A burn is a tissue injury resulting from excessive exposure to thermal, chemical, electrical, or radioactive agents [1]. The transfer of thermal energy over time is proportional to tissue damage.

In the United States, 60,000 to 80,000 people are hospitalized annually for burn care, but only 1,500 to 2,000 people sustain more than 40% total body surface area (TBSA) burns [2]. The elderly population is growing and contributes significantly to the increase in burn related hospitalizations. Among elderly victims, two thirds are flame burned, half have impaired judgment, and three fourths have a concomitant medical condition [2,3]. This population, typically debilitated by limited mobility, is particularly susceptible to large scald injuries, which can be devastating despite their clean appearance [4].

While all human tissue can be burned, the skin is most susceptible and is composed of essentially two distinct layers; the superficial epidermis, which is attached by a basement membrane to the foundation layer—dermis. The epidermis is of ectodermal origin and is invaluable for its vapor barrier, pigment, and immunological functions. While biologically very active, at approximately seven cell layers of keratinocytes, it has little mechanical integrity—the role of the dermis. Fortunately, the epidermis for practical purposes is “immortal” and when mechanically disrupted, will recover anew, without scar. In contrast, the dermis is derived from mesenchymal cells and provides the mechanical integrity to the skin, our “leather” so to speak, and has no native regenerative qualities. Dermis, when injured, repairs by way of scarring. Therefore, the essence of acute burn wound care is to sustain dermal viability.

The term burn will mean “burned skin of partial or full thickness depth.” It is essential to discern between partial thickness and full thickness injuries of the dermis (commonly called second and third degree burns), as the latter requires operative interventions [2,3]. Pale, leathery, and insensate skin are features of full thickness injury, while blistering, weeping, pink and painful burns characterize partial thickness injury. Currently, no technology supersedes clinical experience in making this distinction, however, laser Doppler imaging has been validated in some centers [5]. Furthermore, the injury is dynamic and partial thickness injuries can worsen (“convert”) to full thickness injuries for a variety of reasons.

When the burn injury coincides with blunt trauma, an evaluation for internal hemorrhage, closed head trauma, and long bone fractures is mandatory; the burned skin becomes a secondary concern [6]. Victim extrication from a closed space fire, such as in a bedroom, should make one expect an inhalational injury (see “Inhalation Injury”). The TBSA involved as partial and full thickness skin injury, age, comorbidities, and inhalational injury contributes to the morbidity and mortality of burn victims. Burns involving over 20% TBSA and those with inhalational injury of any burn size are at risk for burn shock (see “Burn Shock” section).

By the 1980s, a paradigm shift toward “early” (within 5 days) operative excision occurred because of the realization that the presence of burned tissue drives “burn shock” [6,7]. During the first half of the twentieth century burn wounds were treated with topical antibiotics and allowed to suppurate from the viable margin; subsequently, bacterial infections causing burn wound sepsis were commonplace [3,7]. The diminution of burn wound sepsis and advances in critical care borrowed from all disciplines have contributed to a remarkable LD50 for 90% TBSA burned in young people and 40% TBSA burned in the elderly [3,8] (Pruitt diagram; Fig. 166.1). Three clinical data points: age more than 60 years, TBSA burned more than 40%, and inhalational injury confer mortality rates over 90% when all three are present and 33% when two factors are present [8]. A rule of thumb with larger burns is a day in the ICU for each percentage of TBSA burned. Mortality usually occurs from multisystem organ failure secondary to sepsis. The substantial reduction in mortality at major burn centers has prompted research focus on improvement in quality of life [7]. Early transfer of patients to regional burn centers as per the guidelines of the American Burn Association has been shown to confer best outcomes [2,9].

Burn shock is a form of vasodilatory shock, akin to “systemic inflammatory response,” and creates an astounding volume requirement for the burned patient. It occurs most commonly with burns of at least 20% TBSA and is essentially universal in larger surface area burns. Increased vascular permeability and decreased capillary oncotic pressure combine to create severe edema, even in non-burned tissues. Kinins, serotonin, histamine, prostaglandins, and oxygen radicals are some of the vasoactive mediators released in response to burn injury and stimulate vascular permeability. Albumin is functionally lost into the interstitium thereby increasing extravascular oncotic pressure compounding the edema [3,10]. Unresuscitated patients perish from hypovolemic shock, historically likened to the demise from cholera; this association contributed to the understanding of the profound dehydration following burn injury [11].

While the resuscitation in burn shock may be conceptualized as optimizing the viability of the partial thickness (second degree) component of the burn injury, treatment is focused on intravascular volume repletion. Central shunting of blood compensates for the anhydremia, yet deprives the injured tissue of perfusion. Under perfusion deprives the partial thickness injury of essential nutrient delivery and gas exchange resulting in conversion of partial thickness injury to full thickness injury—which requires operative repair. Excessive resuscitation compounds tissue edema resulting in the same demise. It seems evolutionary biology has not accounted for intravenous fluid resuscitation, hence the response is maladaptive [12].

The patient’s TBSA burn and weight dictates their fluid requirements for the first 24 hours. A number of methods to calculate the TBSA burned exist. The “rule of nines” and the Lund-Browder scales are useful for contiguous injury, while the palmer surface of the patient’s hand, representing 1% TBSA, is used as a guide in noncontiguous injuries [3] (Fig. 166.2).

Fluid “requirement” should be thought of as that volume needed to optimize organ function; debate continues over appropriate endpoints of resuscitation—most clinicians accept ½ cc per kg per hour of urine output. If the urine output is more than 1 mL per kg per hour, then the rate of infusion should be decreased, this typically occurs by the third post burn day with the return of vascular integrity (See Fig. 166.4 Parkand formula). Thereafter, it is sufficient to limit the infusion and allow the concurrent insensible losses to correct volume overload—judicious diuresis with a loop diuretic may be employed. The timing and use of pressors requires clinical judgment in the face of hypotension despite adequate intravascular volume repletion. In patients with persistent oliguria, preexisting renal failure, or congestive heart failure, a pulmonary artery catheter is advised. While oliguria bodes poorly, excessive urine output should not be admired. If urine output is exceeding expectations, it is good practice to check the urine electrolytes, particularly for glycosuria and treat hyperglycemia accordingly [13]. Tight glucose control between 80 to 120 mg per dL with insulin is advocated [13].

The biological basis of burn wound conversion has not been fully elucidated. It is known that necrosis occurring from direct cellular damage and ischemia is not the only pathway. With cell death in evidence, the presence of apoptotic populations has been identified [14]. Macrophage inducible nitric oxide synthase may be an inciting factor in such apoptosis and its inhibition seems to limit apoptosis in animal models [14,15].

Central venous access is generally necessary because extremity edema makes peripheral access tenuous and is ideally, but not essentially, placed through non-burned tissue.

A number of resuscitative regimens have been advocated, none proven superior to date. Most are iterations of an isotonic solution in the first 12 hours of shock [3,11,15,16].

The use of colloid seems ill advisable in the first 12 hours after injury, as it seems to aggravate water loss into the pulmonary interstitium and potentiates pulmonary edema [3,15,16]. The commonest colloids are albumin, the most popular, and fresh frozen plasma (FFP). Proponents of albumin value its high oncotic pressure and maintenance of intravascular volume. Those against, argue that albumin is lost into the interstitium worsening edema there, possibly aggravating pulmonary edema. Again, the evidence suggests this risk is most pronounced within the first 12 hours post injury. Albumin is generally not used in patients with serum concentrations above 2.5 mg per dL. While FFP has less oncotic potential than albumin it may have a favorable immunomodulatory benefit, resulting in a truncation of the capillary leak associated with burn shock [3]. Both groups state that the use of colloid reduces the total volume of resuscitation and consequently protects against the detriments of excessive water administration. No level I evidence exists for the resuscitative fluid of choice [10]. A prospective, multicenter trial is needed to answer this question [10].

The pathophysiological similarities between septic shock, systemic inflammatory response, and burn shock may have a common pathway that could be interrupted to improve outcomes [17]. Beta blockade, antihistamines, FFP, generous narcosis, nonsteroidal anti-inflammatory agents, glucocorticosteroids and recently, drotrecogin alfa are amongst the many approaches investigated to mitigate this cellular “hysteria” [2,17]. None of these approaches have proven superiority in multicenter prospective trials to date.

The GI tract is an underutilized resuscitative venue and enteral hydration seems to have been forgotten with the advent of improved intravenous therapy [18]. Enteral nutrition and resuscitation may begin on the day of injury with the caution that patients in shock, requiring vasopressors, can develop bowel ischemia and enteral feeds may increase the metabolic needs of the gut, contributing to bowel ischemia and necrosis. Patient’s not tolerating enteral feeds or those with abdominal hypertension (see “Abdominal Compartment Syndrome” section) should be given TPN; this is uncommonly necessary.

Adrenal insufficiency should be suspected when volume repleted hypotension persists despite pressors and is further suggested by concurrent hyponatremia and hyperkalemia. While the characterization of adrenal insufficiency is more expansive in the septic shock literature, numerous case reports and some prospective data support its presence in thermally injured patients. A high mortality exists when disturbances in the hypothalamic-pituitary-adrenal axis are found early in a patient’s burn shock course [19,20]. One need not await the results of a corticotropin stimulation test in the face of circulatory collapse and glucocorticoid supplementation should be initiated. In questionable cases, a corticotropin stimulation test is confirmatory and not skewed by Decadron, which enhances vascular tone but has no mineral corticoid activity unlike hydrocortisone. A single blood cortisol of less than 15 μg/dL, in a stressed patient, is suggestive of insufficiency, and it is probably wise to supplement. Glucocorticoids are known to unfavorably affect skin engraftment, and this risk must be weighed against the patients’ circulatory failure. Vitamin A supplementation seems to limit the unfavorable wound healing delays and atrophy seen with glucocorticosteroid therapy [20,21].