7 Causes of Bedsores and How to Prevent Them from Developing

Bedsores, also called pressure ulcers or pressure injuries, can develop surprisingly fast when constant pressure reduces blood flow to the skin. They often affect people who spend long periods in bed, use wheelchairs, or have limited mobility due to illness, injury, or aging. While bedsores may begin as mild redness or tenderness, they can quickly turn into painful open wounds that are difficult to heal if ignored.

The good news is that most bedsores are preventable with early awareness, consistent skin care, and simple daily habits that reduce pressure on vulnerable areas of the body. Understanding what causes them is one of the most effective ways to stop them before they begin. Bedsores commonly form when pressure, friction, moisture, or poor circulation damage the skin over bony areas such as the hips, tailbone, heels, and elbows.

What Are Bedsores?

Bedsores, also known as pressure ulcers, pressure sores, or pressure injuries, are areas of damaged skin and underlying tissue caused by prolonged pressure on the body. They usually develop when someone stays in the same position for too long, reducing blood flow to the skin and preventing tissues from getting enough oxygen and nutrients. Over time, this lack of circulation can damage the skin and create painful wounds that range from mild redness to deep open sores.

Bedsores most commonly form over bony areas of the body where there is less natural cushioning, such as the tailbone, hips, heels, ankles, elbows, and shoulder blades. People who spend long periods in bed, use wheelchairs, or have limited mobility due to illness, surgery, or aging are at higher risk. Although bedsores can become serious if left untreated, they are often preventable with proper repositioning, skin care, and early attention to warning signs.

Medical professionals generally classify bedsores into stages based on severity, starting with mild skin discoloration and progressing to deeper wounds that may affect muscles or bone in severe cases. Recognizing pressure injuries early is important because prompt treatment can help prevent infection, pain, and long-term complications.

The Signs of Infected Bedsores

Identifying an infection in a pressure ulcer is a high-priority medical event, particularly for individuals already managing chronic venous insufficiency (CVI). In a patient with venous dysfunction, the legs are often already swollen and discolored, which can mask the early redness of a spreading infection. Furthermore, because chronic venous insufficiency with mild cellulitis is a common complication, distinguishing between “stasis changes” and an active, aggressive infection in a bedsore is vital for maintaining chronic venous insufficiency life expectancy.

Local Indicators of Wound Infection

The most immediate signs of infection appear within and directly around the wound bed. While a healing chronic venous insufficiency ulcer may produce some clear or serous fluid, an infected ulcer will transition to producing “purulent drainage.” This pus is typically thicker and can range in color from creamy yellow to dark green.

A secondary local sign is “advancing erythema.” In patients with cvi disease, the skin is often permanently stained a brownish-red (hemosiderin staining). However, an infection will cause a new, brighter red “halo” that is warm to the touch and tender. If this redness expands more than 2 cm from the wound edge, it may indicate that the infection has moved into the deeper skin layers, leading to cellulitis. A foul odor that persists even after the wound has been cleaned is another hallmark of bacterial overgrowth, particularly from anaerobic organisms that thrive in the deep cavities of Stage 3 or Stage 4 ulcers.

Systemic “Red Flag” Symptoms

When an infection moves from the local tissue into the bloodstream, it becomes a systemic threat. This is especially dangerous for elderly patients or those with juvenile chronic venous insufficiency whose immune systems may be compromised.

• Fever and Chills: A core body temperature rising above 38°C (100.4°F) is a primary sign that the body is fighting an infection.

• Mental Status Changes: In older adults, new-onset confusion or lethargy is often the first sign of sepsis (blood poisoning) resulting from an infected bedsore.

• Elevated Heart Rate: Tachycardia (a rapid heart rate) can indicate that the body is under significant physiological stress from a bacterial “bloom.”

Complications: Cellulitis and Osteomyelitis

If the infection is not addressed through aggressive chronic venous insufficiency treatments and targeted antibiotics, it can invade the underlying structures. In Stage 4 ulcers where the bone is exposed, there is a high risk of “osteomyelitis” (bone infection). This condition is notoriously difficult to treat and often requires months of intravenous antibiotics.

Additionally, the presence of chronic venous insufficiency throughout body systems means that the lymphatic drainage is already sluggish. This “logjam” makes it easier for bacteria to spread, potentially leading to necrotizing fasciitis or sepsis, which are life-threatening emergencies.

7 Main Causes of Pressure Ulcers

While bedsores are primarily mechanical injuries caused by external forces, their development is inextricably linked to the patient’s underlying vascular health. For individuals suffering from chronic venous insufficiency (CVI), the risk of tissue breakdown is significantly magnified. The cause of venous stasis aka. poor return of blood to the heart, creates a state of chronic “nutritional bankruptcy” in the legs. When venous dysfunction is present, the tissues are already saturated with metabolic waste and depleted of oxygen, making them far less resilient to the seven primary causes of pressure ulcers.

Sustained Pressure and the Ischemic Cascade

The most direct cause of a bedsore is sustained pressure, which collapses the capillaries and induces ischemia. In a healthy individual, the body signals discomfort, prompting a change in position. However, in patients with chronic venous insufficiency symptoms like severe edema, the extra fluid in the tissues creates a “cushion” of stagnant fluid that actually increases internal tissue pressure.

This makes the skin over the heels or sacrum more susceptible to necrosis because the insufficient venous system is already struggling to clear out fluids. When external pressure is added, the remaining blood flow is snuffed out entirely. Because Hansen’s disease is caused by nerve damage, a similar “painless” breakdown occurs; in CVI, the breakdown is driven by the “toxic” environment of deoxygenated blood and high venous pressure.

The Mechanical Threat: Friction versus Shear

While friction acts as a superficial abrasive, stripping the epidermis like a “sheet burn,” shear is a much more destructive internal force. For patients with cvi disease, the skin is often already compromised by lipodermatosclerosis (hardening of the skin). This “leathery” skin has lost its natural elasticity, making it brittle.

When a patient slides down in bed, the skeleton moves but the skin remains stuck to the linens. Because the skin is stiff from venous dysfunction, the underlying blood vessels are more easily “kinked” or torn. This deep tissue injury is particularly dangerous in the chronic venous insufficiency stages where the skin is thin and waxy, as the damage can occur deep near the bone before any visible signs appear on the surface.

Moisture and Skin Maceration

Excessive moisture from sweat, wound drainage, or incontinence leads to maceration, where the skin becomes waterlogged and soft. This is a critical risk factor for those with chronic venous insufficiency ulcers, as these wounds often “weep” significant amounts of fluid (exudate).

Macerated skin is functionally weak; it is five times more likely to tear under pressure than dry skin. When you combine this moisture with the inflammation seen in chronic venous insufficiency with mild cellulitis, the skin’s barrier is virtually non-existent. Managing this moisture is a fundamental part of chronic venous insufficiency treatments, as it prevents a manageable stasis area from turning into a life-threatening, full-thickness pressure ulcer.

Nutritional Deficit and Dehydration

The skin requires a constant supply of protein, Vitamin C, and Zinc to maintain its structural integrity. In patients with venous deficiency, the transport of these nutrients is impaired by the “logjam” of stagnant blood in the lower extremities. Dehydration further complicates this by reducing overall blood volume, which worsens deep venous reflux and makes the blood “thicker” and harder to move.

A malnourished patient lacks the collagen necessary to repair the minor tears caused by friction. Consequently, their chronic venous insufficiency life expectancy can be impacted not just by the vein disease itself, but by the secondary infections that take hold in these non-healing, nutrient-starved pressure wounds.

How Often Should A Person Be Repositioned to Prevent Skin Breakdown?

The frequency and technique of repositioning are the most critical defensive measures against the development of bedsores. For patients with chronic venous insufficiency (CVI), these intervals are even more vital. Because the cause of venous stasis already keeps the tissues in a state of low oxygenation, any additional interruption in blood flow from external pressure can trigger rapid necrosis. In the context of venous dysfunction, the skin is less “forgiving” than healthy tissue, meaning a delay in turning can quickly escalate through the chronic venous insufficiency stages toward a full-thickness wound.

The “Two-Hour Rule” and Reperfusion

For an individual confined to a bed, the medical standard is repositioning at least every two hours. This schedule is designed to counteract the insufficient venous return by ensuring that no single area of skin is deprived of oxygen for too long. By rotating the patient between their back and sides (the 30-degree lateral position), caregivers allow for “reactive hyperemia”—a temporary flood of oxygenated blood back into the tissues that were just under pressure.

In patients with cvi disease, this reperfusion is essential because the stagnant blood already present in the legs contains metabolic waste that must be “flushed out” by fresh arterial flow. If the two-hour window is missed, the combination of external pressure and internal venous stasis creates a “zone of death” where the skin simply gives up and breaks down.

Wheelchair Frequency and Micro-Shifts

Individuals in wheelchairs face a higher concentration of pressure on a smaller surface area—specifically the ischial tuberosities (sitting bones). Consequently, the repositioning frequency must increase to every 15 to 30 minutes.

Even if a full transfer isn’t possible, “micro-shifts” can be life-saving for the skin. Leaning side-to-side or forward, or performing a “pressure relief push-up” for 10 to 15 seconds, allows the capillaries to refill. For someone with chronic venous insufficiency symptoms like leg heaviness, these shifts also help prevent blood from “pooling” in the pelvis and upper thighs, which can exacerbate deep venous reflux.

Using “Lift, Don’t Drag” to Prevent Shear

The technique used to move a person is just as important as the frequency. Caregivers must always lift the patient using a draw sheet or slide board rather than dragging them across the linens. Dragging creates friction, but more dangerously, it creates “shear”—an internal tearing of the blood vessels.

Since chronic venous insufficiency (CVI) often leads to lipodermatosclerosis (leathery, hardened skin), the tissue is brittle and lacks the “slip” of healthy skin. This makes it far more susceptible to deep tissue injuries during poor transfers. Keeping the head of the bed at or below 30 degrees further minimizes the risk of the patient sliding down, which is a primary source of shear on the sacrum.

Strategic Off-loading with Pillows and Wedges

Proper repositioning also involves “bridging” or “off-loading” bony prominences. Pillows or foam wedges should be placed between the knees and ankles to prevent “kissing” sores, pressure ulcers that form where two bony areas press against each other.

For those with chronic venous insufficiency ulcers, specialized heel-suspension boots (often called “floaters”) are used to keep the heels completely off the mattress. This is vital because the heels are a high-risk zone where venous dysfunction and pressure often intersect to create non-healing wounds that can impact chronic venous insufficiency life expectancy due to the high risk of bone infection (osteomyelitis).

Most Effective Ways to Prevent Bedsores

Preventative skin care and pressure redistribution are the two most effective strategies for preventing bedsores, especially for those with chronic venous insufficiency (CVI). Because cvi disease compromises the skin’s natural barrier and blood supply, the standard “inspection and protection” routine must be even more rigorous. When venous dysfunction is present, the skin is already under stress from internal fluid pressure, making it less resilient to the external “attacks” of moisture and sustained contact.

Daily Skin Inspection: The Early Warning System

The most critical practice is a daily, systematic head-to-toe inspection. For individuals with chronic venous insufficiency symptoms, this inspection should focus heavily on the “gaiter area” (ankles) and heels. The primary warning sign to look for is non-blanchable erythema. This is a red spot that stays red even when you press your finger on it. In healthy skin, the spot would turn white (blanch) as blood is pushed out and then turn red again as it refills.

If it doesn’t turn white, it means the capillaries are already damaged—this is a Stage 1 pressure ulcer. Because Hansen’s disease is caused by nerve damage, a patient may not feel this injury occurring; similarly, in CVI, the heavy, “woody” texture of the skin (lipodermatosclerosis) can hide these early changes. Detecting these shifts in temperature or firmness early is the only way to prevent a minor spot from becoming a deep chronic venous insufficiency ulcer.

Gentle Cleansing and the “Moisture Barrier”

For patients with venous deficiency, the skin is often dry, thin, and prone to “venous eczema.” Cleansing should be done with lukewarm water and a pH-balanced cleanser to avoid stripping away protective oils.

If the patient also deals with incontinence, the skin is at extreme risk. Urine and feces contain enzymes that “digest” the skin, leading to incontinence-associated dermatitis. For these patients, chronic venous insufficiency treatments must include a thick moisture barrier cream containing zinc oxide or dimethicone. This creates a physical shield, ensuring that moisture from the “weeping” of insufficient venous fluid or incontinence does not macerate the skin and lead to breakdown.

Static and Dynamic Support Surfaces

To manage the “mechanical” side of the problem, specialized support surfaces are used to redistribute weight. For those at moderate risk, static surfaces like high-specification foam or gel overlays work by “enveloping” the body. By increasing the surface area in contact with the bed, these surfaces lower the pressure at any single point (like the hip bone).

For high-risk individuals, dynamic surfaces like Alternating Pressure Air Mattresses (APAMs) are used. These systems use a pump to cyclically inflate and deflate different air cells, ensuring that the pressure is constantly moving. This is particularly helpful for patients who cannot move themselves and have chronic venous insufficiency throughout body systems, as it provides a mechanical “pumping” effect that mirrors the relief of manual turning.

Specialized Heel Protection

The heels are one of the most vulnerable spots for anyone with venous dysfunction. Because the heel has very little padding, the cause of venous stasis often results in severe edema that cuts off blood flow to the skin over the bone. “Floating” the heels with specialized foam boots or heel-suspension devices is a best practice. These devices ensure that the heel is suspended in the air, completely removing all pressure. This is a vital component of managing chronic venous insufficiency life expectancy, as a heel ulcer that reaches the bone (osteomyelitis) is a frequent cause of hospitalization and severe decline.

Diet is Important In Bedsores Prevention

Diet serves as the internal scaffolding for skin health, especially when the external circulatory system is compromised by chronic venous insufficiency (CVI). While venous dysfunction creates a “logjam” of stagnant blood in the lower extremities, proper nutrition ensures that the blood actually reaching the tissues is rich in the repair materials needed to prevent bedsores. In the context of cvi disease, where tissues are already under-oxygenated due to deep venous reflux, a nutritional deficit can accelerate the transition from healthy skin to chronic venous insufficiency ulcers.

The Protective Power of Protein and Calories

Protein is the primary raw material for collagen, the “glue” that holds skin cells together. For individuals with insufficient venous flow, the skin is often under constant tension from edema (swelling). Without adequate protein, typically recommended at 1.25 to 1.5 grams per kilogram of body weight, the skin becomes thin and fragile, losing its ability to resist the friction and shear forces that cause bedsores.

Furthermore, maintaining a sufficient caloric intake is a vital part of chronic venous insufficiency treatments. If an individual loses weight rapidly, they lose the “subcutaneous fat pad” that acts as a natural shock absorber over bony prominences like the sacrum and heels. When this padding disappears, the pressure on the capillaries increases significantly, making the formation of a pressure ulcer almost inevitable.

Micronutrients: The Repair Crew

Specific vitamins and minerals act as the “engineers” of skin repair. Because chronic venous insufficiency throughout body systems can lead to chronic inflammation, the demand for these nutrients increases:

• Vitamin C: Essential for strengthening capillary walls. In CVI, where capillaries are already prone to leaking (causing chronic venous insufficiency symptoms like brown staining), Vitamin C helps maintain vascular integrity.

• Zinc: Crucial for cell division. If a minor tear occurs in the “gaiter area” near the ankle, Zinc is required to close that wound before it expands into a named chronic venous insufficiency ulcers name classification.

• Vitamin A: Supports the health of the epithelial cells, the outermost protective layer of the skin.

Hydration and Tissue Perfusion

Hydration is perhaps the most overlooked aspect of a chronic venous insufficiency diagnosis and management plan. Water is the medium that carries oxygen and nutrients to the skin. When a patient is dehydrated, their blood volume drops and their blood becomes more viscous (thicker). This makes it even harder for the insufficient venous system to push blood back up the legs, worsening the cause of venous stasis.

Dehydrated skin also loses its “turgor”, the ability to snap back when pinched. This makes the skin “sticky,” which significantly increases the risk of damage from friction against bed linens. Maintaining a fluid intake of 1.5 to 2 liters per day (unless restricted due to heart or kidney issues) is a fundamental part of preventing the skin breakdown that can lower chronic venous insufficiency life expectancy due to complications like sepsis.

How are Bedsores Diagnosed and Staged?

The diagnosis and staging of bedsores are formal clinical processes that move beyond simple observation to identify the exact depth of tissue destruction. For a patient with chronic venous insufficiency (CVI), this staging is crucial because venous dysfunction can mask the severity of a pressure injury. The “woody” induration and dark pigmentation typical of the advanced chronic venous insufficiency stages can make it difficult to identify the redness of a Stage 1 ulcer, potentially delaying vital chronic venous insufficiency treatments.

Understanding the Stages of Tissue Destruction

The staging system is a progressive scale that measures how far the necrosis has traveled through the layers of the skin and underlying fat, muscle, or bone.

• Stage 1: The skin is intact but shows “non-blanchable erythema.” This is a critical warning sign where the redness does not fade when pressed. In the context of cvi disease, this may be mistaken for simple stasis dermatitis, but the localized nature over a bone (like the ankle) confirms it as a pressure injury.
• Stage 2: This involves “partial-thickness” loss. The epidermis or dermis is broken, often appearing as a shallow pink wound or a clear, fluid-filled blister.
• Stage 3: This is “full-thickness” skin loss. The wound craters down into the subcutaneous fat. While the fat may be visible, the deeper structures like muscle are still protected.
• Stage 4: This is the most severe stage, reaching the “basement” of the body. Bone, tendons, or muscles are exposed or directly palpable. This stage significantly lowers chronic venous insufficiency life expectancy due to the high risk of systemic sepsis and bone infection.

Complex Classifications: Unstageable and DTI

Sometimes, a wound cannot be immediately staged. An Unstageable ulcer occurs when the wound bed is covered in “slough” (yellow/tan dead tissue) or “eschar” (black, leathery scab). Until this dead tissue is removed (debrided), a doctor cannot see how deep the hole actually goes.

A Deep Tissue Injury (DTI) is perhaps the most deceptive. The skin may be intact, but it appears purple or maroon, like a deep bruise. This indicates that the tissue has died from the “inside out,” starting at the bone and moving toward the surface. For someone with deep venous reflux, the dark staining of the skin can make a DTI very hard to spot until the skin suddenly “unroofs” to reveal a deep cavity.

The Braden Scale: Quantifying the Risk

The Braden Scale is the primary tool used during a chronic venous insufficiency diagnosis to predict the likelihood of skin breakdown. It assigns a score from 6 to 23; the lower the score, the higher the risk.

Sensory Perception: Evaluates if the patient can feel the pain of pressure. This is vital for those where Hansen’s disease is caused by nerve damage or where CVI has led to peripheral neuropathy.

• Moisture: Measures exposure to sweat or “weeping” from chronic venous insufficiency ulcers.
• Activity/Mobility: Determines if the patient can move themselves to “off-load” pressure.
• Nutrition: Assesses if the body has enough protein to maintain the skin barrier.
• Friction/Shear: Looks at the risk of the skin tearing when the patient is moved.

By combining the Braden Scale with visual staging, healthcare providers can create a proactive plan. If a patient has a low Braden score and a Stage 1 ulcer, they may be placed on an alternating pressure mattress immediately to prevent the wound from reaching Stage 3 or 4.

The Difference Between Bedsores and Moisture-Associated Skin Damage

Distinguishing between a pressure ulcer and Moisture-Associated Skin Damage (MASD) is a critical skill for anyone managing chronic venous insufficiency (CVI), as the treatments for these conditions are fundamentally different. While both involve skin breakdown, a pressure ulcer is a “bottom-up” injury caused by restricted blood flow, whereas MASD is a “top-down” chemical and mechanical erosion of the skin surface.

Pathophysiology: Pressure vs. Chemical Erosion

The primary difference lies in the source of the damage. A pressure ulcer is caused by ischemia; external pressure collapses the capillaries, starving the tissue of oxygen. This is particularly dangerous in patients with venous dysfunction, where the tissue is already compromised by venous stasis.

In contrast, MASD, which includes Incontinence-Associated Dermatitis (IAD), is caused by the breakdown of the skin’s “acid mantle.” When skin is trapped against moisture (urine, sweat, or “weeping” from chronic venous insufficiency ulcers), it becomes macerated. This makes the skin soft and permeable, allowing bacteria and caustic enzymes to “digest” the epidermis.

Identifying by Location and Shape

The “where” and “what” of the wound provide the most significant diagnostic clues:

• Bedsores: These are almost always found directly over a bony prominence (sacrum, heels, or ankles). They tend to have well-defined, distinct borders and often take on a circular or “crater” shape that mirrors the point of pressure.
• MASD/IAD: These usually occur in “skin folds” or fleshy areas like the perineum and inner thighs. The redness is typically diffuse and irregular, looking more like a sprawling rash or a “sunburn” than a deep hole.

Depth and Tissue Characteristics

The depth of the wound is a major differentiator in a clinical chronic venous insufficiency diagnosis. Pressure ulcers can be quite deep, reaching the fat, muscle, or bone (Stages 3 and 4). Because the injury starts deep and moves outward, the surrounding skin might actually look healthy until the ulcer “breaks” through.

MASD is strictly a superficial, partial-thickness injury. It rarely goes deeper than the very top layers of the skin. However, the skin will appear “macerated”, white, soggy, and wrinkled, and may feature “satellite lesions,” which are small red bumps that indicate a secondary fungal infection has taken root in the damp environment.

Conclusion

Bedsores are more than a skin problem. They can seriously affect comfort, mobility, and overall health if they are allowed to worsen. The encouraging part is that prevention often comes down to small, consistent actions such as changing positions regularly, keeping skin clean and dry, eating well, and checking vulnerable areas for early warning signs. Even people at higher risk can greatly reduce their chances of developing pressure ulcers when caregivers and loved ones stay proactive. Paying attention early can make a meaningful difference and help prevent painful complications later on.

Read more: 7 Common Symptoms of Chronic Venous Insufficiency and What You Can Do About It

FAQ About Bedsores

How quickly can bedsores develop?

Bedsores can develop faster than many people realize, sometimes within hours if pressure on the skin is severe and blood flow becomes restricted. People with limited mobility, poor circulation, or fragile skin may be especially vulnerable. The earliest signs often include redness, tenderness, warmth, or skin discoloration that does not fade after pressure is removed. Catching these warning signs early can help stop a sore from becoming more serious.

What are the first signs of a bedsore?

The first signs of a bedsore usually include skin that looks red, purple, or darker than usual and does not return to normal color after pressure is relieved. The area may feel warm, firm, soft, painful, or unusually tender to the touch. In darker skin tones, discoloration may be harder to spot, so texture and temperature changes become especially important. Regular skin checks can help identify these signs before the skin breaks open.

Can bedsores heal on their own?

Very mild pressure sores may improve if pressure is relieved early and the skin remains protected, but deeper sores usually require medical attention. Without proper care, bedsores can worsen, become infected, and sometimes lead to serious complications. Treatment may include repositioning, wound dressings, pressure-relieving surfaces, nutrition support, and infection prevention. Seeking help early gives the best chance for healing and reduces the risk of long-term damage.

What is the best way to prevent bedsores?

The best prevention strategy combines frequent movement, pressure relief, skin care, and good nutrition. Experts often recommend repositioning every couple of hours for people confined to bed and checking the skin daily for early changes. Keeping skin clean and dry, using pressure-relieving cushions or mattresses, and eating enough protein and nutrients can also help maintain healthy skin. Prevention works best when caregivers and patients stay consistent with these habits.

Are bedsores dangerous?

Yes, bedsores can become dangerous if they are not treated early. Mild sores may stay near the surface of the skin, but advanced pressure ulcers can extend into muscles and even bone, increasing the risk of infection. In severe cases, untreated infections can spread and become life-threatening. This is why early detection and prevention are so important, especially for older adults or people with limited mobility.

Sources

• Mayo Clinic – Bedsores (Pressure Ulcers): Symptoms and Causes
• Mayo Clinic – Bedsores: Diagnosis and Treatment
• Cleveland Clinic – Bedsores (Pressure Injuries)
• MedlinePlus – Preventing Pressure Ulcers
• Johns Hopkins Medicine – Bedsores
• NCBI Bookshelf – Prevention and Management of Pressure Ulcers
• NHS Inform – Pressure Ulcers