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December 16, 2021
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Acute paraspinal compartment syndrome following non-spinal orthopedic surgery

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A 29-year-old non-smoking man with a BMI of 37 kg/m2 and history of bipolar disease sustained a right subtrochanteric femur fracture and pseudoaneurysm of his right proximal femoral artery after a gunshot in December 2016.

He was treated with an intramedullary nail. Subsequently, the patient underwent dynamization of his nail secondary to concern for nonunion in May 2017. Five months later, the patient presented to our institution with continued discomfort and radiographs demonstrating persistent nonunion with a 1.3-cm leg-length discrepancy. Labs were notable for a 25-hydroxy vitamin D level of less than 10 ng/mL, and supplementation was initiated.

Steven D. Jones Jr.
Steven D. Jones Jr.
Donald (DJ) Scholten
Donald (DJ) Scholten

After ruling out infection and correction of nutritional deficiencies, the patient was taken to the OR in December 2017 for hardware removal, repeat biopsy, nonunion repair with grafting (anterior iliac crest bone graft) and proximal femoral blade plate fixation. The surgery was especially complex due to extensive scarring, the patient’s habitus and bony overgrowth at the implant insertion site. The patient was supine on a fracture table with an operative time of 6 hours and 49 minutes, and an estimated blood loss of 2,500 mL. The patient required 1L albumin and 6L crystalloid intraoperatively, as well as 4 units of packed red blood cells postoperatively.

Postoperative day 0 (POD0), the patient complained of increased left lumbar back and left leg pain (nonoperative side), as well as numbness over his left anterior, medial and lateral thigh. On exam, he was found to have decreased left lower extremity strength and sensation. His numbness and decreased strength were thought to be secondary to a positioning-related nerve palsy.

On POD1, the patient continued to complain of left lower back pain, as well as numbness over the left thigh and weakness of knee extension and hip flexion. On exam, he had tenderness to palpation over the paraspinal musculature and changes in his urine color. Creatine kinase (CK), complete blood count, basic metabolic panel and MRI of the lumbar spine were ordered secondary to his pain, as well as concern for possible rhabdomyolysis. Rhabdomyolysis was confirmed by a CK of 94,000 U/L and the patient was found to have an acute kidney injury with a creatine test of 1.52 mg/dL (AKI baseline 0.95 mg/dL). MRI of the lumbar spine obtained demonstrated left paraspinal musculature edema on T2-weighted imaging, prompting spine consultation (Figure 1). On POD2, the patient continued to complain of left lower back pain.

preoperative imaging demonstrating left paraspinal edema at T12-L5 (a) and axial T2 STIR preoperative imaging demonstrating left paraspinal edema at levels L1, L3 and L5
1. Sagittal short-T2 inversion recovery (STIR) preoperative imaging demonstrating left paraspinal edema at T12-L5 (a) and axial T2 STIR preoperative imaging demonstrating left paraspinal edema at levels L1, L3 and L5, respectively (b, c, d) is shown.

Source: Christopher J. Kleck, MD

What is the best next step to manage this patient?

See answer below.

Paraspinal fasciotomy, compartment decompression

Given the patient’s constellation of neuromotor symptoms, MRI findings and progression of rhabdomyolysis/ AKI despite aggressive fluid resuscitation, the decision was made to take him to the OR.

Paraspinal compartment syndrome (PCS) was suspected.

A left Wiltse-based approach was utilized. An incision to the level of the fascia was made 3 cm to the left of midline. The muscle fascia was identified, opened and paraspinal musculature swelled through the fascia. The fascial incision was extended proximally and distally from T12-L5. Muscle health was evaluated and there was no reaction to electrocautery or manual stimulation. At that time, no muscle tissue was excised. The fascial layer was left open, and the subcutaneous and skin layers were closed. A superficial incisional wound vacuum was applied.

Postoperative course

Postoperatively, the patient experienced immediate lumbar pain relief. Motor strength returned except for 4/5 strength of hip flexion. Sensation improved except for decreased sensation over the anterior thigh. His kidney function improved and his CK levels decreased.

Seven days post-fasciotomy, the patient developed progressively worsening leukocytosis and persistent drainage from the left paraspinal incision. Therefore, he was taken back to the OR for incision and debridement. A significant amount of paraspinous musculature was non-viable, excised and cultures were taken. The wound was left open with deep wound vacuum placement. Cultures were positive, necessitating IV antibiotic treatment. The patient again returned to the OR 12 days after paraspinal fasciotomy for repeat irrigation and debridement (I&D), repeat tissue samples, placement of antibiotic beads and wound closure with deep drain placement. The patient was discharged on oral antibiotics.

At his 2-week postoperative appointment, the patient was motor and sensory intact except for 4+/5 strength to his left hip flexors. He complained of mild, intermittent lower back and anterior thigh pain. At his 8-week appointment, he was noted to have dehiscence and drainage from his incision site. This was treated with local wound care, but, given the continued drainage, an MRI was obtained, which demonstrated a persistent fluid collection in his paraspinal musculature and he returned to the OR 4 months after his initial operation for a repeat I&D (Figure 2).

T1-weighted imaging demonstrating a left paraspinal fluid collection with rim-enhancement consistent with abscess
2. Sequential sagittal MRI fluid attenuated inversion recovery T1-weighted imaging demonstrating a left paraspinal fluid collection with rim-enhancement measuring 1.7 cm x 2.1 cm x 9.3 cm (anterior posterior x transverse x craniocaudal), consistent with abscess (a, b), is shown.

The patient was prescribed IV antibiotics and subsequently transitioned to oral antibiotics with repeat MRI imaging demonstrating improvement of fluid collection (Figure 3). The patient’s wound healed without further complication. One and a half years post-fasciotomies, the patient was noted to have a stable motor and sensory exam with minimal, sporadic lower back pain.

postoperative imaging demonstrating resolution of paraspinal abscess with soft tissue scarring
3. Sequential sagittal T2 STIR postoperative imaging demonstrating resolution of paraspinal abscess with soft tissue scarring at T12-L5 (a, b); axial T2-fast recovery fast spin-echo postoperative imaging demonstrating resolution of left paraspinal abscess with soft tissue scarring at levels L1, L3 and L5, respectively (c, d, e), is shown.

Discussion

Lumbar PCS, first described in 1985, is an uncommon cause of severe lower back pain that can be divided into acute and chronic cases. A recent literature review found 23 cases of acute PCS involving mostly male patients with an average age of 32.1 years. Acute PCS can be divided into three subtypes: atraumatic (usually after strenuous physical activity), secondary to direct trauma, and secondary to non-spinal surgery (aortic and gastric bypass surgery). Fifty-three percent of cases were a result of the first category, atraumatic. To our knowledge, there have been only four cases following surgical procedures.

Within the paraspinal compartment lie the erector spinae muscles (spinalis, longissimus and ilicostalis). These muscles are contained within a closed compartment formed by a multilayered thoracolumbar fascia attached medially to the spinous processes and the interspinous ligaments. The thoracolumbar fascia has attachments originating as high as T7 and terminating at the sacrum and iliac crest. Resting pressures have been demonstrated to be 3 mm Hg to 7.95 mm Hg, depending on position, and up to 25 mm Hg during exercise.

Acute PCS presents with severe lower back pain, following trauma, exercise or surgery. Additional symptoms include paraspinal tenderness, fullness or rigidity of the paraspinal region, and motor or sensory changes. Interestingly, it has also been noted that many of these patients had absent or diminished bowel sounds, as well as loss of tactile sensation overlying the paraspinal compartments. Multiple authors have demonstrated significant laboratory abnormalities associated with acute PCS, including elevations in CK, lactate, urine myoglobin, white blood cells and creatinine (Cr).

Imaging, including CT and MRI, has been shown to have a role in suspected acute PCS with these scans demonstrating paraspinal muscle swelling on CT and edema on MRI (best seen on T2-weighted imaging). Compartment pressure monitoring may play a role in diagnosis of these patients and when measured, compartment pressures have ranged from 14.7 mm Hg to 150 mm Hg in those with PCS. While diagnosis of acute PCS can be challenging, a recently published article proposed an algorithm based on the available data. The authors recommended CT and labs (including CK, Bun/Cr, myoglobin and urinalysis), followed by possible MRI and compartment pressure measurements.

Treatment techniques vary among the published cases of PCS, with 12 of the reported cases treated with fasciotomy, nine treated with medical management and two treated with medical management plus hyperbaric oxygen therapy. Of the cases treated with fasciotomy, all had good outcomes, even those found to have muscle necrosis. Those treated with medical management all had residual symptoms and functional impairment at follow-up.

Conclusion

Our patient underwent femoral nonunion repair with prolonged OR time and subsequently developed acute PCS, which has yet to be described following non-spinal orthopedic surgery. Acute PCS should be considered in patients with acute onset lower back pain, especially following surgeries with a prolonged operative time. One should look for increased pain with hip flexion (places the compartment in stretch), tense or tender paraspinal compartments and paravertebral sensory changes (dorsal sensory branch passes through this compartment).

In a postoperative patient, the diagnosis of PCS can be difficult secondary to expected pain, but a high level of suspicion must be maintained. It is important to differentiate from other causes of low back pain, such as disc herniation, retroperitoneal pathology and fracture. It is imperative to do a thorough physical exam combined with laboratory testing such as CK/Cr levels (to evaluate for rhabdomyolysis), transaminase levels, complete blood count and lactate. MRI or CT should also be considered to evaluate for paraspinal muscular edema and other pathology. Although compartment pressure monitoring has not been studied extensively in PCS, previous case reports would indicate that it is typically elevated and may aid in diagnosis.

Despite the fasciotomy resulting in almost immediate resolution of our patient’s lower back pain, this case was complicated by myonecrosis and surgical site infection. The literature suggests that surgical intervention leads to better outcomes than medical management. Based on our experience, we would advocate for a full release of the paraspinal compartment (at least L1 to the iliac crest) and aggressive debridement of necrotic tissue in the case of acute PCS.