Burn Sepsis
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Direct answer
Invasive wound infection is the leading cause of death after the first week post-burn, and burn sepsis is diagnosed on modified criteria because burned patients are inflamed all the time: the American Burn Association 2007 consensus proposes at least three of temperature over 39 degrees C or under 36.5, progressive tachycardia over 110 per minute, progressive tachypnoea over 25 (or high minute ventilation), thrombocytopenia under 100 × 10^9/L (beyond 72 hours after injury), feeding intolerance, and a rising inotrope requirement — in a patient with an infected-looking wound or a suspicious clinical course. Management combines early excision and grafting of the burn (the single most effective anti-infective measure), topical chemotherapy, targeted antimicrobials, and rigorous infection-control, since gram-negative rods, particularly Pseudomonas aeruginosa, and Staphylococcus aureus dominate the burn unit flora.
What you must remember
- Temporal shift in organisms: early — Staphylococcus aureus; after the first week — gram-negative rods (Pseudomonas, Klebsiella, Escherichia coli, Acinetobacter); later — fungal (Candida, Aspergillus) and resistant organisms in prolonged stays.
- Wound infection definitions: colonisation (organisms present without invasion), invasive burn wound infection (organisms invading viable tissue — the surgical emergency), and cellulitis; the historical quantitative culture over 100,000 organisms per gram of tissue and the "rapid eschar separation" of pseudomonal invasion are classical exam fragments.
- Clinical signs of invasive infection: focal patchy black or brown discolouration, rapid eschar separation, conversion of partial- to full-thickness, unexplained hyperglycaemia, and deterioration in a previously stable patient.
- Topical agents: silver sulfadiazine (broad and painless, but transient leucopenia and poor eschar penetration), mafenide acetate (penetrates eschar and covers Pseudomonas, but painful and a carbonic anhydrase inhibitor producing metabolic acidosis), silver nitrate 0.5% (painless but electrolyte leaching — hyponatraemia — and staining), and nanocrystalline silver dressings.
- Systemic antibiotics are not prophylactic in burns — therapeutic for documented infection or clear sepsis; blind prolonged prophylaxis breeds resistance.
- Early tangential excision (within days, staged) with autografting reduces infection, length of stay and mortality in major burns; temporary cover with allograft, xenograft or biosynthetic dressings.
- Burn sepsis physiology: the hypermetabolic state masks classic signs — a "normal" 37 degrees C may be relative hypothermia; the ABA criteria exist precisely because standard SIRS definitions misclassify nearly every burn patient.
How to work through it
Day 9 after a 45% flame burn, a patient who had been feeding and conversing becomes tachypnoeic at 30, has a temperature of 39.4 degrees C, a platelet count that has fallen to 80 × 10^9/L, and starts refusing feeds; the grafted donor site looks fine but a patch of unexcised back eschar has turned soggy and black-edged. Count the ABA boxes: temperature, tachypnoea, thrombocytopenia, feeding intolerance — four met, sepsis presumed. The sequence: cultures from the wound, blood and urine; change of topical therapy to an eschar-penetrating agent or urgent excision of the deteriorating area; empirical broad-spectrum cover aimed at the unit's ecology (anti-pseudomonal beta-lactam plus cover for resistant gram-positives, refined when cultures report); and a surgical plan to excise the offending eschar within 24 hours, because no antibiotic sterilises dead bone and eschar. Alongside, the supportive architecture — enteral nutrition pushed to meet hypermetabolic demands, glucose control, and pressure-area and line care with line changes per protocol. When the wound reports heavy Pseudomonas and the histology shows organisms invading viable fat, the diagnosis is invasive burn wound infection, and the definitive treatment is excision plus grafting, not a longer course of meropenem.
Where students slip
The first slip is applying ward SIRS criteria to burns: every major burn patient is tachycardic and febrile by default, so writing "SIRS = sepsis" earns nothing — the ABA 2007 modified criteria are the expected answer, with the threshold shifts (fever defined above 39, platelets counted only after day three). The second is topical-agent pharmacology: mafenide's carbonic anhydrase inhibition causing metabolic acidosis, and silver sulfadiazine's transient neutropenia or leucopenia, are classic one-liners; candidates who swap them lose easy marks. The third is the prophylaxis reflex — systemic antibiotics "to prevent infection" in a clean burn are wrong; the anti-sepsis intervention is excision, grafting and topical therapy. Fourth, silver nitrate complications (hyponatraemia from its aqueous vehicle) are commonly forgotten.
Frequently asked questions
Which criteria define burn sepsis?
The American Burn Association 2007 criteria: at least three of temperature over 39 or under 36.5 degrees C, tachycardia over 110, tachypnoea over 25 (or rising minute ventilation), thrombocytopenia under 100 × 10^9/L after 72 hours, feeding intolerance, and rising inotrope requirement, with confirmed or suspected infection.
Which organisms dominate late burn wound infections?
Gram-negative rods, especially Pseudomonas aeruginosa, along with Klebsiella, Escherichia coli and Acinetobacter, with fungi such as Candida in prolonged illness; Staphylococcus aureus predominates in the first days.
Why does mafenide acetate carry a metabolic acidosis risk?
It inhibits carbonic anhydrase, producing a compensatory hyperventilation and metabolic acidosis; its advantages are eschar penetration and antipseudomonal activity despite pain on application.
What wound signs indicate invasive infection?
Patchy black or brown discolouration, unexpectedly rapid eschar separation, conversion of partial- to full-thickness injury, periwound cellulitis, and systemic deterioration — confirmed by histology showing organisms in viable tissue.
Why are prophylactic systemic antibiotics avoided in burns?
Because they do not prevent wound colonisation, select resistant flora, and mask treatable infection; control comes from early excision, grafting, topical chemotherapy and infection-control practice instead.