Chapter 22 Manifestation of Gastrointestinal Disease
Principles of Surgery Companion Handbook
MANIFESTATION OF GASTROINTESTINAL DISEASE
|Weight Loss and Cachexia|
|Symptoms Related to Specific Components of the Gastrointestinal Tract|
|Esophagus, Stomach, and Duodenum|
|Small and Large Intestine|
|Upper Gastrointestinal Bleeding|
|Lower Gastrointestinal Bleeding|
|Multiple Organ Failure Syndrome (MOFS)|
Pain is the most common symptom of gastrointestinal disease. The amount and quality of perceived pain are determined by physiologic and psychological variables.
Pain Pathways Pain impulses from the abdomen reach the central nervous system (CNS) through (1) visceral sympathetic afferents and (2) visceral parasympathetic afferents and (3) from the parietal peritoneum, the diaphragm, and the root of the mesentery via somatic afferents of segmental spinal nerves or phrenic nerve. The visceral peritoneum is innervated by autonomic C-type fibers, which are slow transmitters; therefore, the sensation is dull, poorly localized, gradual in onset, and longer in duration. The fibers are insensitive to stimuli such as cutting and crushing; stimuli causing visceral pain include changes in diameter of a hollow viscus perceived as cramping, the stretching of capsules of solid viscera (e.g., subcapsular liver hematoma), ischemia, and chemicals (e.g., acids, alkalis, hypertonic solutions, potassium, and bradykinin). The pain is described as deep in the cutaneous areas and zones supplied by the somatic sensory nerve originating from the same segments of the spinal cord as the visceral afferent fibers from the viscus in question. Autonomic reflexes such as sweating, nausea, vomiting, tachycardia, bradycardia, hypotension, hyperesthesia, and involuntary abdominal muscle contraction may accompany severe visceral or deep somatic pain. Abdominal pain could be visceral pain, referred visceral pain, parietal pain, unreferred parietal pain, or any combination thereof.
The abdominal viscera have bilateral afferent autonomic innovation, except the kidneys, ureter, cecum, and ascending and descending colon, which are unilaterally innovated. Visceral pain usually is perceived as midline because of the embryologic development of the gut; e.g., midgut pain is manifest as periumbilical pain.
Referred Visceral Pain This pain is more localized and is referred to the dermatomes and myotomes that are supplied by the same spinal cord segment as the affected viscus; e.g., increased distention of the abdomen causes abdominal wall discomfort and backache.
Pain sensation is transmitted by A-delta fibers. The pain is well localized; nerve endings are stimulated by chemicals, changes in pH, inflammatory mediators, bacteria, and neutrophil breakdown products.
Referred Parietal Pain This is the result of afferent neurons that innervate two separate, anatomically distinct structures having a common embryologic origin, e.g., left shoulder pain with ruptured spleen.
Pain of intraabdominal origin may arise from the peritoneum, hollow or solid viscera, mesentery, or the pelvic organs and be caused by inflammation, mechanical processes, and vascular disturbances. Extraperitoneal disorders also can manifest as abdominal pain. Common sites of referred pain from intraabdominal pathology are illustrated in Table 22-1.
TABLE 22-1 POSSIBLE ORIGINS FOR REFERRED PAIN
Other pain is back pain as a result of neural infiltration, e.g., infiltration of the celiac plexus by pancreatic cancer or gastric cancer.
ACUTE ABDOMINAL PAIN
Sudden pain is seen with perforation, obstruction, acute arterial ischemia, and acute intraperitoneal bleeding. Pain of gradual onset is seen with inflammatory pathology (Table 22-2). The site and character of pain, radiation, aggravating and relieving factors, and the progression of pain help find the anatomic area and nature of the process; e.g., patients with colic move around compared with patients with peritonitis, who lie still; acute mesenteric vascular ischemia produces pain disproportionate to physical findings. Vomiting, bowel movements, flatus history, menstrual history, previous similar episodes, similar episodes in family members, and medications should be elicited.
TABLE 22-2 DIAGNOSIS RELATED TO THE MODE OF ONSET OF ABDOMINAL PAIN
Physical Examination General Visual Assessment Is the patient looking sick? What is the breathing pattern? What is the state of hydration? Is the patient writhing in pain or lying still? Examine for distention, masses, visible peristalsis, and herniae.
Auscultation This should include the lungs and the abdomen. Crepitations, rales, and bronchial breathing indicate pulmonary pathology with referred pain to the abdomen. Hypoactive bowel sounds are seen with inflammation and ileus (e.g., hypokalemia, hypomagnesia, narcotic overdose). In the early phases of arterial occlusion, bowel sounds are hyperactive and may disappear when gangrene sets in.
Percussion distinguishes between gas and fluid causes of distention; liver dullness is obliterated by large amounts of free air, indicating a hollow viscus perforation.
Examine for masses; make a diligent search for herniae. Remember that light touch is essential when there is peritoneal inflammation. Guarding may be overcome by distracting the patient while palpating. Rebound tenderness indicates inflammation of the parietes, and in advanced stages of peritonitis, boardlike rigidity can occur. Hyperesthesia may be appreciated over the involved intraabdominal viscera. Bimanual pelvic and rectal examinations and stool examination for occult blood are mandatory.
Laboratory Evaluation Complete blood count with differential, pregnancy testing in females of childbearing age, serum electrolytes, serum amylase, lipase and liver profile, sickle cell screening in African-Americans, and an electrocardiogram in all adults are essential.
Radiologic Examination Upright anteroposterior (AP) and lateral chest x-rays and upright and supine abdomen views (free air series) show pulmonary pathology or free air under the diaphragm, abnormal gas patterns (air in the biliary tract indicating gallstone ileus, extraluminal air indicating perforation or abscesses), displaced organs (gastric fundus indented by splenic hematoma), fluid levels of intestinal obstruction, radiopaque ureteric and biliary calculi, appendicular fecaliths, and abnormal vascular calcifications.
Ultrasound is useful in evaluating hepatobiliary and pancreatic disease, appendicitis, and gynecologic abnormalities. Computed tomographic (CT) scan is helpful especially if there is no contraindication to oral or rectal contrast agents. Arteriography is required early in suspected intestinal ischemia. Paracentesis, laparoscopy, culdoscopy, and culdocentesis may be useful, and celiotomy may be indicated in patients who are too sick to undergo prolonged testing.
Symptoms of an acute abdomen may be masked in the pediatric population, in elderly patients, in patients on steroids, and immune-compromised patients.
INTERMITTENT AND RECURRENT PAIN
Hemolytic disorders such as sickle cell disease, autoimmune hemolytic anemia, and thrombotic thrombocytopenia can present with abrupt severe abdominal pain; accompanying muscle spasm and rigidity can mimic an acute abdomen.
Chronic hemolytic anemias, hereditary spherocytosis, and thalassemia can cause abdominal pain, anemia, jaundice, splenomegaly, and cholelithiasis. Acute intermittent porphyria, an inherited dominant disorder, presents as abdominal pain; the mechanism is thought to be an autonomic neuropathy. Attacks are precipitated by drugs (e.g., barbiturates, sulfonamides), starvation, sex hormones, and infection.
Bouts of pain with entirely normal intervals are seen in acute intermittent porphyria, internal hernias, endometriosis, and occasionally, choledocholithiasis. Persistent chronic abdominal pain may be seen with chronic pancreatitis and pancreatic or colon malignancy.
Chronic pain also can be from abdominal wall pathology such as peripheral nerve injuries, hernias, myofascial pain syndromes, the rib tip syndrome, and spontaneous rectus sheath hematoma. In addition, many psychiatric disorders are associated with chronic abdominal pain.
The control of intractable pain could be challenging, e.g., pain from unresectable carcinoma of the pancreas and chronic pancreatitis. Control may require large doses of opiate analgesics. Other modalities include neurologic interruption of the pain pathway (e.g., posterior rhizotomy, spinothalamic tract interruption, prefrontal lobotomy). Mechanical/electrical forms of pain control include the dorsal column stimulator.
Fever indicates illness such as infection, inflammation, auto-immune disease, and neoplasia. In the normal postoperative phase, persistent fever may indicate an infectious complication. Unusually high fever, e.g., malignant hypothermia, could be dangerous.
Pathophysiology Cytokines activated by the inflammatory response and pyrogens from macrophages (interleukin-1, tumor necrosis factor, and interferon) that are released locally within the brain and peripherally into the bloodstream act on the hypothalamus in endocrine fashion. The resulting upward resetting of the thermal regulatory apparatus triggers vasoconstriction that limits heat loss and shivering, which increases heat production.
Patients also may establish the environmental temperature that is most comfortable for them. This temperature is called thermoneutrality. For example, burn patients and patients with large wounds, peritonitis, sepsis, and multi-organ system failure feel cold at temperatures that normal persons consider comfortable because they have a higher thermal regulatory set point.
Clinical Considerations Fevers of gastrointestinal origin usually result from intraabdominal infection, e.g., urinary tract infection, peritonitis. Postoperative fevers are common (1530 percent) in patients after celiotomy, but only 1020 percent of such fevers are from infections such as pulmonary complications, urinary tract infections, wound sepsis, and thrombophlebitis. Twenty percent of fevers of unknown origin are secondary to cancers that are primary or metastatic in the abdomen, e.g., hypernephroma, liver tumors, lymphomas, and carcinoma of the stomach, colon, and pancreas.
Anorexia is seen in many illnesses such as inflammatory diseases (indicates significant inflammation), endocrinopathies such as hyperparathyroidism, and adrenal cortical insufficiency. Anorexia is a manifestation of liver disease, probably mediated by a combination of ammonia and neuropeptide Y (NPY). Anorexia is very common in malignancy and indicates significant tumor burden. Postoperative anorexia may be associated with a loss of taste or poor appetite and may respond to zinc replacement (220 mg daily). Alcohol is a stimulant.
Pathophysiology The physiologic mechanisms that control feeding and satiety are complex and multifaceted, involving receptors in both the brain and the periphery; stimuli include changes in glucose utilization rate, changes in the rate of lipid metabolism, alterations in brain and peripheral peptides, imbalances in plasma and brain amino acid profiles, increases and decreases in neurotransmitter activity, and alterations in cytokine levels. The hypothalamus is the feeding center of the brain; afferents are important for communicating peripheral nutrition-related information from the gastrointestinal tract or from glucose-sensitive cells in the liver. Small decreases in blood glucose levels have been related to the onset of hunger. Increased lipolysis and oxidation of lipids reduce hunger and produce satiety. The obese gene protein (leptin) that is synthesized in adipose sites adversely affects the synthesis and release of hypothalamic NPY, resulting in reduced food intake and increased metabolic rate. Increased dopamine activity and elevated activity in serotonin neurons may inhibit feeding. Multiple peptides also control feeding and satiety; e.g., NPY, endorphins, and galanin stimulate feeding; others, such as cholecystokinin, corticotropin-releasing factor, calcitonin, glucagon, and insulin, produce satiety. Cytokines (e.g., tumor necrosis factor and interleukins) reduce food intake when infused peripherally or injected directly into the hypothalamus. Although many drugs cause anorexia, there is no medication to restore appetite.
Cancer Anorexia It is likely that cancer anorexia results from tumor-induced aberrations of neurochemical mechanisms that normally control hunger and satiety. Aberrations in plasma and brain amino acid profiles have been reported in tumor-bearing organisms. Studies have been unconvincing for cause and effect because some of the aberrations may be the result of the anorexia rather than the cause of it. Factors produced by tumor tissue such as lactic acid and ammonia may produce anorexia. Cytokines also may be involved in tumor-related anorexia/cachexia, although treatment of tumor-bearing mice with tumor necrosis factor antibodies does not prevent the appearance of anorexia. NPY is a very potent appetite stimulator. It is dysfunctional in anorexic tumor-bearing rats.
Patients have significantly negative prognostic implications; a loss of 1015 percent over a 34-month period is indicative of nutritional or immunologic impairment. Inability to carry out normal function, serum albumin levels of less than 3.0 g/dL, and decreased short-turnover proteins (e.g., albumin, transferrin) have seriously negative prognostic implications.
Decreased intake and weight loss may occur in obstruction to the esophagus or be secondary to postprandial pain, chronic infections, and malabsorption. Thyrotoxicosis, Addison's disease, and diabetes mellitus may produce rapid weight loss over a short period. The most common cause of weight loss is malignancy. Up to 70 percent of cancer patients die from the effects of starvation, with infection the final common pathway. Weight loss in the elderly could be from treatable causes such as poorly fitting dentures. In a small percentage of patients, weight loss is of psychological origin.
Hiccups often is transient and benign but can be debilitating if persistent and may be a manifestation of an underlying severe pathologic process. Hiccups reflex consists of the phrenic and vagus nerve and the sympathetic chain from T6T12.
Abdominal conditions such as gastric distention, pancreaticobiliary disease, bowel obstruction, and intraoperative surgical manipulation stimulate the afferent vagal branches. The vagus could be stimulated by intrathoracic pathology such as neoplasms, myocardial infarction, pulmonary edema, and infectious processes. Intraabdominal phrenic nerve stimulation can arise from diaphragmatic hernia or subphrenic abscesses. Within the chest, the phrenic nerve can be irritated by inflammation, tumor, infection, and trauma. Central causes of hiccups include anesthetics, drugs such as intravenous steroids and barbiturates, and metabolic causes such as alcohol toxicity, uremia, hypocalcemia, and hyponatremia. The treatment of hiccups is aimed at the cause, and symptomatic relief may be obtained by nasopharyngeal stimulation and pharmacologic treatment, e.g., chlorpromazine, haloperidol, sodium valproate, or metachlorpromide.
HEARTBURN AND DYSPEPSIA
Frequent heartburn indicates gastroesophageal reflux disease. The defense mechanisms of the esophagus are a competent lower esophageal sphincter (LES), rapid esophageal clearing of refluxed material, neutralization of refluxed acid by bicarbonate-rich saliva, and an intact mucosal diffusion barrier; the most common clinical abnormality is an incompetent LES.
Heartburn is a substernal burning often associated with bitter taste, and when severe, it is associated with regurgitation of gastric contents. A minority of patients with gastroesophageal reflux dysmotility develop esophagitis (19 percent of patients undergoing upper endoscopy for upper abdominal symptoms have esophagitis).
Dyspepsia includes symptoms such as substernal pressure, epigastric distress, nausea, and bloating. Diseases of the esophagus, stomach, duodenum, biliary tree, and pancreas produce the symptoms. Classic esophageal pain radiates directly through to the back between the scapulae. It also can radiate to the left shoulder, mimicking angina. Esophageal disorders can be evaluated with cinefluoroscopy, contrast radiography, endoscopy and biopsy, 24-h pH study, and manometry.
The timing to food helps: Duodenal ulcer pain is relieved by food, and gastric ulcer pain is provoked by food. Fried, fatty, or greasy foods are found to provoke biliary colic. Alcohol may provoke pancreatitis.
Dysphagia (difficulty in swallowing) and painful swallowing (odynophagia) require investigation. Pain accompanying dysphagia is a result of inflammation or spasm. Because of the risk factors for squamous cell cancer of the esophagus, the history should include questions about chronic medications (e.g., nonsteroidal anti-inflammatory drugs), dietary habits, substance abuse, smoking, and the taking of undiluted alcohol. Regurgitation of undigested, foul-smelling food is suggestive of Zenker's diverticulum. A barium swallow should be followed with upper gastrointestinal endoscopy with biopsy; if Barrett's esophagus is suspected, multiple biopsies at various levels should be performed. Studies include manometry and 24-h pH monitoring. The esophagus is the most common part of the gastrointestinal tract to be affected by scleroderma; lower esophageal dysmotility also can occur in association with other connective tissue disorders such as rheumatoid arthritis. Dysphagia lusoria is caused by an aberrant origin of the right subclavian artery or pulmonary artery; it is suspected when there is a posterior indentation of the upper esophagus on barium swallow. If neoplasm is suspected, CT scan of the chest and abdomen and bronchoscopy are indicated. In addition, dysphagia may be a symptom in patients with conversion hysteria, anxiety, and anorexia nervosa.
NAUSEA AND VOMITING
Nausea and vomiting may be related or unrelated to disease of the gastrointestinal (GI) tract. When the GI tract is excessively irritated or overdistended, vomiting may result. Impulses of the GI tract are transmitted by both vagal and sympathetic fibers to the vomiting center in the medulla; motor pulses are transmitted down to cranial nerves V, VII, IX, X, and XII and to the diaphragm and abdominal muscles through the phrenic and spinal nerves. The vomiting center also receives impulses from the higher cortical centers and from the chemoreceptor trigger zone (CTZ) on the floor of the fourth ventricle. Most drug-induced nausea and vomiting is mediated through the CTZ receptor; changes in the directions of motion (through the labyrinthine apparatus), distressing visual input, and foul odors also act through the CTZ on the vomiting center. The same impulses that produce vomiting also produce other autonomic changes such as pallor, perspiration, bradycardia, and hypotension.
Any CNS disorder that leads to increased intracranial pressure (hypoxia) can produce vomiting; inflammation or infectious agents affecting the GI tract, neoplastic disease, or mechanical obstruction can lead to acute nausea and vomiting. Antibiotics such as erythromycin and neomycin may cause nausea and vomiting through direct effects on the GI tract. Pain of any origin may be associated with nausea and vomiting. If bulimia is suspected, psychiatric evaluation is indicated.
Consequences of Vomiting Continued vomiting and resulting hypovolemia can produce hemodynamic instability. Metabolic and electrolyte abnormalities include elevated blood urea nitrogen (BUN) and creatinine levels and metabolic alkalosis (vomitus rich in potassium and hydrogen ions that are also lost in the urine, i.e., paradoxical aciduria). Increased cellular breakdown of protein and the use of fat storage cause a rise in the BUN level and the appearance of ketone bodies, respectively. The initial treatment is with saline solution. Once diuresis is established, potassium is added. Metabolic alkalosis may need correction with ammonium chloride, arginine hydrochloride, and even 0.1 N HCl.
Gaseous Distention, Eructation, and Flatulence Intestinal gas produces symptoms of bloating, left shoulder pain (splenic flexure syndrome), audible bowel sounds, eructation, and flatulence. Postoperative gas pains are not uncommon but usually resolve spontaneously in 34 months.
Chronic belching/eructation may be seen in cholelithiasis, peptic ulcer disease, and esophageal reflux disease. Patients who do not have decreased LES pressure should not undergo fundoplication because the procedure can cause severe distress/gas bloat syndrome. Small intestinal gas is a combination of swallowed gas and gas from bacterial fermentation; the total is less than 1 L/day. Distention of the colon may reflect partial obstruction. Lactase deficiency also can result in eructation and flatulence.
Treatment with activated charcoal, simethicone, and enzymes may be helpful in patients with no correctable cause.
Digestion starts in the stomach. Gastric emptying is achieved within 34 h. In the duodenum and small intestine, 34 L of biliary and pancreatic secretions and 2 L of succus entericus are added per 24 h. Protein absorption occurs in the first 120 cm and carbohydrate absorption within the first 150180 cm. Water absorption is mostly in the right side of the transverse colon. Elimination occurs 2472 h after food digestion.
This is an abnormal retention of fecal material or delay in bowel evacuation compared with usual bowel habits. Investigation is required for a change in bowel habits to rule out neoplastic disease.
Defecation occurs when peristaltic waves move the fecal bolus stored in the sigmoid colon into the rectum. Relaxation of the circular muscles at the rectosigmoid junction and impulses from the rectum via the hypogastric and pelvic nerves to the canda equina generate efferent spinal cord impulses; this results in abdominal and diaphragmatic muscle contraction and voluntary relaxation of the external sphincter. Parasympathetic nerves augment intestinal motility, whereas sympathetic stimulation inhibits it. Anticholinergics and opiates inhibit motility; cholinergic agents, caffeine, nicotine, potassium, and vasopressin stimulate intestinal motility.
Acute Constipation This is often a result of intestinal obstruction. Reflex acute constipation may occur in trauma associated with retroperitoneal hematoma. Painful perianal conditions such as fissures and thrombosed hemorrhoids also cause acute constipation. Other causes of constipation include psychological factors, lack of bulky foods, excess laxatives and drugs, decreased skeletal muscle power, and extrinsic pressure on the GI tract. Intestinal atony is seen in hypokalemia, hypercalcemia, and uremia; collagen and endocrine disorders also can cause intestinal atony (e.g., hypothyroidism). Spinal cord disorders and Hirschprung's disease are examples of neurogenic causes of constipation.
Evaluation includes a history of previous bowel habits; changes in stool caliber, color, and consistency; and the presence of blood, mucus, or undigested fat. Abdominal examination can reveal abdominal distention, and rectal examination may reveal a mass. Stool should be tested for occult blood, and rectosigmoidoscopy (rigid or flexible), barium enema, and colonoscopy may be needed for establishing a diagnosis. Remember to exhibit caution in testing when toxic megacolon or colon perforation is suspected.
Chronic Constipation Congenital disorders, motility disorders, functional problems of the defecatary mechanisms in the pelvic floor, specific problems of the elderly, medications, diverticulosis with chronic scarring, and neoplastic disease are causes of chronic constipation. The age at onset, endoscopy and biopsy, manometry, and motility studies help in the diagnosis. Rectal prolapse and pelvic floor laxity are some of the pelvic floor abnormalities in the elderly resulting in constipation. Laxative abuse, anticholinergic use, and phenothiazine use can result in chronic constipation. A palpable left colon associated with constipation can be seen in chronic diverticulitis with scarring. Chronic constipation in the elderly always should raise a suspicion of neoplastic disease.
Between 5 and 8 L per 24 h is the volume secreted by the stomach, hepatobiliary tree, and small bowel. Profuse diarrhea can result in hemodynamic instability.
Pathophysiology Secretory diarrhea is seen after ileal resection, in pancreatic insufficiency, and from improper mixing of bile and pancreatic juice after a Billroth II gastrectomy. Many pancreatic islet cell tumors also produce secretory diarrhea, e.g., gastrinomas, Werner-Morrison syndrome. Carcinoid tumor produces diarrhea from many of its products such as serotonin, kallikrein, substance P, neuropeptides, and prostaglandins. High plasma calcitonin levels in medullary carcinoma increase jejunal water and electrolyte stimulation, leading to diarrhea; bacterial toxins such as in cholera and Shigella infection, and laxative abuse can cause secretory diarrhea. Exudative diarrhea results from release of serum proteins, blood, or mucus from sites of inflammation, ulceration, or infiltration. Osmotic retention of water can lead to diarrhea, e.g., lactase deficiency. Disordered contact of the luminal contents and the absorptive intestinal surface can lead to diarrhea and is seen after bowel resection, bypasses, and superinfection.
Clinical Evaluation Onset of diarrhea; frequency; associated symptoms such as pain, fever, nausea, and vomiting; family history; and character of the stool are important clues; e.g., diarrhea associated with fever and pain suggests an infectious cause. Small-caliber stools indicate partial distal colonic obstruction. A large amount of mucus with the stool is seen in inflammatory bowel disease, rectal cancer, and villous tumors of the rectum. In the physical examination, look for fever (inflammatory process), skin disorders (pyoderma gangrenosum or erythema nodosum in inflammatory bowel disease), abdominal distention (neoplasm or inflammation), perianal examination for fistulas (Crohn's disease), digital examination of the rectum for a mass, and fecal impaction. A stool test for occult blood may lead to a diagnosis.
Diagnostic Studies Tests include a full blood count, liver chemistry, determinations of serum electrolytes, calcium, phosphorus and magnesium, stool culture, Clostridium difficile toxin determination, stool fat examination, and a stool examination for ova and parasites. Colonoscopy and biopsy are appropriate. Celiotomy and small bowel biopsy may be necessary. Radiologic studies include barium enema and CT scan if pancreatic pathology is suspected.
Treatment This depends on the cause of the diarrhea. Nonspecific therapy includes opiate drugs, correction of fluid and electrolyte abnormalities, indomethacin (prostaglandin synthetase inhibitor), somatostatin (for secretory diarrheas from islet cell tumors of the pancreas), and cholestyramine (bile saltinduced diarrhea).
Intestinal obstruction accounts for 20 percent of surgical admissions. It is classified according to the obstructing agent to the wall of the intestine. Postoperative adhesions are the most common cause of intestinal obstruction; hernias are second, followed by malignant tumors.
Pathophysiology The accumulation of fluid and gas above the point of obstruction and altered bowel motility resulting in loss of fluid and electrolytes from vomiting and sequestration in the bowel are the principle physiologic derangements. Fluid and electrolyte losses are a result of (1) losses into the bowel lumen, (2) losses into the edematous bowel wall, (3) transduction as free peritoneal fluid, and (4) vomiting or nasogastric suction. Significant fluid and electrolyte losses could lead to hypovolemia, renal insufficiency, shock, and death.
Most bowel distention is from fluid sequestration, and some of it is from intestinal gas. Peristalsis increases in an attempt to overcome the obstruction; the higher the obstruction, the more frequent are the high-pitched peristaltic sounds.
Strangulated Obstruction This is seen in adhesive band obstruction, hernia, and volvulus. The obstructed segment of the bowel loses its blood supply; in addition, toxic materials leak into the peritoneal cavity (e.g., exotoxins, endotoxins, toxic hemin breakdown products).
Closed-Loop Obstruction This is a dangerous form of obstruction. Both the afferent and efferent limbs of a loop of bowel are obstructed. There is rapid progression to ischemia of the involved segment, and widespread abdominal distention may be absent.
The physiologic effects on the patient are less traumatic because the colon is mainly a storage organ with minor absorptive and secretory functions. However, progressive distention may be dangerous, especially if the ileocecal valve is competent, because the obstruction becomes that of a closed-loop type and can lead to rupture, especially of the cecum (Laplace's law).
Clinical Manifestations Symptoms are crampy abdominal pain, vomiting, constipation, and abdominal distention. Pain and vomiting occur early in high intestinal obstruction. Constipation and abdominal distention are most common in low intestinal obstruction.
Abdominal distention and hyperactive bowel sounds may be the only finding in simple mechanical obstruction. Fever, tachycardia, localized tenderness, and rebound tenderness suggest compromised bowel. The disappearance of peristalsis in progressive mechanical obstruction indicates gangrenous bowel. In the early postoperative phase, intestinal obstruction is difficult to diagnose.
Laboratory Findings Abnormal tests include elevated BUN level, hemoconcentration, hyponatremia and hypokalemia, high urinary specific gravity, and abnormal acidbase balance depending on the nature of the fluid loss. A very high white blood cell count may indicate the presence of strangulated bowel. High amylase levels may be seen with strangulated bowel, but there is no specific laboratory test indicative of intestinal ischemia.
Management Once nasogastric decompression and intravenous fluid resuscitation have occurred and blood has been drawn for testing, a free air series of the abdomen is obtained; the bowel gas pattern, especially the absence of gas in the rectum, is noted. A barium enema may be done to rule out an obstruction in the colon. Water-soluble contrast examination is contraindicated in obstructed colon because the agent can draw fluid into the intestinal lumen, aggravating the distention.
A central venous line for monitoring fluid needs and fluid administration may be necessary. Patients should have an indwelling bladder catheter. Initial fluid resuscitation is with normal saline or lactated Ringer's solution. Potassium supplements should not be added until a good urine output is established. Appropriate antibiotics should be administered first. If strangulation is suspected, the preceding preparation should be vigorous and fast to get the patient to the operating room quickly.
The majority of small bowel obstructions resolve without operative treatment. The indications to operate are the presence or suspicion of vascular compromise, a patient getting sicker, and the obstruction gone beyond 3 days. With preoperative preparation, the morbidity and mortality are minimal in patients with simple mechanical obstruction when operated on within 24 h of the onset of the disease.
Operative Procedure The timing of the operation is critical. Strangulation, closed-loop obstruction, colon obstruction, and early simple mechanical obstruction require operation as soon as possible. General anesthesia and a generous incision, preferably a long midline, are preferred. The obstruction is relieved with appropriate procedures such as lysis of adhesions, reduction of intersussusption and incarcerated hernia, resection of an obstructive lesion or strangulated bowel, enterotomy for removing obturation such as gallstones, bypass procedure, or enterostomy.
When adhesions are present, multiple sites of obstruction may be encountered. Viability of bowel is determined by the return of color and peristalsis, palpable mesenteric pulses, Doppler evaluations, and fluorescein staining. Reexploration within 24 h may be necessary. At celiotomy, decompression of the bowel is best carried out by advancing the nasogastric tube into the distended proximal small intestine; an alternative is to use a long tube through a proximal jejunostomy.
Postoperative care includes adequate fluid and electrolyte replacement and correction and return of intestinal motility (56 days). Parenteral nutrition may be needed.
The most common type of ileus is adynamic or inhibition ileus from inhibition of normal neuromuscular activities; when the bowel is contracted without coordinated propulsive activity, it is described as spastic ileus. In low floor states or when there is vascular occlusion, ischemic ileus is seen.
Adynamic ileus is common after abdominal operations. Gastric ileus and colonic ileus last for approximately 2 days and 34 days, respectively. Prolonged ileus may result from metabolic causes (e.g., hypokalemia, hyponatremia, hypomagnesia, intraabdominal sepsis, anastomotic leak), drugs (e.g., narcotics), or epidural anesthesia. Adynamic ileus also is seen with retroperitoneal hematoma, spinal fractures, rib fractures, and pelvic fractures. Clinical manifestations include abdominal distention and hypoactive bowel sounds. Abdominal x-rays show copious gas diffusely distributed in the intestine.
Management consists of nasogastric suction or gastrostomy tube drainage, the correction of fluid and electrolyte abnormalities, and parenteral nutrition. Erythromycin (a motilin agonist), bethanechol, vasopressin, metoclopramide, and cisapride are used.
PARTIAL OBSTRUCTION AND PSEUDO-OBSTRUCTION
Partial obstruction or pseudo-obstruction is seen in Crohn's disease and motility disorders, e.g., diabetic and postvagotomy gastroparesis. Symptoms include chronic nausea and vomiting. Abdominal examination may reveal generalized or localized distention.
Chronic intestinal pseudo-obstruction is secondary to abnormalities in the intestinal muscles or the nervous system and is seen in many diseases, including endocrine disorders, chronic infections, autoimmune diseases, neurologic disorders, and paraneoplastic syndromes. Tricyclic antidepressants, opiates, antihistamines, beta-adrenergic agonists, and amitriptyline can cause prolonged pseudo-obstruction. Presenting symptoms include nausea, vomiting, abdominal cramps, and distention. Constipation and diarrhea may occur. Recurrent attacks can lead to chronic obstruction with abdominal distention; if it occurs in the postoperative phase, it can result in multiple unnecessary operations with complications.
No specific test is diagnostic; hypokalemia, hypomagnesemia, and hypoalbuminemia are to be excluded. Endocrine tests, antinuclear antibody determinations, manometric studies, and intestinal biopsies may be necessary. Radiologic studies demonstrate prolonged transit times.
Operation should be avoided unless a specific site of obstruction is identified; support with total parenteral nutrition may be necessary. Many operations have been performed with very poor results. If the pseudo-obstruction is primarily colonic, a subtotal colectomy with ileorectal anastomosis has been found to be the most successful operation.
Bleeding can be occult, presenting as weakness, anemia, and orthostasis, or may be massive with sudden and rapid loss of blood. In one-third of patients it is the first symptom of GI disease, and in 70 percent there is no previous history of bleeding. Fifty percent of GI bleeding stops spontaneously. Hematemesis or vomiting of fresh blood implies bleeding above the ligament of Treitz. Altered blood vomitus is coffee ground emesis. Hematochezia or passage of blood per rectum can be of varied brightness and color and usually is seen in lower GI bleeding. Altered blood presents as black, tarry stool and is seen more commonly in upper GI bleeding. Between 50 and 60 mL of blood is required for a melanotic stool; guaiac-positive stool is seen with 10 mL of bleeding per day. Although iron produces a black stool, the stool is guaiac-negative. The consequences depend on the rate of bleeding and the site of bleeding.
Peptic ulcer disease constitutes one-half to two-thirds of upper GI bleeding, followed by esophageal varices (10 percent). Other causes are nose bleed, Mallory-Weiss tears, reflux esophagitis, gastric neoplasms, and hematobilia. In the over 60 age group, the mortality is 2025 percent. H2-receptor antagonists and proton pump inhibitors decrease the need for elective operations but have not reduced the need for operative treatment for bleeding duodenal ulcers.
Reflux esophagitis more commonly causes chronic occult bleeding. Variceal bleeding is a result of ulceration of the varix secondary to reflux esophagitis or increased pressure within the varix. A failing liver and its inability to synthesize coagulation factors aggravate the bleeding. In 25 percent of patients with cirrhosis and portal hypertension, bleeding can occur from gastritis and gastric or duodenal ulcers. Mallory-Weiss tears in the esophagus are secondary to recurrent vomiting and retching.
Acute gastritis can be seen with nonsteroidal anti-inflammatory drugs, alcohol, steroids, and oral potassium. Chronic gastritis is most commonly associated with H. pylori infection.
Stress ulcers and acute gastroduodenal lesions may be seen in patients in shock, with sepsis, after major surgery, trauma, or burns, and with intracranial pathology; they are the result of decreased gastric blood flow, bile reflux, infection, coagulopathy, and activation of cytocrines.
Among neoplasia, benign lesions such as leiomyomas can present with hematemesis. Dieulafoy's vascular malformations are rare submucosal dilated arterial lesions that can present with massive GI bleeding, as do aortoenteric fistulas. Patients should be questioned about past peptic ulcer disease, medications, alcohol abuse, and the onset of pain and vomiting as it relates to bleeding (in duodenal ulcers, pain disappears with bleeding). Prior aortic reconstructive surgery should raise suspicion for an aortoenteric fistula. Examination focuses on icterus, evidence of liver failure, and evidence of peritonitis.
Resuscitation is by the placement of a wide-bore intravenous line, restoring blood volume, Foley catheter, and nasogastric tube (iced saline lavage of the stomach may be useful). Laboratory tests include complete blood count, prothrombin time (PT), partial thromboplastin time (PTT), blood chemistry, and cross-match of adequate blood.
Esophagogastroduodenoscopy is performed as soon as the patient is hemodynamically stable and is of diagnostic and therapeutic value, e.g., injection or ligation of varices, coagulation of bleeding vessels, etc. Radionuclide scan is unhelpful but may be a useful precursor to arteriography, which can localize the bleeding point.
Specific therapies for variceal bleeding are intravenous vasopressin, Sengstaken-Blakemore tube, transjugular intrahepatic portal systemic shunting (TIPS), and an emergency portal caval shunt. Tamponade is very effective in controlling bleeding from Mallory-Weiss tears. When blood need exceeds 4 units in 24 h and continues, operative treatment should be considered. Operation is tailored to the underlying pathology, e.g., ulcer-reducing operation for duodenal ulcer bleeding, gastric resection for gastritis.
Gastric neutralization with antacids and sucralfate, inhibition of secretion with H2 antagonists and proton pump blockers, the correction of coagulation defects, invasive cardiac monitoring, and ICU care are recommended.
Small intestinal bleeding (1015 percent) is diagnosed by exclusion of upper GI bleeding and colonic bleeding. The causes include vascular malformations, neoplasia, Meckel's diverticula, enteric infections, and ulcers. Investigation includes radionuclide scanning, arteriography, and celiotomy.
Colon bleeding can be acute and massive or chronic. Massive lower GI bleeding occurring in the right colon usually is from angiodysplasia. Diverticular disease is a common cause of massive bleeding from the left colon.
Management starts with fluid resuscitation, placement of a nasogastric tube to rule out upper GI bleeding, Foley catheter placement, and proctosigmoidoscopy. Radionuclide scanning is sensitive and specific but does not pinpoint the site of bleeding accurately. Arteriography is definitive in locating the point of bleeding. CT scan and MRI may be useful. Barium study interferes with endoscopy and angiography. Celiotomy, intraoperative enteroscopy, and colectomy may be indicated if bleeding continues and the site of bleeding cannot be localized.
In chronic lower GI bleeding, neoplasia should be excluded. Investigations include rectosigmoidoscopy, colonoscopy, and barium enema. Rectal and anal bleeding, especially when associated with pain, is from fissures, proctitis, and hemorrhoids. A careful history and physical examination should exclude more proximal colon lesions.
Jaundice (excess bile pigments in the tissues and serum) is recognizable when the serum level of bilirubin approximates 23 mg/dL.
Normal Bilirubin Metabolism Bilirubin is formed when heme is oxidized and the resulting biliverdin reduced. Eighty percent of bilirubin comes from the destruction of red cells, and 20 percent comes from the rapid turnover of hepatic heme proteins and ineffective erythrocytes. Bilirubin, when first formed, is water-insoluble and bound to albumin and is carried to the liver, where the hepatocytes conjugate it to mono-and diglucuronides catalyzed by bilirubin uridine diphosphate glucuronic acid transferase (UDPGA). Conjugated bilirubin is water-soluble, is secreted across the liver canaliculi, and is carried down the bile ducts into the intestines, where bacteria convert the conjugated bilirubin to urobilinogen and urobilin, which are excreted in the feces and urine.
Etiology The causes of jaundice include
Congenital or familial types of hyperbilirubinemia are characterized by increases in unconjugated or conjugated bilirubin. Hemolytic disorders result in increased production of unconjugated bilirubin; pigment gallstones may produce common bile duct obstruction, resulting in an elevated conjugated bilirubin level. Unconjugated hyperbilirubinemia is rarely a surgical condition. The ratio of unconjugated to conjugated bilirubin will not differentiate between intra-or extrahepatic causes of jaundice but may help differentiate between a parenchymal and obstructive etiology. In parenchymal dysfunction, serum transaminase levels are elevated, unlike in obstructive jaundice, where the alkaline phosphatase level is high.
Clinical Manifestations Ask questions concerning loss of appetite (hepatitis), loss of weight, previous episodes of jaundice, the color of urine and stool, exposure to hepatitis, blood transfusions, drug (e.g., chlorpromazine, tetracycline, chlorthiazide, acetaminophen) and alcohol abuse, family history, abdominal pain (painless jaundice in carcinoma of the head of the pancreas), or pruritus (obstructive jaundice). Signs of liver dysfunction, lymph node enlargement, enlargement of the liver and spleen, and a palpable gallbladder (Courvoisier's Law) should be sought on examination.
Laboratory Studies Do a complete blood count and urinalysis (e.g., the presence of bilirubin and absence of urobilinogen indicates obstructive jaundice, the absence of bilirubin but presence of urobilin indicates excessive hemolysis or failure of conjugation); do liver enzyme determinations and fractionated bilirubin levels.
The initial radiologic examination is ultrasound to demonstrate a dilated biliary system and gallstones. If ducts are dilated, endoscopic retrograde cholangiopancreatography (ERCP) or a percutaneous transhepatic cholangiogram (PTC) can be performed depending on the expertise available. Both studies can localize the obstruction and also can be used for therapy, e.g., the removal of stones, sphincterotomy, placement of stent, placement of decompressive tube, obtain biopsies or brushings, and cytology. CT scan identifies masses in the porta hepatis, the head of the pancreas, and the liver. In carcinoma of the pancreas, a dynamic CT scan can define invasion of the portal vein.
This is a progressive, potentially reversible physiologic dysfunction of two or more organs or organ systems. It may be a sequel to resuscitation from an acute life-threatening event, e.g., operations for intraabdominal sepsis, ruptured abdominal aortic aneurysm with hypotension, and intestinal ischemia. Once MOFS is established, the mortality exceeds 70 percent. Although the GI tract may be the primary source of sepsis (e.g., perforated diverticulitis with fecal peritonitis), it also can be an unseen generator of the septic syndrome in a critically ill patient, e.g., bacterial translocation across the gut wall when the immunoregulatory function of the gut is compromised; immunologic activities of the liver also can be impaired in critical illness.
Several organ systems may show impairment. Pulmonary failure is manifest as the acute respiratory distress syndrome; poor urine output and a rise in BUN and creatinine levels indicate renal dysfunction. Liver failure presents as ischemic hepatitis (shock liver) and jaundice combined with associated abnormalities in liver chemistry and coagulation disorders. If septic shock syndrome is not reversed at this point, other organ systems fail. Cardiovascular dysfunction manifests as ventricular failure followed by CNS dysfunction causing altered states of consciousness. Anemia, leukopenia, and thrombocytopenia (heparin can cause thrombocytopenia) indicate hematologic dysfunction. Failure of the GI system may manifest as stress ulceration and diarrhea (exclude pseudomembranous colitis as a cause). Acute pancreatitis is frequent in MOFS. Acalculous cholecystitis may have its origin in mucosal ischemia, stasis, or infection.
For a more detailed discussion, see Fischer JE, Nussbaum MS, Chance WT, and Luchette F: Manifestations of Gastrointestinal Disease, chap. 22 in Principles of Surgery, 7th ed.
Copyright © 1998 McGraw-Hill
Seymour I. Schwartz
Principles of Surgery Companion Handbook