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Compendium June 2012 (Vol 34, No 6)

Clinical Snapshot: Depression and Hemorrhagic Diarrhea in a Thoroughbred Colt

by Kristyn Close, DVM

    Case Presentation

    A critically ill, 2-day-old Thoroughbred colt presented with depression and hemorrhagic diarrhea. Laboratory data revealed severe hemoconcentration consistent with severe dehydration, moderate hyperlactatemia, mild hypocalcemia, and mild leukopenia. Foaling was reported to be normal, and the referring veterinarian reported that the foal had an IgG concentration of 700 mg/dL (normal: >800 mg/dL) on blood testing. Diarrhea was first noted at 1 day of age and became hemorrhagic on the second day. Two days after admission to the hospital, the diarrhea became yellow and watery. Despite intensive therapy, the diarrhea continued until day nine after admission, when the colt’s feces became normal in color and consistency. Seventeen days after initial presentation, the colt displayed signs of moderate to severe colic that persisted intermittently for several days. An exploratory celiotomy was performed on day 24 because of recurrent signs of moderate to severe colic. The colt was humanely euthanized on the surgical table after identification of the lesion in FIGURE A, which was obtained at necropsy.

    left dorsal colon, left ventral colon, and pelvic flexure

    Figure A. A necropsy photograph showing the left dorsal colon (top), left ventral colon (bottom), and pelvic flexure (right). In the ~25-cm segmentally narrowed area in the left dorsal colon, the lumen was <1 cm in diameter.

    1. What is the diagnosis?

    2. What are some infectious agents associated with diarrhea in equine neonates?

    3. Which infectious agents are associated with necrotizing enterocolitis in equine neonates?

    4. Has this lesion been associated with necrotizing enterocolitis?

    Answers and Explanations

    1. The diagnosis was severe, segmental stricture of the left dorsal colon.

    2. Infectious agents associated with diarrhea in equine neonates include Clostridium perfringens, Clostridium difficile, Bacteroides fragilis, Salmonella spp, rotavirus, enterotoxigenic Escherichia coli, Klebsiella spp, and Cryptosporidium parvum.1–3

    3. Necrotizing enterocolitis is generally thought to be caused by the anaerobic bacteria C. difficile, C. perfringens, and B. fragilis.1

    4. It has been theorized that during healing of intestine affected by enterocolitis, a progressive stricture may develop that can be difficult or impossible to distinguish from congenital stricture on histopathologic examination. The human literature includes multiple studies regarding necrotizing enterocolitis in infants and intestinal stricture formation in survivors. Krasna et al4 reported seven cases in which five neonates survived. Of the survivors, three developed colonic stenosis and one developed ileal stenosis. Kosloske et al5 reported that after resolution of acute necrotizing enterocolitis, six of 31 (19%) surviving infants developed colonic stricture. Yeh et al6 described 80 neonatal cases of necrotizing enterocolitis. Of the surviving 61 infants, 12 (20%) developed intestinal strictures.

    1. David JB. Diarrheal diseases. In: Orsini JA, Divers TJ, eds. Equine Emergencies: Treatment and Procedures. 3rd ed. St Louis, MO: Saunders Elsevier; 2008:165-172.

    2. Traub-Dargatz JL. Diarrheal disease in foals. In: Kahn CM, Line S, eds. The Merck Veterinary Manual. 9th ed. Whitehouse Station, NJ: Merck and Co; 2005:241-242.

    3. Wilkins PA. Disorders of foals. In: Reed SM, Bayly WM, Sellon DC, eds. Equine Internal Medicine. 2nd ed. St Louis, MO: Saunders Elsevier; 2004:1417-1419.

    4. Krasna IH, Becker JM, Scheneider KM, et al. Colonic stenosis following necrotizing enterocolitis of the newborn. J Pediatr Surg 1970;5(2):200-206.

    5. Kosloske A, Burnstein J, Bartow S. Intestinal obstruction due to colonic stricture following neonatal necrotizing enterocolitis. Ann Surg 1980;192(2):202-207.

    6. Yeh TC, Chang JH, Kao HA, et al. Necrotizing enterocolitis in infants: clinical outcome and influence on growth and neurodevelopment. J Formos Med Assoc 2004;103(10):761-766.

    References »

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