Two of our local support group members report that their loved ones (one with PDD; one with LBD) have had repeated UTIs and one bout of hyponatremia each. Hyponatremia is a new problem to many of us. "Hyponatremia is an abnormally low concentration of sodium in your blood."*
A "letter to the editor" was published in the March '08 issue of the Journal of American Geriatrics Society on hyponatremia and DLB. Thanks to Forum member Patty, I got a copy of this letter.
The authors provide a case report of one 86-year-old woman who was diagnosed with hyponatremia and probable DLB after a hospital stay where tests were run and her behavior was observed. A test called "The One Day Fluctuation Assessment Scale" was used. I will try to get this as it might be interesting for us. The authors say that this is the only case of DLB with hyponatremia they are aware of! I've copied below the full text of the letter (without a table that provides lab results). You might want to skip the long paragraph that starts "Based on these findings," which is a description of how they diagnosed the hyponatremia. The second to the last paragraph that starts "Finally, we emphasize the following teaching points" is worth reading. I put two definitions after the letter and references.
HYPONATREMIA DUE TO RESET OSMOSTAT IN
DEMENTIA WITH LEWY BODIES
To the Editor: Various central nervous system disorders can
cause the syndrome of inappropriate antidiuresis (SIAD).1
Reset osmostat is considered a subtype of SIAD, in which
unknown central processes lower the osmotic threshold for
antidiuretic hormone (ADH) release, resulting in a continuously
lower serum sodium concentration.1,2
We report a case of hyponatremia due to reset osmostat
in probable dementia with Lewy bodies (DLB), illustrating
how the encountered diagnostic challenges may serve as
teaching points.
An 86-year-old woman presented after a collapse. She
had been lying on the floor for several hours in a hot room.
Her history included ovarian cancer in complete remission
and a transient ischemic attack. Her only medication was
acetylsalicylic acid. She consumed a normal diet and was
not polydipsic.
At presentation, she had a remarkable fluctuating cognition
that shifted between alertness and confusion with
visual hallucinations. She scored 22 points on the Mini-
Mental State Examination.
Physical examination showed symptomatic, orthostatic
hypotension (125/60mmHg supine, 60/40 upright) and
signs of dehydration but was otherwise unremarkable.
Based on these findings and her laboratory data at presenta-
tion (Table 1), a collapse caused by hypovolemia not
due to blood loss was suspected and further substantiated
by the presence of prerenal failure (low fractional excretion
of sodium), hyponatremia, hypokalemia, and evidence of
hyperaldosteronism (high transtubular potassium gradient,
Table 1). An infusion of normal saline with added potassium
normalized renal function and serum potassium within
1 day. From this point, the patient was assessed to be
clinically euvolemic, but hyponatremia, confusion, and ortho-
static hypotension persisted invariably for the remaining
20 days of admission. Therefore, additional diagnostic tests
were performed (Table 1). To investigate whether hypona-
tremia was responsible for confusion, serum sodium was
corrected to 140mmol/L using 3% hypertonic saline and
demeclocycline (rate about 6mmol/d). Neuropsychiatric
symptoms failed to improve, and the patient started to com-
plain of extreme thirst. Moreover, hyponatremia returned each
time therapy was discontinued. When treatment was stopped
for a longer time, serum sodium concentration became regu-
lated at a stable albeit lower setpoint of approximately 129mmol/
L (urinary sodium 42mmol/L, urine osmolality 259mOsm/
kg). Her body weight was also stable during this period.
Finally, 2weeks after admission, subtle signs of parkinsonism
(mainly rigidity) became apparent, which did not respond to
a trial of levodopa.
The following diagnoses were established.
First, the diagnostic criteria for SIAD were met: low
serum osmolality; inappropriate urinary concentration;
hyponatremia during euvolemia; high urinary sodium concen-
tration; and no adrenal, thyroid, pituitary, or renal insufficiency
or diuretic use (Table 1).1 The diagnosis of SIAD was
further refined to reset osmostat based on a normal ADH
concentration and normal water loading test (Table 1).1,2
Second, probable DLB was diagnosed. Of the consensus
criteria for DLB, the central features (dementia), core
features (fluctuating cognition, visual hallucinations, parkin-
sonism), suggestive features (low dopamine transporter
uptake, Table 1), and supportive features (collapse, ortho-
static hypotension) were present.3 The One Day Fluctuation
Assessment Scale also supported the diagnosis.4
To our knowledge, this is the first reported case of hypona-
tremia in a patient with probable DLB and suggests
that its cause is a reset osmostat.
Hyponatremia has been described in multiple-system
atrophy,5 a condition related to DLB. Systematic studies
should reveal how common hyponatremia occurs in DLB,
especially because both conditions are common in elderly
people. Why DLB causes a reset osmostat remains unclear,
but central dopamine metabolism could play a role.6
Finally, we emphasize the following teaching points.
First, an index of suspicion is required to diagnose DLB,
especially because the presenting symptoms may mimic
other medical conditions. Second, the neuropsychiatric
symptoms of DLB resemble those of acute hyponatremia,
risking osmotic demyelination if hyponatremia is corrected
too quickly. Third, both disorders predispose to falls, which
was only recently described in hyponatremia and may be
due to nerve conduction velocity slowing.7 Fourth, this case
highlights the importance of pursuing further diagnostic
testing if no obvious cause for SIAD is found. Measurement
of ADH and a water-loading test are simple approaches to
diagnosing the SIAD subtypes reset osmostat (normal
ADH, normal water loading test) and the recently discovered
nephrogenic SIAD (normal ADH, abnormal water
loading test).1,2 Hyponatremia due to reset osmostat should
be treated conservatively, and DLB may improve with
acetylcholinesterase inhibitors.
In conclusion, hyponatremia due to reset osmostat is a
new finding in DLB, in which adequate diagnosis and treatment
relies on an integrated medical and neurological evaluation.
Ewout J. Hoorn, MD, PhD
Department of Internal Medicine
Erasmus Medical Center
Department of Internal Medicine
Medical Center Rijnmond Zuid
Reinout M. Swart, MD
Department of Internal Medicine
Margriet Westerink, MD
Department of Neurology
Marinus A. van den Dorpel, MD, PhD
Arie Berghout, MD, PhD
Jet J. Bakker, MD
Department of Internal Medicine
Medical Center Rijnmond Zuid
Rotterdam, The Netherlands
REFERENCES
1. Ellison DH, Berl T. Clinical practice. The syndrome of inappropriate antidiuresis.
N Engl J Med 2007;356:2064â2072.
2. Robertson GL. Regulation of arginine vasopressin in the syndrome of inappropriate
antidiuresis. Am J Med 2006;119:S36âS42.
3. McKeith IG, Dickson DW, Lowe J et al. Diagnosis andmanagement of dementia
with Lewy bodies: Third report of the DLB Consortium. Neurology 2005;
65:1863â1872.
4. Walker MP, Ayre GA, Cummings JL et al. The Clinician Assessment of Fluctuation
and the One Day Fluctuation Assessment Scale. Two methods to assess
fluctuating confusion in dementia. Br J Psychiatry 2000;177:252â256.
5. Sone H, Okuda Y, Bannai C et al. Syndrome of inappropriate secretion of
antidiuretic hormone (SIADH) and Gerhardt syndrome associated with Shy-
Drager syndrome. Intern Med 1994;33:773â778.
6. Bridges TE, Hillhouse EW, Jones MT. The effect of dopamine on neurohypophysial
hormone release in vivo and from the rat neural lobe and hypothalamus
in vitro. J Physiol 1976;260:647â666.
7. Renneboog B, Musch W, Vandemergel X et al. Mild chronic hyponatremia
is associated with falls, unsteadiness, and attention deficits. Am J Med 2006;
119:e1âe8.
Robin's notes:
Definitions of two terms used in the letter:
acetylsalicylic acid = aspirin
polydipsic = excessively thirsty
* Here's a link to the Mayo Clinic webpages discussing hyponatremia:
http://www.mayoclinic.com/health/hyponatremia/DS00974
Here are a couple of bits on "reset osmostat" (in the letter's title):
osmostat = "the regulatory centers that control the osmolality of the extracellular fluid." (Dorland's Medical Dictionary for Health Consumers)
"Reset osmostat is a rare condition in acutely ill patients with severe pulmonary, neurologic, or malignant processes. When hyponatremia occurs because of 'reset osmostat,' renal concentrating and diluting capacities are normal but the regulation of arginine vasopressin to maintain serum tonicity takes place at a lower osmolal threshold." (Annals of Internal Medicine)
