Hypochloremia usually manifests when levels are less than 95 meq/L. It is usually caused by excessive diuresis, vomiting, or nasogastric tube drainage. Volume loss results in alkalosis. When Cl - is lost via the urine or gastrointestinal fluids, there is an increase in both Na + and HCO3- resorption secondary to the volume contraction. Na+ may be resorbed in the kidney with either Cl- or HCO3- acid. When Cl- levels become low, the Na+ is exchanged for H+, and HCO3- is accentuated in the renal tubules. This loss of H+ in the urine further worsens the alkalosis. There is also an increased delivery of Na + to the distal nephron for H+ and K+ exchange. This exchange potentiates the loss of H+ and K+ in the urine, exaggerating the alkalosis further. Secondary skin losses from severe sweating or burns, along with states in which sweat has excessive Cl- (cystic fibrosis), often lead to a metabolic alkalosis also.

APPROACH There are no signs or symptoms specific for hypochloremia. However, the clinical approach may be based on the findings of the secondary effects. For example, if a metabolic alkalosis is diagnosed and is judged to be due to volume contraction, the approach is to address the metabolic alkalosis. In fact, [Cl -] can largely be ignored. Vomiting, nasogastric tube drainage, diuretics, or volume depletion may lead to hypochloremia but virtually never without an associated metabolic alkalosis. The symptoms of metabolic alkalosis include muscle weakness, irritability, and hypoventilation. Patients usually present with symptoms of volume depletion from the aforementioned etiologies, and electrolyte levels demonstrate a low [Cl-] and [Na+].

It is important then to determine the urinary [Cl-] because low urinary [Cl-] (less than 10 meq/L) in the setting of metabolic alkalosis implies chloride-responsive alkalosis (see Chap 21, "Acid-Base Disorders"). If the urinary Cl - levels are higher (greater than 40 meq/L), the hypochloremia may be secondary to volume overload or dilution. Increased urinary Cl - may also result from increased mineralocorticoid activity, which leads to the retention of HCO 3- and Na+ at the expense of H+, K+, and Cl-. This results in further positive feedback derangement. The Na+ retention leads to volume expansion that increases the Na+ delivery to the distal tubule. This ultimately leads to a greater exchange with K+ and H+, resulting in more H+ and K+ urinary losses. This acts to further the metabolic alkalosis.

The treatment of Cl--responsive metabolic alkalosis (urinary [Cl-] 10 meq/L) is IV NaCl administration. Generally speaking, emergency practice concerns itself with addressing the acute issues associated with the underlying condition. Chloride deficit per se rarely needs separate or specific consideration in the ED setting. However, as emergency practice extends to the realm of acute extended care, it is worthwhile to note that total body deficit can be determined by:

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