LAUSR

A 17-year-old non-smoker presented with an intractable dry cough. Previous episodes of cough had been clinically diagnosed as asthma and treated with budesonide/formoterol with partial effect. She had no dyspnoea, chest pain or fever. She was obese (body mass index 33 kg/m) and had no previous thoraco-abdominal trauma or surgery. Chest auscultation revealed markedly reduced breath sounds in the right middle and lower zones with bowel sounds heard in the right base. She had left-sided expiratory wheeze. A chest X-ray (CXR) displayed a moderately elevated right hemidiaphragm (Fig. 1A). Two years previously, a CXR revealed mild elevation of the right hemidiaphragm posteriorly. She had a normal CXR at age 3 years. She was empirically treated for an acute asthma exacerbation with oral corticosteroids and inhaled bronchodilators. A fluoroscopic sniff test demonstrated paradoxical elevation of the right hemidiaphragm with deep inspiration suggestive of a right phrenic nerve palsy. After admission, she became more unwell with sinus tachycardia up to 130 beats/min, respiratory rate 20 breaths/min, room air SpO2 98%, blood pressure 140/85 mmHg and she was afebrile. A computed tomography scan showed herniation of her intra-abdominal contents, including the right hepatic lobe, gallbladder, right and transverse colon, into the right hemithorax to the level of T2 consistent with a massive right diaphragmatic hernia (DH) (Fig. 1B). She proceeded to emergency surgery. Her intraoperative course was complicated by severe hypoxia and haemodynamic compromise on induction of general anaesthesia due to impaired venous return as well as right atrial and ventricular compression with tamponade. Laparotomy was performed with decompression of the hernia contents back into the abdomen. The right hemidiaphragm was split at the junction anteromedially between muscular and tendinous portions. The diaphragmatic defect was surgically repaired. The patient made a complete recovery and her cough subsided. Her post-operative CXR (Fig. 1C) and fluoroscopic sniff test were normal. A DH involves the prolapse of abdominal contents into the thoracic cavity due to a congenital or acquired diaphragmatic defect. Congenital DH almost invariably present in infancy or early childhood and are either posterolateral (Bochdalek) or anterior-retrosternal (Morgagni). Acquired DH are most commonly traumatic, infrequently iatrogenic (resulting from thoraco-abdominal surgery) and rarely spontaneous. Spontaneous DH are extremely uncommon but have been reported in the setting of severe coughing or straining and can be life-threatening. In this patient, repeated episodes of raised intra-abdominal pressure caused by Letters to the Editor