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Item Brodifacoum contamination of synthetic cannabinoid causing unexplained coagulopathy in multiple trauma: A case report(Elsevier, 2024-04-01) Thomas, Anthony V.; Johnson, Mackenzie L.; Tincher, Anna M.; Zackariya, Saniya; Khan, Hassaan; Rizvi, Uzma; Thomas, Scott G.; Noveroske, Timothy W.; Fulkerson, Daniel H.; Moore, Ernest E.; Walsh, Mark M.; Medicine, School of MedicineAn 18-year-old female presented to the emergency department after a motor vehicle collision. Initial imaging revealed a liver laceration. Subsequent labs showed significantly elevated prothrombin time, international normalized ratio, and activated partial thromboplastin time. Thromboelastography demonstrated a flatline tracing. The patient denied use of anticoagulation but admitted to synthetic cannabinoid use. It was believed the patient had taken synthetic cannabinoid contaminated by brodifacoum. She was therefore given prothrombin complex concentrate and vitamin K with blood products. The patient underwent sequential embolization, laparotomy, thoracotomy, and repair of the vena cava with a shunt. Thirty minutes postoperatively, her coagulation tests and thromboelastography were much improved. Two and a half hours postoperatively, it was determined she had sustained non-survivable injuries. The patient experienced brain death due to prolonged hypotension as a result of hemorrhagic shock with bleeding exacerbated by brodifacoum. To our knowledge, this is the first case reported of a trauma-induced coagulopathy exacerbated by brodifacoum-contaminated synthetic cannabinoid. Her coagulopathy was clearly not due to trauma alone and contributed greatly to the difficulty in controlling hemorrhage. The synthetic cannabinoid-associated coagulopathy rendered her otherwise potentially survivable injuries fatal. Given the frequency of multiple trauma and the recent increase in the prevalence of synthetic cannabinoid, it can be expected that the incidence of trauma complicated by synthetic cannabinoid-associated coagulopathy will increase in the near future. For patients that present with prolonged prothrombin time and/or activated partial thromboplastin time, it is important to inquire about recent synthetic cannabinoid use.Item Management of Acute Liver Failure: A Pediatric Perspective(Springer, 2018) Bhatt, Heli; Rao, Girish S.; Pediatrics, School of MedicinePurpose of review: Pediatric acute liver failure is a rare, complex, rapidly progressing, and life-threatening illness. Majority of pediatric acute liver failures have unknown etiology. This review intends to discuss the current literature on the challenging aspects of management of acute liver failure. Recent findings: Collaborative multidisciplinary approach for management of patients with pediatric acute liver failure with upfront involvement of transplant hepatologist and critical care specialists can improve outcomes of this fatal disease. Extensive but systematic diagnostic evaluation can help to identify etiology and guide management. Early referral to a transplant center with prompt liver transplant, if indicated, can lead to improved survival in these patients. Summary: Prompt identification and aggressive management of pediatric acute liver failure and related comorbidities can lead to increased transplant-free survival and improved post-transplant outcomes, thus decreasing mortality and morbidity associated with this potential fatal condition.Item Management of COVID-19-associated coagulopathy in persons with haemophilia(Wiley, 2021) Pipe, Steven W.; Kaczmarek, Radoslaw; Srivastava, Alok; Pierce, Glenn F.; Makris, Mike; Hermans, Cedric; Pediatrics, School of MedicineIntroduction: The SARS-CoV-2 coronavirus-induced infection (COVID-19) can be associated with a coagulopathy mainly responsible for pulmonary microvasculature thrombosis and systemic thromboembolic manifestations. The pathophysiology and management of the COVID-19 coagulopathy are likely more complex in patients with inherited bleeding diseases such as haemophilia. These individuals might indeed present with both bleeding and thrombotic complications and require simultaneous antithrombotic and haemostatic treatments. Objective: We propose practical guidance for the diagnosis and management of COVID-19 coagulopathy in persons with haemophilia. Results: Continuation of regular haemostatic treatment is recommended for ambulatory patients. For patients requiring hospital admission and on replacement therapy with factors VIII or IX concentrates, prophylaxis with concentrates should be intensified according to the risk of bleeding complications and associated with prophylactic doses of LMWH. For patients on nonreplacement therapy, emicizumab should be continued and possibly combined with factor VIII and prophylactic doses of LMWH depending on the risk of bleeding and thrombosis. Dose escalation of LMWH tailored to the risk of thrombosis can be employed but not supported by evidence. Conclusions: These practical recommendations are based on the current literature on COVID-19 with its impact on haemostasis, indications and modalities for thromboprophylaxis mainly in nonhaemophilic patients and how that is likely to affect persons with haemophilia in different circumstances. They will need to be tailored to each patient's clinical status and validated in future studies.Item Pediatric Non-Alcoholic Fatty Liver Disease (NAFLD): Trends, Mortality, and Socioeconomic Disparities in the U.S., 1998–2020(MDPI, 2025-01-08) Wasuwanich, Paul; So, Joshua M.; Sadek, Mustafa; Jarasvaraparn, Chaowapong; Rajborirug, Songyos; Quiros-Tejeira, Ruben E.; Karnsakul, Wikrom; Pediatrics, School of MedicineBackground/objectives: We aim to describe the changing inpatient epidemiology of NAFLD in the U.S. and identify major risk factors associated with mortality in the disease among hospitalized pediatric patients. Methods: Hospitalization data from the 1998-2020 National Inpatient Sample were utilized. ICD-9 and ICD-10 codes were used to identify pediatric patients (age less than 18 years old) with NAFLD, and risk factors for mortality were analyzed by logistic regression. Results: We identified 68,869 pediatric hospitalizations involving NAFLD. Among those, 970 (1.4%) died during hospitalization. Hospitalization rates have been rapidly increasing from 1998 to 2020 (incidence rate ratio (IRR): 1.07; 95% CI: 1.06-1.07; p < 0.001). There was a significant difference in mortality based on the type of hospital (rural, non-teaching urban, or teaching urban) in pediatric patients with NAFLD (p < 0.05). Coagulopathy was significantly associated with increased odds of mortality, while age ≥ 12 years, diabetes and obesity were associated with decreased odds of mortality (p < 0.05). Sex, race/ethnicity, hepatitis B, hepatitis C, HIV, and IV drug use were not significantly associated with mortality. Conclusions: Our study has shown ever increasing hospitalization rates for NAFLD in pediatric populations and well as significant risk factors associated with mortality. Further studies should be performed as more data on this patient population are collected.Item Portal vein thrombosis, mortality and hepatic decompensation in patients with cirrhosis: A meta-analysis(Baishideng Publishing Group Co (World Journal of Hepatology), 2015-11-28) Stine, Jonathan G.; Shah, Puja M.; Cornella, Scott L.; Rudnick, Sean R.; Ghabril, Marwan S.; Stukenborg, George J.; Northup, Patrick G.; Department of Medicine, IU School of MedicineAIM: To determine the clinical impact of portal vein thrombosis in terms of both mortality and hepatic decompensations (variceal hemorrhage, ascites, portosystemic encephalopathy) in adult patients with cirrhosis. METHODS: We identified original articles reported through February 2015 in MEDLINE, Scopus, Science Citation Index, AMED, the Cochrane Library, and relevant examples available in the grey literature. Two independent reviewers screened all citations for inclusion criteria and extracted summary data. Random effects odds ratios were calculated to obtain aggregate estimates of effect size across included studies, with 95%CI. RESULTS: A total of 226 citations were identified and reviewed, and 3 studies with 2436 participants were included in the meta-analysis of summary effect. Patients with portal vein thrombosis had an increased risk of mortality (OR = 1.62, 95%CI: 1.11-2.36, P = 0.01). Portal vein thrombosis was associated with an increased risk of ascites (OR = 2.52, 95%CI: 1.63-3.89, P < 0.001). There was insufficient data available to determine the pooled effect on other markers of decompensation including gastroesophageal variceal bleeding or hepatic encephalopathy. CONCLUSION: Portal vein thrombosis appears to increase mortality and ascites, however, the relatively small number of included studies limits more generalizable conclusions. More trials with a direct comparison group are needed.Item Rapid neurological recovery with spontaneous resolution of acute subdural hematoma after severe head trauma: A case report of auto-decompression phenomena(Elsevier, 2025) Obeng-Gyasi, Barnabas; Chinthala, Anoop S.; Christodoulides, Alexei; Ordaz, Josue; Mao, Gordon; Neurological Surgery, School of MedicineIntroduction: The spontaneous resolution of acute subdural hematoma (aSDH) represents an ill-defined but clinically significant phenomenon in traumatic brain injury (TBI). While surgical evacuation remains the standard of care for significant aSDH, rare cases of spontaneous resolution, termed auto-decompression in literature, suggest alternative pathways of hematoma clearance that warrant further investigation. Case presentation: We discuss the case of a 40-year-old male with background seizure disorder who fell off a ladder. His Glasgow Coma Score (GCS) at presentation was 5. Brain Computed Tomography (CT) scan revealed bilateral aSDH and multiple skull fractures. Within 24 h, his GCS quickly improved to 9 T. Repeat brain CT done 72 h post-trauma showed resolution of the aSDH following non-operative management. Discussion: Spontaneous resolution of bilateral aSDH with rapid neurological improvement is a rare but possible occurrence, often attributed to auto-decompression phenomenon in patients with severe head trauma and specific predisposing factors. Our discussion revolves around this patients presentation with polytrauma, complex skull fractures, history of craniotomy, and acute coagulopathy contributing to the spontaneous resolution of the hematoma. Given the complex nature of TBI and the unpredictable course of recovery, clinicians must remain vigilant in continuously reassessing neurological status. Conclusion: This case discusses the unpredictable nature of TBI and highlights the rapid and unexpected resolution of aSDH in a patient with complex neurosurgical history, coagulopathy, and polytrauma. The findings showcase the problems of polytraumatized patients and exemplify the importance of individualized care even when initial signs indicate poor prognosis.Item Traumatic brain injury causes platelet adenosine diphosphate and arachidonic acid receptor inhibition independent of hemorrhagic shock in humans and rats(Wolters Kluwer, 2014) Castellino, Francis J.; Chapman, Michael P.; Donahue, Deborah L.; Thomas, Scott; Moore, Ernest E.; Wohlauer, Max V.; Fritz, Braxton; Yount, Robert; Ploplis, Victoria; Davis, Patrick; Evans, Edward; Walsh, Mark; Biochemistry and Molecular Biology, School of MedicineBackground: Coagulopathy in traumatic brain injury (CTBI) is a well-established phenomenon, but its mechanism is poorly understood. Various studies implicate protein C activation related to the global insult of hemorrhagic shock or brain tissue factor release with resultant platelet dysfunction and depletion of coagulation factors. We hypothesized that the platelet dysfunction of CTBI is a distinct phenomenon from the coagulopathy following hemorrhagic shock. Methods: We used thrombelastography with platelet mapping as a measure of platelet function, assessing the degree of inhibition of the adenosine diphosphate (ADP) and arachidonic acid (AA) receptor pathways. First, we studied the early effect of TBI on platelet inhibition by performing thrombelastography with platelet mapping on rats. We then conducted an analysis of admission blood samples from trauma patients with isolated head injury (n = 70). Patients in shock or on clopidogrel or aspirin were excluded. Results: In rats, ADP receptor inhibition at 15 minutes after injury was 77.6% ± 6.7% versus 39.0% ± 5.3% for controls (p < 0.0001). Humans with severe TBI (Glasgow Coma Scale [GCS] score ≤ 8) showed an increase in ADP receptor inhibition at 93.1% (interquartile range [IQR], 44.8-98.3%; n = 29) compared with 56.5% (IQR, 35-79.1%; n = 41) in milder TBI and 15.5% (IQR, 13.2-29.1%) in controls (p = 0.0014 and p < 0.0001, respectively). No patient had significant hypotension or acidosis. Parallel trends were noted in AA receptor inhibition. Conclusion: Platelet ADP and AA receptor inhibition is a prominent early feature of CTBI in humans and rats and is linked to the severity of brain injury in patients with isolated head trauma. This phenomenon is observed in the absence of hemorrhagic shock or multisystem injury. Thus, TBI alone is shown to be sufficient to induce a profound platelet dysfunction.Item Viscoelastic Hemostatic Assays: A Primer on Legacy and New Generation Devices(MDPI, 2022-02-07) Volod, Oksana; Bunch, Connor M.; Zackariya, Nuha; Moore, Ernest E.; Moore, Hunter B.; Kwaan, Hau C.; Neal, Matthew D.; Al-Fadhl, Mahmoud D.; Patel, Shivani S.; Wiarda, Grant; Al-Fadhl, Hamid D.; McCoy, Max L.; Thomas, Anthony V.; Thomas, Scott G.; Gillespie, Laura; Khan, Rashid Z.; Zamlut, Mahmud; Kamphues, Peter; Fries, Dietmar; Walsh, Mark M.; Medicine, School of MedicineViscoelastic hemostatic assay (VHAs) are whole blood point-of-care tests that have become an essential method for assaying hemostatic competence in liver transplantation, cardiac surgery, and most recently, trauma surgery involving hemorrhagic shock. It has taken more than three-quarters of a century of research and clinical application for this technology to become mainstream in these three clinical areas. Within the last decade, the cup and pin legacy devices, such as thromboelastography (TEG® 5000) and rotational thromboelastometry (ROTEM® delta), have been supplanted not only by cartridge systems (TEG® 6S and ROTEM® sigma), but also by more portable point-of-care bedside testing iterations of these legacy devices (e.g., Sonoclot®, Quantra®, and ClotPro®). Here, the legacy and new generation VHAs are compared on the basis of their unique hemostatic parameters that define contributions of coagulation factors, fibrinogen/fibrin, platelets, and clot lysis as related to the lifespan of a clot. In conclusion, we offer a brief discussion on the meteoric adoption of VHAs across the medical and surgical specialties to address COVID-19-associated coagulopathy.