Electrolyte disturbance

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Electrolyte Disturbance Main Page

Patient Information

Overview

Classification

Hyponatremia
Hypernatremia
Hypokalemia
Hyperkalemia
Hypocalcemia
Hypercalcemia
Hypophosphatemia
Hyperphosphatemia
Hypomagnesemia
Hypermagnesemia

Causes

Diagnosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Synonyms and keywords: abnormal electrolytes, abnormal lytes, lytes

Overview

Electrolytes are electrically charged solutes necessary to maintain body homeostasis. The main electrolytes include Sodium (Na), Potassium (K), Chloride (Cl), Calcium (Ca), Phosphorus (P), and Magnesium (Mg). These electrolytes are involved in multiple physiologic and neurohormonal reactions necessary to maintain neuromuscular, neuronal, myocardial, and acid-base balance. Their balance are mainly regulated by renal and endocrine systems, any changes in their balance may be life threatening. Electrolytes are in balance to achieve neutral electrical charges. Electrolytes could be classified based on their electrical charge to anions and cations. Anions include bicarbonate, chloride, and phosphorus. Cations are calcium, magnesium, potassium, and sodium. Sodium and chloride are the major extracellular ions that has the greatest impact on serum osmolality (solute concentration in 1 liter of water). Calcium and bicarbonate are the other major extracellular electrolytes. Main intracellular electrolytes are potassium, phosphorus, and magnesium.

Causes

Electrolyte Ionic formula Normal limits (mg/dl) Disturbance Common causes
Sodium Na+ 135-145 hyponatremia Hypovolemic
Euvolemic SIADH, glucocorticoid deficiency, psychogenic polydipsia
Hypervolemic CHF, cirrhosis, nephrotic syndrome, renal failure
hypernatremia Extrarenal loss Vomiting, diarrhea, insensible loss
Renal loss Diuretics, diabetes insipidus (central and nephrogenic)
Potassium K+ 3.5-5 hypokalemia Transcellular shifts Insulin therapy, alkalosis
GI loss Diarrhea, laxative abuse, vomiting
Renal loss
hyperkalemia ACE inhibitors, acidosis, addisonian crisis, beta blockers, blood transfusion, cirrhosis, diabetic nephropathy, high potassium diet, malnutrition, renal tubular acidosis type IV, renal failure
Calcium Ca2+ 8.9-10.1 hypocalcemia Hypoparathyroidism, pseudohypoparathyroidism, hypomagnesemia, hypovitaminosis D,

chronic kidney disease, hypoalbuminemia

hypercalcemia Hyperparathyroidism, familial hypocalciuric hypercalcemia, malignancy, Milk-alkali syndrome,

vitamin D toxicity, sarcoidosis, diuretics, lithium

Phosphate PO43- 2.5-4.5 hypophosphatemia Refeeding syndrome, respiratory alkalosis, alcohol abuse, malabsorption
Hyperphosphatemia[1][2] Transcellular shift, tumor lysis syndrome , rhabdomyolysis, hypoparathyroidism, pseudohypoparathyroidism, acute kidney injury, chronic kidney disease
Magnesium Mg2+ 1.5-2.5 Hypomagnesemia[3][4][5] Alcohol use, uncontrolled diabetes mellitus, hypercalcemia, Gitelman syndrome, loop and thiazide diuretics
Hypermagnesemia[6][7] Renal failure, massive oral ingestion

Table of common electrolyte disturbances

Electrolyte Abnormalities and ECG Changes

The most notable feature of hyperkalemia is the "tent shaped" or "peaked" T wave. Delayed ventricular depolarization leads to a widened QRS complex and the P wave becomes wider and flatter. When hyperkalemia becomes severe, the ECG resembles a sine wave as the P wave disappears from view. In contrast, hypokalemia is associated with flattenting of the T wave and the appearance of a U wave. When untreated, hypokalemia may lead to severe arrhythmias.

The fast ventricular depolarization and repolarization associated with hypercalcemia lead to a characteristic shortening of the QT interval. Hypocalcemia has the opposite effect, lengthening the QT interval.

Differentiating electrolyte disturbances from other diseases

Electrolyte disturbance must be differentiated from other causes of headache, altered mental status and seizures such as brain tumors and delirium trmemns.

References

  1. Tsokos GC, Balow JE, Spiegel RJ, Magrath IT (May 1981). "Renal and metabolic complications of undifferentiated and lymphoblastic lymphomas". Medicine (Baltimore). 60 (3): 218–29. PMID 6894477.
  2. Grossman RA, Hamilton RW, Morse BM, Penn AS, Goldberg M (October 1974). "Nontraumatic rhabdomyolysis and acute renal failure". N. Engl. J. Med. 291 (16): 807–11. doi:10.1056/NEJM197410172911601. PMID 4423658.
  3. Shah GM, Kirschenbaum MA (1991). "Renal magnesium wasting associated with therapeutic agents". Miner Electrolyte Metab. 17 (1): 58–64. PMID 1722865.
  4. Elisaf M, Merkouropoulos M, Tsianos EV, Siamopoulos KC (December 1995). "Pathogenetic mechanisms of hypomagnesemia in alcoholic patients". J Trace Elem Med Biol. 9 (4): 210–4. doi:10.1016/S0946-672X(11)80026-X. PMID 8808192.
  5. Tosiello L (June 1996). "Hypomagnesemia and diabetes mellitus. A review of clinical implications". Arch. Intern. Med. 156 (11): 1143–8. PMID 8639008.
  6. RANDALL RE, COHEN MD, SPRAY CC, ROSSMEISL EC (July 1964). "HYPERMAGNESEMIA IN RENAL FAILURE. ETIOLOGY AND TOXIC MANIFESTATIONS". Ann. Intern. Med. 61: 73–88. PMID 14178364.
  7. Clark BA, Brown RS (1992). "Unsuspected morbid hypermagnesemia in elderly patients". Am. J. Nephrol. 12 (5): 336–43. doi:10.1159/000168469. PMID 1489003.

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