Hyponatremia - Na 118 - What Is the Cause?

Author: V. Dimov, M.D., University of Chicago
Reviewer: S. Randhawa, M.D.

Hyponatremia: Case 1

82 yo CF with PMH of Dementia, HTN and DM is admitted for work-up of hyponatremia. Her sodium has been 118 for the last 4 days. She is taking Paxil for depression and she is not on any diuretics.

What is the most likely diagnosis?

Hyponatreamia can be due to many different causes. Paxil can cause SIADH or the patient can have SIADH due to any other cause.

What would you do?

Patient received 1 L of NS. Before IVF, a few tests were ordered: plasma osmolality, urine Na+ and osmolality, specific gravity, plasma uric acid.

What happened?

Laboratory results (click to enlarge the image).

UA (click to enlarge the image).

Uric acid was low which is indicative of SIADH. TSH was normal.

The most likely diagnosis is SIADH and the patient was put on fluid restriction of 1L per day. Her Na increased to 125 mEq/L.

Before diagnosing SIADH, we need to exclude any abnormality of the renal, adrenal or thyroid axis. It is often said that the cause for SIADH is located in one of the 3 body cavities: Head (tumor, meningitis), chest (pneumonia, lung CA), or abdomen.

CT of the head and chest were negative.


Patient was stable, her Na stayed around 125 mEq/L and she was sent to the GeroPsych unit before arranging a NH placement. Paxil was discontinued.

What is generally accepted as a "safe" sodium level before discharging a patient with hyponatremia?

Na+ 125-130, if there are no symptoms.

Hyponatremia Work-up


What is your first assessment? (no labs needed)

Volume status -- this is purely clinical: VS, skin turgor, mucosal membranes, urine output.

Classify hyponatremia according to the volume status.

There are 3 groups:

- Hypovolemic
- Normovolemic
- Hypervolemic

What labwork would you order? Pick just one.


Yes. The next important step is to check urine Na+ (UNa).

Each of these 3 groups has subgroups

Hypovolemic hyponatremia

Renal disease -- UNa high
Extrarenal disease -- sweating, burns -- UNa low -- the kidneys see low volume and try to conserve Na+

Normovolemic hyponatremia

Adrenal insufficiency
SIADH -- UNa is high-normal -- why? -- kidney "see" normal volume
(This group includes all endocrine causes)
PEEP on vent
Psychogenic polydypsia

UNa is WNL -- kidneys see normal volume

Hypervolemic hyponatremia


UNa is low -- the kidney is not a very "smart" organ -- it sees low volume (low perfusion) despite tissue edema (fluid is extravascular), so it tries to keep Na+ (and volume in).

When patient is on diuretics, UNa is high but soon after your stop the diuretic, the UNa may be low.

SIADH Treatment

Fluid restriction 1000 ml/day. Usually this is all it takes to correct Na+.

No NS as IVF.

If symptomatic or seizures -- you have to start NS 3% according to the formula. Correct 12 mEq over 24 hrs. Correct slowly, otherwise the patient may develop CPM (Central Pontine Myelinolysis).

Demeclocycline is effective (causes DI) but not commonly used because it can induce renal failure.

ADH receptor inhibitors, such as conivaptan, are also very effective in increasing sodium concentration in patients with SIADH.

Arginine-vasopressin (ADH) is a hormone that plays an important part in water homoeostasis. The vaptans are non-peptide vasopressin receptor antagonists. V2-receptor antagonists—mozavaptan, lixivaptan, satavaptan, and tolvaptan—induce a highly hypotonic diuresis without affecting the excretion of electrolytes (by contrast with the effects of diuretics). These drugs are all effective in the treatment of euvolemic and hypervolemic hyponatraemia. Conivaptan is a V1a/V2 non-selective vasopressin-receptor antagonist that has been approved by the FDA as an intravenous infusion for the inhospital treatment of euvolemic or hypervolemic hyponatraemia. Source: Lancet, 05/2008.

Related reading

A Case of Central Pontine Myelinolysis, NEJM Images in Clinical Medicine, 1995.
Central Pontine Myelinolysis. NEJM Images in Clinical Medicine, Dec 2008.

Hyponatremia: Case 2

40 yo AAM with a PMH of CHF with EF 25-30% is admitted to the hospital for CHF exacerbation. After a few days of IV diuresis with Lasix, followed by Demadex, his Na+ is 118.

Laboratory results in hyponatremia (click to enlarge the image).

Not surprising? What is the most likely reason?

Diuretic-induced hyponatremia.

Do you notice anything else which is low on the BMP?

Potassium (K+).

That's right. This patient needed daily K+ to counteract the effect of the diuretic. Always check 4 things when you diurese a patient: I/O, Na, K, Mg. Replace accordingly -- K+ up to 4 mEq/L and Mg up to 2.

Why is bicarbonate high?

This is a good example of a contraction alkalosis.

What is the mechanism of contraction alkalosis when diuretics are used?

Dehydration concentrates body electrolytes. Contraction alkalosis occurs when there is loss of relatively large volumes of bicarbonate-free fluid. The plasma bicarbonate concentration rises in this setting because there is contraction of the extracellular volume around a relatively constant quantity of extracellular bicarbonate. Administration of a loop diuretic to induce rapid fluid removal in a markedly edematous patient is the most common cause of a contraction alkalosis. References: eMedicine, UpToDate, first described in 1965 in Ann of IM, click to see the diagram.


Hyponatremia. NEJM 2000.
Hypernatremia. NEJM 2000.
Hyponatremia and Hypernatremia in the Elderly - AFP 2000
Vomiting, Hypertension, Lethargy - NYTimes 6/05

Related reading

Vaprisol (Conivaptan), a vasopressin antagonist, is approved for treatment of hyponatremia. DB’s Medical Rants.
Hyponatremia: must reads for hospital physicians. Notes from Dr. RW, 2005.
Grand Rounds: “Hyponatremia: Something Old, Something New.” The NYU Internal Medicine Blog.
Non-peptide arginine-vasopressin antagonists: the vaptans. The Lancet 2008; 371:1624-1632.
Lowest sodium I have ever seen http://goo.gl/QgJmf
It's summer, make sure to warn all of your SIADH patients about sun sensitivity with demeclocycline. Nephrology blog, 2011.

Published: 03/20/2005
Updated: 05/03/2011


  1. This is a great site for learning. Thank you. Keep up the good work.

  2. It is a great site. please go forword.

  3. This is good info.I had hyponatremia and was givin 0.45 wt%NaCl IV push,).5mg Diazapam IV push and compazine IV push.Fluids were not restricted.Was on Normal saline IV and recovered in 3 days.

  4. You received compazine for nausea, I presume? Nausea is the body's most potent (endogenous) stimulus for ADH secretion. I wonder if severe, prolonged nausea caused your hyponatremia

  5. I had mild nausea prior to being admitted to the ER but this did not cause my electrolyte imbalance.
    This was a beginning symptom of hyponatremia.I then became diapheretic and later confused.

    I am VERY gald to be alive,and I thank God that I had enough sense to get treatment.By the time paramedics got me to ER I was jumping around like Linda Blair.

    I told ER Doc what to give me and he did.

    After all that IV med I passed-out.However,I felt fine when I woke-up.

  6. I developed hyponatremia in the hospital after surgery, iv's and a blood transfusion (although I didn't know it for more than a week). The only blood test I was given in my 3 day hospital stay was checking my red and white blood cells. I knew something was really wrong with me and kept asking for help, but was sent home telling me I would be fine later and to rest. I later understood that a discharge with hyponatremia meant that I was actually sent home from the hospital with the risk of permanant brain damage or death, all because no one bothered to monitor something as basic as my electrolytes! NEVER, NEVER let a friend or loved one leave the hospital after procedures and IV's that would put them at risk for hyponatremia (low blood sodium) without a comprehensive metabolic panel (CMP).

    I was not getting better for over a week (saw a dr. 3 times and still just given the same blood test- rbc and wbc), and was very weak, confused and semi-nauseous, and had lost 6 pounds. My female family physician saw me the following week, gave me comprehensive blood tests and found I was dangerously low in both sodium and chloride. She advised me to use the natural salt I had at home to salt everything I ate or drank and be tested the following day, and my sodium level rose immediately 7 points and out of the severe danger zone, and then gradually over a week or two came up to normal. My body had the wisdom to begin to safely balance my electrolytes when given the means to do so. After reading about the dangers of central pontine myelosis (brain stem herniation and death) that can come from improper IV treatment raising dangerously low sodium levels too quickly, I was glad that I was able to avoid that additional risk and survive the ordeal.

  7. In the second case, there is no urine result. also it is not clear that CHF was worsening or not? Talking about sodium without urine lytes is difficult to interprete.
    In this case I think metolazone should have been stopped first.
    I can see some improvement with replacement of fluid. The follow up is short and patient cannot be left alone with sodium 123.

    Also in hyponatremia on diuretics, FEUrea should be considered.

    But overall thanks for putting this data on.

    Alireza Atef, MD Dallas

  8. Its really a great learning case. Learned lot of things from the above. Tons of Thanks!!!

  9. This is a great site. I came across it preparing for a hyponatremia presentation.

  10. great piece of work.greatly appreciated.

  11. can you correct a low sodium level of 107 and have blood transfusion of 5 pints of blood at same time?