Leslie Kobayashi

The role of rotation thromboelastometry in early prediction of massive transfusion

INTRODUCTION Early prediction of massive transfusion (MT) is critical in the management of severely injured trauma patients. Variables available early after injury including physiologic, laboratory, and rotation thromboelastometric (ROTEM) parameters were evaluated as predictors for the need of MT. METHODS After Institutional Review Board approval, we retrospectively reviewed a cohort of severely injured trauma patients (Injury Severity Score ≥ 16) admitted to a Level I trauma center with available ROTEM measurements on hospital admission during a 1-year study period. Patients with isolated head injury (Abbreviated Injury Scale head ≥ 3 and Abbreviated Injury Scale chest, abdomen, and extremity < 3) and patients with a penetrating mechanism of injury were excluded. Patients who received a MT (≥ 10 units packed red blood cell within 24 hours of admission) were compared with patients who did not. Variables independently associated with MT were identified using stepwise logistic regression. RESULTS A total of 53 patients met inclusion criteria. Of these, 18 patients (34.0%) received a MT and 35 patients (66.0%) did not. Massively transfused patients had significantly lower baseline hemoglobin values (7.9 g/dL ± 0.4 g/dL vs. 11.4 g/dL ± 0.4 g/dL; p < 0.001) and a trend toward higher lactate (4.8 mmol/L ± 0.8 mmol/L vs. 3.0 mmol/L ± 0.3 mmol/L; p = 0.056) and base deficit values (5.9 mmol/L ± 1.1 mmol/L vs. 3.6 mmol/L ± 0.6 mmol/L; p = 0.052). Mean international normalized ratio (1.46 ± 0.07 vs. 1.22 ± 0.05; p = 0.001) and partial thromboplastin times (42.4 seconds ± 5.0 seconds vs. 29.7 seconds ± 1.8 seconds; p < 0.001) were significantly higher in MT patients. Patients receiving a MT had significantly altered ROTEM values on admission compared with non-MT patients. An increase in the clot formation time (471.3 seconds ± 169.9 seconds vs. 178.1 seconds ± 19.9 seconds; p = 0.001), a shortening of the maximum clot firmness (37.5 mm ± 2.9 mm vs. 50.7 mm ± 1.4 mm; p < 0.001), and a shortening of the clot amplitude at all time points (10/20/30 minutes) were observed in massively transfused trauma patients. Variables independently associated with MT included a hemoglobin level ≤ 10 g/dL and an abnormal maximum clot firmness value (area under the receiver operator characteristic curve: 0.831 [95% confidence interval: 0.719-0.942; p < 0.001]). CONCLUSION Hemoglobin ≤ 10 g/dL and an abnormal maximum cloth firmness measured by rotation thromboelastometry on admission reliably predict the need for MT. Prospective validation of the effectiveness of thromboelastometry to guide the transfusion practice after trauma is warranted.

Surgical Strategies for Management of the Open Abdomen

Since the mid-1990s the surgical community has seen a surge in the prevalence of open abdomens (OAs) reported in the surgical literature and in clinical practice. The OA has proven to be effective in decreasing mortality and immediate postoperative complications; however, it may come at the cost of delayed morbidity and the need for further surgical procedures. Indications for leaving the abdomen open have broadened to include damage control surgery, abdominal compartment syndrome, and abdominal sepsis. The surgical options for management of the OA are now more diverse and sophisticated, but there is a lack of prospective randomized controlled trials demonstrating the superiority of any particular method. Additionally, critical care strategies for optimization of the patient with an OA are still being developed. Review of the literature suggests a bimodal distribution of primary closure rates, with early closure dependent on postoperative intensive care management and delayed closure more affected by the choice of the temporary abdominal closure technique. Invariably, a small fraction of patients requiring OA management fail to have primary fascial closure and require some form of biologic fascial bridge with delayed ventral hernia repair in the future.

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.

Necrotizing soft tissue infections: delayed surgical treatment is associated with increased number of surgical debridements and morbidity.

BACKGROUND Early surgical treatment is crucial in the management of necrotizing soft tissue infections (NSTI), a severe, potentially life threatening, rapidly progressive infection. The purpose of this study was to determine the influence of surgical procedure timing on the number of surgical debridements required. METHODS A retrospective study including 47 patients with the diagnosis of NSTI admitted to a large academic hospital from December 2004 to December 2010 was conducted. Demographics, basic laboratories on admission, medical comorbidities, site of infection, and intraoperative culture results were compared between patients with early (≤12 hour) and late (>12 hour) surgical treatment. The x-y plot for the study population and linear regression analyses were used to define the time cut point. Outcomes included the total number of debridements, mortality, hospital length of stay, and complications. Adjustment for confounding factors was done with binary regression logistic model for categorical outcomes and analysis of covariants for continuous outcomes. RESULTS Overall mortality was 17.0%. The average number of surgical debridements in patients with delay surgical treatment >12 hours from the time of emergency department admission was significantly higher than those who had an operation within 12 hours after admission (7.4 ± 2.5 vs. 2.3 ± 1.2; p < 0.001). Delayed surgical debridement was associated with significantly higher mortality, higher incidence of septic shock and renal failure, and more surgical debridements than patients with early surgical debridements. After adjusting for possible confounding factors, the average number of surgical debridements and the presence of septic shock and acute renal failure were still significantly higher in patients in whom surgery was delayed >12 hours. CONCLUSION In patients with NSTI, a delay of surgical treatment of >12 hours is associated with an increased number of surgical debridements and higher incidence of septic shock and acute renal failure.

Erythropoiesis Stimulating Agent Administration Improves Survival After Severe Traumatic Brain Injury: A Matched Case Control Study

Objective:Erythropoiesis stimulating agent (ESA) administration may reduce mortality in severe traumatic brain injury (sTBI). Summary Background Data:It has been established that the administration of ESA in critically ill trauma victims has been associated with improved outcomes. Recent experimental and clinical data showed neuroprotective effects of ESA, however, the literature regarding impact on outcome in sTBI is lacking. Methods:A retrospective matched case control study in patients with sTBI [head Abbreviated Injury Scale (AIS), ≥3] receiving ESA while in the surgical intensive care unit from January 1, 1996 to December 31, 2007 (n = 89), were matched 1 to 2 (n = 178) by age, gender, mechanism of injury, Glasgow Coma Scale, presence of hypotension on admission, Injury Severity Score, AIS for all body regions, and presence of anemia with patients who did not receive the agent. Each cases controls were chosen to have surgical intensive care unit length of stay more than or equal to the time from admission to first dose of ESA. The primary outcome measure in this study was mortality. Results:Cases and controls had similar age, gender, mechanisms of injury, incidence of hypotension, Glasgow Coma Scale on admission, Injury Severity Score, and AIS for all body regions. Although the ESA+ patients experienced protracted hospital length of stay and comparable surgical intensive care unit free days, they demonstrated a significantly lower in-hospital mortality in comparison to controls at 7.9% versus 24.2%, respectively (OR: 0.27; 95% CI = 0.12–0.62; P = 0.001). Conclusions:Erythropoiesis stimulating agent administration in sTBI is associated with a significant in-hospital survival advantage without increase in morbidity. Prospective validation of our findings is warranted.

Abdominal damage control surgery and reconstruction: world society of emergency surgery position paper

Damage control laparotomy was first described by Dr. Harlan Stone in 1983 when he suggested that patients with severe trauma should have their primary procedures abbreviated when coagulopathy was encountered. He recommended temporizing patients with abdominal packing and temporary closure to allow restoration of normal physiology prior to returning to the operating room for definitive repair. The term damage control in the trauma setting was coined by Rotondo et al., in 1993. Studies in subsequent years have validated this technique by demonstrating decreased mortality and immediate post-operative complications. The indications for damage control laparotomy have evolved to encompass abdominal compartment syndrome, abdominal sepsis, vascular and acute care surgery cases. The perioperative critical care provided to these patients, including sedation, paralysis, nutrition, and fluid management strategies may improve closure rates and recovery. In the rare cases of inability to primarily close the abdomen, there are a number of reconstructive strategies that may be used in the acute and chronic phases of abdominal closure.

Thromboembolic prophylaxis with low-molecular-weight heparin in patients with blunt solid abdominal organ injuries undergoing nonoperative management: current practice and outcomes.

BACKGROUND Low-molecular-weight heparins (LMWHs) are effective in preventing thromboembolic complications after trauma. In the nonoperative management (NOM) of blunt solid abdominal organ injuries, the timing of the administration of LMWH remains controversial because of the unknown risk for bleeding. METHODS Retrospective study including patients aged 15 years or older who sustained blunt splenic, liver, and/or kidney injuries from January 2005 to December 2008. Patients were stratified according to the type and severity of organ injuries. NOM failure rates and blood transfusion requirements were compared between patients who got LMWH early (≤3 days), patients who got LMWH late (>3 days), and patients who did not receive LMWH. RESULTS Overall, 312 (63.8%) patients with solid organ injuries had NOM attempted. There were 154 splenic, 144 liver, and 65 kidney injuries (1.2 organs injured per patient). Forty-one patients (13.2%) received LMWH early, 70 patients (22.4%) received LMWH late, and 201 (64.4%) patients did not receive LMWH. The early LMWH group was less severely injured compared with the late LMWH group. However, the distribution of the risk factors for failure of NOM (high-grade injury, large amount of hemoperitoneum, and contrast extravasation) was similar between the three LMWH groups. Overall, 17 of 312 patients (5.4%) failed NOM (7.8% spleen, 2.1% liver, and 3.1% kidney). All but one failure occurred before LMWH administration. After adjustment for demographic differences, the overall blood transfusion requirements for the early LMWH group was significantly lower when compared with patients with late LMWH administration (3.0±5.3 units vs. 6.4±9.9 units; adjusted p=0.027). Pulmonary embolism and deep venous thrombosis occurred in four patients. The mortality rate for patients with splenic, liver, and kidney injuries was 3.2% and did not differ with LMWH application. CONCLUSION In patients with solid abdominal organ injuries undergoing NOM, early use of LMWH does not seem to increase failure rates or blood transfusion requirements.

A Comprehensive review of abdominal infections

Intra-abdominal infection (IAI) describes a diverse set of diseases. It is broadly defined as peritoneal inflammation in response to microorganisms, resulting in purulence in the peritoneal cavity[1]. IAI are classified as uncomplicated or complicated based on the extent of infection[2]. Uncomplicated abdominal infections involve intramural inflammation of the gastrointestinal (GI) tract without anatomic disruption. They are often simple to treat; however, when treatment is delayed or inappropriate, or the infection involves a more virulent nosocomial microbe, the risk of progression into a complicated abdominal infection becomes significant[3, 4]. Complicated abdominal infections extend beyond the source organ into the peritoneal space. They cause peritoneal inflammation, and are associated with localized or diffuse peritonitis[5]. Localized peritonitis often manifests as an abscess with tissue debris, bacteria, neutrophils, macrophages, and exudative fluid contained in a fibrous capsule. Diffuse peritonitis is categorized as primary, secondary or tertiary peritonitis. Primary peritonitis is also known as spontaneous bacterial peritonitis. It is thought to be the result of bacterial translocation across an intact gut wall[6]. These infections are commonly monomicrobial, and the infecting organism is primarily determined by patient demographics. For example, healthy young girls are most often infected by streptococcal organisms, cirrhotics by gram negative or enterococcal organisms, and peritoneal dialysis patients by Staphylococcus aureus[7, 8]. Diagnosis requires peritoneal fluid aspiration. Characteristics of infection include white blood cell count (WBC) > 500 cells/mm3, high lactate, and low glucose levels. Positive peritoneal fluid cultures are definitive, and resolution of infection is marked by peritoneal fluid with < 250 WBC/mm3[9]. Secondary peritonitis is caused by microbial contamination through a perforation, laceration, or necrotic segment of the GI tract[7]. Definitive diagnosis is based on clinical examination and history, and specific diagnoses can be confirmed by radiographic imaging[10]. If a patient is stable enough for transport, computed tomography (CT) scan with intravenous and oral contrast is the standard method of evaluating most intra-abdominal pathologies, such as appendicitis, diverticulitis, and colitis[11]. Suspected biliary pathology is the exception, and ultrasound is the preferred initial imaging modality for this spectrum of disease including acute cholecystitis, emphysematous cholecystitis, and cholangitis. Infections associated with secondary peritonitis are commonly polymicrobial and the infecting organisms are those most commonly associated with the source of contamination (see Table 1). Table 1 Expected organisms according to source Source Expected Organism Primary Peritonitis Young healthy female Streptococcus Cirrhotic Enteric gram negatives Enterococcus CAPD Staphylococcus aureus Secondary peritonitis Stomach and duodenum Streptococcus Lactobacillus Biliary E. coli, Klebsiella, Enterococcus Small Intestine E. coli, Klebsiella, Lactobacillus Streptococci Diptheroids Enterococci Distal ileum and colon Bacteroides fragilis Clostridium spp. E. coli Enterobacter spp. Klebsiella spp. Peptostreptococci Enterococci Teritiary peritonitis Enterococcus Candida Staphylococcus epidermidis Enterobacter Adapted from Weigelt JA [12]. Tertiary peritonitis represents an infection that is persistent or recurrent at least 48 hours after appropriate management of primary or secondary peritonitis. It is more common among critically ill or immunocompromised patients[12]. Because of the poor host defenses, it is also often associated with less virulent organisms, such as Enterococcus, Candida, Staphylococcus epidermidis, and Enterobacter[13]. Intra-abdominal sepsis is an IAI that results in severe sepsis or septic shock[2].

Hypovolemic Shock Resuscitation

Several changes in the way patients with hemorrhagic shock are resuscitated have occurred over the past decades, including permissive hypotension, minimal crystalloid resuscitation, earlier blood transfusion, and higher plasma and platelet-to-red cell ratios. Hemostatic adjuncts, such as tranexamic acid and prothrombin complex, and the use of new methods of assessing coagulopathy are also being incorporated into resuscitation of the bleeding patient. These ideas have been incorporated by many trauma centers into institutional massive transfusion protocols, and adoption of these protocols has resulted in improvements in mortality and morbidity. This article discusses each of these new resuscitation strategies and the evidence supporting their use.