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Basics ⬇

Outline

BASICS

Definition!!navigator!!

Impaired aboral transit of ingesta between the stomach and cecum.

Pathophysiology!!navigator!!

Small intestinal obstruction can be classified according to its degree of vascular involvement as strangulating or nonstrangulating. Whatever the cause, intestinal obstruction leads to distention with gas, fluid, and ingesta; this can compress intramural vasculature, leading to an increase in venous and capillary pressures and resulting in edema and, with time, necrosis of the intestinal wall. Once a certain intraluminal pressure threshold is reached there is net secretion, and more fluid will be sequestered in the lumen. This exacerbates distention and hypovolemia. Additionally, distention produces vascular compromise of the intestinal wall, contributing to adhesion formation. Intestinal distention activates pain receptors. In cases of vascular obstruction, simultaneous occlusion of the intestinal lumen and its blood supply occurs, leading to ischemic injury and possibly necrosis of the affected segment. A combination of pain (sympathetic stimulation) and inflammation results in ileus, further exacerbating the clinical signs.

Systems Affected!!navigator!!

  • GI—vascular obstruction results in congestive and/or ischemic damage of the intestinal wall. Failure to resolve the obstruction will lead to intestinal wall necrosis. Chronic nonvascular obstructions may lead to hypertrophy of the intestinal muscular layer, reducing the intestinal lumen
  • Behavioral—activation of pain receptors is associated with clinical signs of colic
  • Cardiovascular—shock occurs secondary to hypovolemia, endotoxemia, and altered electrolyte balance; with gastric distention, pressure on the vena cava decreases cardiac return, thus cardiac output
  • Respiratory—decreased pulmonary function may be secondary to pressure on the diaphragm from gastric distention or diaphragmatic herniation
  • Endocrine/metabolic—affected patients frequently demonstrate metabolic alkalosis secondary to loss of chloride in intestinal secretions; as the condition progresses and hypovolemia ensues, metabolic lactic acidosis develops
  • Hemic/lymphatic/immune—once tissue pressures exceed venous portal pressures, the small veins, venules, and lymphatics that drain the affected intestine collapse, and net fluid secretion into the bowel is potentiated. Hypovolemia results when excessive fluid is sequestered into the intestinal lumen
  • Renal/urologic—hypovolemia is associated with decreased glomerular filtration rate and renin, angiotensin II, and aldosterone production and secretion

Genetics!!navigator!!

Inflammatory bowel disease—granulomatous enteritis and eosinophilic gastroenteritis.

Geographic Distribution!!navigator!!

Southeastern USA—ileal impaction and proximal enteritis.

Signalment!!navigator!!

  • Any age, sex, or breed
  • Ascarid jejunal impactions are seen most commonly in foals/weanlings/yearlings
  • Small intestinal intussusception and volvulus occur most often in horses < 3 years of age
  • Small intestinal volvulus is most common in foals 2–4 months of age
  • Abdominal tumors usually are identified in older horses
  • 47–71% of horses with epiploic foramen entrapment are < 11 years of age
  • Incidence of strangulating lipoma is 5 times higher in horses > 15 years
  • Inguinal hernias are observed in stallions
  • Proximal enteritis may occur more commonly in stallions
  • Gastrosplenic ligament incarceration of the small intestine has been described most often in male horses
  • Mesoduodenal rents and diaphragmatic hernias can be seen in mares during late gestation
  • Warmbloods, Standardbreds, Tennessee Walking Horses, and American Saddlebreds appear to be predisposed to inguinal herniation

Signs!!navigator!!

Historical Findings

  • Horses with partial obstruction may display subacute, intermittent signs of abdominal pain or vague signs of lethargy, weakness, or weight loss. Transient episodes of abdominal pain may recur over a period of weeks to months and may progress in severity with time
  • Complete small intestinal obstruction is associated with signs of severe, persistent abdominal pain and ileus
  • Recent anthelmintic treatment contributes to ascarid impaction
  • Previous infection with Streptococcus equi can result in abscessation within the small intestinal mesentery (“bastard strangles”)

Physical Examination Findings

  • Clinical signs depend on the lesion present, its location, duration, and severity
  • Most common signs—abdominal discomfort, tachycardia, discolored mucous membranes, prolonged capillary refill time, clinical dehydration, decreased to absent small intestinal borborygmi, gastric reflux from the small intestine (yellow-brown, fetid odor, pH 6–8), and distended loops of small intestine and/or dehydrated colon contents contained within prominent colon haustra on rectal examination

Causes!!navigator!!

Nonstrangulating, Intraluminal Obstruction

  • Impaction—feed, trichobezoar, ascarids, or tapeworms
  • Foreign body
  • Healed duodenal ulcer, with scarring and stricture
  • Granulomatous enteritis

Nonstrangulating, Extraluminal Obstruction

  • Tension on duodenocolic ligament secondary to distention or displacement of the large colon
  • Adhesions—ischemic bowel, peritonitis, prolonged distention, excessive or traumatic surgical manipulation, anastomotic leakage, tissue dehydration, and inappropriate suture or technique
  • Ileal muscular hypertrophy
  • Ileal neurogenic stenosis
  • Ileocecal valve edema or infarction secondary to migrating strongyle larvae
  • Diverticula—traction, pulsion, or Meckel's
  • Mesenteric abscess
  • Neoplasia—pedunculated lipoma, lymphosarcoma, leiomyosarcoma, or carcinoid
  • Intramural hematoma

Strangulating Obstruction

  • Volvulus
  • Herniation—inguinal/scrotal, umbilical, diaphragmatic, epiploic foramen, gastrosplenic, nephrosplenic, or tears in mesentery/omentum/ligaments/fibrous bands/adhesions
  • Intussusceptions
  • Vaginal evisceration

Functional (Ileus)

  • Intestinal distention and ischemia
  • Intestinal inflammation—duodenitis/proximal jejunitis, enterocolitis, surgical manipulation, or resection/anastomosis
  • Endotoxemia
  • Peritonitis
  • Pain—GI, musculoskeletal
  • Drugs—α-adrenergic agonists, opioids
  • General anesthesia
  • Hypovolemia/hypotension
  • Electrolyte imbalances
  • Parasitism

Risk Factors!!navigator!!

Diet

  • Sudden changes in feed or feeding practices
  • Moldy hay or grain
  • Poor quality or low-grade roughage
  • Decreased roughage intake over 24 h
  • Coastal Bermuda hay—ileal impaction (regional)
  • Pelleted feed—impaction
  • Decreased water intake or availability—impaction

Management

Poor deworming program—ascarid impaction, large strongyle migration, and infarction.

Body Condition

Obesity—pedunculated lipoma.

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

Differentiating Similar Signs

GI reflux usually is pathognomonic for small intestinal obstruction.

Differentiating Causes

The ability to differentiate between causes depends on the severity of clinical findings, which may be influenced by location of the lesion, length of intestine involved, and stage of disease.

Abdominal Pain

  • In affected horses, some degree of gastric distention usually is present, which contributes to signs of abdominal pain
  • Abdominal pain may be absent in foals with umbilical or inguinal hernias
  • Biphasic abdominal pain has been associated with ileal impaction
  • Severe, acute abdominal pain usually is associated with strangulating lesions—volvulus
  • Ileocecal intussusception is accompanied by severe, acute abdominal pain, which subsides in 8–12 h to mild, intermittent pain that can persist for weeks to months, until complete obstruction occurs

Clinical Findings

  • Intestinal involvement in an umbilical hernia usually is evident on palpation—pain on palpation of the hernia may indicate a strangulating hernia
  • Inguinal hernias may be accompanied by mild to severe scrotal swelling, palpable loops of intestine within the scrotum, and decreased scrotal temperature because of vascular obstruction

Palpation per Rectum

  • Only the caudal 30–40% of the abdomen is palpable on rectal evaluation, but distention usually pushes affected intestinal segments backwards
  • In cases of small intestinal strangulation, distended loops of small intestine were palpated in 50–98% of horses
  • A thick, tubular structure palpable in the center of the abdomen may indicate ileal impaction, jejunal intussusception, or ileal intussusception
  • Resentment to palpation of the ileocecal region often accompanies ileocecal intussusception
  • Asymmetric inguinal rings, intestine or mesentery extending into an inguinal ring, or inability to identify 1 inguinal ring represent palpation findings in horses with inguinal herniation
  • If ileum is involved in inguinal herniation, the edematous antimesenteric ileocecal band may be palpable entering the ring on the affected side

CBC/Biochemistry/Urinalysis!!navigator!!

  • The WBC count usually is not affected by acute intestinal strangulation or obstruction
  • Leukocytosis/neutrophilia with a left shift may be observed with peritonitis, proximal enteritis, or mesenteric abscessation
  • Leukopenia/neutropenia may develop secondary to intestinal necrosis or endotoxemia
  • Most cases are accompanied by an increased packed cell volume and TP because of fluid sequestration within the bowel
  • Hypoproteinemia may develop as the disease progresses
  • Hypoalbuminemia may be observed with proximal enteritis or mesenteric abscessation
  • Hypergammaglobulinemia may be found with mesenteric abscessation or lymphosarcoma—β- and γ-fractions
  • Decreased potassium and chloride levels occur with intraluminal fluid loss, and decreased sodium and calcium levels occur secondary to extracellular fluid shifts
  • Loss of hydrochloric acid with gastric reflux results in metabolic alkalosis
  • Acute strangulating obstructions associated with release of endotoxin, increased production of lactic acid, and hypoperfusion result in metabolic acidosis
  • If small intestinal obstruction occurs in the region of the hepatopancreatic ampulla, increases in total bilirubin, alkaline phosphatase, and γ-glutamyltransferase may be observed
  • Serum amyloid A concentrations improve the ability to differentiate horses requiring surgical intervention

Other Laboratory Tests!!navigator!!

N/A

Imaging!!navigator!!

  • Abdominal ultrasonography should be used to assess small intestinal wall thickness and movement
  • Edema of the wall of the small intestine (> 3 mm wall thickness), distention, and absence of motility are suggestive of strangulating obstruction
  • Intestinal intussusception may display a characteristic concentric ring or “bull's eye” appearance
  • Abdominal radiography may be useful in distinguishing small from large intestinal problems in foals
  • Contrast radiography in foals may be used to demonstrate GI obstruction

Other Diagnostic Procedures!!navigator!!

Abdominocentesis

  • Normal nucleated cell count for adults ranges from 5000 to 10 000 cells/μL; however, in foals a cell count > 1500 cells/μL is considered elevated
  • As peritonitis and intestinal ischemia progress, the fluid becomes increasingly serosanguineous and cloudy as the cellularity and protein levels increase
  • WBC to TP ratios < 3 and red blood cell to TP ratios < 15 represent nonstrangulating obstructions or proximal enteritis; ratios > 3 or 15, respectively, indicate strangulating lesions
  • Peritoneal fluid may be evaluated cytologically for neoplastic cells
  • Peritoneal lactate concentration higher than the simultaneously measured blood lactate concentration is indicative of intestinal strangulation and ischemia
  • Horses with strangulating obstruction have a higher peritoneal lactate value (> 7 mmol/L) than those with nonstrangulating obstruction (< 3 mmol/L)

Endoscopy

  • May be used to identify duodenal ulcers
  • A 2.5–3.0 m endoscope is needed to visualize this region in adults

Laparoscopy and Celiotomy

May be performed to diagnose and correct the cause of obstruction or for intestinal biopsy.

Treatment ⬆ ⬇

TREATMENT

  • Horses with strangulating lesions will require surgical intervention to correct the lesion
  • Nasogastric decompression is vital. Horses may be transported with nasogastric tubes left in place
  • Exploratory laparotomy is necessary if a surgical lesion can be identified during rectal palpation or abdominocentesis, if abdominal pain becomes uncontrollable, or if there is a lack of response to medical therapy
  • IV fluid therapy is important to maintain hydration and tissue perfusion. Balanced polyionic IV solutions (e.g. lactated Ringer solution) are ideal; rate and quantity depend on the horse's status
  • The decision whether to administer IV fluids before transport depends on the horse's condition. Often, rehydration increases the volume of gastric reflux, so gastric decompression may need to be performed more frequently
  • Hyperimmune serum or polymyxin B (6000 U/kg body weight) may benefit horses with endotoxemia

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

  • Sedation and analgesia may be achieved with xylazine (0.2–1.1 mg/kg IV) or detomidine (0.005–0.02 mg/kg IV); both duration and quality of sedation or analgesia may be enhanced by coadministration of butorphanol tartrate (0.1 mg/kg IV)
  • NSAIDs such as flunixin meglumine (1.1 mg/kg IM or IV BID) or phenylbutazone (2.2–4.4 mg/kg PO or IV BID) may be used for analgesic and anti-inflammatory effects as well as to mediate the effects of endotoxin
  • Endotoxemia also may be treated with polymyxin B (6000 U/kg diluted in 0.5–1.0 L of saline IV BID) or pentoxifylline (8.5 mg/kg PO BID)
  • Specific therapies for ileus, sepsis, gastric ulcers, and laminitis are discussed elsewhere

Contraindications!!navigator!!

Acepromazine for sedation in hypovolemic horses.

Precautions!!navigator!!

  • Continued monitoring after administration of analgesics is important to ensure the drug is not masking signs of pain while the disease process progresses
  • Certain drugs (e.g. xylazine, detomidine, opioids) decrease GI motility
  • Gentamicin, amikacin, and polymyxin B are potential nephrotoxic drugs

Possible Interactions!!navigator!!

N/A

Alternative Drugs!!navigator!!

N/A

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

Depends on cause of obstruction and method of treatment.

Possible Complications!!navigator!!

  • Gastric rupture
  • Intestinal necrosis
  • Abdominal adhesions
  • Thrombophlebitis
  • Laminitis
  • Hypovolemic or endotoxic shock

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Associated Conditions!!navigator!!

  • Endotoxemia
  • Ileus
  • Impaction of the large or small colon secondary to dehydration
  • Laminitis

Age-Related Factors!!navigator!!

N/A

Zoonotic Potential!!navigator!!

N/A

Pregnancy/Fertility/Breeding!!navigator!!

Outcome of pregnancy is determined more by the cardiovascular and metabolic status of the mare and fetus than by the specific cause of the condition.

Synonyms!!navigator!!

N/A

See Also!!navigator!!

  • Acute adult abdominal pain—acute colic Duodenitis–proximal jejunitis (anterior enteritis, proximal enteritis)
  • Endotoxemia
  • Ileus

Abbreviations!!navigator!!

  • GI = gastrointestinal
  • NSAID = nonsteroidal anti-inflammatory drug
  • TP = total protein
  • WBC = white blood cell

Suggested Reading ⬆ ⬇

Desrochers A. White NA. Diagnostic approach to colic. In: Blikslager AT, White NA, Moore JN, Mair TS, eds. The Equine Acute Abdomen, Hoboken, NJ: Wiley-Blackwell, 2017:223–263.

Freeman DE. Small intestine. In: Auer JA, Stick JA, eds. Equine Surgery, 3e. St. Louis, MO: Saunders Elsevier, 2006:401–436.

Author(s) ⬆

Author: Antonio M. Cruz

Consulting Editors: Henry R. Stämpfli and Olimpo Oliver-Espinosa

Acknowledgment: The author and editors acknowledge the prior contribution of Judith B. Keonig and Annette M Sysel.