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Intra-Abdominal Conditions Causing Colic: How They Alter Normal Physiology and Why They Result in Pain
N.A. White
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Take Home Message
The clinical signs created by intestinal injury from obstruction, strangulation, enteritis or peritonitis are manifest from intestinal distention, perfusion alterations, entry of bacteria into the systemic circulation, third space accumulation of fluid or blood and release of inflammatory mediators, all of which create local and systemic cellular dysfunction. Though all types of acute abdominal disease can cause similar clinical signs, each disease classification creates specific changes that can help the clinician diagnose the problem and select appropriate treatment.
The pathophysiologic events that take place during an acute abdominal crisis include intestinal distension, intestinal ischemia, alterations in tissue perfusion and dysfunction of the intestinal epithelium, serosal mesothelium, smooth muscle and enteric nervous system. The classic pathological degeneration is initiated early in the disease by changes in the microvascular permeability, endothelial cell changes, neuron response, and neutrophil activation.1 Cell injury due to microorganisms invading the mucosa initiates enteritis by both local and systemic inflammatory reactions.
Cellular injury was once characterized by the morphologic change it caused. The new paradigm includes cellular responses, which are as much functional as it is structural. The response to a stimulus such as stretch receptors or ischemia is mediated by numerous autocrine and paracrine messengers, which include cytokines, chemokines, prostaglandins, neuropeptides, and proinflammatory substances such as interleukins, tumor necrosis factor (TNFα) complement, histamine, bradykinin, serotonin, and interferon.2 Inflammatory responses to these intercellular messengers are promoted by mucosal cells, fibrocytes, macrophages, mast cells, endothelial cells, neurons, muscle cells and polymorphonuclear cells.2
Though the primary site of intestine injury or dysfunction may create pain and changes in intestinal function, it is clear that there is a systemic cascade of events promoted by inflammatory mediators, which also create clinical signs attributed to an acute abdomen. An understanding of these physiologic and morphologic alterations helps the clinician determine the type of disease, severity, and possible treatments.
Simple Colic
Little is known about the simple colic (often described as “spasmodic colic” or “gas colic”), which makes up as much as 80-85% of colic in horses. Intestinal function is abnormal either due to adynamic ileus or spasm. Gas accumulation is often detected. The pathophysiologic events are not well understood because research to detect intestinal or systemic responses is difficult in these cases, which readily respond to treatment. It is likely that though the intestine does not appear to be injured to the degree detected with obstruction, strangulation or enteritis, the resulting dysfunction appears to create responses with mediators such as prostaglandins. A wide range of signs including heart rate and dehydration can be seen, but lack of change in the blood or peritoneal fluid values suggest that abnormal cell function rather than cell injury is responsible for the clinical signs seen with this type of colic.
Simple Obstruction
Small Intestine
In the small intestine, obstruction of the intestinal lumen usually is due to intraluminal blockage from a dehydrated food mass or extraluminal pressure from adhesions, thickening of the intestinal wall or infection. The immediate response to a physical obstruction is increased motility of the segment of bowel oral (proximal) to the blockage and relaxation of the intestine aboral (distal) to the blockage. The muscular activity of the intestine is increased around the obstruction, increasing intraluminal pressure in this segment of intestine. Distension of the intestine stretches the wall of the intestine and combines with the reflex muscular spasm to initiate colic. Adynamic ileus may cause functional obstruction due to lack of intestinal movement. Though there is not physical blockage, the lack of intestine movement allows accumulation of fluid and gas creating a similar increase in intraluminal pressure with subsequent changes in the intestinal wall.
When the small intestine is obstructed, the enterosystemic circulation of fluid is blocked so that fluid from saliva, stomach fluid, bile, pancreatic fluid, and small intestinal secretion is prevented from passing to the large intestine where it is reabsorbed. Because normal secretion of fluid continues, the small intestine becomes distended oral (proximal) to the blockage. Once the luminal pressure is elevated, the tissue pressure compresses the capillaries and reduces venous drainage. Subsequently, blood flow to the intestine is decreased as the capacitance of the vascular system is decreased. Due to the increased capillary hydrostatic pressure, water from the capillaries, moves from the interstitium into the lymphatic system or the intestinal lumen, or through the serosa into the peritoneal cavity. The increased intraluminal hydrostatic pressure created by the enhanced secretion of fluid then initiates cyclic increases in secretion by continuing to elevate the intraluminal pressure.
Because the fluid secreted is isotonic, there is minimal acute change in serum electrolyte values. The consequences of intestinal distension are dehydration from third-space sequestration of the secreted fluid, mucosal injury, serosal injury, abdominal pain, and increased movement of protein across the serosa into the abdominal cavity. The distension eventually reaches a level that inhibits motility in the affected segment of intestine as well as other portions of the intestinal tract. The clinical signs that result are colic, increased heart rate due to pain and decreased circulatory fluid volume, reduced borborygmi, gastric and intestinal fluid sequestration (gastric reflux), and increased protein concentration in peritoneal fluid. An example of this type of disease process is ileal impaction (Fig. 1).
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