The system of classification categorizes burns into either superficial, partial-thickness, or full-thickness groups. This classification is important to determine the need for surgery. Patients with full-thickness burn require surgery if the burn area is larger than 2 cm. Older patients with thin epidermis and dermis often require surgery. The extent of burn means the total body surface area that is affected by the burn injury. The most popular method to estimate total burn area in older children and adults is the “rule of nines.” According to this rule, a value of 9% body surface area is assigned to the head and neck region, 9% to each arm (including the hand), 18% to each leg (including the foot), and 18% to each side of the trunk (back, chest and abdomen). The Lund and Browder method is employed for children younger than 10 years of age. According to this method, the size of a child’s palm is roughly 1% of the total body surface area (16; 17; 08).
A variety of CNS and peripheral nervous system manifestations has been described. Burn encephalopathy or burn-induced delirium, often hypoxic and metabolic, has extensively been described in the acute phase of burn injury. A retrospective, clinicopathologic study of 139 patients who died following severe burns, reported that 53% of the patients had CNS complications. Cerebral infarcts and hemorrhages, metabolic encephalopathies, central pontine myelinolysis, and cerebral trauma were major central nervous system complications in these patients. Eighteen percent of the patients had pathologic evidence of cerebral infarcts. In almost half of the patients, the infarcts were caused by septic arterial occlusions or other complications of the burn, like disseminated intravascular coagulation and septic shock. In only one third of the cases, infarcts were due to atherosclerosis, atrial fibrillation, or other causes prevalent in the general population. Intracranial hemorrhages were only one fifth as frequent as infarcts and were due to disseminated intravascular coagulation and thrombocytopenia, caused by bacteremia.
Sixteen percent of the patients had a CNS infection. Candida species, Staphylococcus aureus and Pseudomonas aeruginosa caused almost 80% of CNS infections. S. aureus and candida caused cerebral microabscesses and septic infarcts. Pseudomonas aeruginosa caused meningitis and infarcts due to meningitis. The major risk factors for CNS infection were an extensive burn, Staphylococcus aureus endocarditis, and a burn wound infection due to candida or Pseudomonas aeruginosa. Patients with burns of less than 30% of the surface area of their body, those without a systemic infection, and those in the first week after their burn were at low risk (45).
Burn injury-induced CNS complications have also been described in children. Among 287 children with burns, 13 (5%) showed evidence of encephalopathy. The major clinical manifestations were an altered sensorium and seizures. In the majority, symptoms began later than 48 hours after the burn and were accompanied by multiple metabolic abnormalities. Eleven children improved to normal. CNS dysfunction possibly was a result of complex metabolic, hematological, and hemodynamic abnormalities rather than a single metabolic abnormality (32). Hypoxia was the principal determinant in children with burn encephalopathy. Other factors that were responsible for CNS alterations were hypovolemia, sepsis, hyponatremia, and cortical vein thrombosis (03). Systemic inflammatory response syndrome following burn injury may affect dysfunction of microcirculation of body resulting in CNS dysfunction (26). A retrospective study observed that patients with multiple sclerosis and concurrent burn injuries need longer hospital stay and burn triage and treatment (28).
The risk of ischemic stroke is significantly higher in hospitalized patients with burn injury in comparison to the general population. In one case control study, 1763 burn injury patients were matched with 176,300 unexposed patients. The adjusted hazard ratio of ischemic stroke was significantly increased in burn injury patients versus controls (19).
A case series noted correlation between severe burn and occurrence of ischemic optic neuropathy. Medina and coworkers described three patients with severe burns who developed visual loss because of bilateral ischemic optic neuropathy during their hospital stay (31). These patients needed more than 25 L of crystalloid fluid within 24 hours, had multiple bouts of sepsis, and required extended pressor support. The authors postulated that ischemic optic neuropathy possibly developed because of shock, sepsis, and the need for large volume fluid resuscitation. Hughes and colleagues reported another patient with posterior ischemic optic neuropathy following burns (18). They suggested that a high index of suspicion should be kept if a burn patient develops vision loss.
Neuromuscular manifestations are important complications in acute stages as well as later in life as major disabling sequelae. In acute stages, neurologic findings are often missed. Mononeuropathies, mononeuritis multiplex, and polyneuropathies all have been described in burn-injured patients (38). Patients with severe burn injuries are likely to develop rhabdomyolysis and subsequent acute kidney injury (24).
A retrospective study was performed to evaluate neuropathies in patients with burns. Nineteen of a total of 800 patients had signs and symptoms of neuropathy, confirmed on neurophysiological testing. Most patients with neuropathies were severely burned, with 11 patients (69%) having a total burn surface area of greater than 20%. Twenty-eight percent were full thickness burns. Mononeuritis multiplex was the most common finding in these patients, occurring in 11 (69%). Three patients (19%) had an isolated mononeuropathy, one (6%) had a radiculopathy, and one had a generalized axonal polyneuropathy. The length of hospitalization and severity of the burns were the only two factors that correlated with the number of affected nerves (27).
In a cohort of 572 patients with major burn injuries, 64 (11%) of patients had clinical evidence of mononeuropathy or peripheral neuropathy or both. Electrical cause, history of alcohol abuse, and number of days in intensive care were significantly associated with mononeuropathy. The number of days in intensive care and patient age were significantly associated with peripheral neuropathy (25). A system review noted that of the 1533 burn patients, 98 cases (6.39%) later presented with peripheral neuropathy. Thermal and electrical burns were the most common etiologies (41).
Tight dressings can cause compression to superficial nerves, and improper and prolonged positioning can cause excessive stretch of nerves. Thus, proper positioning of patients as well as careful monitoring of wound care can mitigate neuromuscular complications. Poor positioning at the neck and shoulder leads to excessive stretch of the brachial plexus and places the plexus at risk for injury. Also, several bed and intraoperative positions commonly used in the treatment of burn injuries put the patient at risk of developing mononeuropathies or plexopathies. In the upper extremity, the ulnar, median, and radial nerves are common sites for development of mononeuropathies.
Mononeuritis multiplex is an asymmetric neuropathy that involves two or more isolated peripheral nerves. Involvement of multiple nerves after thermal burns has also been noted among patients with greater than 40% total body surface area. The number of nerves involved per patient ranged from 3 to 7. Upper-extremity nerves were more commonly involved than were lower extremity nerves. Mononeuritis multiplex, in burn patients, is thought to result from a combination of circulating neurotoxins, metabolic factors, and mechanical compression (11).
Polyneuropathy in burns patients has also been frequently observed. Polyneuropathy is caused by a combination of direct thermal injury on the nerves, circulating neurotoxins, and changes in distribution of fluid and electrolytes. Critical illness polyneuropathy in burn patients has also been observed. Critical illness polyneuropathy often has a strong link to sepsis, multiple organ failure, and slow ventilatory wean (09). A review on critical care polyneuropathy in burn-injured patients that included a total of 2755 subjects revealed 128 (4.4%) critical care polyneuropathy patients. The factors associated with critical care polyneuropathy in burns were prolonged ventilation, large burns, and sepsis (30).
In the presence of preexisting diabetic neuropathy, the management of lower-extremity burn injuries becomes difficult. Diabetes-associated factors significantly hamper the healing of such wounds. Many of these patients require amputations after their burn injury (39). It has been noted that among patients with isolated lower limb burns, preexisting diabetes mellitus adversely affects the outcome. Patients with lower limb burns and pre-existing diabetes mellitus had a longer hospitalization and increased amputations (36).
Pruritus is a common disabling symptom in the late phases of burns. The exact mechanism of pruritus is not well known. In a prospective cohort study, among 510 burn patients, the reported prevalence rates of mild to severe itching were as high as 87%, 70%, and 67% at 3, 12, and 24 months post-burn event. Significant predictors of itching were deep dermal injury and early posttraumatic stress symptoms. Along with these, total burned surface area and female gender were predictors at 3 months post-burn (42). Axonal sprouting in the dermis is considered a proposed mechanism of pruritus in burn patients.
Burn scars can cause intense pain, even without evidence of underlying nerve damage. Extent of damage by burn injury is the important predicting factor for pain in scars. Scar pain has characteristics of neuropathic pain and is considered caused by an imbalance in C-fibers subtypes. The scar possibly alters the nerve fiber distribution in the damaged tissues, resulting in pain (04). In a retrospective study, 1880 adult patients of burns were analyzed (23). In this study, 113 (6%) of the burn patients developed chronic neuropathic pain over 5 years. Old age, alcohol, substance abuse, smoking, large and severe burns, mechanical ventilation, corrective surgeries, and long hospital stay predicted chronic neuropathic pain following burn injury.
Prognosis and complications
In a retrospective review of 1665 patients with acute burn injuries, authors developed probability estimates for the prediction of mortality based on a minimal set of well-defined variables. Three risk factors for death were identified: (1) age greater than 60 years, (2) more than 40% of body-surface area burned, and (3) inhalation injury. The mortality formula predicts a 90% mortality if all three risk factors were present (37). Approximately 75% of deaths following burn are related to wound infection. Burn patients are also at risk for developing sepsis secondary to pneumonia, catheter-related infections, and suppurative thrombophlebitis (10).
All survivors of burn injuries who had encephalopathic features showed complete neurologic recovery despite severe and prolonged symptoms (03). However, several burn patients suffer long term cognitive dysfunctions, like memory defect. Cognitive dysfunctions affect quality of life. Several reasons have been ascribed for the cognitive dysfunction in the post-burn period; cerebral inflammation, resulting in the destruction of blood-brain barrier, is considered a dominant reason (47). Neuropathy after burn injury can affect strength and function.
Psychiatric disorders are common among burn patients. A study observed that more than 50% of the survivors had some kind of psychiatric disorder 10 years after the burn (34). Posttraumatic stress disorder and depression are common psychiatric disorders in these patients. Body image dissatisfaction is also common in patients with burn injuries. Pain is another serious problem for burn survivors, particularly during the early phases of burn care (12).