What is the workup for sudden onset of bilateral lower extremity weakness, numbness, and lack of sensation?

Workup for Sudden Onset Bilateral Lower Extremity Weakness with Numbness and Sensory Loss

Immediately obtain urgent MRI of the entire spine (cervical through lumbar) to rule out spinal cord compression, which is the most critical time-sensitive diagnosis that can result in permanent paralysis if missed. While vascular etiologies must be considered, the bilateral nature with sensory and motor involvement points primarily to neurologic pathology requiring emergent imaging.

Critical Initial Assessment

Immediate Physical Examination Priorities

• Check for the "5 Ps plus temperature": Pain, paralysis, paresthesias, pulselessness, pallor, and polar (cold extremity) to assess for limb-threatening ischemia 1
• Palpate bilateral femoral, popliteal, dorsalis pedis, and posterior tibial pulses: Absent pulses bilaterally suggest aortic saddle embolus or aortic dissection 2
• Assess motor strength systematically: Document hip flexion/extension, knee flexion/extension, ankle dorsiflexion/plantarflexion, and toe movements bilaterally 1
• Test sensory levels: Identify dermatomal patterns suggesting spinal cord pathology versus peripheral nerve distribution 3
• Evaluate for bladder/bowel dysfunction: Urinary retention or incontinence indicates cauda equina syndrome requiring emergency decompression 3
• Measure skin temperature gradient: Cool extremities suggest arterial insufficiency 4

Urgent Diagnostic Algorithm

Step 1: Obtain ECG immediately - Abnormal ECG findings (particularly U waves, prolonged QT, or ST changes) can point to hypokalemia or thyrotoxic periodic paralysis as systemic causes 5, 6

Step 2: Stat laboratory tests while arranging imaging:

• Serum potassium (hypokalemia causes periodic paralysis) 5, 6
• Thyroid function tests (TSH, free T4) 6
• Complete metabolic panel 5
• Creatine kinase (rhabdomyolysis from prolonged immobility) 3

Step 3: Imaging pathway based on pulse examination:

If pulses are absent or severely diminished bilaterally:

• Obtain CT angiography (CTA) of the aorta and bilateral lower extremities with IV contrast immediately - This is the preferred initial test for acute limb ischemia, providing rapid diagnosis and revascularization planning 7, 1
• CTA evaluates for aortic saddle embolus, aortic dissection, or bilateral iliac/femoral occlusions 7, 8
• Time is tissue: Delays beyond 4-6 hours increase risk of permanent damage and limb loss 7, 4
• Initiate systemic anticoagulation with heparin immediately while awaiting imaging to prevent thrombus propagation 7, 9

If pulses are present:

• Obtain urgent MRI of entire spine (cervical, thoracic, lumbar) with and without contrast - This evaluates for spinal cord compression, epidural abscess, transverse myelitis, or cauda equina syndrome 3
• If MRI is unavailable or contraindicated, obtain CT myelography 3

Step 4: Bedside duplex ultrasound can be performed simultaneously to assess:

• Bilateral common femoral artery patency 1
• Deep venous thrombosis (phlegmasia cerulea dolens can mimic arterial ischemia) 1, 4
• However, ultrasound should not delay definitive imaging 1

Critical Differential Diagnoses by Presentation Pattern

Vascular Emergencies (Cold, Pulseless Extremities)

• Aortic saddle embolus: Sudden onset, absent femoral pulses, history of atrial fibrillation or cardiac disease 2, 1
• Aortic dissection: May present without chest pain, only neurological symptoms from vascular occlusion 8
• Bilateral acute limb ischemia: Rutherford Class IIb (immediately threatened) requires emergency revascularization within 6 hours 7, 9

Neurologic Emergencies (Normal Pulses)

• Spinal cord compression: Trauma, epidural hematoma, tumor, or abscess 3
• Cauda equina syndrome: Saddle anesthesia, bladder/bowel dysfunction 3
• Guillain-Barré syndrome: Ascending paralysis, areflexia 3

Metabolic/Endocrine Causes (Normal Pulses, Abnormal ECG)

• Hypokalemic periodic paralysis: Profound hypokalemia (often <2.5 mEq/L), triggered by carbohydrate/alcohol intake 5, 6
• Thyrotoxic periodic paralysis: Hyperthyroidism with hypokalemia, more common in Asian males but occurs in all ethnicities 6

Compression Neuropathy (History of Prolonged Immobility)

• Bilateral sciatic nerve palsy ("toilet bowl neuropathy"): Prolonged sitting/unusual positioning, medication-facilitated sleep 3
• Gluteal compartment syndrome: Prolonged pressure, rhabdomyolysis 3

Immediate Management Priorities

If vascular etiology suspected:

• Immediate vascular surgery consultation before completing imaging if limb-threatening signs present 7, 4
• Start unfractionated heparin bolus followed by infusion 7, 9
• Prepare for emergency revascularization (catheter-directed thrombolysis, thrombectomy, or surgical bypass) 7, 9
• Presence of paralysis or motor weakness requires immediate surgical intervention, potentially before imaging 7

If neurologic etiology suspected:

• Immediate neurosurgery consultation for potential emergency decompression 3
• Administer IV methylprednisolone if spinal cord injury suspected (within 8 hours of injury) 3

If metabolic etiology confirmed:

• Correct hypokalemia cautiously: Replace potassium at maximum rate of 10-20 mEq/hour with cardiac monitoring 5, 6
• Treat underlying thyrotoxicosis with propranolol and antithyroid medications 6
• Focus on treating the hypokalemia, not the paralysis - motor function returns with potassium normalization 6

Common Pitfalls to Avoid

• Do not assume bilateral symptoms exclude vascular causes: Aortic saddle embolus and aortic dissection present bilaterally 8, 2
• Do not delay imaging for complete laboratory results if pulses are absent - proceed directly to CTA 7
• Do not perform lumbar puncture before imaging if spinal cord compression is suspected - risk of herniation 3
• Do not dismiss resolving symptoms: Transient symptoms can represent impending catastrophic vascular occlusion 2
• Do not overlook functional neurological disorder in the differential, but only after excluding life-threatening causes 1