Cecal diseases that can result in colic

Cecal diseases that can result in colic

14 Cecal diseases that can result in colic RB Edwards INTRODUCTION The cecum is primarily responsible for fluid resorption and the initiation of micr...

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14 Cecal diseases that can result in colic RB Edwards

INTRODUCTION The cecum is primarily responsible for fluid resorption and the initiation of microbial digestion in the horse. Its location in the right caudal quadrant of the abdomen allows partial evaluation through rectal palpation and transabdominal ultrasonography for the diagnosis and monitoring of diseases affecting this portion of the intestinal tract. Reported diseases of the cecum resulting in colic include • tympany • impaction • intussusception • perforation • torsion • volvulus • acidosis • infarction. The cecum is approximately I meter in length and 30 liters in volume in the mature horse. It is divided into three regions • base (cranial or cupula, and caudal portions) • body • apex. The base is tightly attached to the dorsum of the abdominal cavity by mesentery that extends from the 14th rib to the tuber coxae. The right kidney and the pancreas are intimately attached to the mesentery. Mesenteric attachments prevent the complete exteriorization of the cecum, and attachments to the right ventral colon prevent volvulus of-the cecum without accompanying volvulus of the colon. The cecum is a sacculated structure with four teniae (dorsal, ventral,

medial, and lateral). The teniae provide structural support and maintain the conformation of the intestinal tract, and provide directionality to the peristaltic activity through their convergence toward the cecocolic orifice. The teniae also provide the surgeon with a means of anatomically orientating the cecum relative to the ileum and right ventral colon. The dorsal tenia blends with the ileocecal ligament and attaches to the antimesenteric border of the ileum, while the lateral cecal tenia attaches to the lateral free band of the right ventral colon and forms the cecocolic ligament. The blood supply of the cecum is provided by the right and left cecal arteries that are branches of the ileocolic artery. The cecal arteries and veins are located in the medial and lateral teniae of the cecum and supply the respective portions of the cecum. The medial cecal artery provides the majority of the blood supply to the cecal apex. Rete surrounding the cecal veins, arise from the cecal arteries and give rise to a plexus of arteries that supply the cecal tissue. Terminal arteries, located in the submucosa, supply the mucosa, muscularis, and the serosa of the cecum. The arteries penetrate the muscularis mucosa at the base of cecal glands. Capillary networks anastomose at the base of cecal glands to form a honeycomb pattern. The capillary networks drain into venules and submucosal veins. The ileum enters the cecum through the ileocecal orifice at the medial aspect of the cecum at the junction of the cupula and the cecal body. The cecum communicates with the colon through the cecocolic orifice, which is located dorsal to the ileocecal orifice. The cecum is a major site of microbial cellulose digestion in the ihorse leading to volatile fatty acid (VFA) production. VFAs are absorbed in the cecum and colon. The cecum is also a major site of water, sodium, 267



and chloride absorption. Approximately 70 per cent of the water presented to the cecum from the ileum is absorbed before ingesta proceeds into the right ventral colon. The equivalent of a horse's extracellular fluid volume (30 liters) is absorbed by the cecum in 1 day. The mean transit time for ingesta in the cecum has been estimated to be 5 hours. Cecal motility has been studied by the use of visual inspection through cannulae, endoscopy, cinefluoroscopy, indwelling intralumenal monometry, and myoelectric conduction monitoring. A pacemaker in the ventral cecal wall, 10-15 ern from the apex regulates cecal motility. Spike bursts in the cecal body serve to mix the ingesta, while coordinated serial spikes originating in the cecal base propel ingesta toward the apex. Approximately every 3 minutes, a progressive cecal motility pattern can be identified that proceeds from the apex through the body to the caudal base, cranial base and then through the cecocolic orifice into the right ventral colon. Ingesta does not flow from the cecum into the ileum or from the right ventral colon into the cecum. Xylazine and butorphanol each reduce cecal motility for approximately 30 minutes following injection and the combination of xylazine and butorphanol acts synergistically to reduce cecal motility. Neostigmine increases cecal motility for approximately 30 minutes following administration.

Cecal tympany

Respiratory rates will increase secondary to pain and, with severe distention, will be increased in rate because of the inability to move the diaphragm secondary to abdominal distention. Auscultation reveals reduced gastrointestinal sounds, and auscultation and percussion in the region of the right flank will reveal a high resonance 'ping' in the area of the right dorsal and ventral quadrants. Rectal examination will identify palpable distention of the base of the cecum immediately cranial to the pelvic brim and the ventral cecal tenia can be palpated going from the right dorsal region ventrally and to the left.

CLINICAL PATHOLOGY Primary cecal tympany will result in minimal clinicopathologic changes. A stress leukogram (neutrophilic leukocytosis with lymphopenia) may be seen in some cases, and if the tympany is secondary to a distal obstruction the leukogram will most likely reflect the primary disease. A primary respiratory alkalosis may result secondarily to a rapid respiration rate.

GROSS PATHOLOGY Minimal pathology is seen with cecal tympany unless adequate decompression cannot be achieved and this may result in cecal perforation.

DIAGNOSIS AND TREATMENT ETIOLOGY Diagnosis is based on Cecal tympany may be primary or secondary in origin. Primary cecal tympany occurs because of rapid gas production or reduced cecal motility, whereas secondary cecal tympany occurs because of an outflow obstruction (impaction, displacement, or torsion) aboral to the cecum in the digestive tract (large or small colon). Rapid gas production is most commonly seen in horses that are on lush, rapidly growing pasture, high grain diets, or horse exposed to wilted grass.

CLINICAL SIGNS Cecal tympany results in abdominal distention localized primarily to the region of the right flank. Initially pain is intermittent but becomes persistent and more severe as the cecal tympany increases. The heart rate will increase moderately (40-60 bpm) initially but may be greater than 100 bpm with severe distention.


clinical examination (right flank distention, resonance in the region of the cecum on auscultation) • rectal findings consistent with cecal distention without large colon distention.

Many cases of primary cecal distension will respond to the visceral analgesia produced by xylazine (0.20.4 mg/kg i.v.), butorphanol (0.01-0.04 mg/kg i.v.), or detomidine (0.002-0.006 mg/kg). Caution should be used when using detomidine because prolonged visceral analgesia may be produced. Severe cecal distention can occlude the duodenum as it passes caudal to the cecal base. Because of this, a nasogastric tube should be passed to ensure gastric distention is not present. If cecal distention does not readily resolve or if distention continues to worsen, cecal trocarization should be performed. The right flank is auscultated to ensure


that a resonant ping can be localized. A region (about 5 em" in area), centered between the last rib and the tuber coxa at the level of the ventral aspect of the tuber, is clipped and aseptically prepped. Lidocaine or carbocaine is injected subcutaneously, then directed deep through the muscle, and the clipped area is prepped one last time. A I4-gauge, I3-I5-cm catheter and stylet are directed through the body wall until gas escapes. The needle is generally directed across the body wall, perpendicular to the skin surface. Decompression is best accomplished with suction but can be achieved without active suction. When decompression is complete, a broad-spectrum antibiotic should be injected through the lumen prior to removal to reduce the likelihood of cellulitis along the needle track in the body wall.

PROGNOSIS The prognosis is dependent on the cause of the cecal tympany. Primary cecal tympany generally responds to medical management.

PREVENTION Limiting horses' access to lush, rapidly growing grass or large amounts of grain, and avoiding rapid changes in diet can prevent some cases of primary cecal tympany.

Cecal impaction EPIDEMIOLOGY Cecal impactions represent approximately 5 per cent of all large intestinal impactions presented to referral institutions, and 40-55 per cent of all cecal diseases. The literature indicates that this disease is diagnosed and treated more often in institutions on the east and west coasts when compared to those institutions in the central portion of the United States. There is no breed or sex predilection but horses greater than 15 years of age are at a higher risk than younger horses.

• • • • • • • • •


poor dentition poor quality roughage sand ingestion fasting limited access to water parasitic infestation hospitalization for other disorders general anesthesia non-steroidal anti-inflammatory drugs (NSAlDs).

Failure of the normal coordinated motility between the cecum, cecocolic orifice, and the right ventral colon has been suggested as the cause of cecal impaction, however the ability of medical and/or surgical management to restore apparently normal function indicates that this may only account for a limited number of the cecal impactions diagnosed. Cecal impactions have been classified as • type 1 - impactions of dry ingesta filling the cecum • type 2 - impactions resulting from impaired cecal outflow secondary to motility dysfunction. In type 1 impactions, fluid and gas may be able to pass through the impacted viscus from the ileocecal orifice to the cecocolic orifice resulting in the passage of scant, softer than normal feces. Type 2 cecal impactions are more likely to result in spontaneous rupture.

CLINICAL SIGNS The clinical signs associated with cecal impaction can be quite variable, and more importantly some horses with cecal impactions demonstrate mild discomfort prior to spontaneous perforation. A complicating factor is that many horses that develop cecal impactions are often being treated with NSAlDs for other medical conditions and the non-steroidal medications may mask mild abdominal discomfort. Generally, horses will display mild-to-moderate evidence of discomfort • • • • • • •

mild elevation in heart rate (40-50 bpm) watching their flank lying down more often than normal intermittent pawing decreased appetite to complete anorexia reduced gastrointestinal motility scant, semi-formed feces.

CLINICAL PATHOLOGY ETIOLOGY Potential causes or factors that may predispose horses to cecal impactions include

The clinical pathologic changes seen in horses with cecal impactions are minimal. They may have mild hemoconcentration secondary to dehydration and




normal peritoneal fluid unless distention is severe with focal necrosis of the cecum or cecal perforation occurs. However, peritoneal changes may not occur until after cecal perforation.

DIAGNOSIS The diagnosis is made by rectal examination. Palpation of the cecum generally reveals increased tension on the ventral cecal band and firm ingesta filling the cecum.

THERAPY The therapy of choice depends on • the severity of the impaction (firmness of the ingesta within the cecum, size of the cecum on palpation) • duration of the clinical signs • amount of improvement with medical management • factors that may have predisposed the horse to developing a cecal impaction. Severe abdominal discomfort associated with a diagnosis of cecal impaction would be an indication for surgery, however horses with cecal impaction rarely display severe abdominal discomfort. Ultimately, the decision of medical versus surgical management will most likely depend on • the size of the cecum • firmness of the impaction • analysis of the peritoneal fluid.

Medical management The aim of medical management is to soften the ingesta within the cecum and promote progressive motility that will lead to ingesta being propelled into the right ventral colon. Food is withheld and hydration initiated. For the first 24 hours aggressive intravenous fluid administration is given to hydrate the horse. This should limit fluid absorption from the gastrointestinal tract and promote softening of the impacted ingesta. Concurrently, the administration of oral water, electrolytes, mineral oil, or magnesium sulfate is initiated to further promote dissolution of the impaction. Visceral analgesics can be used judiciously to reduce the abdominal discomfort, but xylazine, butorphanol, and the combination of the two have been demonstrated to reduce cecal motility for 30 minutes following administration. The safest analgesic is flunixin meglumine at a rate of 0.250.5 mg/kg i.v, q. 8-12 h. Serial rectal palpation is required to monitor the size of the cecum and the


response of the ingesta to medications. Motility modifiers have been proposed to promote cecal motility once there is some response to medical management. Erythromycin lactobionate (0.5-1.0 mg/kg i.v, in a liter of saline) administered every 2-6 hours for three to four injections, and neostigmine (2-4 mg s.c. q. 1-2 h) have been recommended. In either case, caution must be used when administering these medications because of the risk of promoting cecal perforation. When the impaction has resolved and the cecum has significantly reduced in size, the horse should be started back on feed with intermittent grazing, pelleted feed, and/or hay nets hung outside the stall so that the horse is limited in the rate at which it can eat. The hydration status and the fecal content and consistency of the horse should be monitored closely to ensure that reimpaction does not occur.

Surgical management When medical management is unsuccessful or if clinical findings indicate surgical treatment is necessary, cecal decompression and/or bypass are performed through a ventral midline celiotomy. Surgical management will reduce the incidence of cecal rupture; this is proposed to occur in 40-57 per cent of all cases. Surgical therapy consists of typhlotomy alone or in conjunction with a cecocolic, ileocecal, orjejunocolic (complete or incomplete bypass) anastomosis. Most individuals base the surgical management on 1. the appearance of the cecum at the time of surgery 2. the type of cecal impaction (type 1 versus type 2) 3. the apparent reason for the development of cecal impaction • type 2 cecal impaction implies cecal dysfunction and bypass of these impactions is recommended • if the initiating cause for the cecal impaction can be identified (previous anesthesia, medical problem, transportation) a typhlotomy alone may be used for surgical management.

Typhlotomy Approach to the cecum is through a ventral midline celiotomy (laparotomy). The horse is positioned leaning toward the right to allow better exteriorization of the cecal apex for the typhlotomy. Extreme care must be used when manipulating the cecum when it is grossly distended because perforation can easily occur. The cecum should be isolated from the abdomen with a combination of sterile impervious and barrier drapes to prevent contamination of the abdominal cavity and abdominal wall incision, and moist towels to prevent the exposed cecum from drying. The typhlotomy is


performed by making a 10-12 ern incision near the apex, between the ventral and lateral cecal tenia. Stay sutures are placed at either end of the typhlotomy prior to making the incision. If the cecum can be adequately exteriorized fluid can be slowly introduced into the cecum in a similar fashion to that used with large colon impactions, and the softened ingesta gently manipulated to the typhlotomy incision. The incision is closed in two layers with a TA 90 stapling device followed by an inverting suture pattern, or it may be closed with double inverting suture patterns. In some cases, if the exposed cecum was allowed to dry, contamination of the serosal surface may not be easily removed, and in these instances, a partial typhlectomy may need to be performed. As a prevention carboxymethylcellulose can be applied to the serosal surfaces prior to enterotomy incisions to reduce serosal contamination.

Cecal bypass There are two principal methods used to bypass the cecum • incomplete cecal bypass • complete cecal bypass. Incomplete cecal bypasses may be accomplished by performing a cecocolic anastomosis, an ileocolic anastomosis, or a jejunocolic anastomosis. Complete cecal bypasses are accomplished by transection of the ileum and anastomosing the ileum or jejunum to the right ventral colon. Cecocolic anastomosis has largely been abandoned because of recurrent abdominal discomfort associated with this procedure. Recurrence of impaction is not reported to occur, but 42 per cent of the horses that lived longer than 2 months suffered from recurrent gas distention of the cecum or colon. The only difference between the ileocolic and jejunocolic bypass procedures is the region anastomosed to the right ventral colon. Complete cecal bypass results in cecal atrophy whereas incomplete cecal bypass procedures do not result in significant changes in the cecal size or fill of ingesta. Incomplete cecal bypass procedures still allow ingesta to enter the cecum and may predispose the horse to future impactions. Injejunocolic and ileocolic anastomoses, the respective portion of the small intestine is anastomosed to the right ventral colon between the lateral and medial free bands of the colon with the aboral segment of small intestine facing toward the base of the cecum. The anastomosis can be accomplished with hand suturing or stapling with the GIA 50, 80, or 90 devices. If the GIA 50 is used it must be fired twice, in opposite directions, to ensure adequate stoma size. It is imperative that the staple lines overlap when using the


GIA 50 so that gaps between the small and large intestine do not occur (see Chapter 10). The GIA 80 has longer staples than the GIA 90 and may provide a more secure anastomosis especially when an ileocolic anastomosis is performed. To complete the anastomosis, stay sutures of 2-0 absorbable suture are placed 10 ern apart through the small intestine and right ventral colon to secure the bowel for the anastomosis. Stab incisions are made into the intestinal lumens to allow introduction of the stapler and the stapler is fired as directed. The stab incisions are closed with an inverting suture pattern and the staple line is oversewn with an inverting pattern that incorporates the previously oversewn stab incisions so that the anastomosis is secured with two layers circumferentially. Following completion of the anastomosis, the small intestine should be secured to the surface of the right ventral colon over a distance of 5-10 cm beyond the stoma to prevent kinking at the anastomosis, this has been reported to be a problem postoperatively in some cases if not performed. Closure of the small intestinal mesenteric defect can be accomplished by attaching the mesentery along the cecocolic fold and then the dorsal cecal tenia where it joins the ileocecal fold, with 2-0 absorbable suture in a simple continuous pattern. Horses should be started on feed slowly 36-48 hours after surgery, and initially should be fed grass, pelleted feed, or palatable hay.

PROGNOSIS The prognosis for cecal impaction is guarded because of the unknown etiology of the disease, the risk of spontaneous perforation in cases managed medically, and the chance of recurrence in those cases managed medically or in which a typhlotomy alone or in conjunction with an incomplete bypass is performed. Type 2 cecal impactions generally present with more severe abdominal pain and should be managed surgically because of the increased likelihood of spontaneous perforation. Serial rectal examinations should be performed by the same individual to monitor the progress made in those horses managed medically.

PREVENTION Prevention of cecal impaction is difficult since a definitive cause is not yet known. Since cecal impaction does appear to occur with increased frequency in horses being treated for musculoskeletal diseases, horses having procedures requiring general anesthesia, and horses that have recently been transported, these




horses should be monitored closely for normal appetite, attitude, and fecal consistency and output. Medical management is more likely to be successful in cases where the impaction is discovered early.

Cecocecal and cecocolic intussusceptions (Figure 14.1) EPIDEMIOLOGY It seems unlikely that cecocecal or cecocolic intussusception is either sex or breed specific, although a recent study by Martin et al. (1999) reported a higher incidence in Standardbreds than in other breeds seen by their hospital (55 per cent of the horses with an intussusception versus 30 per cent of the general hospital population). It generally occurs in younger horses, with Martin et al. reporting 63 per cent of the cases of cecocecal and cecocolic intussusception occurring in horses 3 years of age or younger. It can however occur in older horses as well, the range in this study was 7 months to 30 years of age.

ETIOLOGY The cause of cecocecal and cecocolic intussusception is unknown. Like all intussusccptions, a disparity in motility between adjacent segments of bowel results in an intussusception. In horses, organophosphate administration, parasympathomimetic medications, arterial damage by Strongylus vulgaris, infections with Salmonella spp. and Eimeria leukarti, mucosal inflammation secondary to Anaplocephala perfoliata and cyathostomosis, and masses within the cecum have been incriminated for initiating intussusceptions. Tapeworms have been identified in 50-80 per cent of horses suffering from cecocecal and cecocolic intussusceptions, but their role in the etiology ofthis disease remains controversial. Cecal intussusception may occur secondary to the intussusception ofeither the base or the apex into the cecal body, whereas cecocolic intussusception occurs with varying portions ofthe cecum intussuscepting into the right ventral colon.

CLINICAL SIGNS There are three clinical syndromes depending on the severity of abdominal pain reported in horses suffering from cecocecal and cecocolic intussusception

Figure 14.1 Lateral view of the normal cecum and various forms of cecal intussusception, a) normal anatomy - A apex; B body; BS base; C cupula; 0 cecocolic orifice; I ileum; RVC right ventral colon, b) cecocecal intussusception involving the apex, c) cecocecal intussusception involving the cupula, d) cecocolic intussusception (from Milne et al. 1989 Vet. Rec. 125:148-50).



• acute • subacute • chronic wasting form. In the acute and subacute forms the horse displays signs consistent with severe abdominal pain, whereas in the chronic wasting form the clinical signs generally consist of mild intermittent pain and pyrexia, reduced fecal output, and chronic weight loss. In the acute and subacute forms, when vascular compromise occurs to the intussusceptum, the horse demonstrates clinical signs consistent with cardiovascular shock, endotoxemia, and variable degrees of peritonitis. Horses tend to pass a scant amount of soft feces.

CLINICAL PATHOLOGY In the acute and subacute forms horses display clinicopathologic changes consistent with cardiovascular shock and varying degrees of peritonitis. In the chronic wasting form of the disease, horses present with evidence of increasing severity of peritonitis.

GROSS PATHOLOGY Generally the intussusceptum wall becomes thickened with edema and there is histological evidence of submucosal vessel thrombosis and mucosal necrosis.

DIAGNOSIS Diagnosis of cecocecal and cecocolic intussusception can be difficult. The cecum cannot be identified per rectum and the horse may resent palpation of the right dorsal portion of the abdomen. Rectal palpation may reveal a firm mass or edematous bowel in the right dorsal quadrant of the abdomen, but multiple rectal examinations may be required before it is identified. Transabdominal ultrasound is one of the best techniques for confirming cecocecal and cecocolic intussusception. In the report by Martin et al: (1999) two-thirds of horses with confirmed cecal intussusceptions were correctly identified by ultrasonography.

THERAPY Cecocecal intussusceptions involving the apex and body should be reduced and the involved portion of the cecum should be resected. The medial and lateral cecal arteries and veins are double ligated, and the cecum is


resected with automatic stapling devices or by isolating the affected cecum with intestinal clamps and closing in two inverting layers. If the base is involved, then the only option is to invert the affected segment of the cecum and perform a cecal bypass if necessary. A cacel is necessary if the inverted portion of cecum obstructs the cecocolic orifice. Cecocolic intussusceptions are approached by first attempting reduction of the intussusception through traction on the intussusceptum. If it cannot be reduced in a closed manner, the intussusceptum is approached through a colostomy. The safest approach is to suture a plastic drape to the serosal surface of the right ventral colon along the area of the proposed colotomy (generally made through the lateral free band of the right ventral colon). Moistened sterile towels are placed over the plastic drape to absorb contaminants from the colotomy incision during manipulation of the intussusceptum. If the intussusceptum cannot be reduced through the colotomy, the necrotic portion of the cecum is resected within the colon. The resection may be achieved with automatic stapling devices in some cases or by clamping the bowel and suturing. Following reduction of the remaining portion of the cecum further resection may be required in some instances. Final closure of the cecum is accomplished with either an automatic stapling device followed by an inverting suture pattern or two layers of inverting sutures. Martin et al. (1999) reported poor results (0 of 2 survived) when an ileocolostomy was performed to bypass nonreducible cecocolic intussusceptions. An alternative surgical technique involves ligation of the cecal arteries to cause necrosis of the intussuscepted portion of cecum and subsequent sloughing. The medial and lateral cecal arteries and veins are ligated immediately proximal to the intussuscepted portion of the cecum and the serosal margins are closed in two inverting layers. However, based on the study by Martin et al: (1999), all attempts should be made to reduce the cecocolic intussusception as opposed to performing such an intralumenal necrotizing bypass procedure.

PROGNOSIS Historically cecocecal and cecocolic intussusceptions have had a guarded prognosis. The prognosis is dependent on the portion of bowel affected and more importantly the degree of peritonitis prior to surgery and amount of contamination that occurs during surgery. Attempts should be made to reduce the intussusception in a closed manner. If this cannot be accomplished an enterotomy should be performed to reduce the intussusception or resect the affected




portion of intestine so that it can be reduced. If a resection is performed within an enterotomy, following the reduction, it is important to reassess the cecum to ensure that the entire devitalized intestine has been removed. If an ileocolostomy is performed to bypass the cecocolic intussusception, it is important to oversew the cecum on the serosal surface in an attempt to prevent leakage and peritonitis. Cecal intussusceptions have a good prognosis if operated on in a timely manner, prior to the development of peritonitis. It is important that the diagnosis be made prior to the development of peritonitis and a chronic wasting form of the disease.

PREVENTION The cause of intussusceptions is thought to be abnormal motility between adjacent segments of intestine secondary to inflammation or masses. It is unlikely that they can be prevented, however it is important to maintain thorough deworming programs to prevent the development of Anoplocephala perfoliata and cyathostome infestations that may initiate intussusception in some cases.

Post-parturient mares None of the mares reported with cecal perforation in the post-parturient period were observed to have previous clinical signs consistent with cecal impaction. It is hypothesized that cecal trauma at the time of parturition, abnormal motility associated with late gestation leading to impaction, or gas distention with subsequent perforation secondary to increased abdominal pressure associated with parturition leads to perforation. Cecal perforation should be considered in any mare that suffers from acute death with peritonitis.

Foals The foals that suffered cecal perforation were among 17 foals involved in a study investigating gastric ulceration in foals receiving oral phenylbutazone. Two of these foals suffered cecal perforations within 24 hours of being anesthetized for the endoscopic examination of the stomach. These foals had received 8.8 mg/kg phenylbutazone following recovery from anesthesia.

CLINICAL SIGNS Prior to cecal perforation, horses may demonstrate clinical signs consistent with cecal impaction including

Cecal perforation EPIDEMIOLOGY

• • • •

Cecal perforation has been described as an idiopathic event

Clinical signs in horses following cecal perforation are consistent with endotoxic shock, peritonitis, and cardiovascular collapse. These include

• in horses that are hospitalized for management of other medical disorders and receiving NSAIDs • following parturition in mares • following endoscopy in foals.

ETIOLOGY The etiology of cecal perforation is unknown in most cases.

NSAID therapy Cecal perforation may occur in horses being treated for unrelated medical disorders, especially if they are being treated with NSAIDs. These medications may lead to altered cecal motility, or they may mask the development of cecal impaction and predispose horses to perforation by masking the clinical signs. 274

• • • • • • • •

mild abdominal discomfort intermittent inappetence scant-to-soft feces depression.

depression abdominal discomfort shaking sweating tachycardia weak pulse dehydration congested mucous membranes.

Rectal examination may reveal an enlarged cecum impacted with firm feces, gritty material over the serosal surface, and palpation findings consistent with pneumoperitoneum.

CLINICAL PATHOLOGY Prior to cecal perforation there may be no abnormal clinicopathologic findings on examination of a com-



plete blood cell count or abdominal fluid. Following perforation, abdominocentesis and systemic blood work may reveal evidence of plant material within the abdominal fluid, dehydration, and toxic changes in the appearance of peripheral and abdominal white blood cells.

housed and fed in a group situation. In some cases, accidental overfeeding or horses gaining access to large amounts of feed may result in cecal acidosis. Horses on high grain or carbohydrate diets may develop cecal acidosis even when accustomed to the diet.



In most cases of cecal perforation, gross pathology reveals a moderate to severely enlarged cecum with an empty large colon indicating dysfunction ofnormal cecal motility leading to impaction and subsequent perforation. Mares suffering cecal perforation in the peri-parturient period have normal cecal and colon fill ofingesta.

Cecal acidosis occurs following the rapid cecal fermentation of carbohydrates leading to lactic acid production. The amount of grain or other carbohydrate does not appear to be as important as the type and the adjustment of the cecal flora to the fermentation process. Fermentation in the cecum by Lactobacillus, Streptococcus, and Bacillus spp. produces lactic acid that results in the death of the normal flora and sloughing of the cecal mucosa. Endotoxin absorption secondary to gram-negative death and mucosal injury results in the clinical signs seen with cecal acidosis.

DIAGNOSIS A suspicion of cecal perforation can be made based on clinical signs, rectal examination, and evaluation of abdominal fluid. Definitive diagnosis is made by abdominal exploration or post-mortem examination.

THERAPY Because of the severe abdominal contamination cecal perforation cannot be treated in the horse.


CLINICAL SIGNS Mild-to-moderate abdominal pain is often the initial clinical sign displayed by horses suffering from cecal acidosis. More severe abdominal pain will be seen in horses that have acidosis with secondary gastric and or small intestinal distention. In most horses, depression, with injected mucous membranes, tachycardia, tachypnea, and clinical signs consistent with endotoxic shock occur in horses with cecal acidosis. Generally there is a reduction in intestinal sounds and there may be cecal tympany.

Cecal perforation results in death secondary to endotoxic shock and sepsis, or euthanasia.

CLINICAL PATHOLOGY PREVENTION Prevention of cecal perforation in peri-parturient mares is not possible, but in horses hospitalized for other medical disorders, attitude, appetite, fecal consistency and amount should be closely monitored so that the diagnosis of cecal impaction can be identified early in its development.

Cecal acidosis


Elevated packed cell volume (PCV) , neutropenia secondary to endotoxemia, and an elevation of lactic acids resulting in a metabolic acidosis may be present in horses suffering from cecal acidosis.

GROSS PATHOLOGY Over production of lactic acid results in mucosal injury in the cecum and gross loss of cecal mucosa resulting in submucosal edema and hemorrhage.


DIAGNOSIS EPIDEMIOLOGY Cecal acidosis is rarely reported, but is most commonly identified in aggressive or dominant horses that are

The diagnosis is made based on the presenting clinical signs and history of, or evidence of, the horse eating an excessive amount of grain.






Therapy is aimed at providing supportive care and preventing further absorption of endotoxins. Fluid therapy to rehydrate the horse and correct metabolic derangement is indicated. The nasogastric administration of mineral oil and activated charcoal to promote passage of cecal contents and reduce endotoxin absorption is indicated. Flunixin meglumine (0.25-0.5 mg/kg i.v, q. 6 h) should be administered to counteract endotoxemia and reduce the likelihood of the development of laminitis. Other anti-endotoxin therapies include the administration of polymyxin B (6000 IU/kg i.v, in 1 liter of saline or dextrose over 15 min b.i.d.), low molecular weight heparin, and hyperimmune plasma.

Most horses suffering from cecal infarction present with mild abdominal pain, occasionally however, horses also present with depression, diarrhea, or severe abdominal pain and cardiovascular collapse. Abdominal pain will persist and increase in severity over time.

CLINICAL PATHOLOGY Abdominocentesis will reveal elevations in total protein and nucleated cell count consistent with ischemic necrosis.



The prognosis is dependent on the degree of endotoxemia that develops as well as the development of laminitis.

Pathology is consistent with ischemic necrosis secondary to thromboembolic disease.

PREVENTION Cecal acidosis can best be prevented by not feeding grain to horses in groups, thereby preventing the most dominant and aggressive horses from overeating. It can also be avoided by storing grain in a secure area inaccessible to horses.

Cecal infarction

DIAGNOSIS In one report 30 per cent of horses with cecal infarction had a firm mass palpable in the right caudal abdomen, but a preoperative diagnosis is rarely made.

THERAPY A subtotal typhlectomy is performed to remove the affected portion of cecum. All affected tissue must be removed, and progression of infarcted tissue is not reported to occur in this disease.

EPIDEMIOLOGY Cecal infarctions are believed to occur more frequently in young horses than in older horses, although the range of ages reported is 1-12 years.

ETIOLOGY Several studies have suggested that Strongylus vulgaris infestations and larval stages of cyathostomes are associated with cecal infarctions. Initially it was believed that the cecum was prone to infarction because its entire blood supply came from two vessels, but subsequent studies have revealed that the rete system provided extensive collateral circulation and limits cecal infarction to diseases creating extensive thromboembolism. 276

PROGNOSIS Seven of eight horses operated on in one report were discharged from the hospital. If all the affected cecum can be resected, the prognosis is most likely to be dependent on the degree of peritonitis present prior to surgery.

PREVENTION Cecal infarctions secondary to parasitism are best prevented by maintaining proper deworming protocols and pasture stocking rates.


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