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Orthopaedic Surgery - Hip Replacement
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Basics
Total hip arthroplasty, commonly called hip replacement, is a reconstructive procedure used to treat advanced destruction of the hip joint.
Many forms of arthritis and other hip disorders can lead to progressive loss of articular cartilage, resulting in pain, stiffness, impaired walking, and loss of function.
When symptoms become severe and nonoperative treatment no longer provides adequate relief, the damaged joint can be replaced surgically with prosthetic components.
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Age Considerations
Hip replacement is most commonly performed in older adults, although it is increasingly used in younger patients when symptoms are severe.
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Older Patients
Older patients may have a greater burden of medical comorbidity and may therefore have increased perioperative risk from conditions such as:
Cardiovascular disease, pulmonary disease, renal dysfunction, frailty, or osteoporosis.
Preoperative medical optimization is especially important in this population.
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Younger Patients
Patients younger than approximately 50 years have a higher lifetime probability of requiring revision surgery because their expected lifespan may exceed the longevity of the prosthesis.
Their generally higher activity levels may also increase cumulative implant wear.
For this reason, joint-preserving or other alternative strategies should be considered when appropriate.
These may include:
Continued medical management, corrective osteotomy, selected hip-preserving procedures, or, rarely, hip arthrodesis.
Nevertheless, age alone is not an absolute contraindication to total hip arthroplasty when arthritis is severe and disabling.
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Implant Fixation
Hip components may be secured to bone with either:
Cemented fixation or uncemented biologic fixation.
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Cemented Fixation
Bone cement provides immediate mechanical fixation between the implant and bone.
It remains useful in selected patients, particularly those with poor bone quality or certain fracture patterns.
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Uncemented Fixation
Uncemented components have porous or roughened surfaces that permit bone ongrowth or ingrowth.
Over time, biologic fixation develops as host bone integrates with the implant surface.
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Prevention and Delay of Surgery
Progression to hip replacement cannot always be prevented.
However, symptoms and joint loading may sometimes be reduced by:
Weight reduction, low-impact exercise, activity modification, physical therapy, and appropriate treatment of the underlying hip disorder.
These measures may postpone surgery in selected patients.
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Epidemiology
Most hip replacements have historically been performed in patients older than 65 years, although the procedure is now increasingly common in younger adults.
The overall number of total hip arthroplasties continues to increase because of population aging, expanding indications, and favorable long-term outcomes.
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Risk Factors for Hip Disease Requiring Replacement
The risk factors depend on the underlying diagnosis.
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Primary Osteoarthritis
Factors associated with hip osteoarthritis include:
Age, obesity, abnormal hip morphology, previous trauma, and high cumulative mechanical loading.
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Osteonecrosis
Osteonecrosis of the femoral head may be associated with:
Prolonged systemic corticosteroid use, heavy alcohol use, trauma, radiation exposure, and certain hematologic or systemic diseases.
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Femoral Neck Fracture
Osteoporosis predisposes older adults to femoral neck fractures, some of which are treated with hemiarthroplasty or total hip replacement.
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Genetics
Primary hip osteoarthritis appears to have a familial component.
However, there is no simple Mendelian inheritance pattern.
Multiple genetic and environmental factors probably contribute.
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Pathophysiology
Regardless of the underlying cause, end-stage degenerative hip disease shares several important features.
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Cartilage Degeneration
The articular cartilage progressively loses:
Proteoglycans, normal matrix architecture, and mechanical resilience.
This leads to cartilage thinning, fissuring, and eventual loss.
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Subchondral Bone
As cartilage disappears, the underlying bone is subjected to abnormal loading.
This contributes to:
Subchondral sclerosis, cyst formation, osteophytes, deformity, pain, and progressive limitation of motion.
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Etiology
Primary osteoarthritis remains one of the most common indications for total hip arthroplasty.
Other causes of severe hip destruction include:
Post-traumatic arthritis, osteonecrosis, rheumatoid arthritis, sickle cell disease, recurrent hemarthrosis, Paget disease, ankylosing spondylitis, and other inflammatory arthropathies.
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Developmental Causes
Childhood and adolescent hip disorders can produce secondary osteoarthritis years later.
Examples include:
Slipped capital femoral epiphysis, developmental dysplasia of the hip, and Legg–Calvé–Perthes disease.
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Acute Fracture
Some acute displaced femoral neck fractures, particularly in older adults, may be treated directly with:
Hemiarthroplasty or total hip arthroplasty.
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Associated Conditions
Patients requiring hip replacement often have degenerative disease at other sites, including:
The opposite hip, knees, lumbar spine, shoulders, or other upper-extremity joints.
Coexisting musculoskeletal disease may influence rehabilitation and perceived outcome.
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Diagnosis
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Symptoms of Advanced Hip Arthritis
Pain from hip arthritis is classically felt in the:
Groin, anterior thigh, lateral hip, or knee.
Groin pain is particularly characteristic of intra-articular hip disease.
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Activity-Related Pain
Early symptoms are usually aggravated by:
Walking, standing, stair climbing, and other weight-bearing activity.
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Rest and Night Pain
As arthritis becomes advanced, pain may become present:
At rest, during the night, and with minimal activity.
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Walking Limitation
Severe disease may restrict walking to only a few blocks or even less before the patient must stop because of pain.
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Functional Disability
Patients may report difficulty with activities of daily living such as:
Putting on socks or shoes, dressing, grooming, climbing stairs, getting into a car, rising from a chair, and walking outdoors.
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Range of Motion
Advanced disease commonly causes progressive loss of:
Internal rotation, flexion, extension, and abduction.
Internal rotation is often one of the first movements to become painful and restricted.
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Gait
A painful or weak hip may produce:
Antalgic gait, abductor lurch, shortened stance time, or Trendelenburg gait.
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Indications for Considering Hip Replacement
Typical features include:
Severe pain and functional limitation consistent with physical and radiographic findings, failure of appropriate nonoperative treatment, substantial limitation of walking, and difficulty performing daily activities.
The decision to proceed with surgery is based primarily on the patient’s symptoms and functional impairment rather than radiographic severity alone.
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Physical Examination
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Neurovascular Examination
A complete neurologic and vascular assessment of the affected extremity should be documented before surgery.
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Range of Motion
Hip motion should be recorded, including:
Flexion, extension, internal rotation, external rotation, abduction, and adduction.
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Contractures
Fixed flexion or rotational contractures should be identified because they may affect:
Gait, pelvic position, leg length, and surgical planning.
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Leg-Length Discrepancy
True and apparent leg-length discrepancy should be assessed.
Patients should be informed that perfect equalization of leg length cannot always be achieved because joint stability and soft-tissue tension may take priority.
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Gluteal Strength
Hip abductor strength should be assessed, especially the gluteus medius and minimus.
Preexisting abductor weakness can contribute to postoperative limp.
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Gait Examination
The patient’s gait should be observed for:
Antalgia, Trendelenburg pattern, shortening, stiffness, and use of assistive devices.
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Pain With Motion
Advanced arthritis commonly causes pain at the extremes of hip motion.
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Trendelenburg Test
A positive Trendelenburg sign indicates inadequate hip abductor function or painful hip mechanics.
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Stinchfield Test
A resisted straight-leg raise may reproduce groin or anterior thigh pain from an intra-articular hip disorder.
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Laboratory Evaluation Before Surgery
Preoperative testing is individualized according to patient age, health status, and institutional protocol.
Common studies may include:
Complete blood count, electrolytes and renal function, coagulation testing when indicated, and other targeted laboratory studies.
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Additional Preoperative Testing
An electrocardiogram, chest imaging, or urinalysis may be obtained when clinically appropriate rather than routinely in every patient.
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Blood Management
Routine preoperative autologous blood donation is now uncommon.
Modern blood-management strategies may instead include:
Treatment of preoperative anemia, tranexamic acid, careful surgical hemostasis, and restrictive transfusion protocols.
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Imaging
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Plain Radiographs
Standard evaluation generally includes:
AP pelvis and lateral views of the affected hip.
These studies demonstrate:
Joint-space narrowing, osteophytes, subchondral sclerosis, cyst formation, deformity, and bone loss.
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Additional Views
Standing long-leg or other specialized radiographs may be useful when evaluating:
Limb-length discrepancy, deformity, prior osteotomy, complex anatomy, or alignment concerns.
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Differential Diagnosis
Not all hip-region pain is caused by the hip joint.
Important alternative diagnoses include:
Lumbar spinal stenosis, lumbar disc herniation, radiculopathy, greater trochanteric pain syndrome, occult stress fracture, and neoplasm.
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Neoplasm
Occult malignant disorders that may mimic degenerative hip pain include:
Metastatic bone disease, multiple myeloma, and primary bone or soft-tissue tumors.
Atypical pain, particularly severe night pain or systemic symptoms, should prompt further evaluation.
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Nonoperative Treatment Before Surgery
Total hip replacement is usually considered only after reasonable nonoperative measures have failed or become inadequate.
These may include:
Activity modification, weight reduction, NSAIDs, acetaminophen, physical therapy, walking aids, and selected intra-articular corticosteroid injections.
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Physical Therapy
Physical therapy has important roles both before and after arthroplasty.
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Preoperative Therapy
Prehabilitation may improve:
Strength, gait mechanics, familiarity with assistive devices, and postoperative expectations.
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Postoperative Therapy
Rehabilitation emphasizes:
Walking, transfers, hip and lower-extremity strengthening, progressive mobility, balance, and restoration of independence.
Particular attention is given to the:
Hip abductors, flexors, and extensors.
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Assistive Devices
Patients are taught safe use of:
A walker, crutches, or cane, depending on mobility and postoperative instructions.
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Medication
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Postoperative Analgesia
Pain control is generally multimodal and may include:
Acetaminophen, NSAIDs when appropriate, regional anesthesia techniques, and limited opioid medication for breakthrough pain.
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Venous Thromboembolism Prophylaxis
Patients undergoing total hip arthroplasty require prophylaxis against deep venous thrombosis and pulmonary embolism.
Options may include:
Aspirin, low-molecular-weight heparin, direct oral anticoagulants, or other anticoagulants, depending on individual thrombotic and bleeding risk.
Early mobilization and mechanical compression devices are also important.
Routine use of warfarin for every patient is no longer standard practice.
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Surgery
Total hip arthroplasty replaces both the femoral and acetabular sides of the joint.
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Femoral Component
The femoral head and part of the femoral neck are removed.
A prosthetic stem is inserted into the femoral canal and supports a modular head.
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Acetabular Component
The acetabulum is prepared and typically reconstructed with a metal shell.
A bearing liner, usually highly cross-linked polyethylene or ceramic, is inserted into the shell.
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Fixation
Both femoral and acetabular components may be:
Cemented, uncemented, or combined in a hybrid construct.
Fixation choice depends on:
Bone quality, age, anatomy, fracture pattern, and surgeon preference.
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Surgical Approaches
Several approaches may be used successfully.
No single approach is universally superior for every patient.
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Direct Anterior Approach
The direct anterior approach uses an internervous plane near the interval between the sartorius and tensor fascia lata superficially, with deeper dissection toward the anterior hip capsule.
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Structures at Risk
The lateral femoral cutaneous nerve is particularly susceptible to traction or injury and may produce numbness or dysesthesia over the anterolateral thigh.
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Anterolateral Approach
The Watson-Jones approach uses the interval between the:
Tensor fascia lata and gluteus medius.
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Direct Lateral Approach
In the direct lateral or Hardinge approach, part of the anterior abductor mechanism is elevated from the greater trochanter.
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Potential Concerns
Postoperative abductor weakness and limp may occur if healing is incomplete.
The superior gluteal nerve is vulnerable if the dissection extends too proximally.
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Posterior Approach
The posterior approach splits the gluteus maximus and releases the short external rotators to expose the capsule.
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Sciatic Nerve
The sciatic nerve lies near the operative field and must be protected.
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Dislocation
Historically, the posterior approach was associated with a higher dislocation rate.
Modern repair of the posterior capsule and external rotators, larger femoral heads, improved implant positioning, and contemporary techniques have reduced this difference substantially.
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Bearing Surfaces
The bearing surface is formed by the femoral head articulating against the acetabular liner.
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Ceramic or Metal on Polyethylene
A ceramic or metal femoral head articulating with highly cross-linked polyethylene is one of the most widely used modern combinations.
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Polyethylene Wear
Older conventional polyethylene could produce substantial wear debris, leading to:
Osteolysis and implant loosening.
Highly cross-linked polyethylene has substantially reduced wear.
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Metal-on-Metal Bearings
Metal-on-metal total hip bearings are rarely used in contemporary practice because of problems including:
Metal ion release, adverse local tissue reactions, pseudotumor formation, and high failure rates in some implant designs.
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Ceramic-on-Ceramic Bearings
Ceramic-on-ceramic bearings have very low wear.
Potential concerns include:
Noise or squeaking and rare ceramic fracture, although modern ceramics have markedly improved strength.
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Femoral Head Size
Larger femoral heads can increase:
Jump distance, stability, and impingement-free range of motion.
However, head size must be balanced against liner thickness, component design, and bearing mechanics.
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Minimally Invasive and Rapid-Recovery Techniques
Smaller incisions alone do not necessarily explain faster recovery.
Modern recovery has improved largely because of:
Refined surgical techniques, multimodal analgesia, tranexamic acid, early mobilization, standardized rehabilitation, and enhanced-recovery pathways.
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Follow-Up
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Prognosis
Total hip arthroplasty has excellent long-term outcomes.
Most patients experience:
Major pain relief, substantial improvement in walking ability, increased range of motion, and improved quality of life.
Many return to activities that had previously become impossible because of arthritis.
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Implant Longevity
Older studies demonstrated that approximately 85% of some cemented prostheses remained functional at 20 years.
Modern cemented and uncemented implants can both provide excellent long-term survivorship, with outcome strongly influenced by patient age, activity level, implant design, bearing surface, and surgical technique.
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Complications
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Medical Complications
Potential perioperative medical complications include:
Myocardial infarction, pneumonia, urinary retention, ileus, venous thromboembolism, and, rarely, death.
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Leg-Length Discrepancy
A perceived or true limb-length difference may occur after surgery.
Small discrepancies are often tolerated, but larger differences may cause gait disturbance or dissatisfaction.
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Deep Venous Thrombosis and Pulmonary Embolism
DVT and PE remain important complications, although routine chemical prophylaxis, mechanical compression, and early mobilization have greatly reduced risk.
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Infection
Periprosthetic joint infection is a serious complication that may require:
Antibiotic treatment, surgical debridement, implant exchange, or staged revision surgery.
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Dislocation
Dislocation may occur because of:
Component malposition, soft-tissue insufficiency, impingement, neurologic disease, or high-risk movement.
Risk is generally higher after revision arthroplasty than uncomplicated primary surgery.
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Periprosthetic Fracture
Fractures may occur around the femoral or acetabular components either during surgery or later after trauma.
Treatment depends on implant stability and fracture pattern.
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Heterotopic Ossification
Ectopic bone formation around the hip may restrict motion.
Most cases are mild, but severe cases can cause substantial stiffness.
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Implant Loosening
Components may loosen over time because of:
Wear, osteolysis, inadequate initial fixation, infection, or mechanical failure.
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Osteolysis
Particle-induced bone loss may develop around implants, historically most often from polyethylene wear debris.
Modern bearing surfaces have reduced but not eliminated this problem.
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Nerve Injury
Nerve palsy is uncommon.
The sciatic nerve is most frequently involved, although the femoral, obturator, superior gluteal, or lateral femoral cutaneous nerves may also be affected depending on the surgical approach.
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Revision Surgery
Revision may eventually be necessary because of:
Aseptic loosening, infection, recurrent dislocation, fracture, wear, osteolysis, instability, or component failure.
Revision surgery is generally more complex than primary arthroplasty.
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Patient Monitoring
Long-term clinical and radiographic follow-up is important even in patients who feel well.
Radiographs can detect:
Component migration, polyethylene wear, osteolysis, loosening, fracture, and other asymptomatic changes.
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Follow-Up Interval
Periodic radiographic assessment, often every 1–2 years after the early postoperative period, may be appropriate, with timing individualized according to implant age, symptoms, and surgeon preference.
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Dental Procedures and Antibiotic Prophylaxis
Routine antibiotic prophylaxis before dental procedures is not universally recommended for every patient with a total hip replacement.
The decision should be individualized according to current dental and orthopaedic guidance, especially in patients with:
Previous prosthetic joint infection, major immunocompromise, complex revision arthroplasty, or other specific high-risk circumstances.
Good dental hygiene and prompt treatment of active oral infection remain important.
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Orthopaedic Surgery - Hip Pain in the Child
Basics
Hip pain in a child usually refers to discomfort arising from structures around the hip and commonly perceived in the groin, lateral hip, anterolateral thigh, or even the knee.
The groin receives sensory innervation largely through branches of the femoral and obturator nerves, which helps explain why pathology within the hip joint is frequently perceived anteriorly.
Pain may originate from numerous structures, including:
The joint capsule and synovium, pelvis, proximal femur, surrounding muscles and tendons, peripheral nerves, blood vessels, buttock, groin, and pelvic structures.
Because several causes of pediatric hip pain require urgent treatment and may cause permanent disability if diagnosis is delayed, every child with significant hip pain or unexplained limp requires a careful evaluation.
Epidemiology
Transient synovitis is commonly reported as the most frequent cause of acute hip pain in children.
Several important pediatric hip disorders show a male predominance.
Historical male-to-female ratios include approximately:
Transient synovitis: 2:1
SCFE: approximately 2.5:1
Osteomyelitis: approximately 4:1
Legg–Calvé–Perthes disease: approximately 6:1
Septic arthritis also demonstrates a slight male predominance.
Incidence
Transient Synovitis
The lifetime risk of at least one episode of transient synovitis during childhood has been estimated at approximately 3%.
Legg–Calvé–Perthes Disease
Peak incidence occurs at approximately 6 years of age.
Historical incidence is approximately 1 per 1,500 children, although rates vary among populations.
Slipped Capital Femoral Epiphysis
SCFE occurs almost exclusively during preadolescence and adolescence.
Its incidence has historically been estimated at approximately 1 per 10,000 children, although prevalence varies substantially with age, sex, ethnicity, and obesity.
Risk Factors
Risk factors depend on the underlying diagnosis.
Important examples include:
Juvenile inflammatory arthritis, trauma, impaired immune function, obesity, and age.
Obesity, adolescence, and mechanical stress are particularly associated with SCFE.
Genetics
Most causes of pediatric hip pain do not follow a simple hereditary pattern.
A minority of patients with SCFE have a positive family history, historically reported in approximately 4% of cases.
Etiology
The two most common acute causes of hip pain in children are transient synovitis and septic arthritis, but the differential diagnosis is broad.
Transient Synovitis
Transient synovitis is a self-limited inflammatory process involving the hip joint.
Age
The average age at presentation is approximately 6 years, with most cases occurring between 3 and 8 years.
Associations
The disorder may follow:
A recent viral illness, minor trauma, or an allergic or inflammatory stimulus.
In many children, no clear precipitating cause is identified.
Septic Arthritis
Septic arthritis is a bacterial infection of the hip joint and represents an orthopaedic emergency.
Approximately two-thirds of cases historically occur in children younger than 3 years.
Mechanism
Infection may reach the hip by:
Hematogenous spread through the synovial blood supply or direct extension from adjacent osteomyelitis.
Infants
During approximately the first 12–18 months of life, transphyseal vascular channels may permit infection to spread from the proximal femoral metaphysis into the epiphysis and hip joint.
For this reason, concomitant proximal femoral osteomyelitis and septic arthritis are particularly important in infants.
Organisms
The causative organism varies with age and immunization history.
Staphylococcus aureus remains a major pathogen across pediatric age groups.
Historically, neonatal infections were also associated with streptococci and other organisms, while Haemophilus influenzae type b was an important cause before widespread vaccination.
Sexually active adolescents may rarely develop gonococcal septic arthritis.
Legg–Calvé–Perthes Disease
Perthes disease is an idiopathic osteonecrosis of the developing femoral head.
Its exact cause remains unknown.
Proposed contributing mechanisms include:
Vascular interruption, thrombosis, hypercoagulability, repetitive trauma, and other disturbances of femoral-head perfusion.
Slipped Capital Femoral Epiphysis
SCFE results from failure of the proximal femoral physis during adolescent growth.
Potential contributing factors include:
Mechanical stress, physeal weakness during rapid growth, obesity, trauma, and hormonal or metabolic influences.
Approximately 80% of affected patients have historically been described as overweight or obese.
Other Causes of Pediatric Hip Pain
Other etiologic categories include:
Infectious, traumatic, neoplastic, inflammatory, hematologic, developmental, and idiopathic conditions.
Associated Conditions
Transient synovitis may occur in association with:
Current or recent viral illness, minor trauma, or an allergic-type inflammatory event.
Diagnosis
Signs and Symptoms
Hip pathology may produce pain in several locations.
Common sites include:
The groin, greater trochanter, anterolateral thigh, medial thigh, or knee.
An important principle is that knee pain in a child may originate from the hip.
Muscle Guarding
Inflammation or pain within the hip frequently causes involuntary muscle spasm or guarding.
The child may hold the hip in a position that maximizes capsular volume and minimizes discomfort.
Loss of Motion
Both active and passive hip motion may become restricted.
The pattern of restriction can provide diagnostic clues.
Perthes Disease and Hip Dysplasia
Loss of abduction and internal rotation is characteristic.
SCFE
A particularly important finding is obligatory external rotation of the hip during attempted flexion.
As the hip is flexed, the thigh progressively rotates outward.
This finding strongly suggests SCFE.
Weight Bearing
Refusal or inability to bear weight is an important red flag.
Possible causes include:
Septic arthritis, osteomyelitis, fracture, severe transient synovitis, or unstable SCFE.
Limp
The child may have either:
An antalgic painful limp or a relatively painless chronic limp, depending on the disorder.
Muscle Atrophy
Long-standing disease may cause wasting of the:
Thigh, gluteal, or other periarticular musculature.
This finding suggests a more chronic process.
Fever
Fever should raise concern for infection, especially:
Septic arthritis or osteomyelitis.
Absence of fever does not completely exclude infection.
Physical Examination
Inspection
Inspect the child at rest and, when possible, during standing and walking.
Look for:
Abnormal limb position, swelling, erythema, bruising, muscle wasting, limb-length discrepancy, or deformity.
Palpation
Palpate the:
Hip, groin, greater trochanter, buttock, lower back, pelvis, and thigh.
Assess for:
Warmth, focal tenderness, swelling, fluctuance, or tenderness over a bursa or bone.
Resting Position
Document the spontaneous position of the limb.
A child with an irritable hip may hold it in slight flexion, abduction, and external rotation to reduce capsular pressure.
Range of Motion
Active and passive range of motion of both the hip and knee should be examined and compared with the opposite side.
Particular attention should be given to:
Internal rotation, external rotation, abduction, and flexion.
Loss of internal rotation is often one of the earliest findings in many intra-articular hip disorders.
Neurovascular Examination
A complete distal motor, sensory, and vascular examination should be documented.
Weakness, numbness, abnormal reflexes, or poor perfusion may point toward neurologic, spinal, or vascular pathology rather than an isolated joint disorder.
Gait Examination
If the child is able to walk safely, observe the gait.
Assessment may include:
Normal walking, toe walking, heel walking, stride length, stance duration, trunk position, and symmetry.
An antalgic gait is characterized by decreased stance time on the painful side.
Hip Aspiration
If septic arthritis is suspected, urgent aspiration of the hip joint should be considered.
Because the hip is deep, aspiration is usually performed with ultrasound or fluoroscopic guidance.
Fluid should be sent for appropriate microbiologic and laboratory analysis.
Laboratory Tests
Routine blood studies may be normal in:
Transient synovitis, Perthes disease, SCFE, and developmental hip dysplasia.
However, laboratory testing is important when infection is part of the differential diagnosis.
Septic Arthritis Laboratory Findings
Common abnormalities include:
Elevated leukocyte count, neutrophilia or left shift, elevated ESR, and elevated C-reactive protein.
No single blood test confirms or excludes septic arthritis.
Synovial Fluid
The synovial white blood cell count is an important diagnostic measure.
A value greater than approximately 50,000 cells/mm³, particularly with a high neutrophil percentage, strongly raises concern for septic arthritis, although lower counts can still occur with infection.
Blood Cultures
Blood cultures should be obtained early when septic arthritis or osteomyelitis is suspected.
Historically, blood cultures have been positive in approximately 40% of children with septic arthritis or osteomyelitis.
Imaging
Plain Radiographs
Radiographs are commonly the first imaging study for persistent or significant hip pain.
Typical views include an AP pelvis and appropriate lateral hip view, depending on the suspected disorder.
Septic Arthritis
Early plain radiographs may show:
Soft-tissue swelling, capsular distension, or displacement of normal fat planes.
They can also help exclude fracture, SCFE, Perthes disease, or advanced osteomyelitis.
Osteomyelitis
Early radiographs can be normal.
As infection progresses, findings may include:
Loss of normal bone density, cortical or medullary lucency, periosteal reaction, sclerosis, and progressive osseous destruction.
Untreated proximal femoral infection may ultimately damage the femoral head.
Transient Synovitis
AP and lateral radiographs are typically normal or nonspecific.
Their main purpose is to exclude other structural disease.
Ultrasound may demonstrate an effusion but cannot reliably distinguish transient synovitis from septic arthritis.
Legg–Calvé–Perthes Disease
Radiographic abnormalities evolve over time.
Early Findings
Early findings may include:
Failure of expected epiphyseal growth, increased density or sclerosis of the femoral head, and subtle loss of normal contour.
Later Findings
Progressive disease may produce:
Subchondral fracture, fragmentation, femoral-neck shortening, flattening, extrusion, and eventual enlargement or deformity of the femoral head.
Slipped Capital Femoral Epiphysis
Radiographs may show:
Physeal widening or irregularity, osteopenia around the physis, and displacement of the proximal femoral epiphysis relative to the metaphysis.
Both hips should generally be evaluated because bilateral disease is not uncommon.
When an unstable SCFE is suspected, forceful frog-leg positioning should be avoided.
Pathological Findings
Septic Arthritis
Early disease causes synovial inflammation and hypertrophy.
Without rapid treatment, bacterial enzymes and inflammatory mediators can destroy the articular cartilage.
SCFE
The femoral head remains seated within the acetabulum while the proximal femoral metaphysis displaces relative to the epiphysis.
The epiphysis is therefore effectively positioned posteriorly and inferiorly relative to the metaphysis.
Perthes Disease
Progressive femoral-head osteonecrosis can result in:
Flattening, extrusion, fragmentation, and deformity of the capital femoral epiphysis.
Differential Diagnosis
Transient synovitis is common but should remain a diagnosis of exclusion, particularly until infection and other serious conditions have been considered.
Infectious Causes
Important infectious conditions include:
Septic arthritis of the hip, proximal femoral osteomyelitis, pelvic osteomyelitis, sacroiliac septic arthritis, discitis, pyomyositis, and psoas infection or abscess.
Developmental and Mechanical Causes
These include:
Legg–Calvé–Perthes disease, SCFE, developmental hip dysplasia, and early degenerative or chondral disease.
Inflammatory Causes
Consider:
Juvenile idiopathic arthritis and other inflammatory arthropathies.
Neoplastic Causes
Tumors involving the:
Pelvis, spine, proximal femur, or surrounding soft tissues may present with hip or referred knee pain.
Hematologic and Malignant Disorders
Consider:
Sickle cell crisis, leukemia, and lymphoma.
Extra-Articular Causes
Other possibilities include:
Iliopsoas bursitis, greater trochanteric bursitis, pyomyositis, referred lumbar or sacroiliac pain, and other nonarticular disorders.
Treatment
Management depends entirely on the underlying diagnosis.
Transient Synovitis
Transient synovitis is usually self-limited.
Treatment focuses on symptom relief.
Rest
Relative rest and temporary reduction in weight bearing are appropriate until pain improves and a normal or near-normal range of motion returns.
NSAIDs
Anti-inflammatory medication may reduce pain and synovial irritation.
Natural History
Symptoms usually resolve spontaneously.
Failure to improve as expected should prompt reassessment of the diagnosis.
Septic Arthritis
Septic arthritis requires urgent treatment because irreversible cartilage injury can occur rapidly.
Drainage
The infected joint should be aspirated and, when indicated, surgically irrigated and debrided.
Antibiotics
Empiric broad-spectrum intravenous antibiotics are started after appropriate cultures are obtained whenever feasible, then narrowed according to culture and susceptibility results.
The route and total duration of treatment depend on:
The organism, clinical response, inflammatory markers, presence of adjacent osteomyelitis, and local infectious-disease protocols.
Rigid historical treatment durations should not replace clinical and laboratory response.
Positioning
When severe capsular distension has occurred, the hip may temporarily be positioned to reduce discomfort, historically including mild abduction.
Range of Motion
After infection is controlled and drainage is no longer required, gentle range-of-motion exercises are begun to minimize stiffness.
Osteomyelitis
Antibiotic therapy is the primary treatment.
Surgical drainage or debridement may be required when there is:
Abscess formation, necrotic bone, failure of medical treatment, or need for diagnostic tissue sampling.
Legg–Calvé–Perthes Disease
Treatment aims to preserve:
Femoral-head containment, hip range of motion, and the most spherical possible femoral-head shape during healing.
Nonoperative Care
Measures may include:
Activity modification, maintenance of hip motion, treatment of synovitis, and temporary reduction in weight bearing when symptoms are severe.
Traction or bed rest has historically been used during painful episodes, although prolonged immobilization is generally avoided.
Surgery
Selected patients with more extensive disease may require femoral or pelvic reconstruction to improve containment of the femoral head within the acetabulum.
Slipped Capital Femoral Epiphysis
SCFE requires prompt stabilization to prevent further displacement.
Initial Management
Once SCFE is suspected, the child should generally be made non–weight bearing until definitive treatment.
Surgery
The standard treatment for most stable slips is in situ percutaneous screw fixation.
Forceful reduction should be avoided because vascular injury to the femoral head can cause osteonecrosis.
Physical Therapy
Formal physical therapy is not routinely needed for every child with hip pain.
Its role depends on the diagnosis and may include:
Gait retraining, maintenance of range of motion, strengthening, and postoperative rehabilitation.
Medication
Septic Arthritis and Osteomyelitis
Appropriate antimicrobial therapy is essential.
Treatment should be tailored to the likely organism initially and then adjusted to culture results.
Transient Synovitis
NSAIDs may be used for symptomatic relief.
Surgery
Septic Arthritis
Surgical treatment may involve:
Irrigation, debridement, and drainage of the hip joint.
An anterior or other suitable approach may be chosen according to surgeon preference and clinical circumstances.
Osteomyelitis
If operative drainage is necessary, a cortical window may be created to permit:
Culture, curettage, and decompression of infected bone.
Chronic osteomyelitis, although uncommon in children with modern treatment, may require more extensive debridement.
Perthes Disease
Severe disease may require reconstructive surgery involving either the:
Proximal femur, acetabulum, or both to improve containment.
SCFE
Percutaneous in situ fixation is performed to prevent progression of the slip and reduce the risk of additional deformity.
Follow-Up
Prognosis of Septic Arthritis and Osteomyelitis
Early diagnosis and treatment can produce a good outcome.
Delayed or chronic infection may result in permanent deformity.
Prognosis of Perthes Disease
Outcome generally improves when:
The child is younger at disease onset, the necrotic segment is smaller, femoral-head extrusion is minimal, and hip range of motion remains good.
Some residual radiographic deformity may persist even when clinical function is satisfactory.
Prognosis of SCFE
Long-term outcome depends substantially on the severity of the slip and development of complications.
More severe deformity is associated with a greater risk of later femoroacetabular impingement and degenerative arthritis.
Complications
Septic Arthritis and Osteomyelitis
Untreated infection can be devastating in a growing child.
Potential consequences include:
Femoral-head or physeal destruction, limb shortening, joint incongruity, stiffness, deformity, growth disturbance, and early degenerative arthritis.
Cartilage injury can begin very early in the course of untreated bacterial arthritis, reinforcing the need for urgent treatment.
SCFE Complications
Major complications include:
Osteonecrosis and chondrolysis.
Osteonecrosis
Disruption of the femoral-head blood supply may occur as a consequence of the unstable slip or overly aggressive reduction.
Chondrolysis
Chondrolysis is rapid loss of articular cartilage and produces:
Joint-space narrowing, stiffness, contracture, pain, and limp.
Degenerative Arthritis
Patients with SCFE have an increased long-term risk of premature hip osteoarthritis, particularly when residual deformity is substantial.
Patient Monitoring
Septic Arthritis and Osteomyelitis
Clinical recovery should be followed together with inflammatory markers such as:
C-reactive protein and ESR.
A downward trend toward normal supports successful treatment.
Antibiotic duration should be guided by the overall clinical course, inflammatory markers, microbiology, and presence or absence of associated osteomyelitis.
Transient Synovitis
Observation is appropriate when symptoms improve predictably and serious alternative diagnoses have been excluded.
Persistent, recurrent, or worsening symptoms require reevaluation.
Legg–Calvé–Perthes Disease
Children with limited femoral-head involvement may be managed with observation and serial clinical and radiographic assessment.
Historically, involvement of less than approximately 50% of the femoral head has been associated with a more favorable course.
Important Clinical Red Flags
Urgent evaluation is particularly important in a child with:
Fever, inability to bear weight, severe pain with passive hip motion, rapidly progressive symptoms, night pain, systemic illness, significant trauma, or suspected unstable SCFE.
These findings may indicate a condition in which delayed treatment risks permanent damage to the hip.
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Orthopaedic Surgery - Hip Fracture in the Child
Basics
Pediatric hip fractures include fractures of the femoral neck, intertrochanteric region, and subtrochanteric proximal femur.
Femoral-neck fractures in children are rare but serious injuries because disruption of the blood supply to the femoral head can lead to osteonecrosis, nonunion, growth disturbance, coxa vara, and later degenerative arthritis.
Classification
The most commonly used system for pediatric femoral-neck fractures is the Delbet classification, as popularized by Colonna.
Delbet Type I
Type I is a transphyseal separation in which the femoral head separates from the neck through the proximal femoral physis.
It is the least common type and is generally seen in younger children.
A substantial proportion of these injuries are associated with dislocation of the femoral head from the acetabulum.
Delbet Type II
Type II is a transcervical fracture through the middle portion of the femoral neck.
This is the most common pediatric femoral-neck fracture pattern.
Delbet Type III
Type III is a cervicotrochanteric or basicervical fracture occurring near the base of the femoral neck.
It is the second most common pattern.
Delbet Type IV
Type IV is an intertrochanteric fracture, located between the greater and lesser trochanters.
This fracture generally carries a lower risk of osteonecrosis than the more proximal intracapsular types.
Importance of Initial Displacement
The degree of displacement at the time of injury is one of the most important predictors of femoral-head osteonecrosis.
More displaced fractures are more likely to disrupt the vulnerable vascular supply.
Anatomy and Blood Supply
The blood supply of the pediatric femoral head changes substantially during growth.
Early Childhood
At birth, vascular channels arising from the femoral circumflex system travel toward the femoral head through the proximal femoral neck.
The proximal femoral physis acts as a barrier to direct metaphyseal blood vessels entering the epiphysis.
After Approximately 4 Years of Age
By about 4 years of age, the medial femoral circumflex artery, particularly its retinacular branches, provides the dominant blood supply to the femoral head.
These vessels travel along the femoral neck and are vulnerable to injury during fracture or dislocation.
Ligamentum Teres
The artery within the ligamentum teres contributes only a relatively small portion of the total femoral-head blood supply and generally cannot compensate for major disruption of the retinacular vessels.
Surgical Relevance
Capsulotomy itself does not usually compromise the femoral-head circulation provided the important posterosuperior and posteroinferior retinacular vessels along the femoral neck are protected.
Fracture Stability
Approximately half of pediatric hip fractures are initially nondisplaced.
Once displacement occurs, the fracture is generally considered mechanically unstable.
Epidemiology
Pediatric hip fractures account for less than 1% of all fractures in children.
They are far less common than adult hip fractures because healthy pediatric bone is strong and usually requires substantial force to fracture.
Etiology
Approximately 75% of pediatric hip fractures are caused by major trauma.
Typical mechanisms include:
Motor vehicle collisions, pedestrian trauma, falls from significant height, and other high-energy injuries.
Pathologic Fractures
The remaining cases may occur through abnormal bone weakened by disorders such as:
Unicameral bone cyst, aneurysmal bone cyst, fibrous dysplasia, or other osseous lesions.
Nonaccidental Injury
In infants and young children, particularly when the history is inconsistent with the child’s developmental abilities, nonaccidental trauma must be considered.
Associated Conditions
Infants
A hip fracture in an infant should prompt careful assessment for possible nonaccidental injury unless there is a convincing high-energy mechanism.
Children
Because substantial force is usually necessary to fracture the pediatric femoral neck, other associated injuries should be actively sought.
Adolescents
In adolescents, proximal femoral physeal injury may resemble or overlap with slipped capital femoral epiphysis.
Atypical or pathologic slips should raise concern for underlying metabolic or endocrine disease, including:
Hypothyroidism and renal osteodystrophy.
Diagnosis
Signs and Symptoms
The usual presentation is sudden severe hip pain following trauma.
The child may be unable to stand, walk, or move the hip.
Swelling
Swelling may be visible in the:
Inguinal region, proximal thigh, or gluteal area.
Resting Position
The limb is often held in a position of:
External rotation, flexion, and adduction, which may reduce capsular tension and pain.
Motion
With displaced fractures, active hip movement is usually impossible.
Passive movement is markedly painful and restricted, particularly:
Flexion, abduction, and internal rotation.
Crepitus
Pain and occasionally crepitus may be produced with hip motion.
Forceful examination should be avoided.
Infants
Infants may present with pseudoparalysis, refusing to move the involved extremity.
Limb Shortening
The affected leg may appear shortened by approximately 1–2 cm, particularly with a displaced fracture.
External rotation is common.
Physical Examination
Most children with a complete femoral-neck fracture are in substantial pain.
The examination should be gentle and should include assessment for associated injuries.
Incomplete or Nondisplaced Fracture
In patients without an obvious complete fracture, pain may be particularly evident with:
Internal rotation, abduction, and flexion of the hip.
Neurovascular Examination
Distal pulses, capillary refill, motor function, and sensation should be documented before and after reduction or operative treatment.
Imaging
Plain Radiographs
Initial imaging generally includes:
AP pelvis or AP hip and lateral views of the affected hip.
Radiographs may show superior and lateral displacement of the femoral shaft relative to the femoral head.
CT
CT may be helpful for:
Defining fracture comminution, assessing complex fracture geometry, evaluating associated acetabular injury, and determining the direction of femoral-head dislocation.
It is not necessary in every case.
Ultrasound
In newborns and very young infants, ultrasound may be useful because much of the proximal femur remains cartilaginous and therefore poorly visualized on radiographs.
Differential Diagnosis
Important alternatives include:
Slipped capital femoral epiphysis and developmental coxa vara.
Developmental Coxa Vara
Developmental coxa vara may demonstrate a characteristic vertical defect or cleft near the femoral neck and should not be mistaken for an acute fracture.
Treatment
General Principles
Treatment aims to obtain and maintain an anatomic or near-anatomic reduction with stable fixation while minimizing additional injury to the femoral-head blood supply.
Because displaced pediatric femoral-neck fractures are unstable and have a high complication rate, operative fixation is commonly required.
Reduction
Either closed or open reduction may be used.
Reduction should be:
Gentle, accurate, and performed without repeated forceful manipulation.
Residual translation or varus should be avoided because imperfect reduction substantially increases the risk of nonunion and deformity.
Fixation by Age
Implant choice depends on patient age and the size of the femoral neck.
Young Children
In children approximately 2–6 years old, fixation may use:
Smooth pins or small cannulated screws, typically around 4.0–4.5 mm when anatomy permits.
Older Children
In children approximately 7 years and older, larger cannulated screws, historically around 6.5–7.3 mm, may be used when appropriate.
Modern implant size should be individualized to the child’s anatomy.
Spica Casting
A hip spica cast is often added in younger children because the small femoral neck may limit the number or size of implants that can safely be inserted.
The cast provides additional protection against displacement.
Physeal Crossing
Type I
When fixation of a Type I transphyseal injury requires crossing the growth plate, smooth pins are generally preferred, often followed by a spica cast.
Types II–IV
For Types II–IV, implants should ideally avoid crossing the proximal femoral physis when stable fixation can still be achieved.
However, secure fixation takes priority over physeal preservation.
The proximal femoral physis contributes only about 3 mm of longitudinal growth per year, so inadequate fixation should not be accepted merely to avoid crossing it.
Associated Hip Dislocation
When femoral-head dislocation accompanies the fracture, only a gentle attempt at closed reduction should be made.
Repeated manipulations increase the risk of further vascular and physeal injury.
If reduction is unsuccessful, open reduction is indicated.
Surgical Approach
The open approach should generally correspond to the direction of dislocation:
Posterior approach for posterior dislocation and anterior approach for anterior dislocation.
Treatment by Delbet Type
Type I Without Dislocation
A gentle closed or open reduction is followed by fixation with a pin or screw as appropriate for age and anatomy.
Type I With Dislocation
This is one of the highest-risk pediatric hip injuries.
Historical series report osteonecrosis rates approaching 100% in some displaced Type I injuries with dislocation and a very high incidence of later degenerative arthritis.
Reduction
A gentle attempt at closed reduction may use:
Longitudinal traction, abduction, and internal rotation.
If this fails, open reduction and fixation are required.
Type II
Type II transcervical fractures are the most common pediatric femoral-neck fractures.
Most are displaced.
Osteonecrosis Risk
Historical osteonecrosis rates are approximately 50%, with displaced fractures carrying substantially greater risk than nondisplaced injuries.
Treatment
Both displaced and nondisplaced Type II fractures are generally treated with:
Reduction and internal fixation using screws or pins.
Type III
Type III fractures are the second most common pattern.
Historical osteonecrosis rates are approximately 25%.
Displaced Type III
Treatment consists of:
Gentle closed reduction or open reduction followed by internal fixation.
Nondisplaced Type III
Prophylactic screw fixation is commonly recommended because late displacement can occur.
In selected children younger than approximately 8 years, an abduction spica cast may occasionally be considered, but close monitoring is essential because of the risk of:
Late displacement and coxa vara.
Type IV
Intertrochanteric fractures are generally treated with stable fixation appropriate to the child’s size and fracture pattern.
A pediatric hip compression screw or similar fixed-angle device may be used.
Surgical Technique
Imaging
A radiolucent or fracture table with fluoroscopic image intensification is typically used.
Reduction Maneuver
Common reduction principles include:
Longitudinal traction and correction of external rotation, usually with internal rotation.
Acceptable Reduction
No significant translation across the width of the femoral neck should be accepted.
Residual displacement predisposes to progressive varus and nonunion.
Surgical Approaches
For intracapsular reduction of Type II and III fractures, exposure may be obtained through a proximal extension of the tensor fascia lata–gluteal interval or another suitable approach.
Type I and very proximal Type II injuries may require an anterior iliofemoral approach.
Instrumentation
Types I–III
Fixation often uses 2–3 cannulated screws or smooth pins, sized appropriately for the child’s age and anatomy.
Type IV
A pediatric hip compression screw with side plate or other fixed-angle construct may be used.
Age-Specific Management
Ages 7–12 Years
Pediatric hip screw fixation may be combined with a hip spica cast for approximately 8–12 weeks, depending on stability.
Age 13 Years and Older
Older adolescents may often be treated similarly to adults.
A hip screw and side plate or other adult-type fixation may cross the physis if required for stability.
Postoperative casting is usually unnecessary when fixation is secure.
Timing of Surgery
Operative management should generally be performed urgently, usually within 24 hours.
Type I With Dislocation
A Type I injury accompanied by hip dislocation requires immediate treatment because of the extreme risk to femoral-head vascularity.
Osteonecrosis and Timing
Although early reduction is strongly favored, studies have not demonstrated a perfectly consistent relationship between exact operative timing and osteonecrosis.
Initial vascular injury and fracture displacement appear to be major determinants.
Implant Removal
There is no universally mandatory time for implant removal.
When removal is planned, it is commonly performed after solid healing, often within approximately 12–18 months.
Potential reasons include prevention of bony overgrowth around the implant or later stress concentration and refracture.
Neonatal Epiphysiolysis
Neonatal proximal femoral epiphyseal separation is a special injury pattern.
Acute Recognition
If diagnosed before callus forms, gentle skin traction may be used to restore alignment.
Delayed Recognition
If callus is already visible, simple immobilization and observation are usually preferred.
Open reduction is generally avoided because neonatal hips have substantial remodeling potential if the physis remains viable.
Follow-Up
Close monitoring is necessary for growth disturbance and osteonecrosis, although the incidence of osteonecrosis in this particular neonatal pattern may be relatively low.
Follow-Up
The long-term outcome is largely determined by the degree of injury to the femoral-head blood supply.
These patients require prolonged follow-up because major complications may not become apparent for months or years.
Prognosis
The prognosis depends on:
Delbet type, initial displacement, patient age, quality of reduction, vascular injury, development of osteonecrosis, and occurrence of growth arrest.
Complications
Complications occur in as many as approximately 60% of pediatric femoral-neck fractures in some historical series.
The unique and changing blood supply of the developing proximal femur is responsible for many of these problems.
Osteonecrosis
Osteonecrosis is the most common and most devastating complication.
It may involve:
The epiphysis alone, both epiphysis and metaphysis, or the metaphysis with relative sparing of the femoral head.
Incidence
Historical series report osteonecrosis in approximately 42% of pediatric femoral-neck fractures overall, usually becoming apparent within about 9–12 months.
Approximate rates by Delbet type have been reported as:
Type I: nearly 100%
Type II: approximately 52%
Type III: approximately 27%
Type IV: approximately 14%
Rates vary among modern series.
Risk Factors for Osteonecrosis
Factors associated with greater risk include:
Initial fracture displacement, Delbet Types I and II, associated dislocation, and age greater than approximately 10 years.
Ratliff Classification of Osteonecrosis
Ratliff Type I
There is total involvement and collapse of the femoral head.
This carries the worst prognosis and historically represents the most common pattern.
It reflects widespread injury to the lateral epiphyseal blood supply.
Ratliff Type II
Only part of the epiphysis is involved, with limited or minimal collapse.
This may reflect more localized vascular injury, often affecting the anterolateral femoral head.
Ratliff Type III
There is increased sclerosis of the femoral neck from the fracture line to the physis, while the femoral head itself is relatively spared.
This pattern is associated with metaphyseal vascular injury.
Treatment of Osteonecrosis
The goals are to preserve:
Hip motion, femoral-head containment, and joint congruity.
Selected patients may benefit from corrective osteotomy that rotates a less-deformed portion of the femoral head into the weight-bearing zone.
Nonunion
Nonunion occurs in approximately 5–8% of pediatric femoral-neck fractures.
Risk Factors
Closed treatment of displaced Types II and III has historically been associated with higher rates of:
Nonunion, late displacement, and coxa vara.
Stable internal fixation after accurate reduction lowers the risk by preventing varus collapse.
Coxa Vara
Coxa vara may develop because of:
Malunion or growth arrest of the proximal femoral physis.
Remodeling
If the femoral neck-shaft angle is less than approximately 110°, spontaneous remodeling is unlikely to provide adequate correction.
Treatment
In the absence of severe osteonecrosis, a subtrochanteric valgus osteotomy with internal fixation, sometimes combined with bone grafting, can provide good long-term correction.
Premature Physeal Closure
Premature closure of the proximal femoral physis may occur even when implants do not cross the growth plate.
It is often related to the original injury or associated osteonecrosis.
Limb-Length Discrepancy
The proximal femoral physis contributes approximately 3 mm of longitudinal growth per year, representing about 15% of total lower-extremity length growth.
Isolated closure may therefore cause only modest shortening, but combined osteonecrosis and growth disturbance can result in a more substantial limb-length discrepancy.
Growth Monitoring
Children with premature physeal closure should be followed with serial assessment of limb length.
Long-standing monitoring may include:
Standing limb-length imaging or scanograms and bone-age assessment using hand and wrist radiographs.
Contralateral Epiphysiodesis
If a clinically significant projected limb-length inequality develops, contralateral epiphysiodesis may be considered at the appropriate time.
Trochanteric Overgrowth
Growth disturbance can occasionally produce symptomatic relative overgrowth of the greater trochanter.
In selected children older than approximately 8 years, trochanteric advancement or transfer may be considered if abductor mechanics are substantially impaired.
Patient Monitoring
Children with proximal femoral fractures require long-term surveillance for:
Osteonecrosis, nonunion, coxa vara, physeal arrest, limb-length discrepancy, trochanteric overgrowth, deformity, loss of hip motion, and secondary degenerative arthritis.
Follow-up should include serial physical examination and radiographs, particularly throughout the first year, when osteonecrosis often first becomes evident, and subsequently through skeletal growth when significant physeal injury has occurred.
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Orthopaedic Surgery - Traumatic Hip Dislocation
Basics
Traumatic hip dislocation is an orthopaedic emergency in which the femoral head is completely displaced from the acetabulum.
These injuries usually result from high-energy trauma and may occur as an isolated dislocation or as a fracture-dislocation involving the acetabulum, femoral head, or femoral neck.
Because the mechanism is often severe, a complete trauma assessment is essential.
Associated Trauma
Up to approximately 50% of patients may have additional fractures or other major injuries at the time of presentation.
Associated acetabular, femoral head, femoral neck, knee, foot, spinal, thoracic, and abdominal injuries should be actively sought.
Classification
Traumatic hip dislocations are classified primarily according to the direction of displacement.
They may be:
Posterior or anterior, with further description according to associated fractures of the femoral head, femoral neck, or acetabulum.
Prevention
Seat-belt use together with appropriate air-bag protection reduces the risk and severity of injuries sustained in motor vehicle collisions.
Epidemiology
Traumatic hip dislocation is most commonly encountered in young adults exposed to high-energy trauma.
Males are affected more frequently than females.
Posterior Dislocation
Posterior dislocations account for approximately 85–90% of traumatic hip dislocations.
Anterior Dislocation
Anterior dislocations represent approximately 10–15% of cases.
Risk Factors
Major risk factors include:
Motor vehicle collisions, falls from substantial height, pedestrian-versus-vehicle injuries, industrial trauma, and high-energy sports accidents.
Etiology
Approximately 70–90% of traumatic hip dislocations have historically been associated with motor vehicle collisions.
Dashboard Injury
A classic mechanism for posterior dislocation occurs when the patient is seated with the hip and knee flexed.
During rapid deceleration, the knee strikes the dashboard, transmitting an axial force through the femur.
This drives the femoral head posteriorly out of the acetabulum.
Other Mechanisms
Other causes include:
Falls from height, industrial accidents, pedestrian injuries, motorcycle trauma, and sporting injuries.
The direction of force and position of the hip at impact determine whether the femoral head dislocates anteriorly or posteriorly.
Associated Conditions
Because traumatic hip dislocations usually result from high-energy injury, associated abnormalities are common.
Sciatic Nerve Injury
The sciatic nerve is particularly vulnerable in posterior dislocation.
Sciatic nerve dysfunction has been reported in approximately 10–20% of posterior dislocations.
The peroneal division is affected most commonly.
Relationship to Reduction Delay
Prolonged dislocation may increase the likelihood of neurologic injury and other complications.
Musculoskeletal Injuries
Common associated injuries include:
Femoral head fracture, femoral neck fracture, acetabular fracture, ipsilateral knee injury, and foot or ankle injury.
Other Trauma
Chest, abdominal, spinal, and head injuries may also occur and can take priority during initial resuscitation.
Diagnosis
Signs and Symptoms
Patients usually have severe hip pain and inability to move or bear weight on the affected extremity.
Numbness or paresthesias may occur when the sciatic nerve is injured.
Posterior Dislocation Position
The classic posture of a posteriorly dislocated hip is:
Flexion, adduction, and internal rotation.
The affected extremity also typically appears shortened.
Anterior Dislocation Position
An anteriorly dislocated hip usually rests in:
Abduction and marked external rotation, often with some degree of flexion or extension depending on the subtype.
Altered Mental Status
Some patients are obtunded or unconscious because of associated trauma, intoxication, or head injury.
The diagnosis therefore cannot depend solely on patient-reported symptoms.
Careful inspection of limb position and systematic trauma imaging are essential.
Physical Examination
Trauma Survey
A full primary and secondary trauma survey should be performed because associated injuries are common and may be life-threatening.
Limb Position
The position, shortening, and rotational alignment of the lower extremity should be documented before reduction.
Neurovascular Examination
Motor, sensory, and vascular findings should be documented before and after reduction.
Sciatic Nerve
Particular attention should be given to sciatic nerve function.
Motor testing should include:
Ankle dorsiflexion, plantarflexion, great-toe extension, and ankle eversion.
Sensory testing should include the dorsum and plantar aspects of the foot according to tibial and peroneal nerve distribution.
Vascular Status
Distal pulses, capillary refill, skin temperature, and overall limb perfusion should be assessed.
Laboratory Tests
Laboratory studies are directed by the overall trauma evaluation rather than the hip dislocation itself.
A standard trauma panel may be obtained according to injury severity and anticipated operative management.
Imaging
Initial Trauma Radiographs
Imaging commonly includes an AP pelvis as part of the initial trauma evaluation.
Additional imaging is determined by associated injuries.
Hip Radiographs
Dedicated radiographs may include AP and cross-table lateral views.
A cross-table lateral can help establish whether the dislocation is anterior or posterior.
Radiographic Appearance
In a posterior dislocation, projection may make the displaced femoral head appear relatively smaller than the opposite side.
In an anterior dislocation, it may appear somewhat larger.
These findings are secondary to projection and should not replace assessment of the actual displacement pattern.
Associated Acetabular Injury
The acetabulum should be inspected carefully for fracture fragments, wall disruption, or joint incongruity.
When an acetabular fracture is suspected, Judet oblique views may provide additional information, although CT now plays the major role in defining fracture anatomy.
Femoral Neck
The femoral neck must be scrutinized for associated fracture.
An unrecognized femoral neck fracture can be displaced or worsened by forceful reduction.
Intra-Articular Fragments
The joint should be evaluated for:
Osteochondral fragments, femoral-head fractures, acetabular fragments, and asymmetric joint-space widening suggesting an incarcerated fragment.
CT
CT is routinely obtained after reduction in many modern trauma protocols, particularly when there is concern for associated fracture or nonconcentric reduction.
Post-Reduction CT
CT can demonstrate:
Small intra-articular fragments, femoral-head fractures, acetabular fractures, subtle femoral-neck injury, joint congruity, and incarcerated osteochondral material.
Before Open Reduction
If closed reduction fails and open reduction is required, CT may help define fracture anatomy when this can be obtained without creating an unsafe delay.
MRI
MRI is not routinely required during the acute reduction phase.
It may later be useful for evaluating:
Osteonecrosis, cartilage injury, labral injury, occult fracture, or persistent unexplained symptoms.
Differential Diagnosis
Important competing or associated diagnoses include:
Femoral neck fracture, femoral head fracture, acetabular fracture, pelvic fracture, and severe proximal femoral trauma without dislocation.
Treatment
Initial Stabilization
Initial management follows standard trauma principles.
Life-threatening injuries are addressed first.
Once the patient is sufficiently stable, the dislocated hip should be reduced urgently.
Orthopaedic Emergency
Traumatic hip dislocation requires emergent orthopaedic reduction because prolonged displacement increases the risk of femoral-head osteonecrosis and other complications.
Timing
Reduction should be performed as soon as safely possible, ideally within approximately 6 hours of injury when circumstances permit.
Closed Reduction
Closed reduction is the preferred initial treatment when there is no contraindication.
Sedation or Anesthesia
Adequate muscle relaxation is essential.
Reduction may be performed under:
Procedural sedation, regional anesthesia in selected circumstances, or general anesthesia with muscle relaxation.
Reduction Technique
Most techniques use longitudinal or inline traction combined with controlled manipulation of the hip.
The specific maneuver depends on the direction of dislocation and surgeon preference.
Forceful repeated attempts should be avoided.
Contraindications to Forceful Closed Reduction
Reduction should be approached cautiously when there is concern for:
Associated femoral neck fracture, large displaced fracture fragment, or other injury in which manipulation could worsen the fracture.
Stability Assessment
After reduction, the hip should be gently assessed for stability through a safe range of motion.
Instability may suggest an associated acetabular wall fracture, capsular injury, or intra-articular fragment.
Post-Reduction Examination
The neurovascular examination must be repeated immediately after reduction.
Any new deficit should be documented and urgently evaluated.
Post-Reduction Radiographs
Plain radiographs should confirm:
Reduction of the femoral head, restoration of joint congruity, and absence of obvious new fracture displacement.
Post-Reduction CT
CT is then used to assess the congruity of the reduction and to identify occult fracture fragments or intra-articular debris.
Traction
Routine prolonged traction is not required for most simple, stable hip dislocations after successful concentric reduction.
Temporary traction may be considered in selected unstable injuries, painful fracture-dislocations, or situations awaiting definitive fixation.
Definitive Management
After the hip is reduced, management becomes focused on:
Associated fractures, joint stability, intra-articular fragments, cartilage injury, and the patient’s overall trauma condition.
Indications for Surgery
Operative treatment may be required for:
Irreducible dislocation, nonconcentric reduction, incarcerated intra-articular fragments, associated femoral-head fracture requiring fixation or excision, acetabular fracture requiring stabilization, femoral-neck fracture, or persistent post-reduction instability.
Open Reduction
If a satisfactory closed reduction cannot be achieved, open reduction is indicated.
The surgical approach depends on the direction of dislocation, associated fracture pattern, and surgeon preference.
Associated Acetabular Fracture
Acetabular fractures are treated according to displacement, stability, articular congruity, and fracture pattern.
Some require open reduction and internal fixation.
Associated Femoral-Head Fracture
Treatment depends on fragment size, location, displacement, and whether the fragment contributes to the weight-bearing surface.
Options may include:
Fixation, excision of a small nonessential fragment, or more extensive reconstruction.
Activity
Weight-bearing recommendations depend on whether the injury is a simple dislocation or a fracture-dislocation.
Simple Stable Dislocation
After a concentric stable reduction without significant fracture, early protected mobilization and range of motion are generally encouraged.
Weight bearing may be advanced according to the injury pattern and treating surgeon’s protocol.
Fracture-Dislocation
Associated femoral-head or acetabular fractures often require more prolonged protected or restricted weight bearing.
Physical Therapy
Physical therapy commonly includes:
Gait training, protected weight bearing when required, progressive hip range of motion, and later strengthening.
Early controlled motion helps reduce stiffness.
Medication
Analgesics are required during the acute phase.
Opioid medications may be necessary initially because traumatic hip dislocation is extremely painful.
Venous thromboembolism prophylaxis should be considered according to the patient’s overall trauma burden, mobility, and associated injuries.
Follow-Up
Prognosis of Simple Posterior Dislocation
Approximately 70–80% of uncomplicated posterior hip dislocations without associated fracture have historically achieved good or excellent long-term outcomes.
Fracture-Dislocation
Outcome is less favorable when posterior dislocation is associated with acetabular or femoral-head fracture because cartilage injury, instability, and post-traumatic arthritis are more common.
Anterior Dislocation
Anterior dislocations may be associated with substantial femoral-head impaction or cartilage injury.
Long-term outcome depends largely on the degree of articular damage and associated fracture.
Effect of Delayed Reduction
Prognosis worsens as the duration of dislocation increases.
Reduction delayed beyond several hours, particularly beyond approximately 6–12 hours, is associated with greater concern for femoral-head osteonecrosis.
Complications
Post-Traumatic Arthritis
Post-traumatic osteoarthritis is the most common major long-term complication.
Risk is highest in patients with:
Acetabular fractures, femoral-head fractures, chondral injury, nonconcentric reduction, or osteonecrosis.
Osteonecrosis
Avascular necrosis of the femoral head may occur because the injury disrupts its blood supply.
Reported rates vary widely, historically ranging from approximately 1–17% or more depending on injury severity and delay to reduction.
Timing of Reduction
The risk of osteonecrosis increases with prolonged dislocation.
Even prompt reduction cannot eliminate the risk completely because vascular damage may occur at the moment of injury.
Sciatic Nerve Injury
Sciatic nerve palsy occurs most often with posterior dislocation.
Reported rates are approximately 8–20%.
Peroneal Division
The common peroneal component of the sciatic nerve is affected more frequently than the tibial component.
Patients may develop weakness of ankle dorsiflexion and great-toe extension together with sensory loss over the dorsum of the foot.
Electrodiagnostic Testing
If neurologic deficits persist, electromyography and nerve-conduction studies may be obtained after several weeks, often around 3–4 weeks or later, to establish a baseline and aid prognosis.
Recovery
Neurologic recovery is variable.
Some patients recover completely, whereas others have persistent weakness or sensory loss.
Recurrent Dislocation
Recurrent traumatic hip dislocation is uncommon, historically occurring in fewer than approximately 2% of patients.
Heterotopic Ossification
Heterotopic ossification may develop after severe hip trauma or surgery, although it is less common after uncomplicated dislocation alone.
Chondral and Labral Injury
Damage to the acetabular labrum and articular cartilage may occur at the time of dislocation and can contribute to persistent pain and later arthritis even after successful reduction.
Patient Monitoring
Patients require long-term follow-up because osteonecrosis and post-traumatic arthritis may appear months or years after the original injury.
First Year
Clinical examination and serial radiographs may be obtained approximately every 3–4 months during the first year, depending on injury severity.
MRI for Osteonecrosis
MRI is more sensitive than radiographs for early detection of femoral-head osteonecrosis and may be used when symptoms, examination, or radiographs raise concern.
Long-Term Surveillance
Follow-up should assess:
Pain, gait, hip range of motion, neurologic function, femoral-head contour, joint congruity, osteonecrosis, and development of post-traumatic arthritis.
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Orthopaedic Surgery - Hip Avascular Necrosis
Basics
Hip avascular necrosis, also called osteonecrosis of the femoral head, is a condition in which the bone and marrow of the femoral head die because of compromised blood supply.
As the necrotic subchondral bone loses structural strength, the femoral head may collapse. Once collapse occurs, the articular surface becomes incongruent and secondary degenerative arthritis commonly develops.
Classification
Several staging systems are used to describe the extent and progression of femoral-head osteonecrosis.
Ficat and Arlet Classification
Stage I
Plain radiographs are normal, but MRI or other advanced imaging demonstrates osteonecrosis.
There is no collapse of the femoral head.
Stage II
Radiographs show sclerotic or cystic changes within the femoral head, but the articular surface remains intact without subchondral collapse.
Stage III
A subchondral fracture develops beneath the articular surface.
This may appear radiographically as the characteristic crescent sign.
Femoral-head collapse is beginning.
Stage IV
The femoral head has collapsed sufficiently to produce secondary degenerative changes of the hip joint, including joint-space narrowing and acetabular involvement.
Steinberg Classification
The Steinberg system expands on the Ficat and Arlet classification by incorporating lesion size and more detailed stages.
Stage 0
Plain radiographs and bone scintigraphy are normal.
Stage I
Plain radiographs remain normal, but bone scintigraphy or MRI demonstrates osteonecrosis.
Stage II
Radiographs demonstrate sclerosis or cyst formation without subchondral collapse.
Severity can be estimated according to the percentage of the femoral head involved:
A: mild, less than approximately 20%.
B: moderate, approximately 20–40%.
C: severe, greater than approximately 40%.
Stage III
A subchondral fracture or crescent sign is present without substantial flattening of the femoral head.
Extent may be described as:
A: mild, less than approximately 15%.
B: moderate, approximately 15–30%.
C: severe, greater than approximately 30%.
Stage IV
Flattening of the femoral head has occurred, but there is not yet major joint-space narrowing or acetabular involvement.
Severity is based on the amount of surface involvement and depression.
Stage V
Femoral-head flattening is accompanied by joint-space narrowing or acetabular involvement, indicating secondary degenerative arthritis.
Lesion Size
One of the most important prognostic findings on MRI or radiographs is the size and location of the necrotic segment.
Small lesions located away from the primary weight-bearing surface are less likely to collapse than large lesions involving the superior weight-bearing portion of the femoral head.
Prevention
When possible, modifiable risk factors should be addressed.
Corticosteroids
Systemic corticosteroids should be used only when the anticipated benefit for the underlying medical condition outweighs the risk of treatment-related complications.
When long-term corticosteroid therapy is necessary, the lowest effective dose should be used under the direction of the treating medical team.
Alcohol
Heavy alcohol consumption is an important risk factor and should be avoided.
Tobacco
Smoking may adversely affect bone and vascular health and should be discontinued.
Epidemiology
Osteonecrosis of the femoral head occurs more commonly in younger and middle-aged adults than typical primary hip osteoarthritis.
Males are affected more frequently in many series.
Arthroplasty Burden
Osteonecrosis accounts for a meaningful proportion of hip arthroplasties, historically estimated at approximately 5–10% in some series.
Risk Factors
Important risk factors include:
Systemic corticosteroid use, heavy alcohol consumption, hip dislocation, displaced femoral neck fracture, previous surgical disruption of the hip blood supply, decompression sickness, thrombophilic disorders, antiphospholipid syndrome, systemic lupus erythematosus, sickle cell disease, HIV infection, and certain abnormalities of coagulation.
Trauma
Traumatic interruption of the blood supply to the femoral head is a major cause.
Important mechanisms include:
Hip dislocation, displaced femoral neck fracture, and surgical injury to femoral-head vascularity.
Hypercoagulable States
Abnormalities that promote thrombosis may compromise the femoral-head microcirculation.
Examples include:
Protein C or protein S deficiency, activated protein C resistance, antiphospholipid syndrome, and other thrombophilic disorders.
Hematologic Disease
Sickle cell disease is an important cause because repeated vascular occlusion can impair femoral-head perfusion.
Decompression Sickness
Caisson disease or decompression sickness in divers can lead to intravascular gas formation and compromise of osseous blood flow.
Genetics
There is no single inherited pattern for most cases of femoral-head osteonecrosis.
However, inherited thrombophilic disorders may predispose certain patients.
Etiology
The final common mechanism is interruption or compromise of blood flow to the femoral head, followed by ischemia and death of bone and marrow elements.
Corticosteroid-Associated Osteonecrosis
High cumulative exposure to systemic corticosteroids is a well-recognized nontraumatic cause.
The exact mechanism is multifactorial and may involve lipid metabolism, marrow pressure, vascular compromise, and altered bone-cell function.
Alcohol-Associated Osteonecrosis
Heavy alcohol consumption may contribute through lipid abnormalities, marrow changes, and impaired microvascular blood flow.
Gaucher Disease
Marrow infiltration and increased intraosseous pressure can impair circulation in disorders such as Gaucher disease.
Systemic Lupus Erythematosus
Patients with lupus have increased risk related to both the disease process and frequent corticosteroid exposure.
Associated Conditions
HIV infection has been associated with an increased risk of osteonecrosis, potentially related to multiple factors including medication exposure, metabolic abnormalities, and thrombophilia.
Diagnosis
Signs and Symptoms
Some patients are initially asymptomatic, especially in the early pre-collapse stages.
When symptoms develop, they usually reflect irritation or structural failure of the femoral head.
Groin Pain
The most common symptom is deep groin pain.
Pain may radiate into the buttock, thigh, or knee.
Limp
A limp is common as pain increases.
Functional Limitation
Patients may have difficulty walking, running, climbing stairs, or participating in sports.
Advanced disease can substantially impair normal ambulation.
History
Before femoral-head collapse, patients may report gradually increasing atraumatic hip pain.
The history should specifically address corticosteroid exposure, alcohol use, trauma, hematologic disease, autoimmune disease, diving history, and thrombophilic conditions.
After Collapse
Once collapse occurs, the symptoms increasingly resemble those of hip osteoarthritis, including persistent groin pain, stiffness, reduced walking tolerance, and progressive loss of motion.
Physical Examination
Gait
An antalgic limp is common.
Advanced disease may produce compensatory gait changes related to pain, weakness, or loss of hip motion.
Range of Motion
Hip range of motion should be compared with the contralateral side.
Internal Rotation
Painful and reduced internal rotation is a common finding, although it is not specific to osteonecrosis and may occur with many intra-articular hip disorders.
Flexion and Abduction
Flexion and abduction may also become limited as the disease progresses.
Laboratory Tests
There is no serum laboratory test that confirms osteonecrosis.
Coagulation Evaluation
In patients with unexplained or idiopathic osteonecrosis, especially when bilateral or multifocal, evaluation for an underlying thrombophilic disorder may be considered.
Imaging
Plain Radiographs
Initial imaging should include AP and lateral views of the affected hip, usually with an AP pelvis.
Radiographs are particularly useful for detecting:
Subchondral sclerosis, cysts, crescent sign, femoral-head flattening, and secondary arthritis.
Early Disease
Radiographs can remain normal in early osteonecrosis.
A normal radiograph does not exclude the diagnosis when clinical suspicion is high.
MRI
MRI is the most sensitive imaging study for detecting early femoral-head osteonecrosis.
It can identify disease before structural changes appear on radiographs.
T1-Weighted Imaging
On T1-weighted sequences, osteonecrosis often appears as a geographic or wedge-shaped area of low signal intensity.
T2-Weighted Imaging
Fluid-sensitive sequences may demonstrate surrounding high signal related to reactive change or bone marrow edema.
Double-Line Sign
A characteristic MRI finding is the double-line sign, in which a low-signal rim is bordered by a relatively high-signal inner line on T2-weighted images.
Bilateral Imaging
Because nontraumatic osteonecrosis can affect both hips, MRI evaluation of the contralateral femoral head may be appropriate when risk factors are substantial.
Pathological Findings
The final pathologic feature is necrosis of both the osseous trabeculae and marrow elements.
As healing attempts occur at the margin of the lesion, structurally weakened necrotic bone may fail under repetitive weight bearing.
This leads to subchondral fracture and eventual collapse.
Differential Diagnosis
Any process that produces hip pain can mimic osteonecrosis.
Important alternatives include:
Septic arthritis, proximal femoral osteomyelitis, soft-tissue abscess, femoral-neck or femoral-shaft stress fracture, early osteoarthritis, femoroacetabular impingement, and chondrolysis.
Treatment
General Principles
Treatment depends on:
Patient age, symptoms, lesion size, location, cause, degree of femoral-head collapse, and presence of secondary arthritis.
The major distinction is between pre-collapse disease, in which hip-preserving treatment may still be possible, and post-collapse disease, in which arthroplasty is often required.
Remove or Modify the Cause
Whenever possible, reversible risk factors should be addressed.
Corticosteroids
Unnecessary corticosteroid exposure should be reduced or discontinued under the supervision of the physician treating the underlying disease.
Alcohol
Heavy alcohol intake should be stopped.
Tobacco
Smoking cessation should be encouraged.
Activity Modification
Reducing repetitive impact loading may decrease symptoms during early disease.
However, activity modification alone generally does not reliably prevent progression of a large necrotic lesion.
Cane or Crutches
A cane held in the opposite hand can reduce load across the affected hip.
Two crutches may be used temporarily for greater unloading.
Physical Therapy
Physical therapy is useful primarily for:
Gait training, maintenance of motion, strengthening of surrounding musculature, and instruction in assistive-device use.
Forceful weight-bearing exercise over a symptomatic necrotic femoral head should be avoided.
Medication
There is no universally effective medication that reliably reverses established osteonecrosis.
Anticoagulation
Anticoagulation may be considered in carefully selected patients with a documented thrombophilic disorder and early-stage disease, under specialist supervision.
It is not routine treatment for all cases.
Surgery
Surgical treatment is tailored to the stage of disease and the patient’s age and functional demands.
In younger patients with pre-collapse disease, preservation of the native femoral head is emphasized whenever feasible.
Once substantial collapse and arthritis are present, total hip arthroplasty becomes the most reliable treatment.
Core Decompression
Core decompression involves drilling one or more channels into the necrotic area of the femoral head.
The procedure is intended to reduce intraosseous pressure, stimulate vascular ingrowth, and promote healing.
Indications
Core decompression is most effective in early pre-collapse disease with relatively small lesions.
Outcomes are less favorable once substantial subchondral collapse has occurred.
Success
Older series reported success rates of roughly 50–60%, although results vary considerably according to lesion size, stage, and patient selection.
Bone-Grafting Procedures
Various procedures have been developed to support the necrotic femoral head and introduce biologically active bone.
Vascularized Fibular Graft
A vascularized fibular graft may be used in selected young patients with pre-collapse or early-collapse disease.
The operation is technically demanding, and indications vary among centers.
Nonvascularized Bone Grafting
Other techniques include bone grafting through a core tract or through a limited opening in the femoral head or neck.
Trapdoor Procedure
The so-called trapdoor procedure provides direct access to the necrotic segment for removal of dead bone and grafting.
It is used selectively and is not a routine treatment.
Total Hip Arthroplasty
Total hip arthroplasty is the standard treatment for advanced femoral-head collapse with secondary arthritis and disabling symptoms.
Components
Modern total hip replacement typically uses a metal or ceramic femoral head articulating against a highly cross-linked polyethylene or ceramic bearing surface.
Metal-on-metal bearings are generally avoided in contemporary practice because of concerns regarding metal wear debris and adverse local tissue reactions.
Hip Resurfacing
Hip resurfacing has been used in selected younger patients, but indications are limited and the procedure is far less commonly performed than conventional total hip arthroplasty.
Follow-Up
Prognosis
The prognosis depends heavily on whether the femoral head has already collapsed.
Pre-Collapse Disease
Small lesions detected early may remain stable or respond to hip-preserving treatment.
Large lesions involving the weight-bearing dome have a substantially greater risk of progression.
Post-Collapse Disease
Once structural collapse is present, progression toward secondary arthritis is common.
Many symptomatic patients eventually require total hip arthroplasty.
Nonoperative Treatment
Nonoperative management alone frequently fails to prevent progression in symptomatic, structurally significant disease.
It may nevertheless be appropriate for small asymptomatic lesions or patients who are poor surgical candidates.
Complications of Hip-Preserving Procedures
Potential complications include:
Failure of the lesion to heal, continued femoral-head collapse, progression to arthritis, fracture, infection, and need for later arthroplasty.
Complications of Hip Surgery
General operative risks include:
Wound-healing problems, infection, blood loss, neurovascular injury, deep venous thrombosis, and pulmonary embolism.
Complications of Total Hip Arthroplasty
Potential complications include:
Dislocation, infection, periprosthetic fracture, nerve injury, venous thromboembolism, implant wear, osteolysis, and aseptic loosening.
Modern complication rates vary substantially according to patient factors, implant type, and length of follow-up.
Patient Monitoring
Patients with early-stage osteonecrosis should be followed clinically and radiographically for evidence of femoral-head collapse.
An initial follow-up interval of approximately 3–4 months during the first year may be appropriate in higher-risk lesions.
Thereafter, annual or symptom-driven follow-up may be used depending on stability.
Monitoring should assess:
Pain, gait, hip range of motion, lesion size, development of the crescent sign, femoral-head contour, and progression to secondary arthritis.
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Orthopaedic Surgery - Hip Arthritis
Basics
Hip arthritis results from progressive loss of the articular cartilage covering the femoral head and acetabulum.
As cartilage deteriorates, the underlying subchondral bone is increasingly exposed to abnormal mechanical loading. This produces pain with weight bearing, progressive restriction of motion, gait disturbance, and eventually substantial functional disability.
Prevention and Risk Reduction
Although not all hip arthritis can be prevented, symptoms and mechanical stress may be reduced through:
Low-impact exercise, activity modification, maintenance of healthy body weight, and avoidance of repetitive high-impact loading when symptoms are present.
Suitable activities often include swimming, cycling, and walking within a tolerable range.
Epidemiology
Hip arthritis is a common cause of pain and disability in adults.
Some hips appear particularly susceptible because of subtle or overt abnormalities of joint anatomy, including developmental dysplasia and femoroacetabular impingement.
Prevalence
Arthritis overall affects a substantial proportion of the population, with older estimates suggesting that approximately 12% of the U.S. population has some form of arthritis.
The prevalence of symptomatic hip osteoarthritis increases with age.
Risk Factors
Important risk factors and underlying conditions include:
Previous trauma, osteonecrosis, infection, hemophilia, developmental hip dysplasia, femoroacetabular impingement, Legg-Calvé-Perthes disease, slipped capital femoral epiphysis, and inflammatory arthritides.
Inflammatory Arthritis
Inflammatory disorders that may involve the hip include:
Rheumatoid arthritis, systemic lupus erythematosus, and psoriatic arthritis.
Etiology
The exact cause of primary osteoarthritis is multifactorial and incompletely understood.
Contributing factors probably include differences in cartilage biology, genetics, aging, loading patterns, and joint morphology.
Mechanical Factors
Abnormal hip alignment can increase focal contact stress.
Important examples include acetabular dysplasia and femoroacetabular impingement, both of which can lead to premature cartilage and labral damage.
Classification
Hip arthritis can be broadly divided into:
Primary osteoarthritis, inflammatory arthritis, and secondary osteoarthritis.
Primary Osteoarthritis
Primary osteoarthritis develops without a single clearly identifiable initiating disorder, although subtle structural abnormalities may still contribute.
Secondary Osteoarthritis
Secondary osteoarthritis results from an underlying condition such as:
Trauma, dysplasia, osteonecrosis, Perthes disease, slipped capital femoral epiphysis, infection, or femoroacetabular impingement.
Associated Conditions
Patients may also have degenerative disease elsewhere in the musculoskeletal system, particularly:
Lumbar degenerative disc disease and knee osteoarthritis.
These conditions may complicate localization of the primary source of pain.
Diagnosis
Signs and Symptoms
Patients usually present with a deep, diffuse ache around the hip.
The classic location is the anterior groin.
Pain Distribution
Pain may radiate into the:
Buttock, thigh, or knee, often along the medial side of the thigh.
In some patients, knee pain is the predominant complaint despite the underlying pathology being located in the hip.
Gait Symptoms
Patients frequently report:
Limping, fatigue with walking, reduced walking distance, and difficulty with prolonged standing.
Functional Limitation
As hip motion decreases, patients may have difficulty:
Tying shoes, putting on socks, cutting toenails, getting into or out of a car, climbing stairs, or rising from a low chair.
History
The pain of osteoarthritis usually develops gradually over months or years.
It is generally aggravated by activity and relieved by rest, particularly early in the disease.
Activity-Related Pain
Pain with walking, prolonged standing, or other weight-bearing activity is characteristic of hip arthritis.
Night Pain
Advanced osteoarthritis may produce pain at rest or at night.
However, new severe constant pain, especially with systemic symptoms or an atypical clinical pattern, should prompt consideration of infection, tumor, occult fracture, or another diagnosis.
Age
Primary osteoarthritis is most commonly encountered in adults older than approximately 50 years.
Hip arthritis in a younger patient should prompt evaluation for a secondary cause such as trauma, dysplasia, osteonecrosis, Perthes disease, SCFE, or femoroacetabular impingement.
Physical Examination
Range of Motion
Hip range of motion should be measured and compared with the opposite side.
Internal Rotation
Loss of internal rotation is one of the earliest and most characteristic findings of hip osteoarthritis.
Pain with internal rotation is also common.
Flexion
Hip flexion gradually becomes restricted as arthritis progresses.
Flexion Contracture
A fixed flexion contracture should be assessed because it can alter standing posture, pelvic tilt, and lumbar mechanics.
Gait
The patient should be observed for:
Antalgic gait, Trendelenburg pattern, reduced stance time, short stride, or other compensatory abnormalities.
Leg-Length Discrepancy
True and apparent leg lengths should be assessed.
Progressive joint-space loss, deformity, contracture, or pelvic tilt may create actual or functional limb shortening.
Muscle Strength
Hip abductor and flexor strength should be assessed.
Chronic pain and disuse can produce substantial muscle weakness.
Stinchfield Test
A resisted straight-leg raise, commonly called the Stinchfield test, places load across the hip joint.
Reproduction of groin or deep hip pain supports an intra-articular source.
Greater Trochanter Examination
The greater trochanter should be palpated for tenderness.
Localized lateral tenderness suggests greater trochanteric pain syndrome or trochanteric bursitis rather than isolated intra-articular arthritis.
Neurologic Examination
A careful neurologic examination is necessary because lumbar radiculopathy may mimic hip disease.
Straight-Leg Raise
The straight-leg raise test can help identify radicular symptoms, particularly those arising from the lumbar spine.
Spine and Pelvis
The lumbar spine should be examined for:
Tenderness, restricted motion, scoliosis, or radicular signs.
Pelvic tilt should also be assessed because it can affect apparent limb length and hip mechanics.
Laboratory Tests
Routine laboratory studies are generally unnecessary for uncomplicated osteoarthritis.
If inflammatory arthritis is suspected, appropriate rheumatologic testing should be obtained.
Inflammatory Arthritis Evaluation
Depending on the clinical context, studies may include:
ESR, C-reactive protein, rheumatoid factor, anti-CCP antibodies, and other disease-specific tests.
Imaging
Plain Radiographs
Plain radiographs are the first-line imaging study.
A typical evaluation includes an AP pelvis and dedicated AP and lateral views of the involved hip.
Radiographic Features
Characteristic findings include:
Joint-space narrowing, osteophyte formation, subchondral sclerosis, and subchondral cyst formation.
Advanced disease may also produce femoral head deformity and acetabular remodeling.
Lumbar Spine Radiographs
If radiculopathy or substantial spinal pathology is suspected, AP and lateral radiographs of the lumbosacral spine may be useful.
Bone Scintigraphy
Technetium bone scanning can occasionally help identify occult skeletal disease when the patient has severe unexplained pain and the source remains unclear.
Its use has decreased as MRI has become more widely available.
MRI
MRI is useful for evaluating disorders that may not be visible on plain radiographs.
It is particularly effective for detecting:
Osteonecrosis, occult fracture, bone marrow abnormalities, soft-tissue disease, labral pathology, and neoplasm.
The suspected region must be adequately included within the imaging field.
Diagnostic Injection
An intra-articular hip injection containing local anesthetic can be used diagnostically when the source of pain is uncertain.
Substantial temporary pain relief after injection supports the hip joint as the major pain generator.
Differential Diagnosis
The differential diagnosis of hip pain is extensive.
Neoplasm
In younger patients, important malignant bone tumors include:
Osteosarcoma and Ewing sarcoma.
In older adults, consideration should be given to:
Metastatic bone disease and multiple myeloma.
Femoral Neck Stress Fracture
Stress fractures should be considered in:
Runners, military recruits, patients with osteoporosis, and individuals with sudden increases in physical activity.
Greater Trochanteric Pain Syndrome
Lateral hip pain with focal tenderness over the greater trochanter suggests pathology outside the hip joint.
Lumbar Radiculopathy
Pain radiating below the knee, neurologic symptoms, or positive nerve-tension testing increases suspicion for a spinal source.
Treatment
General Principles
Initial treatment is usually nonoperative.
The main goals are to reduce pain, maintain mobility, preserve strength, and delay or avoid surgery when symptoms remain manageable.
Activity Modification
Activities that consistently worsen symptoms should be reduced or modified.
Running, repetitive impact loading, deep squatting, and heavy lifting may need to be limited.
Low-impact activities are generally better tolerated.
Weight Reduction
Weight loss can reduce joint loading and improve mobility in overweight patients.
It may also reduce perioperative risk if arthroplasty is ultimately required.
Cane Use
A cane should generally be held in the hand opposite the affected hip.
This reduces hip abductor demand and can decrease joint reaction forces during walking.
Physical Therapy
Physical therapy may help maintain:
Hip range of motion, muscle strength, gait efficiency, and overall mobility.
Contracture Prevention
Stretching and range-of-motion exercises can help delay development of fixed hip contractures.
Strengthening
Strengthening the hip abductors, extensors, flexors, and surrounding lower-extremity musculature may improve function and prepare the patient for later surgery if necessary.
Medication
Acetaminophen
Acetaminophen may provide symptomatic relief, particularly in patients who cannot take NSAIDs.
NSAIDs
NSAIDs are commonly used for pain relief when there are no contraindications.
They should be used at the lowest effective dose for an appropriate duration, particularly in patients with gastrointestinal, renal, or cardiovascular risk.
Intra-Articular Corticosteroid Injection
Occasional image-guided intra-articular corticosteroid injections may provide temporary relief in selected patients.
They are not a definitive treatment for cartilage loss.
Glucosamine
Glucosamine has been used by some patients with osteoarthritis, although evidence for clinically meaningful benefit in hip osteoarthritis remains inconsistent.
Complementary and Alternative Therapies
A variety of supplements and topical therapies have been studied for osteoarthritis.
Older reports have suggested possible benefit from agents such as:
Devil’s claw, avocado-soybean unsaponifiables, capsaicin, and certain herbal anti-inflammatory preparations.
Evidence is variable, and these products should not replace established treatments.
There is limited evidence supporting magnet or laser therapy, while the role of acupuncture remains uncertain.
Surgery
Surgery is considered when pain and functional limitation remain substantial despite appropriate nonoperative treatment.
Osteonecrosis
In selected patients with early femoral head osteonecrosis before collapse, core decompression may be considered.
Hip-Preserving Osteotomy
Young patients with structural abnormalities may benefit from corrective osteotomy.
Acetabular Dysplasia
A periacetabular osteotomy can improve femoral head coverage and redistribute joint loading in appropriately selected patients with symptomatic dysplasia and preserved cartilage.
Proximal Femoral Deformity
Femoral osteotomy may be useful in selected deformities of the proximal femur.
Femoroacetabular Impingement
Young patients with symptomatic femoroacetabular impingement and limited arthritic change may benefit from procedures that reshape the femoral head-neck junction, acetabulum, or both.
Hip Arthrodesis
Hip fusion has historically been used in selected young, highly active patients when arthroplasty was undesirable.
It is now performed infrequently because of its effects on the lumbar spine, ipsilateral knee, and gait.
Total Hip Arthroplasty
Total hip replacement is the principal surgical treatment for advanced symptomatic hip arthritis.
The diseased femoral head and acetabular cartilage are replaced with prosthetic components.
Follow-Up
Prognosis With Nonoperative Treatment
Patients with mild or early arthritis may obtain substantial symptom relief from:
Activity modification, weight reduction, analgesics, NSAIDs, physical therapy, and assistive devices.
Prognosis After Total Hip Arthroplasty
The prognosis after modern total hip replacement is generally excellent.
Most appropriately selected patients achieve:
Major pain relief, improved range of motion, better walking ability, and substantial improvement in overall function.
Complications of Untreated or Progressive Hip Arthritis
Progressive disease may lead to:
Hip stiffness, flexion contracture, limp, leg-length discrepancy, muscle weakness, reduced walking tolerance, and inability to perform activities of daily living.
Complications of Total Hip Arthroplasty
Potential complications include:
Infection, dislocation, periprosthetic femoral or acetabular fracture, nerve palsy, deep venous thrombosis, pulmonary embolism, heterotopic ossification, implant loosening, liner wear, osteolysis, and stiffness.
Dislocation
Dislocation is an important complication and is generally more common after revision arthroplasty than after uncomplicated primary hip replacement.
Nerve Injury
When nerve palsy occurs, the sciatic nerve is the nerve most commonly affected.
Implant Wear and Osteolysis
Long-term prosthetic wear can generate particulate debris that contributes to bone resorption around the implant.
This process can eventually cause loosening and may require revision surgery.
Patient Monitoring
Patients with hip arthritis should be reassessed when symptoms worsen, function declines, or the pattern of pain changes.
Follow-up should monitor:
Pain severity, walking tolerance, range of motion, gait, muscle strength, limb length, response to nonoperative treatment, and radiographic progression when clinically indicated.
A sudden or atypical increase in pain should prompt evaluation for alternative diagnoses such as occult fracture, osteonecrosis, infection, or neoplasm.
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Orthopaedic Surgery - Heterotopic Ossification
Basics
Heterotopic ossification (HO) is the abnormal formation of mature bone within soft tissues where bone does not normally exist, such as muscle, subcutaneous tissue, or around nerves.
It most commonly develops after major trauma, surgery, traumatic brain injury, or spinal cord injury.
Common Sites
The joints most frequently affected are the:
Hip, elbow, and shoulder.
The resulting ectopic bone may progressively restrict joint motion and, in severe cases, bridge the joint and produce ankylosis.
Epidemiology
Heterotopic ossification is less common in children than in adults and occurs more frequently in males.
Incidence
After major neurologic or traumatic injury, HO has been reported in approximately 10–20% of patients, although incidence varies substantially according to the underlying condition and the population studied.
Clinical onset often occurs within the first several months after injury, with an average onset near 2 months in older series.
Risk Factors
Important risk factors include:
Traumatic brain injury, spinal cord injury, major trauma, previous heterotopic ossification, ankylosing spondylitis, osteoarthritis, extensive osteophyte formation, repeated surgery, certain surgical approaches, and trochanteric osteotomy.
Previous HO
A history of heterotopic ossification after prior surgery substantially increases the risk of recurrence with later procedures.
Genetics
No routine genetic test predicts susceptibility to ordinary post-traumatic or postoperative heterotopic ossification.
However, rare inherited disorders of ectopic bone formation have specific genetic causes.
Etiology
Common precipitating conditions include:
Traumatic brain injury, spinal cord injury, direct musculoskeletal trauma, and major orthopaedic surgery.
The precise biologic mechanism involves abnormal differentiation of local progenitor cells toward bone-forming pathways within inflamed soft tissues.
Associated Conditions
Fibrodysplasia Ossificans Progressiva
Fibrodysplasia ossificans progressiva is a rare genetic disorder characterized by progressive heterotopic bone formation.
It is associated with an activating mutation involving the ACVR1 gene.
This disorder differs substantially from ordinary post-traumatic HO.
Osteoma Cutis
Primary osteoma cutis represents another uncommon disorder in which bone forms within the skin or subcutaneous tissues.
Diagnosis
Signs and Symptoms
Early symptoms are often nonspecific.
Patients may develop:
Increasing pain, progressive stiffness, worsening spasticity, muscle guarding, swelling, and decreasing joint range of motion.
Reduced Range of Motion
Loss of motion is often the earliest and most clinically important finding.
A previously mobile joint may become progressively stiff over days to weeks.
Inflammatory Appearance
During the early phase, the affected area may demonstrate erythema, warmth, swelling, and tenderness, sometimes mimicking infection or thrombosis.
Physical Examination
The examiner should carefully document active and passive range of motion.
The joint should also be assessed for:
Swelling, warmth, erythema, tenderness, spasticity, palpable mass formation, and neurovascular changes.
Neurologic Examination
When HO develops near a major nerve, motor and sensory function should be assessed because progressive ossification may cause nerve entrapment.
Laboratory Tests
Alkaline Phosphatase
Serum alkaline phosphatase may become elevated during active heterotopic bone formation.
The level may begin to rise approximately 2–3 weeks after the inciting injury.
However, this test is nonspecific and cannot establish the diagnosis by itself.
Imaging
Plain Radiographs
Radiographic evidence of new bone may become visible approximately 3–6 weeks after injury, although early films can be normal.
Mature and clearly diagnostic ossification may take several months to become obvious.
Bone Scintigraphy
Bone scintigraphy can detect HO earlier than plain radiographs.
The developing lesion demonstrates intense radionuclide uptake during the metabolically active phase.
Historically, bone scans were also used to assess lesion activity before excision.
CT
CT is particularly useful for defining the location, extent, relationship to surrounding bone and neurovascular structures, and operative anatomy.
Zonal Pattern
A characteristic maturation pattern may be seen, with more mature mineralization at the periphery and a relatively lucent or less mineralized center.
This zonal architecture can help distinguish HO from some malignant soft-tissue tumors.
MRI
MRI appearance varies according to lesion maturity.
Early HO may demonstrate low to intermediate signal on T1-weighted images and high signal on T2 or fluid-sensitive sequences, often with surrounding edema.
As ossification matures, the lesion develops signal characteristics resembling cortical and medullary bone.
Preserved Muscle Architecture
Early lesions may show residual muscle fibers coursing through the abnormal tissue, an appearance sometimes described as a texture sign.
Pathological Findings
Early heterotopic ossification produces an intense inflammatory and proliferative response.
The lesion contains myofibroblasts, fibroblasts, osteoblasts, and developing osteoid and bone.
Diagnostic Pitfall
The high cellularity and rapid growth of early HO can resemble a soft-tissue neoplasm histologically.
Recognition of its characteristic zonal maturation pattern is therefore important.
Differential Diagnosis
Important alternatives include:
Septic arthritis, deep infection, thrombophlebitis or deep venous thrombosis, and soft-tissue neoplasm.
Early HO can resemble all of these conditions clinically.
Treatment
General Principles
Most patients are managed nonoperatively.
The main goals are to:
Maintain functional joint motion, control pain, minimize contracture, and prevent further clinically significant ossification when prophylaxis is appropriate.
Physical Therapy
Gentle range-of-motion exercises are important for preserving mobility.
Therapy should emphasize functional motion without forceful manipulation that causes substantial pain or tissue trauma.
Rehabilitation
Treatment may also include positioning, stretching, strengthening of unaffected muscle groups, and strategies to maintain functional independence.
Analgesia
Analgesics may be used for symptomatic relief.
NSAIDs may provide both pain control and prophylactic benefit in selected postoperative settings.
NSAID Prophylaxis
NSAIDs are commonly used to reduce the risk of heterotopic ossification after high-risk procedures or after surgical excision.
Agents may include:
Indomethacin, naproxen, or other appropriate NSAIDs.
A course of approximately several weeks, often around 6 weeks, has traditionally been used.
Limitations
NSAID prophylaxis may be limited by:
Gastrointestinal intolerance, renal disease, bleeding risk, and other contraindications.
A proportion of patients are unable to complete treatment because of adverse effects.
Radiotherapy
Radiotherapy is primarily used as prophylaxis, not as treatment for mature established HO.
Timing
When selected for prevention after surgery, low-dose radiation is generally administered shortly before or within approximately 72 hours after the operative procedure.
Once mature ectopic bone is established, radiation does not remove the lesion.
Surgery
Surgical excision is considered when HO causes substantial disability.
Indications
Potential indications include:
Severe restriction of joint motion, painful mechanical block, contracture, difficulty with sitting or hygiene, nerve entrapment, or major functional impairment.
Timing of Excision
Historically, surgeons waited at least 6 months or longer for maturation before excision.
Modern practice may permit earlier removal when the lesion is sufficiently mature and symptoms justify intervention, particularly when prolonged delay would lead to permanent contracture or functional loss.
The timing should therefore be individualized according to radiographic maturity, neurologic status, joint function, and recurrence risk.
Operative Planning
CT is often useful before surgery to determine the relationship of the ectopic bone to:
Major vessels, nerves, the joint capsule, and surrounding musculature.
Postoperative Prophylaxis
After excision, prophylaxis is commonly used because recurrence is possible.
Options include:
NSAIDs and/or low-dose radiation therapy, depending on patient factors and institutional practice.
Radiation After Resection
If radiation is chosen, it is generally delivered within approximately 72 hours of surgery.
NSAIDs After Resection
A postoperative NSAID course, often lasting approximately 6 weeks, may be prescribed when not contraindicated.
Follow-Up
Patients who undergo surgical excision should be monitored until the wound has healed and functional range of motion has stabilized.
Continued rehabilitation is important to preserve the motion gained at surgery.
Prognosis
Outcome depends on the location, underlying cause, neurologic status, and extent of ossification.
Most patients with non-neurogenic HO retain reasonable function and never require excision.
Neurogenic HO
Patients with traumatic brain or spinal cord injury may develop more extensive lesions and have a greater risk of severe stiffness or ankylosis.
Complications
Loss of Motion
Progressive ectopic bone can substantially restrict joint motion.
Ankylosis
Severe HO may bridge a joint and result in near-complete or complete ankylosis.
Nerve Entrapment
Ectopic bone may surround or compress a major nerve, producing pain, sensory loss, or motor weakness.
Recurrence
HO may recur after surgical excision, particularly in patients with persistent neurologic risk factors or previous recurrent disease.
Patient Monitoring
Serial clinical examinations should document pain, swelling, range of motion, neurologic status, and functional ability.
Radiographs may be obtained at approximately 1–3-month intervals during the first 6 months when progression or maturation needs to be followed.
Imaging frequency should be individualized according to symptoms, lesion location, and whether surgery is being considered.
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Orthopaedic Surgery - Hemophilia
Basics
Hemophilia is an inherited coagulation-factor deficiency that causes abnormal and prolonged bleeding.
The direct disorder involves the clotting system, but repeated hemorrhage can secondarily affect many organ systems, particularly the joints, muscles, peripheral nerves, and central nervous system.
The age at diagnosis depends largely on disease severity. Severe forms are usually recognized in infancy or early childhood, whereas mild disease may not become apparent until surgery, dental work, or significant trauma.
Classification by Factor Activity
Severity is classified according to the percentage of normal clotting-factor activity.
Severe Hemophilia
Severe disease is defined by <1% normal factor activity.
These patients may experience spontaneous bleeding, particularly into joints and muscles.
Moderate Hemophilia
Moderate disease is characterized by approximately 1–5% factor activity.
Bleeding usually follows relatively minor trauma but may occasionally occur spontaneously.
Mild Hemophilia
Mild disease is associated with >5% factor activity.
Bleeding usually becomes evident only after significant trauma, surgery, or invasive procedures.
Types
Hemophilia A
Hemophilia A, historically called classic hemophilia, results from deficiency or dysfunction of factor VIII.
Hemophilia B
Hemophilia B, historically called Christmas disease, results from deficiency or dysfunction of factor IX.
General Prevention
A major goal of long-term care is prevention of recurrent joint bleeding and development of target joints.
Modern prophylactic factor replacement or other hematologic therapy, together with patient education and appropriate activity modification, can substantially reduce cumulative joint damage.
Epidemiology
The combined frequency of hemophilia has historically been estimated at approximately 1 per 10,000 people, although prevalence varies by population and method of ascertainment.
Males are affected far more commonly because the classic forms are X-linked disorders.
Relative Frequency
Hemophilia A is considerably more common than hemophilia B.
Older series have estimated approximately:
75% hemophilia A, 12% hemophilia B, with the remainder representing other rare coagulation-factor deficiencies.
Risk Factors
The principal risk factor is a positive family history, particularly affected males on the maternal side.
However, new mutations may occur, so absence of a known family history does not exclude the diagnosis.
Genetics
Hemophilia A and B are generally inherited in an X-linked recessive pattern.
Affected males inherit the pathogenic variant through the maternal line, while females are usually carriers, although some carriers can have reduced factor levels and clinically important bleeding.
Etiology
Hemophilia A
Hemophilia A results from a pathogenic variant affecting the F8 gene, leading to factor VIII deficiency.
Hemophilia B
Hemophilia B results from a pathogenic variant affecting the F9 gene, leading to factor IX deficiency.
Diagnosis
Early Presentation
In severe hemophilia, the diagnosis may become apparent during infancy because of excessive bleeding after:
Circumcision, immunizations, oral or lip trauma, venipuncture, or minor falls.
Mild Disease
Patients with milder hemophilia may remain undiagnosed until a major laceration, dental procedure, or operation causes unexpectedly prolonged bleeding.
Recurrent Hemarthrosis
Repeated bleeding into joints is one of the most important long-term manifestations.
The joints most often involved include the:
Knees, ankles, and elbows.
Shoulders may also be affected.
Target Joint
After a joint has bled repeatedly, it becomes increasingly susceptible to additional hemorrhage.
Such a repeatedly affected joint is termed a target joint.
Symptoms of Joint Bleeding
An acute hemarthrosis often begins with deep pain, pressure, or tightness before visible swelling develops.
As blood accumulates, the joint becomes swollen, warm, painful, and increasingly restricted in motion.
Muscle Hemorrhage
Muscle bleeding may cause swelling, pain, loss of motion, and compression of nearby nerves.
Iliopsoas Hemorrhage
An important example is bleeding into the iliopsoas muscle, which may compress the femoral nerve and produce weakness, sensory loss, or femoral neuropraxia.
Chronic Hemophilic Arthropathy
Repeated hemarthroses stimulate synovial hypertrophy and chronic joint damage.
Over years, the affected joint may develop:
Stiffness, flexion contracture, cartilage destruction, subchondral changes, chronic pain, and degenerative arthritis.
Physical Examination
Joint Examination
All major joints should be assessed for:
Effusion, tenderness, warmth, swelling, range-of-motion loss, deformity, and contracture.
Particular attention should be given to the knees, ankles, elbows, and shoulders.
Ankle Examination
An early ankle effusion may be suggested by loss of the normal soft-tissue depressions around the malleoli.
Knee Examination
Knee flexion should be compared bilaterally.
The examiner should also assess whether the patient retains the normal small amount of hyperextension, often approximately 5–10°.
Joint Enlargement
Chronically affected joints may appear enlarged because of:
Synovial hypertrophy, epiphyseal overgrowth related to hyperemia, and atrophy of surrounding muscle.
Bleeding Log
Patients may be encouraged to keep a record of bleeding episodes.
This can help identify development of a target joint and guide prophylactic treatment.
Neurologic Examination
The examiner should look for neurologic sequelae of previous bleeding.
Examples include:
Hemiparesis after intracranial hemorrhage, femoral neuropathy from iliopsoas bleeding, or sciatic neuropathy from deep pelvic or gluteal bleeding.
Laboratory Tests
Factor Assays
Factor VIII or IX activity should be measured and expressed as a percentage of normal activity.
Clinical severity correlates broadly with the residual factor level.
Even relatively low levels, such as approximately 5–10%, may provide substantial protection against spontaneous bleeding compared with severe deficiency.
Inhibitors
If factor activity fails to rise as expected after replacement therapy, a neutralizing inhibitor should be suspected.
An inhibitor is an antibody directed against the replacement clotting factor, most commonly factor VIII.
Surgical Significance of an Inhibitor
The presence of a significant inhibitor complicates hemostatic management and increases the risk of elective surgery.
Procedures should therefore be coordinated with an experienced hematology team.
Additional Long-Term Screening
Historically, patients with hemophilia exposed to plasma-derived blood products were at increased risk for blood-borne infection.
Long-term care should take into account the patient’s status regarding:
Hepatitis, HIV, and factor inhibitors, when clinically relevant.
Pathological Findings
Gross Appearance of the Joint
The synovium of a chronically affected hemophilic joint may appear brown and velvety because of hemosiderin deposition and synovial hypertrophy.
Cartilage Damage
The articular cartilage progressively loses its normal smooth appearance.
Advanced disease may demonstrate erosions and irregular defects.
Microscopy
The synovial lining becomes:
Hypertrophic, hypervascular, and hemosiderin-laden.
The increased vascularity predisposes the joint to further bleeding.
With time, fibrosis develops and contributes to progressive stiffness and loss of motion.
Imaging
Plain radiographs of a hemophilic target joint may demonstrate a progressive sequence of abnormalities.
Early Changes
Initial findings include:
Soft-tissue swelling and periarticular osteopenia.
Intermediate Changes
With recurrent bleeding, radiographs may show:
Epiphyseal enlargement, joint-space narrowing, subchondral irregularity, and cyst formation.
Advanced Changes
Late hemophilic arthropathy resembles severe degenerative joint disease with:
Marked joint-space loss, deformity, subchondral cystic change, and articular destruction.
Differential Diagnosis
Important alternatives include:
Von Willebrand disease, pigmented villonodular synovitis, acquired coagulation-factor inhibitors, and thrombocytopenia.
Treatment
General Principles
Treatment depends on the severity and location of bleeding and should be coordinated closely with hematology.
The principal goals are to:
Stop hemorrhage, prevent recurrent bleeding, preserve joint motion, and avoid long-term arthropathy.
Acute Hemarthrosis
The cornerstone of treatment is prompt clotting-factor replacement or other appropriate hemostatic therapy.
Early treatment limits the amount of blood entering the joint and reduces secondary synovial damage.
Rest and Immobilization
A short period of rest and protective immobilization may be used during the acute painful phase.
Prolonged immobilization should be avoided because it promotes stiffness and muscle wasting.
Range of Motion
Gentle range-of-motion exercises should begin once bleeding and pain have settled.
Joint Aspiration
If a large tense hemarthrosis produces severe pain or threatens joint motion, aspiration may be considered after adequate factor replacement has been established.
The procedure should be performed under sterile conditions with hematologic support.
Compression
Compression and supportive measures may help reduce swelling after bleeding is controlled.
Chronic Hemophilic Synovitis
Repeated bleeding can produce hypertrophic synovium that itself becomes a source of further hemorrhage.
Synovectomy may therefore be considered for persistent target-joint bleeding despite optimized medical treatment.
Synovectomy
Synovectomy removes or ablates diseased hypertrophic synovium in an attempt to reduce recurrent bleeding.
Arthroscopic Synovectomy
In appropriate joints, synovectomy can be performed arthroscopically.
Radiosynovectomy
Injection of a radionuclide into the joint can produce chemical or radiation-induced synovial ablation.
This may reduce bleeding frequency in selected high-risk target joints.
End-Stage Arthropathy
Severely damaged painful joints may require reconstructive surgery.
Arthroplasty
Joint replacement can provide substantial pain relief and improved function, particularly for end-stage knee arthropathy.
Arthrodesis
Fusion may be appropriate for selected end-stage joints, especially the ankle, when painful destruction is severe.
Iliopsoas Hemorrhage
Psoas bleeding associated with femoral neuropraxia is generally treated with:
Hemostatic factor replacement, activity restriction, observation, and serial neurologic examination.
Most cases are managed nonoperatively unless another complication develops.
Compartment Syndrome
Compartment syndrome should be treated according to standard principles.
Because surgery itself carries major bleeding risk, clotting-factor correction should be initiated urgently, followed by decompression when clinically indicated.
Home Prophylaxis
Home treatment programs can substantially reduce the frequency and severity of bleeding episodes.
When the patient and family are appropriately trained, factor or other prescribed hemostatic treatment can be administered promptly at the first sign of bleeding.
Activity
Regular low-impact physical activity is generally beneficial because strong muscles help stabilize joints.
Activities with a high risk of collision or trauma may require modification according to disease severity and hematology guidance.
Physical Therapy
Physical therapy is important for monitoring and maintaining:
Joint range of motion, muscle strength, gait, balance, and overall function.
It is particularly useful after major bleeding episodes or orthopaedic surgery.
Medication
Analgesia
Medications that impair platelet function should generally be avoided unless specifically approved by the treating hematologist.
NSAIDs and Aspirin
Aspirin and many traditional NSAIDs can worsen bleeding because of their antiplatelet effects.
Acetaminophen
Acetaminophen is commonly used for pain control because it does not significantly impair platelet function.
Other analgesic choices should be individualized.
Surgery
Any operation in a patient with hemophilia requires careful perioperative coordination with hematology, including planned factor replacement or other hemostatic therapy before, during, and after the procedure.
Synovectomy
Surgical or radiosynovectomy may be performed for recurrent target-joint bleeding that persists despite adequate prophylaxis.
Total Knee Arthroplasty
Knee replacement may be indicated for severe end-stage hemophilic arthropathy with disabling pain and loss of function.
Ankle Arthrodesis
Fusion can be considered for severe painful ankle degeneration when reconstruction is unlikely to provide reliable function.
Follow-Up
Prognosis
With modern prophylaxis and multidisciplinary care, many patients can maintain substantially better joint function and life expectancy than was historically possible.
Outcome depends on:
Severity of factor deficiency, access to prophylactic treatment, inhibitor development, frequency of bleeding, and established joint damage.
Complications
Neurologic Hemorrhage
Bleeding into the brain or around major peripheral nerves may produce catastrophic neurologic injury.
Intracranial hemorrhage is a medical emergency.
Hemophilic Arthropathy
Repeated hemarthroses can cause:
Joint stiffness, contracture, chronic synovitis, cartilage destruction, and secondary arthritis.
Compartment Syndrome
Deep muscle hemorrhage may increase compartment pressure and threaten nerve and muscle viability.
Peripheral Nerve Compression
Large hematomas can compress nearby nerves, particularly the femoral or sciatic nerve.
Blood-Borne Infection
Historically, transfusion-transmitted hepatitis and HIV were major complications of plasma-derived treatment products.
Modern screening and recombinant therapies have greatly reduced this risk.
Inhibitor Formation
Development of neutralizing antibodies against replacement factor can make bleeding more difficult to control and complicate surgery.
Patient Monitoring
Patients should ideally be followed through a multidisciplinary hemophilia treatment program.
Care commonly involves:
Hematology, orthopaedics, physical therapy or rehabilitation, dentistry, nursing, and social services.
Orthopaedic Monitoring
Follow-up should assess:
Frequency of hemarthrosis, development of target joints, joint range of motion, contractures, muscle strength, gait, pain, and radiographic progression of arthropathy.
Early recognition of recurrent joint bleeding provides the best opportunity to prevent irreversible hemophilic arthropathy.
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Orthopaedic Surgery - Hemangioma
Basics
Hemangioma is a benign vascular lesion that may arise within bone or soft tissue.
In orthopaedic practice, these lesions may involve the axial or appendicular skeleton as well as the surrounding soft tissues.
Many lesions historically labeled hemangiomas, particularly in soft tissue, are now more precisely categorized according to modern vascular-anomaly terminology, but the term remains widely used in musculoskeletal literature.
Age
Hemangiomas can occur at any age, although osseous lesions are most commonly diagnosed during the middle decades of life.
Epidemiology
Hemangiomas are relatively uncommon as symptomatic orthopaedic lesions.
No major difference in prevalence between males and females has been consistently demonstrated.
Risk Factors
No specific environmental or acquired risk factors are known.
Genetics
There is no established hereditary pattern for the typical musculoskeletal hemangioma.
Etiology
The exact cause is unknown.
These lesions are considered benign and nonmetastatic.
Some pathologists regard certain vascular lesions of this type as hamartomatous malformations rather than true neoplasms.
Diagnosis
Signs and Symptoms
Clinical presentation depends on whether the lesion involves bone or soft tissue.
Osseous Hemangioma
A bone lesion may present with a slowly progressive, poorly localized ache or localized swelling.
Many lesions are asymptomatic and found incidentally.
Occasionally, weakening of the involved bone may lead to a pathologic fracture.
Vertebral Hemangioma
Vertebral hemangiomas are commonly incidental findings.
More aggressive lesions can rarely produce vertebral expansion, collapse, epidural extension, pain, or neurologic compromise.
Soft-Tissue Hemangioma
Soft-tissue vascular lesions often present with intermittent swelling, fullness, or a soft mass.
Pain may be absent or mild.
Symptoms and size may fluctuate depending on limb position and venous filling.
Physical Examination
Soft-tissue lesions may feel soft, compressible, fluctuant, or springy on palpation.
Examination is often most informative when the affected limb is placed in a dependent position.
Positional Enlargement
Because the lesion contains vascular channels that fill with blood, it may enlarge when the extremity is dependent and partially collapse with elevation or compression.
After palpation, the lesion may refill gradually.
Laboratory Tests
There are no specific serum laboratory studies that establish the diagnosis of a hemangioma.
Laboratory tests are obtained only when another diagnosis is being considered.
Imaging
Soft-Tissue Lesions
Plain radiographs may be normal or may show indirect evidence of a vascular lesion.
Some lesions produce erosion or remodeling of adjacent bone.
Phleboliths
Rounded calcified thrombi, known as phleboliths, may be visible within soft-tissue vascular lesions.
They are seen in a substantial minority of cases and strongly support a venous vascular lesion when present.
MRI
MRI is the preferred modality for defining the extent and internal characteristics of a soft-tissue vascular lesion.
Gadolinium-enhanced imaging is particularly useful.
MRI Appearance
Typical findings may include serpiginous vascular channels with contrast enhancement.
Lesions may contain substantial fat, producing high signal on T1-weighted images.
Blood-filled vascular spaces and slow-flow components may also produce high signal on fluid-sensitive or T2-weighted sequences.
Osseous Hemangioma
Bone hemangiomas may be solitary or multiple.
They are often expansile and trabeculated and generally produce little or no aggressive periosteal reaction.
Vertebral Radiographic Appearance
A classic vertebral hemangioma demonstrates thickened vertical trabeculae.
On radiographs this produces a “corduroy” or vertically striated appearance.
CT Appearance
Axial CT may show thickened trabeculae seen end-on, creating the characteristic “polka-dot” appearance.
Other Radiographic Patterns
The imaging appearance can vary considerably.
Lesions may appear:
Trabeculated, expansile, “soap-bubble,” osteopenic, or predominantly lytic.
The absence of an aggressive periosteal response and the presence of characteristic internal trabeculation can help suggest the diagnosis.
Pathological Findings
Grossly, these lesions may appear markedly vascular and bloody.
Residual or thickened trabecular bone often passes through the lesion.
Microscopy
Histologic examination typically shows numerous thin-walled vascular channels containing red blood cells.
Depending on the lesion type, channels may be capillary-sized or larger.
Lymphatic channels may also be prominent in some vascular malformations.
Differential Diagnosis
Important considerations include:
Multiple myeloma, infection, simple or aneurysmal bone cyst, primary malignant bone tumor, and metastatic disease.
Other vascular tumors or malformations may also need to be distinguished histologically and radiographically.
Treatment
General Principles
Most asymptomatic osseous hemangiomas do not require treatment.
Management is determined by symptoms, location, structural risk, neurologic involvement, and diagnostic certainty.
Soft-Tissue Lesions
Soft-tissue vascular lesions may recur after surgical excision, particularly when they are diffuse or infiltrative.
For this reason, surgery is avoided when an effective less invasive treatment is available.
Compression
Compression garments or dressings may reduce swelling and discomfort in selected superficial or low-flow lesions.
Sclerotherapy
Image-guided sclerotherapy is commonly used for appropriate symptomatic venous malformations.
Agents vary by lesion characteristics and specialist preference.
Historically, alcohol has been used as a powerful sclerosant, although treatment requires experienced interventional specialists because significant complications are possible.
Osseous Lesions
Hemangiomas of bone rarely require surgical treatment when they are asymptomatic and structurally stable.
Observation is usually appropriate.
Physical Therapy
Physical therapy has no direct role in treating the vascular lesion itself.
It may occasionally be used for rehabilitation when weakness or functional limitation results from associated surgery or fracture.
Surgery
Surgery should generally be reserved for selected situations, such as:
Diagnostic uncertainty requiring biopsy, pathologic fracture, structural compromise, progressive neurologic deficit, severe refractory symptoms, or failure of other treatments.
Biopsy
Biopsy of a suspected vascular lesion requires careful planning because these tumors may bleed significantly.
The imaging appearance should be reviewed thoroughly before biopsy, and the procedure should be coordinated with an experienced musculoskeletal tumor team when diagnosis is uncertain.
Follow-Up
Prognosis
The overall prognosis is excellent because typical hemangiomas are benign and lack metastatic potential.
Recurrence
Local recurrence may occur, particularly in incompletely treated soft-tissue lesions.
Recurrence does not imply malignant transformation.
Complications
Pathologic Fracture
An osseous lesion that substantially weakens bone may rarely produce a pathologic fracture.
Neurologic Compromise
Aggressive vertebral lesions can occasionally cause spinal canal compromise and neurologic deficits.
Bleeding
Because these lesions are vascular, operative or biopsy procedures may be complicated by substantial hemorrhage.
Patient Monitoring
Most stable bone lesions require only observation unless symptoms, fracture risk, or structural changes develop.
Soft-tissue lesions may be followed with serial clinical examinations and MRI, particularly when symptoms or size are changing.
Follow-up intervals such as every 3–6 months initially may be appropriate for symptomatic or recently treated lesions, with longer intervals once stability is established.
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Orthopaedic Surgery - Heel Sores
Basics
Heel sores are pressure-related injuries of the skin and underlying tissues over the calcaneus, usually caused by prolonged loading of the heel.
They occur most often in patients who are bedridden, nonambulatory, critically ill, neurologically impaired, or otherwise unable to reposition the lower extremities independently.
Heel pressure injuries can also develop beneath a lower-extremity cast when padding is inadequate or persistent pressure is concentrated over the posterior heel.
Synonyms
Common terms include heel pressure ulcer, heel ulcer, pressure sore, bedsore, and decubitus ulcer.
The modern term pressure injury is often preferred because significant underlying tissue damage may exist before an open ulcer is visible.
Classification
Pressure injuries are commonly staged according to the depth of tissue involvement.
Stage I
Stage I consists of intact skin with persistent nonblanchable erythema.
The skin may also be painful, warmer or cooler than surrounding tissue, or altered in consistency.
This stage represents early pressure-related injury before actual skin loss has occurred.
Stage II
Stage II involves partial-thickness loss of skin, affecting the epidermis and sometimes part of the dermis.
It may appear as a shallow ulcer, blister, crack, or superficial area of skin breakdown.
Stage III
Stage III represents full-thickness skin loss extending into the subcutaneous tissues.
The ulcer may reach the level of the underlying fascia but does not expose deeper structures such as tendon or bone.
Stage IV
Stage IV pressure injury consists of extensive full-thickness tissue destruction with exposure or direct involvement of bone, tendon, muscle, joint, or other deep structures.
These lesions carry a substantial risk of deep infection and osteomyelitis.
Geriatric Considerations
Older adults are at particularly high risk because of thinner skin, reduced soft-tissue padding, impaired circulation, frailty, and a greater likelihood of immobility or hospitalization.
Comorbidities such as diabetes, neuropathy, peripheral vascular disease, and poor nutrition further increase risk.
Prevention
Prevention is the most important aspect of management.
Early recognition and removal of pressure can prevent superficial tissue injury from progressing to deep ulceration.
Repositioning
Bed-bound patients should be repositioned frequently so that prolonged pressure is not maintained over the same area.
Heel Off-Loading
The heels should be elevated or floated completely off the mattress using appropriate positioning devices or pillows that support the lower leg without concentrating pressure behind the heel.
Cast Precautions
Patients wearing casts should not rest the casted heel continuously on a firm surface.
Any new heel pain, burning, numbness, or pressure sensation beneath a cast should prompt immediate evaluation.
Epidemiology
Heel pressure ulcers are among the more common complications encountered in postoperative, rehabilitative, and long-term-care settings.
They occur particularly frequently in elderly, debilitated, neurologically impaired, or immobilized patients.
Incidence
In hospitalized populations, heel ulcers have been reported in up to approximately 18% of patients in some series.
The exact incidence varies substantially according to patient population and preventive practices.
Risk Factors
Important risk factors include:
Diabetes mellitus, peripheral neuropathy, peripheral vascular disease, malnutrition, immobility, bed-bound status, paralysis, and prolonged postoperative inactivity.
Etiology
Heel sores develop when sustained pressure and shear forces compromise the small blood vessels supplying the skin and soft tissues over the calcaneus.
Pressure
The posterior heel contains relatively little soft-tissue padding between the skin and bone.
When the heel remains against a mattress, cast, or other surface for prolonged periods, local capillary pressure may exceed tissue perfusion pressure.
This produces ischemia, cellular injury, and eventually necrosis.
Shear
Shear forces generated when the limb slides across a bed or within a cast can distort small vessels and further impair blood flow.
Neuropathy
Patients with reduced sensation may not feel the pain that normally prompts repositioning.
As a result, tissue injury may progress substantially before it is recognized.
Vascular Disease
Peripheral arterial disease reduces tissue perfusion and limits the ability of the wound to heal.
Cast-Related Pressure
Pressure injuries may occur beneath casts because of inadequate padding, focal pressure points, swelling, or prolonged resting of the heel against the cast surface.
Associated Conditions
Common associated conditions include:
Paralysis, diabetes mellitus, sensory loss or peripheral neuropathy, contractures, vascular disease, and severe immobility.
Diagnosis
Diagnosis is based primarily on history and direct inspection of the heel.
At-risk patients require repeated skin checks because the earliest stage may be subtle.
History
The lesion may initially present with heel pain, tenderness, burning, or a soft or boggy sensation before visible ulceration develops.
Patients with neuropathy may have no warning pain at all.
High-Risk Patients
Special attention should be given to patients who are:
Bed-bound, postoperative, in an intensive care unit, neurologically impaired, diabetic, neuropathic, malnourished, or immobilized in a cast or brace.
Physical Examination
Inspection
The heel should be inspected for:
Erythema, discoloration, blistering, cracks, skin separation, ulceration, eschar, drainage, or deeper tissue exposure.
Nonblanching Discoloration
A red, maroon, or purple area that does not blanch with pressure is concerning for pressure-related tissue injury.
Persistent discoloration may precede visible skin breakdown.
Tenderness
The heel may be tender before major skin changes develop.
Tenderness in an immobilized or casted patient should therefore be taken seriously.
Advanced Ulcers
More advanced lesions may expose subcutaneous tissue, tendon, muscle, or bone.
The true depth of an ulcer can sometimes be difficult to determine when necrotic tissue or eschar covers the base.
Evaluation for Infection
The wound should be examined for:
Surrounding erythema, warmth, swelling, purulent drainage, malodor, fluctuance, or spreading cellulitis.
Systemic symptoms such as fever or malaise raise further concern for deeper infection.
Joint Involvement
Pain with ankle or hindfoot range of motion may suggest extension into a nearby joint and should raise concern for septic arthritis or deep infection.
Neurologic Examination
A complete motor and sensory examination should be performed.
Loss of protective sensation substantially increases the risk of progression and recurrence.
Vascular Examination
Pulses, capillary refill, skin temperature, and other indicators of limb perfusion should be evaluated.
Poor arterial supply may prevent healing and may alter the surgical plan.
Laboratory Tests
Laboratory studies are guided by clinical suspicion.
Suspected Infection
When infection is suspected, appropriate tests may include:
Complete blood count with differential, erythrocyte sedimentation rate, and C-reactive protein.
Blood cultures may be indicated in patients with systemic illness.
Nutrition
When poor nutritional status is suspected, evaluation may include serum albumin, prealbumin, and broader nutritional assessment.
Laboratory values should be interpreted within the overall clinical context.
Imaging
Plain Radiographs
AP and lateral radiographs of the foot and ankle can help identify underlying bone destruction, fracture, foreign material, or advanced osteomyelitis.
Early superficial pressure injuries usually produce no radiographic abnormalities.
MRI
MRI is particularly useful when osteomyelitis, deep abscess, or extension into adjacent soft tissues is suspected.
It is substantially more sensitive than plain radiography for early marrow abnormalities.
Nuclear Medicine Imaging
Tagged white blood cell studies or other nuclear medicine imaging may be used when the diagnosis of osteomyelitis remains uncertain or MRI cannot be performed.
Debridement and Diagnostic Assessment
Necrotic tissue may need to be removed to determine the actual depth and extent of the ulcer.
Debridement also reduces devitalized tissue that can support bacterial growth and interfere with healing.
Pathological Findings
The fundamental pathologic mechanism is ischemic tissue necrosis caused by prolonged pressure.
Persistent ischemia damages the skin and underlying soft tissues, ultimately producing ulceration.
Infection
In chronically debilitated, diabetic, or neuropathic patients, open ulcers can become infected readily.
Progression may lead to cellulitis, abscess formation, osteomyelitis, or septic arthritis.
Differential Diagnosis
Important alternative or associated diagnoses include:
Osteomyelitis, soft-tissue abscess, cellulitis, fracture, and septic arthritis.
Other causes of heel ulceration, including arterial, neuropathic, and traumatic wounds, should also be considered.
Treatment
General Principles
Treatment begins with complete pressure relief, wound assessment, optimization of perfusion and nutrition, infection control when necessary, and appropriate wound care.
Prevention remains more effective than treatment of an established ulcer.
Pressure Off-Loading
Pressure must be removed from the affected heel.
This can be accomplished with heel-suspension devices, pillows positioned under the calf, specialty mattresses, or other off-loading systems.
Foot Care
Patients with diabetes or neuropathy should perform regular skin inspection and wear appropriately fitted shoes that avoid focal pressure.
Daily Inspection
The feet should be checked daily for redness, blisters, calluses, cracks, or ulceration.
Patients who cannot inspect their own feet require assistance from caregivers.
Cast-Related Heel Pain
A patient in a cast who develops new heel pain should have the cast removed or opened sufficiently to permit direct skin inspection.
Persistent pain should never simply be attributed to the fracture without checking for pressure injury.
Superficial Pressure Injuries
Stage I and many Stage II lesions can often be treated successfully with:
Complete off-loading, protective padding, local wound care, and correction of underlying risk factors.
Deep Ulcers
Stage III and IV lesions often require more aggressive treatment.
This may include serial debridement, specialized dressings, negative-pressure wound therapy in selected cases, treatment of infection, and reconstruction or amputation when tissue destruction is extensive.
Antibiotics
Antibiotics are indicated when there is clinical infection, not merely because an ulcer is present.
Infected heel ulcers may be polymicrobial, especially in patients with diabetes or chronic wounds.
Empiric therapy may therefore require broad coverage initially, followed by adjustment according to culture results and clinical response.
Nursing Care
Nursing staff play a central role in prevention and early recognition.
Essential measures include:
Frequent repositioning, heel off-loading, skin inspection, moisture control, documentation of wounds, and prompt communication of new pressure injuries to the medical team.
Physical Therapy
Physical therapists can help with positioning, pressure relief, transfers, mobility, gait training, and selection of off-loading strategies.
Whirlpool Therapy
Whirlpool therapy was historically used for wound cleansing and debridement.
Modern wound care more commonly favors targeted debridement and moisture-controlled dressings because prolonged soaking may macerate tissue or increase contamination risk.
Nutrition
Adequate caloric and protein intake is important for wound healing.
A nutrition consultation should be considered in patients with weight loss, frailty, low intake, or laboratory evidence suggesting malnutrition.
Surgery
Debridement
Necrotic and infected tissue should be removed when indicated.
Limited soft-tissue debridement may occasionally be performed in a clinic or outpatient setting.
Operative Debridement
Extensive necrosis, deep infection, exposed bone, or suspected osteomyelitis may require formal operative debridement.
Bone Resection
Infected or nonviable calcaneal bone may need to be excised in severe cases.
Amputation
When infection, tissue necrosis, or ischemia cannot be controlled, partial or major amputation may be necessary.
This is generally reserved for advanced limb-threatening disease.
Referral
Patients with complicated heel ulcers may require coordinated care involving:
Orthopaedic surgery, wound-care specialists, vascular surgery, infectious disease, endocrinology, nursing, rehabilitation, and nutrition services.
Prognosis
Stage I and II
Superficial ulcers generally have a favorable prognosis when pressure is removed promptly and underlying risk factors are controlled.
Stage III and IV
Deep ulcers have a poorer prognosis because of the increased likelihood of infection, osteomyelitis, poor healing, and need for surgery.
Factors Affecting Outcome
Prognosis depends on:
Ulcer depth, vascular status, diabetes control, nutritional status, age, mobility, presence of neuropathy, and whether deep infection is present.
Complications
Osteomyelitis
Deep heel ulcers may extend into the calcaneus and cause chronic osteomyelitis.
Septic Arthritis
Spread into adjacent joints may result in septic arthritis.
Cellulitis and Abscess
Local infection may progress into surrounding soft tissues.
Systemic Infection
Severe infected ulcers can cause bacteremia or sepsis, particularly in medically frail patients.
Patient Monitoring
Heel pressure injuries require close and repeated reassessment because progression can occur rapidly when pressure persists.
Monitoring should include:
Wound size and depth, skin color, drainage, surrounding cellulitis, presence of necrotic tissue, vascular status, sensation, pain, nutritional status, and effectiveness of pressure relief.
Any evidence of worsening tissue destruction, systemic infection, exposed bone, or impaired perfusion warrants prompt escalation of treatment.
