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.