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Basics ⬇

Outline

BASICS

Definition!!navigator!!

Signs are associated with discomfort originating within the abdominal cavity. May develop acutely or gradually. Considered chronic when persisting for more than 3–4 days.

Pathophysiology!!navigator!!

  • Most acute abdominal pain originates from the GI tract but may also arise from other systems
  • In the intestinal tract, pain may originate from increased intramural tension, tension on a mesentery, ischemia, inflammation, smooth muscle spasms, or a combination of any of these
  • Causes can be divided into strangulating and nonstrangulating lesions. Nonstrangulating lesions include intraluminal lesions, extraluminal lesions, mural lesions, as well as spasmodic colic, intestinal displacement, ileus, and inflammatory bowel disease. Strangulating lesions, such as torsions and incarcerations, are usually associated with a compromise of local blood supply followed by intestinal necrosis. The necrosis may lead to cardiovascular shock

Systems Affected!!navigator!!

  • Cardiovascular—dehydration and endotoxemia may lead to shock and result in organ failure
  • GI—the large colon and the distal part of the small intestine are commonly involved
  • Other systems can be involved (e.g. urinary system, reproductive tract, hepatobiliary, peritoneum and pleura)

Signalment!!navigator!!

Nonspecific. There may be an age, breed, or sex predisposition for a specific problem.

Signs!!navigator!!

General Comments

May be subtle and easily missed initially. As the disease progresses, changes in clinical parameters, rectal examination findings, transabdominal ultrasound findings, and laboratory data allow a more accurate localization.

Historical Findings

  • Abdominal pain can appear acutely or following an episode of anorexia, depression, and/or decreased fecal output. Recent history of change in the exercise, diet, or availability of drinking water may also be present
  • Mild abdominal pain—decrease in appetite and/or fecal output, mild depression, yawning, extended neck and rolling of the upper lip, teeth grinding, muscle fasciculation
  • Moderate abdominal pain—frequent lying down, pawing, flank watching, groaning, posture for urinating with small quantities of urine passed, kicking the abdomen, attempts to roll
  • Severe abdominal pain—walking in a tight circle, constantly getting up and down, rolling, traumatizing self and handlers, sweating, labored breathing

Physical Examination Findings

Depending on the stage of the disease signs may vary in severity:

  • General findings—abdominal distention, sweating, increased respiratory rate, changes in body temperature, abnormal quality and quantity of feces
  • Cardiovascular findings—tacky mucous membranes, increased capillary refill time, increased heart rate, dehydration, cold extremities. In endotoxemic shock, the cause of pain is likely due to a strangulating lesion or to a severe inflammatory process (colitis, peritonitis)
  • GI findings—increase, decrease, or absence in gut motility, gas-filled resonant viscus on percussion, presence of net gastric reflux on passage of the nasogastric tube. Possible gastric reflux in stomach and small intestinal lesions. Abnormalities on rectal examination—gaseous distention of viscus by gas, liquid, or food; displacement of viscus; thickening of the intestinal wall; presence of tight bands, uterine or renal abnormalities

Causes!!navigator!!

GI

  • Nonstrangulated obstructive lesions:
    • Gastric—ulcers, distention, impaction, rupture, tumor. Small intestine—enterocolitis, ascarid impaction, ileal impaction, ileal hypertrophy, stricture, adhesions. Large colon—ulceration, colitis, impaction, gas distention, mild displacement, left dorsal and right displacement, enterolith, sand impactions. Cecum—impaction, gas distention. Small colon—impaction, enterolith
  • Strangulating obstructive lesions:
    • Small intestine—incarceration into a space/rent in the mesentery/inguinal ring/gastrosplenic ligament/epiploic foramen, strangulation by lipoma, volvulus. Large colon—volvulus, incarceration, thromboembolic infarction. Cecum—intussusception, thromboembolic infarction, torsion. Small colon—strangulating lipoma, submucosal hematoma, thromboembolic infarction

Others

  • Reproductive—uterine torsion, laceration, abortion, parturition, testicular torsion, hematoma in the broad ligament, trauma
  • Renal/urologic—renal/ureteral/bladder/urethral calculi, cystitis, renal inflammatory processes
  • Hepatobiliary—hepatitis, hepatobiliary calculi

Risk Factors!!navigator!!

  • No access to water
  • Sudden change in diet
  • Poor enteric parasite control
  • Pregnancy
  • Previous abdominal surgery
  • Congenital abnormalities
  • Certain medication

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

Other causes of pain that might mimic pain originating from the abdominal cavity include myositis, pleuropneumonia, hemorrhagic shock, rabies, and musculoskeletal injuries.

CBC/Biochemistry/Urinalysis!!navigator!!

  • Increase in packed cell volume and total protein with dehydration
  • Possible hypoproteinemia secondary to GI protein loss
  • Leukopenia in acute inflammation and endotoxemia or leukocytosis in chronic inflammation
  • Metabolic acidosis and production of lactic acid in cardiovascular shock. Metabolic alkalosis and loss of chloride when large amount of gastric reflux is present. Increased lactate concentration in presence of endotoxemia, tissue hypoxia, liver disease
  • Hypokalemia and hypocalcemia, especially if anorexia is present and in lactating mare
  • Hypochloremia and hyponatremia (colitis)
  • Alkaline phosphatase may be increased
  • Azotemia in severe dehydration or acute renal failure

Other Laboratory Tests!!navigator!!

Abdominal Paracentesis

  • Normal fluid has a pale, clear yellow color
  • Increase of the protein level and WBCs is indicative of primary peritonitis or secondary to morphologic change of the viscera
  • Foul-smelling reddish-brown fluid with an increase in the RBCs, WBCs, and protein is indicative of necrotic bowel. Presence of plant materials suggests intestinal rupture
  • Lactate concentration > 1 mmol/L may indicate intestinal ischemia

Urinalysis

A change in specific gravity, increase in leukocyte content, RBCs, and pH may be noticed in cases with renal disease.

Imaging!!navigator!!

Radiographs

May be useful in sand impactions or enteroliths in adults. In foals for localization of gas, fluid distention, impaction, or congenital abnormality (atresia coli).

Ultrasonography

  • Evaluation of—amount and characteristics of abdominal fluid; motility, wall thickness, and diameter of small intestine and its location; motility and wall thickness of the large intestine; nephrosplenic space for presence of intestine; intussusceptions, abscesses, or mass
  • Also useful in evaluating the stomach, kidneys, liver, spleen, uterus, etc.

Endoscopy

Gastroscopy—evaluation of the stomach for ulcers, impaction or tumor. Cystoscopy—evaluation of the urethra, bladder, and opening of the ureters for inflammation or calculi.

Other Diagnostic Procedures!!navigator!!

Exploratory laparotomy/laparoscopy.

Treatment ⬆ ⬇

TREATMENT

  • Horses should be taken off feed until diagnosis/resolution of the underlying problem
  • The history, physical examination, and laboratory results will help differentiate between medical or surgical condition
  • Reasons for exploratory laparotomy—moderate to severe abdominal pain, unresponsiveness to medical treatment, progressive increase in heart rate or heart rates above 60–70/min, cardiovascular compromise or deterioration, presence of moderate to severe gas distention or displacement of the large colon, gas distention of small intestine, gastric reflux, abnormal paracentesis findings
  • Supportive treatment for medical and surgical cases includes pain management, IV fluids, gastric decompression if necessary, electrolyte replenishment, and control of the abdominal pain

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

  • Analgesics—control the abdominal pain
    • NSAIDs initially—flunixin meglumine (0.5–1.1 mg/kg IV, IM every 8 h), α2-blockers such as xylazine (0.25–0.5 mg/kg IV or IM), detomidine (5–10 μg/kg IV or IM), or romifidine (0.02–0.05 mg/kg IV or IM)
    • Narcotic analgesic butorphanol (0.02–0.075 mg/kg IV) in conjunction with the α2-blockers
  • Spasmolytics (indicated in spasmodic colic)—N-butylscopolammonium bromide (0.3 mg/kg)
  • Laxatives—mainly used for impactions:
    • Mineral oil—10 mL/kg via nasogastric tube
    • Osmotic laxative—disodium (0.5 g/kg) or magnesium sulfate (0.5–1 g/kg) in 4 L of warm water via nasogastric tube ideally followed by oral or IV fluid therapy. Dioctyl sodium sulfosuccinate (10–30 mg/kg of a 10% solution). Water, via an indwelling nasogastric tube, if there is no gastric reflux
  • Parenteral fluid treatments—in cases of dehydration or moderate to severe impaction problems, IV fluid (100–150 mL/kg/day). If cardiovascular shock is present, hypertonic saline (2 L of 7% NaCl in an adult horse) prior to balanced electrolyte solutions may be given. Correction of electrolyte imbalances, especially hypokalemia and hypocalcemia, which are important for intestinal motility. Moderate to severe sodium bicarbonate deficit may be corrected as well as low plasma protein level (< 40 g/L)
  • Treatment of endotoxemia—flunixin meglumine 0.25 mg/kg every 6 h
  • Intestinal motility stimulants (see chapter Ileus)
  • Antimicrobial therapy if peritonitis is suspected or surgery is performed

Contraindications!!navigator!!

Acepromazine is contraindicated due to its peripheral vasodilatory effect.

Precautions!!navigator!!

Repeat use of α2-blockers and butorphanol causes prolonged ileus. Repeat dose of NSAIDs, especially in presence of dehydration, can result in gastric or large colon ulceration as well as renal damage.

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

Monitor closely for deterioration of clinical signs and cardiovascular status until resolution of the abdominal pain. Following resolution of these signs, reintroduction to feed should be done gradually.

Possible Complications!!navigator!!

  • Endotoxemia
  • Laminitis
  • Circulatory shock
  • Adhesions
  • GI rupture
  • Peritonitis

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Associated Conditions!!navigator!!

N/A

Age-Related Factors!!navigator!!

Older horses are more predisposed to strangulated lipoma and epiploic foramen entrapment; younger horses are more predisposed to ulcer problems, intussusception, and ascarid impactions.

Zoonotic Potential!!navigator!!

N/A

Pregnancy/Fertility/Breeding!!navigator!!

Mares in late gestation or in the postpartum period are predisposed to large colon torsion. Parturition can present clinical signs similar to a GI accident.

Synonyms!!navigator!!

Colic

Abbreviations!!navigator!!

  • GI = gastrointestinal
  • NSAID = nonsteroidal anti-inflammatory drug
  • RBC = red blood cell
  • WBC = white blood cell

Suggested Reading ⬆ ⬇

Hackett ES. Specific causes of colic. In: Southwood LL, ed. Practical Guide to Equine Colic. Ames, IA: Wiley Blackwell, 2013:204–230.

Mair T, Divers T, Ducharme N. Section 1: Diagnostic procedures in equine gastroenterology. In: Mair T, Divers T, Ducharme N (eds). Manual of Equine Gastroenterology. Philadelphia, PA: WB Saunders, 2002:3–46.

Mair T, Divers T, Ducharme N. Section 4: Colic. In: Mair T, Divers T, Ducharme N (eds). Manual of Equine Gastroenterology. Philadelphia, PA: WB Saunders, 2002:101–141.

Walton RM. Clinical laboratory data. In: Southwood LL, ed. Practical Guide to Equine Colic.Ames, IA: Wiley Blackwell, 2013:78–85.

Author(s) ⬆

Author: Nathalie Coté

Consulting Editors: Henry Stämpfli and Olimpo Oliver-Espinosa