Treating hyponatremic encephalopathy


Category : Acid-Base & Lytes, Attending Rounds, Clinical articles


I am current at the ACP annual meeting, and this morning heard a brilliant grand rounds on hyponatremia – given by Juan Carlos Ayus.  I have found an excellent article in the Southern Medical Journal that he co-authored on treatment of dysnatremias and also provide this Medscape link – Hospital-Acquired Hyponatremia — Why Are Hypotonic Parenteral Fluids Still Being Used?

Hospital-acquired hyponatremia can be lethal. There have been multiple reports of death or permanent neurological impairment in both children and adults. The main factor contributing to the development of hospital-acquired hyponatremia is routine use of hypotonic fluids in patients in whom the excretion of free water, which is retained in response to excess arginine vasopressin (AVP), might be impaired. The practice of administering hypotonic parental fluids was established over 50 years ago, before recognition of the fact that there are numerous potential stimuli for AVP production in most hospitalized patients. Virtually all neurological morbidity resulting from hospital-acquired hyponatremia has been associated with administration of hypotonic fluids. Multiple prospective studies have shown that 0.9% NaCl is effective prophylaxis against hyponatremia. There is not a single report in the literature of neurological complications resulting from the use of 0.9% NaCl in non-neurosurgical patients. Patients at greatest risk of developing hyponatremic encephalopathy following hypotonic fluid administration are children, premenopausal females, postoperative patients, and those with brain injury or infection, pulmonary disease or hypoxemia. When hyponatremic encephalopathy develops, immediate administration of 3% NaCl is essential. In this Review, we discuss the question of why administering hypotonic fluids is unphysiologic and potentially dangerous, the settings in which isotonic fluids should be administered to prevent hyponatremia, and the appropriate treatment of hyponatremic encephalopathy.


Several key points that added to my knowledge:

1. Premenopausal women are more likely to develop hyponatremic encephalopathy – probably secondary to the effect of estrogen on astrocytes – therefore increased cerebral edema for the same level of hyponatremia

2. The cerebral edema can cause non-cardiogenic pulmonary edema – and thus hypoxemia.

3. When hypoxemia occurs, then cerebral blood flow decreases, with potential disastrous results.

4. He argues passionately against the routine use of hypotonic parenteral fluids (see the link above)

5. He argues that the treatment for hyponatremic encephalopathy is 100 cc of hypertonic saline (3%) push, with transfer to the ICU and careful frequent monitoring of sodium levels.  Pulmonary edema is not a contraindication to hypertonic saline if the patient has normal heart size.

This was truly an excellent talk on an infrequent but potentially lethal condition.  He included in the discussion the consideration of marathon runners.  He now recommends that marathon runners to present with altered mental status should receive 100 cc of 3%NS bolus.  According to his presentation this can save lives.  The articles address the risk of demyelinization – and explain how to avoid that complication. 

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Comments (1)

One additional point. All patients receiving continuous intravenous fluid infusions should have a daily serum sodium checked because hyponatremia can develop unpredictably. This especially applies to postoperative patients receiving any type of IV fluid.

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