ADJACENT SEGMENT DISEASE (ASD)
Post-Fusion Degeneration | Radiographic vs Symptomatic | Motion Preservation vs Fusion Extension
ASD CLASSIFICATION
Critical Must-Knows
- Radiographic vs symptomatic ASD - imaging changes far exceed clinical disease
- 2.5% per year symptomatic ASD rate is consistent across studies
- Risk factors include long fusions, sagittal imbalance, stiff segments adjacent to fusion
- Motion preservation devices aim to reduce ASD but long-term evidence lacking
- Treatment is extension of fusion or targeted decompression
Examiner's Pearls
- "Radiographic ASD occurs in 30% at 10 years; only 10-15% become symptomatic
- "Sagittal balance restoration is protective against ASD
- "Fusion to L5 has higher ASD rate at L4-5 than fusion to S1
- "Motion preservation (TDR, dynamic stabilization) may reduce but not eliminate ASD
Clinical Imaging
Imaging Gallery
Critical Adjacent Segment Disease Exam Points
Distinguish Radiographic from Clinical
Radiographic ASD (imaging changes) occurs in up to 30% at 10 years. Symptomatic ASD (causing clinical problems) is much less common at 2.5% per year. Not all radiographic changes require intervention.
Rate and Risk Factors
Symptomatic ASD rate of 2.5% per year is consistent. Risk factors include long fusions, sagittal imbalance, fusion ending at L5 (vs S1), stiff adjacent segments, and pre-existing degeneration.
Sagittal Balance is Key
Restoring sagittal balance at index surgery is protective against ASD. Lumbar lordosis should match pelvic incidence (PI - LL mismatch less than 10 degrees). Fusion in kyphosis accelerates ASD.
Treatment Options
Treatment for symptomatic ASD: extension of fusion to include affected level(s), or targeted decompression if stenosis without instability. Motion preservation at adjacent level remains investigational.
Adjacent Segment Disease At a Glance
| Parameter | Radiographic ASD | Symptomatic ASD |
|---|---|---|
| Definition | Imaging changes at adjacent level | Clinical symptoms from adjacent degeneration |
| Incidence | Up to 30% at 10 years | 2.5% per year (10-15% at 10 years) |
| Clinical significance | May not progress | Requires treatment consideration |
| Management | Observation, optimize factors | Extension of fusion or decompression |
| Reoperation rate | N/A | 10-15% at 10 years |
ASD - Risk Factors
Memory Hook:ASD risk is higher with Age, Sagittal imbalance, and Destabilization
FUSION - Factors Increasing ASD Risk
Memory Hook:FUSION length and position directly affect ASD risk
PROTECT - Reducing ASD Risk
Memory Hook:PROTECT adjacent segments by optimizing fusion parameters
L4-L5 - Common ASD Level
Memory Hook:L4-L5 is the most common ASD level when fusion ends at L5
Overview and Epidemiology
Adjacent segment disease (ASD) refers to the development of degenerative changes at spinal levels immediately adjacent to a previous fusion. It remains one of the most debated topics in spine surgery.
Key concepts:
- Radiographic ASD: Imaging evidence of degeneration (disc space narrowing, osteophytes, facet hypertrophy) at adjacent levels
- Symptomatic ASD: Clinical presentation with pain or neurological symptoms from adjacent level degeneration
- Adjacent segment degeneration: Used interchangeably with radiographic ASD
- Adjacent segment pathology: Symptomatic disease requiring treatment
Epidemiology:
- Radiographic changes: 30% at 10 years, 40-50% at 15-20 years
- Symptomatic disease: 2.5% per year (consistent across studies)
- Reoperation rate: 10-15% at 10 years
- More common cephalad to fusion than caudad
The Fundamental Debate
Is ASD a consequence of altered biomechanics from fusion (iatrogenic) or natural progression of degenerative disease that would have occurred anyway? Evidence suggests both contribute. The high rate of imaging changes with much lower clinical disease rate supports natural history playing a major role.
Pathophysiology and Biomechanics
Biomechanical basis for ASD:
Load transfer hypothesis:
- Fusion eliminates motion at treated segments
- Load and motion transfer to adjacent levels
- Increased stress on adjacent disc and facets
- Accelerated degeneration at these levels
Cadaveric studies show:
- Increased intradiscal pressure at adjacent levels after fusion
- Increased facet joint loading above fusion
- Greater motion at adjacent segments to compensate for fused levels
Fusion Length Matters
Longer fusions create greater stress concentration at transition zones. Each additional fused level increases the mechanical load on remaining mobile segments, potentially accelerating ASD development.
Factors affecting load transfer:
- Fusion length: Longer fusion = greater stress on adjacent levels
- Fusion position: Sagittal balance affects load distribution
- Adjacent segment quality: Pre-existing degeneration is vulnerable
- Rigid vs less rigid constructs: Pedicle screws vs cables/wires
Natural history argument:
- Patients requiring fusion already have degenerative disease
- Adjacent segments may have subclinical degeneration at surgery
- Some ASD represents natural disease progression
- Age-matched controls also develop degeneration
The truth likely involves both biomechanical factors and natural history.
Classification Systems
Patient and surgical factors affecting ASD
| Category | Factor | Impact |
|---|---|---|
| Patient | Age over 60 | Higher baseline degeneration |
| Patient | Pre-existing adjacent degeneration | Most significant risk factor |
| Patient | Obesity | Increased spinal loading |
| Patient | Osteoporosis | Altered load transfer |
| Surgical | Long fusion | Greater stress concentration |
| Surgical | Sagittal imbalance | Abnormal load distribution |
| Surgical | Fusion to L5 (vs S1) | Leaves L4-5 mobile, stressed |
| Surgical | Wide decompression | Destabilizes adjacent facets |
| Surgical | Stiff instrumentation | Greater load transfer |
Pre-existing degeneration at adjacent levels is the strongest predictor of ASD development.
Clinical Assessment
History:
- Timing: Symptom-free interval after index surgery (months to years)
- Location: New or different pain pattern from original surgery
- Character: Axial back pain, radicular symptoms, or both
- Relationship: May mimic original presentation
- Functional impact: Walking distance, activities of daily living
- Previous surgery details: Levels fused, approach, complications
Clinical presentation patterns:
- Stenosis: Neurogenic claudication, radiculopathy
- Disc herniation: Radicular pain, dermatomal sensory changes
- Instability: Mechanical back pain, worse with motion
- Spondylolisthesis: Back pain, radicular symptoms, gait changes
Examination:
Clinical Examination Findings
| Finding | Suggests | Management Implication |
|---|---|---|
| New radiculopathy | Nerve root compression at adjacent level | May need decompression |
| Neurogenic claudication | Central stenosis above fusion | Extension of fusion likely |
| Sagittal imbalance | Failed to restore lordosis at index | Major reconstruction needed |
| Positive extension pain | Instability at adjacent level | Fusion extension required |
| Normal neurological exam | May be discogenic/facetogenic | Consider less invasive options |
Red Flags
Progressive neurological deficit, cauda equina symptoms, or severe instability require urgent assessment and likely intervention. Most ASD presents insidiously with gradual symptom development.
Differential diagnosis:
- Pseudarthrosis at fusion site
- Hardware failure or loosening
- Recurrent stenosis at fused level
- New pathology (tumor, infection, fracture)
- Hip or SI joint pathology
Investigations
First-line imaging
Standing views essential:
- AP and lateral lumbar spine
- Flexion-extension views (dynamic instability)
- Long cassette scoliosis views if deformity
Key findings:
- Disc space narrowing at adjacent levels
- Osteophyte formation
- Endplate sclerosis
- Spondylolisthesis development
- Loss of disc height compared to pre-op
- Sagittal alignment changes
Dynamic instability:
- Greater than 4mm translation or greater than 10 degrees angulation on flexion-extension
Standing radiographs reveal functional alignment and dynamic changes.
Management Algorithm
Initial management for symptomatic ASD
Physical therapy:
- Core strengthening
- Flexibility exercises
- Posture optimization
- Activity modification
Medications:
- NSAIDs
- Neuropathic pain agents (gabapentin, pregabalin)
- Short-term oral steroids for acute exacerbation
- Muscle relaxants
Injections:
- Epidural steroid injections
- Facet joint injections
- Medial branch blocks
- Selective nerve root blocks
Bracing:
- Limited role in lumbar spine
- May provide short-term relief
Approximately 50% of patients with symptomatic ASD may improve with conservative treatment.
Surgical Technique
Extending the fusion cephalad or caudad
Preoperative planning:
- Assess number of levels to add
- Consider sagittal balance correction
- Plan upper instrumented vertebra (UIV)
- Evaluate bone quality
Fusion Extension Steps
Posterior approach extending above or below previous incision. Identify previous hardware. Assess for loosening or pseudarthrosis at original levels.
Evaluate existing instrumentation stability. May need to revise if loose. Connect new segments to existing construct if stable.
Decompress neural elements at affected level(s). Perform adequate foraminotomy if radicular symptoms present.
Place pedicle screws at new levels. Connect to existing construct with rods or rod-to-rod connectors. Consider interbody fusion for stability.
Address sagittal balance if needed. Restore appropriate lordosis. Confirm alignment on imaging.
Extending to sacrum and pelvis may be needed if fusing below L4.
Complications
Complications of revision surgery for ASD
Intraoperative:
- Dural tear (more common in revision)
- Nerve root injury
- Vascular injury (if anterior approach)
- Hardware malposition
Early postoperative:
- Wound infection (higher in revision surgery)
- Hardware failure
- Adjacent level injury from retraction
- Medical complications
Late complications:
- Pseudarthrosis at new fusion
- Hardware loosening
- Recurrent ASD at next level
- Persistent symptoms
Revision surgery for ASD has higher complication rates than primary surgery.
Postoperative Care
After fusion extension surgery
Recovery Phases
Mobilization with PT. DVT prophylaxis. Wound monitoring. Pain management.
Limited bending, twisting, lifting. Walking program. Wound healing. Brace if prescribed.
Gradual activity increase. PT for core strengthening. Fusion assessment on X-ray.
Progressive return to normal activities. Impact activities when fusion solid. Long-term follow-up for next adjacent level.
Bone healing assessment at 3-6 months with standing radiographs.
Outcomes and Prognosis
Treatment Outcomes
| Treatment | Success Rate | Recurrent ASD Risk | Notes |
|---|---|---|---|
| Conservative | 50% | N/A | Initial trial for all |
| Decompression alone | 60-70% | 10-20% need later fusion | Select patients only |
| Fusion extension | 70-80% | Continues at 2.5%/yr | Most common approach |
| Motion preservation | Variable | May be reduced | Limited long-term data |
Prognostic factors:
Factors Affecting Outcomes
| Factor | Better Prognosis | Worse Prognosis |
|---|---|---|
| Symptom duration | Short (less than 6 months) | Prolonged (greater than 2 years) |
| Number of levels | Single level | Multiple levels |
| Sagittal balance | Balanced | Fixed imbalance |
| Bone quality | Normal | Osteoporotic |
| Smoking status | Non-smoker | Current smoker |
| Prior revisions | None | Multiple prior surgeries |
Surgical treatment of ASD is generally effective but carries risk of further ASD at next levels.
Evidence Base
Symptomatic ASD Rate
- 2.5% per year symptomatic ASD rate
- 10-15% reoperation at 10 years
- Radiographic changes far exceed symptomatic disease
- L4-5 most common level
Sagittal Balance and ASD
- PI-LL mismatch increases ASD risk
- Fusion in kyphosis accelerates ASD
- Restoring lordosis is protective
- Sagittal balance assessment essential
Natural History vs Iatrogenic
- Biomechanical changes documented in cadaver studies
- Age-matched controls also develop degeneration
- Pre-existing adjacent degeneration is major risk factor
- Both factors likely contribute
Motion Preservation Effect on ASD
- Lower ASD rate with TDR than fusion in some studies
- Not eliminated - still occurs with TDR
- Patient selection affects outcomes
- Long-term data still maturing
Fusion Length and ASD
- Longer fusion = higher ASD rate
- Each additional level increases risk
- Stress concentration at junctions
- Shortest necessary fusion recommended
Exam Viva Scenarios
Practice these scenarios to excel in your viva examination
Scenario 1: New Symptoms After Fusion
"A 60-year-old woman who had L4-S1 fusion 5 years ago presents with new-onset bilateral leg pain and back pain. She has difficulty walking more than 100 meters. Examination reveals reduced ankle reflexes and sensory changes in the L3 distribution. Her previous surgery was uneventful with good relief of symptoms for the first 4 years."
Scenario 2: Prevention Discussion
"You are planning a L4-L5 fusion for a 55-year-old man with spondylolisthesis. He asks about the risk of needing more surgery in the future because of problems at other levels. How would you counsel him?"
Scenario 3: Surgical Decision Making
"A 58-year-old woman had L5-S1 fusion 8 years ago and now has symptomatic stenosis at L4-5. MRI shows severe stenosis with a 5mm spondylolisthesis at L4-5. Her standing X-rays show positive sagittal balance with loss of lumbar lordosis. How would you approach this?"
MCQ Practice Points
Key facts for MCQs:
- Symptomatic ASD rate: 2.5% per year
- Radiographic ASD at 10 years: approximately 30%
- Reoperation rate: 10-15% at 10 years
- L4-5 is most common ASD level (when fusion ends at L5)
- PI-LL mismatch increases ASD risk
- Pre-existing adjacent degeneration is strongest risk factor
Common MCQ topics:
- Radiographic vs symptomatic ASD distinction
- Risk factors for ASD
- Role of sagittal balance
- Treatment options for symptomatic ASD
- When to decompress alone vs extend fusion
- Prevention strategies
- Fusion length effect on ASD
Key concepts:
- Long fusions have higher ASD rate
- Fusion to L5 (vs S1) has higher ASD at L4-5
- Motion preservation may reduce but not eliminate ASD
- Both iatrogenic and natural history factors contribute
Symptomatic ASD Rate
Q: What is the symptomatic ASD rate after lumbar fusion? A: Approximately 2.5% per year. Radiographic ASD is much more common (~30% at 10 years), but only a fraction become clinically symptomatic.
Strongest Risk Factor
Q: What is the single strongest risk factor for developing ASD? A: Pre-existing degeneration at adjacent levels at the time of index surgery is the strongest predictor.
PI-LL Mismatch
Q: What sagittal parameter mismatch increases ASD risk? A: PI-LL mismatch greater than 10 degrees. Restoring appropriate lumbar lordosis is protective against ASD.
Fusion Length
Q: How does fusion length affect ASD risk? A: Longer fusions have higher ASD rates. Each additional fused level increases stress concentration at transition zones. Use shortest necessary fusion.
Decompression vs Fusion
Q: When can decompression alone be performed for ASD? A: When there is stable stenosis without spondylolisthesis and preserved disc height. Instability requires fusion extension.
Australian Context
Adjacent segment disease represents a significant cause of revision spinal surgery in Australia. The Australian Spine Registry, when fully operational, will provide valuable national data on ASD rates and outcomes.
Management follows international evidence-based guidelines with both conservative and surgical options available through public and private hospital systems. Access to revision spine surgery may involve longer wait times in public systems, with complex cases often managed at quaternary spine centers in metropolitan areas.
Bone health optimization through vitamin D supplementation and treatment of osteoporosis is particularly relevant in the Australian setting. Smoking cessation support through Quitline and general practice is important for prevention and treatment success.
Exam Cheat Sheet
Adjacent Segment Disease
High-Yield Exam Summary
Key Numbers
- •Symptomatic ASD: 2.5% per year
- •Radiographic ASD at 10yr: 30%
- •Reoperation rate: 10-15% at 10yr
- •PI-LL mismatch: less than 10 degrees target
Risk Factors
- •Pre-existing adjacent degeneration (strongest)
- •Long fusion (more levels = more risk)
- •Sagittal imbalance/loss of lordosis
- •Fusion ending at L5 (vs S1)
- •Wide decompression destabilizing facets
Treatment Approach
- •Conservative first: PT, NSAIDs, injections
- •Decompression alone: stable, preserved disc
- •Fusion extension: instability, spondylolisthesis
- •Address sagittal imbalance when present
Prevention Strategies
- •Shortest necessary fusion length
- •Restore appropriate sagittal balance
- •Preserve adjacent facet joints
- •Smoking cessation, weight management
Exam Traps
- •Confusing radiographic and symptomatic ASD
- •Decompression alone with instability
- •Ignoring sagittal balance
- •Not discussing ASD with fusion patients