colonic luminal pressure in horses with strangulating and nonstrangulating obstruction of the large...

Veterinary Surgery 25: 134-14 I, 1996

Colonic Luminal Pressure in Horses With Strangulating and Nonstrangulating Obstruction of the Large Colon

RUSTIN M. MOORE, DVM, PhD, Diplomate ACVS; STEPHEN R. HANCE, DVM, Diplomate ACVS, Diplomate ABVP, JOANNE HARDY, DVM, MS, Diplomate ACVS, BONNIE RUSH MOORE, DVM, MS, Diplomate ACVIM,

ROLF M. EMBERTSON, DVM, Diplomate ACVS, and PETER D. CONSTABLE, BVSC, PhD, Diplomate A C V I M

Colonic luminal pressure (median, range) measured during ventral midline celiotomy in 69 horses with strangulating obstruction (SO) of the large colon (SO; 2 270" large colon volvulus; 27 cm H 2 0 2 to 80 cm H20) was greater ( P = .0023) than that measured in 37 horses with nonstrangulating obstruction (NSO) of the large colon (NSO; I 180" volvulus or a nonstrangulating displacement; I8 cm H,O; 6 to 46 cm H20). Sixty-five percent (45 of 69) of horses with SO and all horses with NSO survived. Survival analysis was restricted to 59 horses with large- colon SO that survived to hospital discharge or met the criteria specified for classification as nonsurvivors. Colonic luminal pressure in nonsurvivors (48.5 cm H20; 34 to 80 cm H20) was higher ( P = .0001) than that measured in survivors ( 1 8 cm H,O; 2 to 50 cm H 2 0 ) of SO. From response operating characteristic curves, a luminal pressure of 38 cm H 2 0 optimized the distribution of horses with SO into survivor and nonsurvivor groups. Sensitivity, specificity, and positive and negative predictive values for a colonic luminal pressure greater than 38 cm H20 in predicting nonsurvival were 0.89, 0.9 1, 0.72 and 0.97, respectively. Measurement of colonic luminal pressure may be useful for predicting survival in horses with colonic volvulus. @Copyright I996 by The American College oJ Veterinary Surgeons

TRANGULATING OBSTRUCTION (SO) and S nonstrangulating obstruction (NSO) of the large colon are common causes of colic in horses.'-' Ap- proximately 50% of the horses requiring surgical intervention for colic have large colon abn~rmalities.~ Yolvulus (> 270") is the only clinically significant cause of large-colon SO whereas partial volvulus (I 11 S O 0 ) , displacement, or both conditions results in large-colon NSO in horses. Large-colon volvulus is associated with mortality in 60% to 80% of affected

horses; high mortality has been associated with severe mucosal injury that occurs during and after ischemia. '.2.4-6 Colonic luminal distention occurs because of accumulation of intestinal gas and fluid caused by luminal obstruction or vascular occlusion or both.2 Accumulation of luminal fluid and gas results in increased colonic luminal pressure because the intestine is not a perfectly compliant organ.' Addi- tionally, the abdominal wall is resistant to expansion; increased intra-abdominal pressure contributes to

~~ ~~ ~ ~

From the Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, OH; and Rood & Riddle Equine Hospital, Lexington, KY.

Dr. RM Moore's present address is Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State LJniversity, Baton Rouge, LA; Dr. BR Moore's present address is Department of Veterinary Clinical Sciences, Kansas State University, h4anhattan, KS; Dr. Constable's present address is Department of Veterinary Clinical Medicine, University of Illinois at Urbana- Champaign, Urbana, IL.

Presented in part at the 29th Annual American College of Veterinary Surgeons Veterinary Scientific Meeting, Washington, DC, October, 1994.

No reprints available. OCopyright 1996 by The American College of Veterinary Surgeons 0 I6 1 -3499/96/2502-0008$3.00/0

134

MOORE ET AL 135

increased luminal pressure by external compression of the intestinal waL8

Luminal distention contributes to compromised intestinal wall and mucosal blood f l o ~ . ~ , ~ Intestinal distention and increased luminal pressure progressively compromises microcirculation initially by compressing venous outflow, which results in edema and further increases in luminal pressure; arteriolar flow is ultimately compromised.8 Increased luminal distention has a more profound effect on mucosal blood flow than on seromuscular flow; blood flow actually shunts from tissues that consume greater amounts of oxygen (mucosa) to low resistance vascular beds that consume small amounts of oxygen (serosa)." Increased luminal pressure in the large colon may exacerbate the ischemia that occurs because of twisting and stretching of the colonic vessels during naturally acquired large-colon volvulus in equids.

Small intestinal luminal pressure is significantly higher in horses that do not survive small intestinal obstruction, and luminal pressure is lower and survival is greater in horses with simple obstruction compared with those with SO ofthe small intestine." Abomasal luminal pressure is significantly higher in cattle with either abomasal volvulus or left displaced abomasum than in normal cattle.' Abomasal luminal pressure is significantly lower in cattle that survive and remain productive than it is in nonsurvivors or in nonproductive cattle with abomasal vol- vuIus.7

Current methods for determination of colonic viability include clinical assessment, fluorescein stain- ing, surface oximetry, Doppler ultrasonographic determination of intestinal blood flow, and histological evaluation of frozen biopsy sections.'2 None of these methods is accurate enough to consistently determine intestinal viability and predict patient survival. Surface oximetry combined with histological evaluation of frozen biopsy specimens has been reported to be the best indicator of large colon viability in horses with large-colon v o l v ~ l u s . ~ ~ ' ~ The use of abomasal luminal pressure measurements is an accurate method for predicting survival in cattle with abomasal vo lvulu~.~ Constable and coworkers reported that a value of 16 mm Hg for abomasal luminal pressure optimizes the distribution of cattle with abomasal volvulus into productive and nonproductive groups7 Measurement of colonic luminal

pressure in horses with large-colon volvulus may improve the clinician's ability to determine colonic viability and accurately predict survival.

The purposes of this study were to determine if colonic luminal pressure is greater in horses with SO compared with NSO; to determine if colonic luminal pressure is greater in nonsurvivors compared with survivors of large-colon SO; and to determine the ideal colonic luminal pressure value to optimize the distribution of horses with large-colon SO into survivor and nonsurvivor groups.

MATERIALS AND METHODS

Criteria .for selection of cases. Luminal gas pressure was measured in the large colon of adult horses admitted to The Ohio State University (OSU) Veterinary Hospital and to Rood & Riddle (R&R) Equine Hospital, between 1991 and 1994, with a diagnosis of either SO (2 270" volvulus) or NSO (5 180" volvulus, left dorsal displacement, right dorsal displacement, or pelvic flexure retro- flexion) of the large colon. Horses with large-colon im- pactions or enteroliths; primary cecal, small intestinal, or small colon disease: or those horses with large-colon SO that had a ruptured colon at the time of surgery were excluded from the study.

Signalment, duration of colic signs, duration of severe abdominal pain from onset to the time of hospital admission. lesion type, and luminal pressure were recorded.

Anesthesia. Horses were anesthetized (halothane or isoflurane in oxygen) and positioned in dorsal recumbency with the rear legs in a relaxed, flexed position.

Colonic luminal gas pressure was measured intra-abdominally after ventral median celiotomy and before exteriorization, rnanipula- tion, or surgical correction of the abnormality. A cali- brated pressure gauge (Pressure Manometer, Spectrum Anesthesia Services, Inc, Louisville, KY) attached to either a 14- or 16-gauge needle by flexible rubber tubing was used to measure colonic luminal pressure. The needle was inserted obliquely through the colon wall by the surgeon whereas the pressure gauge, which was nonstenle, was handled by a surgery suite assistant. Approximately 30 seconds were allowed after needle insertion for equilibra- tion, and then if the value had stabilized, the pressure was recorded. Luminal pressure was recorded at the end of expiration or immediately before mechanical ventilation.

After colonic lurninal pressure was recorded, colonic gas was evacuated by suction, and the abnormality was surgically corrected. The appearance of the large colon serosa and sometimes the mucosa were evaluated in an attempt to assess viability using established

Data collection.

Luminal pressure measurements.

Surgical management.

11 36 LUMINAL PRESSURE IN LARGE COLON OF HORSES

c~iteria.'~ When the colon was determined by clinical assessment to be nonviable, or if the owners chose not to recover the horse, full-thickness biopsy specimens were collected from the pelvic flexure and immediately fixed in 10% buffered formalin. Biopsy specimens were later processed and stained with hematoxylin-eosin for light inicroscopic evaluation. All horses with NSO and most with SO of the large colon were recovered from anesthesia. ]Large colon resection was performed in two horses on the basis of clinical assessment of colonic nonviability. Col- opexy to prevent recurrence of colonic volvulus, was per- Iormed in nine horses at the discretion of the surgeon.14

Perioperative medical management. Horses were treated medically during the perioperative period with antibiotics, flunixin meglumine, and intravenous fluids. Most horses with large-colon SO were administered an- tiendotoxin serum (Endoserum, IMMVAC, Inc, Colum- bia, MO) IV intraoperatively, postoperatively, or both times. Although not quantifiable, we believe that perioperative medical management was similar and adequate nn all horses.

Survivor versus nonsurvivor class$cution. Horses were classified as survivors if they were discharged from the hospital. Nonsurvivors were those horses that died or were euthanatized during the postoperative period and those horses euthanatized during surgery that had a nonviable colon determined by histological examination of colonic biopsy specimens. Criteria for determination of colonic nonviability included loss of 2 97% of the surface epithelium, loss of 2 50% of the depth of the mucosa, or an interstitia1:crypt ratio 2 3: 1, or a combination of these iindice~.~ Horses euthanatized during surgery with colonic biopsy specimens considered to be viable on microscopic examination were excluded from the survival portion of the study, because it was unknown whether they would have survived.

A Mann-Whitney U test was used to compare colonic luminal pressure between horses with NSO and SO, between survivors and nonsurvivors of large-colon SO, and between nonsurvivors of SO and horses euthanatized during surgery without colon biopsy specimens; survival of horses admitted to the two participating hospitals; and duration of clinical signs and severe abdominal pain in horses admitted to the two hospitals. Statistical significance was set at P < .05 for all tests. To evaluate the use ofcolonic luminal pressure as a prognostic indicator, an optimal luminal pressure value was determined by calculating the sensitivity and specificity of various luminal pressure cutoff values and constructing response operating characteristic (ROC) curves. l 5 In this study, the ROC is a plot of the sensitivity versus ( 1 -specificity) 100 of luminal pressure in predicting nonsurvival. 'The optimal luminal pressure value was determined by the point on the ROC curve closest to the upper left-hand

Statisricul unu/yses.

comer, which minimizes the sum of false-positives and false-negatives. Positive (PPV) and negative predictive values (NPV) for nonsurvival were calculated using the optimal luminal pressure value for prevalences of death in different hospital populations of horses with large-colon s0.15

RESULTS

Cases. Colonic luminal pressure was measured in 69 horses with SO (2 270" large-colon volvulus) and 37 horses with NSO (5 180" volvulus or large- colon displacement) of the large colon. Sixty-six of 69 horses with large-colon SO had 2 360" volvulus; the other three horses had a 270" volvulus. The colon in two horses with SO was ruptured at surgery; these horses were excluded from the study. The mean age of horses with SO and NSO were 10.3 (range: 1 to 20 years) and 8.3 years (range: 1 to 20 years), respectively. Sex distribution was as follows: 6 males, 6 geldings, and 57 females for SO, and 7 males, 7 geldings, and 23 females for NSO. Median duration of colic signs was 6.85 (range: 0.5 to 48) hours and median duration of signs of severe pain was 4.64 (range: 0.5 to 18) hours for horses with large-colon SO. Median duration of signs of colic was 17.84 (range: 2 to 72) hours for horses with large-colon NSO. The median duration of signs of severe pain for horses with large-colon SO was 4.5 (range; 0.5 to 18) hours for survivors and 4.75 (range: 2 to 12.5) hours for nonsurvivors; there was no difference (P = .29) in duration of severe pain between survivors and nonsurvivors of large-colon SO. There was a significantly (P = -019) higher duration of severe abdominal pain before hospital admission in horses admitted to OSU (6; 1.5 to 12 hours) versus R&R (3; 0.5 to 1 I hours).

Luminal pressure (median; range) was significantly (P < .0023) greater in horses with SO (27 cm H20; 2 to 80 cm H20) than in horses with NSO (18 cm H20; 6 to 46 cm H20). Sixty-five percent (45 of 69) of all horses with SO and all horses with NSO survived to hospital discharge.

Sixteen horses with large-colon SO were euthanatized during surgery; colonic biopsy specimens (9 horses) were obtained and 7 were histologically classified as nonviable. Eight horses either died or were euthanatized postoperatively, 7 because of toxemia and shock and 1 because of pneumonia. The horse that died from pneumonia

Szirvival analysis.

MOORE ET AL 137

90

80

70

60

50

40

30

20

10

0

ee

8

‘.J

so NSO Fig 1 . Scatter plot of colonic luminal pressure in horses, of known survival status, with strangulating obstruction (SO, n =

59) and large-colon nonstrangulating obstruction (NSO, n = 37). Open circles indicate survivors and solid circles indicate nonsurvivors.

was excluded from survival analysis. Overall, 14 horses with large-colon SO died, were euthanatized postoperatively, or were euthanatized at surgery with colonic biopsy specimens classified as nonviable. There was no difference (P = .49) in colonic luminal pressure between these horses and the seven horses euthanatized intraoperatively that did not have specimens collected (47; 15 to 80 cm H20).

The large colon was resected in two horses. Co- lonic luminal pressure in these two horses was 15 and 42 cm H 2 0 , respectively. The horse with a pressure of 15 cm H20 was euthanatized postoperatively because of pneumonia, and so this horse was excluded from survival analysis. The other horse with a pressure of 42 cm H 2 0 was euthanatized postoperatively because of complications associated with the origmal disease. Colopexy was performed in nine horses; six horses had a colopexy performed because colonic volvulus had recurred, and three horses had a colopexy performed at the time of the first volvulus.

Eight of these horses had a luminal pressure less than 38 cm H20, and one horse had a pressure of 42 cm HzO: all of these horses survived.

Survival analysis was restricted to 59 horses with large-colon SO that either survived to hospital discharge (45 horses) or met the criteria for inclusion as nonsurvivors (14 horses). Ten horses with SO were excluded from survival analysis because they were either euthanatized during surgery and had biopsy specimens that did not meet the histological criteria for being nonviable (2 horses), euthanatized during surgery with no biopsy specimens collected (7 horses), or died postoperatively because of pneumonia ( 1 horse). Luminal pressure in nonsurvivors (48.5 cm H20; 34 to 80 cm H20) was significantly greater (P < .OOOl) than luminal pressure in survivors ( 1 8 cm H20; 2 to 50 cm H20) of large-colon SO (Fig 1). There was a trend toward ( P = .0768) a difference in survival of horses with large-colon SO between horses admitted to OSU (53.3%) and R&R (79.3%).

As determined by ROC curves, a luminal pressure of 38 cm H 2 0 optimized the distribution of horses with large-colon SO into survivor and nonsurvivor groups (Fig 2). Sensitivity and specificity of a colonic luminal pressure greater than 38 cm H 2 0 for pre-

cm ofH20

0 10 20 30 40 50 60 70 80 90 100

100 (1-Specificity) Fig 2. Response operating characteristic curve of colonic luminal pressure values for horses with large-colon strangulating obstruction. *Operating point that maximizes sensitivity and specificity.

!I 38 LUMINAL PRESSURE IN LARGE COLON OF HORSES

diction of postoperative outcome were 0.89 and 0.9 I , respectively. The positive and negative predictive values of a colonic luminal pressure greater than 38 cm H20, with a mortality prevalence of 24%, were 0.72 and 0.97, respectively. Because the positive and negative predictive values of a test depend on prevalence, a plot of positive and negative predictive values versus the prevalence of death of horses with large-colon SO in different hospital populations was constructed (Fig 3).

DISCUSSION

The major findings of this study were that luminal pressure was greater in horses with large-colon SO than in horses with NSO; luminal pressure was greater in nonsurvivors than in survivors of large- colon SO; and measurement of colonic luminal pressure in horses with naturally acquired large-colon SO and NSO can be performed easily and in a timely fashion (approximately 1 to 2 minutes).

The median colonic luminal pressure for nonsurvivors of large-colon SO in our study was 48.5 cm H ~ o , which is higher than the reported median small intestinal luminal pressure of 15.3 cm H20 in non- surviving horses with small intestinal obstruction." An explanation for the difference in magnitude of these pressures may be associated with anatomical differences in these two segments of bowel. It is pos- sible that the microvascular architecture of the colonic mucosa renders it more resistant to increased luminal pressure. It has been shown that the large bowel of piglets maintains fairly normal blood flow up to a luminal pressure of 41 cm H,o, whereas the small intestine seems to be more sensitive to increased luminal pressure.* One potential explanation for this difference is that porcine small intestine mucosa may have a higher metabolic rate than the large intestinal mucosa because of greater enzymatic digestion and absorption. To our knowledge, it is unknown whether the small intestinal mucosa has a greater metabolic rate than the large-colon mucosa in equids; the large-colon mucosa likely has a high metabolic rate attributable to the processes involved in maintenance of normal luminal osmolality and pH, and the absorption of volatile fatty acids.16

Measurement of colonic luminal pressure seems to provide additional useful information for determining potential colonic viability and in formulating a prognosis for survival. Because of the small number

+ PPV

0 10 20 30 40 SO 60 70 80 90 100

Prevalence (%)

Fig 3. Positive (PPV) and negative (NPV) predictive value versus prevalence of death in horses with colonic luminal pressure greater than 38 cm H 2 0 (sensitivity = 0.89, specificity = 0.91). As the prevalence of death increases in a population of horses with large-colon strangulating obstruction, the PPV for luminal pressure values greater than 38 cm H20 becomes more valid in predicting death. Solid vertical line represents prevalence of death (24%) in horses with large-colon SO in the present study.

of horses in which a colon resection was performed it was impossible to determine if luminal pressure measurement may aid the decision for resection. A luminal pressure value of 38 cm H 2 0 optimized the distribution of horses with SO of the large colon into survivor and nonsurvivor groups. Horses with luminal pressure greater than 38 cm H20 were more likely to die than horses with pressures less than 38 cm H20. In fact, 89% of horses with a luminal pressure greater than 38 cm H20 died. Perhaps with further study it can be determined if horses with a colonic luminal pressure greater than 38 cm H 2 0 would survive with large colon resection.

Although 38 cm H 2 0 was the optimal luminal pressure value that discriminated between survivors and nonsurvivors of large-colon SO, the consequence of using this value to determine nonsurvival is that a small number of horses may be euthanatized that would otherwise have survived with appropriate therapy. Response operating characteristic curves are generated from sensitivity and specificity data, therefore, the optimal luminal pressure value is un- affected by differences in prevalence of death in

MOORE ET AL 139

horses with large-colon SO among different hospi- t a l ~ . ' ~ In contrast, positive and negative predictive values are dependent not only on sensitivity and specificity, but also on the prevalence of death; positive predictive value is high if prevalence of death is high, and negative predictive value is high if the prevalence of death is low." Therefore, the prevalence of death of horses with large-colon SO in a given hospital population should be considered before interpretation and application of positive and negative predictive values from the population of horses reported in our study. The validity of using a luminal pressure greater than 38 cm H 2 0 for predicting nonsurvival in horses with large-colon SO in different veterinary hospitals can be determined from a plot of the positive and negative predictive values for nonsurvival of horses with this luminal pressure value versus the prevalence of death in horses in different hospital populations.

The trend toward higher survival for horses with large-colon SO from one of the participating hospitals (R&R) may be because of the difference in elapsed time between onset of severe abdominal pain and hospital admission in horses admitted to the two hospitals, Although from this study it may seem that higher survival at R&R may be associated with a shorter duration of large-colon SO before surgical intervention, other studies have failed to document a correlation between survival and duration of volvulus before surgical correction in horses from a sin- gle hospital population.' Perhaps horses admitted to the hospital with a higher survival rate were of greater economic value, which allowed more intensive medical and supportive care during the postoperative period. Regardless of the reasons for differences between the two hospital populations, we believe pool- ing of data from the two hospitals is unlikely to affect the validity and use of luminal pressure measurements as a prognostic indicator of horses with naturally acquired large-colon SO provided clinicians interpret this information taking into consideration the prevalence of death of horses with large-colon SO in their hospital population.

The correlation between high colonic luminal pressure and nonsurvival is not surprising, because high luminal pressures exacerbate ischemia-induced colonic mucosal necrosis. Colonic luminal pressures above mean mucosal capillary pressure progressively compromise the microcirculation first by obstructing venous outflow, resulting in edema and further in-

creases in luminal pressure, which eventually compromises arteriolar flow.8 Not only does total intestinal blood flow decrease with increasing luminal pressure, but there is a disproportionate decrease in mucosal blood flow.8 Mural blood flow distribution in the porcine small intestine under normal circum- stances is approximately 2: 1 between the mucosa and muscularis.8 Moreover, increased luminal pressure changes blood flow distribution to 1 :4 between mucosa and muscularis.' Oxygen consumption of the small intestine was low when luminal pressures were 40 mm Hg or greater." Taken together, these results indicate that increased luminal pressure causes blood flow to shunt away from portions of the intestinal wall (ie, mucosa) that consume large quantities of oxygen toward lower resistance vascular beds (ie, serosa) that consume smaller amounts of oxygen. This selective mucosal ischemia occurs with luminal pressures similar to those reached during naturally acquired intestinal obstruction." Impair- ment of villus circulation of the small intestinal mucosa occurs when luminal pressure reaches 20 mm Hg; when luminal pressure is further increased, de- rangements in blood flow spread toward the outer layers of the intestinal wall. l o Experimental studies, therefore, clearly show that increased luminal pressure decreases blood flow to intestinal mucosa.8'io These changes would be expected to potentiate he- modynamically mediated reduction in intestinal mucosal blood flow caused by venous and lymphatic obstruction.

Luminal pressure was greater than or equal to 38 cm H,o in three horses with large-colon NSO. There were no apparent deleterious effects of high luminal pressure in the absence of vascular occlusion, because all of these horses survived to hospital discharge. Some may speculate that the greater pressures in SO versus NSO were because of a longer duration of obstruction before surgical intervention, however, in our study the duration of colic signs was longer in horses with NSO. Seemingly, the most likely explanation is that horses with NSO did not have vascular occlusion, and despite the high luminal pressure, mucosal flow was not compromised suffi- ciently to cause severe mucosal injury. Similar findings have been observed in cattle with abomasal volvulus and left displaced abomasum.' In horses, induced luminal fluid distention of the small intestine up to 18 cm H ~ o for 1 hour failed to cause histological or ultrastructural damage to mucosal

1 40 LUMINAL PRESSURE IN LARGE COLON OF HORSES

epithelium like that observed in naturally acquired intestinal obstruction or in experimentally induced intestinal ischemia. l 7 This luminal pressure was similar to the pressure measured in horses with naturally acquired fatal small intestinal obstruction. I '

Experimentally, incremental increases in porcine small and large intestinal luminal pressures of 15, 30,45, and 60 mm Hg caused decreases in mucosal blood flow to approximately 45%, 40%, 30%, and 20% of baseline flow.8 However, even at 60 mm Hg intestinal blood flow was not reduced to a point of critical ischemia.* The intestinal wall is capable of maintaining adequate blood flow at luminal pressures well above a capillary pressure of 15 mm Hg.8 Therefore, other factors, most notably primary vascular occlusion, would seem to contribute more to the development of mucosal injury with intestinal obstruction. The absence of a similar degree of colonic damage in horses with NSO compared with SO, despite comparable luminal pressures in some horses, suggests that for SO, vascular occlusion is responsible for most of the colonic damage, and that sustained high luminal pressure may exacerbate the ischemic injury.

Longer duration of colic signs was not associated with higher luminal pressure measurements. Non- survivors of large-colon SO had higher luminal pressures, but the duration of colic signs or of severe abdominal pain was not different from survivors of SO. Further, duration of colic signs was longer in horses with large-colon NSO when compared with horses with SO. The lower luminal pressures in NSO were likely related to incomplete luminal obstruction, which allowed some aboral movement of luminal contents. The amount of colonic distention associated with large-colon NSO is dependent on the degree of luminal obstruction; some horses with large colon displacements have minimal luminal distention. Likewise, horses with NSO had less severe abdominal pain probably because of incomplete luminal obstruction and the absence of vascular occlusion. Although clinical experience may suggest that the prognosis for survival of horses with large-colon SO is inversely related to the duration before surgical correction, the duration of severe abdominal pain was not significantly different between survivors and nonsurvivors of large-colon SO in this study.

Although the number of mares in this study was significantly higher than the combined number of

males and geldings, the signalment of the horses in this study was similar to previous reports of horses with large-colon volv~lus .~ The relationship between females and the occurrence of large colon SO or NSO is currently unknown.

We conclude from this prospective clinical study that intraoperative measurement of colonic luminal pressure in horses with large-colon SO may be valuable for formulating a prognosis for survival. Luminal pressure measurement may also be useful in determining the need for colon resection. Combining luminal pressure information with other methods for determination of intestinal viability may improve the clinician's ability to accurately assess colonic viability and predict postoperative outcome. Because prevalence of death in different populations of horses with large-colon SO will vary, caution should be observed when using positive and negative predictive values of luminal pressure measurements for prediction of nonsurvival in horses with large-colon volvulus. Clinicians should consider the prevalence of death for horses with large-colon volvulus in their hospital population when using predictive values for a luminal pressure value greater than 38 cm HzO. Future studies appear indicated to compare the prognostic value of colonic luminal pressure with other prognostic indicators, such as preoperative packed cell volume, heart rate, and lactate con- centration. An advantage of using luminal pressure measurement is that it is inexpensive and easy to perform.

ACKNOWLEDGMENT

The authors thank Drs. Warren Beard, Barry Carter, Rick Henniger, Susan Holcombe, and James Lillich for technical assistance.

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colonic luminal pressure in horses with strangulating and nonstrangulating obstruction of the large...

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