increase in brain pH suppresses the stimulus for hyperventilation unless severe hypoxia is present. In

contrast, chronic hypoxia results in hyperventilation even with mildly decreased PCO2 because brain pH

is lowered by metabolic compensation. The two most common causes of hypoxia resulting in respiratory

alkalosis are pulmonary disease and exposure to high altitudes.

Clinical Features

Chronic respiratory alkalosis is usually asymptomatic because compensatory mechanisms are successful

in maintaining pH close to normal. Acute respiratory alkalosis may cause sensations of breathlessness,

dizziness, and nervousness and can result in circumoral and extremity paresthesias, altered levels of

consciousness, and tetany. These signs are related to decreased cerebral blood flow secondary to the

decreased PCO2 and decreased ionized calcium concentration secondary to the increased blood pH.

Compensatory Mechanisms

Tissue buffering is the initial response to a decrease in PCO2

. Red blood cells provide one-third of the

buffering. Consumption of bicarbonate results from cellular liberation of H+. The magnitude of tissue

buffering is weak compared with renal compensation. This is accomplished not by increasing

bicarbonate excretion but by decreasing net acid excretion, namely ammonia. Acute compensation is not

as strong as chronic compensation, which takes at least 3 days to occur.

Acute compensation: Decrease serum HCO3

- by 2 mEq/L per 10 mm Hg reduction in PCO2

Chronic compensation: Decrease serum HCO3

- by 4 to 5 mEq/L per 10 mm Hg reduction in PCO2

Treatment

The underlying stimulus for the hyperventilation should be addressed. The cause of hypoxemia should

be determined and corrected. In acute symptomatic respiratory alkalosis, rebreathing or breathing 5%

CO2

temporarily relieves symptoms. If the condition is secondary to mechanical ventilation, decreasing

tidal volume or respiratory rate should result in resolution of respiratory alkalosis.

Respiratory Acidosis

Respiratory acidosis is defined by a decrease in extracellular pH from a primary increase in PCO2

, due

to inadequate ventilation. Causes of hypoventilation include CNS depression, impaired pulmonary

mechanics, airway obstruction, and chronic obstructive pulmonary disease (COPD). In addition,

inappropriate ventilator settings may result in respiratory acidosis in patients on mechanical ventilation.

Clinical Features

The magnitude of clinical manifestations depends on the chronicity and rate of development of

respiratory acidosis. Acute increases result in cerebral acidosis, manifested by drowsiness, restlessness,

and tremor, as well as stupor or coma in more severe cases. Cerebral vasodilation occurs in response to

acidosis, resulting in increased cerebral blood flow. This may, in turn, result in increased intracranial

blood pressure, headache, and papilledema. Systemic acidosis results in peripheral vasodilatation,

depressed cardiac contractility, and insensitivity to catecholamines.

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Figure 11-8. Acid–base nomogram. Shown are the 95% confidence limits of the normal respiratory and metabolic compensations

for primary acid–base disturbances. (Reproduced with permission from Cogan MG, Rector FC Jr. Acid–base disturbances. In:

Brenner BM, Rector FC Jr, eds. The Kidney. Philadelphia, PA: WB Saunders; 1986:473.)

Compensatory Mechanisms

Increased pCO2

results in increased H2CO3

, which dissociates into H+ and HCO3

-. Cellular exchange of

Na+ and K+ for H+ allows the reaction to continue in this direction with increased extracellular

bicarbonate. This tissue buffering is accomplished within minutes. Persistently elevated PCO2 also

stimulates increased renal acid excretion, primarily the chloride salt of ammonia, and results in

increased renal generation of HCO3

-. Full renal compensation occurs over 3 to 5 days.

Acute compensation: 1 mEq/L HCO3

- per 10 mm Hg PCO2

Chronic compensation ~4 mEq/L for every 10 mm Hg PCO2

Treatment

Treatment should be directed to the underlying cause of hypoventilation. Endotracheal intubation to

achieve adequate ventilation is paramount to the treatment of acute respiratory acidosis of any cause. In

select cases of respiratory acidosis, namely patients with COPD, noninvasive positive pressure

ventilation (i.e., CPAP/BiPAP) has proven effective. However, patients must be able to protect their

airway and have no major concern for aspiration (i.e., not appropriate in the setting of a bowel

obstruction). Furthermore, there must be close follow-up to ensure the acidosis is resolving.

The treatment of chronic, compensated respiratory acidosis may be complicated by the accompanying

hypoxemia. In chronic hypercapnia, the central chemoreceptors may be insensitive, and the

accompanying hypoxemia may supply the main respiratory drive through stimulation of peripheral

chemoreceptors. In such patients, complete correction of the hypoxemia may further suppress

respiration and worsen the respiratory acidosis. In addition, PCO2 should not be normalized rapidly.

Equilibration of cerebral bicarbonate concentration lags behind systemic changes. Thus, even if PCO2

is

normal, cellular and cerebral metabolic alkalosis may develop.

Mixed Acid–Base Disorders

Combinations of two or more of the four primary acid–base disorders may occur and should be

suspected when blood pH approaches normal despite abnormal PCO2 and [HCO3

-], or when

compensatory changes appear to be either excessive or inadequate (Fig. 11-8). Familiarity with the

acid–base disorders associated with various clinical situations and the expectation of mixed

abnormalities allows appropriate interpretation of arterial blood gases and serum electrolyte

determinations.

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Chapter 12

Burns

Benjamin Levi, Mark R. Hemmila, and Stewart C. Wang

Key Points

1 Burn reconstruction remains a challenge given the increased survival of burn patients.

2 Most chemical injuries should be treated with dilution of the chemical rather than neutralization.

3 Frostbite outcomes are improved if patients with threatened extremities are treated with tPA within

24 hours of injury.

4 Resuscitation is of crucial importance for burn patient outcome and physicians must be aware when

to begin resuscitation (>20% TBSA) and to monitor the patient’s response to avoid

overresuscitation.

5 Early excision and grafting within 72 hours of the injury remains a pillar of burn care.

6 Order of burn coverage can affect patient outcome and can help prevent the patient from needing a

tracheostomy.

7 In addition to surgical treatment of hypertrophic scars, new laser technologies allow for scar

rehabilitation improving the quality and pain associated with these scars.

INTRODUCTION

Burn injuries represent a major source of trauma, subsequent scarring and debility throughout the

world. Improved worker safety programs, fire prevention efforts, and fire detection systems have

significantly decreased the prevalence of major burn injuries. Burn patients have also benefited from

recent improvements in surgical critical care in areas such as lung protective ventilation, blood glucose

control, and antibiotic stewardship. Overall, survival after burn injuries remains high, leading to a large

need for improved reconstructive treatment options for burn scar rehabilitation.

EPIDEMIOLOGY

1 Based on the American Burn Association (ABA) National Burn Repository, 450,000 people receive

medical treatment for burns annually. There are 40,000 hospital admissions and 3,400 deaths per year

from fire and smoke inhalation.1 Of these patients, 69% are male, 59% are Caucasian, 20% are African

American, and 15% are Hispanic. The cause of these burn injuries varies with 43% from fire or flame

burns, 34% from scald burns, 9% from contact burns, and 7% are electrical and chemical burns. With

increased safety emphasis in the workplace, only 9% of these injuries occur at work. The majority of

chemical, electrical, and molten burns occur at home and 72% of all burn injuries happen at home. As in

other trauma populations, children are affected to a greater degree. Children under 8 years of age

typically suffer from scald burns caused by spilling of hot liquids. With improved surgical critical care

and understanding of burn injury physiology, over 96% of burn patients survive. Thus, with improved

treatments and survival, there has also been an increased focus on burn reconstruction and scar

management.

Children

Infants and children up to 4 years old comprise almost one-third of burns. Burns are the fifth leading

cause of unintentional nonfatal injury in infants and the third leading cause of fatal injury for newborns

to children 9 years of age. Scald burns caused by hot liquids are the most common cause of pediatric

burns and occur most often in the home.2–5 The number of burns decreases from age 9 until adolescence

and increases again after the age of 15, presumably due to greater exposure to hazards,

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