Strangulation obstruction of the small intestine is frequently fatal because of simultaneous occlusion of the intestinal lumen
and its blood supply, resulting in progressive necrosis of the mucosa, and development of endotoxemia. Among the more common
causes of this condition are strangulating lipomas and entrapment within a natural internal opening or a mesenteric defect.
It has been widely recognized that horses with this type of obstruction are very susceptible to postoperative complications,
most notably endotoxic shock, postoperative ileus, and intra-abdominal adhesions. Despite these complications, short-term
survival rates (generally defined as discharge from the hospital) have dramatically improved over the last decade. However,
long-term survival remains a major concern, particularly because of complications associated with adhesions.
Horses with small intestinal strangulating obstruction typically have moderate and persistent signs of colic, until the latter
stages of the disease process, when they become profoundly depressed. Horses will have progressive signs of endotoxemia, including
congested mucus membranes, delayed capillary refill time, and an elevated heart rate (60-80bpm). In addition, reflux is typically
obtained following passage of a stomach tube, and loops of distended small intestine are usually detected on rectal palpation
of the abdomen. However, these latter findings are variable, depending upon the duration of obstruction, and the location
of the obstruction. For example, horses with ileal obstructions tend to reflux later in the course of the disease process
than horses with a jejunal obstruction. Furthermore, a horse that has an entrapment of small intestine in the epiploic foramen
or a rent in the gastrosplenic ligament may not have palpable loops of small intestine because of the cranial location of
these structures. Abdominocentesis is indicated in horses with suspected strangulation of the small intestine because analysis
of abdominal fluid can provide critical information on the integrity of the intestine. For instance, a horse that has signs
compatible with a small intestinal obstruction, and additionally has serosanguinous abdominal fluid with an elevated protein
level (>2.5mg/dl) is likely to require surgery. A horse that also has an elevated white blood cell count (>10,000cells/μl)
in the abdominal fluid likely has extensive strangulation, or long-standing strangulation.
Treatment should initially be aimed at controlling pain. Short-term analgesics such as xylazine (0.3 – 0.5mg/kg, IV, prn)
and butorphanol (0.05mg/kg, IV, prn) are very useful because of their potency, and because recurrent colic will usually be
detected within the time of the examination (30-60 minutes). The more potent α2 agonist detomidine (5-10μg/kg, IV, prn) is
required for horses that are violently painful, or which have pain recurring within a brief period of time (e.g., 5-15 minutes).
Long-term analgesics such as flunixin meglumine (1.1mg/kg, IV, q12h) are very useful for more prolonged periods of analgesia
and for reducing production of endotoxin-induced prostanoids. However, flunixin meglumine is best utilized following short-duration
analgesics so that recurrent colic can be detected early. In addition, the dose interval is very important considering the
deleterious effect of this drug on both the gastrointestinal mucosa and kidneys, particularly in dehydrated horses.
The second major goal of treatment is to ameliorate signs of shock. Horses with small intestinal strangulating obstruction
are typically at least 6% dehydrated (Table 1), requiring large volumes of isotonic fluids (e.g., 30L in a 500kg horse) to
correct fluid loss or sequestration. Half of the deficit can be administered rapidly (up to 100ml/kg/hr), followed by a reduced
rate for the remainder of the deficit volume (3-5L/ hr). In order to achieve more rapid correction of intravascular volume
depletion, hypertonic saline or an oncotic agent such as hetastarch can be pre- or co-administered with isotonic fluids. However,
these agents do not replace the need for isotonic fluids.
Treatments aimed at reducing the effects of the endotoxin-induced inflammatory cascade include flunixin meglumine and pentoxifylline.
The latter is a phosphodiesterase inhibitor that reduces elaboration of tumor necrosis factor (TNF)-?, although this action
is questionable at the currently recommended dosage (12mg/kg). This drug also has rheologic effects that may reduce the onset
of micro-circulatory disease, including laminitis. Additional treatments that may be used, particularly if endotoxemia is
detected in the early stages, are agents that bind endotoxin. These include hyperimmune serum (antibodies directed against
the core polysaccharide of either J5 Eschericia coli or the Re mutant of Salmonella) and polymixin B (6,000U/kg, IV).