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Management of Intestinal Obstruction in Adult By Bedru.pptx
- 1. Management of Intestinal Obstruction in Adult Presenter: Dr.Bedru (GSR3) Moderator :Dr.Hiwot (Consultant General Surgeon) 1
- 2. Outlines • Introduction • Epidemiology • Pathophysiology • Diagnosis • General management of IO • Management of some specific types of IO • Summary • References 2
- 3. Objectives • To have understanding for proper diagnosis of bowel obstruction • General management approaches of bowel obstruction • Management of common etiologies of bowel obstruction 3
- 4. Introduction • Intestinal obstruction, is a complete or partial mechanical or functional obstruction of the intestines which prevents the normal movement of the products of digestion. • Can affect the small or large or both of bowels. • It remains one of the most common cause of mortality and morbidity in irrespective of the underlying etiologies. • Early recognition and aggressive treatment are crucial in preventing irreversible ischemia and transmural necrosis and thereby in decreasing mortality and long- term morbidity. 4
- 5. Con. Terminologies • Complete vs partial obstruction • Open vs closed loop • Simple vs strangulated • “High” vs Distal vs “low” • Mechanical vs Functional 5
- 6. Epidemiology • Intestinal obstruction account for 1.2% of all surgical diseases and 5% of emergency surgical admissions • Both sexes are equally affected and the condition can occur at any age • In Africa, acute intestinal obstruction accounts for a great proportion of morbidity and mortality. Ethiopia is one of the countries where intestinal obstruction is a major cause of morbidity and mortality. 6
- 7. • The etiologies and thereby the prevalence of bowel obstruction vary widely throughout the world depending on Ethnicity The age group considered, Dietary habits, Geographic location Time of the year 7
- 8. Etiology: Mechanical Intraluminal Intramural Extrinsic Foreign bodies Strictures (IBD, Radiation induced ,TB) Adhesions Worm ball (ascariasis) Tumors(Primary or secondary) Volvulus Gallstones Intussusceptions Fecal impaction Hernias (internal or external ) Carcinomatosis Compression 8
- 9. Functional Paralytic ileus Pseudo-obstruction Intra abdominal inflammation or collection Smooth muscle disorders Abdominal surgery Neurogenic disorders Metabolic causes(Electrolytes imbalance ,uremia ,or hypothyroidism ) Medications (opiods,psychotrotic,anticholinergics) Retroperitoneal inflammation or collections Trauma 9
- 10. Etiology :Developed Countries • 20% of acute Abdomen is bowel obstruction. 80%:SBO • Adhesions :60% • Neoplasms :20% • Incarcerated hernias:10% • Crohn’s :5% • Others :5% 20% :LBO • Malignancies :60% • Diverticular disease:20% • Volvulus :1-5% • Others :15-20% 10
- 11. Pattern of acute abdomen in adult patients in Tikur Anbessa Teaching Hospital, Addis Ababa, Ethiopia.B Kotisso, Z Abdurhaman • One year retrospective study conducted at TASH in 2007 • Results: During the study period there were 587 adult surgical emergency operations of which 214 (36.4%) were laparotomies for acute abdomen. A total of 276 patients were admitted with a diagnosis of acute abdomen of whom the records of 235 patients were retrieved which made the basis of this study. The male to female ratio was 2:1. The ages ranged from 14 years to 84 with a mean of 30.7±14.9. Acute appendicitis accounting for 52% of cases was the leading cause of acute abdomen followed by intestinal obstruction (26%) and perforated Peptic ulcer disease (PPUD) (9%). There were 36 deaths giving an overall mortality rate of 15.3%. A higher mortality rate was observed in patients who presented late. 11
- 12. Surgically Treated Acute Abdomen at Gondar University Hospital, Ethiopia. S. Tsegaye1, M. Osman2, A. Bekele3 • Retrospective study from September 1998 to August 2002 12
- 13. Prevalence, cause ,and management outcome of intestinal obstruction in Adama Hospital,Ethiopia (By Urgessa Soressa and His colleague's) • Hospital based crossectional study of 3 years medical record(January 1,2010 to December 30,2012) • 262 patients admitted with IO • The prevalence of intestinal obstruction was 21.8 % and 4.8 % among patients admitted for acute abdomen surgery and total surgical admissions, respectively. • The mortality rate was 2.5 % (6 of 262). The most common cause of small bowel obstruction was intussusceptions in 48 patients (30.9 %), followed by small bowel volvulus in 47 patients (30.3 %). Large bowel obstruction was caused by sigmoid volvulus in 60 patients (69.0 %) followed by colonic tumor in 12 patients (13.8 %). 13
- 14. Pattern of Non-traumatic Acute Abdomen in Patients from Ayder Comprehensive Specialized Hospital, Northern Ethiopia: A retrospective analysis Girmay Hagos Araaya, G. Temesgen, Mariam Published 2019 • A 2 year retrospective study from 2015 to 2016 • During the study period there were 514 emergency surgical operations of which 439 were laparotomies for none-traumatic acute abdomen. The male to female ratio in patients with acute abdomen was 3:1. The mean age of patients was 28.4±19.5 with a range of 30 days – 88 years. Acute appendicitis accounts for 50.3% of the cases and was the leading cause of acute abdomen followed by intestinal obstruction 34.0% and peritonitis 15.7%. Among the appendicitis, 11.6% of them were perforated appendix, and 4.1% Perforated Peptic Ulcer Disease. The causes of large intestinal obstruction were sigmoid volvulus (28%), colonic cancer (6.1%) and ileo sigmoid knotting (3%) and that of small bowel obstruction were small bowel volvulus (20.7%), adhesion (16.5%), hernia (15.2%) and intussusceptions (10.4%). Late presented patients showed a higher frequency of peritonitis. 14
- 15. Pathophysiology of Intestinal Obstruction 15 Onset of obstruction Accumulation of gas and fluid proximal to the obstruction Increased intraluminal and intramural pressures Impairment of micro perfusion Intestinal perforation Peritonitis Shock sepsis Decreased motility Decreased absorption Hypersecretion Hypovolemia Bacterial overgrowth
- 16. Diagnostic Approach • The diagnostic evaluation should focus on : Distinguish mechanical obstruction from ileus, Determine the etiology of the obstruction Discriminate partial from complete obstruction, and Discriminate simple from strangulating obstruction. 16
- 17. History • Cardinal symptoms….Abdominal pain,vomiting,distension and obstipation/constipation • Previous history of surgery • Rectal bleeding • Bowel habit change 17
- 18. Signs and symptoms of Bowel Obstruction 18
- 19. P/E V/S..PR=Tachycardia/normal BP=hypotensive/normal T=fever/hypothermia HEENT…Dry buccal mucosa Abdomen ..Distension ,surgical scar visible peristalsis Hyper/hypo-active bowel sound Localized/Generalized tenderness PR examination Check hernia sites(especially inguinal, and femoral hernias) 19
- 20. Investigation Laboratory • CBC….Hemoconcentration ,leukocytosis • OFT • Electrolytes 20
- 21. Imaging • To confirm the diagnosis of bowel obstruction • Locate the site of obstruction and • Gain insight into the lesion responsible for the obstruction • Plain Abdominal radiography • CT scan • Contrast studies • Abdominal ultrasound 21
- 22. Plain Films • Has 70% to 80% sensitivity but low specificity • Supine and erect positions • SBO • Dilated loops of small bowel(>3cm) • Centrally located multiple air-fluid levels(“stepladder appearance”) • Paucity of air in the colon 22
- 23. Abdominal x-ray SBO Dilated bowel>3cm Valvulae conniventes Central abdominal pain Multiple air fluid level Paucity/absent gas in the colon LBO Haustral markings Peripheral location 23
- 24. CT-scan • Provide more clinically relevant information. • Sensitivity and specificity >94% • If bowel obstruction is present • Localize the obstructive site • Degree of obstruction • Closed-loop obstruction • Local and regional mets Limitation :low sensitivity for partial obstruction(<50%) 24 oComplications Ischemia Thickened intestinal walls poor flow of contrast media into a section of bowel Necrosis and perforation pneumatosis intestinalis pneumoperitoneum, and mesenteric fat stranding
- 25. General management Bowel rest : NPO Fluid Resuscitation and electrolytes Isotonic fluid should be given iv K+ replacement Catheterize and monitor UOP Invasive hemodynamic monitoring Central venous or pulmonary arterial pressure: unstable patients or those with impaired cardiac, pulmonary or renal function IV broad spectrum antibiotics Peritonitis Once surgery is planned 25
- 26. Non Operative Management • Indications: • No closed loop obstruction • No strangulation • No peritonitis • Partial SBO “The sun should never rise and set on a complete bowel obstruction.” NG tube decompression IV fluid To follow patient condition _If no improvement within 48hours =Operative Mx 65 to 81% success vs 5 to 15% failure 26
- 27. Operative Management • Indication Suspected ischemia/strangulation perforation Closed loop obstruction for those who fail conservative management • Regardless of the etiology, the affected intestine should be examined, and nonviable bowel should be resected. • Criteria suggesting viability are normal color, peristalsis, and marginal arterial pulsations. • Hemodynamically stable patient, short lengths of bowel of questionable viability should be resected, and primary anastomosis of the remaining intestine should be performed • If large segment of the bowel viability is in question, the bowel should be left intact and “second look” after 24 to 48hrs. 27
- 28. Management of some specific causes of intestinal obstruction Sigmoid Volvulus • accounts for 1.9% cases of LBO in US and up to 10 to 50% of cases in developing nation • upto 80% of cases of colonic volvulus , but volvulus can involve the cecum(<20%) or transverse colon • Volvulus occurs when an air-filled segment of the colon twists about its mesentery. • bowel obstruction(180º),which can progress to • strangulation(360º),gangrene,and perforation. Anatomic risk factors A long redundant sigmoid colon Wide mesentery & narrow mesenteric root attachment. advancing age(?due to colonic dysmotility) High fecal load- high fiber diet Constipation Pregnancy HSD 28
- 29. Diagnosis Clinical presentation Acute fulminant Common in young No hx of previous attack Sudden onset, rapid course Constant abdominal pain, minimal distention Subacute progressing • Old, hx of previous attack • Slowly progressing • Prominent abdominal distention Plain AxR • "bent inner tube“ or coffee bean • Contrast enema- “bird’s beak sign” (~100%) • CT scan: ~100%sensitivity and >90% specificity whirl pattern Split wall sign 29
- 30. Treatment: SV • Goals: - • To prevent development of gangrene • to address the anatomic abnormality that led to the volvulus • General management - resuscitation, bowel rest • endoscopic detorsion • flexible sigmoidoscopy/rigid proctoscopy/colonoscopy • blind passage of rectal tube • leave a rectal tube in place with its proximal end beyond the area of twisting. • Outcome: • Recurrence : up to 60% • Mortality : 6.4% (<10%) 30
- 31. • Patients with alarming signs (gangrene,peritonitis,perforation) • Immediate surgical exploration without an attempt to detorse is recommended. If dead bowel is present at laparotomy: Two stage-Hatmann’s procedure - may be the safest operation to perform. Single stage- resection and primary anastomosis 31
- 32. Is primary resection and anastomosis , without proximal stoma safe in gangrenous sigmoid volvulus?(Jitin Bajaj et al(2018)(India) • 6yr,prospectivee ,institution-based study,64 cases • Adults older than 18yr with sigmoid volvulus • Excluded pts : hemodynamical instablity,ASA >III • Primary outcomes: leak(3%),abdominal abscess(3%),wound infection(20%),Mortality(0). • Conclusion : ERPA is a safe and effective option for both viable and gangrenous SV in expert hands and in hemodynamically stable patients. 32
- 33. • Intraoperative finding of Viable sigmoid Non-resective methods Simple detorsion Sigmoidopexy Mesosigmoidoplasty Extraperitonealization Foley Catheter Sigmoidostomy T-Fasteners Sigmoidopexy 33 High recurrence rate:9-44%
- 34. • Overall outcome: Nongangrenous , surgically treated • Mortality rate <10% Gangrenous sigmoid volvulus • Mortality rate : 11-60% 34
- 35. Cecal Volvulus • occurs less commonly than sigmoid volvulus and accounts for approximately 1% of all cases of intestinal obstruction. • Most patients are younger, median age 36yr and M:F-2:1 Etiology and risk factors • Anatomic prerequisite of a mobile cecum/ • Congenital band • Adhesion from previous surgery • Pelvic space occupying lesion / pregnancy 35
- 36. There are three types of cecal volvulus: • Type 1 – axial Type 2 –loop Type 3 – bascule • precipitating factor may be the presence of distal colonic obstruction which occur in one-third to one-half of the cases. • Cecum twist in a clockwise fashion, resulting closed loop and complete obstruction • Clinical presentation- obstipation with sxm of SBO • Tachycardia,fever and diffuse abdominal pain incase of gangrene 36
- 37. •Diagnosis • HX and PE • Imaging • Abdominal xray-classic 37
- 38. Management Depends on status of the pt and bowel • Right hemicolectomy-standard • Ileocolic resection with or without anastomosis • Cecopexy • A tube Cecostomy fixation 38
- 39. Small bowel volvulus • responsible for < 5% of SBO in Western series and over half of SBO in some African and Asian series. • Young adults are primarily affected, with a strong male preponderance. • The incidence of small bowel volvulus is also higher in regions with endemic parasitism, which is known to increase bowel motility. • In 80% of cases the intestinal torsion is clockwise • only a minority of adolescent and adult patients with primary SBO have an identified lack of mesenteric fixation. 39
- 40. Etiology ,risk factor & Pathophysiology • Classified as primary and secondary • High fiber diet/dietary habit • long mesentery with a narrow insertion and a lack of mesenteric fat. • firm, muscular abdomens • Secondary • Postop adhesion is the most common 40
- 41. Pathophysiology: SBV • Theory: 1-rapid filling of a segment of proximal intestine with high-bulk chyme pulls it down into the pelvis and displaces empty distal bowel upward, thereby initiating the torsion. 2-in secondary sbv, the intestine is twisted around an underlying point of fixation; as the loop fills with fluid, peristalsis exacerbates the torsion. 41
- 42. Diagnosis: • Central abdominal pain is almost always present • Bilious Vomiting ,central abdominal distention • Pain out of proportion, fever, tachycardia, peritoneal signs, acidosis, and leukocytosis raises suspicion of bowel ischemia • Abdominal Xray-shows sign of SBO 42
- 43. Treatment: SBV • Suspicion of volvulus clinically or radiographically should prompt immediate exploration because of the associated risk for ischemia. • Viable bowel- derotation • Non-viable bowel • If the patient is hemodynamically stable, short lengths of bowel of questionable viability should be resected and primary anastomosis of the remaining intestine performed • If the viability of a large proportion of the intestine is in question, the bowel of uncertain viability should be left intact and the patient reexplored in 24 to 48 hours in a "second-look" operation • Outcome-over all mortality is 10 to 35% 43
- 44. Adhesions • Abnormal fibrous bands between organs or tissues or both in the abdominal cavity that are normally separated. • Acquired(most common) or congenital)e.g. Ladd bands • 93-100% who undergo transperitoneal surgery will develop post op adhesion • Intraabdominal adhesions related to prior abdominal surgery accounts for up to 75% of cases of SBO. 44
- 45. • Typical adhesions form after peritoneal injury from abdominal surgery. • The risk of SBO due to adhesions depends in part upon the type of surgery being performed and the cause of the SBO • inframesocolic compartment and especially in the pelvic region, such as colonic, rectal, and gynecologic procedures. • a common predisposition to adhesive obstruction is the presence of a prior episode of adhesive obstruction. 45 • Open appendectomy (10.7%) • Open cholecystectomy (6.4%) • ileal pouch–anal anastomosis (19%) • open colectomy (9%). • open operations > laparoscopic surgery
- 46. Pathogenesis of adhesion 46 Damage to peritoneal surfaces induces a repair response Fibrin deposition at the site of injury within 3hrs of the tissue trauma and peaking on day 4 to 5. complete fibrinolysis and resorption of degradation products , reepithelialization a smooth healed tissue surface. connective tissue scars and adhesions develop from in growth of fibroblasts, capillaries, and nerves.
- 47. Types • Fibrinous adhesion-early • Avascular and flimsy • Get resolved completely • Fibrous adhesion • Collagenized and vascularized 47
- 48. Clinical features • Abdominal pain • Colicky • Recurrent • Episodic • Distension • Constipation • Previous surgical scars commonly observed • Imaging X-ray CT-scan 48 Gilroy Bevan triad Pain in the region of old scar Pain gets aggravated or relieved on change of posture Tenderness is elicited by pressure over the scar
- 49. Management • general • Fluid and electrolytes • Bowel rest • NG tube • Urethral catheter • Monitoring • Decide on non operative vs operative mgt • Non operative ~ 80% success rate 49
- 50. Non operative Indications No closed loop obstruction No evidence of bowel ischemia No sign of peritonitis 50 Contraindications Closed loop obstruction Evidence of bowel ischemia Sign of peritonitis LBO Complete obstruction
- 51. 51
- 52. Principles of adhesiolysis 52 • Incision planning-entry into a "virgin" area. • avoiding adhesions and bowel loops adherent to the abdominal wall at the site of prior incisions • Diagnose and resolve the source of the obstruction, resect any nonviable bowel and minimize the occurrence of an incidental enterotomy. • Handle dilated bowel proximal to the point of obstruction gently because the bowel wall can be thin and is easily injured. • Cultures of any cloudy fluid should be obtained. • Ideally, the distal, decompressed bowel loops are identified first and followed to the point of obstruction.
- 53. • Minimizing the chances of injury. • The precise mechanism for the obstruction should be noted • Any internal hernias will require reduction of the herniated intestine and obliteration of the opening that allowed herniation. • After the site of obstruction is relieved, the need for lysis of all remaining adhesions is debatable. 53
- 54. Prevention of adhesion • a good surgical technique(the most effective to date). • Gentle handling of bowel to reduce serosal trauma • Avoidance of unnecessary dissection • Exclusion of foreign material from peritoneal cavity( use of absorbable suture material when possible, avoidance of excessive gauze sponge use,& removal of starch from gloves) • Adequate irrigation and removal of removal of infectious and ischemic debris • Preservation and use of omentum around the site of surgery or in the denuded pelvis. • Use of adhesive barriers such as seprafilm 54
- 55. Intussusception • Intussusception refers to the invagination of a part of the intestine into itself. • leads to obstruction and compromise of mesenteric blood flow, with resultant inflammation and the potential for ischemia of the bowel wall 55
- 56. • It accounts for only 2% of bowel obstruction in the adult population. • An increased incidence of intussusception in patients with HIV/AIDS. • The median age : 6th to 7th decade. • The etiology of intussusception differs greatly between adult and pediatric patients. • Adult intussusception commonly involves a distinct pathologic lead point upto 90%, which is malignant in over half of the cases. 56
- 57. Diagnosis Clinical features • Symptoms are often chronic. • intermittent abdominal pain is the most common presentation in adults. • Other : intermittent partial bowel obstruction and can include nausea, vomiting, melena, weight loss, fever, and constipation 57
- 58. Imaging • Plain abdominal films show small bowel obstruction. • computed tomography (CT). A "target sign" on perpendicular view, a sausage shaped mass when the CT beam is parallel to the longitudinal axis. The distended loop of bowel (intussuscipiens) has a thickened wall because it represents two layers of bowel. 58
- 59. Treatment • Surgical resection using appropriate oncologic techniques is recommended in most cases . • If a benign diagnosis or the patient is at risk for short bowel syndrome, • A combined approach with limited intestinal resections and snare polypectomies is more appropriate. 59
- 60. References 60
Editor's Notes
- via systemic alterations in metabolism,electrolyte balance, or neuroregulatory mechanisms involving both the small and large intestine (generalized ileus).
- For instance, during Ramadan in Ibadan, the most common cause of small bowel obstruction is small bowel volvulus, believed secondary to the combination of a congenitally narrow base of the small bowel mesentery combined with a large volume of oral intake after sundown. Similarly, in the 18- to 30-year-old age group in Miami, FL, intestinal obstruction secondary to ingestion of drug-lled condoms is not an uncommon cause of intestinal obstruction.
- A rare etiology of obstruction is the superior mesenteric artery syndrome, characterized by compression of the third portion of the duodenum by the superior mesenteric artery as it crosses over this portion of the duodenum.
- radiological sign of gallstone ileus is Rigler’s triad, comprising: small bowel obstruction, pneumobilia and an atypical mineral shadow on radiographs of the abdomen.
- Acute abdomen deserving emergency laparotomy is quite common in TAH. Earlier reports from Africa had shown intestinal obstruction as a leading cause. In this study acute appendicitis was found to have taken over at least in the urban setting of Ethiopia. The overall mortality of 15.3% is high and could be attributed to late presentation.
- The abdominal series consists of (a) a radiograph of the abdomen with the patient in a supine position, (b) a radiograph of the abdomen with the patient in an upright position, and (c) a radiograph of the chest with the patient in an upright position.
- Valvulae conniventes –traverse entire lumen of bowel lumen Haustra-crosses only part of the bowel lumen and interdigitate
- Suction with a nasogastric tube empties the stomach, reducing the hazard of pulmonary aspiration of vomitus and minimizing further intestinal distention from swallowed air. Nasogastric decompression in a patient with small bowel obstruction is still considered standard of care.The use of a water-soluble contrast challenge in lower-grade obstructions (i.e., those that have not resolved from nasogastric suction management after 48 hours) has become a more common practice. The challenge requires 100 mL of water-soluble contrast given through the nasogastric tube and follow-up radiographs obtained after 8 and 24 hours. If contrast material still has not passed into the colon after 24 hours, conservative management will probably fail and surgical intervention is likely needed. Patients with a partial intestinal obstruction may be treated conservatively with resuscitation and tube decompression alone. Resolution of symptoms and discharge without the need for surgery have been reported in up to 85% of patients with a partial obstruction. Enteroclysis can assist in determining the degree of obstruction, with higher-grade partial obstructions requiring earlier operative intervention.
- Clinical judgement vs doppler flow In borderline cases, a Doppler probe may be used to check for pulsatile flow to the bowel, and arterial perfusion can be verified by visualizing intravenously administered fluorescein dye in the bowel wall under ultraviolet illumination. Neither technique has, however, been found to be superior to clinical judgment.
- Torsion 180 degrees results in clinical obstruction, and further torsion to 360 degrees causes strangulation. Perforation occurs in areas of necrosis at the point of torsion, within the closed loop, or in the proximal thin walled cecum
- abdominal pain, nausea, abdominal distension, and constipation; vomiting is less common. However, some patients (particularly younger patients) may have a more insidious presentation with recurrent attacks of abdominal pain, with resolution presumably due to spontaneous detorsion [ 15 ]. The disease may not be as apparent in the frail elderly or in patients with neurologic diseases who are unable to express their complaints. The diagnosis is often suspected based upon the clinical presentation and physical examination. The pain associated with sigmoid volvulus is usually continuous and severe, with a superimposed colicky component occurring during peristalsis. The abdomen is usually distended and tympanitic.
- Include a combination of careful resuscitation, urgent diagnosis, and decompression as soon as feasible. Simple volvulus ___decompression with either sigmoidoscope or colonoscope. With decompression manifesting as a sudden rush of flatus and liquid feces via the anus or sigmoidoscope. If no immediate surgery is required, a rectal tube should be placed to prevent further recurrences of the volvulus to allow the continuing decompression of the obstructed colon. The goals of treatment of sigmoid volvulus are to prevent the development of gangrene and to address the anatomic abnormality that led to the volvulus. An effective way to restore the blood supply to the colon is to detorse the volvulus, which can be accomplished by advancing a flexible or rigid sigmoidoscope through the twisted segment. An additional advantage of sigmoidoscopy is assessment of the viability of the colon. Reduction of the sigmoid volvulus using this technique has been successful in 85 to 95 percent of cases in some series . The major problem is recurrence in up to 60 percent of patients . The time to recurrence can vary from hours to weeks; as a result, definitive treatment soon after sigmoidoscopic reduction is advised. Initial sigmoidoscopic reduction of the volvulus converts an emergency procedure into a semiurgent procedure with ample time for bowel preparation and preoperative care. Although surgical resection without decompression has been used at some centers with acceptable outcomes , we favor preoperative decompression whenever feasible.
- Patients with signs and symptoms suggestive of gangrenes bowel. After adequate resuscitation, laparotomy should be done To prevent reperfusion syndrome the resection should be en block With either primary anastomosis or Hartmann’s procedure can be done depending on the patient’s condition and surgeon’s experience . The mortality of this is only slightly higher at 5.5% (primary resection and anastomosis) versus 4.2% (Hartmann’s). The recurrence rate of resectional therapies is almost zero. Clinical evidence of gangrene or perforation mandates immediate surgical exploration without an attempt at endoscopic decompression. Similarly ,the presence of necrotic mucosa,ulceration,or dark blood noted on endoscopy examination suggests strangulation and is an indication for operation. If dead bowel is present at laparotomy, a sigmoid colectomy with end colostomy(Hatmann’s procedure) may be the safest operation to perform.
- The choice of reconstruction should be individualized based on patients clinical parameters. Hartmanns procedure is preferred in the presence of hemodynamic instability,coagulopathy,acidosis,or hypothermia. The technique requires a successful detorsion and decompression of the viable sigmoid colon using a colonoscope. With the colonoscope as a guide, the T-fastener is deployed via the needle. The T-fastener then pulls the sigmoid colon up against the abdominal wall and is tightened on the skin over the cotton pledget (Fig. 13). Three to four T-fasteners are placed 4–5 cm apart, in a triangular disposition . These fasteners are cut at the skin level after 28 days
- The mortality related to sigmoid volvulus is highest (11 to 60 percent in various series) in patients who have developed gangrene. In contrast, the mortality is less than 10 percent in patients treated by surgical resection who have not developed gangrene
- Clinically, the most important precipitating factor may be the presence of distal colonic obstruction. This obstruction reportedly can occur in as many as one-third88 to one-half92 of the cases of cecal volvulus. A cecal volvulus tends to twist in a clockwise fashion, in contrast to the counterclockwise twist of a sigmoid volvulus. The resulting obstruction, however, is similarly of the closed loop and complete type. A cecal bascule is an anterior and superior folding of the mobile cecum over the fixed distal ascending colon (▶ Fig. 28.15). Although tension gangrene may develop, there is no major vessel obstruction. Some authors exclude this condition from being a cecal volvulus because it is not a true volvulus. PATHOPHYSIOLOGY — There are three types of cecal volvulus (figure 1) [4-8]: ●Type 1 – An axial cecal volvulus develops from clockwise axial torsion or twisting of the cecum along its long axis; the volvulized cecum remains in the right lower quadrant. ●Type II – A loop cecal volvulus develops from a torsion or twisting of the cecum and a portion of the terminal ileum, resulting in the cecum being relocated to an ectopic location (typically left upper quadrant) in an inverted orientation. Most, but not all, type II cecal volvuli have a counterclockwise twist [7]. ●Type III – Cecal bascule involves the upward folding of the cecum rather than an axial twisting. Torsion-type cecal volvuli (type I and II) are more common, accounting for approximately 80 percent of all cecal volvuli [7]. Cecal bascules (type III) account for the remaining 20 percent. All three types of cecal volvuli require a mobile cecum and ascending colon, which could be congenital or acquired. ●Congenital mobile cecum is hypothesized to result from failed fusion of the ascending colon mesentery to the posterior parietal peritoneum [15]. Based upon autopsy studies, approximately 10 to 25 percent of the population have a cecum and ascending colon with sufficient mobility to develop a volvulus [16]. A congenital mobile cecum can also cause mobile cecum syndrome [17]. (See 'Differential diagnosis' below.) ●Acquired anatomic abnormalities, such as adhesions from abdominal surgery, can also contribute to the development of a cecal volvulus. Other clinical settings that have been associated with cecal volvulus include pregnancy [18], colonic atony, colonoscopy [19], and Hirschsprung's disease [20]. CLINICAL MANIFESTATIONS Patient presentation — The clinical presentation is highly variable, ranging from insidious, intermittent episodes of abdominal pain to an acute abdominal catastrophe [2,4,11,21-23]. Most patients present with a gradual onset of steady abdominal pain accompanied by episodic cramping pain due to peristalsis. Besides abdominal pain, patients also present with nausea, vomiting, and obstipation [11]. The duration of symptoms can vary from hours to days [24]. The elements of a comprehensive history in a patient with acute abdominal pain are discussed separately. (See "Evaluation of the adult with abdominal pain" and "Evaluation of the adult with abdominal pain in the emergency department", section on 'History'.) Physical examination — The findings on physical examination are also variable. Patients who have bowel ischemia or perforation could have fever or hypotension, while others may have normal vital signs. The abdomen is generally diffusely distended and tympanitic. However, in some patients, the abdomen can be asymmetrically distended with tympany only in the midabdomen or in the right or left upper quadrant. Rebound tenderness can be elicited in patients who have peritonitis or ischemic bowel. The approach to performing a physical examination in patients with acute abdominal pain is discussed separately. (See "Evaluation of the adult with abdominal pain in the emergency department", section on 'Physical examination'.) Laboratory studies — Laboratory studies are not diagnostic of cecal volvulus. However, a significant leukocytosis or metabolic acidosis may indicate the presence of bowel compromise (ischemia, necrosis, or perforation). Hypokalemia and other electrolyte abnormalities may develop after protracted vomiting associated with a bowel obstruction. (See "Evaluation of the adult with abdominal pain in the emergency department", section on 'Laboratory tests'.) DIAGNOSIS — Cecal volvulus should be suspected in patients who present with obstructive symptoms such as abdominal pain, nausea, and vomiting and a physical examination that reveals a distended and tympanitic abdomen. Abdominopelvic computed tomography (CT) is diagnostic of cecal volvulus in 90 percent of patients. The remaining 10 percent of cecal volvuli are diagnosed at the time of surgical exploration [7,22,23,25]. Diagnostic evaluation — The diagnostic evaluation starts with an upright abdominal plain film to identify an obstruction or pneumoperitoneum. In patients who have a pneumoperitoneum on plain film, which is indicative of bowel perforation, no further imaging is necessary. Such patients should be prepared for immediate surgery
- Cecal Volvulus Presentation and Diagnosis The clinical presentation of cecal volvulus is directly linked to the acuity of the presentation and the type of volvulus. Cecal volvulus involves the axial clockwise rotation of the colon around its mesentery. Findings such as abdominal distension, pain, nausea, vomiting, and obstipation can mimic signs and symptoms of small bowel obstruction. If the volvulus is allowed to progress to strangulation, then peritonitis and systemic sepsis will ensue. Diagnosis is first suspected by the classic appearance of a dilated colon in the shape of a “coffee bean” with the apex pointing to the left upper quadrant (Figure 40-7). This classic radiographic finding, however, is present in less than 20% of cases [19]. If the diagnosis is in question, a CE can provide clarity by demonstrating the characteristic column of contrast ending in a “bird beak,” the sight of the torsion, in the right upper quadrant. If CE is unavailable or the diagnosis remains in question, a CT scan may be helpful in establishing the diagnosis. CT may reveal the coffee-bean or bird beak signs, as well as the presence and location of the whirl sign [100]. Due to its ready availability, CT is the first imaging test ordered, on initial presentation, often obviating the need for further imaging. Conversely, in cecal bascule there is no axial twist but an anterior-superior folding of the cecum over the proximal ascending colon, without rotation (Figure 40-19). The cecum is often located in the right upper quadrant on imaging [125]. There is no axial twist of the mesentery and thus these patients often present in subacute fashion. Patients present with intermittent nausea, vomiting, and abdominal pain with
- Cecal volvulus is more dicult to rectify via a colonoscope primarily because of an inability to reach the obstructed right colon. ere is also a higher risk of perforation.197 Consequently, surgery is often required.
- The incidence of small bowel volvulus varies not only by country but also by region within certain countries and correlates with lower socioeconomic status.7 These patterns have been attributed to the high-fiber, vegetarian diet consumed in these populations, as well as to the high proportion of laborers and farmers, who tend to eat infrequent, large meals.7,8 An increased incidence of small bowel volvulus has been observed during Ramadan, when Muslims ingest large quantities of high-fiber food after prolonged fasting.
- The underlying cause of primary SBV is poorly understood, and several anatomic and dietary factors have been implicated. Primary SBV in developing nations correlates with lower socioeconomic status, with a vast majority of affected individuals being laborers and farmers. The consumption of large infrequent meals consisting of vegetables and high-fiber along with manual labor in an upright position has been postulated to account for this condition.6–11 SBV has been observed in Afghanistan during the month of Ramadan, when Muslims ingest large quantities of high-fiber food after prolonged fasting.6 De Souza reported 12 cases of primary SBV over a 2-year period in a Ugandan tribe who consumed a large amount of a beer rich in serotonin.25 A recent review from Spain noted an association of primary SBV with diabetic neuropathy and its altered small bowel motility.16 Anatomically, the small bowel in high-risk populations has been observed to have a longer mobile mesentery with a narrower insertion and a lack of mesenteric fat. Patients with SBV in the Eastern countries have firm, muscular abdomens, theoretically limiting the mobility of bowel in the anteroposterior plane. It is thus postulated that females are less often diagnosed with primary SBV in the developing countries, their abdominal wall laxity from childbearing conferring an advantage.8,14,19,20 These observations support a popular theory that rapid filling of a segment of proximal intestine with high-bulk chyme pulls the heavier loops down into the left pelvis where there is little resistance and displaces the empty distal bowel loops upward toward the right upper abdomen, thereby initiating the torsion around the superior mesenteric vessels.13,14,18 In contrast, secondary SBV is caused by predisposing factors, either congenital or acquired, and is more common than primary SBV in North America and Western Europe. In secondary SBV the intestine is twisted around an underlying point of fixation, and as the loop fills with fluid, peristalsis exacerbates the torsion, causing a closed-loop obstruction. By far the most common cause of secondary SBV are postoperative adhesions.4 Case reports have described a number of other lead points, including small bowel and mesenteric tumors,21,26–29 mesenteric lymph nodes,30 Meckel diverticulum,2,23 malrotation,4,23 small intestinal diverticula,21,22 ascariasis,20,31 tuberculous adhesions,20 and stomas.3 In pregnancy, SBV is the second most common cause of small bowel obstruction after adhesions.21,32 In 56% to 80% of cases of primary SBV the intestinal torsion is clockwise, as it is for neonatal midgut volvulus associated with congenital malrotation.8,14 However, congenital malrotation causing volvulus rarely manifests in delayed fashion. Among all patients hospitalized fo
- Theory: rapid filling of a segment of proximal intestine with high-bulk chyme pulls it down into the pelvis and displaces empty distal bowel upward, thereby initiating the torsion. In contrast, secondary small bowel volvulus is much more common than primary small bowel volvulus in the United States. In secondary small bowel volvulus, the intestine is twisted around an underlying point of fixation; as the loop fills with fluid, peristalsis exacerbates the torsion. By far the most common point of fixation is a postoperative adhesion.
- If the patient is hemodynamically stable, short lengths of bowel of questionable viability should be resected and primary anastomosis of the remaining intestine performed If the viability of a large proportion of the intestine is in question, the bowel of uncertain viability should be left intact and the patient reexplored in 24 to 48 hours in a "second-look" operation At that time, definitive resection of nonviable bowel is completed For patients without ischemic bowel, the optimal treatment is less clear. No prospective, randomized studies or even retrospective studies have addressed the issue of recurrence. It is believed that the formation of intraperitoneal adhesions after laparotomy should prevent most recurrences. For patients without ischemic bowel, the optimal surgical treatment is less clear. Most case series describe simple detorsion of the volvulus without resection, although no long-term follow-up is available to determine recurrence rate. To prevent recurrent volvulus, some authors have described bowel resection in the absence of gangrene while others have performed intestinopexy of long segments of bowel. These procedures run the risk of short gut syndrome and increased risk of adhesive bowel obstruction and must be used with caution. No prospective studies have addressed the issue of recurrence. Two series have reported recurrence rates of 3.9% to 5.4% associated with simple detorsion in primary SBV.16,35 The outcome of SBV likely depends on early diagnosis, patient’s age and physiologic status, associated illnesses, presence of infarcted bowel, and time to surgical intervention. Overall mortality in patients undergoing exploration for SBV ranges from 10% to 35%.1 The mortality for SBV with viable bowel ranges from 0% to 26%,2,7,24,25 whereas it can rise to 40% to 100% in cases of gangrenous bowel.6,8,13,20,24,25 Coe et al. in their population-based study from the United States reported an overall mortality of 7.92% (operative and nonoperative cases). If surgery was performed on the day of admission, the mortality was 4.78%, rising to 6.65% if surgical treatment was delayed to the second day of admission
- Less prevalent etiologies for SBO include hernias,malignant bowel obstruction, and Crohn’s disease.
- Such adhesions are the results of a pathological healing response of the peritoneum upon injury, as opposed to the normal “ad integrum” repair . Typical adhesions form after peritoneal injury from abdominal surgery. Other conditions that may cause peritoneal injury resulting in adhesion formation include radiotherapy, endometriosis, inflammation, and local response to tumors. Adhesions from a non-operative etiology are often part of a more complex pathology that can cause chronic pain and complications as the result of adhesions and other mechanisms The operations associated most frequently with adhesive bowel obstruction are those involving the structures in the inframesocolic compartment and especially in the pelvic region, such as colonic, rectal, and gynecologic procedures. Adhesive bowel obstruction may occur at any time postoperatively after a celiotomy, with reports ranging as early as within the first postoperative month to more than eight decades after the index operation.
- There are several factors involved in mechanisms of adhesion formation. Damage to peritoneal surfaces induces a repair response, which consists of an inflammatory process involving fluid, neutrophils, leukocytes, macrophages, cytokines, mesothelial cells, and tissue and coagulation factors [ 7 ]. The inflammatory response results in fibrin deposition at the site of injury within three hours of the tissue trauma and peaking on postoperative day 4 to 5. If complete fibrinolysis and resorption of degradation products subsequently occur, reepithelialization will result in a smooth healed tissue surface. However, if this process is disturbed, connective tissue scars and adhesions develop from in growth of fibroblasts, capillaries, and nerves. Fibrinolysis may be impaired by thermal injury, desiccation, ischemia, foreign bodies, blood, bacteria, and some drugs; genetic polymorphisms may also play a role in the host's inflammatory and healing response.
- Complete obstructions are associated with a 20% -40% incidence of strangulation.
- To date, the most effective means of limiting the number of adhesions is a good surgical technique.
- COLONIC INTUSSUSCEPTION PATHOPHYSIOLOGY Colonic intussusception is a rare diagnosis in adults. This process occurs when a proximal segment of intestine (intussusceptum) invaginates into a distal segment of intestine (intussuscipiens) with 86% to 90% associated with a pathologic lesion as the lead point.1 The exact mechanism of intussusception in adults is not completely understood. It is proposed that the presence of a stimulus in the lumen of the bowel induces constriction of the bowel proximal to the stimulus and relaxation of the bowel wall distally allowing for invagination of the proximal segment. Intussusception is categorized into two discrete categories: enteric in which solely the jejunum or ileum are involved, and colonic, which includes ileocolic, colocolonic, and colorectal configurations. Often, the stimulus responsible for intussusception in adults is a gastrointestinal (GI) neoplasm with 56% of colonic intussusceptions attributed to malignancy and approximately 19% of enteric intussusceptions related to malignancy. Benign causes include benign GI neoplasms, adhesive disease, Meckel diverticulum, sprue, human immunodeficiency virus (HIV), or idiopathic intussusception Intussusception is a relatively frequent cause of bowel obstruction in infancy, but it accounts for only 2% of bowel obstruction in the adult population. 34 The median age of presentation in adults with intussusception is the sixth to seventh decade. The etiology of intussusception differs greatly between adult and pediatric patients. In the vast majority of adult intussusceptions, there is a demonstrable inflammatory lesion or a neoplasm that serves as the lead point of the intussusception; however, up to 20% of adult cases are idiopathic. 35 Neoplasms causing intussusception in adults are malignant in almost 50% of patients. Although rare in the Western Hemisphere, intussusception is one of the most common causes of bowel obstruction in central Africa, for reasons not yet fully explained. Intussusception is an "internal prolapse" of the bowel, that leads to obstruction and compromise of mesenteric blood flow, with resultant inflammation and the potential for ischemia of the bowel wall [ 27 ]. This occurs when a mass or lead point in the bowel (intussusceptum) is pulled forward by normal peristalsis, with resultant invagination or telescoping of the bowel wall (intussuscipiens). This leads to obstruction and compromise of mesenteric blood flow, with resultant inflammation and the potential for ischemia of the bowel wall
- An increased incidence of intussusception has been reported in patients with acquired immune deficiency syndrome (AIDS) [ 12,13,28 ]. This is due to the high incidence of infectious and neoplastic conditions of the bowel in AIDS patients, such as lymphoid hyperplasia, Kaposi's sarcoma, and non-Hodgkin's lymphoma.
- Symptoms are often chronic; intermittent abdominal pain is the most common presentation in adults. Other common symptoms are those associated with intermittent partial bowel obstruction and can include nausea, vomiting, melena, weight loss, fever, and constipation Plain abdominal films show small bowel obstruction. The diagnosis is most often made with computed tomography (CT) [ 28 ]. A "target sign" may be seen on CT on perpendicular view, while the intussusception will appear as a sausage shaped mass when the CT beam is parallel to the longitudinal axis. The distended loop of bowel (intussuscipiens) has a thickened wall because it represents two layers of bowel. However, target signs are sometimes seen on CT scans of patients who do not have a clinical presentation indicative of bowel obstruction. In such cases, the finding is of little clinical significance and is probably related to normal peristalsis.
- Because of the high percentage of associated malignancy, radiologic decompression is not appropriate in the adult population and surgical resection using appropriate oncologic techniques is recommended in most cases [ 27 ]. However, if a benign diagnosis has been established preoperatively or the patient is at risk for short bowel syndrome, a combined approach with limited intestinal resections and snare polypectomies is more appropriate.