The ambulance company calls in asking your emergency department to prepare for an agitated adult female with known psychiatric history. Depending on where you work, this may involve having security at the ready with physical restraints and your best (strongest?) nurse with Haldol and Ativan in hand, for the patient’s safety and your own. Perhaps a large majority of the time the agitation is simply a sequelae of their psychiatric disturbances, and that is a completely reasonable approach. But what is your approach when the agitated psych patient may have organic pathology? A recent patient encounter in a community ED setting led me to add psychogenic polydipsia with symptomatic hyponatremia to my differential.
Psychogenic polydipsia typically occurs in psychiatric patients who are unaware of or do not admit to excessive water intake, resulting in severely low levels of sodium. Think: direct access to constantly running water, whether at their own home, group home, or a controlled facility such as behavioral hospital or prison.
After caring for this particular patient, I took it upon myself to review how in the world this person’s serum sodium was so low, as low as 104 mEq/L to be exact. According to a 2007 literature review in Endocrine Abstracts, the lowest recorded serum sodium is 99 mEq/L.
Here’s a quick physiology review: When a person has increased water intake due to excessive thirst or psychiatric disturbance, anti-diuretic hormone (ADH) will be suppressed, which will increase free water excretion and the formation of dilute urine. However, if massive water ingestion occurs and exceeds maximal urinary free water excretion, then hyponatremia will develop.
In this setting, urine osmolality will be maximally dilute. Since volume status is normal, renal excretion of sodium is normal however urine sodium concentration will be low due to the dilution of the urine. Fractional excretion of sodium (FENa), if you are feeling adventurous, and order those pesky urine nephrology panels, will be >1%.
Complications from psychogenic polydipsia are secondary to hyponatremia, marked polyuria, and massive urine output. Several problems can exacerbate the already low sodium levels, including psychotic episodes that may cause a transient release of ADH or an increased renal responsiveness to ADH. In addition, multiple psychiatric medications can induce concomitant SIADH, such as SSRIs, worsening the hyponatremia.
Unfortunately, central nervous system tumors may also trigger polydipsia and cause hyponatremia, therefore, neuroimaging is recommended prior to concluding a diagnosis of psychogenic polydipsia. Water restriction tests can prove this diagnosis as there will be rapid resolution of the hyponatremia. Depending on the patient’s length of stay in your emergency department, you may not be the physician making the final decision on the etiology.
Human physiology dictates that the sodium level should be maintained between 138 and 142 mEq/L. When serum sodium levels are less than 130 mEq/L, moderate symptoms will occur, which may include nausea, headache, disorientation, ataxia, and confusion. When levels reach 120 mEq/L or less, severe symptoms such as intractable vomiting, focal neurologic deficits, confusion, seizures, coma, and ultimately respiratory arrest due to brainstem herniation may occur.
The presence of hyponatremia-related symptoms is directly related to the rapidity of onset! In a patient with psychogenic polydipsia, the case is likely acute, as the rapid water ingestion will lower the serum sodium over several hours.
Initial treatment in severe symptomatic cases such as this includes immediate infusion of hypertonic saline, usually 3%, which may run through a large-bore peripheral IV until central access can be obtained. Raising the serum sodium by 4 to 6 mEq/L is recommended to see improvement of neurological symptoms such as seizures or coma. This can be accomplished by initiating 100 mL boluses of hypertonic saline pushed over approximately 10-15 minutes and then a repeat measurement of serum level. Boluses may be repeated.
Frequent sodium checks (at least every 2 hours!) are required. You should aim for an increase of only 6-12 mEq/L in a 24 hour period depending on acuity or chronicity of the hyponatremia. After clinical improvement, stop the hypertonic saline. In the ED, we will likely only have contact with the patient for the first few hours of their care. So remember – if they are symptomatic, hypertonic saline boluses are the standard treatment! Beware the complication of central pontine myelinolysis if sodium correction is too rapid.
Now, back to our patient. Fortunately, the staff accompanying our patient knew her well, and informed us that the behavior and level of agitation was markedly different compared to how she is on a day-to-day basis. This, in part, prompted us to obtain immediate laboratory studies, which demonstrated the serum sodium level of 104 mEq/L. Within several minutes of the labs resulting, the patient began to seize, and we quickly administered 3% hypertonic saline and the seizure activity resolved.
Ultimately, the patient was diagnosed with psychogenic polydipsia leading to severe hyponatremia, and discharged with normal sodium levels within one week. The patient was noted to be on an atypical antipsychotic, which do display some risk of hyponatremia, especially in older adults. She was subsequently switched to another medication with less side effects of electrolyte abnormalities.
We do not always send labs on agitated patients with a psychiatric history as prescription medication noncompliance, illicit drug abuse and acute on chronic psychoses are plausible differential diagnoses. Depending on the chief complaint, history of present illness, as well as historical factors from their collaterals, you may choose to send off labs or obtain imaging to evaluate for organic causes of agitation. After this experience, hyponatremia secondary to psychogenic polydipsia is certainly a cause I will never forget.
Author: Alexis Cates – PGY3. @acates
- This Core EM article by Dr. Anand Swaminathan highlights causes and treatments of hyponatremia.
- Want quick information with bullet point highlights? Try this article on Life in the Fast Lane by Dr. Chris Nickson.
- Have access to EMRAP? This August 2015 Board Review Short has Dr. Mel Herbert discussing hypertonic saline in hyponatremia.
- Hyponatremia and Hypernatremia. In: Stern SC, Cifu AS, Altkorn D. eds.Symptom to Diagnosis: An Evidence-Based Guide, 3e New York, NY: McGraw-Hill; 2014. http://accessmedicine.mhmedical.com/content.aspx?bookid=1088§ionid=61699500. Accessed August 02, 2017.
- Petrino R, Marino R. Fluids and Electrolytes. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e New York, NY: McGraw-Hill; 2016. http://accessmedicine.mhmedical.com/content.aspx?bookid=1658§ionid=109385225. Accessed August 02, 2017.
- Joseph F, Kaliyaperumal M, Moss N, Qedwai F, Hill C, and Khaleeli A. Severe Hyponatremia – How Low Can You Go? Endocrine Abstracts (2007), 13, P 43. Accessed August 03, 2017.
- De Picker L, Van Den Eede F, Dumont G, Moorkens G, Sabbe BG. Antidepressants and the risk of hyponatremia: a class-by-class review of the literature. Psychosomatics. 2014. Nov-Dec;55(6):536-47.
- Quinn CJ, Iyegha UP, Beilman GJ, Cerra FB. Acute correction of hyponatremia secondary to psychogenic polydipsia. The American Journal of Case Reports. 2012;13:69-71. doi:10.12659/AJCR.882772.
- Gandhi S, McArthur E, Reiss JP, et al. Atypical antipsychotic medications and hyponatremia in older adults: a population-based cohort study. Canadian Journal of Kidney Health and Disease. 2016;3:21. doi:10.1186/s40697-016-0111-z.