sodium/ water states Flashcards
hypotonic hyponatraemia versus non-hypotonic hyponatraemia= plasma osmolality levels
hypotonic hyponatraemia= <275 (urine osmolality >100)
non-hypotonic hyponatraemia >275 (urine osmolality <100)
what are non-hypotonic causes of hyponatraemia 5
ethanol- beer potonmania hyperglycaemia pseudohypo-natraemia low sodium intake polydipsia =pure water gain
what is pseudohyponatraemia
paraproteinaemia causes it
2 ways of classifying hyponatraemia
- ECF- hypo, euv, hypervolaemia
2. urine osmolality <20 or >20
causes of hypervolaemia hyponatraemia with a urinary sodium <30 5
Increased interstitial salt
- liver failure
- cirrhosis
- hepato-renal syndrome
- CCF-cardiac
- nephrotic syndrome
mechanism behind hypervolaemic hyponatraemia with <20 urine sodium
due to the above diseases- blood pressure drops
- causes release of AVP which causes salt and water to be retained
- but more water retained than salt
- salt and water excess
causes of euvolaemic hyponatraemia with urine osmolality < serum
(aka trick question= non-hypotonic hyponatraemia) water intoxification -polydipsia -beer potomaina water overload
causes of euvolaemic hyponatraemia with urine osmolality >serum or urine sodium >30
7
- SIADH
- secondary adrenal insufficiency
- hypothyroidsim- myxoedema
- lung disease
- cancer-siadh small cell
- chest
- CNS
causes of hypovolaemic hyponatraemia with urine sodium <30 3 main ones
pre renal: sodium loss in excess of water GI loss 3rd space losses previous diuretic use -diarrhoea -sweat -vomiting -burns -fistula -cirrhosis -SBO -villous adenoma rectum
causes of hyponatraemia hypovolaemic with urine sodium >30 4
renal?: salt and water lost through kidney but more salt loss than water
- kidney failure
- addison’s-primary adrenal failure
- vomiting
- CSWS
treatment for each type of hyponatraemia
hypervolaemic: restrict salt and water
euvolaemic: restrict water
hypovolaemic: give salt and water
2 body compartments
- extracellular: intravascular and intercellular
- intracellular
what compartments should sodium and potassium be found in
sodium=extracellular (so plasma sodium good estimate)
potassium- intracellular (so plasma potassium bad estimate eg in DKA)
hyponatraemia complication of going down too low and the symptoms
=cerebral oedema
- nausea, vomiting, headache and confusion
- reduced consciouscness
- 6th nerve palsy
hyponatraemia complication of coming up too quickly
=central pontine myelinolysis (osmotic demyelination) affects brain stem
symptoms of central pontine myelinolysis
dysarthria mutism dysphagia lethargy mood change spasitc quadriparesis seizure coma death neuro (focal, cranial, bulbar signs)
when does central pontine myelinolysis appear
3-4 days after sodium corrects
how does hyperglycaemia cause hyponatraemia
glucose level high increases osmolality
-> so body pushes sodium down to maintain osmolality level
seen in DKA
classification of mild, moderate and profound hyponatraemia
mild: 130-135
moderate: 125-129
severe <125
moderately severe symptoms of hyponatraemia
nausea without vomiting, confusion headache
severe symptoms of hyponatraemia
vomiting
cardio-resp distress
abnormal and deep somnolence seizure
coma
difference between acute and chronic hyponatraemia and risks
acute: develops <48 hours- more at risk of cerebral oedema
chronic: develops >48 hours more at risk of pontine myelinolysis on repletion
guideline for use of hypertonic fluid for hyponatraemia
-300mls of sodium chloride 1.8% over 30 minutes=hypertonic
-needs urgent treatment
-monitor sodium aim for a 5mmol/l increase in na with no more than 10mmol/l rise in 1st 24 hrs
then 8mmol/l rise every 24 hrs after
-not for hypervolaemic
what should not be used for a hypovolaemic hyponatraemic patient treatment
hypertonic sodium chloride due to already volume depletion
mangement of hypovolaemic hyponatraemia
-fluid but no more than 10mmol/l in first 24 hours
-use an isotonic fluid for resuscitation eg normal saline 0.9% or Hartman or
plasmalyte
-check sodium 4 hourly at least
how is hypovolaemia diagnosed
clinical diagnosis tachycardia hypotension absent JVP postural hypotension
what is management of hyponatraemia based on 2
acute or chronic development
prescence of neurological symptoms
management of euvolaemic hypervolaemia
restrict water
management of hypervolaemic hyponatraemia
restrict salt and water
key difference between CSWS and SIADH
CSWS=hypovolaemic
SIADH=euvolaemic
what causes CSWS
cerebral salt wasting syndrome
sub-arachnoid haemorrhage
management of CSWS
hypovoleamic so give normal saline sodium chloride 0.9%
management of SIADH
euvolaemic so restrict water
diagnoses of SIADH 6 steps
- hypo-osmolality <275 or plasma sodium <135
- inappropriate urinary concen. >100mosmo
- patient euvolaemic
- elevated urinary sodium >30 with normal intake
- exclude hypothyroidism, steroid deficiency through SST and diuretic use
- normal renal and cardiac function
causes of SIADH 5
- drugs related
- pulmonary
- tumours
- CNS disorders
- others
drug related causes of SIADH 3
- stimulate ADH-nicotine, antidepressants, dopamine agonists, MDMA
- potentiate ADH: DDAVP, cyclophosphamide
- ACEI and PPI-omeprazole
pulmonary causes of SIADH
- infection: tb, pneumonia
2. mechanical/ ventilators: ARDS, COPD
tumour causes of SIADH 5
pulmonary mediastinal small cell cancer duodenum pancreas
CNS disorder causes of SIADH 6
- mass lesions
- inflammatory disease
- degenerative disease
- trauma- subarachnoid haemorrhage
- psychosis
- transsphenoidal adenomectomy
what is the triple phase response of transsphenoidal adenomectomy
- CDI
- remission or SIADH
- then recurrence of permanent DI
other cause of SIADH 3
- aids
- strenuous exercise
- idiopathic
management of SIADH 8
- withold meds
- identify and treat underlying cause
- obtain CXR in all patients with SIADH
- CT
- restrict fluid 800-100ml per day
- oral demeclocycline
- loop diuretic and oral sodium chloride alternative
- tolvaptan v2 receptor antagonist for euvolaemic or hypervolaemic not hypovolaemic
management if hyponatraemia is corrected too quickly
discontinue active treatment
consult for sodium free IV infusion of 10ml/kg body weight
-Desmopressin DDAVP 2mcg
causes of hypernatraemia
pure water loss
water gain
hypernatraemia symptoms
reduced cerebral function dehydration dizziness confused weak coma
hypovlaemic causes of hypernatraemia
haemorrhage vomit diarrhoea burns diuretic state fever hyperventilation
iatrogenic causes of hypernatraemia
diuretic therapy
high sodium intake
reduced water intake causes of hypernatraemia
psychosocial-elderly
glycosuria
excessive sweating
euvolaemic causes of hypernatraemia
water deficit alone
Diabetes insipidus
hypervolaemic causes of hypernatraemia
enteral feeds
IV salt
chronic renal failure
management of hypernatraemia
acute= iv fluid isotonic 6% dextrose or hypotonic 0.45% saline
causes of polyuria 4
- DI
- habitual psychogenic
- osmotic diuresis (from glucose DM), mannitol, hypercalcaemia
- renal impairment
definition of polyuria
urine rate >2ml/kg/hour
what receptors does ADH act on in the kidney
v2 receptors
causes of cranial DI 4
inadequate ADH release congenital pituitary/ hypot head injury intracranial infection
nephrogenic DI causes
AND 2 drugs
7
renal insensitivity congenital hypercalcium hypopotasium obstructive uropathy chronic renal failure drugs -lithium -demeclocycline (for SIADH)
criteria for DI
polyuria that is hypotonic <600mosmol/kg when plasma is hypertonic >300mosmol/kg
conditions for the water deprivation test 3
during test for 8 hours
- no fluids and dry snacks
- hourly weight, bp and urine sample
- 2 hourly blood
- then give DDAVP
what would the results be for a water deprivation test for cranial DI
-after dehydration
then
-after giving DDAVP
- <300 after dehydration (no ADH so cant stop loosing water so urine osmolality low)
- after ddavp >600 as stop loosing water
water deprivation test for nephron DI
<300 after dehdration and after DDAVP as problem with the receptors
what would be the result for partial DI
after dehydration would be 300-600
and then after ddavp would be <600
treatment of DI cranial
give DDAVP ie desmopressin
treatment of DI nephrogenic
- thiazide diuretic/ amiloride diuretic to cause increased sodium excretion and water
- indomethacin to lower intra-renal prostaglandins that oppose ADH
- low salt and low protein diet
treatment for partial DI
use meds that promote SIADH eg chlopropamide which may upregulate renal ADH receptors when ADH partially deficient
pathway of ADH release
high plasma osmolality -> adh release -> kidney v2 receptors -> concentrates and retains water
signs of dehydration
- absent jvp
- dry mucosal membranes
- postural hypotension
- tachycardia
- thirst
- reduced skin turgor
- supine hypotension
- oligouria
- organ failure
- dizziness
- dysphagia
signs of volume excess
- hypertension
- tachycardia
- raised jvp
- nausea
- gallop rhythm
- oedema
- third space gain