Infected burn

Despite the great strides made over the last decades in improving survival after thermal injury, infectious complications remain an important cause of morbidity and mortality.

Nearly 50% of all burn deaths are related to infected burn. Several factors contribute to the high incidence and severity of infection in burn patients.

First, a profound immune suppression is induced that is proportional to the extent of burn injury. In addition, the environment at the site of the wound is favorable for the multiplication of infecting organisms, which colonize the wound within 72 hours of injury.

Despite the temptation to administer systemic antibiotics, there is no role for prophylactic systemic antimicrobials. This has no impact on survival and leads to the emergence of resistant organisms. Frequent exposure to antibiotics also establishes an environment favorable for yeast and fungi.

Within 3 days of injury, Gram-positive organisms colonize the wound. Gram-negative organisms then colonize the eschar, and they become dominant by the end of the first week.

The typical flora of burn wounds has changed over the years. Before the advent of penicillin, β-hemolytic streptococci were the most frequent cause of infected burn wound and life-threatening systemic infections. Penicillin largely eliminated mortality due to streptococci, and Staphylococcus aureus became the more common early colonizer.

As broad-spectrum antibiotics effective against Staphylococcus were developed, gram-negative organisms, especially Pseudomonas aeruginosa, became the predominant organisms. These organisms have greater invasive potential due to their production of toxins and proteolytic enzymes.

The use of effective topical agents has reduced the incidence of death secondary to burn wound sepsis, but fungi have emerged as the most common cause of invasive infected burn.

The three most commonly used topical agents used to fight infected burn are silver sulfadiazine (SSD), mafenide acetate, and silver nitrate. SSD is the most frequently used.

It has broad-spectrum activity as well as antifungal properties. SSD is limited by its inability to penetrate the burn eschar. Mafenide acetate has good eschar penetration and can suppress subeschar proliferation of bacteria. Mafenide acetate is a carbonic anhydrase inhibitor that interferes with the renal buffering.

A hyperchloremic metabolic acidosis develops due to the consumption of bicarbonate and chloride retention. A compensatory respiratory alkalosis is generated by hyperventilation but is rarely of clinical significance. Silver nitrate is effective if applied before bacterial penetration into the wound. Side effects of silver nitrate include hyponatremia and methemoglobinemia.

Despite these maneuvers, invasive infected burns still occur. Risk factors include severe injury (>30% total body surface area burn), systemic diseases such as diabetes with poor glycemic control, and delayed excision and grafting of the burn.

The key to successful management of infected burn in the burn patient is early diagnosis. This is best accomplished by daily scheduled monitoring of the burn to identify infected burn at its early stages when surgical and antibiotic therapy will be most effective.

Infected burn is classified as cellulitis, invasive infections, or burn wound impetigo. Cellulitis is diagnosed clinically based on characteristic erythema, edema, and hyperesthesia of unburned skin at the margin of the wound.

Cellulitis unrelated to infected burn may also occur, usually peaking on the second or third day after the burn and then receding; this is rarely accompanied by systemic response. Expanding cellulitis should be treated with the application of mafenide acetate and systemic penicillin if a Beta-hemolytic streptococcus is involved or a broad-spectrum Beta-lactam if specific culture and sensitivity are not available.

A local sign of invasive infected burn is the appearance of dark brown, black, or violaceous discoloration of the wound. Other clinical signs are the conversion of a partial-thickness injury to full thickness and necrosis of previously viable tissue in the wound bed.

Pseudomonas may cause changes in the unburned skin at the wound margin. Infected burns caused by fungi display unexpected rapid eschar separation and rapid centrifugal spread of subcutaneous edema with central necrosis. Vesicular lesions appearing in healing or healed burns on the face are characteristic of herpes simplex virus type 1.

Signs And Symptoms

Once a infected burn is suspected, diagnosis is confirmed by burn wound biopsy. Surface cultures only identify the colonizing organisms present and are therefore inadequate. Quantitative bacterial counts of 105 or greater are suggestive of invasion but only correlate with invasive infection on histologic exam in fewer than 50% of paired samples.

Histologic examination of a burn wound biopsy is the most reliable confirmatory test for invasive infected burn. With a scalpel, a lens-shaped sample of the eschar and unburned underlying/adjacent tissue are obtained from the area of the wound showing the most pronounced changes.

On histologic exam, the presence of microorganisms in unburned tissue is diagnostic. Other findings that indicate infected burn are the presence of hemorrhage, small-vessel thrombosis, and necrosis in unburned tissue. After diagnosis, general supportive treatment is used, and specific systemic antibiotic therapy is initiated based on the institution’s usual flora with subsequent modification as sensitivities return.

Mafenide acetate should be applied to the wound twice daily. Subeschar clysis of a broad-spectrum penicillin may also be employed. Surgical excision should be performed as soon as possible. Topical clotrimazole should be applied when invasive fungi are the culprit microorganisms. Systemic treatment with amphotericin B or other, newer antifungal agents is also used when there is evidence of systemic fungemia.

Burn impetigo occurs after burn healing or grafting and is characterized by multifocal small superficial abscesses. S. aureus is the responsible microbe.

Treatment includes unroofing of abscesses and frequent cleansing followed by application of topical antibiotics. Occasionally, systemic symptoms may be seen when the toxic shock syndrome toxin is produced. In this case intravenous vancomycin is used.

In addition to the previously described clinical situations, appropriate uses of antibiotics in the burn patient include targeted treatment of pulmonary, urinary, and catheter-related infections. In addition, perioperative prophylactic antibiotics should be administered just before wound excision.

These are given based on the findings of transient bacteremia in 21% of patients following wound manipulation, although some studies have shown that bacteremia is rare when there is less than 40% total body surface area burn.

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