| Author: Fawn O. Workman
|
| Author: Fawn O. Workman
|
Chloride is the most abundant anion (negatively charged ion) in extracellular fluid (Alexander et al., 2014). It moves in and out of the cells with sodium and potassium and combines with major cations (positively charged ions) to form sodium chloride, hydrochloric acid, potassium chloride, calcium chloride, and other important compounds. High levels of chloride exist in cerebrospinal fluid (CSF), but the anion can also be found in bile and in gastric and pancreatic juices.
Why it's important
Because of its negative charge, chloride travels with positively charged sodium and helps maintain serum osmolality and water balance. Chloride and sodium also work together to form CSF. The choroid plexus, a tangled mass of tiny blood vessels inside the ventricles of the brain, depends on these two electrolytes to attract water and form the fluid component of CSF.
In the stomach, the gastric mucosa secretes chloride as hydrochloric acid, providing the acid medium necessary for digestion and enzyme activation. Chloride also helps maintain acid-base balance and helps transport carbon dioxide in the red blood cells.
On the level
Serum chloride levels normally range between 98 and 108 mEq/L. Values may vary slightly depending on the laboratory doing the analysis. By comparison, the chloride level inside a cell is 4 mEq/L. Chloride levels remain relatively stable with age. Because chloride balance is closely linked with sodium balance, the levels of both electrolytes usually change in direct proportion to one another.
How the body regulates chloride
Chloride regulation depends on intake and excretion of chloride and reabsorption of chloride ions in the kidneys. The daily chloride requirement for adults is 1.8 to 2.3 g/day per the National Institutes of Health guidelines. Most diets provide sufficient chloride in the form of salt (usually as sodium chloride) or processed foods. (See Dietary sources of chloride.)
Most chloride is absorbed in the intestines, with only a small portion lost in feces. Chloride is present in the stomach in the form of hydrochloric acid, and chloride levels can be influenced by gastrointestinal (GI) disorders (Alexander et al., 2014).
Best buddies
Because chloride and sodium are closely linked, a change in one electrolyte level causes a comparable change in the other. Chloride levels can also be indirectly affected by aldosterone secretion, which causes the renal tubules to reabsorb sodium. As positively charged sodium ions are reabsorbed, negatively charged chloride ions are passively reabsorbed because of their electrical attraction to sodium.
Battling acids and bases
Regulation of chloride levels also involves acid-base balance. Chloride is reabsorbed and excreted in direct opposition to bicarbonate. When chloride levels change, the body attempts to keep its positive-negative balance by making corresponding changes in the levels of bicarbonate (another negatively charged ion) in the kidneys. (Remember, bicarbonate is alkaline.)
When chloride levels decrease, the kidneys retain bicarbonate and bicarbonate levels increase. When chloride levels increase, the kidneys excrete bicarbonate and bicarbonate levels decrease. Therefore, changes in chloride and bicarbonate levels can lead to acidosis or alkalosis. (See Chloride and bicarbonate.)
<98 mEq/LHypochloremia is a deficiency of chloride in extracellular fluid. This occurs when serum chloride levels fall below 98 mEq/L. When serum chloride levels drop, levels of sodium, potassium, calcium, and other electrolytes may also be affected. If much more chloride than sodium is lost, hypochloremic alkalosis may occur.
How it happens
Serum chloride levels drop when chloride intake or absorption decreases or when chloride losses increase. Losses may occur through the skin (chloride is found in sweat), the GI tract, or the kidneys. Changes in sodium levels or acid-base balance also alter chloride levels.
Down with intake
Reduced chloride intake may occur in infants being fed chloride-deficient formula and in people on salt-restricted diets. Patients dependent on IV fluids are also at risk if the fluids lack chloride (e.g., dextrose 5% in water).
Excessive chloride losses can occur with prolonged vomiting, diarrhea, severe diaphoresis, burns, Addison disease, gastric surgery, nasogastric (NG) suctioning, and other GI tube drainage. Severe vomiting can cause a loss of hydrochloric acid from the stomach, an acid deficit in the body, and subsequent metabolic alkalosis. Patients with cystic fibrosis can also lose more chloride than normal. Any prolonged and untreated hypochloremic state can result in a state of hypochloremic alkalosis. (See Dangerous development.)
Hypochloremic alkalosis can affect infants and children as well as adults. (See Hypochloremic alkalosis in infants.) People at risk for hypochloremia include those with prolonged vomiting from pyloric obstruction and those with draining fistulas and ileostomies, which can cause a loss of chloride from the GI tract.
Decreaser medications
Various medications may decrease chloride, including bicarbonate, corticosteroids, laxatives, and theophylline. Diuretics, such as furosemide (Lasix), ethacrynic acid (Edecrin), and hydrochlorothiazide can also cause an excessive loss of chloride from the kidneys. (See Medications associated with hypochloremia.)
Wait, there's more
Other causes of hypochloremia include sodium and potassium deficiency or metabolic alkalosis; conditions that affect acid-base or electrolyte balance, such as untreated diabetic ketoacidosis, water intoxication, and Addison disease; and rapid removal of ascitic fluid (which contains sodium) during paracentesis. Also, patients who have heart failure may develop hypochloremia because serum chloride levels are diluted by excess fluid in the body.
What to look for
Patients who have hypochloremia may exhibit signs and symptoms of acid-base and electrolyte imbalances. You may notice signs of hyponatremia, hypokalemia, or metabolic alkalosis. Alkalosis results in a high pH and to compensate, respirations become slow and shallow as the body tries to retain carbon dioxide and restore a normal pH level.
The nerves also become more excitable, so look for tetany, hyperactive deep tendon reflexes, and muscle hypertonicity. (See Danger signs of hypochloremia.) The patient may have muscle cramps, twitching, fever, weakness, and be agitated or irritable. If hypochloremia goes unrecognized, it can become life-threatening. As the chloride imbalance worsens (along with other imbalances), the patient may suffer arrhythmias, seizures, coma, or respiratory arrest.
What tests show
These diagnostic test results are often associated with hypochloremia:
How it's treated
Treatment for hypochloremia focuses on correcting the underlying cause. Chloride may be replaced through fluid administration or medication therapy. Treatment may be necessary for associated metabolic alkalosis or other electrolyte imbalances.
Chloride may be given orally—for example, in a salty broth. IV medications or normal saline solution may be needed if the patient cannot tolerate oral supplements. To avoid hypernatremia (high sodium level) or to treat hypokalemia, potassium chloride may be administered IV
Addressing the alkalosis
Treatment for associated metabolic alkalosis usually addresses the underlying causes, such as diaphoresis, vomiting or other GI losses, or renal losses. Rarely, metabolic alkalosis may be treated by administering ammonium chloride, an acidifying agent that's used when alkalosis is caused by chloride loss. Medication dosage depends on the severity of the alkalosis. The effects of ammonium chloride last only 3 days. After that, the kidneys begin to excrete the extra acid. (See When treatment doesn't work.)
How you intervene
Monitor patients at risk for hypochloremia, such as those receiving diuretic therapy or NG suctioning. When caring for a patient with hypochloremia, you'll also want to take these actions:
>108 mEq/LHyperchloremia, an excess of chloride in extracellular fluid, occurs when serum chloride levels exceed 108 mEq/L. This condition is associated with other acid-base imbalances, such as metabolic acidosis, and rarely occurs alone.
How it happens
Because chloride regulation and sodium regulation are closely related, hyperchloremia may also be associated with hypernatremia. Chloride and bicarbonate have an inverse relationship, so an excess of chloride ions may be linked to a decrease in bicarbonate. Excess serum chloride results from increased chloride intake or absorption, from acidosis, or from chloride retention by the kidneys.
Up with intake and absorption
Increased intake of chloride in the form of sodium chloride can cause hyperchloremia, especially if water loss from the body occurs at the same time. The water loss raises the chloride level even more. Increased chloride absorption by the bowel can occur in patients who have had anastomoses joining the ureter and intestines. Normal saline contains sodium and chloride in a 1:1 ratio. Hypertonic NaCl IV solution could increase serum chloride (and potentially disproportionately to sodium). The nurse should be aware of the cumulative effects of IV fluids, including those for flushes and diluents, including the effects on Na, Cl, and fluid balance. Kidney function can be adversely affected by hyperchloremia secondary to excessive normal saline infusion (Alexander et al., 2014; Bertschi, 2020).
Conditions that alter electrolyte and acid-base balance and cause metabolic acidosis include dehydration, renal tubular acidosis, diabetes insipidus, kidney failure, respiratory alkalosis, salicylate toxicity, hyperparathyroidism, hyperaldosteronism, and hypernatremia.
Medication-related retention
Several medications can also contribute to hyperchloremia. For example, direct ingestion of ammonium chloride or other medications that contain chloride or cause chloride retention can lead to hyperchloremia. Ion exchange resins that contain sodium, such as Kayexalate, can cause chloride to be exchanged for potassium in the bowel. When chloride follows sodium into the bloodstream, serum chloride levels rise. Carbonic anhydrase inhibitors, such as acetazolamide, also promote chloride retention in the body by increasing bicarbonate ion loss. (See Medications associated with hyperchloremia.)
What to look for
Hyperchloremia rarely produces signs and symptoms on its own. Instead, the major indications are essentially those of metabolic acidosis, including tachypnea; lethargy; thirst; weakness; dehydration; hypotension; diminished cognitive ability; and deep, rapid respirations (Kussmaul respirations).
Left untreated, acidosis can lead to arrhythmias, decreased cardiac output, a further decrease in LOC, and even coma. Metabolic acidosis related to a high chloride level is called hyperchloremic metabolic acidosis. (See Anion gap and metabolic acidosis.)
If a patient has an increased serum chloride level, the serum sodium level is probably high as well, which can lead to fluid retention. The patient also may be agitated and have dyspnea, tachycardia, hypertension, or pitting edema—signs of hypernatremia and hypervolemia.
What tests show
The following diagnostic test results typically occur in hyperchloremia:
In addition, the patient may have a serum pH level less than 7.35, a serum bicarbonate level less than 22 mEq/L, and a normal anion gap (8 to 14 mEq/L). These findings suggest metabolic acidosis.
How it's treated
Treatment for hyperchloremia includes correcting the underlying cause as well as restoring fluid, electrolyte, and acid-base balance. (See Diuretics to the rescue.) A dehydrated patient may receive fluids to dilute the chloride and speed renal excretion of chloride ions. The patient's sodium and chloride intake may also be restricted.
If the patient has normal liver function, the patient may receive an infusion of lactated Ringer solution to convert lactate to bicarbonate in the liver, thereby increasing the base bicarbonate level and correcting acidosis. In severe hyperchloremia, the patient may need IV sodium bicarbonate to raise serum bicarbonate levels. Because bicarbonate and chloride compete for sodium, IV sodium bicarbonate therapy can lead to renal excretion of chloride ions and correction of acidosis.
How you intervene
Try to prevent hyperchloremia by monitoring high-risk patients. If your patient develops a chloride imbalance, follow these steps:
If you answered all five questions correctly, incredible! You're the salt of the Earth when it comes to chloride imbalances.
If you answered four questions correctly, super! You're obviously in the loop about chloride imbalances.
If you answered fewer than four questions correctly, that's okay. Your chloride intake from the chapter is a little low, but the imbalance can be easily corrected by reviewing the chapter.
References
Alexander, M., Corrigan, A. M., Gorski, L. A., & Phillips, L. (2014). Core curriculum for infusion nursing (4th ed.). Lippincott Williams & Wilkins.
Berend, K., van Hulsteijn, L. H., & Gans, R. O. (2012). Chloride: The queen of electrolytes? European Journal of Internal Medicine, 23(3), 203–211. doi:10.1016/j.ejim.2011.11.013
Bertschi, L. A. (2020). Abnormal basic metabolic panel findings: Implications for nursing. AJN, American Journal of Nursing, 120(6), 58–66. https://doi.org/10.1097/01.naj.0000668764.99872.89
Boniatti, M., Cardoso, P. R., Castilho, R. K., & Vieira, S. R. (2011). Is hyperchloremia associated with mortality in critically ill patients? A prospective cohort study. Journal of Critical Care, 26(2), 175–179. doi:10.1016/j.jcrc.2010.04.013
McCallum, L., Jeemon, P., Hastie, C. E., Patel, R. K., Williamson, C., Redzuan, A. M., . . . Padmanabhan, S. (2013). Serum chloride is an independent predictor of mortality in hypertensive patients. Hypertension, 62(5), 836–843. doi:10.1161/HYPERTENSIONAHA.113.01793
McCluskey, S. A., Karkouti, K., Wijeysundera, D., Minkovich, L., Tait, G., & Beattie, W. S. (2013). Hyperchloremia after noncardiac surgery is independently associated with increased morbidity and mortality: A propensity-matched cohort study. Anesthesia and Analgesia, 117(2), 412–421. doi:10.1213/ANE.0b013e318293d81e
McIntosh, E., & Andrews, P. J. (2013). Is sodium chloride worth its salt? Critical Care (London, England), 17(3), 150.
MedlinePlus. (2013). Chloride in diet. http://www.nlm.nih.gov/medlineplus/ency/article/002417.htm
Rai, N., Ashok, A., & Akondi, B. (2020). Consequences of chemical impact of disinfectants: Safe preventive measures against covid-19. Critical Reviews in Toxicology, 50(6), 513–520. https://doi.org/10.1080/10408444.2020.1790499
Seifter, J. R. (2011). Acid-base disorders. In L. Goldman & A. I. Schafer (Eds.), Goldman's Cecil medicine (24th ed., pp. 741–752). Saunders.
Tutay, G. J., Capraro, G., Spirko, B., Garb, J., & Smithline, H. (2013). Electrolyte profile of pediatric patients with hypertrophic pyloric stenosis. Pediatric Emergency Care, 29(4), 465–468. doi:10.1097/PEC.0b013e31828a3006
In this chapter, you'll learn: