PITFALLS IN THEMANAGEMENT OFTRAUMA PATIENTS Keng Sheng Chew, MD, MMED (Emerg Med) Senior Lecturer/Emergency Medicine Physician, School of Medical Sciences, Universiti Sains Malaysia
“The emergency departments unique operating characteristics make it a natural laboratory for the study of error.”- Croskerry P, Sinclair D. Emergency medicine: Apractice prone to error? CJEM 2001; 3 (4):271-6.
Only a fool learns from his own mistakes, a wise manfrom 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) Cognitive properties of Prolonged waiting the mind for bed Affective state Meds errors Admit EMS Fatigue & Shift Procedural errors ED Design workPatient Triage Assessment – Diagnosis –Management - DispositionPresentation Discharge Triage cueing Teamwork Issues Inadequate D/c Overcrowding Lab error plan Information gap Report Delays Follow-up failure
Human Errors (Rasmussen and JensenModel 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 DiagnosticEvaluation 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 MNEMONIC:• P – Psychiatric ‘AEIOU TIPS’• S – Seizures, sepsis
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
FAILURE TO RECOGNIZE EARLYHEMORRHAGE• 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.
INDICATORS OF HYPOPERFUSIONCocchi 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.
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)• 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).
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 FLUIDRESUSCITATION Rapid Response Transient Minimal or No Response minimal ResponseVital signs Return to normal Transient Remain abnormal improvement, then recurEstimated blood 10 – 20% 20 – 40% Severe, >40%lossNeed for more Low High HighcrystalloidNeed for blood Low Moderate to high HighNeed for operative Possibly Likely Highly likelyintervention
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)
GERIATRIC TRAUMA: POTENTIALPITFALLS• 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: POTENTIALPITFALLS• 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: POTENTIALPITFALLS• Clinical manifestations of serious injuries – minimal• Failure to adjust medication dosages, e.g. sedative-hypnotics• Elderly abuse/chronic malnutrition
FAILURE TO RECOGNIZE THE LETHAL TRIAD OF TRAUMA
WHY ACIDOSIS?1. Poor perfusion to the tissues2. 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.