Chapter 46 Shock, Multiple Organ Dysfunction Syndrome, and Burns in Adults

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Chapter 46
Shock, Multiple Organ Dysfunction
Syndrome, and Burns in Adults
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Shock


A condition in which the cardiovascular
system fails to perfuse the tissues
adequately; causes general and widespread
impairment of cellular metabolism
Many factors cause shock

Defective heart function, blood volume changes,
or blood vessel changes
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Shock



Many causes and clinical manifestations
Shock from any cause can progress to organ
failure and death
Untreated severe shock overwhelms the
body’s compensatory mechanisms through
positive-feedback loops that initiate and
maintain a downward physiologic spiral
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Shock

Classified by cause, pathophysiologic
process, or clinical manifestations

Cardiogenic (caused by heart failure)
 Neurogenic or vasogenic (alterations in smooth
muscle tone)
 Anaphylactic (hypersensitivity)
 Septic (caused by infection)
 Hypovolemic (insufficient intravascular fluid)
 Traumatic (components of hypovolemic and
septic)
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Shock

Patient complaints



Weak, “feeling sick,” cold, hot, nauseated, dizzy,
confused, afraid, thirsty, short of breath
Blood pressure, cardiac output, and urinary
output are usually decreased; the respiratory
rate is usually increased
Treatment: correct or remove underlying
cause and provide supportive therapy
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Shock

Impairment of cellular metabolism

Impaired oxygen use regardless of cause
• Aerobic to anaerobic metabolism
• Lose ability to maintain electrochemical gradient
• Sodium and chloride accumulate in the cell

Water follows, thus reducing the extracellular volume
• Potassium exits the cell
• Activated positive-feedback loops impair further oxygen
use

Coagulation pathway activation, decreased circulatory
volume, lysosomal enzyme release
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Shock

Impaired cellular metabolism

Impaired glucose use
• Delivery or uptake
• Cells shift to glycogenolysis, gluconeogenesis, lipolysis
• Gluconeogenesis causes proteins to be used for fuel,
thus are no longer available to maintain cellular structure,
function, repair, and replication

Toxic ammonia and urea production
• Metabolic acidosis

Compensatory mechanism initiated: enables cardiac and
skeletal muscles to use lactic acid as a fuel source but only
for limited time
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Shock

Cardiogenic (heart failure)





Cause: myocardial ischemia, MI, CHF, myocardial or
pericardial infections, dysrhythmias, and drug toxicity
Clinical manifestations caused by inadequate
perfusion to the heart and end organs
As cardiac output decreases, compensatory adaptive
responses activated: renin-angiotensin,
neurohormonal, and sympathetic nervous systems
• Cause fluid retention, systemic vasoconstriction, tachycardia
Catecholamines increase contractility and heart rate
Further stress and metabolic demands on failing
heart
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Cardiogenic Shock
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Shock

Hypovolemic




Insufficient intravascular fluid volume
Loss of whole blood, blood plasma, interstitial
fluid, or fluid sequestration
• Hemorrhage or burns
Compensatory vasoconstriction, increased SVR,
and afterload to improve blood pressure and
perfusion to core organs
If these mechanisms fail, impaired nutrient
delivery and failing cellular metabolism
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Hypovolemic Shock
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Shock

Neurogenic (vasogenic)

Widespread vasodilation from imbalance between
parasympathetic and sympathetic simulation
 Causes persistent vasodilation and creates
relative hypovolemia
• Blood volume unchanged, but amount of space
containing the blood has increased, so SVR decreases
drastically
• Pressure in vessels is inadequate to drive nutrients
across capillary membranes; nutrient delivery to cells is
impaired

Severe pain and stress, anesthesia, and
depressant drugs
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Neurogenic Shock
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Shock

Anaphylactic




Allergen causes extensive immune and inflammatory
response
Widespread hypersensitivity reaction leading to
vasodilation, peripheral pooling, relative hypovolemia
Extravascular effects include constriction of
extravascular smooth muscle
• Constriction often causes respiratory difficulty
More severe due to other pathophysiologic effects
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Anaphylactic Shock
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Shock

Septic





Infectious processes initiate septic shock
Six most common infection sites: lungs, bloodstream,
intravascular catheter, intra-abdominal, urinary tract,
surgical wound
Bacteremia, endotoxins, and exotoxins cause the
host to initiate the inflammatory process
• Complement, coagulation, kinin, and cellular immunity
The inflammatory response initiates and promotes
widespread vasodilation
Symptoms similar to neurogenic/anaphylactic shock
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Multiple Organ Dysfunction
Syndrome (MODS)


Progressive dysfunction of two or more organ
systems due to an uncontrolled inflammatory
response to a severe illness or injury
Shock and sepsis are the most common
causes, but can be from any injury or disease
that initiates massive systemic inflammation

Trauma, major surgery, burns, acute pancreatitis,
acute renal failure, ARDS
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Multiple Organ Dysfunction
Syndrome (MODS)


54% mortality rate if two organ systems are
affected
Mortality rate increases to 100% with five
systems failing
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Multiple Organ Dysfunction
Syndrome (MODS)

Secondary MODS



Progressive organ dysfunction
Result of excessive inflammatory reaction after a
latent period following the initial injury, in organs
distant from the site of the original injury
Thought that the resulting organ trauma is caused by
the host response to a second insult rather than being
a direct result of the primary injury
• Second insult mild but produces immense disproportionate
response because of the previous priming of leukocytes
• Interaction of injured organs leads to a self-perpetuating
inflammation
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Multiple Organ Dysfunction
Syndrome (MODS)





Maldistribution of blood flow
Hypermetabolism
Myocardial depression
Supply-dependent oxygen consumption
Reperfusion injury
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Multiple Organ Dysfunction
Syndrome (MODS)

Treatment



Control initial inflammatory process
Restore intravascular volume
Aimed at providing oxygen and nutrition to support
failing organs
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Burns



General term describing cutaneous injury due
to thermal, chemical, or electrical causes
Multisystem injuries with interaction of shock,
inflammation, immunocompromise
Burns can be thermal or nonthermal
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Burns

Burn wound depth

First-degree burns
• Partial-thickness injury
 Second-degree burns
• Superficial partial-thickness injury
• Deep partial-thickness injury
 Third-degree burns
• Full-thickness injury
• Painless because nerve endings destroyed
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Burns
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Burn Injury

Total body surface area (TBSA)


Rule of nines
Burn injury severity is a combination of age,
medical history, extent and depth of injury,
and body area involved
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Rule of Nines
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Burn Injury

Burn shock






Hypovolemic shock
Decreased cardiac contractility
Cellular response
Metabolic response
Immunologic response
Evaporative water loss
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Burn Injury

Burn shock

Massive edema associated with burn shock is
inevitable with fluid resuscitation
• Failure to administer resuscitation fluid results in irreversible
hypovolemic shock and death


Edema in unburned as well as burned areas
Edema often leads to mechanical airway obstruction;
necessitates tracheal intubation, and increased
severity of the interstitial pulmonary edema
associated with inhalation injury
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Burn Shock
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Burn Shock
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