The underlying cause determines the prognosis of lactic acidosis. In sepsis, elevated lactate levels correlate with mortality. The mortality of lactic acidosis in people taking metformin was previously reported to be 50%, but in more recent reports this was closer to 25%.

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, has some serious complications in lactic acidosis, and in those cases, should be used with great care.

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

Direct removal of lactate from the body (e.g. with hemofiltration) is difficult, with limited evidence for benefit. In type A lactic acidosis, treatment consists of effective management of the underlying cause, and limited evidence supports the use of sodium bicarbonate solutions to improve the pH (which is associated with increased carbon dioxide generation and may reduce the calcium levels).

In type B lactic acidosis produced by medication, withdrawal of the medication may be necessary to resolve the lactic acidosis.

Lactic acidosis in the context of mitochondrial disorders (type B3) may be treated with a ketogenic diet and possibly with dichloroacetate (DCA), although this may be complicated by peripheral neuropathy and has a weak evidence base.

Causes of increased anion gap include:

- Lactic acidosis

- Ketoacidosis

- Chronic renal failure (accumulation of sulfates, phosphates, urea)

- Intoxication:

- Organic acids, salicylates, ethanol, methanol, formaldehyde, ethylene glycol, paraldehyde, isoniazid

- Sulfates, metformin

- Massive rhabdomyolysis

A mnemonic can also be used - MUDPILES

- M-Methanol

- U-Uremia (chronic kidney failure)

- D-Diabetic ketoacidosis

- P-Paraldehyde

- I-Infection, Iron, Isoniazid, Inborn errors of metabolism

- L-Lactic acidosis

- E-Ethylene glycol (Note: Ethanol is sometimes included in this mnemonic, as well, although the acidosis caused by ethanol is actually primarily due to the increased production of lactic acid found in such intoxication.)

- S-Salicylates

Causes include:

The newest mnemonic was proposed in "The Lancet" reflecting current causes of anion gap metabolic acidosis:

- G — glycols (ethylene glycol & propylene glycol)

- O — oxoproline, a metabolite of paracetamol

- L — L-lactate, the chemical responsible for lactic acidosis

- D — D-lactate

- M — methanol

- A — aspirin

- R — renal failure

- K — ketoacidosis, ketones generated from starvation, alcohol, and diabetic ketoacidosis

The mnemonic MUDPILES is commonly used to remember the causes of increased anion gap metabolic acidosis.

- M — Methanol

- U — Uremia (chronic kidney failure)

- D — Diabetic ketoacidosis

- P — Paracetamol, Propylene glycol (used as an inactive stabilizer in many medications; historically, the "P" also stood for Paraldehyde, though this substance is not commonly used today)

- I — Infection, Iron, Isoniazid (which can cause lactic acidosis in overdose), Inborn errors of metabolism (an especially important consideration in pediatric patients)

- L — Lactic acidosis

- E — Ethylene glycol (Note: Ethanol is sometimes included in this mnemonic as well, although the acidosis caused by ethanol is actually primarily due to the increased production of lactic acid found in such intoxication.)

- S — Salicylates

Another frequently used mnemonic is KARMEL.

- K — Ketoacidosis

- A — aspirin

- R — Renal failure

- M — Methanol

- E — Ethylene glycol

- L — Lactic acidosis

Another frequently used mnemonic is KULT.

- K — Ketoacidosis (DKA, AKA)

- U — Uremia

- L — Lactic acidosis

- T — Toxins (Ethylene glycol, methanol, as well as drugs, such as aspirin, Metformin)

The preferred mnemonic of D. Robert Dufour, the chief of the Pathology and Laboratory Medicine Service, Veterans Affairs Medical Center, is DUMPSALE, which omits the I of MUDPILES as the proposed values of *I* are exceedingly rare in clinical practice.

- D — Diabetic ketoacidosis

- U — Uremia

- M — Methanol

- P — Paraldehyde

- S — Salicylates

- A — Alcoholic ketoacidosis

- L — Lactic acidosis

- E — Ethylene Glycol

The mnemonic for the [rare, in comparison] toxins is ACE GIFTs: Aspirin, Cyanide, Ethanolic ketosis, Glycols [ ethylene and propylene ], Isoniazid, Ferrous iron, Toluene. Most of these cause a lactic acidosis.

The primary treatment goal is prevention of hypoglycemia and the secondary metabolic derangements by frequent feedings of foods high in glucose or starch (which is readily digested to glucose). To compensate for the inability of the liver to provide sugar, the total amount of dietary carbohydrate should approximate the 24-hour glucose production rate. The diet should contain approximately 65–70% carbohydrate, 10–15% protein, and 20–25% fat. At least a third of the carbohydrates should be supplied through the night, so that a young child goes no more than 3–4 hours without carbohydrate intake

In the last 30 years, two methods have been used to achieve this goal in young children: (1) continuous nocturnal gastric infusion of glucose or starch; and (2) night-time feedings of uncooked cornstarch. An elemental formula, glucose polymer, and/or cornstarch can be infused continuously through the night at a rate supplying 0.5–0.6 g/kg/h of glucose for an infant, or 0.3–0.4 for an older child. This method requires a nasogastric or gastrostomy tube and pump. Sudden death from hypoglycemia has occurred due to malfunction or disconnection, and periodic cornstarch feedings are now preferred to continuous infusion.

Cornstarch is an inexpensive way to provide gradually digested glucose. One tablespoon contains nearly 9 g carbohydrate (36 calories). Although it is safer, less expensive, and requires no equipment, this method does require that parents arise every 3–4 hours to administer the cornstarch. A typical requirement for a young child is 1.6 g/kg every 4 hours.

Long-term management should eliminate hypoglycemic symptoms and maintain normal growth. Treatment should achieve normal glucose, lactic acid, and electrolyte levels, and only mild elevations of uric acid and triglycerides.

In the United States, hyperkalemia is induced by lethal injection in capital punishment cases. Potassium chloride is the last of the three drugs administered and actually causes death. Injecting potassium chloride into the heart muscle disrupts the signal that causes the heart to beat. This same amount of potassium chloride would do no harm if taken orally and not injected directly into the blood.

Intake of carbohydrates which must be converted to G6P to be utilized (e.g., galactose and fructose) should be minimized. Although elemental formulas are available for infants, many foods contain fructose or galactose in the forms of sucrose or lactose. Adherence becomes a contentious treatment issue after infancy.

Sodium zirconium cyclosilicate (ZS-9) is an investigational selective oral sorbent that binds potassium in the gastrointestinal tract in exchange for sodium and hydrogen ions.

When acidosis is present on blood tests, the first step in determining the cause is determining the anion gap. If the anion gap is high (>12 mEq/L), there are several potential causes.

High anion gap metabolic acidosis is a form of metabolic acidosis characterized by a high anion gap (a medical value based on the concentrations of ions in a patient's serum). An anion gap is usually considered to be high if it is over 12 mEq/L.

High anion gap metabolic acidosis is caused generally by acid produced by the body. More rarely, high anion gap metabolic acidosis may be caused by ingesting methanol or overdosing on aspirin. The Delta Ratio is a formula that can be used to assess elevated anion gap metabolic acidosis and to evaluate whether mixed acid base disorder (metabolic acidosis) is present.

The list of agents that cause high anion gap metabolic acidosis is similar to but broader than the list of agents that cause a serum osmolal gap.

Treatment of uncompensated metabolic acidosis is focused upon correcting the underlying problem. When metabolic acidosis is severe and can no longer be compensated for adequately by the lungs, neutralizing the acidosis with infusions of bicarbonate may be required.

In the fetus, the normal range differs based on which umbilical vessel is sampled (umbilical vein pH is normally 7.25 to 7.45; umbilical artery pH is normally 7.20 to 7.38). In the fetus, the lungs are not used for ventilation. Instead, the placenta performs ventilatory functions (gas exchange). Fetal respiratory acidemia is defined as an umbilical vessel pH of less than 7.20 and an umbilical artery PCO of 66 or higher or umbilical vein PCO of 50 or higher.

In general, the cause of a hyperchloremic metabolic acidosis is a "loss of base", either a gastrointestinal loss or a renal loss.

- Gastrointestinal loss of bicarbonate ()

- Severe diarrhea (vomiting will tend to cause hypochloraemic alkalosis)

- Pancreatic fistula with loss of bicarbonate rich pancreatic fluid

- Nasojejunal tube losses in the context of small bowel obstruction and loss of alkaline proximal small bowel secretions

- Chronic laxative abuse

- Renal causes

- Proximal renal tubular acidosis with failure of resorption

- Distal renal tubular acidosis with failure of secretion

- Long-term use of a carbonic anhydrase inhibitor such as acetazolamide

- Other causes

- Ingestion of ammonium chloride, hydrochloric acid, or other acidifying salts

- The treatment and recovery phases of diabetic ketoacidosis

- Volume resuscitation with 0.9% normal saline provides a chloride load, so that infusing more than 3-4L can cause acidosis

- Hyperalimentation ("i.e.", total parenteral nutrition)

The main causes of hypokalemic acidosis are systemic disorders that can be divided into:

- Carbonic anhydrase inhibitors such as acetazolamide

- Dialysis, in the post-treatment

- Diarrhea

- Renal tubular acidosis

- Treated DKA with insulin therapy

- VIPoma

Hypokalemic acidosis is a normal anion gap metabolic acidosis that has various direct and associated symptoms. Symptoms are associated with hypokalemia instead of hyperkalemia.

Treatment consists of oral bicarbonate supplementation. However, this will increase urinary bicarbonate wasting and may well promote a bicarbonate . The amount of bicarbonate given may have to be very large to stay ahead of the urinary losses. Correction with oral bicarbonate may exacerbate urinary potassium losses and precipitate hypokalemia. As with dRTA, reversal of the chronic acidosis should reverse bone demineralization.

Thiazide diuretics can also be used as treatment by making use of contraction alkalosis caused by them.

Hyperchloremic acidosis is a form of metabolic acidosis associated with a normal anion gap, a decrease in plasma bicarbonate concentration, and an increase in plasma chloride concentration (see anion gap for a fuller explanation). Although plasma anion gap is normal, this condition is often associated with an "increased" urine anion gap, due to the kidney's inability to secrete ammonia.

For most horses, diet has a significant impact on the degree of clinical signs. PSSM horses fed diets high in nonstructural carbohydrates (NSC), which stimulate insulin secretion, have been shown to have increased severity of rhabdomyolysis with exercise. Current recommendations for horses with PSSM include a low-starch, high-fat diet. Low-starch diets produce low blood glucose and insulin levels after eating, which may reduce the amount of glucose taken up by the muscle cells. High fat diets increase free fatty acid concentrations in the blood, which may promote the use of fat for energy (via free fatty acid oxidation) over glucose metabolism. Horses with the most severe clinical signs often show the greatest improvement on the diet.

Dietary recommendations usually include a combination of calorie restriction, reduction of daily NSC content, and an increase in dietary fat. Diet recommendations need to be balanced with the animal's body condition score and exercise level, as it may be beneficial to wait on increasing dietary fat after an obese animal has lost weight. The diet should have <10% of digestible energy coming from NSC, and 15-20% of daily digestible energy coming from fat.

Treatment is typically achieved via diet and exercise, although metformin may be used to reduce insulin levels in some patients (typically where obesity is present). A referral to a dietician is beneficial. Another method used to lower excessively high insulin levels is cinnamon as was demonstrated when supplemented in clinical human trials.

A low carbohydrate diet is particularly effective in reducing hyperinsulinism.

A healthy diet that is low in simple sugars and processed carbohydrates, and high in fiber, and vegetable protein is often recommended. This includes replacing white bread with whole-grain bread, reducing intake of foods composed primarily of starch such as potatoes, and increasing intake of legumes and green vegetables, particularly soy.

Regular monitoring of weight, blood sugar, and insulin are advised, as hyperinsulinemia may develop into diabetes mellitus type 2.

It has been shown in many studies that physical exercise improves insulin sensitivity. The mechanism of exercise on improving insulin sensitivity is not well understood however it is thought that exercise causes the glucose receptor GLUT4 to translocate to the membrane. As more GLUT4 receptors are present on the membrane more glucose is taken up into cells decreasing blood glucose levels which then causes decreased insulin secretion and some alleviation of hyperinsulinemia. Another proposed mechanism of improved insulin sensitivity by exercise is through AMPK activity. The beneficial effect of exercise on hyperinsulinemia was shown in a study by Solomon et al. (2009), where they found that improving fitness through exercise significantly decreases blood insulin concentrations.

The goal for treatment of GSD type 0 is to avoid hypoglycemia. This is accomplished by avoiding fasting by eating every 3-4 hours during the day. At night, uncooked corn starch can be given because it is a complex glucose polymer. This will be acted on slowly by pancreatic amylase and glucose will be absorbed over a 6 hour period.

Glycogen-storage disease type 0 is most commonly diagnosed during infancy and early childhood.

Low temperature is a commonly reported trigger of acute gout: an example would be a day spent standing in cold water, followed by an attack of gout the next morning. This is believed to be due to temperature-dependent precipitation of uric acid crystals in tissues at below normal temperature. Thus, one aim of prevention is to keep the hands and feet warm, and soaking in hot water may be therapeutic.

Horses with PSSM show fewer clinical signs if their exercise is slowly increased over time (i.e. they are slowly conditioned). Additionally, they are much more likely to develop muscle stiffness and rhabdomyolysis if they are exercised after prolonged stall rest.

Horses generally have fewer clinical signs when asked to perform short bouts of work at maximal activity level (aerobic exercise), although they have difficulty achieving maximal speed and tire faster than unaffected horses. They have more muscle damage when asked to perform lower intensity activity over a longer period of time (aerobic activity), due to an energy deficit in the muscle.

Precipitation of uric acid crystals, and conversely their dissolution, is known to be dependent on the concentration of uric acid in solution, pH, sodium concentration, and temperature. Established treatments address these parameters.

It is important for MADD patients to maintain strength and fitness without exercising or working to exhaustion. Learning this balance may be more difficult than normally, as muscle pain and fatigue may be perceived differently from normal individuals.

Symptomatic relief from the effects of MADD may sometimes be achieved by administering ribose orally at a dose of approximately 10 grams per 100 pounds (0.2 g/kg) of body weight per day, and exercise modulation as appropriate. Taken hourly, ribose provides a direct but limited source of energy for the cells. Patients with myoadenylate deaminase deficiency do not retain ribose during heavy exercise, so supplementation may be required to rebuild levels of ATP.

Creatine monohydrate could also be helpful for AMPD patients, as it provides an alternative source of energy for anaerobic muscle tissue and was found to be helpful in the treatment of other, unrelated muscular myopathies.