A 5.5-year-old 23.0-kg (50.6-lb) sexually intact male Bull Terrier was taken to its primary care veterinarian for evaluation because of facial swelling, an inability to close its mouth, and bilateral nasal discharge. The owner reported that 2 days prior to evaluation, the dog had attacked a metal trap that contained a woodchuck. Per the description, the dog had no physical contact with the woodchuck, but no more detailed information was available about the incident. After the incident, the dog was suddenly unable to close his mouth and rapidly developed bilaterally elevated nictitating membranes and severe, diffuse facial swelling. Two years prior to this incident, the dog had similarly attacked a cage containing a woodchuck and developed mild facial swelling.
The primary care veterinarian had performed a CBC, serum biochemical analysis, and skull radiography. Radiography revealed no obvious fractures or abnormalities. Serum biochemical analysis revealed high activities of aspartate aminotransferase (1,256 U/L; reference range, 15 to 66 U/L), alanine aminotransferase (260 U/L; reference range, 12 to 118 U/L), and creatine kinase (80,969 U/L; reference range, 59 to 895 U/L). The CBC revealed neutrophilia (12,136 neutrophils/μL; reference range, 2,060 to 10,600 neutrophils/μL) but no other abnormalities. The dog was then sent home with tramadol hydrochloride (4 mg/kg [1.8 mg/lb], PO, q 8 h) and clindamycin (10 mg/kg [4.5 mg/lb], PO, q 12 h).
Two days later, the dog was brought to a referral hospital because of continued signs of inappetence with no clinical improvement at home. On initial physical examination, the dog appeared bright and alert. Abnormal findings included bilaterally elevated nictitating membranes, an inability to adduct the mandible without assistance, and a fractured left maxillary canine tooth. The masticatory muscles were severely swollen and firm, and signs of pain were elicited on gentle palpation (Figure 1). No superficial wounds or abrasions were identified. Results of neurologic examination confirmed masticatory muscle dysfunction and indicated decreased nasal sensation bilaterally, apparent ophthalmoplegia, and bilaterally miotic but responsive pupils. No other neurologic abnormalities were identified, and results of orthopedic evaluation were unremarkable. Serum electrolyte concentrations were measured, and all were within reference ranges.
The dog was premedicated with oxymorphone (0.1 mg/kg [0.045 mg/lb], IV) in preparation for CT examination of the head, and maropitant citrate (1 mg/kg [0.45 mg/lb], IV) and diphenhydramine (2 mg/kg [0.9 mg/lb], IM) were administered. Anesthesia was induced with propofol (3 mg/kg [1.36 mg/lb], IV) and midazolam (0.3 mg/kg [0.136 mg/lb], IV) and maintained with isoflurane in oxygen. Iohexol contrast medium (2 mL/kg) was administered IV, and CT of the head was performed with a 64-slice CT scanner,a revealing profoundly, bilaterally enlarged temporalis, masseter, and pterygoid muscles. All 3 muscles had a heterogeneous contrast-enhancement pattern (Figure 2). The retropharyngeal lymph nodes appeared mildly enlarged. Both ocular globes were exophthalmic, with the posterior aspect of the left globe slightly deformed. No abnormality was detected in the nasal cavity; therefore, the previously observed nasal discharge was considered transient and likely clinically unimportant. Because compartment syndrome of the masticatory muscles with secondary associated (or consequential) ischemic neuropraxia was suspected, fasciotomy was recommended to the owner and subsequently pursued.
While still anesthetized, the dog was placed in sternal recumbency and the skin over each temporalis muscle was aseptically prepared. An 8-cm dorsal midline incision was made at the level of the temporalis muscle, and the subcutaneous tissues were dissected. Intracompartmental pressures were then measured prior to incision of the temporalis fascia. For this measurement, a standard 20-gauge hypodermic needle connected to a fluid-filled (saline [0.9% NaCl] solution) line, which was connected to an invasive arterial pressure transducer,b was inserted approximately 1 cm deep into the left and then right temporalis muscles, revealing pressures of 72 and 96 mm Hg, respectively. Immediately afterward, a 4-cm, full-thickness incision of the temporalis fascia on the right side was made in a caudal to rostral direction (Figure 3). This process was then repeated for the left temporalis muscle fascia.
After bilateral fascial releases were performed and left open (Figure 3), temporalis muscle compartment pressures were reassessed bilaterally by use of the previously described technique, revealing pressures of 54 and 27 mm Hg in the left and right sides, respectively. A 0.5 × 0.5 × 1-cm section of each temporalis muscle was removed and submitted for histologic examination and complete muscle analysis, including examination of the muscle for underlying inflammation, necrosis, fibrosis, fiber loss, microorganisms, or specific cytoarchitectural abnormalities.
A venous blood sample was also collected for serologic testing for antibody against masticatory 2M muscle fibers. The fascia was left open, and the subcutaneous layer was closed with 3-0 polydixoanonec in a simple continuous pattern. The dermis was closed with 3-0 poliglecaprone 25d in a continuous intradermal pattern.
The skin over the right masseter muscle was then incised in a dorsoventral direction. The fascia was incised in a horizontal direction along the muscle fibers and left open. The subcutaneous layer was closed with 3-0 polydioxanone in a simple continuous pattern. The dermis was closed with 3-0 poliglecaprone 25 in a continuous intradermal pattern. This procedure was then repeated for the left masseter muscle. No intracompartmental pressure measurements were obtained for the masseter muscles. Following surgery, an esophagostomy tubee was placed. A single lateral thoracic radiograph was obtained, evaluation of which revealed appropriate tube placement. The dog was then allowed to recover from anesthesia, with no complications noted.
In the postoperative period, the dog received 1 dose of methylprednisolone acetatef (30 mg/kg [13.6 mg/lb], IV) as well as methadone (0.3 mg/kg, IV, q 6 h) and crystalloid solutiong (60 mL/kg/d [27.3 mL/lb/d], IV). The following morning, the nictitating membranes were no longer elevated, extraocular muscle function and pupillary size were unremarkable, and the dog was observed to eat without any apparent dysphagia (Figure 1). The dog no longer appeared uncomfortable on palpation of the masticatory muscles, but a mildly dropped jaw persisted. It was discharged from the hospital that day with prednisone (0.65 mg/kg [0.3 mg/lb], PO, q 12 h) and codeine (1.3 mg/kg [0.6 mg/lb], PO, q 8 h).
The dog was returned to the referral hospital 1 week after surgery for a recheck examination. All 3 incisions appeared clean, dry, and intact. The previous severe, diffuse facial swelling had completely resolved, and the esophagostomy tube was removed. The owner reported that the dog was doing well at home, appearing comfortable and eating as usual. Results of serologic testing for antibody against 2M muscle fibers were negative (titer, < 1:100). Results of muscle profile analysis were consistent with mild myofiber atrophy and perimysial edema of undetermined origin. No inflammation, necrosis, fibrosis, fiber loss, microorganism, or specific cytoarchitectural abnormalities were identified. Histologic examination of temporalis muscle specimens revealed multifocal swollen eosinophilic myofibers, fragmentation of the sarcoplasm, and occasional myofiber infiltration by macrophages. Rare myofiber mineralization was noted as well as mild to moderate intervening edema with a mild neutrophil and macrophage infiltrate and occasional plump fibroblasts. The microscopic interpretation was consistent with mild to moderate multifocal neutrophilic and histiocytic myositis with myofiber degeneration and necrosis (Figure 4).
At a recheck examination 2 weeks after surgery, the dog was still doing well. No recurrence of swelling, dysphagia, or signs of pain was evident. Results of physical and neurologic examination were unremarkable. The owner had been mistakenly administering prednisone at a higher dose than prescribed (1 mg/kg rather than 0.65 mg/kg), and tapering of prednisone administration over a 12-day period was initiated.
Twenty-six days after surgery, the dog was taken to its primary care veterinarian because of an incisional infection and partial dehiscence along the left masseter muscle. Treatment was initiated at that time with amoxicillin trihydrate-clavulanate potassiumh (21.7 mg/kg [9.9 mg/lb], PO, q 12 h).
Twenty-nine days after surgery, the dog was returned to the referral hospital for a recheck examination, which revealed improvement of the infected incision. Given the amount of time elapsed since surgery, the incisional dehiscence may have been consistent with secondary abscess formation, particularly given the severe muscle trauma. However, because the dog was evaluated elsewhere for the dehiscence, the possibility of secondary abscess formation was not confirmed. Recommendations were made to continue antimicrobial administration and return the dog in 2 weeks for another recheck examination and antibody test, but the owner declined further diagnostic testing. No additional follow-up was pursued by the owner.
The authors thank Drs. Taryn Donovan and Jamie Haddad for assistance with the histologic images and descriptions.
Acute compartment syndrome
Aquilion 64, Toshiba Corp, Tustin, Calif.
Deltran, Utah Medical Products Inc, Midvale, Utah.
PDS, Ethicon, Johnson & Johnson, Somerville, NJ.
Monocryl, Ethicon, Johnson & Johnson, Somerville, NJ.
Esophagostomy feeding tube, MILA International Inc, Florence, Ky.
Solu-Medrol, Pfizer Inc, New York, NY.
Plasmalyte, Zoetis Inc, Florham Park, NJ.
Clavamox, Zoetis Inc, Florham Park, NJ.
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