Hyperchloremic Metabolic Acidosis: More than Just a Simple Dilutional Effect

Fluid resuscitation lies at the heart of acute care medicine. Despite the central role occupied by plasma volume expansion therapeutics, there remains little consensus regarding the ideal fluid for plasma volume expansion. However, the unintended consequences of excessive plasma volume expansion as well as those untoward events directly ascribed to the prescribed fluids have come to the fore. Anasarca, pulmonary edema, myocardial stress, acute lung injury (ALI), acute kidney injury, as well as the secondary abdominal compartment syndrome have all been described as unintended consequences of plasma volume expansion following critical illness or injury [1–3]. It is important to note that these events occur with both crystalloid and colloid therapy, although at different rates. Equally importantly, both crystalloids and colloid may create hyperchloremic metabolic acidosis. It is clear that colloids will do so at a slower rate than crystalloids principally related to their improved efficiency with regard to plasma volume expansion. Since colloid resuscitation generally requires less total volume, less total chloride is delivered and hyperchloremic metabolic acidosis occurs less rapidly. The genesis of hyperchloremic metabolic acidosis, as well as its significance, has been hotly debated over the last several decades [4–6]. Previously, the forces creating hyperchloremic metabolic acidosis were ascribed to simple dilution, and the significance of the acidosis minimized to a laboratory curiosity. Current investigations into hyperchloremic metabolic acidosis and its consequences embrace a diametrically opposed perspective. The focus of this chapter is to explore the mechanisms underpinning hyperchloremic metabolic acidosis as well as the impact of hyperchloremic metabolic acidosis on immunobiology, resuscitation, clotting, and oxygen delivery.