hypochloremia(redirected from Hypochloraemia)
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|Mean LOS:||4.7 days|
|Description:||MEDICAL: Nutritional and Miscellaneous Metabolic Disorders With Major CC|
Hypochloremia is a serum chloride level below 95 mEq/L. Normal serum chloride level is 101 to 112 mEq/L. Chloride is the major anion in the extracellular fluid (ECF). The intracellular level of chloride is only about 2 to 4 mEq/L. Chloride is regulated in the body primarily through its relationship with sodium. Serum levels of both sodium and chloride often parallel each other.
A main function of chloride in the body is to join with hydrogen to form hydrochloric acid (HCl). HCl aids in digestion and activates enzymes, such as salivary amylase. Chloride plays a role in maintaining the serum osmolarity and body water balance. The normal serum osmolarity ranges between 280 and 295 mOsm/L.
Chloride deficit leads to a number of physiological alterations such as ECF volume contraction, potassium depletion, intracellular acidosis, and increased bicarbonate generation. Hypochloremia, similar to hyponatremia, also causes a decrease in the serum osmolarity. This decrease means that there is a decrease in sodium and chloride ions in proportion to water in the ECF. When there is a body water excess, chloride also may be decreased along with sodium, preventing reabsorption of body water by the kidneys.
The most common cause of hypochloremia is gastrointestinal (GI) abnormalities, including prolonged vomiting, nasogastric suctioning, loss of potassium, and diarrhea. Loss of potassium, which occurs as a result of gastric suctioning and vomiting, further leads to hypochloremia because potassium frequently combines with chloride to form potassium chloride (KCl). Chloride is also lost through diarrhea, which has a high chloride content.
Other causes of hypochloremia are dietary changes, renal abnormalities, acid-base imbalances (particularly respiratory acidosis and metabolic alkalosis), and skin losses. Diets low in sodium can contribute to hypochloremia, as can medications such as thiazide and loop diuretics. Another common cause in hospitalized patients is the combination of stopping all oral intake during an illness and placing patients on intravenous (IV) fluid.
Several genetic diseases can result in low blood chloride levels. These include cystic fibrosis. Bartter’s syndrome is a group of several disorders of impaired salt reabsorption in the thick ascending loop of Henle: hypochloremia, hypokalemic metabolic alkalosis, and hypercalciuria. Several genes have been associated with Bartter’s syndrome (bumetanide-sensitive Na-K-2Cl cotransporter SLC12A1, the BSND gene, simultaneous mutation in both the CLCNKA and the CLCNKB genes and the thiazide-sensitive sodium-chloride cotransporter SLC12A3). Congenital adrenal hyperplasia is a heritable disorder of adrenal corticosteroid synthesis that is transmitted in autosomal recessive disorder; it too can result in hypochloremia.
Gender, ethnic/racial, and life span considerations
Infants, children, and adults of both sexes are at risk for developing hypochloremia. Elderly patients are particularly at risk when they are placed on multiple medications or if they have persistent bouts of vomiting and diarrhea. Identify high-risk groups, such as those with GI abnormalities. Note that hospitalized patients across the life span are often at risk because of the treatments, such as nasogastric suction, used to manage their illnesses. There are no known racial and ethnic considerations.
Global health considerations
No data are available.
Ask about any recent signs and symptoms that deviate from past health patterns that could cause hypochloremia, such as vomiting and diarrhea. Ask the patient to list all medications, especially diuretics, which contribute to chloride loss. Obtain a history of past illnesses and surgeries. If the patient is already hospitalized, review the records for prolonged dextrose administration and a history of gastric suctioning.
Physical findings depend on the cause of the chloride deficit. Inspect the patient for tetany-like symptoms, such as tremors and twitching; these neuromuscular symptoms are present with hypochloremia associated with hyponatremia. If hypochloremia is caused by metabolic alkalosis secondary to the loss of gastric secretions, respiratory and neuromuscular symptoms appear. Assess the patient’s respirations and note the depth and rate; the patient’s breathing may become shallow and depressed with severe hypochloremia. If the chloride deficit is not corrected, eventually a decrease in blood pressure occurs.
In most cases, hypochloremia is a result of GI abnormalities. Assess the patient’s tolerance and coping ability to handle the discomfort. If the patient is upset about changes in nerves and muscles, explain that the symptoms disappear when chloride is supplemented.
|Test||Normal Result||Abnormality With Condition||Explanation|
|Serum chloride||101–112 mEq/L||< 95 mEq/L; critical value: < 90 mEq/L||Reflects a deficit in chloride|
|Serum osmolarity||280–295 mOsm/L||< 280 mOsm/L; critical value: < 250 mOsm/L||Reflects decrease in concentration of particles in ECF|
Other Tests: Serum bicarbonate-serum electrolytes, urine electrolytes, urine osmolarity
Primary nursing diagnosis
DiagnosisAltered protection related to neuromuscular changes
OutcomesElectrolyte and acid-base balance; Neurological status: Consciousness; Nutritional status; Fluid balance
InterventionsSurveillance: Risk identification; Surveillance: Safety; Nutrition management; Teaching: Individual; Medication management; Fluid/electrolyte management
Planning and implementation
Treatment of hypochloremia involves treating the underlying cause and replacing the chloride. Careful monitoring of fluid and electrolyte status is critical. Monitor serum chloride levels and report any levels less than 95 mEq/L. Observe for decreases in serum potassium and sodium and note any increase in serum bicarbonate, which indicates metabolic alkalosis. Maintain strict intake and output records, noting any excessive gastric secretion loss, emesis, and diarrhea. Weigh the patient at the same time each day.
In mild hypochloremia, replacement of chloride can be accomplished orally with salty broth. If the condition is severe, IV fluid replacement is necessary. If the patient is hypovolemic, administration of 0.9% sodium chloride increases fluid volume as well as serum chloride levels. Ammonium chloride can also be given for replacement, and if metabolic alkalosis is present, KCl is administered. Dietary changes are seldom necessary.
|Medication or Drug Class||Dosage||Description||Rationale|
|KCl||Oral or IV: 10–40 mEq PO depending on severity of deficit; IV dosages should not exceed 20 mEq/hr except in unusual situations||Electrolyte replacement||Replaces needed electrolytes, particularly in metabolic alkalosis|
|Ammonium chloride||IV dose is dependent on patient’s weight and serum chloride||Electrolyte replacement||Replaces needed electrolytes, particularly in metabolic alkalosis|
Institute safety measures for patients who develop neuromuscular symptoms, with particular attention to changes in level of consciousness and risks to airway patency. Have emergency equipment for airway and breathing maintenance available at all times. Educate those at risk in preventive measures. Teach patients the complications of medication therapy and how to maintain fluid and electrolyte balance nutritionally.
Evidence-Based Practice and Health Policy
Yunos, N.M., Bellomo, R., Hegarty, C., Story D., Ho, L., & Bailey, M. (2012). Association between a chloride-liberal vs chloride-restrictive intravenous fluid administration strategy and kidney injury in critically ill adults. The Journal of the American Medical Association, 308(15), 1566–1572.
- The use of fluids with liberal amounts of chloride, such as 0.9% saline, 4% succinylated gelatin solution, and 4% albumin solution, in critical care settings may increase the risk of renal complications.
- Investigators compared a sample of 760 intensive care unit (ICU) patients who were administered chloride-liberal fluids to 773 ICU patients who were administered chloride-restrictive fluids (lactated or balanced solution, or chloride-poor 20% albumin) following a change in IV fluid protocol.
- During a mean follow-up period of 11 days (interquartile range, 7 to 21 days), patients who received the chloride-liberal fluids had increased mean serum creatinine levels (22.6 µmo/L versus 14.8 µmo/L; p = 0.03), increased incidence of acute kidney injury (AKI) (14% versus 8.4%; p < 0.001), and increased use of renal replacement therapy (RRT) (10% versus 6.3%; p = 0.004) compared to patients who received chloride-restrictive fluids.
- In this sample, chloride-restrictive fluids decreased the risks of AKI and RRT by 48% (95% CI, 0.37 to 0.75; p < 0.001 and 95% CI, 0.33 to 0.81; p = 0.004, respectively).
- Laboratory findings: Serum electrolytes, osmolarity; daily flow sheet for easy day-to-day comparisons
- Physical responses: Respiratory status (rate, quality, depth, ease, breath sounds); vital signs; GI symptoms (nausea, vomiting, diarrhea); muscle strength, signs of muscle twitching, steadiness of gait, ability to perform activities of daily living; fluid balance, intake and output
- Condition of IV site, complications of IV therapy (infection, infiltration phlebitis)
Discharge and home healthcare guidelines
Caregivers of the elderly and infants should be alerted to the effect of vomiting and diarrhea on chloride levels. Teach the patient to report any signs and symptoms of neuromuscular hyperactivity. Teach the patient to maintain a healthy diet with all the components of adequate nutrition. Teach the patient the name, dosage, route, action, and side effects of all medications, particularly those that affect chloride and sodium balance in the body.