Wound debridement is not an emergency, but should be completed no later than 24 h after injury, and is usually performed within hours of admission to a burn center. Wound care should be performed in a dedicated hydrotherapy (shower) facility or in an operating room [28]. Initial wound care is directed at thorough cleansing of the patient using a surgical antiseptic solution, preferably chlorhexidine gluconate; aggressive removal of all foreign material and debris; debridement of blisters, exudate, etc. Burns are then dressed with an antimicrobial cream or dressing. The burn creams of choice are silver sulfadiazine (Silvadene, others) and mafenide acetate (Sulfamylon). An alternative is the use of silver-impregnated dressings.

The extremities are vulnerable to the effects of thermal injury and to the edema formation which subsequently occurs. Evaluation of a burned extremity includes a thorough neurovascular exam. Exercise and elevation combat edema formation and maintain range of motion. By decreasing the elasticity of the skin and by causing edema in the underlying tissue, a burn may exert a tourniquet-like effect and occlude venous outflow and arterial inflow. Progressive diminution in the Doppler signal in an extremity with circumferential deep burns is an indication for escharotomy, performed at the bedside with scalpel or electrocautery through the full thickness of the burned skin and into the subcutaneous tissue (Fig. 30.1). An unusual indication for cervical escharotomy is the patient with full thickness burns of the neck and increased ICP [11].

In patients who have sustained high-voltage electric injury, edema formation beneath the investing fascia typically produces a stony hardness to palpation of the involved muscle compartment, and may be associated with distal paresthesias. In the presence of such findings, fasciotomy, not just escharotomy, may be necessary. Spinal cord injury with either immediate or delayed onset of symptoms has been reported in patients with high-voltage electric injury. Immediate-onset symptoms often clear within 24 h. Those deficits of delayed onset are more apt to be permanent; they range from local paresis to quadriplegia, with motor deficits more common than sensory loss. Clinical presentation may include ascending paralysis or transverse myelitis, and can even resemble amyotrophic lateral sclerosis [29].

Even in the absence of TBI, patients with extensive burns may sustain disruption of the blood–brain barrier (BBB) and consequent cerebral edema during the resuscitation period. Gueugniaud et al. placed epidural ICP monitors in 32 patients with TBSA > 60 % and no history of head injury. Peak ICP values of 31.4 ± 10.4 mm Hg were observed, on average, on day 2 postburn. Mean cerebral perfusion pressure (CPP) reached a nadir of 41.0 ± 10.2 mm Hg, also on day 2. Survival was associated with lower ICP and high CPP [30]. Shin and colleagues measured ICP and cerebral blood flow (CBF) in 8 sheep with 70 % TBSA burns . During the immediate postburn period, CBF was maintained despite a decrease in cardiac output. At the end of the 6 h study, CBF decreased, ICP increased, and cerebrovascular resistance increased. Increased water content was observed in the brain at necropsy. The authors speculated that the mechanism for these changes could include impairment of the BBB, loss of cerebral autoregulatory function, and/or a decrease in the serum sodium concentration induced by large-volume resuscitation with lactated Ringer’s solution [31].

Ding et al. conducted a series of experiments in a rat model directed at understanding the mechanism for postburn neurological complications. Thermal injury caused increased permeability of the BBB to labeled albumin [32]. In the same model, thermal injury caused increases in m-RNA expression of TNF alpha, IL-1 beta, and ICAM-1 in brain homogenates at 3 h, followed by increases in circulating levels at 7 h [33]. Brain edema and increased BBB permeability were associated with expression of matrix metalloproteinase 2 (MMP-2) and MMP-9 in the brain; these gelatinases act to degrade the basal lamina of the BBB [34, 35]. Inhibition of TNF alpha or of MMP-9 protected against the increase in BBB permeability and brain edema, while preserving the basal laminar proteins that comprise the BBB [36]. In another study, there was increased expression of tissue plasminogen activator (tPA) and of urokinase plasminogen activator (uPA) with BBB disruption and brain edema; tPA and uPA may upregulate MMP-9 [37].

Gatson and colleagues evaluated the role of estrogen in protecting against burn-induced brain inflammation in rats. Brain cytokine levels (TNF alpha, IL-1 beta, and IL-6) were much higher than systemic levels, suggesting increased local production. 17 beta-estradiol decreased cytokine levels in the brain, and exerted an anti-apoptotic effect. The possible clinical impact (e.g. on cognitive function) was not assessed [38].

Clinically, burnt patients present with both acute and chronic disturbances of CNS function. Acutely, delirium afflicts many critically ill burn patients and complicates their ICU management. Seventy-seven percent of mechanically ventilated burn patients were diagnosed with delirium using the Confusion Assessment Method in the ICU (CAM-ICU). Benzodiazepine use increased delirium risk [39]. Chronically, approximately one-third of patients admitted with serious burns develop posttraumatic stress disorder (PTSD) . Improved pain control, manifested by increased use of opioids, helps reduce PTSD [40]. Studies from the recent wars in Iraq and Afghanistan showed that PTSD was more common in patients injured in explosions who had both TBI and burns [41]. The mechanism for this association is unknown.

Taken together, these clinical and basic science studies indicate the vulnerability of the CNS to cutaneous burns and burn-associated critical illness. Furthermore, they heighten the level of concern which should attend the patient with burns and TBI.

The hierarchical regionalization of burn care in both the civilian and military medical communities involves the transfer of burn patients with TBI to burn and trauma centers, if necessary by air. Johannigman and colleagues studied the effect of the stresses encountered during long-distance aeromedical transfer on ICP as monitored with intraventricular catheters in 11 critically ill combat casualties with TBI. ICP variability (±50 % of baseline) and instances of ICP > 20 mm Hg were observed throughout flight, but some patients experienced large increases in ICP related to takeoff and landing. ICP variability appeared to be patient-specific, that is, high in some and virtually absent in others. The authors attributed this to the adequacy of sedation and to the extent of previous surgical treatment. To minimize ICP fluctuation, they recommend loading casualties with the head towards the nose of the aircraft, with the head of the litter elevated by at least 30 degrees; adequate sedation; and venting of the intraventricular catheter as needed [42]. For patients with burns and TBI, the intensity of monitoring and the extent of intervention will be dictated by the time postburn and the fluid status of the patient.

In conclusion, the combination of extensive thermal injury and TBI is a particularly challenging scenario. Close collaboration between all members of the multidisciplinary burn and trauma teams is needed to achieve optimal outcomes. Emphasis must be placed on minimizing resuscitation volume, with assiduous monitoring of ICP to prevent cerebral ischemia and to reduce cerebral edema in the ICU and during aeromedical and other transfer procedures. Attention should also be directed toward control of pain and anxiety, maintenance of circulation in muscle compartments, adequate ventilation, early excision and grafting of the burn wound, and prompt institution of rehabilitation programs to maintain and restore function.