1124 - Delayed Diagnosis of Hardware Failure Mimicking White Cord Syndrome in a Postoperative Cervical Fusion Patient: A Case Report

Friday, February 20, 2026

5:00 PM - 6:30 PM AST

Presenting Author(s)

BK

Brandon Khanyan, MD

Medical Student
Stony Brook University Medical School
Great Neck, New York, United States

Co-Author(s)

HA

Hani Abdel-Rahman, DO

Resident Physician
Stony Brook University Hospital
Winchester, Massachusetts, United States
RG

Rahul Gunasekera, DO

Resident
Stonybrook University
Centereach, New York, United States
ER

Etienne B. Rossert, MD

Resident Physician
Stony Brook University Hospital/Medicine
Mineola, New York, United States

Submitter(s)

ER

Etienne B. Rossert, MD

Renaissance School of Medicine at Stony Brook University
Woodbury, New York, United States

Case Diagnosis: Postoperative spinal cord compression due to hardware failure.

Case Description: A 76-year-old male developed progressive neurologic deficits during inpatient rehabilitation following C7–T2 anterior cervical discectomy and fusion for cervical myelopathy. Initially, he had full strength and ambulated with a walker. After a postoperative fall with head trauma, he developed bilateral limb weakness and neuropathic pain. Imaging showed spinal cord edema, and he was treated for presumed white cord syndrome. His hospital course was complicated by ileus, constipation, and urinary retention. Upon transfer to inpatient rehabilitation, he had mild weakness but developed progressive, asymmetric deficits within 48 hours—most notably right lower extremity (1/5 proximal, 2/5 distal) and left upper extremity (3/5), with preserved right upper extremity strength. MRI and CT revealed a vertebral fracture with kyphotic angulation above the fusion site and C7 screws breaching the spinal canal, causing cord compression. He underwent emergent decompression and fusion from C2–T3. By discharge, strength improved except right hip flexor remained 2/5.

Discussions: Although patients in acute inpatient rehabilitation are generally considered medically stable, this case demonstrates the need for maintaining a broad differential when evaluating neurologic decline. While initial imaging supported a diagnosis of white cord syndrome, the emergence of progressive, asymmetric motor deficits raised suspicion for a structural etiology. Serial neurologic examinations were essential in identifying findings inconsistent with reperfusion injury. Repeat imaging revealed hardware failure and kyphotic deformity causing spinal cord compression, necessitating urgent surgical revision. This case illustrates the diagnostic challenges of distinguishing white cord syndrome from mechanical complications and reinforces the importance of frequent exams, timely reassessment, and multidisciplinary coordination in complex postoperative spine care.

Conclusions:

Although patients in inpatient rehabilitation are typically considered medically stable, this case underscores the need for frequent, detailed neurologic examinations. Early identification of subtle deficits enabled timely imaging and intervention, preventing further deterioration and optimizing outcomes.