**5. Dysphagia**

nary artery bypass/valve operation; (e) prolonged mechanical ventilation; (f) emergency sur‐ gery; (g) prolonged pump time; (h) need for intra-aortic balloon pump (IABP) or vasopressors during or after surgery; (i) need for re-exploration following surgery (re-ster‐ notomy or re-thoracotomy); (j) pre-existing gastric ulcer disease; (k) stroke; and (l) postoper‐

ative sepsis/infectious complications including sternal wound infection [3-5, 9-12].

**3. Physiologic and bowel motility changes following cardiac surgery**

dio-thoracic surgical patients [14].

356 Principles and Practice of Cardiothoracic Surgery

Despite significant hemodynamic implications of cardiac surgery, the effects on gastrointes‐ tinal system function are only modest at best. It is important to note that cardiopulmonary bypass impairs small intestinal transport and increases gut permeability, especially when pump times exceed 100 minutes [13]. Intestinal absorption also appears to be affected in car‐

**Figure 1.** Postoperative ileus following thoracoscopic right upper lobe resection. The patient improved markedly fol‐

The incidence of ileus (Figure 1) in cardio-thoracic surgical patients is between 1-2% [15]. Ileus is among the more common complications following cardio-thoracic procedures [16]. Various forms of ileus following CTS constitute approximately 10% of GIC [4]. Gastrointesti‐ nal motility dysfunction following cardio-thoracic procedures can take a number of clinical manifestations, from isolated gastric distention to prolonged bowel dysfunction [9]. It is im‐ portant to note that the appearance of clinically significant new ileus, especially when ac‐ companied by severe abdominal pain, may indicate a more serious underlying problem

lowing 5 days of therapy consisting of nasogastric suction, electrolyte correction and bowel rest.

Dysphagia is a common complaint following cardio-thoracic operations [29]. Undoubtedly, there is an association between history of endotracheal intubation, median sternotomy or thoracotomy incisions, postoperative inflammatory changes in the chest/mediastinum and dysphagia in the CTS patient population. The etiology of postoperative dysphagia is multi‐ factorial, including contributions from gastroesophageal reflux, local tissue trauma from surgery and endotracheal intubation, intraoperative trans-esophageal echocardiography (TEE), and other potential factors such as recurrent/superior laryngeal nerve dysfunction or injury [30]. One of the more interesting contributors to post-CTS dysphagia is the perform‐ ance of intraoperative TEE, with nearly 8 times greater odds of developing dysphagia among patients who underwent TEE versus those who did not [31].

other traditional risk factors such as *H. pylori* infection alone do not seem contributory [39]. Prolonged mechanical ventilation significantly elevates the risk of upper gastrointestinal bleeding [39]. The two most common etiologies of upper gastrointestinal bleeding are duo‐ denal ulceration and gastric erosion. The appearance of gastric erosions following CTS is likely secondary to systemic hypoperfusion with subsequent development of mucosal ische‐

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359

The initial step in diagnosis of gastrointestinal bleeding is the placement of a nasogastric (NG) tube and lavage of gastric contents. This aids in determining if the gastrointestinal hemorrhage is proximal to the ligament of Treitz. Medical therapy is attempted first, and in‐ cludes the administration of H2-receptor blockers or proton pump inhibitors, red blood cell transfusion, correction of coagulopathy, and temporarily withholding anticoagulation when applicable/possible [41, 42]. If medical management fails, upper endoscopy is the next step in evaluation and treatment of potential bleeding source(s) [43]. Endoscopic attempts aimed at stopping the bleeding by cauterization, vasoconstrictive agent injection, or both are usual‐ ly effective [42, 43]. In one report, approximately half of the patient with upper gastrointesti‐ nal bleeding required upper endoscopy with cauterization to stop the hemorrhage while the other half required surgical intervention to control the bleed [32]. Early surgical intervention if patient fails medical and endoscopic treatment or if significant rebleeding occurs, is rec‐ ommended. In general, the presence of continued hemodynamic instability, or a pre-deter‐ mined transfusion threshold (i.e., >4-6 units of packed red blood cells) are utilized as "surgical triggers". Mortality related to gastrointestinal bleeding, even when requiring an

Lower gastrointestinal bleeding following cardio-thoracic procedures is usually approached according to established clinical algorithms [44]. The first step in management is hemody‐ namic resuscitation and normalization of coagulation parameters. The bleeding usually stops following these initial maneuvers. If the bleeding does not stop, the next step is the identification of the source of hemorrhage, either endoscopically [45] or by imaging (nuclear scan versus angiography) [46, 47]. In many cases, the bleeding can be controlled endoscopi‐ cally [48, 49]. Select cases can be treated with endovascular embolization [47]. Surgery should be reserved for refractory cases, with the major determinants for surgery being the failure of non-operative therapies, hemodynamic instability and/or the requirement for

Mesenteric ischemia (Figure 3) is a well known complication of CTS that usually occurs within hours to several days after surgery. The gastrointestinal tract is vulnerable to ische‐ mia because it is often unable to acutely compensate for systemic hypotension. Further, due to the potential for persistent vasoconstriction following the initial "low flow" state, gastro‐ intestinal ischemia may continue despite return of hemodynamic stability (i.e., non-occlu‐ sive mesenteric ischemia or NOMI). Intestinal ischemia may lead to complications such as

mia and erosion [40].

operation has decreased over the past two decades.

transfusion (usually 4-6 units of packed red blood cells) [48, 49].

**8. Mesenteric ischemia**

**Figure 2.** Colonic pseudo-obstruction following cardiac surgery. The first patient (left) presented with increasing ab‐ dominal pain/distention, nausea and vomiting following mitral valve replacement. Abdominal CT showed massively dilated left colon with compressive effect on the surrounding small bowel. The pseudo-obstruction resolved with neo‐ stigmine therapy. The second patient (right) developed diffuse colonic dilatation following coronary artery bypass grafting. His pseudo-obstruction resolved promptly following emergent colonoscopic decompression.
