I. GENERAL CONSIDERATIONS
A. Gastrointestinal (GI) disease is a common clinical problem where signs of vomiting, diarrhea, and anorexia predominate. Rapid diagnosis is essential for symptomatic or specific therapies to be effective. A complete history and physical examination accompanied by appropriate laboratory tests aid in determining the etiology, location, and severity of the disease or disturbance. Endoscopy and mucosal biopsy are frequently required for diagnosis of chronic GI diseases, such as gastritis, malabsorptive syndromes, or idiopathic inflammatory bowel disease (IBD).
B. Nonspecific therapy
1. Correction of fluid and electrolyte balance. Persistent vomiting or watery small bowel diarrhea produces dehydration, electrolyte loss, and disturbances in acid– base balance that should be corrected by parenteral fluid therapy. With severe vomiting, there is variable loss of sodium, chloride, potassium, hydrogen, and bicarbonate that may cause metabolic acidosis. If the pylorus is obstructed, duodenal bicarbonate is retained while continued loss of gastric chloride, potassium, and hydrogen in the vomitus leads to metabolic alkalosis. Oral fluid and electrolyte replacement may suffice in animals having only mild acute diarrhea or if vomiting is infrequent or absent.
2. Resting of the GI tract. Best practice recommendations suggest that withholding food for 24–48 hours in acute GI disturbances is often effective in dogs and cats. Thereafter, feeding a bland diet often and in small amounts is generally indicated for 3–5 days at which time the original diet is gradually introduced. Potential benefits of dietary restriction include decreased gastric secretions, decreased amounts of osmotically active particles in the gut lumen, and the facilitation of mucosal healing (e.g., enterocyte regeneration).
3. Dietary modification
a. Bland diet. A bland, easily digested, low-fat diet such as boiled chicken or white fish or low-fat cottage cheese with rice should be offered after withholding food for 24–48 hours. Limiting dietary fat is important because unabsorbed fatty acids are hydroxylated by colonic bacteria into secretagogues which decrease mucosal absorption and promote increased fecal water loss.
b. Lactose-free diet. Milk products should be eliminated from the diet if there is lactose intolerance or a loss of mucosal brush border lactase from GI disturbances.
c. Insoluble fiber. Increased fiber absorbs water and normalizes intestinal transit in constipation and animals with colitis of diverse causes.
d. Gluten-free diet. Gluten-sensitive enteropathy has been reported to occur in Irish setter dogs. Clinical improvement is observed when affected animals are placed on a cereal-free diet.
4. Provision of nutritional support. Calories, proteins, and vitamins should be supplied to maintain a positive energy and protein balance. Enteral feeding is preferred over parenteral routes since this is most physiologic and prevents atrophy of the intestinal tract. Initial nutrient deficiencies are gauged by use of body condition scores (BCS), and specific nutrient requirements may be estimated by a variety of methods.
5. Symptomatic therapies
a. Protectants and adsorbents. Bismuth-subsalicylate and kaolin-pectin are often administered in acute diarrhea to coat and protect the intestinal mucosa, and because they may reduce intestinal secretions. See more below.
b. Motility modifying drugs. Opiates and opioids (loperamide, diphenoxylate) are used to decrease intestinal motility and secretions associated with acute diarrhea. Anticholinergics should be avoided since they can potentiate ileus. See more below.
c. Antimicrobial therapy. The routine use of antibiotics for treatment of acute or chronic GI disease is not recommended. Animals having severe mucosal injury (parvoviral enteritis) or infection with specific bacterial pathogens
(Campylobacter jejuni) of the GI tract should receive antibiotics. Indiscriminate use of antimicrobials promotes bacterial drug resistance (
Table 11-1).
d. Probiotics. These are live bacterial cultures, which promote beneficial microbial health to the host. The mechanism(s) of action are not fully known and their effects appear to be exquisitely host-specific. Preliminary clinical data supports their use as adjunctive therapy for both acute and chronic diarrhea (see below).
e. Analgesics. Indications include alleviation of visceral pain in animals having diverse causes for GI disease (equine colic, pancreatitis in companion animals). Severe visceral pain is alleviated by morphine or opioid receptor agonists that inhibit nociceptive reflexes at spinal and supraspinal sites within the CNS.
(1) Opiates (see Chapter 4 for more information)
(a) Morphine is used in dogs and cats, IM. Its duration of action is 6 hours in these species. High doses of morphine produce excitement in cats and horses and it is administered at 1/10 of the dose used in dogs (0.05–0.2 mg/kg in cats and horses; 0.5–2 mg/kg in dogs).
(b) Butorphanol is administered IV to horses for the control of colic pain. Butorphanol is a partial agonist for μ-receptors and a full agonist for κ-receptors. Its duration of action is 1–2 hours.
(2) Nonsteroidal anti-inflammatory drugs (NSAIDs). (see Chapter 7 for more information) Flunixin meglumine, or phenylbutazone are given IM or IV to horses for the control of colic pain. They inhibit prostaglandin synthesis by inhibiting the enzyme cyclooxygenase. Duration of action is 1–8 hours, depending on the cause and severity of pain.
(3) Sedatives. Xylazine, detomidine, medetomidine, and romifidine are α2-adrenoreceptor agonists, which produce sedation and analgesia in equine colic. Their duration of action is 1–4 hours following IV or IM administration. (see Chapter 4 for more information).
(4) Spasmolytics. N-butylscopolammonium bromide (Buscopan®) is an antispasmodic and anticholinergic drug used in horses for control of the abdominal pain of colic.
(a) Mechanism of action. Bucospan® competitively inhibits parasympathetic activation of muscarinic receptors on intestinal smooth muscle cells.
(b) Therapeutic uses. Bucospan® is administered IV to horses at a dose of 0.3 mg/kg for control of abdominal pain in colic and simple impactions.
(c) Pharmacokinetics. The plasma t½ of Bucospan® is 6 hours. It is eliminated equally via urine and feces.
(d) Adverse effects. Transient tachycardia and decreased borborygmal sounds may be present for 30 minutes following administration. Bucospan® should not be used in impaction colics associated with ileus or in horses with glaucoma.