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The reader should also see the discussion of porphyrias in the section on neurologic disease, the discussion of nutritional deficiencies in the section on disorders of nutrition, and pediatric disorders such as transesophageal fistula in Chapter 60 and Chapter 77 .
Although preoperative preparation of the GI tract is usually the responsibility of the surgeon and although the GI tract frequently does not need to be extensively evaluated by the anesthesiologist, GI disease can and often does cause derangements in many or all other systems. Such disturbances can affect the safety of anesthesia for the patient. Thus, the anesthesiologist may need to not only optimize the patient's condition through extensive preoperative preparation but also have knowledge of disease
In addition to the vast alterations in fluids, electrolytes, and nutrition that can occur with such diverse GI diseases as neoplasms and pancreatitis, patients with GI disorders can have gastroesophageal reflux disease,[799] bowel obstruction, vomiting, or hypersecretion of acid. These effects may merit rapid induction of anesthesia with the application of cricoid pressure or awake endotracheal intubation, preoperative nasogastric suctioning, or preoperative use of histamine receptor blocking agents (also see Chapter 42 ). Clotting abnormalities may need to be corrected because fat-soluble vitamin K (often malabsorbed) is necessary for the synthesis of factors V, VII, IX, and X in the liver (also see Chapter 55 ). Liver disease is often associated with GI disease and, if severe enough, can also result in a deficiency of clotting factors synthesized by the liver.
Other factors should be remembered in any preoperative evaluation of a patient with GI disease. First, closed spaces containing gas expand by absorbing nitrous oxide. Such expansion can lead to ischemic injury or GI viscus rupture, or both.[800] Second, GI surgery predisposes the patient to sepsis; sepsis and decreased peripheral vascular resistance can lead to massive fluid requirements, cardiac failure, and renal insufficiency. Recently, the wound infection rate has been declining. This decrease may be attributable to the use of better technique, more appropriate prophylactic use of antibiotics, better nutrition, less invasive (laparoscopic and endoscopic) surgery, or surgical resection of even solid tumors.[457] [800] [801] [802] [803] [804] Third, patients with GI disease may have many other associated disorders not directly related to the GI tract. For example, they may be anemic from deficiencies in iron, intrinsic factor, folate, or vitamin B12 . They may also manifest neurologic changes from combined-system disease. Respiration may be impaired because of heavy cigarette smoking, peritonitis, abscess, pulmonary obstruction, previous incisions, aspiration, or pulmonary embolism (as occurs with ulcerative colitis or with thrombophlebitis in the bedridden).[805] These patients may also have hepatitis, cholangitis, side effects from antibiotic drugs or other medications, massive bleeding with anemia and shock, or psychological derangements.
Because GI disease can be accompanied by so many diverse associated disorders, the clinician must clearly search for other system involvement and preoperatively assess and treat such disorders appropriately. Discussion of two specific diseases, ulcerative colitis and carcinoid tumor, will highlight the importance of involvement of other systems in GI disease.
Patients with ulcerative colitis often have psychological problems. They may also have phlebitis; deficiencies in iron, folate, or vitamin B12 ; anemia; or clotting disorders caused by malabsorption. They may be malnourished or dehydrated or have electrolyte abnormalities. In addition, ulcerative colitis can be accompanied by massive bleeding, bowel obstruction or perforation or toxic megacolon causing respiratory compromise, hepatitis, arthritis, iritis, spondylitis, or diabetes secondary to pancreatitis.
The site of origin of carcinoid tumors in more than 75% of patients is the GI tract.[806] Within the GI tract, carcinoid tumors have been documented to occur from the esophagus to the rectum. The most frequent site is the appendix, but carcinoids in this location rarely, if ever metastasize or produce carcinoid syndrome. Tumors arising in the ileocecal region have the highest incidence of metastases. Carcinoid tumors originating from other sites than the GI tract, such as the head and neck, lung, gonads, thymus, breast, and urinary tract, have also been reported. Cardiac involvement, though frequently reported, is usually limited to right-sided valvular and myocardial plaque formation.[807]
Not all patients with carcinoid tumors have symptoms attributable to secretion of hormone by the tumor. Some can, however, and unexpected carcinoid can be manifested during surgery by hypersecretion of gastric fluid.[808] The most comprehensive series in the literature indicates that only 7% of patients have carcinoid syndrome, which typically consists of flushing, diarrhea, and valvular heart disease. Of those with the syndrome, approximately 74% have cutaneous flushing; 68%, intestinal hypermotility; 41%, cardiac symptoms; and 18%, wheezing. Factors influencing symptoms include the location of the tumor and the specific hormones produced and secreted. Although it is generally believed that if patients do not exhibit carcinoid syndrome, the tumors are not producing serotonin (5-hydroxytryptamine [5-HT]), but such may not be the case. Approximately 50% of patients with carcinoid tumors of the GI tract demonstrate evidence of 5-HT production as manifested by elevated urinary levels of 5-hydroxyindoleacetic acid (5-HIAA), a metabolic product of 5-HT. Carcinoid syndrome is usually associated with ileal carcinoid tumors that have metastasized to the liver. Presumably, the liver clears mediators released from the tumor. Impairment of this clearing ability by the metastatic tumor results in carcinoid syndrome.
Most patients with carcinoid tumors and increased urinary 5-HIAA have typical carcinoid tumors originating from the midgut (ileum or jejunum). These patients excrete only small amounts of 5-hydroxytryptophan (5-HTP). Patients with atypical carcinoid tumors that originate in the foregut (bronchus, stomach, and pancreas) excrete large amounts of 5-HT and 5-HTP, as well as moderately higher amounts of 5-HIAA.
Although it is generally agreed that 5-HT is responsible for the diarrhea experienced by patients with carcinoid tumors, other neurohumoral agents may contribute to the flushing and hypotension,[806] including dopamine, histamine, and some of the neuropeptides such as substance P, neurotensin, vasoactive intestinal peptide, and somatostatin.
The net physiologic effect of circulating 5-HT represents a composite of both direct action (mediated by 5-HT receptors) and indirect action (mediated through modulation of adrenergic neurotransmission). The existence of several subtypes of 5-HT receptors may account for the different effects of 5-HT on various serotonin-sensitive tissue beds. Indirect actions are effected through alterations in catecholamine release and depend on the level of circulating 5-HT.
5-HT has little, if any direct effect on the heart. With elevated levels, however, positive chronotropic and inotropic myocardial effects may occur, mediated by the release of noradrenaline (norepinephrine). Effects of serotonin on the vasculature include both vasoconstriction and vasodilation.
Alterations in GI function attributed to 5-HT include increased motility and net intestinal secretion of water, sodium chloride, and potassium. 5-HT reportedly causes bronchoconstriction in many animals, but rarely in humans. Asthmatics are a possible exception. Carcinoid tumors are frequently manifested as diarrhea with fluid and electrolyte abnormalities. Because these tumors secrete vasoactive substances, patients can exhibit hypotension or hypertension along with the flush associated with release of vasoactive substances. Vasoactive substances can be released from the tumor by any number of substances, including catecholamines. Until the 1990s, management of this tumor was a real challenge for the anesthesiologist. Thus, anesthesiologists of that era had to tread a fine line between avoiding substances known to release 5-HT (e.g., d-tubocurarine and morphine) and inducing anesthesia so light that painful stimuli activate a sympathetic stress response.[809] [810] The anesthesiologist also needed to be ready and able to treat hypotension, decreased peripheral vascular resistance, bronchospasm, and hypertension. α-Adrenergic receptor blockade with the phenothiazines, butyrophenones, or phenoxybenzamine and β-adrenergic receptor blockade with propranolol have been advocated to prevent catecholamine-mediated release of vasoactive substances. These practices, however, can lead to hypotension. Nevertheless, that difficulty in managing carcinoid syndrome seemed to change with the availability of a somatostatin analog. In fact, somatostatin is now such a powerful inhibitor of the release of peptides from carcinoid tumors and an inhibitor of the peptic effects on receptor cells that it is the therapy of choice for preoperative, intraoperative, and postoperative management of carcinoid symptoms and crises.[806] [809] However, the ease of management of most patients[806] [809] [810] [811] [812] [813] [814] should not lull the anesthesiologist into being unprepared—in fact, somatostatin has caused problems of its own and has failed to prevent severe hypotension and bronchospasm. [815] [816]
In patients with severe hypotension that is not treatable with somatostatin, the drug of choice is either angiotensin or vasopressin. (Angiotensin is not commercially available in the United States but is an approved drug that is available by contacting Novartis.) However, the vasoactive substances released by carcinoid tumors cause fibrosis of the heart valves that often results in pulmonic stenosis or tricuspid insufficiency. To increase cardiac output in a patient with tricuspid insufficiency, the anesthesiologist should avoid drugs or situations that increase pulmonary vascular resistance (e.g., angiotensin, vasopressin, acidosis, hypercapnia, hypothermia) (also see Chapter 50 and Chapter 51 ). In addition, the production of large amounts of 5-HT (equal to 200 mg/day of 5-HIAA) can lead to the development of niacin deficiency with pellagra (as occurs with diarrhea, dermatitis, and dementia).
Acute elevation of plasma kinin activity in carcinoid patients has been postulated for many years as the explanation for the symptoms of carcinoid syndrome. Physiologic effects of kinins are known to include vasodilation of smaller resistance vessels and stimulation of the release of histamine from mast cells. The latter action potentiates their own vasodilating properties and further reduces systolic and diastolic BP. In addition, increases in vascular permeability may lead to edema. Kinins are not known to affect the myocardium directly.
Steroids have been effective in treating the symptoms of bronchial carcinoid tumors. Although prophylactic preoperative administration and intraoperative therapeutic use have been described, controlled studies of beneficial effects are lacking. Aprotinin, like steroids, inhibits the kallikrein cascade. This drug is believed to be capable of blocking the proteinase activity of kallikrein, and some reports have described a dramatic clinical response.
A subset of patients with symptoms of carcinoid syndrome excrete histamine at increased levels in their urine. Histamine causes vasodilation of small blood vessels, which leads to flushing and decreased total peripheral resistance. Histamine is known to cause bronchoconstriction, particularly in patients with bronchial asthma and other pulmonary diseases. Its role in carcinoid bronchospasm, if any, is uncertain. Histamine receptor blocking drugs have been used with some success in alleviating the flushing associated with carcinoid syndrome. H2 antagonism alone was found to be just as effective as combination therapy in preventing symptoms; pure H1 antagonism, however, was ineffective. These therapies have been relegated to a second-line defense since the use of somatostatin.
Catecholamines aggravate the symptoms of carcinoid syndrome, presumably by stimulating release of hormone by the tumor. The mechanism by which this release occurs remains obscure. Adrenergic receptors have not been demonstrated in carcinoid tumors, nor do these tumors usually have neural innervation. Perhaps adrenergic stimuli work through their mechanical effects on the gut and vessels to stimulate the release of tumor products. Treatment of patients with carcinoid tumors by means of α- and β-adrenergic antagonists has been beneficial in ameliorating flushing in some instances but ineffective in others.
The results of prospective studies on somatostatin to ameliorate the symptoms of carcinoid syndrome have been dramatic. In several case reports involving a total of 46 patients, all but 2 had rapid, dramatic improvement in flushing.[806] [807] [808] [809] [811] [812] [813] [814] Similar results have been obtained in patients with diarrhea. Somatostatin appears to be a major advancement in the treatment of carcinoid syndrome.
It might logically be concluded that preoperative preparation of a patient with carcinoid syndrome would be similar to that for a patient with pheochromocytoma: titration of adrenergic, histaminic, and serotonergic receptor blocking drugs to maximum effect while monitoring
Bronchospasm with or without flushing also develops in many patients when vasoactive substances are released. Thus, a patient with carcinoid tumor may be well or may be severely incapacitated by pulmonary, neurologic, nutritional, fluid, electrolytic, or cardiovascular disturbances.[806] [809] Therefore, although the GI system in itself may not require extensive preoperative preparation, GI disease can cause disturbances in any or all other systems that require extensive preoperative preparation to optimize the patient's condition plus preoperative knowledge of physiology and the effects of diseases to guide patients through the perioperative period smoothly. In addition, the anesthesiologist's understanding of the nature of the surgery probably aids in determining the system involvement caused by the GI disorder.
Another preoperative consideration is that patients with GI diseases (perhaps even more so than those with other diseases) have had to endure the psychosocial trauma of having to live with their disease for long periods or the necessity of facing such a prospect.[817] They need emotional support and holistic kindnesses as much as, if not more than others, without sacrificing scientific rigor in the treatment of their condition. Obtaining relevant psychological data while gathering medical information, sitting (not standing) while taking the history, and empathizing with the patient about how difficult it must be to accomplish tasks with this disease (stressing accomplishments, we have found) legitimize the physician's interests in and support of the patient's pain and other psychosocial issues. The time spent sitting and talking with the patient also allows the anesthesiologist to discuss options for pain therapy with the patient, why systemic morphine might be avoided in a patient with a fresh bowel anastomosis,[818] and other issues that show the anesthesiologist to be both a competent physician and particularly concerned with that patient's well-being. In addition to an appreciation of the organic effects of their disease, attention to emotional support of these patients perioperatively presents opportunities to use one's full skills as a physician to bring about healing.
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