Diffuse acute abdominal pain and palpation of the lower limb pulses: what kind of link?

A 71-year-old woman was referred to our hospital complaining of abrupt onset of diffuse abdominal pain and vomiting. The medical history included arterial hypertension and atrial fibrillation under pharmacological treatment with calcium channel blockers, digoxin, and aspirin. At physical examination, the sensorium was clear, axillary temperature was 36.7°C; arterial blood pressure 140/80 mmHg; pulse 68 bpm, dysrhythmic, no presence of a heart murmur; respiration 18 breaths/min. The chest was clear. Examination of the abdomen revealed diffuse tenderness. The left leg appeared pale and cold, the right lower extremity pulses were normal, but pulses distal to the left femoral artery were absent. On further persistent questioning, the patient reported the presence of pain in the left leg, but she gave no importance to this symptom due to the preponderant abdominal pain. Laboratory data showed a white blood cell count 12 000/mm3 (86% neutrophils); fibrinogen 735 mg/dl; erythrocyte sedimentation rate 60 mm/h; C-reactive protein 10.0 mg/dl. Achest X-ray study, and abdominal ultrasonography were negative. Duplex ultrasonography revealed an acute embolisation of left superficial femoral artery. Selective angiography showed a complete embolic obstruction of the superficial femoral artery and the ileo-colic branch of the superior mesenteric artery (Fig. 1A). Local regional transcatheter thrombolysis was performed in both arteries, giving priority to the mesenteric artery, more sensitive to ischaemic injury. A bolus of 100 000 IU of urokinase was administered, followed by a continuous infusion of 50 000 IU/h. Twelve hours later, partial lysis of the embolus with signs of initial revascularisation were evident (Fig. 1B). Infusion was prolonged, and control at 24 h showed complete recanalisation of the ileo-colic artery and its branches (Fig. 1C). Subsequently, mechanical thrombolysis by means of a straight angiographic guidewire was performed in the femoral artery, followed by a bolus administration of 100 000 IU of urokinase, and continuous perfusion of 50 000 IU/h. Total treatment consisted of 2 600 000 IU of urokinase, with no bleeding and complete recanalisation of both vessels. The patient was discharged a few days later, in good clinical conditions. Acute thromboembolic occlusion of the superior mesenteric artery or one of its branches is a lifethreatening clinical condition, and is the most frequent cause of acute mesenteric ischaemia accounting for 1-2 per 1000 hospital admissions1. Approximately 70% of the cases are due to circulating emboli, and 30% to local thrombosis. In a recent necropsy-based study on a series of fatal acute thromboembolic occlusions, multiple embolism and sources of emboli were present in 94% of cases5. Due to the intestine’s low tolerance to ischaemia, early diagnosis and immediate treatment are crucial keys for patients’ survival. Indeed, the high mortality, recently estimated at 62% in an unselected population, is considered to be due to the non-specificity of the early phase symptoms, and the lack of specific clinical, haematochemical or radiological findings2,3. In our patient, a careful physical examination with the abrupt onset of abdominal pain allowed us to conclude there were multiple emboli leading to a prompt diagnosis and treatment. The clinical triad including a) abdominal pain disproportional to the signs, b) vomiting or diarrhoea, c) and an obvious source of embolisation (atrial fibrillation) was indeed associated with signs suggestive of multiple thromboembolic events4,5. Angiography was both diagnostic and therapeutic due to the efficacy of local thrombolysis in quickly restoring the mesenteric flow. When multiple contemporary emboli are present, mesenteric occlusion should be treated first, since other anatomic regions are better able to tolerate ischaemic damage.