Burns

Michael Tjeuw
A 45-year-old man who was smoking in bed sustained 40% second- and third-degree
burns over his face, neck, chest, and upper extremities. He had a history of hypertension,
angina, and angioplasty of the left main coronary artery 1 year ago. He has smoked three
packs of cigarettes per day for 20 years and he drinks alcohol daily. He is scheduled for
tangential excision of eschar on the third day. Blood pressure, 190/100 mm Hg; heart rate,
120 beats per minute; and weight, 110 kg.

A. Medical Disease and Differential Diagnosis

1. How do you classify the burn injury?
2. How do you express the extent of the burn injury?
3. Should the "rule of nines" be used in children?
4. What is the definition of a major burn according to the American Burn Association?
5. What functions do the skin perform?
6. What pathophysiologic changes accompany major thermal injury?
7. Name some of the known mediators released with thermal injury. What are the responses
to those mediators?
8. What is the prognosis for this patient? What major factors affect his prognosis?
9. What are the most common causes of death?
10. Does this patient have a smoke inhalation burn? How do you make the diagnosis?
11. Could you name some of the chemical products of combustion?
12. What is carbon monoxide poisoning? How do you treat carbon monoxide poisoning?
13. What resuscitative measure would you institute immediately in this patient wiih 40%
burns?
14. What fluid formula would you use?
15. What cardiovascular changes typify the burn injury?
16. Is the immune system affected in burn injury? How?
17. What hematologic changes occur in burn injury?
18. What changes occur in liver function? What are the anesthetic implications of such
changes?
19. What are Curling ulcers? How can they be prevented?
20. What complications are associated with electrical burns?

B. Preoperative Evaluation and Preparation

1. What preoperative preparations would you order? What are particular concerns in this
patient?
2. What are the various operative and management options available for severely burned
patients?
3. What is tangential excision split-thickness skin graft? What are the principles of this
grafting technique?
4. What are the advantages and disadvantages of early tangential excision split-thickness skin
graft?
5. What is this patient's mean arterial blood pressure? How do you calculate it?
6. Are you concerned about this patient's blood pressure? What treatment would you
institute?
7. How do a2-adrenergic agonists work?
8. This patient was ventilated with respirator settings of tidal volume 1,200 mL; respiratory
rate, 20 breaths per minute; FIO2, 60%; and positive end-expiratory pressure, 10 cm H2O.
Arterial blood gas analyses showed the following: pH, 7.25; P02, 56 mm Hg; Pco2, 60 mm
Hg; and 02 saturation, 80%. How would you interpret these arterial blood gas analysis
results? What are the possible causes of high Pco2 and low P02?
9. How do you calculate oxygen content and oxygen delivery? What factors govern the
oxygen delivery to the tissues? What are the causes of tissue hypoxia?
10. What are the symptoms and signs of alcohol withdrawal? Are you concerned that this
patient could develop delirium tremens?
11. How would you prevent the adverse effects of alcohol withdrawal?

C. Intraoperative Management
1. What monitors would you use in the operating room?
2. What information can be obtained from an arterial line and a pulmonary artery catheter?
How are these calculations performed?
3. If the patient had not been incubated, how would you proceed with the anesthetic
induction?
4. Why is awake intubation considered the safest?
5. What anesthetic agents would you use? Discuss inhalation versus intravenous agents.
6. Why are you concerned about the patient's body temperature? What is normothermia for a
burned patient?
7. How is temperature best maintained?
8. What derangements occur with hypothermia?
9. What muscle relaxant would you use?

10. Why is succinylcholine contraindicated in burned patients? For how long should it be
avoided?
11. What other adverse effects are associated with succinylcholine?
12. How are the doses of nondepolarizing muscle relaxants affected by burn injury?
13. How are muscle relaxants such as curare, pancuronium, cisatracurium, vecuronium,
doxacurium, rocuronium, and pipecuronium metabolized and eliminated? Which of them has
significant histamine release?
14. What is the difference between metabolism and elimination of drugs?
15. What complications are associated with electrical burns?

D. Postoperative Management
1. How would you monitor this patient during transport?
2. What is meant by diffusion hypoxia? How do you prevent it?
3. Why do patients often shiver in the recovery room on emergence from anesthesia?
4. Discuss the causes of oliguria in the recovery room.

A. Medical Disease and Differential Diagnosis

A.1. How do you classify the burn injury?
Burns are classified as first, second, or third degree. First-degree, or superficial, burns are
characterized by simple erythema of the skin, with only microscopic destruction of
superficial layers of the epidermis. Second-degree, or partial thickness, burns extend through
the epidermis into the dermis. Even when most of the epithelium is destroyed, regeneration
may occur from epithelial cells surrounding hair follicles or sweat glands. Third-degree, or
full-thickness, burns are characterized by total, irreversible destruction of all the skin, dermal
appendages, and epithelial elements. Spontaneous regeneration of epithelium is not possible
and the burns are described as full-thickness burns. Such burns require the application of skin
grafts if the development of scar tissue is to be avoided. Fourth-degree burns refer to deep
thermal injuries involving fascia, muscle, or bone (Table 54.1).
MacLennan N, Heimbach DM, Cullen BF. Anaesthesia for major thermal injury.
Anesthesiology 1998;89:749-770.
A.2. How do you express the extent of the burn injury?
The extent of the burn injury is expressed as a percentage of the total body surface area
(TBSA) displaying either second- or third-degree burns. It is most commonly estimated by
the "rule of nines" (Fig. 54.1). The major anatomic portions of the adult may be divided into
multiples of 9% of the body surface area. The proportion of each of these areas is estimated
and the sum represents the percentage of the TBSA burn. The percentages of body surface are
as follows:

Head and neck9%

Right upper extremity 9%

Left upper extremity 9%

Right lower extremity 18%

Left lower extremity 18%

Anterior trunk 18%

Posterior trunk18%

Perineum

1%

Table 54.1. Classification of Burn Depth

CLASSIFICATION
BURN DEPTH
OUTCOME
Superficial
First degree
Confined to epidermis
Heals spontaneously
Partial thickness
Second degree
Superficial dermal burn
Epidermis and upper dermis
Heals spontaneously
Deep dermal burn
Epidermis and deep dermis
Requires excision and grafting for rapid return of function
Full thickness
Third-degree burn
Destruction of epidermis and dermis
Wound excision and grafting required
Some limitation of function and scar formation
Fourth-degree burn
Muscle, fascia, bone
Complete excision required.

Limited function
(From MacLennan N. Heimbach DM. Cullen BF. Anesthesia for major thermal injury.
Anesthesiology 1998;89:749-779, with mission.)

Figure 54.1. The rule of nines for determining the percentage of body surface area burned in
adults. (From MacLennan N, Heimbach DM, Cullen BF. Anesthesia for major thermal injury.
Anesthesiology 1998;89:749-770, with permission.)
MacLennan N, Heimbach DM, Cullen BF. Anesthesia for major thermal injury.
Anesthesiology 1998; 89:749-770.

A.3. Should the "rule of nines" be used in children?

The "rule of nines" may not be used to estimate TBSA burns in children because the surface
area of the head and neck in children is significantly larger than 9%, and that of the lower
extremities is smaller. More precise methods, such as the Lund and Browder chart, may be
used to provide greater accuracy by taking into account the changing proportions of the body
from infancy to adulthood (Fig. 54.2).
MacLennan N, Heimbach DM, Cullen BF. Anesthesia for major thermal injury.
Anesthesiology 1998; 89:749-770.

A.4. What is the definition of a major burn according to the American Burn Association? The
American Burn Association defines a major burn as follows:

Full-thickness burns more than 10% TBSA

Partial-thickness burns more than 25% in adults or 20% at extremes of age

Burns involving face, hands, feet, or perineum

Inhalation, chemical, or electrical burns

Burns in patients with serious preexisting medical disorders

Adapted from the American Bum Association Injury Severity Grading System.

Relative percentages of areas affected by growth

(AGE IN YEARS)
A: half of head
B: half of thigh
C: half of leg

Figure 54.2. Diagram and table for determining the percentage of body surface area burned in
children. (From MacLennan N. Heimbach DM, Cullen BF. Anesthesia for major thermal
injury. Anesthesiology I 998;89:749-770, with permission).

A.5. What functions do the skin perform?

The skin is the largest organ of the body, with surface area ranging from 1.3 to 2.0 m2 in the
adult. It protects the invasion of microorganisms. It performs other functions in thermal

regulation, fluid and electrolytes homeostasis, and sensation (touch, temperature, pain). The
skin also has metabolic functions including vitamin D metabolism.
Herndon DN, ed. Total burn care. Philadelphia: WB Saunders, 1996:63-64.

A.6. What pathophysiologic alterations accompany major thermal injury?

The pathophysiologic alterations that accompany major thermal injury are complex. When
destroyed, skin, which is the largest organ of the body, has a systemic impact. Thermal
regulation, fluid and electrolyte homeostasis, and protection against bacterial infection are
affected. Immediately after a burn injury, mediators released from the burn wound contribute
to local inflammation and edema. A large amount of fluid is lost from the vascular
compartment into the burn wound. Sequestration in the extravascular space results in
significant hemoconcentration. Increased secretion of antidiuretic hormone (ADH) may
decrease or even completely inhibit urinary output. It has been shown that during the first 4
days after a bum, an amount of albumin equal to twice the total plasma albumin content is
lost through the wound. Half of this fluid remains sequestered in the extravascular space for 3
weeks or more before returning to the intravascular compartment.
The metabolic rate is markedly increased after the burn injury. Depending on the size of the
burn, the increase in metabolic rate can be doubled or tripled with a proportionate increase in
oxygen consumption and carbon dioxide production. This hypermetabolic state will continue
for weeks or months until full skin coverage is achieved and the tissue repair processes are
complete. Cardiac output is often decreased in patients with major burns. This decrease is not
entirely explained by the rapid reduction in circulating blood volume. It has been shown that
a circulating myocardial-depressant factor exists in both humans and laboratory animals.
Changes in vascular integrity occur in other areas remote from the injury site. The entire
vascular compartment in the body becomes permeable to circulating macromolecules, such as
dextran. This capillary leak syndrome is manifested as edema. In the lung, severe pulmonary
edema can be life threatening.
Pulmonary function decreases markedly. Functional residual capacity is reduced. Both lung
compliance and chest wall compliance decrease markedly. The alveolar-arterial (Pao2
Pao2) oxygen gradient increases. Minute ventilation is increased; it can be as high as 40 L per
minute (normal, 6 L per minute).
Herndon DN, ed. Total burn care. Philadelphia: WB Saunders, 1996:44-52.
MacLennan N, Heimbach DM, Cullen BF. Anesthesia for major thermal injury.
Anesthesiology 1998; 89:749-770.

A.7. Name some of the known mediators released with thermal injury? What are the espouses
to those mediators?
After a thermal injury, mediators released from the burn wound contribute to local
inflammation and edema. Local mediators include histamine, prostaglandins, bradykinin,
nitric oxide, serotonin, and substance P.
In minor burns, the inflammatory process is limited to the wound itself. In major burns, local
injury triggers the release of circulating (systemic) mediators, resulting in a systemic

response. This is characterized by hypermetabolism, immune suppression, and the systemic

inflammatory response syndrome (protein catabolism, sepsis, multiple organ failures).
The systemic mediators are cytokines (interleukins), endotoxin and nitric oxide (Fig. 54.3).
MacLennan N, Heimbach DM, Cullen BF. Anesthesia for major thermal injury.
Anesthesiology 1998; 89:749-770.

A.8. What is the prognosis for this patient? What major factors affect his prognosis?
The prognosis for this patient is very poor. Statistical survival based on TBSA alone would
predict a less than 50% chance of survival. Other factors that affect his prognosis are age, size
and depth of burn, associated pulmonary injury, and preexisting medical disease. In view of
this patient, who had angioplasty for coronary artery disease and hypertension and who is a
heavy smoker and obese, the risk of myocardial infarction is greatly increased.

Mediator Response to Thermal Injury

Minor Burn
Local Mediators
Histamine
Prostaglandins
Bradykinin
Nitric oxide
Serotonin
Substance P
Major burn
Systemic Mediators
Cytokines (interleukins, TNF)
Endotoxin
Nitric oxide
Systemic Response
Immune suppression
Hypermetabolism
Protein catabolism
Sepsis
Multiple organ failure

Figure 54.3. Mediators released with thermal injury and the response to their release. (From
MacLennan N. Heimbach DM. Cullen BE Anesthesia for major thermal injury.
Anesthesiology 1998:89:749-770. with permission.)

A.9. What are the most common causes of death?

With the understanding of vigorous early fluid resuscitation, hypovolemic shock is not
common in United States. The major early cause of death is asphyxia. The most common
cause of long-term mortality is septic complications.

A.10 Does this patient have a smoke inhalation burn? How do you make the diagnosis?
The patient probably sustained a smoke inhalation burn. Smoke inhalation should be highly
suspected in patients who were burned in an enclosed space, received burns of the face, were
burned while under the influence of alcohol or drugs, or lost consciousness at the time of the
accident.
A patient with smoke inhalation often exhibits no physical signs or symptoms during the first
24 hours after the burn. Diagnosis is dependent on a high index of suspicion and careful
physical and laboratory examination. The early symptoms and signs of respiratory tract injury
include singed nasal hair; burned nasal mucosa, lips, and mouth; hoarseness; wheezing; and
brassy cough with soot in the sputum. The posterior pharynx may appear red and the larynx
may appear edematous.
Radiographic findings are usually negative immediately after injury; this is the "clear or lucid
period." Laboratory tests include blood gas analysis, carboxyhemoglobin concentration,
xenon scans, and fiberoptic bronchoscopy.
Herndon DN, ed. Total burn care. Philadelphia: WB Saunders, 1996:184-192.
MacLennan N, Heimbach DM, Cullen BF. Anesthesia for major thermal injury.
Anesthesiology 1998; 89:749-770.

A.11. Could you name some of the chemical products of combustion?

Carbon monoxide is produced by incomplete combustion of carbon-containing compounds
such as wood, coal, and gasoline. Other chemical products of combustion include ammonia,
nitrogen dioxide, sulfur dioxide, and chlorine. These chemicals combine with water to
produce strong acids and alkalines.
MacLennan N, Heimbach DM, Cullen BF. Anesthesia for major thermal injury.
Anesthesiology 1998; 89.749-770.

A.12. What is carbon monoxide poisoning? How do you treat carbon monoxide poisoning?
Carbon monoxide is the leading cause of hypoxia in survivors of burn injuries. Carbon
monoxide has a 200 times greater affinity for hemoglobin than oxygen and therefore
displaces oxygen from its hemoglobin-binding sites. Fortunately, this reaction is a
competitive, reversible one, so oxygen therapy should be instituted immediately. The half-life

for carbon monoxide elimination from hemoglobin can be shortened from 4 hours to 45
minutes with an inspired oxygen concentration of 100%. Although the Pao2 may be normal,
the actual content of oxygen in the blood is markedly reduced.
Fein A, Leff A, Hopewell PC. Pathophysiology and management of the complications
resulting from fire and the inhaled products of combustion: review of the literature. Crit Care
Med 1980; 94:98.
Herndon DN, ed. Total burn care. Philadelphia: WB Saunders, 1996:187.

A.13. What resuscitative measure would you institute immediately in this patient with
40% burns?
Vigorous fluid resuscitation should be instituted immediately to combat the danger of
hypovolemia from translocation of intravascular volume into the burn edema, which acts as a
"third space." Fluid must be administered adequately to ensure good tissue perfusion and
adequate urine output. The airway should be maintained to ensure adequate ventilation. If an
upper airway burn is involved, endotracheal intubation is indicated.

A.14. What fluid formula would you use?

Over the past 30 years, many fluid formulas have been developed as guides to initial
resuscitation in hypovolemic shock after burn injury. Most use various combinations of
crystalloid and colloid solutions, but they differ widely in the colloid/crystalloid ratio and in
the rate of fluid administration. Although much controversy still surrounds the use of "the
solution" for resuscitation in burn shock, scientific investigation supports the need for both
crystalloid and colloid solutions (Table 54.2). Which formula is used to begin such therapy
matters little, as long as it is modified according to the patient's changing requirements. The
Parkland formula, popularized by Baxter, has been adopted in most burn centers because of
its simplicity, reduced cost, and equivalent outcome and is currently the standard against
which new formulas must be compared.

Parkland Formula
First 24 Hours

Electrolyte solution (lactated Ringer's): 4 mL/kg per percentage of body area with
second- and third-degree burn

Administration rate: 1/2 given in the first 8 hours, 1/4 in the second 8 hours, 1/4 in the
third 8 hours

Urine output: maintain at 0.5 to 1.0 mL/kg per hour

Second 24 Hours

Glucose in water: to replace evaporated water loss and maintain serum sodium
concentration of 140 mEq/L

Colloid solutions (e.g., albumin): amount proportional to burn

30% to 50% burn: 0.3 mL/kg per percentage of burn

50% to 70% burn: 0.4 mL/kg per percentage of burn

Larger than 70% burn: 0.5 mL/kg per percentage of burn

Urine output: maintain at 0.5 to 1.0 mL/kg per hour

Herndon DN, ed. Total burn care. Philadelphia: WB Saunders, 1996:53-60.

MacLennan N, Heimbath DM, Cullen BF. Anesthesia for major thermal injury.
Anesthesiology 1998; 89:749-770.
Crystalloid regimens
Parkland
Modified Brooke
Colloid regimens
Evans
Brooke
(From MacLennan N. Heimbach DM, Cullen BF. Anesthesia for major thermal injury.
Anesthesiology 1998;89:749-770. with permission).

A.15. What cardiovascular changes typify the burn injury?

Cardiovascular changes develop in several phases. Acutely, fluid sequestration in the burned
area and from capillary leak is caused by direct thermal destruction of the capillary
membranes. This results in a massive shift of fluids and proteins from the intravascular
compartment to the interstitial spaces. This shift of fluid accounts for the marked decrease in
circulating blood volume, resulting in hypotension or the initial burn shock. Decreased blood
volume and decreased cardiac output would trigger catecholamine release, resulting in severe
vasoconstriction, which may further compromise forward flow and tissue perfusion. Release
of myocardial-depressant factors may further depress cardiac output through its direct action
on myocardial contractility.

Hendon DN, ed. Total burn care. Philadelphia: WB Saunders, 1996:44-52.

Sugi K, Theissen J, Traber LD, et al. Impact of carbon monoxide on cardiopulmonary
dysfunction after smoke inhalation injury. Circ Res 1990;66:69-75.

A.16. Is the immune system affected in burn injury? How?

Both the cellular and the humoral components of the immune system are impaired. The
presence of devitalized tissue greatly increases the risk of wound infection and systemic
sepsis. Endotoxins cause changes in cellular function. Macrophage activity in the alveolar is

impaired. Changes in phagocytic and chemotactic properties of neutrophils have been

demonstrated. Strict antiseptic precautions must be observed in these patients.
Herndon DN, ed. Total burn cure. Philadelphia: WB Saunders, 1996:98-135.

A.17. What hematologic changes occur in burn injury?

Hematologic changes can be seen in erythrocytes (red blood cells [RBCs]), platelets, and the
coagulation mechanism.
Erythrocytes (RBCs): Immediately after injury, the hematocrit level increases as noncellular
fluid translocates into the interstitium. Anemia is more often the case after fluid resuscitation
because of RBC damage and hemolysis during the heating injury. There is shortened RBC
half-life and reduction of production due to circulating inhibitory factors.
Platelets: The platelet count usually decreases because of dilutional and consumption by
formation of microaggregates in the skin and smoke damaged lung. The platelet level returns
to normal by the end of the first week unless sepsis or multiple system organ failure occurs.
Coagulation: Both the thrombotic and the fibrinolytic mechanisms are activated, and clotting
factors decrease. Disseminated intravascular coagulopathy is rare but can occur, particularly
in fourth-degree burns involving structures deep to the skin.
MacLennan N, Heimbach DM, Cullen BF. Anesthesia for major thermal injury.
Anesthesiology 1998; 89:749-770.

A.18. What changes occur in liver function? What are the anesthetic implications of such
changes?
Hypoperfusion during burn shock can result in decreased hepatic function, severely
depressing the detoxification capacity of the liver. Decreased levels.of albumin may result in
greater free fractions of bound drugs such as benzodiazepines and phenytoin. In contrast, the
injury-stimulated rise in the acute-phase reactant a1-acid-glycoprotein increases the binding
of basic drugs such as muscle relaxants, lidocaine, and propranolol.
Herndon DN, ed. Total burn care. Philadelphia: WB Saunders, 1996:150-151.
Martyn JAL The use of neuromuscular relaxants in bum patients. In: Rupp SM, ed. Problems
in anesthesia. Philadelphia: JB Lippincott Co, 1989:482.

A.19. What are Curling ulcers? How can they be prevented?

Curling ulcer is a stress ulcer of the duodenum commonly found after a severe burn. Gastric
ulceration may occur also. Without treatment, the incidence is as high as 80%. The frequency
and severity correlate with the size of the burn. They may present with gastric bleeding. They
can be prevented with prophylactic antacids, Hz-antagonists, and early enteral feeding.
MacLennan N, Heimbach DM, Cullen OF. Anesthesia for major thermal injury.
Anesthesiology 1998, 89:749-770.

A.20. What complications are associated with electrical burns?

The burn from electrical current results from the conversion of electrical energy to thermal
energy. The damages may vary and are determined by the area of contact, the resistances of
the tissues, and the duration of current flow. Often, only the surface entrance and exit sites on
the skirt show visible injury because of the high current concentrations at these points. Deep
tissues such as muscles, tendons, blood vessels, and nerves can be severely injured. Vascular
complications such as thrombosis can be late complications. The heart is particularly
susceptible to electrical damage. Ectopy and congestive heart failure can be signs of electrical
injury.

B. Preoperative Evaluation and Preparation

B.1. What preoperative preparations would you order? What are particular concerns in this
patient?
Preoperative preparations should include a medical history, physical examination, and the
usual concerns regarding cardiac disease, pulmonary disease, renal function, liver function,
anesthetic history, and family history. Of particular concern in this patient are hypertension,
ischemic heart disease, angioplasty of left main coronary artery, and the history of heavy
smoking and heavy alcohol consumption.
The adequacy of fluid volume resuscitation should be assessed.
Hemodynamic stability should have been achieved.
Laboratory tests should include complete blood cell count, platelet count, electrolytes, blood
urea nitrogen, creatinine, coagulation studies, urinalysis, liver function test,
electrocardiogram (ECG), chest radiograph, and arterial and venous blood gases.
Other data that may be helpful include central venous pressure (CVP), pulmonary capillary
wedge pressure (PCWP), cardiac output, and cardiac index (CI).
In view of this patient's left main coronary artery disease, cardiac enzymes studies in
conjunction with cardiologist involvement would be beneficial.

B.2. What are the various operative and management options available for severely burned
patients?
Deep partial-thickness and full-thickness burns will not heal spontaneously and require
excision and skin graft. The burned skin or eschar is a good culture medium 'for bacterial
growth. Although topical antibiotic creams such as silver sulfadiazine can be applied to
control the infection, the definitive treatment is excision of eschar.
The timing and extent of burn wound excision are still debatable; there has been a shift
toward earlier excision and grafting. The most widely used approach involves an initial 48hour period of stabilization, followed by tangential excision split-thickness skin graft
(TE/STSG). The extent of excision is limited to 20%. These procedures are repeated every 2
days until the eschar excision is complete. Some favor very early excision (<24 hours from
the time of burn).
Herndon DN, ed. Total burn care. Philadelphia: WB Saunders, 1996:136-147.

MacLennan N, Heimbach DM, Cullen BF. Anesthesia for major thermal injury.
Anesthesiology 1998; 89:749-770.

B.3. What is tangential excision split-thickness skin graft? What are the principles of this
grafting technique?
TE/STSG is a procedure to debride the dead skin and graft on new layers. The burn eschar is
sharply excised from the underlying subcutaneous tissue. Brisk capillary bleeding signifies
that adequate excision has been achieved and viable tissue uncovered. Skin grafts may be
either full thickness or split (partial) thickness. Full-thickness grafts include all layers of
epidermis and dermis in their sample.
Therefore, the donor site must be closed primarily. Suitable donor sites are the skinfolds of
the axilla and groin. A tissue expander is commonly used to increase the available donor skin.
Full-thickness grafts have the advantage of better cosmesis and durability, and they are useful
when tissue bulk is desired. More commonly, STSGs are used. These grafts are obtained by
slicing the superficial layers of the skin through the level of the dermal pegs. Because
maturation of skin cells occurs as they migrate superficially, the graft has many viable layers
of dermal cells. When placed on a viable bed of subcutaneous tissue, ingrowth of vessels
occurs and the graft remains viable. In addition, because the excision of donor skin is through
the dermis, the deep basement membrane and skin appendages remain intact. Hence, the
donor site will heal on its own, architecturally normal, usually with only mild discoloration.

Herndon DN, ed. Total burn care. Philadelphia: WB Saunders, 1996:142-147.

B.4. What are the advantages and disadvantages of early tangential excision split-thickness
skin graft?
By excising the burn eschar early (within 7 to 10 days), one can remove the bacterial load
quickly and achieve prompt skin coverage with resultant lessening of septic complications;
the hospital and recovery phases are thus shortened. Very early excision (within 24 hours),
however, has the disadvantage of the patient undergoing a major operation during the
resuscitative phase of the injury. The patient is not optimally stabilized, and there is an
increase in anesthetic risk.
Cultured epithelial autografts are an exacting new technique that can be of great use in
patients with large TBSA burns in which donor sites are few in number.
Herndon DN, ed. Total burn care. Philadelphia: WB Saunders, 1996:136-147.

Herndon DN, Barrow RE, Rutan TC, et al. A comparison of conservative versus early
excision A1171 Surg 1989;209(5):547-553.

Munster AM, Weiner SH, Spence RJ. Cultured epidermis for the coverage of massive burn
wounds a single center experience. Ann Surg 1990;211:676-680.

B.5. What is this patient's mean arterial blood pressure? How do you calculate it?
The patient's blood pressure is 190/100 mm Hg; therefore, his mean arterial blood pressure is
130 mm Hg (mean arterial pressure = diastolic pressure + one third of pula pressure, which is
the difference between systolic and diastolic pressure).

B.6. Are you concerned about this patient's blood pressure? What treatment would you
institute?
The blood pressure is quite high (190/100 mm Hg). Knowing that this patient has a history of
ischemic heart disease with symptoms of angina that required angioplasty of the left main
coronary artery 1 year ago, I am very concerned about his hypertension and would like to
control the blood pressure to the normal range.
The following intravenous vasodilators may be used:

Nitroprusside

Nitroglycerine a2-agonist such as clonidine

In view of his tachycardia (heart rate, 120 beats per minute), I would prefer an a2-agonist.
Increased afterload and tachycardia would increase oxygen demand on the heart and increase
the risk of myocardial infarction.
Adequate volume resuscitation should be assessed, so obtaining PCWP, cardiac output, CI,
and systemic vascular resistance would be helpful in instituting treatment.

B.7. How do a2-adrenergic agonists work?

a2-Agonists such as clonidine stimulate the presynaptic a2-receptors centrally in the medulla
of the brainstem and inhibit the release of norepinephrine, thus decreasing sympathetic
outflow from the vasopressor centers in the brainstem. Decreased sympathetic outflow results
in vasodilation, decreased blood pressure, and bradycardia.

Katzung BC, ed. Basic and clinical pharmacology, 8th ed. New York: McGraw-Hill,
2001:160-162.

B.8. This patient was ventilated with respirator settings of tidal volume, 1,200 mL;
respiratory rate, 20 breaths per minute; FIO2, 60%; and positive end-expiratory pressure, 10
cm H20. Arterial blood gas analyses showed the following: pH, 7.25; Po2, 56 mm Hg; PCo2,
60 mm Hg; and 02 saturation, 80%. How would you interpret these arterial blood gas analysis
results? What are the possible causes of high PCo2 and low PO2?
Arterial blood gas analysis results are abnormal. This patient was hypoventilated with high
PCo2 of 60 mm Hg (normal Pco2 is 35 to 45 mm Hg), although the minute volume was 24 L
(1,200 mL x 20.7), the increase in minute volume might not have compensated for his
hypermetabolic state with marked increase in CO2 production.

Ventilation/perfusion mismatch is the most common cause of hypoxemia. Causes of

ventilation/perfusion mismatches range from dead space to shunt. The common causes are
atelectasis, pneumonia, and pulmonary edema.
This patient had respiratory acidosis and probably mild metabolic acidosis. Malposition of
endotracheal tube with single-lung ventilation is a possible cause that should be ruled out.

B.9. How do you calculate oxygen content and oxygen delivery? What factors govern the
oxygen delivery to the tissues? What are the causes of tissue hypoxia?
Oxygen content consists of oxygen in combination with hemoglobin and oxygen dissolved in
plasma and can be expressed as:
Oxygen content (mL/dL) = 1.31 x hemoglobin (g/dL) x 02 saturation (%) + 0.003 x Poe
Normal Cao2 = 20.73 mL/100 mL
Normal C602 = 15.76 mL/100 mL
Oxygen delivery is the product of cardiac output (CO) and arterial oxygen content.
Do2 = C.O x Cao2
= C.O x [(1.31 x hemoglobin x 02 saturation) + 0.003 x Po2]
:

Three main factors govern the oxygen delivery: cardiac output, hemoglobin, and arterial
oxygen saturation.
Tissue hypoxia may be due to the following:

Failure of cardiac output: "stagnant anoxia"

Failure of arterial oxygen saturation: "anoxic anoxia"

Reduction of hemoglobin concentration: "anemic anoxia"

Lumb A. Nunn 's applied respiratory physiology, 5th ed. Oxford: Butterworth Heinemann,
2000:284-285.

B.10. What are the symptoms and signs of alcohol withdrawal? Are you concerned that this
patient could develop delirium tremens?
Minor withdrawal symptoms are anorexia, insomnia, tremors, mild disorientation,
hallucination, and convulsion. These symptoms usually peak within 10 to 30 hours after
cessation of drinking. Major withdrawal symptoms occur later and are characterized by
severe autonomic hyperactivity, which includes anxiety, tachycardia, diaphoresis, tremors,
fever, hallucination, and global convulsion. These major symptoms are also known as
delirium tremens. There is a real concern that this patient could develop withdrawal
syndrome. Early treatment should be instituted.

B.11. How would you prevent the adverse effects of alcohol withdrawal?

Sedatives, such as benzodiazepines, are effective in preventing the withdrawal symptoms. If

autonomic hyperactivity symptoms occur, B-blockers are helpful to attenuate the symptoms,
especially tachycardia and dysrhythmias.

C. Intraoperative Management
C.1. What monitors would you use in the operating room?
The routinely used monitors, such as ECG, blood pressure, temperature, inspired oxygen,
pulse oximetry, and capnography, should be used in this patient. A urinary catheter is essential
to assess urine output. An indwelling arterial line is helpful, because a standard blood
pressure cuff would be difficult to apply over the areas to be grafted and harvested. A
pulmonary artery catheter or CVP catheter is recommended for the severely burned patient,
especially a patient with ischemic heart disease.

C.2. What information can be obtained from an arterial line and a pulmonary artery catheter?
How are these calculations performed?
The arterial line can display direct continuous blood pressure, thereby providing continuous
real-time monitoring of blood pressure. This is most useful in fluctuating hypotensive or
hypertensive situations. In conditions such as atrial fibrillation or ventricular tachycardia,
variations in ventricular response or blood pressure can be recognized instantly. In addition, it
serves as ready vascular access for blood samplingtor example, arterial blood gas analyses,
electrolytes, hematocrit, and blood sugar levels.
Pulmonary artery catheter allows measurement of PCWP. The PCWP parallels left atrial
pressures. Left atrial pressure reflects left ventricular end-diastolic pressure, which is helpful
in assessing the preload status of the left ventricle. CVP, though useful as a rough estimate of
preload, does not correlate with left ventricular end-diastolic pressure when either isolated
right-sided or left-sided cardiac dysfunction occurs.
The multilumen pulmonary artery catheters are capable of measuring CVP and cardiac output
through the thermodilution method. It also permits sampling of mixed venous blood. These
measurements permit calculation of many hemodynamic variables.

A low mixed venous oxygen level (<30 mm Fig) is suggestive of inadequate tissue perfusion.
Miller RD, ed. Anesthesia, 5th ed. New York: Churchill Livingstone, 20&0:1124, 1178, 1185,
1259. 2.3.

C.3. If the patient had not been intubated, how would you proceed with the anesthetic
induction?
One should anticipate a difficult intubation because this patient has burns over his face and
neck. Bums on the face may cause severe edema of the face, pharynx, and larynx, so careful
assessment of the mouth opening, pharynx, and larynx should be performed. The safest way
to secure the airway is to do an awake intubation with topical anesthesia and mild sedation; it
can be achieved with either direct or fiberoptic-guided intubation.

If prolonged postoperative intubation is anticipated, the nasotracheal route should be

considered. A nasotracheal tube is more easily secured in place, is better tolerated by the
patient, and permits better oral hygienic care. Vasoconstriction of the nasal mucosa may be
achieved with phenylephrine drops.

C.4. Why is awake intubation considered the safest?

Awake intubation is considered the safest way to secure an airway because when the patient
is awake and breathing spontaneously, the patient is less likely to obstruct the upper airway
by the tongue and is less likely to have oxygen desaturation. The anesthesiologist does not
have to ventilate using a mask and therefore is less likely to distend the stomach.
If the patient is breathing spontaneously and has adequate oxygenation, the anesthesiologist
has more time to do a proper laryngoscopy or manipulation of the endotracheal tube.
Identifying the passage of air from the glottis may be helpful in blind intubation.

C.5. What anesthetic agents would you use? Discuss inhalation versus intravenous agents.
For the severely burned patient, once the airway is secured, high-dose narcotic-muscle
relaxant technique would be preferred, because this technique offers good intraoperative
hemodynamic stability in critically ill patients, coupled with excellent postoperative
analgesia.
The narcotics such as morphine, meperidine (Demerol), fentanyl, or sufentanil can be used
because they do not depress myocardial contractility, whereas inhalation agents depress the
myocardium. If inhalation agents are chosen, the concentration should be carefully titrated to
prevent loss of cardiovascular compensation.

C.6. Why are you concerned about the patient's body temperature? What is normothermia for
a burned patient?
Massively burned patients with loss of skin have constant evaporation from open surfaces.
They tend to develop severe intraoperative hypothermia. The tendency is exaggerated by the
effects of general anesthesia on the temperature-regulating centers, by vasodilation and by the
cool relatively dry environment of the operating room. The infusion of a large amount of
intravenous fluids at room temperature also contributes to the development of hypothermia.

Normothermia for a burned patient is about 38.5C because the burned patient develops a
resetting of the centrally mediated thermostat.

Herndon DN, ed. Total burn care. Philadelphia: WB Saunders, 1996:140.

C.7. How is temperature best maintained?

Hypothermia is an ever-present problem. Burned patients have lost their natural insulation of
the skin. Heat loss can occur through convection, conduction, and evaporation. Methods to
maintain normothermia should involve active warming and prevention of heat loss. We
administer all fluids and blood transfusions through the blood- and/or fluid-warming device.
A thermal mattress is placed under a single-layer sterile sheet on the operating table and is
prewarmed, although this method is not very effective. Warming the operating room to
temperatures between 24C and 27C with a relative humidity higher than 50% is particularly
effective. The areas of the patient's body not immediately involved in the surgery must be
covered. Heated, humidified circuits are most effective in minimizing the heat loss from
ventilation with cold anesthetic gases.

C.8. What derangements occur with hypothermia?

Hypothermia causes many physiologic changes. Hypothermia decreases metabolism, heart
rate, cardiac output, and blood pressure. At temperatures less than 28C, atrial pacing
becomes irregular and ventricular ectopic increases. Ventricular fibrillation occurs between
25C and 30C in the human adult.
Decreasing the rate of metabolism can prolong the duration of many anesthetic drugs.
Decreased hepatic blood flow could slow the delivery of drugs to the site of metabolism.
Hypothermia shifts the oxygen dissociation curve to the left, resulting in a reduced release of
oxygen by hemoglobin. However, the shift to the left is compensated by two factors, namely
an increase in dissolved oxygen in the plasma and an increase in dissolved carbon dioxide,
which increases acidity and tends to shift the curve to the right.
Miller RD, ed. Anesthesia, 5th ed. New York Churchill Livingstone, 2000:1382.

C.9. What muscle relaxant would you use?

A nondepolarizing muscle relaxant should be used. Depolarizing relaxant should be avoided.
In general, the choice of muscle relaxant should be based on the duration of the operation and
the presence of any coexisting diseases that might affect the elimination of the drug. Muscle
relaxants without histamine release would be preferred, such as vecuronium, rocuronium,
pipecuronium, and doxacurium.

C.10. Why is succinylcholine contraindicated in burned patients? For how long should it be
avoided?
Succinylcholine is contraindicated in burned patients because injection of succinylcholine
may cause a significant transient increase in serum potassium levels as high as 13 mEq/L,
resulting in ventricular tachycardia, fibrillation, and cardiac arrest.
This hyperkalemic response begins about 5 to 15 days after the burn and persists for 2 to 3
months or longer, irrespective of degree and size of bum injury.
The exact mechanism responsible for this response is not known. Gronert and Theye
postulated that the abrupt release of potassium is from the hypersensitive muscle membranes.
Apparently, extrajunctional acetylcholine receptors are found on the muscle membranes of

burned patients. Stimulation of these receptors may mediate the potentially lethal efflux of
potassium.
The exact time period for this hypersensitivity is unclear. Most authors recommend the
avoidance of succinylcholine from 24 to 46 hours after the burn injury and extension of
succinylcholine well until complete healing has occurred. A hyperkalemic response has been
reported in a patient after 480 days. The recommended limit now is extended to about 2 years
after the burned skin has healed.

Gronert GA, Theye RA. Pathophysiology of hyperkalemia induced by succinylcholine.

Anesthesiology 1975;43:89-99.
Miller RD, ed. Anesthesia, 5th ed. New York: Churchill Livingstone, 2000:472.
Schaner PJ, et al. Succinylcholine-induced hyperkalemia in burned patients. Anesth Analg
1969; 48:764-770.
Tohnie JD, et al. Succirtylcholine danger in the burned patient. Anesthesiology 1967;28:467470.

C.11. What other adverse effects are associated with succinylcholine?

Adverse effects of succinylcholine are many. Its side effects are as follows:

Hyperkalemia, particularly following burns, spinal cord injuries and generalized

major trauma: a single case report of a marked hyperkalemic response to succinylcholine in a
patient with a closed head injury without peripheral paralysis

Increased intracranial and intraocular pressures: the practical importance of which is

controversial

Increased intragastric pressure: counterbalanced by the increase in lower esophageal

pressure, which reduces or eliminates the increased risk of regurgitation

Muscle pains: more likely to concern the patient with minor injuries who ambulates
soon after surgery

Prolonged paralysis in patients with atypical pseudocholinesterase

Cardiac arrhythmias, particularly bradycardia after repeated doses

Trigger for malignant hyperthermia

Miller RD, ed. Anesthesia, 5th ed. New York: Churchill Livingstone, 2000:2168.

C.12. How are the doses of nondepolarizing muscle relaxants affected by burn injury?

In general, burn patients show great resistance to the nondepolarizing relaxants. Martyn and
colleagues first reported that burn patients required a five times higher plasma concentration
of D-tubocurarine to attain a given percentage of twitch depression compared with normal
subjects. The dose of pancuronium is increased by 2.5 times.
Although these patients have altered pharmacokinetics and increased plasma protein binding
of the relaxants, most of the increased requirement appears to be due to alterations in the
number and affinity of the junctional receptors. This alteration is quite variable.

Hartman GS. Anesthetic considerations for the burn patient. In: Wellcome trends in
anesthesiology. New York: F & M Projects, December 1990:11.
Martyn JAJ, Liu LMP, Szyfelbein SK, et al. The neuromuscular effects of pancuronium in
burned children. Anesthesiology 198359:561-564.
Martyn JAJ, Szyfelbein SK, Ali HH, et al. Increased D-tubocurarine requirement following
major thermal injury. Anesthesiology 198052:352-355.

C.13. How are the muscle relaxants such as curare, pancuronium, cisatracuriuin, vecuronium,
doxacurium, rocuroniuin, and pipecuronium metabolized and eliminated? Which of them has
significant histamine release?
See Table 54.3.

C.14. What is the difference between metabolism and elimination of drugs?

Drug metabolism is the chemical modification of a substance. There are two phases: Phase 1
metabolism involves chemical reactions of oxidation, reduction, and hydrolysis. Many of
these involve catalysis by the cytochrome P450 system in the liver. Phase II metabolism
involves conjugations, or the combining of endogenous substances with drugs. This is also
known as "the synthetic mode of biotransformation."
Drug elimination involves all processes, which include metabolism, renal and hepatobiliary
excretion, and pulmonary excretion such as CO2 and anesthetic gases.

Herndon UN, ed. Total burn care. Philadelphia: WB Saunders, 1996:401-407.

Miller RD, ed. Anesthesia, 5th ed. New York: Churchill Livingstone, 2000:148-152.

D. Postoperative Management
D.1. How would you monitor this patient during transport?
This patient was most likely intubated, paralyzed, apneic, and still under the influence of
general anesthetic. Monitoring should be directed toward respiration, oxygenation, and
hemodynamics. These can be achieved by a transport monitor capable of monitoring ECG,
blood pressure, CVP, and pulse oximeter. Ventilation should be controlled with an Ambu bag
with supplemental oxygen during transport.

D.2. What is meant by diffusion hypoxia? How do you prevent it?

Fink and colleagues in 1954 first reported diffusion hypoxia during recovery from nitrous
oxide-oxygen anesthesia. A mild degree of hypoxia may develop for more than 10 minutes
when nitrous oxide-oxygen anesthesia is concluded and the patient is allowed to breathe
room air. The arterial oxygen saturation may fall 5% to 10% and often reaches values less
than 90% (Pao2 < 60 mm Hg). This occurs at the time when nitrous oxide is eliminated
rapidly through the lungs. Nitrous oxide is 35 times more soluble in blood than nitrogen.
Therefore, the amount of nitrous oxide diffused from blood to alveoli is much more than the
amount of nitrogen diffused from alveoli to blood. Hence, alveolar oxygen is diluted by
nitrous oxide. Diffusion hypoxia can be prevented by the inhalation of high concentrations of
oxygen for several minutes before the patient is allowed to breathe room air.

Fink R. Diffusion anoxia. Anesthesiology 1955;16:511-519.

Fink R, Carpenter SL, Holiday DA, et al. Diffusion anoxia during recovery from nitrous
oxide-oxygen anesthesia. Fed Proc 1954;13:354.

D.3. Why do patients often shiver in the recovery room on emergence from anesthesia?
Postanesthetic shivering is commonly observed in the recovery room. It is more commonly
seen after receiving inhalational general anesthetics. It is thought that inhalation agents
inhibit the temperature-regulating centers in the hypothalamus, and shivering is a
thermoregulatory response to intraoperative hypothermia (the operating room is always cold).
Shivering is a mechanism to produce heat to maintain normothermic. However, the precise
mechanism of shivering is not fully explained because many patients who shiver are
normothermic. It is postulated that the tremor pattern results from anesthetic-induced
disinhibition of normal descending control over spinal reflexes. Similar non-thermoregulatory
tremor has been seen in women during labor.

Miller RD, ed. Anesthesia, 5th ed. New York: Churchill Livingstone, 2000:1377-1378.

D.4. Discuss the causes of oliguria in the recovery room.

Oliguria is defined arbitrarily as the production of less than 400 mL of urine in 24 hours.
When oliguria occurs, it is a functional manifestation of various clinical entities referred to as
acute renal failure (ARF). The syndrome of ARF may be classified Ltto the following
three groups:

Prerenal ARF (hypovolemic): There is no structural damage to the kidney. The

reduction in renal blood flow results in a reduced filtration rate and a decrease in urinary
flow. It is reversible with volume expansion. However, if untreated, it can progress to the
ischemic form of acute tubular necrosis.


Renal ARF (acute tubular necrosis): There is structural damage to the renal tubules.
The damage may be due to ischemia or nephrotoxic substances.

Postrenal ARF (obstruction of urinary outflow): Pus, tubular debris, clots of blood,
and crystalluria can cause bilateral obstruction of the ureters. The flow of urine is completely
suppressed in contrast to the low flows found in prerenal and renal disease.
One must determine the cause of the oliguria because the management can vary
greatly. To identify the cause of oliguria, one must make a careful assessment of the urinary
sediment. Presence of renal tubular cells, renal tubular cell casts, and pigmented granular
casts is strong evidence for the diagnosis of acute tubular necrosis. A normal urinary sediment
supports a diagnosis of hypovolemic renal failure. Other data, such as CVP, pulmonary artery
diastolic pressure, and PCWP can give valuable information about the state of hydration.