Small Intestine Anatomy and Physiology PDF

EUROPEAN UNIVERSITY CYPRUS Access Provided by: Current Diagnosis & Treatment: Surgery, 15e Chapter 31: Small Intestine Marco Ettore Allaix; Alessandro Fichera ANATOMY Gross Anatomy The small intestine is the portion of the alimentary tract extending from the pylorus to the ileocecal valve, and it consists of three segments: the duodenum, the jejunum (upper twofifths), and the ileum (lower threefifths). The anatomy, physiology, and pathology of the duodenum are discussed in Chapter 25. The duodenum is a retroperitoneal structure that is approximately 25 cm long and is divided into four segments: the bulb and the descending, transverse, and ascending segments. Both the celiac trunk, through the gastroduodenal artery, and the superior mesenteric artery (SMA) supply the duodenum. The jejunum begins at the ligament of Treitz. The jejunum and ileum are suspended on a mobile mesentery covered by a visceral peritoneal lining that extends onto the external surface of the bowel to form the serosa. There is no sharp demarcation between the jejunum and the ileum; as the intestine proceeds distally, the lumen narrows, the mesenteric vascular arcades become more complex, and the circular mucosal folds become shorter and fewer. The mesentery contains fat, blood vessels, lymphatic channels and nodes, and nerves. The jejunum and ileum are supplied by the SMA. Branches within the mesentery anastomose to form arcades, and small straight arteries from these arcades enter the mesenteric border of the gut. Venous blood is drained through the superior mesenteric vein, which then joins the splenic vein behind the pancreas to form the portal vein. Lymphatic drainage is abundant, with several levels following the blood vessels. Elliptical, lymphoid aggregates (Peyer’s patches) are present in the submucosa on the antimesenteric border along the distal ileum, and smaller follicles are evident throughout the remainder of the small intestine. The lymph is drained into the lymph nodes that follow the mesenteric arcade and then into the lymphatic vessels along the SMA. Eventually, the lymph is drained into the cisterna chyli that is located below the diaphragm. The innervation for the small intestine is both sympathetic (fibers from the greater and lesser splanchnic nerves) and parasympathetic (from the right vagus nerve). Although both types of autonomic nerves contain efferent and afferent fibers, only the sympathetic afferents appear to mediate intestinal pain. Microscopic Anatomy The wall of the small intestine consists of four layers: mucosa (innermost), submucosa, muscularis, and serosa (outermost). The mucosa is characterized by circular folds about 10 mm high, named valvulae conniventes, that are taller and more numerous in the proximal jejunum and project into the lumen (Figure 31–1). These folds, combined with the presence of villi on the surface of the valvulae conniventes, increase the absorptive surface area about eight times. There are approximately 2040 villi per square millimeter. They are about 0.51 mm long, and their walls are made up of epithelial cells with tiny projections named microvilli. The epithelial cells enclose a central axis that contains an arteriole surrounded by blood and lymphatic capillaries, known as a lacteal, and fibers from the muscularis mucosae. The microvilli (1 µm in height) amplify the potential absorptive surface area up to 200500 m2 (Figure 31–2). Figure 31–1. Blood supply and luminal surface of the small bowel. The arterial arcades of the small intestine increase in number from one or two in the proximal Downloaded 2024131 5:56 A Your IP is 82.116.202.56 jejunum or five in the distal findingAlessandro that helps to distinguish proximal from distal bowel at operation. Plicae circulares are more Page 1 / 37 Chapter to 31:four Small Intestine, Marcoileum, Ettorea Allaix; Fichera prominent in the jejunum. ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility blood and lymphatic capillaries, known as a lacteal, and fibers from the muscularis mucosae. The microvilli (1 µm in height) amplify the potential EUROPEAN UNIVERSITY CYPRUS absorptive surface area up to 200500 m2 (Figure 31–2). Access Provided by: Figure 31–1. Blood supply and luminal surface of the small bowel. The arterial arcades of the small intestine increase in number from one or two in the proximal jejunum to four or five in the distal ileum, a finding that helps to distinguish proximal from distal bowel at operation. Plicae circulares are more prominent in the jejunum. Figure 31–2. Schematic representation of villi and crypts of Lieberkühn. Downloaded 2024131 5:56 A Your IP is 82.116.202.56 Page 2 / 37 Chapter 31: Small Intestine, Marco Ettore Allaix; Alessandro Fichera ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility The mucosa is microscopically subdivided into three different layers: (1) the muscularis mucosae, the outermost layer, consists of a thin sheet of smooth muscle cells; (2) the lamina propria consists of connective tissue that extends from the base of the crypts up into the intestinal villi; and (3) the EUROPEAN UNIVERSITY CYPRUS Figure 31–2. Access Provided by: Schematic representation of villi and crypts of Lieberkühn. The mucosa is microscopically subdivided into three different layers: (1) the muscularis mucosae, the outermost layer, consists of a thin sheet of smooth muscle cells; (2) the lamina propria consists of connective tissue that extends from the base of the crypts up into the intestinal villi; and (3) the epithelium is the innermost layer. Intestinal epithelium is composed of multiple cell types that rest on a thin basement membrane overlying the lamina propria. There are two major compartments to the intestinal epithelium, the crypt and the villus, each with distinct function and cellular composition. The crypt is populated by cells that are predominantly secretory and that derive from a pluripotent stem cell located above the base of the crypts of Lieberkühn. Paneth cells stay at the base of the crypts; their function is still unknown but may be secretory, as they resemble the zymogensecreting cells of the pancreas. Most of the crypt cells are undifferentiated; some mature into mucussecreting goblet cells and enteroendocrine cells, but the majority become absorptive enterocytes. Enteroendocrine cells include enterochromaffin cells (the most common), N cells that contain neurotensin, L cells (glucagon), and motilin and cholecystokinin (CCK)containing cells. Finally, M cells and T lymphocites play a major role in mucosal cell–mediated immunity. The villus compartment is nonproliferative. Factors that affect enterocyte differentiation include growth factors, hormones, matrix proteins, and luminal nutrients. The life span of enterocytes is 36 days. The submucosa is a dense connective tissue layer populated by different cell types, including fibroblasts, mast cells, lymphocytes, macrophages, eosinophils, and plasma cells. It contains blood vessels, lymphatics, and nerves. Meissner’s submucosal neural plexus interconnects with neural elements from Auerbach’s plexus. The submucosa is the strongest layer of small bowel wall. The muscularis consists of two layers of smooth muscle, a thicker inner circular layer and a thinner outer longitudinal layer. Specialized intercellular junctional structures called gap junctions electrically couple adjacent smooth muscle cells and allow efficient propagation of peristalsis. Ganglion cells and nerve fibers of Auerbach’s myenteric plexus interdigitate between layers and communicate with smaller neural elements between cells. The serosa consists of a single layer of flattened mesothelial cells that covers the small bowel. Johansson ME, et al: Composition and functional role of the mucus layers in the intestine. Cell Mol Life Sci. 2011;68(22):3635–3641. [PubMed: 21947475] Simons BD, et al: Stem cell selfrenewal in intestinal crypt. Exp Cell Res. 2011;317(19):2719–2724. [PubMed: 21787769] PHYSIOLOGY Downloaded 2024131 5:56 A Your IP is 82.116.202.56 Chapter Motility31: Small Intestine, Marco Ettore Allaix; Alessandro Fichera ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility Page 3 / 37 Intestinal motility consists of propulsion of luminal contents (peristalsis) combined with mixing action through segmentation. These functions are accomplished by both the outer longitudinal and inner circular muscle layers of the intestinal wall, mainly under the direct control of the myoenteric 21947475] EUROPEAN UNIVERSITY CYPRUS Access Provided by: Simons BD, et al: Stem cell selfrenewal in intestinal crypt. Exp Cell Res. 2011;317(19):2719–2724. [PubMed: 21787769] PHYSIOLOGY Motility Intestinal motility consists of propulsion of luminal contents (peristalsis) combined with mixing action through segmentation. These functions are accomplished by both the outer longitudinal and inner circular muscle layers of the intestinal wall, mainly under the direct control of the myoenteric nervous plexus. The submucosal nervous plexus is primarily involved in the regulation of secretion and absorption. The extrinsic sympathetic input is excitatory and the peptidergic input likely inhibitory. Intestinal motility is also under positive control by local hormones such as motilin and CCK. Smooth muscles of the small intestine undergo spontaneous oscillations of membrane potentials, known as pacesetter potentials, with progressively decreasing frequency from the duodenum to the ileum. The frequency of pacesetter potentials for the entire small intestine is determined by the duodenum, where they originate. A nerverelated cell type known as the interstitial cell of Cajal appears to play a key role in the generation of pacemaker activity. Small bowel motility varies with the fasted and fed state. During the interdigestive or fasting period, a cyclical pattern of motor activity consisting of three phases is observed. Phase I is resting and lasts for about 80% of the cycle. Phase II, about 15%, consists of random contractions of moderate amplitude. Phase III, about 5%, is a series of brief highpressure waves. This threephase cycle results in a pattern called the migrating motor complex, which is abolished by ingestion of food. In the fed state, the pattern of contraction is more frequent and consistent over time. Rather than beginning from a proximal site and propagating distally, contractions begin at all levels along the small bowel and spread distally. Barrier Function The intestinal epithelium selectively limits the permeation of potentially harmful luminal substances. The anatomic barrier is the intercellular junction complex, a threelevel structure that forms a circumferential seal between adjacent cells: the tight junction faces the lumen, the intermediate junction lies deep to the tight junction, and the desmosome is the innermost element of this complex. Several pathologic conditions can alter the barrier function. Certain bacterial toxins, such as Clostridium difficile, directly perturb the barrier function through disruption of cytoskeletaljunctional interactions, and various cytokines and proinflammatory mediators can also modulate intestinal permeability. Digestion and Absorption Digestion begins in the stomach with the action of gastric acid and pepsin. In the proximal duodenum, ingested food is broken down by pancreatic enzymes such as trypsin, elastase, chymotrypsin, and carboxypeptidases. The activity of intestinal hydrolases and olygopeptidases then accomplishes terminal protein and carbohydrate digestion, and the resulting monosaccharides, amino acids, or di and tripeptides then serve as substrates for Na+ or H+coupled transporters in the apical membrane of absorptive enterocytes. Fat digestion and absorption occur in the proximal small bowel, where pancreatic lipase partially hydrolyzes triglycerides into two fatty acids and a monoglyceride. These substances are solubilized by bile salts to form micelles that diffuse into enterocytes releasing fatty acid and monoglyceride. Triglycerides are transported intracellularly and incorporated along with cellular protein, phospholipid, and cholesterol to form chylomicrons. They then exit the cell to be absorbed by the lymphatic system. Bile salts are reabsorbed into the enterohepatic circulation in the distal ileum by an ileal Na+coupled bile acid transporter. The small bowel receives about 11.5 L/d of ingested fluids and about 8 L of salivary, gastric, and pancreaticobiliary secretions. Most of this fluid is reabsorbed before reaching the colon. Water movement is driven by the active transcellular absorption of Na+ and Cl– and by absorption of nutrients such as glucose and amino acids. The energy for many of these processes derives from the activity of an Na+K+ ATPase, which maintains the low Na+ internal environment that drives uptake via coupled ion exchangers (Na+/H+ and Cl–/HCO3–) and Na+coupled nutrient transporters. Secretion Intestinal crypt cells secrete an isotonic fluid through the active transcellular transport of Cl–. This process lubricates the mucosal surface and facilitates the luminal extrusion of other secreted substances. Diarrhea results when secretion exceeds intestinal absorptive capacity. Immune Function The mucosal immune system is extremely important in defense against toxic and pathogenic threats from the luminal environment. The lamina propria contains numerous immune cells, including plasma cells, mast cells, and lymphocytes, that produce both immunoglobulins and cytokine mediators. Downloaded 2024131 5:56 A Your IP is 82.116.202.56 Page 4 / 37 Chapter 31: Small Intestine, Marco Ettore Allaix; Alessandro Fichera Plasma cells produce immunoglobulin A (IgA) in response food antigens microbes. IgA and immunoglobulin M (IgM) are secreted into the lumen ©2024 McGraw Hill. All Rights Reserved. Terms of Use to Privacy Policy and Notice Accessibility by a mechanism that involves transcytosis through epithelial cells after binding to the polymeric immunoglobulin receptor on the basolateral membrane. Secretory IgA prevents microbial pathogens from penetrating the epithelial layer. IgAantigen interactions also occur within the Immune Function EUROPEAN UNIVERSITY CYPRUS Access Provided by: The mucosal immune system is extremely important in defense against toxic and pathogenic threats from the luminal environment. The lamina propria contains numerous immune cells, including plasma cells, mast cells, and lymphocytes, that produce both immunoglobulins and cytokine mediators. Plasma cells produce immunoglobulin A (IgA) in response to food antigens and microbes. IgA and immunoglobulin M (IgM) are secreted into the lumen by a mechanism that involves transcytosis through epithelial cells after binding to the polymeric immunoglobulin receptor on the basolateral membrane. Secretory IgA prevents microbial pathogens from penetrating the epithelial layer. IgAantigen interactions also occur within the intraepithelial and subepithelial compartments. Intestinal epithelial cells themselves may also contribute to the immune function of the bowel. These cells express major histocompatibility class I and class II molecules on their surface and may function as weak antigenpresenting cells. The epithelial cell layer may transmit important immunoregulatory signals to the underlying lymphocytic population. Specialized cells known as M cells are found overlying Peyer’s patches and act as the major portal of entry for foreign bodies. Specialized membrane invaginations in these cells create a pocket in which lymphocytes and macrophages gather. Luminal substances are immediately delivered to these antigenpresenting cells, and this information is directly conveyed to the underlying follicles. Intraepithelial lymphocytes (IELs) are specialized T cells that reside in the paracellular space between absorptive enterocytes. The precise role of IELs is still uncertain, but they may mediate crosstalk between epithelial cells and the underlying immune and nonimmune cells of the lamina propria. Within the lamina propria and submucosa, mature T cells, B cells, and macrophages carry out traditional cellmediated immune response including phagocytosis, cell killing, and cytokine secretion. Mucosal and connective tissue mast cells produce numerous mediators that contribute to overall immune response and modulate the many functions of the epithelial cells. Neuroendocrine Function The small bowel is a rich source of regulatory peptides that control various aspects of gut function. These substances, released in response to luminal or neural stimuli, exert their biological actions either at distant sites or locally. Secretin is a 27aminoacid peptide released by enteroendocrine cells in the proximal small bowel in response to luminal acidification, bile salts, and fat. Its major function is to stimulate pancreatic ductal alkaline secretion. Secretin inhibits gastric acid secretion and gastrointestinal motility. In addition, it stimulates bile flow by stimulating fluid secretion from cholangiocytes. Other members of the secretin family that share substantial sequence homology and interact with similar receptors include vasoactive intestinal polypeptide (VIP), glucagon, gastric inhibitory polypeptide (GIP), and enteroglucagon. Enteroglucagon and glucagonlike peptides are secreted by neuroendocrine cells in the colon and small bowel and may play an important role in gut adaptation and glucose homeostasis. CCK is released by specialized enteroendocrine cells in response to luminal amino acids and medium to longchain fatty acids. CCK release is inhibited by intraluminal trypsin and bile salts. Two major targets of CCK are the gallbladder and the sphincter of Oddi, where it causes coordinated contraction and relaxation, respectively, to enhance luminal mixing of bile with ingested food. Furthermore, CCK stimulates pancreatic enzyme secretion and cell growth in intestinal mucosa and the pancreas, insulin release, and intestinal motility. Somatostatin is a 14aminoacid peptide that exerts a wide variety of inhibitory functions in the gastrointestinal tract. It is released from specialized enteroendocrine cells, and it acts in paracrine fashion to inhibit intestinal, gastric, and pancreaticobiliary secretion and cell growth. Synthetic forms of somatostatin are used in clinical practice in patients with enterocutaneous and pancreaticobiliary fistulae. Peptide YY is a 36aminoacid peptide secreted by the distal small bowel, and it inhibits gastric acid and pancreatic secretion, as well as several intestinal hormones, and decreases intestinal motility. Motilin is secreted by the duodenum and the proximal jejunum, where it acts to enhance contractility and accelerate gastric emptying. Neurotensin is produced in the ileum and enteric nerves; it appears to affect a variety of enteric functions including gastric acid secretion, gastric emptying, intestinal motility, and secretion. Other peptides (VIP, calcitoninrelated peptide, galanin, bombesin, neuropeptide Y, gastrinreleasing peptides, and substance P) are released from enteric nerves, but their precise role has not been fully clarified. Crenn P, et al: Citrulline as a biomarker of intestinal failure due to enterocyte mass reduction. Clin Nutr. 2008;27:328. [PubMed: 18440672] Edholm T, et al: The incretin hormones GIP and GLP1 in diabetic rats: effects on insulin secretion and small bowel motility. Neurogastroenterol Motil. 2009;21(3):313–321. [PubMed: Downloaded 2024131 5:56 A19126188] Your IP is 82.116.202.56 Chapter 31: Small Intestine, Marco Ettore Allaix; Alessandro Fichera ©2024 McGraw Allintestinal Rights Reserved. Terms Use Privacy 2008;24:164. Policy Notice Accessibility Jones MP, et al:Hill. Small motility. Curr OpinofGastroenterol. [PubMed: 18301266] Page 5 / 37 enteric nerves, but their precise role has not been fully clarified. EUROPEAN UNIVERSITY CYPRUS Access Provided by: Crenn P, et al: Citrulline as a biomarker of intestinal failure due to enterocyte mass reduction. Clin Nutr. 2008;27:328. [PubMed: 18440672] Edholm T, et al: The incretin hormones GIP and GLP1 in diabetic rats: effects on insulin secretion and small bowel motility. Neurogastroenterol Motil. 2009;21(3):313–321. [PubMed: 19126188] Jones MP, et al: Small intestinal motility. Curr Opin Gastroenterol. 2008;24:164. [PubMed: 18301266] SMALL BOWEL OBSTRUCTION General Considerations Small bowel obstruction (SBO) is one of the most common disorders affecting the small bowel. It is characterized by impairment in the normal flow of intraluminal contents and can be divided into mechanical obstruction and paralytic ileus. This distinction is critical for the further management of the patient. Mechanical obstruction implies an extrinsic or intrinsic obstacle that prevents the aboral progression of intestinal contents, and it may be complete or partial. Simple obstruction occludes the lumen only; obstruction with strangulation impairs the blood supply also and leads to necrosis of the intestinal wall. Paralytic (or adynamic) ileus is due to a neurogenic failure of peristalsis to propel intestinal contents with no mechanical obstruction. A. Etiology The causes of mechanical obstruction can be divided into three groups according to the relationship to the intestinal wall: (1) intraluminal; (2) intramural; and (3) extrinsic. The three most common etiologies are intraabdominal adhesions, hernias, and neoplasms. 1. Adhesions. Sixty to seventy five percent of cases of mechanical SBO are secondary to adhesions related to prior abdominal surgery. Lower abdominal and pelvic surgery appears to be associated with a higher incidence of adhesions compared to upper abdominal surgery. Congenital bands are rarely seen in children. 2. Hernia. The most common cause of SBO in patients with no history of prior abdominal surgery is a hernia. A careful search for inguinal, femoral, and umbilical hernias must be made during evaluation of every patient presenting with symptoms consistent with obstruction. Internal hernias into the obturator foramen, the foramen of Winslow, or other anatomic defects must also be considered. In patients who have undergone previous surgery, incisional hernias represent another potential cause of SBO, especially after laparotomy in overweight or obese patients, in patients on steroid therapy, or with wound infections. 3. Neoplasms. Intrinsic small bowel neoplasms can progressively occlude the lumen or serve as a leading point in intussusception. Symptoms may be intermittent, onset of obstruction is slow, and signs of chronic anemia may be present. Peritoneal carcinomatosis from several tumors is an extrinsic cause of SBO due to adhesions of small bowel loops to neoplastic nodules. Other causes of SBO include Crohn disease; intussusception, which is most often seen in children without an organic lesion and rarely in adults with a neoplastic intraluminal lesion; volvulus as a consequence of intestinal malrotation in children or of adhesions in adults; and foreign bodies including bezoars, ingested foreign bodies, and gallstones through a cholecystoduodenal fistula. Gallstone ileus is discussed in Chapter 27. B. Pathophysiology With onset of obstruction, gas and fluid accumulate and distend the intestinal loops proximal to the site of obstruction. Fluid from the extracellular space also fills the lumen proximal to the obstruction, due to the impaired bidirectional flow of salt and water and fluid secretion enhanced by substances (endotoxins, prostaglandins) released from proliferating bacteria in the intestinal lumen. As a consequence, intraluminal and intramural pressures rise until microvascular perfusion to the intestine is impaired, leading to intestinal wall ischemia and ultimately necrosis. Activity of the smooth muscle of the small bowel is increased in an attempt to propel its contents past the obstruction consuming all energy sources. At this point, the intestine becomes atonic and enlarges further. Emesis could be feculent due to bacterial overgrowth—particularly with distal obstruction—as the intestinal dilation progresses proximally (Figure 31–3). Bacterial translocation from the lumen to the mesenteric nodes and the bloodstream occurs, and abdominal distention elevates the diaphragm and impairs respiration, resulting in potential pulmonary complications such as pneumonia and atelectasis. Downloaded 2024131 5:56 A Your IP is 82.116.202.56 Figure 31–3. Chapter 31: Small Intestine, Marco Ettore Allaix; Alessandro Fichera ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility Small bowel obstruction. Variable manifestations of obstruction depend on the level of blockage of the small bowel. Page 6 / 37 Activity of the smooth muscle of the small bowel is increased in an attempt to propel its contents past the obstruction consuming all energy sources. At EUROPEAN UNIVERSITY this point, the intestine becomes atonic and enlarges further. Emesis could be feculent due to bacterial overgrowth—particularly with distal CYPRUS Provided by: obstruction—as the intestinal dilation progresses proximally (Figure 31–3). Bacterial translocation from the lumenAccess to the mesenteric nodes and the bloodstream occurs, and abdominal distention elevates the diaphragm and impairs respiration, resulting in potential pulmonary complications such as pneumonia and atelectasis. Figure 31–3. Small bowel obstruction. Variable manifestations of obstruction depend on the level of blockage of the small bowel. When fullthickness necrosis of the intestinal wall occurs, luminal content with an elevated bacterial load enters the peritoneal cavity and is absorbed by the peritoneum, causing septic shock. The progression of pathophysiologic events when the bowel is strangulated occurs more rapidly than with simple obstruction and is characterized by an acute impairment of venous return initially followed by arterial flow with subsequent ischemia, necrosis, and perforation of the intestinal wall. Clinical Findings Diagnostic evaluation should distinguish mechanical bowel obstruction from ileus, determine the cause of the obstruction, and recognize simple from strangulating obstruction. Accurate diagnosis requires obtaining a detailed history, paying particular attention to medications known to affect intestinal physiology, previous cancer, inflammatory bowel disease, and abdominal surgery, and performing a meticulous physical examination. A. Signs and Symptoms Patients usually present with nausea, vomiting, colicky abdominal pain, and obstipation, although residual gas and stool distal to the obstruction may be expelled. With proximal SBO, emesis is usually profuse, containing undigested food in close temporal association with oral intake; abdominal pain is more often described as upper abdominal discomfort associated with epigastric distension. Distal SBO is characterized by diffuse and poorly localized crampy abdominal pain. Feculent vomiting present in cases of longstanding distal SBO is the consequence of bacterial overgrowth and is pathognomonic for a complete mechanical obstruction. In the presence of strangulation, fever often develops, and previously crampy abdominal pain becomes peritonitis. Initially, vital signs may be normal, but tachycardia and hypotension usually develop as a result of progressive dehydration. Fever is often present with bowel ischemia or perforation. Inspection of the abdomen usually reveals distension that varies based on the site of obstruction and may be absent in cases of proximal obstruction. Peristalsis is usually tremendously increased in the early phases of mechanical SBO, as a result of intensive intestinal muscular contractions. This socalled “peristaltic rush” progressively decreases until it disappears in the late phase of obstruction. The presence of either surgical scars or hernias should be noted, indicating a possible cause of SBO. Rectal examination is essential to detect rectal lesions and to check for the presence of stool. B. Laboratory Findings5:56 A Your IP is 82.116.202.56 Downloaded 2024131 Page 7 / 37 Chapter 31: Small Intestine, Marco Ettore Allaix; Alessandro Fichera ©2024 McGraw Hill.reflect All Rights Reserved. Terms of Use and Privacy Policy Notice Accessibility Laboratory findings intravascular volume depletion dehydration. An elevated hematocrit is indicative of hemoconcentration. Leukocytosis is often the result of dehydration and an acute stress response rather than an underlying infection. Blood chemistries may reveal elevated serum creatinine levels, indicating hypovolemia with prerenal failure. cases of proximal obstruction. Peristalsis is usually tremendously increased in the early phases of mechanical SBO, as a result of intensive intestinal EUROPEAN UNIVERSITY CYPRUS muscular contractions. This socalled “peristaltic rush” progressively decreases until it disappears in the late phase of obstruction. The presence of Access Provided by: either surgical scars or hernias should be noted, indicating a possible cause of SBO. Rectal examination is essential to detect rectal lesions and to check for the presence of stool. B. Laboratory Findings Laboratory findings reflect intravascular volume depletion and dehydration. An elevated hematocrit is indicative of hemoconcentration. Leukocytosis is often the result of dehydration and an acute stress response rather than an underlying infection. Blood chemistries may reveal elevated serum creatinine levels, indicating hypovolemia with prerenal failure. Features of strangulated obstruction or perforation include marked leukocytosis and metabolic acidosis. C. Imaging Studies Plain xrays of the abdomen with the patient in supine and upright positions can confirm the clinical diagnosis of SBO. They reveal dilated small bowel loops with airfluid levels in a ladderlike appearance and a paucity of air in the colon. These features may be minimal or absent in early or highgrade obstructions. Computed tomography (CT) scan of the abdomen and pelvis with both intravenous and oral contrast is recommended in patients with suspected SBO. CT scan can visualize the specific location of the obstruction, showing a discrepancy in the caliber between distended proximal bowel loops and collapsed distal intestine. Moreover, CT scan can also reveal the etiology of SBO and demonstrate signs of strangulation including thickening of the bowel wall, air in the bowel wall or portal venous system, and poor uptake of intravenous contrast by the affected bowel wall. Ascites between dilated bowel loops and in the pelvis is often reported in both simple and strangulated obstruction. Intraperitoneal free air indicates perforation. In patients who fail to improve after 48 hours of conservative treatment, an abdominal xray with watersoluble contrast (Gastrografin) should be obtained for both diagnostic and therapeutic purposes, since it has been demonstrated that the lack of Gastrografin progression into the colon with 24 hours predicts the need for surgery in about 96% of cases. Differential Diagnosis Pain in patients with paralytic ileus is usually not severe but is constant and diffuse, and the abdomen is often distended and mildly tender. If ileus has resulted from an acute intraperitoneal inflammatory process, there should be symptoms and signs of the primary disease as well as the ileus. abdominal xrays show the presence of gas in both the colon and the small bowel. A postoperative ileus may be caused by several factors, including drugs used for anesthesia and analgesia and intraoperative manipulation of intestinal loops and the mesentery. Usually, it is temporary, but if it persists for more than 35 days, diagnostic evaluation to rule out mechanical causes of obstruction is mandatory. Colonic obstruction is usually diagnosed by abdominal xrays that show colonic dilation proximal to the obstructing lesion. In the presence of a competent ileocecal valve, a closed loop obstruction occurs with an elevated risk of perforation of the colon. If the ileocecal valve is incompetent, the distal small bowel will be dilated, and patients will exhibit abdominal distension, nausea, and vomiting. Acute gastroenteritis, acute appendicitis, and acute pancreatitis can mimic simple intestinal obstruction, whereas acute mesenteric ischemia must be considered in the differential of small bowel strangulation. Intestinal pseudoobstruction comprises a spectrum of specific disorders associated with irreversible intestinal dysmotility, in which there are symptoms and signs of intestinal obstruction without evidence for an obstructing lesion. Acute pseudoobstruction of the colon carries the risk of cecal perforation and is discussed in Chapter 32. Chronic pseudoobstruction affecting the small bowel with or without colonic involvement can be idiopathic or secondary to several (sporadic and familial) visceral myopathies and neuropathies that affect intestinal smooth muscle and the intra and extraintestinal nervous system. Systemic disorders such as scleroderma, myxedema, lupus erythematosus, amyloidosis, drug abuse (phenothiazine ingestion), radiation injury, or progressive systemic sclerosis can be complicated by chronic intestinal pseudoobstruction. In addition, cytomegalovirus and EpsteinBarr virus infections can cause chronic intestinal pseudoobstruction. The clinical manifestations of chronic intestinal pseudoobstruction include recurrent episodes of vomiting, crampy abdominal pain, and abdominal distention. The diagnosis is suggested by clinical findings and medical history and confirmed by radiologic and manometric studies. Diagnostic laparoscopic fullthickness biopsy of the small bowel may be required to establish the specific cause of the disease. Therapy focuses on palliation of symptoms and nutritional issues. Downloaded 2024131 5:56 A Your IP is 82.116.202.56 Treatment Page 8 / 37 Chapter 31: Small Intestine, Marco Ettore Allaix; Alessandro Fichera ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility SBO is associated with a marked depletion of liquids caused by decreased oral intake, vomiting, and sequestration of fluid in the bowel lumen. Therefore, vigorous fluid resuscitation and correction of electrolyte disorders (hypochloremic, hypokalemic metabolic alkalosis) are mandatory. A EUROPEAN CYPRUS The clinical manifestations of chronic intestinal pseudoobstruction include recurrent episodes of vomiting, crampy abdominalUNIVERSITY pain, and abdominal Access Provided by: distention. The diagnosis is suggested by clinical findings and medical history and confirmed by radiologic and manometric studies. Diagnostic laparoscopic fullthickness biopsy of the small bowel may be required to establish the specific cause of the disease. Therapy focuses on palliation of symptoms and nutritional issues. Treatment SBO is associated with a marked depletion of liquids caused by decreased oral intake, vomiting, and sequestration of fluid in the bowel lumen. Therefore, vigorous fluid resuscitation and correction of electrolyte disorders (hypochloremic, hypokalemic metabolic alkalosis) are mandatory. A urinary catheter should be placed to monitor urinary output. Gastrointestinal decompression with a nasogastric tube provides relief of symptoms, prevents further gas and fluid accumulation proximally, and decreases the risk of aspiration. Obstruction that occurs in the early postoperative period is usually partial and only rarely associated with strangulation. Therefore, a period of prolonged total parenteral nutrition and hydration is warranted. Patients who have undergone numerous abdominal operations should initially be conservatively treated with decompression, bowel rest, and serial abdominal exams in hopes of avoiding reentering a hostile abdomen. Patients with Crohn disease rarely present with a complete bowel obstruction, and these patients often benefit from steroids or other immunosuppressive therapy. However, if signs suggestive of ischemia are detected, surgery should be promptly undertaken. Finally, management of patients with diffuse carcinomatosis is often challenging and, in most of cases, limited to conservative and palliative treatment. A. Surgery Major predictors for surgery are persistent abdominal pain, persistent abdominal distention, fever, and highgrade obstruction detected by a CT scan. These findings are associated with failure of conservative management and increased risk of bowel strangulation. The surgical procedure performed varies according to the etiology of the obstruction. However, regardless of the cause of obstruction, all small bowel loops must be examined and nonviable segments resected. Criteria suggesting viability include normal pink color, presence of peristalsis, and arterial pulsation. Laparoscopic adhesiolysis may be performed in carefully selected patients by surgeons skilled in this procedure. Generally, however, an open procedure is performed through an incision that is partly dictated by the location of scars from previous operations. If the cause of the obstruction cannot be removed, as in the case of infiltration of vital structures by cancer or in the case of diffuse carcinomatosis, an anastomosis between proximal small bowel and small or large bowel distal to the obstruction (bypass) may be the best procedure in these patients. In some cases, a stoma may be the only choice of treatment. Prognosis The vast majority (> 80%) of patients with adhesive SBO do not need an operation because they improve with medical therapy. Among patients who require surgery, the perioperative mortality rate for nonstrangulating obstruction is less than 5%; most of these deaths occur in elderly patients with significant comorbidities. Strangulating obstruction has a mortality rate of approximately 8% if surgery is performed within 36 hours of the onset of symptoms and 25% if operation is delayed beyond 36 hours. Arung W, et al: Pathophysiology and prevention of postoperative peritoneal adhesions. World J Gastroenterol. 2011;17(41):4545–4553. [PubMed: 22147959] Branco BC, et al: Systematic review and metaanalysis of the diagnostic and therapeutic role of watersoluble contrast agent in adhesive small bowel obstruction. Br J Surg. 2010;97(4):470–478. [PubMed: 20205228] Ezer A, et al: Clinical outcomes of manual bowel decompression (milking) in the mechanical small bowel obstruction: a prospective randomized clinical trial. Am J Surg. 2012;203(1):95–100. [PubMed: 21982997] Maung AA, et al: Evaluation and management of smallbowel obstruction: an Eastern Association for the Surgery of Trauma practice management guideline. J Trauma Acute Care Surg. 2012;73(5 suppl 4):S362–S369. [PubMed: 23114494] Mullan CP, et al: Small bowel obstruction. AJR Am J Roentgenol. 2012;198(2):W105–W117. [PubMed: 22268199] O’Connor DB, et al: The role of laparoscopy in the management of acute smallbowel obstruction: a review of over 2,000 cases. Surg Endosc. 2012;26(1):12–17. [PubMed: 21898013] Downloaded 2024131 5:56 A Your IP is 82.116.202.56 van der Wal JB, et Intestine, al: Adhesion prevention duringAlessandro laparotomy:Fichera longterm followup of a randomized clinical trial. Ann Surg. 2011;253(6):1118–1121. Page 9 / 37 Chapter 31: Small Marco Ettore Allaix; [PubMed: 21502860] ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility Xin L, et al: Indications, detectability, positive findings, total enteroscopy, and complications of diagnostic doubleballoon endoscopy: a systematic Mullan CP, et al: Small bowel obstruction. AJR Am J Roentgenol. 2012;198(2):W105–W117. [PubMed: 22268199] EUROPEAN UNIVERSITY CYPRUS Access Provided by: O’Connor DB, et al: The role of laparoscopy in the management of acute smallbowel obstruction: a review of over 2,000 cases. Surg Endosc. 2012;26(1):12–17. [PubMed: 21898013] van der Wal JB, et al: Adhesion prevention during laparotomy: longterm followup of a randomized clinical trial. Ann Surg. 2011;253(6):1118–1121. [PubMed: 21502860] Xin L, et al: Indications, detectability, positive findings, total enteroscopy, and complications of diagnostic doubleballoon endoscopy: a systematic review of data over the first decade of use. Gastrointest Endosc. 2011;74(3):563–570. [PubMed: 21620401] Zielinski MD, et al: Small bowel obstructionwho needs an operation? A multivariate prediction model. World J Surg. 2010;34(5):910–919. [PubMed: 20217412] CROHN DISEASE General Considerations Crohn disease (CD) is a chronic inflammatory disease that commonly affects the small intestine, colon, rectum, and anus, but it can also involve the stomach, esophagus, and mouth. The most commonly affected location is the terminal ileum, and onefifth of all patients have more than one intestinal segment affected simultaneously. The United States, Canada, and Europe have the highest incidence of CD. The current estimated incidence of CD in the United States is approximately four new cases per year for every 100,000 persons, whereas the prevalence is much higher, between 80 and 150 cases per 100,000. It is much less common in Asia, South America, and Japan, whereas accurate data regarding its incidence in Africa are lacking. The peak age for contracting CD is between 15 and 25 years. Familial clusters of disease are not uncommon, with a 6 to 10fold increase in the risk of CD in firstdegree relatives of those affected by CD or its sister ailment, ulcerative colitis. Although familial aggregations are common, the distribution within families does not indicate a pattern of simple Mendelian inheritance. A. Etiology The etiology of CD is unknown. CD is an altered immune response that results in inflammation and destruction of intestinal tissues. Whether this altered immune response is the result of a primary dysfunction in the gutrelated immune system or whether an unknown pathologic trigger induces an otherwise normal immune system to overreact is still unclear. CD may occur in individuals with a genetic predisposition, whereas environmental triggers may start the pathologic sequence that ultimately manifests as CD. To date, even though an increase in intestinal permeability in both CD patients and their symptomfree firstdegree relatives has been demonstrated, no specific primary defect in the systemic or mucosal immune system has been identified. This may lead to an altered mucosal barrier function with abnormal interactions between the multitude of antigenic substrates normally found in the gut lumen and the immunocompetent tissue of the submucosa. Concerning genetic predisposition, the CARD15/NOD2 gene has been linked to susceptibility to CD. CARD15 is a gene product related to innate immunity, and it is preferentially expressed to Paneth cells of the ileum. Nevertheless, the known mutations of CARD15 are neither necessary nor sufficient to contract the disease. Hence, it appears that the genetic relationship of CARD15/NOD2 to CD is complex and still poorly understood. The hypothesis that infectious agents may play a role, either directly as a primary cause of CD or indirectly as a trigger to stimulate a defective immune system, has always found strength in the identification of noncaseating granulomas as the characteristic histopathologic lesion found in Crohn specimens and in the isolation of Mycobacterium paratuberculosis from resected CD specimens. Nevertheless, even sensitive polymerase chain reaction studies have been unable to provide definitive evidence for the presence of M paratuberculosis–specific DNA in CDaffected segments of the bowel. Other infectious agents, including measles virus, nonpylori Helicobacter species, Pseudomonas, and Listeria monocytogenes have been studied, but none of them has been consistently associated with CD. Although diet modification can ameliorate the symptoms of CD, no dietary factor has been identified as a cause of CD. Smoking, however, has been associated with the development of CD. In addition, smoking is known to exacerbate existing CD and can accelerate the recurrence of disease after resection. Downloaded 2024131 5:56 A Your IP is 82.116.202.56 Chapter 31: Small Intestine, Marco Ettore Allaix; Alessandro Fichera B. Pathology ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility Page 10 / 37 CD has two different phases: the active phase and the remission phase, which is characterized by healing of the inflamed tissue. The histopathologic bowel. Other infectious agents, including measles virus, nonpylori Helicobacter species, Pseudomonas, and Listeria monocytogenes have been EUROPEAN UNIVERSITY CYPRUS studied, but none of them has been consistently associated with CD. Access Provided by: Although diet modification can ameliorate the symptoms of CD, no dietary factor has been identified as a cause of CD. Smoking, however, has been associated with the development of CD. In addition, smoking is known to exacerbate existing CD and can accelerate the recurrence of disease after resection. B. Pathology CD has two different phases: the active phase and the remission phase, which is characterized by healing of the inflamed tissue. The histopathologic examination of the active phase of CD typically shows transmural inflammation characterized by multiple lymphoid aggregates in a thickened and edematous submucosa that can be found within the muscularis propria. Another typical microscopic feature of CD is the noncaseating granuloma. However, it is demonstrated in only 50% of resected specimens and is rarely detected on endoscopic biopsies. Additionally, the presence of granulomas does not correlate with disease activity. Small mucosal ulcerations, called aphthous ulcers, are the earliest gross manifestations of CD. They appear as red spots or focal mucosal depressions, typically directly over submucosal lymphoid aggregates. As the inflammation progresses, the aphthous ulcers enlarge and become stellate. They then coalesce to form longitudinal mucosal ulcerations always along the mesenteric aspect of the bowel lumen. Further progression leads to a serpiginous network of linear ulcerations that surround islands of edematous mucosa producing the classic “cobblestone” appearance. Mucosal ulcerations may penetrate through the submucosa to form intramural channels that can bore deeply into the bowel wall and create sinuses, abscesses, or fistulas. The inflammation of CD also involves the mesentery and regional lymph nodes such that the mesentery may become massively thickened. With early acute intestinal inflammation, the bowel wall is hyperemic and boggy. As the inflammation becomes chronic, fibrotic scarring develops, and the bowel wall becomes thickened and leathery in texture. Clinical Findings A. Symptoms and Signs The clinical presentation and symptoms of CD depend on the involved segment, the pattern and the severity of disease, and the associated complications. The onset of CD is often insidious, and many patients will experience some symptoms for months or even years before the diagnosis is made. The most common complaints are intermittent abdominal pain, bloating, diarrhea, nausea, vomiting, weight loss, and fever. Abdominal pain occurs in 90% of cases: when related to partial obstruction, it is mostly postprandial and crampy in nature, whereas when it is from septic complications, it is typically steady and associated with fever. Weight loss is usually related to food avoidance, but in severe cases, weight loss may be the result of malabsorption. Symptoms can also be related to complications, including abdominal mass, pneumaturia, perianal pain and swelling, or skin rash. Rarely, some patients can experience a more sudden onset of pain in the right lower quadrant, mimicking an acute appendicitis. In patients suspected of having CD, a complete physical exam should include a thorough abdominal evaluation. In cases of ileal CD, tenderness is typically present in the right lower quadrant, and occasionally a palpable mass is present. The oral cavity should be examined for aphthous ulcers, whereas the presence of fistulas, abscesses, or enlarged skin tags should be assessed in the perianal area. A digital rectal examination should assess for the presence of anal strictures, fissures, and rectal mucosal ulcerations. The skin in the extremities should be examined for the presence of erythema nodosum and pyoderma gangrenosum. B. Patterns of Disease Even though CD can be categorized into three general manifestations, such as stricturing, perforating, and inflammatory disease, these three classes do not represent truly distinct forms of the disease. It is typical that the same patient can present with more than one pattern even in the same segment of bowel. Nevertheless, one pattern tends to be predominant in most cases, determining the clinical presentation and affecting the therapeutic options. 1. Stricturing pattern Fibrotic scar tissue is the result of chronic inflammation of CD, and it constricts the intestinal lumen, with cicatricial strictures often referred to as “fibrostenotic lesions.” Patients with a stricturing pattern of disease generally develop partial or complete intestinal obstruction, and hence their symptoms are primarily obstructive in nature. Being the result of scar tissue, these strictures are not reversible with medical therapy, and surgical intervention is often required. 2. Perforating pattern Downloaded 2024131 5:56 A Your IP is 82.116.202.56 Page 11 / 37 Chapter 31:CD Small Intestine, Marco Ettore Allaix; Alessandro Fichera Perforating is characterized by the development of sinus tracts, fistulae, and abscesses. The sinus tracts penetrate through the muscularis propria ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility and give rise to abscesses or to fistulas if they penetrate into surrounding structures. Inflammatory response around the advancing sinus tract typically results in adhesion to surrounding structures; therefore, free perforation with spillage of intestinal contents into the abdominal cavity is uncommon. Fibrotic scar tissue is the result of chronic inflammation of CD, and it constricts the intestinal lumen, with cicatricial strictures often referred to as EUROPEAN UNIVERSITY CYPRUS “fibrostenotic lesions.” Patients with a stricturing pattern of disease generally develop partial or complete intestinal obstruction, and hence their Access Provided by: symptoms are primarily obstructive in nature. Being the result of scar tissue, these strictures are not reversible with medical therapy, and surgical intervention is often required. 2. Perforating pattern Perforating CD is characterized by the development of sinus tracts, fistulae, and abscesses. The sinus tracts penetrate through the muscularis propria and give rise to abscesses or to fistulas if they penetrate into surrounding structures. Inflammatory response around the advancing sinus tract typically results in adhesion to surrounding structures; therefore, free perforation with spillage of intestinal contents into the abdominal cavity is uncommon. Typically, perforating disease is accompanied by a degree of stricture formation, but the fistula or abscess generated by the perforating component of the disease dominates the clinical picture. 3. Inflammatory pattern The inflammatory pattern of CD is characterized by mucosal ulceration and bowel wall thickening. The edema that results from inflammation can lead to an adynamic segment of intestine and luminal narrowing. This pattern often gives rise to obstructive symptoms. Of the three patterns of disease, the inflammatory pattern is much more likely to respond to medical therapy. Other common symptoms and findings include anorexia and weight loss. Patients may develop a palpable mass, usually located in the right lower quadrant, related to an abscess or phlegmon in perforating disease or a thickened loop of intestine in obstructive disease. Evidence of fistulization to the skin, urinary bladder, or vagina may also be elicited with an accurate history and physical exam. C. Laboratory findings There is no specific laboratory test that is diagnostic for CD. The diagnosis is made by a thorough history and physical examination along with intestinal radiography and endoscopy. Advanced imaging studies such as CT scan or magnetic resonance imaging (MRI) can assess or detect some of the complications and manifestations of CD, but they are generally not useful in making the initial diagnosis of CD. D. Imaging Studies Small bowel followthrough or enteroclysis is the best means for assessing the small bowel for CD. The radiographic abnormalities are often distinctive. Mucosal granulations with ulceration and nodularity can be identified in the early stages of the disease. Thickening of the mucosal folds and edema of the bowel wall can be demonstrated as the disease progresses. With more advanced disease, cobblestoning becomes radiographically apparent. Small bowel contrast studies can also provide information regarding enlargement of the mesentery, as well as formation of an inflammatory mass or abscess demonstrated by a general mass effect separating and displacing contrastfilled loops of small intestine. Even though small bowel contrast studies can demonstrate some of the complications of CD, including highgrade strictures and fistulas, they may not identify all such lesions, including ileosigmoid and ileovesical fistulas. In addition, small bowel studies may not demonstrate all the areas of disease with significant strictures. Small bowel radiographs can also help in assessing the extent of the disease by identifying the location and length of involved and uninvolved small bowel and by recognizing whether the disease is continuous or discontinuous, with skip lesions separated by areas of normal intestine. Experienced radiologists can also assess areas of luminal narrowing and determine if they are the result of acute inflammatory swelling or are the result of fibrostenotic scar tissue. Such a distinction provides valuable information regarding the value of medical therapy versus early surgical intervention, as inflammatory stenoses are likely to respond to medical therapy while fibrotic strictures are best treated with surgery. CT findings of uncomplicated CD are nonspecific, and routine CT is not necessary for the diagnosis of CD. CT, however, is very useful in identifying the complications associated with CD, such as thickened and dilated intestinal loops, inflammatory masses, abscesses and hydronephrosis resulting from retroperitoneal fibrosis, and ureteral narrowing (Figure 31–4). CT is also the most sensitive indicator of an enterovesical fistula, as suggested by the presence of air within the urinary bladder. More recently, crosssectional imaging techniques have assumed an increasing role in the imaging of patients with CD. CT enterography (CTE) has been shown to have a higher sensitivity than barium smallbowel followthrough. Based on these findings, CTE is often used combined with ileocolonoscopy as a firstline test for the diagnosis and staging of CD. CTE has several potential advantages over barium studies in the identification of fistulizing disease: CTE does not suffer from superimposition of bowel loops, and it displays the mesentery, retroperitoneum, and abdominal wall musculature, typically involved by fistulas. CTE can also readily identify sinus tracts and abscesses. However, recent concerns about radiationinduced cancer arising from medically related CT in young CD patients have encouraged the use of magnetic resonance enterography (MRE). MRE has the same advantages of CTE but does not require ionizing radiation. Figure 31–4. Computed tomography thickened loop of distal ileum (arrow) causing obstruction of the more proximal small bowel in Downloaded 2024131scan 5:56showing A Your aIPmarkedly is 82.116.202.56 Page 12 / 37 regional enteritis. Chapter 31: Small Intestine, Marco Ettore Allaix; Alessandro Fichera ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility recent concerns about radiationinduced cancer arising from medically related CT in young CD patients have encouraged the use of magnetic EUROPEAN UNIVERSITY CYPRUS resonance enterography (MRE). MRE has the same advantages of CTE but does not require ionizing radiation. Access Provided by: Figure 31–4. Computed tomography scan showing a markedly thickened loop of distal ileum (arrow) causing obstruction of the more proximal small bowel in regional enteritis. E. Endoscopy Although upper endoscopy is useful in the diagnosis of mucosal lesions of the esophagus, stomach, and duodenum, a colonoscopy often allows the evaluation of the terminal ileum. 1. Capsule endoscopy Capsule endoscopy can detect subtle mucosal lesions that may not be apparent on small bowel xrays. The value of capsule endoscopy in the diagnosis of CD has been recently evaluated: the rate of abnormalities detected on capsule endoscopy is higher than that of CTE only for the subgroup of patients with known CD. The need for a preliminary small bowel contrast study to detect asymptomatic partial SBO before the capsule endoscopy and the lack of a clear advantage over other imaging studies limit the utility of capsule endoscopy as a firstline test in CD, and perhaps it is best to reserve this study for patients in whom there is a substantial diagnostic uncertainty. Differential Diagnosis The differential diagnosis includes irritable bowel syndrome, acute appendicitis, intestinal ischemia, pelvic inflammatory disease, endometriosis, and gynecologic malignancies. Other disorders include radiation enteritis, Yersinia infections, intestinal injury from nonsteroidal antiinflammatory drugs (NSAIDs), intestinal tuberculosis, and small bowel tumors. When malignancy is suspected, resection should be undertaken to make the diagnosis certain. The exclusion of intestinal tuberculosis can be difficult, as the inflammation and strictures of the terminal ileum can occur very similarly to CD. A previous exposure to tuberculosis should be evaluated, and a purified protein derivative skin test should be performed, along with chest radiography. Even when the diagnosis of CD is certain, patients who coincidentally are found to also have latent tuberculosis should be treated in accordance with American Thoracic Society guidelines prior to the initiation of immunosuppressive therapy for management of CD. Intestinal injury from NSAIDs can result in focal enteritis with ulcerations and strictures. These manifestations can be very difficult to distinguish from CD of the small bowel and often require resection or biopsy to confirm the diagnosis. Treatment Downloaded 2024131 5:56 A Your IP is 82.116.202.56 Chapter 31: Small Intestine, Marco Ettore Allaix; Alessandro Fichera ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility A. Medical Page 13 / 37 Longlasting symptomatic relief while avoiding excessive morbidity is the goal of medical treatment of CD. Even though CD cannot be cured by medical coincidentally are found to also have latent tuberculosis should be treated in accordance with American Thoracic Society guidelines prior to the initiation of immunosuppressive therapy for management of CD. EUROPEAN UNIVERSITY CYPRUS Access Provided by: Intestinal injury from NSAIDs can result in focal enteritis with ulcerations and strictures. These manifestations can be very difficult to distinguish from CD of the small bowel and often require resection or biopsy to confirm the diagnosis. Treatment A. Medical Longlasting symptomatic relief while avoiding excessive morbidity is the goal of medical treatment of CD. Even though CD cannot be cured by medical treatment, long periods of disease control can be obtained, thus avoiding a surgical intervention. Medical treatment is tailored to the course of the disease, the clinical presentation, and associated complications. Two different CD severity grading systems are used: the Crohn’s Disease Activity Index (CDAI) and the HarveyBradshaw Index. These two scales identify patients with asymptomatic remission, mild to moderate CD, moderate to severe CD, and severefulminant disease. Two different treatment modalities are used for mild to moderate CD: the stepup approach (starting with the least potent drugs) and the topdown approach (starting with more potent drugs, such as biologics or immunomodulators). The latter approach is more frequently used, aiming at minimizing the risk of dependence to glucocorticoids. Corticosteroids have been widely used for controlling acute exacerbations of CD in the short term, but their use is limited due to the risk of serious side effects, including diabetes, osteoporosis, cataracts, osteonecrosis, myopathy, psychosis, opportunistic infections, and adrenal suppression, that are related to the dose and duration of steroid therapy. The majority of patients with active small bowel CD will experience clinical remission with a short course of oral prednisone given in a dose between 0.25 and 0.5 mg/kg/d. For patients unable to take oral medications, methylprednisolone can be administered in adults at doses of 4060 mg given as a daily infusion. Some patients do not respond to corticosteroid therapy (steroidresistant) or experience disease flares when tapering off the medication (steroiddependent). The aminosalicylates include sulfasalazine and 5aminosalicylic acid (5ASA) derivatives. They inhibit leukotriene production by inhibiting 5 lipooxygenase activity and the production of interleukin1 and tumor necrosis factor (TNF). Aminosalicylates are effective in the treatment of mild to moderate CD. 5ASA given in a controlledrelease preparation is also effective as maintenance therapy to prevent recurrence after a flare of disease has been effectively managed either medically or surgically. Aminosalicylates come in a variety of preparations, each designed to deliver the drug in a topical fashion to the affected bowel segments. For instance, Asacol is 5ASA contained within a pHdependent resin that releases the drug in the terminal ileum and colon where the pH is > 7.0. Pentasa is 5ASA contained within ethylcellulosecoated microgranules that slowly releases the active compound throughout the entire small bowel and colon. Azathioprine and 6mercaptopurine (6MP) are immunosuppressive agents that inhibit cytotoxic Tcell and natural killer cell function. These agents are effective in treating mild to moderate CD. Azathioprine given at 2.02.5 mg/kg/d or 6MP in doses of 1.01.5 mg/kg/d will result in a 50%60% response rate in patients with active CD. Both 6MP and azathioprine are also effective in maintaining remission following surgery or successful medical management. Infliximab is a chimeric mousehuman monoclonal antibody to TNF that is a proinflammatory cytokine that may be important in the pathophysiology of CD. Infliximab binds to both free and membranebound TNF and prevents TNF from binding to its cell surface receptors. Clinical trials have demonstrated am 80% response rate with a single dose of infliximab. It is important to note that the doses and dosing intervals of infliximab must be individualized, but a typical regimen would include 5 mg/kg of infliximab given intravenously (IV) at weeks 0, 2, and 6, with a dose of 5 mg/kg every 8 weeks thereafter. Because infliximab is a potent immunosuppressive agent, concerns have been raised about the risk for poor wound healing and postoperative septic complications. Nevertheless, current available data on the perioperative risks associated with infliximab do not seem to support this hypothesis. Other agents that are used with varying success in the treatment of CD include methotrexate, metronidazole, cyclosporine, tacrolimus, and thalidomide. B. Surgical Therapy Similarly to medical treatment, the goal of surgical treatment of CD is to provide longlasting symptomatic relief while avoiding excessive morbidity. Like medical treatment, surgery should be considered palliative. Therefore, treatment of complications and palliation of symptoms while avoiding excessive resection of small bowel should be the main aims of surgical treatment. To avoid excessive loss of small bowel, nonresectional techniques such as strictureplasty may be required. In addition, optimal surgical therapy should be the resection of only the areas of severe and symptomatic CD, leaving behind segments of small bowel affected by mild but asymptomatic CD based Downloaded 2024131 5:56 A Your IP is 82.116.202.56 on the high risks of recurrence and repeated operations. Page 14 / 37 Chapter 31: Small Intestine, Marco Ettore Allaix; Alessandro Fichera ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility Adequate preoperative patient preparation is mandatory to reduce the risk of postoperative complications, assessing the nutritional status, the smoking habits, and the entity of small intestine involvement by CD. Recent evidence shows that preoperative immunosuppressive medications have Similarly to medical treatment, the goal of surgical treatment of CD is to provide longlasting symptomatic relief while avoiding excessive morbidity. EUROPEAN UNIVERSITY CYPRUS Like medical treatment, surgery should be considered palliative. Therefore, treatment of complications and palliation of symptoms while avoiding excessive resection of small bowel should be the main aims of surgical treatment. Access Provided by: To avoid excessive loss of small bowel, nonresectional techniques such as strictureplasty may be required. In addition, optimal surgical therapy should be the resection of only the areas of severe and symptomatic CD, leaving behind segments of small bowel affected by mild but asymptomatic CD based on the high risks of recurrence and repeated operations. Adequate preoperative patient preparation is mandatory to reduce the risk of postoperative complications, assessing the nutritional status, the smoking habits, and the entity of small intestine involvement by CD. Recent evidence shows that preoperative immunosuppressive medications have limited impact on the outcomes and can be safely discontinued before surgery. Patients should always be counselled about the possible need for a stoma construction in both elective and emergent settings. C. Indications for Surgery 1. Failure of medical treatment The most common indications for surgical treatment of CD are the failure to respond to medical treatment and the inability to tolerate effective therapy, due to the occurrence of complications related to the medical treatment or the progression of disease while on maximal medical treatment. Some patients may respond to the initial medical therapy only to rapidly relapse with tapering of the medical treatment. For example, some patients respond well to steroid therapy but become steroiddependent as tapering of the steroid dose results in recurrent symptoms. Due to the severe complications that are virtually inevitable with prolonged steroid treatment, surgery is warranted if the patient cannot be weaned from systemic steroids within 36 months. 2. Intestinal obstruction Partial or complete intestinal obstruction is a common indication for operation. The clinical presentation of chronic partial SBO is much more typical than complete obstruction, and postprandial cramps, abdominal distension, borborygmi, and weight loss are common symptoms. To avoid them, many patients restrict the diet to soft foods or even liquids. In case of partial obstruction primarily due to acute inflammation and bowel wall thickening, initial medical therapy is warranted. If, however, the obstructive symptoms are secondary to highgrade fibrostenotic lesions, surgery is indicated because medical treatment will not reverse these lesions. When complete intestinal obstruction occurs, initial conservative treatment consists of nasogastric decompression and IV hydration along with administration of IV steroids. This treatment leads to decompression of acutely distended and edematous bowel and, in most cases, to resolution of the complete obstruction. However, even patients with complete resolution of the acute obstruction after the initial conservative treatment are at high risk for recurrent episodes of obstruction and are best managed with elective surgery once adequate decompression and resuscitation are achieved. If the obstruction fails to respond to appropriate conservative treatment, then surgery is required. In these situations, a high index of suspicion for small bowel cancer as the cause of the obstruction is mandatory, as obstructions from cancers do not respond to bowel decompression and steroid treatment. 3. Fistulas Intestinal fistulas occur in onethird of CD patients. However, the presence of an intestinal fistula is not in and of itself an indication for surgery. In general, it is the primary indication for surgery if the fistula is in connection with the genitourinary tract, if its drainage causes personal embarrassment and discomfort (enterocutaneous and enterovaginal fistulas), or if a bypass causing intestinal malabsorption is created. Fistulas can be classified according to anatomic site, characteristics of the tract (simple vs complex), and volume of output (high vs low). A lowvolume output is less than 200 mL/24 h, whereas highvolume output is more than 500 mL/24 h. 4. Ileosigmoid fistulas Ileosigmoid fistula is a common complication of perforating CD of the terminal ileum. Typically, the inflamed terminal ileum adheres to the sigmoid colon, which is otherwise healthy. Most ileosigmoid fistulas are small and asymptomatic. These ileosigmoid fistulas do not in and of themselves require operative management. However, large ileosigmoid fistulas can result in bypass of the intestinal contents from the terminal ileum to the distal colon and thus give rise to debilitating diarrhea. Such symptomatic fistulas should be managed surgically, because they often fail to respond to medical therapy. More than half of the ileosigmoid fistulas from CD are recognized intraoperatively. Ileosigmoid fistulas can be managed by simple division of the fistulous adhesion and resection of theIP ileal disease. The defect in the sigmoid colon is then debrided, and simple closure is undertaken. In about 25% Downloaded 2024131 5:56 A Your is 82.116.202.56 Page 15 the / 37 Chapter 31: Small Intestine, Marco Ettore Allaix; of cases, resection of the sigmoid colon is needed,Alessandro particularly Fichera when primary closure of the fistula is at risk for poor healing. This is the case when ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility sigmoid is also involved in CD, when the fistulous opening is particularly large, or when there is extensive fibrosis extending along the sigmoid colon. In addition, fistulous tracts that enter the sigmoid colon in proximity to the mesentery can be difficult to close and often require resection and primary colon, which is otherwise healthy. Most ileosigmoid fistulas are small and asymptomatic. These ileosigmoid fistulas do not in and of themselves EUROPEAN UNIVERSITY CYPRUS require operative management. However, large ileosigmoid fistulas can result in bypass of the intestinal contents from the terminal ileum to the distal Access Provided by: colon and thus give rise to debilitating diarrhea. Such symptomatic fistulas should be managed surgically, because they often fail to respond to medical therapy. More than half of the ileosigmoid fistulas from CD are recognized intraoperatively. Ileosigmoid fistulas can be managed by simple division of the fistulous adhesion and resection of the ileal disease. The defect in the sigmoid colon is then debrided, and simple closure is undertaken. In about 25% of cases, resection of the sigmoid colon is needed, particularly when primary closure of the fistula is at risk for poor healing. This is the case when the sigmoid is also involved in CD, when the fistulous opening is particularly large, or when there is extensive fibrosis extending along the sigmoid colon. In addition, fistulous tracts that enter the sigmoid colon in proximity to the mesentery can be difficult to close and often require resection and primary anastomosis. 5. Ileovesical fistula Ileovesical fistulae occur in approximately 5% of CD patients. Although hematuria and fecaluria are virtually diagnostic of ileovesical fistula, these symptoms are absent in almost 30% of cases. Air within the bladder, as noted on CT scan, is often the best indirect evidence for the presence of an enterovesical fistula, whereas small bowel xrays, cystogram, and cystoscopy often do not detect the fistula. An ileovesical fistula is an indicator of complex fistulizing disease, as most ileovesical fistulas occur along with other enteric fistulae. The necessity for surgery for ileovesical fistula is controversial. Although it is not mandatory to operate on all cases of enterovesical fistulas, surgery is warranted to avoid deterioration of renal function with recurrent infections or if symptoms persist despite appropriate medical therapy. Surgical treatment of ileovesical fistulae requires resection of the ileal disease with closure of the bladder defect. Most ileovesical fistulas involve the dome of the bladder, and thus, debridement and primary closure can be accomplished without any risk of injury to the trigone. Decompression of the bladder with an indwelling Foley catheter should be continued postoperatively until the bladder is confidently healed without leaks. A cystogram taken postoperatively is useful to confirm the seal of the bladder repair, before removing the Foley catheter. 6. Enterovaginal and enterocutaneous fistulas These are rare fistulas caused by perforating small bowel disease draining through the vaginal stump in a female who has previously undergone a hysterectomy or through the abdominal wall, usually at the site of a previous scar. These fistulas often require surgical intervention because they cause physical discomfort and personal embarrassment. Surgical treatment requires resection of the small bowel disease. The vaginal cuff does not need to be closed; the chronic infection along the abdominal wall fistulous tract requires debridement and wide drainage to allow healing by secondary intention. 7. Abscess Intraabdominal CD abscesses tend to have an indolent course with modest fever, abdominal pain, and leukocytosis. In up to 30% of cases, preoperative clinical signs of localized infection are absent and the abscesses are discovered only at the time of operation. When an abscess is suspected or an abdominal mass is palpated, a CT scan should be obtained, as 50% of tender intraabdominal masses will harbor an abscess collection within. The CT scan can detect most chronic abscesses and can also delineate the size and location of the abscess as well as the relationship of the abscess to critical structures such as the ureters, duodenum, and inferior vena cava. In the majority of cases, abscesses are very small collections contained within the area of diseased small bowel and its mesentery. In the case of small intraloop or intramesenteric abscesses, resection of the involved bowel segment and its mesentery often extirpates the abscess such that drains are not necessary and primary anastomosis can be performed without risk. Large abscesses are best managed with CTguided percutaneous drainage. However, an abscess drained percutaneously is very likely to recur or result in an enterocutaneous fistula, and surgical resection is often advised even after successful drainage. Such a fistula may spontaneously close, or it may persist and the intestine may continue to be a source of sepsis. With successful drainage of the abscess, the sepsis often clears well enough that it can be tempting to try to manage the disease without subsequent surgery. In the absence of symptoms, initial nonoperative management after successful percutaneous drainage can be undertaken in carefully selected patients. If drainage through the fistula continues, surgical resection of the affected segment of intestine becomes necessary. 8. Perforation Free perforation is a rare complication of CD, occurring in less than 1% of patients, because the chronic progressive inflammation of CD usually leads to adhesions with adjacent structures, and it is an obvious indication for urgent operation with resection of the diseased segment and exteriorization Downloaded 2024131 A ileostomy. Your IP is The 82.116.202.56 of the proximal bowel as 5:56 an end diagnosis of free perforation is made by detecting a sudden change in the patient’s symptoms along Page 16 / 37 Chapter 31: Small Intestine, Marco Ettore Allaix; Alessandro Fichera with the development of the physical findings of peritonitis or the identification of free intraperitoneal air as demonstrated on plain xrays or CT scan. ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility The use of immunosuppressants and glucocorticosteroids can blunt many of the physical findings of acute perforation; therefore, the index of suspicion for perforation must be higher in immunocompromised patients. segment of intestine becomes necessary. 8. Perforation EUROPEAN UNIVERSITY CYPRUS Access Provided by: Free perforation is a rare complication of CD, occurring in less than 1% of patients, because the chronic progressive inflammation of CD usually leads to adhesions with adjacent structures, and it is an obvious indication for urgent operation with resection of the diseased segment and exteriorization of the proximal bowel as an end ileostomy. The diagnosis of free perforation is made by detecting a sudden change in the patient’s symptoms along with the development of the physical findings of peritonitis or the identification of free intraperitoneal air as demonstrated on plain xrays or CT scan. The use of immunosuppressants and glucocorticosteroids can blunt many of the physical findings of acute perforation; therefore, the index of suspicion for perforation must be higher in immunocompromised patients. Creation of a primary anastomosis even with a proximal protecting loop ileostomy carries a high risk of anastomotic breakdown and should be avoided. Primary closure of the perforation should never be attempted, as sutures will not be able to approximate the edges of the perforated, edematous, and diseased bowel in a satisfactory and tensionfree way and the presence of a distal intestinal stenosis or partial obstruction will cause an increase in the intraluminal pressure at the level of the local repair with subsequent dehiscence. 9. Hemorrhage Hemorrhage is an uncommon complication from small bowel CD. Angiography in the presence of brisk bleeding leads to localization of the site of bleeding. Bleeding from small bowel tends to be indolent with episodic or chronic bleeding requiring intermittent transfusions, but rarely requires emergent surgery. However, because the risk of recurrent bleeding is high, elective resection of the areas of CD is recommended. Finally, risk for bleeding from peptic ulcer disease is increased in patients, particularly in those receiving corticosteroids. 10. Cancer or suspicion of cancer The presence of CD increases the risk of adenocarcinoma of the small bowel. The diagnosis of adenocarcinoma of the small bowel is difficult because symptoms and radiographic findings can be similar to those of the underlying CD. Male patients, patients with longstanding disease, and patients with defunctionalized segments of bowel appear to be at increased risk for small bowel adenocarcinoma. For this reason, bypass surgery should be avoided for CD of the small intestine, and defunctionalized rectal stumps should either be restored to their function or excised. Adenocarcinoma of the small intestine should be suspected in any patient with longstanding disease whose symptoms of obstruction progress after a lengthy quiescent period. 11. Growth retardation Growth retardation occurs in a quarter of children affected by CD. Although steroid treatment may delay growth in children, the major cause of growth retardation in CD patients is due to the malnutrition associated with active intestinal disease. D. Surgical Options 1. Intestinal resection Intestinal resection with anastomosis is the most common surgical procedure performed for the treatment of small bowel CD. In most cases of CD, only limited resections are required with no risk for short bowel syndrome. Only grossly apparent disease should be resected, as wider resections do not improve the surgical outcomes. Grossly normal resection margins with microscopic evidence for CD activity are not associated with early recurrence or other complications. Therefore, intraoperative frozen section of the resection margins is not necessary. The extent of mesenteric dissection does not affect the longterm results. Division of the thickened mesentery of small bowel CD can be the most challenging aspect of the procedure, as identification and dissection of individual mesenteric vessels is often not feasible. A common technique consists of the application of overlapping clamps on either side of the intended line of transection. The mesentery is then divided between the clamps, and the tissue contained within the clamps is suture ligated. In severe cases, a vascular clamp may be used at the root of the small bowel mesentery to obtain proximal control: mattress sutures may then need to be applied to the cut edge of the mesentery to control bleeding. Even when tissuewelding devices such as the LigaSure device are used, mattress sutures in the mesentery are commonly needed for complete hemostasis. 2. Anastomosis There is no consensus regarding the optimal technique for intestinal anastomosis in CD. Recurrent CD after resection of terminal ileum is most likely to occur at the ileocolonic anastomosis or at the preanastomotic ileum. It has been proposed that largecaliber anastomoses require a longer period to stricture down2024131 to a critical5:56 diameter that symptomatic. The argument is made that a longer sidetoside anastomosis may be beneficial over Downloaded A Your IPbecomes is 82.116.202.56 Pageover 17 / 37 Chapter 31: Small Intestine, Marco Ettore Allaix; Alessandro Ficheradata do not indicate a benefit for one particular intestinal configuration an endtoend or endtoside anastomosis. To date, however, clinical ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility another. Intestinal anastomosis for CD cases can be fashioned with a stapling device or may be hand sutured. Under selective conditions, small bowel anastomotic dehiscence rates are less than 1%. In the presence of sepsis, severe scarring, malnutrition, or recent treatment with methotrexate or infliximab, it may be wise to protect the anastomosis with a proximal loop stoma or to forego the anastomosis altogether and bring out an end stoma devices such as the LigaSure device are used, mattress sutures in the mesentery are commonly needed for complete hemostasis. 2. Anastomosis EUROPEAN UNIVERSITY CYPRUS Access Provided by: There is no consensus regarding the optimal technique for intestinal anastomosis in CD. Recurrent CD after resection of terminal ileum is most likely to occur at the ileocolonic anastomosis or at the preanastomotic ileum. It has been proposed that largecaliber anastomoses require a longer period to stricture down to a critical diameter that becomes symptomatic. The argument is made that a longer sidetoside anastomosis may be beneficial over an endtoend or endtoside anastomosis. To date, however, clinical data do not indicate a benefit for one particular intestinal configuration over another. Intestinal anastomosis for CD cases can be fashioned with a stapling device or may be hand sutured. Under selective conditions, small bowel anastomotic dehiscence rates are less than 1%. In the presence of sepsis, severe scarring, malnutrition, or recent treatment with methotrexate or infliximab, it may be wise to protect the anastomosis with a proximal loop stoma or to forego the anastomosis altogether and bring out an end stoma at the point of resection. 3. Bypass procedures Initially conceived to bypass an area of stricture or obstruction, the use of bypass procedures was eventually extended to CD complicated by septic complications. Increased experience with bypass procedures revealed that patients with persistent disease are at higher risk of persistent sepsis and eventually neoplastic transformation. Therefore, bypass procedures were supplanted by limited intestinal resection as the main surgical option in the late 1960s in all intestinal districts except the duodenum, where a simple sidetoside retrocolic gastrojejunostomy adequately relieves the obstructive symptoms. With increased experience in the performance of strictureplasty, duodenal disease is now more and more commonly handled with strictureplasties. 4. Strictureplasty Strictureplasties are best performed when resection would otherwise result in loss of a long segment of bowel with an increased risk for short bowel syndrome, including cases of stricturing disease involving long segments of bowel and patients with multiple prior resections. They are also indicated as a simpler alternative to resection in case of short recurrent disease at a previous ileocolic or enteroenteric anastomosis. There is increased evidence that the acuity of the disease decreases at the site of the strictureplasty and the disease becomes quiescent, maybe in correlation with a simultaneous restoration of absorptive function. The most commonly performed strictureplasty is the HeineckeMikulicz strictureplasty, which is appropriate for short segment strictures of 25 cm in length. A longitudinal incision is made along the antimesenteric border of the stricture extending for 12 cm into the normal elastic bowel on either side of the stricture. Once the enterotomy is made, the area of the stricture should be closely examined to rule out a malignancy. The longitudinal enterotomy of the HeineckeMikulicz strictureplasty is then closed in a transverse fashion with either single or doublelayered sutures. The Finney strictureplasty can be used for strictures up to 15 cm in length. The strictured segment is folded onto itself in a U shape, and a row of seromuscular sutures is placed between the two arms of the U. A longitudinal Ushaped enterotomy is then made paralleling the row of sutures. The mucosal surface is examined, and biopsies are taken as necessary. In essence, the Finney is a short sidetoside functional anastomosis. A very long Finney strictureplasty may result in a functional bypass with a large lateral diverticulum that, in theory, could be at risk for bacterial overgrowth and the blind loop syndrome. However, this theoretical concern has not been observed in clinical practice. Repeated HeineckeMikulicz or Finney strictureplasties to manage multiple strictures should be separated from each other by at least 5 cm, in order to avoid excessive tension on each suture line. Patients with longsegment stricturing disease and multiple strictures grouped close together are best managed with a sidetoside isoperistaltic strictureplasty, also called Michelassi strictureplasty: the segment of stricturing disease is divided at its midpoint. The proximal and distal ends are then drawn onto each other in a sidetoside fashion. Division of some of the mesenteric vascular arcades facilitates the positioning of the two limbs over each other. The proximal and distal loops are then sutured together with a layer of interrupted seromuscular sutures. A longitudinal enterotomy is then made along both of the loops. The intestinal ends are spatulated to provide a smoothly tailored fit to the ultimate closure of the strictureplasty. The outer suture line is reinforced with an interior row of either interrupted or running fullthickness sutures. This inner suture line is continued anteriorly. The anterior closure is then reinforced with an outer layer of interrupted seromuscular sutures to complete the strictureplasty. Other stricturoplasty techniques are the Judd stricturoplasty, the MoskelWalskeNeumayer stricturoplasty, and the Jaboulay stricturoplasty. In appropriately selected patients, perioperative morbidity from strictureplasty appears to be similar to that of resection and primary anastomosis. Specifically, intestinal suture line dehiscence appears to be uncommon with any of the described strictureplasty techniques. The most common postoperative complication directly related to strictureplasty is hemorrhage from the strictureplasty site, in up to 9% of cases. Usually, the gastrointestinal hemorrhage following strictureplasty is minor and can be managed conservatively with transfusions alone. Rarely, a reoperation to Downloaded 2024131 A Your IPisisnecessary. 82.116.202.56 control hemorrhage after5:56 strictureplasty It is by now also well established that strictureplasty techniques provide excellent longterm Page 18 / 37 Chapter 31: Small Intestine, Marco Ettore Allaix; Alessandro Fichera symptomatic relief, which is comparable to resections with anastomosis. ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility 5. Laparoscopy Other stricturoplasty techniques are the Judd stricturoplasty, the MoskelWalskeNeumayer stricturoplasty, and the Jaboulay stricturoplasty. EUROPEAN UNIVERSITY CYPRUS Access Provided by: In appropriately selected patients, perioperative morbidity from strictureplasty appears to be similar to that of resection and primary anastomosis. Specifically, intestinal suture line dehiscence appears to be uncommon with any of the described strictureplasty techniques. The most common postoperative complication directly related to strictureplasty is hemorrhage from the strictureplasty site, in up to 9% of cases. Usually, the gastrointestinal hemorrhage following strictureplasty is minor and can be managed conservatively with transfusions alone. Rarely, a reoperation to control hemorrhage after strictureplasty is necessary. It is by now also well established that strictureplasty techniques provide excellent longterm symptomatic relief, which is comparable to resections with anastomosis. 5. Laparoscopy Most CD patients are well suited for laparoscopy. They are usually young, otherwise healthy, and interested in undergoing an operation that involves minimal scarring, because they are facing the risk of multiple major abdominal operations in their lifetime. The indications for laparoscopic surgery for CD should not differ from conventional open surgery, as described earlier. Contraindications to a laparoscopic approach include patients who are critically ill and unable to tolerate the pneumoperitoneum due to hypotension or hypercarbia, patients with extensive intraabdominal sepsis (abscess, free perforation, or complex fistula), and difficulty in identifying the anatomy (previous surgery, obesity, or adhesions). The same variety of surgical procedures described earlier can be performed laparoscopically. Management of Crohn Disease of the Duodenum Primary CD of the duodenum almost always manifests with stricturing disease that can be managed by strictureplasty or with bypass procedures, whereas resection of the duodenum for CD is almost never required. When CD fistulas involve the duodenum, it is always the result of disease within a distal segment of the small bowel that fistulizes into an otherwise normal duodenum. HeineckeMikulicz strictureplasties can be safely performed in the first, second, and proximal third portions of the duodenum, whereas strictures of the last portion of the duodenum are better handled with a Finney strictureplasty constructed by creating an enteroenterostomy between the fourth portion of the duodenum and the first loop of the jejunum. If the duodenal stricture is lengthy or the tissues around the stricture are too rigid or unyielding, then a strictureplasty should not be performed and an intestinal bypass procedure should be undertaken. The most common bypass procedure performed for duodenal CD is a sidetoside retrocolic gastrojejunostomy. This procedure effectively relieves the symptoms of duodenal obstruction related to CD strictures, but carries a high risk for stomal ulcerations. To lessen the likelihood of ulcerations forming at the anastomosis, it has been recommended that a selective vagotomy be performed along with the gastrojejunostomy in order to reduce the risk of vagotomyrelated diarrhea. If only the third or fourth portions of the duodenum are involved by the structuring CD, a RouxenY duodenojejunostomy to the proximal duodenum is preferred over a gastrojejunostomy, with the Rouxen Y duodenojejunostomy having the advantage of bypassing strictures and eliminating the risk of acidinduced marginal ulceration and the need for vagotomy. Most of these duodenal fistulas are small in caliber and asymptomatic, but larger fistulas may shunt the duodenal contents to the distal small bowel, resulting in malabsorption and diarrhea. In most cases, duodenoenteric fistulas are identified with preoperative small bowel radiography; however, many are discovered only intraoperatively. Most duodenal fistulas are located away from the pancreaticoduodenal margin, and thus these fistulas can be managed by resection of the primary CD with primary closure of the duodenal defect. In case of larger fistulas or fistulas that are involved with a large degree of inflammation, closure with a RouxenY duodenojejunostomy or with a jejunal serosal patch may be required. A. Prognosis The risk for recurrence after surgery is high in CD patients. Most cases of histologic or endoscopically detected recurrences, however, do not produce symptoms of CD. For this reason, histologic or endoscopic evidence of recurrent disease is not typically used as a guide for clinical management. The development of symptoms related to recurrent CD activity is the most commonly applied definition of disease recurrence, because it is the recurrence of symptoms that has the most relevance to the patient. The onset of symptoms of recurrent CD is often insidious, and the severity of symptoms varies greatly. A CDAI greater than 150 is generally accepted as defining clinical recurrence. Once symptoms suggestive of recurrent disease occur, it is necessary to carry out radiologic and endoscopic tests to confirm that the symptoms are in fact related to CD. The clearest end point as a definition of recurrence is the need for reoperation. While reoperation is the most precise definition of recurrence, even this standard does not allow for accurate and reproducible comparisons between series, as some centers may submit patients to surgery earlier than other centers. Reported crude and cumulative recurrence rates vary greatly. Symptomatic recurrence occurs in about 60% of patients at 5 years, and recurrences increase with time such that at 20 years clinical recurrence can occur in between 75% and 95% of cases. Reports of surgical recurrence rates range from Downloaded 5:56 A Your IP isand 82.116.202.56 10%30% at 5 2024131 years, 20%45% at 10 years, 50%70% at 20 years. Recurrent CD is most likely to occur in proximity to the location of the previously Page 19 / 37 Chapter 31: Small Intestine, Marco Ettore Allaix; Alessandro Fichera resected intestinal segment, typically at the anastomosis and preanastomotic bowel, in particular in case of terminal ileal disease. In addition, the ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility length of small bowel involved with recurrent disease parallels the length of disease originally resected. Also, to a lesser degree of concordance, stenotic disease tends to recur as stenotic disease and perforating disease tends to recur as perforating disease. The clearest end point as a definition of recurrence is the need for reoperation. While reoperation is the most precise definition of recurrence, even EUROPEAN UNIVERSITY CYPRUS this standard does not allow for accurate and reproducible comparisons between series, as some centers may submit patients to surgery earlier than other centers. Access Provided by: Reported crude and cumulative recurrence rates vary greatly. Symptomatic recurrence occurs in about 60% of patients at 5 years, and recurrences increase with time such that at 20 years clinical recurrence can occur in between 75% and 95% of cases. Reports of surgical recurrence rates range from 10%30% at 5 years, 20%45% at 10 years, and 50%70% at 20 years. Recurrent CD is most likely to occur in proximity to the location of the previously resected intestinal segment, typically at the anastomosis and preanastomotic bowel, in particular in case of terminal ileal disease. In addition, the length of small bowel involved with recurrent disease parallels the length of disease originally resected. Also, to a lesser degree of concordance, stenotic disease tends to recur as stenotic disease and perforating disease tends to recur as perforating disease. Although many factors that may influence the risk of recurrence have been studied, the cumulative literature has validated very few as true risk factors. Cigarette smoking has a significant effect on the clinical course of CD. Smoking not only exacerbates existing CD, but also has been identified as a risk factor for the development of CD and for endoscopic, symptomatic, and surgical recurrence. Although the mechanism by which smoking results in exacerbation of CD is not known, the risk from smoking appeared to be doserelated, with heavy smokers being at higher risk, and reversible. There is concern that NSAIDs may exacerbate the activity of both ulcerative colitis and CD, but the data are not conclusive. The risk for recurrent disease can be reduced with postoperative maintenance therapy. The most common agents are controlledrelease 5ASA and 6 MP. Maintenance with 5ASA is associated with few side effects, but up to 16 pills have to be taken daily. 6MP is less expensive and is taken on a once daily basis. In addition, 6MP may be more effective in diminishing the risk of recurrence. 6MP, however, is associated with potential bone marrow suppression, so that patients on 6MP maintenance must be followed with periodic blood cell counts. AlHawary M, et al: A new look at Crohn’s disease: novel imaging techniques. Curr Opin Gastroenterol. 2012;28(4):334–340. [PubMed: 22678451] Campbell L, et al: Comparison of conventional and nonconventional strictureplasties in Crohn’s disease: a systematic review and metaanalysis. Dis Colon Rectum. 2012;55(6):714–726. [PubMed: 22595853] Choy PY, et al: Stapled versus handsewn methods for ileocolic anastomoses. Cochrane Database Syst Rev. 2011;9:CD004320. Cunningham MF, et al: Postsurgical recurrence of ileal Crohn’s disease: an update on risk factors and intervention points to a cent

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