mild 130-135 mEq/L
profound < 124
- Acute (< 48 hours) a/w brainstem herniation and death
- Chronic does not herniate: instead see status epilepticus ~ 110 mEq/L; osmotic demyelination from rapid overcorrection
[ ] Labs
- chem 7, ca mag phos
- Osms (serum and urine), Ur Na+, Ur uric acid (if on diuretics)
- CK: low sodium can cause rhabdo
- TSH if c/f hypothyroidism
- Cortisol if c/f adrenal insufficiency (whether primary, i.e. Addison's or CAH, or secondary, i.e. steroids or Sheehan's)
- Urine Legionella, tick panel (Ehrlichia smear), tularemia PCR or titers, HIV if c/f infectious process
[ ] CXR
- a/w small cell lung cancer, Legionella
[ ] fluid restriction
[ ] +/- Foley for UOP
If clearly, truly hypovolemic:
[ ] isotonic fluids +/- K+ (and Mag) repletion
- But beware: Fixing hypovolemia turns off ADH secretion (baroreceptors relax; osm receptors reassert) -> free water in urine -> rapidly increases serum Na+. Can lead to overcorrection. (Especially when other drivers of hyponatremia are also withdrawn, such as SSRIs, HCTZ, or stressors such as seizures, pain or critical illness).
- May see 1L/hr maximally dilute urine appear, which alone will increase serum Na+ by 2 mEq/L/hour or 24 in a day!
- Sterns (AKJD, 2010) suggests preempting water diuresis by giving DDAVP, 1-2 mcg IV.
If profound, symptomatic hyponatremia:
[ ] Head CT if altered
[ ] Need a small, rapid correction:
- 3% NaCl, 100 mL over ~10-30 mins (2 mL/kg to max of 100 mL). MR x 1
- Each 100 mL raises sodium by ~ 2 mEq/L
"Six a Day for Safety"
- Aim for 6 mEQ Na+ increase in 24 hours
- If profound sx: Aim for 6 mEQ increase in six hours and then stop
How do I interpret these labs I've sent?
If urine osms < 100 mOsms, it is dilute urine: Kidneys are losing free water actively, i.e., trying to correct the situation. Think "ways the patient got too much water": water intoxication, hyptonic IV fluids, beer potomania, etc.
If urine osms > 100 mOsms: urine concentrated, kidneys holding onto free water despite having too much. ADH likely active, either "inappropriately" or appropriately.
(See pathophyz below for more discussion.)
Can I sub in NaHCO3 for 3% NaCl? Yes!
- Hypertonic (3%) saline contains 513 mEq/L of Na+
- 8.4% NaHCO3 ("code-cart bicarb") contains 1,000 mEq/L of Na+
- So a 50-mL code cart bicarb amp contains the same sodium load as 100 mL of 3% HTS.
What if I overcorrect horribly?
- Consult renal
- DDAVP, 1-2 mcg IV
- Consider D5W 6ml/kg over 1 hour
What's the pathophyz?
"Bloating or wasting": Hoarding water, or wasting salt.
Arginine Vasopressin (= anti-diuretic hormone, ADH) tells kidneys to retain water. It's also a vasoconstrictor (a pressor). Called out when hypothalamus judges osmolality is high (hypertonic) or, more strongly, when carotid, aortic & renal baroreceptors judge volume is too low.
95% of all cases of hyponatremia (major exceptions: primary polydypsia, renal failure) have elevated ADH levels.
Either it's "inappropriate" (SIADH) or "appropriate", i.e., provoked by decrease in effective circulating volume: Body thinks (correctly or incorrectly) it's hypovolemic.
Drinking too much water:
- Psychiatric problem
- Repleting salty water losses (vomiting, diarrhea, sweating) with free water (or even Gatorade, which still hyptonic)
- Infants given excess tap water in formula, or for gastroenteritis
- Beer potomania: Beer is very hypotonic if it's all you drink and you don't eat much
- Hospital patients given hypotonic IV fluids
Expect copious, maximally dilute urine as body struggles to push out excess water (Ur Na+ < 20, Ur osms < 100 mOsms/L)
Keeping too much water
- ADH inappropriately turned on
- Ecstasy, Carbamazepine (Tegretol) & SSRIs
- Small cell lung cancer (often one of first signs)
- ADH "appropriately" turned on
- Comes out like any other pressor, so in response to EtOH withdrawal, to seizure, to illness, in post-op pts
- Nausea a potent stimulator for ADH
- Edematous disorders can look like hypovolemia to the pituitary gland: CHF, cirrhosis (ascities, portal HTN),
severe nephrotic syndrome
- Loss of volume to GI vomiting, diarrhea, fistulas; to sweating, insensible losses; to bleeding; can all turn on ADH
- ADH given as a medication
- DDAVP analogue, given for bed wetting (you don't urinate much on it), for von Willebrand's disease, and for central
diabetes insipidus (i.e., body makes no ADH, so can't retain water, have dilute urine, are hypernatremic, dehydrated)
- Vasopressin: a pressor in critically ill
- Oxytocyin (Pitocin): Given to induce labor, and also in post-partum hemorrhage to increase uterine tone. Available too
as nasal spray, experimenting with autism, and a/w neurological basis of intimacy, orgasms.
Body is keeping water, so expect low UOP, concentrated urine, (Ur Na+ > 20, Ur osms > 100 mOsms/L)
Wasting too much salt
- Thiazide diuretic
- Kidney failure (ATN or other intrinsic)
Kidney is poisoned so shedding salt +/- lots of water. See diuretics below
Other / Etiology Unclear
- Legionella pneumonia
- Ehrlichiosis, RMSF
- "Cerebral salt wasting" — brain injury causes kidneys to waste salt. Debated if this disease exists at all or is just SIADH.
- Many CNS and pulmonary infections cause SIADH
Various dilutional states:
- hyperlipidemia, IV Ig infusions, mannitol, hyperglycemia, radiocontrast dye
- Correction factor for hyperglycemia: Na+ drops 1.6 mEq/L for every 100 mg/dL of glucose
- ("Pulling labs off same line as the IV fluid bolus" not a likely cause: NS has 154 mEq of Na+, LR 130.)
- Note that often multifactorial: Ultramarathoner repleting salty losses with free water, also getting massive stress response that calls out ADH, also taking NSAIDs that suggest to kidneys a need for more ADH … Ecstasy user at rave, the MDMA direct stim of brain for ADH, drinking water while overexerting, co-ingesting sympathomimetics … Alcoholic post-detox started on SSRIs and HCTZ and sent home, where drinks too much beer, goes into withdrawal (stressor), has a seizure (another stressor) …
The Big Four: HCTZ, SSRIs, Carbamazepine (Tegretol), Ecstasy
- Pathophyz debated, but likely multifactorial:
a) It's a salt-wasting diuretic
b) This lowers BP by induced hypovolemia, which calls out ADH to keep water
c) Also depletes K+; body swaps K+ out of cells and Na+ into cells in response to low K+
- Really the main diuretic to cause hypoNa+. Loop diuretics like Furosemide have only been rarely implicated
- One suggested management strategy: Check uric acid.
- If less than 4 mg/dL, driving force is the diuresis-driven ADH / hypovolemia. Replete hypovolemia with NS + K
- If greater than 4 mg/dL, driving force is the salt wasted. Fluid restrict.
- Believed to stimulate central secretion of ADH
- Other anti-depressants (i.e., TCAs, MOAs) and anti-psychotics also associated. But, they also cause dry mouth in
patients prone to polydypsia, which may be driving force.
- Like SSRIs, stimulates central secretion of ADH
- Actually dose-dependent response
- Oxcarbazepine even worse offender
MDMA / Ecstasy
- Like SSRIs and Carbamazepine, stimulates central secretion of ADH
- But this in patients at raves, sometimes taking other sympathomimetics, often overexerted and hot, and repleting fluid
losses with too much free water
- Several chemo agents, esp. Vincristine, Vinblastin, Cis-Platinum, Cyclophosphamide (patients also told to drink lots of H2O with cyclophosphamide)
- Opioids often mentioned, but a/w nausea, hypotension, stress events that confound
- NSAIDs weakly implicated, mainly in ultramarathoners drinking waters