To the Editor:—
Scheingraber et al. 1have provided further evidence that hyperchloremia causes acidosis and draw attention to this clinical problem. However, the authors suggest that iatrogenic hyperchloremic acidosis may be benign. This may be true in relatively healthy patients subjected to limited hyperchloremic insults, because the hyperchloremia is corrected by the subsequent chloruresis. The concern is the effect of more severe hyperchloremia secondary to aggressive fluid resuscitation in acutely ill patients undergoing major trauma surgery, burn debridements, vascular surgery, and liver transplantation. In vascular surgery, lactic and carbonic acid load from the distal segment may be superimposed on the iatrogenic hyperchloremic acidosis at the time of unclamping the aorta.
Animal studies suggest that hyperchloremia causes renal vasoconstriction 2,3and its affect on other organ functions are not known.
It is a matter of concern that hyperchloremia may be playing a contributory if not a major role in the pathogenesis of renal insufficiency or failure that may be frequently seen in patients requiring massive resuscitation. Until the safety of hyperchloremic acidosis is established, it seems prudent to avoid 0.9% saline during massive resuscitation. This avoidance may be more easily said than done; one consequence of massive resuscitation is increasing hyperkalemia caused by the use of blood products. The hyperkalemia is of special concern if the patient is already in renal failure. Substituting 0.9% saline by the commercially available normochloremic fluids such as lactated Ringer’s injection, Normosol (Abbott), and Plasma-Lyte (Baxter) is likely to compound the problem of hyperkalemia, because these fluids contain potassium. This situation is best exemplified by the the case report where a patient undergoing bilateral nephrectomy for polycystic kidney disease required 20 l normal saline, along with blood products. 4
One means of avoiding hyperchloremia and hyperkalemia is to use a fluid with the following composition: Na+= 140 mEq/l, Cl−= 100 mEq/l, and lactate or bicarbonate = 40 mEq/l. Currently, the only way one can get such normochloremic- and potassium-free fluid is to have the hospital pharmacy prepare it on request from the physician.
Clearly, further studies are needed to better understand the pathophysiology of hyperchloremic metabolic acidosis in acutely ill patients. We think that until such data are available, the conservative and logical approach should be to avoid iatrogenic hyperchloremia. This is more easily achieved if a fluid that is more normal than “normal” saline becomes commercially available.
