Gastrointestinal system
A Carcinoid tumors and carcinoid syndrome
Definition
Carcinoid tumors consist of slow-growing malignancies composed of enterochromaffin cells usually found in the gastrointestinal tract. They may also occur in the lung, pancreas, thymus, and liver. Carcinoid tumors have a low incidence rate of 1.9 per 100,000.
Pathophysiology
Speculation is that the advent and increasing use of proton pump inhibitors is a major contributory factor to the development of carcinoid tumors. A delay of several years frequently occurs before a diagnosis of carcinoid tumor is made. The gastrointestinal tract accounts for about two-thirds of carcinoids. Within the gastrointestinal tract, most tumors occur in the small intestine (41.8%), rectum (27.4%), and stomach (8.7%). Distant metastases may be evident at the time of diagnosis in 12.9% of patients, but better diagnostic techniques have contributed to improved survival rates.
The tumors can secrete several biologically active substances, including serotonin (5-hydroxytryptamine), kallikrein, histamine, prostaglandins, adrenocorticotropic hormone, gastrin, calcitonin, and growth hormone, among others. Approximately 5% to 10% of patients with carcinoid tumors develop carcinoid syndrome.
Clinical manifestations
The manifestations of carcinoid syndrome are in the table on pg. 100 and as follows:
• Episodic cutaneous flushing (kinins, histamine)
• Diarrhea (serotonin, prostaglandins E and F)
• Tricuspid regurgitation, pulmonic stenosis
• Supraventricular tachydysrhythmias (serotonin)
• Bronchoconstriction (serotonin, bradykinin, substance P)
• Hypotension (kinins, histamine)
• Abdominal pain (small bowel obstruction)
• Hypoalbuminemia (pellagra-like skin lesions resulting from niacin deficiency)
Vasoactive peptides released from carcinoid tumors located in the bronchi and ovaries exert a faster effect because of their direct drainage into the portal vein. Carcinoid tumors are also functionally autonomous. Two factors that enhance release of carcinoid hormones are direct physical manipulation of the tumor and β-adrenergic stimulation.
Principal Mediators of Carcinoid Syndrome and Their Clinical Manifestations
| Mediator | Clinical Manifestations |
| Serotonin | Vasoconstriction (coronary artery spasm, hypertension), increased intestinal tone water and electrolyte imbalance (diarrhea), tryptophan deficiency (hypoproteinemia, pellagra) |
| Kallikrein | Vasodilation (hypotension, flushing), bronchoconstriction |
| Histamine | Vasodilation (hypotension, flushing), arrhythmias, bronchoconstriction |
Treatment
Patients with carcinoid syndrome may undergo primary resection of the carcinoid tumor. Examples of other procedures that these patients often undergo include cardiac valve replacement and hepatic resection (e.g., lobectomy) for excision of metastases.
Anesthetic considerations
Many anesthetic techniques have been used successfully in the treatment of patients with carcinoid syndrome (see the following section). Preoperative preparation of the patient requires correction of deficiencies in circulating volume and electrolyte levels. Use of histamine-releasing agents, such as morphine, and atracurium should be avoided. Fasciculations may induce release of carcinoid hormones and are therefore prevented by avoidance of succinylcholine, although it has been used successfully many times, especially for rapid sequence induction.
Anesthetic considerations in carcinoid syndrome
• The most common clinical signs are flushing, wheezing, blood pressure and heart rate changes, and diarrhea.
• Preoperative assessment should include complete blood count, measurement of electrolytes, liver function tests, measurement of blood glucose, electrocardiogram (echocardiogram if indicated), and determination of urine 5-HIAA levels.
• Optimize fluid and electrolyte status and pretreat with octreotide as noted. Continue octreotide throughout the postoperative period. Interferon-α has shown success in controlling some symptoms.
• Both histamine-1 and -2 receptor blockers must be used to fully counteract histamine effects.
• Avoid histamine-releasing agents such as morphine, thiopental, and atracurium.
• Avoid sympathomimetic agents such as ketamine and ephedrine.
• Treat hypotension with an α-receptor agonist such as phenylephrine.
• General anesthesia is preferred over regional anesthesia. Patients with high serotonin levels may exhibit prolonged recovery; therefore, desflurane and sevoflurane, which have rapid recovery profiles, may be beneficial.
• Aggressively maintain normothermia to avoid catecholamine-induced vasoactive mediator release.
• Monitor intraoperative plasma glucose because these patients are prone to hyperglycemia. Treat with insulin as is customary.
Octreotide, a somatostatin analog, is used to blunt the vasoactive and bronchoconstrictive effects of carcinoid tumor products. Octreotide mimics the inhibitory action of somatostatin on the release of several gastrointestinal hormones, as well as those derived from carcinoid tumors. Treatment for 2 weeks preoperatively with a dose of 100 mcg subcutaneously three times a day is standard. If prior therapy was not used, a dose of 50 to 150 mcg subcutaneously is given preoperatively. Intraoperative infusion may be continued at 100 mcg/hr. Bolus doses of 100 to 200 mcg given intravenously may be used for intraoperative carcinoid crises. Lantrotide (which is administered every two weeks) and octreotide LAR (which can be given monthly) are long-acting formulations that are superior in terms of patient acceptance and cost effectiveness.
Patients with hypotension should be treated with an α-adrenergic agonist (e.g., phenylephrine infusion) to avoid hormone release by β-adrenergic stimulation. Bronchospasm resulting from histamine or bradykinin release has been shown to be resistant to ketamine and inhalation anesthetics. Low-dose β2-agonists are effective in bronchodilation and have relatively little influence on carcinoid hormone release. In the presence of high levels of serotonin in carcinoid syndrome, adjustments in anesthetic selection and dosage must be considered if further compromise of cardiovascular function is to be prevented.
B Gallstones and gallbladder disease
Definition
Obstruction of the cystic duct by gallstones results in acute, severe midepigastric pain, typically radiating to the right abdomen. Inspiratory effort usually accentuates the pain (Murphy’s sign).
Clinical manifestations
Increases in plasma bilirubin, alkaline phosphatase, and amylase levels frequently occur. Ileus and localized tenderness may indicate perforation with peritonitis. Leukocytosis and fever are often present. The presence of jaundice indicates complete obstruction of the cystic duct. Symptoms are frequently confused with those of myocardial infarction. Differential diagnosis is accomplished through serial electrocardiogram (ECG) evaluations and laboratory analysis of serum enzymes that are specific to cardiac muscle. Cholescintigraphy (a contrast study that evaluates gallbladder excretion of a radiographically labeled substance) and ultrasonography are often used for clinical confirmation of the diagnosis.
Anesthetic considerations
Patients with symptoms indicative of acute cholecystitis are often volume depleted as a result of intolerance of oral intake, vomiting, and possible preoperative nasogastric evacuation of gastric contents. Dehydration warrants preoperative intravenous fluid replacement. Gastric suction may be warranted in the presence of ileus. The presence of free abdominal air, as determined by abdominal radiography or symptoms of an acute abdomen (fever, ileus, rigid and painful abdomen, vomiting, dehydration), suggests the presence of a ruptured viscus, possibly including perforation of the gallbladder. Under these circumstances, emergency exploratory laparotomy is undertaken.
Cholelithiasis and choledocholithiasis
Acute obstruction of the common bile duct often produces symptoms similar to those seen in patients with cholecystitis. Recurrent bouts of acute cholecystitis induce the development of fibrotic changes in gallbladder structure, thereby impeding the ability of the gallbladder to adequately expel bile. The presence of Charcot’s triad (fever and chills, jaundice, upper quadrant pain) aids in establishing the differential diagnosis in acute ductal obstruction. Weight loss, anorexia, and fatigue complete the symptomatology. Diagnostic modalities include radiography, transhepatic cholangiography, ultrasonography, cholescintigraphy, and computed tomography (CT) scan. A dilated common bile duct and biliary tree are typically observed in these studies.
C Hiatal hernia and gastric reflux
Definitions
Hiatal hernia
A hiatal hernia consists of a defect in the diaphragm that allows a portion of the stomach to migrate upward into the thoracic cavity. Two types of esophageal hiatal hernias are the sliding type (type I), which is formed by the movement of the upper stomach through an enlarged hiatus, and the paraesophageal type (type II), in which the esophagogastric junction remains in normal position but all or part of the stomach moves into the thorax and assumes a paraesophageal position. A third type of hiatal hernia (type III) has been identified that combines the features of a sliding and a paraesophageal hernia. A fourth type of hiatal hernia (type IV) occurs when other organs, such as the colon or small bowel, are contained in the hernia sac that is formed by a large paraesophageal hernia. Hiatal hernia and peptic esophagitis often exist concurrently, although one does not cause the other.
Gastric reflux
Gastric reflux relates to a reduced lower esophageal sphincter tone, which can increase the risk for regurgitation and aspiration. Reflux can occur without the presence of hiatal hernia. The lower sphincter is a physiologic sphincter with no specialized musculature. Tone is 15 to 35 mmHg.
Incidence and prevalence
Types I to IV hiatal hernias are present in 10% of the population, usually without symptoms. Only 5% of the population has reflux symptoms along with a hiatal hernia.
Pathophysiology
In most cases, the cause is unknown, whether the condition is congenital, traumatic, or iatrogenic.
Clinical manifestations
The major symptom is retrosternal pain of a burning quality that commonly occurs after meals. It is assumed that patients with a hiatal hernia are predisposed to developing peptic esophagitis, thereby providing a rationale for surgical correction of this condition. Most patients with hiatal hernia do not have symptoms of reflux esophagitis, however, and do not require H2-agonist and oral antacid therapy. Nevertheless, implementation of aspiration precautions on induction of general anesthesia and emergence is still strongly recommended.
