Management and Complications Associated with Treatment of Cervical Oesophageal Perforations in Horses K

EQUINE VETERINARY EDUCATION / AE / MAY 2013 247

Original Article Management and complications associated with treatment of cervical oesophageal perforations in horses K. Kruger and J. L. Davis* Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, North Carolina, USA. *Corresponding author email: [email protected]

Keywords: horse; oesophageal perforation; enteral nutrition

Summary depressed, tachycardic (84 beats/min), tachypnoeic (54 Six horses were evaluated for colic and anorexia, choke or breaths/min) and dehydrated (capillary refill time 3 s, suspected oesophageal rupture with and without tracheal prolonged skin tent). Complete blood count (CBC) revealed laceration. Clinical findings were variable, but a painful leucopenia characterised by neutropenia with a left shift, and ventral neck swelling was noted in all cases. Two of the horses polycythaemia. Serum chemistry revealed hypocalcaemia. had signs of dehydration and sepsis. Additional findings Palpation per rectum and abdominal ultrasound were within included evidence of previous trauma over the trachea and normal limits. A mild swelling was noted on the ventral aspect oesophagus, ventral neck abscessation, choke and aspiration of the neck that was painful to palpation. During ultrasound pneumonia. A diagnosis of oesophageal perforation was and radiography of the neck, gas was evident in the soft made using endoscopy. Two horses were subjected to tissues surrounding the trachea and oesophagus. Endoscopy euthanasia without treatment. All horses where treatment was revealed a 5 cm long full thickness linear perforation of the attempted received debridement of the oesophageal ventral oesophagus in the mid-cervical region. perforation and surrounding tissues with or without surgical Standing surgery was performed under sedation and local closure of the oesophageal defect. Other therapies included anaesthesia. One approximately 10 cm straight incision was broad spectrum antimicrobials, anti-inflammatory drugs, fluid made through the skin using sharp dissection with a number 10 and nutritional support as well as additional therapeutics for blade scalpel. Further blunt dissection was performed through sepsis and individual complications. Complications included the necrotic subcutaneous and deeper tissues down to the site diverticulum formation, thrombophlebitis, diarrhoea, laryngeal of oesophageal rupture on the ventrolateral aspect of the hemiplegia, azotaemia, aspiration pneumonia, oesophageal neck, approximately 3 cm left of the trachea, for debridement obstruction, weight loss and laminitis. All 4 treated horses and lavage. Another approximately 15 cm straight incision recovered from the oesophageal perforation and are was made directly under the initial incision but further ventrally able to eat a normal diet. Two of the 4 horses have had at the level of the thoracic inlet through the skin and infrequent episodes of recurrent choke. Oesophageal rupture subcutaneous tissue to allow continued drainage of blood should be considered as a differential diagnosis for horses with and debris. The oesophageal tear and surgical wounds were a painful swelling of the ventral neck. With surgical left open to heal by second intention. debridement and adequate supportive care, oesophageal The horse was treated with broad spectrum antibiotics perforation cases can have a fair to good long-term survival, (ampicillin, gentamicin and metronidazole), nonsteroidal although chronic complications can occur, therapy is anti-inflammatory drugs (flunixin meglumine) and anti- prolonged, and a significant economic commitment is endotoxaemic drugs (polymyxin B, hyperimmune plasma). required. Replacement and maintenance polyionic crystalloids, with added calcium gluconate, were administered until the horse was able to maintain hydration from oral water intake on Introduction Day 4. Culture of the affected muscle surrounding the Between 2001 and 2012, 6 horses presented to the North oesophageal tear yielded a heavy growth of Pasteurella Carolina State University Veterinary Teaching Hospital (VTH) multocida and Escherichia coli, both of which were sensitive to with oesophageal perforation in the proximal to mid-cervical ampicillin. region (Table 1). The management of 4 of the cases is Over the first 24 h, the horse remained depressed and described in detail below. The remaining 2 cases were uncomfortable. The heart rate increased to 132 beats/min and subjected to euthanasia without treatment, one at the request copious amounts of serum, mucus and saliva drained from the of his owners due to age (29 years) and financial constraints open wounds. Opioid analgesics (butorphanol) were added and the other due to a poor prognosis. This horse had 4 for additional pain control. Wounds were flushed twice daily separate areas of oesophageal ulceration and tears and signs with sterile saline. Despite continued saliva and serum loss, of severe sepsis, as well as a history of repeated choke. serum electrolytes remained within normal limits. Cellulitis became evident in the pectoral area 3 days after Case 1 presentation. The skin and subcutaneous tissues over this area An 11-year-old Tennessee Walking Horse was referred to VTH proceeded to slough, leaving an open, draining wound. In for an 18 h history of anorexia and colic that did not resolve addition, a malodorous infection developed in the tissues with medical therapy administered by the primary deep to the oesophagus. The tissues were debrided and the veterinarian. On presentation, the horse was moderately wounds were subsequently cleaned twice daily and a dilute

TABLE 1: Summary of cases presented to the North Carolina State University Veterinary Teaching Hospital with a diagnosis of oesophageal rupture

Age (years), Days in Complications Complications Case breed, gender Description of rupture hospital (acute) (chronic) Outcome

1 11, Tennessee Walking 5 cm; ventral 30 Endotoxaemia Recurrent choke Survived Horse, gelding oesophagus; Cellulitis mid-cervical 2 1, Quarter Horse, filly 5 cm; ventral 20 Phlebitis Diarrhoea Survived oesophagus; Diarrhoea Left laryngeal mid-cervical Pyrexia hemiplegia Left laryngeal hemiplegia 3 5, Thoroughbred, mare 1 cm; ventral 37 Subcutaneous – Survived oesophagus; proximal emphysema cervical Periesophageal abscess 4 1.5, Tennessee Walking Two 10 cm; ventral 44 Endotoxaemia Recurrent choke Survived Horse, gelding oesophagus; Cellulitis Laminitis mid-cervical Choke Left laryngeal Aspiration pneumonia hemiplegia Left laryngeal hemiplegia Laminitis Azotaemia 5 29, Quarter Horse 2 cm; lateral oesophagus; <1 – – Subjected to gelding proximal, 3–4 cm distal euthanasia to the larynx 6 1.5, Warmblood, 4 cm; dorsal oesophagus; <1 – – Subjected to gelding distal cervical; multiple euthanasia ulcerations present

iodine solution was applied. Debridement was performed as complication. The neck wounds were manually cleaned of necessary afterwards until the wounds had healed. food particles twice daily and lavaged with water. Surgical After an initial 48 h of fasting, an indwelling nasogastric gauze soaked in dilute iodine solution was packed into the tube was placed and enteral feeding initiated using high fibre large tissue defect surrounding the oesophageal tear. Pectoral pellets soaked in water with added corn oil. Partial parenteral wounds were cleaned daily with chlorhexidine scrub and nutrition consisting of 8.5% amino acids at 250 ml/h as well as necrotic tissue debrided as needed. Wounds were sprayed 10% dextrose in 0.45% NaCl with 10 ml of vitamin B complex with dilute iodine solution on an hourly basis. By Day 26 the added to each litre at 250 ml/h was also started in addition horse had gained back 55 kg. to the abovementioned fluids and continued for 3 days. Despite maintaining a fairly good attitude, a severe, This was designed to provide an additional 25% of the prolonged, neutropenia with a left shift developed after the horse’s maintenance energy requirements (approximately discontinuation of polymyxin B on Day 21. In addition, 8.25 kcal/kg bwt/day). On Day 5, the nasogastric tube was tachycardia persisted at 60–70 beats/min until Day 25 and only removed because of fears that it might be interfering with decreased to 48–52 beats/min at discharge. These healing of the oesophageal rupture. The horse was offered the abnormalities were attributed to continued endotoxaemia as soaked pelleted feed, which he only ate well for the first 24 h, a result of Gram-negative bacterial sepsis. The neutropenia after which his appetite became poor. Metronidazole resolved by Day 27, but the left shift was present until administration was switched to per rectum at this point. Within discharge. Mild anaemia developed on Day 22, and persisted 36 h, the horse became severely depressed and developed until discharge. a thrombocytopenia. Prothrombin time, activated The contracting external skin incision had to be extended thromboplastin time and fibrinogen degradation products approximately 5 cm on Day 27 to re-establish adequate were within normal limits. A stallion catheter was placed drainage. Excessive granulation tissue was also debrided at through the oesophageal wound into the stomach in order to this time. The horse was discharged on Day 30. His diet administer oral medications. The horse’s attitude and platelet consisted of pellets and 30 min of hand grazing several times a count improved over a period of 48 h. The neutropenia day. Flunixin meglumine treatment was continued and owners resolved, but the left shift persisted. Lymphopenia as well as were instructed to continue cleaning and packing the wounds hyperfibrinogenaemia developed. twice daily. On Days 58 and 80, the horse presented to the By Day 10 the horse had lost 75 kg of bodyweight. A clinic for surgical extension of the external wound to allow stomach tube was placed through the oesophageal tear, and continued drainage of feed and saliva. Grazing had to be soaked pellets, corn oil and salt were fed every 4–6 h for 7 days discontinued when grass started to accumulate in the until the tube obstructed and was removed. The horse would oesophageal defect as it decreased in size. Packing of the still not eat adequate amounts of softened feed and was defect was discontinued on Day 80 and wounds were therefore offered dry senior pellets, which he ate without cleaned by hosing with tap water several times a day. The

oesophageal tear was reduced to approximately 1 cm the preceding 3 months on a diet of complete feed pellets diameter after 80 days and was closed completely (along with and sweet feed (fed as a slurry), as well as pasture grass. the external cervical wound) by 114 days. At that time, the Endoscopic examination as well as barium oesophagram oesophageal mucosa appeared intact when examined were performed, and revealed a persistent diverticulum. endoscopically. A diverticulum, with pooled saliva (but no In an attempt to decrease the size of the diverticulum, the feed) was seen as a widened area at the site of the initial horse was anaesthetised and placed in right lateral rupture. The diverticulum at this time had a wide neck and was recumbency. A 15 cm incision was made in the jugular furrow. considered to be a traction diverticulum, which is likely to The cutaneous colli muscle was dissected. Blunt dissection was occur after oesophagotomy or trauma to the oesophagus. used to identify and retract dorsally the left jugular vein and Oesophageal motility was subjectively decreased in the then to identify the left carotid artery and vagosympathetic previously affected area compared to the rest of the trunk. The oesophagus and diverticulum were then isolated oesophagus. by dissection. The diverticulum was identified using an The horse continued to do well on a diet of pellets, grass endoscope placed in the oesophagus. There was no and eventually hay for a period of 7 months before presenting apparent muscular oesophageal wall to suture over the to the VTH for choke and aspiration pneumonia. There was a diverticulum, suggesting that this part of the oesophagus was large amount of impacted grass at the site of the previous lost during the original injury and repair of the wound. Three oesophageal tear, which was lavaged with warm water. layers of 2-0 polytrimethylene carbonate (Maxon) sutures were Thoracic radiographs revealed a broncho-interstitial pattern in placed over the defect in a simple continuous pattern in an the caudoventral lung fields and large fluid pockets were seen attempt to imbricate surrounding soft tissues over the ultrasonographically surrounding the cranioventral lungs. diverticulum. Complete inversion of the diverticulum was not Transtracheal wash yielded suppurative inflammation with achieved due to extensive fibrous adhesions of the degenerate neutrophils and cultured Escherichia coli, surrounding soft tissues to the carotid artery and the lack of Staphylococcus aureus and Enterococcus fecalis. After normal oesophageal muscle layers. A closed suction drain was resolution of the choke, oesophageal endoscopy revealed placed in the incision site adjacent to the oesophagus and intact mucosa in the area of the diverticulum, with reflux exited at a site distal to the incision in an attempt to close any oesophagitis aborally and mild squamous gastric ulcers. dead space. The muscle and subcutaneous tissues were Barium oesophagram confirmed the presence of a closed separately in a simple continuous pattern. The skin was diverticulum, with no evidence of stricture (Fig 1). The neck of closed using staples. The drain yielded very small amounts of the diverticulum had started to contract, creating a flask-like fluid and was pulled 3 days post operatively. The horse was shape, which may have been due to progressive fibrosis of the treated with broad spectrum antibiotics for 7 days post opening, or may have been due to a pulsion component of operatively, as well as flunixin meglumine and ranitidine. the diverticulum developing secondary to the choke episode. Softened complete pelleted feed was administered via The horse was initially treated with potassium penicillin, nasogastric tube for 7 days. The horse had to be tranquilised gentamicin and metronidazole. Based on the culture result, with acepromazine to prevent him from rubbing out the the gentamicin was discontinued and switched to nasogastric tube. Follow-up contrast radiography revealed enrofloxacin. Flunixin meglumine and ranitidine were also that the dimensions of the diverticulum were essentially administered during hospitalisation. The horse made an unchanged after surgical intervention. At discharge the horse uneventful recovery from aspiration pneumonia and the was eating a wet mash of senior pellets 4 times a day as well as owners were counselled to abstain from feeding long-stem fresh grass. The owners were advised to abstain from feeding hay at discharge. Twelve months after the original injury, the hay for at least one month. Three years post operatively the horse presented to the VTH for surgical correction of the horse continued to do well on a diet of wet pellets and grass oesophageal diverticulum due to multiple choke episodes in (summer) or orchard hay (winter), with a significantly decreased incidence of choke episodes subsequent to the corrective surgery (2–3 times per year) compared to several times a month prior to the attempted imbrication. Since the diet remained essentially unchanged, it was thought the attempted imbrication, although not completely successful, had resulted in a scarring and shrinking of the diverticulum once some of the fibrous adhesions had been removed. A repeat oesophagram was not performed, however, and the actual size and shape of the diverticulum was never re-assessed, therefore dietary changes as the cause of the decreased incidence of choke could not be ruled out.

Case 2 A yearling Quarter Horse filly presented for evaluation of a potential oesophageal rupture after her primary veterinarian found feed material surrounding the oesophagus while Fig 1: Double contrast oesophagram of the diverticulum resulting attempting to lance a suspected mid-cervical abscess on the from oesophageal perforation (Case 1). White arrows indicate ventral midline. The horse had received flunixin meglumine barium present in the oesophagus; black arrows indicate the neck and trimethoprim sulfamethoxazole at unknown dosages for of the diverticulum. 48 h prior to presentation. On initial physical examination, all

vital parameters were within normal limits. Endoscopy treated with routine deworming. Three years later, the mare revealed a 5 cm long tear in the mid-cervical oesophagus, was completely normal when examined after foaling. It is communicating with the drainage hole created by the uncertain when the diarrhoea resolved. primary veterinarian and grade 4/4 (complete) left laryngeal paralysis. The only significant bloodwork abnormality was Case 3 hyperfibrinogenaemia. For surgical debridement and A 5-year-old Thoroughbred mare presented for evaluation of a oesophageal closure, the horse was anaesthetised and tracheal laceration 5 days after presumed trauma to the placed in dorsal recumbency. A ventral midline approach to ventral neck. She had been treated with one dose of penicillin, the oesophagus was made by extending the existing skin gentamicin and flunixin meglumine and placed ona5day incision from approximately 5 cm to approximately 12 cm in course of trimethoprim sulfamethoxazole and phenylbutazone length. Underlying tissues were bluntly dissected until the by the primary veterinarian. Two days prior to presentation, a lacerated oesophagus could be visualised. Identification of purulent, malodorous nasal discharge as well as severe the oesophagus was aided by palpation of a nasogastric tube subcutaneous emphysema was noted. Increased respiratory that was placed preoperatively. The wound was copiously noise was also present, which resolved with dexamethasone lavaged and oesophageal edges were apposed in a single and furosemide treatment. The horse started coughing 24 h full-thickness simple continuous suture pattern using 3-0 prior to presentation, but remained afebrile with a good polydioxanone. The incision was lavaged and a drain was appetite throughout. On the morning of presentation, the placed from the oesophageal laceration through a primary veterinarian found a defect in the trachea via subcutaneous pocket extending 10 cm ventral to the incision. endoscopy and was concerned about a possible The surgical incision was left open to heal by second intention. communication with the oesophagus. The neck was bandaged and the bandage changed and the On presentation, physical examination revealed a small, wound flushed out with saline daily. There was some purulent partially healed laceration that ran transversely across the discharge from the wound for 24 h, after which the discharge ventral aspect of the neck at the junction of the cranial and became more serous. The horse was treated with ampicillin middle third of the cervical region. There was diffuse, severe and gentamicin for 9 days post operatively, as well as flunixin swelling of the ventral neck around the trachea, extending to meglumine and ranitidine. After surgery, the horse displayed the throatlatch area as well as subcutaneous emphysema on severe agitation/colic associated with the indwelling both sides of the thorax and between the rami of the nasogastric tube, which was then removed. Partial parenteral mandible. Emphysema of the body wall made thoracic nutrition as described for Case 1 was administered for auscultation and ultrasound difficult to interpret. Complete nutritional support during the first 4 days after surgery. Initial blood count and serum biochemistry revealed a mild mature rates were designed to administer 25% of the daily energy neutrophilia, monocytosis, elevated creatine kinase, requirements for a growing horse (14.625 kcal/kg bwt/day) hyperglycaemia, hypocalcaemia and hyperfibrinogenaemia. and were then increased to provide 50% of the energy Endoscopy revealed a full thickness dorsolateral tracheal requirements on Days 2–4 (29.25 kcal/kg bwt/day). This was defect 60 cm from the external nares involving approximately supplemented with complete feed pellets mixed with water to one-third of the tracheal circumference, with a 1 cm full a very dilute consistency, which the horse drank well. Four days thickness oesophageal perforation at the corresponding level. after surgery, the oesophageal incision dehisced. The horse Cervical radiography revealed subcutaneous emphysema was fed a pelleted gruel via nasogastric tube, which was and a soft tissue defect with an associated abscess dorsal to tolerated well this time without sedation and only water was the trachea and emphysema in the surrounding tissues (Fig 2). offered orally. The neck wound was cleaned with saline-soaked gauze every 6 h and continued to drain saliva and small amounts of purulent material. A right jugular phlebitis, diarrhoea, pyrexia and depression developed 8 days after presentation. Complete blood count and serum biochemistry remained normal and the incision had a healthy bed of granulation tissue. Metronidazole and trimethoprim sulfamethoxazole were added to the treatment regimen on Day 9, when i.v. antibiotics were discontinued. Dry complete feed pellets were introduced on Day 11. Five faecal cultures were negative for Salmonella sp. The diarrhoea continued until discharge on Day 20. At that time, the diet consisted of hay chaff and complete feed pellets, fed from an elevated surface, as well as grazing several times a day. Owners were instructed not to feed hay for a month, followed by gradual re-introduction and to gently clean the neck wound after each feeding. Endoscopy 8 months later revealed normal oesophageal mucosa and there was only a very small external ventral cervical scar. The horse continued to have intermittent watery diarrhoea, despite normal weight gain, on a diet of Timothy hay and sweet feed. During evaluation for chronic diarrhoea, clostridial enterotoxins were not detected and a Fig 2: Cervical subcutaneous emphysema and a dorsal tracheal rectal mucosal biopsy was within normal limits. A faecal egg soft tissue defect with an associated abscess dorsal to the trachea count revealed 25 eggs/g of Parascaris equorum, which was and emphysema in the surrounding tissues (Case 3).

Thoracic radiography revealed a mild pneumomediastinum found. On Day 21, the liquid diet was discontinued and a and emphysema. For surgical debridement, the patient was softened complete pelleted feed was offered, which the anaesthetised and placed in dorsal recumbency. A 15 cm horse ate well for 3 days but then refused to eat. The diet was incision was made over the ventral midline of the neck. The changed to dry complete feed pellets and grazing, which trachea and oesophagus were visualised after blunt dissection was tolerated without complication. The external wound was through the ventral cervical muscles. There was a closed by Day 32 after presentation. At 37 days after initial hemicircumferential laceration of the left side of the trachea presentation, re-check endoscopy was still normal. between 2 tracheal rings. The tracheal rings were intact. Examination of the trachea revealed that the lumen was fully Necrotic tissue, purulent material and debris were meticulously epithelialised. The subcutaneous emphysema was resolving. debrided and removed from the area. There was a 2 cm long Hay was gradually introduced 30 days later without laceration in the ventral oesophageal wall. This laceration was complication. The horse continued to do well 15 months later mostly through the adventitia, but did penetrate the muscle and has had no episodes of choke. layers and mucosa in one small area. The oesophagus was not sutured. A tract was dissected to allow further drainage of the Case 4 previously diagnosed abscess. All wounds were left open to An 18-month-old Tennessee Walking Horse gelding presented allow continued drainage. The horse was treated with for evaluation of possible choke and oesophageal rupture. potassium penicillin and gentamicin for 11 days, followed by The horse was noticed initially to have a swelling under his neck trimethoprim sulfamethoxazole and metronidazole for 18 days. that the primary veterinarian attributed to trauma and treated She also received flunixin meglumine and famotidine with flunixin meglumine. The horse was allowed access to hay (0.5 mg/kg bwt, i.v., q. 8 h for 9 days) followed by ranitidine and water and was eating and drinking without complication. until discharge. The wound was cleaned and manually On the day of presentation, nasal discharge with feed material debrided using gauze moistened with saline twice daily, to was noted at both nostrils. A second veterinarian examined encourage the wound to granulate from the inside out. Enteral the horse and palpated oedema and crepitus along the feed was withheld for 7 days and parenteral nutrition was ventral neck. This veterinarian referred the horse to the VTH for administered at up to 75% of the horse’s daily caloric further evaluation. On presentation, the horse had pyrexia requirements (24.975 kcal/kg bwt/day). Water was withheld for (39.9°C), tachycardia (60 beats/min) and tachypnoea (36 5 days, and fluid requirements were met with intravenous breaths/min) as well as a serosanguineous nasal discharge lactated Ringer’s solution with maintenance amounts of and respiratory distress. A large area of painful, pitting calcium gluconate, potassium chloride and magnesium oedema was present on the ventral aspect of the neck that sulfate added. The perforation in the oesophagus could not extended to the thoracic inlet and pectoral region. be visualised endoscopically on Day 7, but there was an area Oesophageal endoscopy revealed an obstruction 70 cm from of thickened mucosa and absent peristalsis at the level of the external nares. The blockage was successfully resolved previously noted perforation. The tracheal wound was with careful lavage. Repeat endoscopy revealed 2 linear incompletely granulated. Despite the inability to detect an lacerations, each approximately 10 cm long in the ventral oesophageal defect using endoscopy, water and saliva still aspect of the oesophagus extending from approximately drained from the wound. On Day 8, a commercial liquid 85 cm from the external nares further distally (Fig 3a). The enteral formulation (Platinum Performance Enteral wounds subjectively appeared to have preceded the current Immunonutrition Formula)1 was introduced via nasogastric choke episode due to the lack of haemorrhage at the site, as tube. This was fed according to the manufacturer’s directions well as the slight hyperplasia and retraction of the edges. at 1200 g 3 times/day, which delivers 100% of the daily energy Grade 4 left laryngeal hemiplegia was also noted at that time. requirements for a 500 kg horse (32.9 kcal/kg bwt/day). The Thoracic radiographs and ultrasound revealed severe horse developed loose stool, with intermittent small piles of aspiration pneumonia as well as subcutaneous emphysema. normal manure, which persisted until discharge. Otherwise, the Initial CBC revealed mild anaemia and leucopenia. The horse enteral feeding was well tolerated and easy to administer. On received intranasal oxygen therapy at 10 l/min, along with Day 15, endoscopy revealed subjectively improved peristalsis crystalloid fluids at a maintenance rate. He was treated in the oesophagus and normal mucosa. No defect could be with potassium penicillin, gentamicin and metronidazole along

a) b) c) d)

Fig 3: Endoscopic views of oesophageal lacerations (Case 4) at presentation (a), 3 weeks after presentation (b), after surgical intervention (c) and 3 months after presentation (d).

with flunixin meglumine and famotidine. An approximately determine the progression of healing of the lacerations. 10 cm incision was made in the neck over the area of the Granulation tissue was apparent at the edges of the oesophageal laceration during standing surgery and the area lacerations, and they appeared to be adherent to the was cleaned and debrided as described for Case 1. underlying soft tissue structures. At this time, the external edges Forty-eight hours after presentation, CBC revealed a of the oesophageal lacerations were trimmed and sutured in a neutropenia with a degenerative left shift, which was thought 2 layer simple interrupted closure through the mucosa/ to be secondary to endotoxaemia and Gram-negative sepsis. muscularis and serosa using 3-0 polydioxanone with standing Nutrition was provided through intravenous fluids with 5% sedation (Fig 3c). The external skin incision was extended dextrose and electrolytes added. On the third day of approximately 5 cm for adequate drainage. The oesophagus hospitalisation, a nasogastric tube was passed to provide oral was allowed to heal for 5 days and enteral nutrition provided hydration and enteral nutrition using a soaked complete via an indwelling nasogastric tube. After 5 days, the pelleted feed. This was supplemented with a commercial nasogastric tube was removed and the horse was fed liquid enteral feed formulation (Platinum Performance Enteral complete pelleted feed in4lofwater 3 times daily. This was Immunonutrition Formula)1 once it became available. Dosing gradually increased until he was meeting his daily caloric was designed to provide an additional 50% of the growing requirements and maintaining a healthy weight. A small horse’s energy requirements (29.25 kcal/kg bwt/day). The area of the sutured incision (approximately 25%) dehisced horse had to be maintained in a stall on rubber mats to and was allowed to heal via second intention. Forty-four prevent him from eating his bedding. His general condition days after presentation, the horse was discharged with improved over the first week and he was weaned off the instructions to continue feeding fresh grass and a pellet slurry intranasal oxygen and intravenous fluids. Eight days after and to continue the trimethoprim sulfamethoxazole and presentation, the horse showed signs of laminitis, including phenylbutazone and maintain frog supports on the front feet increased digital pulses and lameness bilaterally in the front until recheck in 6 weeks. Radiographic evaluation at that time feet. Lateral radiographs of the front feet revealed bilateral revealed no further sinking; however, there were gas opacities mild sinking of P3 without rotation. No evidence of sinking or along the medial aspect of the hoof wall bilaterally in the front rotation was noted in the hindfeet. The horse was moved to a limbs, worse on the left. A partial hoof wall resection was bedded stall and frog supports were placed on all feet. The performed on the left front foot and both feet were trimmed to analgesic medication was changed from flunixin meglumine attempt to decrease the medial to lateral deviation. Over the to phenylbutazone. Gabapentin (10 mg/kg bwt, per os,q.8h) next 3 months, the horse’s feet were trimmed every 2 weeks. was administered and topical lidocaine patches were applied Radiographs revealed the laminitis had stabilised, but signs of to the front feet due to increased pain. The horse was chronic laminitis, including changes in the tip of P3 and spending an increased amount of time in sternal and lateral osteopenia of the left front foot, along with bilateral concavity recumbency and developed decubital ulcers on the hip, hock of the medial hoof walls had developed. He continued to and carpus that were cleaned daily. Radiographs of the front have mild choke episodes when allowed to eat dry pellets. feet performed 7 days after the initial films showed progression Serial endoscopies showed that the left laryngeal paralysis had of laminitis, with an additional 1.2 and 1.7 mm of sinking improved (grade 2) and the oesophageal mucosa and measured in the left and right front feet, respectively. A medial motility had returned to normal by 4 months after initial to lateral imbalance was noted at this time. Repeat presentation (Fig 3d). Gastric ulcers were noted at this point oesophageal endoscopy at this time revealed some evidence and were successfully treated with omeprazole. Hay had been of healing of the lacerations; however, a large amount of added back into his diet and the horse continued to grow saliva and fluids was still being lost through the incision and and was comfortable on his feet without any additional reflux was intermittently obtained via the nasogastric tube, nonsteroidal anti-inflammatory drugs. preventing administration of oral fluids (Fig 3b). Serum biochemistry at that time revealed azotaemia. Intravenous Discussion fluids were initiated and potassium penicillin and gentamicin This report describes the treatment of oesophageal were discontinued and switched to trimethoprim perforations in 4 out of 6 horses in which treatment was sulfamethoxazole. Phenylbutazone treatment was also attempted and demonstrates some of the associated discontinued and butorphanol was added for additional complications. Oesophageal perforations are rare, but have analgesia. The creatinine concentration increased to 25 mg/l been reported to be idiopathic, or secondary to oesophageal the following day, but returned to normal over the next 9 days. obstruction, nasogastric intubation, retropharyngeal Intravenous fluids were discontinued and the patient’s abscessation, trauma and oesophageal ulceration (Raker and hydration was maintained using oral fluids. Due to continued Sayers 1958; De Moor et al. 1979; van Wuijckhuise-Sjouke 1983; laminitic pain, phenylbutazone treatment was resumed. Since Vrins et al. 1983; Lunn and Peel 1985; Craig et al. 1989; Hardy a high percentage (32%) of calories in the liquid enteral feed et al. 1992; Dechant et al. 1998; Graubner et al. 2011). All 4 formulation came from soluble carbohydrates, the enteral cases in this report presented with swelling of the ventral neck nutrition formulation was changed to a fibre rich gel that was and varying degrees of systemic compromise. Only one horse low in soluble carbohydrates (WellSolve W/G Well-Gel Horse had signs of oesophageal obstruction (Case 4); however, this Supplement)2, due to concerns that the high carbohydrate occurred several days after the initial cervical swelling was feed might worsen the laminitis. This product is designed to noted and was therefore thought to be a secondary provide 100% of the recommended protein, vitamins and complication. Two of the cases in this report were assumed to minerals while being low in sugars and starches. Additional be secondary to unobserved trauma in the ventral neck calories were provided using a complete pelleted feed slurry region, because external lesions were visible. Since a diagnosis with added corn oil. Four weeks after presentation, the horse’s of oesophageal perforation is not always immediately laminitis had stabilised. Endoscopy was performed to apparent, there is frequently a delay prior to treatment. Craig

et al. (1989) reported a range of 1–8 days (mean 3.3 days) prior oesophageal laceration was performed, the incision dehisced to treatment. Similarly, the horses of this report presented for to some degree after surgery. Factors that may influence evaluation and diagnosis approximately 1–5 days after the first dehiscence or oesophageal healing include infection (Cases clinical signs were noted. Endoscopic visualisation of an 1 and 4), mechanical irritation from an indwelling nasogastric oesophageal defect may confirm a suspicion of oesophageal tube or feed (Cases 1–4), lack of serosal covering, or perforation, but the absence thereof should not definitively oesophageal motility. The suture pattern used can also rule it out. The absence of a visible defect in the oesophagus influence dehiscence. Interrupted sutures or suturing multiple at follow-up endoscopy in Case 3 highlights the importance of layers may be more appropriate than a single full thickness ancillary diagnostics (radiography, ultrasound and surgical simple continuous suture, as was used in Case 2. exploration) for diagnosis of small perforations. This has In Case 1, surgery was performed in order to decrease the previously been reported by Stick et al. (1981) in a study of incidence of choke secondary to an oesophageal experimental oesophagostomy in ponies in which 4 of 10 diverticulum that had formed at the previous perforation site. ponies had radiographic evidence of a sinus tract, despite The attempt was unsuccessful; however, due to the loss of endoscopic evidence of mucosal healing. oesophageal muscle layers from severe previous trauma and The basic principles of treatment include: debridement of adherence to the surrounding tissues, including the common infected, contaminated and devitalised tissue; establishment carotid artery. Surgical closure of the oesophagus in Case 3 and maintenance of adequate drainage; treating established was not performed, owing to the small size and quick healing infections and preventing their spread; maintaining fluid and of the perforation. electrolyte balance; and providing nutritional support. Initial Broad spectrum parenteral antibiotic therapy should be surgical management was used in all cases in order to initiated in all cases of oesophageal perforation. Due to the establish adequate drainage from the perforation site and large degree of contamination of the surrounding tissues, remove any infected tissue. Surgical debridement appears to culture may be beneficial, but may also yield an overgrowth of be necessary for long-term survival in cases of oesophageal nonpathogenic bacteria. This was performed at the initial perforation as leakage of saliva and feed into the tissue of the surgical debridement in Case 1, but was not attempted in the neck may result in cellulitis, extension of infection into the other cases. The administration of antibiotics prior to referral thoracic cavity and sepsis unless adequate drainage is may also complicate results. Although no anaerobic bacteria achieved (Lunn and Peel 1985; Craig et al. 1989; Dechant were cultured in Case 1, the closed infection and degree of et al. 1998). In a retrospective report of 11 cases of tissue necrosis present prior to surgical intervention provides an oesophageal perforations, 0 of 7 horses treated only medically ideal environment for anaerobic infections, justifying empiric survived, with 2 of 4 cases surviving after surgical treatment treatment with metronidazole. Case 1 showed a significant (Craig et al. 1989). For the 4 cases in this report, surgical improvement with intragastric metronidazole therapy, which debridement was carried out standing in 2 cases and under would support this conclusion. In cases with large general anaesthesia in 2 cases. While general anaesthesia oesophageal perforations such as Cases 1 and 4, oral therapy may allow for a more complete surgical exploration, the may not be successful due to physical loss of the drug through clinician must balance the patient’s anaesthetic risk, owner the oesophageal defect. Alternatively, the drug may be wishes and financial considerations with increased exposure delivered intragastrically via nasogastric or oesophagotomy and surgical procedural safety. Cases 1 and 4 were judged to tube or stallion urinary catheter. Metronidazole has inferior have increased anaesthetic risk due to systemic compromise bioavailability when administered rectally and therefore the at presentation and therefore standing surgery only was dose should have been increased to maintain the minimal performed. inhibitory concentration above that required to treat common In the 4 cases described above, continued debridement anaerobic pathogens during rectal administration in Case 1 and cleaning of the surgical site was necessary after the initial (Steinman et al. 2000). surgical debridement. To maintain adequate drainage until Aside from surgical debridement and antibiotic therapy, the oesophageal defect has closed completely and prevent the most important and possibly the most difficult aspect of contamination and infection of the surrounding tissues, daily dealing with these cases was fluid and nutritional support. digital debridement using moistened gauze and flushing Frequent monitoring of electrolyte concentrations should be (Cases 2 and 3) or surgical extension of the skin incisions (Cases performed as hyponatraemia and hypochloraemia with 1 and 4) was necessary. It appeared that the skin healed at a subsequent metabolic alkalosis can occur secondary to the more rapid rate than the oesophagus and that without these large loss of saliva through oesophageal fistulations (Stick measures, skin contracture would threaten to close an 2006). The horses in this case series did not develop significant incompletely granulated cavity. electrolyte abnormalities, presumably due to supplementation Surgical correction of the oesophageal perforation can be with intravenous fluid therapy. Finding the best way to provide attempted initially, as in Case 2, or as the case progresses, as adequate nutrition to a oesophageal rupture case remains a in Case 4, in an attempt to shorten the treatment time challenge. Parenteral nutrition was used alone (Case 3)oras required. In a study evaluating oesophageal healing after an adjunct to enteral feeding initially. There may be some oesophagotomy, the mucosa and skin wounds healed faster, advantage to resting the oesophagus completely, but this has and long-term complications such as diverticula, occurred less not been studied in horses. Glucose containing fluids are the frequently when the oesophagostomy was sutured vs. simplest form of parenteral nutrition and were used in 3 of the nonsutured (Stick et al. 1981). In Case 4, surgical correction cases in this report initially. Advanced nutrition support with was performed because healing of the lacerations had added protein and lipids was used in Cases 1–3. However, stopped and adherence of the oesophageal wound edges to prolonged parenteral nutrition is not ideal, as it is expensive, the underlying tissues was thought to be preventing complete and can lead to glucose intolerance, hyperglycaemia and wound healing. In both cases in which surgical closure of the osmotic diuresis (Carr 2009). Enteral feeding should therefore

ideally be used in conjunction with parenteral nutrition in these in all cases, presumably due to feeding changes and liquid cases. Enteral feeding was successfully accomplished for diet administration. The long-term use of antibiotics may also varying periods using an indwelling nasogastric tube in the 4 have contributed to the diarrhoea/weight loss. In Case 2, the cases discussed, however a cervical oesophagostomy tube diarrhoea persisted for at least 8 months after the initial injury, has also been reported to be useful for this purpose (Read which cannot be explained by diet or antibiotics. et al. 2002). The decision to use an indwelling nasogastric tube Oesophageal obstruction with aspiration pneumonia was vs. performing an oesophagostomy distal to the tear was noted on presentation in case 4. Since the horse had been made based on the location of the tears in Cases 1 and 4, seen to eat hay and grain after the cervical swelling was first where the original tears were thought to be too low on the noted, but prior to presentation, this complication probably neck to make accessing the oesophagus below the tear too occurred secondary to the actual rupture. Case 4 also difficult without general anaesthesia. The indwelling developed azotaemia. Fluid loss through the oesophageal nasogastric tube was chosen in these cases instead of placing perforation site, reflux secondary to gastrointestinal ileus and a tube through the tear, due to concerns over possibly causing the administration of potentially nephrotoxic drugs could all additional trauma to the oesophagus at that site, although a have been contributing factors. A review of the literature also small tube was placed through the site in Case 1 for a short reveals other reported complications, including septic pleuritis time to allow administration of oral medications. In Case 2, the (Gonzalez et al. 2008) and carotid artery rupture (Risnes and wound was closed primarily at presentation, and a second Mair 2003). surgery to place an oesophagostomy tube was not thought to Long-term complications included repeated choke be warranted. In Case 3, the original tear was small enough episodes (Cases 1 and 4), laminitis (Case 4) and persistent left that placing a feeding tube through the oesophageal tear laryngeal hemiplegia (Cases 2 and 4), all of which can be would have actually required widening the opening. There career or life ending in the long term. It is interesting to note were several complications associated with the use of that Case 1 choked on grass and Case 4 on dry pellets, but indwelling nasogastric tubes. Cases 1 and 2 appeared to have neither of these horses choked on hay. In the first case extreme pain associated with the indwelling tube in the initial reported here, inversion of an oesophageal diverticulum was phases of treatment. Patient compliance was also a problem complicated by extensive adhesions between the later on in Case 1, but tranquilisation facilitated maintenance oesophagus and carotid artery. The prognosis for horses with of an indwelling tube. Oesophageal perforation has been oesophageal perforations remains guarded and the reported secondary to nasogastric intubation (Craig et al. complication rate is high. In one report of 11 cases, the overall 1989; Hardy et al. 1992), but whether or not an indwelling tube survival rate was 18% (Craig et al. 1989). However, in this will interfere with healing is currently unknown. current case series, 4 out of 6 cases survived. Complications Slurries of commercially available complete pelleted feeds were more severe in the 2 horses with signs of severe systemic were cost effective and provided balanced nutrients as well compromise at presentation that underwent standing surgery as a good source of fibre for Cases 1, 2 and 4. However, only, and those horses had a longer hospital stay. Finances administration of adequate calories through an indwelling also play an important role in treatment. Costs for the initial tube required large volumes of fluids and a large bore tube, hospital stays for these cases ranged from approximately and particulate feeds still tended to obstruct feeding tubes. $5500 (Case 2) to $13,700 (Case 4). This does not include Liquid diets were much easier to administer, and administration repeat visits or treatment of long-term complications. could be achieved through softer, smaller bore tubes that may This report illustrates that with surgical debridement, have caused less mechanical damage to the oesophagus. intensive supportive care and prompt identification and Liquid diets formulated for horses were used to manage 2 of appropriate management, some oesophageal perforation the horses in this report (Cases 3 and 4). The 2 formulations cases can be treated. Owners should be informed of the differed in the calorie and carbohydrate content. Although involved and prolonged treatment required, as well as the the laminitis that developed in Case 4 was probably related to possibility of long-term complications such as chronic chokes the severe endotoxaemia, the low carbohydrate option was secondary to oesophageal strictures or diverticula. useful to prevent possible further insulin resistance that may occur when feeding a high carbohydrate diet. When used Authors’ declaration of interests according to the manufacturer’s directions, these formulations No conflicts of interest have been declared. were easily administered through the nasogastric tube and were associated with minimal complications, mainly soft stool. Manufacturers’ addresses When oral feeding commenced, softer feeds such as slurries of 1Platinum Performance Inc, Buelton, California, USA. complete feed pellets followed by fresh grass were 2Purina Mills LLC Gray Summit, Missouri, USA. preferentially fed; however, not all horses consumed adequate calories if fed a slurry. Hay was withheld for a period References beyond oesophageal healing, but could eventually be Carr, E.A. (2009) Nutrition of critically III horses. Vet. Clin. North. Am.: tolerated by all 4 cases. Equine Pract. 25, 93-108. Short-term complications that occurred included local Craig, D.R., Shivy, D.R., Pankowski, R.L. and Erb, H.N. (1989) Esophageal inflammation with or without abscessation, subcutaneous and disorders in 61 horses. Results of nonsurgical and surgical management. Vet. Surg. 18, 432-438. mediastinal emphysema, and cellulitis in all 4 cases. Endotoxaemia and/or sepsis was noted in 2 out of the 4 cases. De Moor, A., Wouters, L., Mouens, Y. and Verschooten, F. (1979) Surgical treatment of a traumatic oesophageal rupture in a foal. Equine Vet. Left laryngeal hemiplegia was also noted in 2 of the horses and J. 11, 265-266. was presumed to be secondary to inflammation or trauma to Dechant, J.E., MacDonald, D.G., Crawford, W.H. and O’Connor, B.P. the recurrent laryngeal nerve, although pre-existing disease (1998) Pleuritis associated with perforation of an isolated could not be ruled out. Diarrhoea and/or weight loss occurred oesophageal ulcer in a horse. Equine Vet. J. 30, 170-172. Continued on page 236 © 2013 EVJ Ltd