Management of Coagulation and Anticoagulation in Liver Transplantation Candidates.

Hemostasis is a complex balance of clot formation and dissolution that is largely modulated by protein synthesis and degradation in the liver. In the state of end-stage liver disease, there is a disruption of the hemostatic system due to hepatic protein synthetic dysfunction. Because historical clinical laboratory testing often only analyzes a portion of the hemostasis system, the clinician may be misled into believing that cirrhosis patients are imbalanced with a tendency toward bleeding. The modern understanding of hemostasis in cirrhosis involves a rebalance of hemostasis with a tenuous equilibrium between clotting and bleeding, but an equilibrium nonetheless. The clinician should be aware of this rebalance and not depend on limited and flawed laboratory testing in making judgments about the tendency for bleeding or clotting based on these values alone. Prophylactic protocol transfusions including large doses of fresh frozen plasma to "correct" the international normalized ratio are good examples of ineffective and potentially harmful interventions based on an outdated understanding of hemostasis in cirrhosis. Conversely, a thrombotic state is increasingly recognized in patients with cirrhosis, and conditions such as portal vein thrombosis are now becoming important therapeutic targets in many liver transplantation (LT) candidates and other patients with chronic liver disease. This article will introduce the reader to the modern understanding of hemostasis in cirrhosis, describe the common pitfalls and opportunities in treating hemostasis system abnormalities in the LT candidate particularly in regards to preprocedural prophylactic transfusions, and discuss therapeutic targets and interventions for thrombotic complications in the end-stage liver disease population.

Differentiating Clostridium difficile Colitis from Clostridium difficile Colonization in Ulcerative Colitis: A Role for Procalcitonin.

BACKGROUND/AIMS: Clostridium difficile infection (CDI) frequently complicates ulcerative colitis (UC) and can mimic disease flare. Differentiating UC flare from CDI remains a clinical challenge, particularly due to C. difficile colonization. Procalcitonin (PCT) is a serum biomarker for bacterial infections. We hypothesized that PCT would differentiate acute CDI from UC flare and C. difficile colonization. METHODS: A single-center prospective cohort study was conducted from 2013 to 2016. All UC patients with a stool sample for C. difficile testing were eligible. A total of 117 patients were enrolled, while 20 were excluded. Chart review was performed. RESULTS: Among 27 patients with CDI, median PCT was 60.7 (range 26-560.6) pg/mL, while among 90 patients without CDI, median PCT was 56.7 (range 25.1-2,252) pg/mL (p = 0.9). It was found that 14 patients with CDI responded completely to C. difficile treatment (CDI-R), while 8 patients did not and were diagnosed with UC flare (CDI-NR). For CDI-R, median PCT was 104.5 (range 26.3-560.6), compared to 40.3 (range 26.0-116.3) for CDI-NR (p = 0.036). CONCLUSIONS: In UC patients presenting with diarrhea, serum PCT was not significantly higher in UC patients with positive C. difficile testing. However, PCT was significantly elevated in CDI-R versus CDI-NR, suggesting that PCT may have utility in making this discrimination.

Evaluation of the Patient with Markedly Abnormal Liver Enzymes.

Liver enzyme tests are very commonly ordered by physicians, and when they return as abnormal, they can pose a clinical challenge to the provider. Markedly abnormal liver enzymes indicate severe hepatic injury and require immediate evaluation. There are various causes for abnormal liver tests, including infectious, autoimmune, genetic, metabolic, drug, and vascular causes. An understanding of the patterns of aminotransferase and alkaline phosphatase elevations is useful in narrowing the differential diagnosis. A thorough history and physical examination, appropriate blood testing, and imaging are typically key to evaluating the patient with abnormal liver enzymes.

Endoscopic Balloon Dilation Size and Avoidance of Surgery in Stricturing Crohn's Disease.

BACKGROUND: Endoscopic balloon dilation (EBD) is an effective method for treating stricture-related obstruction in Crohn's disease. We aimed to identify factors predictive of successful avoidance of surgery, including endoscopic features, in patients undergoing balloon dilation. METHODS: We performed a retrospective review of patients with symptomatic Crohn's disease-related intestinal strictures undergoing EBD. Clinical, medication use, laboratory, and dilation data, including the minimum and maximum balloon sizes used, and number of balloons used per endoscopic session were collected. Multivariate analysis by Cox proportional hazard regression was used to model future surgical bowel resection. RESULTS: In a total of 135 subjects undergoing 292 dilations, multivariate modeling demonstrated that failure to achieve a maximum dilation of 14 mm or more increased the risk of surgery (hazard ratio [HR] 2.88, 95% confidence limit [CL], 1.10-7.53). Although there was no difference in the risk of future surgery between maximum EBD sizes of 14 to 15 mm and 16 to 18 mm, those reaching 16 to 18 mm exhibited a longer interval between subsequent dilations (mean 240 ± 136.7 versus 456 ± 357.3 d, respectively, P = 0.023). Endoscope passage at index dilation was not predictive of future surgery (HR 0.63, 95% CL, 0.31-1.26). Adjusting for covariates of EBD size, stricture location and type, a C-reactive protein >1.5 mg/dL (HR 2.60, 95% CL, 1.12-5.94), and anti-tumor necrosis factor initiation after index EBD (HR 2.39, 95% CL, 1.09-5.25) increased the risk of future surgery. CONCLUSIONS: Although dilation calibers larger than 14 to 15 mm were not more protective against future surgery, those reaching 16 to 18 mm underwent maintenance dilation less frequently. The risk of surgery associated with post-EBD anti-tumor necrosis factor initiation suggests that effective therapy is often used too late in the disease course.