A pressure ulcer (PU), also known as pressure injury (PI), pressure sore, decubitus ulcer or bed sore, is an area of localized injury to the skin and/or underlying tissue, usually over a bony prominence or related to a medical or other device. A pressure ulcer/injury (PU/PI) can present as intact skin and/or ulcer and may be painful. It occurs as a result of pressure, or pressure in combination with shear. PU/PIs represent a large burden to healthcare systems.
Infected pressure ulcers are a common problem, occurring in 4 to 6 percent of nursing home patients
Patients with hip fractures
Risk Factors for Infection of PU/PI:
Diagnosis of PU/PI is clinical, based on information gathered during history and physical examination. Laboratory tests ordered upon initial assessment help establish a baseline and monitor any chronic underlying medical conditions, as well as the patient’s nutritional status, which may be factors that impair wound healing. Diagnostic tests can be considered when investigating non-healing ulcers and/or complications.
Tissue biopsy or quantitative validated swab technique for culture, obtained after debridement, can be used to diagnose wound infection.
Stage 1:
Stage 2:
Stage 3 or stage 4:
Unstageable:
Deep tissue:
Ensure adequate pressure redistribution on bed and seating surfaces: assess need for a new support surface to reduce the forces of pressure and shear against the patient's body. Select support surfaces according to individual needs/resources and care setting. Reposition patient and encourage mobility if not contraindicated.
Address infection and control bioburden: Interventions to manage PU/PI infection include debridement, topical antiseptics/antimicrobial agents, systemic antibiotics and surgical procedures.
Topic antimicrobials:
See section 'Coding' in topic "Pressure Ulcers/Injuries - Introduction and Assessment"
A pressure ulcer (PU), also known as pressure injury (PI), pressure sore, decubitus ulcer or bed sore, is an area of localized injury to the skin and/or underlying tissue, usually over a bony prominence or related to a medical or other device. A pressure ulcer/injury (PU/PI) can present as intact skin and/or ulcer and may be painful. It occurs as a result of pressure, or pressure in combination with shear. PU/PIs represent a large burden to healthcare systems. It is estimated that PUs/PIs cost the U.S. between $9.1-11.6 billion a year. Despite optimal care, not all PUs/PIs are avoidable.
Incidence: Hospital discharge data from 210 academic medical centers in the USA show decreased incidence rates of PU/PI from 11.8/1000 cases in 2008 to 0.8/1000 cases in 2012.
Prevalence: Data from a sample of 918,621 patients in the USA showed that the overall prevalence of PU/PI at all facilities decreased from 13.5% (2006) to 9.3% (2015)
PUs/PIs develop as a result of an imbalance between an individual's tolerance to external mechanical loads and mechanical loads that exceed this tolerance. PUs/PIs occur over predictable pressure points where bony protuberances are more likely to compress tissues when the patient is in contact with hard surfaces. When the damage threshold of an individual is reached, a series of events occur and result in tissue damage. Tissue deformation may cause immediate muscle damage in susceptible areas/individuals. Cell death due to tissue deformation leads to local inflammatory reactions with edema and increased interstitial pressure. This additional tissue deformation leads to more cell distortion and cellular damage. External mechanical loads cause blood vessels to compress and nutrients cannot be delivered, leading to local hypoxia and tissue damage.
Provide effective local wound care:
Surgical consult is indicated for full thickness ulcers that are extensive or refractory, if important structures are exposed (e.g., vessels, nerve, bone, muscle, fascia) or osteomyelitis is suspected.
Mixed arterial/ venous ulcers occur as a result of both venous and arterial peripheral disease and show clinical manifestations of both conditions. MIxed etiology ulcers are complex and can change very rapidly. In comparison with venous leg ulcers, mixed leg ulcers can be associated with lower health related quality of life, greater mobility impairments, and more deficits in self-care and usual activities.
Mixed arterial venous disease is estimated to affect up to 26% of patients with lower extremity ulcerations.
Patients with mixed etiology ulcers were found to typically be of older age, have lower body mass index, have a history of smoking, and more comorbid conditions than subjects with VLU.
Mixed etiology ulcers arise as a result of the presence venous disease in conjunction with a significant level of arterial disease. Chronic venous insufficiency results in venous hypertension (ambulatory venous pressures of up to 60 to 90 mmHg, as opposed to the normal levels of 20 to 30 mmHg), which can happen due to obstruction to venous flow or venous reflux from dysfunction of venous valves, and/or failure of the "venous pump". Inadequate tissue perfusion plays a major role in the pathogenesis of arterial ulcers.
A full assessment should be completed to determine the etiology of the ulcer and to identify any other disease processes and risk factors for ulceration and delayed wound healing. Assessment should include a comprehensive history of the patient’s current condition, recurrence, past medical and surgical history, medications, and other risk factors related to VLU, AU, PAD, and venous disease. For all patients with suspected chronic limb-threatening ischemia (CLTI)/PAD, guidelines recommend ankle brachial index (ABI) and ankle pressure (AP) and as the first-line screening tests to detect PAD. However, due to the high prevalence of arterial calcification among patients with AU, ischemia should also be documented by at least one of the following non-invasive arterial test modalities: toe pressure, toe brachial index, continuous doppler wave ultrasound, transcutaneous oximetry (TcPO2) or skin pressure perfusion. Venous disease should be documented with duplex ultrasound.
Note: Pitting edema may be present if ulcer is of mixed venous and arterial etiology.
Arterial ulcers, venous ulcers, neuropathic ulcers, pressure ulcers/injuries, metabolic (diabetes mellitus, gout, Gaucher disease, etc), hematologic (Sickle cell anemia, thalassemia, polycythemia vera, leucemia), autoimmune (Rheumatoid arthritis, leukocytoclastic vasculitis, polyarteritis nodosa), exogenous, neoplasia, infection, medication, skin disorders
In patients with mixed arterial and venous disease, revascularization is recommended in a staged fashion. Patients with an ABI > 0.7 should undergo wound care and compression therapy for venous disease, patients with an ABI < 0.7 should be considered for revascularization via an endovascular or open bypass procedure to enhance ulcer healing, and patients with an ABI < 0.5 may need earlier arterial intervention to allow for aggressive compression therapy. After arterial intervention, standard wound care and compression therapy remain crucial to wound healing and the prevention of ulcer recurrence.
Infected arterial ulcers (AU) are leg ulcers that develop due to inadequate blood supply to the skin (arterial insufficiency) and become infected. The decrease in blood supply may be caused by underlying peripheral arterial disease (PAD) that results from narrowing of the arteries to the legs (atherosclerosis), or may be caused by other non-atherosclerotic diseases. It is essential to differentiate AUs from venous leg ulcers (VLUs). Among chronic ulcers, AUs pose the largest financial burden to Medicare in the U.S. In addition to the financial burden, chronic limb-threatening ischemia (CLTI) patients have an increased risk of limb amputation.
Infection of ischemic ulcers is a primary risk factor for major amputation.
Incidence: The monthly incidence rate of AU is estimated to be 1.8 cases per 100 patients with advanced illness
Prevalence: In the United States, the prevalence of AUs among Medicare beneficiaries in 2014 was estimated to be 0.4%.
Patients who are at increased risk of PAD:
Inadequate tissue perfusion plays a major role in the pathogenesis of AUs. AUs are often precipitated by trauma or infection. Limbs with arterial compromise may have minimal but adequate blood flow to maintain tissue viability. Trauma or infection increase demand for blood supply, leading to a non-healing ulcer.
By default, chronic wounds are contaminated by several types of bacteria. Bacterial biofilms are estimated to be present in ~78.2% of chronic wounds.
When the host (patient) does not adequately respond to bacterial contamination, this contamination can turn into colonization, which can further turn into infection.
For all patients with suspected chronic limb-threatening ischemia (CLTI)/PAD, guidelines recommend ankle brachial index (ABI) and ankle pressure (AP) and as the first-line screening tests to detect PAD. However, due to the high prevalence of arterial calcification among patients with AU, ischemia should also be documented by at least one of the following non-invasive arterial test modalities: toe pressure, toe brachial index, continuous doppler wave ultrasound, transcutaneous oximetry (TcPO2) or skin pressure perfusion
Infection: The NERDS mnemonic (Nonhealing ulcer, increased Exudate, Red-friable tissue, Debris, Smell;) can help identify soft tissue infection. If any 3 NERDS are present, superficial soft tissue infection is likely and topical antimicrobial treatment is justified.
The STONEES mnemonic (Size, Temperature, Os (orifice), New breakdown, Exudate, Erythema + edema (cellulitis), Smell) can help identify systemic infection. ystemic antibiotics and topical antimicrobial treatment are justified if 3 or more of the STONEES signs are present.
Mixed ulcers (i.e. ulcer with mixed etiology, for instance, arterial/venous, arterial/neuropathic, etc), diabetic foot ulcer, venous ulcers, pressure ulcers/injuries, skin manifestations of COVID-19 (e.g. chilblains-like lesions, acute limb ischemia due to hypercoagulability)
Infected arterial ulcers have a higher risk of amputation, especially if neuroischemic ulcer. Evaluate need for hospital admission:
See section 'Coding' in topic "Arterial Ulcer - Introduction and Assessment"
Calciphylaxis is a rare but life-threatening calcific vasculopathy affecting the microvessels in the dermis and subcutaneous tissue, characterised by painful cutaneous ischemic lesions. It has an insidious disease course, and detailed medical history and identification of risk factors are essential for its clinical diagnosis. It can mimic many diseases, including warfarin- and heparin-induced skin necrosis, pyoderma gangrenosum, peripheral arterial disease, systemic lupus erythematosus, and antiphospholipid. Most cases of calciphylaxis are in patients with end-stage renal disease (ESRD), who require dialysis. However, it can also occur in other diseases with normal renal function, including autoimmune disease, polyneuropathy, organomegaly, endocrinopathy, monoclonal protein, and skin changes (POEMS) syndrome, cancer, and coronavirus disease 2019. Calciphylaxis not only involves the skin but also the heart, lungs, and other internal organs.
Incidence: rare
Diagnosis
The diagnosis of calciphylaxis is complex and requires careful clinical evaluation and pathological examination. Detailed medical history and identification of risk factors are crucial for its clinical diagnosis. In clinical practice, a biopsy of the deep skin and subcutaneous tissue is essential for the differential diagnosis of calciphylaxis. The histological manifestations of calciphylaxis include skin microvascular or extravascular calcification, thrombosis, and intimal fibrosis. However, routine skin biopsy is not recommended because the biopsy process can induce ulcer formation in the incision area and increase the risk of infection, sepsis, and death. When a biopsy is contraindicated or not diagnostic, radiography, bone scanning, and bone scintigraphy can identify microcalcification and extravascular calcification, which can help confirm the histopathologic results or monitor the treatment response.
Cryoglobulinemic vasculitis is caused by the formation of immunoglobins called cryoglobulins. At temperatures below regular body temperature, cryoglobulins can become solid or gel-like, and can restrict blood flow in the vessels. Cryoglobulinemia typically presents with vasculitis with lower extremity purpura, glomerulonephritis, and peripheral neuropathy.
Prevalence: fewer than 5 cases per 10 000 individuals in Europe and North America
The onset of cryoglobulinemic vasculitis is associated with circulating immunoglobulins that undergo reversible precipitation from plasma or serum upon cooling (below 98.6 F). Most patients diagnosed with type II or type III mixed essential cryoglobulinemia have the disease as an immune response to chronic hepatitis C infection. The cryoglobulins in these patients are enriched with anti–hepatitis C antibody and hepatitis C RNA.. The build up of the immunglobins iin the vessels can result in vascular occlusion and ischemic damage of tissues.
Testing for cryoglobulins is necessary for diagnosis, done via collection of venous blood in citrate, ethylenediamine tetraacetic acid, or oxalate. Keep at 37°C (98.6°F) until the specimen gets to the laboratory. In the laboratory, the sample is then cooled to 4°-5°C (39.2°-41°F) for detection of cryoprotein. Hepatitis panel should be ordered in suspected type II and III cryoglobulinemia. Biopsy may also be helpful.
For type I, the underlying hematologic disease should be treated directly. For mixed cryoglobulinemias, if patients positive for hepatitis C, they should receive antiviral therapy, If negative, other possible underlying infectious, autoimmune, or myeloproliferative diseases should be identified and treated. For severe vasculitis and end-organ involvement, immunosuppressive therapy including systemic steroids and/or rituximab may be used. Cytotoxic agents such as mycophenolate, azathioprine, or cyclophosphamide may be used as a secondary action.
D89.1 – Cryoglobulinemia
Arterial or ischemic leg ulcers (AU) are leg ulcers that develop due to inadequate blood supply to the skin (arterial insufficiency). The decrease in blood supply may be caused by underlying peripheral arterial disease (PAD) that results from narrowing of the arteries to the legs (atherosclerosis), or may be caused by other non-atherosclerotic diseases. It is essential to differentiate AUs from venous leg ulcers (VLUs). Among chronic ulcers, AUs pose the largest financial burden to Medicare in the U.S. In addition to the financial burden, chronic limb-threatening ischemia (CLTI) patients have an increased risk of limb amputation.
Inadequate tissue perfusion plays a major role in the pathogenesis of AUs. AUs are often precipitated by trauma or infection. Limbs with arterial compromise may have minimal but adequate blood flow to maintain tissue viability. Trauma or infection increase demand for blood supply, leading to a non-healing ulcer
Patients with healable AUs should undergo either prompt revascularization or a 4-week trial of conservative treatment followed by revascularization, depending on the WIfI classification. For foot infections involving wet gangrene, abscess, gas, or necrotizing fasciitis urgent surgical debridement is recommended. For non-healable/maintenance AUs, debridement is not recommended.
For all patients (healable, non-healable, maintenance), appropriate local wound care should be implemented to avoid infection and further injury. Interventions to improve circulation in AU patients include:
"It is important to treat the whole patient and not just the 'hole' in the patient."
Dressing selection is just a small part of wound care. Without a holistic, individualized patient assessment and plan that addresses the cause of the ulcer, patient concerns and local wound care, all clinicians’ efforts may not result in complete and timely healing. Thus, it is strongly recommended that dressings be selected after a holistic patient assessment. Assessment can be performed with WoundReference’s Assessment Tool and other tools.
As part of the assessment, clinicians should determine if the ulcer is:
The dressing type will change as the needs of the person and their wound change
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