Dr. Mathes’ letter raises the ultimate question regarding the pathogenesis of fluid administration–associated metabolic acidosis. Unfortunately, this fascinating question cannot be easily resolved with current research technology. The reason is that fluids either come with an abnormally low strong ion difference (SID) in comparison to plasma (plasma SID = 42, saline SID = 0, D5W SID = 0), which inevitably increases the chloride concentration relative to sodium, or they come with so-called buffers, which allow a low chloride fluid to be given, thus leaving the SID essentially unchanged and avoiding acidosis. It is impossible to know whether the acidosis induced by saline or D5W is due to dilution of bicarbonate or a decrease in SID because both happen simultaneously. It is also impossible to know whether the lack of acidosis seen with the administration of fluids, such as plasmalyte or lactated solutions, is due to bicarbonate production or the near normal or normal SID of the solution. It is impossible to prove that the independent variable is either chloride or bicarbonate. We remain uncomfortable with the term “dilutional” acidosis because it implies that what is merely a scientific hypothesis has been proven right. It has not. If anyone can devise the experiment that will convincingly prove which theory is right, we think they should receive the Nobel prize in medicine and chemistry simultaneously!
Dr. Roth raises important clinical issues in relation to fluid administration–associated acidosis. We do not know whether such acidosis is harmful or beneficial, whether we should treat it, and, if we should, how. In fact, we do not know whether we should ever treat any acidosis. 1The degree of acidosis that can be achieved with saline administration alone in human beings is unknown because massive saline administration typically occurs in critically ill patients with other disorders of acid–base balance. Animal models suggest that it can lower the pH to 7.15–7.2. 2Recovery from such acidosis in humans is variable depending on metabolic state, liver function, and renal function. Data from our study 3show that in cardiac surgery patients, even after 3–4 h, this acidosis has not yet fully resolved. In our opinion, the most important aspect of studies like ours is to highlight that fluid therapy can induce a metabolic acidosis and that it must therefore be considered in its differential diagnosis. We are particularly concerned about the possibility of trauma patients who receive large amounts of saline, are then found to have a worsening metabolic acidosis, and are taken for an exploratory laparotomy to exclude intestinal infarction, when the acidosis is mostly iatrogenic.