Gastrointestinal Haemorrhage

The vast majority of postoperative gastrointestinal bleeds are from the upper gut. Patients in the cardiothoracic ICU are more susceptible due to the common use of antiplatelet agents and also instrumentation of the upper GI tract with transoesphageal echo (TOE). The patient with an upper GI bleed may present with frank haematemesis, cardiogenic shock or melaena. It is important not to forget that a significant upper GI bleed can present solely with fresh blood per rectum, thereby mimicking a lower GI bleed. Upper GI bleeds can cause elevations in serum urea levels as well as the more characteristic drop in haemoglobin. Abdominal signs are often lacking and tenderness is normally absent. After resuscitation and correction of any clotting abnormalities, the first line investigation in any significant GI bleed is an upper GI endoscopy to exclude a bleeding peptic ulcer or alternative upper GI pathologies such as oesophageal varices. Should a peptic ulcer be identified, dual-modality therapy is recommended with the options including adrenalin injection, clips or diathermy. High dose proton pump inhibitor therapy should be commenced and Helicobacter pylori eradication therapy started if biopsy (CLO test) results confirm infection. Should the patient suffer a rebleed after primary endoscopy, the options are either repeat endoscopy, interventional radiology (IR) with possible embolisation of the bleeding vessel (usually the gastroduodenal artery) or if these fail, surgery. Surgery involves an upper midline laparotomy and under-running of the bleeding vessel following enterotomy. Alternative diagnoses such as bleeding oesophageal varices can be managed endoscopically with the application of ligation rubber bands in conjunction with medical control of portal venous hypertension.

Significant lower GI bleeds which fail to stop early with resuscitation and correction of clotting abnormalities can be extremely difficult to manage.The use of adjunctive medical therapies can be helpful in these situations, in particular intravenous tranexamic acid can, on occasion, slow down or even stop significant colonic bleeds. It is imperative in situations of massive rectal bleeds to first exclude an upper GI bleed by endoscopy as well as bleeding haemorrhoids by using bedside proctoscopy. Should these tests fail to identify a source for the bleed and if the patient is generally haemodynamically stable, then a CT angiogram should be obtained. In order for this investigation to successfully identify a bleeding point, the patient needs to be bleeding at a rate of >0.5 ml/minute. However, if a location is identified this facilitates the possibility of an IR approach using conventional angiography in conjunction with embolisation. In the absence of IR, CT angiogram can still be of help as it can direct targeted therapeutic colonoscopy or surgical resection. If the bleeding patient is more unstable, or if CT angiogram fails to identify a bleeding location, the next option is therapeutic colonoscopy which can be performed in the operating theatre. Careful wash-out and mucosal inspection can permit diagnosis and therapeutic intervention, with the use of clips and/or adrenaline injection to achieve haemostasis. In the case of a patient continuing to bleed profusely and no active bleeding site identified, the endoscopy can be augmented by a laparotomy to aid wash-out of the colon through the appendix, and should the colon be cleared as a source of bleeding, sequential enterotomy and small bowel endoscopy to identify the site can then be undertaken. However, undertaking a laparotomy when the site of bleeding is not known in advance should be avoided whenever possible.

Mesenteric Ischaemia

Postoperative mesenteric ischaemia carries a very high mortality rate. Two forms of ischaemia are described: occlusive and non-occlusive. Occlusive disease occurs as a result of migration of emboli or the development of de novo thrombus. Non-occlusive disease is more common in this patient group and develops secondary to hypoperfusion from low cardiac output or the use of vasoconstrictors. Occlusive ischaemia tends to follow a very rapid course with the development of acidosis and ultimately intestinal infarction. Non-occlusive disease generally follows a slower clinical trajectory and in the intubated and sedated patient can be problematic to diagnose. In the awake patient, pain, nausea/vomiting and bloody diarrhoea can be present with the pain classically being ‘out of proportion’ to the abdominal signs, which commonly only occur late. However, in the sedated patient the suggestion of non-occlusive ischaemia can be subtle, varying from increasing nasogastric outputs, diarrhoea ± blood or a slowly rising unexplained metabolic acidosis in combination with raised serum lactate. In the stable patient, the investigation of choice if mesenteric ischaemia is suspected is a contrast enhanced CT scan. Endoscopy (both upper and lower) can also be performed if CT is equivocal. Ultimately, however, laparotomy is not uncommonly used as a diagnostic tool in sick patients, and should be considered in a patient where there is a high risk of clinical suspicion for mesenteric ischaemia even if the CT scan is non-diagnostic.

In non-occlusive mesenteric ischaemia, priority should be given to resuscitation and improvement of cardiac output once the diagnosis is made or suspected. If the clinical picture progresses and the patient deteriorates then laparotomy may be the only option for survival.

In both occlusive and non-occlusive mesenteric ischaemia it is not uncommon to find the entire intestine may be non-viable. Depending on the amount of intestine and other associated viscera that have infarcted, the surgical options are either resection with stoma formation accepting the high likelihood of lifelong parenteral nutrition dependency or ‘open-and-shut’ where the degree of ischaemia is extensive and not compatible with ongoing life.

Hepatobiliary (HPB) Complications

Pseudo-obstruction

Pseudo-obstruction or Ogilvie’s syndrome is not common after cardiac surgery but is an important condition to diagnose as failure to treat this appropriately can lead to haemodynamic compromise due to an abdominal compartment syndrome and colonic perforation, which carries a 50% mortality rate. It is defined as massive acute colonic dilatation as a result of an imbalance in the autonomic supply to the colon rather than a true mechanical blockage. The diagnosis is suggested upon the presence of increasing abdominal girth with a tense, tympanic abdomen together with the inability to pass faeces or flatus. Diagnostic confirmation can be made with an abdominal radiograph; however, a CT scan provides greater information and rules out the small possibility of a true mechanical blockage being present (e.g. sigmoid or caecal volvulus). Pseudo-obstruction is more likely to occur in patients with electrolyte imbalances, in particular potassium and magnesium. Indeed sometimes the condition can be adequately treated with restoration of homeostatic levels of these cations alone. Should colonic diameter exceed 10 cm or if the patient (if awake) complains of right iliac fossa tenderness, then urgent intervention is required as the possibility of imminent perforation exists. Generally, endoscopic decompression with a colonoscope can relieve the impending perforation and on occasion a flatus tube is left in situ to aid the ongoing decompression. In the general population the parasympathomimetic neostigmine has been used in refractory cases of pseudo-obstruction; however, the cardiac risk profile of this drug suggests its use may be limited in patients following cardiac surgery. Surgical intervention is only required in cases of perforation where colonic resection, abdominal wash-out and stoma formation are generally required. A drainage caecostomy tube, which can be placed radiologically, is only used in very rare cases of repeated caecal dilatation in a patient where laparotomy is not possible or safe.