What is lactic acidosis and what causes it?
What is lactic acidosis?
Lactic acidosis refers to lactic acid build up in the bloodstream. It is one of the causes of something called ‘metabolic acidosis’. Lactic acid is produced when oxygen levels become low in cells within the areas of the body where metabolism takes place; or in response to overactivity related to adrenaline-like substances or exercise. There are two versions that have these chemical structures.
Why does the body produce lactic acid?
Lactic acid, also called lactate, is a natural byproduct of cellular metabolism. Our cells convert glucose (sugar) to lactate to use for energy in a process called anaerobic glycolysis. They do this when they are in need of immediate energy that cannot be supplied by oxygen.
Aerobic metabolism, which relies on oxygen, is our usual go-to for a steady energy supply, but anaerobic glycolysis is our emergency backup. We might need to tap it for a short burst of intense exercise when our muscles are oxygen-deprived. We also use it when medical conditions deprive our tissues of oxygen.
Definition
Lactic acidosis is defined by:
- Blood lactate levels above 2 mmol/L (severe is >4; normal level <1 mmol/L)
- Blood pH levels below 7.35 (normal is 7.35-7.45).
What is lactic acidosis and what causes it?
Causes
The most common cause of lactic acidosis is severe medical illness in which blood pressure is low and too little oxygen is reaching the body’s tissues. Intense exercise (or convulsions) can also cause temporary lactic acidosis.
More serious lactic acidosis usually results from a medical condition, and there are various types.
Type A
Type A lactic acidosis occurs when your tissues are deprived of oxygen. This most often happens in severe medical illnesses. It can also happen temporarily from excessive exercise.
Diseases that cause the overproduction of lactate include:
- Septic, hypovoalaemic or cardiogenic shock
- Lung disorders that deprive the blood of sufficient oxygen levels
- Haemoglobin disorders that affect the ability of your red blood cells to carry oxygen
- Ischaemic bowel
- Carbon monoxide poisoning.
Type B
Type B lactic acidosis occurs without hypoxia. It has three subcategories.
Type B1 is caused by underlying diseases that inhibit your ability to metabolise lactate, including:
- AKI
- Liver disease
- Thiamine (vitamin B1) deficiency
- Cancer
- HIV/AIDS
- Mitochondrial diseases
- Diabetes-related ketoacidosis.
Type B2 occurs as a side effect of certain drugs and toxins, including:
- Biguanides (e.g. Metformin, a drug used to treat diabetes)
- Cyanide and carbon monoxide poisoning
- Alcohols
- Cocaine
- Nucleoside reverse transcriptase inhibitors (HAART; antiretroviral therapy for HIV/AIDS)
- Beta-adrenergic agonist inhalers (e.g. salbutamol)
- Adrenaline injections, for severe allergic reactions
- Linezolid, an antibiotic
- Propofol, an anaesthetic
- Other drugs: Isoniazid, Salicylates, Sodium Valproate and Sulfasalazine
Type B3 occurs from rare congenital deficiencies of specific enzymes required to metabolise lactate, including:
- Glycogen storage disease
- Fructose-1,6-diphosphatase deficiency
- Pyruvate carboxylase deficiency
- Pyruvate dehydrogenase deficiency
- Oxidative phosphorylation deficiency
- Methylmalonic aciduria.
D-lactic acidosis
Types A and B above refer to a buildup of L-lactate in your blood. L-lactate is the form of lactic acid that is normally produced and broken down by the human body.
Another, rare form of lactic acidosis occurs from a buildup of D-lactate. This type of lactic acid is produced by bacteria in your colon. The bacteria break down carbohydrates during digestion, and D-lactate is the byproduct.
D-lactic acidosis happens when there is an overgrowth of these bacteria. The excess D-lactate is absorbed through your intestines into your bloodstream. D-lactate cannot be broken down by your kidneys or liver, so it just continues to build up in your circulation. This is normally a complication of short gut syndrome.
Clinical features
These are non-specific and dominated by the underlying cause.
But early symptoms of lactic acidosis can include:
- Nausea and vomiting
- Exhaustion and fatigue
- Fast, deep breathing (Kussmaul’s breathing, a ‘respiratory compensation’)
- Muscle cramps and body aches
- Fever greater than 38.5 C is often present when the septic shock is the cause of the lactic acidosis.
More advanced symptoms can include:
Investigations
Tests include a blood test to check lactate, FBC, U+E, LFT, bone, glucose, sepsis screen (including blood cultures and a CXR) and ABG.
Arterial blood gases and the anion gap
In any patient suspected of having a metabolic acidosis, arterial blood gas analysis (including lactate) should be performed. This should include the chloride and bicarbonate level. If the anion gap is elevated, lactic acidosis may be present. An anion gap is considered to be high when over 12 mmol/L (normal is 4-12).
The anion gap is defined as follows:
Sodium + Unmeasured cations = Chloride + Bicarbonate + Unmeasured anions. Rearranged, and we get Anion gap = Sodium – (Chloride + Bicarbonate).
How do you treat lactic acidosis?
If you have transitory lactic acidosis from exertion, shivering or convulsions, this will pass with time. You can treat it at home with rest and hydration.
The main treatment for lactic acidosis is to correct the medical problem that causes the condition. In an emergency setting, lactic acidosis is treated immediately with IV fluids and other resuscitation may be necessary, such as oxygen therapy and IV antibiotics. Intensive care may be necessary.
Prognosis (outlook)
Shock and severe lactic acidosis (pH less than 7.2) often co-exist together, and carry a mortality of about 50%. No survival has been reported for severe lactic acidosis with shock when the pH has fallen under 7.0. Interestingly, this contrasts to lactic acidosis associated with non-shock states, as in metformin-induced lactic acidosis producing pH values of 7.0, where observed mortality is only 25%.
Summary
We have described what is lactic acidosis and what causes it. We hope it has been helpful.
Other resources
This is a more detailed article on lactic acidosis.
Last Reviewed on 28 January 2024