Abnormal coagulation after hepatectomy in patients with normal preoperative coagulation function.

BACKGROUND: To explore the risk factors for postoperative abnormal coagulation (PAC) and establish a predictive model for patients with normal preoperative coagulation function who underwent hepatectomy. MATERIALS AND METHODS: A total of 661 patients with normal preoperative coagulation function who underwent hepatectomy between January 2015 and December 2021 at the First Affiliated Hospital of Sun Yat-sen University were divided into two groups: the postoperative abnormal coagulation group (PAC group, n = 362) and the normal coagulation group (non-PAC group, n = 299). Univariate and multivariate logistic analyses were used to identify the risk factors for PAC. RESULTS: The incidence of PAC in 661 patients who underwent hepatectomy was 54.8% (362/661). The least absolute shrinkage and selection operator (LASSO) method was used for multivariate logistic regression analysis. The preoperative international normalized ratio (INR), intraoperative succinyl gelatin infusion and major hepatectomy were found to be independent risk factors for PAC. A nomogram for predicting the PAC after hepatectomy was constructed. The model presented a receiver operating characteristic (ROC) curve of 0.742 (95% confidence interval (CI): 0.697-0.786) in the training cohort. The validation set demonstrated a promising ROC of 0.711 (95% CI: 0.639-0.783), and the calibration curve closely approximated the true incidence. Decision curve analysis (DCA) was performed to assess the clinical usefulness of the predictive model. The risk of PAC increased when the preoperative international normalized ratio (INR) was greater than 1.025 and the volume of intraoperative succinyl gelatin infusion was greater than 1500 ml. CONCLUSION: The PAC is closely related to the preoperative INR, intraoperative succinyl gelatin infusion and major hepatectomy. A three-factor prediction model was successfully established for predicting the PAC after hepatectomy.

Diagnostic and Prognostic Value of C1q in Sepsis-Induced Coagulopathy.

Early identification of biomarkers that can predict the onset of sepsis-induced coagulopathy (SIC) in septic patients is clinically important. This study endeavors to examine the diagnostic and prognostic utility of serum C1q in the context of SIC. Clinical data from 279 patients diagnosed with sepsis at the Departments of Intensive Care, Respiratory Intensive Care, and Infectious Diseases at the Renmin Hospital of Wuhan University were gathered spanning from January 2022 to January 2024. These patients were categorized into two groups: the SIC group comprising 108 cases and the non-SIC group consisting of 171 cases, based on the presence of SIC. Within the SIC group, patients were further subdivided into a survival group (43 cases) and non-survival group (65 cases). The concentration of serum C1q in the SIC group was significantly lower than that in the non-SIC group. Furthermore, A significant correlation was observed between serum C1q levels and both SIC score and coagulation indices. C1q demonstrated superior diagnostic and prognostic performance for SIC patients, as indicated by a higher area under the curve (AUC). Notably, when combined with CRP, PCT, and SOFA score, C1q displayed the most robust diagnostic efficacy for SIC. Moreover, the combination of C1q with the SOFA score heightened predictive value concerning the 28-day mortality of SIC patients.

Impact of Early Microparticle Release during Isolated Severe Traumatic Brain Injury: Correlation with Coagulopathy and Mortality.

BACKGROUND: Microparticles (MPs) have been implicated in thrombosis and endothelial dysfunction. Their involvement in early coagulopathy and in worsening of outcomes in isolated severe traumatic brain injury (sTBI) patients remains ill defined. OBJECTIVE: We sought to quantify the circulatory MP subtypes derived from platelets (PMPs; CD42), endothelial cells (EMPs; CD62E), and those bearing tissue factor (TFMP; CD142) and analyze their correlation with early coagulopathy, thrombin generation, and in-hospital mortality. MATERIALS AND METHODS: Prospective screening of sTBI patients was done. Blood samples were collected before blood and fluid transfusion. MP enumeration and characterization were performed using flow cytometry, and thrombin-antithrombin complex (TAT) levels were determined using enzyme-linked immunosorbent assay (ELISA). Circulating levels of procoagulant MPs were compared between isolated sTBI patients and age- and gender-matched healthy controls (HC). Patients were stratified according to their PMP, EMP, and TFMP levels, respectively (high ≥HC median and low < HC median). RESULTS: Isolated sTBI resulted in an increased generation of PMPs (456.6 [228-919] vs. 249.1 [198.9-404.5]; P = 0.01) and EMPs (301.5 [118.8-586.7] vs. 140.9 [124.9-286]; P = 0.09) compared to HCs. Also, 5.3% of MPs expressed TF (380 [301-710]) in HCs, compared to 6.6% MPs (484 [159-484]; P = 0.87) in isolated sTBI patients. Early TBI-associated coagulopathy (TBI-AC) was seen in 50 (41.6%) patients. PMP (380 [139-779] vs. 523.9 [334-927]; P = 0.19) and EMP (242 [86-483] vs. 344 [168-605]; P = 0.81) counts were low in patients with TBI-AC, compared to patients without TBI-AC. CONCLUSION: Our results suggest that enhanced cellular activation and procoagulant MP generation are predominant after isolated sTBI. TBI-AC was associated with low plasma PMPs count compared to the count in patients without TBI-AC. Low PMPs may be involved with the development of TBI-AC.

Tackling a deadly global phenomenon: sepsis induced coagulopathy: A narrative review.

Sepsis is a potentially fatal illness marked by organ failure and the two main causes of which are shock and disseminated intravascular coagulation. Multi-organ dysfunction in sepsis is mediated by the inflammatory cytokine storm, while sepsis induced coagulopathy is mediated and accelerated by activation of pro-coagulative mechanisms. Regardless of the severity of sepsis, disseminated intravascular coagulation is a potent predictor of mortality in septic patients. Additionally, oxidative stress in sepsis causes renal ischaemia and eventually acute kidney injury. The first and foremost goal is to initiate resuscitation immediately, with treatment mainly focussing on maintaining a balance of coagulants and anticoagulants. A simpler and more universal diagnostic criteria is likely to improve studies on the spectrum associated with sepsis.

Development and validation of the tic score for early detection of traumatic coagulopathy upon hospital admission: a cohort study.

BACKGROUND: Critically injured patients need rapid and appropriate hemostatic treatment, which requires prompt identification of trauma-induced coagulopathy (TIC) upon hospital admission. We developed and validated the performance of a clinical score based on prehospital resuscitation parameters and vital signs at hospital admission for early diagnosis of TIC. METHODS: The score was derived from a level-1 trauma center registry (training set). It was then validated on data from two other level-1 trauma centers: first on a trauma registry (retrospective validation set), and then on a prospective cohort (prospective validation set). TIC was defined as a PTratio > 1.2 at hospital admission. Prehospital (vital signs and resuscitation care) and admission data (vital signs and laboratory parameters) were collected. We considered parameters independently associated with TIC in the score (binomial logistic regression). We estimated the score's performance for the prediction of TIC. RESULTS: A total of 3489 patients were included, and among these a TIC was observed in 22% (95% CI 21-24%) of cases. Five criteria were identified and included in the TIC Score: Glasgow coma scale < 9, Shock Index > 0.9, hemoglobin < 11 g.dL-1, prehospital fluid volume > 1000 ml, and prehospital use of norepinephrine (yes/no). The score, ranging from 0 and 9 points, had good performance for the identification of TIC (AUC: 0.82, 95% CI: 0.81-0.84) without differences between the three sets used. A score value < 2 had a negative predictive value of 93% and was selected to rule-out TIC. Conversely, a score value ≥ 6 had a positive predictive value of 92% and was selected to indicate TIC. CONCLUSION: The TIC Score is quick and easy to calculate and can accurately identify patients with TIC upon hospital admission.

Improving predictions: Enhancing in-hospital mortality forecast for ICU patients with sepsis-induced coagulopathy using a stacking ensemble model.

The incidence of sepsis-induced coagulopathy (SIC) is high, leading to increased mortality rates and prolonged hospitalization and intensive care unit (ICU) stays. Early identification of SIC patients at risk of in-hospital mortality can improve patient prognosis. The objective of this study is to develop and validate machine learning (ML) models to dynamically predict in-hospital mortality risk in SIC patients. A ML model is established based on the Medical Information Mart for Intensive Care IV (MIMIC-IV) database to predict in-hospital mortality in SIC patients. Utilizing univariate feature selection for feature screening. The optimal model was determined by calculating the area under the curve (AUC) with a 95% confidence interval (CI). The optimal model was interpreted using Shapley Additive Explanation (SHAP) values. Among the 3112 SIC patients included in MIMIC-IV, a total of 757 (25%) patients experienced mortality during their ICU stay. Univariate feature selection helps us to pick out the 20 most critical variables from the original feature. Among the 10 developed machine learning models, the stacking ensemble model exhibited the highest AUC (0.795, 95% CI: 0.763-0.827). Anion gap and age emerged as the most significant features for predicting the mortality risk in SIC. In this study, an ML model was constructed that exhibited excellent performance in predicting in-hospital mortality risk in SIC patients. Specifically, the stacking ensemble model demonstrated superior predictive ability.

A challenging issue in COVID-19 infection: The relationship between PA1-1 and TAFI levels in patients with coagulation disorder: A retrospective and observational study.

COVID-19 disrupts the balance between coagulation and fibrinolysis. Especially in the clinical course of serious disease, plasminogen activator inhibitor-1 (PAI-1), thrombin activatable fibrinolysis inhibitor (TAFI), and tissue plasminogen activator levels increase in association with hypercoagulable state and hypofibrinolysis. This explains the increased incidence of thrombosis seen in COVID-19 infection. In this study, we aimed to examine the changes in PAI-1 and TAFI levels of COVID-19 patients. Department of Infectious Diseases and Clinical Microbiology, University of Health Sciences, Diskapi Yildirim Beyazit Training and Research Hospital-Ankara Turkey, between April 1 and May 7, 2021. Patients who were diagnosed with COVID-19 were included in this retrospective study. TAFI and PAI-1 levels were analyzed from the samples that had been stored at -80 °C formerly. One hundred thirty-five patients diagnosed with COVID-19 and followed up in the service or intensive care unit were included in the study. Thirty-four (25.2%) patients required follow-up in the intensive care unit. Mortality rate was 10.4%, the coagulation tests of these patients were also compared. PA1-1 levels were found to be statistically significantly higher in intensive care unit patients (median: 133 pg/mL vs 31 pg/mL; P < .001), and there was no significant difference in TAFI levels (median:7.31 ng/mL vs 9.80 ng/mL; P = .171) between the 2 groups. TAFI levels were found to be higher in patients who died. In COVID-19 infection, as the severity of the disease increases, the coagulation balance deteriorates and eventually a hypercoagulable state occurs with an increase in PAI-1 and TAFI levels. Markers such as PAI and TAFI can be illuminating in further studies in determining prognosis and mortality and developing new treatment options.

Coagulation profile in hospitalized children with COVID-19: pediatric age dependency and its impact on long COVID development.

Introduction: Pulmonary endotheliopathy and microvascular immunothrombosis play a key role in acute COVID-19. Moreover, persistent endotheliopathy and heightened coagulability frequently occur in individuals recovering from COVID-19, suggesting the intriguing possibility of their role in the development of long COVID. The aim of our study was to investigate the coagulation profile in patients with COVID-19 based on age and their role in the development of long COVID. Methods: We conducted a prospective single-center cohort study from September 2022 to August 2023. The study involved 190 patients younger than 18 years who were hospitalized at the Ternopil City Children's Hospital, Ukraine due to COVID-19. Patients underwent determination of coagulation profile in addition to the general clinical examination. After discharge from the hospital, patients were monitored for the presence of long COVID symptoms. Among the 157 participants who consented for follow-up, 62 patients (39.5%) had long COVID symptoms according to the WHO definition, while the rest (95 patients) did not have symptoms of long COVID (fully recovered). Results: The study revealed the normal count of platelets in the majority of patients (86.8%), whereas abnormalities in the coagulation profile were revealed in 94.5% of children with COVID-19, and these changes were age-dependent. The patients were mostly presented with increased activated partial thromboplastin time (69.1%), prothrombin time (PT) (39.8%) and D-dimer (45.0%). There was no significant difference between the median of platelet levels and coagulation profile indicators between the groups with long COVID and recovered. Among children who developed persistent long COVID symptoms there was a statistically higher percentage of abnormal PT values (53% versus 36.1%, p=0.0432), with no significant differences in other coagulation profile indicators. Abnormal PT along with female gender, comorbidities, especially allergic pathology, nutritional disorder, including obesity, were determined as potential risk factors of the long COVID development (Odds ratio - 2.0611; 95% 1.0179-4.1737, p=0.0445). Conclusions: The study highlights the need for more extensive research into the coagulation profiles of pediatric populations, considering age-specific factors. This could enhance our understanding of thromboinflammation in COVID-19 and its potential contribution to the development of persistent symptoms.

Prognostic gene landscapes and therapeutic insights in sepsis-induced coagulopathy.

BACKGROUND: Sepsis is a common and critical condition encountered in clinical practice that can lead to multi-organ dysfunction. Sepsis-induced coagulopathy (SIC) significantly affects patient outcomes. However, the precise mechanisms remain unclear, making the identification of effective prognostic and therapeutic targets imperative. METHODS: The analysis of transcriptome data from the whole blood of sepsis patients, facilitated the identification of key genes implicated in coagulation. Then we developed a prognostic model and a nomogram to predict patient survival. Consensus clustering classified sepsis patients into three subgroups for comparative analysis of immune function and immune cell infiltration. Single-cell sequencing elucidated alterations in intercellular communication between platelets and immune cells in sepsis, as well as the role of the coagulation-related gene FYN. Real-time quantitative PCR determined the mRNA levels of critical coagulation genes in septic rats' blood. Finally, administration of a FYN agonist to septic rats was observed for its effects on coagulation functions and survival. RESULTS: This study identified four pivotal genes-CFD, FYN, ITGAM, and VSIG4-as significant predictors of survival in patients with sepsis. Among them, CFD, FYN, and ITGAM were underexpressed, while VSIG4 was upregulated in patients with sepsis. Moreover, a nomogram that incorporates the coagulation-related genes (CoRGs) risk score with clinical features of patients accurately predicted survival probabilities. Subgroup analysis of CoRGs expression delineated three molecular sepsis subtypes, each with distinct prognoses and immune profiles. Single-cell sequencing shed light on heightened communication between platelets and monocytes, T cells, and plasmacytoid dendritic cells, alongside reduced interactions with neutrophils in sepsis. The collagen signaling pathway was found to be essential in this dynamic. FYN may affect platelet function by modulating factors such as ELF1, PTCRA, and RASGRP2. The administration of the FYN agonist can effectively improve coagulation dysfunction and survival in septic rats. CONCLUSIONS: The research identifies CoRGs as crucial prognostic markers for sepsis, highlighting the FYN gene's central role in coagulation disorders associated with the condition and suggesting novel therapeutic intervention strategies.

Persistent high sepsis-induced coagulopathy and sequential organ failure assessment scores can predict the 28-day mortality of patients with sepsis: A prospective study.

BACKGROUND: The performance of the sepsis-induced coagulopathy (SIC) and sequential organ failure assessment (SOFA) scores in predicting the prognoses of patients with sepsis has been validated. This study aimed to investigate the time course of SIC and SOFA scores and their association with outcomes in patients with sepsis. METHODS: This prospective study enrolled 209 patients with sepsis admitted to the emergency department. The SIC and SOFA scores of the patients were assessed on days 1, 2, and 4. Patients were categorized into survivor or non-survivor groups based on their 28-day survival. We conducted a generalized estimating equation analysis to evaluate the time course of SIC and SOFA scores and the corresponding differences between the two groups. The predictive value of SIC and SOFA scores at different time points for sepsis prognosis was evaluated. RESULTS: In the non-survivor group, SIC and SOFA scores gradually increased during the first 4 days (P < 0.05). In the survivor group, the SIC and SOFA scores on day 2 were significantly higher than those on day 1 (P < 0.05); however, they decreased on day 4, dropping below the levels observed on day 1 (P < 0.05). The non-survivors showed higher SIC scores on days 2 (P < 0.05) and 4 (P < 0.001) than the survivors, whereas no significant differences were found between the two groups on day 1 (P > 0.05). The performance of SIC scores on day 4 for predicting mortality was more accurate than that on day 2, with areas under the curve of 0.749 (95% confidence interval [CI]: 0.674-0.823), and 0.601 (95% CI: 0.524-0.679), respectively. The SIC scores demonstrated comparable predictive accuracy for 28-day mortality to the SOFA scores on days 2 and 4. Cox proportional hazards models indicated that SIC on day 4 (hazard ratio [HR] = 3.736; 95% CI: 2.025-6.891) was an independent risk factor for 28-day mortality. CONCLUSIONS: The time course of SIC and SOFA scores differed between surviving and non-surviving patients with sepsis, and persistent high SIC and SOFA scores can predict 28-day mortality.

Resuscitation and Care in the Trauma Bay.

Start balanced resuscitation early (pre-hospital if possible), either in the form of whole blood or 1:1:1 ratio. Minimize resuscitation with crystalloid to minimize patient morbidity and mortality. Trauma-induced coagulopathy can be largely avoided with the use of balanced resuscitation, permissive hypotension, and minimized time to hemostasis. Using protocolized "triggers" for massive and ultramassive transfusion will assist in minimizing delays in transfusion of products, achieving balanced ratios, and avoiding trauma induced coagulopathy. Once "audible" bleeding has been addressed, further blood product resuscitation and adjunct replacement should be guided by viscoelastic testing. Early transfusion of whole blood can reduce patient morbidity, mortality, decreases donor exposure, and reduces nursing logistics during transfusions. Adjuncts to resuscitation should be guided by laboratory testing and carefully developed, institution-specific guidelines. These include empiric calcium replacement, tranexamic acid (or other anti-fibrinolytics), and fibrinogen supplementation.

Coagulation and Inflammation in COVID-19: Reciprocal Relationship between Inflammatory and Coagulation Markers.

The coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), formerly known as 2019-nCoV. Numerous cellular and biochemical issues arise after COVID-19 infection. The severe inflammation that is caused by a number of cytokines appears to be one of the key hallmarks of COVID-19. Additionally, people with severe COVID-19 have coagulopathy and fulminant thrombotic events. We briefly reviewed the COVID-19 disease at the beginning of this paper. The inflammation and coagulation markers and their alterations in COVID-19 illness are briefly discussed in the parts that follow. Next, we talked about NETosis, which is a crucial relationship between coagulation and inflammation. In the end, we mentioned the two-way relationship between inflammation and coagulation, as well as the factors involved in it. We suggest that inflammation and coagulation are integrated systems in COVID-19 that act on each other in such a way that not only inflammation can activate coagulation but also coagulation can activate inflammation.

Sepsis-Induced Coagulopathy: A Comprehensive Narrative Review of Pathophysiology, Clinical Presentation, Diagnosis, and Management Strategies.

Physiological hemostasis is a balance between pro- and anticoagulant pathways, and in sepsis, this equilibrium is disturbed, resulting in systemic thrombin generation, impaired anticoagulant activity, and suppression of fibrinolysis, a condition termed sepsis-induced coagulopathy (SIC). SIC is a common complication, being present in 24% of patients with sepsis and 66% of patients with septic shock, and is often associated with poor clinical outcomes and high mortality. 1 , 2 Recent preclinical and clinical studies have generated new insights into the molecular pathogenesis of SIC. In this article, we analyze the complex pathophysiology of SIC with a focus on the role of procoagulant innate immune signaling in hemostatic activation--tissue factor production, thrombin generation, endotheliopathy, and impaired antithrombotic functions. We also review clinical presentations of SIC, the diagnostic scoring system and laboratory tests, the current standard of care, and clinical trials evaluating the efficacies of anticoagulant therapies.

Assessing coagulopathy and endothelial dysfunction in pediatric venous malformation: A thromboelastometry and syndecan-1 study.

OBJECTIVE: The occurrence of unpredictable pain crises are the principal determinant of the quality of life for patients with venous malformations (VM). A definite coagulation phenomenon, characterized by an increase in D-dimer levels and the presence of phleboliths within the malformation, has been previously reported. By applying Virchow's triad and evaluating intralesional samples, our objective is to delineate the coagulation profile and the extent of endothelial dysfunction within the malformation. METHODS: With the authorization of the Ethics Committee, a research project was undertaken on intralesional and extralesional blood samples from 30 pediatric patients afflicted with spongiform VM. Thromboelastometry analyses were performed using ROTEM Sigma, and the concentration of syndecan-1 was determined by ELISA. RESULTS: In the ROTEM analyses, the A5, A10, and maximum clot firmness (MCF) values were below the established reference ranges in the intralesional samples in both the EXTEM and INTEM assays, indicating that intralesional clots had significant instability. Furthermore, during the investigation of the delayed fibrinolysis phase using recombinant tissue plasminogen activator (rtPA) in EXTEM analysis, widespread hyperfibrinolysis was observed intralesional. Additionally, analysis of syndecan-1 showed significant differences between extralesional and intralesional levels (p < .026) and controls (p < .03), suggesting differences in the state of endothelium. CONCLUSIONS: For the first time, we developed a comprehensive understanding of the coagulopathic profile of VM and the role of endothelial dysfunction in its pathogenesis. These findings will enable the implementation of targeted therapies based on the individual coagulation profiles.

Brain-derived extracellular vesicles mediate systemic coagulopathy and inflammation after traumatic brain injury.

Traumatic brain injury (TBI) can induce systemic coagulopathy and inflammation, thereby increasing the risk of mortality and disability. However, the mechanism causing systemic coagulopathy and inflammation following TBI remains unclear. In prior research, we discovered that brain-derived extracellular vesicles (BDEVs), originating from the injured brain, can activate the coagulation cascade and inflammatory cells. In this study, we primarily investigated how BDEVs affect systemic coagulopathy and inflammation in peripheral circulation. The results of cytokines and coagulation function indicated that BDEVs can lead to systemic coagulopathy and inflammation by influencing inflammatory factors and chemokines within 24 h. Furthermore, according to flow cytometry and blood cell counter results, we found that BDEVs induced changes in the blood count such as a reduced number of platelets and leukocytes and an increased percentage of neutrophils, macrophages, activated platelets, circulating platelet-EVs, and leukocyte-derived EVs. We also discovered that eliminating circulating BDEVs with lactadherin helped improve coagulopathy and inflammation, relieved blood cell dysfunction, and decreased the circulating platelet-EVs and leukocyte-derived EVs. Our research provides a novel viewpoint and potential mechanism of TBI-associated secondary damage.

Plasma: indications, controversies, and opportunities.

Plasma is overused as a blood product worldwide; however, data supporting appropriate use of plasma is scant. Its most common utilization is for treatment of coagulopathy in actively bleeding patients; it is also used for coagulation optimization prior to procedures with specific coagulation profile targets. A baseline literature review in PUBMED and Google Scholar was done (1 January 2000 to 1 June 2023), utilizing the following search terms: plasma, fresh frozen plasma, lyophilized plasma, indications, massive transfusion protocol, liver disease, warfarin reversal, cardiothoracic surgery, INR < 2. An initial review of the titles and abstracts excluded all articles that were not focused on transfusional medicine. Additional references were obtained from citations within the retrieved articles. This narrative review discusses the main indications for appropriate plasma use, mainly coagulation factor replacement, major hemorrhage protocol, coagulopathy in liver disease, bleeding in the setting of vitamin K antagonists, among others. The correlation between concentration of coagulation factors and INR, as well as the proper plasma dosing with its volume being weight-based, is also discussed. A high value approach to plasma utilization is supported with a review of the clinical situations where plasma is overutilized or unnecessary. Finally, a discussion of novel plasma products is presented for enhanced awareness.

The Utilisation of INR to identify coagulopathy in burn patients.

Studies conflict on the significance of burn-induced coagulopathy. We posit that burn-induced coagulopathy is associated with injury severity in burns. Our purpose was to characterize coagulopathy profiles in burns and determine relationships between % total burn surface area (TBSA) burned and coagulopathy using the International Normalized Ratio (INR). Burned patients with INR values were identified in the TriNetX database and analyzed by %TBSA burned. Patients with history of transfusions, chronic hepatic failure, and those on anticoagulant medications were excluded. Interquartile ranges for INR in the burned study population were 1.2 (1.0-1.4). An INR of ≥ 1.5 was used to represent those with burn-induced coagulopathy as it fell outside the 3rd quartile. The population was stratified into subgroups using INR levels <1.5 or ≥1.5 on the day of injury. Data are average ± SD analyzed using chi-square; p < .05 was considered significant. There were 7,364 burned patients identified with INR <1.5, and 635 had INR ≥1.5. Comparing TBSA burned groups, burn-induced coagulopathy significantly increased in those with ≥20% TBSA; p = .048 at 20-29% TBSA, p = .0005 at 30-39% TBSA, and p < .0001 for 40% TBSA and above. Age played a significant factor with average age for those with burn-induced coagulopathy 59 ± 21.5 years and 46 ± 21.8 for those without (p < .0001). After matching for age, TBSA, and demographics, the risk of 28 day-mortality was higher in those with burn-induced coagulopathy compared to those without (risk difference 20.9%, p < .0001) and the odd ratio with 95% CI is 4.45 (3.399-5.825). Investigation of conditions associated with burn-induced coagulopathy showed the effect of heart diseases to be significant; 53% of patients with burn-induced coagulopathy had hypertension (p < .0001). Burn-induced coagulopathy increases with %TBSA burned. The information gained firmly reflects a link between %TBSA and burn-induced coagulopathy, which could be useful in prognosis and treatment decisions.