Summary

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. 

Epidemiology

Infected pressure ulcers are a common problem, occurring in 4 to 6 percent of nursing home patients

Risk Factors for PU/PI development

Patients with hip fractures 

• age older than 81 years 
• Patients with neurological conditions (acquired or congenital) that affect mobility:
• Spinal cord injuries (33 - 95% develop PU/PI)
• Spina bifida 
• Elderly patients with immobility and/or cachexia (muscle wasting).
• Lower extremity trauma resulting in bone or soft-tissue injury and subsequent fixation with casting: associated with PU/PI under the cast or on the heels. 
• Patients with COVID-19 requiring intensive care, especially those ventilated in the prone position.

Risk Factors for Infection of PU/PI:

• onset of ulcer: greater risk of infection if ulcer present for more than 4 weeks 
• areas likely to be repeatedly contaminated (eg. near the anus)
• malnutrition and hydration deficits 
• autoimmune disease, immunosuppressants 
• Cardiovascular: hypertension/hypotension, hemodynamic instability, poor diffuse or localized blood perfusion (e.g. generalized atherosclerosis or lower extremity arterial insufficiency), or use of vasopressor infusion
• thyroid disease or diabetes mellitus 

Diagnosis

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. 

Differential Diagnosis

Stage 1: 

• Superficial burn (assess history of exposure)
• Cellulitis (suspect if located on a non-pressure area)
• Post-injury inflammation
• Deep tissue pressure injury
• Non-palpable erythema that blanches on compression

Stage 2: 

• Moisture-associated skin damage (MASD) including incontinence-associated dermatitis (IAD), intertriginous dermatitis (ITD), medical adhesive-related skin injury (MARSI) or traumatic wounds (skin tears, tape burns, excoriations)

Stage 3 or stage 4: 

• Burns, necrotizing fasciitis, calciphylaxis (may have history of rapid development of eschar)
• Infection (abscess)
• Diabetic Foot Ulcer, Venous ulcers, arterial ulcer, Inflammatory Ulcers  (e.g. Pyoderma Gangrenosum)

Unstageable: 

• Arterial ulcer, calciphylaxis 

Deep tissue: 

• Stage 2 pressure ulcers, incontinence-associated dermatitis, skin tears, bruising, hematoma, venous engorgement, arterial insufficiency, necrotising fasciitis and terminal skin ulcers
• COVID-19 dermatologic changes

Management

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:

• If minimal/ light exudate, consider painting wound with antiseptic solution or using a topical antimicrobial agent 
• If moderate or heavy exudate, consider non-adherent antimicrobial dressings (with silver, cadexomer iodine, medical-grade honey, silver, etc)

Summary

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.

Summary

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.

Epidemiology

Risk Factors

• UV radiation exposure
• use of indoor tanning beds
• light skin pigmentation
• freckling
• blue or green eyes 
• red or blond hair 
• poor tanning ability 
• family history 
• history of nonmelanoma skin cancer
• immunosuppression 
• occupational exposure to chemical 
• smoking 
• Parkinson's disease 
• endometriosis
• history of prostate cancer

Diagnosis

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.

Differential Diagnosis

• Common melanocytic nevus
• Atypical melanocytic nevus 
• Traumatized nevus
• blue nevus
• lentigo
• Pigmented basal cell carcinoma
• Pigmented actinic keratosis
• Seborrheic keratosis
• Pyogenic granuloma
• Cherry hemangioma
• Dermatofibroma
• Keratoacanthoma
• Verrucous squamous cell carcinoma of the sole
• Melanonychia striata
• Acral melanocytic nevi
• Subungual hematoma
• Periungual warts

Management

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. 

Summary

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.

Epidemiology

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 

Risk Factors

• light skin types
• ultraviolet (UV) exposure
• solid organ transplantation
• ionizing radiation exposure
• cigarette smoking
• human papillomavirus (HPV)
• chemical exposure (ie, arsenic, mineral oil, coal tar, soot, mechlorethamine, polychlorinated biphenyls, and psoralen plus UVA treatment)
• freckling
• red hair
• immunosuppression such as HIV disease / AIDS
• chronic nonhealing wounds

Pathophysiology

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.

Diagnose

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.

Differential Diagnosis

• Actinic keratoses
• Bowenoid papulosis
• Nummular eczema
• psoriasis
• Inflamed seborrheic keratosis
• Prurigo nodularis
• pyoderma gangrenosum
• Venous stasis ulcers
• Merkel cell carcinoma
• Basal cell carcinoma
• Atypical fibroxanthoma
• Amelanotic melanoma

Summary

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.

Epidemiology

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%.

Risk Factors

Patients who are at increased risk of PAD: 

• 65 years of age or older. 
• 50 to 64 years of age with risk factors for atherosclerosis (i.e., smoking, diabetes mellitus, hypertension, hyperlipidemia, chronic kidney disease) or family history of PAD. 
• younger than 50 years with diabetes mellitus and one or more additional risk factors for atherosclerosis - Patients with known atherosclerotic disease in another vascular bed

Pathophysiology

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

Diagnosis

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

Differential Diagnosis

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)

Management

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:

• Surgical Interventions (Angioplasty, Endarterectomy, Arterial Bypass)
• Management of underlying conditions 
• Medical therapy and aggressive risk factor management
• Nutrition optimization
• Pain management
• Foot, callus and nail care 
• Edema control
• Offloading
• Infection and bioburden control

Summary

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.

Epidemiology

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)

Risk Factors

• Patients with hip fractures 
• age older than 81 years 
• Patients with neurological conditions (acquired or congenital) that affect mobility:
• Spinal cord injuries (33 - 95% develop PU/PI)
• Spina bifida 
• Elderly patients with immobility and/or cachexia (muscle wasting).
• Lower extremity trauma resulting in bone or soft-tissue injury and subsequent fixation with casting: associated with PU/PI under the cast or on the heels. 
• Patients with COVID-19 requiring intensive care, especially those ventilated in the prone position.

Pathophysiology

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

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. 

Differential Diagnosis

Stage 1: 

• Superficial burn (assess history of exposure)
• Cellulitis (suspect if located on a non-pressure area)
• Post-injury inflammation
• Deep tissue pressure injury
• Non-palpable erythema that blanches on compression

Stage 2: 

• Moisture-associated skin damage (MASD) including incontinence-associated dermatitis (IAD), intertriginous dermatitis (ITD), medical adhesive-related skin injury (MARSI) or traumatic wounds (skin tears, tape burns, excoriations)

Stage 3 or stage 4: 

• Burns, necrotizing fasciitis, calciphylaxis (may have history of rapid development of eschar)
• Infection (abscess)
• Diabetic Foot Ulcer, Venous ulcers, arterial ulcer, Inflammatory Ulcers  (e.g. Pyoderma Gangrenosum)

Management

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: 

• For healable, Stage 2 - 4 PUs/PIs, we recommend debridement of devitalized tissue to promote wound healing, when aligned with goals of therapy and not contraindicated (Grade 1C)
• Apply a topical dressing that will manage excess exudate, protect periwound skin and maintain a moist wound bed, with the least amount of dressing changes possible

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: 

• Arterial ulcer, calciphylaxis 

Deep tissue: 

• Stage 2 pressure ulcers, incontinence-associated dermatitis, skin tears, bruising, hematoma, venous engorgement, arterial insufficiency, necrotising fasciitis and terminal skin ulcers
• COVID-19 dermatologic changes

Summary

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.

Epidemiology

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.

Pathophysiology

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.

Diagnosis

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.

Differential Diagnosis

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

Management

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.

Summary

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. 

Epidemiology

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: 

• 65 years of age or older. 
• 50 to 64 years of age with risk factors for atherosclerosis (i.e., smoking, diabetes mellitus, hypertension, hyperlipidemia, chronic kidney disease) or family history of PAD. 
• younger than 50 years with diabetes mellitus and one or more additional risk factors for atherosclerosis - Patients with known atherosclerotic disease in another vascular bed

Pathophysiology

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.

Diagnosis

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.

Differential Diagnosis

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)

Management

Infected arterial ulcers have a higher risk of amputation, especially if neuroischemic ulcer. Evaluate need for hospital admission: 

• If infection is severe (systemic signs of infection, deep space foot infection, wet gangrene - i.e. WiFI Foot Infection 3), patient should be treated as a medical emergency with immediate drainage, debridement, culture, systemic antibiotics and consideration for revascularization. 
• Collect wound culture and initiate empiric antibiotic treatment (e.g. vancomycin and piperacillin/ tazobactan). Adjust antibiotics based on culture results. 
• For patients with hemodynamic instability, immediate amputation may be the only option.
• If infection is non-limb-threatening, blood supply to the foot should be optimized before surgical debridement to ensure that potentially viable tissue is not unnecessarily removed.
• Collect wound culture and initiate empiric antibiotic treatment, adjust antibiotics based on results and signs of improvement
• If AU does not respond with interventions to treat infection (e.g. antibiotics, abscess drainage) or if there is deterioration, revascularization should be strongly considered.