Fatal small bowel ischaemia following laparoscopic cholecystectomy: report of a case

Abstract

Veress needle, trocar insertion, pneumoperitoneum-related complications, biliary injuries apart from haemorrhage, intestinal injuries and lateral thermal injuries are all well described entities following laparoscopic cholecystectomy. The development of intestinal ischaemia following laparoscopic cholecystectomy is rare; this report describes a case of fatal small bowel ischaemia following laparoscopic cholecystectomy and discusses the various possibilities that led to this event.

BACKGROUND

Laparoscopic cholecystectomy is presently the gold standard procedure for cholelithiasis and is probably the most commonly performed laparoscopic procedure worldwide. Biliary and non-biliary complications of laparoscopic cholecystectomy have been well described and include trocar-related complications, haemorrhage, bile duct injuries, hollow and solid visceral injuries, thermal injuries, pneumoperitoneum-induced intrabdominal hypertension and the consequences thereof, cardiopulmonary complications and thromboembolic phenomena.¹ Occasional catastrophic consequences occur following laparoscopic cholecystectomy that may or may not be directly related to the procedure itself. One such event is ischaemia of the small intestine; we describe the cascading events following laparoscopic cholecystectomy in an elderly male and discuss the various possibilities that led to this event.

Surgeons and anaesthetists performing laparoscopic procedures should be familiar with the variety of physiological changes that occur after the induction and during maintenance of carbon dioxide pneumoperitoneum. Proper assessment of the preoperative complaints in correlation with the investigative and clinical findings should be assiduously practiced.

While patient factors appear to play a significant role in the development of this fatal but rare complication, one cannot overemphasise the importance of proper technique during laparoscopic surgery. Meticulous attention to intraoperative manoeuvres, avoidance of steep alterations in patient position, appropriate haemodynamic management and avoiding pneumoperitoneum-induced intra-abdominal hypertension can go a long way in preventing such catastrophic occurrences. Mesenteric ischaemia should be considered in patients developing non-specific abdominal symptoms after laparoscopy with an apparent inconsistency between the physical findings and complaints.

CASE PRESENTATION

An elderly male in his mid 60s presented with a 2 day history of acute onset colicky, upper abdominal pain, radiating to the back, associated with nausea and episodes of moderate grade, intermittent fever without chills or rigors. He had had similar milder episodes in the past; investigations done elsewhere including coronary angiography had revealed mild ischaemic heart disease and he was advised low-dose aspirin. He was a chronic smoker and alcoholic and had given up both 2 years ago. Clinical examination was remarkable for a raised temperature of 100°F and a tender right hypochondrium.

INVESTIGATIONS

Haematological and biochemical investigations revealed a raised white blood cell count (total count 17.8×10⁹/l), normal bilirubin level, liver enzymes and a normal lipid profile. Cardiac enzyme profile was normal except for a raised serum lactic acid dehydrogenase (820 U/l). Ultrasonography of the abdomen revealed cholelithiasis and a non-dilated biliary tree.

TREATMENT

A standard four-port cholecystectomy was carried out with an intra-abdominal carbon dioxide pneumoperitoneum pressure of 12 mmHg. End-tidal carbon dioxide was maintained below 35 mmHg throughout the uneventful 50 min procedure and the patient had no haemodynamic instability. Laparoscopy revealed a normal gastrointestinal tract and an inflamed gallbladder; intraoperative cholangiography was normal. On the second postoperative day, he developed a sudden onset of severe abdominal and retrosternal discomfort associated with 8–10 episodes of greenish semi-formed stools. Clinically, his abdomen was soft and he was haemodynamically stable. His electrocardiograph was normal and cardiac enzymes showed a persistently raised lactic acid dehydrogenase level. Abdominal x ray revealed multiple dilated small bowel loops with air-fluid levels; ultrasound abdomen showed vigorous peristalsis in the dilated small bowel loops. Doppler ultrasound of the mesenteric vessels was inconclusive. A possibility of myocardial/intestinal ischaemia was considered and he was started on fractionated heparin and a titrated drip of nitroglycerine. His pain was unrelenting through the night and a decision to take him up for emergency abdominal exploration was taken. After initial laparoscopic evaluation, abdominal exploration was carried out through a midline laparotomy; gangrenous mid small gut with diffuse mesenteric thickening was noted (fig 1). The main mesenteric arteries and veins appeared normal except for a low volume pulse. Resection of the 90 cm gangrenous bowel and hand-sewn end-to-end anastomosis were carried out after confirming the presence of brisk bleeding from the cut edges of the viable bowel. A decision was taken to carry out a check laparoscopy after 48 h. He was maintained on fractionated heparin in the postoperative period and was progressively showing signs of improvement. On the second postoperative day following the resection, he developed sudden severe haemodynamic instability after an acute episode of retrosternal pain and could not be resuscitated.

Figure 1.

Note the gangrenous small intestine with greenish staining of the serosal surface indicating severe mucosal necrosis.

Gross examination of the resected specimen showed markedly dilated, thinned out segments of small intestine with some segments covered only by serosa. Sections from ileum showed patchy necrosis of varying width and depth. Submucosal oedema, congestion and haemorrhage, along with dense collection of acute inflammatory cells, were seen. Sections from the mesenteric arteries showed grade 1 atherosclerosis without any thrombus.

DISCUSSION

Non-biliary intra-abdominal complications associated with laparoscopic cholecystectomy are well described; intraoperatively, they include enterotomies, liver lacerations, diaphragmatic rupture and haemorrhage, while postoperatively, ileus, small bowel obstruction, and hernia at trocar sites have been reported.¹

The development of small bowel ischaemia following cholecystectomy is a rare complication; a Medline and Index Medicus search revealed eight cases reported thus far following laparoscopic cholecystectomy.^2–8 Considering the vast numbers of laparoscopic cholecystectomies carried out worldwide, the true incidence is probably very low. Most cases reported are in the elderly and a fatal outcome has ensued in all but two cases. (table 1)

Table 1.

List of published cases in the literature of intestinal ischaemia following cholecystectomy

Case report	Age (years)/gender	Procedure (min)	IAP (mmHg)	Reintervention	Extent of ischaemia	Outcome
Paul et al2	68/M	LC (85)	15	Day 4 (laparotomy)	Ileum, right colon	Mortality
Jaffe and Russel3	76/F	LC (70)	?	Day 4 (laparotomy)	Small bowel, right colon	Mortality
Dwerryhouse et al4	36/M	LC (50)	15	Day 2 (laparotomy)	Distal ileum, caecum	Recovered
Schorr6	62/F	LC (40)	?	Day 3 (autopsy)	Small bowel, right colon	Mortality
Thiele and Lang (cited by Andrei and Moshe7)	87/M	LC (?)	?	Day 4	?	Mortality
Andrei VE and Moshe7	72/F	LC (50)	15	Day 8 (laparotomy)	Small bowel	Mortality
Klugewitz (cited by Leduc and Mitchell8)	41/M	LC (?)	?	Day 1 (laparotomy)	Colon	Recovered
Leduc and Mitchell8	57/F	LC (120)	15	Day 3 (autopsy)	Small bowel	Mortality
Present case	64/M	LC (50)	12	Day 4 (laparotomy)	Small bowel	Mortality

IAP, intra-abdominal pressure; LC, laparoscopic cholecystectomy.

Reduced mesenteric perfusion and diminished cardiac output consequent to a raised intra-abdominal pressure, in addition to locally mediated mesenteric vasoconstriction by carbon-dioxide-induced pneumoperitoneum, have been implicated as possible causes of bowel ischaemia following laparoscopic cholecystectomy.^2–8 Recent studies have shown that intra-abdominal hypertension due to raised intra-abdominal pressure can result in mesenteric venous compression promoting increased intestinal permeability leading to bacterial translocation and multiple organ failure thereof.^9–14 Other studies have suggested that levels of intra-abdominal pressure applied on a routine basis during laparoscopic surgery might actually compromise splanchnic oxygenation despite normal systemic oxygen saturation.^10–12 Some studies have actually demonstrated an increase in splanchnic perfusion.¹³ The clinical significance of these physiological consequences is, however, unclear. Exaggeration of these effects by steep alterations in position during laparoscopic cholecystectomy could be an additional factor.¹⁰ In an excellent review on the circulatory and respiratory effects of carbon dioxide insufflation, Gutt et al conclude that the main cardiovascular pathophysiological changes that occur with insufflation correlate with the intra-abdominal pressure and the position of the patient.¹⁴ It is conceivable, but not proven, that the aforementioned physiological consequences are well compensated in patients with previously intact cardiovascular system and become clinically significant in patients with pre-existing atherosclerosis.^2,3,5–7 One has also to consider a possible hypercoagulable state that may arise in the postoperative period, although it remains unclear if carbon-dioxide-induced pneumoperitoneum or intra-abdominal hypertension has a role in inducing such a state. Other factors that may need consideration include abnormalities of the mesentery, such as a short mesentery, or adhesions that might have already induced a low or altered flow state.

While pre-existing thrombosis of an arterial trunk may trigger off critical intestinal ischaemia following carbon dioxide insufflation, acute compromise of the mesenteric circulation of an undetermined nature, and a focal lesion caused by a local insult, are other factors to be considered.

In retrospect, it is impossible to refute the possibility that in some patients the symptoms attributed to cholelithiasis were in fact caused by mesenteric angina. Our patient had multiple risk factors for atherosclerosis and, as in other reports,^2,3,5–8 was elderly. The lack of any apparent intestinal abnormalities on the initial laparoscopy and the rapid onset of symptoms would suggest an acute ischaemic episode. However, the patient reported by Dwerryhouse,⁴ was 36 years old and it seems unlikely that he suffered from mesenteric atherosclerosis. Talbot⁵ presented two cases of intestinal ischaemia following open cholecystectomy as an argument that this complication has nothing to do with the laparoscopic technique. There have been reports of fatal ischaemia following other laparoscopic procedures such as fundoplication and after adhesiolysis during gynaecological procedures,^15,16 and following retroperitoneal sympathectomy¹⁷ and incisional hernia repair¹⁸; the report of fatal ischaemia following laparoscopic fundoplication¹⁵ might have been due to a thromboembolic phenomenon after manipulation of the oesophagus around the hiatus, while the case reported by Hasson et al¹⁶ following laparoscopic adhesiolysis during gynaecological surgery could have been due to a fulminant peritonitis caused by an inadvertent unnoticed enterotomy. The available physiological data, combined with a limited clinical experience, suggest, however, that intestinal ischaemia may be a consequence of laparoscopy.

Unfortunately, establishing an early diagnosis is difficult due to the paucity of abdominal signs until established bowel infarction has occurred. However, the pain is characteristically out of proportion to the physical signs and may be the only indicator of a potential catastrophe and warrants a high degree of clinical suspicion with subsequent aggressive management if one has to salvage such patients.

Concerning preventive measures, Paul et al³ suggested that in patients in whom pre-existing impairment of splanchnic blood flow is suspected it might be wise to use intermittent decompression of gas during pneumoperitoneum or an alternative technique. Junghans et al¹¹ proposed that the head-up position should be avoided if possible to prevent further reduction in cardiac output. The most logical approach would be to perform the procedure using the lowest possible insufflation pressure. In addition to preservation of mesenteric blood flow, such practice has resulted in better postoperative pulmonary function and less pain.^12,14

It would be ideal if we could identify those patients who could develop such ischaemic episodes post-laparoscopy; however, as Leduc⁸ points out, the very small number of cases in which this complication has occurred makes any attempt at screening a futile endeavour, even if reliable screening criteria could be identified.

LEARNING POINTS

• Proper assessment of the preoperative complaints in correlation with the investigative and clinical findings should be assiduously practiced.

• Be aware of physiological changes that occur after the induction and during laparoscopy.

• Meticulous attention to intraoperative manoeuvres, avoidance of steep alterations in patient position, appropriate haemodynamic management and avoiding pneumoperitoneum-induced intra-abdominal hypertension can go a long way in preventing catastrophic occurrences.

• Mesenteric ischaemia should be considered in patients developing non-specific abdominal symptoms after laparoscopy with an apparent inconsistency between the physical findings and complaints.