Atlantoaxial instability, most commonly observed in young, small dog breeds, can result from congenital dens hypoplasia, dens fractures or separations, or malformations or ruptures in the surrounding ligaments (10). The clinical signs vary from neck pain to paralysis, reflecting the degree of compressive and concussive injuries to the spinal cord associated with subluxation (11). In the most severe cases, caudal brainstem signs may present due to trauma to the medulla oblongata and basilar artery (11). Surgical treatment is recommended for patients with neurological deficits, severe neck pain, and those unresponsive to conservative management (13). Surgical treatment involves both dorsal and ventral stabilization techniques, with ventral techniques typically preferred for improved visualization and accessibility of the atlantoaxial junction, lower complication and mortality rates, and infrequent requirements for additional surgery (6,7,11,13). Despite the relative safety of the ventral approach, surgical complication rates can reach 33-53%, and these complications are associated with a high mortality rate (7,13). Complications may include coughing, laryngeal paralysis, gagging, dyspnea, Horner’s syndrome, changes in voice, hemorrhage, and aspiration pneumonia (3,11). Although the detailed incidence of complications has not been published, most complications result from inadvertent damage to adjacent structures, including the larynx, trachea, and neuronal tissue, due to surgical manipulation, implant misplacement, or implant failure (3,7). These may necessitate surgical intervention, such as revision or explantation surgery (3,7). In humans, the risk of these complications is higher during revision surgery (14). Nevertheless, the precise causes and management methods for these complications, especially after explantation surgery, are not yet fully understood.

In this study, a case of canine vagosympathetic trunk (VST) and recurrent laryngeal nerve (RLN) paralysis along with a structural deformity in the retropharyngeal space after a ventral approach for surgical explantation of the atlantoaxial implant is reported. This report describes the clinical course and management of the resulting neurological complications and structural deformities.

A 7-month-old neutered male Poodle presented with severe neck pain that did not respond to conservative treatment and subsequently underwent ventral stabilization surgery for atlantoaxial instability. One year after ventral stabilization surgery, the dog exhibited acute severe cough and vomiting. He had been vaccinated and dewormed, with no history of trauma or exposure to toxins. No significant findings were observed on neurological and physical examinations, including auscultation. Lateral radiographs revealed screw loosening and compression of adjacent structures, including the upper esophagus and airway, caused by the atlantoaxial implant (Fig. 1). Based on these findings, compression from the atlantoaxial implant was determined to be the cause of the clinical signs, leading to the decision to remove the implant. Following explantation surgery, the clinical signs resolved. However, the dog subsequently exhibited significant dyspnea, dysphagia, and dysphonia. The patient experienced difficulty swallowing both food and saliva, which lead to the accumulation of secretions in the airway and worsening of respiratory function. The serum biochemical profile, performed using Catalyst One (IDEXX Laboratories Inc., Westbrook, ME, United States), revealed elevated C-reactive protein (4.2 mg/L; reference interval, 0.1-1.0 mg/L). Thoracic radiographs revealed severe alveolar infiltration in the right middle lobe, suspecting acute aspiration pneumonia. Neurological examination revealed no abnormalities in tongue movement; however, miosis was noted in the right eye (Fig. 2A). Physical examination revealed ipsilateral hyperemia of the ear pinna (Fig. 2B). These findings raised the suspicion of damage to the right sympathetic pathway (partial Horner’s syndrome). Contrast fluoroscopy (OSCAR Prime, GENORAY, Sungnam, Korea) using iohexol showed a delayed swallowing reflex and leakage of contrast material from the hypopharynx into the trachea (Fig. 3A). Gross examination of the larynx via rigid endoscopy revealed hyperemia and reduced movement of the right laryngeal cartilage, confirming the diagnosis of right-sided laryngeal paralysis (Fig. 3B). These findings indicated paralysis of the right recurrent laryngeal nerve. On postoperative day (POD) 15, computed tomography (CT) (Alexion, Toshiba Medical Systems, Japan) was performed for structural evaluation, revealing a structural deformity in the retropharyngeal space ventral to the vertebral body of the second cervical vertebra (C2), measuring 11.9 × 8.9 × 6.1 mm (Fig. 4A). Considering the anatomical features of the right recurrent laryngeal nerve and right vagus nerve, along with the deformity in the retropharyngeal space ventral to C2, the patient’s clinical signs were suspected to be complications arising from the surgical explantation.

Figure 1. Radiographs of the cervical spine prior to the atlantoaxial implant explantation. (A) Right lateral and (B) ventrodorsal views showing implant failure (arrows).

Figure 2. Gross images of the eye (A) and ear (B) after atlantoaxial implant explantation. (A) Miosis observed in the right eye. (B) The right pinna was hyperemic and warm to the touch compared to the left pinna.

Figure 3. Laryngeal paralysis confirmed via contrast fluoroscopy (A) and rigid endoscopy (B) after the atlantoaxial implant explantation. (A) The fluoroscopic image showing contrast medium (asterisk) in the proximal portion of the trachea. (B) The rigid endoscopy revealed decreased movement and hyperemia of the right laryngeal cartilage during inspiration (asterisk).

Figure 4. Mid sagittal-plane computed tomography (CT) images (soft tissue window). (A) On postoperative day (POD) 15, CT revealed the formation of a retropharyngeal space ventral to the vertebral body of the second cervical vertebra (C2), measuring 11.9 × 8.9 × 6.1 mm (arrow). (B) On POD 104, there was a reduction in this space, measuring 8.1 × 5.5 × 3.4 mm (arrow).

Tracheostomy (Yunshin Medical Co., Bucheon, Korea) and gastrostomy feeding tubes (Avanos Medical Co., Georgia, USA) were inserted to relieve dyspnea and assist with enteral feeding. Nebulized normal saline was administered every 6 h for aspiration pneumonia. Amoxicillin-clavulanate (12.5 mg/kg, intravenously, q 12 h; Cramoxin^®, Shinpoong Pharm., Ansan, Korea) and maropitant (1 mg/kg, intravenously, q 12 h; Cerenia^®, Zoetis corp., New Jersey, United States) were also administered. Oropharyngeal and tracheal secretions were suctioned every 6 h through a tracheostomy tube. The patient was fed a liquid diet (Gastrointestinal Low Fat, Royal Canin Veterinary Diet, MO, USA) through a gastrostomy feeding tube for 15 min, four times a day. On POD 6, repeated radiographs showed that the patient had recovered from aspiration pneumonia, and the hyperemia of the right ear pinna had also disappeared. On POD 12, the dyspnea resolved, leading to the removal of the tracheostomy tube. On POD 16, the anisocoria resolved, and the patient began to vocalize as dysphonia started to improve. On POD 37, the patient’s voice fully recovered, and fluoroscopy confirmed the return of normal swallowing function. The gastrostomy tube was removed and the patient was discharged successfully. Following discharge, the CT examination conducted on POD 104 revealed a reduction in the retropharyngeal space, measuring 8.1 × 5.5 × 3.4 mm (Fig. 4B). The patient has remained generally healthy for over 18 months after discharge, with no signs of dyspnea, dysphagia, dysphonia, or Horner’s syndrome.

The ventral approach is a commonly used technique for the surgical stabilization of atlantoaxial instability (11). Neurological damage is a well-documented complication associated with the ventral approach and may occur within the first 48 h postoperatively because of perioperative neuronal trauma caused by surgical manipulation (12,15). This damage can lead to a range of complications, including dyspnea, laryngeal paralysis, and Horner’s syndrome, with severe cases potentially resulting in respiratory failure or cardiac arrest (3,15). In humans, the risk of neurological damage increases during revision procedures for anterior cervical spine surgery (14,15). To the best of our knowledge, the optimal management strategies for complications related to the ventral approach for atlantoaxial implant explantation have not been previously reported in veterinary medicine.

In this case, after surgery for atlantoaxial implant removal via ventral approach, the patient presented with dyspnea, dysphagia, and dysphonia due to right RLN paralysis, as well as right eye miosis and hyperemia of the right ear pinna, indicating right-sided Horner’s syndrome resulting from right VST paralysis. The RLN, a branch of the vagus nerve (CN X), provides sensory, motor, and parasympathetic fibers to the structures of the larynx. RLN paralysis is a known complication of cervical spine surgery (9,14). In humans, RLN paralysis is the most common complication following anterior cervical spine surgery, with an incidence ranging from 0.2% to 24.2% (9,14). Due to the proximity of both RLNs to the esophagus and trachea, these nerves are most often damaged during anterior approaches to the neck, particularly when retraction of the larynx and trachea results in surgical trauma (9,14,15). Horner’s syndrome results from dysfunction of the oculosympathetic pathway, which consists of 3-neuron pathway (19). First-order neurons originate in the hypothalamus and extend to the spinal cord (19). Second-order neurons arise from the first three thoracic spinal cord segments, travel through the thorax and cervical region, and synapse in the cranial cervical ganglion (19). Third-order neurons then travel from the ganglion to the orbit. Symptoms of Horner’s syndrome occur due to dysfunction of the sympathetic pathway (19). Horner’s syndrome is a well-recognized but rare complication of anterior cervical spinal surgery (17,19). In human medicine, the incidence rate in clinical practice is approximately 0.06%, whereas in veterinary practice, only a few case reports exist (17). The low incidence of Horner’s syndrome may be attributed to neuroanatomical factors, as the VST is situated laterally and dorsally to the RLN. In this case, the patient presented with right-sided Horner’s syndrome, likely attributable to an injury to the right VST, suggesting that the symptoms of dysphagia, dyspnea, and dysphonia were likely due to postoperative damage to the adjacent right RLN. This was subsequently confirmed via rigid endoscopy, which revealed right-sided laryngeal paralysis.

In this case, the surgeon approached the midline of the patient from the right side because of right-handedness, which likely resulted in damage to the right VST and RLN. Lateral approaches in cervical surgery elevate the risk of Horner’s syndrome due to the displacement of the sympathetic trunk from the midline (17). Therefore, maintaining a midline approach is generally recommended to minimize the risk of sympathetic nerve damage during surgery (17). In humans, RLN paralysis after anterior cervical spine surgery is reported to be associated with a higher risk of right-sided approaches and revision procedures (14). The right RLN has an anterolateral position and exhibits more variation in course and branching patterns than the left (14). Given the common occurrence of extra-laryngeal branching patterns, misidentification of the branches innervating the trachea, esophagus, or inferior constrictor muscles can lead to iatrogenic injury, resulting in a variety of postoperative symptoms, including dysphagia, dyspnea, and dysphonia (14). This suggests that, in this case, the RLN was damaged during tracheal retraction, and the right-sided approach may have contributed to the occurrence of iatrogenic nerve injury. In human medicine, it has been suggested that periodic release of the retractor after placement may help mitigate the risk of recurrent laryngeal paralysis (2). Therefore, a comprehensive understanding of the neuroanatomy is essential for predicting and preventing potential nerve injuries, thereby guiding optimal clinical practice.

Neurological damage resulting from mechanical injury has rarely been reported in veterinary medicine (2). In the present case, despite nerve damage causing dyspnea and dysphagia, the patient recovered fully after approximately 37 days of symptomatic treatment. A similar case involving cranial nerve IX, X, and XII injuries following ventral stabilization for atlantoaxial instability showed full recovery within one month of revision surgery (2). Additionally, studies on idiopathic trigeminal neuropathy, although unrelated to mechanical injury, suggest that patients with reversible nerve damage typically recover within an average of 22 days (8). Based on these studies, reversible nerve injuries may recover within approximately one month. Therefore, although nerve damage may be life threatening, as demonstrated by the patient in this study, symptomatic management and appropriate treatment should be considered during the recovery period.

On POD 15, CT revealed the formation of a retropharyngeal space as a complication of the ventral approach. To the best of our knowledge, there are no reports on retropharyngeal space formation following cervical ventral approach surgeries in veterinary medicine. However, in human medicine, studies have indicated that pharyngeal diverticulum can occur infrequently, with an incidence of approximately 1.6% (1,16,18). The diagnosis of a pharyngeal diverticulum is typically confirmed through contrast fluoroscopy or CT, which reveals a lateral pharyngeal pouch (4,18). In most cases, pharyngeal diverticula are asymptomatic and do not require treatment (4,18). However, if clinical signs occur, surgical removal becomes necessary, and the prognosis is generally considered favorable (4,18). The most common clinical signs are dysphagia and regurgitation, both of which were observed in the present case (4,18). However, the patient’s symptoms were more likely related to RLN paralysis than to the retropharyngeal space, as contrast fluoroscopy did not reveal any retention of contrast material within that space. In summary, dysphagia is a well-documented complication following ventral approach surgery and is primarily caused by RLN paralysis. However, it can also rarely arise from the presence of a large pharyngeal diverticulum requiring surgical intervention. Therefore, if dysphagia persists for more than three weeks, it is essential to assess the possibility of a pharyngeal diverticulum.

In this case, there was no recurrence of clinical signs related to atlantoaxial instability following the explantation of the atlantoaxial implant. This suggests that the fibrous tissue formation around the atlantoaxial joint during the patient’s growth may have continued to support the stability of the joint after the ventral stabilization surgery (5). Therefore, it is possible that the patient was able to recover conservatively after implant explantation.

This report describes a canine case of VST and RLN paralysis, along with retropharyngeal space deformity, as complications of atlantoaxial implant explantation. A thorough understanding of the neuroanatomy may help predict and prevent potential nerve injuries. If nerve damage is reversible, a recovery period of approximately one month may be required. During this period, appropriate supportive care can facilitate patient recovery.

This study was supported by the National Research Foundation (NRF) of Korea and funded by a grant from the Korean Government (NRF-2022R1G1A10036821131482092640101) and the Basic Science Research Program through the NRF funded by the Ministry of Education (RS-2023-0021971031482092640001).

The datasets used and/or analysed during the current study are available from the corresponding author upon reasonable request.

The authors have no conflicting interests.