Hypernatremia resident survival guide

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Hypernatremia
Resident Survival Guide
Overview
Causes
Diagnosis
Treatment
Do's
Don'ts


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

Overview

Hypernatremia is an electrolyte disturbance consisting of an elevated sodium level in the blood. It is defined as a serum sodium concentration exceeding 145 mEq/L. This is a relatively common problem particularly among young children, older adults, and hospitalized/critically ill who depend upon others to control their water intake.

Causes

Life Threatening Causes

Conditions that may cause death or permanent disability within the next 24 hours

Common Causes

The most common cause of hypernatremia is not an excess of sodium, but a relative deficit of free water in the body. Hypernatremia can be caused by many disease processes and drugs.

  • Water loss into cells due to severe exercise or electroshock-induced seizures[3][4], an effect that is mediated by a transient increase in cell osmolality seizures.
  • Hypernatremia can also occur in cases of primary hypothalamic disease due to impaired thirst (hypodipsia) with or without concurrent diabetes insipidus.

Diagnosis

Shown below is an algorithm summarizing the diagnosis of Hypernatremia:


 
 
 
 
 
Etiology of
Hypernatremia
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Urine Osmolality <600
 
Urine Osmolality >600
 
 
If the criteria for Renal loss & GI loss are not satisfied
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Renal loss
 
Gastrointestinal loss
 
 
Insensible losses like sweat, breathing, Burn unit patients .

Treatment

Summary of Treatment for Hypernatremia based on Volume status


 
 
 
 
 
 
 
 
Hypernatremia
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
ACUTE ONSET
 
 
 
 
 
 
 
CHRONIC ONSET
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
❑ Rapid correction ~ 2-3 mmol/L/hour
❑ Not exceeding 12 mmol/L/hour
 
 
 
 
 
 
 
❑ Slow correction ~ 0.5 mmol/L/hour
❑ Not exceeding 8-10 mmol/L/hour
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Volume Status
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hypovolemia

❑ Fluid resuscitation with a balanced cryatalloid

❑ Then, 5% Dexterose/ Half saline
 
 
Normovolemia

❑ 5% Dexterose

❑ No loop diuretic
 
 
Hypervolemia

❑ 5% Dexterose

❑ loop diuretic
 
 
 


  • It is important that we determine whether hypernatremia is due to
    • Gain of sodium or
    • Loss of free water or
    • Whether a combination of the 2 is present, which will be the case in most patients with ICU-acquired hypernatremia.
      • In any of these cases hypovolemia, volume resuscitation needs to be performed before efforts to correct hypernatremia take place (by the administration of isotonic solutions).
      • If a loss of free water alone is present, it should be treated by the administration of free water in the form of a 5% dextrose solution
      • 5% Dextrose is safe in terms of hemolysis.
      • Distilled water can be given via a central venous line, As an alternative to 5% dextrose.
  • If pure sodium gain is the case, natriuresis should be induced through the application of loop diuretics. At the same time, fluid loss during loop diuretic therapy must be restored with the administration of fluid that is hypotonic to the urine.
  • In critically ill patients who require renal replacement therapy, correction of hypernatremia can be performed by either intermittent or continuous renal replacement therapy.[5]
  • In case of serum glucose levels, which are hard to control, half isotonic saline can be used as an alternative to a 5% dextrose solution to avoid glucose lapses.
  • Addition of loop diuretics along with half isotonic saline to induce natriuresis is recommended.
  • Osmotic diuresis due to urea is often the cause of renal loss of free water and the consequent rise in serum sodium concentration in critically ill patients [6]. This phenomenon can be observed in patients who are tube-fed or in a catabolic state. High amounts of urea are generated and excreted in the urine. This process leads to the high renal output of osmoles and the consequent loss of water as in glucosuria.


 
 
 
 
 
Serum sodium > 145
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Urine output
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Low < 200
 
 
 
High
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
High urine osmolality
 
 
 
Urine osmolality
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hypotonic fluid loss
GI losses nausea, vomiting, renal losses, diuretics
 
Low
 
High
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

Replace Both free water deficit as well as Current ongoing fluid losses.

Calculate the fluid deficit, or the water that the patient has already lost to get to their current sodium.
(% Body Water x Body Weight) x [(Current Na – Target Na)/Target Na]


Calculate the ongoing fluid losses which is how much free water the patient is losing daily as you replete.


Precision method is the electrolyte free water clearance:
Urine volume x (1- (Urine Na + Urine K) / serum Na)
Add ‘fluid deficit’ and ‘ongoing fluid losses’ to find the target water intake for the patient.
It is recommended that dividing by 24 hours and giving hourly as oral free water (preferred) or D5W if the patient is unable to drink or does not have an NG tube.
NOTE, large volumes of D5W may cause osmotic diuresis (through hyperglycemia) and worsen renal water losses.


Target rate for correction of hypernatremia: 10-12 mmol/day is commonly used[7].


A recent study showed no evidence that more rapid correction was associated with greater risk of mortality, cerebral edema, or adverse events[8]
 
Negative water
deprivation test
 
Osmotic diuresis
Collect urine for 24h and calculate a total daily solute excretion
(urine osmolality multiplied by total daily urine volume).


If the total daily solute excretion is >1000 mOsm/day,
then they have an osmotic diuresis (due to high protein feeding, glucosuria, or mannitol).
Glucose Diuresis: Urine Glucose > 250mmol/L or Urine dipstick positive for Glucose
Urea Diuresis: Urine Urea > 250mmol/L and Urine Glucose negative.


Osmotic diuresis can also be caused by Mannitol administration.
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Diabetes insipidus
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
DDAVP
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Increased urine osmolality
 
 
 
 
 
urine osmolality unchanged
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Central Diabetes Insipidus
 
 
 
 
 
Nephrogenic diabetes Insipidus
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Possible Etiologies include Traumatic brain injury, surgery, or Tumors.


Treatment Options include
Desmopressin[9][10][11].
Carbamazepine[12]
Chlorpropamide[13].
Clofibrate[14][15].
Thiazide diuretics[16][17][18].
Indapamide[19].
Indomethacin [20] .
Amiloride[21][22].



Desmopressin is the preferred agent in almost all patients
and is required for symptom control.
Other drugs mentioned above are used in rare instances.


Low-solute diet with or without a thiazide diuretic
can be tried in cases of Partial DI and mild-moderate polyuria and nocturia.
 
 
 
 
 
Possible Etiology:Heriditary causes;Acquired causes like Drugs( lithium, foscarnet, amphotericin B, or ifosfamide);Infilterative disorders;Sickle Cell disease;Hypercalcemia, hypokalemia[23].


Thiazide diuretics in combination with a low salt diet have long been used to treat nephrogenic DI due to lithium.


More recent literature suggests that Acetazolamide may also be effective, and may be useful for patients whose nephrogenic DI is refractory to thiazides.[24].
 
 

Do's

Don'ts

  • Extreme care must be taken to avoid excessively rapid correction or over correction of hypernatremia, which might increase the risk of iatrogenic cerebral edema, with possibly catastrophic consequences.

References

  1. Buckley MS, Leblanc JM, Cawley MJ (2010). "Electrolyte disturbances associated with commonly prescribed medications in the intensive care unit". Crit Care Med. 38 (6 Suppl): S253–64. doi:10.1097/CCM.0b013e3181dda0be. PMID 20502178.
  2. Nelson DC, McGrew WR, Hoyumpa AM (1983). "Hypernatremia and lactulose therapy". JAMA. 249 (10): 1295–8. PMID 6827705.
  3. WELT LG, ORLOFF J, KYDD DM, OLTMAN JE (1950). "An example of cellular hyperosmolarity". J Clin Invest. 29 (7): 935–9. doi:10.1172/JCI102328. PMC 436130. PMID 15436862.
  4. Felig P, Johnson C, Levitt M, Cunningham J, Keefe F, Boglioli B (1982). "Hypernatremia induced by maximal exercise". JAMA. 248 (10): 1209–11. PMID 7109140.
  5. Pazmiño PA, Pazmiño BP (1993). "Treatment of acute hypernatremia with hemodialysis". Am J Nephrol. 13 (4): 260–5. doi:10.1159/000168630. PMID 8267023.
  6. Lindner G, Schwarz C, Funk GC (2012). "Osmotic diuresis due to urea as the cause of hypernatraemia in critically ill patients". Nephrol Dial Transplant. 27 (3): 962–7. doi:10.1093/ndt/gfr428. PMID 21810766.
  7. Adrogué HJ, Madias NE (2000). "Hypernatremia". N Engl J Med. 342 (20): 1493–9. doi:10.1056/NEJM200005183422006. PMID 10816188.
  8. Chauhan K, Pattharanitima P, Patel N, Duffy A, Saha A, Chaudhary K; et al. (2019). "Rate of Correction of Hypernatremia and Health Outcomes in Critically Ill Patients". Clin J Am Soc Nephrol. 14 (5): 656–663. doi:10.2215/CJN.10640918. PMC 6500955 Check |pmc= value (help). PMID 30948456.
  9. De Waele K, Cools M, De Guchtenaere A, Van de Walle J, Raes A, Van Aken S; et al. (2014). "Desmopressin lyophilisate for the treatment of central diabetes insipidus: first experience in very young infants". Int J Endocrinol Metab. 12 (4): e16120. doi:10.5812/ijem.16120. PMC 4338649. PMID 25745483.
  10. Qureshi S, Galiveeti S, Bichet DG, Roth J (2014). "Diabetes insipidus: celebrating a century of vasopressin therapy". Endocrinology. 155 (12): 4605–21. doi:10.1210/en.2014-1385. PMID 25211589.
  11. Kauli R, Laron Z (1974). "A vasopressin analogue in treatment of diabetes insipidus". Arch Dis Child. 49 (6): 482–5. doi:10.1136/adc.49.6.482. PMC 1648779. PMID 4850356.
  12. Meinders AE, Cejka V, Robertson GL (1974). "The antidiuretic action of carbamazepine in man". Clin Sci Mol Med. 47 (4): 289–99. doi:10.1042/cs0470289. PMID 4426163.
  13. Hocken AG, Longson D (1968). "Reduction of free water clearance by chlorporpamide". Br Med J. 1 (5588): 355–6. doi:10.1136/bmj.1.5588.355. PMC 1984885. PMID 5638262.
  14. Moses AM, Howanitz J, van Gemert M, Miller M (1973). "Clofibrate-induced antidiuresis". J Clin Invest. 52 (3): 535–42. doi:10.1172/JCI107213. PMC 302290. PMID 4685079.
  15. Makaryus AN, McFarlane SI (2006). "Diabetes insipidus: diagnosis and treatment of a complex disease". Cleve Clin J Med. 73 (1): 65–71. doi:10.3949/ccjm.73.1.65. PMID 16444918.
  16. Abraham MB, Rao S, Price G, Choong CS (2014). "Efficacy of Hydrochlorothiazide and low renal solute feed in Neonatal Central Diabetes Insipidus with transition to Oral Desmopressin in early infancy". Int J Pediatr Endocrinol. 2014 (1): 11. doi:10.1186/1687-9856-2014-11. PMC 4084573. PMID 25002871.
  17. Al Nofal A, Lteif A (2015). "Thiazide Diuretics in the Management of Young Children with Central Diabetes Insipidus". J Pediatr. 167 (3): 658–61. doi:10.1016/j.jpeds.2015.06.002. PMID 26130110.
  18. O'DOHERTY NJ, ROSSER J, SLATER RJ (1962). "Diabetes insipidus: the influence of chlorothiazide therapy in affected children". Can Med Assoc J. 86: 559–67. PMC 1849045. PMID 14480853.
  19. Saifan C, Nasr R, Mehta S, Sharma Acharya P, Perrera I, Faddoul G | display-authors=etal (2013) Diabetes insipidus: a challenging diagnosis with new drug therapies. ISRN Nephrol 2013 ():797620. DOI:10.5402/2013/797620 PMID: 24977135
  20. Weinstock RS, Moses AM (1990). "Desmopressin and indomethacin therapy for nephrogenic diabetes insipidus in patients receiving lithium carbonate". South Med J. 83 (12): 1475–7. doi:10.1097/00007611-199012000-00026. PMID 2123565.
  21. Kortenoeven ML, Li Y, Shaw S, Gaeggeler HP, Rossier BC, Wetzels JF; et al. (2009). "Amiloride blocks lithium entry through the sodium channel thereby attenuating the resultant nephrogenic diabetes insipidus". Kidney Int. 76 (1): 44–53. doi:10.1038/ki.2009.91. PMID 19367330.
  22. Bedford JJ, Weggery S, Ellis G, McDonald FJ, Joyce PR, Leader JP; et al. (2008). "Lithium-induced nephrogenic diabetes insipidus: renal effects of amiloride". Clin J Am Soc Nephrol. 3 (5): 1324–31. doi:10.2215/CJN.01640408. PMC 2518801. PMID 18596116.
  23. RUBINI ME (1961). "Water excrtion in potassium-deficient man". J Clin Invest. 40: 2215–24. doi:10.1172/JCI104448. PMC 290931. PMID 14494941.
  24. Gordon CE, Vantzelfde S, Francis JM (2016). "Acetazolamide in Lithium-Induced Nephrogenic Diabetes Insipidus". N Engl J Med. 375 (20): 2008–2009. doi:10.1056/NEJMc1609483. PMID 27959610.
  25. Achinger SG, Arieff AI, Kalantar-Zadeh K, Ayus JC (2014). "Desmopressin acetate (DDAVP)-associated hyponatremia and brain damage: a case series". Nephrol Dial Transplant. 29 (12): 2310–5. doi:10.1093/ndt/gfu263. PMID 25107337.

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