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You should not attempt to treat any form of acidosis yourself.

The wrong  treatment for lactic, metablic acidosis, or diabetic ketoacidosis (DKA) can result in complications that may even lead to death!

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By Lahle Wolfe

Sources - Lactic acidosis - Metabolic acidosis

IOH Mini Medical Dictionary

Acidosis (ac·i·do·sis): (as”i-do´sis)  The accumulation of acid and hydrogen ions or depletion of the alkaline reserve (bicarbonate content) in the blood and body tissues, resulting in a decrease in pH.  

Diabetic Ketoacidosis (DKA):  Metabolic acidosis from the accumulation of ketones due to severely depressed insulin levels.  Diabetic ketoacidosis (DKA) results from grossly deficient insulin availability, causing a transition from glucose to lipid oxidation and metabolism.

Metabolic:  Any of the various kinds of acidosis in which the acid-base status of the body shifts toward the acid side because of loss of base or retention of acids other than carbonic acid (fixed or nonvolatile acids), in contrast to respiratory acidosis. Called also nonrespiratory acidosis.

Did you Know?

... that salicylic acid is toxic if ingested in large quantities?  

It is found in small quantities in common everyday items as a food preservative and antiseptic in toothpaste.  It is also a main ingredient in aspirin.  Overdosing on salicylic acid can result in metabolic acidosis.

... that persons following ketogenic,  low-carb diets may suffer from low levels of sodium and potassium due to their diuretic nature?

A combination of any diuretic (medication or diet) along with metformin can quickly induce lactic acidosis.

Medical Books (for sale) from other sources

Clinical Physiology of Acid-Base and Electrolyte Disorders by Rose, Post

Intensive Care Medicine by Irwin and Rippe

The ICU Book by Marino


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Diabetes Complications

Lactic Acidosis and Metabolic Acidosis
Symptoms, Causes & Treatment

Mini Site Index
What is Lactic Acidosis?
What is Metabolic Acidosis?
Signs and Symptoms

Also, See "Diabetic Ketoacidosis."

IOH Health Tip:  It is imperative that any person with diabetes who has elevated blood glucose and ketones in their urine contact their physician immediately.  You cannot "correct" diabetic ketoacidosis, lactic acidosis, or metabolic acidosis simply by drinking more and giving insulin, which in fact, done too quickly or without medical supervision can have fatal results.

A person with any form of acidosis is in a medical state of emergency and requires immediate care.    


What is Lactic Acidosis?

Lactic acidosis is a condition caused by the buildup of lactic acid in the body. It leads to acidification of the blood (acidosis), and is considered a distinct form of metabolic acidosis.

The cells produce lactic acid when they use glucose for energy in the absence of adequate oxygen. If too much lactic acid stays in the body, the balance tips and the person begins to feel ill. The signs of lactic acidosis are deep and rapid breathing, vomiting, and abdominal pain; similar symptoms for diabetic ketoacidosis (DKA).

Lactic acidosis may be caused by diabetic ketoacidosis or liver or kidney disease, as well as some forms of medication, most notably metformin also sold as "Glucophage," which is often prescribed for persons with type 2 diabetes, insulin resistance, and women for polycystic ovarian syndrome (PCOS).

The Cohen-Woods classification (1976) categorises causes of lactic acidosis as follows:

  • Type A: Decreased perfusion or oxygenation
  • Type B:B1: Underlying diseases (sometimes causing type A)
    • B2: Medication  (including metformin [Glucophage]) or intoxication
    • B3: Inborn error of metabolism, including diabetes usually type 1, but also type 2.  



What is Metabolic Acidosis?

Metabolic acidosis is a state in which the blood pH is low (under 7.35) due to increased production of H+ by the body or the inability of the body to form bicarbonate (HCO3-) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general types of acidosis.


Signs and Symptoms

Symptoms are aspecific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite (either anorexia or excessive eating) and weight loss (longer term), muscle weakness and bone pains. A slightly specific finding is when the patient reports rapid breathing, not due to shortness of breath but an unmotivated drive to hyperventilate. Kussmaul respiration is rare, but may indicate ketoacidosis.

Extreme acidosis leads to neurological and cardiac complications:

  • Neurological: lethargy, stupor, coma, seizures.
  • Cardiac: arrhythmias (ventricular tachycardia), decreased response to epinephrine; both lead to hypotension (low blood pressure).

Physical examination occasionally reveals signs of disease, but is otherwise normal. Cranial nerve abnormalities are reported in ethylene glycol poisoning, and retinal edema can be a sign of methanol (methyl alcohol) intoxication. Longstanding chronic metabolic acidosis leads to osteoporosis and can cause fractures.  



Arterial blood gas sampling is essential for the diagnosis. The pH is low (under 7.35) and the bicarbonate levels are decreased (<12 mmol/l). In respiratory acidosis (low blood pH due to decreased clearance of carbon dioxide by the lungs), the bicarbonate is elevated.  An ECG can be useful to anticipate cardiac complications.

Other tests that are relevant in this context are electrolytes (including chloride), glucose, renal function and a full blood count. Urinalysis can reveal acidity (salicylate poisoning) or alkalinity (renal tubular acidosis type I).  In addition, it can show ketones in ketoacidosis.

To distinguish between the main types of metabolic acidosis, a clinical tool called the anion gap is considered very useful. It is calculated by subtracting the chloride and bicarbonate levels from the sodium plus potassium levels.  An elevated anion gap (i.e. > 16 mmol/l) can indicate particular types of metabolic acidosis, particularly certain poisons, lactate acidosis and ketoacidosis.  



The causes are best grouped by their influence on the anion gap:

Increased anion gap

  • lactic acidosis
  • ketoacidosis
  • chronic renal failure(accumulation of sulfates, phosphates, uric acid)
  • intoxication or medication:
    • organic acids(salicylates, ethanol, methanol, formaldehyde, ethylene glycol, paraldehyde, INH, toluene)
    • sulfates, metformin (Glucophage)
  • massive rhabdomyolysis

Normal anion gap

  • longstanding diarrhea  causing dehydration and imbalance (bicarbonate loss)
  • pancreatic fistula
  • uretero-sigmoidostomy
  • RTAtype II and IV
  • intoxication:
    • ammonium chloride
    • acetazolamide(Diamox®)
    • bile acid sequestrants
  • renal failure(occasionally)

The anion gap can be normal in sampling errors of the sodium level, e.g. in extreme hypertriglyceridemia. The anion gap can be increased due to relatively low levels of cations other than sodium and potassium (e.g. calcium or magnesium).  

It is important to note here, the persons following ketogenic low-carb diets may suffer from low levels of sodium and potassium due to their diuretic nature.  A combination of any diuretic (medication or diet) along with metformin can quickly induce lactic acidosis.

Metabolic acidosis is either due to increased generation of acid or an inability to generate sufficient bicarbonate. The body regulates the acidity of the blood by four buffering mechanisms:

  • Blood buffering with bicarbonate. The enzyme carbonic anhydrase maintains the equilibrium between bicarbonate and H2CO3. This is, in turn, converted into carbon dioxide and water.
  • Intracellular buffering by absorption of hydrogen atoms by various molecules, including proteins, phosphates and carbonate in bone.
  • Respiratory compensation: chemoreceptors sense a deranged acid-base system, and there is increased breathing.
  • Renal compensation: finally the kidney produces and excretes ammonium (NH4+) and monophosphate, generating bicarbonate in the process while clearing acid.  



A pH under 7.1 is an emergency, due to the risk of cardiac arrhythmias, and may warrant treatment with intravenous bicarbonate. Bicarbonate is given at 50-100 mmol at a time under scrupulous monitoring of the arterial blood gas readings. This intervention however, is not effective in case of lactic acidosis.

If the acidosis is particularly severe and/or there may be intoxication, consultation with the nephrology (kidney specialists) team is considered useful, as dialysis may clear both the intoxication and the acidosis.

A person with any form of acidosis is in a medical state of emergency and requires immediate care.  

Source: Wikipedia, Lactic Acidosis, edited for content


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