Introduction

Compartment syndrome (CS) is a rare postoperative complication of limb surgery caused by increased pressure within an osteofascial compartment.¹ Hemorrhage or edema within a compartment causes rapid and irreversible neuromuscular damage and often necessitates reoperation. A few veterinary case reports document CS secondary to vascular trauma and neoplasia.^1–3 CS is widely documented in the human medical literature as a postoperative complication and in the acute trauma setting as with crush injury or catastrophic fracture.⁴ To the authors’ knowledge, this is the only report of CS developing postoperatively and secondary to a peripheral arterial aneurysm in the small animal veterinary literature.

Case Report

A 12 yr old male neutered beagle underwent a right lateral fabellar suture (extra-capsular stifle stabilization) with the primary care veterinarian. Postoperative bruising and failure of the correction were noted at 1 wk and referral for revision by a board-certified veterinary surgeon was recommended. A preoperative complete blood count (CBC) was not performed prior to this initial procedure. The patient received carprofen (2.6 mg/kg, per os [PO] q 12 hr) for musculoskeletal pain for 14 wk prior to reevaluation. Obesity (body condition score 8/9), a grade 3/6 cardiac murmur, and an elevation in the enzyme alanine aminotransferase (169 U/L) were noted at referral.⁵ An explant of the right lateral fabellar suture and a right tibial plateau leveling osteotomy (TPLO) were performed without reported complication at a regional orthopedic surgery and sports medicine center. Reported preoperative CBC parameters were within normal limits with a packed cell volume (PCV) of 52%, total protein (TP) of 7.2 g/dL, and platelet count of 272 K/μL. Hydromorphone (0.1 mg/kg, IV q 4 hr), cefazolin (22 mg/kg, IV q 6 hr), and carprofen (2 mg/kg, PO q 12 hr) were administered postoperatively. A 34% decrease in PCV and a significant decrease in blood protein parameters were noted 12 hr postoperatively (PCV 18% and TP 5.2 g/dL). Bruising of the limb and abdomen and a progressive tachycardia developed over the first postoperative day. The development of a severe anemia, progressive regional bruising, and a tachycardia unresponsive to additional analgesia prompted case referral to the Friendship Hospital for Animals intensive care unit (ICU).

On transfer the patient had a persistent tachycardia (140 bpm), was normotensive (130 mm Hg, systolic), and was normothermic (99.5°F). A CBC showed a severe anemia (PCV 18%, clear serum), leukocytosis (25.2 K/μL), and thrombocytopenia (66 K/μL, 3–6 per 100× field). There was no evidence of spherocytosis or auto-agglutination on blood smear analysis. Prothrombin and partial thromobplastin times^a were normal (14 and 69 s) and a screen for tick-borne disease^b was negative. A packed red blood cell (pRBC) transfusion (6 mL/kg), crystalloid fluid therapy^c, and hydromorphone^d (0.2 mg/kg IV q 4 hr) were administered. Twenty-four hours after ICU admission desmopressin^e (1 μg/kg subcutaneously once) was added for treatment of possible platelet dysfunction or other hemostatic impairment.⁶ Forty-eight hours after ICU admission, prednisone^f (1.1 mg/kg PO q 12 hr) was started for suspected immune-mediated thrombocytopenia as repeated CBC tests showed persistent anemia and progressive thrombocytopenia (platelet count of 44 K/μL, 3–5 per 100× field at 24 hr and 33 K/μL, 3–5 per 100× at 48 hr after admission). Doxycycline^g (5 mg/kg PO q 12 hr) antibiotic therapy was started for treatment of possible rickettsial disease. Radiographs showed regional soft tissue swelling and no abnormalities at the TPLO site. The patient was discharged after 5 days with the presumptive diagnosis of immune-mediated thrombocytopenia receiving prednisone, doxycycline, gabapentin^h (10 mg/kg PO q 8–12 hr), and tramadolⁱ (4 mg/kg PO q 8–12 hr). Prior to discharge, anemia had improved, and platelet count had increased (PCV 28% with platelet count of 70 K/μL, 5–7 per 100× field).

Over the subsequent 54 days, the patient re-presented to the urgent care and internal medicine services five times for persistent pain, lameness, bruising, and the development of general proprioceptive deficits in the limb. A regenerative anemia and persistent thrombocytopenia were noted on multiple repeat CBC tests. The patient’s PCV oscillated between 22 and 34% and platelet count oscillated between 68 K/μL, 5–7 per 100× field and 154 K/μL, 10–11 per 100× field across five separate analyses. Repeat prothrombin time/partial thromboplastin time was again normal in this period (11 and 84 s). Repeat radiographs confirmed regional soft tissue swelling and stable postoperative TPLO implant with no evidence of implant failure or osteomyelitis. A second pRBC transfusion (7 mL/kg) was administered, additional oral analgesia (codeine 1.7 mg/kg PO q 12 hr), and additional antibiotic therapy (clindamycin^j [7.5 mg/kg PO q 12 hr], enrofloxacin^k [10 mg/kg PO q 24 hr], and metronidazole^l (12.5 mg/kg PO q 12 hr)] were added to address anemia, pain, possible infectious etiologies, and soft stool during this period.

Fifty-seven days after initial ICU presentation following the development of lethargy and a progressively firm swelling of the limb, a musculoskeletal ultrasound of the caudal thigh was performed. A large pulsating lesion with high-velocity blood flow was found in the caudomedial thigh musculature (Figure 1). A vascular anomaly such as an arterial aneurysm or pseudoandurism was suspected. Characteristics of a dissecting fusiform, saccular aneurysm, or a pseudoaneurysm were found on the ultrasound. The patient was presumptively diagnosed with CS secondary to arterial aneurysm. Pressures in the femoral compartment were not measured. Rehospitalization and amputation were recommended given the chronicity of signs, character of swelling, and neurologic deficits in the limb; however, both were declined. Fasciotomy was not recommended given to the chronicity of the signs and the narrow window during which decompression of the compartment provides benefit to salvage the limb. The term “missed compartment syndrome” has been applied in people with chronic CS leading to severe necrosis of the tissues, as was suspected in this patient at this time point.⁴ The patient re-presented to the urgent care service two additional times in the subsequent 7 days for pain and progressively firm swelling, with amputation repeatedly declined. An emergency right pelvic limb amputation (coxofemoral disarticulation) was performed without complication 66 days after initial ICU presentation. Intramuscular hematoma and regions of suspected muscle necrosis were encountered during the procedure. A third pRBC transfusion (7 mL/kg) was administered intraoperatively. The patient recovered uneventfully and was discharged after 3 days of routine postoperative care. At a recheck 17 days after amputation PCV/TP had returned to within normal limits (36% and 6.7 g/dL, respectively). No complications or concerns were reported at re-examination 61 days after amputation.

View Figure

• Download as Powerpoint
• Download Figure

The limb was submitted for gross pathologic and histopathologic analysis. A massively dilated intramuscular artery and expansile hematoma were found to be compressing adjacent skeletal musculature and fascia and effacing the normal tissue architecture (Figure 2). In the vessel wall, a degenerate tunica media with elastin loss was detected on Van Gieson and Masson trichrome stains assessing vascular collagen and elastin, respectively. A specific focus of vascular rupture communicating with the surrounding hematoma was not detected because of marked tissue necrosis hindering visualization at the suspected rupture site. Development of an aneurysm (possibly caused by surgical vessel ligation) with subsequent aneurysm rupture, or the development of a pseudoaneurysm with breach of the vessel wall at either surgery with the formation of a communicating extravascular hematoma, were reported as the most likely causes of the histopathologic findings. The caudal thigh muscles (hamstring group) showed myocyte atrophy, degeneration, necrosis with macrophagic and fatty infiltration, granulation tissue deposition, and fibrosis demonstrating chronic tissue damage. Histopathology findings were consistent with a diagnosis of CS affecting the femoral compartment. Progression with chronicity causing a massive necrosis of tissues was detected.

View Figure

• Download as Powerpoint
• Download Figure

Discussion

The muscles, blood vessels, and nerves within the extremities are separated into compartments bound by dense connective tissue. Overlapping muscles, fascia, and bone form compartments of a relatively fixed volume. CS occurs when pressure within a compartment is elevated, causing ischemic necrosis of the tissue. Many compartments have been described in the human pelvic limb, and two have been described in the dog (anterior compartment of the crus and femoral compartment).⁷ Emergency fasciotomy is used to allow for tissue expansion outside of the compartment, typically with the acute development of CS. A pressure exceeding 30 mm Hg has been suggested as an indication for emergency fasciotomy in humans; however, techniques comparing compartment pressure with blood pressure may be more accurate in identifying fasciotomy candidates.⁴ Techniques for measuring compartment pressures are routinely used in the emergency and postoperative settings in humans. Similar techniques have been described in the dog but are not widely used in veterinary medicine.¹ Progression of CS with chronicity in people is termed “missed compartment syndrome” and is diagnosed when fasciotomy is no longer indicated because of irreversible tissue damage necessitating another intervention, as with this patient. Severe pain is reliably reported with CS in humans but is commonly masked by analgesia. There are life-threatening systemic implications of CS, notably acute renal failure secondary to rhabdomyolysis reported in humans.^4,8

It is assumed that a combination of intracompartmental bleeding as well as the space occupying nature of the ruptured aneurysm or pseudoaneurysm caused CS in this patient. CS is reported in humans as a complication of vascular trauma from routine orthopedic and other surgeries.^4,9,10 Incorrect placement of the lateral fabellar suture apparatus, which was present for 11 wk after implant failure in this patient, may have incited an aneurysm. Intraoperative trauma to the artery causing pseudoaneurysm formation, or alteration of a congenital vascular anomaly during either procedure, are alternative explanations. Development of a pseudoaneurysm of the femoral artery causing CS in the caudal thigh of a dog has been described after a bite wound injury.³ Several cases of CS have been described in humans secondary to true and false aneurysms of the limb.^9,10

A consumptive thrombocytopenia is suspected to have developed with periodic or progressive thrombosis of the aneurysm or secondary to the expansile hematoma detected adjacent to the abnormal vessel. The patient was treated for an immune-mediated disease before a cause of platelet consumption was determined. Recurrent regenerative anemia was determined to be secondary to hemorrhage from vessel rupture. In this case, early musculoskeletal ultrasound may have prevented the development of CS. Additional imaging such as computed tomography with contrast angiography could have been used to attempt a limb salvaging procedure such resection of the aneurysm or pseudoaneurysm and decompression of the compartment. Repeated measurement of compartment pressures could have demonstrated early CS and provided indication for imaging and decompression.

Conclusion

CS is a rare complication of surgery and has not been reported in the small animal veterinary literature after a routine surgery and secondary to a peripheral arterial aneurysm. Patients with unexplained postoperative limb swelling, especially involving one of the described canine osteofascial compartments, should be evaluated for CS and vascular aberrations such as aneurysm or pseudoaneurysm to reduce the chances of further complication.