lactate and base deficit in trauma

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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 - PowerPoint PPT Presentation

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Lactate and Base Deficit in Trauma

January 19, 2007

James HuffmanEmergency Medicine, PGY-1

Outline

1. Case

2. Lactate Physiology Clinical utility in trauma patients

3. Base Deficit Physiology Clinical utility in trauma patients

4. Summary

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

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)

Question:

How can you tell who is “sick”?

How do you know if we’re making them better?

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).

Lactic Acid History: sour milk

Pathophysiology

Type A Type B

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

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

Clinically…

Useful in guiding resuscitation

Elevated levels are predictive of mortality

Time to normalize levels also strongly predictive

Time to clear lactate <24h 25-48h >48h Did not clear

Mortality 10% 20% 23% 67%

Husain et al. American J of Surgery 185 (2003) 485-491

Predicting Mortality

Base Deficit The amount of strong base that would have to

be added to 1L of blood to normalize the pH

Calculated from pH, PaCO2 and HCO3

-

Usually more positive than -2mEq/L

NOT simply an indirect measure of lactate Elevated in other acidemic states (DKA, ASA tox,

CRD)

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)

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

Which is better?

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

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

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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