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MICHAEL W. ROSS R. REID HANSON, JR.

mesenteric attachment along the medial and lateral cecal bands, respectively. Because both cecal are The equine large intestine consists of the following derived from a single parent vessel without collateral segments (in aboral direction): the , the large input, the cecum is particularly prone to thromboem- colon, and the small colon (Fig. 36-1). Although these bolic disease. segments form a continuum for the passage of digesta The caudal portion of the cecal base and body can from the to the , the three portions are be felt on . The ventral band is considered to be separate structures, anatomically, func- prominent and is palpable per . The cecal body tionally, and surgically. The large intestine of the can be exteriorized through a ventral midline incision; is well developed and can be distinguished from that of however, because of the presence of the dorsal attach- other domestic by the large capacity and shape ment, the base and ileocecal junction can be seen but of the cecum, and length of the small (descending) not exteriorized. colon.' The large intestine is sacculated for most of its length and is approximately 7.5 to 8.0 m long.2 Large Colon Cecum The large colon, measuring between 3 and 4.5 m, The cecum is approximately 1 m long, has a capacity is composed of the right ventral colon (RVC), the left of 16 to 68 L, and occupies the right caudal abdominal ventral colon (LVC), the left dorsal colon (LDC), and quadrant.' The cecum is comma shaped and is divided the right dorsal colon (RDC) and begins at the cecocolic into a base and body. The cecal base has a strong orifice and ends at the . The large colon mesenteric attachment to the dorsal body wall and forms a long U-shaped loop, which is attached to the extends craniad to the level of the fourteenth or fifteenth dorsal body wall at the RDC and RVC. This well- rib.2 The cecal base curves ventrally into the cecal body, developed, voluminous loop is mobile, predisposing the which ends in a cul-de-sac, the apex. The cecal body bowel to anatomic displacements and physical obstruc- has four longitudinal bands (teniae), the dorsal, lateral, tions. The diameter of the large colon varies, with ventral, and medial bands, causing deep sacculations in narrowing occurring at the pelvic flexure, formed be- the body. The ventral band joins the medial near the tween the LVC and the LDC. The RDC narrows before apex. The runs from the antimesenteric entering the transverse colon. The narrow areas are border of the ileum to the dorsal cecal band. The ileum prone to obstruction by digesta or foreign material. enters the medial, ventral aspect of the cecal base and The RVC begins at the cecocolic orifice and courses terminates in the ileocecal orifice. The cecal base is cranioventrally to the sternal flexure, which lies dorsal divided into cranial and caudal portions by a transverse to the xyphoid cartilage. The RVC is sacculated and has fold, arising from the floor of the cecal base, just craniad four bands-medial and lateral mesocolic bands and to the ileocecal junction. The cranial cecal base, or medial and lateral free bands (Fig. 36-2). The RVC is cupula, is voluminous, forms a sigmoid structure, and continuous with the LVC at the sternal flexure. The ends in the cecocolic orifice, which is located caudal in LVC is similar to the RVC in sacculations and bands, the cupula. A well-developed cecocolic (fold) and runs caudally to the pelvic inlet. The LVC joins the runs from the lateral cecal band to the lateral free band LDC at the pelvic flexure. At the pelvic flexure, the of the right ventral colon. Because of its dense dorsal bands of the LVC fade, leaving the pelvic flexure mesenteric attachment, the cecocolic ligament and il- unsacculated and with a narrow . A single meso- eocecal fold, the cecum is immobile without concomitant band is found in the LDC. The LDC runs cranially mobility of adjacent organs. to the diaphragmatic flexure and joins the RDC. Three The cecal blood supply is derived from the cecal bands are found in the moderately sacculated RDC as , a branch of the . The medial and it courses caudodorsally, to end in the transverse colon. lateral cecal arteries (and ) course in a loose The RDC has an enormous diameter described as a -like dilatation.' R. Reid Hanson, Jr. wrote the subsection on the Transverse and Small Colon The ventral and dorsal segments of the colon are under the section on and the section on Surgical Disorders. attached by the intercolonic . The major blood 380 ALIMENTARY SYSTEM

Small colon Transverse colon Left dorsal colon \

FIGURE 36-1. The equine large intestine. Note the mesenteric attachments of the cecum are located at the cecal base and right dorsal colon (Redrawn from Mc- Ilwraith CW: Equine digestive system. In Jennings PB (Ed): The Practice of Large Animal Surgery. Philadel- phia, W. B. Saunders Company, 1984, p 628.)

~pexof cecum supply to the colonic loop running in the mesentery is derived from the , supplying the dorsal colon, and the colic branch from the ileocolic artery, supplying the ventral colon (Fig. 36-2).3 These vessels join at the pelvic flexure. The large colon is much less susceptible to thromboembolic disease because of this anastomosis and an extensive plexus of communications, the rete mirabile (within the intercolonic mesenterv). J,, which is peculiar t; the equine specie^.^ Rectal examination is useful in identifying portions of the large colon in health and disease. The pelvic flexure can be palpated in most normal , and the ventral colon is easily recognized by the distinguishing bands. The RDC can only be felt with extensive impac- tion. With the exception of the initial 15 cm of the RVC and the last 25 cm of the RDC, the entire large colon can be exteriorized through a ventral midline surgical incision.~ ~~

Transversc e and Small Colon

The transverse colon is a constricted portion of large intestine passing from right to left, cranial to the root of the mesentery. The transverse colon joins the voluminous RDC and small colon (SC) and can be felt at surgery but cannot be exteriorized through a ventral midline incision. The SC, a caudal continuation of the transverse colon on the left of the mesenteric root, FIGURE 36-2. Cross-sectional diagram of the equine large intestine, occupies the caudal left quadrant of the along showing longitudinal smooth muscle bands (teniae, dark sections), with the . The SC is approximately 4 m long intercolonic mesentery, and associated vessels. SC, small colon, and and has a diameter of approximately 6 to 8 cm. The associated mesocolon; RDC, right dorsal colon; RVC, right ventral colon; LCA, lateral cecal artery; MCA, medial cecal artery; LVC, mesocolon, which suspends the SC from the dorsal body left ventral colon; LDC, left dorsal colon; RCA, right colic artery, a wall, increases to a midsection width of 80 to 100 cm. branch from the cranial mesenteric artery; CB, colic branch, from the The SC is connected to the by the short ileocolic artery. The ileum is shown with its dorsal mesenteric attach- duodenocolic fold. The SC continues at the pelvic inlet ment and the ileocecal fold, coursing from its antimesenteric band, to the dorsal band of the cecum. The cecocolic ligament courses from as the peritoneal rectum that enlarges to form the the lateral cecal band to the lateral free band of the RVC. (Redrawn ampulla recti. The SC has wide, muscular mesenteric from Habel RE: Applied Veterinary Anatomy. Philadelphia, W. B. and antimesenteric bands and coarse sacculations. Saunders Company, 1986, p 247.) LARGE INTESTINE 381

FIGURE 36-3. Lateral view of the small (descending) colon. 1, arcuate artery; 2, marginal artery; 3, long artery; 4, small branch supplying the mesenteric tenia; 5, secondary arcade; 6, small branch to mesocolon. (Redrawn from Beard WL, Lohse CL, Robertson JT: Vascular anatomy of the in the horse. Vet Surg 18:130, 1989.)

The major arterial supply to the SC is from the mates of the resorptive capacity of the large intestine of caudal mesenteric artery, which divides into two major a 160 kg pony approximate 30 Llday, a volume equal to branches-the and the cranial rectal the extracellular fluid volume (ECF) of the animal.8 artery. The left colic artery supplies the oral 75% of the Fecal averages less than 10% of ileal outflow (Fig. small colon and branches into four to eight arcuate 36-5), and net fluid absorption may approximate 95% arteries that divide again into marginal arteries (Fig. of delivered fluid. Diseases interrupting fluid dynamics 36-3).5.6 The cranial rectal artery courses caudally in could potentially cause life-threatening changes in ECF the small colon mesentery to supply the aboral 25% of and balance. The greatest quantitative net the small colon with similar arcuate and marginal arte- water absorption occurs in the cecum. ries. The joining marginal arteries form one functional Solute transport in the large intestine appears com- artery 1 to 2 cm dorsal to the entire bowel surface, plex but contributes greatly to the transmucosal move- which is obscured from view by mesocolic fat (Fig. 36- ment of water. Although digesta osmolality is main- 4). Marginal arterial overlapping obviates the need for tained at roughly isotonic levels from the cecum to the preservation of the marginal artery when performing SC, concentrations of cations and anions change consid- resection and anastomosis. erably. The Na' concentration decreases markedly, but The SC can be easily recognized on rectal exami- there is a concomitant increase in K+ and NH,- concen- nation by the presence of fecal balls and the thick trations from the cecum to the SC.' Organic antimesenteric band. The oral 30 cm and aboral 30 cm increase in the cecum and ventral colon but then de- of the small colon cannot be exteriorized through a crease in the dorsal and SC. There is a steady increase ventral midline surgical incision. in the concentration. Although osmotic The extrinsic innervation of the large intestine is changes in organic (VFA) production may contrib- derived from the celiacomesenteric plexus, celiac and cranial mesenteric ganglion, and pelvic plexus. The more important intrinsic neurons form the enteric and the myenteric plexus. Extrinsic denervation does not interrupt the intrinsic myoelectric activity of the equine

The two important physiologic functions of the large intestine include (1) storage and absorption of fluid and (2) retention of digesta for microbial . These functions have extreme importance in fluid and electro- lyte balance and nutritional considerations. Complex mechanisms are required to regulate digesta transit, to provide optimal conditions for transport of and fluid, and to allow microbial of di- gesta.' 5 FIGURE 36-4. Cross sectlon of the small colon with vascular anatomy Fluid Absorption shown. 1, marginal artery; 2, secondary arcade; 3, long artery; 4, branch supplying tenia; 5, anastomosis across antimesenteric surface. The most important function of the large intestine (Redrawn from Beard WL, Lohse CL, Robertson JT: Vascular is likely the absorption of large volumes of fluid. Esti- anatomy of the descending colon in the horse. Vet Surg 18:130, 1989.) 382 ALIMENTARY SYSTEM

PONY MAN Marker concentrations are similar in the RVC and LVC, and therefore, the ventral colon is considered a single compartment. Similar marker concentrations in the LDC and RDC are found, and thus, a single dorsal colonic compartment exists. The ventral-dorsal colonic junction, the pelvic flexure, represents a major barrier to the outflow of markers. The dorsal colon preferen- tially retains larger markers. Transit of fluid and partic- ulate markers occurs rapidly through the SC. Experimentally, no retrograde transit of carbon occurs from the ventral colon to the cecum or from the dorsal colon to the ventral colon." Neither polyethylene glycol nor particulate markers are passed in retrograde fashion from cecum to ileum, or from dorsal to ventral colon.10 From these results, it appears likely that the ileocecal junction, cecocolic junction, pelvic flexure, and transverse colon are responsible for the retention of digesta and compartmentalization of the large intestine. Mean transit time in the cecum is approximately 5 hours, whereas mean transit time for the large colon is 50 hours. Fifty percent transit of liquid markers to occurs 24 hours after oral administration, but 50% transit of particulate markers, 2 cm in length, takes greater than 10 days, demonstrating considerable reten- * tion of particulate digesta for microbial digestion (Fig. 1.5 366). This prolonged retention appears to be greater FIGURE 36-5. Net water movement through the large intestine of a than that in the fore stomach^.^^ 70-kg man and 160-kg pony. Both species absorb approximately 90% of ileal outflow, but in the pony, this represents approximately 30 Llday. The volume is roughly equivalent to the animal's extracellular fluid volume. Note the cecum of the pony has greatest net water Motility absorption. (Redrawn from Argenzio RA, Lowe JE, Pickard DW, et al: Digesta passage and water exchange in equine large intestine. Am The motor events of the large intestine are complex J Physiol 22631035, 1974.) and are incompletely understood. Both propulsion (the aboral movement of digesta) and retropulsion (the oral movement of digesta) exist in the cecum and the large ute to net water movement, it appears likely that Na+ colon. transport is the single most important fa~tor.~ Digesta enters the cecum from the ileocecal junc- A net decrease in cecal HCO,- is likely caused by tion, propelled by the migrating action potential com- buffering of organic acids. This buffering reaction plex-a prominent, rapidly progressive electrical event (NaHCO, + HAC + NaAC + H,O + CO, of the ileum.I3 Researchers have identified several mo- [AC:] may aid in absorption of VFA, Na+ and tility patterns of the normal cecum through C0,+.7 An important function of the colon involves or visually through cannulas,I4. Is cinefluoro~copy,'~and acid-base balance. Horses with simple colonic obstruc- indwelling intraluminal monometry, and by monitoring tions may develop metabolic alkalosis, because of dis- myoelectric activity.I7.l8 Coordinated series of spike ruption of colonic buffering ~apacity.~A reduction in bursts occur in the cecal base, which propel digesta to VFA production in horses with colonic diseases may the cecal apex (Fig. 36-7). Several series of spike bursts decrease the normal Cl-:HCO,- exchange mechanism, within the cecal body appear to contribute to nonpro- and lead to a relative decrease in HCO,- se~retion.~.lo gressive, haustra-to-haustra mixing events. A progres- sive motility pattern has been identified, which is initi- ated at the cecal apex, propagated to the cecal body, Microbial Digesti through the caudal and cranial portions of the cecal base, and into the RVC. This pattern occurs once every A major physiologic function of the large intestine 3 minutes in the fed pony, is associated with a loud is retention of fluid and digesta to facilitate important distinctive "rush" of digesta heard on , and microbial digestion. Like colonic fluid dynamics, micro- is likely responsible for the transit of digesta from the bial digestion is regulated by the rate of passage of cecum to the RVC. An electric pacemaker area located digesta through the large intestine. Experimentally, fluid within the ventral 10 to 15 cm of the cecal apex appears (polyethylene glycol) and particulate markers leave the to initiate this progressive motility pattern.I3. l8 Several cecum quickly and are passed to the ventral and dorsal retropulsive patterns, generated from the cranial or colon (Fig. 36-6).8 Marked retention of particulate caudal cecal base, appear to be coupled with this pro- markers occurs in the ventral and dorsal colons, which gressive pattern. are considered the major sites of digesta retention. In the RVC, the aboral, progressive pattern gen- I LARGE INTESTINE 383

FIGURE 36-6. Retention of liquid and particulate markers by the cecum, ven- tral colon segments, and dorsal colon segments (including small colon), and fecal excretion of markers. Liquid markers are passed rapidly from the cecum, and 50% excretion occurred within 3 days after administration. Re- tention of particulate markers increased as marker size increased. Less than 50% excretion of 2-cm markers oc- curred in 10 days. Note relatively greater retention of larger markers in the dorsal colon. (From Argenzio RA, Lowe JE, Pickard DW: Digesta passage and water exchange in equine large intestine. Am J Physiol 226:1035, 1974.)

erated at the cecal apex is rapidly propagated and SSB and LSB may not be useful to describe cecal motor appears to be the dominant motility pattern. Both events. Because of the large size and obvious reservoir propulsion and retropulsion exist in the RVC, indepen- nature of the RDC, strong retropulsion likely exists in dent of the progressive pattern. Progressive motor this area, but the motility of the RDC, transverse colon, events of the RVC likely continue around the sternal and SC has not been characterized. flexure to the LVC and end near the pelvic flexure. Motility of the cecum and large colon is markedly The motor events of the pelvic flexure, LVC, and affected by various pharmacologic agents and physio- LDC have been studied e~tensively.~.14. l9 Coordinated logic changes. Administration of xylazine, an a-2 adre- oral, aboral, and bidirectional pressure peaks exist, nergic agonist, reduces cecal progressive motilityU and originating from the pelvic flexure area, which demon- mechanical activity24 for 30 minutes. Butorphanol, a strates that a colonic pacemaker region may exist here synthetic narcotic agonistlantagonist, reduces cecal pro- (Fig. 36-8).19 Further study by in vitro electromyography gressive motility. The combination of xylazine and bu- demonstrated the existence of an electric pacemaker torphanol further delays return of progressive motility. and direct electric coupling of longitudinal and circular The anticholinesterase neostigmine increases cecal pro- smooth muscle.4-I9 The electric pacemaker initiates pro- gressive motility for approximately 30 minutes. pulsion and retropulsion, impeding the transit of digesta. In the large colon, narcotic agonists increase the Retropulsive spike bursts are likely propagated through resting tone of intestinal muscle, whereas in limited the LVC to the RVC, and propulsive spike bursts may studies of narcotic antagonists, an increase in propulsive continue around the dorsal colons to the transverse motility is seen.25 Xylazine and atropine sulfate reduce colon. motility of the pelvic flexure, whereas neostigmine in- In vivo electromyography of the cecum and large creases progressive motility.21 The acaricide Amitraz colon has demonstrated the existence of long spike causes dissociation of the coordinated pressure peaks of bursts (LSB) which are longer than 5 seconds and short the LVC and LDC. Paralysis of visceral afferent spike bursts (SSB) which are shorter than 5 sec~nds.'~,~~of the pelvic flexure by the use of local anesthetics In the colon, LSB are associated with progressive and decreases coordinated pressure peaks.19 Feeding and simultaneous mechanical activity, whereas SSB result in electrical stimulation of extrinsic supply increase local mixing events. In the cecum, SSB commonly occur intraluminal pressure peaks. Colonic cooling decreases during the progressive motility pattern and the terms conduction velocity and amplitude of pressure peaks.4 384 ALIMENTARY SYSTEM

obstruction of the large intestine represent between 37% to 46% of horses admitted for evaluation of colic or for surgical treatment.27-29The type and severity of obstruc- tion dictate whether medical or surgical management is instituted. Large intestinal obstruction differs from small intestinal obstruction because of the aboral position of the large intestine, the large size of the colonic segments, and different physiologic functions and by-products.

Simple Obstruction

Simple obstruction of the large intestine is common and is caused by impaction with feedstuffs, fibrous foreign material, enteroliths, and . Simple ob- struction also occurs with nonstrangulating displacement of the large colon, although displacement may progress to strangulation obstruction. Functional obstruction, known as spasmodic colic, is a form of simple obstruc- tion. Pathophysiologic changes with simple obstruction vary with severity and duration of the lesion. Partial obstruction, such as cecal impaction, or intermittent enterolith obstruction of the RDC, causes mild patho- physiologic changes. Complete simple obstruction can progress rapidly, however, causing severe clinical signs and irreversible pathophysiologic changes. Abnormal motility, causing or, for example, impaction of the ventral colon, leads to the gradual accumulation of gas from microbial digestion. The large size of the ventral colon allows great quantities of gas to accumulate, causing abdominal distention and colic. Accumulation of digesta and fluid contribute to disten- tion. Intestinal distention can decrease intestinal blood FIGURE 36-7. Myoelectric activity of the cecum and right ventral flow, but in cats, intraluminal pressure increases from colon (RVC) in a pony. Time progresses from left to right. The approximate location of the electrodes correspond to the numbers in 34 to 54 cm H20 are needed for this to occur.30 In the anatomic insert. Two progressive motility patterns (b, b') initiate equine natural obstructions, intraluminal at the cecal apex, the pacemaker region, and progress to sequentially pressure changes of only 4.5 to 21 cm of H,O are involve the cecal body, base, and continue into the RVC. Retrograde found.31 Pressure changes in large intestinal diseases motility patterns (a, a') progress from the cecal base to the apex, may be higher and may contribute to vascular derange- before the progressive pattern, forming a repetitive pattern known as the cecal myoelectric complex. A local haustra-to-haustra pattern (c), ments. Increases in intraluminal pressure could increase likely involving mixing events in the cecal body, is present. (From mural pressure, causing collapse of venules, increased Ross MW, Rutkowski JA, Cullen KK: Myoelectric activity of the hydrostatic pressure, and interstitial edema. In cecum and right ventral colon in female ponies. Am J Vet Res 50:374, the small intestine, mural edema does not develop after 1989.) 4 hours of luminal distention." In ponies with experi- mentally produced pelvic flexure impaction, there is an increase in blood flow to intestinal segments with ob- Experimental Strongylus vulgaris infestation results in str~ction.~~In horses operated on with simple obstruc- severe evidence of thromboembolism but fails to consis- tions, mural edema occurs, although it is not known tently alter colonic m~tility.~,'~Substance P-like immu- whether edema is related to distention or other hemo- noreactivity of enteric neurons is found in submucosal dynamic changes. Initial increases in intestinal blood ganglia, although its relationship to motility is un- flow may contribute to mural congestion and cause known.26 edema. Simple obstruction alters normal fluid and solute absorption. The colon may become secretory, contrib- uting to luminal distention and clinical dehydration. Abnormal fluid dynamics with net fluid and electrolyte Simple obstruction (nonstrangulating), character- loss into the lumen may contribute to disturbances of ized by complete or near-complete occlusion of the motility and further propagate the obstructive process. intestinal lumen, and strangulation obstruction, charac- In simple obstruction, septic or endotoxic shock is terized by vascular compromise of the involved intestine, unusual and does not occur until late when necrosis of occur frequently in the large intestine. Horses with the intestinal segment occurs. Depletion of plasma vol- LARGE INTESTINE 385

FIGURE 36-8. Motor events of the left ventral and left dorsal colon seg- ments and pelvic flexure. Number of motility tracing channels corresponds to the portion of the intraluminal catheters located in anatomic insert. Note the coordinated bidirectional pressure peaks, starting between loci 3-4, corresponding to both propul- sion (4 + 6) and retropulsion (3 + 1). A wandering pacemaker area ex- ists that initiates the bidirectional and unidirectional peaks and is responsi- ble for controlling coordinated motil- ity events in the area of the equine large intestine. (From Sellers AF, Lowe JE, Brondum J: Motor events in equine large colon. Am J Physiol 237:E457. 1979.)

ume and reduction of cardiac output causing obstructions. Therefore, clinical signs may take 24 to 48 clinical signs of dehydration, elevation of the heart rate, hours to develop. and poor peripheral perfusion. These changes generally Abdominal auscultation of horses with simple ob- occur late in most horses with simple obstruction, and struction often reveals an increase in borborygmi early many of the systemic changes may be related to pain in the disease process, followed by a progressive de- rather than to the hemodynamics of fluid loss. crease. In ponies, experimental simple obstruction of Acid-base disturbances occur but are generally not the small intestine produces similar initial increases in severe. The classic metabolic disturbance of horses with electric activity in the oral segment, followed by a colic, namely metabolic acidosis, is uncommon in horses progressive decrease later in the obstructive process.35 with simple obstruction, unless and necrosis of the obstructed segment occurs. Necrosis of the small or large colon can occur with severe impactions. Horses Strangulation Obstruction with cecal perforation secondary to simple obstructions develop cardiovascular collapse and metabolic acidosis. Strangulation obstruction occurs most commonly In horses with spasmodic colic (gaseous distention of due to (torsion) of the large colon (VLC) but the large colon) or impaction of the large colon, mild can affect the cecum and SC as well. Two forms of metabolic alkalosis may occur, secondary to alterations strangulation obstruction exist. Hemorrhagic strangula- of VFA production and normal Cl-:HCO,- exchange tion obstruction occurs when luminal obstruction is mechanism (see the section on Physiology). Severe accompanied by venous occl~sion.~~In this common gaseous distention of the large colon may compress the form, there is a rapid onset of mural edema; thick, dark duodenum, causing partial or complete obstruction. This purple serosa; and purple-black mucosa. The second results in retention of gastric and upper gastrointestinal form, ischemic strangulation obstruction, involves lu- secretions, and may lead to further metabolic alkalosis minal compromise plus venous and arterial occlusion.36 because of sequestration of gastric hydrochloric acid. In ischemic strangulation obstruction, more mild edema Generally, acid-base disturbances are mild. develops, and the bowel serosa becomes gray or blue- The hallmark pathophysiologic changes of horses gray. with simple obstruction, namely, gas distention and In horses with VLC, hemorrhagic strangulation secondary distention of intestinal segments orad to the obstruction is most common but can rapidly progress to obstruction, abdominal distention, pain, progressive de- complete ischemic obstr~ction.~~Therefore, a combina- hydration, slow cardiovascular collapse, and mild acid- tion of pathophysiologic mechanisms is generally base disturbances, progress with the severity of the present. The prognosis in horses with this severe form lesion. Because of the aboral location of the large of disease is poor. intestine relative to the small intestine, cardiovascular Initial venous occlusion causes severe edema of the changes are generally slower to develop. Within the bowel wall and stagnation of blood flow. Vascular oc- large intestine, horses with small colon obstruction de- clusion and low-flow states cause mucosal damage. Al- velop signs more slowly than horses with large colon though mucosal changes have not been studied exten- 386 ALIMENTARY SYSTEM

sively, changes may be similar to those seen in small The pathophysiologic mechanism leading to mu- intestinal occl~sion.~~In the small intestinal villi, a cosal damage during hemorrhagic or ischemic insults is countercurrent exchange mechanism exists owing to the clear, but recently, additional damage caused by return hairpin-like vascular arrange~nent.~~During low-flow of blood flow, or reperfusion injury, has come to light. vascular states, oxygen and other may "short- After surgical correction of strangulation obstruction, circuit7' the villus tip, leaving the tip relatively anoxic further damage may occur. Lipid peroxidation and pro- compared with the villus base.36 During venous occlu- tein denaturation leading to activation and al- sion, this mechanism would explain the initial and most teration of membrane integrity occur, secondary to an severe changes seen at the villus tip.36 In the colon, the increase in superoxide (0,) radicals, hydroxyl radical mucosal architecture is different, but because of the (,OH), single oxygen, and pero~ide.~~.~~.~~ close proximity of arterioles and draining venules, a Normal scavenging systems, including ascorbate, gluta- countercurrent exchange mechanism may exist to ex- thione peroxidase, catalase, and superoxide dismutase plain mucosal damage."38 may be depleted, allowing the build-up of damaging If both venous and arterial occlusion exist, or initial free radicals.36 During the ischemic period, neutrophils venous occlusion progresses to arterial occlusion, more build up and may increase the severity of the reperfusion severe histologic changes result. In horses with ischemic inj~ry.~~,"~In clinical situations, serosal color and gross occlusion or hemorrhagic occlusion, the histologic vascular supply may improve after a strangulated seg- changes may be similar. The equine colonic mucosa may ment is untwisted. However, mucosal and submucosal be approximately 25% more resistant to ischemia than damage continues, leading to ileus, , cardio- the equine small intestinal mu~osa.~~.~~Histologic vascular collapse, and death within 1 to 3 days. For an changes of hemorrhage and edema in the mucosa and in-depth discussion on this subject, please review Chap- , the degree of superficial and crypt cell ter 33. damage, and a measurement that reflects mucosal pres- sure are used to grade large colon da~nage.~~,~'With increasing mucosal edema, there is an increase in inter- stitial-to-crypt ratio, a measurement of the width occu- pied by the interstitium relative to crypt Increas- Cecum ing interstitial-to-crypt ratio, an increase in the percent of superficial colonic mucosal cell sloughing, and an Cecal Impaction increase in crypt cell damage correspond to more severe colonic damage.36 ETIOLOGY Fluid and electrolyte loss accompany progressive The most important disease of the cecum is cecal mucosal damage. In hemorrhagic occlusion, initial fluid impaction (CI), which represents approximately 5% of loss and cardiovascular collapse accompany bowel all intestinal impaction^.^. 45- Cecal impaction generally edema and mucosa damage, causing clinical signs of involves fibrous feedstuffs, but impaction with sand can hypovolemic shock. In horses with advanced hemor- occur. Although classic cases of CI include older horses rhagic occlusion or with ischemic occlusion, extensive with poor dentition and fed poor quality feedstuffs, mucosal damage is accompanied by disruption of the recent reports indicate that younger horses, particularly mucosal barrier. Transmural necrosis occurs, allowing horses hospitalized for other nonrelated disorders, are absorption of endotoxin and, later, enteric at ri~k."~,~'The pathogenesis of CI likely involves a access to the and then to the systemic primary cecal motility dysfunction. Observations at sur- cir~ulation.~~The hepatic reticuloendothelial system, which is normally able to absorb endotoxin efficiently, gery or necropsy reveal a large, digesta-filled cecum and becomes ischemic with cardiovascular deterioration, and a relatively empty RVC (Fig. 36-9). Because only a further endotoxin distribution occurs.40 Endotoxin single motor event is common to the cecum and RVC, causes further deterioration in the hemodynamic, he- interruption of this progressive motility pattern leads to matologic, and blood chemical systems, including hy- cecal filling (see the section on Physiology). Propulsion potension, increased packed cell volume, leukopenia, in the RVC continues, and this segment empties. Al- metabolic acidosis, disseminated intravascular coagula- tered cecal blood flow secondary to parasite damage, tion (DIC), and disruption of glucose metab~lism.~' dietary changes, or other clinical conditions may inter- From both a pathophysiologic and clinical stand- rupt or slow the cecal pacemaker. Transit of small point, the most important consideration in treatment volumes of digesta and gas continue, because oil appears and prognosis is early medical and surgical intervention in the feces and gas accumulation of the cecal base is to limit loss of bowel integrity. Progressive bowel dete- unusual. Initially, digesta is normal in character but may rioration causes clinical signs of cardiovascular collapse, become dry, resembling the expected "impacted di- tachycardia, poor peripheral perfusion, increased capil- gesta." lary refill time, and poor peripheral . Dehydration is accompanied by an increase in packed cell volume HISTORY AND CLINICAL SIGNS (PCV), but with further loss of bowel integrity, loss of plasma protein total (TTP) occurs. Elevation of PCV Typically, horses with CI are intermittently an- may not be accompanied by an increase in plasma orexic, depressed, and show signs of mild abdominal protein, and the increase in PCV/TTP ratio is generally pain, such as looking at the flanks, rolling, and pawing. a poor prognostic sign. Frequently, the horses have experienced a management LARGE INTESTINE 387

FIGURE 36-9. The cecum and large colon. (A), Cecum and large colon from a normal horse, showing, the normal relative size of the organs. (B), Cecum and large colon from a horse with cecal impaction and subsequent perforation. Note the large, digesta filled cecum and relatively empty large colon. A motility dysfunction exists that causes cecal filling but allows colonic emptying. This lesion is found in horses with cecal impaction or cecal perforation secondary to cecal outflow dysfunction.

change or are being treated for unrelated gastrointestinal edge the limitations of medical management, although or musculoskeletal disorders. Vital parameters and lab- one author reports good success.50 Because the chance oratory values are usually within normal limits. of cecal perforation exists with continued cecal filling, Rectal examination is diagnostic, but in rare in- other authors have recommended surgical management, stances, the enlarged cecum cannot be felt. The clinician particularly in horses unresponsive to medical therapy. must differentiate the cecum from other organs such as Earlier surgical techniques included manual massage, the RDC or a displacement of the ventral colon. A firm, sometimes accom~aniedbv water infusion of the im- near-hard viscus is often felt, with a single, distinct band pacted digesta, evacuation of cecal contents by enter- (ventral cecal tenia). The cecum is attached to the dorsal otomy (typhlotomy), and partial to complete typhlec- body wall, and the examiner cannot pass a hand dorsal t~my.~~.47, 49, 51-53 Results with enterotomy and to the impacted mass. Because the colon is usually evacuation of cecal contents, or infusion and massage, empty, it is difficult to feel the pelvic flexure. Fecal were variable, which sparked development of newer production is reduced, and feces range from dry to surgical techniques.'16 These techniques were developed "cow-flop" in nature. Intermittent can occur. to address the pathogenesis of CI, namely the develop- Cecal progressive borborygmi are reduced. ment of a primary cecal motility dysfunction, which is slow to return after surgery. TREATMENT Currently, management of horses with CI depends largely on the result of rectal examination and physical SELECTION.Disagreement exists over the most examination of the patient. If the cecum is small or appropriate treatment of horses with CI. Medical man- moderate in size and the patient's vital parameters are agement has been ad~ocated.~~-'OMost authors acknowl- normal, initial medical management is recommended. 388 ALIMENTARY SYSTEM

Surgery is recommended if the cecum is extremely large, or the digesta is near hard in consistency, in horses with CI refractory to medical management, or in horses with recurrent CI.54 NONSURGICALMANAGEMENT. Successful medi- cal management requires both oral and intravenous fluid therapy, and withholding feed until the cecum returns to normal size, based on rectal examination. Neostig- mine (0.0125 to 0.025 mglkg) may increase cecal pro- gressive motility, and has been used with limited success; however, one should be extremely careful because cecal perforation is a potential sequela. Until it is clinically justified, use of the drug should be restricted to horses with recurrent impaction or when economic constraints restrict surgical intervention. Stimulation of cecal motil- ity by walking and grazing may represent a beneficial adjunctive treatment, although the volume of grass ingested must be closely regulated. Because fasting causes cessation of cecal progressive motility, it may be important to stimulate motility in this manner.13 SURGICALMANAGEMENT. Recently, several sur- gical techniques have been developed to prevent recur- rence of clinical signs and are used in conjunction with surgical techniques such as infusion, massage, or simple evacuati~n.~~-~' FIGURE 36-10. The cecum and origin of the right ventral colon. The Typhlotomy. Typhlotomy may be used alone or dotted areas show the location of the cecocolic anastomosis, a surgical procedure useful for horses with cecal impaction. The anastomosis is in combination with cecocolic, jejunocolic, or ileocolic performed between the lateral (A) and dorsal (B) cecal bands, and anastomoses. Typhlotomy is performed midway be- the lateral (C) and medial (D) free bands of the RVC. The cecocolic tween the ventral and lateral cecal bands, after appro- ligament (E) runs between the lateral cecal band and lateral free band priate draping has been performed to prevent peritoneal of the RVC. (Redrawn from Ross MW, Tate LP, Donawick WJ, et contamination. Peritoneal contamination is generally al: Cecocolic anastomosis for the surgical management of cecal im- more common with typhlotomy incisions than with col- paction in horses. Vet Surg 15:85, 1986.) otomy incisions, because only the apex and body of the cecum can be exteriorized. The surgeon must remember that the cecal base is divided and the cupula (cranial prevent cecal filling, and the complete ileocolic anasto- base) is generally large and digesta filled and needs to mosis with ileal transection was s~perior.~'However, be emptied. the incomplete jejunocolic anastomosis was successful Cecocolic Anastomosis. Cecocolic anastomosis, a in preventing recurrence of CI in one horse.s6 technique developed to avert the possible postoperative In summary, if surgery is required in horses with complications of recurrent CI and perforation, provides CI, typhlotomy and manual evacuation should be fol- an alternative route of digesta transit from the cecum lowed by some form of bypass procedure. Complete to the RVC (Fig. 36-10).55 Generally, the technique is ileocolic anastomosis offers advantages over other pro- combined with typhlotomy and evacuation of cecal con- cedures and has been effective clinically. Incomplete tents. The anastomosis, a combination of hand-sewn ileocolic or jejunocolic anastomoses, or cecocolic anas- seromuscular layer closures and use of the GIA-stapling tomoses remain viable surgical alternative. instrument (U.S. Surgical, Norwalk, CT), is performed between the lateral and dorsal cecal bands, and the - lateral free and lateral mesocolic bands of the RVC. In Cecal Perforation the original report, 12 of 14 horses (86%) survived 2 PATHOGENESIS months or longer and 10 horses (71%) survived longer than 1 year. Four horses had intermittent colic related Cecal perforation (CP), although not considered a to gas distention of the cecum or large colon, but none surgical disease, is a relatively recently characterized, developed recurrent cecal impaction. important cecal disease. Because of the close association Jejunocolic and Ileocolic Anastomoses. Jejuno- of CP to CI, equine surgeons should be familiar with colic'6 or ileocolic anastomosess7represent more recently the pathogenesis of the disease. The pathogenesis of developed surgical techniques designed to completely or CP, a uniformly fatal disease, appears to involve two incompletely bypass the cecum, thus rerouting digesta different pathways: (1) CP may be primarily idiopathic from the aboral small intestine to the colon. Typhlotomy in origin in broodmares near parturition, in which no with cecal evacuation can be performed. Jejunocolic or obvious cecal motility dysfunction exists; and (2) more ileocolic anastomoses can be performed in a side-to-side commonly, CP is secondary to a primary cecal motility fashion, using combined hand-sewn seromuscular layer dysfunction, which although undetected, leads to cecal closures and use of the GIA-stapling instrument. The filling and, later, to perforation. incomplete side-to-side ileocolic anastomosis did not IDIOPATHIC DISEASE. Cecal perforation and LARGE INTESTINE 389

death occurred in 11 horses within 24 hours after Cecocecal and Cecocolic lntunusception parturiti~n58-62and during gestation in one mare.63 In HISTORY AND CLINICAL SIGNS this form of CP, gas accumulation may lead to perfora- tion. The cecum and colon are normal in size, and no Intussusception of the cecal body into the base or accumulation of digesta is found. In women undergoing a continuation of the invagination into the RVC is obstetric procedures, signs of intestinal obstruction and uncommon but requires surgical inter~ention.~~~The late CP may occur. Cecal perforation in horses may be disease is not breed, age, or sex specific. The etiology similar to this form of intestinal pseudo-obstruction is unclear, but various authors have suggested the in- (Ogilvie's syndrome) in humans. volvement of the tapeworm Anoplocephala perfoliata. Mon~mDYSFUNCTION. The most common Tapeworms may cause abnormal motility of the cecum form of CP appears to be related to a dysfunction of if they are present in high number^.^' Tapeworms were cecal motility, leading to filling (impaction) and subse- present in only 3 of 10 horses with intussu~ception.~~A quent perforation. At necropsy examination, the cecum recent report questions the importance of tapeworms, appears large and digesta filled, and the colon is rela- because intussusception occurred in horses not infested tively empty (see Fig. 36-9), similar to that seen in with tapeworms with a frequency of two times that of horses with CI. In a recent study, 22 horses (6 weeks to infested horses.68 Abnormal motility caused by an or- 13 years of age) had signs of CP.61 All horses had a ganophosphate was proposed as a cause of intussuscep- single site of perforation (Fig. 36-11). The majority of tion.(j9 these horses were hospitalized, receiving treatment with Three distinct forms of the disease exist, based on nonsteroidal anti-inflammatory drugs (NSAIDs). Early clinical examination and duration of the clinical signs. signs of the disease may be masked by the analgesic In the acute form, horses have severe properties of NSAIDs, allowing horses actually affected and require immediate attention. Changes in vital pa- with CI to progress to CP. Horses hospitalized with rameters and laboratory values are generally more se- other disorders and treated with NSAIDs also appear vere in this form, and the acute onset may reflect a to be at risk to develop CP. Subtle signs of gastrointes- greater degree of vascular and neural compromise of tinal disease, such as partial anorexia, a reduction in the intussusceptum. In the subacute form, horses are fecal output, a change in fecal quality, or decreased generally depressed and have intermittent abdominal borborygmi, should be carefully investigated. A rectal pain and reduced fecal output. In the chronic form, examination is indicated, but the clinician must remem- horses exhibit weight loss, pyrexia, and mild, intermit- ber that because of colonic emptying, the enlarged tent abdominal pain. When the invaginated portion cecum can assume a more cranial location and may not becomes devitalized, there is an exacerbation of clin- be palpable. ical signs, cardiovascular deterioration, acidosis, and Clinical signs after CP include those seen with changes in peritoneal fluid values. severe endotoxin shock or gram-negative . Al- The clinical signs vary, depending on the time of though complete typhlectomy and peritoneal lavage examination relative to the onset of the disease. Rectal remain theoretical treatment alternatives, euthanasia is examination is most helpful in establishing the diagnosis. most appropriate. Four of eight horses with intussusception had an en- larged viscus felt on rectal examination, and in some horses, the cecum was not palpable at

TREATMENT Surgical management is mandatory for a successful outcome, and in some horses, exploratory surgery is necessary to confirm the diagnosis. At surgery, the cecal apex is not found or a mass may be identified in the cecal base or the origin of the RVC. Manual reduction is often possible. The involved cecum is generally edem- atous, devitalized, and requires resection. Following double ligation of the medial and lateral cecal vessels, the devitalized portion is resected, followed by a double inverting closure of the cecal body. As much as 50% to 60% of the cecum can be removed through a ventral MEDIAL LATERAL midline approach. FIGURE 36-1 I. Diagram of the medial and lateral aspects of the In horses with cecocolic intussusception in which cecum, showing the reported sites of cecal perforation in 17 horses. A single site was identified in each horse. a, dorsal base, 3 horses; b, extramural manual reduction is not possible, an enter- dorsomedial base, 2 horses; c, ventromedial base, 1 horse; d, ventral otomy of the RVC is necessary. The 15- to 20-cm long body, 6 horses; e, lateral body, 3 horses; f, distal lateral body, 2 colotomy incision, made between the medial and lateral horses. The interrupted line indicates the anatomic division between free bands of the RVC, is followed by intraluminal the cecal base and body. The cecum may perforate more frequently along bands, but no location appears particularly at risk. (From Ross resection and closure of the edematous cecal apex. MW, Martin BB, Donawick WJ: Cecal perforation in the horse. J Double ligation of the cecal vessels is required. After I Am Vet Med Assoc 187:249, 1985.) resection and closure, eversion of the cecum through 1 390 ALIMENTARY SYSTEM the cecocolic orifice is usually possible. Once the colot- absence of the dorsal mesenteric attachment of the omy incision is closed, an additional closure of the cecal cecum and subsequent large colon displacement. body is performed. Manual reduction of the intussus- ceptum from within the lumen of the RVC can precede resection in some horses. Large Colon The prognosis is considered favorable, if all of the necrotic cecum can be removed. The pacemaker area, The large colon is particularly prone to simple and necessary for generation of normal cecal motility, wan- strangulation obstruction because of certain physiologic ders over a 40 cm area near the apex in ponies.'' functions. Retention of digesta and water absorption, Therefore, nearly the entire cecal body can be removed. complex motility patterns, the relative lack of mesenteric attachment, and changes in lumen diameter predispose the large colon to disease. Many forms of simple obstruc- Cecal Infarction tion respond favorably to medical management but may Thromboembolic disease of the cecal arteries is rare progress to or be confused with lesions requiring surgical but can occur following damage from S. vulgaris migra- intervention. tion. The arterial supply of the entire cecum arises from the single cecal artery, a precarious vascular arrange- Impaction of the Ventral Large Colon ment. The medial and lateral cecal arteries are located 180 degrees apart and lack extensive communications, ETIOLOGY further predisposing the cecum to vascular insult. The disease can occur in a horse of any age but is Impaction of the ventral colon is one of the most more common in horses younger than 1 year of age. common and important diseases of the equine colon. Clinical signs can vary from those associated with acute, Commonly referred to as pelvic flexure impaction, this severe abdominal pain and cardiovascular collapse, re- form of simple, intraluminal obstruction involves the quiring immediate surgical intervention to low-grade accumulation of digesta in the LVC initially, with sub- abdominal pain, diarrhea, and peritonitis. Peritoneal sequent filling of the sternal flexure and RVC. The fluid changes reflect ischemic necrosis. pathogenesis likely involves interruption or dysfunction Surgical therapy consisting of partial typhlectomy of the pelvic flexure pacemaker region. Impactions are may be successful, if the entire necrotic portion can be unlikely to develop through simple ingestion of dry or removed. Complete typhlectomy after 18th rib resection coarse feedstuffs. A decrease in propulsive motility or in left lateral recumbency is also a consideration. Pro- an increase in retropulsive motility could cause the gressive infarction after surgical removal can occur. The accumulation of digesta. In horses with colonic impac- prognosis in these horses is grave. tion, the digesta appears to be retained just orad tothe pelvic flexure, involving a long segment of the ventral colon, and does not simply involve the pelvic flexure Cecal Torsion alone. The digesta is generally firm and contains fibrous feed material, although sand accumulation can cause a As a primary disease entity, cecal torsion is rare similar lesion. In horses with sand im~actionof this but can occur under unusual situations, such as with area, a shorter segment of colon is involved and the or entrapment of the cecum. Normally, the actual pelvic flexure can be obstructed. Factors such as cecum is relatively immobile and can move only with poor feed quality, poor dentition, reduced water intake, concomitant movement of the RVC and ileum. Re- and parasite damage could cause impaction. Change in cently, cecal torsion was described as a consequence of management conditions such as a stable change, a move hypoplasia of the cecocolic ligament.'O The cecum may from pasture to barn housing, shipping, and systemic be displaced or twisted in horses with volvulus of the diseases may also predispose the large colon to impac- large colon. When this occurs, the axis of rotation tions. involves the dorsal mesenteric attachment of the cecum. The lesions in these horses are often severe, and the prognosis depends on the degree of vascular compro- HISTORY AND CLINICAL FINDINGS mise. If a true cecal torsion is present, partial or com- Typically, horses with impaction of the ventral plete typhlectomy may be necessary. colon exhibit a gradual onset of clinical signs. Often, horses are partially or completely anorexic, and there is Miscellaneous Conditions of the Cecum a gradual decrease in fecal production. Signs of low- grade abdominal pain, such as rolling, pawing, stretch- Adhesion of the cecum to the ventral body wall is ing, and looking at the flanks, are present initially but unusual, except after ventral midline exploratory inci- may progress to signs of severe abdominal pain with sions. Clinicians have suspected cecal adhesion in horses increasing large colon distention. Initial vital parameters with mild, intermittent colic. Rectal examination may are normal, but during painful episodes, heart and reveal chronic cecal malposition. Cecal-cutaneous respiratory rates can be moderately elevated. Initially, is rare but was reported after application of an umbilical auscultation may reveal an increase in borborygmi, but clamp.'l Congenital abnormalities are rare, but with disease progression, intestinal sounds are often the author has observed a single horse with colic due to reduced or absent. It could be shown experimentally LARGE INTESTINE 391

that loud longer borborygmi are associated with colic istering oral and intravenous fluids and analgesic therapy and simultaneous increases in intraluminal pressure of are usually successful. Feed should be withheld until the 40 mm Hg.33 colic subsides, manure production has returned, and the Horses treated early with oral fluid and electrolytes, impaction has resolved, based on rectal examination restriction in oral feed intake, and analgesics to control findings. During resolution of the impaction, semi- abdominal pain generally respond favorably. However, formed and sometimes fluid feces can be passed. Occa- many horses are refractory to early or inadequate treat- sionally, clinicians report mild colic associated with the ment, and clinical signs progress. Signs may progress return of normal motility and resolution of the impac- for 5 to 7 days. Gradual filling of the LVC and RVC tion. with digesta and subsequent gas distention of the ventral The pathogenesis of impactions may, in part, in- colon and cecum occurs with complete obstruction. A volve dehydration of the impacted digesta. Transit of gradual increase in abdominal distention is accompanied dry digesta may be further impeded. Aggressive oral by increased signs of abdominal pain and an elevation fluid therapy (8 L water and electrolytes given via in heart and respiratory rates. Auscultation reveals nasogastric tube, three to four times each day), com- tympanitic sounds, and simultaneous auscultation and bined with intravenous fluid therapy (1 to 2 Llhr), reveal a high-pitched "ping" over the cecum. hydrates the digesta, returns the patient to a more Clinicopathologic changes are generally minimal, but normal systemic hydration status, and may improve local there may be a mild increase in PCV and total protein conditions of the bowel wall that are necessary for levels, indicating mild dehydration. Peritoneal fluid normal motility. changes occur only with advanced impaction and sub- Abdominal pain is controlled by judicious use of sequent devitalization of the colon. Late in the disease, flunixin meglumine in most horses. In some horses, progressive distention of the RVC and cecum may cause however, xylazine administration is needed and effective duodenal compression and passive build-up of gastric for more potent analgesia, but xylazine inhibits progres- sive motility of the colon for a minimum of 30 minutes fluid, but this is unusual. after admini~tration.~~The clinician must avoid giving During rectal examination, the firm, enlarged ter- multiple doses of xylazine or narcotic analgesics, because minal LVC can be readily palpated. Often, the left colon motility dysfunctions may be prolonged. segments are rotated 90 to 180 degrees in horses with SURGICALMANAGEMENT. Surgical management impaction of the ventral colon. The LVC can be iden- is necessary in horses with impaction causing severe tified by the distinct free and mesocolic bands. Rectal abdominal distention, in horses with severe is useful in monitoring progress of the pain, or in horses with progressive cardiovascular dete- impaction. The initial soft, doughy mass may progress rioration or changes in peritoneal fluid values. Ventral to a firm, near-hard, digesta-filled ventral colon. Cecal midline exploratory celiotomy reveals various degrees gas distention can be readily palpated. Occasionally, the of digesta filling of the ventral colon and a small LDC LVC and pelvic flexure are pushed caudally into the (Fig. 36-12). Edema of the intercolonic mesentery and pelvic canal. Rectal examination reveals the firm, im- mild thickening of the bowel wall are commonly en- pacted viscus close to the anus. Obstruction in these countered. Extreme care must be taken not to rupture horses is complicated by additional extraluminal restric- the distended ventral colon during manipulation. To tion of the pelvic canal, resembling a pelvic hernia.72 prevent this fatal sequela, the surgeon should use the arms for bowel handling (see Fig. 33-19), and use large TREATMENT abdominal incisions (up to 45 to 50 cm in some horses). Occasionally, infusion of sterile saline solution and mas- NONSURGICALMANAGEMENT. Horses with im- sage of the digesta result in a successful outcome. paction of the ventral colon should respond favorably Enterotomy combined with evacuation of the accumu- to medical management. Withholding feed and admin- lated digesta is most successful but must be performed

Origin of small colon

FIGURE 36-12. Drawing of the equine cecum and large colon of a horse with impaction of the ventral large colon during colotomy and evacuation. The ventral colon segments are enlarged with firm digesta, whereas the dorsal colon segments are small and relatively empty. The enterotomy is performed between free bands in the terminal left ventral colon and a soft rubber tube is used to provide warm water lavage of the impacted colon. The same technique can be used for impaction of the colon at other sites. (Redrawn from Foerner JJ: Diseases of the large intestine, , and surgical management. Vet Clin North Am Equine Pract 4:130, 1987.) 392 ALIMENTARY SYSTEM

with adequate preparation to avoid excessive contami- SURGICALMANAGEMENT. Surgical management nation. The enterotomy should be performed in the generally involves softening the impacted material with terminal LVC between bands. The pelvic flexure and infusion of saline or water. This process can be per- origin of the LDC should be avoided. Evacuation is formed through a needle and tubing apparatus or with aided by using a hose and large volumes of water. An the aid of a nonsterile assistant passing a hose from the assistant, prepared and gowned for aseptic surgery, is anus. This procedure has been termed a "high-." necessary to aid during manipulation of digesta in the However, if a large volume of digesta or sand is present, RVC. enterotomy may be necessary. Enterotomy in the LVC, The prognosis after surgery is good to excellent. combined with the use of the intraluminal tube, is the Occasionally, a motility dysfunction persists and impac- safest method to avoid possible peritoneal soiling. A ; tion recurs. Medical management is instituted. sterilely prepared assistant to help with manipulation and evacuation of the material is necessary. Removal of Impaction of the Right Dorsal Colon impacted sand by this method is difficult because the I sand tends to settle in this area. I ETIOLOGY Recurrent impaction or obstruction of the RDC The RDC preferentially retains larger digesta par- may be caused by functional obstruction. In a recent 1 ticles and has a large reservoir function for microbial case of recurrent colic, a contracted, corrugated RDC 1 digestion. Strong retropulsion must exist. Marked nar- was detected during emergency celiotomy." A func- rowing of the lumen diameter occurs as the RDC enters tional obstruction of the RDC, postulated to be related the transverse colon. Because of these factors, the RDC to in humans, was suspected. is prone to impaction. Impactions of the right dorsal A side-to-side colocolostomy between the RDC and SC colon are not as common as those of the ventral colon was successful in alleviating clinical signs. but generally consist of very firm digesta or sand. Horses with this disease may respond slowly to medical therapy Fibrous Foreign Body Obstruction I and are at risk for recurrence of the problem. Impaction Obstruction of the RDC, transverse colon, and oral of the RDC may be more common in mares before SC can occur with nondigestible material. Bailing twine, parturition, which suggests that a motility problem may rubber fencing, nylon material, socks, or other nondi- be a factor. An enlarged firm RDC is often found in gestible material cause obstruction. Typically, a hard horses with nonstrangulating displacements or volvulus concretion of fecal material forms around these sub- of the large colon. The pathogenesis may involve a stances. Rubber fencing material causes a classic form primary motility dysfunction of the RDC, digesta and of the disease after horses ingest strands of the polyester gas accumulation, rotation with eventual displacement, and nylon fiber. In one notable outbreak, 28 horses had or volvulus. colic after ingesting the material.74 In one study, 10 of 207 horses with colic had fibrous foreign body impaction. HISTORY AND CLINICAL FINDINGS Affected horses were 3 years of age or younger and had Horses with impaction of the RDC show signs mild colic signs.75In the original description, 2 to 5 years similar to that seen in horses with impactions of the were needed for obstruction to occur after ingestion of cecum or ventral colon. Because of the aboral position the material.74 of the impaction, signs are slow to progress. Intermittent Signs are similar to those seen with impactions, fecal passage indicates that a partial obstruction may including the ability to pass mineral oil around the exist. In horses with advanced disease, secondary duo- offending material, but surgical management is manda- denal obstruction due to enlargement of the RDC may tory. The site of obstruction is nearly always the terminal cause gastric distention. RDC or the transverse or oral SC, sites that are not Rectal examination is most helpful. In the normal directly accessible. One or more enterotomies located horse, the RDC is not palpable. In horses with impac- orally or aborally to the lesion may be needed. Enter- tion, the RDC shifts caudally and may be palpated as a otomy in the dorsal colon, followed by manual retrieval, firm viscus without obvious bands. Occasionally, a me- is most useful. Retrograde flushing or other forms of socolic band with an associated vessel is felt. The ex- hydropulsion are ineffective because the concretions are aminer can usually pass the hand dorsal to the firm tenacious. viscus, a useful technique to help differentiate impaction In horses with long-standing obstruction, the bowel of the RDC from that of the cecum. In these horses, wall may be devitalized, rendering a grave prognosis. If the clinician is most likely palpating the oral portion of the bowel wall is healthy and the offending material can the RDC. be removed, the prognosis is good. In one report, 5 of 10 horses

TREATMENT Enterolith Obstruction NONSURGICALMANAGEMENT. Aggressive medi- cal management as described for horses with impaction ETIOLOGY of the ventral colon can be successful, but horses may Enteroliths, which are large concretions formed be refractory to treatment. Prolonged impaction of the primarily of ammonium phosphate, can ob- RDC may lead to perforation. struct the terminal RDC, transverse colon, or SC. The LARGE INTESTINE 393

mineral is deposited in concentric layers around a nidus Horses stabled in a sandy environment and fed from the of foreign material, such as small pieces of wood or ground appear at risk. Clinicians often associate this chert or a small ~tone.~~.~~Ammonia is continually form of colic with specific geographic areas. Ingested produced in the large colon, and are found sand may cause foreign body or sediment over in abundance in horse feeds. The limiting factor in time to. cause impaction. Offending sand is generally enterolith formation may be the level of magnesium in fine beach sand or clay, but gravel can occasionally be ingested feed or water.76 Enteroliths are formed in two found. basic shapes, spheres or tetrahedra. Clusters can occur, and multiple enteroliths are common. Enteroliths gen- CLINICAL SIGNS - erally are not found in horses younger than 5 years of age and are most common in horses 5 to 10 years of In a recent study, sand colic was diagnosed in 48 age.78 horses, none of which were younger than 1 year of age." Clinical signs range from mild to severe pain and normal to deteriorating cardiovascular status. Rectal CLINICAL SIGNS examination reveals cecal and large colon gas distention. Clinical signs are typical of horses with impaction An impaction could be felt in only seven of 48 horses." colic with one exception. Horses with enteroliths fail to Sand can be present in feces without causing colic. In many horses, surgical exploration is undertaken because pass any feces when complete obstruction occurs. Fail- ure to pass manure for up to 24 hours may alert the of abdominal pain, large colon distention, and deterio- clinician to this form of colic. Typically, signs are inter- rating cardiovascular signs, without an accurate preop- erative diagnosis. Abdominoparacentesis should be per- mittent for several days, and then when complete ob- struction occurs, they progress to become acute. Gas formed carefully, because the heavily laden sand- impacted colon can be lacerated inadvertently. In three and fecal distention of the colon oral to the lesion cause abdominal distention. Vital parameters and laboratory of six horses with inadvertent enterocentesis, sand was data are within normal limits unless the bowel wall found in the fluid, which was diagnostic for the disease.* becomes devitalized. With complete obstruction, severe Abdominoparacentesis should not be performed in abdominal distention, pain, and cardiovascular collapse horses that obviously require surgical intervention or in occur. Rectal examination is most helpful, but the horses in which the procedure may be of low diagnostic enterolith is seldom palpated. value. Auscultation of horses with sand impaction may reveal sounds compatible with sand borb~rygmi.~'.~~ Horses with true sand impaction of the large colon I TREATMENT rarely respond to medical management. Surgical management is necessary; unfortunately, the enterolith lodges in areas that are inaccessible. TREATMENT Therefore, the surgeon must make judicious use of Sand impaction is often a surgical diagnosis and hydropulsion or manual extraction. A technique of may be difficult to treat. Coordinated efforts are needed retrograde flushing of obstructions in the transverse between the surgeon and the assistant surgeon, and both colon by introducing a tube into the SC has been intraluminal and transmural manipulation are needed. described.79 However, the surgeon must be careful be- Judicious, copious intraluminal lavage combined with cause high pressures can cause a rupture of compromised egress tubing in some horses is needed.80 Because sand or normal bowel. Intraluminal retrieval, with the sur- can settle in more than one viscus, multiple enterotomies geon's hand introduced through an enterotomy site in may be needed. Twenty-six of 48 horses had multiple the RDC near the diaphragmatic flexure, is useful when sites of sand impa~tion.~~Single impactions were seen enteroliths lodge in the transverse colon or RDC. Trans- most commonly at the pelvic flexure (14 horses), but mural manipulation and massage to "milk" the entero- when multiple impactions were present, the RDC was lith into the RDC or aborally into a more accessible more frequently involved (15 horses). Sand impaction portion of the SC is useful. Rupture of the bowel can of the pelvic flexure may act as a pendulum, predisposing occur with manipulation, especially in the SC. the horse to volvulus of the colon. Cranial dis~lacement The prognosis is reported to be fair. A 47% success of the pelvic flexure and nonstrangulating and strangu- rate was reported in one with the best results lating colonic displacements were seen in 16 of 48 horses achieved when the enterolith was removed before the with sand impa~tion.~~.Inanother study, 10 of 40 horses bowel became devitalized. After removal of the entero- had volvulus or displacement of the colon.* lith, especially one in the shape of a tetrahedron, the entire large bowel should be palpated for the presence COMPLICATIONS of additional enteroliths. Complications after surgery include recurrence of the disease, peritonitis, diarrhea, and incisional prob- Sand Impaction of the Large Colon lems. The prognosis is guarded to poor for horses with ETIOLOGY true sand impaction requiring s~rgery,'~ and in one I study, the mortality rate was 30%.83 The long-term Sand impaction of the large colon occurs most survival rate was 60% in a recent clinical study, which I commonly at the pelvic flexure and terminal RDC. indicated a relatively high mortality rate compared with 394 ALIMENTARY SYSTEM

other impactions of the large inte~tine.~~Forty-four of Nonstrangulating Colonic Obstruction 48 horses with sand impaction were discharged from the hospital, and follow up on 38 horses revealed a relatively ETIOLOGY low mortality rate (8.3%).80 Clinicians may differ with Because of the length of the bowel and the lack of respect to how they arrive at the diagnosis of sand extensive mesenteric attachments, the gas-distended impaction or to the importance they place on the surgical large colon can twist or become malpositioned, dis- finding of small amounts of sand when other lesions are placed, or incarcerated (entrapped). In a clinical study, present. 32 of 232 horses (14%) undergoing surgery for colic had Minimizing exposure to sand may be important in nonstrangulating displacements of the large colon.85Sev- preventing recurrence. The weekly dosing of the natural eral forms of large colon displacement are recognized fiber psyllium hydrophobic mucilloid is useful that cause similar clinical signs. In conditions such as in removing small amounts of sand from the large colon. impaction and tympanites of the large colon, there can be a 90-degree rotation of the colon without anatomic obstruction. However, 180- to 270-degree rotations of the colon cause anatomic obstruction of the flow of Tympanites of the Large Colon and Cecum digesta and varying degrees of venous stasis. Some forms of nonstrangulating displacements may progress to stran- CLINICAL SIGNS gulating lesions and may simply represent early forms of strangulation obstruction. Primary gas distention of the cecum and large colon occur but are generally short lived and respond to medical management. Occasionally, however, a more CLINICAL SIGNS severe form of tympanites occurs. Clinical signs vary, depending on the degree of abdominal distention. Rectal Each form of displacement has specific character- examination reveals gas distention of the cecum char- istics, but the history and clinical signs are similar. acterized by taut bands. The bowel may shift and assume Horses exhibit signs of displacement for 12 to 24 hours a transverse position in the caudal abdomen. The left before becoming more acutely painful. Generally, low- ventral and dorsal colon segments may rotate 90 de- grade signs of abdominal pain occur that are similar to grees. This anatomic abnormality is confusing, leading those seen in horses with impactions. Horses generally one to suspect a surgical lesion. Generally, no edema respond to symptomatic treatment only to become pain- of the bowel wall is felt. Atropine can cause a particu- ful-once again within several hours. Heart and respira- larly severe form of tympanites and should be used with tory rates are elevated during painful episodes but are ~aution.~"Glycopyrrolate, an antimuscarinic drug used usually normal, until late in the course of the condition. for treatment of horses with increased respiratory secre- The preoperative heart rate was reported in one study tions or bronchoconstriction, can also cause large intes- to be elevated to a mean of 64 beats per minute in tinal stasis, tympanites, and colic. horses with displacement^.^^ Progressive abdominal dis- tention usually causes increased abdominal pain. Occa- sionally, up to 2 to 3 gallons of gastric fluid are obtained by , presumably owing to duo- TREATMENT denal compression by the distended large colon. Tension of the duodenocolic ligament has also been incriminated. Medical management should be undertaken. The Gastric reflux may be more of a problem in horses with horse's response to treatment may be diagnostic. If left dorsal displacement of the lkft colon segments. In auscultation and rectal confirm cecal disten- most horses, gastric distention is not present. tion, cecal trocarization is both therapeutic and diag- Rectal examination is most helpful in establishing a nostic. If the horse responds to treatment, primary diagnosis and distinguishing this form of colic from tympanites is the diagnosis; whereas if distention recurs, tympanites or impaction. Gaseous~distentionof the large tympanites may be secondary to another lesion. Cecal colon and cecum with the associated tight bands is trocarization in the right paralumbar fossa is not without characteristic. Preoperative diagnosis of left dorsal dis- risk, and the peritoneal fluid nucleated cell count may placement and right displacement of the left colon rise dramatically (up to 100,00O/pL) after the proce- portions is possible, but there are no pathognomonic d~re.'~Bowel laceration and subsequent peritonitis can findings on rectal palpation. Most important, the clini- occur; therefore, the procedure should be used judi- cian should note large colon distention, displacement, ciously and sparingly. and mild edema of the bowel wall and make the correct Surgical management may be necessary to alleviate decision for surgical intervention. The diagnosis is con- colonic distention or may be undertaken because of the firmed at surgery. confusing nature of the clinical signs. At surgery, the cecum and colon are usually in the normal anatomic position and needle decompression is performed. Sur- TREATMENT geons often suspect colonic displacement has occurred Surgical correction of the anatomic displacement is but has corrected itself once the horse is rolled into mandatory. The pelvic flexure should be located first, dorsal recumbency. The prognosis is good, but recur- and the remainder of the colon can then be identified. rence is possible if an underlying problem exists. If the pelvic flexure cannot be found, the cecocolic LARGE INTESTINE 395 ligament is found and the surgeon follows the ventral colon to the pelvic flexure. The LVC and LDC are exteriorized, rotated, and placed back into the abdomen in the correct anatomic position. Generally, needle decompression of gas-distended cecum and large colon is adequate, but occasionally, an enterotomy is needed to relieve the accumulation of digesta. The enterotomy should be performed in the terminal LVC. Enterotomy is generally not necessary, because once the displace- ment is corrected, horses quickly regain normal intes- tinal motility. The prognosis of horses with nonstran- gulating displacements is good, and the condition is considered one of the most favorable forms of all surgical problems. The long-term survival rate was 71% in horses with displacement^.^ The survival rate com- pares most favorably with that of horses requiring small intestinal resection and anastomo~is.~In a study of 140 horses, the overall survival rate of small intestinal resec- tion and anastomosis was 22%, although only 11% of horses survived more than 3 years after resection and ana~tomosis.~ Nonsurgical correction of left dorsal displacement has been described (see the section on Left Dorsal Displa~ement).~~,~~Right dorsal and left dorsal displace- ment can recur, requiring additional surgery and possi- ble colopexy. NONSTRANGULATINGVOLVULUS OF THE LARGE COLON. Rotation of the colon between 90 to 270 degrees causes physical obstruction of the colon, inter- rupts digesta transit, and causes gas distention and colic. Nonstrangulating volvulus is one recognized form of displacement of the large colon and is classified as a simple obstruction (Fig. 36-13). Edema and hyperemia of the bowel wall is common, and therefore, partial venous obstruction occurs. Rotation of the colonic axis usually occurs in a clockwise direction when viewed from a caudal position, as if the examiner were perform- ing a rectal examination. This rotation is also seen in horses with strangulating volvulus of the large colon. Obstruction occurs at the sternal and diaphragmatic flexures, although a report describes involvement of the cecum in some h~rses.~Needle decompression is nec- essary in the ventral and dorsal colon segments and the cecum. The surgeon must identify the lesion, exteriorize FIGURE 36-13. Nonstrangulating displacement of the large colon as the colon, and reposition it correctly. viewed from the ventral aspect at exploratory surgery. (A), 180-degree volvulus of the large colon, located at the sternal and diaphragmatic RIGHT DISPLACEMENTOF THE LEF~COLON. flexures. (B), Right displacement of the left colon segments. Without Frequently called right dorsal displacement, this form further rotation or volvulus, this form of displacement may cause of nonstrangulating obstruction may be related to a chronic, intermittent wlic before complete luminal occlusion occurs. motility dysfunction of the RDC. Commonly, the RDC (Redrawn from Hackett RP: Non-strangulating colonic displacement is digesta filled, predisposing the horse to gas distention in horses. J Am Vet Med Assoc 182:235, 1983.) and rotation. Rectal examination reveals a tight band associated with the LVC, traversing across the caudal abdomen and coursing lateral to the cecum. In some and progressive abdominal distention become obvious. horses, the cecum is pushed forward and is not palpable. Medical management including withholding feed, anal- Usually, the ventral cecal band is tight due to cecal gas gesic administration, and occasional trocarization of the distention. Right displacement of the left colon portions gas-distended colon can help resolve the clinical signs. can be a chronic condition and can initially be present However, when the horse is returned to full feed, colic without colic signs. Without concurrent volvulus or recurs. severe gas and digesta accumulation, a malposition of This form of displacement can cause chronic inter- the left colon segments in a U-shaped fashion to the mittent colic. The more typical form involves progressive right impedes but does not stop the transit of digesta large colon distention, secondary abdominal distention, (Fig. 36-13A). With further rotation or with filling of and an increase in abdominal pain, which requires the RDC, a simple obstruction occurs. Signs of colic surgical intervention. Various forms of the displacement 396 ALIMENTARY SYSTEM

are described to include flexion and torsion of the colon In left dorsal displacement of the large colon, portions.89 In the most common form, the pelvic flexure clinical signs may vary from mild to severe, presumably rotates cranially to the right and finally sits tranversely relating to the amount of tension on the renosplenic in the abdomen, thus completing a counterclockwise ligament or the amount of involved intestine. The level rotation (when viewed from the ventral aspect at the of colic is usually compatible with other forms of non- time of surgery). Clockwise rotation can occur but is strangulating displacement, but occasionally, horses are less common. violent. The classic signs found on rectal examination LEFT DORSALDISPLACEMENT OF THE LARGECO- that are associated with this form of displacement in- LON. Left dorsal displacement of the large colon, fre- clude (1) gas-filled LVC and LDC coursing craniodor- quently called renosplenic (nephrosplenic) ligament en- sally over the renosplenic ligament; (2) a ventral and trapment, is a well-recognized form of nonstrangulating medial shift in splenic position; and (3) a tight, gas- displa~ement.~~,87' 90- 91 The etiology is unknown, but distended cecum. However, there are no pathognomonic one possibility includes concomitant splenic contraction signs. With simple tympanites of the large colon, the and gas distention of the LVC and LDC. With dorsal left ventral and dorsal colon segments can assume displacement of the colon and subsequent refilling .of dorsal position in the abdomen, mimicking left dor the , the colon is tra~ped.'~Regardless of etiology, displacement of the large colon. Other large col ~ the lesion involves an entrapment of the LDC and LVC displacements can mimic left dorsal displacement of 1 over the dense, fibrous suspensory ligament between the large colon as well. The lesion may be suspected more and spleen. Occasionally, concurrent impaction frequently than it actually occurs. or volvulus of the colon is present (Fig. 36-14). This Other more subtle clinical findings may lead one to form of displacement can be seen in younger horses, suspect left dorsal displacement. In this form of displace- whereas other forms of displacement are unusual in this ment, horses can have a rather surprising amount of I age category. gastric distention, requiring nasogastric intubation. Rel- ative to the amount of pain and distention, the heart 1 rate is lower than expected. The PCV may be normal or slightly low, despite mild or moderate clinical dehy- dration. Splanchnic or splenic sequestration of red blood cell volume may explain this clinical finding. Abdomi- nocentesis may yield bloody fluid from splenic puncture because of the ventral positioning of the spleen. Occa- sionally, horses with left dorsal displacement of the large colon suffer from intermittent pain, and a more chronic form of colic results. Two forms of correction have been advocated. Surgical exploration, decompression, and repositioning of the colon provide the most direct means of diagnosis and anatomic repositioning, without risking other com- plications reported with nonsurgical management.% At surgery, the LVC and LDC are found dorsal to and entrapped by the renosplenic ligament. The lesion is unequivocal when found and is easily corrected. To free the colon, the surgeon needs to carefully push the spleen medially, while with both hands and arms, gently rock- ing the colon free, bringing the structure first dorsally around the spleen, and then laterally and ventrally. This maneuver is more easily accomplished if the surgeon is standing on the horse's right side during ventral midline exploratory. Both hands are cupped around the colon, after the arms are used to push the spleen to the right (toward the surgeon). A method of nonsurgical correction of left dorsal displacement of the large colon has been de~cribed.~.'~ After inducing general anesthesia, the horse is posi- FIGURE 36-14. Left dorsal displacement of the colon, over the tioned in right lateral recumbency. While providing a renosplenic ligament. (A), Surgeon's view of left dorsal displacement. Occasionally, the digesta in the entrapped portion of the colon is firm, gentle "rocking" motion (shaking) of the abdomen, the requiring enterotomy, or a volvulus of the colon occurs in the horse's limbs are gradually hoisted to a vertical position entrapped portion. (Redrawn from Hackett RP: Non-strangulating and then the horse is rolled into left lateral recumbency. colonic displacement in horses. J Am Vet Med Assoc 182:235, 1983.) After completion of the rolling procedure, the spleen is (B), With concomitant gas distention of the left colon segments and once again against the lateral body wall, now lateral to a medial shift of the spleen, the colon segments become incarcerated dorsal to the renosplenic ligament. LDC, left dorsal colon; LVC, left the LVC and LDC. Occasionally, manipulation by rectal ventral colon. (Redrawn from McIlwraith CW: Equine digestive palpation is needed to free the entrapped colon. In a system. In Jennings PB (Ed): The Practice of Large Animal Surgery. recent clinical study, 5 of 27 horses required rectal Philadelphia, W. B. Saunders Company, 1984, p 638.) manipulation combined with rolling.% Maintenance of R LARGE INTESTINE 397 the dorsal recumbent position for a few minutes may colon can cause gas distention and rotation of the colon. facilitate the correction of the problem. Published com- Unless these areas are carefully palpated, lesions can be plications of the procedure include recurrence, inability easily missed. to free the colon by the technique, cecal torsion, or large colon torsion. Recurrence of left dorsal displacement of the large Adhesions, Abscc and Neoplasia colon and other displacements or volvulus of-the large Nonstrangulating, simple obstruction of the large colon have prompted surgeons to consider stabilizing colon can occur with adhesions, abscessation, or neo- the colon by col~pexy.~',92 In two of nine horses, recur- plastic diseases. Mural abscessation and neoplasia are rence of left dorsal displacement of the large colon was extremely rare. Omental adhesions to various portions found, requiring a second celiotomy. Other reported of the large colon can occur after surgical incision, complications are adhesion formation after surgery in traumatic perforation, or ulceration. Adhesions of the one horse and subsequent large colon necrosis in an- large colon to the body wall can cause partial obstruction other. A technique to obliterate the renosplenic space and displacement. At surgery, adhesions should be was reported to be successful in preventing left dorsal carefully disrupted to avoid penetration of the bowel displacement of the large colon in eight horse^.^',^^ lumen. If chronic scarring is present, intestinal resection Currently, surgical correction and colopexy should be or bypass may be needed. For more information on this undertaken if the condition recurs. Colopexy, however, subject please review Chapter 33. results in a permanent adhesion of the large colon and may have long-term complications (see the section on Colopexy). Strangulation Obstruction of the Large Colon CRANIALDISPLACEMENT OF THE PELVICFLEX- VOLVULUS OF THE LARGE COLON (VLC) URE. At exploratory surgery, the pelvic flexure may be located in the cranial abdomen. A cranial position PATHOGENESIS. Volvulus of the large colon of the pelvic flexure may not be a true lesion and may (sometimes including the cecum) causes one of the most occur secondary to rolling or placing the horse in dorsal acute, devastating forms of colic. By far, the most recumbency. If accompanied by a lesion of another common form of the disease causes acute cardiovascular intestinal segment, without large colon gas distention or deterioration, severe abdominal pain, gross abdominal impaction, the cranial displacement of the pelvic flexure distention, and death within 4 to 24 hours unless the may be incidental. However, in some horses, cranial horse is operated on in a timely fashion. Initially, the displacement of the pelvic flexure with concomitant pathogenesis involves venous occlusion and hemorrhagic impaction or gas distention of the large colon, colic, and strangulation obstruction, but later, progressive arterial no other lesions found at exploratory surgery appears occlusion causes ischemic changes. The colon rotates in to be a true lesion. In one study, eight horses had the clockwise fashion as viewed from behind, looking for- conditi~n.~~Gas distention and associated impaction of ward along the axis formed by the RVC and RDC (Fig. various colonic segments was common. The prognosis 36-15). The volvulus is generally 360 degrees, but sur- is considered good. geons have reported rotations of up to 720 degrees. The OTHERTYPES OF DISPLACEMENT. The colon can classic form of the disease involves a twist at the level rotate or displace into various positions, some of which of the cecocolic ligament, but the axis of rotation can are described, while others seem atypical. Tympanites be at the cecal base. Occasionally, VLC occurs at the can be associated with rotation of the colon. However, sternal and diaphragmatic flexures, but this condition is if large colon distention and an odd form of displacement unusual. are found at surgery, a thorough exploration should be Broodmares, late in gestation or after parturition, performed to rule out other forms of obstruction. Intra- appear at risk of developing VLC. Other forms of luminal obstruction of the terminal RDC or transverse nonstrangulating displacements may also occur in brood-

FIGURE 36-15. The cecum and large colon of a horse with volvulus of the large colon at the level of the cecocolic ligament. Volvulus at this level is the most common form of the disease. Note that clockwise rota- tion of the bowel (as viewed from the caudal aspect of the horse) is most common. Once the horse is in dorsal recumbency, the surgeon untwists the colon in a clock- wise direction as well. RDC, right dorsal colon; RVC, right ventral colon. 398 ALIMENTARY SYSTEM mares. In a recent study of 122 horses with VLC, 73 datory for a successful outcome. Even if surgery is horses were females and 42% had foaled or were preg- undertaken as early as 3 to 4 hours after the onset of nant.94The disease is not restricted to broodmares, but signs, there is no guarantee of a successful result. changes in digestion or visceral positioning during preg- Aggressive intravenous fluid therapy is needed before nancy may predispose mares to the disease. The enlarg- surgery, if possible, to restore blood volume. Reperfu- ing may induce a shift in the position of the large sion injury may cause significant bowel damage after colon or cause partial obstruction of the RDC. Digesta, surgical correction, and some consideration should be gas distention, and secondary rotation of the colon lead given to the administration of free radical scavengers. to strangulation. A change in intestinal motility may A practical choice would be dimethyl sulfoxide (DMSO) occur during pregnancy. Large colon motility dysfunc- (1 gmlkg IV), but recent evidence suggests it is not tion occurs in women during pregnancy, but the condi- effective in preventing injury from either hemorrhagic tion is not known to exist in horses. The history may or ischemic strangulation obstr~ction.~~Broad-spectrum indicate a previous management change such as change intravenous , flunixin meglumine, and corti- in housing or in the type or quality of feedstuffs pro- costeroids are beneficial and should be given before vided. surgery. CLINICALFINDINGS. The clinical signs generally In horses with VLC, induction and early mainte- reflect the duration of the volvulus. Severe, unrelenting nance of general anesthesia are critical and are compli- pain is the most common clinical sign, and based on this cated by the extreme large colon distention and poor factor alone, a decision for surgical intervention is often metabolic state of the patient. Abdominal distention made. Horses sweat profusely and often display skin prevents adequate ventilation and predisposes the horse wounds. Abdominal distention is common and often to ventilation-perfusion mismatches. Blood gas values severe, causing respiratory compromise. The heart rate typically show hypercapnia and inadequate oxygenation. is elevated between 60 and 80 beats per minute but is Rapid release of endotoxin and stagnated venous blood lower than expected for the degree of abdominal pain after untwisting the colon may cause a hypotensive crisis, present. Horses with VLC and high heart rates (greater leading to fatal cardiac arrhythmias. Hypotension is than 65 to 70 beats per minute) accompanied by severe common, and maintenance of anesthesia can be difficult. dehydration (PCV >60%) have a very poor prognosis, Early decompression of the bowel generally helps in because these parameters reflect severe changes in car- improving ventilation, but oxygenation and peripheral diovascular status. In a recent study, there were signifi- perfusion still may be inadequate. Judicious use of cant differences between survivors and nonsurvivors preoperative cecal trocarization may help early in the (values were lower in survivors) in heart rate, respiratory anesthetic management. Efficient and timely surgical rate, capillary refill time, and PCV.94 In this study, the intervention, minimizing surgery time, and aggressive mean duration of clinical signs was 19 hours (range, 2 management of hypotension maximize survival after to 156 hours). Occasionally, horses may have a more surgery. chronic clinical course. Early nonstrangulating lesions Large ventral midline incisions (up to 40 to 50 cm) may progress to strangulation obstruction. are beneficial and allow easier manipulation of the Rectal examination usually reveals large colon dis- distended colon. Early gaseous decompression and un- tention and tight bands coursing transversely in the twisting of the colon should be performed before ma- caudal abdomen. An important finding is edema of the nipulation. The surgeon needs to be gentle in handling colonic wall, which reflects severe venous congestion. the colon, because rupture, particularly of the RDC, Occasionally, rectal examination reveals an empty cau- occurs frequently. As much of the colon as possible dal abdominal quadrant. The empty abdomen leads to should be exteriorized and held by an assistant. The a springy or bouncy feeling of the rectum, resembling surgeon then untwists the colon 360 degrees in a clock- the finding of . In these horses, pain wise direction as viewed from the ventral midline ap- is severe and the colon has shifted forward, causing proach with the horse in dorsal recumbency. A thick, severe compression of the cranial abdominal viscera. In edematous colonic wall; hemorrhagic, congested inter- rare instances, rectal examination reveals edema of the colonic mesentery; and various shades of serosal discol- colon without colonic gas distention. Severe unrelenting oration (from dark purple to greenish gray) are seen. pain is the most consistent sign leading to surgical After untwisting the colon, there is generally some intervention, regardless of the findings on rectal exami- improvement in serosal color, unless complete ischemia nation. or end-stage hemorrhagic strangulation obstruction ex- Examination before surgery may be pre-empted by ists. Generally, a period of 10 to 15 minutes should be unrelenting abdominal pain. Laboratory data generally given to assess bowel viability. Absence of a pulse in reflect dehydration, with protein loss into the bowel wall colonic vessels, failure of the colon to return to its and lumen. Mild metabolic acidosis may become severe normal serosal color, necrotic odor, and black mucosal in advanced disease. Peritoneal fluid can range from color are grave signs, and horses with these signs should normal to serosanguinous in color. Serosanguinous fluid be euthanized. Surface oximetry, if available, may help is common and generally is considered a poor prognostic in predicting possibility of survival in horses with colonic sign. Mean protein levels and nucleated cell counts are strangulation obstruction.% Although clinical evaluation usually slightly elevated, but generally, the clinical of horses with experimental colonic strangulation ob- course is too short to have consistent elevations in these struction would have led to a prediction of poor survival, parameters. a return of serosal surface oxygen tension of greater TREATMENT.Early surgical intervention is man- than 50% of baseline correctly predicted survival in a LARGE INTESTINE 399

high percentage of horses. Recently, microscopic eval- should inhibit the development of intussusception, but I "ation of frozen sections of colonic wall have been abnormal motility, impaction, and parasite lesions may useful in determining colonic viability with the aid of predispose the horse to the disease. Intussusception has clinical assessment of perf~sion.~~ been reported at the pelvic flexure, the LVC, and the Horses with loss of glandular epithelium are un- LDC. These segments may be predisposed to the dis- likely to survive. Resection of the involved colon re- ease. Intussusception is less likely in the right colon mains a possibility, particularly if the volvulus occurs at segments, because the RDC and the RVC have dorsal the diaphragmatic flexure. However, successful resec- mesenteric attachments and the cecocolic ligament at- tion in horses with true VLC at the cecocolic ligament taches to the RVC.' Intussusception may cause initial or at the base of the cecum is difficult because the simple obstruction, but venous obstruction, mural swell- surgeon usually cannot remove all of the necrotic colon. ing, and arterial occlusion lead to strangulation obstruc- A resection of 95% of the colon, as reported, may not tion. Clinical signs and laboratory parameters reflect the be possible,98 because in clinical cases, a minimum of 25 duration of the obstruction. to 30 cm of RDC and RVC are left intact. Although Surgical intervention is mandatory. Manual reduc- close to 95% of the length of the large colon may be tion was successful in one horse,lo2 but usually resection removed in normal horses, removal at this level may and anastomosis are necessary. Both side-to-side or end- leave 15 to 25% of the absorptive surface area severely to-end anastomoses are successful, but end-to-end pro- affected by mucosal damage. Substantial damage to the cedures are difficult because of the disparity in size of RDC and associated endotoxemia reduce the survival the colonic segments. The prognosis is guarded to good, rate in such horses even with the use of resection. depending on the timing of surgery, the degree of j Because of the severity of the lesion, up to 50% of ischemia, and the surgical technique performed. the horses operated on for VLC may be euthanized at the time of surgery. Decompression, untwisting, and LARGE COLON INFARCTION repositioning of the colon are required. If the colon is ~ I filled with digesta, making manipulation difficult, enter- Thromboembolism of the colonic vessels is rare, otomy and evacuation may be needed. Evacuation of but can occur secondary to migration of S. vulgaris the potentially dangerous toxins that may be absorbed larvae. The arterial supply of the colon arises from two after surgery may be desired, but the procedure is not separate branches, forms a loop at the pelvic flexure, 1 mandatory. The RDC is usually large, and evacuation and has extensive communications between the vessels. of this segment is difficult. A colopexy should be con- The vascular supply of the colon is relatively protected sidered if VLC recurs. compared with the cecum. Aggressive management with intravenous fluids, With extensive thromboembolic disease, infarction antimicrobial agents, and anti-inflammatory agents is can occur, causing clinical signs associated with stran- needed after surgery. Because of the high numbers of gulation obstruction. Horses usually suffer from acute ~ anaerobic organisms, metronidazole (15 mglkg, PO, pain but can show depression with chronic pain. Resec- QID) may help in horses with peritonitis or contami- tion and anastomosis are successful if the ischemic nation from enterotomy sites. Endotoxin absorption segment is short. Generally, the LDC and the LVC are from damaged mucosa can complicate recovery. Im- involved, and end-to-end or side-to-side anastomoses munotherapy with J-5 antisera, producing passive im- can be performed after resection. In one horse, end-to- munity with antibodies directed against a core polysac- end colocolostomy was successful after infarction of the charide of gram-negative bacteria, has shown promising LDC.'" Continued thromboembolic disease after sur- early results.99.loo Plasma administration to supplement gery limits the prognosis. protein loss from compromised bowel may help. Early after surgery, hemorrhagic diarrhea, fever, and leuko- penia are common in horses with moderate to severe Large Colon Resection colonic compromise. Continued fecal passage is a good Partial resection of the large colon can be per- prognostic sign, but horses that develop ileus, large formed successfully using both hand-sewn and autosu- colon distention, and abdominal pain after surgery have ture techniq~es.'~.'"Much debate remains, however, a very poor prognosis. Reoperation, decompression, regarding what is called 95%, or near-complete, resec- and large colon resection or euthanasia may be neces- tion of the large col~n.'~~-'~Lesions aboral to the sary. cecocolic ligament can be exteriorized from a ventral PROGNOSIS.The reported survival rate of horses midline incision, and resection is possible. In a recent with VLC ranges from 12% to 34.7%.36,94However, study, 36 of 122 horses had lesions amenable to resection because differences exist with lesion definition and se- from an anatomic ~tandpoint.~~Although the most com- verity grading, survival rates may differ. Actual survival mon site for VLC is the level of the cecocolic ligament, rates for horses with VLC of 360 degrees are likely in the damage extends into the terminal RDC and the oral the 10% to 20% range. portion of the RVC. Resection, even at the cecocolic ligament, leaves necrotic bowel in situ, and endotoxin INTUSSUSCEPTION OF THE LARGE COLON absorption and death are likely. Because the wall is thicker and compromised in horses with VLC, surgical Intussusception of the colon is rare but has been techniques used in horses with experimental resection rep~rted.l~'-'~~The short, strong intercolonic mesentery may fail. 400 ALIMENTARY SYSTEM

Little doubt exists that extensive large colon resec- resectionfi2 Resection was performed at the level of the tion can be performed successfully in normal horses. cecocolic ligament in most horses.l12 Survival decreased Resection at the level of the cecocolic ligament may as the amount of devitalized tissue left in situ in- remove all but 5% to 10% of the length of the large creased.lI2 Large colon resection remains a viable alter- colon but may leave 15% to 20% of the absorptive native to untwisting, enterotomy, and repositioning, but surface area. Five of 10 normal horses survived 18 case selection is important. Hand-sewn techniques months after resection at the cecocolic ligament.lo6 should be considered because edematous, thickened After attaching stay sutures, a side-to-side anasto- colon may not be suitable tissue for the application of mosis is performed between the RDC and the RVC at currently available stapling equipment. the level of the cecocolic ligament, using the GIA autosuture instrument. After completing the anastomo- Colopexy sis and ligating the dorsal and ventral colic arteries, the I large colon is transected using the TA-90 stapling instru- Recurrence of nonstrangulating displacement, or ment (U.S. Surgical, Norwalk, CT) across both the VLC, has led to the development of techniques for RDC and the RLC. This creates a side-to-side anasto- disease prevention. Techniques involving suturing the mosis and two blind colonic ends. In three horses, death dorsal and ventral colon segments together fail to pre- was due to leakage from the staple lines. Modification vent experimentally induced volvulus and induced in application of the TA-90 autosuture device may avert weight loss, and should not be used.". 113 A technique this and other complications such as adhesions to staple of suturing the lateral free band of the LVC to the left lines. Hand-sewn inverting suture lines offer a distinct body wall, approximately 6 cm to the left of midline, is advantage over the use of stapling equipment. Because the currently recommended te~hnique.l'~-"~A nonab- failure occurs with use of stapling equipment in normal sorbable suture, such as #2 polypropylene or nylon is horses, it is likely to occur in horses with thick, edem- preferred, because adhesions caused by absorbable ma- atous large colon after volvulus. Additional information terial tend to mature and lyse over time. on surgical techniques is found in Chapter 33. Colopexy of the LVC may cause weight loss ini- In horses with a large colon resection at the ceco- tially, but the horse regains the weight without compli- colic ligament, digestion of dietary crude protein, cel- cation^."^ Trials to assess digesta passage after colopexv lulose, and phosphorus is decreased.lo8 Fecal water out- revealed digesta was retained on day 4, and variatil put is increased 55%, and total fecal output is increased in the rate of digesta passage within horses decrea 45%. Horses lose weight after surgery but generally are after surgery.Il5 Therefore, after colopexy, stabilizat able to regain weight within 6 months. In these horses, of the large colon may increase transit time initially, out there is a shorter transit time of particulate digesta, and no long-term complications such as impaction of the a decreased overall retention time because of the overall large colon were encountered. decrease in intestinal length and capacity.lo7 In horses Colopexy appears to be safe but has received only with less extensive resection (60%), there is a decrease limited clinical evaluation. The effect of colopexy on in digestion of crude protein, fiber, -free extract, racing animals is unknown currently, but the technique and phosphorus as we11.lW However, horses maintain has been used successfully in brood mare^."^ Special care body weight and develop adaptive digestion ability by 6 must be taken not to penetrate the bowel lumen because months after surgery. leakage and peritonitis may develop. The technique Further studies to evaluate digestion in horses with should not be used if colon viability is q~estionab1e.l'~ extensive large colon resection indicate that grass hay Anecdotal reports of colon rupture near or at the site or alfalfa pellets did not provide adequate digestible of the fixation are worrisome. The technique should be energy.llO.lllAlfalfa hay, with a shorter fermentation reserved for horses with recurrent disease and used only lag time, is recommended, because transit and fermen- after adequate client education has been made available. tation time are reduced in these horses. In summary, horses with a 60% reduction of the length of the colon experience adaptive changes; how- ever, in those with extensive resection (up to 95%), Transverse and Small Colon although adaptive changes occur, feeding alfalfa hay is recommended. Because of the increased fecal water Diseases of the small colon (SC), combined with output, water consumption after surgery is increased. those of the rectum, cause colic in 2.9% to 17.7% of Prognosis after large colon resection depends largely on Obstruction of the SC is caused most fre- the length of resected segment. In horses with less than quently by impactions or fecaliths. 50% removed, the survival rate was 81%, but in horses The diagnosis of small colon disease may be difficult with more than 50% of the colon resected, the survival when it is based only on clinical examination. Horses rate was only 53%.l1° Survival may correlate more with SC obstruction usually exhibit mild colic and pro- closely to the severity of the lesion than to the length gressive abdominal distention. Failure to pass feces can of the resected colon. be an important part of the history, leading the clinician More clinical experience with extensive large colon to suspect a lesion of the small or transverse colon. resection is needed to assess survival after resection in Dehydration is not marked and are within horses in which discolored or damaged tissue is left in normal range. Volvulus or vascular accidents involving situ. In a recent report, hand-sewn techniques resulted the small colon have an abrupt onset and more rapid in survival of 12 of 18 horses undergoing extensive deterioration in vital parameters. LARGE INTESTINE 401

Atresia Coli TREATMENT I I Atresia coli, a rare condition in foals, is seen more NONSURGICALMANAGEMENT. Medical manage- commonly in Thoroughbreds and develops as a result of ment is successful in horses with mild impactions. Ag- gressive oral fluid therapy, sometimes accompanied by I an autosomal recessive inheritance. lZ4 Vascular accidents during fetal development resulting in disruption of blood intravenous fluid administration, and analgesic treat- I supply to the intestine can also produce atresia.lE-ln ment are generally successful. Judicious use of I The lethal white foal syndrome of Paint horses is a in the standing horse have been advocated but are not different disease. The allele responsible for the all-white recommended unless the impaction is near the rectum I color is associated with a deficiency of ganglion cells in and adequate patient restraint is provided. Rectal or the colon myenteric plexus, resulting in thin muscular small colon tearing is a potentially devastating compli- i walls and stenosi~.'~~ cation. Foals with atresia coli often have elevated vital SURGICALMANAGEMENT. If surgical manage- parameters. A digital rectal examination reveals an ment is required, a combination of massage and a absence of feces. Contrast radiography is of limited procedure known as a high enema are generally suc- diagnostic value unless the atresia is in the transverse cessful. A soft rubber hose attached to a garden hose is colon or located aborally.lE gently inserted per rectum by a nonsterile assistant. The Exploratory celiotomy reveals atresia of the colonic surgeon aids in tube passage by transmural manipula- segment. Surgical correction is possible if it is performed tion. Warm water is infused to soften the digesta. early. Concurrent findings include atresia ani, renal Distention and irrigation are continued until the material hypoplasia, or renal ap1a~ia.l~~Disparity in the size of is flushed from the rectum. This procedure is traumatic aboral and oral bowel diameter requires careful approx- to the bowel and occasionally predisposes the horse to imation, using end-to-end or end-to-oblique anastomotic colonic rupture. In horses with more advanced disease, techniques. The side-to-side technique is of value but necrosis of the colon can occur secondary to impaction, may predispose the horse to . which requires resection and anastomosis. The prognosis Resection of the severely dilated oral portion is recom- after surgery is guarded. Recurrence of the impaction, mended to obtain a normal vascularized and functional ileus, and adhesion formation are possible sequelae. intestine.lZ5 Complications arising from surgical correc- Fecaliths. Fecaliths, sometimes 15 to 20 cm in tion include ileus of the dilated oral portion, peritonitis diameter and length, are composed of inspissated fibrous I, resulting from leakage of the anastomosis, chronic in- fecal material that is believed to form as a result of I continence, and . improper fecal ball formation.l18 Fecaliths may develop because of the diet composition and the resistance to flow of digesta through the intestinal tract. Impaction of the Small Colon obstruction of the small colon causes slow, progressive, I intermittent colic. ETIOLOGY Phytoconglobates and . Phytoconglobates are concretions of undigested food fragments and for- Simple obstructions of the SC are usually caused eign particulate matter formed into balls.'" Bezoars are by feed impactions or fecaliths but can also be due to a combination of magnesium ammonium phosphate with enteroliths, foreign bodies, phytobezoars, trichobezoars, a plant fiber (phytobezoars) or animal hair (tricho- and phytocongl~bates.~~-~~~118, 129-133Small colon impac- bezoars). Trichobezoars and phytoconglobates are tion is the most common form of simple obstruction. rare."6. 120 Bezoars have a smooth glistening surface but Ponies appear to be predisposed to SC impaction.27Cold are light colored, unlike the darkly colored enteroliths. weather, limited roughage diets, and lack of water may Small colon obstruction with phytoconglobates and be- predispose horses to the development of impactions. A zoars can cause colic similar to impactions or foreign primary motility problem or vascular insult may lead to body obstruction. the accumulation of digesta. Foreign Body Obstruction. Yearling and weanling horses are prone to ingest foreign materials such as twine, rope, clothing, rubberized fencing materials, and CLINICAL SIGNS tire threads. Twenty-eight horses with SC obstruction were reported from one farm alone due to the ingestion Horses with impactions of the SC have vague signs of nylon tires.74 In 10 horses, ingestion of strips of of anorexia, dullness, and mild abdominal pain. Horses conveyer belt caused foreign body obstr~ction.~~The may exhibit tenesmus if the impaction is near the rec- pitted, uneven surface of the obstructing mass, which is tum. In more chronic impactions, a rapid deterioration surrounded by firm concretions of digesta, lodges against in condition may indicate necrosis of the affected bowel the mucosa. The mass can reach 1 m in length and or the development of gaseous distention of the large weigh up to 7 kg.7S Rupture of the SC can occur easily colon. The diagnosis may be difficult to arrive at before during surgical manipulation. Horses with foreign body surgery. Single or multiple loops of SC with firm, near- obstruction show no clinical signs when the material hard digesta can be felt on rectal examination. Although passes through the small intestine owing to the higher the clinical signs and history may suggest a small colon fluid-to-solid ratio. Horses with foreign body obstruction obstruction, confirmation on rectal examination often is exhibit acute colic if obstruction is complete. The ob- not possible. struction can be preceded by signs of intermittent colic 402 ALIMENTARY SYSTEM if the obstruction is incomplete, or if the material rupture with segmental infarction, and submucosal periodically returns to the RDC.'18 edema.120. 121.130. 138-140 Surgical removal is mandatory. Colotomy in the RDC is necessary to retrieve the foreign body from the INTRAMURAL HEMATOMAS inaccessible area of the large colon. Intraluminal lubri- cants can be useful in relieving the obstruction but may Hematomas of the SC are rare.138.139 The etiology contaminate peritoneal surfaces. is unknown, but rectal or other trauma is p0ssib1e.l~~ Enteroliths. Enteroliths are mineral concretions Intraluminal hematomas not attached to the mucosa can composed primarily of magnesium ammonium phos- easily be manipulated in the rectum and withdrawn phate , which are usually deposited concentrically without entering the bowel. Submucosal hematomas around a foreign material such as a stone or metal. In require resection and anastomosis. a retrospective study, 24 of 30 horses had enteroliths lodged within the small colon, 17 of which were lodged MESOCOLIC RUPTURE in the oral portion of the .n The problem is seen 1 more commonly in horses from 5 to 10 years of age.77. Rupture of the mesocolon with subsequent ischemic '35 The rate of enterolith formation is unknown, but the necrosis of the SC is a rare complication of parturition age of one large concretion (12 x 9 cm) with a nidus of in the mare.116. "'. 120. 140, 142 The parturient mare is a deciduous tooth was estimated to be 4 years.'36 En- predisposed to type I11 or IV , resulting teroliths are not found in horses younger than 3 years from pelvic ligament laxity, increased abdominal pres- of age. In these horses, colonic obstruction occurs more sure, forceful expulsive efforts, and uterine size.129Ex- frequently by foreign materials. cessive tension can cause loss of vascular integrity of the Small enteroliths can be passed in the feces, mesocolon. Eventration of the small intestine or small whereas others may cause obstruction for short periods colon can occur if the bladder, uterus, vagina, or rectum of time and then fall back into the RDC.79 When prolapses or ruptures.'43 Mesenteric tears result in seg- obstruction becomes complete, abdominal pain is per- mental ischemic necrosis of the colon and later rupture. sistent, tympany increases, and the patient's condition Severe injuries of the mesocolon and the SC may result deteriorates. The intestinal wall surrounding the entero- in primary rupture and fatal peritonitis as well.140 lith may undergo pressure necrosis, and if the condition The time from parturition to onset of abdominal is prolonged, the wall may perforate, leading to fatal pain (0 to 24 hours) is variable, and colic may be peritonitis. A surgical approach similar to that described confused with the mild pain associated with uterine for foreign body removal is required for enterolith contraction.'" Mares fail to pass feces and develop removal from the transverse or oral portions of the SC. impaction in the SC. Rectal palpation may not be Retrograde infusion of water through the rectum may diagnostic. Abdominocentesis usually reveals a marked loosen enteroliths that cannot be readily manipulated increase in nucleated cell count and rote in levels. but by hand.79 abdominal hemorrhage may be the' primary finding. Retained Meconium. Retained meconium in foals Exploratory celiotomy is recommended. Resection of is considered a surgical disorder only when medical de~italized~colonand end-to-end anastomosis should be therapy fails. Foals often exhibit tenesmus, intermittent attempted but is often not possible owing to the location colic, and large colon tympany shortly after birth. A of the lesion. may be needed if the lesion is fecal mass can be palpated craniad to the pelvic rim on located aborally. digital rectal examination. The initial goals of therapy are to provide analgesia, to protect the foal from self-mutilation, and to relieve Strangulation Obstruction obstruction. Administration of warm, soapy water, by Strangulation obstruction of the SC is rare and can gravity flow enema through a well-lubricated soft flexible be caused by enlarged or-testicular teratomas in rubber tube is required. The addition of mineral oil or foals and in mature animals."'. '45. 146. 14' Volvulus, her- glycerin but not dioctyl sulfosuccinate may assist niation, intussusception, prolapse, and neoplastic dis- passage of large firm meconium impaction^."^ Enemas ease can cause strangulation obstruction. The initial may have to be repeated. Maintenance oral fluid therapy clinical signs are mild, but the horse's condition deteri- and exercise may stimulate bowel activity. If surgery is orates rapidly unless surgical intervention is undertaken. undertaken, aborally directed massage of the meconium in conjunction with an enema should be carried out before a colotomy is performed.123 VOLVULUS, HERNIATION, AND INTUSSUSCEPTION Small colon volvulus is rare and is usually associated with abnormalities and malpositioning of other organs Vascular Lesions or is due to complications secondary to intra-abdominal adhesions or absce~ses.~'~Secondary impaction can oc- The SC is rarely the site of primary vascular lesions cur oral to the affected segment. Resection of the that cause colic. The caudal mesenteric artery, which diseased segment may be necessary. provides most of the blood supply to the SC, is rarely Internal or external herniation of the SC can cause the site of occlusive verminous arteritis. Vascular lesions strangulation obstruction. The SC can become strangu- seen in the SC are intramural hematomas, mesocolic lated in umbilical or inguinal and tears in the LARGE INTESTINE 403

motic breakdown and leakage as compared with other intestinal segments. 15Z-155 The passage of solid fecal balls through a relatively narrow lumen; increased bacterial concentrations, particularly anaerobic organisms; strong muscular activity; and increased tissue collagenase activ- ity may inhibit healing.153.'56. Is7 Portions of the SC are difficult to exteriorize, and the risk of peritoneal contam- ination is high. The preferred technique involves a two-layer hand- sewn anastomosis. A simple interrupted suture pattern that excludes mucosa is oversewn with a continuous Lembert suture using 0-polydioxanone or other absorb- able suture material (Fig. 36-17). This method produces significantly larger lumen diameters, better anastomotic healing, and minimal intra-abdominal adhesion forma- tion compared with end-to-end triangulated rows of stainless steel staples.Is8 Extensive mesocolic adhesions occur with stapled anastomoses. Complications that oc- cur with single- and double-layer inverting methods of FIGURE 36-16. Small colon intussusception in a Standardbred brood- mare. Notice the dark discolored small colon orad to the intussuscep- SC anastomosis included anastomotic leakage and ste- tion (entering layer). (From Ross MW, Stephens PR, Reimer JM: nosis, respecti~ely.'~~,la Removal of digesta from the Small colon intus~usce~tionin a broodmare: J Am Vet Med Assoc large colon may help minimize stress on the anastomosis 192:372, 1988.) immediately after surgery.

broad ligament, omentum, uterus, and vagina.l19. '"7 124 Incarcerations of the SC can be diagnosed by rectal examination but may be difficult to distinguish from Each surgical condition of the large intestine re- small intestinal lesions. quires specific monitoring and aftercare. Care after large Intussusception of the SC, a lesion similar to type IV rectal prolapse, can cause strangulation obstruction. Rectal examination may reveal the intussusceptum. Ex- ploratory celiotomy, resection, and anastomosis of the small colon was successful in one horse (Fig. 36-16).148

NEOPIASIA Polyps, leiomyomas, and lipomas can occur in the SC. Polyps can be surgically removed without recurrence if they are pedunculated. Lipomas can cause strangula- tion obstruction of the SC in aged horses. Because of a large amount of fat, the mesocolon may be predisposed to lipoma f0rmati0n.l~~

Surgical Procedures COLOTOMY Enterotomy of the SC should be performed through the antimesenteric band, resulting in a quicker comple- tion of the colotomy; easier, more accurate apposition; and less hemorrhage and than in those performed adjacent to the band.lS0,151 Bursting wall tensions of antimesenteric band colotomies are signifi- cantly greater than colotomies of the sacculated por- tion.lS1 The colotomy location is more important than the surgical technique used. Closure of the mucosa as a separate layer facilitates seromuscular layer closure but does not affect the postoperative healing response or lumen diameter in normal horses.'50 FIGURE 36-17. Small colon anastomosis using a 2-layer technique RESECTION AND ANASTOMOSIS with 0-suture material. (A), The first layer is a nonmucosa penetrating simple interrupted pattern. (B), The second layer consists of a contin- Strangulation obstruction of the SC requires reset- uous Cushing suture pattern interrupted at 180 degrees to prevent a tion and anastomosis. The SC may be prone to anasto- pursestring effect. 404 ALIMENTARY SYSTEM colon resection and anastomosis is different than care be staged, and the horse should be slowly reintroduced after enterolith removal, for example. General consid- to its normal diet. Feed is withheld for a minimum of erations include administration, oral fluid ther- 24 hours. If gastric distention does not occur, oral fluid apy, and dietary and management changes. intake can begin approximately 12 hours after surgery. Laxative diets may be considered, but a slow reintro- duction of the horse's regular diet is preferred. Pelleted Antimicrobials feeds may increase fecal water content and decrease intestinal transit time, but some horses do not readily Many of the surgical procedures performed in the consume the diet. large intestine require opening the bowel and perform- ing clean-contaminated surgery. Peritoneal soiling, es- pecially with particulate digesta, should be limited. Copious, continuous lavage and use of appropriate Pharmacologic Stimulation serosal covering with sponges can limit con- tamination, even when the bowel cannot be completely Occasionally, motility dysfunctions persist and exteriorized. The concentration of bacteria, particularly reimpaction may occur, particularly after enterotomy anaerobic species, increases in aboral direction, and for impaction of the ventral or small colon. Medical contamination of the surgical field with pathogenic bac- management is therefore required for these conditions. teria may occur. Therefore, broad-spectrum intravenous The use of neostigmine (0.0125 to 0.025 mglkg, SC, IV antibiotics such as gentamicin (2.2 mglkg, IV, QID) and or IM) to stimulate motility of the large intestine may potassium penicillin (22,000-44,000 IUIkg, IV, QID) improve motility after surgery, but if an enterotomy or are usually sufficient and should be given before and resection and anastomosis have been performed, the continued 3 to 5 days after surgery. Metronidazole (15 surgeon should proceed with caution. Neostigmine in- mglkg, PO, QID) may be useful if anaerobic creases progressive motility of several segments of the is suspected but is not given routinely. Contamination large intestine, but strong contractions might be detri- during enterotomy or resection and anastomosis may mental to healing of the intestine. theoretically contribute to an increased wound infection rate, but this problem has not been observed clinically. Any clean-contaminated procedure, of course, may con- tribute to wound infection or other complications such as hernia formation.

Immediate general complications after surgery in- Management Changes clude dehydration, endotoxemia, peritonitis, ileus, mo- tility dysfunctions, and death. Complications specifically Management changes may help prevent recurrence associated with the large intestine include recurrence of of diseases after surgery. If sand impaction occurs, a the initial problem or inherent complications associated change in housing arrangements and feeding programs with resection, anastomosis, or colotomy incisions. Be- may help prevent recurrence. Avoiding abrupt feeding cause problems of the large intestine can be mild at changes may decrease the potential for motility changes, first, a prolonged clinical course before surgery predis- tympany, and subsequent displacements or volvulus of poses the horse to the development of , the colon. Impactions or other simple obstructions of caused by Salmonella sp. ~ndotoxemia,thrombophle- the large intestine occur in horses after shipping, a bitis, and laminitis may then become apparent. Nonin- change in training program, or are associated with other fectious enterocolitis, associated with mucosal damage unrelated gastrointestinal or musculoskeletal problems. of the large intestine, is common after nonstrangulating Horses resting for orthopedic problems may be prone displacement or early strangulation obstruction of the to development of large intestinal diseases. Careful large colon and can persist for 48 to 72 hours. Leuko- attention should be paid to vague or subtle signs of penia is common, but horses are generally bright and in these horses. Avoiding abrupt afebrile, unlike horses with infectious enterocolitis. dietary changes in broodmares and providing fresh clean Fever on day 1 or 2 after surgery in horses with left water to all horses, particularly during the winter dorsal displacement of the large colon occurs, but no months, are important considerations. firm evidence has been given to explain this response. Feeding horses after large intestinal surgery should Recurrence of nonstrangulating displacement and stran- be carefully considered. Motility dysfunction may cause gulating VLC has led to development of colopexy and diseases of the cecum, the ventral colon, or the RDC. resection techniques. Normal motility may not return for several days after Adhesions, although certainly possible, are gener- surgery. Therefore, the surgeon cannot expect normal ally not as severe in large intestinal surgery as they are motility to return immediately, particularly if an enter- in small intestinal surgery. Omental adhesions occur on otomy and evacuation of accumulated digesta were exposed staple or suture lines at anastomotic sites or performed. Although this particular surgery removes colotomy incisions. Obstructive disease due to adhesions accumulated feedstuffs, it certainly does nothing to occurs but to a lesser extent than after small intestinal correct the primary problem. Feeding, therefore, should surgery. LARGE INTESTINE 405

Clark ES, Thompson SA, Becht JL, et al: Effects of xylazine on cecal mechanical activity and cecal blood flow in healthy hones. Am J Vet Res 49:720, 1988. Roger TW,Bardon TH, Ruckebusch Y: Colonic motor responses in the In general, the prognosis for horses with surgical pony: Relevance of colonic stimulation by opiate antagonists. Am J Vet lesions of the large intestine is better than that associated Res 46:31, 1985. with lesions of the small intestine. Long-term survival Cummings JF, Sellers AF, Lowe JE: Distribution of substance P-like immunoreactivity in the enteric neurons of the large colon of normal and rates (21% to 42%) for horses with VLC compare Amitraz-treated ponies: An immunocytochemical study. Equine Vet J favorably with those after small intestinal surgery (11%). 17:23, 1984. Survival in horses with nonstrangulating lesions of the Tennant B, Wheat JD, Meagher DM: Observations on the causes and incidence of acute intestinal obstructions in the hone. 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