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

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.

•  APS is an autoimmune multisystem disorder characterized by arterial, venous or small vessel thromboembolic events and/or pregnancy morbidity in the presence of persistent antiphospholipid antibodies (aPL). APS occurs as a primary condition or in the setting of an underlying systemic autoimmune disease, particularly systemic lupus erythematosus (SLE)

• Its diagnosis requires the presence of antiphospholipid antibodies (aPL) and clinical manifestations that include thrombotic phenomena and/or recurrent miscarriages.[1,3,4] Clinical manifestations are varied.[1,3,4,5] The most frequent skin lesions in patients with APS are livedo reticularis and skin ulcers.[3,4,5,6]

• Up to 20% of cases of deep vein thrombosis, with and without pulmonary embolism, may be associated with antiphospholipid antibodies

Summary

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.

Epidemiology

Incidence: rare

Risk Factors

• Calcium, phosphorus, parathyroid hormone and bone metabolism disorder
• Drug use (e.g. steroid drugs and immunosuppressive agents, warfarin)
• Utraviolet exposure
• Obesity
• Hypoalbuminemia
• Certain diseases such as systemic lupus erythematosus or antiphospholipid syndrome can also accelerate the progression of calciphylaxis.
  

Pathophysiology

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.

Differential Diagnosis

•  It is essential to differentiate calciphylaxis from skin necrosis caused by other diseases such as calcinosis, autoimmune vasculitis, antiphospholipid antibody syndrome, and warfarin-induced skin necrosis, pyoderma gangrenosum, arterial ulcer, systemic lupus erythematosus.
  

Management

• The management of calciphylaxis requires multidisciplinary cooperation involving nephrology, dermatology, wound care, nutrition, and pain management departments. Currently, there are no clinical practice guidelines for the treatment of calciphylaxis, and treatment methods are mostly based on clinical experience and observational studies.
• It is crucial to maintain serum levels of calcium, phosphate, and PTH within normal ranges to prevent the development of calciphylaxis in patients with chronic renal failure. Hyperphosphatemia control should be prioritised over hypercalcemia control. After management of renal disease, the most common first-line treatment for calciphylaxis is intravenous sodium thiosulfate. Other treatments include wound care management, hyperbaric oxygen therapy, pain management, and close monitoring of calcium and phosphorus levels.
• Wound care is the cornerstone of calciphylaxis treatment and includes removal of necrotic tissue, promotion of wound healing, and prevention of infection. Debridement and the lesion itself can cause intense pain to the patient; hence, the advice of pain experts should be sought. In the later stages of the disease, appropriate palliative treatment is beneficial for patient survival.
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Summary

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.

Epidemiology

Prevalence: fewer than 5 cases per 10 000 individuals in Europe and North America

Risk Factors

• Drug use, more than 90% of cases are associated with Hepatitis C infections 
• occurs more frequently in women
• middle age 
• HIV
• multiple myeloma
• Waldenstrom macroglobulinemia
• lupus
• Sjogren's syndrome

Pathophysiology

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.

Diagnosis

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.

Differential Diagnosis

• Cryofibrinogenemia
• Cholesterol emboli 
• Disseminated intravascular coagulation (DIC)
• Coumadin (warfarin) necrosis
• Purpura fulminans 
• Cocaine levamisole toxicity
• Raynaud disease
• Waldenström macroglobulinemia 
• Livedoid vasculopathy
• Chilblains
• Heparin-induced thrombocytopenia
• Thrombotic thrombocytopenic purpura / hemolytic uremic syndrome
• Homocysteinemia 
• Thrombophilia
• sickle cell disease 
• Leukocytoclastic vasculitis
• Granulomatosis with polyangiitis

Management

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.

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