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Lactate and Base Deficit in Trauma

Lactate and Base Deficit in Trauma. January 19, 2007 James Huffman Emergency Medicine, PGY-1. Outline. Case Lactate Physiology Clinical utility in trauma patients Base Deficit Physiology Clinical utility in trauma patients Summary. Case:. Claresholm, Alberta

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Lactate and Base Deficit in Trauma

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  1. Lactate and Base Deficit in Trauma January 19, 2007 James Huffman Emergency Medicine, PGY-1

  2. Outline • Case • Lactate • Physiology • Clinical utility in trauma patients • Base Deficit • Physiology • Clinical utility in trauma patients • Summary

  3. Case: • Claresholm, Alberta • 28M: MVC >130km/h, restrained, no airbag, EtOH, >30cm passenger space intrusion, BP 88/50 on scene • Heathy otherwise, no meds, NKDA • Vitals: • T: 36.2 C • HR: 104 • RR: 24 • BP: 102/68 • O2: 98% on 15L nrb

  4. Case: • A – Patent. Able to vocalize • B – Bilateral breath sounds • C – Vitals as above. All pulses palpable, CRT 2sec. • D – Moving all four limbs. No signs of head injury. • E – Seat belt sign present. Abdo moderately tender. Pelvis stable. No obvious fractures/open wounds • F – 2 IV’s running wide, Foley in. • Brand new U/S, but not avail (being used by other ED doc for a gyne scan)

  5. Question: How can you tell who is “sick”? How do you know if we’re making them better?

  6. Resuscitation end points: Shock: “An abnormality of the circulatory system that results in inadequate organ perfusion and tissue oxygenation” (ATLS) Inadequate perfusion  inadequate O2 delivery  anaerobic metabolism  acidosis Therefore, resuscitation is complete when O2 debt is repaid, acidosis is eliminated and aerobic metabolism restored. Porter et al. J of Trauma; 44 (1998).

  7. Lactic Acid History: sour milk

  8. Pathophysiology

  9. Decreased O2 delivery Shock (hypovolemia) Severe Anemia Hypoxemia CO poisoning Increased O2 demands Inadequate O2 utilization SIRS DM Malignancy Metabolic Infections Drugs/toxins Other D-Lactic Acidosis Type A Type B

  10. Lactate Pitfalls • Anion Gap • Low albumin lowers the AG • Ethanol • Other Drugs/Toxins • Metformin • Propofol • Beta-2 agonists • Salicylates • Etc. • Inborn errors of metabolism, G6PD deficiency • Sampling location

  11. Clinically… • Useful in guiding resuscitation • Elevated levels are predictive of mortality • Time to normalize levels also strongly predictive Husain et al. American J of Surgery 185 (2003) 485-491

  12. Predicting Mortality

  13. Base Deficit • The amount of strong base that would have to be added to 1L of blood to normalize the pH • Calculated from pH, PaCO2and HCO3- • Usually more positive than -2mEq/L • NOT simply an indirect measure of lactate • Elevated in other acidemic states (DKA, ASA tox, CRD)

  14. Base Deficit • In hemorrhage, this value becomes more negative before we see changes to pH and BP • In pure hemorrhagic and septic shock, BD directly correlates with lactate levels • Severely abnormal BD (≤ 10) in trauma patients is assoc. with significantly higher mortality, rates of ARDS and MOF Davis et al. J of Trauma; 44 (1998)

  15. Base Deficit • Largest clinical series conducted by Rutherford in 1992 • Retrospective review of 3,791 trauma patients • BD of -15 in patients <55 years without HI had significantly increased mortality • If age>55 or HI present, BD of -8 showed significantly increased mortality

  16. Which is better?

  17. Take Home Points • Lactate: • Normalized serum lactate appears to be a suitable end point for resuscitation • High initial lactate and moreover, time to normalize this value are predictive of mortality risk

  18. Take Home Points • Base Deficit: • A large negative BD (<-2mEq/L) may represent early hemorrhage/hypovolemic shock • Very high initial BD (>10-15) in trauma patients represents a significant mortality risk • Resuscitation: • Correction of serum lactate and BD are reasonable markers of resuscitation

  19. References: Adams, B., Bonzani, T. and C. Hunter. 2006. The anion gap does not accurately screen for lactic acidosis in emergency department patients. Emerg Med J. 23; 179-82. Davis J., et al. 1998. Base Deficit is Superior to pH in Evaluating Clearance of Lactic Acidosis after Traumatic shock. J of Trauma. 44; 114-17. Fall, P. and H. Szerlip. 2005. Lactic Acidosis: From sour milk to septic shock. J. of Intensive Care Medicine. 20(5); 255-71. Husain, F., et al. 2003. Serum lactate and base deficit as predictors of mortailty and morbidity. American J of Surgery. 185; 485-91. Jones, A. and J. Kline. 2006. Shock. In Rosen’s Emergency Medicine. Concepts and Clinical Practice (6th Edition). Philadelphia, PA: Mosby Elsevier. Nguyen, B., et al. 2006. Severe Sepsis and Septic Shock: Review of the literature and emergency department management guidelines. Ann of Emergency Medicine. 48(1); 28-54. Porter, J., and R. Ivatury. 1998. In Search of Optimal End Points of Resuscitation in Trauma Patients: A Review. J of Trauma. 44; 908-13.

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