pitfalls in the management of trauma patients2
TRANSCRIPT
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PITFALLS IN THE
MANAGEMENT OF
TRAUMA PATIENTS
Keng Sheng Chew, MD, MMED (Emerg Med)
Senior Lecturer/Emergency Medicine Physician,
School of Medical Sciences, Universiti Sains Malaysia
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“The emergency department's unique
operating characteristics make it a
natural laboratory for the study of
error.”
- Croskerry P, Sinclair D. Emergency medicine: A
practice prone to error? CJEM 2001; 3 (4):271-6.
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Only a fool learns from his
own mistakes, a wise man
from the mistakes of others.
- Otto von Bismarck
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Introduction
• Acute trauma care is often resource-
intensive and time-sensitive
• Patient inflow is unpredictable with periodic
and abrupt surges in volume and/or acuity
• Often doctors in emergency department are
forced to make decisions with limited
information
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Sources of Failure (Adapted from Rosen
et al, 2009)
Triage Patient
Presentation Assessment – Diagnosis –Management - Disposition
Overcrowding
Information gap
Lab error
Report Delays
Affective state
Fatigue & Shift
work
Cognitive properties of
the mind
Procedural errors
Admit
Discharge
Follow-up failure
Meds errors
Teamwork Issues
Inadequate D/c
plan
Prolonged waiting
for bed
ED Design
Triage cueing
EMS
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Human Errors (Rasmussen and Jensen
Model 1974)
• Categorize human errors into three basic groups:
• Skill-based errors
– Technical errors (chipping a tooth during endotracheal
intubation
• Rule-based errors
– Deviations from guidelines or established practice
patterns
• Knowledge-based errors
– Example: errors in judgment and decision-making related
to patient management caused by incorrect interpretation
of data, insufficient knowledge, etc
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Three Erroneous Attitude In Diagnostic
Evaluation of Trauma Patients
• Diagnostic Labeling – The use of a premature (and often presumptive)
diagnostic „label‟ on a patient
• False-negative prediction – Attributing an inappropriately high negative predictive
value on a given physical findings or investigations
• False attribution – Erroneously linking a clinical finding to an
unsubstantiated cause/diagnosis
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DIAGNOSTIC LABELLING
• Is the use of a premature (and often presumptive)
diagnostic „label‟ on a patient
• Labeling can be potentially one of the most
tempting and hazardous errors
• Subsequent healthcare staffs may tend to refer to
the patient by this „label‟ despite the lack of
confirmatory data
• Even when subsequent information conflicts with
the „labeled‟ diagnosis, changing the label may be
impeded by „confirmation‟ bias
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EXAMPLES OF BIASES
• Confirmation bias
– the tendency to look for confirming evidence to support a
diagnosis rather than look for disconfirmation evidence to
refute it, despite the latter often being more persuasive
and definitive
• Blind spot bias
– general belief people have that they are less susceptible
to bias than others
• Ego bias
– overestimating the prognosis of one‟s own patients
compared to a population of similar patients
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FALSE-NEGATIVE PREDICTION
• Attributing an inappropriately high negative
predictive value on a given physical findings or
investigations
• Most of these have insufficient sensitivity to
definitely rule out serious injuries at initial
presentation
• Examples:
– Abdomen soft, non-tender intra-abd unlikely
– Heart rate normal hemorrhagic shock unlikely
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FALSE ATTRIBUTION
• Refers to erroneously linking a clinical finding
to an unrelated cause.
• Often due to selectively using certain clinical
information
• For example: attributing loss of
consciousness due cerebral concussion in a
patient with post-MVA without considering
other causes.
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CAUSES OF ALTERED MENTAL STATUS
• A – Alcohol, acidosis
• E – Electrolyte imbalances, endocrine
• I – Infective, insulin
• O – Opiates, oxygen
• U – Uremia
• T – Trauma, toxins
• I – Inflammatory
• P – Psychiatric
• S – Seizures, sepsis
MNEMONIC:
‘AEIOU TIPS’
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HOW TO REDUCE HUMAN ERRORS
• Patients should generally be managed according to
the worst “reasonable case”
• Listen carefully, but always remain a bit skeptical
about the history
– Falls are not always falls
• Constantly reassess, never assume “stability”
• Never become married to the initial diagnosis
• Maintain the “clock speed”
• Constantly upgrading your knowledge bank
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HEMORRHAGIC SHOCK IN
TRAUMA
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FAILURE TO RECOGNIZE EARLY
HEMORRHAGE
• An early presentation of normotension may create
the illusion of hemodynamic stability, even when
30% to 40% circulating blood volume loss may
have lost before the onset of hypotension
• A normal BP may be abnormal in the setting of
acute pain and stress (sympathetic overactivity)
• BP = CO * TPR
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HYPOTENSION
• Fit, young patients may lose 40% of their blood
volume before the systolic blood pressure (SBP)
drops below 100 mmHg
• Elderly may become hypotensive with volume loss
of as little as 10%
• Committee on Trauma, American College of Surgeons. Advanced
trauma life support program for doctors. Chicago: American College of
Surgeons; 1997.
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Cocchi MN, Kimlin E, Walsh M et al. Identification and resuscitation of the trauma patient in shock.
Emerg Med Clin North Am 2007; 25 (3):623-42, vii.
INDICATORS OF HYPOPERFUSION
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TACHYCARDIA
• In a study by Victorino et al, up to 35% of trauma
patients with hypotension did not display
tachycardia.
• Trauma patients without hypovolemia may display
tachycardia because of fear, pain etc whereas
those with extreme age and on meds (beta
blockers) may have „„relative bradycardia‟‟
• Victorino GP, Battistella FD, Wisner DH. Does tachycardia correlate with
hypotension after trauma? J Am Coll Surg 2003;196(5):679–84.
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SHOCK INDEX
• Ratio of heart rate to SBP
• Shock Index = HR/SBP
• Help identify hypoperfused patients with more
subtle vital sign abnormalities.
• A shock index of >0.9 has been found to be more
sensitive than traditional vital sign
• Rady MY, Smithline HA, Blake H, et al. A comparison of the shock index
and conventional vital signs to identify acute, critical illness in the
emergency department. Ann Emerg Med 1994;24(4):685–90.
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SHOCK INDEX
• A large retrospective study was unable to
demonstrate an advantage of shock index over
traditional vital sign analysis in trauma patients • King RW, Plewa MC, Buderer NM, et al. Shock index as a marker for significant injury in
trauma patients. Acad Emerg Med 1996;3(11):1041–5.
• While the presence of vital sign abnormalities may
indicate shock, the absence of these
abnormalities does not completely exclude
occult hypoperfusion in the traumatic patient. • Blow O, Magliore L, Claridge JA, et al. The golden hour and the silver day: detection and
correction of occult hypoperfusion within 24 hours improves outcome from major trauma. J
Trauma 1999;47(5):964–9.
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• Mean arterial pressure (MAP) is a better
representation than SBP for organ perfusion status
• MAP = Diastolic BP + 1/3(Systolic BP – Diastolic
BP).
• MAP = 1/3(Systolic BP) + 2/3(Diastolic BP)
• Using MAP avoids the deception of a seemingly
normal systolic blood pressure.
– A patient with a BP of 80/60 (MAP=66) is actually
perfusing their organs better than a patient with a BP
of 110/30 (MAP=56).
MEAN ARTERIAL PRESSURE (MAP)
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METABOLIC MARKERS
• Metabolic markers of hypoperfusion include
bicarbonate, base deficit, and lactic
acidosis.
• With inadequate perfusion, cells will begin
anaerobic metabolism and generate lactic acids
• Callaway et al report a mortality of 38% in
normotensive elderly trauma patients with
initial lactic acid levels of >4 mmol/dL. • Callaway D, Rosen C, Baker C, et al. Lactic acidosis predicts mortality in
normotensive elderly patients with traumatic injury. Acad Emerg Med
2007;14(S152).
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LACTATE
• Effective lactate clearance has been found
to be associated with lower mortality levels
in trauma, sepsis, and postcardiac arrest
• Husain FA, Martin MJ, Mullenix PS, et al. Serum lactate and base deficit
as predictors of mortality and morbidity. Am J Surg 2003;185(5):485–91.
• Abramson D, Scalea TM, Hitchcock R, et al. Lactate clearance and
survival following injury. J Trauma 1993;35(4):584–8, [discussion: 588–
9].
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LACTATE
• Although normal pH is a good indicator of
adequate fluid volume, serum lactate level
is a better indicator of the depth and
duration of shock.
• The rate at which shock patients normalize
lactate is correlated strongly with outcome.
• Abramson D, Scalea TM, Hitchcock R, et al. Lactate clearance and
survival following injury. J Trauma 1993;35:584–8.
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CONFOUNDING FACTORS
• Some patients with significant hypoperfusion
without high lactate level.
• Conditions are associated with elevated lactic acid
levels without associated tissue hypoperfusion
– Seizure
– severe respiratory distress
– certain medications (ie, anti-retrovirals, metformin, linazolid,
albuterol)
– thiamine deficiency
– carbon monoxide or cyanide toxicity, and diabetic
ketoacidosis
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RESPONSES TO INITIAL FLUID
RESUSCITATION
Rapid Response Transient
Response Minimal or No
minimal Response
Vital signs Return to normal Transient
improvement, then recur
Remain abnormal
Estimated blood
loss 10 – 20% 20 – 40% Severe, >40%
Need for more
crystalloid Low High High
Need for blood Low Moderate to high High
Need for operative
intervention Possibly Likely Highly likely
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• Knowledge about age-specific vital signs is
important to prevent misguided assumption
• Hypotension is defined as systolic BP below 5th
percentile specific for age:
SBP < 70 + (2 * age) mmHg
[Normal SBP ~ 80 + (2*age) mmHg]
• Estimating the weight for a child in kg:
Less than 8 years: (2*age) + 8
8 years and above: (3*age)
PEDIATRIC TRAUMA
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• Minimal or limited physiologic reserve.
– Profound hypovolemia can occur even in
setting of “normal” blood pressure
• Narrow therapeutic window for cardiac
preload
• Cortical atrophy potentially delay clinical
manifestations of serious intracranial
hemorrhage
GERIATRIC TRAUMA: POTENTIAL
PITFALLS
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• Ventilatory failure & respiratory arrest
may occur suddenly concurrently with
chest/abdominal trauma, etc.
• Myocardial demand ischemia may results
from severe pain, etc.
• Decrease in connective tissue integrity,
less tamponade effect
– The blood loss can be excessive and is often
overlooked
GERIATRIC TRAUMA: POTENTIAL
PITFALLS
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• Clinical manifestations of serious injuries –
minimal
• Failure to adjust medication dosages, e.g.
sedative-hypnotics
• Elderly abuse/chronic malnutrition
GERIATRIC TRAUMA: POTENTIAL
PITFALLS
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FAILURE TO RECOGNIZE THE
LETHAL TRIAD OF TRAUMA
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WHY ACIDOSIS?
1. Poor perfusion to the tissues
2. Decreased cardiac output, anemia, and hypoxemia anaerobic metabolism lactic acidosis.
3. Resuscitation with unbalanced crystalloids such as normal saline hyperchloremic acidosis
• Ho, A.M., et al., Excessive use of normal saline in managing traumatized patients in shock: a preventable contributor to
acidosis. J Trauma, 2001. 51(1): p. 173-7.
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THE DANGERS OF ACIDOSIS
• Severe acidosis can further diminish
cardiac output and make catecholamines
less effective • Adrogue, H.J. and N.E. Madias, Management of life-threatening
acid-base disorders. Second of two parts. N Engl J Med, 1998.
338(2): p. 107-11.
• The most dangerous effect of acidosis is the
induction of coagulopathy
– Hess, J.R. and J.H. Lawson, The coagulopathy of trauma versus
disseminated intravascular coagulation. J Trauma, 2006. 60(6
Suppl): p. S12-9.
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THE DANGERS OF ACIDOSIS
• Our body‟s coagulation system does not
work in an acidic milieu.
• When the pH drops from 7.4 to 7.0, the
activity of portions of the coagulation
cascade decreases by 55-70%
• Meng, Z.H., et al., The effect of temperature and pH on the activity of
factor VIIa: implications for the efficacy of high-dose factor VIIa in
hypothermic and acidotic patients. J Trauma, 2003. 55(5): p. 886-91.
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DANGERS OF HYPOTHERMIA
• The reactions of the coagulation cascade are
all temperature dependent; as temperature
drops, bleeding increases dramatically.
• Hypothermia can cause relative
thrombocytopenia by inducing platelet
sequestration and also causes qualitative
platelet dysfunction. • Ferrara, A., et al., Hypothermia and acidosis worsen
coagulopathy in the patient requiring massive transfusion. Am J
Surg, 1990. 160(5): p. 515-8.
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COAGULOPATHY
• In addition to the coagulopathy induced by
acidosis, hypothermia, and the direct loss of
clotting factors from bleeding, the ability to
clot is further compromised by dilution and
consumption.
• Dilutional coagulopathy takes place any time
we infuse fluid or products that do not
contain clotting factors (e.g. crystalloid,
colloid, PRBCs, and platelets)
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COAGULOPATHY
• Traumatized tissues and the shock state
can abnormally activate the clotting cascade
and cause fibrinolysis out of proportion to
the injury and in areas distant to the site of
bleeding - consumptive coagulopathy
(DIVC)
• Gando, S., et al., Posttrauma coagulation and fibrinolysis. Crit Care
Med, 1992. 20(5): p. 594-600.
• Kapsch, D.N., et al., Fibrinolytic response to trauma. Surgery, 1984.
95(4): p. 473-8.
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QUESTION?