Decubitus ulcers, commonly called bedsores or pressure injuries, are caused by sustained pressure on the skin that cuts off blood flow to the tissue. When external pressure on the body exceeds roughly 32 mmHg, the tiny capillaries that deliver oxygen to skin and muscle become compressed and occluded. Without oxygen, the tissue begins accumulating toxic waste products, and if the pressure isn’t relieved, the cells die. This basic mechanism, called ischemic necrosis, is the root cause of every pressure ulcer, but several other forces and health conditions make the damage happen faster and heal slower.
How Pressure Starves Tissue of Blood
Your smallest blood vessels need only a modest amount of outside force to collapse. Venous return, the flow carrying deoxygenated blood back toward the heart, can be blocked at pressures as low as 8 to 12 mmHg. Arterial inflow shuts down at around 32 mmHg. For context, simply lying motionless on a standard hospital mattress can generate pressures well above those thresholds at bony contact points like the tailbone, heels, and hips.
Once blood stops flowing, a cascade starts. Cells deprived of oxygen switch to less efficient energy production, generating acidic byproducts. Waste accumulates. If the pressure is brief, blood rushes back in when you shift position and the tissue recovers. But when someone cannot move, or doesn’t feel the discomfort that normally triggers a position change, the tissue progresses from reversible injury to permanent cell death. The longer the pressure lasts, the deeper the damage extends, potentially reaching fat, muscle, and even bone.
Shear and Friction: The Hidden Amplifiers
Pressure alone isn’t the only mechanical force at work. Shear and friction act as accomplices that dramatically lower the amount of pressure needed to cause harm.
Shear occurs when bone and deeper tissue slide in one direction while the skin stays put, held in place by friction against a surface. A common example is a person slowly sliding down in a reclined hospital bed or chair. When the head of the bed is raised above 30 degrees, gravity pulls the body downward, but the skin on the back grips the sheet. The tissue layers between bone and skin stretch and distort, kinking blood vessels and cutting off flow at pressures far below the usual 32 mmHg threshold.
Friction is the surface force that resists one material sliding against another. On its own, friction strips the outermost skin layer, creating blisters and shallow erosions. These superficial wounds then serve as entry points for deeper pressure damage. The combination of pressure, shear, and friction together is more destructive than any single force alone.
Moisture and Skin Breakdown
Skin that stays damp from sweat, urine, or wound drainage becomes structurally weaker and more vulnerable to mechanical forces. Prolonged moisture causes the outermost skin layer to swell and soften, a process called maceration. This swelling disrupts the protective lipid barrier between skin cells, raises the coefficient of friction against sheets and clothing, and makes the skin less able to withstand even moderate pressure or shear. Skin temperatures above 35°C (95°F) compound the problem by increasing sweating and further reducing the mechanical stiffness of the skin’s outer layer.
This is why incontinence is such a strong risk factor. A person who is both immobile and incontinent faces a combination of chemical irritation from urine or stool, persistent moisture weakening the skin, and continuous pressure on vulnerable areas. Each factor reinforces the others.
Who Is Most Vulnerable
The underlying cause of pressure ulcers is always mechanical, but certain health conditions dramatically increase a person’s susceptibility. Risk factors fall into two broad categories: things that keep you from moving and things that weaken your tissue’s ability to survive temporary blood loss.
Immobility is the single biggest risk factor. Any condition that limits your ability to shift position, whether it’s a spinal cord injury, stroke, heavy sedation, general anesthesia, or even a fractured hip, puts you at risk. Reduced sensation matters just as much as reduced movement. People with nerve damage from diabetes, paralysis, or pain medications may not feel the discomfort that would normally prompt a position change. Patients in intensive care units face the highest rates, with prevalence between 5% and 30% depending on the facility.
Conditions that impair blood flow make tissue less resilient once pressure is applied. Peripheral arterial disease is particularly dangerous because it not only reduces oxygen delivery under normal conditions but also slows the tissue’s ability to recover after pressure is removed. Heart failure similarly reduces perfusion to the extremities. People with diabetes face a double threat: impaired circulation and reduced sensation in the feet and legs. Case-control studies have found that patients with peripheral arterial disease are at higher risk of both developing ulcers and experiencing poor wound healing afterward.
How Nutrition Plays a Role
Malnutrition doesn’t directly cause pressure ulcers, but it significantly lowers the threshold at which they develop and dramatically slows healing. Your body needs a steady supply of protein, calories, and specific micronutrients to maintain skin integrity and repair damaged tissue. When those are lacking, skin becomes thinner, less elastic, and more easily injured.
Unplanned weight loss is one of the strongest warning signs. Losing 5% or more of body weight in a single month, or 10% over six months, signals the kind of protein-calorie deficit that leaves tissue vulnerable. Low blood albumin levels, a marker of protein status, are among the most powerful predictors of pressure ulcer development. One study found that albumin levels below 3.1 g/dL predicted ulcer formation and were associated with higher mortality.
Specific nutrients play distinct roles in keeping skin intact. Vitamin C is essential for building collagen, the structural protein that gives skin its strength, and for maintaining the immune response that fights wound infections. Vitamin A supports immune function and collagen production. Zinc aids in cell division and tissue repair. Deficiencies in any of these slow wound healing and increase the chance that a small area of pressure damage will progress to a larger, deeper ulcer.
Where Pressure Ulcers Develop
Pressure ulcers form over bony prominences, the places where bone sits close to the skin surface with little cushioning fat or muscle in between. The exact location depends on body position. For someone lying on their back, the sacrum (tailbone), heels, and back of the head are the most common sites. Side-lying positions put the hips, ankles, and ears at risk. Sitting concentrates force on the ischial tuberosities, the “sit bones” at the base of the pelvis. In European and American hospitals, prevalence ranges from about 4% to 23% of patients, with long-term care facilities and ICUs seeing the highest rates.
How Ulcers Progress in Stages
Pressure ulcers are classified into stages based on depth of tissue damage. Understanding these stages helps explain what the progression from early warning sign to serious wound actually looks like.
- Stage 1: The skin is intact but has a persistent area of redness that doesn’t fade when pressed. On darker skin tones, the discolored area may appear different from surrounding skin without obvious redness. The area may feel warmer, firmer, or softer than nearby tissue.
- Stage 2: The skin has broken open or formed a blister. The wound is shallow with a pink or red base, and it hasn’t yet penetrated below the second layer of skin.
- Stage 3: The wound extends through the full thickness of the skin into the fat layer beneath. Bone, tendon, and muscle aren’t yet visible, but the ulcer may have tunneling beneath the surface.
- Stage 4: The deepest and most severe. Bone, tendon, or muscle is exposed at the base of the wound. These ulcers often involve extensive tunneling and tissue destruction.
A separate category, deep tissue injury, appears as a purple or maroon area of intact skin or a blood-filled blister. This signals damage that started in the deeper layers and is working its way outward, sometimes rapidly worsening over the following days even after pressure is relieved.
Complications of Untreated Ulcers
A pressure ulcer that reaches Stage 3 or 4 is no longer just a skin problem. The open wound becomes a pathway for bacteria to enter the body. Cellulitis, an infection of the surrounding skin and soft tissue, is one of the more common complications. If bacteria reach the bloodstream, the result can be sepsis, a life-threatening systemic infection. Deep ulcers near joints or bone can lead to osteomyelitis (bone infection) or septic arthritis. In rare cases, sinus tracts form, connecting the surface wound to deeper structures and creating conditions for necrotizing fasciitis or endocarditis. Some cases ultimately require amputation.
Preventing the Root Cause
Because the fundamental cause is sustained pressure, prevention centers on reducing how much pressure the body experiences and how long it lasts. Repositioning every two hours is the most basic intervention for bedridden patients. Specialized support surfaces, from high-density foam mattresses to alternating-pressure air systems, work by either spreading body weight across a larger area or mechanically cycling pressure so no single spot is compressed for too long. Some systems combine both approaches, allowing caregivers to adjust the mode based on a patient’s changing needs.
Equally important is addressing the contributing factors: keeping skin clean and dry, managing incontinence promptly, ensuring adequate protein and calorie intake, and treating conditions that impair circulation. For people with reduced sensation from paralysis or neuropathy, extra vigilance is needed because the body’s natural alarm system, pain, isn’t functioning to trigger movement.