Over a 24-month period, serum tumor necrosis factor (TNF) activity was determined in 289 horses with colic attributable to gastrointestinal tract disease. Serum TNF activity was quantitated by use of a modified in vitro cytotoxicity bioassay, using WEHI 164 clone-13 murine fibrosarcoma cells. Causes for colic, determined by clinical and laboratory evaluation, exploratory celiotomy, or necropsy included: gastrointestinal tract rupture (GTR); ileal impaction; small intestinal strangulating obstruction (SIO); proximal enteritis (PE); transient small intestinal distention; large-colon displacement; large-colon vovulus; large-colon impaction; colitis; small-colon obstruction; peritonitis; and unknown. Each diagnosis was placed into 1 of 3 lesion categories: inflammatory disorders (GTR, PE, colitis, peritonitis); strangulating intestinal obstruction (SIO, large-colon volvulus); and nonstrangulating intestinal obstruction (ileal impaction, transient small intestinal distension, large-colon displacement, large-colon impaction, small-colon obstruction, unknown). The prevalence of high serum TNF activity and/or mortality were evaluated. Differences were tested at significance level of P < 0.05. Approximately 20% of the 289 horses has serum TNF activity greater than that found in clinically normal horses (> 2.5 U/ml). Twenty-three horses (8%) had marked increase in serum TNF activity (greater than or equal to 10 U/ml) which was more prevalent among horses with SIO and PE than in horses of other diagnostic groups, except those with GTR. Mortality and marked increase in serum TNF activity were greater in horses with intestinal inflammatory disorders or strangulating intestinal obstruction than in horses with nonstrangulating intestinal obstruction. Similarly, a greater proportion of the horses that died had markedly high serum TNF activity than did horses that lived. Mortality of horses with serum TNF greater than or equal to 10 U/ml was greater than that of horses with serum TNF activity < 10 U/ml. Results indicate possible association between colic and serum TNF activity in horses and that high mortality may be associated with horses with markedly increased serum TNF activity.

A 3-year-old female Thoroughbred racehorse was presented following the accidental oral and skin administration of amitraz. This case report describes the clinical signs and the treatment of this horse. Clinical signs of amitraz toxicosis are associated with the stimulation of alpha2-adrenergic receptors. Amitraz is seldom fatal because the effects can be reversed by alpha2-adrenergic antagonists. The horse displayed typical clinical signs of colic, including pawing, small hard drops, tranquillisation, depression, ataxia, muscular incoordination and impaction colic lasting up to 7 days. The syndrome was accompanied by mild dehydration. The horse survived after persistent symptomatic treatment, including the giving of intravenous fluids, antibiotics, multiple doses of mineral oil per os, nonsteroidal anti-inflammatory drugs and dexamethasone intramuscularly and intravenously.

Diaphragmatic hernias, whether congenital or acquired (traumatic), are rarely observed in the horse. Acquired diaphragmatic hernias typically occur secondary to trauma or an increase in intra-abdominal pressure due to falling, heavy exercise, or parturition. Diaphragmatic herniorrhaphy is difficult to perform in adult horses and the horses with symptomatic diaphragmatic hernias usually die. A 10-year old, 340 kg, Jeju horse (crossbred) broodmare with sudden onset of gait disorder and a moderate emaciation was examined. Findings on physical examination included conjunctivitis, dehydration, shallow breathing, dyspnea, weaken heart beat, lack of auscultatable sounds from the gastrointestinal tract, and anorexia. Rectal temperature was 38.4℃ and respiratory rates were moderately increased. There were slight signs of acute colic. The broodmare died one day after non-specific treatment of fluids, nutriment, antibiotics and non-steroidal anti-inflammatory drug. The cause of death was strangulation of the small intestine through a diaphragmatic hernia. The rent was about 2 cm in diameter and located in the central right part of diaphragm. Around 60 cm of small intestine was protruded into thoracic cavity through the rent. The cause of the hernia could not be ascertained. The broodmare had been pastured with many other horses, and the groom had not noticed any aggressive behavior among them. It was, however, speculated that trauma by stallion's attack may have been the cause of the diaphragmatic hernia, because the new horse may be the object of behaviors ranging from mild threats to seriously aggressive kicking, squealing, rearing, and biting.

A variety of enteric diseases may result in the manifestation of abdominal pain in horse. An acute colic in a 5-month-old Thoroughbred filly is described. The filly was presented with acute colic characterized by rolling and pawing. Next day she suffered from severe abdominal pain and subsequently died. Post mortem examination revealed very heavy ascarid, Parascaris equorum (P. equorum) infection in small intestine. In addition, it is also noted the presence of P. equorum in the stomach. Infection due to P. equorum manifests itself in foals between 6-8 weeks and one year of age.

A 3-day-old Appaloosa colt was examined because of acute onset of ataxia, left-sided head tilt, fever and heart murmur. The foal continued to nurse but became increasingly depressed and mild colic. On plain radiological examination, the foal was normal. Uroperitoneum was diagnosed following abdominocentesis. Postmortem examination revealed bladder rupture. The lesion was in the dorsomedial part of the bladder wall. We suggested that the cause of bladder rupture was parturient trauma. Even though the rupture was associated with trauma, the margin of rupture of bladder was clearly smooth and regular.