The most important approach to managing a metabolic acidosis is to treat the underlying disorder. Then with supportive management, the body will correct the acid-base disorder. Accurate analysis & diagnosis is essential to ensure the correct treatment is used. Fortunately, in most cases this is not particularly difficult in principle. Remember though that a patient with a severe metabolic acidosis may be very seriously ill and even with optimal management the patient may not survive.
Some examples of specific treatments for underlying disorders:
The detailed treatment of the various specific disorders is not considered here, but the important message is that the treatment of each underlying disorder differs so an accurate diagnosis is essential for selection of correct treatment. Treatment of the underlying disorder will result in correction of the metabolic acidosis (ie the bicarbonate level will return to normal).
So where does this bicarbonate come from? There are three usual sources:
1. Kidney: Renal generation of new bicarbonate
This usually occurs as a consequence of an increase in ammonium excretion.
2. Liver: Hepatic metabolism of acid anions to produce bicarbonate
The normal liver has a large capacity to metabolise many organic acid anions (eg lactate, ketoanions) with the result that bicarbonate is regenerated in the liver. In severe ketoacidosis there is often a large loss of ketoanions due to the hyperglycaemia induced osmotic diuresis. This leaves a shortfall of ketoanions to be used to regenerate bicarbonate as a consequence of their metabolism in the kidney.
3. Exogenous Administration of sodium bicarbonate
This is the time honoured method to 'speed up' the return of bicarbonate levels to normal. Indeed, this may be useful in mineral acidosis (hyperchloraemic metabolic acidosis) where there are no endogenous acid anions which can be metabolised by the liver. However, in most other cases of metabolic acidosis this administration is either not helpful or may be disadvantageous.
Following the above stricture in clinical practice may be very difficult. A severe lactic acidosis may be associated with a very high risk of death no matter how careful the management. If the patient dies there are often those who will criticise. Development of (institutional) evidence-based protocols or guidelines can be useful to aid in selection of agreed treatments.
Administration of sodium bicarbonate may be useful in treatment of severe hyperkalaemia. Such hyperkalaemia may be immediately life-threatening. Calcium gluconate will be more rapidly protective against serious arrhythmias.
It should be noted that correction of a metabolic acidosis does not necessarily involve renal excretion of acid or renal regeneration of bicarbonate because of the role of hepatic metabolism of some anions. For example, in lactic acidosis and ketoacidosis, treatment results in significant correction because of predominantly hepatic metabolism of the acid anions to regenerate bicarbonate. If acid anions have been lost in the urine, then renal regeneration of bicarbonate is very important for correction of the acid-base disorder.
In a severe ketoacidosis, there is a large loss of ketoanions in the urine. When the disorder is treated (fluids & insulin) there is a relative deficiency of acid anions which can be metabolised in the liver with regeneration of bicarbonate. Consequently, it is common to find that treatment results in a rapid correction (few hours) of the hyperglycaemia and the hypovolaemia but the acidosis may take over 24 hours to return to normal. This is because 'new' bicarbonate has to be regenerated by the kidneys and this takes longer to correct the bicarbonate deficit. There has been a past tendency to speed up the process by administration of intravenousNaHCO3 solution but this is not necessary and has not been shown to have any advantage.
The liver has several important roles in acid-base metabolism and its importance is generally understated in texts. Metabolism of other bicarbonate precursors (eg citrate from blood transfusion, acetate from 'Plasmalyte 148' solution) also occurs in the liver. The liver is the major site for the synthesis of plasma proteins and this is very significant for acid-base physiology (see also Section 10.6).
Note: 'Plasmalyte 148' is an IV fluid that is available in some countries. It is used as an ECF replacement fluid. It is similar to Hartmann's solution in that it contains a bicarbonate precursor (acetate in Plasmalyte; lactate in Hartmanns). Differences from Hartmanns are that Plasmalyte has a [Na+] of 140mmol/l and contains Mg++ instead of Ca++.