sodium Flashcards
What’s the most abundant, osmotically important extracellular cation?
sodium
accounts for 86% of plasma osmolality
disorders of sodium are associated with increased mortality & length of hospital stay
How to assess a hyponatremic pt? how to manage?
ENDOCRINOLOGiST should guide Ix & management of hyponatremia
History:
symptoms (non-specific, frequently hyponatremia is an incidental finding (symptoms uncommon with serum sodium [] >125mmol/L: nausea, headache, vomiting, confusion, muscle cramps- in severe cases, seizure & coma)
Medical issues (eg. diarrhoea/vomiting, Addison’s, cirrhosis, heart failure, renal failure, hyperproteinaemia)
medications/drugs (eg. AEDs, PPIs, diuretics, antibiotics, SSRIs)
drinking habits
Examination:
if severe: hyporeflexia, confusion/drowsiness/reduced GCS, seizures, coma
volume status (HR, BP incl postural hypoT, skin turgidity, evidence oedema)
signs of other disease processes that may be associated
Investigations:
urea
electrolytes
paired (serum & urine) osmolalities & urinary sodium
-If the pt is hypervolaemic & the urinary sodium is low (<20mmol/L), it means increased interstitial salt (Ddx incl cirrhosis, CCF). If urine Na+ >20mmol/L, DDx= cerebral salt wasting, renal failure, diuretics.
-if ECF volume normal, consider water intoxication/primary polydypsia, hypothyroidism, hypotonic fluids (if low urine osmolality) or SIADH if urine osmolality normal or high (normally excess water would result in urine osmololity <100mOsmol/kg) since SIADH causes inappropriate water retention (eg. CNS, malignancy)- other Ddx if urine osmolality higher= glucocorticoid insufficiency.
-If ECF volume decreased & low urinary sodium, pre-renal (eg. diarrhoea, sweat, burns, SBO), while urine Na+ >20mmol/L is renal (eg, renal failure, Addison’s) or drugs (eg. diuretics)
-factitious: hyperglycaemia/lipidaemia/proteinaemia/glycine washout for TURP or hysteroscopy
urine dip (proteins, ketones)
blood glucose
TSH
ACTH
cortisol
consider other Ix depending on findings: short synacthen, ECG, CXR, abdo US, CT head/thorax/abdo/plevis, echo
Rx:
specific Rx depends on the cause
restore normal sodium & water balance in a well0controlled monitored environment
At what rate should sodium be increased?
maximum 4-6mmol/24hrs, 12-14mmol/L per 48hrs, 14-16mmol/L per 72hrs, to reduce risk myelinolysis
best managed in critical care environment with art line
endocrinologist should guide Ix & management of hyponatremia
What are the classifications of hyponatremia?
Mild: 130-135mmol/L
moderate 125-129mmol/L
severe <=125mmol/L
may be hypertonic (dilutional), isotonic (pseudohyponatremia), hypotonic hypervolaemic, euvolaemic, hypovolaemic)
What’s normal ECF sodium? total body sodium content? daily requirement?
134-146mmol/L
58mmol/kg
2mmol/kg
How to estimate osmolality (mosmoles/kg of solvent)?
2x (Na + K) + glucose + urea (mOsm/kg)
What’s normal serum osmolality? what change in osmolality may stimulate water reabsorption? what does hypovolaemia stimulate?
280-290mosmol/kg
increase in ECF osmolality as small as 1-2% may stimulate the posterior pituitary to relate ADH which stimulates V2 receptors on distal nephron to increase water reabsorption via aquaporin-2 channels.
thirst is also stimulated
renin secretion (from renal JG cells) is stimulated due to hypovolaemia. Renin converts angiotensinogen to angiotensin I which, via ACE, is converted to angiotensin II, stimulating adrenal cortex to release aldosterone.
renal cortex also detects decreased plasma sodium, stimulating aldosterone secretion, a mineralocorticoid which acts on principal cells in CDs to increase Na reabsorption (& water via osmosis) & also causes sodium absorption from sweat, saliva & colon.
What’s normal urine osmolality?
50-1400 mOsmol/kg
What are the 3 basic mechanisms through which someone can develop hyponatremia?
- gaining excess water in isolation (eg, SIADH, dextrose infusion)
- gaining water in excess of gaining Na+ (eg. liver failure, CCF, nephrotic syndrome)
- sodium depletion to a greater extent than water depletion (renal: cerebral salt wasting syndrome, diuretics. non-renal: GI losses, sweat losses, “3rd space” (burn, pancreatitis, trauma)
examples of hypotonic hypovolaemic hyponatremia?
diarrhoea
vomiting
sweat
burns
pancreatitis
trauma
if urine Na+ >40mmol/L, consider:
Addison’s
cerebral salt wasting syndrome
diuretics
*may be >1x so important to exclude other pathologies eg. hypothyroidism
examples of hypotonic euvolaemic hyponatremia?
SIADH
hypothyroidism
glucocorticoid insufficiency
hypotonic fluids
drugs (diuretics, PPIs, AEDs, antibiotics, SSRIs)
examples of hypotonic hypervolaemic hyponatremia?
cirrhosis
heart failure
nephrotic syndrome
renal failure
pregnancy
examples of isotonic pseudohyponatremia?
hyperlipidaemia
hyperproteinaemia (multiple myeloma & recent immunoglobulin therapy)
examples of hypertonic dilutional hyponatremia?
severe hyperglycaemia
glycine washout (TURP, hysteroscopy)
mannitol
What’s the short synacthen test?
test of adrenal insufficiency
measure serum cortisol before & after injection of synthetic ACTH
What’s normal urea?
5 to 20 mg/dl, or 1.8 to 7.1 mmol/L
What’s normal creatinine?
62-115µmol/L for men & 53-97µmol/L for women
Diagnostic criteria for SIADH?
hyponatremia, due to water retention due to elevated ADH
clinical euvolaemia or hypervolaemia
serum osmolality <275mOsmol/kg (DECREASED)
urine osmolality >100mOxm/kg
urinary Na+ >30mmol/L (INCREASED)
normal urine output
normal thyroid/adrenal function
no use of diuretics within 1/52 of testing
How to manage SIADH?
seek cause
commence H2O restriction (1L/24hr)
if Na+ not increasing, demeclocycline can be added- a tetracycline antibiotic that causes nephrogenic diabetes insidious by inhibiting ADH action in the nephron
if still not improving, under endocrine advice, consider V2 receptor antagonist tolvaptan (side effects nausea, weakness, hyperK, postural hypoT)
How is cerebral salt wasting distinguished from SIADH?
mechanism= excess secretion of Na & H2O
Manifests as:
polyuria
hypovolaemia
usually associated with recent intracranial surgery
usually self-limiting, corrects with isotonic saline
similar to SIADH as hypotonic hyponatremia with high urinary Na & high urine osmolality.
What are some causes of SIADH?
Intracranial: trauma, tumor, SAH, CVA, post-surgical, epilepsy
pulmonary: pneumonia, TB, abscess
malignancy: small cell lung cancer, lymphoma, GI or GU tract
drugs/toxins: desmopressin, PPIs, SSRIs, sodium valproate, levetiracetam, ecstasy, oxytocin
misc: HIV, acute intermittent porphyria, GBS
what’s plasma osmolality normally maintained at?
280 –295 mOsmol/kg
What happens with TURP syndrome?
glycine 1.5% may be used in high volumes (favourable osmotic characteristics)
It’s an inhibitory CNS transmitter, is absorbed through the vascular prostate
initially a transient dilutional hypervolaemic hypotonic hyponatremia as it’s a hypotonic (200mOsmol/kg) salt-free solution
the unmetabolised portion then causes a natriuresis & osmotic diuresis–> hypovolaemic hypertonic hyponatremia
Symptoms of TURP syndrome are due to the initial hypo-osmolar state and by the CNS effects of glycine. ammonia, a metabolite of glycine, may contribute to cerebral depression.
The osmolar gap may be high due to unmeasured glycine.
If symptomatic or hypo-osmolar, need to manage in critical care, consider frusemide but if that worsens Na+, mannitol is an option (aim to maintain -ve free water balance)
For each 3.5mmol/L increase in glucose, by how much do [Na] decrease?
1mmol/L
Diagnostic criteria for diabetes insipidus?
high serum sodium (>145mmol/L)
increased urine volume
high serum osmolality
low urine osmolality
what may cause low plasma osmolality and low urine osmolality (less than half the plasma osmolality)?
water overload, polydypsia
what may cause low plasma osmolality and low urine osmolality (less than half the plasma osmolality)?
water overload, polydypsia
SS_NS 1.12: Describe the mechanism and management of disorders of sodium control detected after neurosurgery
SIADH may be caused by intracranial (trauma, tumour, CVA, post-surgery, epilepsy), pulmonary (TB, abscess, pneumonia), malignancy (small cell lung Ca, GI or GU tract), drugs (desmopressin, PPIs, SSRIs, Na valproate, keppra, ecstasy, oxytocin), misc (HIV, acute intermittent porphyria, GBS)
diagnostic criteria?
hypoNa
low serum osmolality (<275)
high urine Na (>30)
high urine osmolality (>100)
euvolaemic or hypervolaemic
NORMAL urine output
Asymptomatic hypoNa in SIADH is usually Mx with H2O restriction (1L/24hrs) General measures= identify/treat any underlying causes, drugs that could contribute to hyponatremia, reduce electrolyte-free water, oral salt tablets, consider loop diuretics (these may help to lower urine osmolality & increase water excretion by impairing renal responsiveness to ADH & interfering with countercurrent concentrating mechanism)
but in SAH/cerebral trauma H2O restriction can —> intravasc vol contraction & vasospasm SO in this case is treated with HTS. Rx depends on symptom severity (want to rapidly correct if seizures, coma (most likely if <120mmol/L) or if intracranial disease & can’t tolerate brain swelling)- give 50-100mL bolus of 3% HTS (aim for a 5mmol/L increase, repeat up to 2x more @ 10-minute intervals aiming to reverse severe symptoms eg. seizures. potential complication= rapid over-correction, max rate 8mmol incr Na+/day). If chronic, infusion at 15-30mL/hr if chronic (24-hr increase of 5mmol/L), with inpatient monitoring & frequent serum monitoring 1-2 hourly.
If sodium isn’t increasing, further endocrine advice- consider demeclocycline (a tetracycline that causes nephrogenic DI by (-) ADH action in nephron) can be added (but may be nephrotoxic, cause N&V & photosensitivity& onset days to weeks), or V2 receptor antagonist tolvaptan, w side effects nausea, weakness, hyperK, postural hypoT). Once able, pt can take salt tablets.
How’s cerebral salt wasting characterised?
HypoNa
low serum osmolality
High urine Na
high urine osmolality
DISTINCTION FROM SIADH: HYPOVOLAEMIA which appropriately triggers release of ADH, POLYURIA
How common is it?
it may occur in pts with CNS disease, esp SAH, however it’s a much less common cause of hyponatremia in pts w cerebral injury cf SIADH.
Clinically, CSW= hypoT, decr skin turgor, elevated Hct, despite a urine [Na] that isn’t low.
typical onset time?
within 10 days following neurosurg procedure or event
how about typical onset of SIADH?
after neurosurgery, most severe on 6th or 7th postop day.
Aim to restore volume (which may or not dilute the urine due to suppression of ADH release- this may not occur if there’s SIADH overlap). Rx with isotonic saline for volume repletion but may require HTS & fludrocortisone to counteract diuresis & natriuresis. Any patient with CSW with active intracranial pathology should have 3% HTS to incr serum Na & ensure there is no reduction in ECF volume. Once able, pt can take salt tablets.
What’s the natural history of CSW?
transient- resolution in 3-4wks, so long-term therapy not necessary.
How is diabetes insipidus diagnosed?
HIGH serum sodium (>145), high serum osmolality, incr urine volume & low urine osmolality
what may cause low plasma & urine osmolality (< half of plasma osmolality)?
water overload
What are other differential for hyponatremia after neurosurgeon aside from CSW & SIADH?
adrenal insufficiency: hyper secretion of ADH due to any cause of cortisol deficiency or hypoaldosteronism, only get hyperkalaemia with primary adrenal disease.
excessive hypotonic or isotonic fluid fluids
