Infections - usual / unusual
Recommendations
| Identify and Treat the Cause | ||
|---|---|---|
| 1 | Implement a regular wound assessment protocol that allows early identification of critical colonization or infection. | Level of Evidence Not Assessed |
| 2 | Identify critical colonization or infection through clinical evaluation and support the diagnosis with microbiologic data. | Level of Evidence Not Assessed |
| 3 | Manage infected wounds effectively by addressing host factors, preparing the wound bed and instituting appropriate antimicrobial therapy. | Level of Evidence Not Assessed |
| 4 | Diagnose infectious ulcers based on history, clinical characteristics, culture and sensitivity, and biopsy. | Level of Evidence Not Assessed |
| 5 | Treat infected wounds with systemic empiric antibiotic therapy followed by individualized treatment once culture results are available. | Level of Evidence Not Assessed |
| 6 | Treat suspected infection in diabetic ulcers with broad-spectrum antibiotic therapy. | Level of Evidence Not Assessed |
| Address patient-centered Concerns | ||
|---|---|---|
| 7 | Communicate (patients, family, caregivers) to establish a social support system with realistic expectations for healing and to prevent leg ulcer recurrences. | Level of Evidence Not Assessed |
| 8 | Assess / control pain and optimize activities of daily living | Level of Evidence Not Assessed |
| Provide Local Wound Care | ||
|---|---|---|
| 9 | Consider the possibility of resistant organisms when wound infection is unresponsive to treatment. | Level of Evidence Not Assessed |
| Provide Organizational Support | ||
|---|---|---|
| 10 | Consult appropriate disciplines to maximize healing (e.g. mobility and nutrition). | Level of Evidence Not Assessed |
Background
Infection may cause an ulcer or delay its healing. It is critical to identify infection and the causative organism.Infected chronic ulcers
Although high microbe numbers and virulence contribute to tissue invasion, the most important determinant of infection in chronic wounds is reduced host resistance. Local and systemic factors affecting resistance include the following:
♦ Increasing wound size increases the microbial burden and risk of infection.
♦ Specific wound locations, such as the plantar surface of the foot, perineum or sacrum, increase the risk of infection.
♦ Wound age >6 weeks is associated with increased risk of infection and polymicrobial flora.
♦ Inadequate perfusion favours microbial proliferation and increases the risk of infection.
♦ The presence of devitalized tissue and foreign bodies predisposes to infection.
♦ Behavioural determinants, such as depression, poor nutrition, alcohol abuse, smoking and poor hygiene interfere with healing.
♦ Financial resources may affect healability of wound, such as the ability to purchase offloading devices.
♦ Various comorbidities can reduce host defences, presdisposing to infection.
Assessment of infection in a chronic wound is based on clinical evaluation and supported by microbiological data. Signs of infection include delayed healing, increased serous drainage and inflammation, increased tenderness, friable or bleeding granulation tissue, foul odour, and increased wound breakdown. Infection must be differentiated from inflammatory processes, such as pyoderma gangrenosum and acute Charcot foot. Moderately severely infected wounds may also have a rim of cellulitis with increased erythema, swelling, and local skin temperature. Severe infection may be associated with systemic signs of sepsis.
Effective management of chronic wounds depends on recognizing critical colonization and infection early, addressing contributing host factors, preparing the wound bed, and instituting appropriate antimicrobial therapy. Topical antibiotic agents are redundant in treating infected wounds when systemic antibiotic therapy is used.
Initial empiric systemic antibiotic therapy should be individualized once detailed culture and sensitivity information is available. Gram-positive organisms usually cause infections in wounds that have been present for less than 1 month. Polymicrobial infection is usually found in wounds that have been present for more than 1 month. Wounds in immunosuppressed individuals should be assumed to have a polymicrobial infection. Broad-spectrum antibiotic therapy is appropriate for suspected infection in patients with diabetes, as diabetic foot infections are polymicrobial. Specific microbiologic data are required to select antibiotic therapy for extensive and longstanding infection. Resistance should be suspected when an infected wound does not respond to appropriate antimicrobial treatment. Repeat culture and sensitivity can identify the resistant organism and treatment options.
Infectious ulcers
Ulcers may also be caused by infection, especially in patients with a history of immunodeficiency, tropical travel, trauma, insect bite or surgery. Bacteria, viruses, fungi and protozoa may cause infectious ulcers.
♦ Bacteria
◊ Necrotizing fasciitis may develop at the site of a recent surgical incision or traumatic wound, or it may complicate a chronic wound. Group A β-hemolytic streptococci are usually the cause of this surgical emergency, but other organisms have also been found. Patients are usually unwell with fever and chills. Apparent cellulitis quickly develops into blisters or black necrotic areas. Rapid diagnosis, surgical debridement, broad-spectrum antibiotic therapy, and treatment of shock and septicemia are required. Specific antibiotic therapy is instituted when culture and sensitivity data are available.
◊ Ecthyma, an ulcerative infection caused by Group A β-hemolytic streptococci (Pseudomonas aeruginosa in immunocompromised patients) starts as blood blisters with a red halo and develops into black-crusted ulcers surrounded by erythema. Gram stain, culture and biopsy can confirm the diagnosis.
◊ Cutaneous anthrax: Bacillus anthracis can produce lesions resembling insect bites that develop into necrotic ulcers with a depressed centre. Gram stain and culture confirm the diagnosis. Oral ciprofloxacin is the treatment of choice.
◊ Syphilis: Ulcers (gummas) in tertiary syphilis (Treponema pallidum) may heal spontaneously with scarring, and new lesions continue to develop. Penicillin is the treatment of choice.
◊ Tropical ulcer: This polymicrobial (Fusobacterium, Bacillus fusiformis, Treponema vincentii), rapidly expanding, painful ulcer on the lower leg may develop from minor trauma in individuals living in the tropics. Treatment consists of tetracycline and metronidazole.
◊ Yaws: This condition is similar to tropical ulcer, except for the presence of multiple lesions due to Treponema pertenue. Yaws is most often seen in Central and West Africa in children under 15 years of age.
◊ Mycobacterial ulcers:
• Mycobacterium tuberculosis: Tuberculous chancres, lupus vulgaris, erythema induratum of Bazin, scrofuloderma
• Mycobacterium leprae: Neuropathic ulcers in lepromatous leprosy
• Mycobacterium ulcerans: Buruli ulcer, an indolent ulcer seen in tropical and subtropical areas
• Mycobacterium marinum: (an atypical mycobacterium) Fish-tank granuloma, a solitary, slowly growing, largely asymptomatic ulcer developing at the site of minor trauma that occurs while cleaning a fish tank or swimming pool. Doxycycline or minocycline are the usual treatment.
♦ Fungi
◊ Blastomycosis: Inhalation of, or direct skin contact with Blastomyces dermatitidis may lead to a single, slow-growing, asymptomatic ulcer. Biopsy can aid in diagnosis, and chest x-ray is necessary to identify or rule out simultaneous pulmonary disease.
◊ Sporotrichosis: Skin nodules or ulcers, often distributed along lymphatics, are caused by Sporothrix schenkii (present in the soil). Biopsy confirms the diagnosis.
◊ Histoplasmosis: This pulmonary infection, caused by Histoplasma capsulatum (present in the soil) may be accompanied by skin involvement and ulceration in immunocompromised individuals.
◊ Dermatophytes: Tinea capitis, usually due to Trichophyton or Microsporum, may present as superficial pustules, with development of a deep abscess, hair loss and scarring. Systemic antifungal therapy is required.
♦ Viruses
◊ Herpes simplex, herpes varicella zoster and cytomegalovirus may cause ulcerating skin lesions in immunocompromised individuals.
◊ Epstein-Barr virus may cause persistent genital ulcerations.
◊ Orf, a virus of sheep and goats may cause ulcerating skin lesions, especially on the hands of animal handlers.
♦ Protozoa
◊ Leishmaniasis: A sand fly bite can transmit Leishmania, which can produce cutaneous, mucocutaneous, and visceral disease. Skin lesions may be highly variable. Leishmaniasis is seen in South America and the Middle East.
References
| Essential Publications |
|---|
| 1 | Kaposi’s Sarcoma |
Quality Indicator
|
Type: Case-control study (2 groups) |
| Newton R, Carpenter L, Casabonne D, Beral V, Babiker A, Darbyshire J, Weller I, Weiss R, Kwan A, Bourboulia D, Munoz F, Lagos D, Boshoff C. A prospective study of Kaposi’s sarcoma-associated herpesvirus and Epstein-Barr virus in adults with human immunodeficiency virus-1. British Journal of Cancer; 2006: 94(10) 1504-9. | |||
| This purpose of this study was to investigate using data collected prospectively, the evolution of antibody response to Karposi’s Sarcoma associated herpes virus (KSHV) and to Epstein Bar Virus (EBV) in HIV infected individuals, who subsequently developed Karposi’s Sacroma or non-Hodgkin’s Lymphoma compared to that in HIV infected controls without cancer. No significant association was found between anti-EBV-VCA antibodies and non-Hodgkin’s lymphoma or Kaposi’s sarcoma in HIV seropositive adults. Among HIV infected people, high levels of antibodies against KSHV appear strongly associated with subsequent risk of Kaposi’s sarcoma but not with non-Hodgkin’s lymphoma. | |||
| 2 | Kaposi’s Sarcoma |
Quality Indicator
|
Type: RCT |
| Cooley T, Henry D, Margaret T, Sun S, O’Connell M, Rackoff W. A randomized, double-blind study of pegylated liposomal doxorubicin for the treatment of AIDS-related Kaposi’s sarcoma. The Oncologist; 2007: 12 114-23. | |||
| Pegylated liposomal doxorubicin was found to be safe and effective for the treatment of AIDS-related KS, with most patients experiencing clinical benefit defined as an improvement from baseline in at least one of five AIDS-related KS symptom categories that lasted for  28 days in the absence of disease progression or severe drug-induced toxicity, tumour response or both. Results from this study indicate that even in the era of highly active antiretroviral therapy (HAART). Chemotherapy still plays an important role in the treatment of advanced AIDS-related KS. | |||