Approach to metabolic acidosis: Clinical sciences

Metabolic acidosis refers to an increase in hydrogen ion concentration and a decrease in bicarbonate concentration in the blood. This can cause the pH to fall below 7.35 and serum bicarbonate level under 22 milliequivalents per liter. As a reference bicarbonates normally range from 22 to 27 miliequivalents per liter. Metabolic acidosis can be classified as either normal anion gap metabolic acidosis, which occurs in conditions like renal tubular acidosis, or elevated anion gap metabolic acidosis, which is seen in conditions like ketoacidosis.

If a patient presents with a chief concern suggesting metabolic acidosis, first perform an ABCDE assessment to determine if they are unstable.

If your patient is unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, put your patient on continuous vital sign monitoring, and provide supplemental oxygen, if needed. Here’s a clinical pearl! Severe cases might present with nausea, vomiting, lethargy, and tachypnea; and might need treatment with hemodialysis.

Let’s move on to stable patients. First, obtain a focused history and physical exam and order labs, including an arterial blood gas analysis or ABG, and CMP.

Patients may report diarrhea and vomiting, or they may have a history of diabetes mellitus. The physical exam might reveal signs of dehydration, such as dry oral mucous membranes and decreased skin turgor, and there might be an increased respiratory rate as the body tries to compensate for the acidosis.

If the ABG shows an arterial pH below 7.35 and the CMP shows decreased serum bicarbonate, typically below 22 milliequivalents per liter, that’s metabolic acidosis.

Here’s a clinical pearl! In metabolic acidosis, the body tries to compensate by increasing the rate and depth of breathing, which eliminates CO2 and lowers the pCO2.

To assess if the compensation is adequate, use the Winter formula: the range of expected pCO2 is equal to 1.5 times the bicarbonate level, plus 8, and plus or minus 2. If the measured pCO2 falls within this calculated range, the respiratory compensation is adequate. On the flip side, if the measured pCO2 is higher than calculated, there might be both metabolic and respiratory acidosis occurring at the same time.

Lastly, if the measured pCO2 is lower than calculated, your patient might be having concurrent metabolic acidosis and respiratory alkalosis.

Now that you know your patient has metabolic acidosis, your next step is to calculate the anion gap. The normal anion gap is due to the difference between unmeasured anions like sulfate, phosphate, albumin, and organic anions and cations such as potassium, magnesium, and calcium. Therefore, fluctuations in these unmeasured anions and cations may influence the anion gap. To calculate use this formula: serum sodium minus the sum of the serum chloride and bicarbonate.

Okay, let’s go over a normal anion gap range. A normal anion gap ranges from 4 to 12 milliequivalents per liter. If your patient has a normal anion gap, look for the specific cause. To remember the causes of normal anion gap metabolic acidosis, use the mnemonic HARDUPS. H stands for hyperalimentation, which is the delivery of nutrients into the vein, hypoadrenalism and hypoaldosteronism; A for acetazolamide, R for renal tubular acidosis, D for diarrhea, U for ureterostomies, P for post-hypocapnic state, and finally, S stands for spironolactone as well as saline infusion.

Okay, let’s first go over iatrogenic causes, referring to hyperalimentation, saline infusion, and acetazolamide. In such cases, patients might have a recent history of receiving total parenteral nutrition or TPN, or infusion of a large volume of IV normal saline When amino acids in TPN are metabolized, a lot of hydrogen ions are released which decreases the pH. Next, saline in large amounts can dilute the serum bicarbonate concentration and disrupt the body's acid-base balance due to excess chloride administered relative to sodium. Additionally, they might report taking medications, such as carbonic anhydrase inhibitors, like acetazolamide, or potassium-sparing diuretics, like amiloride. If this is the case, your patient’s metabolic acidosis is due to iatrogenic causes.

Moving on to renal tubular acidosis, which causes metabolic acidosis due to either impairment of hydrogen secretion like in types 1 and 4 or bicarbonate absorption like in type 2.

These patients often report muscle weakness, and possibly a history of recurrent urinary tract infections and kidney stones. Their CMP may show slightly elevated BUN and creatinine.
With these findings, consider renal tubular acidosis, and calculate the eGFR.
Normal eGFR, meaning above 60 milliliters per minute, confirms your diagnosis of renal tubular acidosis.

Next up is gastrointestinal loss of bicarbonate through diarrhea. Patients typically report profuse diarrhea, while the physical exam may show signs of dehydration, like dry mucous membranes or decreased skin turgor. Additionally, CMP reveals decreased sodium and potassium levels. If you see these findings, the patient’s metabolic acidosis is due to gastrointestinal loss of bicarbonate.

Let's go over an elevated anion gap range. Let’s start with methanol and ethylene glycol toxicity.

Alright, let’s take a step back to the anion gap, and have a look at individuals with an anion gap of more than 12 milliequivalents per liter. In this case, your patient has an elevated anion gap metabolic acidosis. To remember the causes, use a mnemonic GOLD MARK. G stands for glycols, O for oxoproline, L for L-lactate, D for D-lactate, M for methanol, A for aspirin, R for renal failure, and lastly, K stands for ketoacidosis.