Abstract
An 81-year-old female with a history of type I diabetes mellitus underwent mitral valve repair and tricuspid annuloplasty for severe mitral and tricuspid regurgitation. A nasogastric tube was inserted on postoperative day 2, and enteral feeding was initiated. She complained about severe abdominal pain on postoperative day 7. Contrast-enhanced computed tomography revealed a massive hepatic portal venous gas and pneumatosis intestinalis of the small intestine. Emergency laparotomy showed no evidence of transmural necrosis. Bowel resection was not performed. On the next day, computed tomography showed an almost complete resolution of the portal venous gas and pneumatosis intestinalis. She was discharged home.
Learning objective
Cardiac surgeons should still be aware that enteral feeding is a potential risk factor for pneumatosis intestinalis and hepatic portal venous gas as a sign of non-occlusive mesenteric ischemia due to impaired blood supply, intestinal distension, and toxic mucosal injury.
Keywords: Non-occlusive mesenteric ischemia, Pneumatosis intestinalis, Hepatic portal venous gas, Enteral feeding
Introduction
Non-occlusive mesenteric ischemia (NOMI) is a well-known life-threatening condition with a high mortality rate. This rarely occurs following cardiac surgery due to multifactorial causes [1], [2], [3], [4]. Herein, a survivor having pneumatosis intestinalis and hepatic portal venous gas which finally may lead to NOMI associated with enteral feeding after a valve surgery was described. This relationship is unrecognized in the field of cardiac surgery.
Case report
An informed consent was obtained from the patient
An 81-year-old female was admitted electively to receive heart valve surgery for severe mitral regurgitation (MR) and moderate tricuspid regurgitation (TR). She had complained about progressive dyspnea on exertion over the past few months. The patient was significant for type I diabetes mellitus on insulin and has hypertension. The results of blood work were within normal limits. Electrocardiogram showed sinus at 94 beats/min. Transthoracic echocardiography showed severe MR due to failed P2 and moderate TR with preserved left ventricular function. Small amount of calcification at the origin of the superior mesenteric artery without significant stenosis was observed on preoperative computed tomography (CT). Coronary artery disease was insignificant. The patient underwent mitral valve repair and tricuspid annuloplasty, which were successful. The duration of cardiopulmonary bypass and aortic cross clamp was 177 and 124 min, respectively. She was extubated 16 h after the surgery and was transferred to a ward on postoperative day (POD) 1. However, she had experienced difficulty in swallowing, which required the insertion of a nasogastric tube on POD 2. Intermittent (three times/day) enteral feeding with Isocal (Nestle HealthScoence, Tokyo, JP) support (1.5 kcal/ml) was initiated with intensive insulin therapy for her diabetes mellitus. At each time, 267 ml of nutrition was given. Blood sugar was well-controlled, which was <200 mg/dL. She was started on warfarin for annuloplasty rings, beta-blocker, and angiotensin-converting enzyme inhibitor. Up until POD 6, she was doing well with enteral feeding despite frequent loose stools, for which a medicine was prescribed. She complained about the onset of acute severe abdominal pain on POD 7. At that time, her blood pressure was stable, and blood work was improving. Arterial blood gas analysis showed no signs of metabolic acidosis. Intravenous prostaglandin was started, and enteral feeding was discontinued. Contrast-enhanced CT in the arterial and venous phase revealed a massive hepatic portal venous gas and pneumatosis intestinalis of the small intestine (Fig. 1A and B). Gas was also seen inside inferior vena cava and superior mesenteric vein.
Fig. 1.
Contrast-enhanced computed tomography in the arterial (A) and venous phase (B) shows a massive portal venous gas and pneumatosis intestinalis. Gas is also seen inside inferior vena cava and superior mesenteric vein.
Computed tomography on the next day after emergency laparotomy demonstrates almost complete resolution of the portal venous gas and pneumatosis intestinalis (C).
Although she had paroxysmal atrial fibrillation postoperatively, there was no evidence of thromboembolism in the superior mesenteric artery on CT. NOMI was strongly suspected and, so general surgeons were consulted to fix the ongoing issue. At emergency laparotomy, we observed patchy ischemic area in serosa and pneumatosis intestinalis at around 100 cm from the cecum. A slight bloody ascites was observed as well. Fortunately, there was no evidence of intramural necrosis of the small intestine. No other finding of ischemia in the large intestine was observed. Therefore, resection of the small intestine was not performed. She was transferred to an intensive care unit to closely monitor her. On the next day, CT showed an almost complete resolution of the massive portal venous gas and pneumatosis intestinalis (Fig. 1C). She did not complain about abdominal pain after that. Enteral feeding with Peptamen (Nestle HealthScoence, Tokyo, JP) standard (1.5 kcal/ml) was resumed intermittently at 10 mL/h for six hours with total parenteral nutrition, aiming at 1200 kcal per day on POD 15. Increased volume at 15 ml/h for six hours was started three days after the initiation of the feeding. The volume of intermittent feeding gradually increased, while the volume of total parenteral nutrition decreased. We switched to take oral intake gradually with support of enteral feeding alone. No abdominal symptoms developed during the course. Regular diet resumed on POD 31. Transthoracic echocardiography before discharge showed trivial MR and TR with preserved left ventricular function. She was discharged on POD 37.
Discussion
To the best of our knowledge, this is the first description of a survivor having pneumatosis intestinalis and hepatic portal venous gas, which finally may lead to NOMI associated with enteral feeding in the field of cardiac surgery.
The incidence rate of NOMI after cardiovascular surgery has been reported to be <0.5 % [1], [2], [3], [4]. The potential risk factors for NOMI include advanced age, diabetes mellitus, atrial fibrillation, peripheral vascular disease, elevated creatinine level, intraaortic balloon pumping, longer duration of cardiopulmonary bypass, and use of significant inotropic support according to data in the cardiovascular journals [1], [2], [3]. The mortality rate is high, reaching up to 94 % [1]. The mechanism of NOMI is unlclear, but alterations in intestinal microcirculation induced by cardiopulmonary bypass or vasopressor treatment were proposed to cause NOMI after cardiovascular surgery in patients with the above-mentioned risks [5]. However, we were not able to find articles about cardiovascular surgery to consider enteral feeding as a risk for NOMI.
On the contrary, the incidence rate of bowel necrosis mostly caused by NOMI ranges from 1.2 % to 1.7 % in oncologic surgery [6], [7], where a case of NOMI and associated findings of pneumatosis intestinalis and hepatic portal venous gas by enteral feeding has been reported [8]. A diagnosis of NOMI was made at a median of six days from initiation of enteral feeding. The mortality rate due to NOMI associated with enteral feeding was 49 % [8].
The possible mechanisms of the finding of pneumatosis intestinalis and hepatic portal venous gas and NOMI associated with enteral feeding are as follows: First, include the increased energy demands in combination with a decreased oxygen supply due to hypoperfusion or inadequate resuscitation. Second, and the osmotic gradient with a rapid fluid shift into the intestinal lumen or excessive bacterial fermentation, leading to intestinal distension and toxic mucosal injury [8].
In this case, the patient was doing well without the inotropes in the ward except being fed through a nasogastric tube. Finally, she developed pneumatosis intestinalis and hepatic portal venous gas on POD 7. Her findings on CT were assumed to be related to enteral feeding because her loose stools persisted after starting, which was consistent with one of the proposed mechanisms (a rapid fluid shift into the intestine) of pneumatosis intestinalis and hepatic portal venous gas associated with enteral feeding [8]. The findings of pneumatosis intestinalis and portal venous gas on CT supported the diagnosis of NOMI [8], [9]. However, we did not perform selective angiography of superior mesenteric artery, which was required for a diagnosis of NOMI [9]. Therefore, we were unable to come to an exact diagnosis of NOMI in this case. The only difference between this patient and others who had some risk factors for NOMI in the literature was enteral feeding. Enteral feeding was not considered as a cause of NOMI and associated findings because loose stools are common when enteral feeding was started. Before this event, we gave feeding at higher rate. As we thought that the higher rate of feeding could cause the mechanisms of NOMI described above, feeding was slowly started after the event.
Initially, it was attempted to be managed medically as usual, with continuation of enteral feeding. With a rapid suspicion of NOMI during the time of sudden onset of abdominal pain and pneumatosis intestinalis and hepatic portal venous gas on CT, ischemia did not become transmural, and a bowel resection was not required.
Findings of pneumatosis intestinalis and hepatic portal venous gas with NOMI related to enteral feeding were seen more frequently in the field of general surgery than in the field of cardiac surgery [6], [7], [8]. Nonetheless, cardiac surgeons should still be aware that enteral feeding is a potential risk for pneumatosis intestinalis and hepatic portal venous gas which finally leads to NOMI due to impaired blood supply, intestinal distension, and toxic mucosal injury as we mentioned above.
Conclusion
A survivor of pneumatosis intestinalis and hepatic portal venous gas associated with enteral feeding after a valve surgery was described. This relationship is unrecognized in the field of cardiac surgery. Once these findings are found, enteral feeding should be stopped immediately.
Funding
This research received no graft from any funding agency in the public, commercial, or non-for-profit sectors.
Declaration of competing interest
The authors have no conflict of interest to declare.
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