Hypernatremia resident survival guide: Difference between revisions

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{{familytree | | | | E01 | | | E02 | | | E03 | | | |E01='''Hypovolemia'''<br><br>❑ Fluid resuscitation with a balanced cryatalloid<br><br>❑ Then, 5% Dexterose/ Half saline|E02='''Normovolemia'''<br><br>❑ 5% Dexterose <br><br> ❑ No loop diuretic|E03='''Hypervolemia'''<br><br>❑ 5% Dexterose <br><br> ❑ loop diuretic}}
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<br>NOTE, large volumes of D5W may cause osmotic diuresis (through hyperglycemia) and worsen renal water losses.
<br>NOTE, large volumes of D5W may cause osmotic diuresis (through hyperglycemia) and worsen renal water losses.


<br>Target rate for correction of hypernatremia: 10-12 mmol/day is a commonly used<ref name="pmid10816188">{{cite journal| author=Adrogué HJ, Madias NE| title=Hypernatremia. | journal=N Engl J Med | year= 2000 | volume= 342 | issue= 20 | pages= 1493-9 | pmid=10816188 | doi=10.1056/NEJM200005183422006 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10816188  }} </ref>.
<br>Target rate for correction of hypernatremia: 10-12 mmol/day is commonly used<ref name="pmid10816188">{{cite journal| author=Adrogué HJ, Madias NE| title=Hypernatremia. | journal=N Engl J Med | year= 2000 | volume= 342 | issue= 20 | pages= 1493-9 | pmid=10816188 | doi=10.1056/NEJM200005183422006 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10816188  }} </ref>.
<br>A recent study showed no evidence that more rapid correction was associated with greater risk of mortality, cerebral edema, or adverse events<ref name="pmid30948456">{{cite journal| author=Chauhan K, Pattharanitima P, Patel N, Duffy A, Saha A, Chaudhary K | display-authors=etal| title=Rate of Correction of Hypernatremia and Health Outcomes in Critically Ill Patients. | journal=Clin J Am Soc Nephrol | year= 2019 | volume= 14 | issue= 5 | pages= 656-663 | pmid=30948456 | doi=10.2215/CJN.10640918 | pmc=6500955 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30948456  }} </ref>  
<br>A recent study showed no evidence that more rapid correction was associated with greater risk of mortality, cerebral edema, or adverse events<ref name="pmid30948456">{{cite journal| author=Chauhan K, Pattharanitima P, Patel N, Duffy A, Saha A, Chaudhary K | display-authors=etal| title=Rate of Correction of Hypernatremia and Health Outcomes in Critically Ill Patients. | journal=Clin J Am Soc Nephrol | year= 2019 | volume= 14 | issue= 5 | pages= 656-663 | pmid=30948456 | doi=10.2215/CJN.10640918 | pmc=6500955 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30948456  }} </ref>  



Revision as of 10:35, 9 August 2020

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 according to the the [...] guidelines.


 
 
 
 
 
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
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
❑ Fluid resuscitation with a balanced cryatalloid
❑ Then, 5% Dexterose/ Half saline
 
 
❑ 5% Dexterose

❑ No loop diuretic
 
 
❑ 5% Dexterose

❑ loop diuretic
 
 
 


  • In general, it should be determined 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 case of hypovolemia, volume resuscitation by the administration of isotonic solutions should be performed before efforts to correct hypernatremia take place.
    • 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, which is safe in terms of hemolysis.
    • As an alternative to 5% dextrose, distilled water can be given via a central venous line.
  • 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
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Treat with Desmopressin &..
 
 
 
 
 
Causes of Nephrogenic DI:Heriditary causes;Drugs like lithium, foscarnet, amphotericin B, or ifosfamide;Hypercalcemia, hypokalemia[9].


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.[10].
 
 

Do's

Don'ts

Extreme care must be taken to avoid excessively rapid correction or overcorrection 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. RUBINI ME (1961). "Water excrtion in potassium-deficient man". J Clin Invest. 40: 2215–24. doi:10.1172/JCI104448. PMC 290931. PMID 14494941.
  10. 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.

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