Colonoscopy Principles and Practice - part 10 potx

Chapter 49: Infections and Other Noninflammatory-Bowel-Disease Colitides 593 large. Therapy is dependent on prevention of impaction (Fig. 49.19). Preparation artifacts The preparation for colonoscopy can induce mucosal changes in the rectum which could be mistaken for IBD. They are not friable, and regress within days of the procedure (Fig. 49.20). References 1 Reinus JF, Brandt LJ. Diarrhea. In: Raskin, JB, Nord, HJ, eds. Colonoscopy: Principles and Techniques. New York: Igaku- Shoin, 1995: 241–63. 2 Nostrant TT, Kumar NB, Appelman HD. Histopathology differentiates acute self-limited colitis from ulcerative colitis. Gastroenterology 1987; 92: 318–28. 3 Surawicz CM, Haggitt RC, Husseman M, McFarland LV. Mucosal biopsy diagnosis of colitis: acute self-limited colitis and idiopathic inflammatory bowel disease. Gastroentero- logy 1994; 107: 755–63. 4 Cohen MB, Giannella RA. Bacterial infections. pathophysiology, clinical features, and treatment. In: Phillips SF, Pemberton JH, Shorter RG, eds. The Large Intestine: Physi- ology, Pathophysiology, and Disease. New York: Raven, 1991: 395–428. 5 Maguire TM, Wensel RH, Malcolm N et al. Massive gastrointestinal hemorrhage, cecal ulcers and salmonella colitis. J Clin Gastroenterol 1985; 7: 249–50. 6 Wolf DC, Gianella RA. Antibiotic therapy for bacterial enterocolitis: a comprehensive review. Am J Gastroenterol 1993; 88: 1667–83. 7 Levine MM, DuPont HL, Formal SB et al. Pathogenesis of Shigella dysenteriae I (Shiga) dysentery. J Infect Dis 1973; 127: 261–70. 8 Rout WR, Formal SB, Giannella RA, Dammin GJ. Pathophysiology of Shigella diarrhea in the rhesus monkey: intestinal transport, morphological and bacteriological studies. Gastroenterology 1975; 68: 270–8. 9 Barrett-Connor EB, Connor JD. Extraintestinal manifestations of shigellosis. Am J Gastroenterol 1970; 53: 234– 45. 10 Speelman P, Kabir I, Islam M. Distribution and spread of colonic lesions in shigellosis: a colonoscopic study. J Infect Dis 1984; 150: 899–903. 11 Blaser MJ, Wells JG, Feldman RA, Pollard RA, Allen JR. Campylobacter enteritis in the United States: a multicenter study. Ann Intern Med 1983; 98: 360–5. 12 Robinson DA. Infective doses of Campylobacter jejuni in milk. Br J Med 1981; 282: 1584. 13 Black RE, Levine MM, Clements ML, Hughes TP, Blaser MJ. Experimental Campylobacter jejuni infection in humans. J Infect Dis 1988; 157: 472–9. Fig. 49.18 Angioectasias of radiation proctopathy over the prostate gland. (Courtesy of David M. Martin MD, “Atlas of Gastrointestinal Endoscopy,” www.EndoAtlas.com.) Fig. 49.20 Typical red-ring signs of a phospho-soda prep. as seen in the rectum. (Courtesy of David M. Martin MD, “Atlas of Gastrointestinal Endoscopy,” www.EndoAtlas.com.) Fig. 49.19 Stercoral ulcer due to fecal impaction. 594 Section 12: Clinical Use of Colonoscopy 14 Karmali MA, Fleming PC. Campylobacter enteritis in children. J Pediatr 1979; 94: 527–53. 15 McKinley MJ, Taylor M, Sangree MH. Toxic megacolon with Campylobacter colitis. Connecticut Med 1980; 44: 496–7. 16 Mee AS, Shield M, Burke M. Campylobacter colitis: differenti- ation from acute inflammatory bowel disease. J R Soc Med 1985; 78: 217–23. 17 Waye JD. The differential diagnosis of inflammatory and infectious colitis. In: Sivak MV, ed. Gastroenterologic Endo- scopy, 1st edn. Philadelphia: WB Saunders, 1987: 881–99. 18 Loss RW Jr, Mangla JC, Pereira M. Campylobacter colitis pre- senting as inflammatory bowel disease with segmental colonic ulcerations. Gastroenterology 1980; 79: 138–40. 19 Hannuksela M, Ahvonen P. Skin manifestations in human yersiniosis. Ann Clin Res 1975; 7: 368–73. 20 Spira TJ, Kabins SA. Yersinia enterocolitica septicemia with septic arthritis. Arch Intern Med 1976; 136: 1305–8. 21 Vantrappen G, Ponette E, Geboes K, Bertrand P. Yersinia enteritis and enterocolitis: gastroenterological aspects. Gast- roenterology 1977; 72: 220–7. 22 Simmonds SD, Noble MA, Freeman HJ. Gastrointestinal features of culture-positive Yersinia enterocolitica infection. Gastroenterology 1987; 92: 112–17. 23 Matsumoto T, Iida M, Matsui T et al. Endoscopic findings in Yersinia enterocolitica enterocolitis. Gastrointest Endosc 1990; 36: 583–7. 24 Vantrappen G, Geboes K, Ponette E. Yersinia enteritis. Med Clin North Am 1982; 66: 639–53. 25 Hoogkamp-Korstanje JA. Antibiotics in Yersinia enterocolitica infections. J Antimicrob Chemother 1987; 20: 123–31. 26 DuPont HL, Formal SB, Hornick RB et al. Pathogenesis of Escherichia coli diarrhea. N Engl J Med 1971; 285: 1–9. 27 Tullock EF Jr, Ryan KJ, Formal SB, Franklin FA. Invasive enteropathic Escherichia coli dysentery. An outbreak in 28 adults. Ann Intern Med 1973; 79: 13–17. 28 Snyder JD, Wells JG, Yashuk J, Puhr N, Blake PA. Outbreak of invasive Escherichia coli gastroenteritis on a cruise ship. Am J Trop Med Hyg 1984; 33: 281–4. 29 Griffin PM, Ostroff SM, Tauxe RV et al. Illness associated with Escherichia coli O157: H7 infections. A broad clinical spectrum. Ann Intern Medical 1988; 109: 705–12. 30 Griffin PM, Olmstead LC, Petras RE. Escherichia coli O157. H7-associated colitisaa clinical and histological study of 11 cases. Gastroenterology 1990; 99: 142–9. 31 Tarr PI, Neill MA, Clausen CR, Watkins SL, Christie DL, Hickman RO. Escherichia coli O157. H7 and the hemolytic uremic syndrome: importance of early cultures in establish- ing the etiology. J Infect Dis 1990; 162: 553–6. 32 Martin DL, MacDonald DL, White KE, Soler JT, Osterholm MT. The epidemiology and clinical aspects of the hemolytic uremic syndrome in Minnesota. N Engl J Med 1990; 323: 1161–7. 33 Ryan CA, Tauxe RV, Hosek GW et al. Escherichia coli O157: H7 diarrhea in a nursing home: clinical, epidemiological, and pathological findings. J Infect Dis 1986; 154: 631–8. 34 Bentley G, Webster JH. Gastro-intestinal tuberculosis: a 10- year review. Br J Surg 1967; 54: 90–6. 35 Goldberg J. Colonoscopic diagnosis of colonic tuberculosis. Gastrointest Endosc 1984; 30: 216. 36 Gomez-Rubio M, de Cuenca B, Opio V, Ulloa J, Garcia J. Colonic tuberculosis. An unusual endoscopic diagnosis. Endoscopy 1993; 25: 377. 37 Tabrisky J, Lindstrom RR, Peters R, Lachman RS. Tuber- culosis enteritis: review of a protean disease. Am J Gastro- enterol 1975; 63: 49–57. 38 Ferentzi CV, Sieck JO, Ali MA. Colonoscopic diagnosis and medical treatment of ten patients with colonic tuberculosis. Endoscopy 1988; 20: 62–5. 39 Shah S, Thomas V, Mathan M et al. Colonoscopic study of 50 patients with colonic tuberculosis. Gut 1992; 33: 347–51. 40 Eboda MA, Akande B. Massive lower gastrointestinal hemorrhage from abdominal tuberculosis. Trop Geogr Med 1991; 43: 307–9. 41 Chutkan RK, Balba NH. Infectious Diseases of the Colon. In: DiMarino AJ, Benjamin SB, eds. Gastrointestinal Disease: an Endoscopic Approach, 2nd edn. Thorofare, NJ: Slack, 2002: 795–814. 42 Hamer DH, Gorbach SL. Infectious diarrhea and bacterial food poisoning. In: Feldman M, Friedman LS, Sleisenger MH, eds. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management, 7th edn. Phil- adelphia: WB Saunders, 2002: 1864–913. 43 Bhargava DK, Tandon HD, Chawla TC, Shriniwas Tandon BN, Kapur BM. Diagnosis of ileocecal and colonic tuberculosis by colonoscopy. Gastrointest Endosc 1985; 31: 68–70. 44 Pettengell KE, Pirie D, Simjee AE. Colonoscopic features of early intestinal tuberculosis. Report of 11 cases. S Afr Med J 1991; 79: 279–80. 45 Breiter JR, Hajjar JJ. Segmental tuberculosis of the colon diagnosed by colonoscopy. Am J Gastroenterol 1981; 76: 369–73. 46 Zyngier FR, Liberal MH, Dechoum A. Tuberculous colitis manifested by skip-lesions of the colon. Gastrointest Endosc 1986; 32: 375. 47 Franklin GO, Mohapatra M, Perrillo RP. Colonic tuberculosis diagnosed by colonoscopic biopsy. Gastroenterology 1979; 76: 362–4. 48 Bhargava DK, Shriniwas Chawla TC, Tandon BN, Kapur BM. Intestinal tuberculosis: bacteriological study of tissue obtained by colonoscopy and during surgery. J Trop Med Hyg 1985; 88: 249–52. 49 Bartlett JG. Pseudomembranous enterocolitis and antibiotic-associated diarrhea. In: Feldman M, Friedman LS, Sleisenger MH, eds. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management , 7th edn. Philadelphia: WB Saunders, 2002: 1914–31. 50 Tedesco FJ, Corless JK, Brownstein RE. Rectal sparing in antibiotic-associated pseudomembranous colitis: a prospective study. Gastroenterology 1982; 83: 1259–60. 51 Burbige EJ, Radigan JJ. Antibiotic-associated colitis with normal-appearing rectum. Dis Colon Rectum 1981; 24: 198– 200. 52 Bartlett JG, Tedesco FJ, Shull S, Lowe B, Chang T. Symp- tomatic relapse after oral vancomycin therapy of antibiotic- associated pseudomembranous colitis. Gastroenterology 1980; 78: 431–4. 53 Bartlett JG. Treatment of antibiotic-associated pseudomembranous colitis. Rev Infect Dis 1984; 6: S235–41. 54 Wenisch C, Parschalk B, Hasenhundl M, Hirschl AM, Graninger W. Comparison of vancomycin, teicoplanin, metronidazole, and fusidic acid for the treatment of Clostridium difficile-associated diarrhea. Clin Infect Dis 1996; 22: 813–18. Chapter 49: Infections and Other Noninflammatory-Bowel-Disease Colitides 595 and comparison to collagenous colitis. Dig Dis Sci 1989; 34: 1730–8. 69 Noyer CM, Brandt LJ. Systemic, iatrogenic, and unusual disorders of the colon. In: DiMarino AJ, Benjamin SB, eds. Gastrointestinal Disease: An Endoscopic Approach, 2nd edn. Thorofare, NJ: Slack, 2002: 915–40. 70 Brandt LJ, Boley SJ, Goldberg L et al. Colitis in the elderly: a reappraisal. Am J Gastroenterol 1981; 76: 239–45. 71 Berman LG, Burdick D, Heitzman ER, Prior JT. A critical reappraisal of sigmoid peridiverticulitis. Surg Gynecol Obstet 1968; 127: 481–91. 72 Stollman NS, Raskin JB. Diverticular disease. In: DiMarino AJ, Benjamin SB, eds. Gastrointestinal Disease: An Endoscopic Approach, 2nd edn. Thorofare, NJ: Slack, 2002: 859–79. 73 Imperiali G, Meucci G, Alvisi C et al. Segmental colitis associated with diverticula: a prospective study. Am J Gastro- enterol 2000; 95: 1014–16. 74 McFarland LV, Elmer GW, Surawicz CM. Breaking the cycle: treatment strategies for 163 cases of recurrent Clostridium difficile disease. Am J Gastroenterol 2002; 97: 1769–75. 75 Baert F, Schmit A, D’Haens G et al. Budesonide in collagenous colitis: a double-blind placebo-controlled trial with histologic follow-up. Gastroenterology 2002; 122: 20–5. 76 Harig JM, Soergel KH, Komorowski RA, Wood CM. Treatment of diversion colitis with short chain fatty acid irrigation. N Engl J Med 1989; 320: 23–8. 77 Gibson GR, Whitacre EB, Ricotti CA. Colitis induced by nonsteroidal anti-inflammatory drugs. Arch Intern Med 1992; 152: 625–32. 78 Clarkston W, Bonacini M, Peterson I. Colitis due to Histoplasma capsulatum in the acquired immune deficiency syndrome. Am J Gastroenterol 1991; 86: 913. 79 Blaser, MJ, Smith, PD, Ravdin, JI. Viral infections. In: Blaser MJ, Smith PD, Ravdin JI et al., eds. Infections of the GI Tract. New York: Raven Press, 1995. 80 Wilcox CM, Schwartz DA, Costonis G, Thompson SE 3rd. Chronic unexplained diarrhea in human immunodeficiency virus infection: determination of the best diagnostic approach. Gastroenterology 1996; 110: 30–7. 81 Horsburgh CR. Epidemiology of Mycobacterium avium com- plex disease. Am J Med 1997; 102: 11–15. 55 Blumencranz H, Kasen L, Romeu J, Waye JD, LeLeiko NS. The role of endoscopy in suspected amebiasis. Am J Gas- troenterol 1983; 78: 15–18. 56 Luterman L, Alsumait AR, Daly DS, Goresky CA. Colo- noscopic features of cecal amebomas. Gastrointest Endosc 1985; 31: 204–6. 57 Nebel OT, el-Masry NA, Castell DO, Farid Z, Fornes MF, Sparks HA. Schistosomal colonic polyposis: endoscopic and histologic characteristics. Gastrointest Endosc 1974; 20: 99– 101. 58 Mohamed AR, al Karawi M, Yasawy MI. Schistosomal colonic disease. Gut 1990; 31: 439–42. 59 Surawicz CM, Myerson D. Self-limited cytomegalovirus colitis in immunocompetent individuals. Gastroenterology 1988; 94: 194–9. 60 Akdamar K, Martin RJ, Ichinose H. Syphilitic proctitis. Am J Dig Dis 1977; 22: 701–4. 61 Martin EG, Kallet HI. Primary syphilis of the anorectal region. JAMA 1925; 84: 1556. 62 Nazemi MM, Musher DM, Schell KF, Milo S. Syphilitic proctitis in a homosexual. JAMA 1975; 231: 389. 63 Rompalo AM, Price CB, Roberts PL, Stamm WE. Poten- tial value of rectal-screening cultures for Chlamydia tra- chomatis in homosexual men. J Infect Dis 1986; 153: 888–92. 64 Fried R, Surawicz C. Proctitis and sexually transmissible intestinal disease. In: Feldman M, Friedman LS, Sleisenger MH, eds. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management, 7th edn. Phil- adelphia: WB Saunders, 2002: 2263–75. 65 Levine JS, Smith PD, Brugge WR. Chronic proctitis in male homosexuals due to lymphogranuloma venereum. Gastro- enterology 1980; 79: 563–5. 66 Giardiello FM, Hansen FC III, Lazenby AJ et al. Collagenous colitis in the setting of nonsteroidal anti-inflammatory drugs and antibiotics. Dig Dis Sci 1990; 35: 257–60. 67 Tanaka M, Mazzoleni G, Riddell RH. Distribution of collagenous colitis: utility of flexible sigmoidoscopy. Gut 1992; 33: 65–70. 68 Giardiello FM, Lazenby AJ, Bayless TM et al. Lymphocytic (microscopic) colitis: clinicopathologic study of 18 patients 596 Introduction Sir William Heneage Ogilvie first described acute colonic pseudo-obstruction (ACPO) in 1948 in two patients with far-advanced intraabdominal malignancies [1]. He was the first to postulate an underlying imbalance between the sympathetic and parasympathic innervation of the colon as the cause of this disorder. Ogilvie’s patients, however, developed subacute symptoms over the course of 2 months and thus represent an atypical presentation of what we now recognize as ACPO. The hallmark features of ACPO consist of acute colonic dilation in the absence of a mechanical etiology. This condition is increasingly recognized and is associated with substan- tial morbidity and mortality. Epidemiology and predisposing factors The exact incidence of ACPO in hospitalized patients is unknown. Vanek and Al-Salti [2] analyzed 400 cases of ACPO and found that it occurred most commonly in the sixth decade and was more common in men than women. More than 90% of patients had significant comorbid disease, thought to be contributing to the syndrome. About 50% of cases occurred in the post- operative state. The diverse underlying medical and surgical problems associated with ACPO are listed in Table 50.1. Pathophysiology The pathophysiology of ACPO is still not entirely under- stood but there is evidence of an imbalance between the sympathetic and parasympathic nervous system, which leads to a functional obstruction caused by atony of the distal colon followed by progressive dilation of the cecum and ascending colon [1,3]. Ogilvie favored the sympathetic deprivation theory, leading to unopposed parasympathic stimulation and thereby resulting in “excessive and probably incoor- dinated contraction” of the distal colon [1] mimicking obstruction. More recent theories postulate either an impairment of the sacral parasympathetic outflow [3–5] or excessive sympathetic stimulation [6,7]. The clinical presentation of ACPO resembles Hirschsprung’s disease, supporting the hypothesis of impaired parasympathetic function [5], which is also supported by the commonly observed transition point at the level of the splenic flexure. The parasympathetic innervation of the colon distal to the splenic flexure is via the pelvic splanchnic nerves whereas the more proximal colon is innervated by the vagus (Fig. 50.1). The proponents of the sympathetic stimulation theory [6,7] argue that right-sided colonic motility is impaired Chapter 50 Acute Colonic Pseudo-obstruction Hubert Nietsch and Michael B. Kimmey Table 50.1 Causes of acute colonic pseudo-obstruction [2,11,17,18,33,45–50]. Neurologic Parkinson’s disease Alzheimer’s disease Cerebrovascular accident Multiple sclerosis Spinal cord disease Craniotomy Cardiovascular Myocardial infarction Congestive heart failure Post cardiac arrest Respiratory Pneumonia Mechanical ventilation Acute respiratory distress syndrome Metabolic Hyponatremia Hypocalcemia Hypomagnesemia Liver failure Renal failure Hypothyroidism Infective/inflammatory Acute cholecystitis Pelvic abscess Spontaneous bacterial peritonitis Acute pancreatitis Sepsis Herpes zoster Appendicitis Neoplasia Retroperitoneal Metastatic cancer Post surgical Cardiac surgery Cesarian section Gynecologic surgery Pelvic surgery Organ transplantation Orthopedic surgery Post traumatic Pelvic trauma Spinal cord injury Femoral fracture Drugs Narcotics Tricyclic antidepressants Phenothiazines Antiparkinson agents Calcium channel blockers Benzodiazepines Clonidine Vincristine Colonoscopy Principles and Practice Edited by Jerome D. Waye, Douglas K. Rex, Christopher B. Williams Copyright © 2003 Blackwell Publishing Ltd Chapter 50: Acute Colonic Pseudo-obstruction 597 by excessive sympathetic inhibition. This theory is supported by animal experiments performed in the 1920s and 1930s [8] showing increased colonic peristalsis after spinal anesthesia, which leads to a temporary paralysis of sympathetic input. This was the rationale for the induction of spinal anesthesia as a successful treatment of adynamic ileus in Europe in the 1920s. Clinical presentation ACPO is usually seen in middle-aged to elderly critically ill patients in the intensive care unit or postoperatively and is exacerbated by immobility and narcotic pain medications. Symptoms usually develop gradually over 3–7 days. Significant abdominal distension is seen in all patients, associated with pain (83%), vomiting (57%), constipation (51%), and fever (37%). The bowel sounds are variable and can be normal or hyperactive (40%), hypoactive (31%), high-pitched (17%), or absent (12%) [2]. If peritoneal signs are present, transmural ischemia or perforation should be suspected. Diagnosis Abdominal examination shows significant distension in all patients, with variable degrees of tenderness. The presence or quality of bowel sounds is also variable. Peritoneal signs are suggestive of transmural ischemia or perforation and mandate surgical consultation. The diagnosis is confirmed by plain abdominal radiographs, which typically show significant distension of the colon with predominance of the right side in the absence of mechanical obstruction (Fig. 50.2). A cut-off sign at the splenic flexure is frequently observed [5]. Initial studies suggested that a cecal diameter of greater than 12 cm increases the risk of perforation sub- stantially [9]. The case series by Vanek and Al-Salti [2] reported no cecal perforation with a cecal diameter < 12 cm, 7% perforation risk with cecal diameters of 12–14 cm, and 23% perforation risk with a cecal diameter > 14 cm. However, more recent reports suggest that the duration of significant cecal dilation is more predictive of ischemia than the cecal diameter per se [10]. A water-soluble contrast enema should be cauti- ously performed to confirm the functional etiology, if a mechanical obstruction (absence of rectal air) cannot be entirely excluded by the initial radiographs. Barium should not be administered, because this could Superior mesenteric ganglion T10 11 12 L1 2 T10 11 12 L1 2 Vagus nerves Celiac ganglion Inferior mesenteric ganglion Pudendal nerves S2 3 4 S2 3 4 Pelvic plexus T10-12 Fig. 50.1 Schematic diagram illustrating colonic innervation. Parasympathetic pathways (stimulatory/prokinetic): prevertebral ganglia and sacral nerves (red) and vagus (yellow). Sympathetic pathways (inhibitory): thoracic spinal cord to inferior mesenteric plexus and pelvic plexus (green). Fig. 50.2 Abdominal radiograph of patient with acute colonic pseudo-obstruction following internal fixation of a fractured femur. 598 Section 12: Clinical Use of Colonoscopy complicate surgery if perforation is present and endoscopic decompression if this is required. Complications The dreaded complication of progressive colonic dilation is transmural ischemia followed by perforation. However, the frequency of this complication, which requires emergency colonic resection, has significantly decreased in recent case series. The risk of perforation was initially reported to be as high as 13% with a mortality of 43% [11]. A summary of more recent studies shows a perforation risk of 3% [12]. The surgical mortality may be as high as 40–50%, if perforation occurs [13]. Management Supportive medical care Initial management for the first 24–48 h is conservative, with close attention to correcting any fluid and elec- trolyte imbalances that may be present. The medication list should be carefully scrutinized and drugs that might delay intestinal transit, such as anticholinergics or opiates, should be discontinued if possible [14]. The abdominal examination needs to be followed carefully and daily abdominal radiographs obtained to monitor for progressive dilation and evidence of perforation. The introduction of a nasogastric tube for decompression is advisable for most patients, and in selected cases a rectal tube might also be of help. Mobilization of the patient with frequent turning might facilitate the passage of flatus. Success rates of supportive management are variable but can be as high as 96%, as reported in a cohort of cancer patients from Sloan-Kettering Cancer Center [15]. Pharmacotherapy When colonic dilation persists or progresses despite conservative therapy, specific pharmacotherapy to stimul- ate the parasympathic innervation of the colon should be attempted (Table 50.2). Catchpole [16] first proposed the combined use of a sympathetic blocker (guanethidine) followed by a cholinesterase inhibitor (neostigmine) to correct the sympathetic/parasympathic imbalance. Sub- sequent small case series suggested that a majority of patients with ACPO could be effectively treated using neostigmine [17–19]. A double-blind, randomized, placebo-controlled clinical trial reported by Ponec and colleagues [20] con- clusively showed a dramatic improvement of clinical status and colonic distension in the majority of patients treated with intravenous neostigmine, making endoscopic intervention unnecessary in most cases. In this study, patients were treated with 2 mg of neostigmine administered over a few minutes by slow intravenous push. Patients were monitored continuously by electrocardiography with atropine available at the bedside, as symptomatic bradycardia is the most significant adverse effect of this treatment. Of 11 patients who received neostigmine, 10 (91%) had prompt colonic decompression with a median time to response of only 4 min, whereas none of the patients receiving placebo (saline) had a clinical response. Seven patients in the placebo group and the one patient in the neostigmine group who failed initial response received open-label neostigmine 3 h after the initial infusion, with prompt colonic decompression noted in all patients. Only two patients developed recurrent symptoms requiring colonoscopic decompression [20]. Several studies have since confirmed the safety of neostigmine for the treatment of ACPO, reporting Number of Initial decompression Recurrence Medication Reference patients (%) (%) Erythromycin Armstrong et al. [27] 2 100 0 Bonacini et al. [28] 1 100 0 Rovira et al. [29] 2 100 0 Cisapride MacColl et al. [7] 1 100 0 Pelkmans et al. [30] 2 0 0 Mazloum et al. [31] 1 100 0 Neostigmine Hutchinson & Griffiths [17] 11 72 0 Stephenson et al. [18] 12 83 16 Turegano-Fuentes et al. [19] 16 75 0 Ponec et al. [20] 21 81 11 Paran et al. [21] 11 82 0 Trevisani et al. [22] 28 93 0 Abeyta et al. [23] 8 87 0 Van der Spoel et al. [24] 24 79 0 Table 50.2 Reports of pharmacotherapy of acute colonic pseudo-obstruction. Chapter 50: Acute Colonic Pseudo-obstruction 599 successful colonic decompression in 79–93% of cases. Several different neostigmine infusion protocols have been used, including 2-mg and 2.5-mg intravenous boluses and 2.5 mg administered over 60 min [21–24], all with similar success rates. Recurrence of colonic distension following successful decompression using neostigmine occurs in up to 16% of patients. In these situations, neostigmine can be safely readministered, leading to colonic decompression in approximately two-thirds of cases [21,23]. The observed adverse effects of neostigmine, like other cholinesterase inhibitors, include excessive saliva- tion (38%), vomiting (9%), abdominal pain (62%), bradycardia (9%), and bronchospasm. Patients must therefore be closely monitored during drug administration with continuous electrocardiography and atropine available at the bedside [20]. Symptomatic bradycardia responds to administration of atropine, but this also leads to a reversal of any benefit of neostigmine in relieving colonic dilation. The coadministration of glycopyrrolate, an antimuscarinic anticholinergic agent, seems to decrease the incidence of bradycardia without reducing neostigmine’s efficacy [25,26]. Suitable candidates for neostigmine administration are hence patients with ACPO who have no evidence of mechanical bowel obstruction, a resting heart rate greater than 60 beats per minute with a systolic blood pressure greater than 90 mmHg, and no active bronchospasm [14,20]. Neostigmine is contraindicated in patients on β-blockers and those who have significant acidosis or recent myocardial ischemia, because of the risk of inducing cardiac arrhythmias [18]. Anecdotal case reports with other prokinetic agents show variable success rates in the treatment of ACPO. Intravenous erythromycin, which acts as a motilin receptor agonist, showed some success in a total of five reported cases [27–29]. The efficacy of intravenous cisapride, no longer available in the USA, was highly variable in case reports of five patients [7,30,31]. The new 5-hydroxytryptamine 5-HT 4 receptor agon- ists (tegaserod, prucalopride) might be theoretically useful for stimulating colonic motility in the setting of ACPO, but no data are yet available with the use of these medications in ACPO [14]. Colonoscopic decompression Pharmacologic treatment of ACPO has markedly re- duced the need for urgent colonoscopic decompression. While previously considered to be the treatment of choice for progressive colonic dilation, it is now usually reserved for patients who have failed treatment with neostigmine (Fig. 50.3). No randomized comparative studies of colonoscopic decompression with neostigmine or other treatment modalities are available. A summary of 11 retrospective studies involving 264 patients shows a high initial success rate for colonoscopic decompression (64–100%), with an average recurrence rate of 23% (range 13–65%) (Table 50.3). Complications were reported in 3% [32,33]. The largest single-center series from the Mayo Clinic shows a similar experience in 50 patients, with an overall success rate of 88% complicated Conservative measures (NG, rectal tube, stop narcotics, mobilize patient) Success Stop Fail Bradycardia, active bronchospasm, renal failure? Yes No Colonoscopic decompression Fail Neostigmine 2.0 mg IV Fig. 50.3 Algorithm for management of acute colonic pseudo- obstruction. Number of Initial Complications Reference patients success Recurrence (death) Surgery Kukora & Dent [51] 6 5 (83%) 0 0 1 (17%) Nivatvongs et al. [5] 22 19 (86%) 4 (21%) 0 4 (18%) Strodel et al. [35] 44 32 (73%) 5 (13%) 5% (2%) 9 (20%) Starling [52] 17 17 (100%) 3 (18%) 12% 0 Bode [55] 22 20 (91%) 4 (20%) 5% (5%) 3 (14%) Nakhgevany [53] 10 9 (90%) 0 0 1 (10%) Fausel & Goff [54] 12 11 (91%) 3 (25%) 0 2 (17%) Nano et al. [47] 17 13 (76%) 6 (46%) 0 0 Gosche et al. [32] 19 17 (89%) 11 (65%) 5% 2 (11%) Jetmore et al. [33] 45 29 (64%) 13 (29%) 0 5 (11%) Geller et al. [34] 50 39 (78%) 9 (18%) 2% (2%) 1 (2%) Total 264 83% 23% 3% (1%) 11% Table 50.3 Reports of colonoscopic decompression of acute colonic pseudo-obstruction. 600 Section 12: Clinical Use of Colonoscopy by one procedure-related perforation. The overall hos- pital mortality is 30% [34]. Colonoscopic decompression is technically more chal- lenging compared with routine colonoscopy since the colon is unprepared and the patients are often critically ill, necessitating performance of the procedure in an intensive care unit. Enemas are not very helpful in preparation for colonoscopy and should be done gently, if at all, due to the risk of perforation. Liquid stool must be suctioned and irrigated at the time of colonoscopy in most cases. Air insufflation should be kept to a minimum to prevent further cecal dilation, which could potentially precipitate perforation. It is important to reach the hepatic flexure in order to achieve significant decompression, although cecal intubation is not required [35]. Jetmore and colleagues [33] reported that colonic decompression was almost twice as successful if the ascending colon was reached (initial success 71% vs. 37%). If mucosal changes suggestive of acute ischemia are encountered, the procedure should be terminated and the patient referred for emergency colectomy. The overall decrease in cecal diameter following colonoscopic decompression is generally quite modest, with an average reduction of only 2 cm [36]. Up to 40% of patients develop recurrence of colonic distension after initial successful colonoscopic decompression. This led to the introduction of decompression tubes, which are inserted at the time of the initial procedure. Harig and colleagues [37] performed a randomized trial in 20 patients comparing endoscopic decompression alone vs. additional insertion of a modified enteroclysis catheter and demonstrated a reduction in the recurrence of colonic dilation from 44% to 0%. Decom- pression tubes remained in place for an average of 3–4 days without any reported complications. The two most commonly used decompression tubes are a modified enteroclysis catheter, with additional side holes at the tip or a 14F colon decompression kit (Wilson-Cook Medical, Winston-Salem, NC). A flexible guidewire is placed through the endoscope channel and the tip is directed into the cecum under fluoroscopy. The endoscope is then slowly withdrawn leaving the wire in place. Fluoroscopy is helpful in keeping the wire straight during complete withdrawal of the colonoscope. The decompression tube is then advanced under fluoroscopic guidance, using traction on the wire to keep it straight while the tube is advanced. The decompression tube is than taped to the patient’s buttock and connected to low intermittent suction. It is advisable to flush the tube with water every 4 h to prevent clogging with stool. Fig. 50.4 (a) Abdominal radiograph of patient with acute colonic pseudo-obstruction following bone marrow transplantation for leukemia. (b) Abdominal radiograph of same patient immediately following colonoscopy at which time a 14F decompression tube was placed. (a) (b) Chapter 50: Acute Colonic Pseudo-obstruction 601 The patient’s clinical status should be followed carefully with daily abdominal radiographs (Fig. 50.4). The catheters are usually left in situ for 2–4 days, until colon decompression is complete and underlying reversible contributors to ACPO are reversed. Use of larger tubes up to 40F in diameter (Levacuator, Mallinckrodt Medical, St Louis, MO) has been described in case reports, with more rapid decompression and less tube clogging [38]. A minority of patients may not respond to these measures and if there is suspicion of acute ischemia or perforation the patient should be referred for immediate surgery. Percutaneous cecostomy In the absence of ischemia or perforation, percutaneous cecostomy (PCC) should be considered as a minimally invasive alternative to surgery in those critically ill patients where induction of general anesthesia poses a significant risk. Both transperitoneal and retroperitoneal approaches for PCC have been described [39–41]. The early work by VanSonnenberg and colleagues [42] showed the technical feasibility and safety of PCC tubes. The theoretically safer retroperitoneal approach did not lead to a lower risk of peritonitis than the anterior transperitoneal approach [42]. The technique was recently refined by using additional T-fasteners, which allow for better colonic apposition to the abdominal wall, thereby potentially reducing the risk of fecal soilage of the abdominal cavity [43]. No studies comparing the efficacy and safety of pharmacotherapy, endoscopic intervention, radiographically guided PCC, and surgery are available. Surgery Peritoneal signs or free air on abdominal radiography are clear indications for laparotomy and colectomy [2]. The definitive surgical management depends on the viability of the cecum and ascending colon at the time of exploration. Partial colectomy is indicated for transmural ischemia and perforation but carries a high mortality in these critically ill patients. Surgical decompression in the absence of perforation, through an open or laparoscopic cecostomy, is an alternative to colectomy if the local expertise is not available to perform com- puted tomography-guided PCC [44]. Prognosis The overall mortality of ACPO remains approximately 30%, despite the recent advances in its management [2,34]. This reflects the severity of the underlying disease process leading to ACPO and is not directly related to the colonic complications. The impact of pharmacologic therapy on the outcome of patients with ACPO has not yet been fully assessed. References 1 Ogilvie H. 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Neostigmine: safe and effective treatment for acute colonic pseudo-obstruction. Dis Colon Rectum 2000; 43: 599–603. 602 Section 12: Clinical Use of Colonoscopy 39 Crass JE, Simmons RL, Mathis PF, Charles WM. Per- cutaneous decompression of the colon using CT guidance in Ogilvie syndrome. AJR Am J Roentgenol 1985; 144: 475–6. 40 Casola G, Withers C, vanSonnenberg E, Herba MJ, Saba RM, Brown RA. Percutaneous cecostomy for decompression of the massively distended cecum. Radiology 1986; 158: 793–4. 41 Haaga JR, Bick JR, Zollinger RM. CT-guided percutaneous catheter cecostomy. Gastrointest Radiol 1987; 12: 166–8. 42 VanSonnenberg E, Varney RR, Casola G et al. Percutaneous cecostomy for Ogilvie syndrome: laboratory observations and clinical experience. Radiology 1990; 175: 679–82. 43 Chevallier P, Marcy PY, Francois E et al. Controlled transperitoneal percutaneous cecostomy as a therapeutic alternative to endoscopic decompression of Ogilvie’s syndrome. 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Neostigmine resolves critical illness-related colonic ileus in intensive care patients with multiple organ failure: a prospective, double-blind, placebo-controlled trial. Intensive Care Med 2001; 27: 822–7. 25 Ostheimer GW. A comparison of glycopyrrolate and atropine during reversal of nondepolarizing neuromuscular block with neostigmine. Anesth Analg 1977; 56: 182–6. 26 Mirakur RK, Briggs LP, Clarke RS, Dundee JW, Johnston HM. Comparison of atropine and glycopyrrolate in a mix- ture with pyridostigmine for the antagonism of neuromuscular block. Br J Anaesth 1981; 53: 1315–20. 27 Armstrong DN, Ballantyne GH, Modlin IM. Erythromycin for reflex ileus in Ogilvie’s syndrome (letter). Lancet 1991; 337: 378. 28 Bonacini M, Smith OJ, Pritchard T. Erythromycin as therapy for acute colonic pseudo-obstruction (Ogilvie’s syndrome). J Clin Gastroenterol 1991; 13: 475–6. 29 Rovira A, Lopez A, Cambray C, Gimeno C. Acute colonic pseudo-obstruction (Ogilvie’s syndrome) treated with erythromycin. 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[...]... dilation of multiple NSAID-induced colonic strictures: case report and review of literature on NSAID-related colopathy Gastrointest Endosc 1999; 50: 120–3 Weinstock LB, Hammoud Z, Brandwin L Nonsteroidal anti-inflammatory drug-induced colonic stricture and ulceration treated with balloon dilatation and prednisone Gastrointest Endosc 1999; 50: 564–6 622 Section 12: Clinical Use of Colonoscopy 26 Smith JA,... self-expandable metallic stents before scheduled surgery Results of a multicenter study Radiology 1999; 210: 65 – 9 44 Binkert CA, Ledermann H, Jost R, Saurenmann P, Decurtins M, Zollikofer CL Acute colonic obstruction: clinical aspects and cost-effectiveness of preoperative and palliative treatment with self-expanding metallic stents A preliminary report Radiology 1998; 206: 199–204 45 Martinez-Santos... are similar, pediatric colonoscopy is different from colonoscopy in adults in many aspects, such as preparation, sedation, technique, and spectrum of therapeutic manipulations Indications for colonoscopy Indications for diagnostic and therapeutic colonoscopy are listed in Table 53.1 Although colon cancer is not one of the usual indications for colonoscopy in children, colonoscopy and biopsy are performed... therapeutic endoscopic procedures and SEMS placement to assist with these procedures Nonfluoroscopic-guided stent placement Non-TTS stent placement For distal left-sided lesions, the area may be accessed entirely under endoscopic guidance [60] If the endoscope cannot be passed through the lesion, the stricture Fig 52.4 Endoscopic view of through-the-scope placement of self-expandable metal stent for palliation... usually involves clear liquids and milk of magnesia Milk of magnesia 1.0 ml/ kg of body weight is given two nights before the procedure and mid-day the day before the procedure Magnesium citrate may also be used in children above 1 year of age This may be divided in two doses and given 24 and 12 h before the colonoscopy It is best given cold and over ice, or mixed with lemon/lime-type soft drinks Some individuals... Full and continuous monitoring is necessary during the procedure Sedation is begun after baseline vital signs are obtained The most commonly used sedation for colonoscopy includes use of tranquilizers for relief of anxiety and narcotics for sedation-analgesia The narcotic of choice is fentanyl, which is rapid acting with a short half-life and minimal side effects It rarely causes nausea and vomiting and. .. useful to perform a colonoscopy in children safely and effectively: 1 The intubated colon adopts configuration and shape according to manipulations and movements with the colonoscope, and the pattern of these changes are predictable, as well as the direction in which the colonoscope tip should be moved Chapter 53: Pediatric Colonoscopy Table 53.3 Steps to ensure complete and successful colonoscopy in children... occur to the mucosa with the passage of the instrument, and if abnormalities are not identified beforehand, one is always left wondering whether what one sees is due to colonoscopy, versus the underlying pathology Risks and complications of colonoscopy The potential risks and complications of colonoscopy include bleeding, perforation, infection, and difficulties with sedation (such as paradoxical reaction... an air-filled dilated proximal bowel, the catheter is advanced over the guidewire through the lesion After removal of the guidewire, water-soluble radiographic contrast is injected (b) 620 Section 12: Clinical Use of Colonoscopy (a) (b) (c) (d) Fig 52.5 Endoscopic placement of a through-the-scope stent using fluoroscopic guidance: (a) endoscope is advanced to the site of the lesion and a guidewire and. .. in patients with longstanding inflammatory bowel disease Patients who have undergone small intestinal transplantation may need to undergo ileoscopy and or colonoscopy to obtain specimens from transplanted bowel to look for rejection and evidence of lymphoproliferative disease When diagnostic colonoscopy is not indicated Colonoscopy is not indicated in patients with: • acute self-limited diarrhea; • gastrointestinal . friable, and regress within days of the procedure (Fig. 49.20). References 1 Reinus JF, Brandt LJ. Diarrhea. In: Raskin, JB, Nord, HJ, eds. Colonoscopy: Principles and Techniques. New York: Igaku- Shoin,. Pathophysiology/Diagnosis/Management, 7th edn. Phil- adelphia: WB Saunders, 2002: 1864–913. 43 Bhargava DK, Tandon HD, Chawla TC, Shriniwas Tandon BN, Kapur BM. Diagnosis of ileocecal and colonic tuberculosis by colonoscopy. Gastrointest. recognized and is associated with substan- tial morbidity and mortality. Epidemiology and predisposing factors The exact incidence of ACPO in hospitalized patients is unknown. Vanek and Al-Salti

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