Hip-Spine Syndrome

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Hip-Spine Syndrome (HSS) describes the clinical challenge presented by patients experiencing concurrent symptomatic pathology in both the hip joint and the lumbar spine. First conceptualized by Offierski and MacNab in 1983, this syndrome highlights the diagnostic and therapeutic difficulties arising from overlapping pain patterns and the complex biomechanical relationship between these two regions. Common presentations include combinations of low back pain, buttock pain, groin pain, and radiating lower extremity symptoms, making it difficult to pinpoint the primary pain generator. The prevalence of conditions contributing to HSS, such as hip osteoarthritis (OA) and degenerative lumbar spinal stenosis (LSS), is increasing, particularly within the aging population. Hence it is likewise common for both hip and lumbar spine problems to co-exist. This demographic trend underscores the growing clinical significance of HSS.

Crucially, HSS represents more than just the coexistence of two separate pathologies; it implies a functional and biomechanical interdependence mediated by the lumbopelvic complex. Pathological changes or altered mechanics in the hip can induce compensatory changes and stress in the lumbar spine, and conversely, spinal pathology can significantly impact hip joint function and loading. This intricate relationship is particularly relevant when considering major surgical interventions like total hip arthroplasty (THA) or lumbar spine surgery (decompression or fusion), as procedures addressing one region can have profound, sometimes adverse, effects on the other. For instance, pre-existing spinal fusion is a known risk factor for instability after THA.

Classification

The term "Hip-Spine Syndrome" was introduced by Offierski and MacNab in 1983 to describe patients, typically older adults, presenting with concurrent symptomatic hip osteoarthritis and degenerative lumbar spine disease, often lumbar stenosis. Their initial work highlighted the diagnostic challenge posed by overlapping low back and groin pain originating from these distinct but potentially interrelated sources. Since this original description, the concept has broadened considerably. The modern understanding of HSS encompasses a wider spectrum of pathologies in both regions. Hip pathologies now include not only OA but also conditions like femoroacetabular impingement (FAI), acetabular labral tears, hip dysplasia, and avascular necrosis. Similarly, relevant lumbar spine pathologies extend beyond stenosis to include facet arthropathy, symptomatic disc disease (annular tears and endplate disease), spondylolisthesis, and sacroiliac joint dysfunction.

A distinction is sometimes made between Hip-Spine Syndrome (HSS), where the primary pathology or driver of symptoms originates in the hip, and Spine-Hip Syndrome (SHS), where the primary pathology resides in the spine. This distinction emphasizes the directionality of the biomechanical influence, although in many clinical scenarios, the relationship is bidirectional or difficult to ascertain definitively.

Offierski and MacNab proposed a classification system based on their retrospective review, categorizing HSS presentations into four types:

1. Simple HSS: Pathologic changes exist concurrently in the hip and lumbar spine, but clinical evaluation clearly identifies either the hip or the spine as the predominant source of the patient's disability. Treatment targeted at the primary source is expected to provide significant relief.  
2. Complex HSS: Coexisting hip and spine pathologies are present, but the primary source of disability is unclear even after initial clinical assessment. Further diagnostic investigations, such as selective injections, are typically required to differentiate the main pain generator.
3. Secondary HSS: The hip and spine pathologies are interdependent, with dysfunction or deformity in one region directly causing or exacerbating symptoms in the other. A classic example is a hip flexion contracture leading to compensatory lumbar hyperlordosis, which in turn may cause or worsen facet joint pain or foraminal stenosis, particularly at L3-L4. Similarly, spinal deformity like scoliosis can alter pelvic orientation and hip mechanics.
4. Misdiagnosed HSS: This category refers to situations where the primary pain generator was incorrectly identified, leading to inappropriate or ineffective treatment and persistent symptoms.

While this classification provides a useful historical framework, the complexity of biomechanical interactions revealed by modern analysis of spinopelvic parameters and mobility suggests its limitations. he "Secondary" category hints at the biomechanical link, but the dynamic interplay, especially involving non-arthritic hip conditions like FAI and the variable contributions of the spine and pelvis to movement, requires a more nuanced understanding. The newer Bordeau classification attempts to incorporate spinopelvic parameters and mobility to better stratify patients, but is mainly for patients undergoing THA.

Pathomechanics

The foundation of HSS lies in the integrated function of the lumbopelvic complex (LPC) – the anatomical and functional unit comprising the lumbar spine, the pelvis, and the hip joints. The pelvis serves as the critical link, connecting the lower extremities (via the hip joints) to the axial skeleton (via the lumbosacral junction). The concept of the spine-hip relation (SHR) describes the dynamic interaction between the spine/pelvis and the hips. Because the pelvis is a shared structure, any change in the position, alignment, or mobility of the lumbar spine affects pelvic orientation, which in turn influences the functional orientation of the acetabulum and hip joint mechanics. Conversely, changes in hip joint mobility or alignment necessitate compensatory adjustments in pelvic and lumbar spine posture and movement. This interconnectedness means that pathology in one area rarely exists in isolation; it almost inevitably affects the function and loading of the adjacent region. Understanding this pelvic role is central to comprehending HSS, as quantified by spinopelvic parameters.

The kinematic relationship between the lumbar spine and the hip joints during sagittal plane movements, known as the lumbopelvic rhythm or hip-spine coordination, exemplifies this biomechanical link. Coordinated motion between the femur, pelvis, and spine allows for a greater functional range of motion than any single segment could achieve alone.

During forward bending (e.g., touching toes with knees straight), the movement is typically initiated by flexion of the lumbar spine, followed by anterior tilting of the pelvis at the hip joints. This coordinated sequence is controlled by eccentric contraction of the lumbar erector spinae and hip extensor muscles (gluteals, hamstrings) to counterbalance gravity, while hip flexors contract concentrically.

Returning to the upright position involves a reversal of this rhythm: initiation occurs with posterior pelvic tilting driven by concentric contraction of the hip extensors, followed by active extension of the lumbar spine. Hip flexors contract eccentrically to control the movement.

Dysfunction within this system, such as tightness of the hip flexors or weakness of the hip extensors or lumbar extensors, disrupts the normal rhythm. For example, if hip extensors are weak, initiating the return to standing may overload the lumbar extensors. Conversely, limited hip flexion (e.g., due to hamstring tightness or hip pathology) may force excessive lumbar flexion during forward bending. Similarly, limited hip extension (e.g., due to hip flexor contracture or anterior hip pathology) forces compensatory lumbar extension (hyperlordosis) or anterior pelvic tilt during standing or gait. This altered distribution of movement and load increases mechanical stress on either the spinal structures (discs, facets, foramina) or the hip joint, contributing to the development or exacerbation of pain and degenerative changes characteristic of HSS.

Secondary HSS

Hip Pathology Leading to Spine Compensation

When the hip joint is affected by pathology that restricts its motion or alters its alignment, the lumbar spine and pelvis must compensate to maintain function, potentially leading to spinal symptoms or degeneration.

Hip Stiffness / Osteoarthritis: OA often leads to pain and reduced hip range of motion (ROM), particularly flexion, extension, and internal rotation. This stiffness forces the LPC to increase its contribution to movement. For example, limited hip flexion may necessitate increased lumbar flexion during activities like sitting down. Limited hip extension during gait forces increased pelvic motion (anterior tilt) and compensatory changes in LL (often increased lordosis initially, but potentially decreased lordosis with associated pelvic retroversion in stiff hips trying to maintain upright posture). This altered lumbopelvic rhythm and increased spinal motion can overload facet joints, discs, and ligaments, contributing to LBP and potentially accelerating degenerative changes. Hip OA also leads to characteristic gait alterations (e.g., decreased speed, step length, hip extension) that further impact spinal loading.  

Hip Flexion Contracture: A common finding in hip pathology, this limits terminal hip extension. To achieve an upright stance, the body compensates by increasing anterior pelvic tilt and subsequently increasing lumbar lordosis (hyperlordosis). This sustained hyperlordosis increases compressive loads on the posterior elements of the lumbar spine (facet joints) and can narrow the intervertebral foramina, leading to facetogenic pain or symptoms of nerve root impingement (radiculopathy), especially at the L3-L4 or L4-L5 .

Femoroacetabular Impingement (FAI), Ischiofemoral Impingement (IFI), and Abnormal Femoral Version: These non-arthritic hip conditions can also drive spinal compensation. Cam-type FAI limits hip flexion, potentially forcing increased pelvic posterior tilt or lumbar flexion during activities requiring deep hip flexion. IFI limits hip extension, potentially causing increased lumbar extension or anterior pelvic tilt during terminal stance or activities involving hip extension. Abnormal femoral version (anteversion or retroversion) alters rotational kinematics and can affect hip flexion/extension limits. These limitations in hip motion necessitate compensatory movements in the pelvis and lumbar spine, leading to increased stress transmission and potentially LBP. Cadaveric studies simulating IFI demonstrated increased facet joint loading (L3-S1) during hip extension, while simulated cam FAI increased lumbar disc loading during hip flexion. Altered femoral version was also shown to impact lumbar facet loading levels.

Spine Pathology Leading to Hip Compensation

Conversely, primary spinal pathology, particularly conditions affecting sagittal alignment or mobility, can force compensatory changes at the hip joint, increasing the risk of hip symptoms or complications, especially after THA.

Lumbar Stiffness / Fusion: Degenerative changes leading to a stiff lumbar spine ("biological arthrodesis") or surgical spinal fusion significantly reduce the contribution of the lumbar spine and pelvis to overall sagittal plane motion. To achieve necessary functional movements like transitioning from standing to sitting (which normally involves pelvic retroversion and lumbar flattening), the hip joints must undergo a greater range of flexion and extension. This increased demand on hip ROM, often occurring with an abnormally oriented pelvis due to the spinal condition, significantly elevates the risk of impingement (either bone-on-bone or prosthesis-on-bone/prosthesis-on-prosthesis) and subsequent instability or dislocation, particularly following THA. The risk is particularly high in patients with long spinal fusions (multiple levels), especially those extending to the sacrum. Dislocation rates after THA in patients with prior LSF are reported to be significantly higher than in patients without spinal fusion.  

Loss of Lumbar Lordosis / Flatback Deformity: Defined by an insufficient LL relative to PI (PI-LL mismatch > 10°), flatback deformity alters spinopelvic alignment. It is often associated with compensatory pelvic retroversion (increased PT) to maintain upright balance. This posterior pelvic tilt functionally retroverts the acetabulum, decreasing anterior coverage and increasing posterior coverage. This altered orientation increases the risk of anterior impingement during extension and posterior instability/dislocation during flexion activities, especially after THA. Patients may compensate by increasing hip extension while standing.

Sagittal Imbalance: An increased SVA signifies that the body's center of gravity is shifted anteriorly. The body attempts to compensate through mechanisms like pelvic retroversion (increased PT), reducing residual LL, extending the hips, and flexing the knees and ankles. These compensations are energy-inefficient and place abnormal stresses on the hip joints and surrounding musculature.  

Bidirectionality

The relationship between hip and spine pathology is often bidirectional, creating a potential vicious cycle. Hip dysfunction can lead to compensatory spinal mechanics that accelerate spinal degeneration , while spinal dysfunction can lead to compensatory hip mechanics that increase stress on the hip joint, potentially causing pain, accelerating hip degeneration, or leading to THA complications. Some cadaveric evidence suggests that lumbar degenerative disc disease often precedes the development of hip OA, implying that altered spinal biomechanics may be a causative factor in hip degeneration in many individuals.

Epidemiology

While the precise prevalence of Hip-Spine Syndrome as a distinct clinical entity remains unknown, the underlying components – degenerative conditions of the hip and lumbar spine – are exceedingly common, particularly as the population ages.

Given the high prevalence of both hip OA and LSS individually, their co-occurrence (multimorbidity) is expectedly common. Systematic reviews attempting to quantify this overlap have found wide-ranging prevalence estimates (0% to 54%), heavily influenced by the case definitions used (clinical symptoms, imaging findings, or combined) and whether LSS or hip/knee OA was considered the primary (index) condition.

HSS is traditionally associated with older adults due to the degenerative nature of the initially described pathologies (OA and LSS). However, the underlying biomechanical principles of hip-spine interaction are relevant across age groups. Younger individuals, including athletes, can present with concurrent hip pathologies (e.g., FAI, labral tears, dysplasia) and lumbar spine issues (e.g., especially internal disc disruption, but also spondylolysis, and facet pain) that influence each other biomechanically.

Clinical Features

Patients with Hip-Spine Syndrome typically present with a constellation of symptoms involving the lower back, pelvis, groin, and lower extremities. A hallmark of the condition is the significant overlap in pain referral patterns between hip and lumbar spine pathologies, making clinical differentiation challenging. Pain can manifest in the low back, buttocks, groin, anterior, posterior, or lateral thigh, and frequently radiates to the knee or even below the knee, regardless of the primary source. Always consider somatic referred pain.

History

While overlap is common, certain features are more characteristic of a primary hip problem:

Pain Location: Groin pain is a relatively specific indicator of hip pathology, reported in up to 84% of hip OA patients and associated with a sevenfold higher likelihood of having a hip disorder (alone or combined with spine) versus a spine-only disorder. However, buttock pain is also very common, identified as the most frequent site of referred pain (71%) in one study of patients with confirmed intra-articular hip pathology. Thigh pain (anterior, lateral, or posterior) is also frequent. Pain referred below the knee occurs in a substantial minority (up to 47%) of patients with hip OA. Pain originating from the hip rarely refers to the lumbar spine itself. The "C-sign," where the patient cups their hand over the greater trochanter with fingers pointing towards the groin, is often associated with intra-articular hip pathology.  

Pain Character and Triggers: Hip pain is often described as a deep ache, typically exacerbated by weight-bearing activities like walking or standing, and by movements involving hip rotation or end-range motion. Patients often report difficulty with activities requiring hip flexion and rotation, such as putting on shoes and socks, or getting in and out of a car. Mechanical symptoms like clicking, snapping, or catching suggest intra-articular issues like labral tears or loose bodies. Morning stiffness, usually lasting less than 60 minutes, can be present. Pain provoked by pivoting, prolonged sitting, or transitioning from sitting to standing is also common. Startup pain (initial pain upon walking that transiently improves then worsens) may suggest a loose THA component.

The following features may be suggestive of a primary spinal source:

Pain Location: Low back pain is common, often radiating into the buttock(s) and lower extremity(ies) in a dermatomal or sclerotomal pattern. Groin pain is relatively uncommon with lumbar pathology, unless it involves the upper lumbar nerve roots (L1, L2) due to foraminal stenosis or a high disc herniation.

Pain Character and Triggers: Neurogenic claudication is the classic symptom of LSS: buttock or leg pain (often bilateral, but can be unilateral) that worsens with walking or prolonged standing and is relieved by sitting or leaning forward (spinal flexion), such as when pushing a shopping cart ("shopping cart sign"). Pain described as burning, tingling, electric shock-like, or associated with numbness or weakness strongly suggests nerve root involvement (radiculopathy). Symptoms are often aggravated by lumbar extension (standing, walking downhill) and relieved by flexion (sitting, bending forward). Startup back or buttock pain may indicate spinal instability.

Examination

Gait: Observe for an antalgic gait (shortened stance phase on the affected side), which suggests painful hip loading. A limp is common with hip pathology. Trendelenburg gait (pelvic drop on the swing side) indicates hip abductor weakness, which can stem from hip pathology (pain inhibition, muscle pathology) or L5 radiculopathy.

Range of Motion (ROM): Assess active and passive hip ROM in all planes. Limited internal rotation (IR) in flexion is a sensitive sign for intra-articular hip pathology (OA, FAI). Pain reproduction at the end-range of IR is also highly suggestive. Reduced hip flexion and extension ROM are also common findings. Assess for hip flexion contracture using the Thomas test or Ely's test. Studies show reduced hip flexion and IR ROM correlate with worse LBP-related functional scores.

Strength Testing: Evaluate strength of key hip muscle groups: flexors (iliopsoas - L1-3), extensors (gluteus maximus - S1), abductors (gluteus medius/minimus - L5), adductors, and rotators. Weakness, particularly in abductors and extensors, may be present due to pain inhibition or deconditioning.

Provocative Maneuvers: Several tests aim to reproduce hip pain by stressing specific structures. Note: Sensitivity and specificity values can vary significantly between studies due to differences in patient populations, reference standards, and test execution. These tests should be interpreted within the full clinical context.

Key Provocative Tests in Hip-Spine Syndrome Evaluation

Test Name	Brief Procedure Description	Positive Finding / Interpretation	Primary Target Pathology	Reported Diagnostic Accuracy Range (Sensitivity / Specificity)
Hip Tests
FADIR Test	Passive hip flexion, adduction, and internal rotation	Reproduction of anterior groin/hip pain	Femoroacetabular Impingement (FAI), Anterior Labral Tear	Sensitivity: 59-100% / Specificity: 4-75% (Good screening tool )
FABER (Patrick's) Test	Supine, figure-4 position (flexion, abduction, ER), stabilize contralateral ASIS, apply posterior force to knee	Reproduction of groin pain (hip), SIJ pain (SIJ), or posterior hip pain	Intra-articular Hip Pathology, Iliopsoas Strain, SI Joint Dysfunction	Sensitivity: 82-89% / Specificity: Low (e.g., <35%)
Internal Rotation Overpressure	Passive hip internal rotation at 90° flexion, apply overpressure at end range	Reproduction of hip/groin pain	Intra-articular Hip Pathology	Sensitivity: High (e.g., 0.91) / Specificity: Low
Spine Tests
Straight Leg Raise (SLR)	Supine, passive lifting of extended leg	Reproduction of radicular leg pain (below knee) between 30-70° hip flexion	Sciatic Nerve / L5, S1 Nerve Root Irritation (esp. Disc Herniation)	Sensitivity: 84-92% / Specificity: 26-78% (High sensitivity makes negative test useful for ruling out. Lower sensitivity in LSS )
Femoral Nerve Stretch Test	Prone or side-lying, passive knee flexion +/- hip extension	Reproduction of anterior thigh pain	Femoral Nerve / L2, L3, L4 Nerve Root Irritation	Sensitivity: High (e.g., 86-100%) / Specificity: Moderate (e.g., 64-83%) (False positives with hip flexor tightness. Lower sensitivity in LSS )
Slump Test	Seated slumped posture with sequential cervical flexion, knee extension, ankle dorsiflexion	Reproduction of radicular symptoms, altered by neck position changes	Sciatic Nerve / Dural Sensitivit	Accuracy varies depending on criteria and population.

Investigations

Plain Radiographs

These are the recommended initial imaging modality.

Hip: Standard views include an anteroposterior (AP) pelvis and a lateral view (cross-table or frog-leg). Weight-bearing views can better assess joint space narrowing in OA. Radiographs can reveal signs of OA (osteophytes, joint space narrowing, subchondral cysts), FAI morphology (cam lesion, pincer lesion, acetabular version), signs suggestive of avascular necrosis (subchondral lucency, femoral head collapse), or fractures.  

Spine: AP and lateral views of the lumbar spine are standard. They assess overall alignment (lordosis, scoliosis), disc height, facet joint arthropathy, osteophytes, spondylolisthesis, and fractures. Critically, for assessing sagittal balance and spinopelvic relationships, standing full-length lateral spine radiographs (including the pelvis and femoral heads) are essential. These allow measurement of PI, PT, SS, LL, and SVA. Sitting lateral radiographs are also necessary to evaluate spinopelvic mobility by comparing parameters between standing and sitting positions (e.g., calculating ΔSS or ΔPT).

MRI

Hip: MRI is superior for evaluating soft tissues like the labrum (MR Arthrography is often preferred for labral tears), cartilage, tendons, and muscles. It is the most sensitive modality for detecting early avascular necrosis, stress fractures, bone marrow edema, bursitis, tendinopathy, and tumors. MRI can show muscle edema associated with impingement syndromes like IFI (quadratus femoris edema).

Spine: MRI is the gold standard for evaluating neural elements (spinal cord, nerve roots) and intervertebral discs. It clearly depicts disc herniations, spinal stenosis (central, foraminal, lateral recess), nerve root compression, ligamentum flavum hypertrophy, facet joint effusions/cysts, infections, and tumors.

CT and EOS

Hip: Useful for precise assessment of bony morphology in FAI, measuring femoral and acetabular version, evaluating complex fractures, and pre-operative planning or post-operative assessment of THA components.

Spine: Excellent for visualizing bony elements like osteophytes, facet arthropathy, pars defects (spondylolysis), and assessing the status of spinal fusion. CT Myelography (CT after intrathecal contrast injection) can be used to evaluate stenosis and nerve compression if MRI is contraindicated or inconclusive.

EOS Imaging: This technology provides low-dose, simultaneous biplanar (AP and lateral) radiographic images in functional weight-bearing positions (standing, sitting). It allows for accurate 3D reconstruction and precise measurement of spinopelvic parameters and assessment of changes between positions, making it ideal for evaluating sagittal balance and spinopelvic mobility in HSS patients, particularly when THA is being considered.

Diagnostic Injections

When the clinical picture and imaging findings remain ambiguous regarding the primary pain source (i.e., complex HSS), diagnostic injections are invaluable tools. Image guidance (fluoroscopy or ultrasound) is strongly recommended to ensure accurate needle placement.

The interpretation of diagnostic injections requires careful consideration of the magnitude, duration, and nature of pain relief, correlated with the patient's typical symptoms. False positives (placebo effect) and false negatives (inaccurate placement, insufficient anesthetic volume/concentration) can occur.

Hip Injection: A significant reduction in the patient's typical pain (commonly defined as ≥50% or ≥80% relief on a visual analog scale) immediately following the anesthetic component strongly implicates the hip joint as a major pain generator. This positive response has high reported diagnostic accuracy for identifying intra-articular pathology and predicting a successful outcome after THA, with sensitivity often cited around 90% and specificity/positive predictive value approaching 100% in some studies (see Hip Osteoarthritis for more detail). Failure to achieve significant relief suggests an extra-articular hip source or a non-hip origin (e.g., spine). It is crucial to assess the anesthetic response for diagnosis; the steroid effect is primarily therapeutic and occurs later. Potential chondrotoxicity of local anesthetics warrants caution, especially in non-arthritic hips.

Medial Branch Blocks: Medial branch blocks are the most well studied for diagnosis facet joint origin of pain. Dual comparative blocks with different duration anaesthetics are used with double blinding. Complete abolition of pain (100%) is the gold standard, but some centres use 80% relief as a criterion. Anything below 80% as a cut off is not evidence based.

Selective Nerve Root Blocks: This is controversial because one cannot be sure that only one nerve root has been blocked. A positive response can be supportive for diagnosing radicular pain from referred hip pain, but the diagnostic value is not as strong as for intra-articular hip and medial branch blocks.

Management

Full discussion of management of all relevant conditions is outside the scope of this article. However one highly relevant challenge is managing HSS patients requiring treatment (especially surgery) for both hip and spine is determining the optimal sequence. There is no universal consensus, and evidence from comparative studies is conflicting, leading to considerable debate among surgeons.

Arguments for THA First:

• Potential LBP Relief: THA can alleviate or resolve concurrent LBP in a significant proportion of patients (up to 82% in some studies), potentially obviating the need for subsequent spine surgery.  
• Addressing Hip Drivers: Correcting hip pathology (e.g., releasing flexion contractures, restoring motion) may improve spinopelvic alignment and reduce compensatory stress on the spine.
• Lower THA Dislocation Risk: Performing THA before LSF avoids operating on a hip adjacent to a stiffened or fused spine, which is associated with a higher risk of postoperative THA dislocation. Database studies suggest LSF after THA has a lower dislocation rate than THA after LSF.
• Facilitating Spine Surgery: A mobile, pain-free hip may make positioning and recovery from subsequent spine surgery easier.

Arguments for Spine Surgery First:

• Prioritizing Neurological Deficits: Urgent or progressive neurological symptoms (weakness, myelopathy, severe claudication) generally warrant prioritizing spinal decompression/stabilization.
• Optimizing Pelvic Alignment for THA: Correcting significant spinal deformity or sagittal imbalance first may restore more normal pelvic orientation, potentially allowing for more accurate and stable THA component placement.
• Potential Reduction in Spine Reoperation: Some evidence suggests that addressing severe hip OA after LSF may increase the risk of subsequent spinal revision surgery, potentially favoring spine surgery first in some scenarios.
• Patient-Reported Outcomes: At least one cohort study reported better health-related quality of life outcomes when LSS surgery preceded THA.

Summary

Hip-Spine Syndrome represents a challenging clinical scenario characterized by the coexistence of symptomatic hip and lumbar spine pathologies. The overlapping pain referral patterns frequently complicate diagnosis, necessitating a comprehensive approach that integrates a detailed history, a thorough physical examination of both the hip and spine regions, and judicious use of targeted imaging and diagnostic injections to accurately identify the primary source(s) of pain.

Understanding the intricate biomechanical relationship mediated by the lumbopelvic complex is fundamental to grasping the pathophysiology of HSS. Alterations in spinopelvic alignment (quantified by parameters like PI, PT, SS, LL, SVA) and mobility play crucial roles, as pathology or stiffness in one region often leads to compensatory stress and potential secondary pathology in the other. This interdependence is particularly critical when planning surgical interventions like THA, where abnormal spinopelvic mechanics, especially spinal stiffness or fusion, significantly increase the risk of complications such as impingement and dislocation.

Management should be individualized, typically beginning with a trial of comprehensive conservative therapy focusing on physical therapy tailored to address specific hip and spine impairments, alongside appropriate pharmacotherapy for symptom control. Surgical intervention is reserved for patients with refractory symptoms or specific indications like progressive neurological deficits or advanced joint destruction. The optimal sequence for performing hip versus spine surgery in patients requiring both remains controversial, lacking definitive high-level evidence. The decision requires careful consideration of the predominant symptoms, neurological status, severity of each pathology, planned surgical extent, and patient factors, often benefiting from multidisciplinary input.

While favorable outcomes are achievable with both conservative and surgical management, the prognosis for HSS patients may be tempered compared to those with isolated hip or spine conditions. The presence of co-pathology, particularly prior spinal fusion, is associated with potentially inferior results and higher complication rates for subsequent hip surgery (THA or arthroscopy). Nonetheless, significant functional improvements and pain relief are attainable with accurate diagnosis and appropriately targeted treatment strategies. Continued research into optimal diagnostic algorithms, refined surgical techniques considering spinopelvic dynamics, and evidence-based sequencing protocols is needed to further improve outcomes for this complex patient population.

Resources

Hip Spine Syndrome - McCurdy 2024.pdf - 671 KB (f)

Hip-spinesyndrome - Mccullough 2012.pdf - 346 KB (f)

Differentiating hip from lumbar spine pathology - Buckland 2017.pdf - 861 KB (f)

Hip spine syndrome sagittal balance - Abdallah 2020.pdf - 540 KB (f)

Spine hip relations - Riviere 2018.pdf - 1.02 MB (f)

Literature Review

Literature Review

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