Intestinal Obstruction

By definition, intestinal obstruction implies the failure of ingesta or intestinal secretions to move in a normal aboral direction [1]. Obstructions are typically classified by their duration, their severity, and their location. Partial or incomplete obstruction is incomplete occlusion of the bowel lumen that allows limited passage of fluid or gas. Complete obstruction is total occlusion of the intestinal lumen, with failure of gas or fluid to pass the point of obstruction. Blockage in the duodenum or upper jejunum constitutes a high intestinal obstruction; blockage in the midjejunal area constitutes a midintestinal obstruction; and blockage in the distal jejunum, ileum, or ileocecal junction constitutes a low intestinal obstruction.

In terms of pathophysiologic changes, obstructions are usually best described as either simple mechanical or strangulating [1]. Simple mechanical obstruction is partial or complete obstruction of the bowel lumen, but the blood supply to the intestinal wall is usually not impaired. Conversely, with strangulation obstruction, the circulation to the involved segment of intestine is impaired, and usually complete obstruction is present.

Etiology of Simple Mechanical Obstruction

The causes of mechanical obstruction can be subdivided into three general categories: intraluminal mechanical obstruction, intramural mechanical obstruction, and extramural mechanical obstruction (Fig. 35-1) [2].

Figure 35.1. Types of mechanical obstruction. A. An intraluminal obstruction caused by a foreign body. B. An intramural obstruction created by neoplasia or granuloma. C. An extra-mural obstruction caused by an extramural mass (top) or kinking of the bowel wall to adhesions (below).

Intraluminal mechanical obstruction 

Intraluminal mechanical obstruction is the most common type in small animals. The oropharyngeal opening is larger than any other orifice in the alimentary tract and foreign bodies such as bones, balls, or corncobs can traverse the esophagus and stomach and become lodged in the smaller-diameter intestine. Large intraluminal foreign bodies often cause signs consistent with complete luminal obstruction, although slow aboral passage of the foreign body may occur. Polypoid intestinal masses or linear foreign bodies such as string may cause partial or incomplete luminal obstruction. In cats, benign adenomatous polyps of the upper duodenum can cause intermittent hematotemesis [3]. The trailing end of linear foreign bodies often becomes anchored over the base of the tongue or in the pyloric antrum. Normal intestinal peristalsis moves the foreign body distally, but because it is fixed proximally the bowel plicates itself along the length of the foreign body [4].

Intramural mechanical obstruction 

Intramural mechanical obstruction is most commonly caused by intestinal wall neoplasia or fungal granulomas. Intestinal neoplasms such as adenocarcinoma, leiomyoma, leiomyosarcoma, fibrosarcoma, and lymphosarcoma commonly invade the muscular layer of the intestinal wall. These tumors not only compromise lumen diameter, they also reduce the pliability of the intestinal wall at that point, reducing its distensibility and likening the occurrence of intussusception. In the Southeastern United States, intestinal granulomas caused by the algae Pythium species, is a common cause of intestinal obstruction. This obligate organism creates mural thickening and fibrosis that interferes with normal intestinal absorption and also prevents normal intestinal distention. Both intestinal neoplasms and fungal granulomas tend to cause incomplete mechanical obstruction. Onset of clinical signs is often delayed or insidious [4].

Extraluminal small intestinal obstruction 

Extraluminal small intestinal obstruction resulting from adhesions is a potential sequel of elective abdominal surgery. Because of this, there is increasing emphasis on minimally invasive laparoscopy techniques in human and veterinary medicine. Most experimental and clinical studies in people found a reduction of adhesions with laparoscopy versus laparotomy [5]. Although adhesions do occur in the dog and cat abdomen following laparotomy, functional obstruction is less common. Studies of intestinal transit times after planned enteroplication techniques for intussusception in dogs have shown that no delay occurs in actual transit time when planned adhesions are created [6]. Clinical signs relating to extraluminal obstruction in small animals are more often a result of compression because of pancreatic abscess or neoplasia or translocation of the bowel through rents in the mesentery or through hernias in the diaphragm, umbilicus, or inguinal or femoral triangle region. These latter translocations usually lead to strangulation obstruction.

Pathophysiology of Mechanical Obstruction

Accumulation of Gas and Fluid

Complete intraluminal mechanical obstruction results in distention of the bowel proximal (oral) to the obstruction, owing to accumulation of gas and fluid (Fig. 35-2). The gas accumulating proximal (oral) to the obstruction consists of swallowed air (72%) and gas formed in the body (28%).1 Of the gas formed in the body, it is estimated that approximately 70% is gas that diffuses from the blood into the bowel lumen, and a smaller percentage (30%) results from intramural decomposition of food material by bacteria. The gas in the distended bowel is composed principally of nitrogen (70%), oxygen (10% to 12%), and hydrogen (1% to 3%), which mimics those percentages seen in atmospheric air. Additionally, small amounts of carbon dioxide (6% to 9%) can be formed from neutralization of bicarbonate in the bowel lumen. Organic gases such as methane (1%) or hydrogen sulfide (1% to 10%) when present are the result of low-level bacterial fermentation [1].

Figure 35.2. The pathophysiology of simple mechanical obstruction associated with an intraluminal foreign body.

Fluid accumulation is a result not only of retention of ingested fluids but also of the significant production of secretions in the upper gastrointestinal tract. It is estimated that a 40 kg dog actually produces in excess of 2100 ml of secretions per day. Most of these secretions are reabsorbed in the lower jejunum and ileum; only an estimated 4% to 1% of the water volume reaches the colon [7]. Water transport in the gut is normally passively regulated, principally by hydrostatic pressure gradients that are created mainly by solute transfer. The intracellular solute pathway that allows passive diffusion between the pores and tight junctions of epithelial cells is controlled by electrochemical, osmotic, and hydrostatic pressure gradients.

During mechanical obstruction, the absorption of water from the gut lumen is reduced by several mechanisms. Transport of solutes through the epithelial cells is impaired, which normally occurs by active transport via sodium ion membrane pumps or brush border membrane carriers. Intraluminal osmolality is usually increased and additive factors such as lymphatic and venous congestion also reduce the absorption of solutes [8]. In addition, intestinal mucosal secretion is increased owing to the cyclic AMP mechanism. Factors believed to contribute to increased secretion and decreased absorption include increased concentration of intraluminal bacterial enterotoxins, increased levels of bile and fatty acids, or products of tissue ischemia [9]. The distended bowel may lose its ability to absorb fluids within 24 hours after onset of obstruction.

Normal intraluminal pressure in the canine small bowel is 2 to 4 mm Hg. It is estimated that normal peristalsis may produce pressures in the range of 15 to 25 mm Hg. Three days after creation of a total obstruction, intraluminal pressure in the small bowel of dogs can be as high as 44 mm Hg [10]. During vomiting it can rise as high as 95 mm Hg. Rapid lymphatic and capillary stasis occurs when intraluminal pressure reaches 30 mm Hg, and total occlusion of venous drainage occurs at 50 mm Hg [9]. Because the arterial supply is not affected, capillary congestion can occur at the microcirculatory level. The increased hydrostatic pressure at the capillary bed level produces a net shift of fluid into the interstitium, resulting in bowel wall edema. Eventually, fluid can shift not only from the bowel wall into the lumen but also through the serosal surface into the peritoneal cavity.

Increases in pressure also cause circulatory impairment of the submucosa and muscular layers of the bowel wall. Early impairment of the villous circulation within the mucosa is seen when the pressure reaches 20 mm Hg. Reductions in mesenteric and submucosal blood flow occur when the intraluminal pressures reach 30 mm Hg. Oxygenation of the intestinal mucosa decreases significantly when the intraluminal pressure exceeds 40 mm Hg. At 44 mm Hg arteriovenous shunting occurs at the mucosal villous base. Therefore, selective mucosal ischemia can follow simple mechanical obstruction if intraluminal pressure rises above 40 mm Hg. Because in naturally occurring mechanical obstruction physiologic pressure probably does not exceed 50 mm Hg, full-thickness devitalization of the wall usually does not occur in the dilated proximal segment [10].

Reduced Motility and Bacterial Overgrowth

The bowel responds to gaseous and fluid distention with periodic bursts of neuromuscular activity, resulting in peristaltic rushes. These wave-like movements begin in the proximal bowel and traverse the entire length of intestine above the point of obstruction. Periods of hyperactivity are then followed by quiescent periods of varying duration. Experimental studies in dogs have shown increased myoelectric activity above the point of obstruction. The intestine distal to the obstruction simultaneously exhibits reduced peristaltic activity. With increased distention from prolonged obstruction, clusters of intense myoelectric activity are felt by the patient as intermittent cramps (colic). It is believed that this phenomenon is largely caused by stimulation of the proximal bowel through cholinergic pathways and by inhibition of the bowel distal to the obstruction through noncholinergic nonadrenergic pathways [11].

Small intestinal stasis may lead to luminal bacterial overgrowth. In normal intestinal mucosa, bacteria and their enterotoxins are not able to cross the mucosal barrier. In the impaired mucosal barrier, a potential exists for increased permeability and migration of bacteria and their toxic products into the systemic circulation or the peritoneal cavity [1]. Decompression of the distention usually allows reversal of the circulatory changes and provides for rapid mucosal regeneration [10]. However, if necrosis of the bowel wall occurs owing to prolonged severe distention or direct pressure from the obstructing object, the mucosal barrier may break down and transmural migration of bacteria and endotoxins beneath the obstructing foreign body may occur.

Level of Obstruction and Electrolyte Loss

The classic clinical signs associated with high (duodenal and proximal jejunal) obstruction are described as frequent vomiting that begins soon after the onset of obstruction. Yet experimental data support the observation that dogs and cats with high intestinal obstruction may not begin vomiting for 24 to 72 hours. Electrolyte loss is closely associated with the level of obstruction. With obstructions at the pylorus, gastric fluids that are rich in potassium, sodium, hydrogen, and chloride ions are vomited. Hypochloremic, hypokalemic, moderately hyponatremic metabolic alkalosis with dehydration may result in early stages [4]. Animals that vomit profusely do not survive as long as those that do not vomit at all [8].

Severe vomiting associated with duodenal and proximal jejunal obstruction causes loss of gastric hydrochloric acid and bicarbonate-rich alkaline pancreatic secretions. Dehydration with mild metabolic acidosis usually results. With continued fluid depletion, progressive hypovolemic shock occurs. The major cause of mortality from upper small-intestinal obstruction is associated with this severe and rapid hypovolemia. Dogs with experimental complete upper intestinal occlusion usually died within 3 or 4 days without crystalloid fluid therapy [8]. Mortality was greatly reduced with parenteral infusion of physiologic saline or lactated Ringer's solution. Experimental reinfusion of vomitus into the dog's bowel below the obstruction was also life saving [8].

With low small-intestinal obstruction, the onset of vomiting may not occur until 2 or 3 days after onset of obstruction and it is often intermittent. The distention usually is gaseous during the initial 24 hours, but thereafter is accompanied by loss of varying quantities of fluid into the bowel lumen. Fluid sequestered in low intestinal obstructions is usually mildly hyperosmotic and similar in composition to plasma. Analysis of intraluminal fluid after experimental low obstruction in dogs reveals a mean level of sodium of 140 mEq/L; of potassium, 16.8 mEq/L; and of albumin, 3.6 mg/dl [8]. The sequestration of these fluids from the upper gastrointestinal tract and the increase in secretion of new fluid electrolytes and protein cause a net loss of these compounds. The intraluminal fluid volume increases as the obstruction persists, although some sequestered fluid may move orally and eventually reach a nondistended loop of bowel, where normal reabsorption occurs. Lethargy and anorexia are often apparent in dogs with low intestinal obstruction. These animals exhibit steady weight loss and drink but do not eat. Dogs with experimentally created complete low intestinal obstructions may survive three weeks or longer if adequate water is provided [9].

Evaluating Intestinal Viability

Intestinal viability is best evaluated after decompressing the dilated loops of bowel and removing the obstruction. In most cases of simple non strangulated obstruction, bowel viability is maintained and the appearance of dark distended loops of bowel improves rapidly after enterotomy and removal of the obstruction. Questionable areas of bowel viability are assessed with standard clinical criteria, including bowel-wall color, presence of arterial pulsations, and presence of intestinal peristalsis. The continued presence of intestinal myoelectric activity is the most important parameter of viability [4]. The pinch test should be performed on questionable areas of intestine, to determine whether smooth muscle contraction and peristalsis can be initiated.

Experimentally, bowel-wall viability has been assessed using temperature probes, pH monitors, Doppler devices, intravenous vital dyes, and surface oximetry. Fluorescein dye given intravenously through a peripheral vein at a dose of 20 mg/kg has been shown to be beneficial in determining intestinal wall (but not gastric wall) viability, particularly if the ischemia is mainly arterial versus venous in origin [10]. The tissues are subjected to 365-nm ultraviolet light (Wood's lamp). Normal bowel wall viability is represented by a bright green glow with smooth, uniform fluorescence. Areas of the bowel are considered viable if they have a normal or fine granular fluorescent pattern. Areas of bowel are considered non viable if they have a patchy density where areas of non fluorescence exceed 3 mm diameter or where only perivascular fluorescence is seen [12]. Pulse oximetry has also been utilized as a feasible technique to evaluate experimental intestinal ischemia in dogs. Dogs with bowel segment values exceeding PO2 of 85% in general survived, whereas those with values lower than this had statistically higher incidence of ischemia and anastomotic breakdown. All anastomoses performed in segments with PO2 values of 60 to 70% failed [13].

Strangulation Obstruction

Causes and Classification

By definition, strangulation obstruction implies an obstructive process with loss of vascular integrity to the bowel wall. Common causes include intussusception, traumatic avulsion of the mesentery, mesenteric arteriothrombosis, mesenteric (intestinal) volvulus, and strangulated diaphragmatic, inguinal, or abdominal hernia. Foreign bodies can also create local small discrete areas of "pressure" strangulation necrosis. Strangulation obstruction may occur secondary to venous obstruction or thrombosis, arterial obstruction or thrombosis, or a combination of both. If the strangulating process incorporates the mesenteric vessels, devitalization of large segments of the intestinal tract may occur. Strangulation obstruction should be considered a medical and surgical emergency. Death is often rapid, the result of hypovolemia and septic shock secondary to devitalization of the intestinal wall.

Pathophysiology

Pathophysiologic changes as described under simple mechanical obstruction occur proximal to the strangulation obstruction in addition to the direct changes attributable to the strangulated bowel segment. Partial venous occlusion, such as that caused by partially strangulated hernia or intussusception, is a common type of intestinal strangulation in small animals. With venous occlusion alone, the arterial supply remains intact, allowing bowel-wall edema and sequestration of blood in the intestinal wall. Motility changes in the bowel wall are proportional to the duration of venous obstruction. Spike activity and motility of the affected bowel segment may be initially increased. As tissue hypoxia progresses, cyanosis becomes evident and motility gradually decreases until it ceases completely.

With complete venous occlusion or thrombosis, wall edema, hemorrhage, and mucosal epithelial sloughing can occur as early as 1 to 3 hours after the insult. The strangulated loop then gradually becomes more turgid, and whole blood begins accumulating in the bowel lumen and extravasating into the peritoneal cavity (Fig. 35-3). The bowel wall becomes visibly thickened and dark red to blue. Eight to 12 hours after complete venous occlusion the bowel segment turns black and distends maximally. When complete arterial occlusion occurs, as with mesenteric volvulus, full-thickness ischemia of the bowel wall occurs and bacteria and red cells invade all layers of the wall within 20 hours of strangulation.

Figure 35.3. The pathophysiology of strangulation obstruction associated with intestinal volvulus.

Translocation of Bacteria

The flora in the proximal small bowel consists primarily of gram-positive, facultative bacteria, whereas the distal small intestine contains primarily aerobic coliforms and anaerobic species. Organisms that are normally found in the terminal intestine, move to upper levels of the small intestine. Marked increases in aerobic coliform bacteria and Streptococcus species occur, in addition to large increases in anaerobic Clostridia and Bacillus species. Small intestinal bacterial concentrations that normally range from 102 to 104 per milliliter liquid secretion may increase to 108 to 1011 per milliliter within just 6 hours after the onset of strangulation [14]. A massive proliferation of resident bacteria also occurs within the strangulated section of bowel. Bacteria, particularly Clostridium perfringens, play a key role in the mortality of strangulation obstruction because germ-free animals live significantly longer than those with normal intestinal flora in experimental models.

Loss of mucosal function leads to passage of viable bacteria or endotoxins through the epithelial mucosa into the lamina propria and then to the intra-abdominal cavity and systemic circulation. Bacterial translocation does occur in simple mechanical obstruction of the small bowel or colon. In strangulation obstruction, the loss of gut barrier function occurs more severely compared with simple obstruction because the ischemia promotes the rapid destruction of the intestinal epithelium. Three mechanisms that promote bacterial translocation have been identified:

1. Intestinal bacterial overgrowth;
2. Increased permeability of the intestinal mucosal barrier; and
3. Deficiencies in host immune defenses [14].

Clinical Presentation

Clinically, free peritoneal fluid begins to accumulate shortly after the development of strangulation obstruction. Initially, the fluid is a transudate resulting from effusion from serosal vessels secondary to venous congestion or obstruction. The initial fluid is pink, clear, and odorless, and relatively low in protein. As the length of time of strangulation obstruction increases, the appearance of the fluid changes: it becomes black and has a foul odor. This is thought to be caused by filtration of lumen contents through the devitalized bowel wall [14]. After prolonged strangulation obstruction, hypoxia in the intestinal wall results in complete breakdown of the mucosal barrier. With arterial thrombosis, full-thickness necrosis occurs, as does perforation and septic peritonitis, with resultant inflammatory cells, ingesta, and bacteria.

Many experimental and clinical studies have independently proposed the hypothesis that the loss of gut barrier function and the consequent translocation of bacteria and their products may play an important role in the development of multiple organ failure (MOF) in strangulation obstruction. Evidence is growing that loss of gut barrier function to bacteria and or "endotoxins" might induce a local intestinal inflammatory response and lead to the subsequent release of cytokines (TNF, IL-1, 1L-6, IL-8, etc.) [15]. Strangulation obstruction has been shown to cause increased release of IL-6 to intestinal venous blood in pigs [16].

Plasma lactate has been shown to be of value in the diagnosis of gastrointestinal ischemia. In dogs with GDV, serum lactate values of more than 6 mm/L have been shown to be a positive predictor of gastric necrosis [17]. Likewise, peritoneal lactate levels in dogs with experimentally induced ischemia of the small intestine were found to be highly predictive for intestinal ischemia in these animals [18].

Treatment

Treatment for strangulated intestinal obstruction involves not only fluid and electrolyte support but also aggressive antibiotic therapy, and possibly nonsteroidal anti-inflammatory drugs. If massive blood loss has taken place, blood transfusions may also be warranted. Early surgical removal of the devitalized section of bowel wall is essential. In experimental models of strangulated obstruction in dogs, death is delayed by the administration of broad-spectrum systemic antibiotics, particularly the aminoglycoside derivatives in combination with penicillins and metronidazole or third-generation cephalosporins.

Intestinal Pseudo-obstruction

Chronic intestinal pseudo-obstruction is a syndrome, originally described in humans, characterized by chronic or recurrent symptoms of intestinal obstruction. The obstruction occurs in the absence of both organic luminal obstruction and a recognized underlying disease. Although previously limited to the human literature, the disease syndrome has been described in two dogs and a cat [19-21]. Clinical manifestations result from delayed intestinal transit caused by disordered motility. Although all portions of the alimentary tract can be affected, the small bowel is most often involved. In some cases of pseudo-obstruction no pathologic abnormality can be found. In other cases, histologic examination has shown two distinct pathologic abnormalities. In humans, one pathologic subtype includes direct degeneration of intramural neurons, which are specifically associated with arrangement of the myenteric plexus, the celiac ganglion, the spinal cord, and even the brain. This type of chronic pseudo-obstruction has been labeled "visceral neuropathy". The second type of idiopathic intestinal pseudo-obstruction is caused by degeneration of intestinal smooth muscle cells -- so-called visceral myopathy. Histologic sections of bowel of this type have shown vacuolization of the smooth muscle and atrophy of muscle fibers in both the longitudinal and circular muscle layers of the bowel wall. All affected animals had chronic vomiting and weight loss with concurrent dilatation of the small intestine. In a mixed breed dog, atrophy of cecal smooth muscle fibers as well as infiltration of plasma cell lymphocytes and macrophages and mild lymphoplasmacytic enteritis were present [19]. In an English bulldog, both atrophy and fibrosis with monocellular infiltrate were noted from the duodenum to the colon [20]. In a cat, a regional jejunal area also displayed marked atrophy of the outer longitudinal muscular layer along with fibroplasia and vacuolar degeneration consistent with visceral myopathy in humans [21]. Clinical signs of idiopathic intestinal pseudo-obstruction in man include abdominal pain, constipation, diarrhea, and vomiting. In the acute stages, abdominal distention may occur. Surgery is usually avoided if possible; it is rarely beneficial. Stimulation of the gastrointestinal smooth muscle by prokinetic agents such as metoclopramide or cisapride might be helpful, as might nutritional support, in the form of enteral hyperalimentation. Results of surgery in animals have been similarly unsuccessful.