Vulvar calcinosis cutis in a female dog with urinary incontinence secondary to an ectopic ureter

Abstract

A 2-year-old, spayed female standard schnauzer dog was presented with a history of urinary incontinence and painful whitish lesions localized to the vulvar region. An ectopic ureter was diagnosed by cystoscopy. Histopathology of the biopsy specimens from the vulvar lesions was compatible with calcinosis cutis. Seven weeks following the cystoscopic laser ablation of the ectopic ureter and resolution of the urinary incontinence, the calcinosis cutis lesions completely resolved without any specific treatment. To the authors’ knowledge, vulvar calcinosis cutis secondary to urinary incontinence has not been previously reported in a dog.

Key clinical message:

This is the first case report in the veterinary literature of vulvar calcinosis cutis in a female dog due to urinary incontinence.

Calcinosis cutis has been described as an inappropriate deposition of inorganic mineral salts (calcium phosphate) within the skin. Calcinosis cutis can be divided into 4 categories (metastatic, iatrogenic, dystrophic, and idiopathic) based on the etiology and mechanism of deposition of mineral (1,2). The pathomechanism of calcinosis cutis is not well-understood, and the hypotheses vary according to the type of calcinosis cutis.

The purpose of this case report is to describe an unusual presentation of vulvar calcinosis cutis suspected to be dystrophic in origin secondary to urinary incontinence caused by an ectopic ureter.

Case description

A 2-year-old, 13.5-kg, spayed female standard schnauzer dog was referred for urinary incontinence and painful lesions localized to the vulvar region. Urinary incontinence had been present since adoption when the dog was 8 wk old. The owner also reported intermittent hematuria and severe dysuria, as well as scooting behavior and vulvar licking. The dog was spayed at 6 mo of age and had not been in heat. The owner consulted a veterinarian because of the dog’s urinary incontinence and dysuria 2 mo before referral. White painful plaques involving the vulvar mucosa and the skin of the genital region and a small nodule on the left side of the vulvar labium were noted. No significant abnormalities were detected on complete blood (cell) count (CBC) and serum biochemical panel; a urinalysis revealed mild pyuria. A urine culture and sensitivity (urine collected by cystocentesis) revealed alpha hemolytic Streptoccocus. Abdominal radiographs showed no urinary tract abnormalities. The dog was treated with cephalexin (Apo-Cephalex; Apotex, Toronto, Ontario), 24.5 mg/kg body weight (BW), PO, q12h, for 3 wk. Three weeks prior to referral, the dog was presented to another veterinarian who referred the dog to our clinic. The urinary incontinence, skin and mucosal lesions in the vulvar region were still present. A second urinalysis showed that there was persistent pyuria. The dog was then treated with amoxicillin-clavulanate (Clavaseptin; Vétoquinol, Lavaltrie, Quebec), 13.8 mg/kg BW, PO, q12h, for 2 wk and tramadol (Ultram; McKesson, Saint-Laurent, Quebec) 1.8 mg/kg BW, PO, q12h, for 5 d. No clinical improvement was noted.

At the time of the initial presentation, the fur around the genital region, hind limbs, and tail was soaked with urine. The physical examination findings were unremarkable. The dermatological examination revealed mucocutaneous lesions consisting of 3 well-defined firm plaques covered with white chalky material and occasional erosions/ulcers limited to the genital region (Figure 1A). The lesions were painful and the dog was uncomfortable during manipulation.

Figure 1.

Vulvar region of dog with calcinosis cutis. A — Day 1: well-defined skin plaques covered with fine whitish granular material and erosions/ulcers (arrows). B — Day 49: complete resolution of the mucocutaneous lesions following correction of the ectopic ureter and complete resolution of the urinary incontinence.

Cytological examination of impression smears of the lesions revealed mixed inflammation (degenerate neutrophils and macrophages) with a few free cocci-shaped bacteria. Trichography was negative for parasites. A serum biochemical panel and CBC showed no significant abnormalities. Analysis of the urine sample obtained via cystocentesis revealed a high specific gravity (1.060), neutral pH (7.5), and an unremarkable urine sediment. A urine culture showed no growth. An ultrasound examination of the urinary tract showed findings compatible with a left ectopic ureter.

Cystoscopy was performed under general anesthesia. The whitish plaque lesions were visible and extended along the ventral surface of the vestibule towards the urethral papilla. The lesions were ulcerated and bled easily when touched with the scope. A paramesonephric remnant was identified. Upon entering the urethra, the opening of the left ectopic ureter was seen. The right ureteral papilla opened within the trigone. Cystoscopic laser ablation of the ectopic ureter was performed with a diode laser following confirmation of its intramural course by fluoroscopy. Retrograde contrast urethrocystography was performed to confirm correct positioning of the ureteral opening within the bladder. The paramesonephric remnant was also laser ablated.

One 3-mm punch biopsy of the whitish lesion along the vaginal mucosa was taken following the cystoscopy and fixed in 10% formalin for histological examination. Histologic examination of the skin biopsy showed the presence of a severe inflammatory reaction in the dermis consisting mostly of neutrophils and macrophages. Small areas of mineralization (Figure 2) were present among the inflammatory reaction and many small blood vessels of the dermis were thrombosed. The overlying epidermis displayed vacuolar degeneration. These findings were compatible with calcinosis cutis. In skin lesions of calcinosis cutis, the epidermis often shows acanthosis with ulceration and possibly extrusion of mineral through the epidermis in chronic lesions. Coalescing lakes of basophilic granular mineral generally surrounded by a granulomatous inflammation are found in the dermis. When necessary, Von Kossa’s stain can confirm the presence of calcification (2).

Figure 2.

Vulvar biopsy. Photomicrograph of the calcium deposits (brown material) present in the dermis of the vulva as revealed by the von Kossa special stain (400×, high power field).

Due to the potential link between the lesions of calcinosis cutis and the local irritation caused by the urinary incontinence, no treatment was deemed necessary for the mucocutaneous lesions.

Following the procedures, tramadol (Ultram; McKesson), 1.8 mg/kg BW, PO, q12h, for 10 d and meloxicam (Metacam oral suspension; Boehringer Ingelheim, Burlington, Ontario), 0.1 mg/kg BW, PO, q24h for 5 d was prescribed for analgesia. Amoxicillin-clavulanate (Clavaseptin; Vétoquinol), 13.8 mg/kg BW, PO, q12h, was prescribed for 7 d in order to prevent infection following the cystoscopy. Phenylpropanolamine (Propalin oral suspension; Vétoquinol), 1.5 mg/kg BW, PO, q8h, was prescribed after the procedure because of mild persistent urinary incontinence. Seven weeks after the cystoscopic intervention, the dog was presented to the dermatology service for a recheck of the mucocutaneous lesions. The lesions compatible with calcinosis cutis had completely resolved without any specific treatment, and the urinary incontinence was well-controlled (Figure 1B). A follow-up 2 y after the initial presentation confirmed that the urinary incontinence was managed with weekly administration of diethylstilbestrol (Stilbestrol tablets; Ormond Veterinary Supplies, Ancaster, Ontario), 1 mg PO, and the dog remained lesion-free.

Discussion

To the authors’ knowledge, this is the first time that calcinosis cutis localized to the vulvar region and secondary to urinary incontinence is reported in a dog.

In the human medical literature, calcinosis cutis involving the genital skin and mucosa in women has been reported (3,4). One case was described as idiopathic vulvar calcinosis and the lesion was removed surgically (3). A second case involving the outermost surface of the vulva in an elderly woman with a vesicovaginal fistula was reported as dystrophic calcinosis cutis. In the latter case, pain and uncontrolled urinary incontinence were associated with the skin calcification. The authors considered that the calcinosis was secondary to the friction and chemical stimuli (contact with urine and feces), which created an environment suitable for the formation of calculi in the vaginal cavity and over the area in contact with the incontinence pads. Because the tissue damage was deemed to play an important role in the deposition of calcium, the authors identified it as dystrophic calcinosis (4).

In the veterinary literature, calcinosis cutis is an uncommon disorder in dogs classically categorized based on the suspected etiology. Dystrophic calcinosis cutis occurs as a result of local tissue damage (trauma, necrosis, inflammation, or neoplasia) without hypercalcemia or hyperphosphatemia and is often associated with iatrogenic or endogenous hyperadrenocorticism (5). Iatrogenic calcinosis cutis is a separate group implying a direct contact of the skin with substances containing mineral salts (6,7). Although most cases of calcinosis cutis are classified as idiopathic, it has been proposed that they are in fact often secondary to dystrophic calcification.

In the present case, there was no history of exposure to substances containing mineral salts that would have led to an iatrogenic calcinosis cutis. In addition, a metastatic calcinosis cutis is considered unlikely as serum phosphorus and calcium were within the reference ranges. In our case, we hypothesized that the underlying cause of the calcinosis cutis was the chronic irritation of the genital skin and mucosa secondary to the severe, persistent and long-standing urine scalding. Although the presence of minerals in urine and/or urease-producing bacteria might have played a role in the formation of calcium deposition, the last urine bacterial culture showed no growth in this dog. Tissue damage and irritation caused by chemical stimuli was considered as a prerequisite for the development of the calcium formation in the vaginal mucocutaneous region in our patient. In this case, the licking and scooting behavior may also have contributed to tissue damage but would not explain the calcium deposits on the ventral surface of the vestibule right up to the urethral papilla. The remarkable regression of the vulvar lesions after surgical correction of ectopic ureter was also suggestive of calcinosis cutis secondary to the constant irritation localized in the vulvar area, which was again in favor of a dystrophic type of calcification.

Given that calcinosis cutis is usually an uncommon disorder, there is a notable lack of scientific reports, and unfortunately no standard therapy is described. The therapeutic approach is largely based upon expert opinions and single case reports. The recognition and the proper correction of the underlying urinary disorder in this case were essential for the resolution of the incontinence and skin lesions. No specific treatment was prescribed to address the calcinosis cutis lesions and a rapid resolution of the mucocutaneous lesions followed the control of the urinary incontinence.

In conclusion, we suggest that the distribution and resolution of the vulvar lesions following the correction of the ectopic ureter in this case were suggestive of a dystrophic calcinosis cutis secondary to irritation mainly caused by urinary incontinence. Many aspects concerning the etiology, the pathophysiology and the treatment of calcinosis cutis remain unclear. Other clinical reports and future studies would be useful to clarify the pathogenesis of calcinosis cutis. CVJ