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 infection. 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 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 burn wound infections.

The three most commonly used topical agents used to fight wound infections 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.