Complications
Managing large burns entails successful management of a series of complications while the wound is progressively closed. Most complications are related to sepsis.[99] Neutropenia, thrombocytopenia, and disseminated intravascular coagulation are common indicators of impending sepsis and should prompt appropriate investigations and treatment. Topical antimicrobial agents are rarely the cause. Global immunologic deficits associated with burn injury contribute to a high rate of infectious complications. Prompt wound closure is the best prophylaxis.
The most common wound infection in small outpatient burns is cellulitis, usually caused by Staphylococcus aureus. This infection presents with expanding wound erythema, which, if untreated, will progress to lymphangitis and systemic toxicity. All suspected burn infections require aggressive management, which may include admission, intravenous antibiotics, observation, and surgery excision if wounds are deep.
May occur with or without antecedent inhalation injury and is treated with pulmonary hygiene and antibiotics.[102]
Occurs as a result of bacterial invasion of cartilage and results in the rapid loss of viable tissue. Prevented by the routine use of topical mafenide acetate on burned ears.
Hepatic dysfunction, as the result of transient hepatic blood flow deficits and manifested as transaminase elevations, is extremely common during resuscitation from large burns. Resolves with volume restitution.
Can be encountered as sepsis without localized symptoms or signs accompanied by rising cholestatic chemistries. A standard radiographic evaluation can be followed by bedside percutaneous cholecystostomy in patients in unstable condition.
May occur as the result of splanchnic blood flow deficits that degrade mucosal defenses. Extremely common and often life-threatening if routine histamine receptor blockers and antacids are not administered.
Minimized by maintaining bladder catheters only when absolutely required. Treated with appropriate antibiotics. Neither catheterization nor colonic diversion is routinely required for the treatment of perineal and genital burns.
Candida cystitis occurs in patients treated with bladder catheters and broad-spectrum antibiotics. Catheter change and amphotericin irrigation for 5 days is generally successful.
If infections are recurrent, upper tracts should be screened by ultrasonography.
Occurs in up to 30% of patients and generally resolves with supportive therapy when the possibility of anoxia, metabolic disturbance, and structural lesions are eliminated by appropriate studies.
Most commonly result from hyponatremia or abrupt benzodiazepine withdrawal. Prevention is the best treatment.
Early acute renal failure follows inadequate perfusion during resuscitation or myoglobinuria. Treatment is with careful fluid and electrolyte support and occasional dialysis.
Late renal failure complicates sepsis and multi-organ failure or the use of nephrotoxic agents. Treatment is with careful fluid and electrolyte support and occasional dialysis. Protein loads are ideally not reduced to facilitate treatment, because this may impair wound healing.
Occurs as the result of hemorrhage into the gland. Presents with hypotension, fever, hyponatremia, and hyperkalemia. Diagnosis is by adrenocorticotropic hormone-stimulated and random serum cortisol level determination. Treatment is glucocorticoid replacement at stress levels with empiric tapered reduction.
Occurs with fever and bacteremia without signs of local infection. Diagnosis may require ultrasonography or surgical exposure of peripheral veins.
Occurs with fever and bacteremia without signs of local infection. Diagnosis may require ultrasonography or surgical exposure of peripheral veins.
Infrequent in patients with large burns, so routine prophylaxis is not currently recommended. Iatrogenic catheter insertion complications are minimized by meticulous technique. Catheter-related DVT is minimized by using the smallest possible catheter.
Can progress to infarction. Results from inadequate resuscitation and splanchnic blood flow deficits.
Corneal ulceration, which develops after initial epithelial injury or later exposure as the result of ectropion, can progress to full-thickness corneal destruction if secondary infection occurs. This is prevented by careful globe lubrication with topical antibiotics in the former case, and acute lid release in the latter.
Other eye-related complications include ectropion, from progressive contraction of burned ocular adnexa, which results in exposure of the globe. This requires acute eyelid release. Tarsorrhaphy is rarely helpful and may result in injury to the tarsal plate as contraction forces pull out tarsorrhaphy sutures. Symblepharon, or scarring of the lid to the denuded conjunctiva after chemical burns or corneal epithelial defects that complicate toxic epidermal necrolysis, is prevented by daily exam and adhesion disruption with a fine glass rod.
Rarely, abdominal compartment syndrome can develop, usually in patients with very large injuries and delayed resuscitation.
May occur, particularly in preadolescent boys, and is best treated with beta-blockers, after inadequate pain and anxiety treatment are excluded.
A major cause of long-term functional and cosmetic deformities seen in burn patients. This poorly understood process is heralded by a secondary increase in neovascularity 9 to 13 weeks after epithelialization.
Treatment options include compression garments, massage, judicious steroid injections, topical silicone products, and scar release and resurfacing procedures.[100]
Develops weeks after injury and is encountered most commonly around deeply burned major joints such as the triceps tendon. Accompanied by pain and decreased range of motion. Most patients respond to physical therapy, but some require excision of heterotopic bone to achieve full function.
A squamous cell carcinoma that occurs in chronic ulcerated open areas in old burn wounds.
May occur early after the injury as the result of inhalation of noxious chemicals or later in the course of therapy as the result of sepsis or pneumonia.
Late hepatic failure, beginning with elevations of cholestatic chemistries and progressing through frank liver failure, complicates sepsis and multi-organ failure.
Pancreatitis, beginning with amylase and lipase elevations and ileus and progressing through hemorrhagic pancreatitis, is generally coincident with splanchnic blood flow deficits early and sepsis-induced organ failures later in the hospital course.
Some peripheral nerve injuries occur from direct thermal injury or compression from compartment syndrome, overlying nonelastic eschar, or improper splinting techniques.
Delayed peripheral nerve and spinal cord deficits develop weeks or months after high-voltage injury as the result of small vessel injury and demyelinization.
Occurs in up to 30% of patients and is probably exacerbated by inadequate treatment of pain and anxiety. Symptoms include hypervigilance, reliving the incident, night terrors, and chronic fearfulness. Recognition and treatment with supportive psychotherapy and pharmacotherapy greatly facilitates recovery.[101]
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