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Basics ⬇

Outline

BASICS

Definition!!navigator!!

  • Malabsorption or malassimilation from the intestine occurs when there is diffuse or localized intestinal disease that inhibits the transference of nutrients from the intestinal lumen to the vasculature
  • Transient malabsorption occurs with enteritis caused by viral and bacterial agents
  • Chronic malabsorption is caused by parasitism, infiltrative bowel diseases, amyloidosis, and neoplasia. Besides parasitism, the causes of chronic inflammatory bowel disease are uncommon
  • The small intestine is usually affected in the chronic diseases; however, the large intestine may also be involved

Pathophysiology!!navigator!!

  • Malabsorption is caused by loss of the intestinal absorptive area (villus atrophy), loss of absorptive villus epithelial cells, and enlargement of junctional areas between epithelial cells
  • Thickening of the intestinal wall with edema, hypertrophy, inflammatory cells, or fibrous tissue inhibits the absorptive capacity
  • Blockage of normal lymphatic drainage (lymphangiectasia) and decreased intestinal blood flow due to verminous arteritis may be involved
  • Horses that have had extensive small intestinal resection may also suffer from malabsorption
  • Viral and bacterial infections of the bowel wall can result in the temporary loss of the absorptive capacity of the small intestine
  • Chronic malabsorption is caused by uncontrolled immune reactions (infiltrative bowel diseases, such as lymphocytic/plasmacytic enteritis, granulomatous enteritis, or eosinophilic granulomatous enteritis)
    • The initiating factors in this group of diseases are unknown; however, allergens or infectious agents have been considered stimuli
    • Chronic diseases include infections with Mycobacterium avium, Mycobacterium avium ssp. paratuberculosis, and fungi (Aspergillus spp., Histoplasma spp.)
    • Alimentary neoplasia may also cause similar signs
  • Transient malabsorption may result in short-term weight loss, delayed growth, and diarrhea. These problems should resolve once the infection and immune reaction subside and the intestines achieve normal structure and function
  • The signs of chronic malabsorption persist; however, the progression and severity may vary. A hallmark of chronic disease is hypoproteinemia resulting from decreased protein intake (due to inappetence), malabsorption of nutrients, and protein loss into the bowel. Decreased albumin production may occur due to negative feedback mechanisms in response to elevated globulin levels, thus maintaining plasma oncotic pressure. Other disease entities cause protein-losing enteropathy than malabsorptive diseases

Systems Affected!!navigator!!

GI

Normal feces or diarrhea if diffuse colonic involvement with weight loss.

Endocrine/Metabolic

Altered protein levels and ratios.

Hemic/Lymphatic/Immune

Lymphadenopathy with neoplasia or granulomatous disease.

Hepatobiliary

Decreased feed intake may cause mild increase in bilirubin; eosinophilic epitheliotropic disease may affect many organs, including the liver.

Musculoskeletal

  • Weight loss
  • Muscle atrophy

Skin/Exocrine

Owing to malnutrition, vasculitis, or inflammatory cell infiltration.

Behavioral

Mild depressed demeanor.

Signalment!!navigator!!

Any breed or sex; younger horses usually involved (1–6 years).

Signs!!navigator!!

  • Colic
  • Cutaneous lesions—alopecia; rough, dry haircoat
  • Dermatitis
  • Coronitis
  • Depressed demeanor
  • Diarrhea or normal feces
  • Edema
  • Lethargy
  • Lymphadenopathy
  • Pyrexia
  • Weakness
  • Weight loss

Causes!!navigator!!

  • Parasitic damage due to Strongylus spp. or cyathostomes. Parascaris equorum may cause disease in young horses
  • Infiltrative diseases may be due to an allergic response or uncontrolled response to an infectious agent
  • Proliferative enteropathy due to infection with Lawsonia intracellularis has been increasingly identified in the young horse (see chapter Lawsonia intracellularis infections in foals). This organism is occasionally identified as a cause of disease in the nonjuvenile horse. Familial occurrence has been reported
  • The causes of alimentary neoplasia, such as lymphosarcoma, are unknown

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

A detailed history and physical examination are required. Initially, common causes of weight loss should be considered, such as inadequate nutritional intake for metabolic demands (poor feed quality, bad dentition, competition for food). Many other diseases should be considered using a systematic approach.

Differential diagnoses for hypoproteinemia include:

  • Decreased protein absorption (inadequate intake, gastroenteric disease), decreased production (liver failure), sequestration into third spaces (pleural cavity, peritoneal cavity, abscesses), or loss (alimentary or renal)
  • Protein-losing enteropathy may be caused by acute/subacute colitis, parasitism, NSAID use, GI neoplasia (lymphosarcoma, adenocarcinoma), infiltrative bowel disease, tuberculosis, or congestive heart failure
  • Chronic proliferative bowel disease is caused by Lawsonia infection and chronic infiltrative bowel disease is caused by lymphocytic/plasmacytic enteritis, eosinophilic granulomatous enteritis, and granulomatous enteritis

CBC/Biochemistry/Urinalysis!!navigator!!

CBC

Common findings include neutrophilia, anemia (due to chronic inflammatory disease or blood loss from ulcerations), and hypoproteinemia. The neutrophil level can be high, normal, or low.

Biochemistry

  • Hypoalbuminemia
  • Globulin level—low, normal, or elevated
  • Fibrinogen—mild elevation
  • Hypocalcemia (due to loss of protein-bound calcium)
  • Elevations of hepatobiliary parameters:
    • γ-Glutamyltransferase
    • Aspartate amino transferase
    • Alkaline phosphatase
    • Bilirubin (conjugated)
    • Lactate dehydrogenase, glutamate dehydrogenase, inositol dehydrogenase (sorbitol dehydrogenase)
    • Bile acids
    • Serum amyloid A protein—normal to elevated

Urinalysis

Normal

Abdominal Fluid Analysis

Normal

Fecal Examination

Identification of large or small strongyles; if present, strongyles do not necessary pinpoint parasites as the cause of malabsorption.

Ultrasonography

Determine thickness of wall of small intestine and the presence of masses.

Carbohydrate Absorption Tests

Horse should be fasted for at least 12 h but not >24 h. A blood sample should be collected before the administration of the sugar, then at 30 min intervals for up to 4 h. Water intake should be restricted for the initial 2 h of the test period. Low or no absorption levels are consistent with delayed gastric emptying, enteric disease, or delayed intestinal transit. In addition to absorption, distribution, metabolism, and excretion are important factors to consider.

d-Xylose Absorption Test

Give 0.5 g/kg as a 10% solution via nasogastric tube. Samples may be collected into heparinized tubes. A peak is expected at approximately 60 min.

Glucose Absorption Test

Give 1 g/kg as a 20% solution via nasogastric tube. Collect blood samples into tubes containing sodium fluoride to prevent cellular metabolism of glucose. Heparinized samples can be used if the glucose level is determined immediately after collection. Normal absorption is a 2-fold increase in the baseline glucose level within 90–120 min. Low levels may occur if there is metabolism of the glucose in the lumen. Levels also reflect the metabolic/endocrinologic status of the animal.

Rectal Mucosal Biopsy

Use uterine biopsy forceps or other instrument (bottle cap, syringe-case cap); collect mucosal sample from dorsal or lateral rectal wall in region of retroperitoneal space (30 cm orad to anus). Samples with infiltration of lymphocytes, plasmacytes, eosinophils, and/or histocytes may represent diffuse disease. Negative sample is nondiagnostic, necessitating intestinal biopsy.

Small Intestinal Biopsy

Requires general anesthesia, celiotomy, and full-thickness biopsies. Risks of anesthesia, surgery, and poor wound healing due to catabolic state with hypoalbuminemia. Laparoscopic techniques have been described.

Treatment ⬆ ⬇

TREATMENT

Symptomatic care or specific treatment for transient diseases.

Diet

Consider feeding highly digestible feed; high-protein feed; high-quality fiber should be fed for colonic digestion. Multiple small feedings should be given. Intestinal resection for localized small intestinal disease.

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

Anthelmintics

Treatment should be appropriate for the specific parasite; repeat treatment may be required for encysted stages of nematode:

  • Ivermectin—0.2 mg/kg PO
  • Moxidectin—0.4 mg/kg. Consider prior treatment with prednisolone or dexamethasone if treating for encysted cyathostomes
  • Fenbendazole—10 mg/kg PO once daily for 5 days
  • Pyrantel tartrate—2.2 mg/kg/day. Used as a preventative; other anthelmintics should be used to kill adult worms
  • Note that anthelmintic resistance has become prevalent in some geographic areas. Treatment recommendations may be adjusted accordingly

Corticosteroids

  • Infiltrative bowel disease
  • Prednisolone—1–2 mg/kg PO, IM BID
  • Dexamethasone—0.05–0.2 mg/kg PO SID or by parenteral administration

Antibiotics

Trimethoprim–sulfonamide 30 mg/kg PO or IV every 12 h.

Contraindications!!navigator!!

Corticosteroids have been associated with laminitis.

Possible Interactions!!navigator!!

N/A

Alternative Drugs!!navigator!!

N/A

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

  • Appetite
  • Demeanor
  • Feces
  • Body condition

Possible Complications!!navigator!!

Drug-associated (immunosuppression; laminitis; Cushing or Addison disease).

Expected Course and Prognosis!!navigator!!

  • Parasitism—poor to good
  • Infiltrative bowel disease—poor
  • Neoplasia—poor

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Associated Conditions!!navigator!!

N/A

Age-Related Factors!!navigator!!

N/A

Zoonotic Potential!!navigator!!

May be possible if shedding mycobacterial organisms or Salmonella spp.

Pregnancy/Fertility/Breeding!!navigator!!

Debilitation may lead to infertility, early embryonic death, or abortion.

Synonyms!!navigator!!

  • Chronic inflammatory bowel disease
  • Granulomatous bowel disease
  • Infiltrative bowel disease

Abbreviations!!navigator!!

  • GI = gastrointestinal
  • NSAID = nonsteroidal anti-inflammatory drug

Suggested Reading ⬆ ⬇

Brown CM. The diagnostic value of the d-xylose absorption test in horses with unexplained chronic weight loss. Br Vet J 1992;148:41–44.

Kaikkonen R, Niinisto K, Sykes B, et al. Diagnostic evaluation and short-term outcome as indicators of long-term prognosis in horses with findings suggestive of inflammatory bowel disease treated with corticosteroid and anthelmintics. Acta Vet Scan 2014;56:35.

Kalck KA. Inflammatory bowel disease in horses. Vet Clin North Am Equine Pract 2009;25:303–315.

Lindberg R, Nygren A, Persson SG. Rectal biopsy diagnosis in horses with clinical signs of intestinal disorders: a retrospective study of 116 cases. Equine Vet J 1996;28:275–284.

MacAllister CG, Mosier D, Qualls Jr CW, Cowell RL. Lymphocytic-plasmacytic enteritis in two horses. J Am Vet Med Assoc 1990;196:1995–1998.

Schumacher J, Moll HD, Spano JS, et al. Effect of intestinal resection on two juvenile horses with granulomatous enteritis. J Vet Int Med 1990;4:153–156.

Sweeney RW. Laboratory evaluation of malassimilation in horses. Vet Clin North Am Equine Pract 1987;3:507–515.

Author(s) ⬆

Author: Daniel G. Kenney

Consulting Editors: Henry Stampfli and Olimpo Oliver-Espinosa