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An ocular examination on the left was impossible due to its closure and lid swelling. Crepitus was appreciated in the periorbital and upper left maxillary regions without tenderness, ecchymosis or other craniofacial abnormalities. CT imaging of the head was obtained within 12?h (figure 2). This axial image exhibited extensive left-sided orbital and facial emphysema. No fracture was seen, but the lamina papyracea contained air. It was hypothesised that a microfracture created a portal for the forced air entry into the soft tissues. Figure?2 Axial CT image of the brain with extensive left-sided orbital and facial emphysema. Learning points Subcutaneous emphysema may develop after diving with compressed gas.1 Any gas-filled, non-compliant space in the body is at risk for air extravasation from barotraumas, obeying Boyle's Law.1�C3 Diving with compressed gases may result in pulmonary overinflation syndrome (different pathophysiology than decompression sickness) with potential life-threatening complications including gas embolism, pneumothorax or mediastinal emphysema.1 Footnotes Contributors: VM (PGY-3 radiology resident) assisted with obtaining the CT image with meprobamate correct selection of scan to upload for publication. Competing interests: None. Patient consent: Obtained. Provenance and peer review: Not commissioned; externally peer reviewed.""The 12-lead ECG on admission to the cardiac care unit was normal (figure 1), and an echocardiogram showed no wall motion abnormalities (figure 2). The major results of blood testing are shown in table 1. Postcardiac arrest blood tests revealed an increased serum transaminase, lactate dehydrogenase, creatine phosphokinase and white?cell count. A troponin T test was negative. Four days following her admission, VF recurred following prominent ST segment elevation on the ECG. In this episode, as well, the patient did not report any anginal symptoms (figure 3). The VF was immediately defibrillated with an external defibrillator, and the ST segment elevation normalised after successful defibrillation. An echocardiogram also demonstrated normal wall motion, and blood tests showed no abnormality at that time. A coronary angiography was performed, which appeared normal; however, an acetylcholine provocation test induced multivessel coronary artery spasms (figure 4). A signal-averaged ECG was negative (figure 5). As a result of these findings, transient myocardial ischaemia owing to coronary artery spasm was considered to be the cause of the VF. Table?1 The major data of blood tests on the admission due to the first episode of ventricular fibrillation Figure?1 The 12-lead ECG results on admission. The ECG did not indicate ischaemic changes, pre-excitation or repolarisation abnormalities such as short or long QT, J wave or Brugada syndrome. Figure?2 Echocardiogram at admission, indicating completely normal heart function.