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6/12/2017
1
Slide 1JSOMTC, SWMG(A)
Complications of TraumaPFN: SOMTRL0F
Hours: 4.0
Instructor:
Slide 2JSOMTC, SWMG(A)
Terminal Learning Objective
Action: Communicate knowledge of Shock
Condition: Given a lecture in a classroom environment
Standard: Received a minimum score of 75% on the written exam IAW course standards
Slide 3JSOMTC, SWMG(A)
References
Trauma, 6th Edition, January 2008
Basic Immunology, January 2007
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Slide 4JSOMTC, SWMG(A)
References
Access Emergency Medicine, JSOMTC Learning Platform, 1 March 2011
Slide 5JSOMTC, SWMG(A)
Reason
Slide 6JSOMTC, SWMG(A)
Agenda
Define shock
Identify types of shock
Understand the shock state
Recognize the patient at risk
Identify fluid shifts and acid‐base balance disturbance associated with the shock state
Recognize the development of coagulopathy
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Slide 7JSOMTC, SWMG(A)
Agenda
Understand the effects of hypothermia
Describe hemorrhage and the four stages of hemorrhagic shock
Identify the stages, pathophysiology, clinical presentation and management of SIRS, sepsis and septic shock
Recall the SOCM fluid resuscitation protocol
Slide 8JSOMTC, SWMG(A)
Agenda
Identify the body fluids and fluid imbalances
Identify the risk factors, pathophysiology and management of multiple organ dysfunction syndrome (MODS)
Recognize acute renal failure (ARF)
Identify the cause and management of traumatic cardiac arrest
Slide 9JSOMTC, SWMG(A)
Agenda
Define the four respiratory complications relevant to trauma
Identify the pathophysiology, clinical presentation and management of acute respiratory distress syndrome (ARDS)
Identify the pathophysiology, risk factors, clinical presentation and management of pulmonary embolism
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Slide 10JSOMTC, SWMG(A)
Definition of Shock
Slide 11JSOMTC, SWMG(A)
Definition of Shock
Failure of the cardiovascular system to deliver enough oxygen and nutrients to meet the metabolic needs of the cells
Simply stated, shock can be defined as inadequate tissue perfusion
Slide 12JSOMTC, SWMG(A)
Definition of Shock
Shock is not adequately described or diagnosed by a single parameter: Pulse rate or blood pressure
Cardiac function
Hypovolemia or capillary refill
Temperature or skin color
Loss of systemic vascular resistance
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Slide 13JSOMTC, SWMG(A)
Etiology of Shock
More than 100 types of shock have been described
Often classified by the cause of the syndrome
Bottom Line: Regardless of the classification the underlying defect is ALWAYS inadequate tissue perfusion
Slide 14JSOMTC, SWMG(A)
Identify Types of Shock
Slide 15JSOMTC, SWMG(A)
Types of Shock
More than 100 TYPES OF SHOCK have been described
Often classified by the cause of the syndrome
Two or more types are often combined
•Hypovolemia may occur with septic shock
• Elements of cardiogenic shock frequently occur in other types of shock
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Slide 16JSOMTC, SWMG(A)
4 "Classic" Categories of Shock
Hypovolemic Hemorrhagic
Non‐hemorrhagic
Distributive Septic
Non‐septic
Cardiogenic Cardiomyopathic
Arrhythmogenic
Mechanical
Obstructive Pulmonary vascular
Mechanical
Slide 17JSOMTC, SWMG(A)
Hypovolemic Shock
Occurs when rapid loss of fluids results in inadequate circulating volume and subsequent inadequate perfusion. Hemorrhagic Shock
Non‐Hemorrhagic Shock
Slide 18JSOMTC, SWMG(A)
Hypovolemic Shock
Hemorrhagic Shock ‐ Reduced intravascular volume from blood loss and results in shock
Blunt Trauma
Penetrating trauma
Upper/lower GI bleeds
Ruptured abdominal aortic aneurysm
Aortic‐enteric fistulas
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Slide 19JSOMTC, SWMG(A)
Hypovolemic Shock
Non‐Hemorrhagic Shock ‐ Reduced intravascular volume from fluid loss other than blood can also cause shock
GI losses; diarrhea, vomiting
Skin losses; heat stroke, burns
Renal losses; diuresis
Third space losses; crush injury, cirrhosis, pancreatitis, Intestinal obstruction
Slide 20JSOMTC, SWMG(A)
Distributive Shock
Characterized by severe peripheral vasodilation (vasodilatory shock).
Septic
Non‐Septic
Slide 21JSOMTC, SWMG(A)
Distributive Shock
Septic Shock ‐ Is a clinical syndrome that occurs as part of the body's immune and inflammatory response to invasive or severe localized infection, typically from bacterial or fungal pathogens.
Sepsis is the most common cause of distributive shock.
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Slide 22JSOMTC, SWMG(A)
Distributive Shock
Non‐Septic Shock
Neurogenic
Anaphylactic
Drug/Toxin Induced
Endocrine
Psychogenic
Slide 23JSOMTC, SWMG(A)
Distributive Shock
Neurogenic Shock ‐ Diminished tissue perfusion as a result of loss of vasomotor tone to peripheral arterial beds
Usually due to injuries to the spinal cord
Disrupt sympathetic regulation of peripheral vascular tone resulting in HoTN
Below pink warm and dry; Above pale cool and clammy
Slide 24JSOMTC, SWMG(A)
Distributive Shock
Anaphylactic Shock ‐ Defined as a serious allergic or hypersensitivity reaction that is rapid in onset and may cause death.
IgE mediated
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Slide 25JSOMTC, SWMG(A)
Distributive Shock
Psychogenic Shock ‐ Non–life‐threatening causes include receiving bad news or seeing something unpleasant such as blood
Caused by a sudden reaction of the nervous system
Produces temporary vascular dilation
Results in fainting (syncope)
Slide 26JSOMTC, SWMG(A)
Obstructive Shock
Due to a mechanical obstruction of the circulation impending venous return to the heart or preventing cardiac filling
Divided into 2 general etiologies
Pulmonary vascular
Mechanical
Slide 27JSOMTC, SWMG(A)
Obstructive Shock
Pulmonary vascular ‐ Obstructive shock due to right ventricular failure secondary to high pulmonary vascular resistance Pulmonary Embolism (PE)
Severe Pulmonary HTN
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Slide 28JSOMTC, SWMG(A)
Obstructive Shock
Mechanical ‐ Primary physiologic disturbance causing reduced preload
Tension pneumothorax
Pericardial tamponade
Constrictive pericarditis
Restrictive cardiomyopathy
Slide 29JSOMTC, SWMG(A)
Cardiogenic Shock
Results when a failure of the circulatory pump leading to diminished forward flow and subsequent tissue hypoxia, in the setting of adequate intravascular volume
Cardiac pump failure is diverse and generally divided into 3 categories:Cardiomyopathy
Arrhythmic
Mechanical
Slide 30JSOMTC, SWMG(A)
Cardiogenic Shock
Cardiomyopathy ‐
Myocardial Ischemia (MI)
Severe heart failure
Myocarditis
Prolonged cardiac ischemia
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Slide 31JSOMTC, SWMG(A)
Cardiogenic Shock
Mechanical ‐
Aortic or mitral valve insufficiency
Valvular rupture
Critical aortic stenosis
Arrythmogenic ‐
Tachyarrhythmias
Bradyarrhythmias
Slide 32JSOMTC, SWMG(A)
Understand The Shock State
Slide 33JSOMTC, SWMG(A)
Inciting Event
Temperature
Trauma
Infection
Pain Hypoxia
Acidosis
Hypoglycemia
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Slide 34JSOMTC, SWMG(A)
Afferent Signaling
Baroreceptors
Chemoreceptors
Slide 35JSOMTC, SWMG(A)
Efferent Signaling
ANS ‐> SNS ‐> Catecholamines
Cardiovascular response
Neuroendocrine response
Immunological response
Inflammatory response
Cellular effect
Slide 36JSOMTC, SWMG(A)
SNS Response
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Slide 37JSOMTC, SWMG(A)
Cardiovascular Response
Alpha 1 – Systemic Vasoconstriction
Beta 1 – Increased HR, Contractility and Conduction Velocity
Beta 2 ‐ Bronchodilation, coronary artery dilation
Triggers the release of catecholamine's and initiating the RAS
SNS Response
Slide 38JSOMTC, SWMG(A)
Renin‐Angiotensin‐Aldosterone System
Renal hypoxia!
(less than 80mm Hg)
Hypotension!
Neuroendocrine Response
Slide 39JSOMTC, SWMG(A)
Glucose Production
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Slide 40JSOMTC, SWMG(A)
Immunological Response
1. Infection or insult established
2. Organisms proliferate
3. Toxins release
4. Toxins activate macrophages
5. Cytokines are released
6. Systemic activation occurs
Slide 41JSOMTC, SWMG(A)
Immunological Response
“The microorganisms that seem to have it
in for us . . . turn out . . . to be rather
more like bystanders. . . . It is our
response to their presence that makes
the disease. Our arsenals for fighting
off bacteria are so powerful . . . that
we are more in danger from them than
the invaders.”
Slide 42JSOMTC, SWMG(A)
Immunological / Inflammatory Response
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Slide 43JSOMTC, SWMG(A)
Recognize the Patient at Risk
Slide 44JSOMTC, SWMG(A)
Patients At Risk
Despite aggressive hemodynamic support, broad‐spectrum potent antibiotics, and surgical treatment, the mortality rate of septic shock remains high
Overall mortality rates exceed 20%
30‐45% of patients in Septic Shock die within 1 month of presentation
60‐90% of patients in Cardiogenic Shock die within 1 month of presentation
Slide 45JSOMTC, SWMG(A)
Patients At Risk
With a contemporary understanding of shock the combat medic can recognize its manifestation at earlier stages and initiate expert timely interventions regardless of the inciting factor
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Slide 46JSOMTC, SWMG(A)
Patient At Risk
Early detection and avoidance of the lethal triad
Five Trigger Points:
Acidosis (base deficit greater than 6)
Coagulopathy (INR greater than 1.5)
Hypothermia (temperature less than 96o)
HoTN (BP less than 90mmHg)
Hemoglobin (less than 11g)
Slide 47JSOMTC, SWMG(A)
Patient At Risk
DeathAcidosis Hypothermia
Coagulopathy
Slide 48JSOMTC, SWMG(A)
Injury 1st Event Recovery
Activation2nd Event
Infection2nd Event
Early MOF
Late MOF
Innate Immune System
Adaptive Immune System
SIRS
CARS
Pro
-infla
mm
atio
n
• Tissue Disruption• Cellular Shock• Blood component
transfusion• Coagulation• Genotype
Progression of the Shock State
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Slide 49JSOMTC, SWMG(A)
Identify Fluid Shifts and Acid‐Base Balance Disturbances Associated
with the Shock State
DeathAcidosis Hypothermia
Coagulopathy
Slide 50JSOMTC, SWMG(A)
Chemoreceptors
Chemoreceptors located throughout the body are sensitive to CO2, pH, and O2 and send impulses to the CVCC via sensory nerves which excite Sympathetic and Parasympathetic Divisions of ANS
Slide 51JSOMTC, SWMG(A)
Normal Cellular Function
Na+
Cl -
K+
Na+
Cl -
K+
ATP
ADP
K+
Na+
Leaky Channels, Gated Channels and Pumps
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Slide 52JSOMTC, SWMG(A)
Cellular Swelling
Slide 53JSOMTC, SWMG(A)
Acid‐Base Balance
Acid is a substance that releases H+ ions
CO2, lactic, ketones, urine, saliva, stomach acid
Base (alkali) is a substance that releases hydroxyl (OH‐) ions
Bicarbonate, blood
Slide 54JSOMTC, SWMG(A)
Acid‐Base Balance
Neutral pH is 7.0, < 7.0 is acidic and > 7.0 is alkali
Anatomical pH below 7.35 represents acidosis, above 7.45 represents alkalosis
The body has 3 systems to maintain homeostasis; bicarbonate, urinary and respiratory buffer systems.
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Slide 55JSOMTC, SWMG(A)
Hydrogen Ion Homeostasis
H+Metabolism Metabolism
HemoglobinProtein
Slide 56JSOMTC, SWMG(A)
O2 Transport
O2 diffuses from alveoli to blood where 4 molecules of O2 bind with hemoglobin and are transported to the left heart and out to the system
98.5% of oxygen binds with hemoglobin (oxyhemoglobin) while only 1.5% is dissolved in the blood
Saturation ?
Slide 57JSOMTC, SWMG(A)
Oxygen Saturation
S%O2 is the percent saturation of hemoglobin with oxygen
S%O2 and PaO2 positively correlated but not physiologically linear (oxyhemoglobindissociation curve)
Pulse oximetry can be misleading with hypovolemia S%O2 may be good but PaO2 may be low so perfusion is poor
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Slide 58JSOMTC, SWMG(A)
Gas Exchange in the Tissue
40 mmHg
45 mmHg
40 mmHg
95 mmHg
Slide 59JSOMTC, SWMG(A)
Gas Exchange in the Lungs
100 mmHg
40 mmHg45 mmHg
40 mmHg
Slide 60JSOMTC, SWMG(A)
Recognize the Development of Coagulopathy
DeathAcidosis Hypothermia
Coagulopathy
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Slide 61JSOMTC, SWMG(A)
Traumatic Coagulopathy
Traditional Driving Factors
Massive fluid resuscitation
Clotting factor dilution
Clotting factor consumption
Hypothermia
Acidosis
Slide 62JSOMTC, SWMG(A)
Coagulation Disorders
Disseminated Intravascular Coagulopathies (DIC)
Bleeding disorder resulting from the widespread over stimulation of the body's clotting and anti‐clotting mechanisms
Hemodilution
Increase in the volume of plasma, resulting in a reduced concentration of red blood cells in the blood
Slide 63JSOMTC, SWMG(A)
Disseminated Intravascular Coagulopathies (DIC)
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Slide 64JSOMTC, SWMG(A)
DIC
Is considered an acquired bleeding disorder
Is not a disease entity but an event that can accompany various disease processes
Is an alteration in the blood clotting mechanism (abnormal acceleration of the coagulation cascade, resulting in thrombosis)
Clotting and hemorrhage occur simultaneously
Slide 65JSOMTC, SWMG(A)
Common Causes of DIC
Sepsis from a variety of organisms (bacterial, fungal, viral, and parasitic)
Malignancy
Trauma, especially to the CNS
Obstetrical complications
Intravascular hemolysis, often due to acute hemolytic transfusion reaction (AHTR) in the setting of ABO incompatible transfusion
Slide 66JSOMTC, SWMG(A)
Main features of DIC in 118 Patients
Dysfunction Feature Affected Patient %
Bleeding 64%
Renal dysfunction 25%
Hepatic dysfunction 19%
Respiratory dysfunction 16%
Shock 14%
CNS dysfunction 2%
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Slide 67JSOMTC, SWMG(A)
Pathogenesis of DIC
Procoagulant exposure
Coagulation
Fibrinolysis
End organ damage
Slide 68JSOMTC, SWMG(A)
Systemic Activation of Coagulation
Slide 69JSOMTC, SWMG(A)
DIC Clinical Presentation
Epistaxis
Gingival bleeding
Mucosal bleeding
Cough
Dyspnea
Confusion, disorientation
Fever
Bruising, petechiae
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Slide 70JSOMTC, SWMG(A)
DIC Management
The basic treatment involves addressing the already existing conditions, which may be more than one
Medications associated with treatment:
Anticoagulants
Blood components
Antifibrinolytics
Heparin (Adult: 80‐100 U/kg SC q4‐6h or 20,000‐30,000 U/d IV continuous infusion)
Slide 71JSOMTC, SWMG(A)
Petechiae Associated with DIC
Slide 72JSOMTC, SWMG(A)
Understand the Effects of Hypothermia
DeathAcidosis Hypothermia
Coagulopathy
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Slide 73JSOMTC, SWMG(A)
Hypothermia
Many causes exist with trauma
Altered central thermoregulation
Prolonged exposure to low ambient temp.
Decreased heat production due to shock
Inadequately warmed fluids
Slide 74JSOMTC, SWMG(A)
Hypothermia
Coagulation effects from hypothermia
Enzymatic reactions of the coagulation cascade are temperature dependent.
Functionally optimal at 37oC or 98.6oF
1oC corresponds to a decrease in clotting factors by 10%
Hypothermia also affects both platelet function and fibrinolysis
Slide 75JSOMTC, SWMG(A)
Hypothermia Prevention
Minimize exposure; keep gear on/with casualty if feasible
Replace wet with dry clothing; place on insulating surface if able
‘Ready‐Heat Blanket’ to torso & ‘Heat‐Reflective Shell’(HRS) from HPMK
No HRS? Blizzard Survival Blanket and ‘Ready‐Heat’ combination
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Slide 76JSOMTC, SWMG(A)
Hypothermia Prevention
Aforementioned items not available?
Dry Blanket
Poncho Liner
Sleeping Bag
Anything that retains heat and keeps casualty dry!
Warm IV fluids are preferred if fluid therapy required
Slide 77JSOMTC, SWMG(A)
Describe Hemorrhage and the Four Stages of Hemorrhagic Shock
Slide 78JSOMTC, SWMG(A)
Hemorrhagic Shock
The most common cause of shock in the trauma patient is loss of circulating volume from hemorrhage
The most common form of combat related shock
Shock in a trauma patient with blunt or penetrating trauma should be presumed to be hemorrhage until proven otherwise
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Slide 79JSOMTC, SWMG(A)
Fractures and Blood Loss
Pelvic Fx: 2,000 mL
Femur Fx: 1,500 mL
Humerus Fx: 750 mL
Tibia/Fibula: 750 mL
Large Contusions: 500 mL
Slide 80JSOMTC, SWMG(A)
Stage 1
15% loss of Circulating Blood Volume 70 kg pt = 500‐750 mL blood loss
The healthy human system can easily compensate for such a blood loss volume by constricting the vascular beds, especially on the venous side.
Slide 81JSOMTC, SWMG(A)
Stage 2
15‐25% loss of Circulating Blood Volume 750‐1250 mL blood loss
The first line of compensatory responses can no longer maintain an adequate BP.
A strong release of catecholaminesincreases peripheral vasoconstriction.
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Slide 82JSOMTC, SWMG(A)
Stage 3
25‐35% loss of Circulating Blood Volume 1250‐1750 mL
Compensatory mechanisms can no longer cope with the loss.
Rapid tachycardia as the blood pressure begins to drop even more.
Slide 83JSOMTC, SWMG(A)
Stage 4
Greater than 35% Circulating Blood Volume Loss >1750 mL
The patients pulse is barely palpable, if one can be found at all and moving rapidly to unconsciousness.
Slide 84JSOMTC, SWMG(A)
Compensated Shock
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Slide 85JSOMTC, SWMG(A)
Compensated Shock/Stage 1
15% loss of CBV 70 kg pt = 500‐750 mL blood loss
Compensation phase LOC intact (usually)
Vasoconstriction
Normal BP, Pulse Pressure, Respirations
Slight Elevation of Pulse
Release of catecholamine• Epinephrine• Norepinephrine• Anxiety, slightly pale and clammy skin
Slide 86JSOMTC, SWMG(A)
Decompensated Shock
Slide 87JSOMTC, SWMG(A)
Decompensated/Stage 2
15‐25% loss of CBV 750‐1250 mL blood loss
Early Decompensation LOC deterioration
Unable to maintain BP (unstable)
Tachycardia & Tachypnea
Decreased pulse strength
Narrowing pulse pressure?
Significant catecholamine release• Increase systemic peripheral resistance
• Cool, clammy skin & thirst
• Increased anxiety and agitation
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Slide 88JSOMTC, SWMG(A)
Decompensated Shock
Marked increase in heart, respiratory rate, and a decrease BP.
Prolonged capillary refill
Blood flow to critical organs drop
• Decreased urine output (decreased flow to kidneys) continues or worsens
• Generally altered mental status secondary to blood loss is seen in this stage (decreased flow to brain)
Slide 89JSOMTC, SWMG(A)
Late Decompensated/Stage 3
25‐35% loss of CBV 1250‐1750 mL
Late Decompensation Significant LOC deterioration
Compensatory mechanism unable to cope with loss
Slide 90JSOMTC, SWMG(A)
Late Decompensated
Classic ShockWeak, thread, and rapid PULSE
•Narrowing pulse pressure
Tachypnea
Tachycardia
Anxiety, restlessness
Decreased LOC and AMS
Pale, cool, and clammy skin
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Slide 91JSOMTC, SWMG(A)
Irreversible Shock
Slide 92JSOMTC, SWMG(A)
Irreversible/Stage 4
Greater than 35%Loss CBV >1750 mL
Irreversible Pulse pressure: Barely palpable
Respiration: Rapid, shallow, and ineffective
LOC: Lethargic, confused, unresponsive
Bradycardia Skin: Cool, clammy, and very pale
Unlikely survival due to DIC
Slide 93JSOMTC, SWMG(A)
Irreversible Shock
Signs and symptoms
Bradycardia (HALLMARK)
Serious dysrhythmias
Frank hypotension
Pale, cold, and clammy skin
Noticeably delayed or absence of capillary refill
Cardiopulmonary collapse is usually imminent
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Slide 94JSOMTC, SWMG(A)
Variations in Physiological Responses to Shock
Age and relative health
General physical condition
Preexisting diseases
Medications
Environment
Slide 95JSOMTC, SWMG(A)
Variations in Physiological Responses to Shock
Ability to activate compensatory mechanismsOlder adults are less able to compensate (develop hypotension early)
Children compensate longer but deteriorate faster
Medications may interfere with compensatory mechanisms
Slide 96JSOMTC, SWMG(A)
Pre‐existing condition
Rate of blood loss
Patient Types Pregnant
• >50% blood volume than normal
• Fetus deprived of good circulation when mother is compensating
Athletes• Greater fluid and cardiac capacity
Variations in Physiological Responses to Shock
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Slide 97JSOMTC, SWMG(A)
Patient TypesObese
• CBV is based on IDEAL weight
Children
• CBV 8‐9% of body weight
• Poor compensatory mechanisms
• TREAT AGGRESSIVELY
Elderly
• Decreased CBV
•Medications: Beta Blockers, BP, & Anticoagulants
Variations in Physiological Responses to Shock
Slide 98JSOMTC, SWMG(A)
Identify the Stages, Pathophysiology, Clinical
Presentation and Management of SIRS, Sepsis, and Septic Shock
Slide 99JSOMTC, SWMG(A)
Septic Shock Progression
SIRS
Sepsis
Severe Sepsis
Septic Shock
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Slide 100JSOMTC, SWMG(A)
SIRS, Sepsis and Septic ShockInterrelationship
Slide 101JSOMTC, SWMG(A)
Septic Shock Stages
Systemic Inflammatory Response Syndrome (SIRS)
2 or more of the following:
• Temperature of > 38C or < 36C
• Heart Rate of > 90 bpm• Respiratory Rate of > 20 per minute
•WBC count > 12,000uL or < 4,000uL or 10% immature forms
Slide 102JSOMTC, SWMG(A)
Septic Shock Stages (cont)
Sepsis
SIRS plus culture documented infection
Severe Sepsis
Sepsis plus organ dysfunction, hypotension, or hypoperfusion (including but not limited to lactic acidosis, oliguria, or acute mental status change)
Septic Shock
Hypotension (despite fluid resuscitation efforts) and hypoperfusion
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Slide 103JSOMTC, SWMG(A)
SIRS, Sepsis and Septic Shock Management
Slide 104JSOMTC, SWMG(A)
Management Therapy
Stabilize airway and breathing
Intubation
Oxygen administration
Consider mechanical ventilation
Septic Shock:
Initial crystalloid fluid challenge (1‐2 Liters) for a period of 30‐60 minutes
Monitor Ins and Outs: maintain 30‐50cc/hr
Monitor for fluid overload (dyspnea, pulmonary rales, or pulmonary edema)
Slide 105JSOMTC, SWMG(A)
Management (cont)
The fluid algorithm is a guide for fluid therapy
It is only a guide and the casualties response or non‐response should be taken into account along with the long term ramifications of any treatment
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Slide 106JSOMTC, SWMG(A)
Management Keys
Early recognition of infection
Challenging in special populations (children and elderly)
Early antibiotic therapy (within 1st hour of recognition)
Maintaining adequate tissue perfusion with fluid therapy
Slide 107JSOMTC, SWMG(A)
Antibiotic Therapy
Broad spectrum antibiotics covering gram‐positive, gram‐negative, and anaerobic bacteria
Antibiotic resistant bacteria are a concern (MRSA: Methicillin‐Resistant Staphylococcus Aureus)
Slide 108JSOMTC, SWMG(A)
Antibiotics
Choices
Ertapenem, also known as Invanz (Beta‐lactam) 1gm given over 30 min IV
MRSA: Vancomycin
Linezolid
Extended Spectrum Penicillins: Ticarcillin
Piperacillin
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Slide 109JSOMTC, SWMG(A)
Persistent Hypotension
Consider Vasopressors (1ST Line)
Norepinephrine
Dopamine
2nd Line Vasopressors:
Epinephrine
Vasopressin (also known as ADH, Antidiuretic Hormone)
Slide 110JSOMTC, SWMG(A)
Recall the SOCM Fluid Resuscitation Protocol
Slide 111JSOMTC, SWMG(A)
SOCM Fluid Resuscitation Protocol for Multisystem Trauma
This protocol was designed to assist the management of patients with potential uncontrolled internal hemorrhage as a result of blunt or penetrating body cavity trauma or a significant external hemorrhage now controlled.
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Slide 112JSOMTC, SWMG(A)
The Fluid Algorithm
The SOCM fluid algorithm provides a means to increase the vascular volume (blood pressure) and to help perfusion of vital organs, such as the kidneys
Careful attention and a conscious thought process for fluid administration will enable the SOCM to find the “happy medium” for vascular volume, limiting hemodilution consequences
Slide 113JSOMTC, SWMG(A)
SOCM Fluid Protocol
Purpose:
To guide resuscitation of hypotensive patients to a coherent mental status or palpable radial pulse.
To guide resuscitation of hypotensive patients with TBI
Slide 114JSOMTC, SWMG(A)
SOCM Fluid Protocol
All adult casualties in hemorrhagic shock should be resuscitated to; Systolic BP of at 80‐90 mmHg systolic
Improved mental status
Palpable radial pulse
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Slide 115JSOMTC, SWMG(A)
SOCM Fluid Protocol Overview
The preferred fluids for resuscitation of casualties in hemorrhagic shock;
1. Whole blood
2. 1:1:1 Plasma, RBC, and platelets
3. 1:1 Plasma and RBC's
4. Reconstituted FDP, liquid plasma, thawed plasma alone or RBC's alone
5. Hextend
6. LR or Plasma‐Lyte A
Slide 116JSOMTC, SWMG(A)
SOCM Fluid Protocol
Patients without TBI or found to be non‐symptomatic of hemorrhagic shock or without weak/absent radial pulse;
1. Establish IV access (Saline Lock)
2. No IV fluids are immediately necessary
3. Fluids by mouth are permissible if the casualty is conscious and can swallow.
Slide 117JSOMTC, SWMG(A)
SOCM Fluid Protocol
Hemorrhagic shock and/or absent radial pulse (Systolic BP < 80 mmHg) without TBI;
Administer 500 ml IV Bolus
Immediately reassess for;
1. Palpable radial pulse, or
2. Improved mental status, or
3. Systolic BP of 80‐90mmHg
Discontinue when one OR more of the above has been achieved
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Slide 118JSOMTC, SWMG(A)
SOCM Fluid Protocol
If the end state has not been achieved then repeat one more 500 ml IV Bolus.
If 1000 ml of fluids have been administered and blood products are still unavailable then continue resuscitation with Hextendor crystalloid solution as needed to maintain the target BP or to produce clinical improvement.
Slide 119JSOMTC, SWMG(A)
SOCM Fluid Protocol
Patients with TBI or and concomitant hemorrhagic shock or with absent radial pulse (Systolic BP < 80 mmHg);Administer 500 ml IV Bolus
Immediately reassess for;
1. Normal radial pulse
2. Systolic BP of at least 90 mmHg
Discontinue when one OR more of the above has been achieved
Slide 120JSOMTC, SWMG(A)
Special Considerations
Burn patients can receive either crystalloid or colloid infusions. Burn patients that require fluid resuscitation due to trauma must first be brought to 80‐90 mmHg prior to beginning the Parkland infusion. Renal output should guide treatment if the patient requires significant fluids to achieve 80‐90 mm Hg (hemodilutionrisk is great).
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Slide 121JSOMTC, SWMG(A)
Special Considerations
Battlefield fluid triage terminology
Rapid Responder
Transient Responder
Non‐Responder
Slide 122JSOMTC, SWMG(A)
Crystalloid vs. Colloid BLOOD VOLUME in 1 hour
1000cc
500cc
500cc
500cc
200 600 1000
INFUSIONVOLUME
Ringer’s Lactate
5% Albumin
Hextend
Packed cells Blood
Slide 123JSOMTC, SWMG(A)
Hextend
ProsMore volume replacement capability
500cc bolus creates 800cc volume increase
Stays in vascular space for up to 8 hours• Only 200cc of a 1000cc bolus of Saline will remain in the vascular space after 1 hour
Medic can carry less fluid
ConsCost $.61 cents for 1 liter Ringers, $27.50 for 500cc Hextend
Leaky capillary syndrome. Reverse fluid shift.
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SOCM Fluid Algorithm (Trauma)Administration Precedence1. Whole Blood2. Plasma : RBC : Platelets
(1:1:1) ratio3. Plasma : RBC (1:1) ratio4. Plasma or RBC's alone5. Hextend6. Crystalloids
1. Establish IV access (Saline Lock)
2. No IV fluids are immediately necessary
3. Fluids by mouth are permissible if the casualty is conscious and can swallow
Hemorrhagic Shockand/or
Absent radial pulse*(Systolic BP < 80
mmHg)
NO
YES
Suspected or Known
TBINO YES
1 unit blood productor
500ml IV bolus
1 unit blood productor
500ml IV bolus
Immediately reassess for;1. Palpable radial pulse*, or2. Improved mental status, or3. Systolic BP of 80-90 mmHg
Immediately reassess for;1. Normal radial pulse*, or2. Systolic BP of 90 mmHg
NO NO
Discontinue when one OR more of the above has been achieved
Discontinue when one OR more of the above has been achieved
YESYES
* Although assessing the radial pulse is a quick indicator for shock especially in the field, obtaining a BP is a better indicator especially in the clinic.
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Identify the Body Fluids and Fluid Imbalances
Slide 126JSOMTC, SWMG(A)
Water
Water is the main component of body mass:
Accounts for 50%‐60% of body weight in adults
The healthy body maintains a constant balance between intake and excretion of water
The water gained each day is approximately equal to the water lost
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Water
The body gains water by:
Drinking fluids (primary source)
Ingesting food containing moisture
Forming water through the oxidation of hydrogen in foods during the metabolic process
The body loses water by:
Kidneys as urine
Feces
Skin as perspiration
Exhaled air as vapor
Excretion of tears and saliva
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Fluid Imbalances
Two abnormal states of body fluid balance can occur:
Dehydration
Over hydration
Slide 129JSOMTC, SWMG(A)
Orthostatic Vital Signs
Variation in what is considered abnormal:
Pulse rate increase greater than 15‐20 from lying to standing
Systolic BP decrease of greater than 10‐20 mm Hg from lying to standing
Diastolic BP decrease of greater than 10‐15mm Hg from lying to standing
The greater the difference the higher the specificity and the lower the sensitivity
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Dehydration
Can be classified as:
Isotonic‐excessive loss of sodium and water in equal amounts (diarrhea)
Hypernatremic‐ (more salt than water) loss of water in excess of sodium (sweat losses, diuretics)
Hyponatremic‐ (more water than salt) loss of sodium in excess of water (diuretics)
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Isotonic Dehydration
Causes
Severe or long‐term vomiting or diarrhea
Signs and symptoms:
Dry skin
Poor skin turgor (“doughy” skin)
Longitudinal wrinkles or furrows of the tongue
Oliguria (urinary output‐‐100‐400 ml/24hr) Anuria (urinary output‐‐100 ml or less in 24 hr)
Depressed or sunken fontanelles (“soft spot”) in infants
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Isotonic Dehydration
Treatment:
IV infusion of an isotonic solution that has a solute concentration equal to that of blood (usually NS)
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Hypernatremic Dehydration
Causes:
Excessive use or misuse of diuretics
Excessive loss of water with little loss of salt (sweat is about 1/4 ‐ 1/3 normal saline)
Profuse, watery diarrhea
Inhalation or ingestion of saltwater (e.g., near‐drowning) may cause hypernatremia without dehydration
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Hypernatremic Dehydration
Signs and Symptoms:
Dry, sticky mucous membranes
Flushed skin
Intense thirst
Oliguria or anuria
Treatment:
Volume replacement with isotonic or occasional hypotonic solutions, based on serum sodium levels and the clinical condition of the patient
Slide 135JSOMTC, SWMG(A)
Hyponatremic Dehydration
Causes:
Use of diuretics
Increased water intake
Inhalation or ingestion of fresh water (e.g., near‐drowning)
Signs and Symptoms:
Abdominal or muscle cramps
Seizures
Rapid, thready pulse
Cyanosis
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Hyponatremic Dehydration
Treatment:
IV fluid replacement with normal saline or lactated Ringer's solution
Occasionally hypertonic saline, e.g., when seizures caused by hyponatremia occur
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Orthostatic Vital Signs
Variation in what is considered abnormal:
Pulse rate increase greater than 15‐20 from lying to standing
Systolic BP decrease of greater than 10‐20 mm Hg from lying to standing
Diastolic BP decrease of greater than 10‐15mm Hg from lying to standing
The greater the difference the higher the specificity and the lower the sensitivity
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Over Hydration
An increase in body water with a decrease in solute concentration
Causes:
IV administration of excessive fluid
Impaired cardiac function
Impaired renal function
Some endocrine dysfunction's
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Over Hydration
Signs and Symptoms:
Shortness of breath
Puffy eyelids
Edema
Polyuria (voiding a large volume of urine in a given time)
Moist crackles (rales)
Acute weight gain
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Over Hydration
Treatment:
Depends on the cause
Excessive water administration and certain endocrine problems are treated with water restriction
Cardiac or renal impairment may be treated with diuretics
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Over Hydration
Treatment:
Profound hyponatremia associated with over hydration (serum sodium level less than 120 mEq/L and associated seizures or altered consciousness) may require administration of hypertonic saline
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Fluids
Concentrations of particles within the intracellular and extracellular spaces regulate movement of fluids
Fluid volume is controlled by hormones, kidneys and thirst mechanism
1. ADH
2. Aldosterone
Hypervolemia is too much fluid volume and hypovolemia is too little
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Identify the Risk Factors, Pathophysiology and Management of Multiple Organ Dysfunction
Syndrome (MODS)
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Injury 1st Event Recovery
Activation2nd Event
Infection2nd Event
Early MOF
Late MOF
Innate Immune System
Adaptive Immune System
SIRS
CARS
Pro
-infla
mm
atio
n
• Tissue Disruption• Cellular Shock• Blood component
transfusion• Coagulation• Genotype
Progression of the Shock State
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Compensatory Anti‐Inflammatory Response Syndrome (CARS)
Counter‐regulation of SIRS anti‐inflammatory mediators
If exaggerated immunoparalysis occurs (CARS) diminished or no immunosurveillance
Microorganisms can easily invade the body during this period
Patients are prone to developing sepsis with subsequent septic shock
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Classification of MODS
Immediate Type (Primary): Dysfunction are happened simultaneously in two or more organs due to primary disease.
Delayed Type (Secondary): Dysfunction happened in an organ, other organs sequentially happened dysfunction or failure.
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Four clinical phases in MODS
Stage 1 the patient has increased volume requirements and mild respiratory alkalosis which is accompanied by oliguria, hyperglycemia and increased insulin requirements.
Stage 2 the patient is tachypneic, hypocapnic and hypoxemic. Moderate liver dysfunction and possible hematologic abnormalities.
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Four clinical phases in MODS
Stage 3 the patient develops shock with azotemia and acid‐base disturbances. Significant coagulation abnormalities.
Stage 4 the patient is vasopressor dependent and oliguric or anuric. Ischemic colitis and lactic acidosis follow.
Slide 149JSOMTC, SWMG(A)
Manifestation of MODS
Organ
Heart
Peripheral circulation
Lung
Kidney
Gastro‐intestine
Liver
Brain
Coagulation
Symptoms
Acute heart failure
Shock
ARDS
ARF
Stress ulcers / GIT paralysis
Acute hepatic failure
CNS failure
DIC
Slide 150JSOMTC, SWMG(A)
Multi‐Organ Dysfunction Risk factors
Increased age
Injury severity
Number of units of RBC’s transfused
Base deficit
Lactate levels
Obesity
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Recognize Acute Renal Failure (ARF)
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Acute Renal Failure
Abrupt or rapid decline in renal filtration function
First sign of injury to kidney is decreasedurine production
Microvascular changes and Inflammation play the usual role in injury
Slide 153JSOMTC, SWMG(A)
Renal Failure Categories
Pre‐renal: Sudden and severe drop in BP or interruption of blood flow
Intra‐renal: Direct damage due to inflammation, toxins, drugs, infection
Post‐renal: Enlarged prostate, stones, tumor, or injury
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Renal Failure Management
As a SOCM, we are concerned with renal function at all times
The best treatment at this time is initiation of fluid therapy and minimizing hypovolemia
The time window for intervention is 6 hours
Dialysis is a consideration when the SOCM may be in an environment that supports this intervention
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Identify the Cause and Management of Traumatic Cardiac Arrest
Slide 156JSOMTC, SWMG(A)
Cardiac Arrest
Myocardial dysfunction is defined according to 4 factors
Preload
Afterload
Contractility
Heart rate
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Common Causes
Systemic hypovolemia (inadequate preload), secondary to hemorrhage or third space losses is the most common factors of cardiac arrest in the trauma patient
Evolving ischemia may affect contractility
Blunt trauma to the heart may lead to contractile dysfunction and decreased cardiac output
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Management Considerations
Urine output is markedly decreased from hypoperfusion. Restoring vascular volume aids the heart and other organs immensely
With volume replacement, patient temperature is of major concern and study after study confirms that hypothermia induces suppression of diastolic and systolic function
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Define the Four Respiratory Complications Relevant to Trauma
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Respiratory Complications
Acute Respiratory Distress Syndrome (ARDS)
Acute, hypoxemic respiratory failure following systemic or pulmonary insult without evidence of heart failure
Pulmonary embolism (PE)
A complication that results from a block in the main artery supplying the lungs, or one of its branches
Slide 161JSOMTC, SWMG(A)
Respiratory Complications (cont)
Air embolism
Obstruction of the circulatory system caused by an air bubble from trauma, surgery, hypodermic injection or diving
Fat embolism
Condition in which fat blocks an artery; fat can enter the blood stream after a long bone is fractured or adipose tissue is injured
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Identify the Pathophysiology, Clinical Presentation and
Management of Acute Respiratory Distress Syndrome (ARDS)
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ARDS
Most severe form of acute lung injury
Pro‐inflammatory cytokines are considered to be pivotal in the lung injury.
ARDS is typically associated with sepsis and other underlying conditions
Characterized by inflammation of the lung parenchyma leading to impaired gas exchange
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ARDS Pathophysiology
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Pathophysiology (cont)
Inflammation of the epithelial membrane causes inefficiency of oxygen and waste exchange
A widening interstitium allows neutrophils and other molecules to decrease exchange processes
Inactivated surfactant collapses and diminishes the alveoli functioning
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ARDS Presentation
Acute onset (12‐24 hours)
Dyspnea
Tachypnea
Intercostal retractions
Crackles heard while auscultating
Chest radiographs show “bilateral infiltrates”
Marked hypoxemia refractory to oxygen therapy
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Radiographic Pulmonary Infiltrates
Presents within 12‐24 hours
Mortality rate: 42% (ICU 37%)
ARDS associated with sepsis has mortality rate approaching 90%
X‐ray presentation of the lungs features diffuse patchy nature
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ARDS Management
Identification and specific treatment of the underlying secondary conditions (sepsis)
Meticulous supportive care
Intubation
Low tidal volume mechanical ventilation (6ml/kg of ideal body weight)
Maintain SpO2 above 88%
Prone positioning may be considered
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ARDS Management (cont) Targeted Antibiotic therapy should be administered
PEEP therapy (Positive End Expiratory Pressure) In ARDS, three populations of alveoli can be distinguished. There are normal alveoli which are always inflated and engaging in gas exchange, flooded alveoli which can never be used for gas exchange, and partially flooded alveoli that can be "recruited" to participate in gas exchange.
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Controversial Management Options
Systemic Corticosteroids is a treatment that has had limited and inconsistent results
The routine use of corticosteroids with ARDS is not recommended
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Identify the Pathophysiology, Risk Factors, Clinical Presentation and
Management of Pulmonary Embolism
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Embolism Basics
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Embolism Basics (cont)
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Pulmonary Embolism
Incidence is 1 per 1000 per year
Massive acute PE mortality rate 30‐60%
Non‐massive mortality rate is <5%
Largest risk group is African Americans at 50%
PE affects both men and women at the same rate
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Pulmonary Embolism
Most of the time, the block is due to a blood clot (thrombus) that has detached itself from the deep veins in the legs and traveled all the way to the lungs
This process is known as venous thromboembolism
Related to DVT (Deep Vein Thrombosis)
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Virchow Triad
Pulmonary Embolism is triggered by 3 main causes:
Venostasis
Hypercoagulability
Vessel wall inflammation (injury to the intima)
Slide 177JSOMTC, SWMG(A)
Remember the Virchow Triad in relation these risk factors:
Trauma
• Spinal cord injury
• Catheters• Postoperative
Old Age
PE Risk Factors
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PE Risk Factors (cont)
Oral Contraceptives
Smoking
Pregnancy
Hypercoagulable state due to venous stasis and altered levels of circulating clotting factors
3rd trimester is highest risk
Unexplained respiratory symptoms should trigger action
Reduced Mobility
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PE Presentation
Clinical evaluation for PE is very difficult
Statistically predictive physical signs:
Unilateral leg swelling
Hypoxemia (Saturation <95%)
Pulse > 94 bpm
Symptoms
Shortness of Breath
Chest pain beneath the sternum or under the ribs that worsens with deep breathing
Hemoptysis (coughing of blood)
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CTPA View of Pulmonary Embolism
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PE Management
Transport to medical facility
If risk of bleeding is low: give low molecular weight heparin (enoxaparin) 1mg/kg, BID, SQ
Administer supplemental O2; increase SPO2 above 92%
Thrombolytics for massive PE (tPA)
Surgical Removal at a Level III facility
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Air Embolism
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Traumatic Air Embolism
Gas bubbles in the vascular system
Air embolism can occur whenever a blood vessel is open and a pressure gradient exists favoring entry of gas
Because the pressure in most arteries and veins is greater than atmospheric pressure, an air embolism does not always happen when a blood vessel is injured
Pressure gradients are the key
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Traumatic Air Embolism
Trauma may cause the pressure gradient to change and air to enter the vascular space
Blast injuries
Pressure changes in the thorax (tension pneumothorax)
Use of a ventilator for trauma patients
Holding your breath while ascending from a dive (Boyle’s Law)
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Air Embolism Pathophysiology
A compromise occurs within the vascular space and air enters the system
In 20%‐30% of the population there exists the foramen ovale
Air may enter the left ventricle and flow to the brain
Slide 186JSOMTC, SWMG(A)
Air Embolism Presentation
The location of the air embolism is key:
Brain
• Neurologic deficiencies
• Loss of consciousness
• Convulsions• Stroke
Heart
• Heart attack
• Irregular heart beat
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Air Embolism Presentation (cont)
Other signs:
Low blood pressure
Extreme fatigue
Shortness of breath
Blurred vision
Hypoxia
Chest pain
Irregular breathing
Slide 188JSOMTC, SWMG(A)
Radiographic Air EmbolismNote the radiolucent (dark) area within the right
side of the heart (arrows).
Slide 189JSOMTC, SWMG(A)
Air Embolism Management
Oxygen (considering hyperbaric therapy)
Ventilation must be performed with care and observations of a worsening patient condition
ACLS
Supportive measures
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Fat Embolism
Slide 191JSOMTC, SWMG(A)
Fat Embolism Theories
Mechanical Theory
Large fat droplets are released into the venous system.
Microvascular lodging of droplets produces local ischemia and inflammation
Biochemical Theory
Hormonal changes caused by trauma and/or sepsis cause systemic release of free fatty acids
The biochemical theory helps explain non‐traumatic fat embolism
Slide 192JSOMTC, SWMG(A)
Fat Embolism Presentation
Frequency 3‐4%
Mortality rate 10‐20%
Signs and symptoms:
Altered mental status
Dyspnea, hypoxia, tachypnea
Febrile
Petechiae (20‐50%) usually in axillae first
Retinal hemorrhages
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Fat Embolism Possible Causes
Surgery (orthopedic interventions)
Burns
Blunt Trauma
Fractures (closed or open)
Liposuction
Decompression Sickness
Diabetes Mellitus
Slide 194JSOMTC, SWMG(A)
Fat Embolism Management
Supportive in nature:
Oxygen (Pulse Ox monitoring)
Vascular volume monitoring (crystalloid or colloid)
Ventilatory Management
Blood if needed
Preventative measures: early surgical fixation by the surgeon
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Damage Control Surgery
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Damage Control for Trauma
“The central tenet of damage control surgery is that patients die from a triad of coagulopathy, hypothermia and metabolic acidosis. Once this metabolic failure has become established it is extremely difficult to control haemorrhage and correct the derangements. If the patient is to survive the operation must be foreshortened so that they can be transferred to a critical care facility where they can be warmed and the hypothermia and acidosis is corrected. Once this is achieved the definitive surgical procedure can be carried out as necessary ‐ the 'staged procedure'.”
http://www.trauma.org/archive/resus/DCSoverview.html
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Damage Control Principles
Phase I ‐ Initial Exploration
Rapid control of active hemorrhage and contamination.
Phase II ‐ Secondary Resuscitation
Correction of coagulopathy and acidosis
Phase III ‐ Definitive Operations
Definitive repair of injuries (usually 48‐72h after initial operation)
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In Theatre Damage Control
Surgeons in your theatre of operations will perform damage control at:
FST
CSH
Where ever the surgeon may set up within the battle space
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Essential Concepts in Shock Management
Early definitive control of the airway must be achieved
Delays in control of active hemorrhage increase mortality;
Poorly corrected hypoperfusion increases morbidity and mortality
Excessive fluid resuscitation exacerbates problems
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Questions?
Slide 201JSOMTC, SWMG(A)
Agenda
Define shock
Identify types of shock
Understand the shock state
Recognize the patient at risk
Identify fluid shifts and acid‐base balance disturbance associated with the shock state
Recognize the development of coagulopathy
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Agenda
Understand the effects of hypothermia
Describe hemorrhage and the four stages of hemorrhagic shock
Identify the stages, pathophysiology, clinical presentation and management of SIRS, sepsis and septic shock
Recall the SOCM fluid resuscitation protocol
Slide 203JSOMTC, SWMG(A)
Agenda
Identify the body fluids and fluid imbalances
Identify the risk factors, pathophysiology and management of multiple organ dysfunction syndrome (MODS)
Recognize acute renal failure (ARF)
Identify the cause and management of traumatic cardiac arrest
Slide 204JSOMTC, SWMG(A)
Agenda
Define the four respiratory complications relevant to trauma
Identify the pathophysiology, clinical presentation and management of acute respiratory distress syndrome (ARDS)
Identify the pathophysiology, risk factors, clinical presentation and management of pulmonary embolism
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Reason
Slide 206JSOMTC, SWMG(A)
References
Trauma, 6th Edition, January 2008
Basic Immunology, January 2007
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References
Access Emergency Medicine, JSOMTC Learning Platform, 1 March 2011
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Terminal Learning Objective
Action: Communicate knowledge of Shock
Condition: Given a lecture in a classroom environment
Standard: Received a minimum score of 75% on the written exam IAW course standards
Slide 209JSOMTC, SWMG(A)
Complications of TraumaPFN: SOMTRL0F
Hours: 4.0
Instructor: