1. 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

2. “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.

3. Only a fool learns from his
own mistakes, a wise man
from the mistakes of others.
- Otto von Bismarck

6. 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

7. Sources of Failure (Adapted from Rosen
et al, 2009)
Cognitive properties of Prolonged waiting
the mind for bed
Affective state Meds errors
Admit
EMS Fatigue & Shift Procedural errors
ED Design work
Patient
Triage Assessment – Diagnosis –Management - Disposition
Presentation
Discharge
Triage cueing Teamwork Issues
Inadequate D/c
Overcrowding
Lab error plan
Information gap Report Delays Follow-up failure

8. 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

9. 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

10. 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

11. 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

12. 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

13. 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.

14. 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 MNEMONIC:
• P – Psychiatric ‘AEIOU TIPS’
• S – Seizures, sepsis

15. 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

16. HEMORRHAGIC SHOCK IN
TRAUMA

17. 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

19. 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.

20. INDICATORS OF HYPOPERFUSION
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.

21. 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.

22. 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.

23. 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.

24. MEAN ARTERIAL PRESSURE (MAP)
• 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).

25. 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).

26. 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].

27. 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.

28. 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

29. RESPONSES TO INITIAL FLUID
RESUSCITATION
Rapid Response Transient Minimal or No
Response minimal Response
Vital signs Return to normal Transient Remain abnormal
improvement, then
recur
Estimated blood 10 – 20% 20 – 40% Severe, >40%
loss
Need for more Low High High
crystalloid
Need for blood Low Moderate to high High
Need for operative Possibly Likely Highly likely
intervention

30. PEDIATRIC TRAUMA
• 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)

31. GERIATRIC TRAUMA: POTENTIAL
PITFALLS
• 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

32. GERIATRIC TRAUMA: POTENTIAL
PITFALLS
• 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

33. GERIATRIC TRAUMA: POTENTIAL
PITFALLS
• Clinical manifestations of serious injuries –
minimal
• Failure to adjust medication dosages, e.g.
sedative-hypnotics
• Elderly abuse/chronic malnutrition

34. FAILURE TO RECOGNIZE THE
LETHAL TRIAD OF TRAUMA

35. 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.

36. 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.

37. 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.

38. 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.

39. 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)

40. 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.

41. QUESTION?