What is metabolic acidosis?
Metabolic acidosis refers to the clinical disturbance, in which body fluids become too acidic. Metabolic acidosis is not an illness itself, but a sign of an underlying disease process. Normally the body has several mechanisms to control the pH (acidity or alkalinity) of the blood and tissue fluid around 7.4. However, when these mechanisms fail either due to an excessive buildup of acids or failure of alkalis (bases) to neutralize the acids, metabolic acidosis will ensure. It can be seen in a range of conditions ranging from kidney dysfunction to diabetes mellitus and even cancer. Metabolic acidosis is potentially fatal if left untreated.
Acidity in the Body
The acidity or strength of an acid can be determined in terms of hydrogen ion concentration (H+). In the body fluids, hydrogen ion concentration (H+) is around 40 nEq/L. These levels are maintained within very narrow limits. Maintaining H+ ion concentration is crucial as more H+ can bind to different enzymes in the body and affect the metabolic reactions adversely.
A larger concentration of H+ will also lead to formation of more H2CO3 (carbonic acid) and decrease HCO3- (bicarbonate – a base) concentration, as shown in the equation given above. Bicarbonate (HCO3-) is a base (alkaline) that acts as a buffer to prevent acidity.
Decreased HCO3- (bicarbonate ion) concentration will result in metabolic acidosis, a condition which can impair many body functions. Increased acidity beyond the body’s ability to neutralize it even when the HCO3- (bicarbonate ion) concentration is normal will also lead to metabolic acidosis.
Types of Anion Gap
Anion gap is the difference in the measured cations (positively charged ions, like H+) and the measured anions (negatively charged ions, like HCO3-) in body fluids. If there are unmeasured anions (like in acids), they can cause anion gap.
Therefore if in some condition, concentration of measured anions (like HCO3-) decreases and concentration of unmeasured anions (the acid anions) increases, the anion gap will increase. This also may lead to metabolic acidosis.
Depending on the anion gap, metabolic acidosis can be either :
- High anion gap due to ketoacidosis, lactic acidosis, kidney failure resulting in a higher than normal acid production and accumulation within the body.
- Normal anion gap due to problems with kidneys or gastrointestinal tract leading to a loss of bicarbonate ions that would neutralize acids.
Ways to Control Acidity
H+ concentration is maintained in following 3 ways:
- Alveolar ventilation (through lungs), which controls CO2 pressure (PaCO2). CO2 can combine with water present in body fluids to make H2CO3.
- H+ excretion by kidneys, which controls [HCO3-] concentration in blood.
Buffering is defined as keeping the acid-base concentration within normal limits with the help of buffers, which are weak acids or bases. Buffers can control pH changes by taking up or releasing H+ to prevent metabolic acidosis.
If H+ increases, HCO3- can bind to H+ to form H2CO3, thus minimizing the pH change. In this way buffers can prevent metabolic acidosis by blunting pH changes, which may result from the constant addition of acids and bases to body fluids.
In healthy people, blood pH is maintained around 7.4. An increase in H+ or a fall in pH is termed acidemia, which is caused by acidosis. In metabolic acidosis blood HCO3- concentration decreases, which increases H+ concentration. High H+ levels can eventually disturb body metabolism.
Signs and Symptoms
Metabolic acidosis presents following non-specific symptoms:
- Chest pain
- Heart palpitations
- Bone pain
- Nausea, vomiting, diarrhea, and decreased appetite
- Stunted growth and rickets in children (in chronic metabolic acidosis)
- Coma and low blood pressure (in acute severe metabolic acidosis)
- Dry skin
Severe metabolic acidosis can lead to coma, shock or death.
Causes of Metabolic Acidosis
Causes can be grouped as:
- Non-anion gap metabolic acidosis: Due to loss of HCO3- from either the gastrointestinal tract tract or the kidneys, chronic kidney failure, diarrhea, pancreatic fistula, use of drugs called carbonic anhydrase inhibitors
- High anion gap metabolic acidosis: Due to formation of too much lactic acid or ketone bodies, kidney failure, intake of some substances (like salicylate, methanol, formaldehyde, ethylene glycol, metformin), muscle damage
- Diabetic ketoacidosis: Due to buildup of acidic ketone bodies in uncontrolled type 1 diabetes.
- Lactic acidosis: Due to buildup of lactic acid caused by alcoholism, cancer, strenuous and prolonged exercising, low blood sugar, liver failure, intake of drugs (like salicylates), seizures, and prolonged lack of oxygen from heart failure, shock, or severe anemia
- Tubular acidosis: Due to kidney disease, kidney stones, poisoning (by aspirin, ethylene glycol, or methanol), and severe dehydration
Tests and Diagnosis
The following tests can be performed to diagnose metabolic acidosis:
- Lab tests can detect low concentration of HCO3-, low pH, and levels of iron, lactic acid and salicylate. It can also reveal presence of ketoacids in the blood and the urine.
- Abdominal x-rays, CT scans, or ultrasound images of kidneys, ureters, and bladder may detect kidney stones.
- Electrocardiogram (ECG) may show heart beat abnormalities arising due to electrolyte imbalances (like excessive potassium).
Treatment options can be grouped as:
- Acute metabolic acidosis is treated by alkali therapy, which increases and maintains the plasma pH alkaline or more than 7.2. Alkali therapy is the main treatment for patients with respiratory failure and elderly patients suffering from metabolic acidosis.
- Sodium bicarbonate (NaHCO3) is commonly given to treat metabolic acidosis.
- Treating underlying disorder controls serum pH in patients suffering from high anion gap acidosis, which results from accumulation of lactate, organic acids, and ketones.
- Tromethamine (THAM) treats severe metabolic acidosis by combining with H+ to form a bicarbonate buffer. However, it may have severe side-effects like hyperkalemia (too much potassium) and hypoglycemia (low blood sugar). The drug is not given to patients with poor kidney function.
- Citrate salts are given to patients with both low potassium and metabolic acidosis; however they may affect patients with kidney impairment adversely.
- Thiazide diuretics can be given to control HCO3- wasting.
- Normal serum potassium level is maintained by a low-K+ diet and by stopping drugs (like ACE inhibitors, NSAIDs) that can cause hyperkalemia or high blood potassium.
- Fludrocortisone may be given to increase potassium secretion, but it increases sodium retention.
- Starvation and alcoholism-related ketoacidosis is treated by intravenously administering glucose.
- Insulin may also be given to such patients to promote glucose uptake by cells and to reduce production of ketone bodies.
- Lactic acidosis is controlled by treating the underlying disorder.
- Salicylate poisoning is managed with alkali therapy and by increasing urine pH. NaHCO3, activated charcoal, or acetazolamide increase the excreted salicylate. Activated charcoal absorbs salicylate. In acute salicylate toxicity, hemodialysis may be done.
- In case of ethylene glycol or methanol poisoning, fomepizole or ethanol may be given. Patients with these conditions are also given folate (vitamin B9), thiamine (vitamin B1), and pyridoxine (vitamin B6).