Percutaneous puncture of the axillary artery has proved a useful approach for angiographic examination of both proximal and distal portions of the aorta and its branches (1–3). Significant injury to the brachial plexus was not encountered until recently when Staal and his co-workers (4) reported two cases following axillary angiography. Two additional cases of similar plexus deficits following axillary angiography are presented below to suggest strongly immediate surgical exploration of the axilla should evidence of significant brachial plexus injury appear after axillary artery puncture. The necessity for prompt surgical intervention derives from the inverse correlation between duration of nervous deficit and probability of return of function. Case I: A 78-year-old white woman was admitted on Jan. 25, 1966, with a one-year history of episodic burning pain in all of the left toes. The pain was accompanied by their reddening, and it was worse at night or following exercise. A sensation of coldness and numbness in the left foot was constant, but there had been no foot or leg ulcerations. Past medical history included a myocardial infarction in 1956 and mild diabetes mellitus, currently controlled by diet and 500 mg of tolbutamide per day. The blood pressure, which had been elevated for the preceding twenty-five years, was being regulated by 10 mg of guanethidine sulfate per day. On physical examination the patient was noted to be of slight build and oriented. Blood pressure while sitting was 210/80 mm of mercury in both arms; the pulse was 88 and irregular. There was a systolic high-pitched bruit over the right carotid artery. Examination of the heart revealed cardiomegaly and a soft basal systolic murmur. Bilateral femoral arterial systolic bruits were heard. The skin over both legs was atrophic, and there was marked rubor in the left foot. The temperature of the left foot was less than that of the right foot. No ulcers were noted on either leg. Both radial pulses were present and equal. The popliteal, dorsalis pedis, and posterior tibial pulses were absent bilaterally. Pertinent laboratory data included a fasting blood sugar of 107 mg per 100 ml, blood urea nitrogen of 20 mg per 100 ml, and creatinine of 1.1 mg per 100 ml. Prothrombin time was 72 per cent. An electrocardiogram showed atrial fibrillation with a rapid ventricular rate and occasional ventricular extra-systoles, with patterns suggestive of left ventricular hypertrophy and ischemia. Chest roentgenograms disclosed the heart to be top normal size with prominent pulmonary vasculature. Roentgenographic examination of the abdomen demonstrated extensive calcification of the abdominal aorta and pelvic vessels without evidence of aneurysm formation. On Jan. 26, left axillary arteriography was attempted through two separate skin punctures.