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InternalMed_Harrison. Preoperative risk factors influencing postoperative mortality rates include higher American Society of Anesthesiologists (ASA) physical status class (Table 353-2) and preexisting organ failure. In patients who are low risk (ASA P1 and P2), surgical therapy can be offered to those who do not rapidly improve on medical therapy. For uncomplicated diverticular disease, medical therapy can be continued beyond two attacks without an increased risk of perforation requiring a AmERiCAn SoCiETy of AnESTHESioloGiSTS PHySiCAl STATuS ClASSifiCATion SySTEm colostomy. However, patients on immunosuppressive therapy, in chronic renal failure, or with a collagen-vascular disease have a fivefold greater risk of perforation during recurrent attacks. Surgical therapy is indicated in all low-surgical-risk patients with complicated diverticular disease.


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InternalMed_Harrison. The goals of surgical management of diverticular disease include controlling sepsis, eliminating complications such as fistula or obstruction, removing the diseased colonic segment, and restoring intestinal continuity. These goals must be obtained while minimizing morbidity rate, length of hospitalization, and cost in addition to maximizing survival and quality of life. Table 353-3 lists the operations most commonly indicated based on the Hinchey classification and the predicted morbidity and mortality rates. Surgical objectives include removal of the diseased sigmoid down to the rectosigmoid junction. Failure to do this may result in recurrent disease. The current options for uncomplicated diverticular disease include an open sigmoid resection or a laparoscopic sigmoid resection. The benefits of laparoscopic resection over open surgical techniques include early discharge (by at least 1 day), less narcotic use, less postoperative complications, and an earlier return to work.


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InternalMed_Harrison. The options for the surgical management of complicated diverticular disease (Fig. 353-3) include the following: (1) proximal diversion of the fecal stream with an ileostomy or colostomy and sutured omental patch with drainage, (2) resection with colostomy and mucous fistula or closure of distal bowel with formation of a Hartmann’s pouch, (3) resection with anastomosis (coloproctostomy), or (4) resection with anastomosis and diversion (coloproctostomy with loop ileostomy or colostomy). Laparoscopic techniques have been used for complicated diverticular disease; however, higher conversion rates to open techniques have been reported.


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InternalMed_Harrison. Patients with Hinchey stages I and II disease are managed with percutaneous drainage followed by resection with anastomosis about 6 weeks later. Current guidelines put forth by the American Society of Colon and Rectal Surgeons suggest, in addition to antibiotic therapy, CT-guided percutaneous drainage of diverticular abscesses that are greater than 3 cm and have a well-defined wall. Abscesses that are less than 3 cm may resolve with antibiotic therapy alone. Contraindications to percutaneous drainage are no percutaneous access route, pneumoperitoneum, and fecal peritonitis. I Resection with primary 3.8 22 anastomosis without diverting stoma II Resection with primary 3.8 30 anastomosis +/− diversion III Hartmann’s procedure vs — 0 vs. 6 mortality diverting colostomy and omental pedal graft IV Hartmann’s procedure vs — 6 vs. 2 mortality diverting colostomy and omental pedicle graft


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InternalMed_Harrison. III Hartmann’s procedure vs — 0 vs. 6 mortality diverting colostomy and omental pedal graft IV Hartmann’s procedure vs — 6 vs. 2 mortality diverting colostomy and omental pedicle graft FIGURE 353-3 Methods of surgical management of complicated diverticular disease. (1) Drainage, omental pedicle graft, and proxi-mal diversion. (2) Hartmann’s procedure. (3) Sigmoid resection with coloproctostomy. (4) Sigmoid resection with coloproctostomy and proximal diversion.


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InternalMed_Harrison. Urgent operative intervention is undertaken if patients develop generalized peritonitis, and most will need to be managed with a Hartmann’s procedure (resection of the sigmoid colon with end colostomy and rectal stump). In selected cases, nonoperative therapy may be considered. In one nonrandomized study, nonoperative management of isolated paracolic abscesses (Hinchey stage I) was associated with only a 20% recurrence rate at 2 years. More than 80% of patients with distant abscesses (Hinchey stage II) required surgical resection for recurrent symptoms.


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InternalMed_Harrison. Hinchey stage III disease is managed with a Hartmann’s procedure or with primary anastomosis and proximal diversion. If the patient has significant comorbidities, making operative intervention risky, a limited procedure including intraoperative peritoneal lavage (irrigation), omental patch to the oversewn perforation, and proximal diversion of the fecal stream with either an ileostomy or transverse colostomy can be performed. No anastomosis of any type should be attempted in Hinchey stage IV disease. A limited approach to these patients is associated with a decreased mortality rate.


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InternalMed_Harrison. Recurrent Symptoms Recurrent abdominal symptoms following surgical resection for diverticular disease occur in 10% of patients. Recurrent diverticular disease develops in patients following inadequate surgical resection. A retained segment of diseased rectosigmoid colon is associated with twice the incidence of recurrence. The presence of irritable bowel syndrome may also cause recurrence of initial symptoms. Patients undergoing surgical resection for presumed diverticulitis and symptoms of chronic abdominal cramping and irregular loose bowel movements consistent with irritable bowel syndrome have poorer functional outcomes.


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InternalMed_Harrison. RECTAL PROLAPSE (PROCIDENTIA) Incidence and Epidemiology Rectal prolapse is six times more common in women than in men. The incidence of rectal prolapse peaks in women >60 years. Women with rectal prolapse have a higher incidence 1974 of associated pelvic floor disorders including urinary incontinence, rectocele, cystocele, and enterocele. About 20% of children with rectal prolapse will have cystic fibrosis. All children presenting with prolapse should undergo a sweat chloride test. Less common associations include Ehlers-Danlos syndrome, solitary rectal ulcer syndrome, congenital hypothyroidism, Hirschsprung’s disease, dementia, mental retardation, and schizophrenia.


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InternalMed_Harrison. Anatomy and Pathophysiology Rectal prolapse (procidentia) is a circumferential, full-thickness protrusion of the rectal wall through the anal orifice. It is often associated with a redundant sigmoid colon, pelvic laxity, and a deep rectovaginal septum (pouch of Douglas). Initially, rectal prolapse was felt to be the result of early internal rectal intussusception, which occurs in the upper to mid rectum. This was considered to be the first step in an inevitable progression to full-thickness external prolapse. However, only 1 of 38 patients with internal prolapse followed for >5 years developed full-thickness prolapse. Others have suggested that full-thickness prolapse is the result of damage to the nerve supply to the pelvic floor muscles or pudendal nerves from repeated stretching with straining to defecate. Damage to the pudendal nerves would weaken the pelvic floor muscles, including the external anal sphincter muscles. Bilateral pudendal nerve injury is more significantly


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InternalMed_Harrison. with straining to defecate. Damage to the pudendal nerves would weaken the pelvic floor muscles, including the external anal sphincter muscles. Bilateral pudendal nerve injury is more significantly associated with prolapse and incontinence than unilateral injury.


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InternalMed_Harrison. Presentation and Evaluation In external prolapse, the majority of patient complaints include anal mass, bleeding per rectum, and poor perianal hygiene. Prolapse of the rectum usually occurs following defecation and will spontaneously reduce or require the patient to manually reduce the prolapse. Constipation occurs in ~30–67% of patients with rectal prolapse. Differing degrees of fecal incontinence occur in 50–70% of patients. Patients with internal rectal prolapse will present with symptoms of both constipation and incontinence. Other associated findings include outlet obstruction (anismus) in 30%, colonic inertia in 10%, and solitary rectal ulcer syndrome in 12%.


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InternalMed_Harrison. Office evaluation is best performed after the patient has been given an enema, which enables the prolapse to protrude. An important distinction should be made between full-thickness rectal prolapse and isolated mucosal prolapse associated with hemorrhoidal disease (Fig. 353-4). Mucosal prolapse is known for radial grooves rather than circumferential folds around the anus and is due to increased laxity of the connective tissue between the submucosa and underlying muscle of the anal canal. The evaluation of prolapse should also include cystoproctography and colonoscopy. These examinations evaluate for associated pelvic floor disorders and rule out a malignancy or a polyp as the lead point for prolapse. If rectal prolapse is associated with chronic constipation, the patient should undergo a defecating proctogram and a sitzmark study. This will evaluate for the presence of anismus or colonic inertia. Anismus is the result of attempting to defecate against a closed pelvic floor and is also


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InternalMed_Harrison. proctogram and a sitzmark study. This will evaluate for the presence of anismus or colonic inertia. Anismus is the result of attempting to defecate against a closed pelvic floor and is also known as nonrelaxing puborectalis. This can be seen when straightening of the rectum fails to occur on fluoroscopy while the patient is attempting to defecate. In colonic inertia, a sitzmark study will demonstrate retention of >20% of markers on abdominal x-ray 5 days after swallowing. For patients with fecal incontinence, endoanal ultrasound and manometric evaluation, including pudendal nerve testing of their anal sphincter muscles, may be performed before surgery for prolapse (see “Fecal Incontinence,” below).


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InternalMed_Harrison. The medical approach to the management of rectal prolapse is limited and includes stool-bulking agents or fiber supplementation to ease the process of evacuation. Surgical correction of rectal prolapse is the mainstay of therapy. Two approaches are commonly considered, transabdominal and transperineal. Transabdominal approaches have been associated with lower recurrence rates, but some patients with significant comorbidities are better served by a transperineal approach. Common transperineal approaches include a transanal proctectomy (Altmeier procedure), mucosal proctectomy (Delorme FIGURE 353-4 Degrees of rectal prolapse. Mucosal prolapse only (A, B, sagittal view). Full-thickness prolapse associated with redundant rectosigmoid and deep pouch of Douglas (C, D, sagittal view).


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InternalMed_Harrison. procedure), or placement of a Tirsch wire encircling the anus. The goal of the transperineal approach is to remove the redundant rectosigmoid colon. Common transabdominal approaches include presacral suture or mesh rectopexy (Ripstein) with (Frykman-Goldberg) or without resection of the redundant sigmoid. Colon resection, in general, is reserved for patients with constipation and outlet obstruction. Ventral rectopexy is an effective method of abdominal repair of full-thickness prolapse that does not require sigmoid resection (see description below). This repair may have improved functional results over other abdominal repairs. Transabdominal procedures can be performed effectively with laparoscopic and, more recently, robotic techniques without increased incidence of recurrence. The goal of the transabdominal approach is to restore normal anatomy by removing redundant bowel and reattaching the supportive tissue of the rectum to the presacral fascia. The final alternative is abdominal


InternalMed_Harrison

InternalMed_Harrison. of the transabdominal approach is to restore normal anatomy by removing redundant bowel and reattaching the supportive tissue of the rectum to the presacral fascia. The final alternative is abdominal proctectomy with end-sigmoid colostomy. If total colonic inertia is present, as defined by a history of constipation and a positive sitzmark study, a subtotal colectomy with an ileosigmoid or rectal anastomosis may be required at the time of rectopexy.


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InternalMed_Harrison. Previously, the presence of internal rectal prolapse identified on imaging studies has been considered a nonsurgical disorder and biofeedback was recommended. However, only one-third of patients will have successful resolution of symptoms from biofeedback. Two surgical procedures more effective than biofeedback are the Stapled Transanal Rectal Resection (STARR) and the Laparoscopic Ventral Rectopexy (LVR). The STARR procedure (Fig. 353-5) is performed through the anus in patients with internal prolapse. A circular stapling device is inserted through the anus; the internal prolapse is identified and ligated with the stapling device. LVR (Fig. 353-6) is performed through an abdominal approach. An opening in the peritoneum is created on the left side of the recto-sigmoid junction, and this opening continues down anterior on the rectum into the pouch of Douglas. No rectal mobilization is performed, thus avoiding any autonomic nerve injury. Mesh is secured to the anterior and lateral


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InternalMed_Harrison. opening continues down anterior on the rectum into the pouch of Douglas. No rectal mobilization is performed, thus avoiding any autonomic nerve injury. Mesh is secured to the anterior and lateral portion of the rectum, the vaginal fornix, and the sacral promontory, allowing for closure of the rectovaginal septum and correction of the internal prolapse. In both procedures, recurrence at 1 year was low (<10%) and symptoms improved in more than three-fourths of patients.


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InternalMed_Harrison. FIGURE 353-5 Stapled transanal rectal resection. Schematic of placement of the circular stapling device. FECAL INCONTINENCE Incidence and Epidemiology Fecal incontinence is the involuntary passage of fecal material for at least 1 month in an individual with a developmental age of at least 4 years. The prevalence of fecal incontinence in the United States is 0.5–11%. The majority of patients are women and


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InternalMed_Harrison. FIGURE 353-6 Laparoscopic ventral rectopexy (LVR). To reduce the internal prolapse and close any rectovaginal septal defect, the pouch of Douglas is opened and mesh is secured to the anterolateral rec-tum, vaginal fornix, and sacrum. (From A D’Hoore et al: Br J Surg 91:1500, 2004.) • Myopathies, above the age of 65. A higher incidence of incontinence is seen among parous women. One-half of patients with fecal incontinence also suffer from urinary incontinence. The majority of incontinence is a result of obstetric injury to the pelvic floor, either while carrying a fetus or during the delivery. An anatomic sphincter defect may occur in up to 32% of women following childbirth regardless of visible damage to the perineum. Risk factors at the time of delivery include prolonged labor, the use of forceps, and the need for an episiotomy. Symptoms of incontinence can present after two or more decades following obstetric injury. Medical conditions known to contribute to the development of


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InternalMed_Harrison. use of forceps, and the need for an episiotomy. Symptoms of incontinence can present after two or more decades following obstetric injury. Medical conditions known to contribute to the development of fecal incontinence are listed in Table 353-4.


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InternalMed_Harrison. Anatomy and Pathophysiology The anal sphincter complex is made up of the internal and external anal sphincter. The internal sphincter is smooth muscle and a continuation of the circular fibers of the rectal wall. It is innervated by the intestinal myenteric plexus and is therefore not under voluntary control. The external anal sphincter is formed in continuation with the levator ani muscles and is under voluntary control. The pudendal nerve supplies motor innervation to the external anal sphincter. Obstetric injury may result in tearing of the muscle fibers anteriorly at the time of the delivery. This results in an obvious anterior defect on endoanal ultrasound. Injury may also be the result of stretching of the pudendal nerves during pregnancy or delivery of the fetus through the birth canal.


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InternalMed_Harrison. Presentation and Evaluation Patients may suffer with varying degrees of fecal incontinence. Minor incontinence includes incontinence to flatus and occasional seepage of liquid stool. Major incontinence is frequent inability to control solid waste. As a result of fecal incontinence, patients suffer from poor perianal hygiene. Beyond the immediate problems associated with fecal incontinence, these patients are often withdrawn and suffer from depression. For this reason, quality-of-life measures are an important component in the evaluation of patients with fecal incontinence.


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InternalMed_Harrison. The evaluation of fecal incontinence should include a thorough history and physical exam including digital rectal examination (DRE). Weak sphincter tone on DRE and loss of the “anal wink” reflex (S1-level control) may indicate a neurogenic dysfunction. Perianal scars may represent surgical injury. Other studies helpful in the diagnosis of fecal incontinence include anal manometry, pudendal nerve terminal motor latency (PNTML), and endoanal ultrasound. Centers that care for patients with fecal incontinence will have an anorectal physiology laboratory that uses standardized methods of evaluating anorectal physiology. Anorectal manometry (ARM) measures resting and squeeze pressures within the anal canal using an intraluminal water-perfused catheter. Current methods of ARM include use of a three-dimensional, high-resolution system with a 12-catheter perfusion system, which allows physiologic delineation of anatomic abnormalities.


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InternalMed_Harrison. 1976 Pudendal nerve studies evaluate the function of the nerves innervating the anal canal using a finger electrode placed in the anal canal. Stretch injuries to these nerves will result in a delayed response of the sphincter muscle to a stimulus, indicating a prolonged latency. Finally, endoanal ultrasound will evaluate the extent of the injury to the sphincter muscles before surgical repair. Unfortunately, all of these investigations are user-dependent, and very few studies demonstrate that these studies predict outcome following an intervention. Magnetic resonance imaging (MRI) has been used, but its routine use for imaging in fecal incontinence is not well established. Rarely does a pelvic floor disorder exist alone. The majority of patients with fecal incontinence will have some degree of urinary incontinence. Similarly, fecal incontinence is a part of the spectrum of pelvic organ prolapse. For this reason, patients may present with symptoms of obstructed defecation as well as


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InternalMed_Harrison. of urinary incontinence. Similarly, fecal incontinence is a part of the spectrum of pelvic organ prolapse. For this reason, patients may present with symptoms of obstructed defecation as well as fecal incontinence. Careful evaluation including dynamic MRI or cinedefecography should be performed to search for other associated defects. Surgical repair of incontinence without attention to other associated defects may decrease the success of the repair.


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InternalMed_Harrison. Medical management of fecal incontinence includes strategies to bulk up the stool, which help in increasing fecal sensation. These include fiber supplementation, loperamide, diphenoxylate, and bile acid binders. These agents harden the stool and delay frequency of bowel movements and are helpful in patients with minimal to mild symptoms. Furthermore, patients can be offered a form of physical therapy called biofeedback. This therapy helps strengthen the external sphincter muscle while training the patient to relax with defecation to avoid unnecessary straining and further injury to the sphincter muscles. Biofeedback has had variable success and is dependent on the motivation of the patient. At a minimum, biofeedback is risk free and safe. Most patients will have some improvement. For this reason, it should be incorporated into the initial recommendation to all patients with fecal incontinence.


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InternalMed_Harrison. The “gold standard” for the treatment of fecal incontinence with an isolated sphincter defect has been the overlapping sphincteroplasty. The external anal sphincter muscle and scar tissue as well as any identifiable internal sphincter muscle are dissected free from the surrounding adipose and connective tissue and then an overlapping repair is performed in an attempt to rebuild the muscular ring and restore its function. Long-term results following overlapping sphincteroplasty show about a 50% failure rate over 5 years. Poorer outcome has been seen in patients with prolonged pudendal nerve terminal motor latency.


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InternalMed_Harrison. Sacral neuromodulation, collagen-enhancing injectables, radio-frequency therapy, and the artificial bowel sphincter are other options. Sacral nerve stimulation and the artificial bowel sphincter are both adaptations of procedures developed for the management of urinary incontinence. Sacral nerve stimulation is ideally suited for patients with intact but weak anal sphincters. A temporary nerve stimulator is placed on the third sacral nerve. If there is at least a 50% improvement in symptoms, a permanent nerve stimulator is placed under the skin. The artificial bowel sphincter is a cuff and reservoir apparatus that allows for manual inflation of a cuff placed around the anus, increasing anal tone. This allows the patient to manually close off the anal canal until defecation is necessary. Long-term results for sacral stimulation have been promising, with nearly 80% of patients having a reduction in incontinence episodes by at least 50%. This reduction has been sustainable in studies out


InternalMed_Harrison

InternalMed_Harrison. results for sacral stimulation have been promising, with nearly 80% of patients having a reduction in incontinence episodes by at least 50%. This reduction has been sustainable in studies out to 5 years. Unfortunately, the artificial bowel sphincter has been associated with a 30% infection rate. Accordingly, implantation is performed less often.


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InternalMed_Harrison. Collagen-enhancing injectables have been around for several years. The largest open trial involved 115 incontinent patients treated with nonanimal stabilized hyaluronic acid (NASHA/DX) gel. In this study, patients underwent injections of NASHA/DX (Solesta) into the anal mucosa and were followed for 12 months. The results were promising, with over 50% achieving greater than 50% reduction in incontinence episodes, and these results were sustainable up to 2 years. This method is another less invasive therapy for patients with fecal incontinence. Radiofrequency energy delivery to the anal canal in patients with fecal incontinence aids in the development and restructuring of collagen fibers and provides tensile strength to the sphincter muscles. The radiofrequency is delivered as an office procedure with sedation. The results have been variable, with 20–50% of patients having a sustained reduction in incontinence episodes for 5 years.


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InternalMed_Harrison. Finally, the use of stem cells to increase the bulk of the sphincter muscles is currently being tested. Stem cells can be harvested from the patient’s own muscle, grown, and then implanted into their sphincter complex. Concern for cost and the need for an additional procedure dampen enthusiasm. Trial results are awaited. HEMORRHOIDAL DISEASE Incidence and Epidemiology Symptomatic hemorrhoids affect >1 million individuals in the Western world per year. The prevalence of hemorrhoidal disease is not selective for age or sex. However, age is known to be a risk factor. The prevalence of hemorrhoidal disease is less in underdeveloped countries. The typical low-fiber, high-fat Western diet is associated with constipation and straining and the development of symptomatic hemorrhoids.


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InternalMed_Harrison. Anatomy and Pathophysiology Hemorrhoidal cushions are a normal part of the anal canal. The vascular structures contained within this tissue aid in continence by preventing damage to the sphincter muscle. Three main hemorrhoidal complexes traverse the anal canal—the left lateral, the right anterior, and the right posterior. Engorgement and straining lead to prolapse of this tissue into the anal canal. Over time, the anatomic support system of the hemorrhoidal complex weakens, exposing this tissue to the outside of the anal canal where it is susceptible to injury. Hemorrhoids are commonly classified as external or internal. External hemorrhoids originate below the dentate line and are covered with squamous epithelium and are associated with an internal component. External hemorrhoids are painful when thrombosed. Internal hemorrhoids originate above the dentate line and are covered with mucosa and transitional zone epithelium and represent majority of hemorrhoids. The standard


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InternalMed_Harrison. are painful when thrombosed. Internal hemorrhoids originate above the dentate line and are covered with mucosa and transitional zone epithelium and represent majority of hemorrhoids. The standard classification of hemorrhoidal disease is based on the progression of the disease from their normal internal location to the prolapsing external position (Table 353-5).


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InternalMed_Harrison. Presentation and Evaluation Patients commonly present to a physician for two reasons: bleeding and protrusion. Pain is less common than with fissures and, if present, is described as a dull ache from engorgement of the hemorrhoidal tissue. Severe pain may indicate a thrombosed hemorrhoid. Hemorrhoidal bleeding is described as painless bright red blood seen either in the toilet or upon wiping. Occasional patients can present with significant bleeding, which may be a cause of anemia; however, the presence of a colonic neoplasm must be ruled out in anemic patients. Patients who present with a protruding mass complain about inability to maintain perianal hygiene and are often concerned about the presence of a malignancy.


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InternalMed_Harrison. The diagnosis of hemorrhoidal disease is made on physical examination. Inspection of the perianal region for evidence of thrombosis or excoriation is performed, followed by a careful digital examination. Anoscopy is performed paying particular attention to the known position of hemorrhoidal disease. The patient is asked to strain. If this is difficult for the patient, the maneuver can be performed while sitting on a toilet. The physician is notified when the tissue prolapses. It is important to differentiate the circumferential appearance of a full-thickness rectal prolapse from the radial nature of prolapsing hemorrhoids (see “Rectal Prolapse,” above). The stage and location of the hemorrhoidal complexes are defined.


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InternalMed_Harrison. The treatment for bleeding hemorrhoids is based on the stage of the disease (Table 353-5). In all patients with bleeding, the possibility of other causes must be considered. In young patients without a family history of colorectal cancer, the hemorrhoidal disease may be treated first and a colonoscopic examination performed if the bleeding continues. Older patients who have not had colorectal cancer screening should undergo colonoscopy or flexible sigmoidoscopy.


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InternalMed_Harrison. With rare exceptions, the acutely thrombosed hemorrhoid can be excised within the first 72 h by performing an elliptical excision. Sitz baths, fiber, and stool softeners are prescribed. Additional therapy for bleeding hemorrhoids includes the office procedures of banding and sclerotherapy. Sensation begins at the dentate line; therefore, banding or sclerotherapy can be performed without discomfort in the office. Bands are placed around the engorged tissue, causing ischemia and fibrosis. This aids in fixing the tissue proximally in the anal canal. Patients may complain of a dull ache for 24 h following band application. During sclerotherapy, 1–2 mL of a sclerosant (usually sodium tetradecyl sulfate) is injected using a 25-gauge needle into the submucosa of the hemorrhoidal complex. Care must be taken not to inject the anal canal circumferentially, or stenosis may occur.


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InternalMed_Harrison. For surgical management of hemorrhoidal disease, excisional hemorrhoidectomy, transhemorrhoidal dearterialization (THD), or stapled hemorrhoidectomy (“the procedure for prolapse or hemorrhoids” [PPH]) is the procedure of choice. All surgical methods of management are equally effective in the treatment of symptomatic thirdand fourth-degree hemorrhoids. However, because the sutured hemorrhoidectomy involves the removal of redundant tissue down to the anal verge, unpleasant anal skin tags are removed as well. The stapled hemorrhoidectomy is associated with less discomfort; however, this procedure does not remove anal skin tags. THD uses ultrasound guidance to ligate the blood supply to the anal tissue, hence reducing hemorrhoidal engorgement. No procedures on hemorrhoids should be done in patients who are immunocompromised or who have active proctitis. Furthermore, emergent hemorrhoidectomy for bleeding hemorrhoids is associated with a higher complication rate.


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InternalMed_Harrison. Acute complications associated with the treatment of hemorrhoids include pain, infection, recurrent bleeding, and urinary retention. Care should be taken to place bands properly and to avoid overhydration in patients undergoing operative hemorrhoidectomy. Late complications include fecal incontinence as a result of injury to the sphincter during the dissection. Anal stenosis may develop from overzealous excision, with loss of mucosal skin bridges for reepithelialization. Finally, an ectropion (prolapse of rectal mucosa from the anal canal) may develop. Patients with an ectropion complain of a “wet” anus as a result of inability to prevent soiling once the rectal mucosa is exposed below the dentate line. FIGURE 353-7 Common locations of anorectal abscess (left) and fistula in ano (right).


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InternalMed_Harrison. FIGURE 353-7 Common locations of anorectal abscess (left) and fistula in ano (right). ANORECTAL ABSCESS Incidence and Epidemiology The development of a perianal abscess is more common in men than women by a ratio of 3:1. The peak incidence is in the third to fifth decade of life. Perianal pain associated with the presence of an abscess accounts for 15% of office visits to a colorectal surgeon. The disease is more prevalent in immunocompromised patients such as those with diabetes, hematologic disorders, or inflammatory bowel disease and persons who are HIV positive. These disorders should be considered in patients with recurrent perianal infections.


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InternalMed_Harrison. Anatomy and Pathophysiology An anorectal abscess is an abnormal fluid-containing cavity in the anorectal region. Anorectal abscess results from an infection involving the glands surrounding the anal canal. Normally, these glands release mucus into the anal canal, which aids in defecation. When stool accidentally enters the anal glands, the glands become infected and an abscess develops. Anorectal abscesses are perianal in 40–50% of patients, ischiorectal in 20–25%, intersphincteric in 2–5%, and supralevator in 2.5% (Fig. 353-7).


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InternalMed_Harrison. Presentation and Evaluation Perianal pain and fever are the hallmarks of an abscess. Patients may have difficulty voiding and have blood in the stool. A prostatic abscess may present with similar complaints, including dysuria. Patients with a prostatic abscess will often have a history of recurrent sexually transmitted diseases. On physical examination, a large fluctuant area is usually readily visible. Routine laboratory evaluation shows an elevated white blood cell count. Diagnostic procedures are rarely necessary unless evaluating a recurrent abscess. A CT scan or MRI has an accuracy of 80% in determining incomplete drainage. If there is a concern about the presence of inflammatory bowel disease, a rigid or flexible sigmoidoscopic examination may be done at the time of drainage to evaluate for inflammation within the rectosigmoid region. A more complete evaluation for Crohn’s disease would include a full colonoscopy and small-bowel series.


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InternalMed_Harrison. As with all abscesses, the “gold standard” is drainage. Office drainage of an uncomplicated anorectal abscess may suffice. A small incision close to the anal verge is made, and a Mallenkot drain is advanced into the abscess cavity. For patients who have a complicated abscess or who are diabetic or immunocompromised, drainage should be performed in an operating room under anesthesia. These patients are at greater risk for developing necrotizing fasciitis. There is limited role of antibiotics in management of anorectal abscesses. The antibiotics are only warranted in patients who are 1978 immunocompromised or have prosthetic heart valves, artificial joints, diabetes, or inflammatory bowel disease.


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InternalMed_Harrison. FISTULA IN ANO Incidence and Epidemiology The incidence and prevalence of fistulating perianal disease parallels the incidence of anorectal abscess, estimating to be 1 in 10,000 individuals. Some 30–40% of abscesses will give rise to fistula in ano. Although the majority of the fistulas are cryptoglandular in origin, 10% are associated with IBD, tuberculosis, malignancy, and radiation. Anatomy and Pathophysiology A fistula in ano is defined as a communication of an abscess cavity with an identifiable internal opening within the anal canal. This identifiable opening is most commonly located at the dentate line where the anal glands enter the anal canal. Patients experiencing continuous drainage following the treatment of a perianal abscess likely have a fistula in ano. These fistulas are classified by their relationship to the anal sphincter muscles, with 70% being intersphincteric, 23% transsphincteric, 5% suprasphincteric, and 2% extrasphincteric (Fig. 353-7).


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InternalMed_Harrison. Presentation and Evaluation A patient with a fistula in ano will complain of constant drainage from the perianal region associated with a firm mass. The drainage may increase with defecation. Perianal hygiene is difficult to maintain. Examination under anesthesia is the best way to evaluate a fistula. At the time of the examination, anoscopy is performed to look for an internal opening. Diluted hydrogen peroxide will aid in identifying such an opening. In lieu of anesthesia, MRI with an endoanal coil will also identify tracts in 80% of the cases. After drainage of an abscess with insertion of a Mallenkot catheter, a fistulagram through the catheter can be obtained in search of an occult fistula tract. Goodsall’s rule states that a posterior external fistula will enter the anal canal in the posterior midline, whereas an anterior fistula will enter at the nearest crypt. A fistula exiting >3 cm from the anal verge may have a complicated upward extension and may not obey Goodsall’s rule.


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InternalMed_Harrison. A newly diagnosed draining fistula is best managed with placement of a seton, a vessel loop or silk tie placed through the fistula tract, which maintains the tract open and quiets down the surrounding inflammation that occurs from repeated blockage of the tract. Once the inflammation is less, the exact relationship of the fistula tract to the anal sphincters can be ascertained. A simple fistulotomy can be performed for intersphincteric and low (less than one-third of the muscle) transsphincteric fistulas without compromising continence. For a higher transsphincteric fistula, an anorectal advancement flap in combination with a drainage catheter or fibrin glue may be used. Very long (>2 cm) and narrow tracts respond better to fibrin glue than shorter tracts. Simple ligation of the internal fistula tract (LIFT procedure) has also been used in the management of simple fistula with good success.


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InternalMed_Harrison. Patients should be maintained on stool-bulking agents, nonnarcotic pain medication, and sitz baths following surgery for a fistula. Early complications from these procedures include urinary retention and bleeding. Later complications are rare (<10%) and include temporary and permanent incontinence. Recurrence is 0–18% following fistulotomy and 20–30% following anorectal advancement flap and the LIFT procedure, ANAL FISSURE Incidence and Epidemiology Anal fissures occur at all ages but are more common in the third through the fifth decades. A fissure is the most common cause of rectal bleeding in infancy. The prevalence is equal in males and females. It is associated with constipation, diarrhea, infectious etiologies, perianal trauma, and Crohn’s disease.


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InternalMed_Harrison. Anatomy and Pathophysiology Trauma to the anal canal occurs following defecation. This injury occurs in the anterior or, more commonly, the posterior anal canal. Irritation caused by the trauma to the anal canal results in an increased resting pressure of the internal sphincter. The blood supply to the sphincter and anal mucosa enters laterally. Therefore, increased anal sphincter tone results in a relative ischemia in the region of the fissure and leads to poor healing of the anal injury. A fissure that is not in the posterior or anterior position should raise suspicion for other causes, including tuberculosis, syphilis, Crohn’s disease, and malignancy.


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InternalMed_Harrison. Presentation and Evaluation A fissure can be easily diagnosed on history alone. The classic complaint is pain, which is strongly associated with defecation and is relentless. The bright red bleeding that can be associated with a fissure is less extensive than that associated with hemorrhoids. On examination, most fissures are located in either the posterior or anterior position. A lateral fissure is worrisome because it may have a less benign nature, and systemic disorders should be ruled out. A chronic fissure is indicated by the presence of a hypertrophied anal papilla at the proximal end of the fissure and a sentinel pile or skin tag at the distal end. Often the circular fibers of the hypertrophied internal sphincter are visible within the base of the fissure. If anal manometry is performed, elevation in anal resting pressure and a sawtooth deformity with paradoxical contractions of the sphincter muscles are pathognomonic.


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InternalMed_Harrison. The management of the acute fissure is conservative. Stool softeners for those with constipation, increased dietary fiber, topical anesthetics, glucocorticoids, and sitz baths are prescribed and will heal 60–90% of fissures. Chronic fissures are those present for >6 weeks. These can be treated with modalities aimed at decreasing the anal canal resting pressure including nifedipine or nitroglycerin ointment applied three times a day and botulinum toxin type A, up to 20 units, injected into the internal sphincter on each side of the fissure. Surgical management includes anal dilatation and lateral internal sphincterotomy. Usually, one-third of the internal sphincter muscle is divided; it is easily identified because it is hypertrophied. Recurrence rates from medical therapy are higher, but this is offset by a risk of incontinence following sphincterotomy. Lateral internal sphincterotomy may lead to incontinence more commonly in women.


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InternalMed_Harrison. We would like to thank Cory Sandore for providing some illustrations for this chapter. Gregory Bulkley, MD, contributed to this chapter in an earlier edition and some of that material has been retained here. Rizwan Ahmed, Mahmoud Malas Intestinal ischemia occurs when splanchnic perfusion fails to meet the metabolic demands of the intestines, resulting in ischemic tissue injury. Mesenteric ischemia affects 2–3 people per 100,000, and the incidence of mesenteric ischemia is bound to increase in the aging population. Delay in diagnosis and management results in a high mortality, and prompt interventions may be life-saving. Intestinal ischemia is further classified based on etiology, which dictates management: (1) arterioocclusive mesenteric ischemia, (2) nonocclusive mesenteric ischemia, and (3) mesenteric venous thrombosis.


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InternalMed_Harrison. Risk factors for arterioocclusive mesenteric ischemia are generally acute in onset and include atrial fibrillation, recent myocardial infarction, valvular heart disease, and recent cardiac or vascular catheterization, all of which result in embolic clots reaching the mesenteric circulation. Nonocclusive mesenteric ischemia, also known as “intestinal angina,” is generally more insidious and most often seen in the aging population affected by atherosclerotic disease. Patients with chronic atherosclerotic disease could also suffer an acute insult from emboli leading to complete occlusion. Nonocclusive mesenteric ischemia is also seen in patients receiving high-dose vasopressor infusions, patients with cardiogenic or septic shock, and patients with cocaine overdose. Nonocclusive mesenteric ischemia is the most prevalent gastrointestinal disease complicating cardiovascular surgery. The incidence of ischemic colitis following elective aortic repair is 5–9%, and the incidence triples in


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InternalMed_Harrison. ischemia is the most prevalent gastrointestinal disease complicating cardiovascular surgery. The incidence of ischemic colitis following elective aortic repair is 5–9%, and the incidence triples in patients following emergent repair. Mesenteric venous thrombosis is less common and is associated with the presence of a hypercoagulable state including protein C or S deficiency, antithrombin III deficiency, polycythemia vera, and carcinoma.


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InternalMed_Harrison. The blood supply to the intestines is depicted in Fig. 354-1. To prevent ischemic injury, extensive collateralization occurs between major mesenteric trunks and branches of the mesenteric arcades. Collateral vessels within the small bowel are numerous and meet within the duodenum and the bed of the pancreas. Collateral vessels within the colon meet at the splenic flexure and descending/sigmoid colon. These areas, which are inherently at risk for decreased blood flow, are known as Griffiths’ point and Sudeck’s point, respectively, and are the most common locations for colonic ischemia (Fig. 354-1, shaded areas). The splanchnic circulation can receive up to 30% of the cardiac output. Protective responses to prevent intestinal ischemia include abundant Left Phrenic a. Aorta


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InternalMed_Harrison. Left Phrenic a. Aorta Right Phrenic a. Marginal a. Arch of Riolan IIAPancreatico-duodenal a. Griffiths’ point Sudeck’s point SMAIMAHemorrhoidal aa. Superior Middle Inferior Celiac trunk Splenic a. FIGURE 354-1 Blood supply to the intestines includes the celiac artery, superior mesenteric artery (SMA), inferior mesenteric artery (IMA), and branches of the internal iliac artery (IIA). Griffiths’ and Sudeck’s points, indicated by shaded areas, are watershed areas with-in the colonic blood supply and common locations for ischemia. collateralization, autoregulation of blood flow, and the ability to 1979 increase oxygen extraction from the blood.


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InternalMed_Harrison. collateralization, autoregulation of blood flow, and the ability to 1979 increase oxygen extraction from the blood. Occlusive ischemia is a result of disruption of blood flow by an embolus or progressive thrombosis in a major artery supplying the intestine. Emboli originate from the heart in more than 75% of cases and lodge preferentially in the superior mesenteric artery just distal to the origin of the middle colic artery. Progressive thrombosis of at least two of the major vessels supplying the intestine is required for the development of chronic intestinal angina. Nonocclusive ischemia is disproportionate mesenteric vasoconstriction (arteriolar vasospasm) in response to a severe physiologic stress such as shock. If left untreated, early mucosal stress ulceration will progress to full-thickness injury. Even in the early stages of ischemia, there is translocation of bacteria across the intestinal mucosa, resulting in bacteremia that can lead to sepsis.


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InternalMed_Harrison. PRESENTATION, EVALUATION, AND MANAGEMENT Intestinal ischemia remains one of the most challenging diagnoses. The mortality rate is greater than 50%. The most significant indicator of survival is the timeliness of diagnosis and treatment. An overview of diagnosis and management of each form of intestinal ischemia is given in Table 354-1.


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InternalMed_Harrison. Acute mesenteric ischemia resulting from arterial embolus or thrombosis presents with severe acute, nonremitting abdominal pain strikingly out of proportion to the physical findings. Associated symptoms may include nausea and vomiting, transient diarrhea, anorexia, and bloody stools. With the exception of minimal abdominal distention and hypoactive bowel sounds, early abdominal examination is unimpressive. Later findings will demonstrate peritonitis and cardiovascular collapse. In the evaluation of acute intestinal ischemia, routine laboratory tests should be obtained, including complete blood count, serum chemistry, coagulation profile, arterial blood gas, amylase, lipase, lactic acid, blood type and cross match, and cardiac enzymes. Regardless of the need for urgent surgery, emergent admission to a monitored bed or intensive care unit is recommended for resuscitation and further evaluation. If the diagnosis of intestinal ischemia is being considered, consultation with a surgical


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InternalMed_Harrison. admission to a monitored bed or intensive care unit is recommended for resuscitation and further evaluation. If the diagnosis of intestinal ischemia is being considered, consultation with a surgical service is necessary. Often the decision to operate is made on a high index of suspicion from the history and physical exam despite normal laboratory findings.


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InternalMed_Harrison. Other diagnostic modalities that may be useful in diagnosis but should not delay surgical therapy include electrocardiogram (ECG), echocardiogram, abdominal radiographs, computed tomography (CT), and mesenteric angiography. More recently, mesentery duplex scanning and visible light spectroscopy during colonoscopy have been demonstrated to be beneficial. The ECG may demonstrate an arrhythmia, indicating the possible source of the emboli. A plain abdominal film may show evidence of free intraperitoneal air, indicating a perforated viscus and the need for emergent exploration. Earlier features of intestinal ischemia seen on abdominal radiographs include bowel-wall edema, known as “thumbprinting.” If the ischemia progresses, air can be seen within the bowel wall (pneumatosis intestinalis) and within the portal venous system. Other features include calcifications of the aorta and its tributaries, indicating atherosclerotic disease. With the administration of oral and IV contrast, dynamic


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InternalMed_Harrison. within the portal venous system. Other features include calcifications of the aorta and its tributaries, indicating atherosclerotic disease. With the administration of oral and IV contrast, dynamic CT angiography with three-dimensional reconstruction is a highly sensitive test for intestinal ischemia. In acute embolic disease, mesenteric angiography is best performed intraoperatively. A mesenteric duplex scan demonstrating a high peak velocity of flow in the superior mesenteric artery (SMA) is associated with an approximately 80% positive predictive value of mesenteric ischemia. More significantly, a negative duplex scan virtually precludes the diagnosis of mesenteric ischemia. Duplex imaging serves as a screening test; further investigations with angiography are needed. The biggest limitation of duplex scanning is body habitus; in obese patients, imaging is poor yield. However, in patients with chronic disease, “food fear” often leads to a decreased appetite and therefore less


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InternalMed_Harrison. limitation of duplex scanning is body habitus; in obese patients, imaging is poor yield. However, in patients with chronic disease, “food fear” often leads to a decreased appetite and therefore less abdominal fat, and duplex imaging is very high yield. The endoscopic techniques using visible light spectroscopy can be used in the diagnosis of chronic ischemia. When suspecting mesenteric ischemia involving the colon, performing an endoscopy to evaluate up to the splenic


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InternalMed_Harrison. Treatment of Treatment of Systemic Condition Key to Early Diagnosis Underlying Cause Treatment of Specific Lesion Consequence 1. 2. Angiography with venous phase Vasospasm: Angiography Hypoperfusion: Spiral CT or colonoscopy Endovascular approach: thrombolysis, angioplasty and stenting Source: Modified from GB Bulkley, in JL Cameron (ed): Current Surgical Therapy, 2nd ed. Toronto, BC Decker, 1986. flexure is high yield. This is often an excellent diagnostic tool in patients with chronic renal insufficiency who cannot tolerate IV contrast.


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InternalMed_Harrison. The “gold standard” for the diagnosis of acute arterial occlusive disease is angiography, and management is laparotomy. Surgical exploration should not be delayed if suspicion of acute occlusive mesenteric ischemia is high or evidence of clinical deterioration or frank peritonitis is present. The goal of operative exploration is to resect compromised bowel and restore blood supply. The entire length of the small and large bowel beginning at the ligament of Treitz should be evaluated. The pattern of intestinal ischemia may indicate the level of arterial occlusion. In the case of SMA occlusion where the embolus usually lies just proximal to the origin of the middle colic artery, the proximal jejunum is often spared while the remainder of the small bowel to the transverse colon will be ischemic. The surgical management of acute mesenteric ischemia of the small bowel is embolectomy via arteriotomy; a small incision is made in the artery through which the clot is retrieved. Another way to


InternalMed_Harrison

InternalMed_Harrison. The surgical management of acute mesenteric ischemia of the small bowel is embolectomy via arteriotomy; a small incision is made in the artery through which the clot is retrieved. Another way to manage acute thrombosis is thrombolysis therapy and angioplasty, with stent placement. However, this approach is more commonly applied to treat chronic mesenteric ischemia. If this is unsuccessful, a bypass from the aorta or iliac artery to the SMA is performed.


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InternalMed_Harrison. Nonocclusive or vasospastic mesenteric ischemia presents with generalized abdominal pain, anorexia, bloody stools, and abdominal distention. Often these patients are obtunded, and physical findings may not assist in the diagnosis. The presence of a leukocytosis, metabolic acidosis, elevated amylase or creatinine phosphokinase levels, and/or lactic acidosis is useful in support of the diagnosis of advanced intestinal ischemia; however, these markers may not be indicative of either reversible ischemia or frank necrosis. Investigational markers for intestinal ischemia include D-dimer, glutathione S-transferase, platelet-activating factor (PAF), and mucosal pH monitoring. Regardless of the need for urgent surgery, emergent admission to a monitored bed or intensive care unit is recommended for resuscitation and further evaluation. Early manifestations of intestinal ischemia include fluid sequestration within the bowel wall leading to a loss of interstitial volume. Aggressive fluid


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InternalMed_Harrison. for resuscitation and further evaluation. Early manifestations of intestinal ischemia include fluid sequestration within the bowel wall leading to a loss of interstitial volume. Aggressive fluid resuscitation may be necessary. To optimize oxygen delivery, nasal O2 and blood transfusions may be given. Broad-spectrum antibiotics should be given to provide sufficient coverage for enteric pathogens, including gram-negative and anaerobic organisms. Frequent monitoring of the patient’s vital signs, urine output, blood gases, and lactate levels is paramount, as is frequent abdominal examination. All vasoconstricting agents should be avoided; fluid resuscitation is the intervention of choice to maintain hemodynamics.


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InternalMed_Harrison. If ischemic colitis is a concern, colonoscopy should be performed to assess the integrity of the colon mucosa. Visualization of the rectosigmoid region may demonstrate decreased mucosal integrity, associated more commonly with nonocclusive mesenteric ischemia, or, on occasion, occlusive disease as a result of acute loss of inferior mesenteric arterial flow following aortic surgery. Ischemia of the colonic mucosa is graded as mild with minimal mucosal erythema or as moderate with pale mucosal ulcerations and evidence of extension to the muscular layer of the bowel wall. Severe ischemic colitis presents with severe ulcerations resulting in black or green discoloration of the mucosa, consistent with full-thickness bowel-wall necrosis. The degree of reversibility can be predicted from the mucosal findings: mild erythema is nearly 100% reversible, moderate is approximately 50% reversible, and frank necrosis is simply dead bowel. Follow-up colonoscopy can be performed to rule out


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InternalMed_Harrison. the mucosal findings: mild erythema is nearly 100% reversible, moderate is approximately 50% reversible, and frank necrosis is simply dead bowel. Follow-up colonoscopy can be performed to rule out progression of ischemic colitis.


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InternalMed_Harrison. Laparotomy for nonocclusive mesenteric ischemia is warranted for signs of peritonitis or worsening endoscopic findings and if the patient’s condition does not improve with aggressive resuscitation. Ischemic colitis is optimally treated with resection of the ischemic bowel and formation of a proximal stoma. Primary anastomosis should not be performed in patients with acute intestinal ischemia.


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InternalMed_Harrison. Patients with mesenteric venous thrombosis may present with a gradual or sudden onset. Symptoms include vague abdominal pain, nausea, and vomiting. Examination findings include abdominal distention with mild to moderate tenderness and signs of dehydration. The diagnosis of mesenteric thrombosis is frequently made on abdominal spiral CT with oral and IV contrast. Findings on CT angiography with venous phase include bowel-wall thickening and ascites. Intravenous contrast will demonstrate a delayed arterial phase and clot within the superior mesenteric vein. The goal of management is to optimize hemodynamics and correct electrolyte abnormalities with massive fluid resuscitation. Intravenous antibiotics as well as anticoagulation should be initiated. If laparotomy is performed and 1981 mesenteric venous thrombosis is suspected, heparin anticoagulation is Acute intestinal obstruction immediately initiated, and compromised bowel is resected. Of all acute


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InternalMed_Harrison. Danny O. Jacobs intestinal disorders, mesenteric venous insufficiency is associated with the best prognosis.


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InternalMed_Harrison. Chronic intestinal ischemia presents with intestinal angina or postprandial abdominal pain associated with need for increased blood flow to the intestine following meals. Patients report abdominal cramping and pain following ingestion of a meal. Weight loss and chronic diarrhea may also be noted. Abdominal pain without weight loss is not chronic mesenteric angina. Physical examination will often reveal a malnourished patient with an abdominal bruit as well as other manifestations of atherosclerosis. Duplex ultrasound evaluation of the mesenteric vessels has gained in popularity. It is important to perform the test fasting because the presence of increased bowel gas prevents adequate visualization of flow disturbances within the vessels or the lack of a vasodilation response to feeding during the test. This tool is frequently used as a screening test for patients with symptoms suggestive of chronic mesenteric ischemia. The gold standard for confirmation of mesenteric arterial occlusion


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InternalMed_Harrison. the test. This tool is frequently used as a screening test for patients with symptoms suggestive of chronic mesenteric ischemia. The gold standard for confirmation of mesenteric arterial occlusion is mesenteric angiography. Evaluation with mesenteric angiography allows for identification and possible intervention for the treatment of atherosclerosis within the vessel lumen and will also evaluate the patency of remaining mesenteric vessels. The use of mesenteric angiography may be limited in the presence of renal failure or contrast allergy. Magnetic resonance angiography is an alternative if the administration of contrast dye is contraindicated.


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InternalMed_Harrison. The management of chronic intestinal ischemia includes medical management of atherosclerotic disease by exercise, cessation of smoking, and antiplatelet and lipid-lowering medications. A full cardiac evaluation should be performed before intervention on chronic mesenteric ischemia. Newer endovascular procedures may avoid an operative intervention in selected patient populations. Angioplasty with endovascular stenting in the treatment of chronic mesenteric ischemia is associated with an 80% long-term success rate. In patients requiring surgical exploration, the approach used is determined by findings of the mesenteric angiogram. The entire length of the small and large bowel should be evaluated, beginning at the ligament of Treitz. Restoration of blood flow at the time of laparotomy is accomplished with mesenteric vessel endarterectomy or bypass.


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InternalMed_Harrison. Determination of intestinal viability intraoperatively in patients with suspected intestinal ischemia can be challenging. After revascularization, the bowel wall should be observed for return of a pink color and peristalsis. Palpation of major arterial mesenteric vessels can be performed, as well as applying a Doppler flowmeter to the antimesenteric border of the bowel wall, but neither is a definitive indicator of viability. In equivocal cases, 1 g of IV sodium fluorescein is administered, and the pattern of bowel reperfusion is observed under ultraviolet illumination with a standard (3600 A) Wood’s lamp. An area of nonfluorescence >5 mm in diameter suggests nonviability. If doubt persists, reexploration performed 24–48 h following surgery will allow demarcation of nonviable bowel. Primary intestinal anastomosis in patients with ischemic bowel is always worrisome; thus, delayed bowel reconstruction and reanastomosis should be deferred to the time of second-look laparotomy.


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InternalMed_Harrison. We thank Cory Sandore for providing the illustration for this chapter. Susan Gearhart contributed to this chapter in the 18th edition. Morbidity and mortality from acute intestinal obstruction have been decreasing over the past several decades. Nevertheless, the diagnosis can still be challenging, and the type of complications that patients suffer has not changed significantly. The extent of mechanical obstruction is typically described as partial, high-grade, or complete—generally correlating with the risk of complications and the urgency with which the underlying disease process must be addressed. Obstruction is also commonly described as being either “simple” or, alternatively, “strangulated” if vascular insufficiency and intestinal ischemia are evident.


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InternalMed_Harrison. Acute intestinal obstruction occurs either mechanically from blockage or from intestinal dysmotility when there is no blockage. In the latter instance, the abnormality is described as being functional. Mechanical bowel obstruction may be caused by extrinsic processes, intrinsic abnormalities of the bowel wall, or intraluminal abnormalities (Table 355-1). Within each of these broad categories are many diseases that can impede intestinal propulsion. Intrinsic diseases that can cause intestinal obstruction are usually congenital, inflammatory, neoplastic, or traumatic in origin, although intussusception and radiation injury can also be etiologic. Primary small-bowel cancers rarely cause acute obstruction.


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InternalMed_Harrison. Acute intestinal obstruction accounts for approximately 1–3 % of all hospitalizations and a quarter of all urgent or emergent general surgery admissions. Approximately 80% of cases involve the small bowel, and about one-third of these patients show evidence of significant ischemia. The mortality rate for patients with strangulation who are operated on within 24–30 h of the onset of symptoms is approximately 8% but triples shortly thereafter. Extrinsic diseases most commonly cause mechanical obstruction of the small intestine. In the United States and Europe, almost all cases are caused by postoperative adhesions (>50%), carcinomatosis, or herniation of the anterior abdominal wall. Carcinomatosis most often originates from the ovary, pancreas, stomach, or colon, although rarely, metastasis from distant organs like the breast and skin can occur. Adhesions are responsible for >90% of cases of early postoperative obstruction that require intervention.


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InternalMed_Harrison. Operations of the lower abdomen, including appendectomy and colorectal and gynecologic procedures, are especially likely to create Adhesions (especially due to previous abdominal surgery), internal or external hernias, neoplasms (including carcinomatosis and extraintestinal malignancies, mostly commonly ovarian), endometriosis or intraperitoneal abscesses, and idiopathic sclerosis Congenital (e.g., malrotation, atresia, stenosis, intestinal duplication, cyst formation, and congenital bands—the latter rarely in adults) Inflammation (e.g., inflammatory bowel disease, especially Crohn’s disease, but also diverticulitis, radiation, tuberculosis, lymphogranuloma venereum, and schistosomiasis) Neoplasia (note: primary small-bowel cancer is rare; obstructive colon cancer may mimic small-bowel obstruction if the ileocecal valve is incompetent) Traumatic (e.g., hematoma formation, anastomotic strictures)


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InternalMed_Harrison. Traumatic (e.g., hematoma formation, anastomotic strictures) Other, including intussusception (where the lead point is typically a polyp or tumor in adults), volvulus, obstruction of duodenum by superior mesenteric artery, radiation or ischemic injury, and aganglionosis, which is Hirschsprung’s disease Bezoars, feces, foreign bodies including inspissated barium, gallstones (entering the lumen via a cholecystoenteric fistula), enteroliths adhesions that can cause bowel obstruction (Table 355-2). Overall, small-bowel obstruction is slightly more common in women. The risk of internal herniation is increased by abdominal procedures such as laparoscopic or open Roux-en-Y gastric bypass. Although laparoscopic procedures may generate fewer postoperative adhesions compared with open surgery, the risk of obstructive adhesion formation is not eliminated.


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InternalMed_Harrison. In many patients who are successfully treated for adhesive small-bowel obstruction, obstruction will recur. The rate varies according to how patients were initially managed. Approximately 20% of patients who were treated conservatively and between 5 and 30% of patients who were managed operatively will require readmission within 10 years.


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InternalMed_Harrison. Volvulus, which occurs when bowel twists on its mesenteric axis, can cause partial or complete obstruction and vascular insufficiency. The sigmoid colon is most commonly affected, accounting for approximately two-thirds of all cases of volvulus and 4% of all cases of large-bowel obstruction. The cecum and terminal ileum can also volvulize, or the cecum alone may be involved as a cecal bascule. Risk factors include institutionalization, the presence of neuropsychiatric conditions requiring psychotropic medication, chronic constipation, and aging; patients typically present in their seventies or eighties. Colonic volvulus is more common in Eastern Europe, Russia, and Africa than it is in the United States. It is rare for adhesions or hernias to obstruct the colon. Cancer of the descending colon and rectum is responsible for approximately two-thirds of all cases, followed by diverticulitis and volvulus.


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InternalMed_Harrison. Functional obstruction, also known as ileus and pseudo-obstruction, is present when dysmotility prevents intestinal contents from being propelled distally and no mechanical blockage exists. Ileus that occurs after intraabdominal surgery is the most commonly identified form of functional bowel obstruction, although there are many other causes (Table 355-3). Although postoperative ileus is most often transient, Intraabdominal procedures, lumbar spinal injuries, or surgical procedures on the lumbar spine and pelvis Metabolic or electrolyte abnormalities, especially hypokalemia and hypo magnesemia, but also hyponatremia, uremia, and severe hyperglycemia Drugs such as opiates, antihistamines, and some psychotropic (e.g., haloperi dol, tricyclic antidepressants) and anticholinergic agents Intraoperative radiation (likely due to muscle damage) Ileus secondary to hereditary or acquired visceral myopathies and neuropa


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InternalMed_Harrison. Intraoperative radiation (likely due to muscle damage) Ileus secondary to hereditary or acquired visceral myopathies and neuropa Some collagen vascular diseases such as lupus erythematosus or scleroderma it is the most common reason why hospital discharge is delayed. Pseudo-obstruction of the colon, also known as Ogilvie’s syndrome, is a relatively rare disease. Some patients with Ogilvie’s syndrome have colonic dysmotility due to abnormalities of their autonomic nervous system that may be inherited.


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InternalMed_Harrison. The manifestations of acute intestinal obstruction depend on the nature of the underlying disease process, its location, and changes in blood flow (Fig. 355-1). Increased intestinal contractility, which occurs proximally and distal to the obstruction, is a characteristic response. Subsequently, intestinal peristalsis slows as the intestine or stomach proximal to the point of obstruction dilates and fills with gastrointestinal secretions and swallowed air. Although swallowed air is the primary contributor to intestinal distension, intraluminal air may also accumulate from fermentation, local carbon dioxide production, and altered gaseous diffusion.


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InternalMed_Harrison. Intraluminal dilation also increases intraluminal pressure. When luminal pressure exceeds venous pressure, venous and lymphatic drainage is impeded. Edema ensues, and the bowel wall proximal to the site of blockage may become hypoxemic. Epithelial necrosis can be identified within 12 h of obstruction. Ultimately, arterial blood supply may become so compromised that full-thickness ischemia, necrosis, and perforation result. Stasis increases the bacteria counts within the jejunum and ileum. The most commonly cultured intraluminal organisms are Escherichia coli, Streptococcus faecalis, and Klebsiella, which may also be recovered from mesenteric lymph nodes and other more distant sites.


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InternalMed_Harrison. Other manifestations depend on the degree of hypovolemia, the patient’s metabolic response, and the presence or absence of associated intestinal ischemia. Inflammatory edema eventually increases the production of reactive oxygen species and activates neutrophils and macrophages, which accumulate within the bowel wall. Their accumulation, along with changes in innate immunity, disrupts secretory and neuromotor processes. Dehydration is caused by loss of the normal intestinal absorptive capacity as well as fluid accumulation in the gastric or intestinal wall and intraperitoneally.


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InternalMed_Harrison. Anorexia and emesis tend to exacerbate intravascular volume depletion. In the worst case scenario that is most commonly identified after distal obstruction, emesis leads to losses of gastric potassium, hydrogen, and chloride, while dehydration stimulates proximal renal tubule bicarbonate reabsorption. Intraperitoneal fluid accumulation, especially in patients with severe distal bowel obstruction, may increase intraabdominal pressure enough to elevate the diaphragm and inhibit respiration and to impede systemic venous return and promote vascular instability. Severe hemodynamic compromise may elicit a systemic inflammatory response and generalized microvascular leakage.


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InternalMed_Harrison. Closed-loop obstruction results when the proximal and distal openings of a given bowel segment are both occluded, e.g., due to volvulus or a hernia. It is the most common precursor for strangulation, but not every closed loop strangulates. The risk of vascular insufficiency, systemic inflammation, hemodynamic compromise, and irreversible intestinal ischemia is much greater in patients with closed-loop obstruction. Pathologic changes may occur more rapidly, and emergency intervention is indicated. Irreversible bowel ischemia progresses to transmural necrosis even if the obstruction is relieved. It is also important to remember that patients with high-grade distal colonic obstruction who have competent ileocecal valves may present with closed-loop obstruction. In the latter instance, the cecum may progressively dilate such that ischemic necrosis results in cecal perforation. This risk is generally greatest when the cecal diameter exceeds 12 cm, as informed by Laplace’s law. Patients


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InternalMed_Harrison. cecum may progressively dilate such that ischemic necrosis results in cecal perforation. This risk is generally greatest when the cecal diameter exceeds 12 cm, as informed by Laplace’s law. Patients with distal colonic obstruction whose ileocecal valves are incompetent tend to present later in the course of disease and mimic patients with distal small-bowel obstruction.


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InternalMed_Harrison. Even though the presenting signs and symptoms can be misleading, many patients with acute obstruction can be accurately diagnosed after a thorough history and physical examination is performed. Early Point of obstruction from extrinsic, intrinsic, or intraluminal disease Patients with distal obstruction may still discharge intraluminal contents FIGURE 355-1 Pathophysiologic changes of small-bowel obstruction. recognition allows earlier treatment that decreases the risk of progression or other excess morbidity. Small-bowel obstruction with strangulation can be especially difficult to diagnosis promptly.


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InternalMed_Harrison. recognition allows earlier treatment that decreases the risk of progression or other excess morbidity. Small-bowel obstruction with strangulation can be especially difficult to diagnosis promptly. The cardinal signs are colicky abdominal pain, abdominal distention, emesis, and obstipation. More intraluminal fluid accumulates in patients with distal obstruction, which typically leads to greater distention, more discomfort, and delayed emesis. This emesis is feculent when there is bacterial overgrowth. Patients with more proximal obstruction commonly present with less abdominal distention but more pronounced vomiting. Elements of the history that might be helpful include any prior history of surgery, including herniorrhaphy, as well as any history of cancer or inflammatory bowel disease.


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InternalMed_Harrison. Most patients, even with simple obstruction, appear to be critically ill. Many may be oliguric, hypotensive, and tachycardic because of severe intravascular volume depletion. Fever is worrisome for strangulation or systemic inflammatory changes. Bowel sounds and bowel functional activity are notoriously difficult to interpret. Classically, many patients with early small-bowel obstruction will have high-pitched, “musical” tinkling bowel sounds and peristaltic “rushes” known as borborygmi. Later in the course of disease, the bowel sounds may be absent or hypoactive as peristaltic activity decreases. This is in contrast to the common findings in patients with ileus or pseudo-obstruction where bowel sounds are typically absent or hypoactive from the beginning. Lastly, patients with partial blockage may continue to pass flatus and stool, and those with complete blockage may evacuate bowel contents present downstream beyond their obstruction.


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InternalMed_Harrison. All surgical incisions should be examined. The presence of a tender abdominal or groin mass strongly suggests that an incarcerated hernia may be the cause of obstruction. The presence of tenderness Collapsed bowel distal to obstruction should increase the concern about the presence of complications such as ischemia, necrosis, or peritonitis. Severe pain with localization or signs of peritoneal irritation is suspicious for strangulated or closed-loop obstruction. It is important to remember that the discomfort may be out of proportion to physical findings mimicking the complaints of patients with acute mesenteric ischemia. Every patient should have a rectal examination. Patients with colonic volvulus present with the classic manifestations of closed-loop obstruction: severe abdominal pain, vomiting, and obstipation. Asymmetrical abdominal distension and a tympanic mass may be evident.


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InternalMed_Harrison. Patients with ileus or pseudo-obstruction may have signs and symptoms similar to those of bowel obstruction. Although abdominal distention is present, colicky abdominal pain is typically absent, and patients may not have nausea or emesis. Ongoing, regular discharge of stool or flatus can sometimes help distinguish patients with ileus from those with complete mechanical bowel obstruction.


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InternalMed_Harrison. Laboratory testing should include a complete blood count and serum electrolyte and creatinine measurements. Serial assessments are often useful. Mild hemoconcentration and slight elevation of the white blood cell count commonly occur after simple bowel obstruction. Emesis and dehydration may cause hypokalemia, hypochloremia, elevated blood urea nitrogen–to–creatinine ratios, and metabolic alkalosis. Patients may be hyponatremic on admission because many have attempted to rehydrate themselves with hypotonic fluids. The presence of guaiac-positive stools and iron-deficiency anemia are strongly suggestive of malignancy.


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InternalMed_Harrison. Higher white blood cell counts with the presence of immature forms or the presence of metabolic acidosis are worrisome for severe volume 1984 depletion or ischemic necrosis and sepsis. At this time, there are no laboratory tests that are especially useful for identifying the presence of simple or strangulated obstruction, although increases in serum D-lactate, creatine kinase bb isoenzymes, or intestinal fatty acid binding protein levels may be suggestive of the latter. In all cases, when considering diagnostic imaging, the key is not to delay surgical consultation and operative intervention when the patient’s signs or symptoms strongly suggest that high-grade or complete obstruction or bowel compromise is present. Plain films of the abdomen, which must include upright or cross-table lateral views, can be completed quickly and may confirm the clinical suspicion 60% of the time. Interpretation immediately after operation is difficult. A “staircasing” pattern of dilated air and


InternalMed_Harrison

InternalMed_Harrison. lateral views, can be completed quickly and may confirm the clinical suspicion 60% of the time. Interpretation immediately after operation is difficult. A “staircasing” pattern of dilated air and fluid-filled small-bowel loops >2.5 cm in diameter with little or no air seen in the colon are classical findings in patients with small-bowel obstruction, although findings may be equivocal in some patients with documented disease. Little bowel gas appears in patients with proximal bowel obstruction or in patients whose intestinal lumens are filled with fluid. Upright plain films of the abdomen of patients with large-bowel obstruction typically show colon dilatation. Small-bowel air-fluid levels will not be obvious if the ileocecal valve is competent. Although it can be difficult to distinguish from ileus, small-bowel obstruction is more likely when air-fluid levels are seen without significant colonic distension. Free air suggests that perforation has occurred in patients who have not


InternalMed_Harrison

InternalMed_Harrison. from ileus, small-bowel obstruction is more likely when air-fluid levels are seen without significant colonic distension. Free air suggests that perforation has occurred in patients who have not recently undergone surgical procedures. Radiopaque foreign bodies or enteroliths may be visualized. A gas-filled, “coffee bean”–shaped dilated shadow may be seen in patients with volvulus. More sophisticated imaging can be beneficial when the diagnosis is unclear. Magnetic resonance imaging has been used to diagnose small-bowel obstruction, but it is more expensive and, typically, provides less spatial resolution. Ultrasonographic evaluations are especially difficult to interpret but may be sensitive and appropriate studies to evaluate patients who are pregnant or for whom x-ray exposure is otherwise contraindicated or inappropriate. Computed tomography (CT) is the most commonly used imaging modality. Its sensitivity for detecting bowel obstruction is approximately 95% (78–100%) in patients


InternalMed_Harrison

InternalMed_Harrison. contraindicated or inappropriate. Computed tomography (CT) is the most commonly used imaging modality. Its sensitivity for detecting bowel obstruction is approximately 95% (78–100%) in patients with high-grade obstruction, with a specificity of 96% and an accuracy of ≥95%. Its accuracy in diagnosing closed-loop obstruction is much lower (60%). Examples of some CT images are reproduced in Fig. 355-2. It may also provide useful information regarding location or identify particular circumstances where surgical intervention is needed urgently. Patients who have evidence of contrast appearing within the cecum within 4–24 h of oral administration can be expected to improve with high sensitivity and specificity (~95% each). For example, contrast studies may demonstrate a “bird’s beak,” a “c-loop,” or “whorl” deformity on CT imaging at the site where twisting obstructs the lumen when a colonic volvulus is present. CT imaging with enteral and IV contrast can also identify ischemia. Altered


InternalMed_Harrison

InternalMed_Harrison. or “whorl” deformity on CT imaging at the site where twisting obstructs the lumen when a colonic volvulus is present. CT imaging with enteral and IV contrast can also identify ischemia. Altered bowel wall enhancement is the most specific early finding, but its sensitivity is low. Mesenteric venous gas, pneumoperitoneum, and pneumatosis intestinalis are late findings indicating the presence of bowel necrosis. CT scanning after a water-soluble contrast enema may help distinguish ileus or pseudo-obstruction from distal large-bowel obstruction in patients who present with evidence of small-bowel and colonic distention. CT enteroclysis can accurately identify neoplasia as a cause of bowel obstruction. Contrast enemas or colonoscopies are almost always needed to identify causes of acute colonic obstruction. Barium studies are generally contraindicated in patients with firm evidence of complete or high-grade bowel obstruction, especially when they present acutely. Barium should never be


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InternalMed_Harrison. obstruction. Barium studies are generally contraindicated in patients with firm evidence of complete or high-grade bowel obstruction, especially when they present acutely. Barium should never be given orally to a patient with possible obstruction until that diagnosis has been excluded. In every other case, such investigations should only be performed in exceptional circumstances and with great caution because patients with significant obstruction may develop barium concretions as an additional source of blockage and some who would have otherwise recovered will require operative intervention. Barium opacification also renders cross-sectional imaging studies or angiography uninterpretable.


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InternalMed_Harrison. FIGURE 355-2 Computed tomography with oral and intravenous contrast demonstrating (A) evidence of small-bowel dilatation with air-fluid levels consistent with a small-bowel obstruction; (B) a partial small-bowel obstruction from an incarcerated ventral hernia (arrow); and (C) decompressed bowel seen distal to the hernia (arrow). (From W Silen: Acute intestinal obstruction, in DL Longo et al [eds]: Harrison’s Principles of Internal Medicine, 18th ed. New York, McGraw-Hill, 2012.)


InternalMed_Harrison

InternalMed_Harrison. An improved understanding of the pathophysiology of bowel obstruction and the importance of fluid resuscitation, electrolyte repletion, intestinal decompression, and the selected use of antibiotics have likely contributed to a reduction in the mortality from acute bowel obstruction. Every patient should be stabilized as quickly as possible. Nasogastric tube suction decompresses the stomach, minimizes further distention from swallowed air, improves patient comfort, and reduces the risk of aspiration. Urine output should be assessed using a Foley catheter. In some cases, for example, in patients with cardiac disease, central venous pressures should be monitored. The use of antibiotics is controversial, although prophylactic administration is warranted if surgery is required. Complete bowel obstruction is an indication for intervention. Stenting may be possible and warranted for some patients with high-grade obstruction due to unresectable stage IV malignancy. Stenting may also allow


InternalMed_Harrison

InternalMed_Harrison. obstruction is an indication for intervention. Stenting may be possible and warranted for some patients with high-grade obstruction due to unresectable stage IV malignancy. Stenting may also allow elective mechanical bowel preparation before surgery is undertaken. Because treatment options are so variable, it is helpful to make as precise a diagnosis as possible preoperatively.


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InternalMed_Harrison. Patients with ileus are treated supportively with intravenous fluids and nasogastric decompression while any underlying pathology is treated. Pharmacologic therapy is not yet proven to be efficacious or cost-effective. However, peripherally active μ-opioid receptor antagonists (e.g., alvimopan and methylnaltrexone) may accelerate gastrointestinal recovery in some patients who have undergone abdominal surgery.


InternalMed_Harrison

InternalMed_Harrison. Neostigmine is an acetylcholinsterase inhibitor that increases cholinergic (parasympathetic) activity, which can stimulate colonic motility. Some studies have shown it to be moderately effective in alleviating acute colonic pseudo-obstruction. It is the most common therapeutic approach and can be used once it is certain that there is no mechanical obstruction. Cardiac monitoring is required, and atropine should be immediately available. Intravenous administration induces defecation and flatus within 10 min in the majority of patients who will respond. Sympathetic blockade by epidural anesthesia can successfully ameliorate pseudo-obstruction in some patients.


InternalMed_Harrison

InternalMed_Harrison. Patients with sigmoid volvulus can often be decompressed using a flexible tube inserted through a rigid proctoscope or using a flexible sigmoidoscope. Successful decompression results in sudden release of gas and fluid with evidence of decreased abdominal distension and allows definitive correction to be scheduled electively. Cecal volvulus most often requires laparotomy or laparoscopic correction.


InternalMed_Harrison

InternalMed_Harrison. Approximately 60–80% of selected patients with mechanical bowel obstruction can be successfully treated conservatively. Indeed, most cases of radiation-induced obstruction should also be managed nonoperatively if possible. In most circumstances, early consultation with a general surgeon is prudent when there is concern about strangulation obstruction or other abnormality that needs to be addressed urgently. Deterioration signifies a need for intervention. At this time, the decision as to whether the patient can continue to be treated nonoperatively can only be based on clinical judgment, although, as described earlier, imaging studies can sometimes be helpful. The frequency of major complications after operation ranges from 12 to 47%, with greater risk being attributed to resection therapies and the patient’s overall health. Risk is increased for patients with American Society of Anesthesiologists (ASA) class III or higher.


InternalMed_Harrison

InternalMed_Harrison. At operation, dilation proximal to the site of blockage with distal collapse is a defining feature of bowel obstruction. Intraoperative strategies depend on the underlying problem and range from lysis of adhesions to resection with or without diverting ostomy to primary resection with anastomosis. Resection is warranted when there is concern about the bowel’s viability after the obstructive process is relieved. Laparoscopic approaches can be useful for patients with early obstruction when extensive adhesions are not expected to be present. Some patients with high-grade obstruction secondary to malignant disease that is not amendable to resection 1985 will benefit from bypass procedures.


InternalMed_Harrison

InternalMed_Harrison. Primary resection is prudent. Careful manual reduction of any involved bowel may limit the amount of intestine that needs to be removed. A proximal ostomy may be required if unprepped colon is involved. Only 60% of patients with gallstone ileus obstruct in the ileum. The most common site of intestinal obstruction in patients with gallstone “ileus” is the ileum (60% of patients). The gallstone enters the intestinal tract most often via a cholecystoduodenal fistula. It can usually be removed by operative enterolithotomy. Addressing the gallbladder disease during urgent or emergent surgery is not recommended.


InternalMed_Harrison

InternalMed_Harrison. Early postoperative mechanical bowel obstruction is that which occurs within the first 6 weeks of operation. Most are partial and can be expected to resolve spontaneously. It tends to respond and behave differently from classic mechanical bowel obstruction and may be very difficult to distinguish from postoperative ileus. A higher index of suspicion for a definitive site of obstruction is warranted for patients who undergo laparoscopic surgical procedures. Patients who first had ileus and then subsequently develop obstructive symptoms after an initial return of normal bowel function are more likely to have true postoperative small-bowel obstruction. The longer it takes for a patient’s obstructive symptoms to resolve after hospitalization, the more likely the patient is to require surgical intervention. The wisdom and expertise of Dr. William Silen are gratefully acknowledged. Danny O. Jacobs


InternalMed_Harrison

InternalMed_Harrison. The wisdom and expertise of Dr. William Silen are gratefully acknowledged. Danny O. Jacobs Appendicitis occurs more frequently in Westernized societies. Although its incidence is decreasing for uncertain reasons, acute appendicitis remains the most common emergency general surgical disease affecting the abdomen, with a rate of approximately 100 per 100,000 person-years in Europe and the Americas or about 11 cases per 10,000 people annually. Approximately 9% of men and 7% of women will experience an episode during their lifetime. Appendicitis occurs most commonly in 10to 19-year-olds, although the average age at diagnosis appears to be gradually increasing, as is the frequency of the disease in African Americans, Asians, and Native Americans. Overall, 70% of patients are less than 30 years old and most are men; the male-to-female ratio is 1.4:1.


InternalMed_Harrison

InternalMed_Harrison. One of the more common complications and most important causes of excess morbidity and mortality is perforation, whether it is contained and localized or unconstrained within the peritoneal cavity. In contrast to the trend observed for appendicitis and appendectomy, the incidence of perforated appendicitis (~20 cases per 100,000 person-years) is increasing. The explanation for this phenomenon is unknown. Approximately 20% of all patients have evidence of perforation at presentation, but the percentage risk is much higher in patients under 5 or over 65 years of age.


InternalMed_Harrison

InternalMed_Harrison. 1986 PATHOGENESIS OF APPENDICITIS AND APPENDICEAL PERFORATION Appendicitis was first described in 1886 by Reginald Fitz. Its etiology is still not completely understood. Fecaliths, incompletely digested food residue, lymphoid hyperplasia, intraluminal scarring, tumors, bacteria, viruses, and inflammatory bowel disease have all been associated with inflammation of the appendix and appendicitis. Although not proven, obstruction of the appendiceal lumen is believed to be an important step in the development of appendicitis. In some cases, obstruction leads to bacterial overgrowth and luminal distension, with an increase in intraluminal pressure that can inhibit the flow of lymph and blood in some cases. Then, vascular thrombosis and ischemic necrosis with perforation of the distal appendix may occur. Any perforation that occurs near the base of the appendix should raise concerns about another disease process. Most patients who will perforate do so before they are evaluated by surgeons.


InternalMed_Harrison

InternalMed_Harrison. may occur. Any perforation that occurs near the base of the appendix should raise concerns about another disease process. Most patients who will perforate do so before they are evaluated by surgeons. Appendiceal fecaliths (or appendicoliths) are found in approximately 50% of patients with gangrenous appendicitis who perforate but are rarely identified in those who have simple disease. As mentioned earlier, the incidence of perforated, but not simple, appendicitis is increasing. The rate of perforated and nonperforated appendicitis is correlated in men but not in women. Together these observations suggest that the underlying pathophysiologic processes are different and that simple appendicitis does not always progress to perforation. Furthermore, some cases of simple acute appendicitis may resolve spontaneously or with antibiotic therapy, and recurrent disease is remotely possible. The relative frequency of these events is unknown. When perforation occurs, the resultant leak may be


InternalMed_Harrison

InternalMed_Harrison. may resolve spontaneously or with antibiotic therapy, and recurrent disease is remotely possible. The relative frequency of these events is unknown. When perforation occurs, the resultant leak may be contained by the omentum or other surrounding tissues to form an abscess. Free perforation normally causes severe peritonitis. These patients may also develop infective suppurative thrombosis of the portal vein and its tributaries along with intrahepatic abscesses. The prognosis of the very unfortunate patients who develop this dreaded complication is very poor.


InternalMed_Harrison

InternalMed_Harrison. More refined approaches to diagnosis, supportive care, and surgical intervention are likely responsible for the remarkable decrease in the risk of mortality from simple appendicitis to currently less than 1%. Nevertheless, it is still important to identify patients who might have appendicitis as early as possible to minimize their risk of developing complications. Patients who have had symptoms for more than 48 h are more likely to perforate. Appendicitis should be included in the differential diagnosis of abdominal pain for every patient in any age group unless it is certain that the organ has been previously removed (Table 356-1).


InternalMed_Harrison

InternalMed_Harrison. Appendicitis should be included in the differential diagnosis of abdominal pain for every patient in any age group unless it is certain that the organ has been previously removed (Table 356-1). The appendix’s anatomical location, which varies, directly influences how the patient presents for care. Where the appendix can be “found” ranges from local differences in how the appendiceal body and tip lie relative to its attachment to the cecum (Figs. 356-1 and 356-2), to where the appendix is actually situated in the peritoneal cavity—for example, from its typical location in the right lower quadrant, to the pelvis, right flank, right upper quadrant (as may be observed during Ruptured ovarian cyst or other cystic Hepatitis disease of the ovaries Kidney disease, including Small-bowel obstruction nephrolithiasis 0.5% FIGURE 356-1 Regional anatomical variations of the appendix.


InternalMed_Harrison

InternalMed_Harrison. Kidney disease, including Small-bowel obstruction nephrolithiasis 0.5% FIGURE 356-1 Regional anatomical variations of the appendix. pregnancy), or even the left side of the abdomen for patients with malrotation or who have severely redundant colons. Because the differential diagnosis of appendicitis is so extensive, deciding if a patient has appendicitis can be difficult (Table 356-2). Soliciting an appropriate history requires detecting symptoms that might suggest alternative diagnoses. Patients with appendicitis may not have any abdominal discomfort early in the disease process. Furthermore, many patients may not present with the classically described history or physical findings.


InternalMed_Harrison

InternalMed_Harrison. What is the classic history? Nonspecific complaints occur first. Patients may notice changes in bowel habits or malaise and vague, perhaps intermittent, crampy, abdominal pain in the epigastric or periumbilical region. The pain subsequently migrates to the right lower quadrant over 12–24 h, where it is sharper and can be definitively localized as transmural inflammation when the appendix irritates the parietal peritoneum. Parietal peritoneal irritation may be associated with local muscle rigidity and stiffness. Patients with appendicitis FIGURE 356-2 Locations of the appendix and cecum.


InternalMed_Harrison

InternalMed_Harrison. FIGURE 356-2 Locations of the appendix and cecum. Migration of pain to right lower 50–60% quadrant will most often observe that their nausea, if present, followed the development of abdominal pain, which can help distinguish them from patients with gastroenteritis, for example, where nausea occurs first. Emesis, if present, also occurs after the onset of pain and is typically mild and scant. Thus, timing of the onset of symptoms and the characteristics of the patient’s pain and any associated findings must be rigorously assessed. Anorexia is so common that the diagnosis of appendicitis should be questioned in its absence.


InternalMed_Harrison

InternalMed_Harrison. Arriving at the correct diagnosis is even more challenging when the appendix is not located in the right lower quadrant, in women of childbearing age, and in the very young or elderly. Because the differential diagnosis of appendicitis is so broad, often the key question to answer expeditiously is whether the patient has appendicitis or some other condition that requires immediate operative intervention. A major concern is that the likelihood of a delay in diagnosis is greater if the appendix is unusually positioned. All patients should undergo a rectal examination. An inflamed appendix located behind the cecum or below the pelvic brim may prompt very little tenderness of the anterior abdominal wall.


InternalMed_Harrison

InternalMed_Harrison. Patients with pelvic appendicitis are more likely to present with dysuria, urinary frequency, diarrhea, or tenesmus. They may only experience pain in the suprapubic region on palpation or on rectal or pelvic examination. A pelvic examination in women is mandatory to rule out conditions affecting urogynecologic organs that can cause abdominal pain and mimic appendicitis such as pelvic inflammatory disease, ectopic pregnancy, and ovarian torsion. The relative frequencies of some presenting signs are displayed in Table 356-3. Patients with simple appendicitis normally only appear mildly ill with a pulse and temperature that are usually only slightly above normal. The provider should be concerned about other disease processes beside appendicitis or the presence of complications such as perforation, phlegmon, or abscess formation if the temperature is >38.3°C (~101°F) and if there are rigors.