assess the incidence and risk factors for adhesive small bowel obstruction (SBO) following laparotomy.MethodsThe PubMed database was systematically reviewed to identify studies in the English literature delineating the incidence of adhesive SBO and reporting risk factors for the development of this morbidity.ResultsA total of 446,331 abdominal operations were eligible for inclusion in this analysis. The overall incidence of SBO was 4.6%. The risk of SBO was highly influenced by the type of procedure, with ileal pouch–anal anastomosis being associated with the highest incidence of SBO (1,018 out of 5,268 cases or 19.3%), followed by open colectomy (11,491 out of 121,085 cases or 9.5%). Gynecological procedures were associated with an overall incidence of 11.1% (4,297 out of 38,751 cases) and ranged from 23.9% in open adnexal surgery, to 0.1% after cesarean section. The technique of the procedure (open vs. laparoscopic) also played a major role in the development of adhesive SBO. The incidence was 7.1% in open cholecystectomies vs. 0.2% in laparoscopic; 15.6% in open total abdominal hysterectomies vs. 0.0% in laparoscopic; and 23.9% in open adnexal operations vs. 0.0% in laparoscopic. There was no difference in SBO following laparoscopic or open appendectomies (1.4% vs. 1.3%). Separate closure of the peritoneum, spillage and retention of gallstones during cholecystectomy, and the use of starched gloves all increase the risk for adhesion formation. There is not enough evidence regarding the role of age, gender, and presence of cancer in adhesion formation.ConclusionAdhesion-related morbidity comprises a significant burden on healthcare resources and prevention is of major importance, especially in high-risk patients. Preventive techniques and special barriers should be considered in high-risk cases.

Pediatric vs adult vascular trauma: a National Trauma Databank review

INTRODUCTION The purpose of this study was to examine nationwide data on vascular injuries in children and to compare pediatric and adult patients with respect to the incidence, injury mechanisms, and outcomes. METHODS This is a National Trauma Databank analysis based on dataset version 7.0 (spanning a 5-year period ending December 2006). Pediatric patients under the age of 16 with at least one reported diagnosis of a vascular injury were compared to the adult cohort aged 16 and greater with a vascular injury. RESULTS During the study period, of 251,787 injured patients younger than 16 years, 1138 (0.6%) had a vascular injury. The incidence in patients 16 years or older was significantly higher, at 1.6% (P < .01). Compared to the adult vascular patients, pediatric patients had a significantly lower Injury Severity Score (16.8 +/- 14.9 vs 26.3 +/- 16.7, P < .001) and encountered less frequently penetrating injuries (41.8% vs 51.2%, P < .001). The most commonly injured vessels in the pediatric population were vessels of the upper extremity (424 patients or 37.9%). The overall incidence of thoracic aortic injuries in children was seven-fold lower compared to the incidence in adults (0.03% vs 0.21%). After adjusting for confounding factors, pediatric patients demonstrated improved survival following vascular injuries (adjusted odds ratio, 0.60; 95% CI, 0.45-0.79; P < .001). No significant difference was identified in the rate of amputation between pediatric and adult patients who had sustained upper or lower extremity vascular injuries. CONCLUSION Vascular trauma in the pediatric population is uncommon, occurring in only 0.6% of all pediatric trauma patients. Although less frequent than adults, a significant proportion was due to penetrating injury. Vessels of the upper extremity were the most commonly injured and were associated with low mortality. Injuries of the thoracic aorta are rare. Overall, pediatric patients had an improved adjusted mortality when compared to adults.

Time course of coagulopathy in isolated severe traumatic brain injury.

BACKGROUND Time aspects of coagulopathy following severe traumatic brain injury (sTBI) are ill defined throughout the literature. Thus, the aim of this study was to evaluate the time course of coagulopathy following isolated sTBI and its relationship to in-hospital outcomes. METHODS Retrospective analysis of patients sustaining isolated sTBI (head AIS 3, extracranial injuries AIS < 3). TBI coagulopathy was defined as thrombocytopenia and/or elevated international normalised ratio (INR) and/or prolonged activated partial thromboplastin time (aPTT). Incidence, onset and duration of sTBI-coagulopathy and its impact on morbidity and mortality were analysed. RESULTS Overall, 45.7% (n = 127) of the 278 patients included developed coagulopathy. Coagulopathy occurred 23.1 ± 2.2 h [range: 0.1–108.2 h (0–4.5 days)] post-admission with a mean duration of 68.0 ± 7.4 h[range: 2.6–531.4 h (0.1–22.1 days)]. The time interval to onset of coagulopathy decreased significantly with increasing head injury severity (p = 0.015). Early coagulation abnormalities occurring within 12 h of admission along with markers of devastating head injury including head AIS 5, penetrating injury mechanism, subdural hematoma, and a low GCS on admission proved to be independent risk factors for mortality. CONCLUSIONS The sTBI-associated coagulopathy may ensue as late as 5 days after injury with a prolonged duration (>72 h) in 30% of patients. Early coagulopathy occurring within 12 h after injury is a marker of increased morbidity and poor outcomes. Pertinent prolonged screening of this sequela is warranted.

Early coagulopathy after isolated severe traumatic brain injury: relationship with hypoperfusion challenged.

INTRODUCTION The purpose of this study was to examine the incidence of tissue hypoperfusion in victims of severe traumatic brain injury (sTBI) and to determine the associations between hypoperfusion and TBI coagulopathy. METHODS This is a retrospective analysis of a prospectively collected cohort admitted to the surgical intensive care unit from June 2005 to December 2007 sustaining isolated sTBI, defined as sTBI [head Abbreviated Injury Scale (AIS) ≥ 3] with chest, abdomen, and extremity AIS < 3. Criteria for TBI-associated early coagulopathy included isolated sTBI in conjunction with thrombocytopenia (platelet count < 100,000 per mm³) or elevated international normalized ratio > 1.2 or prolonged activated partial thromboplastin time > 36 seconds at admission. Hypoperfusion was defined by the presence of an arterial base deficit (BD) > 6 mmol/L. Univariate and multivariate analysis was performed to identify associations among hypoperfusion, coagulopathy, and mortality. RESULTS A total of 132 patients met the study criteria. TBI-associated early coagulopathy occurred in 48 patients (36.4%). With increasing head injury severity, the incidence of coagulopathy increased in a stepwise fashion. Mean BD values and mean lactate values were significantly higher among patients with coagulopathy compared with their noncoagulopathic counterparts at hospital admission. The coagulopathic cohort presented more frequently with a BD > 6 mmol/L at admission (39.6% vs. 20.2%, p = 0.016). In the stepwise logistic regression analysis, head AIS = 5 and an admission BD > 6 mmol/L were independently associated with early coagulopathy. Coagulopathy was associated with increased mortality in patients after blunt head trauma, adjusted odds ratio (95% confidence interval): 3.79 (1.06-13.51); adjusted p = 0.04. CONCLUSION Hypoperfusion is an independent risk factor for the development of early coagulopathy in patients with isolated sTBI. Nevertheless, early coagulopathy after sTBI does not occur exclusively in patients experiencing tissue hypoperfusion.

Incidence and clinical predictors for tracheostomy after cervical spinal cord injury: a National Trauma Databank review.

BACKGROUND The purpose of this study was to determine the incidence and identify clinical predictors for the need for tracheostomy after cervical spinal cord injury (CSCI). METHODS The National Trauma Databank version 7.0 (2002-2006) was used to identify all patients who sustained a CSCI. Patients with severe traumatic brain injury (TBI) were excluded. Demographics, clinical data, and outcomes were abstracted. Patients requiring tracheostomy were compared with those who did not require tracheostomy. Logistic regression analysis was used to identify independent predictors for the need of tracheostomy. RESULTS There were 5,265 eligible patients. Of these, 1,082 (20.6%) required tracheostomy and 4,174 (79.4%) did not. The majority patients were men and blunt trauma predominated. Patients requiring tracheostomy had a higher Injury Severity Score (ISS) (33.5±17.7 vs. 24.4±16.2, p<0.001) and required intubation more frequently on scene and Emergency Department (ED) (4.2 vs. 1.4%, p<0.001 and 31.1 vs. 7.9%, p<0.001, respectively). Patients requiring tracheostomy had higher rates of complete CSCI at C1-C4 (18.2 vs. 8.4%, p<0.001) and C5-C7 levels (37.8 vs. 16.9%, p<0.001). Patients requiring tracheostomy had more ventilation days, longer intensive care unit and hospital lengths of stay, but lower mortality. Intubation on scene or ED, complete CSCI at C1-C4 or C5-C7 levels, ISS≥16, facial fracture, and thoracic trauma were identified as independent predictors for the need of tracheostomy. CONCLUSION After CSCI, a fifth of patients will require tracheostomy. Intubation on scene or ED, complete CSCI at C1-C4 or C5-C7 levels, ISS≥16, facial fracture, and thoracic trauma were independently associated with the need for tracheostomy.

Early vasopressor use in critical injury is associated with mortality independent from volume status.

BACKGROUND Complications of excessive crystalloid after critical injury have increased interest in vasopressor support. However, it is hypothesized that vasopressor use in patients who are under-resuscitated is associated with death. We performed this study to determine whether volume status is associated with increased mortality in the critically injured exposed to early vasopressors. METHODS The intensive care unit database at a Level I center was queried for all adult admissions surviving for >24 hours from January 1, 2001, to December 31, 2008. Patients with spinal cord injury and severe traumatic brain injury were excluded. The vasopressor group [Vaso (+)] was exposed to dopamine, epinephrine, phenylephrine, norepinephrine, or arginine vasopressin within 24 hours of admission. Demographic and injury data were studied including intensive care unit admission central venous pressure. Hypovolemia [Hypov (+)] was considered an admission central venous pressure ≤8 mm Hg. The Vaso (+) group was analyzed to determine whether Hypov (+) was independently associated with death. RESULTS Of 1,349 eligible patients, 26% (351) were Vaso (+). Mortality was 43.6% (153) in the Vaso (+) versus 4.2% (42) in the Vaso (-) group (17.60 [12.10-25.60], <0.01). Vasopressor exposure was associated with death independent of injury severity. In Vaso (+) patients, Hypov (+) was not associated with mortality, whereas Emergency Department admission Glasgow Coma Scale ≤8 and multiple vasopressor use were. CONCLUSIONS Vasopressor exposure early after critical injury is independently associated with death and mortality is increased regardless of fluid status. Although it is not advisable to withhold support with impending cardiovascular collapse, use of any vasopressor during ongoing resuscitation should be approached with extreme caution regardless of volume status.