Published on Jan 10, 2023 and last reviewed on Feb 02, 2023 - 7 min read
Metabolic acidosis is a condition in which the body's fluids have an abnormally high acid level. Read the article to know more.
Acid-base disorders, such as metabolic acidosis, are defined as disruptions in the normal balance of acidity in the blood. Acidosis is defined as any condition that results in a rise in the serum hydrogen ion concentration. The term acidemia refers to the total acid-base condition of the serum pH.
Metabolic acidosis is a clinical condition defined by an increase in the acidity of the blood plasma. This condition should be regarded as an undiagnosed underlying disease condition.
There are various types of metabolic acidosis, which are as follows:
1. Ketoacidosis: Ketoacidosis is metabolic acidosis with a significant anion gap that occurs due to an excessive concentration of ketone bodies in the blood (keto-anions). A state of increased ketogenesis is established when hepatic lipid metabolism shifts to one of increased ketogenesis. As a result, acetoacetate, beta-hydroxybutyrate, and acetone, among other ketones, are excreted into the bloodstream.
There are subtypes of ketoacidosis depending upon the underlying cause, which are:
2. Lactic Acidosis: Lactate is primarily metabolized in the liver (60 percent) and kidneys (40 percent). One-half of the carbon dioxide is turned into glucose (gluconeogenesis), while the other half is metabolized further to CO2 and water in the citric acid cycle. Lactic acidosis can occur as a result of the following factors:
Excessive synthesis of lactate in the tissues.
Lactate metabolism in the liver is hampered.
3. Hyperchloraemic Metabolic Acidosis: The anion gap is normal in the presence of hyperchloraemic acidosis (in most cases). The anion that takes the place of the titrated bicarbonate is chloride, and because this is taken into account in the anion gap calculation, the anion gap is considered normal. Hyperchloremic acidosis can be caused due to:
The increase in anions will be too little to cause the anion gap to move out of the reference range.
It is also possible that acid anions will migrate throughout the cell in exchange for chloride.
This may be due to the wide standard range of the anion gap.
4. Renal Tubular Acidosis (RTA): In the case of RTA, a deficiency in the proximal tubule. Bicarbonate reabsorption, as well as a defect in distal tubule hydrogen ion secretion, or both, is responsible for the acidosis. There is a resultant metabolic acidosis that is hyperchloremic (increase in chloride ion concentration) and has a normal to moderately reduced GFR (glomerular filtration rate). There is an average anion gap in this type of acidosis. Whenever the pH of urine is greater than 7.0 despite metabolic acidosis, RTA is a common cause of suspicion for this condition.
5. Metabolic Acidosis Due to Drugs and Toxins: Many drugs and toxins have been identified as direct or indirect causes of metabolic acidosis with a significant anion gap. It is essential to consider these medications when making a differential diagnosis for a HAGMA (high-anion gap metabolic acidosis). Methanol, ethylene glycol, and salicylates are the three most prevalent substances to consider. Isopropyl alcohol and butoxyethanol are two more poisons that can cause acidosis in humans. Toluene also induces acidosis, and the anion gap may be normal or increased depending on the concentration.
Production of an excessive amount of acid leads to this condition known as metabolic acidosis. It can also occur if the kidneys cannot eliminate enough acid from the body on their own. There are various kinds of metabolic acidosis, which includes:
Diabetic acidosis (also known as diabetic ketoacidosis or DKA) occurs when substances known as ketone bodies (which are acidic) accumulate in the bloodstream as a result of uncontrolled diabetes.
Kidney disease is a severe condition that can cause uremia, distal renal tubular acidosis, or proximal renal tubular acidosis.
Hyperchloremic acidosis is produced by the excretion of an excessive amount of sodium bicarbonate from the body, which can occur due to prolonged diarrhea.
Lactic acidosis occurs when the body produces too much lactic acid.
Aspirin poisoning, ethylene glycol poisoning, and methanol poisoning are all possibilities.
Dehydration to a dangerous level can also cause metabolic acidosis.
The majority of the symptoms are produced by the disease or condition that is causing the metabolic acidosis in the first place. The most common cause of fast breathing is metabolic acidosis itself. Although the symptoms of metabolic acidosis might vary, the following are frequently seen by those who are affected by the condition:
Breathing at a rapid pace.
Feeling sluggish and exhausted with no desire to eat.
The sick feeling in the stomach.
Lactic acidosis is caused by an accumulation of lactic acid in the body. Muscle cells and red blood cells are the primary sources of lactic acid production. When the body breaks down carbohydrates to use for energy when oxygen levels are low, it results in the formation of ketones.
Any of the following can cause it:
Carbon monoxide poisoning (a medical emergency.)
Excessive use of alcoholic beverages.
Exercising for an extended period.
Failure of the liver.
Hypoglycemia (a state of low blood sugar).
Salicylates, Metformin, and antiretrovirals usage for longterm.
MELAS is a very rare genetic mitochondrial disorder that affects energy production.
Shock, cardiac failure, or severe anemia can result in a prolonged absence of oxygen.
These tests can aid in the diagnosis of acidosis. They can also tell whether the problem is caused by a respiratory problem or a metabolic problem. The tests that may be performed are:
A test for arterial blood gas.
The most fundamental metabolic panel (a group of blood tests that measure the sodium and potassium levels, kidney function, and other chemicals and functions).
Ketones in the blood.
Test for lactic acid.
Ketones in the urine.
The pH of urine.
The goal of treatment for metabolic acidosis is to:
Replace lost fluid and electrolyte balance.
Get carbohydrate and lipid metabolism back on track.
Treat the root cause of the problem.
Manage certain complications that may arise.
The treatment of metabolic acidosis depends on the underlying condition. The use of alkali (base) therapy in treating acute metabolic acidosis is usually recommended to increase and maintain the plasma pH at or above 7.20.
Sodium Bicarbonate Therapy: Sodium bicarbonate can be delivered intravenously to elevate the serum HCO3- level sufficiently to raise the pH to greater than 7.20. Continued correction is dependent on the specific case and may not be necessary if the underlying cause is curable or if the patient is asymptomatic (not experiencing symptoms). Sodium bicarbonate can be delivered intravenously to elevate the serum.
Potassium Citrate Therapy: Potassium citrate can be beneficial when acidosis is associated with hypokalemia; however, it should be taken with caution in the case of renal impairment and avoided entirely when hyperkalemia is present.
Chronic Metabolic Acidosis: When treating patients with chronic metabolic acidosis, oral alkali delivery is the primary treatment method. The most frequent alkali formulations for oral therapy are NaHCO3 pills and NaHCO3 solutions. These are available in two different strengths: 325 mg and 650 mg.
Tromethamine (THAM): THAM forms a bicarbonate buffer when it comes into contact with hydrogen ions. In order to prevent and rectify systemic acidosis, this medication is taken. A 0.3-mol/L IV solution with 18 g (150 mEq) per 500 mL (0.3 mEq per mL) of the active ingredient is available.
Diet: Consumption of fruits and vegetables regularly helps reduce the body's acid load. Because fruits and vegetables produce alkali, whereas meals such as meat, eggs, cheese, and cereal grains stimulate the body to produce acid, it is recommended that these items should be avoided.
Treatment Depending on Acidosis:
Not every type of acidosis requires the same treatment. The treatment differs based on the type of acidosis one is presented with and the conditions related to that particular acidosis.
Diabetic Ketoacidosis: In the case of diabetic ketoacidosis (DKA), insulin is provided intravenously to increase cellular uptake of glucose, minimize gluconeogenesis, and prevent lipolysis and the generation of ketone bodies, all of which are detrimental to the patient's health. Aside from that, normal saline is supplied to replenish extracellular volume; potassium and phosphate replacement may also be required.
Lactic Acidosis: The primary goal of therapy is to correct the underlying disease or condition. The restoration of tissue perfusion is critical in treating individuals suffering from tissue hypoxia. If the underlying cause of lactic acidosis is identified and addressed, the liver can use lactic acid to create HCO3 on an equimolar basis once again. A significant consideration is that rebound alkalosis might occur if the patient receives an excessive amount of alkali while suffering from acidemia.
Salicylate Poisoning: For various reasons, alkali therapy is an essential component of treatment in cases of salicylate overdose. Acidemia is corrected, and the quantity of salicylate that crosses the blood-brain barrier is reduced as a result. It is also possible to increase the excretion of salicylate by administering multiple doses of activated charcoal at 0.25 to 1 g/kg every two to four hours.
Methanol or Ethylene Glycol Poisoning: Treatment should be initiated as soon as possible in order to avoid any neurologic complications. A powerful inhibitor of alcohol dehydrogenase, Fomepizole (4-methyl pyrazole; Antizol), is now the primary treatment, even though it is significantly more expensive than ethanol. Fomepizole is administered as a loading dose and repeated multiple times until the toxin levels have decreased considerably.
The care of metabolic acidosis should focus on identifying and treating the underlying cause of the acid-base imbalance. Because there are so many potential causes, an interprofessional team effort is the most effective way to manage the condition. The result is determined by the etiology, the severity of the patient's disease, and the responsiveness to treatment.
Last reviewed at:
02 Feb 2023 - 7 min read
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