Pathophysiology of

Trauma Management

Eko – Adi – Achie – Ita

Ati – Adib – Tizi - Huntal

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 Case Study
 Taxi Driver, 50 yrs old
 Multiple Trauma, no seatbelt
 Primary Survey:
 A : free
 B : respiratory distress, breath sound (-) left hemi-thorax
 C : shock
 D : anxious
 E : multiple abrasion on left anterior hemi-thorax
Secondary Survey:
Thorax : multiple abrasion on left anterior hemi-thorax
Abd : multiple abrasion on right upper quadrant; tenderness
Extr : bruises on both upper arm, pain on the hip

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 Recognition: Mechanisms of Injury
 Simple Classifications  Classification by True
of Mechanisms Mechanism
 Cause Related  Force / Energy Related
 Motor Vehicle (Kinematics)
Accident/Crash  Deceleration vs
 Fall Acceleration
 Stabbing  Blunt vs. Penetrating
 Useful in initial  Blast
assessment  Thermal/Chemical

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 Predicting Severity of Injury
 Incident Biomechanics
 Ejection from Vehicle
 Death of other occupant
 Falls > 10 feet
 Pedestrian (> 20 mph)
 High energy Transfer: Head on, T-bone; Significant Intrusion
 Prolonged Extrication/Transport
 Co-Morbid Factors
 Extremes of Age
 Underlying Disease & Poor General Health
 Pregnancy
 Environmental Extremes
 Protective Devices
 TIME

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 Kinematics
 Physical Laws
 Newton’s First Law
 A body at rest or a body in motion will remain in that state until acted
upon by an outside force
 Multiple collisions
 Conservation of energy
 Energy cannot be created nor destroyed
 It can change form
 Force
 Force = Mass x Acceleration
 Force = Mass x Deceleration
 Kinetic energy (KE)
 KE = ½ m x V2
 What factor has the greatest influence on KE?

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 Energy Transfer
 Cavitation
 Energy exchange  particle motion
 Temporary / Permanent cavity
 Depends on the number of particles & Density of bodies
involved
 Air Density: Lungs, Intestinal Tract
 Water Density: Vascular system, Liver, Spleen, Muscle
 Solid Density: Bone, asphalt, steel
 Area of Interaction: Shape, Position, or Fragmentation of Object
 Blunt
 Tissue not penetrated
 Cavitation away from site of impact
 Cavitation in direction of impact
 Penetrating
 Tissue penetrated
 Cavitation at 90o to bullet pathway
 Tissue inline to penetration is crushed

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 Lateral Impact

Frontal Collision

Rear-End Collisions

Rotational & Roll-Over

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 Organ Collisions

 Blunt Trauma
 Compression
 Change in Velocity
 Acceleration or Deceleration
 Shear or Avulsion
 Restraint System
 Seat belt
 Airbag

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 Core Problems
 Breathing Problems  Respiratory System
 Circulation Problems  Cardiovascular System
 Shock
 Internal Bleeding

 Neurologic Problems  Nervous System

 Anxious

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 Associated Problems
  Tissue Perfusion
 Metabolic Problems
 Acid-Base imbalance
 Energy Metabolism: Lysis of Glocose, Lipid, Protein

 Hemostatic Problems
 Coagulation Disorders  DIC
 Middle Aged Person  Altered Physiologic
Mechanism

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 Multiple Trauma

Internal Breathing Direct Neuro Trauma

Bleeding Problems

Aging
CV problems Problems

SHOCK O2  Anxious

ACID/BASE METABOLIC COAGULATION

IMBALANCE DISORDER DISORDER

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 Pathophysiology of Thoracic
Trauma
 Blunt Trauma
 Results from kinetic energy forces
 Subdivision Mechanisms
 Blast
 Pressure wave causes tissue disruption
 Tear blood vessels & disrupt alveolar tissue
 Disruption of tracheobronchial tree
 Traumatic diaphragm rupture
 Crush (Compression)
 Body is compressed between an object and a hard surface
 Direct injury of chest wall and internal structures
 Deceleration
 Body in motion strikes a fixed object
 Blunt trauma to chest wall
 Internal structures continue in motion
 Ligamentum Arteriosum shears aorta
 Age Factors
 Pediatric Thorax: More cartilage = Absorbs forces
 Geriatric Thorax: Calcification & osteoporosis = More fractures
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 Possible Thoracic Injury
 Pneumothorax
 Tension ?
 Hemothorax
 Flail Chest
 Lung Contusion
 Diaphragmatic Rupture

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 Pathophysiology of Thoracic
Trauma Chest Wall Injuries
 Pulmonary Contusion
 Most Common result of blunt injury
 Signs & Symptoms
 Erythema
 Ecchymosis
 DYSPNEA
 PAIN on breathing
 Limited breath sounds
 HYPOVENTILATION
 BIGGEST CONCERN = “HURTS TO BREATHE”
 Crepitus
 Paradoxical chest wall motion

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 Pathophysiology of Thoracic
Trauma Chest Wall Injuries
 Rib Fractures
 >50% of significant chest trauma cases due to blunt trauma
 Compressional forces flex and fracture ribs at weakest points
 Ribs 1-3 requires great force to fracture
 Possible underlying lung injury
 Ribs 4-9 are most commonly fractured
 Ribs 9-12 less likely to be fractured
 Transmit energy of trauma to internal organs
 If fractured, suspect liver and spleen injury
 Hypoventilation is COMMON due to PAIN

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 Pathophysiology of Thoracic
Trauma Chest Wall Injuries
 Flail Chest
 Segment of the chest that becomes free to move with the
pressure changes of respiration
 Three or more adjacent rib fracture in two or more places
 Serious chest wall injury with underlying pulmonary injury
 Reduces volume of respiration
 Adds to increased mortality
 Paradoxical flail segment movement
 Positive pressure ventilation can restore tidal volume

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 Flail Chest

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 Pathophysiology of Thoracic
Trauma Pulmonary Injuries
 Simple Pneumothorax
 Closed Pneumothorax  Progresses into Tension
Pneumothorax
 Disruption of lung tissue  air leaks into the pleural space
 Progressive Pathology
 Air accumulates in pleural space
 Lung collapses
 Alveoli collapse (atelectasis)
 Reduced oxygen and carbon dioxide exchange
 Ventilation/Perfusion Mismatch
 Increased ventilation but no alveolar perfusion
 Reduced respiratory efficiency results in HYPOXIA

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 Pathophysiology of Thoracic
Trauma Pulmonary Injuries
 Open Pneumothorax
 Free passage of air between atmosphere and pleural space
 Air replaces lung tissue
 Mediastinum shifts to uninjured side
 Air will be drawn through wound if wound is 2/3 diameter
of the trachea or larger
 Signs & Symptoms
 Penetrating chest trauma
 Sucking chest wound
 Frothy blood at wound site
 Severe Dyspnea
 Hypovolemia

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 Pathophysiology of Thoracic
Trauma Pulmonary Injuries
 Tension Pneumothorax
 Build-up of air under pressure in the thorax.
 Excessive pressure reduces effectiveness of
respiration
 Air is unable to escape from inside the pleural space

 Progression of Simple or Open Pneumothorax

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 Pathophysiology of Thoracic
Trauma Pulmonary Injuries
Tension Pneumothorax Signs & Symptoms

 Dyspnea  Diminished then absent

 Tachypnea at first breath sounds on injured side
 Progressive  Cyanosis
ventilation/perfusion  Diaphoresis
mismatch  Hypotension
 Atelectasis on uninjured  Hypovolemia
side  Tracheal Shifting
 Hypoxemia  LATE SIGN
 Hyperinflation of injured
side of chest
 Hyperresonance of injured
side of chest
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 Pathophysiology of Thoracic
Trauma Pulmonary Injuries
 Hemothorax
 Accumulation of blood in the pleural space
 Serious hemorrhage may accumulate 1,500 mL of blood
 Mortality rate of 75%
 Each side of thorax may hold up to 3,000 mL
 Blood loss in thorax causes a decrease in tidal volume
 Ventilation/Perfusion Mismatch & Shock
 Typically accompanies pneumothorax
 Hemopneumothorax

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 Pathophysiology of Thoracic
Trauma Pulmonary Injuries
Hemothorax Signs & Symptoms
 Blunt or penetrating chest trauma
 Shock
 Dyspnea
 Tachycardia

 Tachypnea

 Diaphoresis

 Hypotension

 Dull to percussion over injured side

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 Pathophysiology of Thoracic Trauma
Cardiovascular Injuries
 Pericardial Tamponade
 Restriction to cardiac filling caused by blood or other fluid
within the pericardium
 Occurs in <2% of all serious chest trauma
 However, very high mortality
 Results from tear in the coronary artery or penetration of
myocardium
 Blood seeps into pericardium and is unable to escape
 200-300 ml of blood can restrict effectiveness of cardiac contractions
 Removing as little as 20 ml can provide relief

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 Pathophysiology of Thoracic
Trauma Cardiovascular Injuries
Pericardial Tamponade Signs & Symptoms

 Dyspnea  Kussmaul’s sign

 Possible cyanosis
 Beck’s Triad
 JVD
 Distant heart tones
 Hypotension or
narrowing pulse pressure
 Weak, thready pulse
 Shock
 Decrease or absence of JVD
during inspiration
 Pulsus Paradoxus
 Drop in SBP >10 during
inspiration
 Due to increase in CO2 during
inspiration
 Electrical Alterans
 P, QRS, & T amplitude changes
in every other cardiac cycle
 PEA

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 Circulation Problems
 Circulatory Shock due to
 Internal Bleeding
 Possible Lung Injury, Diaphragmatic Rupture, Cardiac
Injury
 Liver Injury, most common with no seatbelt accident

 Hollow organ injury, less common

 Right Kidney Injury

 Obstructive Shock
 Tension Pneumothorax
 Pericardial Tamponade

 Possible Pelvic Fracture

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 Liver injury
 50% cases bleeding will stop spontaneously.
 Unstable patients DPL

 Stable patients without peritoneal sign CT Scan

 Small, non deep laceration ( stage I – III ) simple

suture.
 More severe ( stage IV – VI ) complex procedure

 Consider PACKING if shock, metabolic derangement

and coagulopathy
 REMEMBER: Liver can regenerate itself in injury up to
80%  through cell proliferation ( cells cycle)

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 Postoperative complications of liver injury
 Metabolic : hyperglicemia.
 Due to stress hormone release, including glucagon,
epinephrine,and cortisol gluco-neogenesis
 Peripheral glucose use decrease ( insulin resistance )
 Pulmonary complication
 Postoperative bleeding and coagulopathyderangement
of protein synthesis in liver due to trauma clotting
disorder.
 Billiary fistula
 Hemobilia
 Subdiphragmatic and intraparenchymal abscess

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Blunt trauma: 80-90%
Rapid deceleration / Direct blow
Trauma to back/flank/lower
thorax/ upper abdomen

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 Coagulopathy
 Coagulopathy often develops after significant bleeding
 Due to core hypothermia which inhibits clotting
cascade
 Clotting abnormalities and deficiencies of coagulation
factors  significant when core body temperature
<34ºC  decreased plasma TXA2 levels and
prolonged bleeding times
 Tissue hypoperfusion and metabolic acidosis 
consumption of clotting factors  DIC

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 The Bloody Vicious Cycle
Major torso trauma

Active hemorrhage

Progressive coagulopathy
Iatrogenic factors
Core hypothermia
Cellular shock
Metabolic acidosis Tissue injury

Contact activation Massive transfusion

Clotting factor Pre-existing disease

deficiencies
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 DIC
 Most prone to DIC:
- shock
- receive massive transfusion
- undergone a difficult operative procedure
- tranfusion reactions

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 Endothelial Damage Coagulation cascade Tissue Injury

Kinin

Vascular
Effect Thrombin

Fibrinogen Fibrin Fibrin split product

Plasminogen Plasmin

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 Stimulus

Direct Endothelial damage

Activation of coagulation cascade Inadequate concentration

of inhibitors

Adequate concentration
of inhibitors Activation
Other
DIC
Biological
Pathway
DIC “aborted”

Decompensated

Normal hemostatic Compensated

mechanism restored
Hemorrhagic
Over-compensated
diathesis

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 Cuthberson’s Two Phase
 Ebb Phase
 Initially after trauma
 Physiologic response to restore tissue perfusion and
circulating volume
 Flow Phase
 Begins once the patients has successfully resuscitated
 Catabolic  hyperdinamic response (hypermetabolism,
hyperglycemia, sodium/water retention)
 Anabolic  the return of normal homeostasis

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 Metabolic Response
 Shock Phase
 Hypoperfusion (Hemorrhage and Tissue injury)
 Resuscitation Phase
 Active vol. resuscitation and operations to stop hemorrhage
 Elaboration of inflammatory mediators
 Hypermetabolic Phase
  symphatetic activity
  catecholamines, cortisol, insulin   protein catabolism, negative
nitrogen balance, lypolisis
 Acutely, to protect the individual  if too long, lead to MODS
 MODS
 Sustained overexpression of injury-induced mediators
 Development of infections
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 First Hit Seccond Hit

Recovery

Tissue Injury
SIRS
MOF

Unable to Resuscitate

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 Characteristics of Metabolic
Stress
Hormonal Metabolic Chemical

 Catecholamines  REE  pH
 Glucagon Hyperglycemia Prostanoids

 Corticosterioids Ketoacidosis Leukotrienes

Insulin Resistance Uremia Cytokines

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 Change in Energy Requirements
Due to Disease or Injury
 Resting energy expenditure
increased by 10-50% (injury
factor) Skeletal Trauma

Major Burn
 to support increased metabolic
workload Multitrauma

 An additional allowance is Closed Head Injury

added for activity (activity Sepsis

factor) Elective Surgery

 20 % if confined to bed Starvation

 30 % if ambulatory -20 0 20 40 60 80
% Above Usual Requirement

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 Post Injury Hypercatabolism
“NITROGEN DEATH”
 Muscle mass
 Visceral Protein
 Organ Function
 Immune Response
“INFECTION”
MULTIPLE ORGAN FAILURE

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 Protein requirements are altered
to accommodate:
 Immune response
 Increased metabolic activity
 Replacement of damaged cells
 Replacement of protein losses
 perspiration, blood, exudates, renal, intestinal
  if anorexia accompanies fever/infection

  by muscle proteolysis
 up to 35 g/day with metabolic stress

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 TRAUMA MANAGEMENT

OXIGENATION
THROUGH…
 A AIRWAY AND C – SPINE CONTROL
 B BREATHING
 C CIRCULATION AND HEMORRHAGE CONTROL
 D DISABILITY
 E EXPOSURE

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 Airway Management
 PATTENCY OF AIRWAY
 TRIPLE AIRWAY MANOUVRE
 ADDITIONAL TOOLS
 NEEDLE CRYCOTHYROTOMY
 ENDO-TRACHEAL/NASO-TRACHEAL TUBE

 C-SPINE CONTROL
 SUSPECT SPINAL INJURY UNLESS PROVEN
OTHERWISE

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 Breathing Management
 BREATHING AND VENTILATION
A PATENT AIRWAY ALONE DOES NOT ENSURE ADEQUATE VENTILATION
THE TRAUMA PATIENT NEEDS ADEQUATE GAS EXCHANGE
EXAMINE THE CHEST WALL
AUSCULTATE THE LUNGS
PERCUSS FOR AIR / BLOOD
MAJOR INJURIES : TENSION PNEUMOTHORAX
FLAIL CHEST
MASSIVE HAEMOTHORAX
OPEN PNEUMOTHORAX
MINOR INJURIES : RIB FRACTURES
SIMPLE HAEMO / PNEUMOTHORAX
PULMONARY CONTUSION

DYSPNOEIC/TACHYPNOEIC (RR = 35)  INTUBATE+VENTILATE

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 Management of the Chest Injury
Patient
 Open Pneumothorax
 High flow O2
 Cover site with sterile
occlusive dressing taped
on three sides
 Progressive airway
management if indicated

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 Management of the Chest Injury
Patient
 Tension Pneumothorax
 Confirmation
 Auscultaton & Percussion
 Pleural Decompression
 2nd intercostal space in mid-
clavicular line
 TOP OF RIB
 Consider multiple
decompression sites if patient
remains symptomatic
 Large over the needle
catheter: 14ga
 Create a one-way-valve:
Glove tip or Heimlich valve

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 Circulation Management
 CIRCULATION AND CONTROL OF BLOOD LOSS
HAEMODYNAMIC STATUS

ALL HYPOTENSION IS HYPOVOLEMIC UNLESS PROVEN OTHERWISE

ALL INJURED PATIENTS GET OXYGEN

MONITOR SpO2
PLACE LARGE LINES – REMEMBER Poisoulle’s Law
PERIPHERAL OR CENTRAL
CUT DOWNS / FLOW RATES / SITE OF ACCESS
BASELINE BLOODS

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 MAINTAINING BODY TEMP.

 Keep as close to normal as possible

 Protect patient from elements
 Remove wet clothing
 Cover patient, but don’t get them too warm,
causing vasodilation

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Circulation Management… Con’t
 CONTROL BLEEDING
DIRECT PRESSURE  TOURNIQUETS  CLAMPS
(prevent further vascular injury and reperfusion injury)
PNEUMATIC ANTI SHOCK GARMENT (PASG)
THINK OF THE SITE THORAX
ABDOMEN
RETROPERITONEUM
FRACTURE SITE
PENETRATING THORAX

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 Airway

Pressure to
external hemorrhage

IVs – Fluid/Blood THORACOTOMY

Chest Tube On Going Hemorrhage

Distended Abdomen
LAPARATOMY
DPL/US
Abdomen

X-ray Pelvis
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 Multi-Systems Trauma
 If you don’t know the diagnosis. . .
 treat the signs and symptoms

Open, clear, maintain airway

Maximize oxygenation,
ventilation
Maximize perfusion
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 THE RESUSCITATION PHASE

 FLUIDS – CRYSTALLOID  COLLOID BLOOD

 STOP HYPOVOLEMIA AND HAEMORRHAGE !!!

 ALMOST ALL SHOCK IN TRAUMA IS HYPOVOLEMIC IN ORIGIN !!!!

 THE WAY TO STOP BLEEDING IS TO INTERVENE, NOT CONTINUE

WITH FLUIDS

 WE OPERATE TO RESTORE INTRAVASCULAR VOLUME

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 MONITORING DURING RESUSCITATION

 VITAL SIGN MONITORING

 HEART RATE
 BLOOD PRESSURE
 RESPIRATION RATE
 TEMPERATURE
 FLUID INTAKE  IV LINE and ORAL
 TUBES
‘ a tube and a finger in every orifice ‘
URINARY CATHETERS  URINARY OUTPUT
NASOGASTRIC DECOMPRESSION

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 After Resuscitation…
 Pain Control
 Nutritional Support
 Energy sources: Glucose
 Protein !!!

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