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J Thorac Cardiovasc Surg 1994;108:899-906
© 1994 Mosby, Inc.

SURGERY FOR ACQUIRED HEART DISEASE

Gastrointestinal complications after coronary artery bypass grafting

Meyrin-Geneva, Switzerland

From the Cardiovascular Surgery Unit, Hôpital de la Tour, Meyrin-Geneva & Clinique de Genolier, Genolier, Switzerland.

Received for publication March 18, 1994. Accepted for publication July 12, 1994. Address for reprints: Jan T. Christenson, MD, Hôpital de la Tour, Cardiovascular Surgery Unit, 1 Avenue J.-D. Maillard, CH-1217 Meyrin, Geneva, Switzerland.

Abstract

Clinical variables were studied in 3129 patients undergoing coronary artery bypass grafting to identify patients at risk of abdominal complications and common etiologic factors in the development of such complications. Seventy-three gastrointestinal complications occurred (2.3%), with an overall mortality rate of 16.4% compared with a mortality rate of 3.4% for all patients undergoing bypass grafting (p < 0.001). Cholecystitis and intestinal ischemia were the most frequently encountered complications. Multivariate analysis demonstrated that preoperative hypertension, New York Heart Association classes III and IV, preoperative left ventricular ejection fraction less than 40%, age greater than 70 years, reoperation, and urgent operation as independently and significantly associated with gastrointestinal complications. In contradiction to previous reports, no significant correlation existed between gastrointestinal complications and cardiopulmonary bypass time, 99.8 ± 35.8 versus 101.2 ± 39.8 minutes. Perioperative myocardial infarction and immediate postoperative hypotension with low cardiac output necessitating substantial inotropic pharmacologic support or intraaortic balloon pumping were significantly more prevalent in patients who had gastrointestinal complications (all p < 0.001). Furthermore, multivariate analysis revealed that postoperative low cardiac output was a significant, independent predictor in the development of gastrointestinal complications of any kind after coronary artery bypass grafting. Postoperative splanchnic hypoperfusion could therefore be a common etiologic factor. (J THORACCARDIOVASCSURG1994;108:899-906)

The number of cardiac operations for which cardiopulmonary bypass (CPB) is used has been rapidly increasing in recent decades, mainly because of an increased number of coronary bypass grafting (CABG) procedures. Both mortality and morbidity after cardiac operations today are low. Various types of postoperative complications after cardiac operations, such as hematologic, renal, cardiac, neurologic, and pulmonary complications, have been extensively discussed in the literature, ^1-3 whereas gastrointestinal (GI) complications have been less commonly addressed. GI complications are not prevalent (0.3% to 3%), ^4-8 but they are associated with a high overall mortality (12% to 67%). ^9-12 Several etiologic and risk factors for the development of GI complications have been suggested, such as preexisting disease, prolonged CBP time, perioperative hypoperfusion and hypotension, valve surgery, and use of vasopressor substances. ^7,8,10,13,14

The present study was undertaken to evaluate clinical variables to identify patients at risk of abdominal complications and to try to identify a common etiologic factor in developing various GI complications after cardiac operations. Patients undergoing valve operations and combined cardiac procedures were excluded from this study.

PATIENTS AND METHODS

From January 1, 1984, to April 30, 1993, 3129 patients underwent CABG, performed by one surgical team, at Hôpital de la Tour, Geneva, and since May 1990 at Clinique de Genolier, Switzerland, as well. Only patients with GI system complications that arose within 30 days of the CABG procedure and on their initial hospitalization were considered for this study. The GI complications were defined as follows: (1) upper GI tract hemorrhage manifested by hematemesis or melena, associated with a decrease in the hemoglobin level of 2 gm and with endoscopic or radiographic confirmation of the diagnosis; (2) acute cholecystitis, calculus, or acalculus, with leukocytosis and positive ultrasonographic, radiographic, or computed tomographic findings; (3) acute pancreatitis manifested by abdominal pain, elevated urinary or serum amylase levels, and positive ultrasonographic or computed tomographic findings; (4) liver failure with or without demonstrable liver necrosis and without any other major abdominal complications, manifested by progressive cholestatic jaundice, rising liver function test values, and uncorrectable coagulopathy; (5) paralytic ileus lasting more than 4 days and resulting in a significant prolongation of hospitalization; and (6) intestinal ischemia or infarction, with or without intestinal necrosis and confirmed by laparotomy, endoscopy, or autopsy. Eight of these patients had hemorrhage of the lower GI tract (fresh rectal bleeding with a decrease in the hemoglobin level of -2 gm.

Transient abdominal distention, medication-induced nausea or vomiting, and diarrhea were not regarded as GI complications. Transient postoperative liver dysfunction (serum-bilirubin >26 µmol/L and serum alkaline phosphatase >175 U/L) without a picture of fulminant liver failure was not regarded as an isolated GI complication.

All patients received prophylactic antibiotics and cephalosporin (Mandokef or Rocephine) at induction of anesthesia and twice daily for 48 hours after the operation. Nasogastric tubes were placed in all patients. Antacids and H₂ blockers were routinely administered for prophylaxis against stress ulcerations.

Anesthesia
Preoperative medication consisted of morphine 0.1 to 0.15 mg/kg subcutaneously and midazolam 0.1 to 0.2 mg/kg orally. Anesthesia was induced with flunitrazepam 0.02 to 0.06 mg/kg and maintained with fentanyl 4 to 10 µg/kg and flunitrazepam. Muscle relaxation was provided by pancuronium 0.1 mg/kg. Ventilation was controlled with a minute volume of 0.1 L/kg body weight and an inspired oxygen fraction of 100% before and after CPB. When the patient was weaned from CPB, nitroglycerin 1 to 3 mg/hr and dopamine 1 to 4 µg/kg per minute were administered intravenously during the first 12 to 24 hours.

Routinely the patients were extubated within 24 hours and oral fluids were started. Twenty-four hours after the operation, the majority of patients were receiving a light oral diet with routine postoperative medications (eg., furosemide 40 mg daily).

CPB technique
All operations were undertaken through a median sternotomy. CPB was achieved with a hollow-fiber membrane oxygenator. Initially core cooling to 28° C was used, but during the later period of the series the majority of the operations were performed with normothermia (rectal temperature kept at 37° C at all times). During CPB nonpulsatile flow from the pump-oxygenator was maintained at 2.4 L/min per square meter. Lungs were ventilated with a minute volume of 0.01 L/min at an inspired oxygen fraction of 21%. Mean arterial pressure was maintained during CPB between 60 and 70 mm Hg. Regitine, nitroglycerin, and isoflurane were used as vasodilators and phenylephrine (Neo-Synephrine) as a vasoconstrictor. Use of these drugs did not differ between the groups of patients who subsequently had GI complications and those who did not. Nifedipine (Adalat, 10 mg) was administered at the time of implantation of the internal mammary artery, whenever used. During CPB, the hematocrit value was kept minimally at 22% to 25%, potassium concentration at 5.5 to 6.0 mg/dl, and diuresis was maintained at 100 to 150 ml/hr with furosemide used as necessary.

Myocardial preservation was achieved by using cold (4° C) crystalloid cardioplegic solution (St. Thomas' solution), with 1 ml procainamide and 100 mg allopurinol, together with topical myocardial cooling with iced saline solution. Cardioplegic solution was reinfused every 30 minutes during the crossclamping period or whenever electrical activity resumed. The aortic crossclamping time and CPB time were carefully noted in all cases.

During the postoperative period, patients had routine hematologic investigations and any GI or other system complications were recorded. Low perioperative cardiac output was defined as a cardiac index less than 2.0 L/min per square meter and the need for inotropic pharmacologic support other than the routinely used dopamine dose, 1 to 4 µg/kg per minute (kidney dose), with or without the addition of an intraaortic balloon pump. The inotropic pharmacologic support was divided into three groups: (1) minimal support—dopamine alone, 5 to 10 µg/kg per minute; (2) moderate support—dopamine combined with dobutamine; and (3) maximal support—a three-drug combination of dopamine, dobutamine, and norepinephrine as the intravenous infusion.

Statistical analysis
Univariate testing of variables was performed with ² analysis or Fisher's exact test for discrete variables. The unpaired t test or one-way analysis of variance was used for continuous variables. ¹⁵ A probability value less than 0.05 was regarded as significant. Stepwise logistic regression analysis was then used to further test significant variables in a multivariate situation. ^15,16 Any variables that had trends associated with GI complications were included in stepwise logistic multivariate regression. Age was added and analyzed in decades. In a similar fashion, all patients with postoperative low cardiac output as indicated by decreased cardiac index or hypovolemic hypotension (hemorrhage necessitating reexploration and with documented hypovolemic shock) were identified and tested by multivariate analysis to determine if postoperative hypotension also could be an independent predictor for GI complications when analyzed in conjunction with preoperative variables.

RESULTS

Seventy-three GI complications occurred, an incidence of 2.3%. The most common GI complications were acute cholecystitis and intestinal ischemia (23% each), followed by paralytic ileus (22%). Twelve deaths occurred, for an overall mortality rate of 16.4% in this group, compared with a mortality rate of 3.4% for all patients undergoing CABG during the same time period in our institution (p < 0.001) (Table I). The highest mortality was found in the group of patients who had isolated fulminant liver failure/necrosis (75%), followed by intestinal ischemia/infarction (30%) and acute cholecystitis (18%); acute pancreatitis and upper GI tract bleeding resulted in no deaths. Upper GI tract hemorrhage occurred in general on the fourth postoperative day (range 2 to 8 days) and all patients were successfully managed conservatively. Acute cholecystitis (mostly acalculus) was diagnosed on average 5.3 days after the operation (range 2 to 13 days). Eight patients were operated on with either cholecystectomy or tube drainage. Two of the eight patients subsequently died, both having necrosis of parts of the gallbladder and peritonitis. One third of the patients who had cholecystitis (35%) required reoperation. Acute pancreatitis was predominantly seen after reoperative CABG (75%). The diagnosis was made 5 days after the operation (range 3 to 8 days). In one patient laparotomy and drainage of the pancreas were performed. Fulminant isolated liver failure with or without demonstrable liver necrosis was a rare GI complication (5.5%), with a late onset and the highest mortality. Diagnosis was made on average on the sixth postoperative day (range 3 to 24 days). Paralytic ileus was in all instances managed conservatively. One patient died in this group, but of an unrelated cause, a postoperative myocardial infarction. Intestinal ischemia was also diagnosed relatively late, 5.3 days after the operation (range 2 to 15 days). Eleven patients underwent laparotomy and intestinal resections and two of them subsequently died. Three other patients died in this group. In their case the diagnosis was made too late and surgical intervention was no longer feasible. There was no statistically significant difference in aortic crossclamping time and CPB time for the different types of GI complications, nor was there a difference between patients having GI complications and those not. In our series, GI complications never occurred as an isolated complication but always in conjunction with, for example, perioperative myocardial infarction, postoperative low cardiac output, or hypovolemic shock. To identify risk factors for GI complications after CABG, we first compared patients with and without these complications. There was no difference regarding age and sex distribution. Significantly more patients who had hypertension and who smoked belonged to the group with GI complications. Furthermore, a significantly larger number of the patients who subsequently had GI complications had a worse preoperative cardiac condition and function, with a higher number of emergency operations and reoperative CABG procedures. The incidence of concomitant peripheral vascular disease did not differ between the groups (Table II). Operative data for the two groups are presented in Table III. No statistically significant differences were noted in aortic crossclamping time, CPB time, normo thermic and hypothermic CPB, or perfusion pressures (69 ± 8 versus 68 ± 7 mm Hg—the average of measurements obtained every 15 minutes during the CPB run) between the groups

Table IV

Table V

Table V

Table VI

Postoperative hypotension (low cardiac output caused by poor cardiac performance and postoperative hypovolemic shock) was also analyzed by multivariate logistic regression, and it was found that postoperative low cardiac output (p = 0.001) and postoperative hypovolemic hypotension (p = 0.008) were both additional significant and independent predictors for the development of GI complications (see Table IV). Thus these findings indicate that splanchnic hypoperfusion could be a major cause of postoperative GI complications that occur after coronary operations.

DISCUSSION

GI complications are relatively rare after CABG procedures, 2.3% in this series of 3129 CABGs, which corresponds well with earlier reports. ^4-7 However, these complications are associated with a high mortality. In the series we studied, the overall mortality was 16.4%, which is lower than previously reported. ^8-13 One reason for the lower figure could be that we are routinely using antacid and H₂ blockers for gastric protection. This protocol has led to a lesser number of upper GI tract bleedings and no mortality, which contradicts earlier reports. ^8,10 Several authors have also reported upper GI tract bleeding to be the most common GI complication. ^5,9,10,13 The incidence of pancreatitis has been reported to be 0.2% to 5.2%, ^17,18 but recently Castillo and coworkers ¹⁹ demonstrated that pancreatic cellular damage occurs in a much higher frequency after cardiac operations, 27%. However, abdominal signs and symptoms were present in only 7.7% in their group of 300 patients, which corresponds well with the 11% found in our series. We have also found that acute pancreatitis and cholecystitis occurred more frequently after reoperative CABG than after first-time CABG, a phenomenon also experienced by others, but not easily explainable. Acute cholecystitis and significant paralytic ileus are common among the GI complications after cardiac operations, 23% and 22% respectively, in our series, corresponding well with previous reports. ^4,8,12 Intestinal ischemia is a relatively common GI complication, 23% in our series, with a substantial delay in diagnosis and often with a fatal outcome (30% mortality), as also described by others. ^5,6,10,11

The cause of most GI complications after cardiac procedures appears to be visceral hypoperfusion. Several authors have reported that a prolonged CPB time is a significant risk factor for the development of postoperative GI complications. ^7,8,10,12 It has been speculated that a reduced cardiac output during CPB may result in shunting of blood flow away from the splanchnic bed toward areas of higher priority, such as the brain. ¹⁴ However, in our series CPB time did not differ at all between patients who subsequently had a postoperative GI complication and those who did not have any such complication, regardless of extremes. Thus there must be other etiologic risk factors present. Another clinical risk factor for GI complications has been said to be valve surgery, ^8,10 in which a possibility of embolization may alsobe present. In our study, patients undergoing valve surgery or combined surgery were excluded and we evaluated only patients who had CABG. Postoperative low cardiac output, hypotension caused by bleeding, extensive need for postoperative vasopressors, and intraaortic balloon pump support during or after the operation are other risk factors for GI complications mentioned in the literature. ^7,8,10,12,18 This corresponds well with our findings. We have observed a significantly higher incidence of perioperative myocardial infarction, postoperative low cardiac output, use of intraaortic balloon pump, and need for inotropic pharmacologic support, as well as a higher incidence of reexploration for postoperative bleeding (with a documented period of hypovolemic shock), in patients who subsequently had GI complications compared with those who did not. Other perioperative complications, including neurologic events (e.g., stroke), did not differ. This observation suggests that postoperative hypoperfusion of the splanchnic bed could be an important etiologic factor.

Using multivariate logistic regression analysis, we have identified age greater than 70 years, hypertension together with a poor preoperative cardiac condition (NYHA class III or IV, LVEF <40%), reoperative CABG, and need for emergency operations as significant, independent risk factors. Concomitant peripheral vascular disease was not found to be a significant independent factor. This lack, together with absence of an overrepresentation of postoperative neurologic events, makes atherosclerotic embolization unlikely as an etiologic factor, a result that somewhat contradicts a recent report. ²⁰ Poor preoperative left ventricular function, emergency operations, and hypertensive disease were also significantly overrepresented in patients who had abdominal complications and who eventually died, when compared with the survivors.

There are several indications that splanchnic hypoperfusion is the important etiologic factor in the development of intestinal ischemia. Lipopolysaccharide or endotoxin is always present in large amounts in the intestines and can leak out from the lumen into the portal circulation if the mucosal barrier is damaged. ²¹ Experimental data indicate that splanchnic hypoperfusion during shock does cause mucosal ischemia. ²² When endotoxin from the intestines leaks into the portal circulation, it will pass through the liver and under normal conditions be destroyed by the Kupffer cells of the reticuloendothelial system in the hepatic sinusoids. However, if the amount of endotoxin is too large or the reticuloendothelial system is depressed, endotoxin can translocate into the systemic circulation.

Ohri and coworkers ¹⁴ have recently demonstrated that transcellular transport in the small intestine was impaired and gut permeability was increased during CPB in 41 patients undergoing cardiac operations. These findings coincided with a mucosal hypoperfusion.

Multivariate regression analysis demonstrated that postoperative low cardiac output and hypovolemic hypotension were independent, significant predictors of GI complications. This observation suggests that splanchnic hypoperfusion could be a common denominator in the cause of all types of GI complications in cardiac surgery. When comparing the group of patients who subsequently had postoperative intestinal ischemia with the group of patients who had other postoperative abdominal complications, we found no differences whatsoever between the groups. The literature contains a great deal of support for the concept that ischemia caused by splanchnic hypoperfusion is a common cause for all abdominal complications seen after CABG. ^4,14,19,23 It should certainly also be mentioned that vasopressors, used in controlling refractory hypotension, produce by themselves a marked splanchnic vascular constriction and thereby lower the mucosal perfusion further. ¹³

From our series of 3129 CABG procedures it can be concluded that postoperative GI complications are relatively rare (2.3%) but associated with a significant mortality rate (16.4%). Clinical, independent risk factors appear to be concomitant hypertensive disease, preoperative NYHA functional class III or IV, LVEF less than 40%, reoperative CABG, emergency operation, and age 70 years or older. With appropriate gastric protection, upper GI tract complications were rarely observed in our series; cholecystitis and intestinal ischemia were the most frequently encountered GI complications. In contrast to others, we did not find that the CPB time is an important risk factor. However, immediate postoperative hypotension, with a low cardiac output necessitating inotropic pharmacologic support or intraaortic balloon pump insertion, was found to be an etiologic factor. The common etiologic factor in GI complications of any kind after CABG operations seems to be splanchnic hypoperfusion, leading to ischemia and ultimately gangrene/necrosis, breakdown of the intestinal mucosa, and translocation of endotoxins into the systemic circulation. This in its turn could play an important role in the development of adult respiratory distress syndrome and ultimately death after multiorgan failure.

On the basis of the results of the present study some clinical suggestions may be put forward, which may lower the number of abdominal complications after CABG: (1) preoperative identification of patients at risk, as described earlier; (2) restrictive use of traditional inotropic drugs and evaluation of new substances, for example, splanchnic vascular dilating inotropic drugs such as dopexamine ²⁴; (3) early mobilization of the GI tract, with enteral feeding rather than parenteral ²⁵; (4) early support with an intraaortic balloon pump in patients with perioperative and postoperative low cardiac output syndrome; (5) early rethoracotomy in case of postoperative hemorrhage to avoid hypovolemia and massive blood transfusions; (6) liberal use of endoscopic and laparoscopic examinations, whenever GI complications are suspected, because early diagnosis and thereby treatment seem to be essential to lower the mortality rate.

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