Introduction

Diseases of the salivary gland or duct are uncommon in small animals compared with humans.^1–4 In particular, diseases related to the parotid salivary gland or duct are extremely rare in dogs; only a few cases in dogs have been reported in veterinary literature.^4,5 This report describes a dog with parotid duct ectasia that likely developed subsequently to parotid duct stenosis following ductal incision for sialolith removal.

Case Report

A 3 yr old, 21 kg, spayed female Brittany was presented with a lump on her right cheek of 1 yr duration that would fluctuate in size. The referring veterinarian found a small stone embedded in the right parotid duct by palpation and removed the stone via ductal incision from the oral cavity. After removal of the sialolith, the incision in the duct was closed with 4-0 polydioxanone^a. Three months after surgery, the soft, cylindrical mass was found on her right cheek again, and the mass got bigger when the dog ate. The dog was treated with clindamycin (10 mg/kg per os [PO] q 12 hr) and tramadol (3 mg/kg PO q 12 hr) for 14 days, but the swelling did not resolve. The dog was referred to the University of Konkuk Veterinary Medical Teaching Hospital.

At referral, the right cheek swelling was present, but the dog was otherwise healthy with normal temperature, heart rate, and respiratory rate. The soft-tissue swelling was over the area of the parotid duct on the right side of the face (Figure 1). The cylindrical mass extended from the base of the right ear and to the near the lateral canthus where it tapered to a point.

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Routine hematology and biochemistry profiles were within normal limits. Skull radiographs showed faint mineral opacity ∼1 mm in diameter lateral to the right mandible on the rostrocaudal view (Figure 2). The density was presumed to be a retained sialolith or dystrophic mineralization within the previous surgical site. A 2 × 3 cm ovoid soft-tissue swelling was seen dorsolateral to the mineral opacity. Aspiration of the mass yielded a thick, yellow/tan, mucopurulent fluid. Cytology of the fluid revealed moderately degenerate neutrophils admixed with streaming cellular debris and a basophilic, mucus-like material. No infectious organisms were seen. Microbiological culture resulted in no aerobic or anaerobic growth.

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The dog was premedicated with intravenous dexmedetomidine (4.9 µg/kg) and buprenorphine (0.01 mg/kg). General anesthesia was induced with intravenous propofol (6 mg/kg) and maintained with inhalant isoflurane and oxygen. Cefazolin (20 mg/kg IV) and meloxicam (0.1 mL/kg IV) were administered before surgery. The right side of the face was aseptically prepared, and a carbon dioxide laser^b was used to make the skin incision and dissection. Hemostasis was achieved with electrosurgery and the laser^b. The plastysma muscle and surrounding fascia were incised to dissect the mass from its most rostral and caudal aspects (Figure 3A). The caudal end of the mass was connected to the parotid salivary gland and the rostral portion of the mass tapered to a point that looked like a stricture grossly (Figure 3B). After excision of the rostral end of the mass by the laser^b, the caudal end of the mass was ligated with 3-0 polydioxanone^a and excised immediately rostral to the ligation. An ∼5 mm portion of the parotid gland was removed with the mass. The center of the mass contained mucopurulent fluid with a yellow/tan color similar to what had been aspirated preoperatively (Figure 3C). No sialolith was found inside the mass. The excised mass was submitted for histologic examination. A series of 3-0 polydioxanone^a cruciate sutures was placed in order to eliminate dead space. Intradermal sutures with 3-0 polyglecaprone 25^c were then placed, and the skin was closed with 3-0 nylon^d. The dog recovered uneventfully from anesthesia without perioperative complications. For postoperative analgesia, a continuous rate infusion of buprenorphine (1.6 µg/kg/hr) and lidocaine (1.2 mg/kg/hr) was administered for 24 hr after surgery. Additionally, intravenous cefazolin (20 mg/kg q 8 hr) was administered postoperatively during hospitalization while awaiting culture results. Two days after surgery, the dog was discharged with medications including tramadol (3 mg/kg PO q 12 hr), carprofen (2.2 mg/kg PO q 12 hr), and clavamox (12.5 mg/kg PO q 12 hr). The antibiotic was discontinued when the culture revealed no growth.

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Histopathological examination of the excised tissue revealed a linear fibrous connective tissue lined by columnar epithelium with small to moderate numbers of neutrophils, compatible with duct ectasia (Figure 4A). The fibrous tissue was more abundant in the rostral stenotic region, which was presumed to be the previous surgical site. The parotid salivary gland was normal with distended duct contained inspissated saliva (Figure 4B).

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At discharge from the hospital, the facial swelling was completely resolved. However, the dog had some mild facial paresis on the right side involving only the inferior palpebrum and commissure of the mouth. Facial paresis was improved 2 wk after surgery, and there were no neurological deficits, and no recurrence of the facial swelling 4 mo after surgery.

Discussion

Salivary duct ectasia, defined as a dilated salivary duct, is a rarely reported condition in dogs compared with humans.⁶ In human medicine, salivary duct ectasia is a relatively common disease of the parotid duct, so-called “Stensen’s duct,” as a consequence of intraductal obstruction as a result of sialolith, polyp (papilloma), or ductal stenosis.^7,8 Ductal stenosis can occur secondary to ductal trauma, ductal inflammation, or following sialolithotomy with subsequent ductal fibrosis.⁶ In dogs, the causes of the parotid duct ectasia are similar to those in humans, including parotid duct sialolith, and inflammation around parotid duct and/or its papilla.^4,5,9,10 Additional reported causes in dogs include: transposed parotid duct ligation,¹¹ foreign body trauma,¹² secondary to maxillectomy surgery,¹³ and carnassial abscess¹⁴. In this report, the dog had a history of parotid sailolith and its removal by ductal incision and suturing. Ductal stenosis as a result of the ductal fibrosis occurred at the sialolith extraction site; therefore, it was highly suspected that parotid duct ectasia developed following ductal incision and closure for sialolith removal. Additionally, inappropriate surgical technique of the initial surgery might have encouraged the ductal stenosis. For example, 4-0 polydioxanone used in the initial surgery may have been too large and too long lasting for ductal suturing and as a result could have contributed to the resulting stricture. Another possible cause for parotid duct ectasia in this dog is a small retained sialolith, as was suspected on preoperative radiographs. A retained sialolith could have obstructed the duct and caused eventual ectasia. However, no sialolith was found at surgery or upon examination of the excised surgical specimen.

Salivary duct ectasia can be mistaken as a sialocele because both may appear as cystic structures containing saliva, with similar gross characteristics and aspiration results.⁶ However, there are several differences between the salivary duct ectasia and sialocele. Sialocele results when saliva leaks from a damaged salivary gland or duct and is retained in the surrounding tissue forming a cavity,¹¹ whereas salivary duct ectasia is a dilated salivary duct containing an increased amount of saliva.⁶ Therefore, a sialocele is grossly observed as a relatively round and diffuse mass while salivary duct ectasia is observed as a cylindrical mass or cord-like structure.^4,6 The location of a sialocele is often inconsistent with the location of the salivary duct, whereas the location of duct ectasia is exactly the same as the location of the affected salivary duct.⁵ Salivary duct ectasia is definitively differentiated from sailocele via histopathology, whereas salivary duct ectasia has an epithelial lining with cuboidal epithelial cells, and sialocele has no epithelial lining.^4,15 In the dog reported here, the lesion was grossly distinguished from sialocele because of its cylindrical shape with a well-defined boundary and its location in the exact path of the parotid duct. In addition, an epithelial lining was demonstrated on histologic examination, confirming the mass to be parotid duct ectasia.

In human medicine, the degree of the duct dilation is different depending on the severity of the obstruction, duct elasticity, and the status of the attached gland.⁶ The severity of the obstruction depends on the severity of the causes such as sialoliths, polyps, or most commonly duct stenosis.⁷ The degree of the duct stenosis depends on the degree of ductal fibrosis, which reduces the duct elasticity so that the duct cannot be stretched normally at the stenotic region.⁶ On the other hand, the duct proximal to the fibrosis has normal elasticity, allowing this portion of the duct to dilate more readily. The result is called the “sausage effect” based on its “sausage- like” appearance.⁶ If the attached gland is normal, moderate-to-extensive dilation of the duct is possible as a result of the active glandular secretion, whereas an atrophied or inflamed gland produces less saliva, resulting in little or no duct dilation.⁶ The “sausage effect” was noted in the parotid duct of this dog. The reason for this appearance, based on the histological findings, was the stenosis of the rostral portion of the parotid duct in association with a normal parotid salivary gland. The stenotic region showed abundant fibrous tissue causing ductal stricture and the decrease of duct elasticity, whereas the parotid duct caudal to the stenosis distended extensively. The normal parotid gland of this dog contributed to dilation of the parotid duct because of the active secretion of saliva. If the ductal fibrosis was not significant and glandular secretions were decreased, parotid duct ectasia might not be prominent.

The treatment method is selected based on the location of the stricture and the extent of ductal dilation.⁸ In humans, traditional options for salivary duct ectasia include reimplantation of the duct into buccal mucosa, proximal duct ligation, and parotidectomy.⁸ If the stricture occurs near the parotid duct orifice or in the parotid duct near the oral cavity, reimplantation of the duct is a valid procedure.⁶ If the stricture occurs toward the parotid gland, reimplantation may not be possible, and ductal ligation at the hilus of the parotid gland can be used.⁶ However, in humans, parotidectomy is preferred to the ductal ligation because ductal ligation can be technically difficult, have inconsistent results, and can cause significant facial scarring.⁶ Recently, minimally invasive techniques such as balloon dilation and endoscopic sialodochoplasty have been used effectively to enlarge ductal stricture in humans.^16,17 However, several limitations prevent routine use including expensive equipment and possible iatrogenic ductal perforation.⁸

In veterinary medicine, similar surgical options can be used to treat the parotid duct disease as in humans including reimplantation as well as marsupialization of the affected duct, ductal ligation, and parotidectomy.^4,11,8 Previously reported dogs with the parotid duct ectasia were treated by marsupialization by incising the dilated parotid duct and anastomosing it to the labial mucosa via an intraoral approach.^4,5 Marsupialization is simple and easy to perform, and it maintains the physiologic function of the salivary duct. However, if the intraoral approach to the dilated duct is not possible, parotid duct ligation or parotidectomy should be chosen.^1,8 Unlike in human medicine, in veterinary medicine, parotid duct ligation is the simplest and quickest, easiest and most effective technique to treat parotid salivary gland and duct disease such as sialocele and fistula.^1,2,18 Ligation usually causes back pressure, which makes the secretory cells of the affected salivary gland atrophy progressively.^1,2,19–22 With few complications and high efficacy, parotid duct ligation can be used alternatively to parotidectomy.^1,18,23 Parotidectomy is always accompanied by the risk of facial or trigeminal nerve injury; therefore, it should be chosen carefully, specifically only when there is a lesion in the parotid gland itself.² In this report, the dog was successfully treated with the removal and ligation of the affected parotid duct. Marsupialization could not be applied because it was not possible to approach the dilated section of the parotid duct intraorally. Parotidectomy was not a treatment option in the case of this report as a result of the invasiveness of the procedure and potential postoperative complication of facial nerve injury. Additionally, there was no abnormality in the affected parotid gland such as sialoadenitis or abscess to suggest that the gland should be removed.

The most serious complication of parotid gland/duct excision is facial nerve injury because facial or trigeminal nerve branches are located close to the parotid duct and gland, predisposing them to damage during parotid duct and gland removal.¹ The possibility and degree of the complication is usually higher for parotidectomy than for parotid duct excision because the main facial nerve is distributed around the parotid gland anatomically. Therefore, in case of removal of parotid salivary gland/duct, pet owners must be educated about the clinical signs of potential facial paresis or paralysis such as absent palpebral reflex, wide palpebral fissure, and drooping of the lip that could occur postoperatively.¹ The dog of this report had mild facial paresis after the parotid duct removal. It was presumed that the branch of facial nerve around the parotid duct sustained blunt trauma during duct dissection because dysfunction was minimal and resolved quickly. Collateral thermal damage from the laser could have been responsible for the temporary facial palsy, but this nerve or its branches were not visualized during surgery. The carbon dioxide laser was used because of precise hemorrhage control during incision that allowed optimal visualization in the surgical field. The blood-free field afforded by the laser facilitated precise identification and avoidance of regional structures including nerves. The average depth of thermal damage from the CO₂ laser is ∼0.2 mm; therefore, if branches of the facial nerve were seen in the surgical field, it is likely that they could be avoided before the laser invoked thermal damage to them.²⁴

Conclusion

This case study reports canine parotid duct ectasia that likely developed subsequently to parotid duct stenosis after the removal of parotid sialoliths. This case was successfully treated with parotid duct ligation at the hilus of the parotid gland and removal of the dilated parotid duct. This report illustrates that parotid duct ligation combined with the removal of the dilated portion of a parotid duct can be an effective surgical option for treatment of parotid duct ectasia in the presence of a normal parotid salivary gland.