MECHANISMS OF INJURY: Predicting Injury Patterns Donald H. Jenkins, MD Trauma Director Saint Marys...
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MECHANISMS OF INJURY: Predicting Injury Patterns Donald H. Jenkins, MD Trauma Director Saint Marys Hospital Mayo Clinic Rochester MN Zumbro Valley Chapter Emergency Nurses Conference 9 April 2014
MECHANISMS OF INJURY: Predicting Injury Patterns Donald H. Jenkins, MD Trauma Director Saint Marys Hospital Mayo Clinic Rochester MN Zumbro Valley Chapter
MECHANISMS OF INJURY: Predicting Injury Patterns Donald H.
Jenkins, MD Trauma Director Saint Marys Hospital Mayo Clinic
Rochester MN Zumbro Valley Chapter Emergency Nurses Conference 9
April 2014
Slide 2
Acknowledgements COL David Burris, USUHS COL John Holcomb, ISR
(Retired, Houston TX) Col Deb Mueller, UTSA Hasan Alam, MD, USUHS
John Hess, MD, Univ of Maryland Dustin Smoot MD and Scott Zietlow
MD, Mayo Clinic, Rochester
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Slide 4
Blood transfusion as a predictor of injury mortality 1 in 400
injured people die 1 in 50 of the hospitalized injured die 20% of
transfused injured die 40% of injured who receive more than 10 U
RBC die
Slide 5
As blood use increases, mortality increases. Other predictors
of mortality, such as ISS, become less discriminant.
Slide 6
Stopping bleeding is important- Mortality Increases as
Transfusion Increases Storage limitations = Old blood is bad
Adverse immunologic effects potassium Transport limitations Further
dilutes coagulation factors Eastridge et al, submitted, 2005 Como
et al. Blood transfusion rates in the care of acute trauma.
Transfusion. 2004 Jun;44(6):809-13.
Slide 7
Epidemiology Tri-modal Distribution of Death First Peak - 50%
of Deaths Within seconds to minutes Occur at the scene Causes
Severe CNS Heart Aorta Great vessels
Slide 8
Epidemiology Trimodal Distribution of Death Second Peak - 30%
of Deaths Within minutes to hours Preventable causes
Subdural/Epidural hematoma Hemo/pneumothorax Splenic injury Pelvic
fracture Multiple injuries associated w/ significant blood
loss
Slide 9
Epidemiology Third Peak - 20% of Deaths Several days to weeks
following injury Causes Sepsis Multiple Organ Failure Syndrome
Slide 10
Breaking the Bloody Vicious Cycle Control hemorrhage Use best
possible resuscitation practice Prevent hypothermia Prevent
hemodilution Treat coagulopathy Hemorrahge Resuscitation
Hemodilution & Hypothermia Coagulo- pathy
Slide 11
Pathophysiology of Shock hemorrhage decreased O 2 delivery to
cells conversion from aerobic to anaerobic metabolism change in the
NaKATPase pump in cell membrane and loss of transmembrane potential
influx of H 2 O and Na into the cell from the interstitium
Slide 12
Pathophysiology of Shock (cont.) vascular space depleted and
cannot recover fluid from the interstitial space decreased venous
return decreased CO compensation with increased SVR increased
tissue hypoxia
Slide 13
The human coagulation system is slow and weak Clotting takes
time (2-10 minutes in the best of circumstances) Clots are
physically weak There is limited clotting material to work with
(even in the whole body) 10 grams of fibrinogen total 15 mL of
platelets total in normal individuals
Slide 14
Coagulopathy of Trauma Majority (90%) Pro-thrombotic State DVT
/ PE Hemorrhagic State (10%) Bleeding Ongoing hypotension
Coagulopathy of trauma is dynamic
Slide 15
Coagulopathy on Presentation An initial INR 1.5 reliably
predicts those military casualties who will require MT. Pts who
have a significant injury present with a coagulopathy. Severity of
injury and mortality is linearly associated with the degree of the
initial coagulopathy. - Schreiber MA, Perkins JP, Kiraly L,
Underwood SJ, Wade CE, Holcomb JB. Early Predictors of Massive
Transfusion in Combat Casualties. Submitted, J Trauma. - Brohi K,
et al. Acute traumatic coagulopathy. J Trauma. 2003.
Slide 16
Coagulopathy and Trauma Derangements in coagulation occur
rapidly after trauma By the time of arrival at the ED, 28% (2,994
of 10,790) of trauma patients had a detectable coagulopathy that
was associated with poor outcome (MacLeod et al., 2003)
Slide 17
Background Brohi K et al. J Trauma, June 2003. Coagulopathy
associated with increased mortality even after adjusting for
ISS
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Summary of Epidemiology Truncal Hemorrhage is the unresolved
problem Massive transfusion is more common in military than
civilian Still only 5-10% of all admissions MT leads to increased
mortality NEED Early Diagnosis and Rapid Effective Treatment
Slide 21
What Fluid Should We Carry?
Slide 22
World War I -etiology of shock investigatedtoxins? - primary
fluid salt solution - British also used a colloid 6% gum acacia in
saline -Cannon W, Frawer J, Cowell E. The preventive treatment of
wound shock. JAMA 1918;70:618-621.
Slide 23
World War II -hypovolemia identified as cause of shock -Plasma
recommended as primary fluid for resuscitation -Whole blood
approved eventuallyEdward Churchill
Slide 24
Korean War -improved resuscitation resulted in improved
survival -organ dysfunction such as renal failure seen more
often
Slide 25
Vietnam -larger volumes administered -Decreased renal failure
-Emergence of Da Nang lung
Slide 26
Class I Class II Class III Class IV Blood Loss 2000 % Blood Vol
40% Pulse 100 >120 >140 BP nl nl Pulse Pres. nl RR 14-20
20-3030-40 >35 UOP >30cc/hr 20-30 5-15 negligible CNS nl
anxious confused lethargic Fluid Choice crystalloid crystalloid
crystalloid crystalloid & blood & blood Hemorrhagic Shock
Classifications
Slide 27
Volume Resuscitation Resuscitation Agents Crystalloids Isotonic
Hypertonic Saline Colloids Albumin Hetastarch Blood and Coagulation
factors
Slide 28
Crystalloids are not a great Resuscitation Fluid for Severely
Injured Casualties Isotonic crystalloids induce more inflammation
than hypertonic crystalloids, colloids or blood products in
resuscitative models (in vitro and animal data) Rhee et al. Crit
Care Med. 2000. Coimbra et al. Trauma. 1997.
Slide 29
Volume Resuscitation - Response Responders Sustained
improvement in perfusion Likely have stopped bleeding May need
definitive surgery Transient responders Temporary improvement in
perfusion Continued bleeding, surgery Start blood transfusion
Emergent
Slide 30
Volume Resuscitation - Response Nonresponders No improvement in
perfusion Massive ongoing blood loss Immediate surgery &
transfusion Consider futility of resuscitation
Slide 31
Hypotensive Resuscitation Time Honored technique developed by
Military physicians during WWI and WWII Maximizing the
resuscitation benefit to the mitochondria while minimizing
rebleeding by avoiding popping the clot Supported by a significant
body of scientific data. This approach preserves the resuscitation
fluid within the vascular system Logistically sound by preventing
needless waste of blood and fluids. -Holcomb JB. Fluid
Resuscitation in Modern Combat Casualty Care: Lessons Learned From
Somalia. J Trauma. 2003 May. -Sondeen JL, Coppes VG, Holcomb JB.
Blood Pressure at which Rebleeding Occurs after Resuscitation in
Swine with Aortic Injury. J Trauma. 2003. -NATO Emergency War
Surgery Handbook. 2004.
Slide 32
Controlled Resuscitation Use prior to definitive hemorrhage
control to achieve & maintain adequate perfusion Regains
consciousness (follows commands) Palpable radial pulse SBP ~ 80-90
mm Hg / MAP ~ 60 mm Hg NOT a substitute for definitive surgical
control -Bickell WH, Wall MJ, Pepe PE, et al. Immediate versus
delayed fluid resuscitation for hypotensive patients with
penetrating torso injuries. NEJM 1994.
Slide 33
Volume Resuscitation-End Points SBP > 100 mm Hg, MAP > 70
mm Hg SaO 2 > 92% Normothermia Urine output Correction of
acidosis Base deficit < 2 Serum lactate < 2.5 mmol/L Clinical
coagulopathy resolved
Slide 34
Shock in Trauma Hemorrhage Most preventable deaths during war
STOP the bleeding Tension pneumothorax Cardiac tamponade
Slide 35
Resuscitation on the Battlefield 1.Use TCCC concepts
Tourniquets, hemostatic dressings, pressure, etc Needle
thoracentesis Airway Evacuation 2.Damage Control Resuscitation
1.Hypotensive resuscitation 2.Hemostatic resuscitation Its all
about stopping bleeding
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Extremity blast injury
Slide 38
Blast Injuries (IED)
Slide 39
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Slide 42
Summary of Epidemiology Truncal Hemorrhage is the unresolved
problem Massive transfusion is more common in military than
civilian Still only 5-7% of all admissions MT leads to increased
mortality NEED Early Diagnosis and Rapid Effective Treatment
Slide 43
Standard Resuscitation of Injured Casualties A, B, Cs Dx and
treat Injury Resuscitate Casualties Hypothermic, coagulopathic,
acidotic LR then PRBCs LR Diarrhea fluid from 1880 Acidotic No
clotting factors 200 ml intravascular at 60 min after infusion
proinflammatory PRBCs Doesnt carry much O2 for 24 hrs Each unit
increases MOF Old blood = High K+ Acidotic No clotting factors
Anticoagulant Trigger was a systolic BP of 90 or less Standard
resuscitation approach was to escalate use of fluids that only make
the patient worse 2000 LR (3:1) then PRBC (10 units) then FFP (1-4
units)
Slide 44
Changing Resuscitation Practices from Crystalloid to Blood
products Damage Control Resuscitation: The need for specific blood
products to treat the coagulopathy of trauma Hess, JR, Holcomb JB,
Hoyt DB. Transfusion, June 2006 The cellular, metabolic, and
systemic consequences of aggressive fluid resuscitation strategies.
Cotton BA et. al. Shock. Aug 2006 Damage Control Resuscitation:
Directly Addressing the Coagulopathy of Trauma Holcomb, JB, et. al.
J Trauma, submitted
Slide 45
Dilution is inevitable when giving blood components Whole blood
500 mL Hct 38-50% Plts 150-400K Plasma coag factors = 100% 1500 mg
fibrinogen Components 1 U pRBC = 335 mL with Hct 55% 1 U platelets
= 50mL with 5.5 x 10 10 plts 1 U plasma = 275mL with 80% coag
activity 750 mg fibrinogen Thus: 1U pRBC + 1U platelets + 1U FFP =
660mL with Hct 29%, Plts 88K/L, and Coag activity 65%.
Slide 46
Fresh Frozen Plasma -- Electrolytes (mmol/L) average unit of
FFP ~ 300cc Na165 (48mmol/unit) K3.3 (1.0mmol/unit) Glucose20
Calcium1.8 Citrate20 Lactate3 pH7.2-7.4 (LR 6.5, NS 5.0)
Phosphate3.63 British Society for Hematology 1994 Coagulopathy of
Trauma Strategies for Treatment
Mechanism of Wounding Missile or fragment destroys tissue by
passing through and crushing it (PERMANENT CAVITY) Cross-sectional
area of the permanent cavity is comparable to the presenting area
of the missile, and is the same for ALL tissue types Not the only
mechanism of wounding
Slide 65
After passage of the projectile, the walls of the permanent
cavity are stretched radially outward creating a temporary cavity,
wider with higher velocities Damage in the temporary cavity results
from stretching of the tissue A tissues elasticity determines the
damage the tissue sustains
Slide 66
Slide 67
The bullet created a permanent cavity with 8 mm diameter but
there was no observed temporary cavity STUDY I The bullet entered
the paraffin block from left side and stayed at the upper corner of
the paraffin block
Slide 68
Water and body tissues are 800-900 times more dense then air.
so that the rotation force can be more 800-900 times and in this
environment the missiles balance impair and thumbling movement
starts Air Density 1.26 kg / m 3 Water Density 1000 kg / m 3
Slide 69
The thumbling movement causing the bullet creates a large
surface and the bullet loosing velocity transfers energy to the
environment with pressure.
Slide 70
G3 missile M 16 missile AK-47 missile p t t p t p t Temporary
cavity was started on 15th cm with 14 cm diameter M16 missile has
two temporary cavities which started on 4th cm with 7 and 11 cm
diameter AK-47 missiles temporary cavity was started on 11th cm
with 13 cm diameter
Slide 71
Same stretch in one tissue (muscle) may cause little injury,
may result devastating injury in another (liver, brain); tissue
traversed is important Zone of temporary cavitation is analogous to
an area of blunt trauma around the projectiles tract Summation of
the two types of tissue disruption gives the wounding potential of
the missile
Slide 72
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Other Wounding Mechanisms Fragmentation/ Expansion some
missiles are designed to fragment or expand dum-dums,
hollow-points, non-jacketed some fragments despite copper jacket
fragments cause multiple tracts of permanent and temporary cavities
when they expand the permanent cavity is made wider
Slide 75
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Yaw Yaw is the deviation in the longitudinal axis of the bullet
from its line of flight (tumbling) Yaw is usually 180 degrees and
can be caused by striking foliage or tissue It increases the area
of permanent and temporary cavitation
Slide 78
But for barrels with grooves, missiles goes straightly after a
while.
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Extremity blast injury
Slide 89
Blast Injuries (IED)
Slide 90
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Slide 93
Shotgun Injuries Shotgun shells have a big powder charge with a
large mass of lead balls destructive potential depends on range at
close range, it can cause a large wound with severe disruption of
anatomy by direct crush alone long range (>25m) cause usually
only skin wounds wadding is a projectile too
Slide 94
Slide 95
STAB WOUNDS Similar injury pattern Lower energy = lower injury
Look for defense wounds to hands
Slide 96
IMPALEMENT Very dramatic Do not remove object until in OR
Survivable injuries if patient alive initially Contaminated wounds
Difficulty in transport
