Mesenteric ischemia caused by heparin-induced thrombocytopenia

Ahmed M, et al. Mesenteric Ischemia Caused by Heparin-induced Thrombocytopenia: A Case Report. Cureus. 2019 Jan 16;11(1):e3900.

“The incidence of HIT incidence is 0.1% – 5% in patients receiving heparin with 35% – 50% of those patients developing thrombosis. It should always be suspected in patients receiving heparin who develop a new onset thrombocytopenia with platelet counts are less than 150,000, or there is a drop of 50% or more in the platelet count, venous or arterial thrombosis, skin necrosis at the site of the injection, and if the patient develops acute systemic reactions after intravenous (IV) administration of heparin (fever, chills, tachycardia, hypertension, dyspnea, cardiopulmonary arrest). Antibody formation typically requires four or more days of exposure to heparin and presents with a dropping platelet count within five to 14 days. HIT is subdivided into two subtypes: HIT Type I (none immune and usually resolves spontaneously in few days) and HIT Type II which is immune-mediated (immunoglobulin G (IgG) antibody against heparin-platelet factor 4 (PF4) complex) resulting in excessive thrombin generation that leads to venous or arterial thrombosis [5].

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Mortality and treatment outcome following surgical interventions for acute mesenteric ischemia.

Beaulieu RJ, et al. Comparison of open and endovascular treatment of acute mesenteric ischemia. J Vasc Surg. 2014 Jan;59(1):159-64. Erratum in: J Vasc Surg. 2014 Jul;60(1):273.

Full-text for Emory users.

Results: Of 23,744 patients presenting with AMI, 4665 underwent interventional treatment from 2005 through 2009. Of these patients, 57.1% were female, and the mean age was 70.5 years. A total of 679 patients underwent vascular intervention; 514 (75.7%) underwent open surgery and 165 (24.3%) underwent endovascular treatment overall during the study period. The proportion of patients undergoing endovascular repair increased from 11.9% of patients in 2005 to 30.0% in 2009. Severity of comorbidities, as measured by the Charlson index, did not differ significantly between the treatment groups. Mortality was significantly more commonly associated with open revascularization compared with endovascular intervention (39.3% vs 24.9%; P = .01). Length of stay was also significantly longer in the patient group undergoing open revascularization (12.9 vs 17.1 days; P = .006). During the study time period, 14.4% of patients undergoing endovascular procedures required bowel resection compared with 33.4% for open revascularization (P < .001). Endovascular repair was also less commonly associated with requirement for TPN support (13.7% vs 24.4%; P = .025).

Conclusions: Endovascular intervention for AMI had increased significantly in the modern era. Among AMI patients undergoing revascularization, endovascular treatment was associated with decreased mortality and shorter length of stay. Furthermore, endovascular intervention was associated with lower rates of bowel resection and need for TPN. Further research is warranted to determine if increased use of endovascular repair could improve overall and gastrointestinal outcomes among patients requiring vascular repair for AMI.

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