BACKGROUND:Venous Thromboembolism (VTE) is a serious complication after free tissue transfer to the head and neck (H&N). However, an optimal antithrombotic prophylaxis protocol is not defined in the literature. Enoxaparin 30 mg twice daily (BID) and heparin 5000 IU three times daily (TID) are among the most commonly used regimens for chemoprophylaxis. However, no studies compare these two agents in the H&N population. METHODS:A cohort study of patients who underwent free tissue transfer to H&N from 2012 to 2021 and received either enoxaparin 30 mg BID or Heparin 5000 IU TID postoperatively. Postoperative VTE and hematoma events were recorded within 30 days of index surgery. The cohort was divided into two groups based on chemoprophylaxis. VTE and hematoma rates were compared between the groups. RESULTS:Out of 895 patients, 737 met the inclusion criteria. The mean age and Caprini score were 60.6 [SD 12.5] years and 6.5 [SD 1.7], respectively. 234 [31.88%] were female. VTE and hematoma rates among all patients were 4.47% and 5.56%, respectively. The mean Caprini score between the enoxaparin (n = 664) and heparin (n = 73) groups was not statistically significant (6.5 ± 1.7 vs.6.3 ± 1.3, p = 0.457). The VTE rate in the enoxaparin group was significantly lower than in the heparin group (3.9% vs. 9.6%; OR: 2.602, 95% CI: 1.087-6.225). Hematoma rates were similar between the two groups (5.5% vs. 5.6%; OR: 0.982, 95% CI: 0.339-2.838). CONCLUSIONS:Enoxaparin 30 mg BID was associated with a lower VTE rate while maintaining a similar hematoma rate compared to heparin 5000 units TID. This association may support the use of enoxaparin over heparin for VTE chemoprophylaxis in H&N reconstruction.

BACKGROUND:Intravascular large B-cell lymphoma (IVLBCL) is a rare subtype of extranodal B-cell lymphoma, which has traditionally been associated with poor outcomes. Despite increasing recognition, IVLBCL requires a high degree of clinical suspicion on the part of the clinician for its diagnosis.CASE SERIES:We present four patient cases: A 69-year-old female with constitutional symptoms and cognitive decline; a 78-year-old female with kidney injury and constitutional symptoms whose disease rapidly progressed to multiorgan failure and death; a 70-year-old asymptomatic female with an incidentally found, enlarged thyroid; and a 63-year-old male with cytopenia and constitutional symptoms. Retrospective chart analysis was performed on these four patients diagnosed with IVLBCL at our Institute to identify the pathognomonic features of the disease and compare these to the published evidence. IVLBCL has a heterogeneous presentation, as seen in our four patients. The disease is characterized by the exclusive presence of malignant cells inside the blood vessels and lack of organ infiltration. Traditional preliminary diagnostic modalities such as imaging are usually inconclusive, given the paucity of lymphomatous aggregates. A bone marrow biopsy, random skin biopsies, or a focal organ biopsy in appropriate cases is required for diagnosis. Immunosuppression might play a role in the pathogenesis. Timely initiation of aggressive cancer-directed therapy was associated with improved outcomes. Monitoring for disease response and relapse continues to be a challenge.CONCLUSION:Our mini-series highlights the significance of timely diagnosis and intervention in IVLBCL and emphasizes the importance of further research to determine its association with immunosuppression.

Background Existing evidence indicates Black patients have higher incidence of pulmonary embolism (PE) and PE‐related mortality compared with other races/ethnicities, yet disparities in presenting severity and treatment remain incompletely understood. Methods and Results We retrospectively queried a multihospital healthcare system for all hospitalizations for acute PE (2012–2019). Of 10 329 hospitalizations, 8743 met inclusion criteria. Black patients (14.3%) were significantly younger (54.6±17.8 versus 63.1±16.6 years; P<0.001) and more female (56.1% versus 51.6%; P=0.003) compared with White patients. Using ordinal regression, Black race was significantly associated with higher PE severity after matching 1:3 on age and sex (1210:3264; odds ratio [OR], 1.08; 95% CI, 1.03–1.14), adjusting for clinical (OR, 1.13; 95% CI, 1.01–1.27), and socioeconomic (OR, 1.05; 95% CI, 1.05–1.35) characteristics. Among intermediate and high‐severity PE, Black race was associated with a decreased risk of intervention controlling for the competing risk of mortality and censoring on hospital discharge. This effect was modified by PE severity (P value <0.001), with a lower and higher risk of intervention for intermediate and high‐severity PE, respectively. Race was not associated with in‐hospital mortality (OR, 0.84; 95% CI, 0.69–1.02). Conclusions Black patients hospitalized with PE are younger with a higher severity of disease compared with White patients. Although Black patients are less likely to receive an intervention overall, this differed depending on PE severity with higher risk of intervention only for life‐threatening PE. This suggests nuanced racial disparities in management of PE and highlights the complexities of healthcare inequalities.

Anti-factor Xa (anti-Xa) monitoring of unfractionated heparin (UFH) is associated with less time to achieve therapeutic anticoagulation compared to the activated partial thromboplastin time (aPTT). However, it is unknown whether clinical outcomes differ between these methods of monitoring. The aim of this research was to compare the rate of venous thrombosis and bleeding events in patients that received UFH monitored by anti-Xa compared to the aPTT. A retrospective review of electronic health records identified adult patients that received UFH given intravenously (IV) for ≥2 days, with either anti-Xa or aPTT monitoring at an academic tertiary care hospital. This was a pre/post study design conducted between January 1 to December 30, 2014 (aPTT), and January 1 to December 30, 2016 (anti-Xa). All UFH adjustments were based on institutional nomograms. The primary outcome was venous thrombosis and the secondary outcome was bleeding, both of which occurred between UFH administration and discharge from the index hospitalization. A total of 2500 patients were in the anti-Xa group and 2847 patients aPTT group. Venous thrombosis occurred in 10.2% vs 10.8% of patients in the anti-Xa and aPTT groups, respectively (P = .49). Bleeding occurred in 33.7% vs 33.6% of patients in the anti-Xa and aPTT groups, respectively (P = .94). Anti-Xa monitoring was not an independent predictor of either outcome in multivariate logistic regression analyses. Our study found no difference in clinical outcomes between anti-Xa and aPTT-based monitoring of UFH IV.

INTRODUCTION:Performing therapeutic plasma exchange (TPE) with albumin replacement decreases coagulation factor and platelet levels. No defined guidelines exist regarding laboratory testing to assess hemostasis in patients undergoing TPE. MATERIALS AND METHODS:A survey to evaluate hemostasis testing with TPE was distributed using online survey software. One response per institution was analyzed based on a hierarchical algorithm, excluding membrane filtration users, resulting in a maximum of 120 respondents per question. Descriptive analysis was performed with results reported as the number and/or frequency (%) of respondents to each question. RESULTS:The practices represented vary by institution type, number of apheresis procedures per year, and performance of TPE on children. Prior to TPE planned with albumin replacement, many respondents obtain laboratory studies for almost all patients (54.9% outpatients and 68.7% inpatients); however, some do not routinely obtain laboratory studies (9.7% outpatients and 4.4% inpatients). Hemoglobin/hematocrit, platelet count, fibrinogen, partial thromboplastin time (aPTT), and international normalized ratio (INR) are obtained prior to all TPE by 62.5%, 53.4%, 31.0%, 18.1%, and 17.7% of respondents, respectively; however, 1.0%, 8.7%, 29.0%, 38.3%, and 35.4%, respectively, do not routinely obtain these studies. Variation was observed in laboratory threshold values for action; the most common reported were hemoglobin/hematocrit <7 g/dL or 21% (31.0%), platelet count <50 × 109 /L (24.1%), fibrinogen <100 mg/dL (65.3%), aPTT >reference range and >1.5 times reference range (tied, 28.1%), and INR >1.5 (20.7%). CONCLUSIONS:Practice variation exists in hemostasis laboratory testing and threshold values for action with TPE. Further studies are needed to determine optimal hemostasis testing strategies with TPE.

Background: Little data exist on the use of direct oral anticoagulant (DOAC) factor Xa inhibitors for submassive pulmonary embolism (PE) after catheter-directed thrombolysis (CDT). The objective of this evaluation was to determine whether the transition from parenteral anticoagulation to DOACs for submassive PE after CDT would decrease hospital length of stay (LOS) compared to warfarin. Methods: A retrospective review of patients diagnosed with submassive PE who underwent CDT was conducted from January 1, 2012, to February 28, 2017. Hospital LOS and major and minor bleeding events were recorded during hospitalization and at 90 days. Results: Sixty-two patients met the inclusion criteria, 36 in warfarin group and 26 in the DOAC group. Overall, patients receiving rivaroxaban or apixaban had a shorter median hospital LOS compared to warfarin (4.0 vs 6.1 days, P = .002). In the multivariate regression analysis, administration of DOAC was an independent predictor of decreased hospital LOS, β: −2.1, 95% confidence interval (−3.5 to −0.7). Conclusion: Among patients with submassive PE, initiation of a DOAC shortly after CDT may result in a decreased hospital LOS compared to parenterally bridged warfarin.

The purpose of this study was to compare the performance of anti-factor Xa concentration versus activated partial thromboplastin time (aPTT) monitoring with multiple indication-specific heparin nomograms. This was a prospective, nonrandomized study with historical control at a large academic medical center. A total of 201 patients who received intravenous heparin in the cardiology units were included. The prospective cohort included patients (n = 101) with anti-factor Xa (anti-Xa) monitoring, and the historical control group included patients (n = 100) who had aPTT monitoring. Patients in the prospective group had both anti-Xa and aPTT samples drawn, but anti-Xa was used for dosing adjustment. The anti-Xa cohort achieved a significantly faster time to therapeutic range (P < .01) and required fewer dose adjustments per 24-hour period compared to the aPTT control (P = .01). Results were consistent across heparin nomograms. The overall discordance rate between the 2 tests was 49%. No significant differences in clinical outcomes were observed. In summary, anti-Xa monitoring improved the time to therapeutic anticoagulation and led to fewer dose adjustments compared to the aPTT with multiple indication-based heparin nomograms.

The present study extends our previous investigation of circulating antibody/fibrinogen/C1q complexes (FgIgC) associated with thrombosis in a heterophenotypic AαR16C proband, by focusing on the molecular and functional characteristics of the FgIgC, isolated by cryoprecipitation, FgIgC components were demonstrated by SDS-PAGE and by rotary shadowing electron microscopy. Affinity chromatography was used to isolate IgG and fibrinogen from FgIgC. Thrombin-induced clots were examined by scanning electron microscopy and turbidity measurements. IgG/fibrinogen binding was measured by ELISA. Fibrinogen Aα1-19 peptides, cleaved by thrombin from fragment N-DSK, were examined by mass spectrometry. Clot stiffness, platelet release of P-selectin, and fibrinogen self-assembly were assessed by thromboelastography, flow cytometry, and atomic force microscopy, respectively. The FgIgC effects included the following: increased P-selectin release from gel-sieved platelets, finer fiber networks and decreased stiffness of its clots, and marked inhibition of fibrinogen self-assembly. The abnormal proband fibrinogen structure displayed phosphorylated AαR16C-AαR16C homodimers and AαR16C-glutathione heterodimers. ELISA measurements disclosed pronounced binding by proband fibrinogen to proband IgG, which was blocked by the IgG's Fab fragment and by proband, but not by normal plasmic fragment E1. There was appreciable, but much weaker, binding to normal fibrinogen, to its fragments E1, and D1, and to homodimeric AαR16C fibrinogen. The antibody's primary target epitope included heterodimeric AαR16C-glutathione; a secondary epitope resided in the D region. Moreover, both the enhanced platelet activation (i.e. increased P-selectin release induced by FgIgC) and the highly phosphorylated FpA (i.e. resulting in its accelerated release by thrombin) may have contributed to the thrombotic diathesis.

Introduction: Heparin-induced thrombocytopenia (HIT) is a rare diagnosis, however commonly tested. We hypothesize that the 4T score, a diagnostic tool to diagnose HIT, is underutilized by clinicians. This may subsequently lead to unnecessary testing for HIT, administration of costly alternative anticoagulants, and mislabeling of heparin as allergy. We present preliminary data of our quality improvement study. Our aim was to analyze patients previously labeled with heparin allergy and analyze the 4T's scores, optical density values (OD), and serotonin release assay (SRA) results.

Prothrombin complex concentrates (PCCs) are indicated for urgent reversal of warfarin and used for reversal of novel oral anticoagulants, in patients with acute major bleeding or need for an urgent procedure. The research goal was to evaluate effectiveness and safety outcomes with PCC usage at our institution. A retrospective review of electronic medical records identified patients that received a PCC commercially available in the United States (KCentra ® or Profilnine ® ) at twelve hospitals in a tertiary care health system from July 1, 2013 to April 30, 2014. A total of 193 patients received PCC, of which 184 patients received four-factor PCC. The patient population was 48 % male and 75 % Caucasian, with a mean age of 73 years old. Clinical outcomes of interest included time to achieve a target INR ≤1.3, time to Hgb >7 g/dL, and incidence of thromboembolism. A total of 143 patients were on warfarin (74.1 %) at baseline, whereas 18 patients (9.3 %) were taking a novel anticoagulant. Target INR of ≤1.3 was achieved in 125 patients (65.8 %), within a median time of 8.03 h (IQR 3.38–34.07). Among patients with a baseline Hgb <7 g/L ( n = 13), the median time to Hgb >7 g/dL was 8.48 h (IQR 6.95–13.00). Eight patients (4.1 %) developed an acute venous thromboembolism following PCC administration. INR reversal was achieved in approximately two-thirds of patients, with a low incidence of venous thromboembolism. Four-factor PCC is a viable alternative to plasma.

Introduction: Deep vein thrombosis (DVT) is an important cause of the morbidity and mortality in the United States (US). National estimates of 30-day readmissions in DVT patients in the US are unknown. The objective of our study was to estimate readmission rates and identify causes, predictors and cost of readmissions in DVT patients.

Introduction: Pulmonary Embolism (PE) is an important cause of the morbidity and mortality in the United States (US). National estimates of 30-day readmissions in PE patients in the US are unknown. The objective of our study was to estimate readmission rates and identify causes, predictors and cost of readmissions in PE patients.

Rectus sheath hematoma (RSH) develops due to rupture of epigastric arteries or the rectus muscle. Although RSH incidence rate is low, it poses a significant diagnostic dilemma. We evaluated the risk factors for RSH, its presentation, management, and outcomes for 115 patients hospitalized with confirmed RSH by computed tomography scan between January 2005 and June 2009. More than three-fourth (77.4%) of the patients were on anticoagulation therapy, 58.3% patients had chronic kidney disease (CKD) stage ≥3, 51.3% had abdominal injections, 41.7% were on steroids/immunosuppressant therapy, 37.4% had abdominal surgery/trauma, 33.9% had cough, femoral puncture was performed in 31.3% of patients, and 29.5% were on antiplatelet therapy. Rectus sheath hematoma was not an attributable cause in any of the 17 deaths. Mortality was significantly higher in patients with CKD stage ≥3 ( P = .03) or who required transfusion ( P = .007). Better understanding of RSH risk factors will facilitate early diagnoses and improve management.

In this retrospective study; we evaluate the effects of heparin therapy on hexagonal lipid neutralization test. We identified 8000 patients in our hospital system that had been evaluated for lupus anticoagulants. Among these patients we found 100 patients who had been evaluated for lupus anticoagulants while they were on and off unfractionated (UFH) heparin. 23% had positive result of hexagonal lipid neutralization test before receiving heparin while 59% had positive result of hexagonal lipid neutralization test after receiving heparin. We conclude that there is an association between heparin therapy and positive result of hexagonal lipid neutralization test.

Venous thromboembolism (VTE) is an important cause of morbidity and mortality in the United States (US). The increasing rates of VTE in the US resulted in the surgeon general issuing a call to action to reduce VTE in 2008. The objective of our study was to analyze the national trends of inpatient VTE in the US from 2004 to 2013 (5 years before and after 2008). We used the dataset National Inpatient Sample, Healthcare Cost and Utilization Project and measured trends of inpatient VTE by annual % change using joinpoint regression software. From 2004 to 2013 the National Inpatient Sample contained data on 78 million hospitalizations (weighted n = 385 million). In these 1.6 million had a diagnosis of VTE (2.0%, weighted n = 7.7 million) including 1.2 million with deep venous thrombosis (DVT) (1.53%, weighted n = 5.9 million) and 588,878 with pulmonary embolism (PE) (0.74%, weighted n = 2.8 million). Joinpoint regression analysis showed that rates of DVT and PE are increasing consistently from 2004 to 2013(1.27% to 1.80% for DVT and 0.52% to 0.92% for PE). The increasing rates of DVT and PE were consistent in all subgroups except few exceptions. In conclusion inpatient VTE rates continue to rise even after 5 years from the surgeon general's a call to action except in certain high-risk patients. Further research is needed to curb the VTE in patients especially among those perceived to be at lower risk of VTE. (C) 2019 Elsevier Inc. All rights reserved.

In this retrospective study; we evaluate cardiac disorders and systemic hypertension in JAK2 V617F positive patients. We identified 1000 patients in our hospital system that had been evaluated for JAK2 V617F mutation. Among these patients we found 100 JAK2 V617F positive patients and 100 JAK2 V617F negative patients matched by age and gender. Cardiac disorders were characterized as coronary artery disease (CAD), atrial fibrillation (Afib), heart failure (HF), and myocardial infarction (MI). As well as cardiac disorders and systemic hypertension (HTN), we considered the other thrombotic events such as stroke, deep vein thrombosis (DVT), pulmonary embolism (PE) and peripheral arterial disease (PAD). We conclude that there is an association between JAK2 V617F mutation and HTN, CAD, DVT, PAD, HF and Afib.

Schistocytes are associated with micro angiopathic hemolytic processes. In this retrospective study; we evaluate the association of schistocytosis in the peripheral blood smear of patients before and after dialysis. We identified 7000 patients in our hospital system that underwent dialysis. The peripheral blood smears of 153 who were evaluable for the presence of schistocytosis prior to and after dialysis. Ninety seven patients had alternative reasons to have schistocytosis. Among the remaining 50 patients, 14% had schistocytes present prior to begin dialysis and 86% after one or more dialysis episodes. We conclude that the presence of schistocytes in the peripheral blood prior to dialysis is likely due to the underlying cause of renal impairment or other co-morbidity. However, upon initiation of dialysis the proportion of patients with schistocytosis is markedly increased and is likely due to the fragmentation of red cells during the dialysis procedure.

Abstract Background: Venous thromboembolism (VTE) is an important cause of morbidity and mortality in patients with hematologic malignancies (HMs). The national burden of inpatient VTE in patients with HMs is not known. Methods: We used the National Inpatient Sample (NIS), one of the largest publicly-available inpatient dataset in United States (U.S.), which represents a 20% stratified random sample of discharges from all hospitals, excluding rehabilitation and long-term acute care hospitals. The NIS is drawn from all States participating in Healthcare Cost and Utilization Project, representing more than 95 percent of the U.S. population. Discharge weights are used to generate national estimates. Patients with HMs were identified using ICD9 codes published by NIS and VTE was defined by ICD9 codes 451 - 453 and 415.1. Annual rates of inpatient VTE were calculated from 1993 to 2012 by HM type. Multivariate odds of inpatient VTE was determined by logistic regression controlling for confounders (age, sex, Charlson co-morbidity index, metastasis, chemotherapy, transfusion of blood products, major operating room procedure, primary hypercoagulable state, disseminated intravascular coagulation, heparin induced thrombocytopenia and thrombosis, antiphospholipid syndrome, obesity and calendar year). The malignancies with non-specific designation (e.g. unspecified leukemia) or with less than 1000 patients (weighted number) were excluded from results. Results: 8.42million hospitalized patients (weighted number) with HMs were identified, and 335,240had VTE (3.98%). In patients with HMs, rates of inpatient VTE increased from 2.59% to 5.22% between 1993 and 2012 (p<0.01). A detailed analysis of VTE rates for various HMs is presented in Table 1. The HMs with highest odds of inpatient VTE are peripheral T-cell lymphoma (PTCL), anaplastic large cell lymphoma (ALCL) and primary central nervous system (CNS) lymphoma (OR 1.56, 1.53, and 1.39, p<0.05) as compared to all other HM. Among leukemias, hairy cell leukemia had higher odds of VTE (OR 1.19, p<0.05). The HMs with the least odds of VTE were acute lymphoid leukemia, chronic monocytic leukemia and plasma cell leukemia (OR 0.65, 0.66 and 0.71, p<0.05). The HMs with the highest rates of VTE were PTCL, large cell lymphoma and ALCL (6.96%, 6.35% and 6.27%). The HMs with lowest rate of VTE were megakaryocytic leukemia, acute lymphoid leukemia and acute monocytic leukemia (1.42%, 2.04%, and 2.73%). Conclusions: Our study provides national estimates of inpatient VTE in HM, which are increasing over the last 20 years. Certain HMs have higher rates and odds of VTE as compared to others. Identification of these differences provides valuable information for the use of prophylaxis in HM with high risk of VTE. Table 1. Multivariate Odds and Rates of Inpatient Venous Thromboembolism in Patients with Hematologic Malignancies (Total weighted N = 8.42 million) Hematologic malignancy Inpatient VTE rate (%) Adjusted OR (95% CI) of inpatient VTE compared to all other HM Hodgkin's disease Hodgkin's disease - lymphocyte rich 3.86 1.15 (0.82 - 1.61) Hodgkin's disease - nodular sclerosing 4.04 1.3 (1.18 - 1.43) Hodgkin's disease - mixed cellularity 4.02 1.22 (0.89 - 1.68) Hodgkin's disease - lymphocyte depleted 3.88 1.14 (0.73 - 1.77) Non-hodgkin's lymphoma Nodular lymphoma 4.89 1.2 (1.13 - 1.28) Mycosis fungoides 4.83 1.25 (1.16 - 1.35) Sezary's disease 3.99 1.08 (0.72 - 1.62) Peripheral t-cell lymphoma 6.96 1.56 (1.32 - 1.85) Burkitt's lymphoma 3.44 1.05 (0.97 - 1.15) Marginal zone lymphoma 5.57 1.07 (0.91 - 1.26) Mantle cell lymphoma 4.91 1.03 (0.92 - 1.15) Primary CNS lymphoma 6.18 1.39 (1.18 - 1.64) Anaplastic large cell lymphoma 6.27 1.53 (1.21 - 1.94) Large cell lymphoma 6.35 1.36 (1.22 - 1.51) Sarcoma Myeloid sarcoma 4.24 1.14 (0.9 - 1.44) Myeloma and leukemia Multiple myeloma 4.57 1.14 (1.1 - 1.18) Plasma cell leukemia 2.85 0.71 (0.5 - 1) Lymphoid leukemia - acute 2.04 0.65 (0.61 - 0.69) Lymphoid leukemia - chronic 3.43 0.76 (0.73 - 0.78) Myeloid leukemia - acute 3.71 0.97 (0.93 - 1) Myeloid leukemia - chronic 2.93 0.72 (0.68 - 0.76) Monocytic leukemia - acute 2.73 0.75 (0.59 - 0.96) Monocytic leukemia - chronic 2.74 0.66 (0.44 - 0.98) Erythrocytic leukemia - acute 2.95 0.81 (0.5 - 1.32) Megakaryocytic leukemia 1.42 0.48 (0.23 - 1.02) Hairy cell leukemia 4.72 1.19 (1.07 - 1.32) Disclosures No relevant conflicts of interest to declare.