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.

Protein C content and plasminogen activity were measured in plasma from 100 horses with signs of colic. Data were analyzed by grouping horses 4 ways. Each horse was allotted to 1 of 2 outcome groups (survivors and nonsurvivors), 1 of 3 broad-category diagnosis groups (inflammatory disorders, strangulating obstructions, and all other gastrointestinal disorders), and 1 of 2 clinical management groups (medical and surgical). In a fourth grouping, all horses (although numbers of horses included in each subgroup were small) were assigned either to specific diagnostic groups that had high expectation for activated hemostasis (intestinal ischemia, endotoxemia, jugular thrombosis, peritoneal adhesions, and laminitis) or to a control group, in which active hemostasis was unlikely. Within 2 to 24 hours after admission, nonsurvivors developed lower protein C content than did survivors. Protein C content and plasminogen activity became low during hospitalization in horses with strangulating obstructions and in horses having surgery. The results from the grouping by specific diagnosis must be considered pilot data because the numbers of horses in each subgroup were small. Although not statistically significant, trends were noticed in protein C and plasminogen: (1) horses with intestinal ischemia and endotoxemia developed low protein C content and plasminogen activity, (2) protein C content became low in horses that developed peritoneal adhesions or laminitis, and (3) plasminogen activity became low in horses that developed jugular thrombosis. Low protein C content or low plasminogen activity, or both, may be useful as predictors for outcome and for these specific complications of equine colic. Protein C content and plasminogen activity were often normal at admission, but decreased by 2 to 24 hours; therefore, the hemostatic alterations appear to be an effect, rather than a cause of the gastrointestinal disorders. A return to normal values over several days may signify clinical improvement.

A survey of 1,965 equine colic cases was conducted from August 1985 to July 1986 at 10 equine referral centers located throughout the United States. The purpose of this study was to develop and validate a multivariable model for the need for surgery. Two-thirds of the cases were randomly selected for model development (1,336), whereas the remaining cases (629) were used only for subsequent validation of the model. If a lesion requiring surgical correction was found at either surgery or necropsy, the case for the horse was classified as surgical, otherwise the case was classified as medical. Only variables that were significant (P < 0.05) in an initial bivariable screening procedure were considered in the model development. Because of the large number of missing values in the data set, only variables for which there were < 400 missing values were considered in the multivariable analysis. A multivariable logistic regression model was constructed by use of a stepwise algorithm. The model used 640 cases and included variables: rectal findings, signs of abdominal pain, peripheral pulse strength, and abdominal sounds. The likelihood ratio for surgery was calculated for each horse in the validation data set, using the logistic regression equation. Using Bayes theorem, the posttest probability was calculated, using the likelihood ratio as the test odds and the prevalence of surgery cases (at each institution) as an estimate of the pretest odds. A Hosmer-Lemeshow goodness-of-fit X2 statistic indicated that the model fit the validation data set poorly, as demonstrated by the large X2 value of 26.7 (P < 0.001). However, when the expected proportion of surgical cases was compared with the observed proportion of surgical cases in each of 10 increments of risk, the model's performance appeared satisfactory.

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.