1. Physical obstruction of the small intestine usually occurs by impacted food material, stricture, or foreign body (Box 2.1), thereby preventing the passage of the large volumes of fluid produced in the upper alimentary tract from reaching the absorptive surfaces of the lower intestine so that it becomes sequestered or maybe lost by nasogastric reflux.

2. During one day this volume almost equals the extracellular volume of the horse (approximately 125 L).

3. Systemically, the prime concern in simple obstruction is depletion of plasma volume and reduction in cardiac output together with acid–base disturbances.

4. Gas production by bacterial action continues and is even enhanced by the static medium. With continued secretion of fluids and build-up of gas, the intraluminal hydrostatic pressure (IHP) increases and distends the bowel.

5. As stretch receptors in the distended intestinal wall are activated, the pain increases and becomes continuous.

6. Peristaltic waves diminish and then cease altogether as the intestinal lumen is progressively filled, leaving an atonic rapidly distending tube.

7. Once IHP increases to above 15 cm H₂O, absorption of water by the mucosa stops and instead water begins to flow from the mucosa into the lumen.

8. The increasing pressure and expanding volume of fluid causes reflux into the stomach – how soon after the onset of the obstruction depends on where along the small intestine it is located.

9. Increased vascular hydrostatic pressure in the bowel promotes leakage of protein-rich plasma into the peritoneal fluid. Few leucocytes and no erythrocytes appear in the peritoneal fluid within the first 12–24 hours but may become more numerous with the progression of degenerative changes and vascular compromise of the intestinal wall.

10. Damage may be sufficient to allow absorption of endotoxins and cause production of prostaglandins and leukotrienes which may further compromise cardiovascular function. However, endotoxic shock plays only a very limited part in the fatal outcome of unrelieved simple obstruction. Hypovolaemia and altered blood electrolytes are the usual causes of cardiovascular collapse.

• In general, proximal obstructions have a more acute onset, produce greater pain, generate a greater volume of gastric fluid sequestration and have a more rapidly fatal course than distal obstructions. In proximal obstructions, large quantities of chloride are lost particularly if gastric reflux is removed by a nasogastric tube, resulting in metabolic alkalosis.

• Later the metabolic disturbance becomes complicated by acidosis secondary to hypoperfusion.

• Clinical signs resulting from distal small intestine obstructions develop more slowly and are generally less severe due to the compliance of the intestine and the ability to continue some fluid absorption until IHP initiates secretion.

• Established distal small intestine obstructions are characterized by metabolic acidosis with low serum concentrations of HCO₃.

1. Simple obstruction of the large intestine (Box 2.2) is usually due to impaction with food material, enteroliths or other intraluminal masses, or a change in position of the colon, e.g. nephrosplenic entrapment (left dorsal displacement of the large colon), and may be partial or complete.

2. In general the clinical signs or rate of systemic degeneration are much less dramatic in simple obstruction of the large intestine than in simple obstruction of the small intestine.

3. Incomplete obstruction allows the passage of small amounts of ingesta and gas.

4. Dehydration is mild at first because water still passes into the caecum where it is readily absorbed.

5. The production of volatile fatty acids and gas by bacterial fermentation is reduced due to decreased amounts of ingesta.

6. If the obstruction becomes complete, ingesta, and particularly gas, accumulate much more rapidly. Distension becomes marked and may become so great as to exert pressure on the diaphragm and vena cava, resulting in impaired pulmonary function and venous return to the heart.

7. Prolonged and/or marked distension of the caecum and colon may cause interference with mucosal perfusion leading to devitalization and possibly fatal rupture.

1. Strangulating obstructions of the small intestine include incarcerations, intussusceptions and volvulus (Box 2.1) and represent a common cause of acute abdominal crisis.

2. The same fluid retention which occurs due to simple obstruction with eventual reflux into the stomach is present, but because vascular compromise of the intestine is present at the outset, the pathophysiological changes associated with strangulation obstruction are more acute and severe.

3. The incidence of mortality of surgical cases with strangulation obstruction can be high.

4. The vascular compromise may be venous, or venous and arterial, but typical lesions cause venous occlusion before arterial occlusion with consequent venous congestion.

5. Within minutes of strangulation occurring the involved segment of bowel and its mesentery become deep red as veins and venules are distended with blood. If there is immediate concurrent arterial occlusion the intestine becomes cyanotic.

6. More often, thicker walled arteries and arterioles resist compression and continue to pump blood into the distended veins and venules. As the involved intestine is engorged with blood, vascular stasis quickly develops, and the segment becomes red/black in colour. Almost immediately, the vascular endothelium becomes more permeable, and plasma diffuses into the tissue.

7. Within a few hours degeneration of vascular epithelium becomes so extensive that blood pours out of the distended vessel into the tissue (venous infarction stage) and eventually into the lumen.

• The epithelial cells slough in sheets starting at the tip of the villus and working towards the crypts.

• Within 4–5 hours the mucosal epithelium is completely necrotic.

• By 6–7 hours the degenerative effects of hypoxia have extended through the external muscle layer.

• Early in the development of the ischaemic lesions, the bacteria and endotoxins readily gain entry to the circulation via viable tissue adjacent to the lesion.

• By 6 hours or possibly earlier, as the muscularis degenerates, bacteria and toxins leak through the serosa into the peritoneal cavity from which they are readily absorbed.

• Release of endotoxins into the general circulation results in damage to endothelial cells and platelets. Platelets are immediately stimulated and release the potent vasoconstrictor substances, thromboxane and serotonin. Damage to the endothelium increases vascular permeability, prostacyclin is released, and neutrophils are stimulated, especially in the lungs and site of intestinal injury.

• The endotoxic shock is dose-related and is more severe the greater the length of bowel involved.

• The heart rate increases progressively, and pulse quality deteriorates.

• Mucous membranes become congested, and the capillary refill time increases.

• The PCV and total protein also rise progressively, and the respiratory rate increases in response to developing metabolic acidosis.

• At first the peritoneal fluid is slightly serosanguinous with a mild increase in protein and leucocytes. As the strangulation process continues, all these substances increase dramatically, and the fluid becomes flocculent and turbid. Toxic neutrophils indicate leakage of toxins and bacteria.

• The clinical course is rapid, and most horses with an untreated strangulating obstruction of the small intestine die within 24–30 hours of the onset of disease from irreversible endotoxaemic shock / systemic inflammatory response syndrome and marked vascular collapse. However, the deterioration in the animal’s condition is such that for surgical correction to be successful, it must be carried out within a few hours of the obstruction occurring. Eighty per cent or more of affected horses may recover if operated upon within 8 hours.

1. Strangulating obstructions of the large intestine (Box 2.2) include intussusception of the caecum, torsion and volvulus of the large colon and incarceration of the small colon.

2. The pathophysiology is similar to that previously described for the small intestine, but there are points of variance.

3. The rate of systemic deterioration can vary markedly between caecocaecal intussusception in which it is slow, and 360° torsion of the large colon which is the most rapidly fatal of all the intestinal obstructions of the horse.

4. Such is the size of the submucosal space in the large colon that venous occlusion can result in the horse losing half its circulating blood volume into the wall of the gut within 4 hours of a 360° torsion occurring.

5. Hypovolaemia is rapidly profound, and the mucous membranes become pale and cyanotic.

6. The degeneration of the large surface area of bowel wall allows massive leakage of endotoxin and bacteria into the peritoneal cavity, and the effects of endotoxaemia are added to those of the hypovolaemia.

7. Because of the short clinical course prior to death, rupture is not normally seen.

• Relief of visceral pain in horses with severe colic is essential on humane grounds and to minimize injury to the horse and attending personnel during evaluation and therapy.

• The most satisfactory method of pain relief is the correction of the cause of increased intramural tension resulting from distension or spasm. However, this may take time, and it is frequently necessary to achieve temporary relief of severe pain chemotherapeutically to allow a thorough clinical examination without risk of injury to the horse and attending personnel.

• It is important to select a drug which will accomplish the desired effect without creating complications such as depressing gut activity, predisposing to hypovolaemic shock or, most important, masking the signs of developing endotoxaemia.

Dipyrone: Dipyrone is a very weak analgesic drug that provides only short-term relief in a few cases of very mild abdominal pain. Combined with hyoscine N-butylbromide it is effective in relieving intestinal spasm. Its failure to help reduce or stop pain in individual cases should signal that a condition exists which is more serious than a simple intestinal spasm or tympanic colic.

Phenylbutazone: Phenylbutazone provides no greater relief from visceral pain than does dipyrone. However, the toxic side-effects of phenylbutazone are numerous and include gastrointestinal ulceration and nephrotoxicity. For this reason the dosage should not exceed 4.4 mg/kg every 12 hours.

Meloxicam: Meloxicam is available in Europe for the alleviation and relief of pain associated with musculoskeletal disorders and colic. Meloxicam selectively inhibits cyclooxygenase-2 (COX-2) over COX-1, and therefore has a lower risk of side-effects compared to phenylbutazone or flunixin meglumine. The analgesic effects are equivalent to phenylbutazone.

Firocoxib: Firocoxib is a selective COX-2 inhibitor available in north America for control of pain associated with musculoskeletal disorders. There is currently no official approval for its use for control of pain associated with colic.

Flunixin meglumine:

Xylazine:

Detomidine:

Romifidine: Romifidine has a similar action to xylazine and detomidine. At a dose of 40–80 µg/kg IV it provides potent analgesia lasting 1–3 hours.

Acepromazine: Phenothiazine tranquillizers have a peripheral vasodilatory effect and so are contraindicated in horses with reduced circulatory volume because they block the life-saving vasoconstriction which maintains arterial blood pressure and assures, within limits, perfusion of vital organs.

Morphine:

Pethidine: Pethidine is a narcotic agonist with few side-effects and provides slight to moderate analgesia of relatively short duration in horses with abdominal pain. Used repeatedly it can potentiate obstructions due to impactions by reducing colonic activity.

Butorphanol:

Pentazocine: Pentazocine is a partial agonist which is more effective than dipyrone but less effective than xylazine and flunixin in relieving visceral pain.

Atropine: Atropine is not recommended for use in horses with colic because its effect in relaxing the intestinal wall and preventing contractions can last for several hours or even days creating tympany and complicating the initial problem with ileus.

Hyoscine:

Mineral oil: Mineral oil (liquid paraffin) is the most frequently used laxative in equine practice and is administered at a dose rate of 10 mL/kg by nasogastric tube. Its effects are considered mild, and it is safe for prolonged use. Vegetable oils can be used in the same way.

Psyllium hydrophilic mucilloid:

Osmotic laxatives: Magnesium sulphate and common salt can be used as an osmotic laxative in horses, but because, undiluted, they will cause enteritis by osmotic damage to the mucosal cells, each dosage of 0.5–1.0 g/kg should be diluted in 4 litres of warm water and administered by nasogastric tube.

Dioctyl sodium succinate (DSS):

Intravenous and enteral fluids: Balanced electrolyte solution administered intravenously will sometimes provide a stimulus for intestinal motility. This treatment works particularly well for colon impaction and appears to stimulate motility in cases of ileus of the caecum and large colon. ‘Overhydration’ with Hartmann’s solution at 40–80 L every 24 hours helps to provide secretion of fluid to soften hardened impactions, however when fluid therapy is stopped, the horse may suffer a rebound dehydration. Continuous or repeated administration of enteral fluid by nasogastric tube can also be used in the treatment of impactions.

Neostigmine methyl sulphate:

The preferred method of correcting postoperative ileus is to specifically antagonize the inhibiting neurogenic or hormonal processes.

Metoclopramide: Metoclopramide appears to have a beneficial effect on stomach emptying and small intestinal motility when used as a constant drip infusion at 0.1 mg/kg/hour over several hours or constantly until some response is seen. Higher doses up to 0.5 mg/kg can cause untoward nervous signs.

Domperidone: Domperidone, a newer dopaminergic antagonist does not cross the blood–brain barrier and at a dose rate of 0.2 mg/kg IV has been shown to block dopaminergic receptors and prevent postoperative ileus induced experimentally. It has potential for use in clinical cases.

Cisapride:

Erythromicin:

Lidocaine: