Chapter 25 Small Intestine
Principles of Surgery Companion Handbook
|Digestion and Absorption|
|Jejunal and Ileal Diverticula|
|Small Bowel Ulcerations|
|Pneumatosis Cystoides Intestinalis|
|Blind Loop Syndrome|
|Short Bowel Syndrome|
The duodenum is 20 cm long, the jejunum is 100110 cm long, and the ileum is 150160 cm long. The jejunoileum extends from the ligament of Treitz (the peritoneal fold at the duodenojejunal junction) to the ileocecal valve. The jejunum is larger and thicker than the ileum and has only one to two vascular arcades versus four to five in the ileum. The small bowel is tethered by the mesentery, which carries the vascular and lymphatic supply. The mesentery travels obliquely from the left of L2 to the right of the S1 joint; it is normally very mobile. The blood supply to the jejunum and ileum is via the superior mesenteric artery, which also supplies the proximal transverse colon. Vascular arcades in the mesentery provide collateral supply. Venous drainage parallels the arterial supply, leading to the superior mesenteric vein, which joins the splenic vein behind the pancreas to form the portal vein. Lymphatic drainage is from the bowel wall (lacteals), through the mesenteric nodes, to the superior mesenteric nodes, into the cisterna chyli, and finally to the thoracic duct. Mucosal folds form circumferential transverse plicae circulares. Innervation is parasympathetic (vagus, celiac ganglia) and affects secretion and motility. Sympathetics come from the splanchnic nerves via the celiac plexus, affect secretion and bowel and vascular motility, and carry pain afferents.
Serosa This is the outermost, visceral peritoneum that encircles the jejunum, covering the duodenum only anteriorly.
Muscularis This consists of a thin outer longitudinal layer and a thicker inner circular smooth muscle layer. Auerbach's plexus lies between the layers.
Submucosa This is a layer of fibroelastic connective tissue with vessels, nerves (Meissner's plexus), and lymphatics. Strongest component of bowel wall.
Mucosa This contains transverse folds with fingerlike villi. Cells of villi have microvilli (brush border) and glycocalyx fuzz, which increase surface area. Villi are largest in the duodenum. The mucosa is composed of three distinct layers.
Muscularis Mucosae This is the deepest mucosal layer, a thin sheet of muscle.
Lamina Propria This is a continuous connective tissue layer between the muscularis mucosae and the epithelium. It contains plasma cells, lymphocytes, eosinophils, macrophages, fibroblasts, and smooth muscle and serves to support the epithelium and act as an immunogenic barrier.
Epithelium This is the one layer of cells covering the villi and lining the crypts of Lieberkuhn. The crypts contain goblet cells (mucous), enterochromaffin cells (endocrine), Paneth cells (zymogen granules), and basal undifferentiated cells. New cells march up the crypt onto the villus, taking 37 days. Villi have endocrine, goblet, and absorptive cells covered by microvilli, which are covered by glycocalyx fuzz. Absorptive cells contain digestive enzymes and some specific absorption receptors (Fig. 25-1).
FIGURE 25-1 Schematic diagram of an intestinal absorptive cell. (From Trier JS et al, in Sleisenger MH, Fordtran JS (eds): Gastrointestinal Disease: Pathophysiology, Diagnosis, Management. Philadelphia, Saunders, 1983, chap. 48, with permission.)
Pace-setter potentials originate in the duodenum, initiate contractions, and propel food through the small bowel via segmentation (short segment contraction with to and fro mixing) and peristalsis (aboral migration of contraction wave and food bolus). The migrating myoelectric complex (MMC) sweeps the entire bowel during fasting. This is all under neurohumoral control, stimulated by motilin. Vagal cholinergics are excitatory; vagal peptidergics are inhibitory. Gastrin, cholecystokinin, and motilin stimulate muscular activity; secretin and glucagon inhibit it.
Fat Pancreatic lipase hydrolyzes triglycerides; components combine with bile salts to form micelles. A micelle then traverses the cell membrane passively by diffusion and then disaggregates, releasing bile salts back into the lumen and fatty acids and monoglycerides into the cell. The cell then reforms the triglycerides and combines these with cholesterol, phospholipids, and apoproteins to form chylomicrons, which exit cells and enter the lacteals. Small fatty acids can enter capillaries to the portal vein directly. Bile salts are resorbed into the enterohepatic circulation in distal ileum. Of a 5-g bile salt pool, 0.5 g is lost daily; the pool recirculates six times in 24 h.
Protein Gastric acid denatures proteins, and pepsin begins proteolysis. Pancreatic proteases (trypsinogen, activated by enterokinase to trypsin, and endopeptidases, exopeptidases) further digest proteins, yielding amino acids and two to six residue peptides. Active transport brings di- and tripeptides into absorptive cells.
Carbohydrate Pancreatic amylase rapidly digests carbohydrates in the duodenum. Brush border enzymes complete the digestion into hexoses, which are specifically transported into epithelial cells.
Water and Electrolytes Water, bile, and gastric, salivary, and intestinal fluids contribute up to 810 L/day of water, most of which is absorbed. Water is osmotically and hydrostatically absorbed or may diffuse passively. Sodium and chloride are absorbed by coupling to organic solutes or by active transport. Bicarbonate is absorbed by sodium-hydrogen exchange. Calcium is absorbed via active transport in the duodenum and jejunum, facilitated by parathormone (PTH) and vitamin D. Potassium is absorbed by passive diffusion.
Small bowel mucosa releases a wealth of hormones into blood (endocrine), via local discharge (paracrine), or as neurotransmitters.
Secretin This is a 27-amino acid peptide released from small bowel mucosa by acidification or contact with fat. Secretin stimulates pancreatic water and bicarbonate release, which neutralizes gastric acid. It also stimulates bile flow and inhibits gastrin release, gastric acid, and motility.
Cholecystokinin This is released by mucosa in response to amino acids and fatty acids. Cholecystokinin causes gallbladder contraction with relaxation of the sphincter of Oddi and pancreatic enzyme secretion. It also is trophic for bowel mucosa and pancreas and stimulates motility and the release of insulin.
Other Peptides Gastric inhibitory peptide (GIP) is released by glucose and fat and stimulates insulin release. It also enhances the oral versus intravenous response to glucose load. Others released by the small bowel include vasoactive intestinal peptide (VIP), enteroglucagon, motilin (intestinal smooth muscle contraction), bombesin, somatostatin (paracrine inhibitory peptide), neurotensin, and peptide YY (PYY).
The mucosa prevents pathogen entrance. It is a major source of immunoglobulin, produced by plasma cells in the lamina propria. M cells overlying lymphocytes in Peyer's patches exposed to antigens migrate to regional nodes, to the bloodstream, and then return to redistribute in the lamina propria to elaborate specific antibody.
Crohn's disease is a chronic inflammatory disease of the small or large intestine with acute exacerbations and spontaneous remissions. The true etiologic agent is unknown. Symptoms include intermittent, sometimes disabling diarrhea associated with meals, weight loss, and abdominal pain. This is the most common surgical disease of the small intestine. The risk is increased 30 times in siblings and 13 times in first-degree relatives.
Pathology The disease consists of mucosal and submucosal inflammation with aphthous ulcers. It progresses to transmural involvement with intense mononuclear cell infiltration and linear ulcers that, when severe, may coalesce resulting in cobblestone mucosa. The wall thickens and becomes edematous. Noncaseating granulomas appear late in the bowel wall and nodes. The mesentery becomes thick and short. Fat wraps from the mesenteric to the antimesenteric border. Scarring and fibrosis occur, narrowing the lumen. Typically, involved areas are not contiguous (skip lesions). Involved loops become adherent, matted, and may have internal fistulas.
In young adults, the symptoms include abdominal pain (intermittent, crampy), diarrhea (85 percent), and weight loss. The small bowel alone is affected in 30 percent, ileocolitis is seen in 55 percent, and the colon only is affected in 15 percent. The disease may involve any enteric mucosa, including the mouth and anus. Anal fissures, fistulas, and perianal abscesses are common. Extra abdominal manifestations include arthritis, uveitis, iritis, hepatitis, erythema nodosum, and pyoderma gangrenosum. Stools rarely contain pus, mucus, or blood (as in ulcerative colitis). Fever is seen in one-third of patients. In addition, patients may present with pain, intestinal obstruction, abscess, or a fistula to bowel, bladder, or skin. Free perforation is rare.
Diagnosis Small bowel barium follow-through shows nodular contour, luminal narrowing, linear ulcers, sinuses and clefts, and cobblestoning. Enteroclysis (double-contrast small bowel x-ray) is more sensitive. Barium enema may be useful. Acute ileitis is inflammation of the terminal ileum, which can mimic appendicitis but is self-limited and does not lead to Crohn's disease.
Treatment Nonsurgical treatment consists of combinations of anti-inflammatory, antineoplastic, and antibiotic agents such as sulfasalazine (Azulfidine), corticosteroids (for acute exacerbations), azathioprine, 6-mercaptopurine, cyclosporine, and metronidazole. Patients with obstructive symptoms are treated with bowel rest, hyperalimentation, nasogastric decompression, and pulsed steroids. Surgery is reserved for complete obstruction (rare) or for chronic high-grade partial obstruction (more common). Appendectomy (alone) is to be avoided with active appendiceal or cecal disease but should be performed otherwise. Operation is indicated for such complications as obstruction, pain, abscess, fistula, perforation, bleeding, perianal disease, growth retardation, refractory disease, or complications of nonsurgical therapy. More than 70 percent of all Crohn's patients ultimately require surgery. Intraoperatively, only grossly involved intestine should be removed; wide resections are to be avoided. Stomas are rarely needed for small bowel Crohn's disease. Bypass with exclusion is not used.
Prognosis Surgical therapy is not curative. Recurrence at 5, 10, 15, and 25 years is 29, 52, 64, and 84 percent, respectively, after surgery. The disease burns out with advancing age, especially age greater than 50 years. Ileal Crohn's disease increases the risk of adenocarcinoma more than 60-fold.
This entity is rare in Western countries. It is seen mostly as a secondary infection in pulmonary tuberculosis patients. The ileocecal region is involved most often, usually with caseating granulomas. The disease may produce a hypertrophic reaction with luminal stenosis, ulceration, or both. Ulceration produces diarrhea and pain alternating with constipation. Treatment is with combination chemotherapy. Surgery is reserved for perforation, obstruction, or hemorrhage.
This disease is caused by Salmonella typhosa, with ulceration of Peyer's patches, splenomegaly, and mesenteric adenopathy. It is rare in Western patients. Treatment is Bactrim or amoxicillin. Patients may have gross hemorrhage, and ileal perforation is seen in 2 percent.
Primary small bowel neoplasms are very rare. The colon is affected 40 times more than the small intestine. Symptoms are often vague: epigastric pain, nausea, vomiting, colic, diarrhea, bleeding (usually occult). The most common reasons for operation are obstruction, bleeding, and pain. Benign tumors cause intussusception in adults; malignant tumors directly obstruct the bowel. Diagnosis is difficult. Endoscopy is useful for duodenal and proximal jejunal lesions; the rest of the bowel requires small bowel barium radiographs.
Benign neoplasms are either of epithelial or connective tissue origin. Most often they are adenomas, leiomyomas, or lipomas (Table 25-1). Often these cause no symptoms unless they cause obstruction by intussusception; they also may bleed (one-third are occult). Surgery is indicated if the diagnosis is made or suspected. Most often simple segmental resection is used.
TABLE 25-1 TYPES AND RELATIVE FREQUENCY OF SMALL BOWEL BENIGN NEOPLASMS
These consist of true adenomas, villous adenomas, or Brunner's gland adenomas (hyperplastic duodenal glandular proliferation without malignant potential); 20 percent are seen in the duodenum. Most are asymptomatic. Villous adenomas have 3555 percent malignant potential.
These are benign, single smooth muscle lesions. Most commonly present with bleeding.
This syndrome consists of mucocutaneous melanotic pigmentation (circumoral, buccal, palms, soles, perianal) and gastrointestinal polyps. It occurs by simple dominant inheritance. Polyps are multiple jejunal, ileal, and rectal and are hamartomas. They may cause intussusception or bleeding. Curative resection usually is not possible. Surgery is indicated for obstruction or bleeding.
Metastatic lesions (ovarian, colonic, gastric, breast, lung primary) are the most common. Primary malignancies include adenocarcinomas, carcinoids, sarcomas, and lymphomas. Patients have diarrhea with mucus/tenesmus, obstruction, and chronic blood loss. Usually there is an insidious presentation. Treatment is wide resection, including nodes. Duodenal lesions require pancreaticoduodenectomy. Palliative resections are done for relief of symptoms/obstruction. Overall survival is poor (average 20 percent 5-year survival). Periampullary carcinoma may have up to 40 percent 5-year survival.
Approximately 50 percent of small bowel malignancies are adenocarcinomas. They are seen mostly in the duodenum and proximal jejunum; 50 percent of duodenal carcinomas involve the ampulla and are associated with intermittent jaundice. Jejunal lesions are associated with obstruction.
Sarcomas comprise 20 percent of small bowel malignancies; leiomyosarcomas are most common. They may bleed or obstruct.
Lymphomas comprise 1015 percent of small bowel malignancies. They are most common in the ileum. They may be primary small bowel neoplasms or part of systemic disease.
Carcinoids arise from enterochromaffin (Kulchitsky) cells. They occur as often as adenocarcinomas of the small bowel. Their malignant potential is variable. They secrete serotonin and substance P. Carcinoid syndrome (i.e., flushing, bronchospasm, diarrhea, vasomotor collapse, hepatomegaly, and right-sided heart valvular disease) occurs in less than 5 percent. (Hepatic metastasis is likely present before the syndrome occurs.) Carcinoids arise in the appendix (46 percent), ileum (28 percent), and rectum (17 percent). Appendiceal tumors metastasize 3 percent of the time as compared with ileal carcinoids (35 percent metastatic rate). Of those less than 1 cm in diameter (75 percent of gastrointestinal carcinoids), only 2 percent metastasize. Gross appearance is a yellow or tan, round, hard submucosal nodule. Often asymptomatic, but can cause abdominal pain, obstruction, diarrhea, and weight loss; carcinoid syndrome is rare.
Diagnosis A small bowel series, mesenteric arteriograms, and computed tomographic scans are useful. Urine examination for 5-hydroxyindoleacetic acid (5-HIAA) with or without pentagastrin stimulation is used for diagnosis of syndrome.
Malignant carcinoid syndrome is rare, occurring in only 69 percent of carcinoid patients. It is seen most often with small bowel disease and hepatic metastasis. Symptoms include hepatomegaly, diarrhea, flushing, right-sided heart valvular disease, and asthma. Symptoms are due to serotonin, substance P, and possibly bradykinin and prostaglandins E and F.
Treatment Primary carcinoids less than 1 cm in size are treated by segmental small bowel resection. Larger lesions or lesions with involved nodes require wide bowel excision with inclusion of mesentery. Appendiceal carcinoids less than 2 cm in size require only simple appendectomy; if carcinoids are more than 2 cm in size, the patient should have a right hemicolectomy. Carcinoid syndrome may be treated by curative or palliative resection or with long-acting somatostatin.
Prognosis Overall survival rate is 54 percent, with 75 percent for local disease, 59 percent for regional spread, and 19 percent for distal spread. Because of the indolent nature of the disease, debulking and palliative resections are used.
Congenital diverticula are true, composed of all layers; acquired diverticula are false, because only mucosa and submucosa protrude through a muscular defect. Meckel's and duodenal diverticula are the most common diverticula of the small bowel.
Incidence is 1020 percent in autopsy series; 90 percent are asymptomatic; and less than 5 percent require operative intervention. Between 67 and 75 percent are found in the periampullary region on the medial wall. Manifestations may be obstruction, perforation, or bleeding. Those associated with the ampulla may produce cholangitis, pancreatitis, and recurrent choledocholithiasis from stasis or choledochal sphincter dysfunction. Surgical therapy is diverticulectomy or extended sphincteroplasty for those involving the ampulla.
These are less common than those in the duodenum. Multiple false diverticula may occur and lead to jejunal pseudo-obstruction and dyskinesia.
This is the most common true diverticulum of the gastrointestinal tract. It is congenital, from incomplete closure of the omphalomes-enteric or vitelline duct. Usually it is located 23 ft from ileocecal valve and is 112 cm long. It may have heterotropic gastric mucosa or pancreatic tissue. Overall, it is seen in 2 percent of population. Complications include intestinal obstruction (via volvulus or intussusception), bleeding (gastric mucosa produces acid, ulcer is in adjacent ileum), or acute diverticulitis. Meckel's diverticulum in a hernia is a Littre hernia. Diagnosis is via enteroclysis or technetium-99m pertechnetate scan. Complications of Meckel's are often confused with acute appendicitis. Asymptomatic Meckel's diverticulum found incidentally at surgery should not be removed.
Most of these ulcerations are due to drugs (enteric-coated potassium or corticosteroids), vascular disorders, Crohn's disease, syphillis, typhoid fever, tuberculosis, lymphoma, gastrinoma, or Meckel's diverticulum. Nonspecific ulcers may be found in the terminal ileum. Treatment is for complications, pain, obstruction, bleeding, and perforation.
Most often fistulas are due to surgical trauma; less than 2 percent are associated with Crohn's disease. Complications include sepsis, fluid and electrolyte imbalances, skin breakdown, and malnutrition. Overall, intestinal fistulas have more than 20 percent mortality, even with total parenteral nutrition (TPN). The key to successful management is fluid, electrolyte, and nutritional maintenance with control of sepsis. Proximal fistulas have higher output (> 500 mL/day) and more severe complications. A gastrointestinal series is essential to identify the anatomic location of the fistula. Treatment includes drainage of the fistula or cavity, TPN, bowel rest, and skin protection. Somatostatin may be helpful. Factors that prevent spontaneous closure are high output, distal obstruction, marked disruption in intestinal integrity, inflammation (undrained abscess, active granulomatous disease), a foreign body in the tract, cancer, radiated tissue, a short tract (< 2.5 cm), or epithelialization of the tract. Fewer than 30 percent close spontaneously, and most that do close, do so in about 3 weeks.
This is an uncommon condition manifested by multiple gas-filled cysts (submucosal, subserosal) in the gastrointestinal tract. It is most often associated with other conditions, and usually it does not require surgical therapy.
Bacterial overgrowth in a stagnant area of small bowel produces diarrhea, steatorrhea, anemia, weight loss, abdominal pain, vitamin deficiencies (especially B12), and neurologic disorders. This is usually secondary to strictures, fistulas, blind pouches (postoperative), or diverticula.
After massive, often emergent small bowel resection (volvulus, mesenteric vascular occlusion, Crohn's disease), short bowel syndrome may arise. Hallmarks are diarrhea, fluid and electrolyte deficiencies, and malnutrition. Usually up to 70 percent resection can be tolerated if the terminal ileum and ileocecal valve are preserved. Loss of the terminal ileum leads to abnormalities of vitamin B12 and bile salt absorption. Jejunal resection is better tolerated than ileal resection. After resection, adaptation occurs: Villi lengthen, and cell number and renewal increase, thus increasing the absorptive surface. Luminal feeding (especially glutamine), pancreaticobiliary secretions, and certain hormones (cholecystokinin, secretin, neurotensin, PYY) appear to be trophic and necessary for adaptation. Adaptation does not occur with TPN alone.
Treatment Treatment includes prevention with conservative resection of marginally viable bowel and second look operations to reassess such intestine; early on, treatment is corrective for fluid and electrolyte losses and TPN. Early enteral nutrition is essential. Elemental diets or polymeric diets are useful. Milk products should be avoided. Fat-soluble vitamin supplementation is often needed. Vitamin B12 injections may be used. Histamine H2 blockers may diminish diarrhea from rapid transit. Certain amino acids (glutamine) may specifically aid in adaptation.
Jejunoileostomy for the treatment of morbid obesity has been almost completely abandoned. Long-term complications include liver failure, death, cirrhosis, hyperoxaluria, renal calculi, avitaminoses, blind loop syndrome, pancreatitis, and gallstones, among many others. Morbid obesity is now treated with gastric partitioning or gastric bypass. Supermorbidly obese patients can be treated initially with intestinal bypass. A previously constructed jejunoileal bypass should be taken down, and intestinal continuity should be restored if significant metabolic imbalances or hepatic failure exists. There is some early evidence that partial ileal bypass (200 cm) may be useful in refractory hyperlipidemia.
For a more detailed discussion, see Evers BM, Townsend CM Jr, Thompson JC: Small Intestine, chap. 25 in Principles of Surgery, 7th ed.
Copyright © 1998 McGraw-Hill
Seymour I. Schwartz
Principles of Surgery Companion Handbook