Neurocritical Care
Fluid
Restriction
PO Sodium
IV Sodium
Demeclocycline
Vasopressin
(V)-Antagonists
Dose
< 1500 mL/day
4–16 g/day (1
g = 17 mEq of
Na)
0.9%–3% at
0.5–1.5 mL/
kg/hr
300 mg every 12
hr up to 1200 mg/
day
Conivaptan:
20–40 mg IV daily
Tolvaptan:
15–60 mg PO
daily (Intensive
2014;40:320-31)
Efficacy
Modest, delayed
(over 2+ days)
Modest, more
effective for
CSWS (over 2+
days)
Modest, more
effective for CSWS
(over 2+ days)
Modest, delayed
(over 1 wk)
Modest, prompt
over the first 24
hr
Common
adverse
effects
Thirst
Thirst,
diarrhea,
nausea,
vomiting
Fluid overload,
hyperchloremia
GI upset,
hepatotoxicity,
nephrotoxicity,
photosensitivity
Thirst;
conivaptan
Infusion pain
Common
considerations
Difficult
to ensure
adherence;
caution for
permitting
hypovolemia
in patients
with cerebral
perfusion needs
such as SAH,
TBI
Poor
palatability
when taken by
mouth
≤ 3% sodium
chloride may be
given through
peripheral IV line;
The smallest-
bore IV in the
largest available
vessel should be
used. Central
line remains the
preferred access, if
available
Chelation
occurs with
coadministered
cations;
nephrotoxicity has
been reported
Cost; drug-drug
interactions are
common; risk of
overcorrection of
Na > 8 mEq/24
hours; tolvaptan
should not be
used > 30 days
in patients with
liver disease due
to risk of life-
threatening liver
injury
ADH = antidiuretic hormone; IV = intravenous(ly); PO = oral(ly); SAH = subarachnoid hemorrhage; TBI = traumatic brain injury.
Treatment of SIADH can be challenging in neurocritical care patients such as those with subarachnoid
hemorrhage (SAH) and TBI.
because of prioritizing a euvolemic volume status to optimize cerebral perfusion pressure (CPP). This
is particularly important when treating elevated ICP or cerebral vasospasm.
Hypertonic sodium solutions are often needed to raise serum sodium.
A practice-based study evaluated the impact of various hyponatremia treatments on the serum sodium
concentration (Neurocrit Care 2017;27:242-8). Hypertonic saline solutions were commonly used and
most effectively increased the serum sodium.
Etiology is largely unknown, but speculation typically focuses on the increased secretion of natriuretic
peptides, causing loss of sodium at the renal distal tubules.
Typical causes include TBI, SAH, and brain tumor.