What could cause bilateral symmetric ankle dorsiflexion weakness after high‑energy trauma with pelvic fracture and large pelvic hematoma, when imaging shows no lumbar spine or nerve‑root compression?

Bilateral Symmetric Ankle Dorsiflexion Weakness After Pelvic Trauma

The most likely cause is traumatic lumbosacral plexopathy from direct compression or stretch injury by the pelvic hematoma itself, even without visible nerve root compression on imaging. 1, 2

Primary Mechanism: Lumbosacral Plexus Injury from Hematoma

Large pelvic hematomas can directly compress or stretch the lumbosacral plexus branches that innervate ankle dorsiflexion (L4-L5 nerve roots forming the common peroneal nerve via the sciatic nerve), producing bilateral symmetric weakness when the hematoma is centrally located or bilateral. 2

Key Pathophysiologic Points:

• High-energy pelvic trauma commonly causes stretching injuries or nerve compression from adjacent hematoma, even when imaging shows no direct nerve root compression at the spinal level. 2
• The lumbosacral plexus lies in close proximity to the pelvic bones and can be injured by mass effect from hematoma, local inflammation, and traumatic edema without requiring actual bony impingement. 2
• Bilateral symmetric presentation suggests either a large midline/bilateral hematoma affecting both sides of the plexus, or injury to the cauda equina/conus (though you state no spinal compression was seen). 1

Critical Diagnostic Limitation: Timing of Imaging

Your current imaging may be falsely negative because acute-phase MRI (within days of trauma) is notoriously poor at visualizing plexus injuries due to hemorrhage and soft-tissue edema obscuring the nerve structures. 1, 3

Optimal Imaging Strategy:

• Delay dedicated lumbosacral plexus MRI until approximately 1 month post-trauma to allow hemorrhage clearance and pseudomeningocele formation (a key sign of nerve avulsion), which dramatically improves diagnostic accuracy. 1, 3
• Standard lumbar spine MRI protocols are insufficient—you need dedicated lumbosacral plexus imaging sequences with diffusion-weighted neurography to detect intraneural signal abnormalities and plexus pathology. 1
• Acute imaging (3 days post-injury) has reduced sensitivity because blood products and edema mask the plexus; waiting 3-4 weeks yields superior visualization. 3

Differential Diagnosis to Consider

1. Compartment Syndrome of Fascial Spaces (Less Likely Given Bilateral Symmetry)

• Fascial compartments can compress the sciatic nerve and its branches (including the common peroneal nerve responsible for dorsiflexion), though this typically presents unilaterally unless there is bilateral lower extremity involvement. 4

2. Avulsion Injuries at Muscle Attachment Sites

• Ischial tuberosity avulsion fractures (hamstring origin) can cause sciatic nerve compression from local hematoma and inflammation, potentially affecting dorsiflexion if the injury extends to involve the common peroneal division. 2
• Check for avulsion fractures at the ischial tuberosity, greater trochanter (gluteal nerve injury), or inferior pubic symphysis (obturator nerve) on your imaging. 2

3. Bilateral Sciatic Nerve Stretch Injury

• High-energy pelvic fractures with significant displacement can stretch the sciatic nerves bilaterally, particularly in vertical shear or "open-book" fracture patterns with sacroiliac joint disruption. 4, 5

Clinical Management Algorithm

Immediate Actions:

1. Rule out cauda equina syndrome (saddle anesthesia, bowel/bladder dysfunction)—this would mandate urgent repeat imaging despite the acute phase limitations. 3
2. Monitor for rapidly progressive neurological deficit—worsening weakness requires emergent re-evaluation. 3
3. Ensure hemodynamic stability and hemorrhage control—pelvic hematomas in unstable fractures can be life-threatening. 1

Short-Term (Next 2-4 Weeks):

• Conservative management with pain control and physical therapy is appropriate while awaiting optimal imaging timing, provided no red flags emerge. 3
• Serial neurological examinations to detect any progression or emergence of cauda equina signs. 3

At 1 Month Post-Trauma:

• Obtain dedicated lumbosacral plexus MRI with diffusion-weighted neurography to definitively characterize the plexus injury. 1, 3
• Look specifically for nerve discontinuity, root avulsion, pseudomeningocele, intraneural signal abnormality, and compressive hematoma or scarring. 1, 2
• Detection of complete nerve rupture or avulsion may necessitate surgical intervention rather than continued conservative management. 2

Electrodiagnostic Testing:

• Consider EMG/nerve conduction studies at 3-4 weeks post-injury to complement imaging and assess for active denervation, which correlates with MRI findings of plexopathy. 1

Common Pitfalls to Avoid

• Do not rely solely on acute-phase lumbar spine MRI to exclude plexus injury—standard protocols miss plexopathy, and timing is suboptimal. 1, 3
• Do not assume that absence of bony nerve root compression excludes neurological injury—soft-tissue hematoma and plexus stretch are common mechanisms. 2
• Do not delay recognition of cauda equina syndrome—this is the one scenario requiring immediate imaging despite technical limitations. 3
• Do not forget that pelvic fractures are markers of high-energy trauma with frequent associated injuries—75% have concomitant head, thorax, abdominal, or genitourinary injuries requiring multisystem evaluation. 1

Prognosis Considerations

Functional outcomes depend heavily on whether the injury represents nerve stretch (better prognosis with conservative management) versus complete rupture or avulsion (often requiring surgical reconstruction). 1, 2 Delayed optimal imaging at 1 month is essential to make this critical distinction and guide definitive treatment planning. 3