28 terms

Bowel Obstruction


Terms in this set (...)

History of crampy abdominal pain relieved by emesis and a previous abdominal surgery - DD?
Small-bowel obstruction (SBO) until proven otherwise. Other possibilities include adynamic ileus, large-bowel obstruction (LBO), volvulus, gastroenteritis, pancreatitis, and mesenteric vascular occlusion.
Most common causes of SBO
In adults, postoperative adhesions are the most common cause of SBO, producing up to two thirds of cases (26% to 64%); next are incarcerated hernia (6% to 21%) and neoplasms. Inflammatory bowel disease, diverticulitis, gallstone ileus, and bezoars are other less common causes of SBO.
What are the three most salient features of SBO on history, and why is it important to recognize them?
history of abdominal pain, obstipation, and emesis typify SBO. More frequently than not the diagnosis must be made by history alone because the physical examination and laboratory tests are not diagnostic.
Why is testing for blood in stools important?
Heme-positive stool may be an early indication of ischemic bowel. The mucosal layer of the bowel wall is most susceptible to ischemia and may bleed before full-thickness bowel injury occurs. Also, in elderly patients, one should keep in mind cancer as a possible cause of bowel obstruction.
What is the significance of the quality of the bowel sounds?
In the early period of obstruction, peristalsis is increased, and hyperactive bowel sounds can be heard as the intestines attempt to overcome the obstruction. As the bowel distends, reflex inhibition of bowel motility results in a quiet abdomen. The quality of the bowel sounds does not help in differentiating between a partial and a complete obstruction.
What are the most common physical findings associated with SBO?
Dehydration (e.g., low-grade fever, dry skin turgor or mucosa, tachycardia). Other than distention, the abdominal examination is most commonly equivocal (i.e., moderate subjective discomfort upon palpation without a bona fide tenderness or rebound).
Why does SBO not usually produce significant abdominal tenderness? How is this related to the pathophysiology of SBO?
Regardless of the cause, SBO results in either (a) simple distal intestinal obstruction with proximal distention and no vascular compromise or (b) strangulation of bowel or closed-loop intestinal obstruction. The consequences of intestinal obstruction and distention are decreased luminal fluid resorption and increased intraluminal fluid secretion (e.g., intestinal distention, nausea, emesis), overall fluid and electrolyte abnormality from fluid shifting into the interstitial third space, and dehydration, and luminal fluid stasis and overgrowth of bacteria (i.e., foul-smelling vomitus). Intestinal obstruction and proximal distention alone cause crampy abdominal pain. Mesenteric vascular occlusion due to strangulation or closed-loop bowel ischemia causes significant pain but not the same degree of tenderness.
Increasing pain in SBO. Should we wait for peritonitis?
It is critically important that severe and increasing abdominal pain, even without significant tenderness, is treated surgically. Waiting for signs of peritonitis such as abdominal tenderness, rebound tenderness, or systemic signs of inflammation (e.g., fever or increased leukocyte count) leads to catastrophic delay, as these signs portend that the ischemic bowel may have already progressed to necrosis or perforation
How does a physician decide whether the patient is a candidate for surgery?
The decision to operate depends on the index of suspicion for bowel strangulation, closed-loop obstruction, and ischemic bowel. It is difficult to make the diagnosis of strangulation and ischemic bowel with just history and physical examination.
Clearly, abdominal pain associated with fever, leukocytosis, acidosis, peritoneal sign, and shock are all indications of bowel necrosis and necessitate surgical exploration. Generally speaking, even in the absence of these physical signs, unrelenting and increasing abdominal pain with obstipation and radiographic signs of SBO indicate surgery. Unless there are extenuating circumstances to the contrary, complete bowel obstruction should not be dismissed without exploratory surgery.
Which laboratory abnormalities are anticipated?
Signs of dehydration from emesis and shifting of fluid into the third space are common, such as mildly elevated hematocrit and normal or upper normal white blood cell count. Blood chemistries may show prerenal azotemia (blood urea nitrogen-creatinine ratio [BUN-Cr] above 20) and hypochloremic, hypokalemic metabolic alkalosis from ongoing emesis of acidic gastric juice.
What are the salient features of SBO on the kidney, ureter, and bladder and upright abdominal radiographs?
Radiographic examination of a patient with SBO indicates (a) multiple loops of distended small bowel in a stepladder pattern, which (b) layer out on the upright film showing air-fluid levels, and (c) absence of colonic air or stool. Other findings, such as free air under the right diaphragm from bowel perforation, are looked for as part of the routine radiographic evaluation.
Is it possible for the abdominal radiographs of SBO not to show any air-fluid levels?
Yes. Sometimes early in the course of SBO, effective emesis and relief of intraluminal fluid can give a normal-appearing bowel gas pattern. Also, completely fluid-filled loops of bowel can give a ground glass appearance on radiograph without the air-fluid levels.
What is the significance of loops of distended small bowel and air in the colon and rectum if they are visible on abdominal radiographs?
Raise the possibility of adynamic ileus or partial SBO.
If the abdominal radiographs show loops of distended small bowel, distended cecum, and colon up to the descending colon, yet no rectal air or stool, what is the significance?
The possibility of LBO increases in the differential diagnosis. However, colonic air does not rule out SBO because colonic air is sometimes seen in the early phase of SBO.
What are the causes of LBO?
Sigmoid or cecal volvulus, obstructive colon cancer, obstruction from inflammatory reactions to diverticulitis or ulcerative colitis, fecal impaction or foreign body obstruction, sliding hernia, intraperitoneal adhesions (e.g., postsurgical adhesions, endometriosis). Children face a host of congenital problems, such as Hirschsprung's disease, imperforate anus, and meconium ileus.
Workup for LBO?
In addition to review of history, workup includes rectal examination and proctosigmoidoscopy to look for distal rectosigmoid disease. If the distal segment is normal in the presence of LBO, barium enema or colonoscopy is helpful to determine the more proximal colonic lesions.
Treatments for Large-Bowel Obstruction?
The treatments must achieve two therapeutic goals: relieving the obstruction and addressing the underlying problem. For example, in the case of a septic and metabolically deranged patient with obstructive colon cancer, the obstruction can be dealt with by placing a diverting colostomy proximal to the point of obstruction, and the definitive resection may be performed as a second procedure. Or, if the bowel preparation status and the patient's physiologic state are optimal, the cancerous segment may be resected and a primary anastomosis performed. A complete knowledge of the entire colon is necessary before beginning any definitive treatment for obstructive colon cancer. In cecal volvulus, on the other hand, the bowel may simply be untwisted and cecopexy performed. The management of LBO is very different from that of SBO, thus it is important to distinguish the two.
What is the difference between complete and partial SBO?
Partial SBO is distinguished from complete SBO by passage of flatus through the rectum and radiographic presence of air or stool in the colon despite the loops of distended small bowel. These indicate partial blockage of the intestines, allowing distal passage of some air and fluid.
Complete SBO is associated with a significant risk of strangulation and bowel ischemia. The incidence of necrotic bowel in patients with complete SBO has been reported to be as high as 30% (3). Patients with partial obstruction have a much lower incidence of ischemic complications. Accordingly, partial SBO may be treated conservatively, whereas a complete SBO requires timely operative intervention.
Does complete SBO always require operation?
Complete SBO does not always require operation. For patients who have had multiple episodes of SBO and who have been successfully managed without operation, it may be worthwhile to try an initial period of conservative management with nasogastric decompression. In such patients, proceed to surgery if pain becomes worse or if obstipation continues for 3 or 4 days without clinical progress. Generally speaking, however, the maxim "do not let the sun set or rise on bowel obstruction" holds true for complete SBO.
How accurate are the various radiographic studies in diagnosing SBO?
The overall sensitivity of plain abdominal radiograph is only 66%. Low-grade SBO can be interpreted as normal 21% of the time. Only 13% of complete SBO is interpreted as "definite SBO."
Barium enteroclysis is very accurate. Enteroclysis has a sensitivity of 100% and specificity of 88%. It can also predict the distance and etiology of obstruction in 86% to 88% of patients.
Abdominal CT scan appears to be more inconsistent in terms of accuracy. There have been reports touting that its accuracy is as high as 90%. For high-grade or complete SBO, the sensitivity may be as high as 88%. But for a low-grade SBO, the sensitivity is as low as 48%. Overall, the accuracy has been found to be as low as 66%, with sensitivity of 68% and specificity of 78%.
Considering such inconsistent accuracy with abdominal CT alone, some have advocated the use of CT enteroclysis with the oral contrast infused directly into the intestines through a long NGT. CT enteroclysis is suggested to have an accuracy as high as the barium enteroclysis with the added benefits of visualizing closed loop obstructions and localizing the lesions in a three-dimensional map, a piece of information helpful to a laparoscopic surgeon
What should the surgeon seek during exploration?
First, the cause of obstruction should be determined. Most commonly, it is due to surgical adhesions. If that is not the case, the physician should search for other causes, such as hernias or neoplasms.
Second, the point of obstruction should be determined. This is the point at which the proximal dilated bowel collapses distally. Sometimes the transition zone is abrupt, as in the case of kinking or twisting, but it can spread over a segment, at which point the cause may be less certain. The possibility of multiple points and closed-loop obstruction must be entertained and ruled out. The entire bowel must be visualized.
Third, evidence of bowel necrosis must be evaluated.
How can viable bowel be distinguished from the nonviable segment?
Although the pink peristaltic bowel is obviously viable and the bluish-black necrotic bowel is easily recognized to be nonviable, it can be difficult to distinguish ischemia from necrosis. The presence of peristalsis, the color of the bowel, and vigorous bleeding from cut edges are all clinical clues of viability. Intraoperative Doppler examination, fluorescein staining, and monitoring of the myoelectric activity of the bowel are all tests aimed at making the recognition of viable bowel easier. When bowel viability is questionable, the bowel may be left in place and the patient taken back to the operating room 12 to 24 hours later for a second look
Do biosynthetic products reduce the chance of adhesion formation?
The use of hyaluronic acid-carboxymethylcellulose membrane (Seprafilm) reduces the severity of dense adhesions following abdominal and pelvic surgeries. Theoretically, this would minimize the future occurrence of SBO. Wide adoption of these "anti-adhesion" products has not been the case, however. The product is expensive, and usually between 4 to 10 units of application are required.
There has been some question as to whether an anti-adhesion product increases the infectious complications. In a large prospective randomized trial, the product was found to be safe with respect to abscess formation; however, fistula and peritonitis occurred more frequently in the group using the product.
Finally, there is no long-term data on the reduction of the incidence of future bowel obstruction. This remains an area of controversy with divergent opinions among experts
What are possible complications following surgery for SBO?
Recurrence, postischemic bowel stenosis, and other postsurgical complications such as wound infection, atelectasis, pneumonia, and urinary tract infection may follow surgery for SBO.
What is the incidence of recurrent SBO after the first episode from postsurgical adhesions is treated by celiotomy and lysis of adhesions?
The recurrence rate is probably 10% to 15%, which is higher than the incidence of the first episode.
What is the incidence of developing the first episode of SBO after an initial abdominal surgery?
Over a lifetime, the incidence of developing SBO following abdominal surgery is approximately 5%.
What is the risk of mortality from surgery for SBO?
The risk of mortality depends on the patient's comorbid factors (e.g., age, cardiopulmonary status); the preoperative hemodynamic and electrolyte derangement; and the extent of bowel ischemia, necrosis, and sepsis. Surgical mortality from uncomplicated SBO in a relatively healthy patient is less than 1%. Mortality from complicated septic SBO in compromised patients, on the other hand, can be much, much higher, such that the overall mortality from surgical decompression of SBO averages 9% to 13%.
ABG interpretation:
PO2, 75 mm Hg; PCO2, 46 mm Hg; pH, 7.48; bicarbonate, 33 mEq
Metabolic alkalosis. This is a common sequela in a postsurgical patient who undergoes vigorous diuresis, losing both salt and water. Sodium is lost in the proximal tubule, much of which is resorbed in the distal tubule. Resorption of sodium in the distal tubule is counterbalanced by active excretion of hydrogen, which leads to acidic urine and metabolic alkalosis. The treatment is to decrease the diuretic dose, infuse saline as appropriate for the overall goal of volume status, and supplement potassium.