Abstract

A 25-year-old male soccer player was admitted to the emergency department (ED) after a ventricular fibrillation out-of-hospital cardiac arrest (OHCA) caused probably by previously unrecognized parvovirus B19-positive myocarditis. The patient collapsed without prodrome just before the start of a match but no basic life support was provided. After 80 min of resuscitation with fractionated administration of 14 mg adrenaline the return of spontaneous circulation (ROSC) could be achieved by the emergency medical services personnel. Physical findings in the ED included a distended abdomen and the absence of bowel sounds. Contrast enhanced computed tomography (CT) of the abdomen revealed hepatic portal venous gas and band-like pneumatoses in the gastric wall (Fig. 1a ), air in the portal confluence and perigastric veins (Fig. 1b), a paralytic ileus with massive dilatation of the stomach, small bowel and colon, wall thickening of the ascending colon up to 10 mm, and a small amount of ascites. A follow-up CT 24 h later showed no remains of the hepatic portal venous gas or pneumatoses and the clinical signs of peritonitis regressed fully. Although neither hepatic portal venous gas nor pneumatosis intestinalis are individually diagnostic of bowel ischaemia, the combination of these CT findings are highly suggestive of transmural bowel infarction [[1]Wiesner W. Mortele K.J. Glickman J.N. Ji H. Ros P.R. Pneumatosis intestinalis and portomesenteric venous gas in intestinal ischemia: correlation of CT findings with severity of ischemia and clinical outcome.Am J Roentgenol. 2001; 177: 1319-1323Crossref PubMed Scopus (252) Google Scholar]. Its cause therefore warrants urgent diagnosis and will usually require surgical management with high mortality. Hepatic portal venous gas and pneumatosis intestinalis have also been described less frequently in non-ischaemic conditions [[2]Kinoshita H. Shinozaki M. Tanimura H. et al.Clinical features and management of hepatic portal venous gas.Arch Surg. 2001; 136: 1410-1414Crossref PubMed Scopus (168) Google Scholar] and after prolonged cardiopulmonary resuscitation (CPR). Lai and colleagues described the fatal outcome of two patients, in whom the post-resuscitation course was complicated by hepatic portal venous gas and pneumatosis intestinalis [[3]Lai C.F. Chang W.T. Liang P.C. Lien W.C. Wang H.P. Chen W.J. Pneumatosis intestinalis and hepatic portal venous gas after CPR.Am J Emerg Med. 2005; 23: 177-181Abstract Full Text Full Text PDF PubMed Scopus (11) Google Scholar]. The authors suggested that in patients receiving prolonged CPR and high cumulative doses of adrenaline the decreased mesenteric perfusion may have induced bowel ischaemia or even necrotizing enterocolitis. Based on the present case, we propose a different pathogenic mechanism for the development of hepatic portal venous gas after prolonged CPR. The clinical and radiographic findings indicate that in our patient the source of the gastric emphysema and hepatic portal venous gas was primarily the distension of the stomach during CPR. Besides the mechanical compression, bag-mask ventilation with improper neck positioning before tracheal intubation might cause gastric inflation and bowel distension (Fig. 1). It has previously been suggested that severe bowel distension may cause mucosal tears, thus allowing the entry of air into the intramural part of stomach or bowel [[4]Radin R.D. Rosen R.S. Halls J.M. Acute gastric dilatation: a rare cause of portal venous gas.Am J Roentgenol. 1987; 148: 279-280Crossref PubMed Scopus (29) Google Scholar]. Emphysema in the gastric wall without air in the wall of the large and small bowel supports this conclusion because the stomach's blood supply arises from several arteries and is less prone to ischaemia than the small and large bowel, in particular. The present case suggests that the source of hepatic portal venous gas and gastric emphysema in some patients may be primarily the mechanical trauma provided by resuscitation and bag-mask ventilation, a condition that requires no specific treatment. Doctors should be aware of this phenomenon especially in the absence of risk factors predisposing to mesenteric ischaemia. None to declare.

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