(A) Decreased cardiac output
(B) Decreased systemic vascular resistance
(C) Increased peripheral blood flow
(D) Increased plasma volume
(E) Increased urine output

The correct response is Option A.

Patients with acute burn shock exhibit hemodynamic changes similar to those seen with hypovolemic shock. Management should focus on volume resuscitation and maintenance of tissue perfusion.

Following burn injury, cardiac output is decreased to 40% to 60% of normal as a result of decreased plasma volume and increased systemic vascular resistance. The release of myocardial depressants further diminishes cardiac output. In addition, angiotensin II, catecholamines, neuropeptide Y, and vasopressin all act on arterial smooth muscle to cause vasoconstriction.

Decreased plasma volume and capillary pressure occur as a result of factors released from both injured and uninjured tissue and excessive fluid shifting that occurs within the first hour after injury. Although the total body water level remains constant, there is an increase in cell water content of 70% to 80%. Volume resuscitation is required to maintain tissue perfusion; unfortunately, this will also exacerbate burn wound edema.

Decreased urine output is caused by inadequate fluid resuscitation and occurs as a response to decreased tissue perfusion and increased systemic vascular resistance. Aggressive volume replacement is required during the first 24 to 48 hours after injury to restore intravascular fluid.

References
1. Kramer GC, Lund T, Herndon DN. Pathophysiology of burn shock and burn edema. In: Herndon DN, ed. Total Burn Care. 2nd ed. Philadelphia, Pa: WB Saunders Co; 2002:79-85.
2. Salisbury RE. Thermal burns. In: McCarthy JG, ed. Plastic Surgery. Philadelphia, Pa: WB Saunders Co;1990;2:791-795.

A 26-year-old man who weighs 80 kg (176 lb) is brought to the emergency department three hours after sustaining superficial burns involving 20% total body surface area (TBSA), partial-thickness burns involving 15% TBSA, and full-thickness burns involving 25% TBSA. According to the Parkland formula, which of the following is the most appropriate method of fluid resuscitation for this patient?

(A) Administration of lactated Ringer’s solution 800 mL/hr for the next eight hours
(B) Administration of lactated Ringer’s solution 1300 mL/hr for the next five hours
(C) Administration of hypertonic saline solution 1000 mL/hr for the next 12 hours
(D) Administration of hypertonic saline solution 1500 mL/hr for the next five hours
(E) Administration of hypertonic saline solution 600 mL/hr for the next eight hours

The correct response is Option B.

In a patient who has second- and/or third-degree burn injuries that cover more than 20% of the total body surface area (TBSA), acute fluid resuscitation should be performed with administration of lactated Ringer’s solution during the initial 24 hours after injury. The Parkland formula is used to estimate the amount of fluid required. According to this formula, lactated Ringer’s solution 4 mL/kg/% TBSA burned should be administered during the first 24 hours. A total of 50% of the solution should be administered during the first eight-hour period and the remaining 50% over the next 16 hours.

An 80-kg patient who has burns involving 40% TBSA (second-degree burns involving 15% TBSA and third-degree burns involving 25% TBSA) will require 12,800 mL of fluid during the first 24 hours: 6400 mL during the first eight hours and 3200 mL in both the second and third eight-hour periods. Because he received no fluid during the first three hours immediately following injury, 6400 mL of lactated Ringer’s solution, or 1280 mL/hr, should be administered over the next five hours in order to adequately resuscitate the patient.

Vital signs and urine output should also be monitored in this patient to determine the success of resuscitation efforts.

Administration of hypertonic saline solution for fluid resuscitation in burn patients is controversial and is not universally recommended.

References
1. Cioffi WG. What’s new in surgery: burns and metabolism. J Am Coll Surg. 2001;192:241-254.
2. Demling RH. Fluid resuscitation. In: Bostwick JA, ed. The Art and Science of Burn Care. Rockville, Md: Aspen Publishers; 1987.

Silver sulfadiazine is administered topically to a patient with severe burns of the trunk and upper extremities. Which of the following is the most likely adverse effect?

(A) Hyponatremia
(B) Metabolic acidosis
(C) Metabolic alkalosis
(D) Neutropenia
(E) Pain with application

The correct response is Option D.

The most likely adverse effect of treatment of severe burns with topical application of silver sulfadiazine (Silvadene) is neutropenia, a self-limiting condition that is not thought to increase mortality in burn patients. Silver sulfadiazine is an effective treatment because it has a broad spectrum of activity and a low incidence of development of resistant organisms. Application is painless, and wound dressings are not required.

Hyponatremia occurs with administration of silver nitrate, a topical agent that is applied painlessly and has no resistance to organisms but penetrates tissue poorly. Metabolic acidosis and pain with application are adverse effects of topical administration of mafenide acetate (Sulfamylon), which provides excellent penetration of burn eschar. Metabolic alkalosis does not occur with application of silver sulfadiazine.

References
1. Petri WA. Antimicrobial agents. In: Hardman JG, Limbird LE, Gilman AG, eds. The Pharmacologic Basis of Therapeutics. New York, NY: McGraw-Hill, Inc; 2001:1171-1192.
2. Salisbury RE. Thermal burns. In: McCarthy JG, ed. Plastic Surgery. Philadelphia, Pa: WB Saunders Co; 1990;1:787-813.

A 24-year-old woman has been hospitalized for the past week because she has toxic epidermal necrolysis syndrome involving 90% of total body surface area (TBSA) with sparing of the lower legs and feet. She has been mechanically ventilated, and her hands have been splinted in a functional position except during passive occupational therapy. Following discontinuation of the ventilation, this patient’s hands should be splinted for how long to prevent contractures?

(A) 6 weeks
(B) 3 months
(C) 6 months
(D) 1 year
(E) No additional splinting is required

The correct response is Option E.

Toxic epidermal necrolysis syndrome is an uncommon systemic condition characterized by acute inflammation of the skin and mucous membranes and sometimes the bowel and respiratory epithelium. In patients who develop this life-threatening condition, the mortality rate ranges from 20% to 60%. Although it is thought to be caused by an adverse reaction to an antibiotic, anti-inflammatory agent, or anticonvulsant, other factors, including viral, bacterial, and fungal infections and neoplasms, have also been implicated.

Patients with toxic epidermal necrolysis syndrome have sloughing of the skin at the dermal-epidermal junction. However, because injury occurs only to the level of the superficial dermis, the skin will heal without contracture. Therefore, no additional splinting is required following discontinuation of ventilation. Long-term sequelae of this condition include complications involving the eyes and fingernails and changes in skin pigmentation.

References
1. Ducic I, Shalom A, Rising W, et al. Outcome of patients with toxic epidermal necrolysis syndrome revisited. Plast Reconstr Surg. 2002;110:768-773.
2. Sheridan RL, Schulz JT, Ryan CM, et al. Long-term consequences of toxic epidermal necrolysis in children. Pediatr. 2002;109:74-78.

An otherwise healthy 25-year-old man sustains second- and third-degree burns over 60% of total body surface area (TBSA). Which of the following immunologic responses is LEAST likely in this patient?

(A) Activation of helper T lymphocytes
(B) Increased circulating immunoglobulin G (IgG) level
(C) Increased interleukin-7 (IL-7) level
(D) Redistribution of T lymphocytes in the peripheral blood
(E) Suppression of circulating T lymphocytes

The correct response is Option B.

One immunologic response anticipated in this 25-year-old man who has sustained a 60% TBSA burn is impairment of cell-mediated immunity resulting from impairment of T-lymphocyte function. This manifests in burn patients as a delay in allograft rejection, suppression of the graft-versus-host response, and development of skin hypersensitivity reactions. Alterations in T-lymphocyte function include overall suppression of circulating T lymphocytes and a redistribution of T lymphocytes within peripheral blood and tissue compartments.

The initial response to significant burn injury is activation of helper T lymphocytes. B lymphocytes undergo functional changes resulting from the profound decrease in immunoglobulin levels following thermal injury. Although all classes of immunoglobulins are decreased, immunoglobulin G (IgG) levels exhibit the greatest decrease. This decrease can be attributed to plasma leakage, increased protein turnover, and decreased synthesis of IgG by B lymphocytes.

Interleukin-7 levels are increased during the first week after injury; this results in a decrease in the proliferative capacity of B lymphocytes.

References
1. Munster AM. Alteration of the immune system in burns and implications for therapy. Eur J Pediatr Surg. 1994;4:231-242.
2. Shankar R, Amin CS, Gamelli RL. Hematologic, hematopoietic, and acute phase response. In: Herndon DN, ed. Total Burn Care. 2nd ed. Philadelphia, Pa: WB Saunders Co; 2002:334-335.
3. Sparkes BG. Immunological responses to thermal injury. Burns. 1997;23:106-113.

A 26-year-old man is brought to the emergency department with significant pain in the forearms 90 minutes after spilling hydrofluoric acid on his forearms at work. Immediately after the accident, the affected areas were copiously irrigated with water.

The most appropriate initial management is topical administration of which of the following agents?

(A) Calcium gluconate gel
(B) Mineral oil
(C) Polyethylene glycol
(D) Silver nitrate
(E) Silver sulfadiazine

The correct response is Option A.

This patient has severe pain after sustaining chemical burn injuries from a hydrofluoric acid spill. Hydrofluoric acid is a strong chemical agent used primarily in industries such as electronics manufacturing and glassworks but also found in rust remover and other household items. The mechanism of action of this chemical involves binding of fluoride ions to intracellular calcium and magnesium. The fluoride ions leech calcium and magnesium from the bones, causing cellular death and producing severe pain that may not develop until several hours after initial exposure. In addition, the cellular death leads to the release of potassium, resulting in hypocalcemia, hypomagnesemia, and hyperkalemia. Any patient who has sustained hydrofluoric acid burns should be hospitalized and monitored closely because of the risk for arrhythmia associated with these electrolyte imbalances.

The most appropriate initial management is copious irrigation of the involved areas with water or saline followed by administration of calcium gluconate. This agent, which neutralizes the hydrofluoric acid by binding to the affected fluoride ions, can be applied topically as a gel, infused intra-arterially, or infiltrated beneath the burn eschar. Because relief of pain is a primary goal of treatment, analgesic and anesthetic agents should not be administered, as the patient will be unable to judge the pain-relieving effect of the calcium gluconate.

Application of mineral oil is appropriate for patients with phenol burns. Irrigation with water is contraindicated in these patients because it can dilute the phenol, resulting in deeper penetration and increased tissue damage. Creosol burns should be treated with topical application of polyethylene glycol. Silver sulfadiazine is used in the treatment of thermal burns involving disruption of the skin and soft tissues. Silver nitrate is effective for cauterization of pyogenic granulomas.

References
1. Achauer BM. The burned hand. In: Green DP, Hotchkiss RN, Pederson WC, eds. Operative Hand Surgery. 4th ed. New York, NY: Churchill Livingstone, Inc; 1999;2:2045-2060.
2. Concannon MJ. Common hand problems. In: Common Hand Problems in Primary Care. Philadelphia, Pa: Hanley & Belfus, Inc; 1999;8:161.
3. Concannon MJ, Hurov J, eds. Hand Pearls. Philadelphia Pa: Hanley & Belfus; 2002;104.
4. Hojer J, Personne M, Hulten P, et al. Topical treatments for hydrofluoric acid burns: a blind controlled experimental study. J Toxicol Clin Toxicol. 2002;40:861-866.
5. Lin TM, Tsai CC, Lin SD, et al. Continuous intra-arterial infusion therapy in hydrofluoric acid burns. J Occup Environ Med. 2000;42:892-297.
6. Sanz-Gallen P, Nogue S, Munne P, et al. Hypocalcaemia and hypomagnesaemia due to hydrofluoric acid. Occup Med(Lond). 2001;51:294-295.