Severe oesophageal stricture after sedation with xylazine and endoscopic management in a cat

Abstract

Case summary

An 18-month-old castrated domestic shorthair cat was presented to the veterinarian for regurgitation after solid food consumption, 3 days after sedation with xylazine for diagnostic evaluation of chronic upper respiratory disease. Treatment with antibiotics, sucralfate and metoclopramide by the referring veterinarian did not lead to any clinical improvement. Oesophagoscopy 3 weeks after initial sedation with xylazine revealed an oesophageal stricture, which, based on history and after excluding other potential causes, was attributed to oesophagitis resulting from gastro-oesophageal reflux during sedation. The prevalence of gastro-oesophageal reflux in cats under general anaesthesia is in the range of 12–33%; however, the condition has been less studied in this species compared with dogs. The cat in this report underwent several successful balloon dilatation sessions, which corrected the stricture. The cat remains asymptomatic 1 year later.

Relevance and novel information

To our knowledge, this is the first reported case of oesophageal stricture formation after a single xylazine administration in cats. This case highlights the importance of considering gastro-oesophageal reflux and subsequent oesophagitis as a potential complication of sedation and anaesthesia in cats, and the need for prompt diagnosis and management to prevent oesophageal strictures.

Introduction

Gastro-oesophageal reflux (GOR), defined as the retrograde flow of gastric content through the lower oesophageal sphincter (LES),^{1 –3} is a common anaesthetic complication in dogs and cats.^{3 –7} GOR is often silent and underdiagnosed if regurgitation or postanaesthetic complications are absent. Mild oesophageal damage may go unnoticed in the absence of overt clinical signs or without oesophagoscopy or pH-metry.

The prevalence of GOR in cats is in the range of 12–33%,^{6 –10} while it has been reported in up to 57% of dogs under general anaesthesia.^{3 –5,11,12} Risk factors in cats include propofol or thiopentone use, ⁶ airway devices (laryngeal masks, endotracheal tubes)^8,9 and anaesthetic-related changes in LES and barrier pressure.^13,14 In dogs, GOR risk increases with prolonged fasting,^4,15,16 specific anaesthetic agents (opioids, anticholinergics, propofol)^4,10,11,17 and procedure type.^3,11

GOR may lead to oesophagitis, stricture and severe extraoesophageal complications, such as rhinitis, aspir-ation pneumonia, pleural effusion or pneumomediastinum after oesophageal perforation.^{5,18 –22}

This case report describes an oesophageal stricture in a cat after xylazine sedation, which was successfully managed using balloon dilatation. To our knowledge, this is the first published report of oesophageal stricture formation following sedation in a dog or cat.

Case description

An 18-month-old castrated male domestic shorthair cat was presented with a history of regurgitation after dry food consumption. The cat had a longstanding history of chronic upper respiratory disease with nasal discharge and coughing, without any previously reported gastrointestinal signs.

The respiratory signs first appeared when the cat was 7 months old. Initial treatment by the primary veterinarian included amoxicillin trihydrate/clavulanate potassium (20 mg/kg PO q12h for 10 days, Synulox; Zoetis), with no clinical improvement. Subsequently, the cat received two monthly injections of methylprednisolone (1 mg/kg SC, Depo Medrol; Zoetis), which led to only slight improvement. Over the next 8–9 months, the cat continued to experience intermittent mild episodes of upper respiratory signs. At 18 months of age, 11 months after the initial onset of respiratory signs and because of the persistence of upper respiratory signs, the cat was sedated for blood collection and thoracic radiographs by the primary veterinarian. Sedation was necessary because the cat was not cooperative. Xylazine (1.5 mg/kg IM, Xylazine; Neocell) was the sole anaesthetic administered, after overnight fasting. Sedation was adequate for blood sampling and no general anaesthesia was required. No vomiting was observed during or after sedation. The procedure lasted 40 mins, and the cat recovered without the use of an α₂-antagonist. Sedation and recovery were deemed uneventful, and complete blood count, biochemical profile and radiographic evalu-ation were unremarkable. The cat was prescribed amoxicillin/clavulanate tablets (20 mg/kg PO q12h) for another 10 days.

Three days after sedation, the cat exhibited signs of regurgitation after the consumption of dry food and water. The veterinarian administered dexamethasone (0.1 mg/kg SC q24h, Dexamethasone; Provet) for 3 days and sucralfate suspension (0.5 g PO q12h, Peptonorm; Uni-Pharma) and metoclopramide syrup (0.25 mg/kg PO q12h, Primperan; Sanofi-Aventis) for 2 weeks, while amoxicillin trihydrate/clavulanate potassium (8.75 mg/kg SC q24h, Synulox RTU; Zoetis) was administered for 5 days. The owner was advised to feed the cat exclusively wet food. Despite these interventions, regurgitation signs persisted, occurring two to four times daily, most frequently after food or water intake, and 2 weeks later, the patient was referred for oesophagoscopy. The timeline of events is presented in Figure 1.

Figure 1.

Timeline diagram illustrating the progression of clinical signs and interventions in the case. Time intervals are expressed in days

For oesophagoscopy, the cat was premedicated with dexmedetomidine (15 μg/kg, Dexdomitor; Zoetis) combined with buprenorphine (20 μg/kg IM, Bupaq; Neocell). Anaesthesia was induced with propofol (1 mg/kg IV, Propofol; Fresenius) followed by incremental doses of 1 mg/kg IV to effect. The total amount of propofol administered to allow tracheal intubation was 3 mg/kg. Intubation was performed with a cuffed tube of 3.5 mm, and anaesthesia was maintained with isoflurane (Iso-Vet; Biovet) in oxygen through a T-piece breathing system. During anaesthesia, crystalloid lactated Ringer’s solution was infused at a dose of 5 ml/kg/h.

A single severe oesophageal stricture was observed in the mid oesophagus (Figure 2) with the diameter of the oesophageal lumen at the stricture site estimated at approximately 3–4 mm. No active oesophagitis was visible at that time. The stricture was managed using balloon dilation catheters (Encore 26 Inflation Device with the CRE PRO Wireguided Oesophageal Balloon Dilation Catheter 6–11 mm; Boston Scientific), with a standard technique previously described by Leib et al. ²³ A total of eight oesophagoscopy-guided treatment sessions (every 1–2 weeks) were necessary to achieve adequate dilation. At each session, incremental adjustments were used to achieve adequate dilation of the stricture, while monitoring the resulting damage to the oesophageal mucosa. During the first session, dilation of the stricture was performed at 6, 7 and 8 mm. The next three sessions were performed at 8, 9 and 10 mm, and the last four sessions were performed at 9, 10 and 11 mm. During the first three dilation sessions, significant oesophageal mucosal tearing and haemorrhage were observed. Management included prednisolone (1 mg/kg PO q24h, Adelcort; Adelco) with a tapering schedule, along with sucralfate (250 mg PO q12h) and esomeprazole (1 mg/kg PO q12h, Nexium; Vianex) for 3 weeks to prevent fibrosis and stricture reformation. In the final five dilation sessions, only mild to moderate haemorrhage was noted (Figures 3–5). The inner diameter of the oesophagus during the last oesophagoscopy session was 12 mm. The anaesthetic protocol used in all sessions consisted of intramuscular administration of dexmedetomidine and buprenorphine as previously described. After each session, buprenorphine was administered via the transmucosal route (20 μg/kg q8h for 3 days). The cat was fed a highly palatable wet diet, although not in a postural feeding position, throughout the dilation period. After each treatment session, regurgitation progressively improved and had fully resolved by the final session. The cat subsequently exhibited normal eating and drinking behaviour. One year after the initial balloon dilation session, the cat remains asymptomatic.

Figure 2.

(a,b) Severe oesophageal stricture identified on oesophagoscopy

Figure 3.

Balloon dilation of the oesophageal stricture

Figure 4.

Severe oesophagitis after one of the balloon dilation sessions

Figure 5.

(a,b) Oesophageal lumen after the final dilation session

Discussion

To our knowledge, this is the first report of oesophageal stricture formation following xylazine-only administration in a cat. Postanaesthesia oesophageal strictures in cats and dogs can result from GOR-related oesopha-gitis.^5,18,24,25 Up to 71% of cats presenting for endoscopic balloon dilation had strictures attributed to anaesthesia-related GOR.^18,23,26,27

The choice of anaesthetic is an important factor predisposing to GOR by decreasing LES tone. Three reports describing suspected anaesthesia-associated oesophageal strictures in cats revealed a history of xylazine administration either in combination with ketamine and atropine^18,28 or ketamine alone. ²⁹ The effect of α₂-adrenergic agonists on LES pressure is unclear. Hashim and Waterman ¹⁴ reported that in cats treated with a combination of ketamine, xylazine and atropine, a reduced barrier pressure was observed compared with the use of ketamine alone. LES pressure was also reduced in dogs treated with xylazine.^4,30 Although not investigated in cats, studies in dogs have reported GOR with dexmedetomidine-based protocols; ¹⁷ however, higher reflux prevalence has been observed in dogs premedicated with acepromazine. ³¹ Furthermore, Croffie et al ³² noted decreased LES pressure after administration of oral midazolam, as well as intramuscular meperidine, promethazine and chlorpromazine in cats. Interestingly, no general anaesthetic agent was administered in the present case. To our knowledge, all reported GOR cases in dogs and cats include induction agents.^4,7,14 However, GOR cannot be ruled out when sedatives alone are used. This case highlights that sedation only may, in rare cases, result in oesophageal stricture, presumably due to GOR.

Another important consideration is the emesis-inducing properties of xylazine. ³³ Vomiting before anaesthesia may reduce the risk of GOR by emptying the stomach content. However, emesis during sedation could result in residual gastric acid in the oesophageal lumen. ¹¹ Combined with depression of oesophageal protective mechanisms like salivation and oesophageal peristalsis, this may predispose to oesophagitis. ³⁴ In this case, the cat did not vomit after xylazine administration, so the likelihood of vomiting-induced oesophagitis is not considered relevant.

Other factors linked to GOR include procedure type and recumbency. In the present case, the cat was sedated for thoracic imaging, a procedure type weakly associated with GOR in dogs. ¹⁷ However, there are limited data on reflux prevalence during diagnostic imaging in feline patients. Stricture formation has been reported after ovariohysterectomy in cats,^18,28 while in another study, 6/9 cases of stricture formation were associated with prior administration of anaesthesia for various surgical procedures. ²⁷ Although no strong correlation between recumbency and GOR exists, frequent repositioning during imaging may provoke regurgitation.^3,17

Procedure duration appears unrelated to the likelihood of reflux, ³ although it may affect the oesophagus as the refluxate remains in contact with the mucosa for a longer period. In our case, we hypothesise that the absence of an antagonist and a prolonged recovery likely extended exposure of the oesophagus to the refluxate.

Most GOR studies in dogs indicate that reflux occurs soon after induction. According to one study, 90% of dogs experienced reflux within 40 mins after induction, while another study noted a median onset of GOR within 10 mins.^3,11 In 6/40 cats, GOR had already occurred by the time the pH electrode was introduced into the oesophagus, approximately 5 mins after induction. ⁹ Similarly, a recent study reported that 29/119 dogs that experienced GOR had already refluxed during probe insertion. ¹⁷ Therefore, reflux during premedication cannot be excluded. However, the combination of anaesthetics administered likely increases the prevalence of reflux due to their combined effects.^4,11,17

Other causes of oesophagitis and stricture formation were considered but excluded. Oesophagoscopy revealed no foreign bodies, and the cat, being strictly indoors, had no exposure to corrosive agents or signs of toxicity. Although the patient was on long-term antibiotic therapy, amoxicillin/clavulanic acid is not commonly associated with pill-induced oesophagitis.^35,36 Moreover, the onset of clinical signs 3 days after sedation are consistent with the reported onset of anaesthesia-related oesophagitis (1–32 days after anaesthesia).^1,5,19,25 Based on the sequence of events and oesophagoscopic findings, xylazine-associated GOR is considered the primary contributing factor to stricture formation in this cat.

Conclusions

This is the first reported case of oesophagitis and stricture formation after a single administration of xylazine in a cat. Although rare, GOR and stricture formation after sedation should be considered a possible complication.