logo

Hyponatremia

Sodium: (Normal range: 136 - 145 meq/l)

Sodium plays a vital role in maintaining the concentration and volume of the extracellular fluid (ECF).  It is the main cation of the ECF and a major determinant of ECF osmolality. Sodium is important in maintaining irritability and conduction of nerve and muscle tissue and assists with the regulation of acid-base balance. The average daily intake far exceeds the normal daily requirements. The kidneys are responsible for excreting the excess and are capable of conserving sodium during periods of extreme  sodium restriction. The kidneys accomplish this primarily through regulation of water intake/excretion.  If the serum sodium falls, the kidneys respond by excreting water. If the serum sodium increases (increased osmolality)---thirst center is stimulated--increased ADH release by the posterior pituitary---acts on kidney to conserve water. Aldosterone also plays a key role by regulating Na+/ECF volume. Its release causes the kidneys to conserve water and sodium which results in increased ECF volume.  Because changes in serum sodium levels typically reflect changes in body water balance, gains or losses of total body sodium are not necessarily reflected by the serum sodium level. 
Hyponatremia: (Serum sodium less than 136 meq/L)
Clinical indicators and treatment depend on the cause of hyponatremia and whether or not it is associated with a normal, decreased or increased ECF volume.
Signs and symptoms: neurologic symptoms usually do not occur until the serum sodium level has dropped to approximately 120-125 meq/L.  Hyponatremia with decreased ECF volume: irritability, apprehension, dizziness, postural hypotension, dry mucus membranes, cold and clammy skin, tremors, seizures.  Hyponatremia with normal or increased ECF volume: headache, lassitude, apathy, confusion, weakness, edema, weight gain, elevated blood pressure, muscle cramps, convulsions. 
History and risk factors: diarrhea, fistulas, vomiting, NG suction, diuretics, adrenal insufficiency, skin losses (burns, wound drainage), other.   Note: hyperlipidemia, hyperproteinemia, and hyperglycemia may cause a pseudo-hyponatremia. This must be ruled out before determining therapy. For every 100 mg/dl increase in glucose, the sodium is diluted by 1.6 meq/L.  
Diagnostic tests: serum sodium will be less than 136 meq/L.  Serum osmolality will be decreased except in cases of pseudo-hyponatremia, azotemia, or toxins that increase osmolality (example: ethanol). Urine specific gravity will be decreased because of the kidneys attempt to excrete excess water. Urine sodium: decreased (except in SIADH and adrenal insufficiency).
Collaborative management: The goal of therapy is to get the patient out of immediate danger (eg return the sodium level to greater than 120 meq/L) and then gradually return the serum sodium to a normal level and restore normal ECF volume.

Hyponatremia with increased ECF volume and edema

Hypervolemia: low serum serum osmolality (< 280 ), urine sodium < 10 mmol/L, Usually associated  with: CHF, cirrhosis, or acute/chronic renal failure.)

Therapeutic options: 
1) For mild cases only (serum sodium > 120 meq/L):  Water restriction (limit to 500 to 1500 ml/ 24 hours) and furosemide 40-80 IV/ oral once daily (20-400 mg/day). 
2) Patients with CHF, cirrhosis, nephrotic syndrome who usually have excessive ECF volume have few symptoms referable to hyponatremia. Usually water restriction combined with treatment of the underlying disorder is successful.
3) If severe symptomatic hyponatremia is present (sodium level < 115 meq/L) in the volume overloaded patient: Continue water restriction. Also infuse 3% hypertonic saline. 
Calculate sodium deficit: 0.6 x (weight in kg) x (desired sodium - Actual sodium)
     Use 0.5 for females.    Desired range= 120 - 125 meq/L.
When hyponatremia is symptomatic and acute (< 24 hours in duration), the serum sodium may be raised safely to 120-125 meq/L in 24 hours or less. In patients with symptomatic chronic hyponatremia, or hyponatremia of unknown duration, the serum sodium should be raised slowly (0.5 meq/L/hr) to about 120-125 meq/L in order to avoid CNS complications (cerebral edema, pontine myelinolysis, seizures) and/or pulmonary edema. The total increase in these patients should not exceed 10-12 meq/L in 24 hours or <20-25 meq/L over 48 hours.  Thereafter, the hypertonic saline is stopped, and the serum sodium is allowed to rise more slowly (eg over several days) in response to continued restriction of free water. In all cases, the serum sodium should be corrected only halfway to normal in the initial 24 hours (120-125 meq/L) to prevent the complications listed above.

Example calculations:
80kg patient; serum sodium=110 meq\L ; male; desired target= 120 meq/L.
    1)   0.6 x 80kg x (120-110)= 480 meq  (total needed)
    2)  Amount needed to increase serum level by 0.5 meq/L/hr =
           0.6 x 80 x 0.5= 24 meq.  (rate should be 24 meq/hr)
    3)  3% hypertonic saline contains 513 meq/Liter
         [desired rate/hr]/513 x 1000= # ml/hr  //      Total meq/rate/hr 
                                                                           =infusion time.

           Therefore:  24 meq/hr  x 1000= 47 ml/hr
                                 513
            Length of infusion=  480 meq/ 24 meq=  20 hours
           Final order: infuse 3% hypertonic saline at 47 ml/hr for 20 hours.
              When infusion is complete, discontinue. Continue with fluid 
               restriction.

Hyponatremia with isovolemia

Low osmolarity (<280), urine sodium < 10 mmol: water intoxication; urine sodium > 20: SIADH, hypothyroidism, renal failure, addisons disease, drugs.
Mild: (serum level > 120 meq/L; asymptomatic): furosemide 80mg IV once or twice daily and  Normal saline + 20-40meq KCL/liter  infused at 65-150 ml/hr (correct deficit at 0.5 meq/L/hr or less.)
SIADH: fluid restriction 500-750ml/ day.  Demeclocycline 300 to 600mg twice daily. Use caution in patients with hepatic disease. In emergency situations (sodium < 115) use hypertonic saline (see above) and furosemide.
Symptomatic patients: hypertonic saline and furosemide as above. or hypertonic saline and water restriction.
 

Hyponatremia with hypovolemia

Low serum osmolarity (<280).  Urine sodium < 10 mmol: vomiting, diarrhea, 3rd space/respiratory/skin loss.  Urine sodium > 20: diuretics, renal injury, RTA, adrenal insufficiency.
If volume depleted give 500 to 3000 ml of normal saline at 500 ml/hr until no longer orthostatic, then give normal saline ( + 20-40 meq KCL/ liter) at 65 to 150 ml/hr until desired level is reached (note: in mild cases, target a level of 130 meq/ Liter). Each liter of normal saline contains 154 meq. May use the calculations above to determine approximate length of therapy. If severe hyponatremia is present (<115 meq/L) start hypertonic saline using the dosing guidelines above
References

1.  Adrogue HJ, Madias NE. Hyponatremia. N Engl J Med. 2000 May 25;342(21):1581-9. 
2.  Arieff AI, Ayus JC. Pathogenesis of hyponatremic encephalopathy: current concepts. Chest 1993;103(2):607-10 
3.  Ayus JC, Arieff AI. Pathogenesis and prevention of hyponatremic encephalopathy. Endocrinol Metab Clin North Am. 1993 Jun;22(2):425-46. 
4.  own RG. Disorders of water and sodium balance.
Postgrad Med. 1993 Mar;93(4):227-8, 231-4, 239-40.
5.  Ellis SJ. Extrapontine myelinolysis after correction of chronic hyponatraemia with isotonic saline. Br J Clin Pract. 1995 Jan-Feb;49(1):49-50.
6.  Engquist A.  From plasma [Na+] to diagnosis and treatment.
Acta Anaesthesiol Scand Suppl. 1995;107:273-9. 
7.  Faber MD, Kupin WL, Heilig CW, Narins RG. Common fluid-electrolyte and acid-base problems in the intensive care unit: selected issues.
Semin Nephrol. 1994 Jan;14(1):8-22. 
8.  Heneghan C, Goldrick P, Pham H. Management of acute symptomatic hyponatremia. BMJ. 1994 Jan 15;308(6922):203. 
9.  InneraritySA, Stark JL. Fluids and Electrolytes: A Study and Learning Tool. 1990 Springhouse Corp, PA 19477-0908.
10.  Keyes, J. Fluid, Electrolyte, and Acid-Base Regulation: Physiology & Pathophysiology. Boston: Jones & Bartless Publishers, Inc., 1985.
11.  Laureno R. Myelinolysis is due to rapid correction of hyponatremia.
Am J Med. 1993 Feb;94(2):225-7
12.  Leier CV, Dei Cas L, Metra M. Clinical relevance and management of the major electrolyte abnormalities in congestive heart failure: hyponatremia, hypokalemia, and hypomagnesemia. Am Heart J. 1994 Sep;128(3):564-74.
13.  Lohr JW. Osmotic demyelination syndrome following correction of hyponatremia: association with hypokalemia. Am J Med. 1994 May;96(5):408-13. 
14.  Muller RJ, Donner TW. Correction rate of severe hyponatremia and central pontine myelinolysis. Am J Psychiatry. 1992 May;149(5):715-6. 
15.  Norris MK. Evaluating sodium levels.
Nursing. 1992  Jul;22(7):20. 
16.  Oh MS, Kim HJ, Carroll HJ. Recommendations for treatment of symptomatic hyponatremia. Nephron 1995;70(2):143-50 
17.  Sivakumar V, Rajshekhar V, Chandy MJ.Management of neurosurgical patients with hyponatremia and natriuresis. Neurosurgery. 1994 Feb;34(2):269-74.
18.  Sterns RH. Treating hyponatremia: why haste makes waste.
South Med J. 1994 Dec;87(12):1283-7
19.  Sterns RH, Cappuccio JD, Silver SM, Cohen EP. Neurologic sequelae after treatment of severe hyponatremia: a multicenter perspective. J Am Soc Nephrol. 1994 Feb;4(8):1522-30.

Disclaimer

The authors make no claims of the accuracy of the information contained herein; and these suggested doses are not a substitute for clinical judgement. Neither GlobalRPh Inc. nor any other party involved in the preparation of this program shall be liable for any special, consequential, or exemplary damages resulting in whole or part from any user's use of or reliance upon this material.PLEASE READ THE DISCLAIMER CAREFULLY BEFORE ACCESSING OR USING THIS SITE. BY ACCESSING OR USING THIS SITE, YOU AGREE TO BE BOUND BY THE TERMS AND CONDITIONS SET FORTH IN THE DISCLAIMER.   Read the disclaimer
more Career Center image description
Medical Calculators - A thru Z
Lab Values - A thru Z