Epidural pneumatosis as a consequence of cocaine use.

1 of 2 DESCRIPTION A previously healthy 22-year-old gentlemen was referred to the surgical department following acute onset epigastric pain. The initial onset of pain was followed by an episode of vomiting and wretching lasting an hour. On examination, although the abdomen was tender in the epigastrium there was no evidence of peritonitis. Crepitus was evident in the neck and anterior chest wall due to extensive subcutaneous emphysema. Plain radiographs illustrated linear lucencies tracking in the neck and chest, but no pneumothorax or free intra-abdominal air. CT illustrated marked subcutaneous emphysema throughout the mediastinum and neck (fi gures 1 and 2). Furthermore free air was identifi ed in the spinal canal. Gastroscopy and contrast swallow did not identify any oesophageal perforation. After further careful history taking, the patient admitted cocaine abuse. The patient was treated conservatively and symptoms resolved after 48 h. The mechanism of cocaine-induced subcutaneous emphysema is believed to be secondary to barotrauma; after deep inhalation and Valsalva maneouvre in order to increase uptake and the euphoriant effect, or cough triggered by the sniffed substance. This resulting increased intra-alveolar pressure causes rupture of a distended alveolus into the lung interstitium. Air then dissects along the pulmonary vasculature toward the hilum and then extravasates into the posterior mediastinum. It may then travel through the neural formamina into the epidural space. Air thus freely communicates via the neural foramina and collects in the epidural space. 1 – 3 This case illustrates a previously unreported complication of cocaine use and highlights the diffi culty in differentiating between oesophageal perforation which produces similar clinical and radiological appearances. Learning points