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[1][2][3] 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[4][5][6] Hypoparathyroidism, pseudohypoparathyroidism, hypomagnesemia, hypovitaminosis D,

chronic kidney disease, hypoalbuminemia

Hypercalcemia[7][8][9][10] Hyperparathyroidism, familial hypocalciuric hypercalcemia, malignancy, Milk-alkali syndrome,

vitamin D toxicity, sarcoidosis, diuretics, lithium

Phosphate PO43- 2.5-4.5 Hypophosphatemia[11][12][13] Refeeding syndrome, respiratory alkalosis, alcohol abuse, malabsorption
Hyperphosphatemia[14][15] Transcellular shift, tumor lysis syndrome , rhabdomyolysis, hypoparathyroidism, pseudohypoparathyroidism, acute kidney injury, chronic kidney disease
Magnesium Mg2+ 1.5-2.5 Hypomagnesemia[16][17][18] Alcohol use, uncontrolled diabetes mellitus, hypercalcemia, Gitelman syndrome, loop and thiazide diuretics
Hypermagnesemia[19][20] 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. ↑ Smellie WS (March 2007). "Spurious hyperkalaemia". BMJ. 334 (7595): 693–5. doi:10.1136/bmj.39119.607986.47. PMC 1839224. PMID 17395950.
  2. ↑ Gonick HC, Kleeman CR, Rubini ME, Maxwell MH (May 1971). "Functional impairment in chronic renal disease. 3. Studies of potassium excretion". Am. J. Med. Sci. 261 (5): 281–90. PMID 5092154.
  3. ↑ Arthur S, Greenberg A (June 1990). "Hyperkalemia associated with intravenous labetalol therapy for acute hypertension in renal transplant recipients". Clin. Nephrol. 33 (6): 269–71. PMID 2376088.
  4. ↑ Riccardi D, Brown EM (March 2010). "Physiology and pathophysiology of the calcium-sensing receptor in the kidney". Am. J. Physiol. Renal Physiol. 298 (3): F485–99. doi:10.1152/ajprenal.00608.2009. PMC 2838589. PMID 19923405.
  5. ↑ Neufeld M, Maclaren NK, Blizzard RM (September 1981). "Two types of autoimmune Addison's disease associated with different polyglandular autoimmune (PGA) syndromes". Medicine (Baltimore). 60 (5): 355–62. PMID 7024719.
  6. ↑ Cholst IN, Steinberg SF, Tropper PJ, Fox HE, Segre GV, Bilezikian JP (May 1984). "The influence of hypermagnesemia on serum calcium and parathyroid hormone levels in human subjects". N. Engl. J. Med. 310 (19): 1221–5. doi:10.1056/NEJM198405103101904. PMID 6709029.
  7. ↑ Meric F, Yap P, Bia MJ (November 1990). "Etiology of hypercalcemia in hemodialysis patients on calcium carbonate therapy". Am. J. Kidney Dis. 16 (5): 459–64. PMID 2239937.
  8. ↑ Glendenning P, Gutteridge DH, Retallack RW, Stuckey BG, Kermode DG, Kent GN (April 1998). "High prevalence of normal total calcium and intact PTH in 60 patients with proven primary hyperparathyroidism: a challenge to current diagnostic criteria". Aust N Z J Med. 28 (2): 173–8. PMID 9612524.
  9. ↑ Alikhan Z, Singh A (October 1996). "Hyperthyroidism manifested as hypercalcemia". South. Med. J. 89 (10): 997–8. PMID 8865795.
  10. ↑ Distler W (1989). "[The climacteric--physiology or pathology?]". Arch. Gynecol. Obstet. (in German). 245 (1–4): 947–52. PMID 2679445.
  11. ↑ Marinella MA (2005). "Refeeding syndrome and hypophosphatemia". J Intensive Care Med. 20 (3): 155–9. doi:10.1177/0885066605275326. PMID 15888903.
  12. ↑ MOSTELLAR ME, TUTTLE EP (January 1964). "EFFECTS OF ALKALOSIS ON PLASMA CONCENTRATION AND URINARY EXCRETION OF INORGANIC PHOSPHATE IN MAN". J. Clin. Invest. 43: 138–49. doi:10.1172/JCI104888. PMC 289504. PMID 14105225.
  13. ↑ Murer H, Lötscher M, Kaissling B, Levi M, Kempson SA, Biber J (June 1996). "Renal brush border membrane Na/Pi-cotransport: molecular aspects in PTH-dependent and dietary regulation". Kidney Int. 49 (6): 1769–73. PMID 8743494.
  14. ↑ 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.
  15. ↑ 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.
  16. ↑ Shah GM, Kirschenbaum MA (1991). "Renal magnesium wasting associated with therapeutic agents". Miner Electrolyte Metab. 17 (1): 58–64. PMID 1722865.
  17. ↑ 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.
  18. ↑ Tosiello L (June 1996). "Hypomagnesemia and diabetes mellitus. A review of clinical implications". Arch. Intern. Med. 156 (11): 1143–8. PMID 8639008.
  19. ↑ 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.
  20. ↑ 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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