LACTIC ACIDOSIS

✓ Medically ReviewedDISEASEID: MDBT0247🚨 TRIAGE: EMERGENCYICD-10: E87.2

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Definition

CLINICAL DEFINITION

A metabolic acidosis characterised by an accumulation of lactate and a decrease in serum bicarbonate, typically defined by an arterial pH < 7.35 and a serum lactate concentration > 4 mmol/L, reflecting an imbalance between lactate production and clearance.

IN PLAIN ENGLISH

A condition where lactic acid builds up in the blood, making it too acidic. This usually happens when the body's cells are not getting enough oxygen or cannot use oxygen properly to make energy.

COMMON MISCONCEPTION / WHAT IT DOES NOT MEAN

Lactic acidosis is NOT simply an elevated lactate level (hyperlactataemia) without acidemia; it requires a concurrent drop in blood pH. It is also NOT a primary respiratory acidosis, although the two can coexist.

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Word Breakdown

lact-

=milk (from Latin 'lac', referring to lactic acid first isolated from sour milk)

-osis

=abnormal condition or disease (from Greek '-osis')

Literal Meaning: An abnormal condition of lactic acid

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Abbreviations

LA=Lactic Acidosis — general abbreviation, though context-dependent and often confused with other terms

LAC=Lactate — common shorthand for serum lactate levels in critical care settings

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Synonyms & Variants

Hyperlactataemia with acidemia›

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Category-Specific Context

As a metabolic disturbance, lactic acidosis represents a failure of cellular energy metabolism or impaired hepatic and renal clearance. It is traditionally divided into Type A (hypoxic or hypoperfusion states) and Type B (non-hypoxic, related to toxins, drugs, or underlying diseases) to guide clinical investigation and management.

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Clinical Context & Usage

CLINICAL SETTINGS

Intensive Care UnitEmergency DepartmentOperating TheatreOncology WardEndocrinology Clinic

USAGE & DOCUMENTATION NOTES

Often documented as 'lactic acidosis' or 'elevated lactate with acidemia'. In critical care notes, clinicians frequently refer to 'lactate clearance' (e.g., 'lactate cleared by 20% over 2 hours') rather than just the absolute value. Arterial or venous blood gas is used to confirm the acidemia, while serum lactate is measured separately.

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Primary Causes & Pathophysiology

PATHOPHYSIOLOGY

Lactic acid is the end-product of anaerobic glycolysis. Under normal conditions, pyruvate enters the mitochondria and is oxidised via the Krebs cycle. When oxygen delivery is inadequate (Type A) or mitochondrial function is impaired (Type B), pyruvate is converted to lactate by lactate dehydrogenase to regenerate NAD+ and allow glycolysis to continue. Lactate is normally cleared primarily by the liver via gluconeogenesis and oxidation, and to a lesser extent by the kidneys. Lactic acidosis develops when lactate production exceeds hepatic and renal clearance capacity, leading to an accumulation of hydrogen ions that consume serum bicarbonate and lower blood pH.

PRIMARY CAUSES

Tissue hypoxia and shock (cardiogenic, hypovolaemic, septic, obstructive)

Global or regional hypoperfusion limits oxygen delivery to tissues, forcing a shift from aerobic metabolism to anaerobic glycolysis (Type A lactic acidosis).

Severe hypoxaemia (e.g., severe asthma, ARDS, carbon monoxide poisoning)

Inadequate arterial oxygen tension impairs mitochondrial oxidative phosphorylation despite adequate perfusion.

Seizures or extreme physical exertion

Transiently massive increase in muscular glycolytic rate exceeds hepatic clearance capacity, usually self-limiting.

Malignancy (e.g., lymphoma, leukaemia)

Warburg effect — tumour cells preferentially utilise aerobic glycolysis, producing large amounts of lactate even in the presence of oxygen (Type B).

Thiamine (Vitamin B1) deficiency

Thiamine is a required cofactor for pyruvate dehydrogenase; its absence prevents pyruvate from entering the Krebs cycle, shunting it to lactate.

Liver failure

Impaired hepatic clearance of lactate via the Cori cycle, reducing the body's ability to metabolise the daily lactate load.

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Drug-Induced Causes

💊 Metformin ↗

Mechanism: Inhibits mitochondrial complex I, impairing oxidative phosphorylation and promoting anaerobic metabolism; risk is highest in acute kidney injury or overdose.

→ Discontinue metformin. Consider haemodialysis in severe cases (lactate > 20 mmol/L, pH < 7.0, or failure to improve) to remove the drug and correct acidosis.

💊 Nucleoside reverse transcriptase inhibitors (NRTIs) ↗

Mechanism: Inhibit mitochondrial DNA polymerase gamma, leading to mitochondrial toxicity and impaired aerobic metabolism.

→ Discontinue the offending antiretroviral agent. Provide supportive care and consider bicarbonate therapy if severely acidotic.

💊 Beta-2 agonists (e.g., salbutamol) ↗

Mechanism: Stimulate glycogenolysis and glycolysis, increasing pyruvate production that exceeds mitochondrial oxidation capacity (Type B).

→ Reduce dose or discontinue if clinically feasible; usually self-limiting once the drug is stopped.

💊 Linezolid ↗

Mechanism: Prolonged use (> 2 weeks) can cause mitochondrial toxicity by inhibiting bacterial and mitochondrial protein synthesis.

→ Discontinue linezolid. Lactate levels typically normalise over days to weeks after cessation.

💊 Propofol ↗

Mechanism: Impairs mitochondrial fatty acid oxidation and electron transport chain function, especially with high doses or prolonged infusions (Propofol Infusion Syndrome).

→ Stop propofol infusion immediately. Provide supportive critical care, including haemodialysis or ECMO in refractory cases.

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Epidemiology

Prevalence:Common in critically ill patients; hyperlactataemia (> 2 mmol/L) is present in up to 30-40% of ICU admissions, while frank lactic acidosis (lactate > 4 mmol/L with acidemia) occurs in approximately 5-10% of ICU patients and is strongly associated with sepsis and shock.

Age Group:All ages, but incidence of shock-related lactic acidosis peaks in older adults due to higher prevalence of sepsis, cardiovascular disease, and polypharmacy.

Sex Predilection:Equal

Geographic Distribution:Globally uniform, though incidence of specific causes (e.g., infectious diseases causing sepsis, HIV-related NRTI toxicity, or malnutrition-related thiamine deficiency) varies by region.

Red Flags & Triage ★

TRIAGE LEVEL

🚨 EMERGENCY

DO NOT MISS — LIFE-THREATENING PRESENTATIONS

Occult mesenteric ischaemia — elderly patients with atrial fibrillation or severe atherosclerosis presenting with unexplained lactic acidosis and vague abdominal pain require urgent CT angiography, as bowel necrosis is rapidly fatal.
Metformin-associated lactic acidosis (MALA) — patients with acute kidney injury taking metformin can develop severe, refractory lactic acidosis; early nephrology consultation for haemodialysis is critical.

URGENT EVALUATION TRIGGERS

Serum lactate > 4 mmol/L in a patient with suspected infection (indicates severe sepsis or septic shock).
Failure of lactate to decrease by at least 10-20% after 2 hours of adequate fluid resuscitation.
Lactic acidosis accompanied by altered mental status, severe hypotension, or oliguria.

Contraindications & Precautions

CONTRAINDICATIONS

Routine use of sodium bicarbonate for lactic acidosis with pH > 7.1 is generally not recommended
as it can cause intracellular acidosis (via CO2 generation)
hypernatraemia
and volume overload without improving outcomes.

SPECIAL PRECAUTIONS

Interpret lactate levels in the context of liver function; patients with cirrhosis may have chronically elevated baseline lactate due to impaired clearance
not necessarily acute hypoperfusion.
Avoid relying solely on a single lactate value; serial measurements (lactate clearance) are required to assess the adequacy of resuscitation.
Be aware that venous lactate can be slightly higher than arterial lactate; use consistent sampling sites for serial trending.

Complications

DOWNSTREAM CLINICAL COMPLICATIONS

Cardiovascular collapse — severe acidemia (pH < 7.1) depresses myocardial contractility and causes vasoplegia
worsening shock.
Hyperkalaemia — extracellular shift of potassium in exchange for hydrogen ions as the body attempts to buffer the acidosis.
Acute kidney injury — renal hypoperfusion and direct tubular toxicity from severe acidemia and shock.
Encephalopathy — altered mental status and depressed consciousness due to severe acidemia and underlying shock.

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Reference Ranges

NORMAL RANGESerum lactate: 0.5–1.0 mmol/L (or up to 2.0 mmol/L depending on the laboratory reference range). Arterial pH: 7.35–7.45.

CRITICAL (PANIC) VALUESerum lactate > 4.0 mmol/L in the context of suspected infection or shock indicates severe tissue hypoperfusion and requires immediate resuscitation. Arterial pH < 7.10 indicates severe acidemia with risk of cardiovascular collapse.

UNIT OF MEASUREMENTmmol/L (SI), mg/dL (conventional; 1 mmol/L = 9 mg/dL)

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Confused With (LASA & DDx) ★

LEXICAL (LASA) — SIMILAR NAMES

Diabetic Ketoacidosis (DKA)

Both present as high anion gap metabolic acidosis. DKA is distinguished by hyperglycaemia and significant ketonaemia, whereas lactic acidosis has elevated lactate without primary ketosis.

Hyperlactataemia

Often used interchangeably in casual speech, but hyperlactataemia refers only to elevated lactate levels without the requisite acidemia that defines lactic acidosis.

CLINICAL DIFFERENTIAL DIAGNOSES (DDx)

Diabetic Ketoacidosis (DKA)

Key Distinguishing Feature: High anion gap metabolic acidosis with marked hyperglycaemia and positive serum or urine ketones; lactate may be mildly elevated but is not the primary driver.

Toxic alcohol ingestion (Methanol, Ethylene glycol)

Key Distinguishing Feature: High anion gap metabolic acidosis with a high osmolar gap; specific toxicology screens or clinical history confirm the diagnosis.

Salicylate toxicity

Key Distinguishing Feature: Mixed primary respiratory alkalosis and high anion gap metabolic acidosis; history of aspirin ingestion and elevated serum salicylate levels.

Uraemic acidosis

Key Distinguishing Feature: High anion gap metabolic acidosis in the setting of severe renal failure, with markedly elevated blood urea and creatinine, without primary lactate elevation.

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Clinical Pearls

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Lactate is not solely a marker of hypoxia; it is also produced during accelerated glycolysis (e.g., from beta-agonist use, seizures, or severe stress) even when tissue oxygenation is adequate. Always correlate the lactate level with the clinical picture of perfusion.

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The Cohen and Woods classification divides lactic acidosis into Type A (clinical evidence of tissue hypoperfusion or hypoxia) and Type B (no clinical evidence of hypoperfusion, associated with drugs, toxins, or systemic diseases). This distinction guides the diagnostic workup.

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D-Lactic acidosis is a rare variant seen in patients with short bowel syndrome. Standard hospital lactate assays only measure L-lactate, so a patient with D-lactic acidosis will present with a high anion gap metabolic acidosis and neurological symptoms, but a 'normal' serum lactate level.

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In trauma and shock, lactate clearance (the percentage decrease in lactate over time) is a stronger predictor of survival than the initial absolute lactate value. A failure to clear lactate suggests ongoing occult hypoperfusion or impaired hepatic function.

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Example Usage & SOAP

CLINICAL SENTENCE

"The patient presented with septic shock secondary to perforated diverticulitis, complicated by a severe Type A lactic acidosis with an initial lactate of 6.8 mmol/L and pH of 7.18, which improved to 3.2 mmol/L following aggressive fluid resuscitation and source control."

IN A SOAP NOTE

S: 68-year-old male with increasing abdominal pain, confusion, and decreased urine output over the past 12 hours. O: T 38.9°C, HR 118 bpm, BP 85/50 mmHg, RR 24/min. Abdomen diffusely tender with guarding. VBG shows pH 7.15, pCO2 28 mmHg, HCO3 12 mmol/L. Serum lactate 7.2 mmol/L. WBC 18.5 x 10^9/L. A: Septic shock likely secondary to acute intra-abdominal pathology, with severe lactic acidosis indicating profound tissue hypoperfusion. P: 1. Administer 30 mL/kg IV balanced crystalloid. 2. Start noradrenaline infusion to maintain MAP > 65 mmHg. 3. Broad-spectrum IV antibiotics (piperacillin-tazobactam). 4. Urgent CT abdomen/pelvis and surgical consultation for source control. 5. Recheck lactate in 2 hours.

DIFFERENTIAL DIAGNOSIS CONTEXT

Differential for high anion gap metabolic acidosis with elevated lactate: (1) Type A lactic acidosis (evaluate for shock, hypoxia, regional ischaemia); (2) Type B lactic acidosis (review medications like metformin or NRTIs, check for occult malignancy or liver failure); (3) Mixed acid-base disorder (e.g., concurrent DKA or toxic alcohol ingestion, which can also elevate lactate secondary to shock or mitochondrial toxicity).

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Prognosis

SHORT-TERM OUTCOME

Highly dependent on the underlying cause and reversibility. In septic shock, a failure to clear lactate by at least 10-20% within the first 2-6 hours of resuscitation is associated with significantly higher short-term mortality.

LONG-TERM PROGNOSIS

If the underlying cause (e.g., sepsis, ischaemia) is reversed and the patient survives the acute episode, long-term prognosis is determined by the residual organ damage (e.g., post-sepsis syndrome, amputations from ischaemic limbs) rather than the lactic acidosis itself.

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References & Coding

ICD-10 DIAGNOSTIC CODE

E87.2

LITERATURE CITATIONS & GUIDELINES

[1]Kraut JA, Madias NE. Lactic acidosis. N Engl J Med. 2014;371(24):2309-2318.

[2]Andersen LW, Mackenhauer J, Roberts JC, et al. Etiology and therapeutic approach to elevated lactate. Mayo Clin Proc. 2013;88(9):1021-1037.

[3]Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med. 2021;49(11):e1067-e1143.

MEDICAL DISCLAIMER — This content is intended for educational purposes and qualified healthcare professionals only. Always refer to current clinical diagnostic criteria, institutional protocols, and official guidelines. Medobo is not responsible for clinical decisions made based on this content.