Mediastinal tamponade due to gastric distension.

Abstract

A 75-year-old woman was admitted to our hospital under the care of the general surgeons. She gave a history of 6 h continuous epigastric pain radiating to the left iliac fossa accompanied by coffee-ground vomiting. She described at least 10 previous episodes of this pain, but each time the symptoms had resolved spontaneously with oral antacids and application of a hot water bottle. She was documented as having a past medical history of diverticular disease and reflux oesophagitis (seen at endoscopy 8 months previously), for which she took a maintenance dose of omeprazole and regular metoclopramide. She had no history of cardiac or respiratory problems. On examination, the patient was apyrexial and cardiovascularly stable. The only positive findings were dullness to percussion and decreased air entry at the left base, as well as mild epigastric tenderness. Bowel sounds were normal. Blood indices at that time were within the normal range, except for a raised white cell count of 20.4. Chest X-ray revealed a significant portion of the left lower hemithorax contained stomach protruding above the level of the diaphragm as well as possibly a segment of large bowel (Fig. 1). The provisional diagnosis was of gastritis with what appeared to be an accompanying diaphragmatic defect. Initially, the patient was treated conservatively with intravenous fluids and ranitidine. A nasogastric tube was not inserted. The patient was also scheduled for endoscopy the following day. Over the course of the next 24 h, however, the patient became increasingly unwell. She became pyrexial with worsening epigastric pain and increasing dyspnoea. Thirty-six hours after admission, the patient suffered a cardiac arrest. Cardiopulmonary resuscitation was commenced and the patient was initially found to be in asystole. There was no response to epinephrine and atropine. No pulse was present on cardiac compression. At tracheal intubation, the patient was seen to have aspirated gastric contents. Following insertion of a nasogastric tube, large volumes of air and fluid were aspirated, at which point sinus rhythm with a palpable pulse appeared. The patient was transferred to ITU for ventilatory and inotropic support. A chest X-ray at that time showed correct positioning of the nasogastric tube, with no obvious diaphragmatic abnormality. Over the next 24 h, the patient remained cardiovascularly stable. Upper GI endoscopy was undertaken on the day following admission to ITU. On insufflating the stomach the patient suffered a profound cardiovascular collapse with an arterial blood pressure of 30/10 mmHg. She required immediate resuscitation with epinephrine. Examination revealed an absence of chest wall expansion and breath sounds on the left side. The stomach was deflated via the endoscope and the blood pressure improved dramatically. Following endoscopy, anteroposterior and lateral chest X-rays demonstrated persistent massive gastric expansion into the left hemithorax (2, 3). The nasogastric tube was reinserted and the stomach fully decompressed. During endoscopy, compressed air is used to insufflate the lumen of the gut. A typical flow rate of 1–2 l.min−1 is produced from a driving pressure of 0.3 bar. This pressure is significantly greater than normal intrathoracic pressure and is clearly capable of causing severe organ dysfunction. We believe that, in this patient, massive gastric expansion into the left hemithorax decreased cardiac return and produced profound cardiovascular collapse via a similar mechanism to a tension pneumothorax. At the time of the initial cardiac arrest this gastric expansion may well have resulted from air swallowing. The subsequent collapse during endoscopy was undoubtedly caused by gastric expansion due to insufflation of air. A repeat endoscopy and insertion of a nasojejunal feeding tube was successfully performed 2 days later. Limited gas insufflation and simultaneous administration of intravenous epinephrine avoided cardiovascular compromise.