Ischemic Toe Ulceration Due to Foreign Body Embolus From Hydrophilic Polymer-Coated Intravascular Device.

Hydrophilic polymer coatings are now widely applied to catheters and other intravascular devices used in neurovascular, cardiovascular, and peripheral vascular procedures. Emboli consisting of these materials have been previously identified in biopsies and autopsies following pulmonary infarction, stroke, gangrene, or death. We report a case involving a nonhealing foot ulcer that appeared following cardiac catheterization, stenting, and automatic implanted cardiac defibrillator (AICD) implantation in a patient without other evidence of significant peripheral artery disease. An 85-year-old woman with chronic atrial fibrillation, aortic valve stenosis, and coronary artery disease underwent coronary stenting and AICD implantation for ventricular tachycardia and syncope. She developed a toe ulcer shortly thereafter, which did not respond to standard treatment. A histological examination following amputation of the toe found amorphous basophilic material in capillaries adjacent to the edge of the ulcer, which was similar to material associated with hydrophilic polymer coatings. Ischemia and infarcts following endovascular procedures should not be presumed to result from thrombus or vascular disease, even if intravascular devices appear intact or properly placed after the procedure. To help establish the incidence of ischemia caused by hydrophilic polymer device coatings, if excision of ischemic or infarcted tissue after endovascular procedures using coated devices becomes necessary, the tissue should be evaluated microscopically. Surgeons should also consider the tolerance of distal organs to infarct or ischemia when selecting coated intravascular devices.

Hemosiderosis is associated with accelerated decompensation and decreased survival in patients with cirrhosis.

AIM: Although hepatic iron deposition unrelated to hereditary hemochromatosis is commonly observed in cirrhosis, its clinical significance is unclear. The aim of this study was to examine the outcomes of cirrhotic patients with and without hemosiderosis. METHODS: Patients with an initial liver biopsy demonstrating cirrhosis between January 1993 and December 1997 were identified using the Department of Pathology database. Based on iron staining, patients were characterized as siderotic or nonsiderotic. Charts were reviewed to determine outcomes. RESULTS: Siderotic patients had significantly higher Child-Pugh (CP) and model for end-stage liver disease (MELD) scores. Their median survival without transplant was 23 months vs. 85 months in the nonsiderotics (P<0.0001, confidence interval: 95%). On univariate analysis, siderosis was associated with a hazard ratio of 2.74 (P<0.0001). On multivariate analysis, the effect of siderosis was reduced but remained significant after correction for the CP or MELD score (hazard ratios 1.82 and 2.06, P=0.05 and 0.02, respectively). Child's A cirrhotics with hemosiderosis decompensated more rapidly and had shorter median survival than those without siderosis (P=0.007 and P=0.01, respectively). CONCLUSIONS: The presence of siderosis is associated with more advanced liver dysfunction. Even when the effects of baseline liver function are taken into account, siderosis is associated with decreased survival and more rapid decompensation in cirrhosis.

Detection of factor V leiden and prothrombin gene mutations in patients who died with thrombotic events.

CONTEXT: Individuals with factor V or prothrombin gene mutations are at increased risk for thrombotic events. Furthermore, the risk of recurrent deep venous thrombosis in heterozygous carriers of both factor V Leiden and prothrombin gene mutations is high enough that some investigators suggest lifelong warfarin prophylaxis for these individuals, even with a single spontaneous thrombotic event. OBJECTIVES: To assess the incidence of factor V Leiden and prothrombin gene mutations in an autopsy population and to determine if these tests can prove useful in identification of at-risk family members. DESIGN: We analyzed factor V Leiden and prothrombin gene mutations in 45 patients who died with or of thrombotic events, using archival tissue and multiplex allele-specific polymerase chain reaction amplification. The wild-type factor V gene was amplified in all 45 patients, whereas the wild-type prothrombin gene was amplified in 29 patients. RESULTS: Two patients (4.4%) who died with thrombotic events at the ages of 35 and 92 years were heterozygous for factor V gene mutation. Two additional patients (6.7%), who died with thrombotic events at the ages of 26 and 39 years, were heterozygous for prothrombin gene mutation. Patients homozygous for either factor V or prothrombin gene or simultaneously heterozygous for both genes were not detected in our study. CONCLUSIONS: Our findings suggest that screening the relatives of elderly patients who die with thrombotic events would not be cost-effective because of the low incidence of these mutations in the autopsy population. However, because the incidence of these mutations appeared significantly more frequently among individuals who died at 39 years or younger, testing the relatives of this subset of patients may prove useful for detection of at-risk individuals who would benefit from preventive anticoagulation therapy.