Chapter 56. Anesthesia for Gastrointestinal Surgery

1. Diseases of the gastrointestinal system frequently result in abnormal gastric function, with potentially increased anesthetic risk caused by increased intragastric pressure, delayed gastric emptying, gastric dilation, and increased gastric secretion.

2. Although volume, pH, and amount of particulate matter in the aspirate appear to be the 3 most important factors determining the severity of the pulmonary insult, overall the medical fragility of the patient is often the most important determinant influencing the clinical course and outcome of pulmonary aspiration.

3. Extensive bowel, pancreatic, or esophageal resections entail considerable morbidity, with potential serious postoperative complications such as hemorrhage, coagulopathy, and hepatic, renal, pulmonary, or cardiovascular failure.

4. Laparoscopy entails the installation of gas (usually CO2) into the peritoneal cavity with physiologic changes resulting from this gas under pressure and subsequent surgical positioning. Hemodynamic compromise can occur, which, although rare, can be catastrophic.

5. The systemic inflammatory response syndrome/multiorgan dysfunction syndrome continuum is often accompanied by gastrointestinal mucosal ischemia and the release of mediators that further compromise both splanchnic and systemic perfusion. Anesthetic care of these patients is especially challenging.

6. If the lower esophageal sphincter is not functioning properly, or if a hiatal hernia exists, stomach contents may reflux into the esophagus and pharynx during anesthesia and surgery, increasing the potential for serious aspiration pneumonia.

7. Narcotics have intestinal side effects that are well recognized. Lower esophageal sphincter tone is decreased. Gastric emptying is impaired because of decreased propulsive motility and increased tone in the antrum of the stomach.

8. During laparoscopy, the development of pneumothorax and/or pneumomediastinum is a serious and/or potentially life-threatening complication. When either is suspected, from hemodynamic deterioration or from the presence of subcutaneous emphysema, especially of the neck and face, aggressive investigation (auscultation, chest radiograph) and management (eg, chest tube for tension pneumothorax) should be undertaken. Procedures on the lower esophagus may be more likely to result in these complications. Conversion to an open procedure is usually required.

9. Approximately 40% of patients with gastroesophageal reflux have delayed gastric emptying, and in approximately one-third of these, the delay is clinically significant.

10. Maneuvers necessary for blunt esophagectomy are capable of causing serious hemodynamic and ventilatory compromise and require appropriate monitoring of blood pressure and respiration.

11. Bariatric surgery patients may have significant medical problems and their perioperative care can be quite challenging. Newer procedures continue to lessen morbidity and mortality.

Gastrointestinal (GI) surgical practice has evolved dramatically with experience and technology. Newer techniques result in less physiologic trespass and more rapid return to full activities, and the trend continues. Current robotics-assisted laparoscopic surgery will be augmented by remotely controlled natural orifice transluminal endoscopic surgery (NOTES).1

The GI system includes an amazingly complex neurochemical system with far-reaching implications on homeostasis and well-being.2 Furthermore, from routine appendectomies to advanced robotic-assisted natural orifice hepatic resections,3 GI surgery occupies a major percentage of the operative time in most hospitals. Therefore, providing anesthesia care for patients requiring these procedures represents a great portion of the anesthesiologist's time and attention. From routine to sophisticated procedures, this chapter illustrates and discusses preoperative, intraoperative, and postoperative considerations. A discussion of the effects of anesthesia administration on GI function is followed by important surgical and anesthetic considerations of specific GI surgical procedures.

Mastication begins the process of digestion. Inadequately swallowed and regurgitant material may be in the pharynx. Pulmonary aspiration of oropharyngeal, esophageal, or gastric contents is an extremely important issue for all patients receiving anesthesia care, and especially those with gastrointestinal disorders/symptoms.

Local and general anesthesia depress sensation of the upper digestive system, starting with trigeminal innervations of the nasopharynx. The posterior third of the tongue and oral pharynx are innervated by the glossopharyngeal nerve, which accompanies the carotid sheath emerging from the jugular foramen. The superior laryngeal nerve innervates the tongue base and inferior epiglottis to the vocal cords. The recurrent laryngeal nerve innervates from the vocal cords distally. The remaining larynx and trachea are innervated by penetrating branches of the vagus. Any local (eg, pharyngeal tumor) or general (eg, cerebral vascular accident or metabolic toxin) pathology affecting the innervation of these areas increases risks of perioperative mishandling of oropharyngeal secretions and fluids, and an increased potential aspiration pneumonitis.

Proper functioning of the esophagus and the lower esophageal sphincter (LES) is a concern during anesthesia care. If the esophagus is dilated because of obstruction by tumor, destruction of neural mechanisms (eg, achalasia), or existence of a diverticulum (Fig. 56-1), particulate matter will remain for hours (if not days) after ingestion, and secretions will not pass normally to the stomach. If the LES is not functioning properly and/or if a hiatal hernia exists, stomach contents may reflux into the esophagus and even the pharynx during anesthesia and surgery, increasing the potential for serious aspiration pneumonia. During an operative procedure, placement of a cuffed endotracheal tube during surgical procedures protects the airway from such materials. When an obstruction(s) is present, endotracheal intubation should occur with the patient awake (eg, direct oral, blind nasal, or fiberoptic bronchoscopy) or via a rapid sequence method with the patient anesthetized. With the awake method, sedation should be limited or avoided altogether, especially in patients with a "full" stomach, proximal obstruction, esophageal diverticulum, or altered consciousness. Emptying the gastric or esophageal contents (eg, nasogastric tube, Sengstaken-Blakemore tube) when feasible should decrease the volume and nature of any fluid available for reflux.4 In any patient with known hiatal hernia or LES dysfunction, or when the stomach or esophagus is suspected to contain fluid or particulate matter, an attempt should also be made to aspirate the material before emergence from anesthesia. In addition, extubation should occur only after swallowing, adequate strength, and the ability to follow commands are apparent.

Many surgical approaches to the esophagus require a thoracotomy and a laparotomy, the lateral position, and a method of collapsing 1 lung. In addition, a temporary esophageal dilator may be requested intraoperatively by the surgeon; a nasogastric or naso-"intestinal" tube will need to be positioned at some point during the procedure to maintain continuity above and below the anastomosis. Such procedures can be demanding and require considerable preoperative planning. Discussion with the primary surgeon both before arriving in the operating room and during the "Team Time Out" can be very helpful for all involved.

Management of Acid Reflux

Abdominal surgery has been associated with as much as 75% of the perioperative mortality related to aspiration pneumonitis.5 In addition, fasting gastric volume can be large in patients with GI disorders, especially duodenal ulcer disease.6 Many other conditions, some directly related to the GI tract, are associated with some risk of regurgitation of esophageal or stomach contents and ultimate pulmonary aspiration (Box 56-1). In these conditions, an inadequate initial clearance or the return of a substance to the pharynx may be followed by ineffective removal with subsequent passage through the glottic opening into the lungs.7 Mortality associated with aspiration ranges from 3% to 70%8 and the true incidence and morbidity are not well quantified. A large European study suggests that the actual incidence is considerably lower, approximately 0.05%.9 Unrecognized or "silent" regurgitation typically occurs, as does subsequent aspiration.10,11

The volume, pH, and amount of particulate matter in the aspirate appear to be the 3 most important factors determining the severity of the pulmonary insult. Particulate matter obstructs airways and quickly leads to ventilation and perfusion mismatching, hypoxia, hemorrhagic edema, and sometimes acute pulmonary hypertension.12 Traditionally, gastric volumes greater than 25 mL and pH less than 2.5 have been associated with the most severe pneumonitis,13 although more recent data suggest that greater volumes of nonparticulate aspirated fluid would be tolerated when the pH is greater than 2.5.12,14

In addressing the problem of aspiration during the delivery of anesthesia, anesthesiologists have focused on 4 areas: (1) reduction of the acid content and volume of the stomach contents, (2) improvement of intestinal motility, (3) prevention of reflux into the pharynx, and (4) a better understanding of gastric emptying.

Although antacids increase gastric pH, particulate (ie, opaque) antacids produce severe aspiration damage similar to that of gastric acid.21 The use of clear antacids is just as effective in increasing pH but is associated with only mild pulmonary changes if aspirated.15

Histamine-2 (H2)-blocking agents are effective in reducing the acidity and, to a lesser extent, the volume of gastric fluid. Typical agents used include cimetidine and ranitidine.16,17 None of these agents has much effect on the acidity of material already present in the stomach (eg, that found in the trauma patient or patients requiring other emergency surgery) but may decrease intraoperative acid production if given before surgery. Oral therapy seems to be as effective (and considerably less expensive) as intravenous (IV) or intramuscular forms when premedication by the oral route is suitable. Administration the night before and the morning of surgery consistently increases gastric pH to above 2.5. Rapid administration of cimetidine is associated with hypotension,18 bradycardia, and cardiac arrest. Ranitidine appears to have a lesser incidence of similar side effects. Mechanisms may include blockage of the inotropic and chronotropic responses of stimulation of myocardial H2 receptors.19 These agents alter the metabolism or kinetics of various drugs, including the cytochrome P450 system,20 lidocaine,21 nifedipine,22 theophylline, warfarin, and phenytoin. Although atropine and glycopyrrolate decrease gastric acid production somewhat, they generally are not used for this specific purpose because they also decrease LES tone.

Rapid-acting intravenous proton pump inhibitors are effective in reducing gastric volume and increasing gastric pH. In a prospective, randomized, controlled trial, proton pump inhibitors were compared with H2 antagonists. After intravenous administration 1 hour prior to surgery, pantoprazole 40 mg (Protonix) and ranitidine 50 mg (Zantac) were compared. Gastric aspirate pHs were 5.3 and 4.8 and residual volumes 8 mL and 15 mL, respectively, measured just after induction of anesthesia. This was compared with an IV saline control. Patients receiving pantoprazole and ranitidine had statistically greater gastric pH and less gastric volume than control patients (5 mL IV saline with gastric aspirate pH 3.7 and 29 mL volume), but there was no statistical difference between the pantoprazole and ranitidine groups.23 Although both proton pump and H2 inhibition may be used to reduce perioperative gastric acid, neither seems to be superior.

Gastric and intestinal motility are stimulated by metoclopramide, which acts centrally by inhibiting dopamine and in the gut by releasing acetylcholine. LES tone also increases, but the pylorus and duodenum relax. Metoclopramide usually is administered concurrently with an H2 blocker.

Preventing refluxed material from reaching the pharynx is the goal of cricoid pressure (the Sellick maneuver) and rapid sequence intubation. When properly performed, cricoid pressure should provide a barrier for at least 100 cm H2O of esophageal pressure.24 Pressure should not be released until the cuff is inflated and until correct placement has been verified by appropriate observations, including auscultation and capnometry. However, a meta-analysis of 241 peer-reviewed articles found little evidence that rapid-sequence intubation provided protection against aspiration. Furthermore, in a controlled, blinded, randomized crossover study comparing the Sellick and BURP (backward, upward, and right-sided pressure on the thyroid cartilage) maneuvers, the BURP maneuver and cricoid pressure worsened the laryngoscopic view in 30% of cases, cricoid pressure alone worsened the view in 12.5% of cases, and there was no difference in 65% of cases.25,26 Although the protocol of rapid-sequence intubation is generally valued as an important tool to prevent aspiration, anesthesiologists continue to evaluate the relative values of drug dosage, manual ventilation, cricoid pressure, and patient position in an attempt to maximize patient safety A recent volunteer study suggests that compression of the alimentary tract does occur during both midline and lateral displacement of the cricoid cartilage.6 The application of cricoid pressure appears to have a net positive value, but experience in its application is important.

As more is learned about the physiology of gastric emptying, the tradition of overnight fasting for elective surgery has come into question.27-31 Residual gastric volumes may be acceptable after 2 to 4 hours of fasting, and the addition of H2 blockers lowers pH as well. One should not extrapolate from such information directly to the emergency patient or the patient with a full stomach. The aspiration of particulate matter produces such a devastating insult in the lung that, except for the most urgent situations, 6 to 8 hours of fasting after solid foods is recommended. Even after this waiting period, the stomach often still contains food and large amounts of fluid.

Bowel Distension

Nitrous oxide (N2O) administration is associated with an increase in intraluminal gas volume. Experimentally, in dogs, bowel gas volume increases approximately 75% to 100% after 2 hours of 70% to 80% N2O, and by 100% to 200% after 4 hours.32 Normally, luminal contents include approximately 100 mL of gas, mostly swallowed air; aerophagia or bowel obstruction greatly increases this volume. Clinically, N2O use results in a slow increase in bowel distension and intraluminal pressure. The principal surgical consequence is difficulty with abdominal closure at the completion of a procedure. During extreme conditions (eg, obstruction with distended bowel), increased intraluminal pressure may lead to bowel ischemia. N2O use during abdominal surgery, if needed, should be limited to the initial 10 to 15 minutes at induction and intubation, and during the period of abdominal wall closure at the completion of the surgical procedure. (See Endoscopy section for issues regarding N2O during laparoscopy.)

Bowel Motility

Anticholinesterase drugs (eg, neostigmine) are necessary for the reversal of residual nondepolarizing muscular blockade. Although relatively safe, the parasympathetic stimulation of anticholinesterase drugs can have undesirable side effects. Bradycardia occurs so often that it is anticipated and managed before its occurrence by the administration of a parasympatholytic drug (eg, atropine or glycopyrrolate) prophylactically before administration of a neuromuscular blockade reversal agent. This parasympathetic stimulation also affects intestinal motility, increasing the frequency and pressure of peristaltic waves, especially in the colon. For unknown reasons, diseased colon (eg, from ulcerative colitis, diverticulitis) appears to be more susceptible to this effect. This has led to considerable debate over the potential for cholinesterase inhibitors to cause breakdown of colonic anastomoses.33 Fortunately, residual anesthetic agents and pretreatment with parasympatholytic agents (atropine, glycopyrrolate) attenuate this response. Inadequate perfusion of the anastomotic site, infection, and underlying tissue abnormality are now thought to be more significant issues.

Thiopental increases the electrical and mechanical activity of the duodenum and jejunum in experimental studies, and atropine premedication decreases the response. Ketamine has little effect on GI motility, and oral diazepam reduces gastric emptying and increases small bowel transit time.34

Narcotics have significant intestinal side effects. LES tone is decreased.35 Gastric emptying is impaired36 because of decreased propulsive motility and increased tone in the antrum of the stomach. The duodenum and the small intestine undergo a decrease in propulsive contractions, whereas the amplitude of rhythmic segmental nonpropulsive contractions often is enhanced, which results in an increase in resting tone and can cause peristaltic spasms. The proximal small bowel is more affected than the distal part, and the tone of the ileocecal valve is increased. Parasympatholytic agents can partially abolish these effects. In the large intestine, the narcotic effects can be more pronounced; peristaltic waves are decreased or absent. The amplitude of rhythmic nonpropulsive contractions is increased, often to the point of spasm. Anal tone also is increased. Again, diseased bowel appears more susceptible to such effects.37

High spinal or epidural anesthesia promotes hyperperistaltic activity because of blockade of sympathetic innervation. The unopposed parasympathetic activity may cause nausea and vomiting in approximately 20% of patients, for whom atropine may be effective. Because of the increased peristaltic activity, controversy has arisen over the effects of spinal or epidural anesthesia on anastomotic breakdown, especially in colon surgery. Some data suggest that this problem is not significantly increased with regional anesthesia and that colonic blood flow is improved by spinal or epidural anesthesia.38 Others disagree with these findings. Many believe that axial anesthesia is the emerging standard for early postoperative pain control.

Postoperative ileus is probably associated with manual trauma during laparotomy or from increased splanchnic nerve discharge in other procedures. Gastric peristalsis returns within 24 to 48 hours, and colonic activity returns after 48 hours, beginning at the cecum and progressing caudally. Small bowel motility returns more rapidly, and sometimes enteral tube feedings can be initiated within 24 hours. This ileus can lead to mild abdominal distension and absent bowel sounds for as long as 48 to 72 hours. Passage of flatus, cramping, and return of appetite suggest the return of normal peristaltic activity.39

Although neuraxial narcotics generally are recommended for pain relief in most patients, the side effects of pruritus, urinary retention, and especially respiratory depression are problematic in some. Effects are presumably through local spinal cord receptors and via more central mechanisms after rostral spread in the cerebrospinal fluid or systemic absorption. Although used extensively and successfully in patients undergoing all forms of surgery, including many varieties of abdominal surgery,19,40 there are animal data that document alterations in intestinal motility associated with neuraxial narcotics,41 and at least 1 note of caution in humans.41 Most studies conclude that postoperative epidural anesthesia and analgesia directed by an anesthesiologist, compared with intravenous anesthesia administered by a surgeon, provides superior analgesia and decreases postoperative ileus, but does not reduce mortality or major morbidity, especially after major abdominal and cardiac surgical procedures43,44 Postoperative epidural analgesia, in conjunction with a comprehensive program of preoperative counseling, no bowel preparation, carbohydrate clear liquids (until 2 hours before surgery), perioperative oxygen supplementation, nonopioid analgesia, minimal surgical drains and nasogastric tubes, early removal of urinary catheters, standard laxatives and prokinetic agents, and early ambulation, can reduce length of stay.44

Biliary Effects

Therapeutic doses of the opioids can cause a marked increase in biliary tract pressure in susceptible patients. For example, 10 mg of subcutaneous morphine can produce a 10-fold increase in common bile duct pressure within 15 minutes that can last 2 or more hours.45 This effect results from opiate receptor-mediated mechanisms that cause spasm of the sphincter of Oddi. Fentanyl and alfentanil also increase common bile duct pressure.46,47 The general importance of this effect on intraoperative cholangiograms is uncertain, but fentanyl-supplemented anesthesia is associated with a 3% surgical failure rate.48 Considering the possibility of opioid-induced sphincter of Oddi spasm after a cholycystectomy or endoscopic retrograde cholangiography may avoid additional unnecessary and/or potentially dangerous procedures.49

Meperidine increases biliary tract pressure via mechanisms that are not receptor mediated. Opiate antagonists (eg, naloxone) can reverse this opiate-related increase in biliary tract pressure (except for that caused by meperidine)50 but also may reverse general analgesic effects. Sublingual nitroglycerin (0.6 mg) decreases the elevated intrabiliary pressure, but atropine only partially attenuates the response. Glucagon (1-3 mg), titrated to effect, also reverses opiate-related biliary spasm.

Respiratory Function

Frequently, abdominal procedures are conducted with the patient supine, which decreases functional residual capacity (FRC) by 0.5 to 1.0 L. The relationship of FRC to closing volume contributes to the alveolar–arterial oxygen difference and shunt.51,52 This augments the 15% to 20% decrease in FRC associated with general anesthesia,53 which continues postoperatively.54,55 The Trendelenburg position, along with intra-abdominal retractors or packings, aggravates this problem even further56 because more of the lung assumes zone III conditions. Patients with elevated pulmonary arterial pressure (eg, mitral stenosis) generally do not tolerate the Trendelenburg position. Diaphragmatic impairment and abdominal pain contribute to the potential for major respiratory embarrassment after abdominal surgery and, at least initially, are intensified by any negative effects from residual inhalation agents, IV anesthetics, and neuromuscular blockade. After upper abdominal surgery, vital capacity remains abnormal for more than 1 week.57,58 Experimental data demonstrate that excessive fluid administration contributes to hypoxemia if fluid accumulates in the lungs and leads to increasing arteriovenous shunting.59 However, no rigorous evidence exists favoring either the amount or type (colloid vs crystalloid) of intravenous fluid, in spite of decades of controvery.60,61

Gastrointestinal Endocrinology

The understanding of GI endocrine tumors has expanded dramatically since original descriptions of the carcinoid syndrome several decades ago. That clinical syndrome (including flushing, diarrhea, telangiectasias, bronchoconstriction, and fibrous endocardial plaques) has traditionally been said to originate from metastatic carcinoid tumors in the GI system, pancreas, biliary vessels, bronchi, ovaries, and testes via release of vasoactive hormones into systemic circulation. Cardiac involvement (primarily right-sided valvular) is actually noted in more than 50% of patients by echocardiography and may require valvular surgery.

In the gastrointestinal tract, at least 14 endocrine cell types produce numerous peptide hormones such as gastrin, glucagon, somatostatin, secretin, and vasoactive intestinal peptide (VIP). The hormonal and/or neurotransmitter functions are complex and tumor presentation is uncommon; excellent references detail their complexity, management, and uncommon clinical syndromes.62-65 Most produce small amounts of neuroendocrine substances and do not result in clinical symptoms until late stages of disease. Fortunately, aggressive malignancy is relatively infrequent; these tumors tend to have an indolent course. An increasing number of such lesions are being discovered before biochemical clinical symptoms. In addition to these endocrine/neuroendocrine tumors (terms considered synonymous), there are also pancreatic islet cell tumors. Duodenal gastrinomas can be associated with multiple endocrine neoplasia type-1 and may or may not result in the Zollinger-Ellison syndrome. Somatostatinomas may be associated with neurofibromatosis.

These gastroenteropancreatic neuroendocrine tumors have a yearly incidence of 1.0 to 2.6 per 100000 people from gastrointestinal origin, with an additional 0.2 to 0.4 per 100000 people from the pancreas. Because only approximately 10% of the 100000 people produce bioactive hormones, diagnosis often occurs late after metastasis has occurred. There is emerging evidence of distinct molecular genetic differences between GI and pancreatic neuroendocrine tumors.66

Therapy of functional tumors involves controlling symptoms, which includes somatostatin analogues for carcinoid syndrome, watery diarrhea syndrome ("VIPomas"), and hyperglucagonemia.67 For those with gastrinoma (Zollinger-Ellison syndrome), proton pump inhibitors have improved therapy of high acid production. In addition to true insulinomas, some other neuroendocrine tumors may secrete a chemical that behaves like insulin.

Surgical treatment includes attempts to discover/remove the primary tumor, regional lymph nodes, and appropriate distant metastases, for example, liver tumors. This includes liver resection and both cryoablation and radiofrequency ablation. Impressive improvements in symptomatology can occur, and depending on cell type, meaningful 5-year survival may result.68

Anesthesia management of this broad group of patients requires an understanding of the biochemical abnormalities noted, the clinical/potential clinical manifestations, the medical therapy being used, the surgical/diagnostic procedure(s) contemplated, and the ability to monitor hemodynamics and lab values (eg, glucose) closely in the operating room/perioperative environment.

For the carcinoid syndrome, a nonhistamine-releasing anxiolytic can be used to reduce the catecholamine levels. The somatostatin analogue octreotide,69 odansetron (5-HT3 antagonist),70 and remifentanil71 have been found useful in perioperative suppression of carcinoid signs and symptoms.

The Esophagus

The esophagus extends from the pharynx at the level of C6 to the gastroesophageal junction. The hypopharynx courses from the level of the epiglottis to the upper border of the esophagus and funnels food into the esophagus. Swallowing begins as a voluntary process as food and liquid pass through the mouth, which initiates a complex and normally coordinated sequence of involuntary discharges through cranial nerves V, VII, X, and XII to the oropharynx and the esophagus. The upper third of the esophagus contains striated musculature, the lower third has smooth muscle, and the middle third has a mixed muscular supply. Motor innervation is supplied by the vagus nerves. Striated muscle is innervated by preganglionic fibers and smooth muscle by postganglionic fibers from the Auerbach plexus.

In adults, the upper esophageal sphincter (UES) is approximately 3 cm in length and consists of the cricopharyngeal muscle (striated), a portion of the inferior constrictor muscle superiorly, and circular esophageal muscles inferiorly.72,73 The primary function of the UES is controlled by the swallowing mechanism in general, but its resting tone is increased in response to esophageal distension or acid from gastroesophageal reflux74 and decreases during sleep.75

The lower end of the esophagus (3-5 cm in length) acts as a functional LES. Thickness of the smooth muscle layers increases in this area, and circular fibers develop considerable tension. Control of the LES tone is complex and chiefly results from vagal cholinergic and myogenic mechanisms, although prostaglandins,76 neuropeptides (eg, vasoactive intestinal peptide),77 GI hormones (eg, gastrin, motilin),78 the progesterones and estrogens of pregnancy, and thyroid-stimulating hormone79 are among substances known or suspected of affecting LES tone. Material enters the esophagus after voluntary propulsion by the tongue into the hypopharynx. With relaxation of the UES (resting tone, approximately 20-60 mm Hg), food enters the esophagus and is moved along by primary peristaltic waves (25-80 mm Hg). LES relaxation (resting tone, 10-20 mm Hg) occurs, and the bolus enters the stomach. This whole process takes only 4 to 8 seconds. Secondary peristaltic waves serve to move residual matter through and into the stomach. Figure 56-2 depicts normal esophageal motility.

Acid Reflux and Hiatal Herniation

Reflux of material from the stomach into the esophagus is a complex topic and is covered in depth in other texts.80 Criteria for diagnosis include those of reflux symptoms (Box 56-2) and the results of various tests, including radiographic studies, endoscopy, biopsy, manometry, and prolonged esophageal pH monitoring. The pH test demonstrates that virtually all healthy subjects have episodes during daily activity when their esophagus is exposed to pH less than 4. This exposure is increased during awake upright activity, especially after eating, and occurs during supine sleep activity,115 when swallowing frequency is diminished and less effective (Table 56-1). Reflux is associated with pressure gradients between the abdomen (positive pressure) and the thorax (intermittently negative pressure), and with poorly understood episodes of "transient lower esophageal relaxation."82-86 pH testing also detects those patients with reflux of alkaline duodenal material into the stomach and esophagus.87

The etiology for increased exposure of the esophagus to acid material and ultimately to the risks of acid and particulate matter aspiration can involve 1 of several mechanisms (Box 56-3). The mechanical competence of the LES depends on intrinsic tone (normally >5 mm Hg88), the overall length of the LES muscular segment (normally ≥3 cm), the portion of that segment that is intra-abdominal (at least 1 cm), and interaction with the cardia of the stomach, which should transmit intra-abdominal pressure to the distal LES.87,89-91 The most common abnormality is decreased LES tone, but even normal LES tone can be affected by the other mechanisms.100

Esophageal clearance of reflux material depends on swallowing, gravity, intrinsic motor activity, salivation, and whether a hiatal hernia is present. Although the frequency of acid reflux may be greater during the day, the duration of episodes is longer when the patient is in the supine position because of loss of gravitational effects. Additionally, any disease that affects the motor activity of the esophagus may lead to impaired clearance of acid material (Box 56-4), with resultant effects on the esophageal mucosa and potential for aspiration. Saliva is important in neutralizing the small amounts of acid refluxed with peristalsis even in healthy persons, and clearance of this acid is prolonged when saliva is removed by suctioning.93 The salivation stimulated by heartburn (termed water brash) can lead to repetitive swallowing, aerophagia, and gastric distension with further reflux.94 Perioperatively, the presence of a nasogastric/orogastric tube may contribute to reflux of gastric contents and the risk of aspiration, and has been challenged as a routine practice.95,96

The presence of a hiatal hernia is associated with additional abnormalities (Fig. 56-3). The hernia produces a defect in esophageal propulsion that results in inadequate acid clearance and longer transit time.97 The retreat of all or part of the distal LES into the chest impairs the ability of the lower third of the LES, in concert with the cardia of the stomach, to impart extrinsic abdominal pressure and enhance sphincter function. If intrinsic LES tone also is decreased, a setup exists for major reflux of acid material and, ultimately, for the development of aspiration pneumonia. Despite this, most patients with hiatal hernias are asymptomatic.98

Certain abnormalities of gastric function also can result in acid reflux through a normal gastroesophageal junction or by exacerbating preexisting LES abnormalities (Box 56-5). Normally, the body and fundus of the stomach are able to adapt to a large volume of material with minimal increases in pressure, although a previous vagotomy interferes with the active relaxation necessary for this to occur, and greater intragastric pressures occur with lesser volumes.99 Outlet obstruction of the stomach more obviously leads to increases in pressure, which occurs normally with vomiting, but also with pyloric stenosis in newborns and obstructing ulcers or tumors in patients of any age.

Delayed gastric emptying leads to persistence of gastric acid and foodstuffs. The causes are varied80 (Box 56-6) but yield a similar effect. As larger volumes accumulate and persist for a longer period, the potential for reflux through either a normal or abnormal LES increases. Approximately 40% of patients with gastroesophageal reflux have delayed gastric emptying,100,101 and in approximately one-third of these, the delay is clinically significant. Those rare patients with postviral gastroparesis also may have serious autonomic neuropathy.102 Patients with various neurologic illnesses may manifest a variety of GI motility abnormalities.103

As the stomach dilates from any cause, the relationship between the cardia and abdominal portion of the LES changes, which results in decreased maintenance of proper LES tone and increased risk of reflux. In addition to the conditions already mentioned, aerophagia from several causes also may lead to gastric distension. Normally, each pharyngeal swallow results in several cubic centimeters of swallowed air. Patients with reflux may habitually swallow (water brash; some even chew gum to stimulate saliva) to clear acid and can develop air-induced gastric distension, which can exacerbate their reflux. Other patients with decreased saliva formation (eg, with Sjögren syndrome) or after head and neck irradiation may swallow excessively with resultant aerophagia. Loss of secondary peristalsis, which can occur with diabetes mellitus and collagen vascular diseases, also leads to inordinate swallowing in an effort to propel food along, again with resultant aerophagia.

Gastric acid hypersecretion plays a role in some patients with gastroesophageal reflux who have a mechanically normal LES, and is a complicating factor in other patients with abnormal LES function.104,105

The most serious acute consequence of acid reflux is the risk of aspiration of stomach contents. Chronic complications include esophagitis, stricture formation, Barrett esophagus (with risk of esophageal cancer), and chronic pulmonary disease from repeated episodes of aspiration. Aspects of surgical management are discussed next.

Surgical Procedures of the Esophagus

Several surgical procedures for patients with esophageal disease are worthy of specific mention, but an extensive discussion of all approaches is beyond the scope of this text.106 Patient positioning, site of incision, and whether the esophagus will be transected are important to the anesthesiologist in all esophageal procedures.

Several approaches exist for the management of reflux disease. The Nissen-type (360-degree gastric fundoplication) procedure may be approached abdominally (open or more commonly via laparoscopy) or through a left posterolateral thoracotomy. During the abdominal approach, severe liver retraction typically occurs, and the reverse Trendelenburg position is useful to the surgeon. The transthoracic approach may be used for repeat procedures, in obese patients, and when esophageal shortening is suspected. The Belsey-type (240-degree fundoplication) procedure also is approached from a left lateral chest incision. For any of these procedures, the anesthesiologist may be asked to pass a bougie through the pharynx into the distal esophagus to the area of surgical manipulation so that the repair can be sized. Should the restoration tend to slide back into the chest because the esophagus is too short, a lengthening procedure (eg, colon interposition) may be required. Except for this latter maneuver, the esophagus is not transected for these procedures. Laparoscopic and robotically assisted laparoscopic operations have increased in quantity and complexity.107 Because of restrictions in patient positioning and the shear mass of the robotic devices, access to the patient during these procedures may be suboptimal. Attempts to use endoscopically placed devices have generally failed to produce long-term symptom relief.108 Although 2-year data in a small study with the "Esophyx" device for treating small hiatal hernias with mild to moderate reflux disease demonstrated results comparable with the Nissen-type fundoplication, additional trials are needed.109 As NOTES (natural orifice transluminal endoscopic surgery) technologies expand, antireflux surgery may be of historical interest, like vagotomy and antrectomy is for benign ulcers. Heightened awareness of the operative field is required by the anesthesiologist because the surgeon may be viewing only the video projection at a platform physically removed from the patient.

Several techniques are used for patients with esophageal cancer. For lesions of the distal esophagus, the Ivor-Lewis/McKeown-type repair (Fig. 56-4) includes an anterior abdominal incision followed by a right thoracotomy. The McKeown-type is similar but adds a right neck incision to facilitate the anastomosis of the stomach to the cervical esophageal remnant. Either procedure may include extensive node dissection in the chest, entry into the pericardium or the opposite chest, and thoracic duct ligation. Single-lung ventilation may facilitate operative exposure. Blunt esophagectomy (Fig. 56-5) is used for cervical esophageal disease, for lower-third esophageal carcinoma, and in early noninvasive disease. Abdominal and left cervical incisions are made, and extensive "blind" bimanual dissection through the chest is performed. Bleeding or tracheal injury may necessitate an emergent thoracotomy. Postoperative recurrent nerve injury is described in 10% of patients.110 In 600 patients undergoing surgical resection for esophageal cancer with and without preoperative chemotherapy, aspiration pneumonia, adult respiratory distress syndrome, cardiovascular events, and neurological accidents were the most common complications: patients less than 60 years old had the fewest complications and patients older than 70 years had the most.111

Peptic Ulcer Disease and Duodenal and Gastric Carcinoma

Millions of Americans have symptoms of acid and peptic ulcer disease,112 and annual direct and indirect costs exceed $3.4 billion.113 Duodenal ulcer disease (DUD) occurs 2 to 3 times more often in men than in women, and mortality rates may be somewhat greater in nonwhites aged up to about 65 years. Genetic (eg, family history, blood group O, human leukocyte antigen [HLA] types B5 and B12) and environmental (eg, smoking, aspirin, nonsteroidal anti-inflammatory drugs [NSAIDs]) factors are involved in DUD. Chronic pulmonary disease, cirrhosis, renal transplantation, and possibly high psychological stress also may increase the incidence of ulcer disease. Resting and stimulated secretion of acid are increased114,115 in common DUD and in patients with gastrinoma (Zollinger-Ellison syndrome—see Gastrointestinal Endocrinology section). The number of parietal cells secreting acid may be increased. The rapid emptying of stomach contents in some patients with DUD may overwhelm duodenal buffering and clearance mechanisms. Because these patients appear to have reduced duodenal bicarbonate secretion,116 they are predisposed to ulceration.117

Gastric ulcers occur only one-third to one-fifth as often as duodenal ulcers, and causal factors in gastric ulcer disease (GUD) are largely unrelated to those for DUD. Genetic, psychological, and hypersecretion of acid are not factors for most patients. The largest group of patients with GUD has normal to low secretion of acid and evidence of decreased gastric mucosal defenses against acid and pepsin-related endothelial injury. GUD tends to occur in older patients, and possibly as a result, the mortality rate is higher. GUD is associated with gastritis and with gastric carcinoma. Aspirin is clearly a risk factor,118 as may be NSAIDs; both are thought to work via inhibition of prostaglandin synthesis. Pyloric function may be defective in patients with GUD, permitting reflux of duodenal, biliary, and pancreatic secretions into the stomach, initiating gastritis, and, ultimately, ulcerations.119 Smoking reduces pyloric sphincter tone and increases the risk of bleeding from ulcers.120 DUD and GUD are associated with Helicobacter pylori infection121 and elimination of H pylori is a focus of treatment.

Medical Treatment

The medical treatment of patients with ulcer disease involves dietary and environmental restrictions (eg, avoiding aspirin, NSAIDs, smoking, alcohol; limiting caffeine, anxiety) and medication. Antacids, H2-receptor antagonists, and coating agents (eg, sucralfate) are useful in patients with DUD or GUD. Protein pump (H, K-ATPase) inhibition (eg, omeprazole) has become important as an extremely potent inhibitor of gastric acid secretion in the patient with DUD. Exogenous prostaglandins ultimately may have a role. Bleeding patients undergo endoscopic procedures with the potential for cauterization. At arteriography, selective administration of vasopressor (eg, vasopressin into the left gastric artery) or embolization may be warranted. Multiple trials support the suppression of acid production in the critically ill patient, especially those receiving anticoagulation or on mechanical ventilation. However, there is insufficient data to support proton pump inhibitors over H2 antagonists, but in the acutely bleeding patient, proton pump inhibitors are quite effective as prophylaxis and superior to H2 antagonists.122 Although proton pump inhibitor treatment has been associated with rare reports of interstitial nephritis, hepatitis, and fundic gland polyps, long-term treatment with these drugs is safe when an indication exists for lengthy inhibition of acid secretion.11

Surgical Treatment

Several procedures and variations are performed for the management of DUD (Box 56-7). Duration of symptoms, gastric outlet obstruction, perforation,123 and hemorrhage impose specific considerations, as do various known complications of these procedures (Box 56-8). For example, after a truncal or selective vagotomy, approximately 20% of patients will have clinically impaired gastric emptying if a drainage procedure also is not performed.

Erosive gastritis is a common problem. Therapy involves appropriate blood and volume resuscitation, gastric irrigation with saline, and instillation of antacids. When bleeding does not stop or recurs, endoscopic evaluation and cauterization may suffice. If not, angiography may allow visualization of the damaged vessel for embolization or continuous infusion of intraarterial vasopressin. Surgical procedures for hemorrhagic gastritis are required in 10% to 20% of patients. No single technique is considered the procedure of choice, and decisions regarding the nature of the procedure selected may require open visualization of the focal versus diffuse nature of the bleeding. Total gastrectomy, partial gastrectomy with vagotomy, vagotomy and pyloroplasty, devascularization, and simple oversew procedures all have advocates.

Surgical therapy for patients with gastric ulcer generally involves ulcer removal and antrectomy (ie, distal gastrectomy) with direct anastomosis to the duodenum (Billroth I procedure). Unless features of hypersection of acid exist, a vagotomy generally is not performed. Perforation can be managed with excision and simple closure in debilitated elderly patients or more definitively in younger stable patients. If malignancy is encountered, an appropriate procedure should be performed.

Gastric carcinoma generally is divided into 2 broad categories. Early carcinoma is confined to the gastric mucosa or submucosa, regardless of size or of lymph node seeding. Many of these patients are curable surgically. A subtotal gastrectomy is warranted for localized disease, and a total gastrectomy is needed for more extensive involvement. Surgical therapy for advanced gastric carcinoma is generally less successful because less than 10% of patients survive 5 years. Procedures vary as to the extent of gastric resection and to the aggressiveness of lymph node and adjacent organ resection.124-125 Some studies suggest improved survival for patients undergoing palliative resections even when a cure is not possible.

Cholecystitis, Gallstone Disease, Cholecystectomy, and Biliary Disease

Approximately 20 million Americans have cholelithiasis, and another 800000 are diagnosed with it each year. Many predisposing factors exist (Box 56-9). The 3 basic types of gallstones are cholesterol, pigment, and mixed. The last category represents approximately 75% of all affected patients. Catalysts for stone formation include decreased gallbladder motility with stasis, increased gallbladder mucous secretion, altered epithelial ion transport, and possibly increased gallbladder synthesis of prostaglandins126 and increased biliary calcium.127

Diagnosis

Clinical cholecystitis is classically associated with obstruction of the cystic duct (eg, from stone, edema, sludge, fibrosis) and subsequent epithelial injury, enzyme release, and inflammatory response.128 In approximately 75% of patients, cholecystitis is self-limiting and resolves over approximately 1 week, but 5% to 10% of patients develop serious complications, including empyema, cholangitis, gangrene, or perforation. Positive cultures are found in approximately 20% to 30% of patients younger than 50 years of age, in greater than 50% of patients older than 70 years of age,181 in 20% to 40% of those with chronic disease, and in 60% to 70% of those with acute cholecystitis.129,130 Gram-negative organisms predominate. An overriding focus in evaluating patients is detecting cystic duct obstruction. Abdominal ultrasonography is extremely useful in detecting cholelithiasis, and technetium scans in detecting cystic duct obstruction (even in patients with elevated bilirubin levels). Plain abdominal films, oral cholecystography, and IV cholangiography are more limited as diagnostic tools.

Treatment

Oral therapy using deoxycholic acid analogues results in cholelitholysis because of their ability to decrease the rate-limiting enzyme in cholesterol synthesis, coenzyme A reductase. This is effective in some patients. Although it is recognized that asymptomatic gallstones frequently exist, management options are debated. Some studies document that about one-third of these patients will develop complications requiring urgent surgery. Others note that morbidity and mortality are lower after elective procedures in younger patients,103,131 although most suggest that routine prophylactic cholecystectomy for asymptomatic disease is not required.132

Cholecystectomy generally is performed within several days of onset of symptoms. Approximately 25% of patients develop recurrent cholecystitis if surgery is delayed, and 1 in 8 will require emergency cholecystectomy.133-134 Despite the risks associated with older patients, conservative management (eg, delayed surgery) in the elderly population may be inadvisable; gallbladder empyema, perforation, sepsis, and cardiovascular complications occur more often in this group.135-137

Lithotripsy with high-frequency shock waves disintegrates some gallstones. General anesthesia usually is not needed, but sedation and analgesia with appropriate monitoring are required.138 Although laparoscopic cholecystectomy17 has become the staple of gallbladder removal, management considerations are similar to those of any laparoscopic procedure (Box 56-10).

Open laparotomy is generally reserved for more complicated considerations (eg, abscess, perforation, need for intraoperative cholangiogram or bile duct exploration, suspected anatomic abnormalities, obesity). In addition, laparotomy remains the backup procedure for other procedures that fail or for patients with complications. Surgical manipulation of the abdominal viscera has been associated with various circulatory changes, including bradycardia and hypotension.

Transvaginal NOTES (natural orifice translumenal endoscopic surgical) cholecystectomy minimizes visible scars and expands the surgeon's arsenal in the healthy patient.12 In the high-risk patient, ultrasound-guided percutaneous cholecystostomy may be a valuable bridging alternative.13 The surgical and anesthesia team must discuss appropriate patient selection for NOTES, standard laparoscopic, open, or percutaneous surgical care of cholecystitis.

Biliary Tract Cancer

As many as 2000 new cases of gallbladder carcinoma may be seen in the United States annually. Patients are likely to be elderly women who have associated gallstones. Because of early metastasis, most patients are unresectable at presentation, and their 5-year survival rate is extremely low. Patients with microscopic disease have a much better prognosis. Palliative procedures are difficult for those with advanced disease; biliary decompression stents are placed for bile drainage.

Extrahepatic bile duct cancer survival rate depends on the location of the tumor. Survival improves from proximal to distal common duct sites and is best with a papillary morphology. Patients may undergo 1 or more laparotomies before arrival at a tertiary/definitive treatment center. Surgical management generally involves some form of biliary-enteric anastomosis (eg, Roux-en-Y hepaticojejunostomy, Roux-en-Y choledochojejunostomy, Whipple procedure, palliative silastic tube drainage) depending on the tumor's location.

Strictures of the Biliary Tract and Sclerosing Cholangitis

Benign strictures of the biliary tract result from various causes, including surgical trauma, inflammation from calculi, biliary tract infection (eg, bacterial cholangitis), blunt or penetrating abdominal trauma, toxic injury during hepatic arterial infusion therapy, and sclerosing cholangitis. Eighty percent of patients have symptoms within 1 year of the associated surgery or trauma.139 Symptoms and signs include abnormal biliary drainage or bile leakage immediately postoperatively and variable evidence of biliary obstruction and abnormal liver function in all patients. Painless jaundice and cholangitis are seen less often. Cholangiography should define biliary tree anatomy, and the placement of a ring catheter permits drainage and management of infection preoperatively.

When patients have an acute stricture after surgery, operative treatment may consist of the resection of a short segment of bile duct or a segmental duct ligation. More involved injuries usually demand creation of a Roux-en-Y jejunal limb and T-tube of transhepatic drainage catheters. Later in the postinjury period, extensive adhesions often are present, necessitating tedious dissection. Again, surgical management requires the creation of a Roux-en-Y loop and decompression via T-tube, ring catheter, or a transhepatic silastic stent.

Endoscopic Procedures

Endoscopic abdominal procedures leave inconspicuous scars and result in less postoperative pain with shorter hospitalizations, decreased hospital costs,140,141 and even immunologic advantages.142 As "minimally invasive" surgical techniques, reduced risk is implied, but endoscopic surgery involves the instillation of gas under pressure into a "closed" cavity, a process that may initiate unique physiologic responses and potential complications.

Diagnostic examination, cholecystectomy, vagotomy, appendectomy, adrenalectomy, nephrectomy, bariatric procedures, liver resection, pancreatic surgery, colectomy and hiatal, diaphragmatic, and inguinal hernia repair are among the abdominal procedures being performed with laparoscopic equipment. Each procedure has its own indications and conversion rates to an open method (eg, 1.0%-6.9% conversion to laparotomy with laparoscopic cholecystectomy).143

The physiologic changes associated with laparoscopy include those associated with tilting the patient to facilitate instrumentation and surgical exposure, the pressure effects of instilled gas, and the systemic effects of the gas—almost universally CO2—that is instilled (and absorbed or embolized). In addition, careful positioning of the extremities and torso is a shared responsibility of the surgical team and the anesthesia team.

The head-down position (ie, Trendelenburg) reduces vital capacity because of the increased weight of the abdominal contents on the diaphragm.144 This effect is more pronounced in elderly, obese, and debilitated patients. In those undergoing open procedures, it is made worse by the placement of retractors and surgical packing under the diaphragm. In addition to this encroachment on lung expansion, right mainstem bronchial intubation can occur. Either of these can be associated with hypoxemia.145 In contrast, the head-up position redistributes central blood volume peripherally and further aggravates any impairment of venous return created by the pneumoperitoneum.

The instillation of CO2 to create an intentional pneumoperitoneum carries with it a number of physiologic side effects and complications (Box 56-11). Mechanical injury at the time of trocar insertion can lead to bleeding or bowel perforation. Bleeding also can occur from injury to vessels encountered during surgical instrumentation and dissection. With current laparoscopic equipment, intra-abdominal pressure is maintained between 12 and 15 mm Hg (17-22 cm H2O). Because of leaks around the various cannulae, enormous gas volumes (≥50 L)146 may be required during the course of the procedure to generate this relatively low pressure. Such pressures and the resulting abdominal distension may disturb the protective function of the gastroesophageal junction. The hemodynamic changes associated with this pneumoperitoneum depend on a number of factors, including the resulting intra-abdominal pressure, the amount of CO2 absorbed, the patient's level of hydration, the type of ventilation, and the nature of the surgery. Cardiac function during insufflation of peritoneal CO2 has been studied primarily in healthy (eg, no known cardiac disease) patients using a variety of cardiac function measurements (dye dilution, impedance cardiography, transesophageal echocardiography, and pulmonary artery catheters). Unfortunately, none of the studies have controlled well for the level of anesthesia at the various stages of the procedures and have managed hypercapnia differently. Most studies,147-150 but not all,151,152 report a decrease in left ventricular function and cardiac output (cardiac output decreased 7%-24%). Similarly, most studies found an increase in central venous pressure (redistribution of abdominal blood volume), with an increase in systemic vascular resistance and mean arterial pressure. In addition, with assumption of the reverse Trendelenburg position, cardiac index may decrease by 50% of preanesthesia and preinsufflation values.149 Left ventricular end-diastolic, right atrial, and pulmonary capillary wedge pressures dramatically decrease after assumption of the reverse Trendelenburg position.153 Venous stasis of the lower extremities also occurs, with attendant concerns for embolic phenomenon.154 Patients with cardiovascular disease will have responses to laparoscopy that are affected by the extent of cardiac reserve, baseline medications, level of hydration, and their response to the anesthesia medications used.155 The potential deleterious effects of hypercapnia on cardiac function (eg, increased sympathetic activity, myocardial depression) may further complicate laparoscopy in those with cardiovascular disease.

During retroperitoneoscopic adrenalectomy (prone–jackknife position or lateral), a small (<10 cm) cavity in the lumbodorsal fascia is created with a distension balloon trocar. CO2 is insufflated to a pressure of 15 to 20 mm Hg. Unlike laparoscopy, stroke volume and cardiac output appear to increase with insufflation, as do mean arterial pressure, central venous pressure, and pulmonary artery pressure. No change was noted in pulmonary capillary wedge pressure, heart rate, and systemic vascular resistance.156

Relatively small CO2 emboli have been detected by transesophageal echocardiography in 69% of patients, classified by the American Society of Anesthesiologists as physical status P1 to P3, who undergo laparoscopic cholecystectomy.157 Fatal massive CO2 embolism has been reported,158 including a report of death from delayed CO2 embolism associated with gas trapping in the portal circulation.159 With time, subcutaneous or mediastinal emphysema and pneumothorax may develop, with associated hypoxemia, hypotension, and cardiovascular collapse. The incidence of extraperitoneal insufflation of CO2 has been reported to range from as little as 0.4% to 2%160 to 20% to 64%,161 and is more likely during lengthy procedures such as fundoplication.162 The development of pneumothorax and/or pneumomediastinum during endoscopic surgery is a serious and potentially life-threatening complication. When either is suspected, from hemodynamic deterioration or from the presence of subcutaneous emphysema, especially of the neck and face, aggressive investigation (auscultation, chest radiograph) and management (eg, chest tube for tension pneumothorax; conversion to an open procedure) should be undertaken. Procedures on the lower esophagus are more likely to result in these complications.163

Ventilation and pulmonary function are important concerns during laparoscopy. With conventional open laparotomy, it is well accepted that upper abdominal surgery is associated with postoperative pulmonary dysfunction in approximately 50% of patients.163 This dysfunction is related to impaired diaphragmatic function, pain, type of incision, and decreased FRC.164-166 Pulmonary function is also impaired after laparoscopic cholecystectomy, with sustained decreases in forced vital capacity, peak expiratory flow, and forced expiratory volume in 1 second (FEV1) noted 24 hours after surgery; fortunately, these changes are only approximately 50% of those seen in conventional open cholecystectomy.167

The exogenous CO2 insufflated during laparoscopy is soluble in blood and after transperitoneal absorption is presented to the lungs for excretion. End-tidal CO2 (ETCO2) increases from 0% to 30%168,169 when minute ventilation is held constant. Increasing ventilation by as much as 30% may be necessary to keep the ETCO2 in the mid-30s (mm Hg) range.170

During laparoscopy, an overriding anesthetic concern is the preservation of ventilation, which tends to be impaired by surgical positioning and abdominal distension. This almost always means general anesthesia with endotracheal intubation.17 Not only does this provide protection for the airway, but it permits adequate measurement of ETCO2 and manipulation of ventilation as needed. Routine intraoperative monitoring (ETCO2, pulse oximetry, blood pressure, airway pressure) should be adequate for the expected physiologic changes encountered in most patients. The anesthesiologist should be aware of the insufflating pressure being used and should be alerted if an unusual amount of CO2 is required.

It is theoretically sound to avoid N2O for at least 2 reasons. First, it diffuses into the abdominal cavity in concentrations sufficient to support combustion of intestinal gas172,173; second, it will diffuse into CO2 bubbles and emboli, increasing their size and the potential for an obstructive event.

Adequate muscle relaxation is required during laparoscopy so that spontaneous respiratory effort does not impair the surgical procedure or risk increasing the gradient for embolic gas to enter the central circulation.

Despite the limited surgical incision(s), postoperative muscle pain remains a problem, even in children.174 This has not been eliminated by avoiding succinylcholine or by manipulation of other anesthetic regimens.175 Nausea and vomiting is common after laparoscopy, especially in women, and it appears that women are at increased risk for this during their menses.176

Droperidol, a dopamine receptor antagonist, has been found to decrease nausea and vomiting in nonmenstruating women, but not during menses. However, the low risk of QT interval prolongation and torsades des pointes has led to a recent Food and Drug Administration (FDA) black box warning, yet at lower dosages maintains clinical utility. Because serotonin has been implicated in several premenstrual syndromes, serotonin antagonist therapy (eg, ondansetron) can be beneficial.

In the rare event of catastrophic hemodynamic collapse during laparoscopy, several possible causes should be considered. During laparoscopy, hemorrhage can be obvious or occult (eg, retroperitoneal). Pneumothorax, massive CO2embolus, and pneumomediastinum may occur. Initial therapy includes releasing the pressurized pneumoperitoneum (ie, conversion to open procedure). For pneumothorax, a thoracentesis should be performed. If massive embolization occurs, N2O, if used, should be discontinued immediately and cardiopulmonary resuscitation should be performed. The patient should be placed in the left lateral position. Attempts at embolus retrieval should be made through central venous access, if available. If these measures do not provide sustained benefit, even cardiopulmonary bypass, if available, may be necessary.

Laparoendoscopic single-site surgery (LESS) uses one port side to minimize pain. Natural orifice translumenal endoscopic surgery (NOTES) uses a natural orifice to access the abdominal cavity.177 Endoscopists have experience in endoscopic ultrasound-guided pancreatic biopsy, endoscopic retrograde cholangiograms, and stenting. Gynecologists have experience with transvaginal hysterectomies. Gastrointestinal surgeons are using transvaginal and transgastric NOTES for cholecystectomies, sigmoidectomies, appendectomies, liver biopsies, and tubal ligation.178 As instrumentation and techniques evolve, LESS and NOTES will be used more frequently. The GI anesthesiologist must remain cognizant of limitations and a steep learning curve for natural orifice surgery in order to minimize the risk of infection (eg, the perioperative administration of appropriate antibiotics), and must be prepared to recognize and manage intraperitoneal hemorrhage, compression syndromes, and more prolonged procedures.179

Bariatric Procedures

Ten percent of all health costs in the United States are related to treating obesity and obesity-related complications.180 Perioperative care of the extremely obese (body mass index [BMI] >40 kg/m2) presents multiple challenges. A myriad of comorbidities including obstructive sleep apnea, diabetes, dyslipidemia, hypertension, atherosclerosis, cardiomyopathy, cholecystitis, nonalcoholic steatohepatitis, and certain cancers181 make this a formidable group of patients.

Bariatric surgery refers to procedures of the stomach or intestines designed to result in weight loss. Initial attempts at such surgery (eg, jejunoileal bypass) induced malabsorption and rapid weight loss, but the resulting blind loop syndrome limited its long-term acceptability. Some advocate adjustable gastric banding, whereas others advocate a procedure involving the so-called duodenal switch. Variations on the theme of a Roux-en-Y gastric bypass may be the most frequently used method in the United States. With the advent and increasing use of laparoscopic approaches, the early postoperative course and recovery have been greatly improved. Ultimately, the goal has been to balance restriction of food intake and malabsorption for enhanced patient acceptance and success of therapy.182 NOTES endoluminal and transgastric procedures are now being performed that include banding, botulism toxin injection, and electrode implantation.183,184

Peripheral venous access is often difficult or impossible and central venous access is required. Central access can be very challenging because of an inability to properly appreciate anatomical landmarks; however, such access has been greatly facilitated by the use of ultrasound guidance.185,186 Measurement of an accurate blood pressure may require invasive access. Unsurprisingly, the physical mass of the extremely obese patient requires appropriate bed selection and positioning because of the risk of compression neurologic injuries.187

One misconception associated with anesthesia for the extremely obese involves airway management; with increasing bariatric surgical experience, extreme obesity no longer is an independent risk factor for difficult intubations. In more than 750 patients without airway pathology, no correlation between BMI and difficult intubation was noted.188 In fact, of 100 direct laryngoscopies of patients with BMI greater than 40 kg/m2, only 1 intubation failed and only 12 intubations were deemed challenging (not significantly different from the general population).189 Morbidities associated with obstructive sleep apnea include hypoxemia, pulmonary hypertension, and cor pulmonale.

Extreme obesity is associated with significant cardiovascular perioperative risks. More than 50% of these patients are hypertensive.190 (See Chapter 23 for a detailed discussion of the preoperative assessment of the obese patient.) The Framingham study indicated that for every increased increment in body mass index (weight in kg/height in m2), a 5% to 7% increased risk of congestive heart failure exists.191 An "X" syndrome of massive obesity that includes glucose intolerance, hypertension, hyperlipidemia, and microalbuminemia has been described; it is strongly associated with coronary artery disease.16 Such findings suggest the potential positive benefits of bariatric surgery: for example, for every kilogram of weight loss, systolic pressure decreases 0.5%, serum glucose decreases 0.2 mM, low-density lipoprotein cholesterol decreases 0.7%, and high-density lipoprotein cholesterol increases 0.25.192 In spite of these potential long-term benefits, bariatric surgery still has significant perioperative risk: mortality 1.5%, pulmonary embolism 1.14%, and small bowel obstruction and anastomotic leaks 3% each.193 In addition, there are both short- and long-term metabolic and nutritional issues that vary with the procedure type and can be of concern.194,195

Mean weight loss for patients undergoing all forms of bariatric surgery has been reported to be approximately 61% of excess body weight, and maintenance of weight loss far exceeds that from medical treatments alone. Significant improvements in diabetes, hyperlipidemia, hypertension, and obstructive sleep apnea are usually expected. Improvements in other comorbidities, such as fatty infiltration of the liver, respiratory and asthmatic symptoms, and cardiomyopathy are more modest. Emerging studies suggest a reduction in mortality associated with bariatric surgery and a clear improvement in quality of life.183,196 and many consider such surgery the only cure for morbid obesity (Fig. 56-6).

Advances in bariatric surgery using endoscopy and NOTES have the potential to improve cosmesis and postoperative recovery. The natural orifice incision used in NOTES procedures may be very beneficial in obese patients if it reduces the high rate of incision-related hernia formation.197 The first human transvaginal endoscopic sleeve gastrectomies were reported in 4 patients, taking 90 to 100 minutes to perform and a 2-day hospital stay.198 Note that intrinsic challenges include entry visualization, complication management, infection prevention, and patient positioning; these are magnified in the bariatric population, but provide a promising future.

The Pancreas and Pancreatic Surgery

Pancreatitis

Although the treatment of acute pancreatitis is primarily medical, surgery may be required for such conditions as draining an abscess. Emerging evidence suggests that early surgery may not be as high a risk as previously thought.199 Patients with pancreatitis are extremely ill with severe abdominal pain and may have fever, nausea and vomiting, jaundice, hypotension, ileus, and external distortion of the stomach on radiographs. Management includes nasogastric suction, maintenance of intravascular volume, anticipation of respiratory insufficiency,200-202 analgesia, and nutritional support.

The patient with chronic pancreatitis may have incapacitating upper abdominal pain radiating to the back, which can be continuous or intermittent, especially after eating. Forty percent of patients have diabetes from loss of pancreatic tissue.203 Exocrine function may be sufficiently abnormal to require pancreatic enzyme replacement. Obstructions, strictures, and dilations of the pancreatic ductal system are thought to produce the pain through sympathetic pathways. Several surgical procedures have evolved to decompress the ducts and remove damaged pancreas. A caudal pancreatojejunostomy204 uses a Roux-en-Y loop to decompress the tail of the pancreas. With the Puestow-type205 procedure (Fig. 56-7), the Roux-en-Y limb envelops the pancreas distally, allowing pancreatic ducts to be opened longitudinally for drainage into the loop. For both of these procedures, a splenectomy and excision of the tail of the pancreas are necessary for technical reasons. A modification of the Puestow procedure206 (Partington procedure) allows the tail of the pancreas and the spleen to be spared. Postoperatively, some patients require insulin and pancreatic enzyme replacement. Other patients with severe chronic pancreatitis require a near-total pancreatectomy or a pancreatoduodenectomy to remove sufficient tissue to relieve pain. Patients with pseudocyst of the pancreas require drainage of the cyst through a Roux-en-Y loop or directly into the stomach. Alternatively, a distal cyst may be removed by a partial pancreatectomy.

Other Conditions

Cancer of the pancreas and periampullary area is a frequently diagnosed problem with, unfortunately, an increasing incidence. Approximately 25 000 patients are diagnosed each year in the United States. Diagnosis usually is suggested by ultrasonography or computed tomography. Magnetic resonance imaging, endoscopic retrograde cholangiopancreatography, or percutaneous transhepatic cholangiography may yield information concerning the site and etiology of bile duct obstruction. Percutaneous fine-needle aspiration biopsy may be performed with the aid of ultrasound examination or computed tomography. Despite this array of tests, determination of the extent of disease and often the tissue diagnosis should await a thorough intraoperative examination. Only then can the necessary procedure be decided. The cure rate is 5% or less, largely because of relatively vague and general symptoms before the onset of jaundice, which greatly narrows the diagnostic possibilities. By the time the diagnosis is suspected, the lesion may be unresectable. Because only small lesions of the head of the pancreas or ampullary area are resectable, and because many of the remaining patients still require a palliative procedure to relieve obstructive jaundice, a considerable number of these patients undergo laparotomy.

Most procedures aimed at a cure are termed a pancreatoduodenectomy (Fig. 56-8; ie, Whipple procedure). Variations include total pancreatectomy, regional pancreatectomy, and similar procedures that preserve the pylorus of the stomach. These are long, extensive bowel resections that cause considerable morbidity. Serious postoperative complications include hemorrhage, coagulopathy, and hepatic, renal, pulmonary, and cardiovascular failure. Invasive monitoring and postoperative intensive care are generally required. Thoracic epidural analgesia can be an important component of postoperative management.

With the advent of improved laparoscopic instrumentation and techniques, a comparison of laparoscopic to open distal pancreatectomies demonstrated no differences in the positive margin (eg, remaining local malignancy) rate, operative time, or fistula formation rate. Laparoscopic distal pancreatectomies were associated with less blood loss, shorter hospital stay, and overall fewer complications.207,208

Endocrine disease of the pancreas also is managed surgically. An insulinoma is the most common of these diseases. Because this tumor secretes insulin autonomously, spontaneous hypoglycemia is seen, with symptoms caused by decreased blood sugar levels and the resultant burst of catecholamine release. The differential diagnosis for hypoglycemia is extensive, but once insulinoma is diagnosed, management is surgical. Benign tumors are either enucleated or resected with a margin of pancreas. When no tumor is found at laparotomy, a distal or near-total pancreatectomy is performed, depending on the histology. Malignant disease may be surgically debulked with subsequent chemotherapy.

The Zollinger-Ellison syndrome results from a pancreatic or duodenal tumor (gastrinoma) that secretes excessive gastrin. Symptoms usually are abdominal pain and possibly diarrhea. Associated endocrinopathies include multiple endocrine neoplasia syndrome type 1 (MEN 1: parathyroid, pituitary, adrenal) and MEN 2 (medullary carcinoma of the thyroid, parathyroid adenoma, pheochromocytoma). Medical management involves H2-receptor antagonists or proton pump blocker therapy. Surgical management involves vagotomy and pyloroplasty when no tumor is discovered at laparotomy or major resection procedures when a localized tumor is found. The presence of metastatic disease and MEN syndromes dictates medical therapy.

Other endocrine tumors of the pancreas include VIP (VIPoma), glucagonoma, and somatostatinoma. Surgical considerations are similar to those for insulinoma and gastrinoma (see Gastrointestinal Endocrinology section).

Pancreas Transplantation

Pancreas transplantation (PTX)209 has become a surgical treatment for type 1 diabetes mellitus.210 Most patients receive their PTX with or shortly after a renal transplantation, although some have received a pancreas before becoming uremic (such treatment is controversial).211

Evaluation of patients before PTX includes extensive assessment of the cardiovascular system because the incidence of coronary artery disease in young diabetic patients with end-stage renal disease is high.212 Active infection (eg, dental abscess, peritonitis, osteomyelitis, decubitus ulcers) should be sought and managed before transplantation. Secondary diabetic complications (eg, retinopathy) should be documented and quantified in an effort to gauge the effects of the transplant process on their progression. Recipient contraindications include malignancy and active infection, with concern for those with blindness, advanced cardiovascular disease, and major amputation.

Donor organs typically come from patients younger than 55 years of age without major atherosclerosis of the celiac axis, abdominal contamination, pancreatic injury or pancreatitis, or diabetes. Neither donor serum glucose nor amylase appears to have predictive value for ultimate function in the recipient.213 Earlier competition between harvesting teams for the liver or pancreas has been largely resolved by techniques permitting simultaneous retrieval of the liver and the pancreas.214

There are several approaches to implanting the pancreas. Some drain the pancreas enterically via a Roux-en-Y loop. Reexploration is frequent with this procedure because of a high incidence of complications. Assessment of organ function and rejection is difficult. Other centers perform PTX via a bladder drainage procedure (Fig. 56-9). Some use direct draining of the pancreatic duct into the ureter or bladder, whereas others use a small "button" of duodenum or a closed duodenal segment for union with the bladder. Vascular anastomoses are with the iliac vessels, similar to a renal transplantation. Hypertension, abnormal renal function, and all the sequelae of diabetes mellitus and its management make this a challenging group of patients.

Perioperatively, patients undergoing PTX need to have appropriate cardiovascular monitoring and a regimented approach to managing serum glucose levels. This may entail insulin infusion protocols and frequent intraoperative glucose determinations in an attempt to prevent hypoglycemia and hyperglycemia. Glucose-containing solutions are avoided unless the glucose level is lowered to less than 60 mg/dL. With reperfusion of the new pancreas, a dramatic increase occurs in blood sugar levels for reasons not entirely understood, so it is also prudent to monitor glucose levels frequently for the first hour or so after reperfusion. Postoperatively, the patient is treated in an intensive care setting.215-217 (See Chapter 59 for an in-depth discussion of pancreas transplantation.)

Small Bowel Transplantation

Because of extremely poor outcomes in patients with extensive bowel resection for acute and chronic disease, and because of success in other solid-organ transplantation, small bowel transplantation has been pursued by a few selective academic centers. Candidate patients have intestinal failure and have significant complications from total parenteral nutrition. Furthermore, these patients have one of the highest mortality rates of any patients waiting for solid organs.218 Candidate organs are difficult to acquire because the intestine is sensitive to pressor-induced ischemia that may occur during aggressive intensive care, both before and after brain-death declaration. (See Chapter 59 for a detailed discussion of small bowel transplantation.)

Small bowel transplantation may be coupled with liver or en bloc visceral organ transplantation. Anesthesia for small bowel transplantation with liver or en bloc visceral transplantation is similar to orthotopic liver transplantation. (See Chapter 57 for a detailed discussion of liver transplantation.) For isolated small bowel transplantation, significant lysis of adhesions and vascular anastomoses require adequate perfusion pressure and fluid resuscitation.219

Children with intestinal failure and total parenteral nutrition–induced liver disease who are without venous access have the highest mortality of solid organ candidates. A recent small report of living related hepatic/intestinal transplantation in 13 donors and 10 recipients noted no donor complications, 100% 1- and 2-year recipient survival, and 80% intestinal graft survival (1 intestinal graft was successfully reimplanted). The same institution reported a 60% and 50% 1- and 3-year survival, respectively, for living related intestinal transplantation.220

Surgical technique of en bloc visceral transplantation and the exclusion of the colon aided the improvement of small bowel transplantation.219 But the greatest advances, as with other solid-organ transplantation, have occurred because of improvements in immunosuppression, which have led to longer organ and patient survival. Tacrolimus, mycophenolate, rapamycin, daclizumab, alemtuzumab, interleukin-2 antagonists, and steroids represent novel increments in immunosuppression developed in the last 20 years. Others have used donor bone marrow infusion with ex vivo graft irradiation as adjuvant therapies to improve small bowel survival.219,221

Preoperative screening and aggressive therapy for cytomegalovirus and Epstein-Barr virus are also important considerations for extending organ and patient survival.222,223

Gastrointestinal Bleeding

GI bleeding often represents a major diagnostic and therapeutic challenge. Initial signs may be hematemesis, melena, hematochezia, or occult blood in the stool. A loss as little as 60 mL per day can result in a black stool, and less than 10 mL can result in a positive hemoccult test. Many patients with GI bleeding are elderly or debilitated, and symptomatic hemorrhage causes major stress to other organ systems (eg, cardiac, renal, central nervous).

Upper Tract Bleeding

The list of potential etiologies for upper GI hemorrhage is lengthy, but the 4 most common causes appear to be peptic ulcer disease, erosive gastritis, esophageal varices, and Mallory-Weiss tears of the esophagus.224 Other causes include malignancy, blood dyscrasias, hemostatic disorders, aortoenteric fistulas, Dieulafoy syndrome, and collagen vascular diseases. In 1 series, 12% of patients with upper GI bleeding had chronic renal failure and bled from angiodysplastic lesions of the stomach and duodenum. It usually is stated that if the patient's systolic pressure is less than 100 mm Hg, with a pulse greater than 100 beats/min (ie, a loss of 2 or 3 units or more of blood) and red or maroon stools, then the mortality rate is greater than 20% and surgical intervention is necessary in more than 50% of patients.225 Chronic lung, renal, cardiac, and liver disease and age older than 60 years add to this burden.

Diagnosis is aided by esophagogastroduodenoscopy in the first 24 hours. Management includes volume replacement and attention to illness in other systems. Some patients may receive parenteral vasopressin, such as an arterial infusion after angiography locates a bleeding ulcer or Mallory-Weiss tear, or an IV infusion for variceal bleeding. Varices often can be controlled with a Sengstaken-Blakemore tube, usually in preparation for more definitive management, such as sclerotherapy. Vasopressin often is still infusing when patients arrive for surgery to control bleeding. Vasopressin increases splanchnic and hepatic arteriolar resistance while decreasing portal venous pressure and hepatic blood flow. After a bolus dose, effects may last for approximately 1 hour.226 Worrisome side effects of vasopressin include coronary artery vasoconstriction with myocardial infarction, a potential complication of its use in patients with myocardial ischemia. Intestinal and extremity ischemia also can occur.227,228

Lower Tract Bleeding

The more frequent causes of lower GI bleeding are anorectal polyps, colonic polyps, colorectal cancer, inflammatory bowel disease, submucosal angiodysplasia, and diverticular disease. In children, juvenile polyps, Meckel diverticulum, and arteriovenous malformations are additional causes. Because the bleeding often is intermittent, diagnostic evaluation may be frustratingly negative. Endoscopy, radiographic examinations, and selective angiography are among the diagnostic and therapeutic (eg, electrocoagulation, embolization) modalities. Technetium-99m–labeled erythrocyte scans appear to be useful for slow, recurrent lower GI bleeding. Surgical procedures are directed toward the suspected diagnosis. Infrequently, when troublesome and symptomatic bleeding persists without a diagnosis, laparotomy may be undertaken for intraoperative endoscopy. Video camera capsule endoscopy and balloon enteroscopy have revolutionized lower tract bleeding diagnosis. The entire small bowel, or nearly so, can be visualized with a double balloon enteroscope making it the nonsurgical gold standard for evaluation of the deep small bowel.229

Gastrointestinal Obstructive Disease

Impaired GI transit results from various conditions causing pseudo-obstruction (ie, decreased motility) and paralytic ileus, and those producing varying degrees of mechanical obstruction (Box 56-12). Considerable variation exists within each of these broad categories, and associated illness can be extensive.

Pseudo-obstruction and paralytic ileus generally represent intestinal motility disorders, and the list of causes is long (Box 56-13).303 Patients with pseudo-obstruction usually have an insidious clinical course that evolves over months and years for the primary disease and for any coexisting GI manifestations. In general, remissions and exacerbations often occur.

Paralytic ileus tends to be acute in onset and to develop in patients with no suspected predisposing disease process. Although probably caused by neurohumoral mechanisms, paralytic ileus is not well understood. The most common ileus is that seen after intra-abdominal operations. Length of hospitalization following abdominal surgery depends on several factors including pain control, presence of mechanical devices (drains, catheters, and intervenous tubes), and postoperative ileus. In 2000, the Health Care Financing Administration demonstrated that 161 000 Medicare patients underwent major intra-abdominal operative procedures costing more than $1 billion. Postoperative ileus has the potential to play a significant role in length of hospitalization, morbidity, mortality, and cost.

Normal gastrointestinal motility is an integration of smooth muscle contraction, neural input, hormonal signals, and an enteric nervous system. The digestive system has as many neurons (Auerbach and Meissner plexus) as the spinal cord. After an intra-abdominal operation, the electrical disorganization and ineffective coordination of propulsion characterizing an ileus usually resolves after 4 to 5 days.231 The small intestine usually recovers motility within a few hours. The stomach resumes its ability to empty after about 24 hours, but the colon may not regain effective motility for 48 hours or longer.232-234

Physical manipulation of the abdominal viscera, opioids, catecholamines, and inhalational anesthesia decrease bowel motility.235 To date, there is no specific treatment for postoperative ileus. Nasogastric tubes historically have been inserted to reduce pulmonary complication, hasten bowel function return, increase patient comfort, and shorten hospital stay. In fact, a Cochrane analysis (4194 patients, 2108 routine nasogastric tube, 2087 no or selective tubes) demonstrated that not having a nasogastric tube after a procedure hastened return of bowel function (P < 0.001) and marginally decreased pulmonary complications (P = 0.07).236 Early ambulation is an inexpensive therapy that decreases risk of thromboembolism and may be psychologically helpful for patients, but does not appear to benefit patients in resolution of postoperative ileus.237 In 1928 Steinbrok et al reported treatment of ileus by splanchnic epidural anesthesia. Although there have been suggestions that sympathectomy from epidural anesthesia will cause an increase in anastomotic leaks, an analysis of 12 trials with 562 patients failed to find an association between epidural anesthesia and anastomotic breakdown.238 Furthermore, when compared with patients who were receiving patient-controlled parenteral opioids, epidural analgesia provided better postoperative pain control.239

Although neostigmine, metoclopramide, cisapride, erythromycin, ceruletide, somatostatin, laxatives, and nonsteroidal anti-inflammatory agents have theoretical advantages for enhancing GI motility, investigations have not demonstrated useful effects in humans.231 It is well established that opioids acutely and chronically slow gastrointestinal motility. Administration of peripheral opioid antagonists appears to lead to a faster return of bowel function and faster hospital discharge, without an increase in readmissions, and with no difference in pain scores.239,240

Other abdominal causes of paralytic ileus include blunt trauma, bowel perforation, bile peritonitis, and intra-abdominal sepsis. Nonabdominal causes include lobar pneumonia, myocardial infarction, massive trauma, generalized sepsis, and electrolyte abnormalities such as hypophosphatemia and hypokalemia.

Mechanical obstruction is a vexing diagnostic problem that generally requires surgical intervention. Simple obstruction implies adequate blood flow to the obstructed area, whereas strangulation connotes insufficient circulation to the area. Obturated obstruction is caused by an intraluminal foreign body. Mechanical obstruction tends to be acute, with fairly rapid progression to complete obstruction.

Approximately 60% to 80% of obstruction occurs in the small intestine.241 Pain, distension, emesis, and obstipation typically are present. Volume loss, tachycardia, and electrolyte disturbances can occur from severe vomiting and the massive volumes that are sequestered in strangulated bowel.

Approximately 7 to 9 L of fluid are presented to the gut daily242 from varied sources (Table 56-2). With obstruction, not only is reabsorption hindered, but intestinal fluid secretion may be increased.243 In addition, rapid infusion of IV fluids, which may be necessary for hemodynamic support, has been reported to increase secretion.244 Once intraluminal pressure exceeds approximately 20 cm H2O, reabsorption fails.245

Because intestinal fluid has a tonicity and electrolyte composition similar to extracellular fluids, acid-base and electrolyte disturbances generally are not severe. Duodenal obstruction can lead to hypokalemic alkalosis resulting from severe emesis. In addition, once strangulation occurs (and no definitive criteria exist for this diagnosis), necrosis of bowel and bacterial proliferation contribute to rapid sequestration of fluid and colloid in the affected bowel and peritoneal cavity. Together with vomiting, this can produce marked depletion of intravascular volume and the potential for renal and cardiovascular instability.

Other conditions can mimic small bowel obstruction (Box 56-14), making the diagnosis difficult. This especially applies to elderly patients, who often have only minimal evidence of peritoneal irritation.

Acute large bowel obstruction is associated with pain, distension, vomiting, and obstipation, although large bowel obstruction can be more insidious than small bowel obstruction and may present without pain but with "overflow" diarrhea. Fifty percent or more of large bowel obstructions result from colorectal cancer, with much of the rest caused by diverticulitis, volvulus, and fecal impaction.246 Small bowel obstruction may occur concurrently. An incompetent ileocecal valve may permit the eventual development of feculent vomiting.

Management includes decompression of the stomach, appropriate IV fluids, and attention to conditions in other systems (eg, infection, renal and cardiovascular problems). Depending on the patient's age and the severity of illness or suspected intervention, invasive hemodynamic monitoring may be warranted.

Patients with GI motility disorders and those with obvious obstruction are at risk for regurgitation and aspiration during the induction and maintenance of anesthesia and postoperatively. The anesthesiologist should be aware of the potential for such difficulty with this group of patients and treat appropriately. At the least, this would include the omission of oral premedication and the use of postoperative (and preoperative when indicated) nasogastric suctioning. Anesthesia should be induced using awake intubation or rapid sequence considerations.

Many severely ill patients require emergency surgical intervention for life-threatening conditions such as abdominal trauma, resection of nonviable bowel, relief of obstruction or strangulation, drainage of an abscess, or removal of a severely inflamed gallbladder. In addition to their abdominal disorder, they may be intubated in an intensive care unit, may have evidence of organ system failure (eg, pulmonary, renal, central nervous system, and major metabolic changes), or may be older with serious cardiac and vascular disease. Many behave as if they have a severe infection whether or not one is eventually discovered. In the past, varying etiologies have been suggested, including gram-negative sepsis, endotoxemia, sepsis syndrome, and multiple system organ failure. Because of the many similarities among such patients, even for those whose clinical course falls outside these diagnoses (eg, patients with gram-positive sepsis, viral or fungal infection, or no infection at all), other explanations have been sought.

Common to many of these patients is evidence of major inflammatory mediator production and release by polymorphonuclear leukocytes, macrophages, monocytes, platelets, and the endothelium. The cyclooxygenase pathway has important effects. More than 30 such mediators have been identified, with cytokines such as tumor necrosis factor; interleukins-1, -6, and -8; substance P; granulocyte-macrophage colony-stimulating factor; interferon; and platelet-activating factor among the most studied.247,248

It has been suggested that the systemic inflammatory response syndrome (SIRS) represents the earliest, fairly nonspecific phase of a process that may lead to organ dysfunction and, ultimately, organ failure. Currently, the diagnosis of SIRS requires that 2 of the findings in Box 56-15 be present.249 Systemic inflammatory response syndrome and multiple organ failure appear to be the ends of a hierarchical continuum with an increasing inflammatory response to infectious and noninfectious stimuli. Initially organ dysfunction is more functional than permanent, organ failure and mortality increase with increasing inflammatory response.250-252

The GI tract is a vulnerable organ system. Any insult to adequate core tissue perfusion (eg, hemorrhage, cardiac arrest, cardiopulmonary bypass) may result in severe or relative hypotension, with ensuing GI mucosal ischemia. Endogenous vasoconstrictors may be released253 (Box 56-16), which may affect the splanchnic bed more consistently than others.254-257 Reperfusion after shock may be associated with oxygen and free radical mucosal damage. In addition, so-called myocardial depressant factors can be released from the pancreas and possibly the small intestine, which further contribute to tissue hypoperfusion and low cardiac output syndrome. As much as 15% to 65% of the circulating volume can redistribute to damaged bowel during this process. Although inadequate perfusion limits delivery of oxygen for cellular processes, other mechanisms that directly affect mitochondria may have similar effects even with relatively adequate (or increased) perfusion. A host of factors affect the mitochondria, including reactive oxygen species, local PO2, levels of adenosine triphosphate, and hormonal influences such as thyroid, catecholamines, corticosteroids, and leptins. Nitric oxide is a strong inhibitor of mitochondrial electron transport. If insufficient energy is available to fuel metabolism, critical thresholds of adenosine triphosphate result and cellular dysfunction and death ensue.

Although the systemic cardiovascular response demanded by these conditions usually is hyperdynamic, it often is inadequate, either because metabolic requirements are too high (or because of end-organ inability to use oxygen) or because of limitations imposed by evolving or underlying myocardial dysfunction. Management of these patients is beyond the scope of this chapter. When the anesthesiologist encounters these patients, they frequently are already receiving vasopressor and inotropic support. Intraoperative care includes intensive evaluation of oxygen delivery, optimization of volume and cardiovascular function, and avoidance of drugs and agents that will further compromise their already tenuous status.258,259

The complex physiologic and metabolic interactions of the GI tract and other organ system functions can present fascinating challenges for the anesthesiologist. Because GI surgery often can seem so benign, it is perhaps more difficult to remain "tuned in" to such concerns. The rewards of good patient care should be sufficient incentive to reexamine important issues in GI surgery and anesthesia from time to time.

• Block BM, Liu SS, Rowlingson AJ, Cowan AR, Cowan JA Jr, Wu CL. Efficacy of postoperative epidural analgesia: a meta-analysis. JAMA. 2003;290:2455-2463.
• Cash BD. Evidence-based medicine as it applies to acid suppression in the hospitalized patient. Crit Care Med. 2002;30:S373-S378.
• Goyal RK, Hirano I. The enteric nervous system. N Engl J Med. 1996;334:1106.
• Mokdad AH, Bowman BA, Ford ES, Vinicor F, Marks JS, Koplan JP. The continuing epidemics of obesity and diabetes in the United States. JAMA. 2001;286:1195-1200.
• Ng A, Smith G. Gastroesophageal reflux and aspiration of gastric contents in anesthetic practice. Anesth Analg. 2001;93:494-513.
• Rangel-Frausto MS, Pittet D, Costigan M, et al. The natural history of the systemic inflammatory response syndrome (SIRS): a prospective study. JAMA. 1995;273:117.
• Shah M, Simha V, Garg A. Long-term impact of bariatric surgery on body weight, comorbidities, and nutritional status [review]. J Clin Endocrinol Metab. 2006;91:4223-4231.
• Singer M, De Santis V, Vitale D, Jeffcoate W. Multiorgan failure is an adaptive, endocrine-mediated, metabolic response to overwhelming systemic inflammation. Lancet. 2004;363:545–548.
• Sollinger HW. Pancreas transplantation in humans. In: Moody FG, ed. Surgical Treatment of Digestive Disease. 2nd ed. Chicago, IL: Mosby-Year Book; 1990:577-598.