Introduction

Implanted microchips are a widely used method of domestic animal identification.¹ Microchips are usually implanted by hypodermic needle injection in the subcutaneous tissue on the dorsal midline between the scapulae.² Microchips are relatively safe, permanent, reliable, and unalterable, and implantation involves minimal discomfort. Adverse effects have been reported to include migration, loss, failure to function, infection, swelling, fracture, and neoplasia.^1–4 The clinical features, laboratory, radiographic, ultrasonographic, and histopathologic findings of a dog with a dorsal cervical mass surrounding a microchip are reported herein. To the authors' knowledge, this is the first reported case of a granulomatous inflammatory response to a microchip occurring 8 yr after implantation.

Case Report

An 8 yr old neutered male springer spaniel was referred to our institution for evaluation of a dorsal cervical mass. The mass was first noticed 4 mo prior to presentation and had increased slightly in size. On presentation, physical exam revealed a large (9 × 6 cm) mass in the dorsal neck. Palpation of the mass elicited a mild amount of pain. The mass was not attached to overlying skin but firmly attached to underlying tissues. No pain was elicited on manipulation of the neck. The dog also had multiple subcutaneous nodules, which had been diagnosed as lipomas. A microchip scanner placed over the mass confirmed that a microchip was present in the vicinity of the mass. The owner reported that the microchip had been implanted approximately 8 yr prior.

Thoracic radiographs, cervical radiographs, fine-needle aspiration, and ultrasonographic evaluation of the mass were performed. Interpretation of thoracic radiographs revealed no abnormalities of concern. Interpretation of cervical radiographs revealed a soft-tissue mass dorsal to C3–C7. A metal opacity (microchip) was present within the plane of the mass (Figure 1). Ultrasound of the dorsal neck revealed a large, thick-walled, cavitated mass (Figure 2). Within the cavitated area, there was a 13.2 mm hyperechoic linear structure that had reverberation consistent with metal. The size and appearance were compatible with the microchip transponder seen on radiographs. The sonographic assessment was a metallic foreign body (microchip suspected) surrounded by fluid and a thick wall. A fine-needle aspirate was performed under ultrasound guidance. Interpretation of the fine-needle aspirate revealed pyogranulomatous inflammation and no etiologic agents. Surgical removal of the mass was recommended.

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The patient was placed under general anesthesia. The mass and overlying skin were removed by marginal excision without complication. The excised tissue was placed in a sterile container and radiographed to confirm the presence of the microchip within the mass. The tissue was then submitted for culture and histopathologic examination. The cultured tissue grew two colonies of Staphylococcus pseudintermedius, susceptible to all antibiotics tested. The microchip was carefully dissected from the mass. On inspection, a crack in the glass case and blood within the microchip were found. On histopathologic examination of the tissue, mature granulation tissue and fibrous connective tissue with prominent, congested vessels surrounded by muscle and fat were found. A central cavity was present within the tissue and contained numerous large, foamy macrophages, scattered aggregates of neutrophils, lymphocytes, plasma cells, and hemorrhage. A Gram stain was performed on the tissue, and low numbers of intracellular gram-positive coccoid bacteria were identified within the mass. The surrounding muscle was multifocally atrophic with degenerate myocytes. The morphological diagnosis was a focal, severe, chronic granulomatous panniculitis with granulation tissue formation. No evidence of neoplasia was detected.

Discussion

This case highlights the importance of considering inflammation as a differential diagnosis in a dog with a microchip-associated mass. Initially, we suspected neoplasia in this dog. Although rare, neoplasia associated with foreign materials has been reported in association with microchips, retained surgical sponges, metallic implants, and vaccines.^5–8 The present case documents inflammation as another differential for a late-developing response in a dog after microchip implantation.

The response to microchip implantation has been well studied in dogs. Immediately following microchip implantation, an inflammatory response occurs.⁹ The inflammatory response resolves within 3 mo of microchip implantation.⁹ After the inflammatory response resolves, a connective tissue capsule forms around the microchip.⁹ This capsule is formed of collagen, elastin, and fibroblasts.⁹ Formation of the connective tissue capsule is typically complete within 12 mo of implantation.⁹ In most dogs, no further response is detected. Several potential explanations for the granulomatous inflammation associated with this dog's microchip exist.

A crack in the bioglass capsule was detected after removal of the microchip in this dog. A microchip transponder consists of a microchip and a small coil, which functions as an antenna enclosed in a bioglass cylinder.² Bioglass is used to enclose microchips because it is insoluble and biocompatible.² Cracking of the bioglass portion of the microchip is very rare.³ Previously, only one dog with an implanted microchip had been reported to experience a crack in the bioglass capsule.² In that dog, continuous inflammation at the site of implantation was exhibited.² Following removal of the dog's cracked microchip, histology of the surrounding tissue demonstrated chronic inflammation.⁵ In that dog, the reaction was observed 16 wk after implantation, but it was unknown when the bioglass fractured. The presence of inflammation surrounding the microchip with cracked bioglass indicates that in a dog, when subcutaneous tissue is exposed to a fractured microchip capsule, an inflammatory response may mount. The fractured bioglass capsule or its contents (the microchip and antenna coil) may be less inert than the outside surface of the bioglass capsule. In the dog in the present report, when the bioglass fractured, the inflammatory response may have reinitiated.

In the dog in the present study, no cause of the cracked bioglass was determined. The location of the microchip was in the approximate location of a collar. It would be unusual for a collar to fracture the small microchip embedded into the underlying tissue, but it is a possible explanation, as the dog was not known to have experienced other trauma. Fracture of the bioglass capsule prior to or during implantation seems improbable, as no swelling or tissue changes were detected for 8 yr.

Concurrent infection is considered likely, as two colonies of bacteria were isolated on culture, and gram-positive bacteria were identified on histopathologic examination of the tissue. The infection likely did not originate from the microchip or its interior contents, as the microchip is sterilized prior to distribution. Infection may have been hematogenously deposited at the site of the microchip transponder, similar to hematogenous deposition at surgical implants. The deposition of bacteria may have led to the granulomatous inflammatory reaction, as a walled-off abscess containing the microchip. Alternatively, bacteria may have been iatrogenically introduced during fine-needle aspiration. The fine-needle aspiration was performed 4 days prior to surgical excision, allowing the possibility of iatrogenic introduction of bacteria and bacterial proliferation. Further, no bacteria were seen on examination of the cytologic sample obtained during fine-needle aspiration.

Neoplasia was the main differential diagnosis at the time of presentation based on signalment, microchip implantation 8 yr prior, and previous reports of microchip-associated neoplasia.^1,4 In dogs with microchip-associated neoplasia, foreign body–induced tumorigenesis is the proposed mechanism and consists of two phases.^9,10 First, there is an acute cellular reaction with phagocytically active macrophages (phase 1), followed by macrophage dormancy and fibrous encapsulation of the foreign body (phase 2).¹⁰ In foreign body tumorigenesis, the formation of the fibrous capsule is linked to neoplastic development.¹⁰ Because neoplasia associated with a foreign body was a primary differential in this case, it would have been prudent to perform a biopsy of the mass. A biopsy may have provided information to help determine margins for the mass removal. Many foreign body neoplasias would be better addressed by performing a wide resection with deep margins, rather than the marginal resection performed here. A preoperative biopsy could have determined the need for wide resection and deep margins.

Conclusion

Of the millions of pets implanted with microchips, serious reactions are very rare.^3,11 Veterinarians should inform owners of potential complications, however rare, and encourage owners to monitor the site of microchip implantation. When reactions occur, veterinarians should consider granuloma formation at the site of the microchip, even when the microchip has been in place for a long period of time. Further study regarding tissue response to fractured bioglass may be warranted if additional reports of pyogranulomatous inflammation occur in response to microchips. When considering differential diagnoses for dogs with masses in the area of microchips, neoplasia should not be the only differential, as inflammation can occur as a late-developing response if the microchip becomes damaged.