Red cell distribution width and outcome in patients with septic shock.

INTRODUCTION: Red cell distribution width (RDW) is reflective of systemic inflammation. The objective of this study was to investigate the association between RDW (on day 1 of development of septic shock) and mortality. METHODS: A total of 279 patients with septic shock were included. We categorized the patients into quintiles based on RDW as follows: <13.5%, 13.5% to 15.5%, 15.6% to 17.5%, 17.5% to 19.4%, and >19.4%. RESULTS: Red cell distribution width was a strong predictor of hospital mortality with a significant risk gradient across RDW quintiles after multivariable adjustment: RDW 13.5% to 15.5% (odds ratio [OR], 4.6; 95% confidence interval [CI], 1.0-23.4; P = .06); RDW 15.6% to 17.5% (OR, 8.0; 95% CI, 1.5-41.6; P = .01); RDW 17.6% to 19.4% (OR, 25.3; 95% CI, 4.3-149.2; P < .001); and RDW >19.4% (OR, 12.3; 95% CI, 2.1-73.3; P = .006), all relative to patients with RDW <13.5%. Similar significant robust associations were present for intensive care unit mortality. Estimating the receiver-operating characteristic area under the curve (AUC) showed that RDW has very good discriminative power for hospital mortality (AUC = 0.74). The AUC was 0.69 for Acute Physiologic and Chronic Health Evaluation II (APACHE II) and 0.69 for sequential organ failure assessment (SOFA). When adding RDW to APACHE II, the AUC increased from 0.69 to 0.77. CONCLUSIONS: Red cell distribution width on day 1 of septic shock is a robust predictor of mortality. The RDW is inexpensive and commonly measured. The RDW fared better than either APACHE II or SOFA, and the sum of RDW and APACHE II was a stronger predictor of mortality than either one alone.

Giant left ventricular pseudoaneurysm.

Left ventricular (LV) pseudoaneurysm (PS) is an uncommon, often fatal complication associated with myocardial infarction, cardiothoracic surgery, trauma, and, rarely, infective endocarditis. A 28-year-old man with prior history of bioprosthetic mitral valve replacement presented with congestive heart failure and bacteremia with Abiotrophia granulitica. Transesophageal echocardiogram showed bioprosthesis dysfunction, large vegetations, mitral regurgitation, and probable PS. Cardiac and chest CT confirmed a PS communicating with the left ventricle Patient had pulseless electrical activity and died. Autopsy showed a giant PS with layered thrombus and pseudo-endothelialized cavity. Our case highlights the importance of multimodality imaging as an important tool in management of PS.

Coagulopathy does not protect against venous thromboembolism in hospitalized patients with chronic liver disease.

BACKGROUND: It is uncertain whether pathologically prolonged international normalized ratio (INR) seen in chronic liver disease (CLD) protects against venous thromboembolism (VTE). Previous studies reported VTE incidence of 0.5% to 1.9% in patients with CLD. We sought to evaluate VTE incidence among hospitalized patients with CLD according to INR levels. METHODS: This was a retrospective cohort study performed at a tertiary university hospital. We included all adult patients admitted with a primary diagnosis of CLD over a 7-year period. The primary outcome was the development of VTE during hospital stay. Patients were divided into quartiles according to their highest admission INR. VTE events and prophylaxis rates were compared among INR quartiles. RESULTS: During the allotted 7-year period, we included 190 patients. Of these, 12 developed VTE events, yielding a VTE incidence of 6.3%. There was no significant difference in the incidence of VTE between INR quartiles. Hospital mortality rates were higher in the higher INR quartiles than in the lower ones (P < .001), but hospital length of stay was not significantly different. Of the patients with documented VTE, one (4.2%) was Child-Pugh stage A, three (4.6%) were stage B, and eight (8.0%) were stage C (P = .602). VTE prophylaxis was not used in 75% of patients. CONCLUSIONS: An elevated INR in the setting of CLD does not appear to protect against the development of hospital-acquired VTE. The notion that "auto-anticoagulation" protects against VTE is unfounded. Use of DVT prophylaxis was extremely low in this population.