While seating-acquired pressure injuries (PIs) over the ischial tuberosities are a traditional focus of spinal cord injury (SCI) rehabilitation, the heels represent an urgent clinical priority. Heel PIs are among the most frequent secondary complications in both acute and long-term SCI care, often resulting in catastrophic loss of independence and immense healthcare expenditure. Effective management demands a sophisticated understanding of how denervation and physiological changes post-injury compromise the skin’s ability to tolerate mechanical load.
1. The Silent Priority: Why Heels Are at Risk
The heels are uniquely vulnerable due to a lack of the significant subcutaneous fat and muscle found in the gluteal region. In the SCI population, this vulnerability is immediately exacerbated by systemic physiological changes. Muscle atrophy is a primary driver of risk; the volume of damaged muscle increases exponentially with the degree of atrophy. This loss of natural protective cushioning, combined with calcaneal (or ischial tuberosity) flattening, ensures that external pressure is transmitted more intensely to the underlying soft tissues.
Biological Risk Factors
- Muscle Atrophy: Significant reduction in tissue volume decreases the area available to redistribute pressure and increases internal tissue stress.
- Calcaneal Flattening: Changes in bone morphology further concentrate pressure, accelerating the rate of deep tissue damage.
- Vascular Dysregulation: SCI causes profound subcutaneous blood flow dysregulation, impairing the body’s ability to maintain skin perfusion during pressure loading.
- Collagen Catabolism: A rapid increase in collagen breakdown and a decrease in skin elasticity reduce the skin’s tensile strength and ability to tolerate mechanical trauma.
2. Assessment First: Evaluating Perfusion and Microcirculation
A comprehensive vascular and nutritional assessment is a mandatory clinical prerequisite before implementing offloading or treatment strategies. SCI causes microvascular dysfunction; patients typically exhibit increased resting skin temperature but decreased skin temperature reactivity in the lower extremities. Furthermore, the “reactive hyperemia response”—the increase in blood flow following occlusion—is significantly weakened, especially in sacral and lower extremity skin, leading to dangerously slow recovery times.
Clinical Assessment Checklist
- [ ] Temperature Reactivity: Evaluate for increased resting skin temperature and the characteristic lack of reactivity to thermal or mechanical stimuli.
- [ ] Perfusion Integrity: Assess capillary refill and distal pulses; note that autonomic dysfunction impairs the normal vascular response to pressure.
- [ ] Autonomic Dysreflexia Screening: For injuries at T6 or above, monitor for signs of autonomic dysreflexia (sudden hypertension, bradycardia, headache), as a heel PI is a primary inciting stimulus for this life-threatening condition.
- [ ] Nutritional Status: Use the Canadian Nutrition Screening Tool (CNST) to identify risk; refer to the Subjective Global Assessment (SGA) as the criterion standard for a definitive diagnosis of malnutrition.
- [ ] Edema and Induration: Check for localized bogginess or swelling that increases internal tissue strain.
3. Decoding the Surface: Stage 1 PI vs. Deep Tissue Injury (DTI)
Precise diagnostic distinction is critical for establishing an effective care plan. Differentiating between a superficial Stage 1 injury and a suspected Deep Tissue Injury (DTI) is vital, as DTIs originate at the bone-muscle interface and may involve discontinuous fascia.
| Stage 1 Pressure Injury | Suspected Deep Tissue Injury (DTI) |
| Visual Presentation: Intact skin with non-blanchable erythema (redness). In SCI, this signifies a critical warning of impending breakdown. | Visual Presentation: Purple or maroon localized area of discoloured intact skin or a blood-filled blister. |
| Tissue Depth: Superficial; limited to the epidermis and upper dermis. Reversible with immediate and total offloading. | Tissue Depth: Deep; damage starts at the bone-muscle interface. Ultrasound may reveal heterogeneous hypoechoic areas or discontinuous fascia. |
| Clinical Significance: Indicates a failure of current prevention protocols; serves as the final opportunity for intervention before tissue loss. | Clinical Significance: A “hidden” injury that frequently evolves into a Stage III or IV ulcer despite aggressive treatment. |
4. The Golden Rule of the Ischemic Heel: Why Stable Eschar Stays
In the context of SCI, the management of dry, stable eschar on the heels requires a strictly conservative approach.
Clinical Red Flag: Stable Eschar Debridement is strictly contraindicated for dry, stable, intact eschar on the heels. In the SCI population, reduced tissue oxygenation and impaired microcirculation make these limbs highly susceptible to complications. Stable eschar serves as the body’s natural protective cover; premature debridement in an ischemic limb significantly increases the risk of osteomyelitis and systemic infection. If there is no erythema, fluctuance, or drainage, the eschar must remain undisturbed.
5. Mechanical Protection: Offloading Devices and Support Surfaces
Protecting the heels requires moving beyond standard mattress selection to achieve total redistribution or removal of mechanical load.
Best Practices for Recumbent Positioning
- Suspending the Heels (“Floating”): This is the preferred gold-standard method for complete pressure removal.
- Pillows must be placed under the calves to ensure the heels are completely free of the bed surface.
- Frequent skin checks of the Achilles tendon and calf are mandatory to ensure no secondary pressure points are created.
- Heel Offloading Devices:
- Heel Boots: These provide protective padding but require constant monitoring to prevent secondary breakdown from the device itself.
- Suspension Boots: Specifically designed to maintain the “floating” position while simultaneously ensuring proper foot alignment to prevent foot drop.
- Support Surface Selection:
- Active Technology: Powered surfaces (e.g., alternating pressure) that change load distribution cyclically are recommended for patients with limited repositioning ability.
- Reactive Technology: Non-powered surfaces (e.g., high-density foam) that redistribute load in response to the patient’s weight.
- Multizoned Mattresses: These are the preferred surfaces for heel management as they allow for specialized, lower-pressure redistribution in the heel section compared to the torso.
6. Systemic Support: Nutrition as a Preventive Tool
Nutritional status is an independent and significant predictor of PI development. Malnutrition is associated with twice the odds of developing a PI in hospitalized patients. Screening must occur immediately upon admission.
The Canadian Nutrition Screening Tool (CNST)
- Have you lost weight in the past 6 months without trying to lose this weight?
- Have you been eating less than usual for more than a week? Two “YES” answers indicate a high risk of malnutrition and require immediate referral to a Dietitian for assessment against the Subjective Global Assessment (SGA) standard.
Implementing nutritional support—specifically high-protein supplements providing 1000 to 2000 kJ/d—is both a clinical and economic mandate. Recent data indicates that nutritional support is cost-saving at AU $425 per patient, primarily by reducing PI incidence and avoiding the costs of extended hospital stays and complex wound care.
7. Conclusion: The Interprofessional Mandate
Heel pressure injuries are a multi-factorial crisis that cannot be managed in isolation. The gold standard for care is a collaborative, interprofessional team—including the Physiatrist, Wound Nurse, OT/PT, and Dietitian—working across the continuum of care. Specialized SCI units consistently produce superior outcomes, characterized by lower rates of secondary complications and higher functional gains.
Clinical Takeaways
- Total Offloading is Mandatory: Floating the heels using calf pillows is the most effective prevention strategy for recumbent patients.
- Screen for Nutrition Early: Use the CNST to identify risks; nutritional intervention is cost-saving at AU $425 per patient.
- Respect Stable Eschar: Debridement is strictly contraindicated for dry, intact heel eschar due to the high risk of osteomyelitis.
- Monitor Physiological Indicators: Be vigilant for increased resting skin temperature and signs of autonomic dysreflexia triggered by heel PIs.
- Utilize Advanced Diagnostics: Where available, use ultrasound to detect subclinical markers like discontinuous fascia before a DTI reaches the surface.