When Gut Attacks - All Ages, All Comers

Take Home Message—Gastrointestinal conditions may be acute or chronic, painful or seemingly benign, have no systemic effects or be responsible for profound losses in condition or performance potential. When acute, establishing a diagnosis, preserving life and controlling pain are first and foremost. When chronic, the management plan may be difficult to formulate and achieve only intermittent success. Clinical findings should be interpreted in relation to the historical information available. Confirming a definitive diagnosis before action is required may not be obtainable.

Author’s address—Rood and Riddle Equine Hospital, PO Box 12070, Lexington, KY 40580-2070; e-mail: pmorresey@roodandriddle.com.

I. INTRODUCTION

Acute or chronic gastrointestinal pathology is a common and potentially life-threatening affliction of the horse, with the majority of horses suffering from one of these conditions sometime during their lives. The majority of gastrointestinal conditions are amenable to medical management and in some cases this may be chronic in nature, however acutely painful conditions may indicate an intestinal accident is present necessitating surgical intervention.

II. COLIC The degree of pain shown during a gastrointestinal condition will largely determine the approach to diagnosis and management. The presence of intractable abdominal pain necessitates surgical exploration.

History

Signalment: Geriatric horses may have a similar admission cardiovascular status compared to mature horses (heart rate, packed cell volume, plasma creatinine and blood lactate concentration) but a more serious cause of colic underlying the episode Increased occurrence of enteroliths in Arabians and miniature breeds has been demonstrated. 

Management changes and potential triggers: transport, administration of medications for concurrent conditions (antimicrobials, anti-inflammatories), and changes in social structure by the addition or removal of other horses may precipitate colic. More frequently, recent feed or water changes may be incriminated.

Pattern of colic episode(s): How often and over what time period has the colic been apparent (isolated episode versus chronic intermittent over months)? Are episodes similar or signs random? Is there a temporal relationship to estrous cyclic activity (actual or perceived)? Fecal production: Decrease in volume or frequency of fecal production is suggestive of decreased dietary intake (inappetence, inability to prehend food, competition), or prolonged intestinal passage (motility disorders, obstructive processes, increased fecal density).

Pain

Duration: The duration of signs of colic prior to evaluation has been associated with survival. 

Severity and frequency: In many prognostic models, the degree of pain affects survival. Horses vary in their pain responses, so it is useful to know if this episode is consistent with other colic episodes (is it more or less severe?)

Response to analgesics: What is the duration and completeness of response to analgesics? Alpha-2 adrenergic agonists have a rapid onset and may provide visceral analgesia for prolonged periods. Flunixin meglumine has been shown to provide less visceral analgesia. 

Clinical Examination

In one referral center colic study, there was a significant association between predicted survival and outcome based on clinical impression, and this correlation improved with increased case exposure. 

Vital signs: Rectal temperature is widely variable, ranging from elevated with acute infectious involvement to hypothermic in the presence of severe hypovolemia or devitalized bowel. Cardiovascular parameters are significant predictors of mortality in multiple studies. Heart rate is variably elevated (individual pain tolerance) and alone cannot be relied upon to predict outcome. Hypovolemia may be responsible (are signs of circulatory compromise present?). Paradoxically, a normal heart rate may be present with significant gastrointestinal compromise. Pulse quality can be assessed peripherally at the distal extremities or the facial artery along the mandible. Poor pulse pressure is suggestive of endotoxic shock, hypovolemia or cardiac compromise.11 A bounding pulse indicates the early stages of endotoxemia before decompensation occurs.