Colic Pathophysiology in Horses

Pathophysiology

It is important to understand the pathophysiology of gastrointestinal obstructions in order to clinically assess the patient and formulate a treatment plan. Abnormalities of the equine gastrointestinal tract which prevent the progression of intestinal contents, constitutes an obstruction. Obstructions can be physical or functional and they can be broadly divided into simple obstructions, strangulating obstructions, and non-strangulating infarctions. Paralytic or adynamic ileus are functional obstructions. They can be due to an inflammatory disease, idiopathic or caused by serosal irritation from surgical manipulation.

Simple Obstruction

This is characterised by a physical obstruction of the intestine with no initial vascular compromise to the affected bowel. A simple obstruction can be due to impacted food material, stricture formation, or foreign bodies. The primary pathophysiological abnormality caused by this obstruction is related to the trapping of fluid within the intestine, oral to the obstruction. This is due to the large amount of fluid produced in the upper gastro-intestinal tract (around 125L daily), and the fact that this fluid cannot reach the absorptive surfaces of the large intestine downstream from the obstruction. This fluid becomes sequestrated or can be lost by nasogastric reflux. The first problem with this degree of fluid loss from circulation is one of decreased plasma volume, leading to a reduced cardiac output, and acid-base disturbances.

There are also serious effects on the intestine itself. The continued secretion of trapped fluids and the gas production from bacteria cause an increase in the intraluminal hydrostatic pressure and distends the intestine. It is this distension, and subsequent activation of stretch receptors within the intestinal wall, that leads to the associated pain. Peristalsis is reduced and subsequently stops all together as the affected bowel continues to fill with fluid and results in reflux into the stomach. With progressive distension of the intestinal wall, there is occlusion of blood vessels, firstly veins, then arteries. The difference in time to onset of occlusion is due to the relatively more rigid walls of arteries compared with veins. This impairment of blood supply leads firstly to hyperaemia and congestion, and ultimately to ischaemic necrosis and cellular death. The poor blood supply also has effects on the vascular endothelium, resulting in an increased permeability. This results initially in leakage of plasma, and eventually blood into the intestinal lumen. The damage may also allow for the absorption of gram-negative bacteria and endotoxins into the circulation, causing the release of prostaglandins and leucotrienes, which lead to further cardiovascular and systemic effects. Hypovolaemia and acid-base disturbances are the major causes of cardiovascular collapse. Endotoxaemia plays a limited role in the death of cases with a simple obstruction.

The location and degree of the obstruction (partial or complete) determines the severity of the clinical signs. Proximal obstructions of the small intestine produce greater pain and have an acute onset of clinical signs. They have a more rapidly fatal course than distal obstructions. A large quantity of gastric fluid is produced and sequestrated in cases of proximal obstructions. This fluid contains a large quantity of chloride. The acidic gastric fluid can be lost by a nasogastric tube and will result in an initial metabolic alkalosis for the patient. As the disease progresses and the horse becomes hypoperfused, the acid-base abnormality is further complicated by acidosis. Distal obstructions of the small intestine produce less painful clinical signs with a slower onset. The fluid lost by nasogastric intubation is high in bicarbonate and has an alkaline pH. Distal small intestinal obstructions can be identified by a metabolic acidosis and low serum concentrations of bicarbonate.

Simple obstructions of the large intestine produce milder clinical signs compared to the small intestine and have a slower rate of deterioration. Partial obstructions allow for the passage of some ingesta and gas and hence the clinical signs and level of dehydration are milder as some ingesta and water can pass into the caecum. If the obstruction becomes complete, the gas and ingesta cannot pass and cause intestinal distention. This exerts a pressure on the diaphragm which impairs pulmonary function and inhibits the venous return to the heart by compressing of the vena cava. If these cases are untreated, the distention can become so marked that there is a fatal risk of rupture of the devitalised portions of colon or caecum.

Strangulating Infarction

Strangulating infarctions have all the same pathological features as a simple obstruction, but the bloody supply is immediately affected and so they often present as an acute abdominal crisis. The patholphysiological changes are more acute and severe and the mortality rate of cases that go to surgery, is high. Common causes of strangulating obstruction are incarcerations, intussusceptions and intestinal volvulus.

Both arteries and veins may be effected immediately, or progressively as in simple obstruction. Venous occlusion makes the affected segment of bowel a deep red color. If there is arterial occlusion as well, the intestine becomes cyanotic. Vascular stasis quickly pursues and the bowel becomes red/black. Immediately, the vascular epithelium starts to degenerate and becomes more permeable. Plasma is lost into the tissue. Within a few hours, the damage is so severe that that blood is lost out of the vessel into the tissue and then the lumen (venous infacrction stage).

The subsequent hypoxia causes degeneration of the mucosal villi and within hours, the mucosal epithelium is completely necrotic. As time passes, the degeneration continues through the different layers of the intestinal wall and the barrier is compromised. Gram-negative bacteria and endotoxins enter the circulation and cause damage to the endothelium and platelets. The platelets release potent vasoconstricor substances (thromboxane and serotonin). The vascular epithelium releases prostacyclins in response to the damage. The prostacyclins cause a massive release of neutrophils systemically but predominantly in the lungs and affected portion of bowel. These mediators are responsible for the horse going into endotoxic shock that is apparrent clinically. It is dose-related and more severe with larger portions of gut involved.

The clinical signs are acute in onset and of severe unrelenting pain that shows no or little reponse to analgesia. The rate of deterioration is rapid and untreated cases of small intestinal strangulation will die in 24-36 hours of the onset of clinical signs. Surgical correction must be carried out within a few hours of the strangulation occurring if it is to be successful. Strangulation of the large intestine has a similar pathophysiology to that of the small intestine.

Non-strangulating Infarction

In a non-strangulating infarction, blood supply to a section of intestine is occluded, without any obstruction to ingesta present within the intestinal lumen. The most common cause is infection with Strongylus vulgaris larvae, which develop within the (primarily cranial)mesenteric artery.

References

• Edwards B. (2009), Diagnosis and Pathophysiology of Intestinal Obstruction, in Equine Gastroenterology courtesy of the University of Liverpool, pp 3-18
• Meuller E, Moore J. N, (2008) Classification and Pathophysiology of Colic, Gastrointestinal Emergencies and Other Causes of Colic, in Equine Emergencies- Treatments and Procedures, 3rd Edition, Eds Orsini J. A, Divers T.J, Saunders Elsevier, pp 107