Factor V Leiden and morbid obesity in fatal postoperative pulmonary embolism

Hypothesis: Currently, the risk for postoperative acute pulmonary embolism (APE) is assessed clinically. We hypothesize that the expensive screening f or the most common genetic thrombophilic clotting defect (factor V Leiden; R(506)Q) after exclusion of established clinical risk factors does not offe r additional benefit to surgical patients. Design: We reviewed protocols and histories from 8249 consecutive autopsies performed at the Mayo Clinic, Rochester, Minn. All patients who died of AP E after routine surgery and who lacked any other clinical risk factors for APE were included and compared with matched controls. Genomic DNA was extra cted from archival tissues and examined for R(506)Q by polymerase chain rea ction amplification, restriction enzyme digestion, and direct sequencing. Results: Acute pulmonary embolism was the immediate cause of death in 454 p atients (5.5%). Of those, 32 (7.0%) had undergone routine surgery. These pa tients represent less than 0.07% of all case-adjusted surgical procedures i n the same period. The rate of postoperative death from APE was higher afte r neurosurgical procedures (0.3%) than all other procedures (0.04%). Sixtee n patients (50.0%) were morbidly obese. Only 1 patient was heterozygous and none were homozygous for R(506)Q. Conclusions: (1) Fatal APE is uncommon in surgical patients lacking clinica lly apparent risk factors for venous thromboembolism. (2) Neurosurgical pat ients are at increased risk for postoperative APE. (3) Morbid obesity is a major independent risk factor in cases of sudden death from APE postoperati vely. (4) Routine preoperative screening for R(506)Q ill the factor V gene does not appear to offer additional benefit in surgical patients without cl inically recognizable thromboembolic risk factor(s).