Zygomatic Sialadenitis as a Rare Cause of Exophthalmos in a Dog

ABSTRACT

Objective

To describe the clinical presentation, diagnostic findings, and surgical management of zygomatic sialadenitis associated with retrobulbar disease in a dog following extensive dental extractions.

Animals Studied

A 10‐year‐old spayed female Cavalier King Charles Spaniel.

Procedures

The dog was evaluated for acute‐onset right‐sided exophthalmos that developed after a recent dental procedure involving 15 extractions. Ophthalmic examination identified marked exophthalmos, pain on opening of the mouth, lagophthalmos, and a superficial corneal ulcer. Computed tomography (CT) of the head was performed and revealed a tubular fluid‐filled structure likely consistent with a retrobulbar abscess and right‐sided zygomatic sialadenitis. Samples for cytology and culture were obtained. Initial medical management included intravenous fluids, broad‐spectrum systemic antibiotics, analgesics, topical antibiotics, and ocular antihypertensive medications.

Results

Cytology revealed septic suppurative inflammation. Microbial culture identified Bacteroides pyogenes , an anaerobic organism not typically associated with antimicrobial resistance. Histopathology confirmed subacute zygomatic sialadenitis with associated cellulitis. Due to progressive clinical deterioration and vision loss, transpalpebral exenteration with zygomatic sialoadenectomy was performed. Postoperative recovery was uneventful, with complete resolution of periocular swelling and pain on follow‐up examination.

Conclusions

Zygomatic sialadenitis should be considered a differential diagnosis for retrobulbar disease in dogs, particularly when cases are refractory to medical management. In this case, persistent salivary secretions likely contributed to ongoing inflammation and clinical signs. Advanced imaging facilitated accurate diagnosis, and surgical removal of the affected gland was necessary for definitive resolution.

1. Introduction

Zygomatic sialadenitis, while uncommon, represents a clinically significant cause of orbital disease in dogs that can mimic more common conditions and complicate management [1, 2, 3]. The zygomatic salivary gland is ventrolateral to the globe, where it rests on the dorsolateral surface of the medial pterygoid muscle and forms much of the orbital floor [2, 4]. Any change in the size of the gland, secondary to inflammation or infection, can lead to globe displacement. The resultant clinical signs, including exophthalmos, decreased retropulsion, third eyelid protrusion, and pain upon mouth opening, are the same as those observed in other retrobulbar inflammatory conditions [1, 2]. In more advanced cases, systemic signs such as lethargy, anorexia, and pyrexia may also be present [1, 2].

Although multiple etiologies including trauma, immune‐mediated, and systemic or local infection have been suggested, the etiology remains largely unknown [2]. Due to the overlap of clinical signs with other retrobulbar diseases, advanced imaging modalities such as ultrasonography, computed tomography (CT), or magnetic resonance imaging (MRI) are necessary for definitive diagnosis [2, 3].

This case report describes a case of zygomatic sialadenitis in a dog, which presented after routine periodontal treatment and was unresponsive to medical treatment for retrobulbar cellulitis. This report highlights zygomatic sialadenitis as an important element of the differential diagnosis for orbital disease in dogs and offers practical clues that can prompt earlier surgical intervention and improve the likelihood of globe preservation.

2. Case Summary

A 10‐year‐old female spayed Cavalier King Charles Spaniel dog was presented to a tertiary referral hospital for evaluation of progressive exophthalmos of the right eye (OD—oculus dexter). One week prior to presentation, the primary veterinarian had carried out an anesthetized periodontal treatment and extraction of 15 teeth. Carprofen (4 mg/kg PO q24 h, for 6 days) and clindamycin (11 mg/kg PO q12 h, for 1 week) were prescribed at discharge. Four days prior to presentation, the patient returned to the primary veterinarian for evaluation of lethargy and hyporexia. Mild pain was noted in the mandibular right quadrant in the mouth. Vital signs and the remainder of the physical exam were recorded as normal. Maropitant (2 mg/kg PO q24 h, for 4 days) and gabapentin (14 mg/kg PO q12‐24 h, for 3 to 6 days) were prescribed. Following discharge, progressive periorbital swelling leading to exophthalmos OD was noted. Hours before presentation to the hospital, the patient again presented to the primary veterinarian, who noted discomfort when opening the mouth, buphthalmia, a raised third eyelid, and decreased retropulsion OD. Emergency referral to an ophthalmologist was recommended.

Upon presentation to the referral hospital, the patient was quiet but responsive with a rectal temperature of 103.5°F. On physical examination there was a Grade V/VI systolic heart murmur. There was severe exophthalmos and lagophthalmos, a superficial corneal ulcer, accompanied by firm, warm periocular swelling, a raised and hyperemic third eyelid, marked chemosis of the bulbar conjunctiva, and moderate aqueous humor flare (2–3+) and cell (2+) (Figure 1). The menace response and dazzle reflex were absent OD. Examination findings of the left eye (OS—oculus sinister) were largely unremarkable, except for the presence of asteroid hyalosis. The intraocular pressures were 98 mmHg OD and 17 mmHg OS (TonoVet: Icare, Finland Oy). High‐frequency ultrasound biomicroscopy with a 29–71 MHz probe (UHF70; Visual Sonics Vevo MD; Fujifilm, WA, USA) was performed to evaluate the iridocorneal angle and associated structures. Evaluation revealed multifocal hyperechoic suspended debris in the anterior chamber, a diffusely hyperechoic and thickened iris, and complete ciliary cleft collapse (Figure 2). A complete blood count (CBC) and a chemistry panel revealed a mild normocytic, normochromic non‐regenerative anemia, macrothrombocytopenia, mild neutrophilia with a left shift, and a mild lymphocytosis.

FIGURE 1.

Gross image of the right eye (oculus dexter, OD) of a 10‐year‐old female spayed Cavalier King Charles Spaniel presented for evaluation of progressive exophthalmos. Notable findings include severe exophthalmos, a raised and hyperemic third eyelid, and marked chemosis of the bulbar conjunctiva. Moderate lagophthalmos is present, leading to corneal desiccation and the development of a geographic axial superficial corneal ulcer. Additionally, miosis is observed that corresponds to anterior uveitis.

FIGURE 2.

High‐frequency ultrasound biomicroscopy (29–71 MHz) from the nasal iridocorneal angle. Multifocal hyperechoic debris is present within the anterior chamber (AC), with a diffusely hyperechoic, thickened iris (black asterisk) indicating anterior uveitis. There are no discernable ciliary cleft structures present (boxed).

The patient was hospitalized for medical therapy and to perform an anesthetized computed tomography (CT) scan of the head the following day. Intravenous (IV) fluids (0.45% NaCl with added 0.05 mEq/kg/h KCl) were started at a low maintenance rate (30 mL/kg/day) to avoid fluid overload in light of previously diagnosed mitral valve disease. Overnight therapy included ampicillin/sulbactam (30 mg/kg every 8 h), enrofloxacin (10 mg/kg every 24 h), methadone (0.3 mg/kg every 6 h), ondansetron (0.5 mg/kg every 8 h), maropitant (1 mg/kg every 24 h), intraocular pressure‐lowering agents (dorzolamide and timolol OD every 8 h, and latanoprost OD every 24 h), topical antibiotics (neomycin‐polymyxin‐bacitracin ophthalmic ointment OD every 8 h), and a topical carbomer gel lubricant (OD every hour).

The following morning, the patient was dull with no improvement of the exophthalmos OD. Intraocular pressure was 40 mmHg OD (TonoVet). An anesthetized CT scan was performed. A nonionic iodinated contrast medium (iohexol; Omnipaque 350 mg/mL; Chicago, IL) was administered intravenously at a dose of 2 mL/kg. All CT images were acquired with a 64‐slice multidetector CT scanner (SOMATOM Sensation 64, Siemens Medical Systems, Malvern, PA). Acquisition parameters included 130 kVp, 38 mA, an exposure time of 1500 ms, and a helical pitch of 0.55. Images were reconstructed with a 161 mm reconstruction diameter and a 512 × 512 image matrix. Images were reconstructed with a soft‐tissue algorithm at 1.0 mm slice thickness (window width 400 HU; window level 40 HU) and a bone algorithm at 0.75 mm slice thickness (window width 2000 HU; window level 400 HU). CT revealed a large, branching, tubular, fluid‐filled, peripherally contrast‐enhancing structure within the soft tissues along the right margin of the calvarium and medial orbital wall causing marked exophthalmos OD and compression of the globe and ophthalmic plexus with regional cellulitis, myositis, and right zygomatic sialadenitis (Figure 3). The right zygomatic salivary gland was mildly enlarged, showed mildly reduced contrast enhancement relative to the contralateral side, and was displaced rostromedially, and the right deep facial vein within the gland was not identified, likely secondary to compression; overall, these findings were considered most consistent with zygomatic sialadenitis. There was no evidence of foreign material within the structure. Septic retrobulbar cellulitis and abscess formation were prioritized and suspected to be related to the patient's history of dental disease and recent dental surgery. Neoplastic etiologies could not be excluded but were considered unlikely due to the acute onset of clinical signs. There was moderate periodontal disease of both maxillary first molars, multiple absent teeth including: incisors, rostral premolars, and caudal molars consistent with the reported extractions, and multiple retained roots in the maxillary right and both mandibular quadrants. There was moderate bilateral mandibular, medial retropharyngeal, and parotid lymphadenopathy, more pronounced on the right, and was considered to be most likely reactive.

FIGURE 3.

Transverse (A, C) and dorsal (B, D) post‐contrast CT images. Severe soft tissue swelling involving the right side of the face and head is present (white arrows), with a branching, tubular, fluid‐filled, peripherally contrast‐enhancing structure along the right calvarial margin and medial orbital wall (black arrows). Marked right‐sided exophthalmos and compression of the globe are noted. The right ophthalmic plexus and deep facial vein are not identified, likely secondary to compression (black asterisk: Normal left ophthalmic plexus; white arrowhead: Normal deep facial vein). The right zygomatic salivary gland is mildly enlarged and demonstrates rostromedial displacement and mildly reduced contrast enhancement relative to the contralateral side (white asterisk).

The CT of the head was followed by ultrasound‐guided sampling of the retrobulbar region. Approximately 6 mL of thick sanguinopurulent fluid was aspirated. Following aspiration, there was no obvious improvement of the exophthalmos OD. In an attempt to continue to drain the fluid, a small incision through the nasal bulbar conjunctiva with Wescott tenotomy scissors was made. Only a small amount of additional fluid drained out through the incision. A temporary tarsorrhaphy was placed at the lateral canthus OD due to persistent lagophthalmos. Cytologic analysis of the aspirated fluid revealed necrotic debris and septic suppurative inflammation with both cocci and rod bacteria. A portion of the aspirated fluid was submitted for anaerobic and aerobic culture and antibiotic susceptibility.

The patient recovered uneventfully from general anesthesia and was hospitalized for continued medical therapy. Changes made to the original hospitalization plan included decreased dose and frequency of methadone (0.2 mg/kg every 8 h), and the addition of dexamethasone SP (0.1 mg/kg every 24 h).

Due to a lack of improvement in clinical signs during the next 2 days, further evaluation of the CT and a case review from a board‐certified veterinary dentist was pursued. Based on concerns for a zygomatic salivary gland infection and the grave prognosis for vision OD, transpalpebral exenteration OD and right‐sided zygomatic sialoadenectomy were recommended. Following removal of the globe, the ventral periorbital fascia was dissected to reveal the zygomatic salivary gland. The attachments around the gland were dissected using a combination of blunt and sharp dissection, and a dental periosteal elevator was used to elevate the gland off the zygomatic arch. The gland was then transected at its base. On gross evaluation, the salivary gland was friable, and mottled purple and pink. The orbit was flushed thoroughly with sterile saline solution. Prior to complete closure, a bupivacaine splash block was administered into the orbit. The patient recovered uneventfully from general anesthesia and was discharged the following day with a 14 day course of amoxicillin clavulanate (18 mg/kg q12h), and enrofloxacin (10 mg/kg q24 h), a 7 day course of gabapentin (10 mg/kg q8‐12 h), and a tapering dose of prednisone (1.4 mg/kg/day for 2 days, 0.7 mg/kg for 4 days, then 0.35 mg/kg for 4 days). The microbial culture results had returned on the day of discharge and had revealed B. pyogenes. Susceptibility to antibiotics was not evaluated since the organism did not meet requirements for routine susceptibility testing.

Histologic evaluation of the eye revealed neutrophilic keratitis, a pre‐iridal fibrovascular membrane (PIFM), and infiltration of melanomacrophages in the trabecular meshwork (Figure 4A,B). The retina did not appear atrophied, but there was evidence of optic nerve damage evidenced by myelin swelling and spheroid formation (Figure 4C,D).

FIGURE 4.

Histology of ocular lesions. (A) While the angle is open, the ciliary cleft (three arrowheads) is narrowed, and the trabecular meshwork (star) is partially collapsed and infiltrated by pigment‐laden macrophages (yellow dashed line). 20× objective. (B) The anterior surface of the iris is lined by non‐pigmented spindle cells with occasional empty vascular lumen (arrows). 60× objective. (C) The posterior portion of the optic nerve (to the left of the black dashed line) has increased white spaces indicative of myelin swelling. 10× objective. (D) Higher magnification of the affected portion of the optic nerve confirms myelin swelling with occasional swollen axons, or spheroids (black arrows). 60× objective.

Histologic evaluation of the zygomatic salivary gland and third eyelid revealed marked adenitis, conjunctivitis, and cellulitis as well as acinar atrophy of the salivary gland (Figure 5). Due to the chronicity of lesions within the salivary gland compared to that within the third eyelid and the tracking of inflammation along the fascial planes of musculature and adipose tissue, primary sialadenitis was considered most likely. No overt infectious etiologies were observed.

FIGURE 5.

Histology of periocular adnexa. (A) Nictitans. The conjunctiva is regionally ulcerated, and the underlying stroma is expanded and distorted by proliferative granulation tissue (asterix) mixed with hemorrhage overlain by a hemorrhagic and serocellular crust (arrow). 4× objective. (B) Orbital soft tissue and striated muscle (bottom of image). Expanding the interstitium and extending into the perimysium of the adjacent striated muscle is regionally extensive edema mixed with neutrophilic inflammation. There are multiple fibrin thrombi (arrows). 10× objective. (C) Zygomatic salivary gland. The acini are diffusely atrophied with multifocal dilated lumen (arrows). Non‐atrophied acinus outlined by black circle. The dilated lumen contain low numbers of neutrophils and macrophages (arrowheads). The interstitium contains mild edema and pigment‐laden macrophages (asterix). 20× objective.

The patient presented for an incisional recheck approximately 2 weeks after discharge. The incision was intact, the periorbital swelling had resolved, and the patient was nonpainful on palpation of the enucleation site.

3. Discussion

This case highlights zygomatic sialadenitis as a rare but important differential diagnosis for retrobulbar disease in dogs, particularly when cases are refractory to medical management. Due to its anatomic location and proximity to the globe, the clinical signs corresponding to zygomatic sialadenitis closely resemble those of other retrobulbar diseases [1, 2, 3]. For this reason, advanced imaging, either CT or magnetic resonance imaging (MRI), is essential for diagnosis.

In the present case, several findings support the hypothesis that the infection developed secondary to dental surgery. The major zygomatic papillae are located just caudal to the parotid salivary gland papilla and dorsal to the last maxillary molar [5]. This location corresponds with the CT findings in this case that identified a retained tooth root, and moderate periodontal disease in this region. Although no intraoperative complications were reported by the primary veterinarian, an unrecognized penetrating injury to the zygomatic salivary gland, its duct, or adjacent periorbital tissues during dental extraction cannot be excluded as a potential inciting cause.

Additional evidence to support this is the identification of B. pyogenes, an obligate anaerobe, which is a part of the oral microbiome in cats and dogs [6, 7]. This supports the hypothesis that oral bacteria may have ascended via the zygomatic duct, leading to infection of the gland and formation of a sialocele. Histopathology further supports this hypothesis, as lesions were more chronic within the salivary gland than the third eyelid, with inflammation tracking along adjacent fascial planes, consistent with primary sialadenitis (Figure 5). However, the proposed dental origin remains a presumptive etiology. Other possibilities include a resistant infection or a small foreign body not identifiable on CT [8, 9].

Bacteroides species have been identified in refractory cases of retrobulbar abscesses in dogs [8]. In humans, B. pyogenes has been associated with a range of infections often resulting in hospitalization and the need for intravenous antibiotics [7, 10]. Anaerobic bacterial susceptibility testing is not routinely performed in veterinary medicine due to the specialized handling and laboratory equipment required [11]. In human medicine, resistance of Bacteroides species to commonly used antibiotics, including amoxicillin‐clavulanic acid and clindamycin, is a growing concern [7]. In this case, there is no definitive way to determine whether antibiotic resistance contributed to the patient's clinical outcome or if the poor response to treatment was secondary to sialocele formation and static saliva.

Dogs with orbital abscesses typically respond within two to 3 days to broad‐spectrum antibiotic therapy, anti‐inflammatories, and analgesics [1, 2]. Amoxicillin–clavulanic acid is recommended as an appropriate empirical antibiotic, though other broad‐spectrum agents can be used [2, 11]. In this case, appropriate intravenous therapy was initiated, but clinical improvement was not achieved, which raised suspicion for static saliva from a sialocele contributing to persistent swelling. It's also possible that the viscous nature of the fluid could have hindered effective drainage through the small conjunctival incision.

Surgical intervention involving removal of the zygomatic salivary gland is indicated in refractory cases. In a previous case series describing 11 cases of zygomatic sialadenitis, two cases were refractory to medical therapy and had to be surgically addressed via a lateral orbitotomy with zygomatic gland removal [1]. Various surgical approaches have been described to remove the zygomatic salivary gland while sparing the globe [5, 12]. In the present case the patient was already blind due to uveitis, secondary glaucoma, and presumed optic nerve damage from compressive ischemia, so a globe salvaging procedure was not attempted. Exenteration with concurrent zygomatic sialoadenectomy was therefore pursued. Had the disease been recognized earlier, globe‐sparing surgery may have been considered.

In the above case report glaucoma was diagnosed on presentation based on a markedly elevated intraocular pressure of 98 mmHg. In dogs with inflammatory orbital disease intraocular pressure is generally described as normotensive, so the profound ocular hypertension in this case likely reflects an advanced and atypical manifestation of the disease [1]. The combination of severe retrobulbar inflammation, periorbital swelling, markedly elevated intraocular pressure, and vision loss could be considered consistent with orbital compartment syndrome [13, 14]. Orbital compartment syndrome is more commonly described in humans and occurs when a rapid increase in intraorbital pressure secondary to severe orbital disease compromises the optic nerve and orbital vasculature, potentially resulting in irreversible vision loss [13, 14]. This syndrome has also been reported in two dogs with periorbital and facial abscessation, both of which developed permanent unilateral blindness [14].

The histologically noted myelin swelling and spheroid formation in the optic nerve is consistent with significant damage, presumed secondary to compression from severe retrobulbar inflammation (Figure 4). The arterial and venous supply to the globe run parallel to the optic nerve [12]; thus compression of these structures may have resulted in both impaired ocular perfusion and venous congestion. Obstruction of venous outflow, the terminus of aqueous fluid drainage, may have contributed to the development of acute glaucoma [15].

Additionally, ischemia has been shown to induce the expression of vascular endothelial growth factor (VEGF) as well as other pro‐inflammatory cytokines [16, 17, 18]. VEGF, in particular, has been implicated in the formation of pre‐iridial fibrovascular membranes (PIFM) which develop on the anterior surface of the iris and obstruct the iridocorneal angle and aqueous humor outflow, leading to secondary glaucoma [17, 18]. This mechanism was supported by high‐frequency ultrasound findings in this case which demonstrated complete collapse of the ciliary cleft and marked uveitis. Although PFIMs are typically reported in dogs with chronic inflammation of 2 weeks or longer [17], the severe inflammatory and ischemic insult associated with acute retrobulbar cellulitis in this patient may have accelerated PIFM formation.

Although many clinical signs overlap with other orbital diseases, important diagnostic clues include a history of dental disease or procedures near the zygomatic papilla and lack of improvement despite appropriate medical therapy. In the same case series referenced earlier, 4 of 11 dogs with zygomatic sialadenitis had visible swelling of the papilla intraorally, which may provide an additional diagnostic aid but was not assessed in this patient [2].

This case report underscores the diagnostic and therapeutic challenges associated with zygomatic sialadenitis and its potential to cause severe and sight threatening ocular complications. While uncommon, it should be considered as a differential diagnosis in dogs with orbital disease that do not respond to medical management. This case report emphasizes the need for early recognition, advanced imaging, and surgical intervention in refractory cases to optimize clinical outcomes.

Author Contributions

Danielle Meritet: writing – review and editing. Hans D. Westermeyer: writing – review and editing, conceptualization, investigation, writing – original draft, supervision. Katrina E. V. Jones: conceptualization, writing – original draft, investigation, writing – review and editing. Manabu Kurihara: writing – review and editing.

Disclosure

The authors have not used AI to generate any part of the manuscript.

Ethics Statement

Animal owners or owners' representatives provided written consent for the treatment provided and for the publication of data and images.

Data Availability Statement

Data sharing not applicable to this article as no datasets were generated or analyzed during the current study.