COMPLICATIONS of the lithotomy position are well-known and include lower extremity compartment syndrome, peroneal nerve dysfunction, femoral neuropathy, and deep vein thrombosis. 1The main risk factor for such complications is duration of surgery longer than 4 h. These complications may be explained by direct nervous or muscular compression or by decreased arterial and venous blood flow in the lower extremities.

We describe a case of acute arterial ischemia occurring after brief urologic surgery in the lithotomy position in a patient presenting with a severe lower limb arteritis. To our knowledge, only one previous case of lower extremity arterial thrombosis has been reported (Canterbury et al.  2).

A 46-yr-old man with American Society of Anesthesiologists physical status III was scheduled to undergo transurethral resection of a bladder tumor. The patient had several cardiovascular risk factors: active smoking, hypercholesterolemia, diabetes mellitus, and hypertension. He had a clinical history of severe arteritis (bilateral calf pain after 300 m walking). Arterial ultrasonography performed 6 months before surgery showed patent iliac vessels, several femoropopliteal stenoses, occlusion of the right superficial femoral artery, and severe distal atherosclerosis. He was in sinus rhythm. His medical treatment included verapamil, taken until the day of surgery, and aspirin, which was discontinued 15 days before surgery.

Bladder transurethral resection was performed with general anesthesia with the patient in the high lithotomy position. Anesthesia was induced with propofol and sufentanil and maintained with desflurane and nitrous oxide. A laryngeal mask airway was placed. Blood pressure was measured from the right arm with use of an oscillometric method. Systolic blood pressure was higher than 110 mmHg during the entire procedure. No vasoconstrictor drugs were used. No arrhythmia occurred. Because the tumor was located near the right ureteral ostium, the right obturator nerve was stimulated four times during the procedure, resulting in transient contractions of the right adductor muscles. The patient was kept in the high lithotomy position for 50 min. Emergence from anesthesia was uneventful. After arrival in the recovery room, the patient reported right calf pain. The right foot and leg were pale and cold, with sensory and motor dysfunction; right pedal and popliteal pulses were absent. The calf showed no muscular tension. Pulse rate was regular at 55 beats/min, arterial blood pressure was 130/70 mmHg, and electrocardiography showed no changes as compared with preoperative electrocardiography. Acute arterial ischemia was confirmed by acoustic ultrasonography. Arteriography was performed immediately and showed thrombosis of the initial part of the right external iliac artery and severe distal arteritis with developed collateral branches. Doppler ultrasonographic examination showed normal venous blood flow and no evidence of deep vein thrombosis. Intravenous ilomedin (prostacyclin analog) and heparin were administered. This treatment was followed by an improvement in motor function and cutaneous temperature. Nevertheless, subacute ischemia and sensory disorders were still present. Iliofemoral bypass and lumbar sympathectomy were performed successfully 2 days later. Intravenous ilomedin and heparin were infused postoperatively. The patient was discharged from the hospital after regaining normal motor and sensory functions of the right leg.

We have described a complication of the high (but not exaggerated) lithotomy position in a short urologic procedure. Neurologic, venous, and muscular complications have been described extensively, usually in patients kept in the lithotomy position for more than 4 h. 1These complications usually are explained by local compression, distortion of nervous or vascular elements by exaggerated flexion of the thighs, and decrease in perfusion pressure in the lower extremities.

In the current case, several factors may have contributed to acute arterial ischemia. First, the patient had atherosclerotic disease. As shown by Halliwill et al. , 3the lithotomy position decreases lower extremity perfusion pressure in young, healthy volunteers. Canterbury et al.  2described a case of lower extremity arterial thrombosis after a 40-min surgery with the patient in the lithotomy position, explained by popliteal vessel angulation. In their study of 100 patients, they showed that the ankle–arm index (ankle/arm systolic blood pressure ratio) decreased significantly immediately after placing the lower extremities in the lithotomy position and remained abnormal throughout surgery. The decrease in blood flow was more pronounced in patients with arterial calcifications. We can suppose reasonably that severe hypoperfusion of the lower extremities occurred in our patient and was not detected because blood pressure measured at the brachial artery remained in the normal range. Because the patient probably had an abnormal systolic blood flow, the lithotomy position may have critically decreased blood flow in the lower extremities and possibly contributed to the constitution of arterial thrombosis.

Several studies have shown that the femoral nerve and vessels can be distorted in the lithotomy position. Hopper et al.  4provided anatomic explanations for femoral neuropathy after a procedure in the lithotomy position. In cadaver studies, flexing, abducting, and externally rotating thighs have been shown to angulate (80–90°) the femoral nerve and vessels. 5,6In a study of 177 cases in which the exaggerated lithotomy position was used, Angermeier et al.  1described four thromboembolic complications that were possibly caused by venous compression. Nilsson et al.  7found that filling the bladder with irrigation fluid with the patient in the lithotomy position resulted in echographic signs of iliac venous obstruction. In the case reported herein, all these mechanical factors may explain a decrease in blood flow in a compressed iliac artery. Another hypothesis is the possibility of an atherosclerotic plaque rupture caused by angulation and compression of the artery. Transient contractions of adductors during bladder resection by obturator nerve stimulation also may have contributed to a plaque rupture. This hypothesis is supported by the finding that the complication occurred during a short surgical procedure.

The recent discontinuation of acetylsalicylic acid before surgery may have facilitated the occurrence of arterial thrombosis. Experimental studies 8have shown that fibrin gel porosity may be increased after discontinuation of antiplatelet drugs and may explain accelerated thrombosis in patients with coronary artery disease. Beving et al.  9demonstrated that high levels of arachidonic acid metabolite are produced by platelets 1 to 2 weeks after discontinuation of acetylsalicylic acid. This abnormally high platelet activity after discontinuation of acetylsalicylic acid might increase the risk of thrombosis.

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