Hyponatraemia Flashcards

1
Q

What is mild/moderate/severe hyponatraemia

A
  • Mild: serum sodium concentration of 130-135 mmol/L
    • Moderate: serum sodium concentration of 125-129 mmol/L
    • Severe: serum sodium less than 125mmol/L

IT IS ONLY CLINICALLY SIGNIFICANT IF <125 OR FALLEN RAPIDLY (>20MMOL/L IN 24HOURS)

Hyponatraemia can lead to shift of H2O into cells, with cell swelling ie. cerebral oedema.

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2
Q

What is acute/chronic hyponatraemia

A

• Acute — duration of less than 48 hours.
• Chronic — duration of 48 hours or more.
In practice, most cases of hyponatraemia will be of undetermined duration and should be considered chronic unless there is clinical evidence suggesting otherwise

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3
Q

What is another way to classify hyponatraemia

A
  • Hypertonic or hyperosmolar hyponatraemia (high serum osmolality).
  • Pseudo-hyponatraemia or isotonic hyponatraemia (normal serum osmolality).
  • Hypotonic or true hyponatraemia (low serum osmolality)
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4
Q

How is hypotonic/true hyponatraemia classified?

A
Hypovolemic hyponatraemia (volume depletion).
 Hypervolemic hyponatraemia (volume overload).
Euvolemic hyponatraemia (normal volume status).
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5
Q

What is pseudohyponatraemia?

A

artifactually (falsely) low serum sodium concentration due to hyperproteinaemia (multiple myeloma is the most common cause) or hypertriglyceridemia

AKA normal serum osmolality

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6
Q

What is hypertonic or hyperosmolar hyponatraemia?

A

caused by severe hyperglycaemia (the high levels of glucose draw intracellular water into the extracellular space) or administration of an active osmolyte (such as mannitol)

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7
Q

What is hypovolemic hypotonic hyponatraemia caused by

A

Occurs when the total body water and sodium are both decrease but relative decrease in total body sodium is > than the decrease in total body water
○ Medications especially thiazides
○ Endocrine disorders (primary adrenal insufficiency)
○ Cerebral salt wasting ( a rare cause of hyponatremia from CNS insult e.g aneurysmal SAH, or TBI or surgery)
○ Severe D/V
○ Sweating and extensive skin burns
○ Salt wasting nephropathies e.g tubulopathy after chemotherapy
○ Third space loss e.g bowel obstruction, pancreatitis, severe hypalbuminaemia, sepsis, muscle trauma

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8
Q

What is hypervolemia hypotonic hyponatraemia caused by?

A

occurs when the total body water and sodium are both increase, but the relative increase in total body water > increase in total body sodium- leads to oedema
○ Congestive heart failure
○ Liver disease (cirrhosis with ascites)
○ Kidney disease (AKI, CKD, nephrotic syndrome )

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9
Q

What is euvolemia hypotonic hyponatraemia caused by?

A

Euvolemia (normal volume status) hyponatraemia occurs when total body water increases but total body sodium remains the same, therefore a dilutional effect
○ Drugs e.g SSRI, thiazides
○ SIADH
○ Endocrine disorder secondary adrenal insufficiency, hypothyroidism
○ High water low solute intake e.g primary polydipsia, anorexia nervosa, beer potomania (excessive beer consumption with a low solute diet)

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10
Q

How can you diagnose SIADH?

A

• Euvolemia: No evidence of volume depletion or oedema
• Hyponatraemia
• Hypo osmolarlity
• Inappropriately high urine osmolality and excessive renal excretion of NA+ (Urine >20Na)
• Normal renal, adrenal, pituitary, thyroid
• Not on any drugs (diuretics, antidiuretics)
• Causes are usually:
○ small cell lung cancer,
○ Atypical pneumonia (legionella)
○ Brain damage (e.g Meningitis/SAH), drugs (carbamazepine, SSRI)
• Diagnosis of exclusion!
• Clinical and biochemical improvement on fluid restriction
Treat the underlying cause give tovaptan (competitive ADH receptor antagonist!)

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11
Q

Drugs associated with hyponatraemia? What increase ADH secretion

A
○ Anticonvulsants: carbamazepine 
		○ Anti neoplastics: cyclophosphamide 
		○ Hypoglycaemics: sulphonylureas 
		○ Narcotics: morphine 
               ○ Antipsychotics (such as haloperidol and phenothiazines).
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12
Q

Drugs associated with hyponatraemia? What potentiate ADH

A

○ Tricyclic
○ SSRIs: prozacs
○ Paracetamol
Indomethacin

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13
Q

Drugs associated with hyponatraemia? Diuretics which prevent sodium reabsorption

A

○ Thiazides
○ Frusemide
○ K+ sparing (amiloride, spironolactone)

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14
Q

What is the clinical presentation of hyponatraemia?

A

Usually asymptomatic and picked up incidentally on a blood test
Non specific and related to severity, rate of onset, and intrinsic ability of CNS to adapt to changing osmolar stress and range and degree of comorbidities
• Rapid changes in sodium levels or severe hyponatraemia can cause symptoms such as vomiting, drowsiness, headache, seizures, coma, and cardio-respiratory arrest due to cerebral oedema and raised intracranial pressure.
• Chronic mild hyponatraemia can lead to gait instability, falls, and concentration and cognitive deficits.
Nausea, lethargy, headache, dizziness, postural hypotension, malaise, stupor, ataxia, confusion, psychosis, coma, seizure

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15
Q

What does ADH do?

A

It increases the reabsorption of water by the kidney and prevents excessive loss of water from the body.

• Hyponatraemia is usually associated with a disturbance in ADH secretion
○ ADH disturbances can be physiological (for example hypovolaemia), pathological (for example heart failure), or iatrogenic (for example use of thiazide diuretics)

In most cases of hyponatraemia, there is an inability to suppress ADH
However, in rare cases, ADH is suppressed but there is either excess water intake (primary polydipsia) or a reduced threshold for the release of ADH (reset osmate syndrome) that impairs renal excretion of excess water
The underlying mechanism leading to hyponatraemia depends on the underlying cause

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16
Q

What are the steps in assessing hyponatraemia

A
  1. Check the osmolality- for true hyponatraemia
  2. Check the volume status for hypotonic hyponatraemia
  3. Check the urine sodium/osmality for assessing if it is a problem with the kidney
17
Q

What is step 1 of assessing hyponatraemia

A
  1. Check the serum osmolality

This is a measure of the number of osmotically active solute particles (such as sodium) per kilogram of serum to differentiate between hypertonic (or hyperosmolar) hyponatraemia, pseudo-hyponatraemia (or osmotic hyponatraemia), and hypotonic (or true) hyponatraemia.

A. Serum osmolality >295 mmol/kg (high osmolality) indicates hypertonic hyponatraemia.
○ Consider hyperglycaemia as a spurious cause of hyponatraemia, due to movement of water from the intracellular to extra-cellular space.
○ Administration of hypertonic fluids (such as mannitol and sorbitol) can also cause hypertonic hyponatraemia.

B. Serum osmolality between 275–295 mOsmol/kg (normal osmolality) indicates pseudo-hyponatraemia.
○ Pseudo-hyponatraemia is an artifactually (falsely) low serum sodium concentration due to hyperproteinaemia (in conditions such as multiple myeloma) or hypertriglyceridaemia. The abnormally high concentrations of proteins or lipids in the blood interfere with the accurate measurement of sodium.

C. TRUE Serum osmolality < 275 mmol/kg (low osmolality) indicates hypotonic hyponatraemia.

18
Q

What is step 2 of assessing hyponatraemia

A

Check the volume status for hypotonic hyponatraemia

Assess for pulse rate, postural changes in blood pressure, jugular venous pressure, presence or absence of oedema, and clinical signs of dehydration.

Hypovolaemia= tachycardia, postural hypotension, dry skin and mucous membranes, low urine output, decreased jugular venous pressure, and reduced skin turgor.

Hypervolaemia = peripheral, sacral, and pulmonary oedema, ascites, significant weight gain, and raised jugular venous pressure.

19
Q

What is step 3 of assessing hyponatraemia

A

Check the urine sodium.osmolality

Urine osmolality =measure of the number of osmotically active solute particles (such as sodium) per kilogram of urine, estimate of antidiuretic hormone (ADH) activity and can be used to evaluate the cause of hyponatraemia.

Urinary sodium =concentration of sodium in a litre of urine
Urinary sodium + Volume status may help differentiate the underlying cause of hyponatraemia.

20
Q

what does hypovolaemic hyponatraemia with high urinary sodium >20 suggest

A
LOOSING IN KIDNEYS!
Renal failure 
Diuretic excess 
Osmolar diuresis 
Mineralocorticoid deficiency 
Cerebral salt wasting 
Salt wasting nephropathies
21
Q

what does hypovolaemic hyponatraemia with low urinary sodium <20 suggest

A
GI loss 
Skin loss
Haemorrhagic 
Third spacing 
Diuretic
22
Q

what does euvolaemic hyponatraemia with high sodium >20 in urine suggest

A

SIADH
hypothyroidism
Glucocorticoid deficiency
Diuretics

23
Q

what does euvolaemic hyponatraemia with low sodium <20 in urine suggest

A

Primary polydipsia
Beer potomania
Iatrogenic

24
Q

What does hypervolaemic hyponatraemia with high sodium >20 in urine suggest

A

renal failure

25
Q

What does hypervolaemia hyponatraemia with low sodium <20 in urine suggest

A

Liver failure
Nephrotic syndrome
HF

26
Q

What are some other investigations you can do

A
Urinalysis for urine protein/blood for renal disease
TFTs for hypothyroidism
 Serum cortisol for addison's 
 BNP for Heart failure
LFTs for liver failure
27
Q

What are four questions you need to ask yourself with hyponatraemia?

A
  1. Are they symptomatic/ severe hyponatremia (Do they need Critical Care Assessment?)
  2. What’s the serum osmolality (Is it true hyponatremia?)
  3. What’s the volume status (what type of hyponatremia?)
    What’s the urinary sodium/osmolality (what’s the cause?)
28
Q

Hypovolaemic hyponatraemia treatment

A
FLUID REPLACE
• Give IV 0.9% NaCl
• Restore to normotension
•  Stop diuretics 
•  Give anti-emetics if necessary 
• Severe: hypertonic saline

The amount of Na+ required in hypovolaemic hyponatraemia is determined as follows: Na+ requirement (mmol) = 0.6 x body weight in kg x (desired Na+ - actual Na+ )

Calculate volume of 0.9% saline (150 mmol/L) to be given over 24 hr from this formula.

29
Q

Euvolaemic hyponatraemia treatment

A

• 1st line: Restrict fluid to 1L/day
• Stop diuretics
• HYPOTHYROID: Give liothyronine or L-thyroxine if hypothyroid
• MINERALCORTICOID DEFICIENCY: Replace corticosteroid
• Consider oral sodium
• 2nd Line: vasopressin reducer (demeclocycline 300 mg – 600 mg bd)
Conivaptan can be considered following discussion with the renal team; appropriate adjustments for liver or renal impairment must be made

30
Q

Hypervolaemia hyponatraemia treatment

A
• 1st line: Restrict fluid to 1L/day 
• Restrict sodium intake 
• Give diuretic as necessary 
•  Replace K+ loss 
 Treat underlying disease
31
Q

What is a complication of hyponatraemia

A

Cerebral odema is a life threatening complication of severe and/or acute hyponatraemia
○ If hyponatraemia is severe (less than 125 mmol/L) or develops acutely (in less than 48 hours), the brain does not have time to adapt and cerebral oedema occurs.
Cerebral oedema and raised intracranial pressure can lead to symptoms of vomiting, headache, drowsiness, seizures, coma, and cardio-respiratory arrest

32
Q

What is a complication of chronic hyponatraemia

A

Complications of chronic hyponatraemia: increased falls, bone fractures, osteoporosis, even mild can lead to gait disturbance, falls, [] and cognitive deficits

33
Q

What is central pontine myelinolysis how can this be prevented?

A

plasma sodium is not allowed to increase by 8mmol in 24hrs, should only be 4-6mmol/L
○ Typically 2 days after and usually irreversible: altered mental status, reduced motor functioning (paraparesis, quadriparesis), dysphagia, and/or abnormalities of balance, and can lead to permanent neurological dysfunction, seizures, confusion, and coma
patients are awake but are unable to move or verbally communicate, also called ‘Locked-in syndrome’

34
Q

How many mmols in 24hrs corrected

A

Do not increase the serum sodium by more than 8 mmol per 24 hours as this risks permanent neurological damage (osmotic demyelination)

35
Q

What is the appropriate response of the sodium in the urine to hyponatraemia?

A

Low urinary sodium is an appropriate response to hyponatraemia (i.e. the body is conserving sodium) due to the renin-angiotensin-aldosterone system & ADH being secreted which conserves water (diluting the sodium further). The body releases these hormones whenever it senses the circulating volume and/or pressure isn’t quite right.