Hyponatremia

 

Hyponatremia is a common finding, occurring as plasma Na+ levels fall below 135 mmol/L. This can result in water intoxication.

45% of patients had other electrolyte abnormalities.



 

Causes and Risk Factors

 

Hyponatremia can be hypo- iso-, or hyper-osmolar.

 

Hypo-osmolar (dilutional) hyponatremia, is the most common cause, and is due to excess water in comparison to sodium. It is further categorized according to volume status:

Excretion may be impaired due to reduced GFR, reduced effective circulating volume, impaired sodium-chloride reabsorption in the renal diluting segments, or inappropriate ADH secretion. This causes a retention of water but not sodium.

Surgery can induce hyponatremia via SIADH and can be exacerbated by delivery of excess sodium-free fluids.

 

Iso-osmolar hyponatremia is due to retention of large volume fluid due to osmotic agents such as mannitol. Pseudohyponatriema can also be a lab artifact with severe hyperlipidemia or paraproteinemia.

 

Hyper-osmolar (false) hyponatremia is due to extra ECF osmoles which draw water and dilute plasma sodium. Glucose is the usual agent. Each 10 mmol increase in blood glucose leads to a 3 mm decrease in sodium. Other dilutional factors are  hyperlipidemia and paraproteins. 

 

 

 

Signs, Symptoms, and Diagnosis

Signs and symptoms depend on degree and rapidity of onset.

 

  • history
  • physical exam
  • lab investigations
  • diagnostic imaging

History

Neurologic symptoms are the most substantial following cerebral edema. They include:

  • headache
  • nausea and loss of appetite
  • malaise
  • lethargy
  • weakness
  • muscle cramps
  • somnolence
  • disorientation
  • personality change

Physical Exam

ECF volume status assessment is important to determine cause.

Depressed reflexes and decreased LOC can be followed by seizures, coma, respiratory arrest, brainstem herniation, and death.

Lab Investigations

 

Bloodwork

  • electrolytes
  • glucose
  • lipids
  • creatinine (will rise in hypovolemic patients)
  • osmolality
  • thyroid levels
  • 8 am cortisol - Addison's
  • paraproteins

urinalysis

  • osmolality: will be maximally dilulte if euvolemic; should be quite concentrated if hypovolemic
  • sodium concentration <10-20 mmol/L suggests volume depletion

 

Diagnostic Imaging

 

CXR if SIADH is suspected

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Treatments

 

It is important to treat the underlying cause of hyponatremia. This is the primary treatment in hypervolemic hyponatremia.

Monitor serum Na frequently.

 

by giving IV saline. However, this must be done gradually. A sudden restoration of blood volume has the potential to inhibit ADH secretion, causing prompt dieuresis and dramatic increase in plasma sodium concentration. This may lead to central pontine myelinolysis, characterized by major neurologic damage.

 

Assess total body water

 

A general rule of thumb: One litre of HTS raises serum sodium by 10.

 

 

1) Important to determine if the hyponatremia is acute or chronic

Acute (<48 hrs)

Increase by 5 mM/L over 3 hrs

Then increase Na conc to 130 mmol/L in the first 24 hrs.  The rate of this increase is not what makes the difference.  If the situation is acute, it is safe to incr the Na conc. to 130 mmol/L in 24 hrs.

Once at 130 mmol/L --> STOP

 

Chronic (>48 hrs)

Increase the Na conc not by more than 6-8 mM/day.

Depending on the situation (elderly, cachectic, hypokalemia), it may be safer to correct even less than 6 mM/L per day

So,
1. fluid restrict to < 1 L/day
2. If patient has both hyponatremia and hypokalemia, treat the hypokalemia
and then wait.  The K given will increase the Na due to shift of Na out
of cells and need to count the K as Na.
3. if you think the patient is chronic hypoNa and has symptoms - you
could increase Na by 3 - 5 mM over 3 hours, but then stop - no further
correction for the rest of the 24 hours.

 

 

 

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Consequences and Course

 

Hyponatremia is a poor prognosticator for CHF.

Asymptomatic hyponatremia can increase rates of falls.

 

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References

 

Lab. risk factors for hospital mortality in acutely admitted patients. QJM 2007.