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

“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.

Only a fool learns from his

own mistakes, a wise man

from the mistakes of others.

- Otto von Bismarck

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

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

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

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

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

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

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

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.

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’

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

HEMORRHAGIC SHOCK IN

TRAUMA

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

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.

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

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.

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.

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.

• 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)

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).

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].

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.

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

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

• 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

• 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

• 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

• Clinical manifestations of serious injuries –

minimal

• Failure to adjust medication dosages, e.g.

sedative-hypnotics

• Elderly abuse/chronic malnutrition

GERIATRIC TRAUMA: POTENTIAL

PITFALLS

FAILURE TO RECOGNIZE THE

LETHAL TRIAD OF TRAUMA

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.

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.

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.

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.

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)

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.

QUESTION?