Abstract
A 5-year-old cat presented with haemorrhagic left aural discharge, 2 days following a road traffic accident. Otoscopic examination identified disruption of the external ear canal at the auricular/annular cartilage junction. This was managed by total ear canal ablation and lateral bulla osteotomy. Left sided facial nerve deficits were present following surgery. Eighteen months postoperatively there were no auricular problems, however facial nerve deficits persisted.
There are no previous reports describing management of acute separation at the auricular/annular cartilage junction of the external ear in the cat or dog. This case report describes the presentation, diagnosis and surgical management of an acute ear canal separation at the auricular/annular junction of the external ear canal in a cat.
A 5-year-old, male neutered, 4.5 kg, Domestic Short Hair cat presented with drooling and inability to close its mouth, two days after a road traffic accident. Upon clinical examination the patient was quiet, responsive, had dry oral mucous membranes, reduced skin pliability and was estimated to be 10% dehydrated. Pain, moderate soft tissue swelling and superficial skin abrasions of the rostral mandible with malocclusion of the rostral maxilla and mandible due to suspected mandibular symphyseal fracture, were also identified. No cranial nerve deficits were present. Left sided haemorrhagic aural discharge was observed. The left external ear was more loosely attached to the skull than the contra-lateral ear, and palpation of the area elicited moderate discomfort. Limited otoscopic examination revealed haemorrhagic discharge within the vertical ear canal.
Fluid deficits were corrected with intravenous Hartmann's solution (Aquapharm No.11, Animal care). Analgesia was provided with 4 mg/kg carprofen (Rimadyl, Pfizer) and 0.01 mg/kg Buprenorphine, given every 8 h (Vetergesic, Animalcare) and antimicrobial therapy was with 20 mg/kg cephalexin (Ceporex, Smith-Kline and Beecham), all of which were administered by subcutaneous injection.
After stabilisation, a complete blood count and serum biochemistry were obtained, revealing no abnormalities. The patient was pre-medicated with 0.1 mg/kg Acepromazine Maleate (ACP, C-Vet) administered intramuscularly, and anaesthesia induced with 6 mg/kg propofol intravenously (Rapinovet, Schering-Plough). Following intubation, anaesthesia was maintained with halothane vaporised in an oxygen and nitrous oxide carrier mixture (33%/66%) via an Ayres T-piece. Intravenous Hartmann's solution was administered intravenously at a rate of 3 ml/kg/h for the duration of anaesthesia.
Otoscopic examination revealed complete separation of the auricular from the annular cartilage of the external ear, which allowed visualisation of the masseter muscle and the annular cartilage, which was observed in its normal position. Re-direction of the otoscope into the horizontal canal revealed a ruptured tympanic membrane. Based on these findings, a diagnosis of complete separation of the auricular from annular cartilage was made.
Left lateral oblique and dorsoventral skull radiographs were obtained. The former was unremarkable, while the latter confirmed mandibular symphyseal fracture and demonstrated soft tissue swelling and pockets of air around the base of the vertical ear canal (Fig. 1). Thoracic radiographs were unremarkable.

Dorsoventral radiograph of the skull demonstrating soft tissue swelling and pockets of air around the base of the vertical ear canal.
The mandibular symphyseal fracture was repaired routinely with a circumferential cerclage wire (Scott, 1998). Postoperative radiographs revealed satisfactory fracture reduction and implant placement and temporary extubation revealed normal oral occlusion.
The left side of the face and pinna were prepared for surgery, and a total ear canal ablation (TECA) was performed. Blunt dissection allowed the auricular cartilage to be freed from its attachments until the level of avulsion was reached, at which point it was removed from the surgical field. The annular cartilage was then grasped with artery forceps and gentle traction facilitated close perichondrial dissection. The facial nerve was identified and gently retracted from the surgical field with Gelpi retractors. The annular cartilage was amputated from the external acoustic meatus and lateral bulla osteotomy (LBO) performed. The surgical field was flushed with sterile saline and the wound closed routinely. The pinna was scrolled during closure, allowing erect ear carriage to be maintained, achieving satisfactory postoperative appearance.
After surgery, analgesia was provided with 0.01 mg/kg buprenorphine (Vetergesic, Animalcare) administered subcutaneously, three times daily for 24 h. On recovery from anaesthesia there was absence of palpebral reflex in the left eye, indicative of facial nerve dysfunction. Oral prehension and mastication were normal the day after surgery. A 7-day course of 50 mg cephalexin, per os, twice daily was started. The patient was discharged on the third postoperative day.
At suture removal, fourteen days after surgery, absence of palpebral reflex in the left eye and drooping of the left upper lip demonstrated persistence of facial nerve dysfunction. Nictitating membrane function was normal and Schirmer tear test result within normal limits. At re-examination 6 weeks and 14 weeks after surgery, no abnormalities other than persistence of the left sided facial nerve deficits were detected. Telephone follow up eighteen months after surgery revealed the patient to have no problems related to the ear, however left sided facial nerve deficits persisted.
Discussion
Discontinuity of the external ear canal is an uncommon diagnosis, with three recorded cases in the cat (Kyles, 2001; Smeak, 1997) and nine in the dog (Boothe et al., 1996; Connery et al., 2001; McCarthy et al., 1995). All cases resulted from known or suspected external trauma. Disruption can occur at the auricular/annular cartilage junction (Boothe et al., 1996; Connery et al., 2001; Kyles, 2001) or at the attachment of the annular cartilage to the external acoustic meatus (McCarthy et al., 1995; Smeak, 1997), the former being more common, perhaps as their ligamentous connection is more susceptible to trauma (Boothe et al., 1996).
Diagnosis, management and outcome of acute traumatic ear canal separation is poorly described in the literature, with only one previous report (Smeak, 1997) describing separation of the annular cartilage from the external acoustic meatus, of 1 weeks duration, in a cat. All other reports describe diagnosis, management and outcome of chronic cases, where para-aural abscessation/fistulation are present (Boothe et al., 1996; Connery et al., 2001; Kyles, 2001; McCarthy et al., 1995).
Smeak (1997) recorded presence of haemorrhagic aural discharge with the acute presentation of ear canal disruption. Its presence has also been mentioned by owners of patients with chronic disease, as a historical observation from the time of trauma (Boothe et al., 1996; McCarthy et al., 1995). In this case, haemorrhagic aural discharge prompted early otoscopic examination, which was diagnostic for discontinuity of the external ear canal, in common with findings by Smeak (1997). In previous reports, dorsoventral and open mouth rostrocaudal skull radiographic views have identified soft tissue opacity and obliteration of the horizontal ear canal in both the acute (Smeak, 1997) and chronic presentations (Connery et al., 2001; Kyles, 2001; McCarthy et al., 1995). The horizontal and vertical canals were still visible on dorsoventral radiographs in this case, although soft tissue swelling and pockets of air around the base of the vertical ear canal were suggestive of trauma in this region.
Site of separation is considered an important factor in surgical decision making (Smeak, 1997). In this case, with absence of horizontal canal and bulla disease, isolation of the opening of the horizontal canal and its anastomosis to the skin as described by Boothe et al. (1996) or vertical canal ablation would have provided a satisfactory drainage route for otic secretions. Alternatively, Kyles (2001) described horizontal canal ablation and lateral bulla osteotomy as an effective treatment for chronic cases of separation at the auricular/annular junction, while preserving the blind ending vertical canal for aesthetic reasons. With chronicity, cicatrical sealing of the separated ends of the ear canal occurs, however at what stage and how long this takes to occur is not known. With an acute presentation, procedures used by Kyles (2001) and Boothe et al. (1996) would not address communication between the external environment and deeper tissues, which would still persist postoperatively, perhaps predisposing to future complications, such as para-aural abscessation/fistulation.
Intra-operatively, following excision of the vertical ear canal, the traumatised and frayed separated end of the annular cartilage was debrided and approximated to the skin wound. The required debridement reduced the functional length of the annular cartilage, creating excessive tension at this proposed site of anastomosis. Excessive tension may predispose to stenosis of the stoma, necessitating revision surgery, as was recorded in 2/5 cases by Boothe et al. (1996).
TECA with or without bulla surgery is indicated in patients with severe trauma to the ear canal (Smeak and Kerpsack, 1993). It can be used for separation at any level, and in combination with ventral bulla osteotomy successfully managed the acute separation described by Smeak (1997) and in combination with LBO has been used to manage chronic cases with para-aural abscessation/fistulation (Connery et al., 2001; McCarthy et al., 1995).
Despite the absence of bulla disease TECA alone was not performed as residual aural secretory epithelium may be left within the short osseous ear canal, a risk factor towards development of para-aural abscessation (Smeak and Kerpsack, 1993). LBO, in combination with TECA allows complete removal of aural integument lining the short osseous ear canal and bulla epithelium through the same surgical approach (Smeak and Kerpsack, 1993).
TECA and LBO is not a benign procedure with overall complication rates of 29% (White and Pomeroy, 1990) to 82% (Smeak and DeHoff, 1986). Williams and White (1992) cited ipsilateral neurological disorders [facial nerve neuropraxia (22%)/paralysis (39%) and Horner's Syndrome (17%)]—as the most common postoperative complication.
Facial nerve neuropraxia or paralysis is most likely the result of excessive trauma to the nerve (Smeak and Kerpsack, 1993; Williams and White, 1992), during dissection of the annular cartilage. Deficits present at 4 weeks postoperatively suggest permanent dysfunction (Smeak and Kerpsack, 1993). Facial nerve trauma may or may not adversely affect lacrimation (Barnett and Crispin, 1998). Normal lacrimation and passive third eyelid movement provided tear film distribution, preventing development of corneal pathology in this patient.
In conclusion, when haemorrhagic aural discharge is observed following trauma, prompt otoscopic examination allows early diagnosis of ear canal separation, facilitating early surgical intervention and the prevention of para-aural abscessation/fistulation. In common with previous reported cases, the prognosis following surgery was very good, with unexceptional postoperative complications.
Footnotes
Acknowledgement
The author would like to thank Dylan Clements and Dr Elizabeth Welsh for their review of the manuscript.
