Should I treat this lactate?

Good posts start with good questions. Have an ER question? Send it here.

KEY

🔍- Deep Dive

📌- Clinical Application

🔸 - Weak Evidence

🔹 - Strong Evidence

📑 - Evidence summaries

✅ - Recommended treatment

⚠️ - Critical Information

You were about to discharge the patient.

Then the nurse hands you an ABG.

Lactate: 4 mmol/L.

Now what?

Panic? Fluids? Admission? ICU call?

Before reacting to the number, let’s demystify lactate.

Jump to what matters ⏬

First: what is lactate?

Glucose metabolism begins with glycolysis, producing pyruvate.

Under normal conditions, pyruvate is converted to acetyl-CoA and enters the Krebs cycle for oxidative phosphorylation.

When there is insufficient oxygen, or when glycolysis outpaces mitochondrial capacity, pyruvate is converted to lactate.

This reaction is catalysed by lactate dehydrogenase (LDH):

pyruvate ↔ lactate

When glycolysis accelerates — stress, catecholamines, exercise, illness — lactate production increases.

What happens to all the lactate produced?

Used for energy: It is continuously converted back to pyruvate and used for energy

Converted to glucose: It is metabolised mainly by the liver (and to a lesser extent the kidneys) where it is converted back to glucose

⚠️

Lactate is not a waste product. It is a metabolic fuel.

Is lactate toxic?

No.

Lactate itself is not harmful.

🔍

In some settings — such as traumatic brain injury or severe hypoglycaemia — elevated lactate may even be protective, acting as an alternative energy substrate.

What is hyperlactataemia?

Normal lactate = 0.3–1.8 mmol/L.

⚠️

Hyperlactataemia = > 2 mmol/L

When lactate rises above baseline, it reflects either:

increased production, or

decreased clearance.

⚠️

This alteration may be adaptive, not pathological.

But doesn’t lactate cause acidosis?

This is commonly misunderstood.

The idea that “lactic acidosis = lactate causes acidosis” is an oversimplification.

Lactate production does not generate hydrogen ions

The acidosis seen with hyperlactataemia results from ATP hydrolysis when oxidative phosphorylation is impaired.

🔍

Under normal conditions, hydrogen ions generated during glycolysis are consumed during mitochondrial oxidative phosphorylation.

When oxidative pathways fail or cannot keep up with metabolic demand:

hydrogen ions accumulate

acidosis develops

lactate rises in parallel

⚠️

So Lactate is a marker, not the poison.

Why does lactate increase?

This is traditionally explained using the Cohen & Woods classification.

🔍

Type A — Inadequate oxygen delivery

Type B — No evidence of tissue hypoxia

B1 -Disease-related
B2 - Drugs & toxin
(B3 exists, but is beyond the scope of this article.)

This classification is useful — but not always ED-friendly.

A more ED-useful way to think about lactate

In the ED, lactate accumulates because of an imbalance between production and clearance.

Broad mechanisms

1️⃣ Increased production

2️⃣ Decreased clearance

3️⃣ Mixed pathology

1️⃣ Increased lactate production

Type A: With inadequate oxygen delivery (Hypoperfusion or Hypoxia)

This is the category we fear most.

Any shock state

Cardiac arrest

Regional hypoperfusion (e.g. mesenteric ischaemia)

Severe hypoxaemia or anaemia

Impaired oxygen utilisation (e.g. carbon monoxide poisoning)

Generalised seizures

Intense anaerobic muscular activity

Here, lactate reflects true tissue hypoxia.

Type B: Without tissue hypoxia

B1 : Disease-related

LUKE — leukaemia, lymphoma

TIPS — thiamine deficiency, infection, pancreatitis, short bowel

DKA

B2: Drugs & toxins (common ED offenders)

β-agonists (salbutamol)

Adrenaline

Salicylates

Ethanol (especially chronic use)

2️⃣ Decreased clearance

Lactate clearance is primarily hepatic, with a smaller renal contribution.

Causes include:

Hepatic failure

Renal Failure

These patients are:

less tolerant of hypotension

more prone to sepsis

poorly equipped to handle physiological stress

⚠️

An elevated lactate here often warrants aggressive evaluation, even if vital signs appear acceptable.

3️⃣ Mixed pathology

(Impaired oxidative phosphorylation ± impaired clearance)

Examples:

Sepsis

Ethanol

Metformin

Severe pancreatitis

Sepsis — a special case

This explains why lactate can be elevated even when blood pressure and oxygenation look normal.

Why are we so concerned about lactate?

Because lactate predicts death

Regardless of the underlying cause, not just sepsis.

🔍

At higher levels, lactate usually signals:

severe physiological stress

impaired oxygen delivery or utilisation

or failure of clearance

Across multiple studies:

Elevated lactate is consistently associated with increased mortality

Lactate clearance is associated with improved outcomes

This is why lactate features prominently in sepsis guidelines, though the controversies are beyond the scope of this article.

Lactate and occult sepsis

Lactate is especially useful for detecting occult severe sepsis, particularly when ≥ 4 mmol/L.

These patients may have normal blood pressure and appear “not that sick”

Yet carry a high risk of deterioration and death.

Lactate often flags danger before vital signs do.

⚠️

A lactate ≥ 4 usually means something bad is happening — even if the patient looks fine.

But not all high lactates mean the same thing

So let’s simplify this into two ED questions:

When does lactate lie?

When does lactate kill?

When does lactate lie?

Some ED situations cause transient hyperlactataemia.

Examples:

β-agonist use (acute asthma)

Post-ictal state

Extreme physical exertion

In these cases:

Lactate may be markedly elevated

Rapid clearance is expected in 1-2 hrs

The degree of lactate elevation does not correlate with outcome

But failure to clear should prompt re-evaluation.

✅

Any test showing an elevated lactate level should be repeated.

When does lactate kill?

Sepsis

Any shock state (cardiogenic, hypovolaemic, obstructive)

Mesenteric ischaemia

Necrotising soft-tissue infection

Toxicological causes

In many of these, lactate is not just a marker —

it may be the earliest warning sign.

⚠️

Lactate levels may also provide false reassurance because not all patients with hypoperfusion will generate elevated lactate levels.

What matters

Instead of reacting to the number, ask three questions.

1️⃣ Is this shock or hypoperfusion — overt or occult?

Think broadly:

Cardiac arrest

Any shock state

Limb or mesenteric ischaemia

Compartment syndrome

Major trauma

Burns and inhalational injury

Cyanide or other cellular hypoxia states

Do not be reassured by normal vital signs.

If you are unsure → assume hypoperfusion until proven otherwise and resuscitate.

2️⃣ Does this lactate reflect dangerous pathology that needs treatment or admission?

If lactate is not from hypoperfusion, decide whether it is signalling disease.

Ask:

Is there ongoing overproduction?
(Malignancy, Pancreatitis, Toxicologic causes)

Is there impaired clearance?
(Hepatic failure, Renal failure)

Is this a mixed picture?
(Sepsis, Ethanol, Metformin, Severe pancreatitis)

In these cases:

Lactate is not benign

Have a low threshold for admission

Continue resuscitation and targeted therapy
(e.g. thiamine, source control, stop offending agents)

3️⃣ Can this lactate be explained by a reversible cause — and does it clear?

Only ask this after the first two.

Examples:

β-agonist use

Post-ictal state

Exertional lactate

Here, lactate may be high — but rapid clearance is expected.

Prove it.

Repeat lactate after time or resuscitation

Failure to clear = wrong diagnosis until proven otherwise

Want to Read More?

Wardi, Gabriel, et al. "Demystifying lactate in the emergency department." Annals of Emergency Medicine 75.2 (2020): 287-298.
(Highly recommended for a practical ED-focused understanding of lactate, it is well worth your time.)

Yartsev A. Causes of acidosis in hyperlactataemia Deranged Physiology Published January 15, 2018.

Farkas J. Understanding lactate in sepsis & Using it to our advantage. EMCrit PulmCrit. Published July 5, 2015.

Carden R. Lactate = LactHATE. St Emlyn’s. September 5, 2015.

Yartsev A. Metabolic origins and metabolic fate of lactate. Deranged Physiology. Published June 14, 2015

Stiller RH, Luks AM, Çoruh B. All that raises lactate is not sepsis. ATS Scholar. 2023 Jun 12;4(3):385-386. doi:10.34197/ats-scholar.2023-0032OT. PMID: 37795127.