The classification of burns, treatment of infected burns and its complications.

In medicine, a burn is a type of injury caused by heat, cold, electricity, chemicals or radiation (e.g. sunburn).

Classification of Burns:

1^st Degree Burn: Limited to redness (erythema), a white plaque and minor pain at site of injury. Only extend into the epidermis.

2^nd Degree Burn: Superficial blistering of the skin, filled with clear fluid. Involve superficial (papillary) dermis & may involve deep (reticular) dermis layer.

3^rd Degree Burn: Charring of the skin & produce hard, leather-like eschars (scabs that has separated from the unaffected part of the body. May contain purple fluid. Painless as nerve endings have been destroyed

Burns that injure the tissues underlying the skin, such as the muscles or bones, are sometimes categorized as fourth-degree burns. These burns are additionally broken down into three additional degrees: fourth-degree burns result in the skin being irretrievably lost, fifth-degree burns result in muscle being irretrievably lost, and sixth-degree burns result in bone being charred.

A newer classification of "Superficial Thickness", "Partial Thickness" (which is divided into superficial and deep categories) and "Full Thickness" relates more precisely to the epidermis, dermis and subcutaneous layers of skin.

Nomenclature	Traditional Nomenclature	Depth	Clinical Findings
Superficial Thickness	1st Degree	Epidermis involvement	Erythema, minor pain, lack of blisters
Partial Thickness – Superficial	2nd Degree	Superficial (papillary) dermis	Blisters, clear fluid & pain
Partial Thickness – Deep	2nd Degree	Deep (reticular) dermis	Whiter appearance, with decreased pain. Difficult to distinguish from full thickness
Full Thickness	3rd or 4th Degree	Dermis & underlying tissue & possibly fascia, bone or muscle	Hard, leather-like eschar, purple fluid, no sensation

Treatment of Infected Burns:

Medical Care:

• Bacterial infection

• Cellulitis: Apply topical mafenide acetate burn cream twice daily, and administer systemic antibiotic therapy until the infection resolves. Most cases of burn wound cellulitis are caused by group A beta-hemolytic streptococci, which can be treated with penicillin. If specific cultures and sensitivities are not known, a broad-spectrum beta-lactam antibiotic should be administered.

• Colonization of nonviable tissue: The wound should be debrided, followed by the application of silver sulfadiazine cream every 12 hours. Wounds that are colonized more heavily or those that deteriorate should be treated with mafenide acetate. The topical creams should be removed daily, and the wound should be cleansed with a surgical detergent.

• Invasion of viable tissue: The infected wound should be excised surgically. Antimicrobial coverage should be started prior to excision to prevent hematogenous spread and organ seeding.
• Gram-negative infections: Invasive infections caused by gram-negative organisms should be treated with topical mafenide acetate to ensure penetration of the burn eschar. Subeschar clysis with an antibiotic solution prior to surgical excision may be helpful. The antibiotic solution is injected below the eschar 6-12 hours before surgery and again immediately prior to the procedure.
• Gram-positive infections: Invasive gram-positive infections are characterized by suppurative foci in the burned tissue. These infections require administration of appropriate systemic antibiotics and debridement, followed by a topical application of mupirocin, mafenide acetate, or silver sulfadiazine.

• Fungal infection

• Colonization of nonviable tissue: Candidal species rarely invade tissue and, therefore, do not require surgical excision. Wounds colonized with candidal species are treated with a twice-daily application of a topical antifungal cream, such as clotrimazole or ciclopirox olamine. Alternatively, mafenide acetate mixed with nystatin powder is effective for topical treatment of superficial fungal infections.
• Invasion of viable tissue: Filamentous fungi, including Aspergillus and the agents associated with mucormycosis, are responsible for most invasive fungal burn wound infections. The treatment of invasive fungal infection is analogous to invasive bacterial infection, ie, surgical excision of the infected burn wound followed by application of topical antimicrobial therapy (clotrimazole or ciclopirox olamine). Systemic dissemination or extensive tissue involvement necessitates administration of systemic amphotericin B.

Surgical Care:

• Invasive bacterial or fungal burn wound infections are treated with surgical excision to the level of viable tissue.

• Wounds that can be excised completely should be covered with an allograft (transplanted cells, tissues or organs are sourced from a genetically non-identical member of the same species) or autograft (Tissue transplanted from one part of the body to another in the same individual).

• If complete removal of the infected tissue is not possible, 5% mafenide acetate should be applied, and the wound should be reexamined in 24 hours for possible repeat excision.

• With aggressive fungal infections, particularly mucormycosis, radical debridement of muscle, including limb amputation may be necessary to control infection.

Diet: The basal metabolic rate is increased 100% above the reference range in patients with burns of greater than 40% TBSA.

• Enteral feeding of a high-caloric diet through a nasogastric tube should be instituted within the first 12 hours after injury. The feedings should include a high-protein component (2 g/kg/d) and 3-10 times the recommended daily allowance of vitamins and minerals, particularly zinc (7 mg/d).

• In severely injured patients, supplementation with omega-3 fatty acids and arginine has been shown to decrease sepsis.

Activity: Patients may be as active as they can tolerate. Aggressive physical therapy of extremity injuries is paramount.

Complications:

• Systemic spread and seeding of distant organs or invasion of muscle may occur; limb amputation may be required.

• Sepsis can contribute to multisystem organ failure and death.

• Methicillin-resistant S aureus infection

• Methicillin-resistant S aureus (MRSA) infection is a serious and increasingly common cause of nosocomial infection in patients with large burn wounds.

• The incidence of MRSA colonization and subsequent infection has increased dramatically in the last decade, primarily because of antibiotic selective pressure in critically ill hospitalized patients.

• Risk factors that have been associated with MRSA colonization or infection include age, coma, invasive procedures, and extended hospitalization.

• MRSA colonization/infection rates may be reduced by early eschar excision, wound closure, bacterial wound surveillance, and strict enforcement of infection control procedures.

• Systemic vancomycin therapy and topical application of mupirocin cream are indicated for burn wounds infected with MRSA.

• Hospital personnel who have been demonstrated to harbor MRSA should receive mupirocin nasal ointment until surveillance culture results are negative.

References: Burn Wound Infections 'http://www.emedicine.com/med/topic258.htm'
Burn (Injury) 'http://en.wikipedia.org/wiki/Burn_%28injury%29'