Diaa M. El-Mowafi Associate Professor, Obstetrics and GynaecologyDepartment of Obstetrics and Gynecology, Benha Faculty of MedicineLecturer and Researcher, Wayne State University, Detroit, Michigan, USAFellow, Geneva University, Switzerland
Michael P. DiamondProfessor and DirectorDivision of Reproductive Endocrinology and Infertility, Department of Obstetrics and GynecologyWayne State University, Detroit, Michigan, USA
Intestinal obstruction is a broad term, which entails cessation of the normal progression of the intestinal contents. Intestinal obstruction can be segregated into complete and incomplete blockage, and be due to mechanical or functional etiologies.
Mechanical obstruction is a term usually applied when there is an actual physical barrier blocking the intestinal lumen, such as bands of adhesion, strangulated hernias, and pressure from pelvic tumors. In contrast, adynamic ileus is used to describe disorders of propulsive motility of the bowel.
Mechanical Intestinal Obstruction
Intestinal obstruction is one of the more common and potentially fatal complications following gynecologic surgery. Forty years ago, mortality rate of 40% to 60% was not uncommon. Currently, the mortality rate has decreased but is still between 10% to 20% for all patients with obstruction of the small intestine.1
Adhesions, usually secondary to previous surgical procedures, are the most common cause of intestinal obstructions in the United States, and are responsible for 49% to 74% of small bowel obstruction in industrial countries.2 Menzies and Ellis3 reported that 93% of 210 patients who had previously undergone abdominal operations had substantial peritoneal adhesions at the time of reoperation. Gynecologic procedures, appendectomies, and other intestinal operations are the three most common type of surgical procedures performed before these occurrences.4,5 Lo et al,6 in 1966, reported a series in which 21% of patients with small bowel obstruction secondary to adhesions have had some form of gynecologic surgery. Melody,7 in 1957, reported that abdominal hysterectomy is the most common operation, which was associated with postoperative intestinal obstruction among 487 gynecological surgeries. In 1983, Ratcliff et al.,15 reviewed 59 cases of admitted women who underwent exploratory laparotomy for relief of small bowel obstruction. They found that 49 patients (83%) had previous abdominal surgery. Of these 49 patients, 38 (78%) had some type of obstetric or gynecologic abdominal procedure, of which 33 of the 49 (67%) had previously undergone a total abdominal hysterectomy.
In 1994, Monk et al.,8 reported that postoperative adhesions occur in 60% to 90% of patients undergoing major gynecologic surgery. The incidence of adhesion-related intestinal obstruction after gynecologic surgery for benign conditions without hysterectomy was approximately 0.3%, increased to 2% to 3% among patients who underwent hysterectomy, and was as high as 5% if a radical hysterectomy was performed.
ADYNAMIC ILEUS
Some degree of adynamic ileus occurs after any intra-abdominal operation as well as in association with nearly all cases of intra-abdominal inflammation. The recovery of motor function of the intestines depends on many factors, including the length of the operation, the extent of handling of the bowel, the degree of chemical and bacterial peritonitis, and the underlying disease. After abdominal operations the patient usually feels hungry and passes flatus within the first three postoperative days. If the patient is not interested in eating, denies flatus and the abdomen is distended and has inaudible intestinal sounds, further diagnostic procedure may be called for. Radiography of adynamic ileus shows distention of both the small and large bowel, with scattered air-fluid levels.
The treatment consists of correction of any electrolyte imbalance, if present, as low serum potassium or sodium as well as hypomagnesemia and severe protein depletion can cause bowel atony. Ambulation, systemic and localized intestinal stimulation by rectal suppositories may be helpful. Otherwise, nasogastric intubation for decompression may be needed.1
PATHOPHYSIOLOGY OF INTESTINAL OBSTRUCTION
Obstruction of the small intestine causes collection of intestinal contents proximal to the obstruction leading to intestinal distention. Swallowed air, that represents over 70% of the air in the gastrointestinal tract, increases this distention. Because the veins and arteries enter the intestinal wall tangentially, the tension on them increases rapidly with distention. The veins, having the lower pressure, show the effect of the increase in tension first. As they are stretched, resistance in them increases, and flow slows down. Fluid rich in protein and salt begins to exude from the capillaries resulting in edema. Intraluminal fluid accumulation increases from both active secretion and decreased absorption. Subsequently, blood cells begin to escape from the capillaries, venous flow finally stops, and as arterial flow continues, blood accumulates in the wall and in the lumen of the bowel. If this process continues unabated gangrene occurs, intestinal integrity is lost and peritonitis quickly follows.1 Importantly, even in the absence of food and liquid ingestion, the volume within the gastrointestinal tract may continue to expand. The total volume of daily secretions into the normal gastrointestinal tract is estimated to be about 10 liters. As much as 7-8 liters of fluid can easily be sequestered in the bowel with intestinal obstruction.
Stagnant bowel contents in a distended loop of ileum show an increase in the number of bacteria. As long as the mucosa is intact and viable, the bacteria are harmless; however, increased intraluminal pressure for a sustained period will produce patchy areas of necrosis that allow some of the intestinal contents to escape into the peritoneal cavity. The main avenue of sepsis from intestinal obstruction is absorption from the peritoneal cavity and not the venous and lymphatic system.9
PATHOPHYSIOLOGY OF ADHESION FORMATION
Following peritoneal injury, the microvasculature beneath the mesothelium becomes disrupted. This is followed by extravasation of serum and cellular elements. Within 3 hours, this proteinaceous fluid coagulates, producing fibrinous bands between abutting surfaces.10 Twelve hours later; polymorphonuclear cells are entangled in fibrin strands, which are subsequently replaced with a macrophage infiltrate. By 48 hours after peritoneal injury, the wound surface is covered with a layer of macrophages.8 In normal peritoneal healing, the fibrinolytic system is triggered to lyse these fibrinous strands within 72 hours of the insult. Within the initial 5 days, re-epithelization of the peritoneal injury occurs. Interestingly, it appears that centripetal growth from the margin of peritoneal wounds contributes little to the healing p; the new mesothelium is derived from the metaplasia of subperitoneal perivascular connective tissue cells that resemble primitive mesenchymal cells.11 Disruption of the existing equilibrium between fibrin deposition and fibrinolysis leads to persistence of the fibrinous strands, which then becomes infiltrated by proliferating fibrobiasts. Subsequently, vascularization and cellular ingrowth occur, and an adhesion is created.10
During mesothelial repair, macrophages and lymphocytes produce growth factors that modulate fibroblast proliferation and collagen synthesis, including platelet-derived growth factor, transforming growth factor-b , fibroblast growth factor, epidermal growth factor, interleukin-l, and tumor necrosis factor-a .12,13 Prostaglandins, particularly prostaglandin E2, are also involved in normal and abnormal mesothelial repair,14,15 most likely through a separate mechanism not related to fibroblast proliferation.16
Adequate blood supply is critical for normal fibrinolysis to occur. Peritoneal injurischemia interferes with fibrinolysis and leads to organization rather than resolution of the fibrin-cellular matrix.8 Ischemia may also induce adhesion formation by stimulating the growth of blood vessels form a non-ischemic to an ischemic site.17 Ischemia may result from excessive handling, crushing, ligating, suturing, cauterizing, or stripping of the peritoneum.
Foreign body reaction causes excessive formation of the fibrin coagulum that stimulates the development of adhesions. Common foreign bodies include sutures as well as cornstarch powder and lint from drapes, caps, gown, masks, and laparotomy pads. It is interesting that foreign bodies in the absence of peritoneal injury are an infrequent cause of adhesion formation.17
The presence of intraperitoneal blood has also been proposed to play a role in adhesion formation, although its actual contribution is not clear. However, free blood in the peritoneal cavity generally does not lead to adhesions, except in the presence of tissue ischemia.19
Infection may result in the development of adhesions by causing the release of proteolytic enzymes, which lead to ischemia and tissue damage, resulting in the formation of adhesions.5
In summary, ischemia seems to play the central role in adhesions formation and factors that compromise blood flow within the area of tissue injury lead to the development of adhesions. Thermal injury,20,21 infection,22 foreign body reaction,22,23 radiation induced endarteritis,24 and impairment of the fibrinolytic activity, all probably act via inducing ischemia to enhance adhesion formation. The thermal effect on adhesion formation called the question about optimal method to achieve hemostasis; is it cautery or sutures as both are incriminated in the etiology of development of adhesions.
DIAGNOSIS OF INTESTINAL OBSTRUCTION
The initial symptom of intestinal obstruction is sudden onset of crampy abdominal pain. This pain is intermittent, with intervals devoid of it which are longer than the periods of pain. The pain is classically periumbilical for a midgut obstruction. Vomiting may accompany the onset of pain with the possibility of recurrence if obstruction persists.
Inspection of the abdomen usually shows distention in persistent obstruction. Loops of intestine with visible peristalsis may be seen beneath the abdominal wall in the very thin patient. High-pitched, tinkling, or metallic intestinal sounds are characteristic of obstruction and occasionally can be heard without a stethoscope. These sounds represent the existence of the air-fluid interface. Motility with violent bursts of peristalsis occurs proximal to the obstruction. The duration of quiet intervals between bursts of peristalsis may suggest the level of obstruction; in high obstruction the time may be 3 to 5 minutes, whereas in low obstruction it may be 10 to 15 minutes.1 Palpation in the early stage of the disease may disclose no tenderness. As distention progresses, it is usual to find tenderness over the point of obstruction.
X-ray study demonstrating distended loop(s) of intestine with air-fluid levels, is suggestive of a mechanical obstruction, whereas grossly dilated loops of small bowel with gas in the colon is typically found is adynamic ileus.7 Computed tomography (CT) was used recently to diagnose postoperative intestinal obstruction due to adhesions.25 The CT findings that suggest strangulated obstruction are serrated beaks, mesenteric edema or vascular engorgement, and moderate to severe bowel wall thickening. In contrast, simple obstruction could be assumed when the beak is smooth, there are no mesenteric changes, and the bowel wall is normal or mildly thickened.
PERITONEAL CLOSURE AND ADHESIVE INTESTINAL OBSTRUCTION
Suturing the parietal peritoneum of the anterior abdominal wall at completion of gynecologic and obstetric surgery was always a tradition. Intuitive logic suggests that it will be of benefit to re-establish normal anatomical relationships and to prevent adhesion formation between the intestines and/or uterus and fascia. However, data supporting this hypothesis is lacking, and in fact it may be incorrect. Importantly, reperitonalization also places pelvic and abdominal contents within the abdominal cavity, and possibly makes fascial closure easier.
The microscopic cellular studies in animals have demonstrated that the broad peritoneal repairative process is different from that of the edge-to-edge skin cicatrization.26 When left undisturbed, peritoneal defects demonstrate mesothelial integrity (reperitonization) by 48 hours and complete indistinguishable healing i.e. without scaring can be achieved by 5 days.27, 28
Adhesions are caused by ischemia, inflammation, and infection rather than by open surfaces. Re-approximation of peritoneal edges or repair of defects via grafts, even with suture material considered to be minimally reactive, results in increased tissue ischemia and foreign-body tissue reaction, and may lead to increased adhesion formation at the site of reperitonization.29
Pietrantini and co-workers30 compared 127 patient in whom the peritoneum was left unsutured after cesarean section with another 121 patients in whom it had been closed with a continuous 000 polyglactin suture. There were no postoperative differences between the two groups regarding the incidence of wound infection, dehiscence, endometritis, ileus, and length of hospital stay. They concluded that peritoneal closure at cesarean delivery provides no postoperative benefits, while unnecessarily lengthening surgical time, anesthesia exposure, and increasing patient costs. Finally, they advocated the elimination of closure of the parietal peritoneum from cesarean technique. However, they did actually evaluate the issue of the frequency of adhesion development as a function of peritoneal closure.
Hull and Yarner31 extended this modality to non-closure of the visceral and parietal peritoneum during lower segment cesarean section. In their randomized study on 113 patients, 59 patient were assigned to closure of both the visceral and parietal peritoneum with absorbable suture. The other 51 patients were left with no peritoneal closure. The incidence of postoperative fever, endometritis, or wound infection was not different between the two groups. The numbers of oral analgesic doses was significantly greater with closure of the peritoneum than without. The frequency with which postoperative lieus was diagnosed in each group was similar. Bowel stimulants were administered more frequently to the closure than to the non-closure patients. The average operating time was shorter for the open group than for the closure one.
Stricker et al32 reviewed 100 cases of female intestinal obstruction where they found that postoperative adhesions was the most common cause being present (59%). Fifty-six percent of those patients had a prior gynecologic surgery, most commonly abdominal hysterectomy. From 11 patients who had records from their previous operation, 9 patients had peritoneal closure; among these patients adhesions were found always to the site of reperitonization. In the 2 patients iwhom the peritoneum was left open, the adhesions causing the obstruction were found away form the site of reperitonization. In their study, Tulandi and others33 confirmed that non-closure of the parietal peritoneum after gynecologic surgery, as compared to closure using chromic cut gut suture did not increase adhesion formation found at second-look laparoscopy
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