Shock, Multiple Organ Dysfunction Syndrome, and Burns in Adults Chapter 46 Mosby items and derived...

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

Chapter 46Chapter 46

Mosby items and derived items © 2010, 2006 by Mosby, Inc., an affiliate of Elsevier Inc.Mosby items and derived items © 2010, 2006 by Mosby, Inc., an affiliate of Elsevier Inc.

22Mosby items and derived items © 2010, 2006 by Mosby, Inc., an affiliate of Elsevier Inc.Mosby items and derived items © 2010, 2006 by Mosby, Inc., an affiliate of Elsevier Inc.

ShockShock A condition in which the cardiovascular A condition in which the cardiovascular

system fails to perfuse the tissues system fails to perfuse the tissues adequately; causes general and widespread adequately; causes general and widespread impairment of cellular metabolismimpairment of cellular metabolism

Many factors cause shockMany factors cause shock Defective heart function, blood volume changes, Defective heart function, blood volume changes,

or blood vessel changesor blood vessel changes


ShockShock Many causes and clinical manifestationsMany causes and clinical manifestations Shock from any cause can progress to organ Shock from any cause can progress to organ

failure and deathfailure and death Untreated severe shock overwhelms the Untreated severe shock overwhelms the

body’s compensatory mechanisms through body’s compensatory mechanisms through positive-feedback loops that initiate and positive-feedback loops that initiate and maintain a downward physiologic spiral maintain a downward physiologic spiral


ShockShock Classified by cause, pathophysiologic Classified by cause, pathophysiologic

process, or clinical manifestationsprocess, or clinical manifestations Cardiogenic (caused by heart failure)Cardiogenic (caused by heart failure) Neurogenic or vasogenic (alterations in smooth Neurogenic or vasogenic (alterations in smooth

muscle tone)muscle tone) Anaphylactic (hypersensitivity)Anaphylactic (hypersensitivity) Septic (caused by infection)Septic (caused by infection) Hypovolemic (insufficient intravascular fluid)Hypovolemic (insufficient intravascular fluid) Traumatic (components of hypovolemic and Traumatic (components of hypovolemic and

septic)septic)


ShockShock Patient complaintsPatient complaints

Weak, “feeling sick,” cold, hot, nauseated, dizzy, Weak, “feeling sick,” cold, hot, nauseated, dizzy, confused, afraid, thirsty, short of breathconfused, afraid, thirsty, short of breath

Blood pressure, cardiac output, and urinary Blood pressure, cardiac output, and urinary output are usually decreased; the respiratory output are usually decreased; the respiratory rate is usually increasedrate is usually increased

Treatment: correct or remove underlying Treatment: correct or remove underlying cause and provide supportive therapycause and provide supportive therapy


ShockShock Impairment of cellular metabolismImpairment of cellular metabolism

Impaired oxygen use regardless of causeImpaired oxygen use regardless of cause• Aerobic to anaerobic metabolismAerobic to anaerobic metabolism

• Lose ability to maintain electrochemical gradientLose ability to maintain electrochemical gradient

• Sodium and chloride accumulate in the cellSodium and chloride accumulate in the cell Water follows, thus reducing the extracellular volume Water follows, thus reducing the extracellular volume

• Potassium exits the cellPotassium exits the cell

• Activated positive-feedback loops impair further oxygen Activated positive-feedback loops impair further oxygen useuse

Coagulation pathway activation, decreased circulatory Coagulation pathway activation, decreased circulatory volume, lysosomal enzyme releasevolume, lysosomal enzyme release


ShockShock Impaired cellular metabolismImpaired cellular metabolism

Impaired glucose useImpaired glucose use• Delivery or uptakeDelivery or uptake

• Cells shift to glycogenolysis, gluconeogenesis, lipolysisCells shift to glycogenolysis, gluconeogenesis, lipolysis

• Gluconeogenesis causes proteins to be used for fuel, Gluconeogenesis causes proteins to be used for fuel, thus are no longer available to maintain cellular thus are no longer available to maintain cellular structure, function, repair, and replication structure, function, repair, and replication

Toxic ammonia and urea productionToxic ammonia and urea production

• Metabolic acidosisMetabolic acidosis Compensatory mechanism initiated: enables cardiac and Compensatory mechanism initiated: enables cardiac and

skeletal muscles to use lactic acid as a fuel source but only skeletal muscles to use lactic acid as a fuel source but only for limited timefor limited time


ShockShock Cardiogenic (heart failure)Cardiogenic (heart failure)

Cause: myocardial ischemia, MI, CHF, myocardial or Cause: myocardial ischemia, MI, CHF, myocardial or pericardial infections, dysrhythmias, and drug toxicitypericardial infections, dysrhythmias, and drug toxicity

Clinical manifestations caused by inadequate Clinical manifestations caused by inadequate perfusion to the heart and end organs perfusion to the heart and end organs

As cardiac output decreases, compensatory adaptive As cardiac output decreases, compensatory adaptive responses activated: renin-angiotensin, responses activated: renin-angiotensin, neurohormonal, and sympathetic nervous systemsneurohormonal, and sympathetic nervous systems• Cause fluid retention, systemic vasoconstriction, tachycardiaCause fluid retention, systemic vasoconstriction, tachycardia

Catecholamines increase contractility and heart rateCatecholamines increase contractility and heart rate Further stress and metabolic demands on failing heart Further stress and metabolic demands on failing heart


Cardiogenic ShockCardiogenic Shock


ShockShock Hypovolemic Hypovolemic

Insufficient intravascular fluid volumeInsufficient intravascular fluid volume Loss of whole blood, blood plasma, interstitial Loss of whole blood, blood plasma, interstitial

fluid, or fluid sequestrationfluid, or fluid sequestration• Hemorrhage or burnsHemorrhage or burns

Compensatory vasoconstriction, increased SVR, Compensatory vasoconstriction, increased SVR, and afterload to improve blood pressure and and afterload to improve blood pressure and perfusion to core organsperfusion to core organs

If these mechanisms fail, impaired nutrient delivery If these mechanisms fail, impaired nutrient delivery and failing cellular metabolismand failing cellular metabolism


Hypovolemic ShockHypovolemic Shock


ShockShock Neurogenic (vasogenic) Neurogenic (vasogenic)

Widespread vasodilation from imbalance between Widespread vasodilation from imbalance between parasympathetic and sympathetic simulationparasympathetic and sympathetic simulation

Causes persistent vasodilation and creates Causes persistent vasodilation and creates relative hypovolemiarelative hypovolemia• Blood volume unchanged, but amount of space Blood volume unchanged, but amount of space

containing the blood has increased, so SVR decreases containing the blood has increased, so SVR decreases drasticallydrastically

• Pressure in vessels is inadequate to drive nutrients Pressure in vessels is inadequate to drive nutrients across capillary membranes; nutrient delivery to cells is across capillary membranes; nutrient delivery to cells is impairedimpaired

Severe pain and stress, anesthesia, and Severe pain and stress, anesthesia, and depressant drugsdepressant drugs


Neurogenic ShockNeurogenic Shock


ShockShock

AnaphylacticAnaphylactic Allergen causes extensive immune and inflammatory Allergen causes extensive immune and inflammatory

response response Widespread hypersensitivity reaction leading to Widespread hypersensitivity reaction leading to

vasodilation, peripheral pooling, relative hypovolemiavasodilation, peripheral pooling, relative hypovolemia Extravascular effects include constriction of Extravascular effects include constriction of

extravascular smooth muscleextravascular smooth muscle• Constriction often causes respiratory difficulty Constriction often causes respiratory difficulty

More severe due to other pathophysiologic effectsMore severe due to other pathophysiologic effects


Anaphylactic ShockAnaphylactic Shock


ShockShock

SepticSeptic Infectious processes initiate septic shockInfectious processes initiate septic shock Six most common infection sites: lungs, bloodstream, Six most common infection sites: lungs, bloodstream,

intravascular catheter, intra-abdominal, urinary tract, intravascular catheter, intra-abdominal, urinary tract, surgical woundsurgical wound

Bacteremia, endotoxins, and exotoxins cause the host to Bacteremia, endotoxins, and exotoxins cause the host to initiate the inflammatory processinitiate the inflammatory process• Complement, coagulation, kinin, and cellular immunity Complement, coagulation, kinin, and cellular immunity

The inflammatory response initiates and promotes The inflammatory response initiates and promotes widespread vasodilationwidespread vasodilation

Symptoms similar to neurogenic/anaphylactic shockSymptoms similar to neurogenic/anaphylactic shock


Multiple Organ Dysfunction Multiple Organ Dysfunction Syndrome (MODS)Syndrome (MODS)

Progressive dysfunction of two or more organ Progressive dysfunction of two or more organ systems due to an uncontrolled inflammatory systems due to an uncontrolled inflammatory response to a severe illness or injuryresponse to a severe illness or injury

Shock and sepsis are the most common Shock and sepsis are the most common causes, but can be from any injury or disease causes, but can be from any injury or disease that initiates massive systemic inflammationthat initiates massive systemic inflammation Trauma, major surgery, burns, acute pancreatitis, Trauma, major surgery, burns, acute pancreatitis,

acute renal failure, ARDSacute renal failure, ARDS



54% mortality rate if two organ systems are 54% mortality rate if two organ systems are affectedaffected

Mortality rate increases to 100% with five Mortality rate increases to 100% with five systems failingsystems failing



Secondary MODS Secondary MODS Progressive organ dysfunction Progressive organ dysfunction Result of excessive inflammatory reaction after a Result of excessive inflammatory reaction after a

latent period following the initial injury, in organs latent period following the initial injury, in organs distant from the site of the original injurydistant from the site of the original injury

Thought that the resulting organ trauma is caused by Thought that the resulting organ trauma is caused by the host response to a second insult rather than being the host response to a second insult rather than being a direct result of the primary injury a direct result of the primary injury • Second insult mild but produces immense disproportionate Second insult mild but produces immense disproportionate

response because of the previous priming of leukocytesresponse because of the previous priming of leukocytes

• Interaction of injured organs leads to a self-perpetuating Interaction of injured organs leads to a self-perpetuating inflammationinflammation



Maldistribution of blood flowMaldistribution of blood flow HypermetabolismHypermetabolism Myocardial depressionMyocardial depression Supply-dependent oxygen consumptionSupply-dependent oxygen consumption Reperfusion injuryReperfusion injury



TreatmentTreatment Control initial inflammatory processControl initial inflammatory process Restore intravascular volumeRestore intravascular volume Aimed at providing oxygen and nutrition to support Aimed at providing oxygen and nutrition to support

failing organsfailing organs


BurnsBurns General term describing cutaneous injury due General term describing cutaneous injury due

to thermal, chemical, or electrical causesto thermal, chemical, or electrical causes Multisystem injuries with interaction of shock, Multisystem injuries with interaction of shock,

inflammation, immunocompromiseinflammation, immunocompromise Burns can be thermal or nonthermalBurns can be thermal or nonthermal


BurnsBurns Burn wound depthBurn wound depth

First-degree burnsFirst-degree burns• Partial-thickness injuryPartial-thickness injury

Second-degree burnsSecond-degree burns• Superficial partial-thickness injurySuperficial partial-thickness injury• Deep partial-thickness injuryDeep partial-thickness injury

Third-degree burnsThird-degree burns• Full-thickness injuryFull-thickness injury• Painless because nerve endings destroyedPainless because nerve endings destroyed


BurnsBurns


Burn InjuryBurn Injury Total body surface area (TBSA)Total body surface area (TBSA)

Rule of ninesRule of nines Burn injury severity is a combination of age, Burn injury severity is a combination of age,

medical history, extent and depth of injury, medical history, extent and depth of injury, and body area involvedand body area involved


Rule of NinesRule of Nines


Burn InjuryBurn Injury Burn shockBurn shock

Hypovolemic shockHypovolemic shock Decreased cardiac contractilityDecreased cardiac contractility

Cellular responseCellular response Metabolic responseMetabolic response Immunologic responseImmunologic response Evaporative water lossEvaporative water loss


Burn InjuryBurn Injury

Burn shockBurn shock Massive edema associated with burn shock is Massive edema associated with burn shock is

inevitable with fluid resuscitationinevitable with fluid resuscitation• Failure to administer resuscitation fluid results in irreversible Failure to administer resuscitation fluid results in irreversible

hypovolemic shock and deathhypovolemic shock and death

Edema in unburned as well as burned areas Edema in unburned as well as burned areas Edema often leads to mechanical airway obstruction; Edema often leads to mechanical airway obstruction;

necessitates tracheal intubation, and increased necessitates tracheal intubation, and increased severity of the interstitial pulmonary edema severity of the interstitial pulmonary edema associated with inhalation injuryassociated with inhalation injury


Burn ShockBurn Shock

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