Chapter 48: Shock, Multiple Organ Dysfunction Syndrome, and Burns in Adults

MULTIPLE CHOICE
1. What is the final outcome of impaired cellular metabolism?
a. Cellular alterations in the heart and brain
b. Buildup of cellular waste products
c. Cellular alterations in the vasculature structures and kidneys
d. Impairment of urine excretion
ANS: B

The common pathway in all types of shock is impairment of cellular metabolism as a result of
decreased delivery of oxygen and nutrients, which are frequently coupled with an increased
demand, the consumption of oxygen and nutrients, and a decreased removal of cellular waste
products. Of the options available, this selection is the only accurate outcome.
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2. Which clinical manifestation of septic shock confirms an elevation in immune system

response?
a. Tachycardia
b. Increased white blood cell count

c. Low respiratory rate

d. Hypothermia

ANS: B

Clinical manifestations common in septic shock are fever, high heart rate, high respiratory
rate, or elevations in immune responses, such as increased white blood cells and circulating
blood glucose.
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3. The release of catecholamine by the adrenal glands compensate for which initial effects of

hypovolemic shock?
Interstitial fluid moves out of the vascular compartment.
Systemic vascular resistance is decreased.
Heart rate is increased.
Water excretion is increased.

a.
b.
c.
d.

ANS: C

Compensatory mechanisms (see Figure 48-3) initially offset hypovolemia. Heart rate and
systemic vascular resistance increase as a result of catecholamine release by the adrenal
glands, which boosts cardiac output and tissue perfusion pressures. Compelled by a decrease
in capillary hydrostatic pressures, interstitial fluid moves into the vascular compartment. The
liver and spleen add to blood volume by disgorging stored red blood cells and plasma. In the
kidneys, renin (through several intermediaries) stimulates aldosterone release and the
retention of sodium and therefore water, whereas antidiuretic hormone (ADH), or vasopressin,
from the posterior pituitary gland increases water retention. Data on the compensation of
ADH, however, show that as shock worsens, ADH in plasma decreases.
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4. Hypovolemic shock begins to develop when intravascular volume has decreased by what

percentage?
a. 5
b. 10

c. 15
d. 20

ANS: C

Hypovolemic shock begins to develop when intravascular volume has decreased by

approximately 15%.
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5. What type of shock develops as a result of the overstimulation of the parasympathetic nervous

system or the understimulation of the sympathetic nervous system?

c. Anaphylactic
d. Vasogenic

a. Septic
b. Cardiogenic
ANS: D

Only vasogenic shock refers to a widespread and massive vasodilation resulting from an
imbalance between parasympathetic and sympathetic stimulation of vascular smooth muscle.
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6. What is the clinical hallmark of neurogenic shock as a result of the overstimulation of the

parasympathetic nervous system?

a. Vasoconstriction
b. Vasodilation

c. Increased metabolism
d. Respiratory distress

ANS: B

Neurogenic shock refers to a widespread and massive vasodilation that results from an
imbalance between parasympathetic and sympathetic stimulation of vascular smooth muscle.
None of the other options are related to this condition.
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7. Which form of shock is often more severe than other forms because of its sudden, rapid

systemic vasodilation?
a. Septic
b. Hypovolemic

c. Anaphylactic
d. Neurogenic

ANS: C

Anaphylactic shock is often more severe than other types of shock because the
hypersensitivity reaction, which triggers vasodilation, has other pathophysiologic effects that
rapidly involve the entire body. This action is not associated with the other options.
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8. What type of shock is related to a decrease in systemic vascular resistance?

a. Septic
c. Hypovolemic
b. Cardiogenic
d. Heart failure
ANS: A

Clinical manifestations of only septic shock are persistent low arterial pressure, low systemic
vascular resistance from vasodilation, and an alteration in oxygen extraction by all cells.

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9. For which type of shock would antihistamines and corticosteroids be prescribed?

a. Septic
c. Hypovolemic
b. Anaphylactic
d. Cardiogenic
ANS: B

Only anaphylactic shock responds to the administration of epinephrine to decrease mast cell
and basophil degranulation. Antihistamines and steroids are administered to stop the
inflammatory reaction.
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10. Which condition is best defined as a clinical syndrome involving a systemic response to

infection, which is manifested by two or more of the systemic inflammatory response

syndrome criteria?
a. Bacteremia
c. Septicemia
b. Sepsis
d. Septic shock
ANS: B

Of the options available, only sepsis is best defined as a systemic response to infection that is
manifested by two or more criteria of the systemic inflammatory response syndrome.
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REF: Page 1676 | Table 48-1

11. In septic shock, which mediators are antiinflammatory?

a. Interleukin (IL)4 (IL-4), IL-10, and IL-13
b. Tumor necrosis factoralpha (TNF-) and granulocyte cell-stimulating factor
c. IL-1, IL-2, and IL-6
d. Prostaglandin, leukotrienes, and bradykinin
ANS: A

In septic shock, the only antiinflammatory mediators released include lipopolysaccharidebinding protein; IL-1 receptor antagonist; soluble cluster of differentiation 14 (CD-14); type 2
IL-1 receptor; leukotriene 4-receptor antagonist; IL-4, IL-10, and IL-13; and soluble TNF.
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12. What mechanism causes organ injury in primary multiple organ dysfunction syndrome

(MODS)?
a. Impaired immune response
b. Impaired glucose use

c. Impaired perfusion
d. Impaired ventilation

ANS: C

In primary MODS, the organ injury is directly associated with a specific insult, most often
ischemia or impaired perfusion from an episode of shock or trauma, thermal injury, soft-tissue
necrosis, or invasive infection. None of the other options accurately identifies the cause of
MODS.
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13. In secondary multiple organ dysfunction syndrome (MODS), what stimulates the normal

endothelial cells to change to a proinflammatory state?

Interleukin (IL)4 (IL-4) and IL-13
IL-1, IL-6, and tumor necrosis factor (TNF)
Interferon gamma (IFN-) and granulocyte cell-stimulating factor
Prostaglandin, leukotrienes, histamine, and bradykinin

a.
b.
c.
d.

ANS: B

Normal endothelial cells have little interaction with leukocytes except when stimulated by
TNF, IL-1, and IL-6. This selection is the only option that accurately describes what
stimulates the normal endothelial cells to change to a proinflammatory state.
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14. What stimulates the respiratory burst and production of highly toxic free radicals in the

multiple organ dysfunction syndrome (MODS)?

Neutrophils adhering to the endothelium
Activation of the complement cascade
Release of prostaglandins, thromboxanes, and leukotrienes
Activation of the fibrinolytic system

a.
b.
c.
d.

ANS: A

The accumulation of activated neutrophils in organs is thought to play a key role in the
pathogenetic development of MODS. When neutrophils adhere to the endothelium, they
undergo a respiratory burst (oxidative burst) and release oxygen radicals. The respiratory burst
occurs as the activated neutrophil experiences a sudden increase in oxidative metabolism,
producing large quantities of highly toxic oxygen free radicals. This selection is the only
option that accurately identifies the stimulant of the respiratory burst that results in the
production of toxic free radicals.
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15. In multiple organ dysfunction syndrome (MODS), the gut hypothesis attempts to explain

which phenomena?
Paralytic ileus
Translocation of bacteria
Maldistribution of blood flow
Massive diarrhea accompanying septic shock

a.
b.
c.
d.

ANS: B

The loss of intestinal barrier function leads to the systemic spread of bacteria and/or endotoxin
from the gut (systemic endotoxemia). This phenomenon is called translocation of bacteria.
The gut hypothesis provides a possible explanation for the fact that an infectious focus is not
always found in individuals with MODS. The gut hypothesis is not related to any other option.
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16. Blistering of the skin within minutes occurs in which type of burn injury?
a. First degree
c. Deep second degree
b. Superficial second degree
d. Third degree
ANS: B

The hallmark of superficial partial-thickness injury is the appearance of thin-walled, fluidfilled blisters that develop within only a few minutes after injury. Blistering that occurs within
minutes of the burn injury is not a defining characteristic of the other options.
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17. Which form of shock occurs from an acute burn injury?

a. Hypovolemic
c. Cardiogenic
b. Septic
d. Vasogenic
ANS: A

Burn shock consists of a hypovolemic cardiovascular component and a cellular component.

Hypovolemia associated with burn shock results from massive fluid losses from the
circulating blood volume. The other forms of shock are not directly related to an acute burn
injury.
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18. Which fluid is most often used in fluid resuscitation after a major burn injury?
a. Saline
c. Lactated Ringer solution
b. Albumin
d. Dextrose in water
ANS: C

Lactated Ringer solution is used most often because it closely approximates extracellular
fluid, the repository of fluid leaving the circulatory system during this phase of extensive
edema formation (see Table 48-4). The other options are not most often used in fluid
resuscitation after major burns.
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19. What is the most reliable criterion of adequate fluid resuscitation after a major burn injury?
a. Blood pressure
c. Respiratory rate
b. Pulse rate
d. Urine output
ANS: D

The most reliable criterion for adequate resuscitation of burn shock is urine output. None of
the remaining options are considered reliable.
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20. The endpoint of burn shock is defined as the time when the individual is able to do which of

the following?
Maintain adequate blood pressure for 4 hours.
Maintain adequate urine output for 2 hours.
Manage pain without narcotics.
Manage pain during dressing changes.

a.
b.
c.
d.

ANS: B

The endpoint of burn shock is defined as the state in which the individual is able to maintain
adequate urine output for 2 hours with the intravenous fluid administration rate equal to the
individuals calculated maintenance rate (see Box 48-4). None of the remaining options are
defined as the endpoint of burn shock.

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21. Which condition does a burn injury create for an extended period?
a. Hypervolemia
c. Hyponatremia
b. Hypermetabolism
d. Hypotension
ANS: B

Of the options available, a burn injury induces a hypermetabolic state that persists until wound
closure.
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22. What effect does a fatal burn injury have on interleukins (ILs)?
a. Decreases levels of IL-2, which may decrease T helper 1 (Th1) lymphocytes.
b. Decreases levels of IL-4, which causes a shift in production from Th1 to Th2

lymphocytes.
c. Decreases levels of IL-6, which produces cytokines.
d. Decreases levels of IL-12, which stimulates the production of immunoglobulins.
ANS: A

A fatal burn injury has often shown decreased levels of IL-2, which may result in decreased
Th1 lymphocytes. This option is the only accurate description of the effect a fatal burn injury
has on ILs.
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23. Daily evaporative water loss after a burn injury is approximately how many times the normal?
a. 5
c. 15
b. 10
d. 20
ANS: D

Moncrief and Mason attempted to determine the magnitude of such a loss and determined that
daily evaporative water loss was in the range of 20 times normal in the early phase of injury,
with gradual decreases as wound closure is achieved.
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24. What is the significance of a high level of interleukin 1 (IL-1) in a patient who has

experienced severe burns?

a. Prognosis is poor.
b. Antibiotic therapy is required.

c. Urinary function is improved.

d. They are less at risk for death.

ANS: D

The level of IL-1 inversely correlates with burn survival; low levels may be associated with a
higher mortality. This selection is the only option that accurately identifies the significance of
a high level of IL-1.
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25. What is the purpose of monitoring procalcitonin (PCT) levels in a patient after a burn?
a. To help evaluate the potential risk for respiratory complications

b. To justify the initiation of antibiotic therapy

c. To determine when discontinuing antibiotic use is feasible
d. To help in the selection of appropriate antibiotic therapy agents
ANS: C

Seeking to decrease the use of antibiotics in the patient who is critically ill and thus prevent
resistance to antibiotics is an important strategy in treating infection. Recent research suggests
that monitoring serial PCT levels, a precursor hormone to calcitonin, may be used to shorten
antibiotic use in the treatment of respiratory infections. PCT, normally not discernible on
assay, when elevated may indicate specific proinflammatory response during a bacterial
infection. PCT levels should not be used as an indicator to start antibiotics; however, if
monitored sequentially at the start of empiric antibiotics and then dropped to low levels, then
discontinuation may be clinically indicated.
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26. How many milliliters of fluid replacement per hour does a 70-kg adult with a 50% total body

surface area burn and a body surface area of 2 m require?

a. 150
c. 350
b. 275
d. 500
ANS: B

A 70-kg adult with a 50% total body surface area burn and a body surface area of 2 m requires
the following:
Basal = (1500 ml/day) (2 m2 body surface area) = 3000 ml/24 hr or 125 ml/hr
Evaporative = (25 + 50% total body surface burn)
(2m2 total body surface area) = (75) (2) = 150 ml/hr
Total maintenance fluids = 125 ml + 150 ml = 275 ml/hr
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REF: Page 1690 | Box 48-4

MULTIPLE RESPONSE
27. A patient will be referred to the burn unit when which criteria are met? (Select all that apply.)
a. Patient is older than 5 years of age.
b. The burn involves the face or a major joint.
c. The source of the burn is electrical.
d. Partial thickness burns are on more than 10% of the total body surface area

(TBSA).
e. Patient has a life-threatening trauma injury.
ANS: B, C, D

A burn unit may treat adults or children or both. Burn injuries that should be referred to a burn
unit include the following: partial-thickness burns on more than 10% TBSA, burns that
involve the face, hands, feet, genitalia, perineum, or major joints, and electrical burns,
including lightning injury. If the trauma poses the greater immediate risk, then the patients
condition may be initially stabilized in a trauma center before being transferred to a burn
center.
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REF: Page 1689 | Box 48-3

28. Which feedback loop will further impair oxygen in all types of shock? (Select all that apply.)
a. Activation of the fibrinolytic cascade
b. Increased circulating volume
c. Hypermetabolic state
d. Lysosomal enzyme release
e. Activation of the clotting cascade
ANS: D, E

Both positive and negative compensatory mechanisms, such as anaerobic metabolism,

lysosomal enzyme release, decreased intravascular volume, and activation of the clotting
cascade, may further impair oxygen delivery and use. The remaining options are not related to
impaired oxygen delivery.
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MATCHING

Match the types of shock with the corresponding descriptions. Terms can be used more than
once.
______ A. Cardiogenic
______ B. Hypovolemic
______ C. Neurogenic
______ D. Anaphylactic
______ E. Septic
29.
30.
31.
32.
33.

Follows a systemic inflammatory response.

Follows widespread hypersensitivity reaction.
Follows myocardial infarction.
Follows major burns.
Follows parasympathetic stimulation.

29. ANS: E
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MSC: Septic shock begins with systemic inflammatory response syndrome. It then evolves into
sepsis, into severe sepsis, and finally into septic shock.
30. ANS: D
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MSC: Anaphylactic shock is the outcome of a widespread hypersensitivity reaction known as
anaphylaxis.
31. ANS: A
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MSC: Cardiogenic shock results from the inability of the heart to pump adequate blood to tissues and
end organs. This type of shock occurs from any cause, the most common being within hours of an
acute myocardial infarction or severe episode of myocardial ischemia.
32. ANS: B
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MSC: Hypovolemia associated with burn shock results from massive fluid losses from the circulating
blood volume.
33. ANS: C
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MSC: Any factor that stimulates parasympathetic activity or inhibits sympathetic activity of vascular
smooth muscle can cause neurogenic shock.