Elevated blood lactate (usually >4 mmol/L) causing an anion gapmetabolic acidosis (arterial pH <7.35 with low bicarbonate).
Signals severe illness—it's the most commonmetabolic acidosis in ICU patients. High lactate reflects tissue hypoperfusion and correlates with worse outcomes (the higher/longer the elevation, the higher the mortality risk). Frequently appears on exams as a marker of shock or drug toxicity.
Critically ill patients in shock (septic, cardiogenic, etc.) often have lactic acidosis due to poor perfusion. Clues include hypotension, tachycardia, and signs of hypoperfusion (cool clammy skin, delayed capillary refill) in Type A lactic acidosis.
Can also occur without obvious hypoxia: Type B lactic acidosis in contexts like severe liver/renal failure, metformin use (especially in CKD), malignancy, or post-seizure exertion (transient). These involve lactate overproduction or decreased clearance despite adequate perfusion.
Lab: High serum lactate (e.g., >4 mmol/L is significant) with an anion gapmetabolic acidosis on ABG/CMP (low HCO₃⁻, low pH). Mild elevations (2–4 mmol/L) without acidosis are called hyperlactatemia.
Confirm lactic acidosis: measure serum lactate in any high anion gap metabolic acidosis or shocked patient. Calculate the anion gap (correct for low albumin) and obtain an ABG to assess pH severity.
Find the cause (Type A vs B): If signs of hypoperfusion (hypotension, hypoxia) → Type A (tissue hypoxia); address immediately (fluids, oxygen, treat shock). If perfusion is intact → Type B; look for other causes (toxins, organ failure, thiamine deficiency, etc.).
Consider contributing factors: For example, give thiamine if deficiency is possible (alcoholics), review medications (metformin, beta-agonists, HIV NRTIs, etc.), and evaluate liver/kidney function (impaired lactate clearance).
uremic acidosis from renal failure (↑BUN/Cr, cannot excrete acids)
Toxic alcohol poisoning
e.g., methanol (vision loss) or ethylene glycol (oxalate crystals in urine) → severe anion gap acidosis
Restore perfusion: In shock, give aggressive IV fluids, improve oxygenation, and use vasopressors if needed to improve tissue perfusion. Treat the underlying cause (e.g., antibiotics for sepsis, revascularization for ischemia).
Remove offending causes: Stop any causative drugs or toxins (e.g., metformin); administer antidotes if applicable (100% O₂ for CO poisoning, antidote for cyanide, thiamine for B1 deficiency, etc.).
Bicarbonate: Reserved for severe acidosis (pH < ~6.9). IV sodium bicarbonate can temporize extreme acidemia, but avoid overuse (may cause CO₂ buildup and paradoxical CNS acidosis). Focus on definitive treatment of the cause.
Dialysis: In refractory or toxin-induced cases, consider renal replacement therapy to help clear lactate and correct acidosis (e.g., in metformin toxicity or profound shock with AKI).
Mnemonic: MUDPILES for high anion gap acidosis causes (Methanol, Uremia, DKA, Propylene glycol, INH/Iron, Lactic acidosis, Ethylene glycol, Salicylates).
In septic shock, lactate clearance (lactate dropping with treatment) is a good sign; persistently high lactate indicates poor prognosis.
Thiamine (vitamin B1) is needed to metabolize pyruvate; deficiency (e.g., in alcoholics) can lead to lactic buildup – always replete B1 when suspecting malnutrition.
Lactate ≥4 mmol/L with hypotension – sign of critical illness (e.g., septic shock). High lactate plus shock = high mortality risk → requires ICU-level aggressive management.
Arterial pH <7.1 (with high lactate) – severe acidosis can depress cardiac contractility and catecholamine response. Watch for arrhythmias and cardiovascular collapse; consider emergent dialysis or bicarbonate.
Suspect lactic acidosis in any ill patient with high anion gap metabolic acidosis or signs of poor perfusion.
Measure serum lactate and get an ABG to confirm acidosis (lactate >2 mmol/L, especially >4, with pH <7.35).
If lactate is elevated, assess perfusion/oxygenation: hypotension or hypoxia suggests Type A (hypoperfusion); if perfusion is normal, think Type B causes.
Treat the underlying cause promptly: e.g., broad-spectrum antibiotics + fluids for sepsis, restore circulation for ischemia, stop offending drugs (metformin, etc.), give thiamine if needed, etc.
Monitor lactate trends as you resuscitate. If lactate remains high or patient deteriorates, escalate care (ICU, consider vasopressors, mechanical support, or dialysis as needed).
Septic shock – A febrile, hypotensive patient with high lactate (~6 mmol/L) and anion gap metabolic acidosis despite fluids → Type A lactic acidosis from inadequate tissue perfusion (lactate as a marker of severe sepsis).
Metformin overdose – A type 2 diabetic on metformin (with CKD) presents with confusion and deep rapid breathing; labs show pH ~7.1, anion gap 24, lactate very high → Metformin-associated lactic acidosis (Type B; biguanide accumulation impairs lactate clearance).
Case 1
A 68-year-old man with type 2 diabetes (on metformin) and stage 4 CKD is brought in for altered mental status and rapid breathing.
Diagram of L-lactic acid synthesis: low oxygen causes pyruvate to convert to lactate via LDH. Dichloroacetate (DCA) activates pyruvate dehydrogenase (with thiamine as cofactor) to reduce lactate production.