Terminal Learning Objective - JSOMTCslides.jsomtc.org/SOMTRL0F/SOMTRL0F.pdf · JSOMTC, SWMG(A) Slide 22 Distributive Shock Non‐Septic Shock Neurogenic Anaphylactic Drug/Toxin Induced

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Slide 1JSOMTC, SWMG(A)

Complications of TraumaPFN: SOMTRL0F

Hours: 4.0

Instructor:


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


References

Trauma, 6th Edition, January 2008

Basic Immunology, January 2007

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References

Access Emergency Medicine, JSOMTC Learning Platform, 1 March 2011


Reason


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


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


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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Definition of Shock


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


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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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


Identify Types of Shock


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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4 "Classic" Categories of Shock

Hypovolemic Hemorrhagic

Non‐hemorrhagic

Distributive Septic

Non‐septic

Cardiogenic Cardiomyopathic

Arrhythmogenic

Mechanical

Obstructive Pulmonary vascular

Mechanical


Hypovolemic Shock

Occurs when rapid loss of fluids results in inadequate circulating volume and subsequent inadequate perfusion. Hemorrhagic Shock

Non‐Hemorrhagic Shock


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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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


Distributive Shock

Characterized by severe peripheral vasodilation (vasodilatory shock).

Septic

Non‐Septic


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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Distributive Shock

Non‐Septic Shock

Neurogenic

Anaphylactic

Drug/Toxin Induced

Endocrine

Psychogenic


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


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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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)


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


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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Obstructive Shock

Mechanical ‐ Primary physiologic disturbance causing reduced preload

Tension pneumothorax

Pericardial tamponade

Constrictive pericarditis

Restrictive cardiomyopathy


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


Cardiogenic Shock

Cardiomyopathy ‐

Myocardial Ischemia (MI)

Severe heart failure

Myocarditis

Prolonged cardiac ischemia

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Cardiogenic Shock

Mechanical ‐

Aortic or mitral valve insufficiency

Valvular rupture

Critical aortic stenosis

Arrythmogenic ‐

Tachyarrhythmias

Bradyarrhythmias


Understand The Shock State


Inciting Event

Temperature

Trauma

Infection

Pain Hypoxia

Acidosis

Hypoglycemia

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Afferent Signaling

Baroreceptors

Chemoreceptors


Efferent Signaling

ANS ‐> SNS ‐> Catecholamines

Cardiovascular response

Neuroendocrine response

Immunological response

Inflammatory response

Cellular effect


SNS Response

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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


Renin‐Angiotensin‐Aldosterone System

Renal hypoxia!

(less than 80mm Hg)

Hypotension!

Neuroendocrine Response


Glucose Production

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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


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.”


Immunological / Inflammatory Response

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Recognize the Patient at Risk


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


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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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)


Patient At Risk

DeathAcidosis Hypothermia

Coagulopathy


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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Identify Fluid Shifts and Acid‐Base Balance Disturbances Associated

with the Shock State


Coagulopathy


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


Normal Cellular Function

Na+

Cl -

K+

Na+

Cl -

K+

ATP

ADP

K+

Na+

Leaky Channels, Gated Channels and Pumps

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Cellular Swelling


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


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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Hydrogen Ion Homeostasis

H+Metabolism Metabolism

HemoglobinProtein


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 ?


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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Gas Exchange in the Tissue

40 mmHg

45 mmHg

40 mmHg

95 mmHg


Gas Exchange in the Lungs

100 mmHg

40 mmHg45 mmHg

40 mmHg


Recognize the Development of Coagulopathy


Coagulopathy

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Traumatic Coagulopathy

Traditional Driving Factors

Massive fluid resuscitation

Clotting factor dilution

Clotting factor consumption

Hypothermia

Acidosis


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


Disseminated Intravascular Coagulopathies (DIC)

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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


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


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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Pathogenesis of DIC

Procoagulant exposure

Coagulation

Fibrinolysis

End organ damage


Systemic Activation of Coagulation


DIC Clinical Presentation

Epistaxis

Gingival bleeding

Mucosal bleeding

Cough

Dyspnea

Confusion, disorientation

Fever

Bruising, petechiae

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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)


Petechiae Associated with DIC


Understand the Effects of Hypothermia


Coagulopathy

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Hypothermia

Many causes exist with trauma

Altered central thermoregulation

Prolonged exposure to low ambient temp.

Decreased heat production due to shock

Inadequately warmed fluids


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


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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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


Describe Hemorrhage and the Four Stages of Hemorrhagic Shock


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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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


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.


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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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.


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.


Compensated Shock

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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


Decompensated Shock


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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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)


Late Decompensated/Stage 3

25‐35% loss of CBV 1250‐1750 mL

Late Decompensation Significant LOC deterioration

Compensatory mechanism unable to cope with loss


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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Irreversible Shock


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


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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Variations in Physiological Responses to Shock

Age and relative health

General physical condition

Preexisting diseases

Medications

Environment



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


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


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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



Identify the Stages, Pathophysiology, Clinical

Presentation and Management of SIRS, Sepsis, and Septic Shock


Septic Shock Progression

SIRS

Sepsis

Severe Sepsis

Septic Shock

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SIRS, Sepsis and Septic ShockInterrelationship


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


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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SIRS, Sepsis and Septic Shock Management


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)


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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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


Antibiotic Therapy

Broad spectrum antibiotics covering gram‐positive, gram‐negative, and anaerobic bacteria

Antibiotic resistant bacteria are a concern (MRSA: Methicillin‐Resistant Staphylococcus Aureus)


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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Persistent Hypotension

Consider Vasopressors (1ST Line)

Norepinephrine

Dopamine

2nd Line Vasopressors:

Epinephrine

Vasopressin (also known as ADH, Antidiuretic Hormone)


Recall the SOCM Fluid Resuscitation Protocol


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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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


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


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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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


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.


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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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.


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



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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Special Considerations

Battlefield fluid triage terminology

Rapid Responder

Transient Responder

Non‐Responder


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


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



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.


Identify the Body Fluids and Fluid Imbalances


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


Fluid Imbalances

Two abnormal states of body fluid balance can occur:

Dehydration

Over hydration


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)


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


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


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


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


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


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


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


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


Identify the Risk Factors, Pathophysiology and Management of Multiple Organ Dysfunction

Syndrome (MODS)


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


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.


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.


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


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)


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


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


Identify the Cause and Management of Traumatic Cardiac Arrest


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


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


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


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


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


ARDS Pathophysiology


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


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


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.


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


Identify the Pathophysiology, Risk Factors, Clinical Presentation and

Management of Pulmonary Embolism

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Embolism Basics


Embolism Basics (cont)


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)


Virchow Triad

Pulmonary Embolism is triggered by 3 main causes:

Venostasis

Hypercoagulability

Vessel wall inflammation (injury to the intima)


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


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)


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


Air Embolism


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)


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


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


Radiographic Air EmbolismNote the radiolucent (dark) area within the right

side of the heart (arrows).


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


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


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


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


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


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)


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


Questions?


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


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


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


References

Trauma, 6th Edition, January 2008

Basic Immunology, January 2007


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


Complications of TraumaPFN: SOMTRL0F

Hours: 4.0

Instructor:

Terminal Learning Objective - JSOMTCslides.jsomtc.org/SOMTRL0F/SOMTRL0F.pdf · JSOMTC, SWMG(A) Slide 22 Distributive Shock Non‐Septic Shock Neurogenic Anaphylactic Drug/Toxin Induced

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