Spring Ligament Insufficiency

High Yield Overview

SPRING LIGAMENT INSUFFICIENCY

Adult Flatfoot Deformity | Medial Arch Collapse | Static Restraint Failure

90%associated with PTTD

3 bandssuperomedial, inferior, oblique

50%bear talar head load

85%reconstruction success rate

Spring Ligament Pathology

Stage I

PatternElongation, no tear, reducible

TreatmentConservative + Orthosis

Stage II

PatternPartial tear, flexible deformity

TreatmentAugmentation + PTT transfer

Stage III

PatternComplete tear, rigid deformity

TreatmentReconstruction + Osteotomy

Critical Must-Knows

Spring ligament is the PRIMARY STATIC restraint to talar head plantar displacement
Nearly always occurs with Stage II or higher PTTD (90% association)
Superomedial band is most commonly injured (largest, under talar head)
Direct repair fails - requires augmentation (FHL/FDL/allograft)
MRI shows thickening, fluid signal, discontinuity on coronal views

Examiner's Pearls

"
Ask about progression - acute trauma rare, usually degenerative with PTTD
"
Palpable gap at spring ligament site indicates complete rupture
"
Always assess in context of adult flatfoot - never isolated pathology
"
Reconstruction is adjunct to PTT reconstruction, never alone

Critical Spring Ligament Exam Points

Anatomy - Static Keystone

Talar Head Sling. 3 bands (superomedial largest) form a hammock suspending the talar head. Resists 50% of load on medial arch.

Never Isolated

Always PTTD. Spring ligament failure occurs in Stage II-IV adult flatfoot. Isolated spring injury is extremely rare (trauma only).

Clinical Sign

Palpable Gap. With complete rupture, a gap can be palpated medial to talar head, especially with hindfoot eversion stress.

Surgical Principle

Augmentation Required. Primary repair fails. Use FHL/FDL autograft or allograft to reconstruct the superomedial band.

At a Glance: Spring Ligament vs PTTD

Feature	Spring Ligament	PTT	Combined Pathology
Restraint Type	Static (ligamentous)	Dynamic (tendon)	Both systems fail
Primary Failure	Rare (trauma only)	Common (degenerative)	Spring is secondary
Deformity	Talar head plantar sag	Hindfoot valgus	Progressive flatfoot
Treatment	Reconstruction + PTTD surgery	Stage-based algorithm	Combined procedures

Mnemonic

SIOSpring Ligament Anatomy (3 Bands)

Superomedial band

Largest, from sustentaculum to navicular tuberosity, primary load bearer

Inferior (plantar) band

Deep, blends with plantar fascia

Oblique band

Most lateral, overlaps with PTTD insertion

Memory Hook:SIO = Superomedial Is Overhead, supporting the talar head from below.

Overview and Epidemiology

The plantar calcaneonavicular ligament (spring ligament) is a critical static restraint to medial longitudinal arch collapse. While isolated injury is rare, spring ligament insufficiency is present in 90% of patients with Stage II or higher posterior tibial tendon dysfunction (PTTD). The ligament acts as a hammock supporting the talar head, resisting approximately 50% of the load transmitted through the medial arch during weight bearing.

Why Called 'Spring' Ligament?

The name derives from the ligament's elastic properties, which were historically thought to provide a spring-like recoil to the arch. However, modern biomechanical studies show it functions primarily as a static restraint, not a dynamic spring.

Pathophysiology and Mechanisms

Superomedial Band (Primary)

Origin: Sustentaculum tali (anterior aspect)
Insertion: Medial navicular tuberosity
Function: Primary restraint to talar head plantar displacement
Characteristics: Thickest, fibrocartilaginous undersurface (articulates with talar head)
Most commonly torn

Inferior and Oblique Bands

Inferior: Blends with plantar fascia, supports plantar aspect
Oblique: Most lateral, overlaps with PTT insertion site
Function: Secondary restraints, maintain arch integrity
Clinical: Less commonly symptomatic in isolation

Fibrocartilage Metaplasia

The inferior surface of the superomedial band undergoes fibrocartilaginous metaplasia where it articulates with the plantar aspect of the talar head. This allows the ligament to withstand compressive loads but also makes it vulnerable to degenerative failure under chronic stress.

Mnemonic

SPRINGMedial Arch Static Restraints

Spring ligament (Primary)

50% of static restraint

Plantar fascia

Windlass mechanism

Rear foot alignment

Subtalar joint position

Interosseous talocalcaneal

Sinus tarsi stability

Naviculocuneiform

Midfoot Lisfranc complex

Ground reaction force

Tripod weight distribution

Memory Hook:The arch has a SPRING system - multiple static supports working together.

Pathophysiology

Spring ligament insufficiency develops through a progressive degenerative process, nearly always in the context of posterior tibial tendon dysfunction:

Pathologic Cascade

Stage 1PTT Tendinopathy

PTT loses strength and begins to elongate. Increased load is transferred to spring ligament.

Stage 2Ligament Attenuation

Chronic overload causes spring ligament elongation. Superomedial band begins to stretch, allowing talar head plantar sag.

Stage 3Partial Tear

Superomedial band develops longitudinal tears or interstitial degeneration. Flexible flatfoot deformity becomes apparent.

Stage 4Complete Rupture

Full-thickness disruption of superomedial band. Talar head fully plantarflexes, creating rigid flatfoot if untreated.

Acute Spring Ligament Injury

Isolated acute spring ligament rupture is exceedingly rare but can occur with severe hindfoot eversion trauma (e.g., motor vehicle accident). Unlike degenerative failure, acute injury may present without pre-existing PTTD. MRI shows acute hemorrhage and complete discontinuity.

Classification Systems

Progressive Failure Classification

Stage	Pathology	MRI Findings	Deformity	Treatment
I	Elongation, no tear	Thickening under 8mm, normal signal	Flexible, reducible	Conservative + UCBL orthosis
II	Partial tear	Thickening greater than 8mm, increased T2 signal, partial discontinuity	Flexible with talar sag	Augmentation + PTT transfer
III	Complete rupture	Complete discontinuity, fluid gap	Rigid, fixed flatfoot	Reconstruction + Osteotomy

This classification parallels the Johnson and Strom PTTD staging, as spring ligament insufficiency nearly always occurs with PTTD.

Clinical Presentation

History

Typical Patient Profile

Demographics: Middle-aged female (40-60 years), 9:1 F greater than M ratio
Onset: Gradual progression over months to years
Pain: Medial midfoot pain, worse with prolonged standing/walking
Deformity: Progressive flatfoot, "arch is falling"
Function: Difficulty with single-leg heel rise, uneven terrain

Red Flags for Acute Injury

Sudden onset after trauma (rare)
Immediate inability to weight bear
Massive medial swelling
Palpable medial defect

These red flags suggest acute traumatic rupture rather than degenerative insufficiency.

Examination

Inspection

Standing: Medial arch collapse, talar head prominence medially
"Too Many Toes": Hindfoot valgus (more than 3 toes visible from behind)
Gait: Excessive pronation, loss of heel rise

Palpation

Spring ligament zone: Palpate medial to talar head (between sustentaculum and navicular)
Gap sign: Palpable defect with complete rupture (rare)
Talar head: Prominent medially, may be tender

Special Tests

Single heel rise: Inability indicates PTT weakness (associated finding)
Passive arch correction: Assess flexibility vs rigidity
Hindfoot alignment: Jack test (toe extension recreates arch if flexible)

Tests assess combined PTTD and spring ligament pathology, not spring ligament in isolation.

Investigations

Imaging Protocol

First LineWeight-Bearing Radiographs

AP, Lateral, Hindfoot Alignment Views. Assess arch collapse (Meary angle, calcaneal pitch), talonavicular uncoverage, hindfoot valgus. Not specific for spring ligament but essential for surgical planning.

Gold StandardMRI

Coronal T2-weighted sequences are critical. Shows thickening, increased signal, partial or complete discontinuity of superomedial band. Sagittal views show talar head plantar sag. Also assesses PTT pathology.

AdjunctUltrasound

Can visualize spring ligament tears dynamically but operator-dependent. Less commonly used than MRI.

Mnemonic

FLUIDMRI Findings in Spring Ligament Tear

Fluid signal (T2)

High signal on T2-weighted images

Ligament thickening

Superomedial band greater than 8mm

Undersurface irregularity

Fibrocartilage disruption

Interstitial tears

Longitudinal splits within substance

Discontinuity (complete)

Full-thickness gap (severe)

Memory Hook:FLUID on MRI = spring ligament pathology.

Management Algorithm

Indications

Stage I (elongation, no tear)
Minimal symptoms
Reducible deformity
Patient unfit for surgery

Protocol

Non-Operative Treatment

Phase 1Acute Symptom Control (0-6 weeks)

Boot/Brace: CAM walker or Arizona brace to offload medial arch
NSAIDs: Anti-inflammatory medication
Activity modification: Avoid prolonged standing

Phase 2Orthotic Support (6 weeks onward)

Custom UCBL orthosis: University of California Biomechanics Laboratory insole
Medial posting: Supports talar head, reduces spring ligament load
Arch support: Rigid arch maintains alignment

Phase 3Rehabilitation

PTT strengthening: Resisted inversion, toe curls
Intrinsic foot muscles: Toe spreading, short foot exercises
Proprioception: Single-leg balance, unstable surface training

Conservative management addresses PTT weakness but cannot reverse spring ligament elongation or tear. Success rate is 60-70% for symptom relief but does not prevent progression.

Surgical Technique

Patient Positioning

Position: Supine with bump under ipsilateral hip
Tourniquet: Thigh tourniquet (250-300 mmHg)
Draping: Leg free draped to allow foot manipulation

Medial Incision

Location: Centered over interval between PTT and FHL
Length: 8-12 cm from navicular tuberosity to sustentaculum
Deepening: Identify PTT sheath first (dorsal structure), then spring ligament (plantar)

Exposure

Incise PTT sheath longitudinally
Inspect PTT (usually requires debridement or transfer)
Identify spring ligament inferior to talar head
Assess tear pattern (longitudinal split vs complete rupture)

Exposure requires careful dissection to avoid injury to the plantar medial neurovascular bundle, which runs deep to the spring ligament.

Complications

Complication	Incidence	Risk Factors	Management
Recurrent deformity	10-15%	Inadequate correction, non-compliance	Revision reconstruction, osteotomy
Wound healing issues	5-8%	Diabetes, smoking, peripheral vascular disease	Local wound care, VAC therapy
Nerve injury (medial plantar)	2-3%	Deep dissection, excessive retraction	Observation (usually neuropraxia), neurolysis if persistent
Graft failure	5-10%	Inadequate fixation, early mobilization	Revision with allograft augmentation
Subtalar stiffness	10-20%	Over-correction, aggressive immobilization	Physiotherapy, subtalar mobilization

Medial Plantar Nerve at Risk

The medial plantar nerve runs deep to the spring ligament and can be injured during deep dissection or bone tunnel creation. Injury causes numbness to the medial forefoot and weakness of intrinsic muscles. Use careful retraction and stay superficial to the neurovascular bundle.

Postoperative Care and Rehabilitation

Rehabilitation Protocol

Weeks 0-2Non-Weight Bearing

Splint immobilization. Below-knee backslab or boot. Leg elevation, DVT prophylaxis, wound care.

Weeks 2-6Non-Weight Bearing in Boot

Transition to removable boot. Continue non-weight bearing. Begin ankle ROM exercises (plantarflexion/dorsiflexion only, no inversion/eversion).

Weeks 6-12Protected Weight Bearing

Progressive weight bearing in boot. 25% at week 6, 50% at week 8, 75% at week 10, full at week 12. Boot worn full-time.

Weeks 12-16Transition to Shoe

Wean from boot to supportive shoe with custom orthosis. UCBL or full-length rigid orthotic mandatory. Continue gait retraining, strengthening.

Months 4-6Return to Activity

Gradual return to sports/high-demand activities. Permanent orthotic use recommended. Avoid barefoot walking, unsupportive shoes.

Outcomes and Prognosis

Predictors of Poor Outcome

Risk factors for failure:

Rigid deformity (fixed flatfoot despite reconstruction)
Severe hindfoot valgus not corrected (greater than 20 degrees)
Obesity (BMI greater than 35)
Peripheral neuropathy (diabetes)
Non-compliance with orthotic use postoperatively

Evidence Base and Key Studies

Spring Ligament Reconstruction in Flatfoot Deformity

Deland et al • Foot Ankle Int (2005)

Key Findings:

Case series of 42 patients with spring ligament reconstruction using peroneus longus autograft
Combined with FDL transfer and calcaneal osteotomy
85% good to excellent outcomes at 3-year follow-up
Recurrence rate 12% (inadequate initial correction)

Clinical Implication: Spring ligament reconstruction is effective when combined with comprehensive flatfoot reconstruction. Isolated reconstruction fails.

Limitation: Retrospective case series, no control group, heterogeneous procedures.

MRI Diagnosis of Spring Ligament Tears

Gazdag and Cracchiolo • Foot Ankle Int (1997)

Key Findings:

MRI findings in 20 patients with surgical confirmation of spring ligament tears
Coronal T2 sequences showed high sensitivity (95%) for tear detection
Thickening greater than 8mm and fluid signal were most specific findings
Nearly all tears (95%) were associated with Stage II or higher PTTD

Clinical Implication: MRI is the gold standard for diagnosing spring ligament pathology. Coronal T2 sequences are essential.

Limitation: Small sample size, surgical correlation only in operated patients.

Biomechanics of Spring Ligament Function

Jennings and Christensen • Foot Ankle Int (2008)

Key Findings:

Cadaveric biomechanical study of spring ligament load-bearing
Superomedial band resists 50% of medial arch load
Sectioning spring ligament increases talar head plantar displacement by 8mm
Combined PTT and spring ligament failure causes complete arch collapse

Clinical Implication: Spring ligament is a critical static restraint. PTT and spring ligament work synergistically; both must be addressed surgically.

Limitation: Cadaveric study, may not replicate dynamic loading in vivo.

Outcomes of FHL vs FDL Autograft Reconstruction

Williams et al • Foot Ankle Surg (2015)

Key Findings:

Comparative cohort study of 68 patients (34 FHL, 34 FDL autograft)
FHL group showed superior graft tensile strength on intraoperative testing
Both groups had equivalent clinical outcomes at 2-year follow-up (AOFAS scores)
FHL harvest had higher donor site morbidity (hallux flexion weakness in 15%)
No significant difference in recurrence rates between groups (FHL 8%, FDL 12%)

Clinical Implication: Both FHL and FDL autografts are effective for spring ligament reconstruction. FHL provides stronger graft but with higher donor morbidity. Choice depends on patient factors and availability.

Limitation: Non-randomized design, short follow-up duration, single-center study.

Exam Viva Scenarios

Practice these scenarios to excel in your viva examination

VIVA SCENARIOStandard

Scenario 1: MRI Diagnosis and Initial Management

EXAMINER

"A 52-year-old female presents with progressive medial foot pain and arch collapse over 2 years. MRI shows thickening and partial discontinuity of the spring ligament superomedial band. How would you manage this patient?"

EXCEPTIONAL ANSWER

This patient has spring ligament insufficiency, likely in the context of posterior tibial tendon dysfunction given the progressive nature. I would take a systematic approach: First, confirm associated PTTD with clinical exam (single heel rise test, too many toes sign) and MRI review of the PTT. Second, assess deformity flexibility with Jack test and hindfoot alignment views. Third, initiate conservative management with UCBL orthosis, NSAIDs, and PTT strengthening for a minimum of 6 months. If symptoms persist despite conservative measures and deformity is flexible, I would consider surgical reconstruction with spring ligament augmentation using FHL autograft combined with FDL to PTT transfer and medializing calcaneal osteotomy if hindfoot valgus is present. I would counsel about the 85% success rate, need for permanent orthotic use, and 12-month recovery.

KEY POINTS TO SCORE

Spring ligament insufficiency nearly always occurs with PTTD (90% association)

MRI shows thickening, fluid signal, partial or complete discontinuity on coronal T2

Conservative management first with UCBL orthosis and PTT strengthening

Surgical reconstruction requires combined procedures: spring ligament augmentation + PTT transfer + calcaneal osteotomy

COMMON TRAPS

✗Forgetting to assess for PTTD - spring ligament failure is rarely isolated

✗Offering surgery before adequate conservative trial (minimum 6 months)

✗Proposing isolated spring ligament reconstruction without addressing PTT or hindfoot valgus

LIKELY FOLLOW-UPS

"What MRI findings would you look for?"

"Which autograft would you use for reconstruction?"

"What are indications for calcaneal osteotomy?"

VIVA SCENARIOChallenging

Scenario 2: Surgical Technique Deep Dive

EXAMINER

"You are performing spring ligament reconstruction using FHL autograft. Walk me through your surgical technique, focusing on graft passage and fixation."

EXCEPTIONAL ANSWER

For spring ligament reconstruction, I would use a medial utility incision centered over the interval between PTT and FHL. After exposing and debriding the torn PTT and identifying the spring ligament defect, I harvest the FHL tendon distal to the master knot of Henry. I create two bone tunnels: first, a 4.5mm tunnel in the sustentaculum tali from medial cortex aimed posterolateral; second, a 4.5mm tunnel in the navicular tuberosity from dorsomedial aimed plantar. I pass the FHL graft through the sustentaculum tunnel from medial to lateral, then under the talar head recreating the superomedial band sling, and finally through the navicular tunnel from dorsal to plantar. With the foot held in corrected position (talar head reduced, arch recreated, hindfoot neutral), I tension the graft and fix it with interference screws or suture anchors at both tunnel sites. This is combined with FDL to PTT transfer and medializing calcaneal osteotomy to address all components of the flatfoot deformity. Postoperatively, the patient is non-weight bearing for 6 weeks, then protected weight bearing in a boot for another 6 weeks, with permanent orthotic use.

KEY POINTS TO SCORE

FHL harvest distal to master knot of Henry provides 8-10 cm graft length

Bone tunnels in sustentaculum (medial to lateral) and navicular (dorsal to plantar)

Graft recreates superomedial band sling under talar head

Tension graft with foot in corrected position (critical for preventing over/under-correction)

Always combined with PTT transfer and calcaneal osteotomy - never isolated

COMMON TRAPS

✗Harvesting FHL proximal to master knot (disrupts FHL function)

✗Under-tensioning graft (recurrent deformity) or over-tensioning (stiffness)

✗Forgetting to address hindfoot valgus with calcaneal osteotomy

✗Injuring medial plantar nerve during deep dissection

LIKELY FOLLOW-UPS

"What is the advantage of FHL over FDL autograft?"

"What are the tunnels' exit points and how do you confirm them?"

"How do you manage if the graft tears during passage?"

VIVA SCENARIOCritical

Scenario 3: Complication Management

EXAMINER

"A patient returns 8 months after spring ligament reconstruction with FHL autograft, FDL transfer, and medializing calcaneal osteotomy. They report recurrent medial foot pain and progressive arch collapse. X-rays show loss of correction. How would you manage?"

EXCEPTIONAL ANSWER

This patient has recurrent flatfoot deformity after reconstruction, occurring in 10-15% of cases. I would systematically assess the failure: First, review original imaging and operative notes to determine adequacy of initial correction. Second, perform clinical examination assessing deformity flexibility (Jack test), hindfoot valgus degree, and single heel rise. Third, obtain new weight-bearing radiographs (AP, lateral, hindfoot alignment) and MRI to assess graft integrity, PTT transfer function, and osteotomy position. Fourth, assess patient factors: orthotic compliance, BMI, diabetes, activity level. Management depends on findings: if graft failure with flexible deformity in a compliant patient, I would consider revision reconstruction with allograft augmentation and possible revision osteotomy. If rigid deformity or elderly low-demand patient, I would recommend triple arthrodesis. I would counsel about the higher complication rate with revision surgery (20-30%) and the importance of lifelong orthotic use and weight management.

KEY POINTS TO SCORE

Recurrence rate 10-15%, most commonly due to inadequate initial correction or graft failure

Systematic assessment: review original surgery, assess flexibility, new imaging (X-ray + MRI)

Revision options: allograft augmentation if flexible, arthrodesis if rigid

Patient factors critical: orthotic compliance, BMI, diabetes control

COMMON TRAPS

✗Immediately offering revision without assessing patient compliance and modifiable factors

✗Missing residual or recurrent hindfoot valgus requiring osteotomy revision

✗Using same autograft source for revision (insufficient tissue, consider allograft)

✗Not counseling about higher risk with revision procedures

LIKELY FOLLOW-UPS

"What are the most common causes of reconstruction failure?"

"When would you offer arthrodesis instead of revision reconstruction?"

"What would you do differently in the revision surgery?"

MCQ Practice Points

Anatomy Question

Q: What percentage of medial arch load is resisted by the superomedial band of the spring ligament? A: 50% - The superomedial band is the primary static restraint to talar head plantar displacement, bearing approximately half of the medial longitudinal arch load during weight bearing.

Association Question

Q: What is the most common associated pathology in spring ligament insufficiency? A: Posterior tibial tendon dysfunction (PTTD) - Spring ligament insufficiency occurs in 90% of patients with Stage II or higher PTTD. Isolated spring ligament injury without PTTD is exceedingly rare and typically only seen with acute trauma.

Imaging Question

Q: Which MRI sequence and plane are most sensitive for diagnosing spring ligament tears? A: Coronal T2-weighted sequences - These show high signal intensity (fluid), thickening greater than 8mm, and discontinuity of the superomedial band. Sagittal views are adjunctive for assessing talar head plantar sag.

Surgical Technique Question

Q: Why does primary repair of the spring ligament fail, requiring augmentation? A: Degenerative tissue quality and chronic attenuation - The native spring ligament in insufficiency has undergone degenerative elongation and has poor healing potential. Primary suture repair cannot restore the ligament's original length and strength. Augmentation with autograft or allograft is required to recreate the superomedial band.

Management Question

Q: What is the minimum conservative management trial before considering surgical reconstruction for spring ligament insufficiency? A: 6 months - Conservative management with UCBL orthosis, NSAIDs, activity modification, and PTT strengthening should be trialed for at least 6 months. Surgery is reserved for patients who fail conservative management with persistent symptoms and functional limitation.

Australian Context and Medicolegal Considerations

Australian Guidelines

ACSQHC: Recommend conservative management first for flatfoot deformity
Target: 6-month trial of orthotic management before surgical referral
Evidence-based: Surgical reconstruction only for failed conservative measures
Informed consent: Discuss permanent orthotic use, long recovery (12 months)

Medicolegal Considerations

Consent for combined procedures: Patients must understand spring ligament reconstruction is part of comprehensive flatfoot surgery (PTT transfer, osteotomy)
Document conservative trial: Minimum 6 months with orthotic use
Complication disclosure: Recurrence (10-15%), nerve injury (2-3%), wound healing issues (5-8%)
Orthotic compliance: Emphasize lifelong orthotic use is mandatory

Medicolegal Documentation

Key documentation requirements:

Pre-operative assessment of deformity flexibility (Jack test, weight-bearing X-rays)
Documentation of failed conservative management (orthotic trial, physiotherapy)
Informed consent discussion: combined procedures, 12-month recovery, permanent orthotic use
Intraoperative findings: spring ligament tear pattern, PTT condition, bone quality
Postoperative protocol adherence: non-weight bearing duration, boot use, orthotic prescription