Sodium Imbalances Flashcards
State the symptoms of hypernatraemia
- Lethargy
- Weakness
- Confusion
- Hyperreflexia
- Reduced consciosness
- Seizures
- Coma
To help us think about causes of hypernatraemia, we can think about:
- Hypovolaemic hypernatraemia
- Euvolaemic hypernatraemia
- Hypervolaemiac hypernatraemia
… state some example causes in each category
Hypovolaemia hypernatraemia
- Renal water losses e.g. osmotic diuresis such as with NG tube, loop diuretics, HHS
- Non-renal water losses e.g. sweating, burns, diarrhoea, fistulas
Euvolaemic hypernatraemia
- Renal losses e.g. diabetes insipidus,
- Extra-renal losses e.g. insensible respiratory loses
Hypervolaemic hypernatraemia (Na gain)
- Primary hyperaldosteronism, Cushing’s, hypertonic dialysis, hypertonic sodium bicarb, NaCl tablets, excessive saline
The high serum Na+ concentration in hypernatraemia causes fluid to move out of cells into vasculature; describe two consequences of this
- Cellular dehydartion (high Na+ in plasma draws water out of cells)
- Creates vascular shear stress leading to bleeding and thrombosis
Diabetes insipidius can cause hypernatraemia (but doesn’t always). Diabetes insipidus can be split into cranial DI and nephrogenic DI. State some potential causes of each
Cranial DI
- Trauma/post-op
- Tumour
- Infection
- Cerebral sarcoid or TB
- Cerebral vasculitis (SLE)
Nephrogenic DI
- Congenital
- Drugs e.g. lithium, amphoterecin
- Hypokalaemia
- Hypercalcaemia
What does a pt need to have to support a diagnosis of diabetes insipidus?
- Urine volume >3L /24hr
- High serum osmolality (>295mOsm/kg)
- Low urine osmolality (<300mOsm/kg)
*DI excluded if urine somolality >600mOsm/kg or double serum osmolality
What specific test can we do to confirm diagnose diabetes insipdus?
Water Deprivation Test
Part 1
- Pt comes in in the morning:
- Empty bladder, record vol & osmolality
- Take serum osmolality
- Record pts weight
- Pt must then not drink
- Record weight & urine osmolality every hr
- Record serum osmolality every 2hr
- If pt has diabetes insipidus won’t have usual actions of ADH (inserteing aquaporins into CD) hence pt won’t be able to concentrate urine and osmolality of urine will be low
Part 2
Pt is then given synthetic vasopressin to help distinguish between neurogenic & nephrogenic diabetes insipidus:
- Neurogenic: urine osmolality will increase
- Nephrogenic: no response to vasopressin
What investigations would you do for someone with suspected hypernatraemia, include:
- Bedside
- Bloods
- Imaging
(where appropriate)
Bedside
- Urine osmolalilty: help determine cause
- Urine electrolytes: so you can determine electrolyte free water
- Urine flow rate: needs careful monitoring
Bloods
- U&Es
- Serum osmolarity: hypernatraemia also associated with serum osmolarity
Imaging
- MRI or CT brain: reccommended in all pts with diabetes insipidous to identify cause. Look for cerebral bleeding too- caused by hypernatraemia
What would the following suggest about cause of hypernatraemia:
- Low urine osmolality/ urine osmolality < plasma osmolality
- Urine osmolality > plasma osmolality
- Urine osmolality roughly = plasma osmolality
- Low urine osmolality suggests diabetes insipidus
- Pure volume depletion not due to diabetes insipidus e.g. due to GI losses
- Inability of renal system to concentrate urine; could be due to e.g. renal failure, osmotic diuersis, diuretics
Discuss the management of hypernatraemia
- If patient hypovolaemic, give 0.9% NaCl first to correct hypovolaemia (relatively hyponatraemic in hypernatraemic patient)
- If not hypovolaemic, 4% or 5% dextrose should be given (must monitor for hyperglycaemia)
Can use free water deficit calculation to help assess severity of water depletion.
*NOTE: FC initially said first line is ideally oral fluids (water)- consider NG it pt can’t swallow but this is not on any guidelines
At what rate/time scale should you aim to correct water deficit/hypovolaemia in hypernatraemia?
At what rate should you aim to correct Na+ in hypernatraemia?
At what rate/time scale should you aim to correct hypernatraemia?
- Correct water deficit/hypovolaemia over 24-48hrs
- Aim to correct sodium no more than 12mmol/24hr (0.5mmol/hr)
- Aim to correct sodium over 48-72hrs
State and describe the main complication of hypernatraemia
HINT: it is treatment related
Cerebral odema; if treating chornic hypernatraemia the lowering of serum osmolality too quickly can lead to water moving into brain cells causing them to swell.
State some symptoms of hyponatraemia
NOTE: initially anorexia, nausea and malaise followed by others.
- Headache
- Nausea/vomiting
- General malaise
- Decreased strength
- Gait disturbance
- Reversible ataxia
- Anorexia
- Confusion
- Seizures
- Coma
What is pseudohyponatraemia?
State some possible causes of pseudohyponatraemia
- Falsely low Na+ levels
- Causes:
- High lipids
- Myeloma
- Hyperglycaemia
- Uraemia
- Hyperprtoeinaemia
Like with hypernatraemia, we can classify causesof hyponatraemia into hypovolaemic, euvolaemic and hypervolaemic; state some example causes of each
*More important to consider fluid balance when assessing for cause of hyponatraemia
Hypovolaemic Hyponatraemia
- Renal losses
- Diuretics (thiazides), osmotic diuresis (glucose, urea), Addison’s
- Non renal losses
- Diarrhoea, vomiting, sweating, third spaces losses (burns, small bowel obstruction, pancreatitis)
Euvolaemic Hyponatraemia
- Hypothyroidism
- Primary polydipsia/water overload (urine osmolality <100)
- Adrenal insufficiency
- SIADH (NOTE: carbamezapine can cause SIADH and therefore cause hyponatraemia)
Hypervolaemic Hyponatraemia
- Congestive cardiac failure
- Nephrotic syndrome
- Liver cirrhosis
State what investigtions you would do if you suspect hyponatraemia, include:
- Bedside
- Bloods
- Imaging
Bedside
- Urine Na+
- Urine osmolality
- Serum osmolality
Bloods
- Plasma osmolality
- U&Es: hypokalaemia can potentiate ADH release
- TSH: hypothyroidism can cause euvolaemic hyponatraemia
- 9am cortisol: adrenal insufficiency
- Magnesium: hypomagnesaemia can potentiate ADH release
- Calcium: can cause psuedohyponatraemia
- Albumin: hyperproteinaemia can cause pseudohyponatraemia
- Glucose: hyperglycaemia can cause psuedohyponatraemia
- LFTs:
Imaging
- CT head or chest: if suspect SIADH
We can use the urine Na+ concentration, in combination with pts volume status, to further narrow down causes of hyponatraemia. State what each of the following would indicate:
- Hypovolaemic with urine [Na+] <20mmol/L
- Hypovolaemic with urine [Na+] >20mmol/L
- Hypervolaemic with urine [Na+] <20mmol/L
- Hypervolaemic with urine [Na+] >20mmol/L
- Hypovolaemic with urine [Na+] <20mmol/L
- Non-renal losses e.g. GI losses
- Hypovolaemic with urine [Na+] >20mmol/L
- Renal losses e.g. diuretics
- Hypervolaemic with urine [Na+] <20mmol/L
- Non-renal e.g. CCF, cirrhosis, neprhotic syndrome
- Hypervolaemic with urine [Na+] >20mmol/L
- Renal e.g. AKI, CKD,
Treatment of hyponatraemia is the same regardless of if it occurs acutely and pt is symptomatic or if it occurs chronically and pt is asymptomatic; true or false?
FALSE
Treat acute and/or symptomatic different to chronic and/or asymptomatic
What time period do we consider hyponataemia to be acute?
What time period do we consider hyponatraemia to be chronic?
- Acute <48hr
- Chronic >48hr
Discuss the management of acute or symptomatic hyponatraemia; think about how management differs for severe and mild symptoms
Acute hyponatraemia and moderate or severe symptoms: seek expert help (e.g. ICU) hypertonic saline IV +/- furosemide
Acute and asymptomatic or have mild symptoms: isotonic IV fluids (e.g. 0.9% NaCl) +/- furosemide
AND TREAT UNDERLYING CAUSE
Discuss the management of chronic (>48hrs) hyponatraemia without severe symptoms:
- Hypovolaemic hyponatraemia
- Euvolaemic hyponatraemia
- Hypervolaemic hyponatraemia
Hypovolaemic Hyponatraemia
-
Isotonic IV fluid
- Can give boluses of 250ml-1000ml if pt is very hypotensive. Then do infustion at a rate of 0.5-1ml/kg/hr) - BMJ says.
- Or if pt doesn’t need boluses, do infusion of isotonic IV fluid at 1-3ml/kg/hr (workbook)
- Treat underlying cause
Euvolaemic Hyponatraemia
- Fluid restriction (~500ml less than their urine output)
- Treat underlying cause
- If fluid restriction doesn’t work consider ADH antagonist
Hypervolaemic Hyponatraemia
- Fluid restriction (~500ml less than their urine output)
- Treat underlying cause
- Consider loop diuretic or spironolactone
- Consider vasopressin antagonist
What Na+ correction, in mmol/L, should you aim for in a 24hr period when correcting hyponatraemia?
Aim to correct 8mmol/L in 24hr
**PASSMED says 4-6mmol/l per 24hrs. Some guidelines say in severe can correct up to 10mmol first 24hr then 8mmol/24hr thereafter
State some potential complications of hyponataemia
- Cerebral oedema: if serum sodium changes rapidly (e.g. pt has acute hyponatraemia) the brain doesn’t have time to adapt causing water to move into brain cells- this is why pts can have seizures, comas etc…
- Increased risk of falls in elderly
- Long term chornic hyponatraemia associated with osteoporosis
State a potential complication of correcting hyponatraemia too quickly
Central pontine/osmotic myelinolysis:
- Irreversible and often fatal pontine demyelination
- Seen in malnourished alcoholics or rapid correction of sodium
- Symptoms usually occur after 2 days:
- Lethargy
- Confusion
- Pseudobulbar palsy (dysarthria, dysphagia)
- Para or quadrapesis
- Locked in syndrome
- Coma
Explain how SIADH secretion leads to euvolaemic hyponatraemia
- Excessive ADH causing water reabsorption in the collecting ducts
- Dilutes Na+ in blood so leads to hyponatraemia
- The excessive water reabsorption is not enough to case hypervolaemic hyponatraemia hence end up with euvolaemic hyponatraemia
State two possible sources of ADH in SIADH
- Posterior pituitary secreting too much ADH
- ADH from ectopic site e.g small cell lung cancer
State some potential causes of SIADH
- Post-operative from major surgery (abdo or thoracic)
- Infection, particularly atypical pneumonia and lung abscesses
- Head injury
- Medications (thiazide diuretics, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDs, PPIs)
- Malignancy, particularly small cell lung cancer
- CNS disorders e.g. meningitis, SAH, stroke
SIADH is a diagnosis of exclusion; explain how we arrive at this diagnosis- include tests/results that use do to rule out other causes
- U&Es show hyponatraemia
- Euvolaemic state
- Urine Na+ and osmolality= high
- Other causes of hyponatraemia need to be excluded:
- Negative short synacthen test to exclude adrenal insufficiency
- Normal thyroid function tests
- No history of diuretic use
- No diarrhoea, vomiting, burns, fistula or excessive sweating
- No excessive water intake
- No chronic kidney disease or acute kidney injury
Discuss the management of hyponatraemia casued by SIADH
SIADH causes euvolaemic hyponatraemia hence treat as we would treat any euvolaemic hyponatraemia with few extra considerations:
- Fluid restrict (usually <800ml a day)
- May give furosemide
- Tolvaptans (ADH antagonists)
- Demeclocycline (tetracycline antibiotic that inhibits ADH) *RARELY USED
Tolvaptans are very powerful and can cause rapid increase in Na+ hence they are usually initiated by specialist endocrinologist and Na+ levels must be monitored every few hours; true or false?
True
Disuss how you could assess a pts fluid balance- think about signs that would suggest pt is underfilled or overfilled
Discuss the management of diabetes insipidus
- Pts should be investigated for pituitary disease & managed as appropriate
- Cranial DI
- Desmopressin (trade name DDAVP)
- Nephrogenic DI
- Underlying cause should be considered and reveresed where possible
- Advise pt to drink according to thirst and keep up with water loss
- Low salt & low protein diet
- Diuretics e.g. Thiazides (in DI they increase concentration of urine and decrease amount passed from body)
- NSAIDs
