Pressure ulcers and gangrene

• A pressure injury is localised damage to skin and underlying soft tissue, usually over a bony prominence or under a device, caused by intense or prolonged pressure, often with shear. The old term "pressure ulcer" was changed to "pressure injury" because damage can begin while the skin is still intact. ^{[2][5] [7]}
• Pressure injuries are staged by depth from 1 to 4, with extra categories for unstageable injury, deep tissue injury, medical-device-related injury and mucosal injury. ^[6][2]
• Gangrene is death of tissue. Dry gangrene is ischaemic and dry; wet gangrene is soft, infected and swollen; gas gangrene is a rapidly lethal myonecrosis caused most often by Clostridium perfringens. ^[8][9][10]
• Prevention beats treatment: turn patients, redistribute pressure, protect skin, feed them, and reassess risk whenever the clinical situation changes. ^[1][12]
• Treatment of an established pressure injury is stage-driven: cleanse, debride necrotic tissue, keep a warm moist wound bed, treat infection only when there are clinical signs, and offload the pressure. ^[1][6]
• Wet and gas gangrene need prompt surgical debridement plus antibiotics; penicillin plus clindamycin is the standard combination for confirmed clostridial gas gangrene. ^[9][11]

By the end of this page you should be able to:

1. Define a pressure injury, list its typical sites, and explain why pressure, shear, friction and moisture combine to cause it.
2. Stage a pressure injury correctly, including the categories that cannot be staged or that are not a linear progression.
3. Explain the Braden and Norton concepts and the thinking behind turning schedules and support surfaces.
4. Describe a stepwise approach to diagnosing and caring for a pressure injury, including when to debride and when not to give antibiotics.
5. Distinguish dry, wet and gas gangrene clinically and microbiologically, and outline the surgical and antimicrobial management of each.
6. Recognise red flags, prognostic markers including the LRINEC score, and the needs of older adults, children and low-resource settings.

The traditional word "decubitus ulcer", still used on book page B2:79, describes the same process. Modern practice endorsed by the National Pressure Injury Advisory Panel, the European Pressure Ulcer Advisory Panel and the Pan Pacific Pressure Injury Alliance uses "pressure injury" because damage now has a name before the skin breaks: stage 1 changes and deep tissue injury can occur with intact skin. ^[2][5]

The staging system in use is the NPIAP (formerly NPUAP) system, first agreed in 1989 and revised in 2016 to match the new terminology. It separates injuries by depth of tissue damage. A higher number means deeper damage, but the system is not a timeline. A pressure injury can appear first as a stage 3 or 4 lesion, and healing does not run backwards from stage 4 to stage 1. ^[6][2]

Gangrene, by contrast, is the localised death of body tissue, usually from ischaemia, infection, or both. The three clinically useful types are:

• Dry gangrene: coagulative necrosis from inadequate blood supply. Dry, black and sharply demarcated, without significant infection.
• Wet gangrene: tissue necrosis complicated by bacterial infection, with swelling, moisture, discharge and spreading inflammation.
• Gas gangrene: myonecrosis caused by gas-forming organisms, most often Clostridium perfringens, with crepitus, severe pain and systemic toxicity. ^[8][9][10]

Pressure injuries are common and costly. They affect up to 3 million adults in the United States each year and have a prevalence of 5 to 15 percent among hospitalised patients, with higher figures in intensive care units and some long-term care settings. ^[6] A continuing medical education review in the American Academy of Dermatology (AAD) series reminds readers that, despite decades of prevention research, pressure injuries remain common in hospitals and the community and often become chronic, recurrent wounds. ^[3][4]

Your reader can reason about the scale rather than memorising a single number: in one UK series of 209 patients, half of pressure ulcers had healed by 12 months, but success varied sharply by stage (100 percent for stage 1, 69 percent for stage 2, 41 percent for stage 3, 21 percent for stage 4 and 36 percent for unstageable). ^[5] Pressure injuries also carry a heavy mortality signal in advanced wound sepsis: infection is the most common complication of a pressure injury, and osteomyelitis underlies a delayed-healing wound in up to 32 percent of cases. ^[6]

Dry gangrene accompanies chronic limb-threatening ischaemia, especially in people with diabetes and atherosclerosis. Wet (infective) gangrene can complicate any break in the skin, from trauma to surgery to intravenous drug use. Gas gangrene is rare but devastating, affecting muscle after deep injury; in World War I it complicated about 6 percent of open fractures and 1 percent of all open wounds. ^[9][10]

The cause of a pressure injury is mechanical, but the machinery is biological. Four forces interact:

• Pressure. Soft tissue is compressed between bone and an external surface. Pressures that exceed normal capillary closing pressure (about 12 to 32 mm Hg) reduce oxygenation and choke the microcirculation. If compression is not relieved, a pressure injury can develop in as little as 3 to 4 hours. ^[6]
• Shear. When a patient slides down in bed or in a chair, the deeper tissues move with gravity while the skin stays against the surface. The opposing forces stretch and tear small vessels inside the tissue, more than on the skin; shear is a major contributor, not a direct sole cause. ^[6][7]
• Friction. Rubbing against clothing or bedding erodes the epidermis and superficial dermis and turns minor skin tears into entry points for deeper pressure damage. ^[6][7]
• Moisture. Sweat, incontinence and exudate macerate the stratum corneum and raise friction, creating a softer surface through which pressure and shear reach deeper tissues. ^[6][7]

Muscle is more susceptible to ischaemia under compression than skin, so some pressure injuries start deep in muscle and only surface later. After ischaemia, reperfusion triggers neutrophils and oedema; temperature, skin thickness, tissue stiffness and vascular reactivity all modify how much damage results. Neonates and people older than 65 years have especially vulnerable skin. ^[6]

Because these forces act through risk factors, NICE CG179 lists adults at risk when they are admitted to secondary care or care homes, or have risk factors in any setting: significantly limited mobility; significant loss of sensation; a previous or current pressure ulcer; nutritional deficiency; inability to reposition themselves; or significant cognitive impairment. Neonates, infants, children and young people are assessed under the same categories, using scales validated for their age. ^[1][12]

Risk factors cluster into recognisable groups:

• Mobility and sensation (bed rest, paralysis, coma, spinal cord injury, sedation, cognitive impairment, neuropathy).
• Tissue perfusion (peripheral arterial disease, diabetes, venous insufficiency, dehydration).
• Nutrition (low intake, albumin under 3.5 g/dL or weight under 80 percent of ideal). ^[6]
• Skin conditions (incontinence, moisture, friction, tapes and devices).
• Age extremes (under 1 year and over 65 years), with children who have cerebral palsy, spina bifida or spinal cord injury at particular risk. ^[6]
• Medical devices: masks, tubes, collars, splints, orthoses and even bed rails can produce a medical device-related pressure injury that mirrors the device's shape. ^[7]

Gangrene has its own causes. Dry gangrene follows chronic or acute reduction in arterial supply: atherosclerosis, embolism, thrombosis, vasculitis, connective tissue disease, smoking, diabetes and exposure to extreme cold. Wet gangrene follows bacterial invasion of necrotic or ischaemic tissue, often polymicrobial. Gas gangrene follows contamination of deep, devitalised muscle with clostridial spores, usually after trauma or surgery, though spontaneous cases occur in the setting of colorectal or genitourinary disease. ^[8][9][10]

Normal tissue tolerance. Under normal conditions the skin and subcutaneous tissue tolerate routine pressure from sitting or lying because the body shifts, microvessels reopen, and nutrients and oxygen are delivered. Capillary pressure has to be overcome for injury to begin.

Step one: occlusion. Sustained pressure collapses capillaries; blood flow stops; the tissue becomes hypoxic. Because muscle tolerates ischaemia less well than skin, deep muscle can die before the skin breaks. ^[6]

Step two: inflammatory injury. Ischaemia triggers neutrophils and oedema. When pressure is relieved and blood returns, reperfusion adds further damage. The eventual lesion can therefore be much larger and deeper than the visible skin change suggests. ^[6]

Step three: clinical expression. The visible stage depends on how much of the depth axis has died: intact but non-blanching erythema (stage 1), exposed dermis (stage 2), full-thickness fat (stage 3), exposed fascia, muscle, tendon or bone (stage 4). ^[6]

Step four: gangrene. If ischaemia is not corrected, coagulative necrosis sets in and the tissue desiccates into the black, leathery eschar of dry gangrene. If bacteria colonise the dead tissue, autolysis and bacterial proteases turn it into wet gangrene; gas-forming organisms such as C. perfringens generate toxins that further thrombose vessels, create an anaerobic niche, and spread rapidly along fascial planes. ^[8][9][10]

The earlier you see a pressure injury, the simpler it is to treat. Good examination is systematic.

History. Ask about mobility, sensation, incontinence, recent surgery or hospitalisation, nutrition, weight change, pain, fever, and previous pressure injuries. Ask about devices: masks, tubes, dressings, footwear and splints. Ask about diabetes, vascular disease, smoking, and medications that affect perfusion or consciousness. ^[6][1]

Skin inspection. Examine all skin over bony prominences and under devices, in good lighting. Pay attention to the sacrum, ischial tuberosities, greater trochanters, heels, malleoli, occiput, scapulae, ears and elbows. In stage 1 the skin is intact but erythema does not blanch under finger pressure or diascopy, and it may be warmer, cooler, firmer, softer or more tender than the surrounding skin; the colour change can be subtle or different in darker skin tones. ^[1][6]

Pressure points in children need special attention around the occiput, where pressure injury can develop quickly in neonates and infants. ^[1]

Examination of the wound, when open, records site, shape, size, depth, edges, undermining or tunnelling, slough or eschar, exudate (amount, colour, odour), pain, and the condition of the surrounding skin. Document surface area with a tracing or photograph. Estimate depth, but do not routinely measure wound volume. ^[1][7]

Vascular examination for gangrene. In dry gangrene the limb or digit is cool and pale on elevation, shows dependent rubor when lowered, has delayed capillary refill, lost hair and absent or reduced distal pulses. Pain, paraesthesia, paralysis and a pulseless limb in acute ischaemia are an emergency. ^[8][10]

Wet gangrene starts as cellulitis: erythema, swelling, pain and warmth; bullae, haemorrhagic or clear, follow, then ecchymosis, skin necrosis and numbness, with systemic toxicity. Foul-smelling discharge and gas in the tissues point to anaerobes. Gas gangrene declares itself with severe pain out of proportion, tense swelling, brown or purple skin change, haemorrhagic bullae, crepitus, fever, tachycardia and confusion. ^[9][10]

No blood test proves a pressure injury; diagnosis is clinical. ^[6] The purpose of testing is to find complications, to stage and measure, and to guide management.

The LRINEC table uses these cut-offs exactly: CRP over 150 mg/L scores 4; white cells over 25 x10^9/L score 2; haemoglobin under 11 g/dL scores 2; sodium under 135 mmol/L scores 2; creatinine above 1.6 mg/dL scores 2; glucose above 180 mg/dL scores 1. ^[9]

Differential diagnosis matters in two different situations: a skin change is suspected to be a pressure injury, or an open wound is suspected to be something else.

Prevention follows NICE CG179 and the 2019 international guideline (EPUAP/NPIAP/PPPIA), which contains 114 evidence-based recommendations, 62 good practice statements and 20 quality indicators. ^[2]

NICE CG179 recommends:

• Be aware that all patients are potentially at risk. ^[1]
• Carry out and document a risk assessment for adults admitted to secondary care or care homes, and in other settings if risk factors are present; neonates, infants, children and young people are assessed in the same way. ^[1]
• Use a validated scale to support, not replace, clinical judgement: the Braden scale, the Waterlow score or the Norton risk-assessment scale in adults; the Braden Q scale in children. CKS also notes the NWCSP recommendation of the PURPOSE-T tool for adults. ^[1][7]
• Reassess risk whenever there is a change in clinical status, for example after surgery, after deterioration of an underlying disease, or with a change in mobility. ^[1][7]
• Offer adults assessed as high risk a skin assessment by a trained professional, checking areas of pressure, colour change including non-blanchable erythema which may appear differently in darker skin, and variations in heat, firmness and moisture. Use finger palpation or diascopy to decide whether erythema is blanchable; start preventative action for non-blanching erythema and repeat the skin assessment at least every 2 hours until it resolves. ^[1]
• Encourage position change at least every 6 hours if at risk, and at least every 4 hours if at high risk; neonates and infants at risk need repositioning at least every 4 hours. ^{[1] [7]}
• Do not offer skin massage or rubbing to prevent a pressure ulcer at any age. ^[1]
• Do not offer nutritional supplements or intravenous or subcutaneous fluids specifically to prevent a pressure ulcer when intake and hydration are adequate; but provide an individualised care plan, timely information, equipment and training. ^[1]
• Use a high-specification foam mattress for adults admitted to secondary care, or assessed as high risk in primary and community care; consider high-specification foam theatre mattresses and appropriate cushions and surfaces for children. ^[1]
• Consider pressure offloading for heels and the seating needs of people who sit for prolonged periods. Barrier preparations may be used when moisture lesions or incontinence-associated dermatitis are a risk. ^[1]

In practice, pressure should not rest on any bony surface for more than about 2 hours. Patients who cannot move themselves need a written repositioning schedule, and should be turned even on low-pressure mattresses; turned patients are placed at a 30 degree angle to the mattress to avoid direct trochanteric pressure, with minimal head-of-bed elevation to reduce shear. Lifting devices or bed linen rather than dragging prevent friction. ^[6]

Support surfaces are described in detail in the Merck Manual and related sources. Static surfaces (foam, gel, water overlays) spread load; dynamic surfaces (alternating air, low-air-loss, air-fluidised beds) additionally reduce heat and moisture and are indicated for deeper or non-healing injuries. ^[6] Evidence connecting any particular mattress to lower pressure-ulcer risk is of low certainty, so support surfaces are combined with repositioning and nursing care rather than used alone. ^{[6] [9]}

Patient and carer information is a NICE priority. People at high risk and their families need timely, tailored information on causes, early signs, prevention and the implications of having a pressure ulcer, delivered by a trained professional and demonstrated with the actual equipment. ^[1]

Risk scales themselves deserve cautious interpretation. The Braden and Norton scales (and Braden Q in children) are widely used and sensible, but NICE CG179 presents them as support to clinical judgement, not as replacements. The Merck Manual is explicit that, although these scales are considered standard care, they have not been shown to prevent more pressure injuries than skilled clinical assessment alone; combining a scale with expert judgement is recommended. ^[1][6] A Norton score under 14 indicates high risk. ^[6] This is one place to show a learner how to use numbers humbly rather than by rote.

NICE CG179's management pathway is summarised as a quality standard, with the British Association of Dermatologists (BAD) among its supporting organisations. ^[12][1]

• Measure and stage. Document the surface area by a validated method such as tracing or photograph, estimate depth and undermining, and categorise with a validated system such as the NPUAP/EPUAP system; repeat and document on every assessment. ^[1][7]
• Nutrition and hydration. Offer a nutritional assessment by a dietitian or other trained professional. Offer supplements only to those with a nutritional deficiency, and food or advice for adequate intake otherwise. Treat fluid balance so that hydration is adequate. ^[1][6]
• Pressure redistribution. Use high-specification foam mattresses; if these are not enough, consider a dynamic support surface. Never use standard foam for someone with a pressure ulcer. Consider seating and cushion needs. ^[1][6]
• Wound bed and debridement. Assess whether to debride based on the amount of necrotic tissue, the category, size and extent of the ulcer, tolerance and comorbidities. Use autolytic debridement with a suitable dressing, and consider sharp debridement if autolysis will take too long. Wet-to-dry gauze, larval therapy and enzymatic debridement are not routinely used; larval (maggot) therapy is considered if sharp debridement is contraindicated or if there is associated vascular insufficiency. ^[1][6]
• Dressings. Discuss choice with the patient and carers, taking account of pain, position, exudate and frequency of change. Consider dressings that promote a warm, moist healing environment for category 2, 3 and 4 ulcers. Do not use gauze dressings. ^[1]
• Adjuncts to avoid. Do not routinely use negative pressure wound therapy except where fewer dressing changes are needed with a heavily exuding wound. Do not offer electrotherapy or hyperbaric oxygen therapy for a pressure ulcer in adults. Do not routinely use topical antiseptics or antimicrobials. ^[1][6]
• Antibiotics. These are for clinical infection, not for healing the wound. ^[1][6]

NICE CG179 applies the same principles to neonates, infants, children and young people: measure and stage; offer an age-related nutritional assessment; consider autolytic debridement before sharp debridement by trained staff; provide specialist support surfaces, with dynamic surfaces where needed; do not routinely use negative pressure wound therapy, electrotherapy or hyperbaric oxygen; dress for a warm moist environment. Systemic antibiotics are considered for local or systemic infection. ^[1]

For neonates specifically: do not use iodine dressings, and treat iodine dressings as contraindicated in this group. ^[1]

The Merck Manual and Mervis and Phillips' AAD review provide practical wound-care detail consistent with NICE. Clean with normal saline; avoid antiseptics such as iodine or hydrogen peroxide that damage granulation tissue, although newer hypochlorous acid cleansers are designed to reduce microbial load without harming normal cells. Remove necrotic tissue by mechanical methods (irrigation at adequate pressure, hydrotherapy), sharp debridement (bedside for modest eschar, theatre for deep or extensive wounds), autolytic debridement with occlusive dressings, enzymatic agents such as collagenase, or biological (maggot) debridement when bone, tendons or joints are exposed and sharp debridement is contraindicated. Match dressings to depth and exudate: transparent films or hydrogels for shallow low-exudate wounds; foam and alginate for deeper, more exudative wounds. ^[6][4]

Control of infection is a recurring decision point. All pressure injuries are heavily colonised, so routine wound culture is not recommended; rising inflammatory markers, tenderness, erythema, exudate, foul odour, fever or leukocytosis should instead raise the suspicion of infection. Surface swabs reflect colonisation; tissue culture and blood culture guide treatment if cellulitis, bacteraemia or osteomyelitis is suspected. ^[6]

Nutrition deserves emphasis because wound healing is protein-hungry: oral, nasogastric or parenteral routes should supply 1.25 to 1.5 g of protein per kg per day in patients with pressure injuries, especially stage 3 and 4. Undernutrition should be screened with history and examination rather than with albumin or prealbumin alone, which are not reliable by themselves. ^[6]

For deep or non-healing wounds, surgery (grafts or myocutaneous or fasciocutaneous or perforator flaps, after optimising nutrition and comorbidity) and careful offloading are the only routes to closure. ^[6][4]

Dry gangrene is the natural endpoint of inadequate blood supply: chronic arterial disease, an acute embolus or thrombosis, severe vasoconstriction from cold or drugs, or calciphylaxis. It is dry, black and sharply demarcated, with a line of separation where the dead tissue ends and viable tissue begins. Early ischaemia presents as a pale paralysed pulseless limb if acute, or as blue, grey or purple patches, blisters or ulcers at the digits if more distal. The skin is thin, dry, shiny, cool and hairless; pulses are reduced or absent. ^[8]

Investigate the circulation as in peripheral arterial disease: physical examination, ECG, ankle-brachial pressure index (1.0 to 1.4 normal, 0.5 to 0.8 mild to moderate disease, lower than 0.5 severe), vascular ultrasound, angiography, CT or MRI angiography, and echocardiography if an embolic source is suspected. ^[8]

Management centres on blood flow and tissue protection, not on antibiotics, because dry gangrene is not primarily infected. Revascularisation (embolectomy, balloon angioplasty or stent, arterial bypass), removal of thrombus, and hyperbaric oxygen if used, together with medical therapy: antiplatelets, statins, treatment of diabetes, cessation of vasoconstrictive medicines and smoking. Dry gangrene of limited extent may be left to demarcate before amputation; extensive or spreading necrosis needs surgical debridement with or without amputation. ^[8]

Wet gangrene is tissue necrosis complicated by infection, usually polymicrobial (gram-positive cocci, gram-negative rods and anaerobes, including clostridia), or monomicrobial (group A streptococcus, staphylococci, or marine gram-negative organisms in coastal regions). It affects older, sicker patients with diabetes, vascular disease, trauma, surgery (especially bowel or gallbladder), abscesses, fistulae, bites or immunosuppression. ^[9]

Clinically it begins looking like cellulitis and then accelerates: discolouration from blue to black, haemorrhagic bullae, foul-smelling discharge, ecchymosis preceding necrosis, crepitus from gas in tissues, cutaneous anaesthesia, pain out of proportion, swelling beyond the erythema, systemic toxicity, confusion, fever, hypotension and persistent severe pain. The early signs that should prompt urgent surgical exploration are haemorrhagic bullae, ecchymosis preceding necrosis, crepitus and numb skin. Progression despite antibiotics is a clue. ^[9]

Diagnosis relies on surgery rather than imaging. Laboratory tests include blood cultures to identify organisms. The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score combines C-reactive protein, white cell count, haemoglobin, serum sodium, creatinine and glucose; a score of 6 or more carries a 92 percent positive predictive value and 96 percent negative predictive value. Imaging (plain films, CT or MRI) may show subcutaneous gas or fascial thickening but has a limited role, and small exploratory incisions help when the diagnosis is uncertain. Surgical exploration with fascial separation remains the gold standard. ^[9]

Treatment is centred on radical surgical debridement with or without amputation, broad-spectrum antimicrobial therapy (penicillin G, clindamycin, vancomycin and gentamicin may be used as empiric cover for meticillin-resistant Staphylococcus aureus, gram-negative, gram-positive and anaerobic organisms) and haemodynamic support. Additional options include maggot debridement therapy, vascular surgery to improve perfusion, hyperbaric oxygen (especially in diabetes or vascular disease), intravenous immunoglobulin to bind Toxin A and B, and treatment of underlying diabetes. ^[9]

Gas gangrene is a special, most severe form of wet gangrene. It is caused most often by Clostridium perfringens, which proliferates in injured muscle; clostridia release alpha toxin and others that induce thrombosis and myonecrosis, lowering pH and encouraging further bacterial growth. Historically it complicated 6 percent of open fractures and 1 percent of open wounds. Clinical hallmarks are severe pain, tense swelling, brown or purple skin change, crepitus and systemic sepsis. ^[9][10][11]

The IDSA 2014 skin and soft tissue infection guidelines recommend urgent surgical exploration and debridement of suspected gas gangrene, definitive antimicrobial therapy with penicillin plus clindamycin for documented clostridial myonecrosis, and state that hyperbaric oxygen is not recommended because it has not been proven to benefit the patient and may delay resuscitation and debridement. ^[11] StatPearls, which summarises IDSA alongside other sources, adds that the combination covers Clostridium and group A streptococcus, that penicillin plus clindamycin is given for 10 to 14 days once those organisms are identified, that clindamycin is important for toxin inhibition but should not be used alone because of inducible resistance, and that empiric therapy should be broadened for MRSA and gram-negative organisms, particularly in people with diabetes. ^[10] StatPearls also notes reported mortality of about 20 to 30 percent with treatment and near 100 percent without, and that early antibiotics plus early surgical debridement reduce the fatality rate to about 30 percent, with some authors reporting 5 to 10 percent with adjunctive hyperbaric oxygen; the IDSA position on hyperbaric oxygen, however, remains that it is not recommended. ^[10][11] Where strong sources disagree, state both positions and let the local team decide.

The combination is used because experimental work found clindamycin, tetracycline and chloramphenicol more effective than penicillin at suppressing toxin formation, but about 5 percent of C. perfringens strains are clindamycin resistant, so penicillin is added. ^[11][10]

This small table is where learners lose marks, so set it out clearly. ^{[1][6][9][11]}

Pressure injury complications include:

• Infection: cellulitis, abscess, bursitis, septic arthritis, bacteraemia, meningitis, endocarditis. ^[6]
• Osteomyelitis in up to 32 percent of delayed-healing wounds. ^[6]
• Marjolin (squamous cell) ulcer in a long-standing scar. ^[6]
• Sinus tracts communicating with deeper structures such as bowel. ^[6]
• Tissue calcification. ^[6]
• Chronic pain, poor quality of life, depression, prolonged length of stay and high cost. ^[3][6]

Gangrene complications depend on type:

• Dry gangrene can become secondarily infected and convert to wet gangrene; recurrence of ischaemia is likely, especially with diabetes. ^[8]
• Wet gangrene can progress to septic shock, multi-organ failure and death within hours. ^[9]
• Gas gangrene and necrotising fasciitis carry a mortality around 20 to 30 percent even with treatment, and close to 100 percent without. ^[10]

The Anaya clinical score for infective gangrene predicts outcome: heart rate above 110, temperature below 36 degrees C, serum creatinine above 1.5 mg/dL, age above 50, white cell count above 40,000 per microlitre, or haematocrit above 50 percent. Few findings mean about a 6 percent risk of death; several mean up to 88 percent. ^[9]

For pressure injuries, the prognosis of early-stage disease is excellent with timely treatment, but healing takes weeks; stage 3 and 4 injuries take much longer. Prognosis worsens when care cannot be optimised or when undernutrition, diabetes and peripheral arterial disease are present. ^[6][5] In the UK series cited, healing rates by 12 months were 100 percent for stage 1, 69 percent for stage 2, 41 percent for stage 3, 21 percent for stage 4 and 36 percent for unstageable. ^[5]

For gangrene, prognosis depends on how much tissue is involved, the cause, and how quickly treatment starts. Amputation rates after critical limb ischaemia in people with diabetes reach up to 50 percent within a year and 20 to 25 percent die within that year; non-diabetic patients with rest pain, ulcers or gangrene also have substantial amputation rates during follow-up. Ray amputations in diabetic wet gangrene recur more often than isolated toe amputations. Predictors of death in gas gangrene of the lower limb include sepsis at presentation, leukocytosis and hyperglycaemia. ^[10]

There is no population screening programme for pressure injury in the way that there is for cancer. Instead, prevention is operational: risk assessment on entry to care and on clinical change, a turning and support-surface plan, skin care, nutrition, pressure monitoring and patient education. NICE frames this as a quality standard, with BAD among its supporting organisations. ^[1][12]

For peripheral arterial disease, which drives dry gangrene, the pathway is different: identify tissue loss (ulceration or gangrene) as a symptom of peripheral arterial disease, assess with ankle-brachial pressure index, and arrange revascularisation. ^[12] Diabetic foot programmes add annual foot checks and stratification into low, moderate, high and "active" risk (active includes gangrene). ^[12]

• Older adults. Skin is thinner, perfusion is poorer, and comorbidity is common. Risk scales help but should not replace bedside assessment. ^[6]
• Neonates and infants. Risk is reassessed differently (occipital area, repositioning at least every 4 hours, high-specification cot mattresses and pads); iodine dressings are contraindicated in neonates. ^[1]
• Children and young people. Use Braden Q, reposition every 4 hours or more often if high risk, and involve play specialists if repositioning is refused. ^[1]
• Pregnancy. Pressure injury is uncommon but can occur with epidural catheters, prolonged labour or operative delivery; positioning, support surfaces and careful monitoring apply. Vasoconstrictive therapy for shock can precipitate peripheral symmetrical gangrene. ^[10]
• People with impaired sensation or mobility, such as those with spinal cord injury, need lifelong skin care, positioning and equipment. ^[1]
• Low-resource settings. Repositioning, basic support mattresses, heel offloading with folded towels or water bags, daily skin checks, and adequate protein food are the high-value interventions. Sharp surgical debridement and antibiotics are usually available; advanced support surfaces and negative-pressure therapy are not. Hyperbaric oxygen should not delay surgery. ^[1][6][9]