Hypernatremia resident survival guide

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.

• Free water loss in form of
  Diarrhea
  Diabetes insipidus
  Osmotic diuresis due to glycosuria, urea, mannitol administration
  Loop diuretics,
  Renal Insufficiency
  Upper Gastrointestinal losses.

• Primary sodium excess is a rare cause of hypernatremia and can be due to
  Massive salt ingestion
  Mineralocorticoid excess
  Administration of hypertonic sodium-containing solutions.
• Nasogastric Suction
• Drains
• Chest Tubes
• Burns
• Isotonic solutions such as 0.9% saline
• Sodium Rich antibiotics (example: Fosfomycin)
• Overzealous administration of lactulose

• Water loss into cells due to severe exercise or electroshock-induced seizures, 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.
• 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 . 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. A recent study showed no evidence that more rapid correction was associated with greater risk of mortality, cerebral edema, or adverse events

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. ❑ Carbamazepine ❑ Chlorpropamide. ❑ Clofibrate. ❑ Thiazide diuretics. ❑ Indapamide. ❑ Indomethacin . ❑ Amiloride. 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. 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..

Do's

• Monitoring of the serum sodium concentration is recommended particularly in infants and young children in order to prevent water retention.
• Plasma sodium needs to be carefully monitored: hyponatremia is a potential risk in patients which could lead to brain injury.

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