Escharotomies, fasciotomies and carpal tunnel release in burn patients--review of the literature and presentation of an algorithm for surgical decision making.

Escharotomies are usually performed in patients with circumferential third degree burns of the extremities or anterior trunk. Fasciotomies are recommended for patients who sustained high voltage (or associated crush) injuries, with entrance or exit wounds in one or more extremities. Carpal tunnel release is practiced routinely in some services for cases of electrical injury. We have reviewed the literature which provides relatively little information as to when should these procedures actually be performed and what would happen if they were not done. We present a series of patients treated at our institution when an algorithm was used for surgical decision making as to when (or not) to operate (perform an escharotomy, a fasciotomy or a carpal tunnel release), based on clinical signs and monitoring alternatives, using the oximeter and the Doppler flowmeter. 13 938 burn patients were treated at our institution during the year of 2005. Of these, 571, with an average of 22.3 % TBSA, were treated as inpatients. Of these, 58 (10.3 %) had circumferential or electrical burns of one or more extremities. Patients were monitored hourly from admission and decision to operate was based on clinical signs and in absent or below 90 % oximetry, regardless of Doppler flow signs. 68 % were males, 6 (11.3 %) patients had immediate escharotomies, while 4 (7.5 %) had immediate fasciotomies. 2 of these patients were operated regardless of positive Doppler sign but no oximetry. All patients recovered oximetry over 90 % immediately after the operations. 3 patients had negative Doppler sign but oximetry > 90 % and were not operated. 3 patients had carpal tunnel releases based on oximetry < 90 % and symptoms of compression of the median nerve. Patients who were not operated fared well with no signs or symptoms of impairment of circulation or nerve damage up to their 3 and 6 months reevaluations.

Chemotactic mediator requirements in lung injury following skin burns in rats.

Partial-thickness skin burns have been shown to induce neutrophil-dependent microvascular injury both locally (skin) and systemically (lung). In the present study, interventional measures to block inflammatory chemoattractants were employed to define the pathophysiologic role of these mediators in the development of secondary lung injury following thermal injury of skin. Rats were treated with blocking antibodies to either C5a or to the alpha-chemokines, keratinocyte-derived cytokine (KC), or macrophage inflammatory protein-2 (MIP-2). To study the role of platelet activating factor, a receptor antagonist (PAF-Ra) was utilized. The development of lung vascular injury following thermal injury to skin was significantly attenuated by treatment with anti-C5a (84%), anti-KC (67%), and anti-MIP-2 (77%), but treatment with PAF-Ra had no protective effects. Protective interventions were paralleled by significant reductions in the tissue buildup of myeloperoxidase. When bronchoalveolar lavage fluids from thermally injured rats were evaluated, elevations in TNF;ZA and IL-1 were found and were determined to be C5a-dependent (but unaffected by treatment with PAF-Ra). These studies indicate that lung tissue injury after thermal skin burns is dependent on chemotactic mediators. The data also suggest that lung expression of TNFalpha and IL-1 after thermal injury of skin is C5a-dependent.

Role of chemotactic factors in neutrophil activation after thermal injury in rats.

Acute thermal trauma is well known to produce evidence of a "systemic inflammatory response" in vivo, as manifested by evidence of complement activation, appearance in plasma of a variety of inflammatory factors, and development of multi-organ injury. The current studies were focused on acute thermal injury of rat skin and factors responsible for accompanying activation of blood neutrophils. Acute thermal injury of rat skin resulted in a time-dependent loss of L-selectin and up-regulation of Mac-1 (CD11b/CD18) on blood neutrophils, with no changes in LFA-1 (CD11a/CD18). The loss of L-selectin was prevented by blockade of C5a but not by blockade of the alpha-chemokine, macrophage inflammatory protein-2 (MIP-2). C5a, the alpha chemokines, MIP-2 and keratinocyte-derived cytokine (KC), and platelet activating factor (PAF) contributed to up-regulation of blood neutrophil Mac-1. Blocking interventions against these mediators also blunted the degree of neutropenia developing after thermal trauma. These data suggest that activation of blood neutrophils after thermal trauma is related to the role of several chemotactic mediators. These studies may provide clues regarding factors responsible for development of the "systemic inflammatory response syndrome" after thermal injury in the experimental model employed.

Requirement for C5a in lung vascular injury following thermal trauma to rat skin.

Previous studies in rats have shown that deep second degree dermal burns, involving 28-30% of total body surface area, result in systemic complement activation, appearance in plasma of chemotactic activity, sequestration of blood neutrophils in lung capillaries, and development of neutrophil-dependent dermal vascular and lung vascular injury. Although blockade of complement activation or depletion of complement before skin burns has resulted in significant attenuation of tissue injury both locally and distally (in lung), a role for C5a in these events is unclear. In the following studies, we demonstrate the presence of C5a and neutrophil chemotactic activity in serum and in lung homogenates after thermal injury. C5a has also been found in bronchoalveolar lavage fluids of thermally injured animals. Treatment of animals with a polyclonal neutralizing rabbit antibody to rat C5a was lung protective. The protective effects of the antibody (anti-C5a) were associated with diminished vascular permeability changes, as well as reduced tissue build-up of myeloperoxidase. Anti-C5a also prevented up-regulation of lung vascular ICAM-1 (intercellular adhesion molecule-1) in skin-burned rats. These observations indicate that C5a is essential for development of neutrophil accumulation and vascular permeability increases in distant (lung) organs after thermal trauma to skin. The protective effects of anti-C5a in lung, appear to be related to prevention of up-regulation of vascular ICAM-1. Accordingly, C5a may represent a target for clinical approaches in the treatment of organ injury following thermal trauma.

Inhibition of neutrophil chemotaxis by plasma of burned patients: effect of blood transfusion practice.

Incubation of normal human neutrophils with plasma from burned patients markedly reduced the ability of the cells to respond to a chemotactic stimulus in vitro. Previous transfusion of the patients with packed red blood cells did not alter the inhibited locomotion of neutrophils, whereas transfusion with normal plasma alone attenuated or even abolished the inhibitory activity. The finding provides direct evidence for the involvement of circulating suppressive factors in neutrophil chemotaxis, rendering burned patients more susceptible to infections. In addition, it stresses the relevance of plasma transfusion in clinical management and infection control following thermal injury.