Burns represent a unique but common traumatic injury that is second only to motor vehicle acci-dents as the leading source of accidental death. Temperature and duration of heat contact determine the extent of burn injury. Children (because of a high body surface area to body mass ratio) and the elderly (whose thinner skin allows deeper burns from simi-lar thermal insult) are at greater risk for major burn injury. The pathophysiological and hemodynamic responses to burn injuries are unique and warrant specialized burn care that can be optimally provided only at burn treatment centers, particularly when more than 20% of a patient’s body surface area is involved in second- or third-degree burns. A basic understanding of burn pathophysiology and of resus-citation requirements, especially early initiation of therapies such as oxygen administration and aggres-sive fluid resuscitation, will improve patient survival.
Burns are classified as first, second, or third degree. First-degree burns are injuries that do not penetrate the epidermis (eg, sunburns and superficial thermal injuries). Fluid replacement for these burns is not necessary, and the area of first-degree burns should not be included in calculating fluid replace-ment requirements when extensive, more significant burns are also present. Second-degree burns are par-tial-thickness injuries (superficial or deep) that pen-etrate the epidermis, extend into the dermis for some depth, and are associated with blistering. Fluid replacement therapy is indicated for patients with second-degree burns when more than 20% of total body surface area (TBSA) is involved. Skin grafting also may be necessary in some cases of second-degree burns, depending upon size and location of the wounds. Third-degree burns are those in which the thermal injury penetrates the full thickness of the dermis. Nerves, blood vessels, lymphatic channels, and other deep structures may have been destroyed, creating a severe, but insensate, wound (although surrounding tissue may be very painful). Debridement and skin grafting are nearly always required for recovery of patients from third-degree burns.
Major burns (a second- or third-degree burn involving 20% TBSA) induce a unique hemo-dynamic response. Cardiac output declines by up to 50% within 30 minutes in response to massive vaso-constriction, inducing a state of normovolemic hypoperfusion (burn shock). Survival depends on restoration of circulating volume and infusion of crystalloid fluids according to recommended proto-cols . This intense hemodynamic response may be poorly tolerated by patients with significant underlying medical conditions. If intra-venous fluid therapy is provided, cardiac function returns to normal within 48 h of the injury, then typically progresses to a hyperdynamic physiology as the metabolic challenge of healing
begins. Plasma volume and urine output are also reduced early on after major burn injuries.In contrast to fl uid management for blunt and penetrating trauma, which discourages use ofcrystalloid fluids, burn fluid resuscitation empha-sizes the use of crystalloids, particularly lactated Ringer’s solution, in preference to albumin, hydroxy-ethyl starch, hypertonic saline, and blood. Following burn injuries, kidney failure is more common when hypertonic saline is used during initial fluid resusci-tation, death is higher when blood is administered, and outcomes are unchanged when albumin is used in resuscitation.
Fluid resuscitation is continuous over the first 24 h following injury. Two formulas are commonly used to guide burn injury fluid resuscitation, the Parkland and the modified Brooke. Both require an understanding of the so-called rule of nines (Figure 39–6) to calculate resuscitation volumes. The (adult) Parkland protocol recommends 4 mL/kg/% TBSA burned to be given in the first 24 h, with half the volume given in the first 8 h and the remaining amount over the following 16 h. The (adult) modi-fied Brooke protocol recommends 2 mL/kg/% TBSA,with administration of half the calculated volume beginning in the first 8 h and the remainder over the following 16 h. Both formulas use urine output as a reliable indicator of fluid resuscitation, target-ing (adult) urine production of 0.5–1.0 mL/kg/h as indications of adequate circulating volume. If adult urine output exceeds 1.0 mL/kg/h, the infusion is slowed. In both protocols, an amount equal to half the volume administered in the first 24 h is infused in the second 24-h period following injury, with con-tinued attention to maintaining adult urine output at 0.5–1.0 mL/kg/h. The formula for fluid resuscitation of children is the same as that for adults, but children weighing less than 30 kg should receive 5% dextrose in Ringer’s lactate as their resuscitation fluid and tar-get urine output should be 1.0 mL/kg/h. The target urine output for infants younger than 1 year of age is 1–2 mL/kg/h.
The Parkland and modified Brooke protocols both use urine output as an indicator for adequate fluid resuscitation. However, circumstances may arise in which the volume of fluid administered exceeds the intended volumes. For example, initial fluid resusci-tation volumes may be miscalculated if first-degree burns are mistakenly incorporated into the TBSA value. Prolonged use of sedatives and sedative infu-sions may also result in hypotension that is treated with additional fluids rather than vasoconstrictors. The phenomenon of fluid creep occurs when intra-venous fluid therapy volumes are increased beyond intended calculations in response to various hemo-dynamic changes. Fluid creep is associated with abdominal compartment syndrome and pulmo-nary complications, which represent resuscitation morbidity.
Abdominal compartment syndrome is a risk for pediatric patients, adults with circumferential abdominal burns, and patients receiving intrave-nous fluid volumes greater than 6 mL/kg/% TBSA. Intraabdominal pressure can be determined by measuring intraluminal bladder pressure using a Foley catheter. The transducer is connected to a 3-way stopcock at the point where the Foley cath-eter connects to the drainage tube. After the trans-ducer is zeroed at the pelvic brim, 20 mL of fluid is instilled to distend the bladder. Intraabdominal pressure readings are taken 60 s after fluid installa-tion, allowing the bladder to relax. Intraabdominal pressures exceeding 20 mmHg warrant abdominal cavity decompression. However, an abdominal sur-gical procedure places the burn patient at high risk for intraabdominal Pseudomonas infection, particu-larly if the laparotomy incision is near burned tissue.
Excessive resuscitative fluid volumes are associated with an increased incidence of pneumonia. Patients with severe burns frequently have pulmonary injury related to the burn. Decreased tracheal ciliary activ-ity, the presence of resuscitation-induced pulmo-nary edema, reduced immunocompetence, and tracheal intubation predispose the burn patient to pneumonia. Abdominal compartment syndrome can have an adverse impact on pulmonary function. Intravenous fluid administration volumes must be monitored closely and documented to be consistent with American Burn Association recommendations (ie, the Parkland or modified Brooke protocol).Fluid administration that exceeds recommenda-tions warrants careful review of the rationale for the increased fluid therapy volume, including assess-ment of possible causes for hypotension (eg, sepsis) or reduced urine output (eg, abdominal compart-ment syndrome).
Carbon monoxide poisoning should be con-sidered in all serious burn injury cases, as wellas with lesser TBSA burns occurring in enclosed spaces. Unconsciousness or decreased levels of con-sciousness following burn injuries should be pre-sumed to represent carbon monoxide poisoning, prompting endotracheal intubation and mechanical ventilation with high inspired concentration oxy-gen therapy. Carbon monoxide binds to hemoglo-bin with an affinity approximately 250 times that of oxygen. The resultant carboxyhemoglobin (HbCO) leaves less hemoglobin available to bind with oxygen (HbO2) and shifts the O2–Hb dissociation curve to the left; both of these processes result in impaired availability of oxygen molecules at the local tissue level. Pulse oximetry provides a falsely elevated indication of oxygen saturation in the setting of carbon monoxide exposure because of its inability to distinguish between HbO2 and HbCO. If carbon monoxide poisoning is suspected, HbCO can be directly measured via arterial or venous blood gas analysis. HbCO concentrations below 10% are usu-ally not clinically significant. However, with high inspired oxygen concentrations, HbCO levels of 20% correspond to a hemoglobin oxygen satura-tion of 80%; intubation and mechanical ventilation is indicated in such circumstances to improve local tissue oxygenation and enhance carbon monoxide elimination. Death from carbon monoxide poison-ing occurs at HbCO levels of 60%.
A primary characteristic of all burn patients is an inability to regulate temperature. The resuscitation environment must be maintained near body tem-perature through the use of radiant warming, forced air warming devices, and fluid warming devices.
Assessment of the patient begins with inspec-tion of the airway. Although the face may be burned (singed facial hair, nasal vibrissae), facial burns are not an indication for tracheal intubation. The need for urgent airway management, mechanical venti-lation, and oxygen therapy is indicated by hoarse voice, dyspnea, tachypnea, or altered level of con-sciousness. Arterial blood gases should be obtained early in the treatment process to assess HbCO levels.
Mechanical ventilation should be adjusted to afford adequate oxygenation at the lowest tidal volumes.
Tracheal intubation in the early period follow-ing burn injury (up to the first 48 h) can be facili-tated with succinylcholine for paralysis. In patients with significant burns (>20% TBSA), injuries and disruption of neuromuscular end plates occur fol-
lowed by upregulation of acetylcholine receptors.
Beyond 48 h after a major burn, succinylcho-line administration is likely to produce potentially lethal elevation of serum potassium levels. Analgesia for burn patients is challengingbecause of concerns about opioid tolerance and psy-chosocial complications. Multimodal approaches are often advantageous. Regional analgesia may provide benefit, although in the early postburn period this technique may mask the symptoms of compartment syndrome or other clinical signs and symptoms.
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