Transcript lactate - Calgary Emergency Medicine

HYPERLACTATEMIA
Renie Traiforos, R3
Lab rounds
August 28, 2008
OUTLINE
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Case
Definitions – lactate, hyperlactatemia, lactic acidosis.
Pathophysiology
Causes of elevated lactate/lactic acidosis.
Significance of elevated lactate
Source of blood for sampling the lactate??
Summary/take home message
CASE
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57 yr old female c/o difficulty breathing x 2 days. Hx of cough, sore
throat & nasal congestion.
Past med significant for smoking & ?COPD
Brought in by EMS – worsening SOB and chest pain.
Initial assessment: diaphoretic, appears slightly distressed. RR 22-24,
HR 128, 113/79, T36.9
CASE – cont’d
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Hgb 180, Wbc 37, bands 13, platelets 178,
creatinine 189, Na 128, K 4.9, Cl 90, CO2 20
ABG 7.26/46/90/20/-7. lactate 3.5
CXR – large LLL consolidation
CASE – cont’d
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Worsens in the ED (Incr RR, then fatigued, more tachycardic,
developed hypotension)
Rpt ABG: 7.17/53/92/19/-11. lactate 5
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Intubated for impending respiratory failure. ICU admission.
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DEFINITIONS
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LACTATE: A three carbon intermediary of carbohydrate
metabolism, generated from pyruvate with lactate dehydrogenase as
a catalyst.
Under normal circumstances, it made in skeletal muscle, brain, skin &
erythrocytes and it metabolized in the liver & kidney.
N levels: <2 mmol/L (various cutoffs reported)
HYPERLACTATEMIA then is a blood lactate level greater than
2 mmol/L.
 Sometimes see this subdivided into
“mild to moderate” is 2-4 mmol/L and “severe” hyperlactatemia
is > 4 mmol/L
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DEFINITIONS
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LACTIC ACIDOSIS:
[lactate] >4 mmol/L + metabolic acidosis
Occurs when lactate production exceeds lactate use or
metabolism
Classically seen as a wide anion gap metabolic acidosis
LACTATE FORMATION
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Glycolysis converts glucose into pyruvate.
Pyruvate may be transported across mitochondrial membranes and
metabolized in Krebs cycle (aerobic cond’ns).
Or under anaerobic conditions, pyruvate is oxidized to lactate by
lactate dehydrogenase. This is a reversible reaction within the liver &
kidney, requiring the coenzyme NAD+ (the Cori cycle)
LACTATE FORMATION
The Cori Cycle
Causes of Hyperlactatemia
Elevated lactate can occur due to:
 excessive tissue lactate production
 impaired hepatic metabolism of lactate
In most clinical cases it is probable that both processes are contributing.
Almost always discussed in the texts as a differential for lactic acidosis.
But just remember that depending on buffer reserves and concurrent
acid-base disturbances, hyperlactatemia may or may not be associated
with acidemia.
CLASSIFICATION of LACTIC ACIDOSIS
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Cohen – Woods classification system
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Type A: Due to tissue hypoxia
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Tissue hypoperfusion (global – shock, hypotension, cardiac arrest.
regional – mesenteric ischemia)
Reduced tissue 02 delivery (hypoxemia, severe anemia, CO
poisoning)
Anaerobic muscular activity (seizures, extreme exercise)
LACTIC ACIDOSIS – classification
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Type B: Not due to tissue hypoxia. 3 subtypes:
B1- is due to systemic disorders (note – can lead to Type A) Eg, renal or
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B2- is due to medications/intoxications. Eg, cyanide, salicylates,
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B3 - is due to hereditary inborn errors of metabolism. Eg, G-6-PD, biotin
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hepatic dysfunction, sepsis, DM, neoplasms, severe malnutrition
methanol, ethanol, ethylene glycol, anti-retrovirals, INH, nitroprusside, biguanides.
deficiency, mitochondrial disorders.
Significance of elevated lactate
In a recent paper on severe sepsis and septic shock by Talan et al (Infec Dis
Clin North America 2008), it states that elevated lactate levels in sepsis “are
associated with poor prognosis”… and “hyperlactatemia is not always
accompanied by a low bicarb level and/or elevated AG and thus, a
lactate level should be considered if severe sepsis is suspected.”
Significance of elevated lactate
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Studies have shown that anion gap does NOT accurately screen for
either lactic acidosis or hyperlactatemia in critically ill patients (Adams et al,
Emerg Med J 2006, and Iberti et al, Crit Care Med 1990)
ie – can see a clinically significant rise in lactate without a wide anion gap metabolic acidosis and
potentially even with no acidosis.
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Lactic acidosis or lactate > 4 mmol/L has often been regarded as a sign
of poor prognosis (in trauma, sepsis and other shock states)
Significance of elevated lactate
Not all high lactate levels predict poor outcome though. Keep
clinical setting in mind. Eg: elevated lactate in setting of
seizure – can be high (30 mmol/L!) but clear within few hrs likely b/c problem only d/t excess production not impaired
lactate metabolism.
Drawing a lactate level
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any evidence for arterial vs central venous vs venous sampling???
Good correlation b/t arterial & central venous samples (Middleton et al,
Emerg Med J, 2006) – this was true for pH, bicarb, BE & lactate values.
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One study (Gallagher et al, Ann of Emerg Med 1997) studied the agreement between
peripheral venous and arterial lactate levels and concluded “caution
should be used in substitution of V-LACT for A-LACT”. In particular found
that N venous lactate closely correlate with arterial lactate but that elevated venous levels did not.
Drawing a lactate level
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Another study (Lavery et al, J Am Coll Surg 2000) found that in trauma
patients venous lactate is “an excellent approximation for”
arterial lactate.
It is suggested that in the setting of resuscitating a shock
patient in the ED, better to follow central venous or arterial
lactate levels. Do we do this?
TAKE HOME POINTS
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Elevated levels of lactate – many causes. Often a sign of hypoxia.
Often associated with bad outcomes.
Recognize that patient does not have to have wide AG acidosis or
acidosis at all to have a significant hyperlactatemia. Espec true in early
sepsis.
It may matter where you draw your lactate level from. ABG/CVBG
often considered better than VBG. VBG okay if N level.
 QUESTIONS??????