redazione@vetpedia.it +39-0372-40-35-36/37/47
  • Disciplina: Chirurgia
  • Specie: Cane

The outer and middle ear diseases of the dog and cat are frequently associated with allergic skin diseases and atopy. Particular attention to these conditions is therefore essential, as surgical treatment is usually the last resort and must in any case be accompanied by the management of the underlying dermatological problem.

Ear surgery is rarely an emergency procedure, or one that must be performed in the immediate future. This said, traumatic injuries causing the avulsion of the ear canal may require an earlier and more urgent intervention.

In the dog, inflammatory or atopic diseases of the external auditory canal are the most frequent ear diseases. Although less frequently, trauma or neoplastic lesions may also affect the ear pinna. In general, middle ear diseases of the dog result from the involvement of the tympanic bulla by processes originating in the outer ear canal. In the cat, instead, inflammatory polyps originate in the middle ear to then secondarily involve the outer ear through the tympanic membrane, and the nasopharynx through the auditory tubes. Neoplastic diseases that can affect both the outer and middle ear include squamous cell carcinoma and carcinoma of the ceruminous glands.


OUTER AND MIDDLE EAR SURGICAL DISORDERS OF THE DOG AND CAT
  • CONGENITAL STENOSIS OF THE EAR CANAL (Sharpei & Chow)
  • OTITIS EXTERNA & MEDIA (Spaniels and all breeds predisposed to INFLAMMATORY POLYPS) (cats < 3 years of age)
  • TRAUMATIC INJURY OF THE EAR CANAL (e.g., bite wounds)
  • NEOPLASMS (squamous cell carcinoma & ceruminous gland carcinoma)

 

OTITIS EXTERNA


The term otitis externa (OE) defines an inflammatory process affecting the pinna and the external auditory canal. The inflammation of these structures produces a cascade of events that makes the ear a favourable environment for the multiplication of pathogenic microorganisms, with a progressive occlusion of the auditory meatus. In the course of otitis externa the temperature inside the duct increases significantly, accompanied by a concomitant rise in relative humidity. This favours bacterial proliferation, mainly Staphylococcus aureus and Pseudomonas spp., then followed by changes also in the fungal flora, with specifically an increased prevalence of Malassezia pachydermatis.

The inflammation is accompanied by oedema and by an infiltration of inflammatory cells that progressively accumulates in the form of exudate. The ability of microorganisms to develop resistant strains that can proliferate even in unfavourable conditions allows the progression of the infection. In the course of chronic otitis, a series of progressive pathological alterations are observed, including varying degrees of glandular hyperplasia and ectasia, fibrosis and calcification of the external auditory canals.

The triggering event of otitis externa can be represented by a single causative agent or instead be the result of the sum of several factors. These factors are classified into four groups: predisposing factors, primary causes, secondary causes and perpetuating factors.

Predisposing factors are those conditions that increase the risk of developing otitis externa. Alone, these factors are not capable of causing the disease; in association with primary or secondary causes they may however contribute to its development and may promote relapses.

OTITIS EXTERNA: PREDISPOSING FACTORS

  • ANATOMICAL CONFORMATIONOF THE PINNA and of the EAR CANAL
  • CLIMATIC CONDITIONS SUCH AS INCREASED HUMIDITY and ENVIRONMENTAL TEMPERATURE
  • PRESENCE OF EXCESSIVE HAIR IN THE EAR CANAL
  • TRAUMATIC INJURY OF THE EAR CANAL (e.g., bite wounds)
  • EAR CANAL OBSTRUTIVE CONDITIONS

Primary causes include all those conditions which are causal, even alone, of otitis externa.


OTITIS EXTERNA: PRIMARY CAUSES
  • PARASITES
  • ALLERGIC DISEASE
  • ENDOCRINOPATHIES
  • AUTOIMMUNE DISEASES
  • FOREIGN BODIES
  • SEBACEOUS GLAND HYPERPLASIA

Secondary causes include all those agents and factors that by overlapping with the primary and predisposing causes may contribute to the development of otitis externa. They include bacteria, yeasts or adverse contact reactions that can result from the use of auricular preparations.

Perpetuating factors hinder the healing of otitis and include the concomitant presence of otitis media and/or the presence of progressive pathological alterations such as oedema, dermofibrosis, ceruminous and sebaceous gland hyperplasia.

The prevalence of otitis externa in the cat is significantly lower compared to that of the dog. The prevalence of the disease differs between the two species, probably because of the different ear canal anatomy and microclimate, but also because of the various factors that are commonly involved in the development of this condition. The different ear anatomy and length and diameter of the outer ear canal between the dog and the cat certainly play a key role in ear disease susceptibility and surely influences the diagnostic and therapeutic approach.

 

OTITIS MEDIA


Otitis media (OM) is a disease of the middle ear; it is frequent but unfortunately it is often under diagnosed. Important differences in the aetiology of the disease exist between the cat and the dog, determining a different diagnostic and therapeutic approach in the two species. For example, in the dog, OM is frequently the consequence of a descending bacterial infection, while in the cat it is often associated with the presence of inflammatory proliferations within the middle ear.

The middle ear is an air-filled cavity interposed between the outer and the inner ear in the petrous portion of the temporal bone. Separated from the outer ear by the tympanic membrane, and from the inner ear by the round (cochlear) and oval (vestibular) windows, the middle ear communicates with the nasopharynx via the auditory tube, also known as the Eustachian tube.

The tympanic membrane is a thin and semi-transparent membranous structure that separates the outer ear from the middle ear. It is divided into two parts:

  • pars tensa: of greater size, shiny, with the handle of the malleus visible;
  • pars flaccida: more opaque, pink or white, it can be quite prominent in the dog.

The middle ear is formed by the tympanic cavities, by the opening of the auditory tube and by the ossicular chain (malleus, incus and stapes), with their associated muscles and ligaments.

The tympanic cavities include:

  • epitympanic recess: dorsal to the TM, it is occupied by the malleus, incus and the chorda tympani (branch of the facial nerve);
  • ventral cavity: located within the tympanic bulla of the temporal bone, it contains the opening of the auditory tube. In the cat, this cavity is separated into two compartments by a thin, incomplete bony septum: the dorsolateral and the ventromedial compartments (Fig. 1).

The periosteum of the tympanic cavity is covered by a lamina propria consisting of a modified respiratory system-type epithelium (simple squamous or cuboidal epithelium with rare cilliate and secretory cells). Consequently, in the course of chronic inflammation of the middle ear not only is an accumulation of keratin secondary to epithelial hyperplasia present, but also of mucus.

The auditory tube starts in the dorsolateral wall of the nasopharynx and ends in the rostrodorsomedial wall of the tympanic bulla; it is is lined with an epithelium similar to that of the nasopharynx (cuboidal, pseudostratified mucociliary epithelium). Cilliate cells are more numerous in the proximal part of the tube, a factor that certainly helps to limit the upward migration of bacteria from the upper respiratory tract. Its function is to balance air pressure on both sides of the tympanic membrane; this is achieved through its proximal opening, which is regulated by the action of the levator and tensor veli palatini muscles.

The ossicular chain, consisting of the malleus, incus and stapes, and the two associated muscles (the tensor tympani and the stapedius), connect the eardrum to the vestibular window and transmit vibrations from the membrane to the perilymph fluid of the inner ear (Fig. 2).

In the course of otitis media the epithelium lining the tympanic cavity becomes hyperplastic and cells increase their secretory capacity. The connective tissue becomes oedematous and infiltrated by inflammatory cells.

As a consequence ofthese events an exudate is formed. Epithelial breaks are at times present, allowing the proliferation of connective tissue, which generates granulation tissue that can propagate within the tympanic cavity.

The most frequent causesof otitis media differ considerably between the dog and the cat. This difference certainly reflects differences in the aetiology of auricular diseases. In summary, the causes of OM in the dog and cat can be classified into primary and secondary causes.

OTITIS MEDIA: PRIMARY CAUSES

  • MASSES:
    • INFLAMMATORY POLYPS
    • NEOPLASMS
  • ALTERATIONS OF HOMEOSTASIS:
    • PRIMARY SECRETORY OTITIS MEDIA
    • FOREIGN BODY, TRAUMA
  • FOREIGN BODIES
  • SEBACEOUS GLANDS HYPERPLASIA

Secondary causes include bacteria and yeasts, just as in otitis externa.

Most frequent causes of OM in the dog:

  • Extension of an otitis externa (no doubt the most common cause of OM in the dog).
  • Inflammatory polyps: rare and usually present in adult males. The aetiology and pathogenesis are unknown. Although they may form de novo, in some cases they are associated with a chronic inflammation of the ear. The clinical signs may be bilateral or unilateral and attributable to an OM with or without an OE. The infectious agents can reach the middle ear hematogenously (very rare), through the auditory tube or the tympanic membrane.
  • Neoplasms: not very common; they usually consist in the progression of a neoplasm originating in the ear canal.
  • Primary secretory OM: its aetiology and pathogenesis is unknown, however the most likely causes are an increased mucus production secondary to chronic inflammation or its decreased drainage as a result of a decreased diameter of the auditory tube (stenosis of inflammatory origin or anatomical alteration). The most commonly affected dog breed is the Cavalier King Charles Spaniel and the clinical signs include neck pain, neurological signs, pruritus with or without signs of OE. The diagnosis is by examination of the tympanic membrane, which is intact but bulging, and by myringotomy, that highlights an accumulation of mucus within the cavity. Treatment consists in the removal of the mucus by lavage of the tympanic bullae.
  • Congenital palatine defects: in the dog these defects may be a predisposing factor for diseases of the middle ear.

The most frequent causes of OM in the cat are:

  • Inflammatory polyps: this is the most frequent cause of OM in the cat. The presence of polyps in the middle ear is frequently associated with secondary bacterial OM, which in most cases disappears after the surgical removal of the polyps.
  • Infection of the upper airways: infections of the nasopharynx are frequently associated with ascending infections (through the auditory tube) of the middle ear.
  • Neoplasms: few cases have been described, among which carcinoma and lymphoma.
  • Congenital palatine defects: only described in one cat. In this species the prevalence of congenital palatine defects is very low compared to the dog.

CLINICAL SIGNS ASSOCIATED WITH OUTER AND MIDDLE EAR DISEASES OF THE DOG AND CAT         
  • Head TILTING and SHAKING
  • EAR SCRATCHING
  • PRESENCE OF FOUL-SMELLING PURULENT OR HAEMORRHAGIC EXUDATE (Malassezia infections)
  • EAR PAIN ON PALPATION (Pseudomonas infections)
  • LOCAL SWELLING AND BLEEDING (traumatic lesions)
  • EVIDENT TISSUE PROLIFERATIONS (neopasms and hyperplasia)
  • DYSPHAGIA AND RESPIRATORY SOUNDS (nasopharyngeal polyps of the cat)
  • PAIN when OPENING THE MOUTH and on PALPATION of the TEMPOROMANDIBULAR JOINT (otitis media)
  • FACIAL NERVE DEFICITS (absence of blink reflex, lip and palpebral ptosis)
  • HORNER'S SYNDROME
  • PERIPHERAL AND CENTRAL VESTIBULAR SIGNS (loss of balance, nystagmus, rolling).

The evaluation of the patient with an outer or middle ear disease of surgical interest may include: general physical examination, comprehensive dermatological examination and investigation of the ear, otoscopy or video-otoscopy, radiography, computed tomography (CT) or magnetic resonance imaging (MRI).

The observation of the subject at a distance allows to appreciate any particular head position, such as a head tilt, which may be suggestive of otitis media, while a sharp and aggressive reaction evoked by the simple act of touching the affected ear is suggestive of the presence of severe pain.

The skin of the pinna is often involved in the inflammatory process; lesions that may be observed inlcude redness, skin thickening and self-induced trauma.

Palpation of the ear canal allows to appreciate the possible presence of proliferative alterations and/or calcifications as well as to assess the presence of itching or pain.

Otoscopy allows to examine the external ear canal, to identify the presence of foreign bodies and to assess the integrity of the tympanic membrane. It should however be noted that with this examination the tympanic membrane is at times not fully visible; in doubtful cases special investigations such as video otoscopy are necessary.

Myringotomy is a procedure that consists in making an incision in the tympanic membrane in order to collect tissue samples for cytology/histology and culture examinations (Fig. 3). The description of the myringotomy execution technique is beyond the scope of this article.

Radiography remains the most commonly used diagnostic imaging modality used by the veterinarian. It is of easy execution and it is cost effective. Its sensitivity (70%) is however inferior to that of CT or MRI. The radiographic views necessary are a dorsoventral view, an open-mouth view and a lateral-oblique view, the latter being certainly the most sensitive. An increased radiopacity within the tympanic cavity is suggestive of the presence of exudate or of soft tissue, such as inflammatory polyps. Another sign of middle ear disease is the presence of bone alterations such as lysis or bone proliferation (Fig. 4). The radiographic study should be performed before the flushing of the ear, as in an animal with a tympanic membrane lesion the leakage of fluid within the middle ear could result in misinterpretation of the radiographs. A limitation of radiographic studies is the presence of sclerotic alterations observed in the bullae of older dogs, which cannot be differentiated from proliferative lesions present in the course of otitis media.

CT and MRI are considered complementary examinations. Their sensitivity is higher than that of radiographs. CT allows an accurate assessment of bony structures, while MRI provides a better soft tissue contrast resolution (Figs. 5, 6 and 7).

The surgical treatment of outer and middle ear diseases entails the complete excision of the external auditory canal (TECA- Total Ear Canal Ablation) associated with the opening of the latero-ventral wall of the tympanic bulla (LBO- Lateral Bulla Osteotomy) in order to allow the surgical cleaning of the tissue/material contained in it. In the cat, given the higher prevalence of pathologies affecting the tympanic bulla, the most frequently performed surgical treatment is VBO (Ventral Bulla Osteotomy). Techniques used in the past, such as the Zepp procedure or the vertical ear canal resection are no longer indicated or habitual and therefore will not be described in this dissertation.

 

TECA-LBO (Total Ear Canal Ablation - Lateral Bulla Osteotomy)


Dogs with bilateral chronic otitis should be treated with two different surgical sessions, separated by a period of at least 4 weeks. Apart from ensuring better post-operative pain management, this strategy also allows to reduce the risk of respiratory problems, which could result from the oedema or swelling of the surgical area. It is important to remember that patients with chronic ear disorders are at risk for profuse intraoperative bleeding.


TECA-LBO: INDICATIONS IN THE DOG
  • END-STAGE OTITIS: (end-stage chronic proliferative otitis) obstruction of the horizontal and vertical canal.
  • PERSISTENT OTITIS EXTERNA NOTWITHSTANDING MEDICAL TREATMENT
  • NEOPLASMS
  • AUDITORY CANAL COLLAPSE and STENOSIS
  • SEVERE TRAUMA OF THE AUDITORY CANAL  
  • PARA-AURICULAR ABSCESS
  • INTRACTABLE OTITIS MEDIA

TECA-LBO: INDICATIONS IN THE CAT
  • NEOPLASMS (ceruminous gland ACA, SCC)
  • POLYPS (middle and outer ear, nasopharynx)
  • CHRONIC OTITIS EXTERNA and MEDIA

SURGICAL TECHNIQUE
The pinnain its entirety and the side of the head must be shaved and aseptically prepared for surgery. The dog is placed in lateral recumbency, with a pillow under the head in order to tilt it by around 30 degrees (Fig. 8). With a scalpel blade No. 10, a circular incision is made around the opening of the external auditory canal that includes all the hyperplastic tissue of the pinna (Fig. 9); the sharp incision must include the cartilage. One must be careful not to compromise the vascularity by resecting by mistake the vessels located on the dorsal surface at the base of the pinna.

Completed the incision, the cartilage is grasped with a Babcock or Backhaus tissue holding forceps, so as to allow the movement of the cartilage when necessary during the dissection of the ear canal (Fig. 10). The first step is the dissection of the vertical ear canal (A). The muscles are gently separated from the ear canal, trying to stay as adherent as possible to the cartilage, so as not to damage the facial nerve. The blunt dissection is made with Metzenbaum scissors proceeding towards the horizontal portion (B) of the canal. It is important to remember that the facial nerve exits the skull through the stylomastoid foramen, caudal to the auditory meatus, and runs caudally and ventrally to the horizontal ear canal, in close proximity of the junction between the horizontal and the vertical canal (Figs. 11 and 12).

In this region, traction of the soft tissues must be exerted very gently, in order to avoid neuropraxia. Gelpi retractors may be used, but they should be placed superficially with regard to the facial nerve. The author of this article also frequently uses Langenbeck retractors. For blood loss control the use of bipolar electrocautery is recommeded, however its use must be avoided when in proximity of the facial nerve. Once the blunt dissection of the ear canal has been completed an incision is made with a No. 11 blade in the transition point between the horizontal canal and the osseus portion of the acoustic meatus. It is advisable to make the incision of the ear canal in its most caudal portion, so as to reduce the risk of injuring important structures such as blood vessels and the facial nerve. The complete removal of the canal is performed by resecting ¼ of the circumference of the canal at a time, until complete separation from the base of the bone. Another important anatomical aspect to consider is the presence of the retroarticular vein that originates from the retroarticular foramen which is cranial to the osseus portion of the acoustic meatus and caudal to the temporomandibular joint (Figs. 11 and 12).

Once the ear canal ablation has been completed, the surgery is continued with the removal of the osseus portion of the auditory meatus, using bone rongeurs and being careful to avoid damaging the facial nerve (Fig. 13). It is also important not to damage the external carotid artery and the maxillary vein. In case of injury to these vessels, profuse bleeding will occur. The management of this complication requires the suspension of the intervention and compression of the region with gauzes soaked in saline solution for at least 5 minutes.

In order to perform the lateral tympanic bulla osteotomy the soft tissues are elevated from the bone base of the tympanic bulla with a periosteal elevator and a rongeur is used to open the ventrolateral portion of the bulla by about 1-1.5 cm. Do not use the rongeur to remove the rostral portion of the bulla as there is the risk of injuring the epitympanic recess. Once the osteotomy of the bulla has been performed, it is imperative to completely remove the residues and the lining epithelium of the bulla. This is done with the aid of a curette or Volkmann spoon and hemostats in order to grasp the tissue fragments in depth. Equally important is to take a sample from the bulla to be sent for histology and bacteriology. The removal of the inner lining of the bulla allows the exposure of the white and translucent bony wall of the tympanic cavity. Once the debridement of the bulla has been completed a low pressure (to avoid barotrauma) pre-warmed saline flushing is performed and the surgical wound is then closed with monofilament absorbable suture material such as poliglecaprone 25 3-0 or 4-0 depending on the size of the patient.

The skin suture must be accurate and must completely cover the exposed cartilage (Figs. 14 and 15). The skin may be sutured with monofilament absorbable suture material such as poliglecaprone or with non-absorbable monofilament suture material such as nylon, with a simple interrupted suturing technique. The use of drains or bandages is not necessary.

The applicationof ice packs on the surgical area, wrapped in a soft towel, for 10 minutes every 4 hours for the first 24 hours and then every 6-8 hours for the next three days, is instead recommended. Also recommended is the administration of a broad-spectrum antibiotic, which may then be changed if necessary on the basis of the culture results. In the post-operative period it is also necessary to monitor the presence or absence of the palpebral reflex, the eventual presence of additional signs of paralysis/neuropraxia of the facial nerve as well as of any palpebral and lip ptosis. In case of palpebral reflex deficit the use of an ophthalmic lubricant until complete recovery of the reflex is necessary.


TECA-LBO: COMPLICATIONS
  • INTRA-OPERATIVE:
    • HAEMORRHAGE
    • FACIAL NERVE INJURY
    • THICKENING OF THE HORIZONTAL CANAL THAT MAKES THE DISSECTION DIFFICULT WITH THE RISK OF FACIAL NERVE INJURY
  • SHORT-TERM (1-14 DAYS):
    • FACIAL NERVE DEFICIT
    • VESTIBULAR SYNDROME Fig. 16
    • HAEMORRHAGE Figs. 17-18
    • WOUND DEHISCENCE
    • PINNA NECROSIS
  • LONG-TERM:
    • FACIAL NERVE PARALYSIS
    • PARA-AURAL ABSCESS
    • HEAD TILT
    • SCRATCHING AND EAR PAIN

 

VBO (Ventral Bulla Osteotomy)


VBO is the electivesurgical procedure for the treatment of middle ear diseases. Although the procedure can be performed in both species (dog and cat), it is more frequently performed in the cat. In fact, as already described, middle ear diseases of the dog are almost always related to disorders of the external ear canal and the tendency is therefore to combine a lateral approach to the tympanic bulla with the ablation of the ear canal.


VBO: INDICATIONS IN THE CAT
  • MIDDLE EAR DISEASES:
    • NASOPHARYNGEAL POLYPS
    • NEOPLASMS
    • TYMPANIC BULLA OSTEOMYELITIS
    • OTITIS MEDIA REFRACTORY TO TREATMENT

SURGICAL ANATOMY
In view of the complexity and delicacy of this anatomical region, before approaching this type of surgery it is recommended to revise the surgical anatomy of the area involved. The tympanic bulla of the cat consists of two compartments: the dorsolateral and the ventromedial compartments, separated by an osseus septum inside the bulla (Fig. 19). However, the septum is not intact dorsally, and the two compartments communicate through a fissure. Postganglionic sympathetic nerve fibres, originating from the cranial cervical ganglion, run together with the internal carotid artery and pass through the tympano-occipital foramen, caudal to the bulla, between it and the petrous bone, and join the glossopharyngeal nerve (Fig. 20). They penetrate the tympanic bulla at the level of the oval promontory, medial to the septal fissure, and give rise to the tympanic plexus. The tympanic plexus is exposed on the surface of the oval promontory and this makes the fibres particularly vulnerable to surgical insult. A lesion of this plexus is the underlying cause of Horner's syndrome, characterized by miosis, protrusion of the third eyelid, enophthalmos and palpebral ptosis. The tympanic plexus crosses the promontory and enters the dorsolateral compartment through the fissure before reaching the eye, joining the ophthalmic branch of the trigeminal nerve. Through the tympanic bulla also run parasympathetic fibres that innervate the parotid and mandibular gland. Parasympathetic fibres are less frequently affected by iatrogenic damage.

SURGICAL TECHNIQUE
To perform the surgery the patient is positioned in dorsal recumbency, with a soft support under the cervical region in order to extend the neck and maximize the exposure of the area. All the cervical, intermandibular and submandibular areas must be clipped and aseptically prepared for surgery (Fig. 21). The tympanic bulla is at the centre of an imaginary triangle the sides of which join the larynx, mandibular angle and chin. A 3-5 cm incision is made within this area. The incision is paramedian, parallel to the trachea and exactly above the bulla (Fig. 22). The dissection continues through the platysma and the sphincter muscles of the neck. The mandibular salivary gland and the bifurcation of the linguofacial vein meet at this point and are retracted laterally. The surgery continues via blunt dissection, separating the digastric muscle from the styloglossus muscle laterally and from the hyoglossus muscle medially. Medial to the hyoglossus muscle is the hypoglossal nerve, which is not to be damaged and is to be gently retracted medially (Fig. 23).

Once the tympanic bulla has been reached, recognizable by its bone consistency and for the particular spherical shape, two Gelpi retractors are gently applied to keep the soft tissues apart, and a periosteal elevator is used to free the tympanic bulla from the periosteal lining (Fig. 24). Steinmann pins mounted on a hand drill or a very large-size needle (16 gauge) are then used to open the tympanic bulla. The bulla is entered being careful not to break through the contralateral wall and hence the inner ear at the level of the ventromedial compartment (Figs. 25 and 26).

The initial opening is then expanded with a small rongeur or with a mosquito forceps with small teeth. As soon as the opening is complete a sterile sample should be taken for the execution of a bacteriological examination and for an antibiogram test (always!). The liquid content of the bulla is suctioned with an aspirator and the curettage of the tympanic bulla is performed with a small Volkmann spoon and surgical tweezers, removing the pathologic tissue that will be sent for the histological examination (always!!!). Once again, the curettage should be performed gently. A violent curettage at the level of the oval promontory can in fact result in injury to the tympanic plexus with consequent Horner's syndrome. The septum that separates the two compartments in the cat is removed with the aid of a very fine rongeur or with mosquito forceps (Fig. 26).

Once the curettage has been completed the bulla is lavaged. The flushing pressure must be contained in order to avoid any barotrauma. The surgical incision is routinely closed with an absorbable monofilament suture. The skin may be be sutured with nylon, metal staples or glue.

VBO: COMPLICATIONS

  • HORNER’S SYNDROME Fig. 27
  • VESTIBULAR SYNDROME (head tilt, nistagmus, ataxia)
  • RELAPSE OF THE RHINOPHARINGEAL POLYP
  • OTITIS MEDIA
  • HAEMORRHAGE
  • DAMAGED HYPOGLOSSAL NERVE
  • DAMAGED FACIAL NERVE
  • FISTULAE

 

Suggested reading


  1. Bellah JR. Surgical disesaes of the ear. Standards of care emergency and critical care medicine 2006;Vol 8.5:1-12.
  2. Donnelly KE. Feline inflammatory polyps and ventral bulla osteotomy. Compendium Continuing Education for Veterinarians 2006;June:446-454.
  3. Ordeix L. Otite esterna nel gatto. Societa’ Italiana di Dermatologia Veterinaria 2005.
  4. Ordeix L. Otite esterna e media nel cane e nel gatto. Societa’ Italiana di Dermatologia Veterinaria 2005.
  5. Scarampella F. Otite esterna nel cane. Societa’ Italiana di Dermatologia Veterinaria 2005.
  6. Smeak DD. Lateral approach to the subtotal bulla osteotomy in dogs: anatomy and procedural details. Compendium Continuing Education for veterinarians 2005;May:377-385.