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.
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.
Stage 1:
Stage 2:
Stage 3 or stage 4:
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.
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.
Unstageable:
Deep tissue:
See section 'Coding' in topic "Pressure Ulcers/Injuries - Introduction and Assessment"
Soft tissue sarcomas are a rare but heterogeneous family of malignant tumors that are predominantly found beneath the skin, with very few tumors originating in the dermal layers. While there are many different types of soft tissue sarcoma, some that predominantly affect the skin include epithelioid sarcoma, low-grade myxofibrosarcomas, and dermatofibrosarcoma protuberans. The most common presenting complaint for a soft tissue sarcoma is a gradually enlarging, painless mass. These tumors can become quite large. Some patients complain of pain or symptoms associated with compression by the mass, including paresthesias or edema in an extremity.
Malignant melanomas are the most serious form of skin cancer. Melanomas form when melanocytes begin to grown out of control. Early diagnosis of melanoma is crucial to improve patient outcomes and save lives. It's likely that a combination of factors, including environmental and genetic factors, causes melanoma. It is believed that exposure to ultraviolet (UV) radiation from the sun and from tanning lamps and beds is the leading cause of melanoma.
Melanomas are typically diagnosed through clinician assessment of the skin lesion with the unaided eye, often based on the “ABCDE rule”:
A: asymmetry, B: irregular border, C: color variations, D: diameter >6 mm, and E: elevated surface
The use of a skin surface microscope or a dermascope may improve visualization of the lesion and aid in diagnosis. A biopsy is needed to confirm the diagnosis.
Primary melanomas are typically treated with surgical excision, which yields a high survival rate. However, following metastasis, surgical excision of the tumor only yields about 10% five-year survival, so metastatic melanomas are medically managed by chemotherapeutics. Dacarbazine, dimethyltriazeno-imidazol carboxamide (DTIC), is an alkylating agent and the only monochemotherapy approved by the FDA for treating melanomas.
See "Malignant melanoma of skin C43"
Squamous cell carcinoma (SCC) is the second most common type of skin cancer worldwide. SCC is a malignant tumor arising from epidermal keratinocytes. While the majority of SCCs can be easily and successfully treated, if left untreated SCCs can become invasive, grow into deeper layers of skin, and spread to other areas of the body.
The lifetime risk of developing SCC is 9%-14% for men and 4%-9% for women.
In Europe: 9 to 96 per 100,000 male inhabitants and 5 to 68 per 100,000 female inhabitants
In Australia: 499 per 100,000 for men and 291 per 100,000 in women
SCC occurs when DNA damage from exposure to ultraviolet radiation or other damaging agents trigger abnormal changes and unregulated growth in the squamous cells of the epidermis.
The skin of patients with SCC will often display evidence of sun exposure such as rhytides, actinic keratoses, and solar lentigines. Although clinical and dermoscopic findings may strongly suggest a diagnosis of SCC, histopathologic examination is necessary to confirm the diagnosis. Shave, punch, or excisional biopsies may be used.
See "2022 ICD-10-CM Diagnosis Code C44.329"
A skin tear is defined as a traumatic wound caused by mechanical forces, including removal of adhesives. Skin tears are acute wounds with the potential to be closed by primary intention, and they can vary based on depth. Individuals suffering from skin tears may experience increased pain and decreased quality of life. Populations at the highest risk for skin tears include those at extremes of age and the critically or chronically ill. These individuals are at a higher risk for developing secondary wound infections and have co-morbidities
Incidence: The incidence of STs among elderly people living in long-term care facilities has been reported to range between 2.23 to 92%.
Prevalence: Existing studies report prevalence varying from 3.9% and 26%
Although STs can occur in any age group, it is most prevalent in age extremes (elderly and very young).The most prevalent risk factor for skin tears is old age, followed by impaired mobility, falls and accidental injuries, previous STs, cognitive deficit/dementia, dependence in transfers, and upper limbs
Dermal thinning results in reduction of the blood supply to the area, along with reduction of the number of nerve endings and collagen. These changes lead to decreased sensation, temperature, tightness and moisture control, and increased propensity for lesions such as ecchymosis and senile purpura.
Skin tear occurs when an extrinsic factor leads to frictional forces that are greater than those tolerated by the skin.
Diagnosis of a ST is clinical, based on history and physical examination. Errors persist in the correct identification of STs, which results in underreporting, diagnostic errors and inadequate management of wound care. There is no consensus at the moment on the need for laboratory investigations or imaging to assist in the diagnosis of ST.
Stage 2 Pressure Ulcers/Injuries, deep tissue injury, incontinence-associated dermatitis, bruising, hematoma, terminal ulcers
For all skin tear patients (with healable, non-healable or maintenance ST), expert consensus recommends that healthcare professionals identify and implement a personalized treatment plan that corrects the underlying causes or co-factors affecting skin integrity, and that takes into consideration the patient’s needs, the wound, and environmental/system challenges.
Adequate local wound care is accomplished with the following steps:
For ISTAP type 2 skin tears, clinicians might opt to cover the wound bed with pieces of the skin flap (used as skin grafts) to promote wound healing.
Currently, there is no ICD-10 code for STs. As skin tear is an acute wound, it is typically coded as a superficial injury.
Polyarteris nodosa (PAN) is a multisystem disease with symptoms including fever, sweats, weight loss, and severe muscle and joint aches/pains. It can also cause skin abnormalities such as purpura, livedo reticularis, ulcers, nodules or gangrene, mostly located on the legs and can be very painful.
PAN is a necrotizing vasculitis of medium-sized and occasionally small arteries. The exact cause is unknown, but it likely involves immune complex deposition, autoantibodies, inflammatory mediators, and adhesion molecules.
A skin biopsy should be used to identify vasculitis in the small/medium vessels. PAN should be considered in a patient who presents with the following symptoms: fever, weight loss, myalgias, arthralgias, and signs of multiorgan involvement such as neurologic dysfunction, skin lesions, abdominal pain, renal insufficiency, and hypertension.
Provide local wound care to any skin ulcerations. Surgery may be required for the debridement of necrotic tissue or in the context of an acute abdomen. The use of graduated compression stockings may be helpful. Systemic corticosteroids may be used to treat mild disease. For severe systemic disease, methylprednisolone may be administered followed by prednisone.
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:
Tissue biopsy or quantitative validated swab technique for culture, obtained after debridement, can be used to diagnose wound infection.
Address infection and control bioburden: Interventions to manage PU/PI infection include debridement, topical antiseptics/antimicrobial agents, systemic antibiotics and surgical procedures.
Topic antimicrobials:
Pemphygus is an autoimmune skin disorder that is characterized by acantholysis of the epidermis that results in superficial blisters, crusted erosions, and scale in a seborrheic distribution (ie, scalp, face, and upper trunk). Lesions usually start on the trunk.
In patients with pemphigus, antibodies, mostly immunoglobulin G4 (IgG4), are created that damage cells of the epidermis and mucous membranes. This causes dissolution of the bridges between epidermal cells, resulting in the formation of crusted lesions and blisters on the skin.
Skin biopsy for both hematoxylin and eosin (H&E) stain and direct immunofluoresnce (DIF) should be performed. Serum antibodies to desmoglein 1 (Dsg1) can be detected by enzyme-linked immunoassay (ELISA) in the majority of patients.
If the distribution of lesions is limited and symptoms are mild, pemphygus can typically be treated with a topical corticosteroid. In more severe cases, systemic therapy, such as administration of prednisone or prednisolone, may be required. In all cases, sun avoidance/protection measures should be implemented.
L10.2 – Pemphigus foliaceous
Immunoglobulin A vasculitis (IgAV), formerly called Henoch-Schönlein purpura, is a necrotizing small-vessel vasculitis most common in young children. IgAV is characterized by the presence of palpable purpura, abdominal pain, arthritis, and hematuria. Erythema may be subtle in darker skin colors, and edematous papules and plaques may be the sole clinical finding.
incidence: 140 cases/million persons. in childhood, 3-26 per 100 000
Risk Factors:
IgAV is characterized by characterized by IgA1-immune deposits, complement factors and neutrophil infiltration in the small blood vessels. Immmunoglobin A collects in small blood vessels causing them to become inflamed and leak blood. Incidence of IgAV is twice as high during fall and winter, suggesting an environmental trigger associated to climate. It is unclear what causes the onset of IgA deposits.
Diagnosis is largely clinical. Look for palpable purpura over areas such as the buttocks and legs and over pressure points, in the setting of a recent upper respiratory tract infection, and consider the diagnosis for any patient presenting with widespread palpable purpura, arthralgias of the knees and ankles, and colicky abdominal pain and/or a positive urinalysis. A skin biopsy shows leukocytoclastic vasculitis, and direct immunofluorescence (DIF) shows IgA deposits. The biopsy should be performed on a lesion that is less than 24 hours old.
IgAV in children is typically self-limited, and treatment is usually not needed in mild episodes. Involvement of the renal and gastrointestinal systems can cause complications, so these cases may warrant the us of systemic immunosuppressants.
D69.0 – Allergic purpura
Basal cell carcinoma (BCC) is a common type of skin cancer arising from the basal layer of the epidermis. While basal cell carcinoma rarely metasticizes, the tumor is often locally invasive, aggressive, and destructive of skin and the surrounding structures, including bone. Those who have this condition are at higher risk of developing further basal cell carcinoma and other malignancies in the future.
Incidence shows marked geographical variation:
Mutations in several tumor suppressor genes and proto-oncogenes are thought to be the cause of BCC formation. In most cases, alteration of genes causing hyperactivation of the hedgehog (HH) protein family, a highly conserved developmental pathway involved in organogenesis, tissue repair, and including PTCH1 receptor, SMO signal transducer, and GLI transcription factors, are linked to BCC formation. The TP53 tumor suppressor gene is also commonly involved in the pathogenesis of BCC. Mutations in PTCH1 and TP53 are in most cases consistent with ultraviolet (UV) radiation-induced mutagenesis. These UV signature mutations include base substitutions of C>T at dipyrimidine sites and CC>TT tandem base substitutions.
PTCH1 encodes a protein acting as a transmembrane receptor for the HH protein family. Sonic hedgehog (SHH), the most studied HH ligand, binds a cell membrane receptor complex that is formed by PTCH and a second protein, smoothened (SMO), relieving the inhibition of the pathway induced by unbound PTC1 and thus activating the HH pathway. However, the mechanism by which HH signal overexpression leads to tumorigenesis is unclear.
Diagnosis of BCC can typically be made based on clinical examination. A dermatoscope may be used to assist the clinical diagnosis. Dermoscopic features of BCC include the lack of a pigmented network and the presence of one or more findings that are characteristic of BCC, such as arborizing vessels, blue-gray ovoid nests, and ulceration.
A skin biopsy is typically performed to confirm the diagnosis and determine the histological subtype.
Surgical:
Non-surgical:
See "2022 ICD-10-CM Diagnosis Code C44.310"
Pyoderma gangrenosum is a rare but serious primary ulcerating condition of the skin that falls into the category of neutrophilic dermatoses. Pyoderma gangrenosum is often associated with systemic diseases including inflammatory bowel disease, arthritis, and myeloproliferative disorders.
Incidence: estimated to occur in 3-10 patients per million population per year
Prevalence: estimated to be of 0.01% among adult patients in the U.S
Current pyoderma gangrenosum pathogenic hypothesis is that the disease is autoimmune in nature with defects in cell-mediated immunity, neutrophil and monocyte function and humoral immunity. A patient’s genetic background can lead to aberrant activation of innate-immune complexes (inflammasomes). The activated immune system leads to increased levels of dermal cytokines and resultant neutrophilic tissue infiltration. Other inducers of pyoderma gangrenosum include drugs such as granulocyte colony stimulating factor, isotretinoin, propylthiouracil and sunitinib. Cocaine has also been implicated as a common agent to trigger pyoderma gangrenosum.
Pyoderma gangrenosum presents with several variations and is easy to misdiagnose. Diagnosis of pyoderma gangrenosum is based mainly on clinical findings because biopsies show no specific diagnostic features. however, a biopsy is indicated for all potential cases in order to exclude other conditions such as malignancy, infections, or cutaneous vasculitis.
add in diagnostic criteria from WR
Currently, there is no definitive guideline or gold standard in management of pyoderma gangrenosum, as data from controlled clinical trials are scarce.
Local wound care:
For simple/ limited pyoderma gangrenosum: use topical therapy, agents include:
For more severe cases, see above plus consider:
Sytemic therapy agents:
Targeted Therapy:
See section 'Coding' in topic "Pyoderma Gangrenosum - 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
Granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA) are both necrotizing vasculitides that typically affect small-sized arteries and vary in terms of organ manifestations and severity. The most commonly and severely affected organs include the upper and lower respiratory tract and the kidneys. Because of their strong association with antineutrophil cytoplasmic autoantibody (ANCA), they are also referred to as ANCA-associated vasculitis (AAV). Patients typically present with symptoms including fever, malaise, anorexia, weight loss, myalgias, and arthralgias.
Incidence: GPA: 0.4 to 11.9 cases per million person-years
MPA: 0.5 to 24.0 cases per million person-years
Prevalence: GPA: 2.3 to 146.0 cases per million persons
MPA: 9.0 to 94.0 cases per million persons
GPA Risk Factors:
MPA:
GPA and MPA are two types of ANCA-associated vasculitis, or AAV. AAV causes inflammation of the small blood vessels. The presence of ANCAs in the bloodstream cause neutrophils to stick and clump to the walls of small blood vessels in different tissues and organs of the body, leading to inflammation and narrowing and/or weakening of the vessels.
The diagnosis of GPA and MPA is based upon the combination of characteristic clinical findings, laboratory tests, and imaging studies.
Testing for ANCA should be performed in any adult patient who presents with symptoms suggestive of a vasculitis. In clinical practice, ANCA can be detected using an indirect immunofluorescence (IIF) assay or antigen-specific enzyme-linked immunosorbent assays (ELISAs) for proteinase 3 (PR3) and myeloperoxidase (MPO).
Whenever possible, the diagnosis of GPA or MPA should be confirmed by biopsy of a site of suspected active disease. Histologic examination of tissue obtained by biopsy of an affected organ (usually kidney, skin, or lung) remains the most definitive method to establish a diagnosis.
The overall management approach is the use of systemic glucocorticoids plus cyclophosphamide or rituximab. Induction of remission is followed by maintenance therapy using medications such as azathioprine, methotrexate, or rituximab.
See "2022 ICD-10-CM Diagnosis Code M31.7"
"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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