History
An 8-year-old 46.2-kg (101.6-lb) spayed female German Shepherd Dog was referred for evaluation because of an inability to open its mouth (trismus) and signs of pain on manipulation of the mouth. The owner reported that 1 month earlier, the dog showed signs of pain when touched around the mouth; however, the referring veterinarian identified no underlying abnormalities and prescribed prednisone (0.43 mg/kg [0.20 mg/lb], PO, q 12 h for 3 days, then 0.43 mg/kg, PO, q 48 h for 1 week). Signs of pain resolved; however, the dog developed excessive polyuria and polydipsia, and prednisone was discontinued. Days later, signs of pain returned, and the dog was treated with carprofen (2.1 mg/kg [0.95 mg/lb], PO, q 12 h). Approximately 1 month after the initial examination, swelling around the eyes and muzzle was noticed. Results of evaluation by the referring veterinarian were within reference limits, with the exception of the dog being hyperthermic (39.4°C [103.0°F]; reference range, 38.3° to 39.2°C [101.0° to 102.5°F]) and having subcutaneous edema around the eyes and muzzle. Dexamethasone sodium phosphate (0.52 mg/kg [0.24 mg/lb], IV) and diphenhydramine hydrochloride (2.1 mg/kg, IM) were administered, and by 24 hours later, the dog's edema had resolved. The referring veterinarian performed a comprehensive oral health assessment and treatment, the extent of which was not conveyed. A week later, the dog again showed signs of pain when touched around its mouth and could not open it much. The owner reported that despite the limited mandibular mobility, the dog was able to eat canned food and drink water. The dog was returned to the referring veterinarian and anesthetized for an oral examination; however, despite general anesthesia, the dog's mouth could not be opened more than approximately 2 cm. After recovery from anesthesia, the dog was referred for further evaluation.
On referral examination, the dog was hyperthermic (39.6°C [103.3°F]) and resisted manipulation of its mouth, which could not be opened > 2 cm. Subjectively, the temporalis muscles were mildly atrophied; however, on palpation, the muscles felt clinically normal and no signs of pain were elicited. No swelling of the face or muzzle was evident, and there were no other remarkable findings on physical examination.
Results of a CBC indicated leukocytosis (19.4 × 103 WBCs/μL; reference range, 4.2 × 103 to 12.9 × 103 WBCs/μL), with neutrophilia (15.9 × 103 neutrophils/μL; reference range, 2.7 × 103 to 8.5 × 103 neutrophils/μL) and monocytosis (1.55 × 103 monocytes/μL; reference range, 0.10 × 103 to 1.00 × 103 monocytes/μL). Serum biochemical analyses revealed hypoalbuminemia (2.4 g/dL; reference range, 3.3 to 4.2 g/dL) and hyperglobulinemia (4.0 g/dL; reference range, 1.8 to 3.0 g/dL). Thoracic radiography revealed no abnormalities.
The dog was anesthetized and underwent MRIa of the head (Figure 1). The multiplanar sequences obtained were T2-weighted (T2W), proton density–weighted images with the Dixon technique (use of in-phase and out-of-phase cycling to image water vs fat) for fat suppression, and T1-weighted (T1W) fluid-attenuated inversion recovery. Following administration of gadopentetate dimeglumineb (0.10 mmol/kg [0.05 mmol/lb], IV), T1W fluid-attenuated inversion recovery and a 3-D spoiled gradient sequence (3-D volumetric interpolated breath-hold examination [VIBE]) images were obtained.
Transverse precontrast T2-weighted (T2W; A), T2W with Dixon technique for fat suppression (B), and T1-weighted (T1W; C) and postcontrast T1W with Dixon technique for fat suppression (D) images from MRI at the level of the temporomandibular joints of an 8-year-old 46.2-kg (101.6-lb) spayed female German Shepherd Dog with trismus. The dog's right is to the left of the images.
Citation: Journal of the American Veterinary Medical Association 256, 6; 10.2460/javma.256.6.647
Determine whether additional imaging studies are required, or make your diagnosis from Figure 1—then turn the page →
Diagnostic Imaging Findings and Interpretation
The dog's right temporalis muscle had heterogeneous hyperintense signal on T2W and proton density–weighted images (both with and without fat suppression), isointense signal on precontrast T1W images, and diffuse homogenous contrast medium enhancement (Figure 2). These signal intensities were also evident in the dorsomedial aspect of the left temporalis muscle. The tendon of the right temporalis muscle at the attachment on the coronoid process of the ramus of the mandible was thickened and disrupted by multiple foci of heterogeneous hyperintense signal on T2W images. Extending caudomedially from the dorsal aspect of the right coronoid process was a complex, branching tract-like lesion that centrally had hyperintense signal on T2W images and hypointense signal on T1W images and that peripherally had contrast medium enhancement. In the subcutaneous tissue dorsal to the external sagittal crest of the skull, there were multiple, large, fluid-filled structures that had heterogeneous hyperintense signals on T2W images and hypointense signals on T1W images and that had strong peripheral contrast medium enhancement. A small focal area of lysis of the frontal bone adjacent to the fluid-filled structures was identified on the 3-D VIBE sequence (not shown). A small amount of fluid or mucus (compared with muscle, the material's signal was hyperintense on T2W images and isointense on T1W images) was present in the right frontal sinus. The right mandibular, parotid, and medial retropharyngeal lymph nodes were moderately enlarged.
Same images as in Figure 1. The right temporalis muscle (asterisk) has heterogeneous hyperintense signal on T2W and T2W fat-suppression images (A and B) and shows enhancement on T1W images with fat suppression (D). Similar signal intensities and contrast enhancement are evident in the dorsomedial aspect of the left temporalis muscle. The tendon of the right temporalis muscle attaching to the coronoid process is thickened (arrowhead; A through D), with focal disruptions on T2W images (A and B) and isointense signal (compared with muscle) on the precontrast T1W image (C). Adjacent to the external sagittal crest are fluid-filled structures (arrow; A though D) that display contrast enhancement (D).
Citation: Journal of the American Veterinary Medical Association 256, 6; 10.2460/javma.256.6.647
Findings on MRI were consistent with myositis involving primarily the right temporalis muscle and to a lesser extent the left temporalis muscle. Given the asymmetric involvement of the temporalis muscles, the dog's myositis was likely caused by an infection rather than an immune-mediated process. In addition, findings for the fluid-filled structures in the subcutaneous tissue dorsal to the external sagittal crest were consistent with abscesses, and those for the focal area of lysis of the frontal bone were consistent with osteomyelitis. Infectious myositis (eg, possibly from an unidentified foreign body) was prioritized over immune-mediated myositis, and the fluid or mucus accumulation in the right frontal sinus may have represented sinusitis attributed to potential osteomyelitis.
Treatment and Outcome
Cytologic evaluation of a fine-needle aspirate sample of the subcutaneous fluid revealed suppurative inflammation. A biopsy of the right temporalis muscle was performed, and results of histologic evaluation indicated myositis and fibrosis. The inflammation and fibrosis were multifocal and characterized by neutrophils, plasma cells, macrophages, and fewer lymphocytes and mast cells that infiltrated between and around individual myofibers. In some areas, inflammatory cells infiltrated around hypereosinophilic, vacuolated, and fragmented myofibers. Bacterial culture and susceptibility testing of a biopsy sample of the affected temporalis muscle yielded growth of Actinomyces hordeovulneris susceptible to amoxicillin.
The dog was treated with amoxicillin–clavulanic acid (20.0 mg/kg [9.1 mg/lb], PO, q 12 h) and meloxicam (0.1 mg/kg [0.05 mg/lb], PO, q 24 h). After 1 week of treatment, the dog's mandibular mobility remained unchanged; however, the dog appeared comfortable and continued to eat canned food and drink water. Antimicrobial treatment was continued, and after 1 month of antimicrobial treatment, the owner reported that the dog was able to open its mouth to a near normal extent. Two months after diagnosis of myositis and continued antimicrobial treatment, the owner reported that the dog had normal mobility of its lower jaw. Antimicrobial treatment was continued for an additional month, then discontinued. Two weeks after antimicrobial treatment was discontinued, the owner reported that the dog's mobility of its lower jaw remained normal.
Comments
In dogs, temporalis myositis combined with abscess formation is most commonly attributed to penetrating injuries from activities such as stick chewing. Clinical signs include pyrexia, facial swelling, and signs of pain or reluctance to open the mouth.1–3 In the dog of the present report, trismus that also persisted during general anesthesia was attributed to myositis, myofiber degeneration, and fibrosis in the temporalis muscle. Although definitive evidence of foreign material in the temporalis muscle was not observed, the area of peripheral contrast enhancement surrounding a hypointense region observed on 3-D VIBE MRI images was suggestive of foreign material or a tract related to migration of a previous foreign body.4
Actinomyces spp are gram-positive, acid-fast–negative filamentous bacteria. In addition to being commensal organisms of the oral cavity, A hordeovulneris has been isolated from infections associated with migrating plant awns.5,6 Retrospectively, the owner reported that the dog of the present report frequently chewed on sticks. It was possible that trauma associated with stick chewing inoculated commensal A hordeovulneris organisms from the dog's oral cavity into the temporalis muscle. Alternatively, the organism may have been directly inoculated into the temporalis muscle by a penetrating wound.
Findings in the dog of the present report highlighted the utility of MRI in dogs with trismus. A common differential diagnosis for trismus in dogs is masticatory muscle myositis (MMM), an immune-mediated myositis involving the muscles of mastication.7 In MMM, the immune-mediated process is directed against type 2M muscle fibers that are unique to muscles of mastication.7 With MMM, the muscles of mastication contain multifocal areas of ill-defined hyperintense signal on T2W MRI images and have heterogeneous contrast enhancement.8 Microscopically, MMM consists of inflammation composed of lymphocytes, histiocytes, and macrophages, with rare neutrophils.9,10 In some dogs, eosinophilic inflammation is observed.10 Definitive diagnosis is based on positive results for serologic tests for autoantibodies directed against type 2M myofibers. Other differential diagnoses for trismus are disorders (eg, osteoarthritis, intra-articular ankylosis, or extra-articular ankylosis secondary to trauma or neoplasia) involving the temporomandibular joint and restricting mandibular mobility.11 Cross-sectional diagnostic imaging often provides a definitive diagnosis of temporomandibular joint abnormalities, and in the dog of the present report, MRI was pursued over CT given the superior soft tissue resolution of MRI. However, the soft tissue lesions in this dog may have been observed on CT. Additionally, CT may have better defined the lysis of the dog's frontal bone.
In the dog of the present report, the history and clinical examination findings substantially overlapped with those of dogs with MMM. Consequently, the combination of finding from MRI, histologic evaluation, and bacterial culture and susceptibility testing were paramount in establishing a definitive diagnosis. Moreover, the high sensitivity and specificity of serologic testing for autoantibodies directed against type 2M myofibers could help exclude MMM from consideration.7,8 In short, MRI of the head should be strongly considered in dogs with trismus. The finding of only a single muscle with hyperintense signal on T2W MRI should prompt clinicians to consider an underlying infectious cause. To help prevent secondary fibrosis, altered mandibular function, and trismus, empirical treatment with antimicrobials and NSAIDs may be considered while waiting for results from histologic evaluation and bacterial culture and susceptibility testing.
Footnotes
3.0-T MRI, Skyra, Siemens Medical Solutions, Malvern, Pa.
Magnevist, Bayer HealthCare LLC, Whippany, NJ.
References
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