Sodium Imbalances Flashcards

1
Q

State the symptoms of hypernatraemia

A
  • Lethargy
  • Weakness
  • Confusion
  • Hyperreflexia
  • Reduced consciosness
  • Seizures
  • Coma
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2
Q

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

A

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
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3
Q

The high serum Na+ concentration in hypernatraemia causes fluid to move out of cells into vasculature; describe two consequences of this

A
  • Cellular dehydartion (high Na+ in plasma draws water out of cells)
  • Creates vascular shear stress leading to bleeding and thrombosis
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4
Q

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

A

Cranial DI

  • Trauma/post-op
  • Tumour
  • Infection
  • Cerebral sarcoid or TB
  • Cerebral vasculitis (SLE)

Nephrogenic DI

  • Congenital
  • Drugs e.g. lithium, amphoterecin
  • Hypokalaemia
  • Hypercalcaemia
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5
Q

What does a pt need to have to support a diagnosis of diabetes insipidus?

A
  • 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

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6
Q

What specific test can we do to confirm diagnose diabetes insipdus?

A

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
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7
Q

What investigations would you do for someone with suspected hypernatraemia, include:

  • Bedside
  • Bloods
  • Imaging

(where appropriate)

A

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
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8
Q

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
A
  • 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
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9
Q

Discuss the management of hypernatraemia

A
  • 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

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10
Q

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?

A
  • 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
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11
Q

State and describe the main complication of hypernatraemia

HINT: it is treatment related

A

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.

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12
Q

State some symptoms of hyponatraemia

A

NOTE: initially anorexia, nausea and malaise followed by others.

  • Headache
  • Nausea/vomiting
  • General malaise
  • Decreased strength
  • Gait disturbance
  • Reversible ataxia
  • Anorexia
  • Confusion
  • Seizures
  • Coma
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13
Q

What is pseudohyponatraemia?

State some possible causes of pseudohyponatraemia

A
  • Falsely low Na+ levels
  • Causes:
    • High lipids
    • Myeloma
    • Hyperglycaemia
    • Uraemia
    • Hyperprtoeinaemia
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14
Q

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

A

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
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15
Q

State what investigtions you would do if you suspect hyponatraemia, include:

  • Bedside
  • Bloods
  • Imaging
A

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
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16
Q

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
A
  • 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,
17
Q

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?

A

FALSE

Treat acute and/or symptomatic different to chronic and/or asymptomatic

18
Q

What time period do we consider hyponataemia to be acute?

What time period do we consider hyponatraemia to be chronic?

A
  • Acute <48hr
  • Chronic >48hr
19
Q

Discuss the management of acute or symptomatic hyponatraemia; think about how management differs for severe and mild symptoms

A

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

20
Q

Discuss the management of chronic (>48hrs) hyponatraemia without severe symptoms:

  • Hypovolaemic hyponatraemia
  • Euvolaemic hyponatraemia
  • Hypervolaemic hyponatraemia
A

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
21
Q

What Na+ correction, in mmol/L, should you aim for in a 24hr period when correcting hyponatraemia?

A

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

22
Q

State some potential complications of hyponataemia

A
  • 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
23
Q

State a potential complication of correcting hyponatraemia too quickly

A

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
24
Q

Explain how SIADH secretion leads to euvolaemic hyponatraemia

A
  • 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
25
Q

State two possible sources of ADH in SIADH

A
  • Posterior pituitary secreting too much ADH
  • ADH from ectopic site e.g small cell lung cancer
26
Q

State some potential causes of SIADH

A
  • 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
27
Q

SIADH is a diagnosis of exclusion; explain how we arrive at this diagnosis- include tests/results that use do to rule out other causes

A
  • 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
28
Q

Discuss the management of hyponatraemia casued by SIADH

A

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
29
Q

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?

A

True

30
Q

Disuss how you could assess a pts fluid balance- think about signs that would suggest pt is underfilled or overfilled

A
31
Q

Discuss the management of diabetes insipidus

A
  • 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
32
Q
A