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FFICM > Hyponatraemia > Flashcards

Hyponatraemia Flashcards

1
Q

What is the normal range of serum sodium?

A

135 - 145 mmol/L

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2
Q

What is the typical total sodium in the human body (in mmol/Kg)

A

~ 60 mmol/Kg

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3
Q

What is the daily maintenance requirement of sodium? (in mmol/Kg/day)

A

1-2 mmol/Kg/day

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4
Q

Define hyponatraemia

A

A true serum sodium concentration < 135 mmol/L

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5
Q

How common is hyponatraemia in acute hospital admissions?

A

Very. It is either a primary presentation or co-presentation in up to 30% of all acute hospital admissions. Making it the most common electrolyte abnormality by far.

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6
Q

Under normal physiological conditions, what percentage does sodium contribute to plasma osmolality?

A

~ 85%

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7
Q

How might you classify hyponatraemia?

A

There are 5 different domains against which you can classify hyponatraemia:
1. Serum Na concentration
2. Symptoms
3. Measured serum osmolality
4. Volume status
5. Rate of onset

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8
Q

What are the classifications of hyponatraemia by serum Na concentration?

A
  • Mild (Na 130 - 135 mmol/L)
  • Moderate (Na 125 - 129 mmol/L)
  • Profound (Na < 125 mmol/L)

Note, “profound” is preferred to “severe” to avoid conflating with classification by symptoms, where “severe” is used.

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9
Q

What are the classifications of hyponatraemia by symptoms?

A
  • Moderately severe: nausea (without vomiting), confusion or headache
  • Severe: Vomiting, cardio-respiratory distress, deep somnolence, seizures, coma
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10
Q

What are the classifications of hyponatraemia by measured serum osmolality?

A
  • Hypotonic: < 275 mOsm/Kg
  • Non-hypotonic:
    • Iso-tonic: 275-295 mOsm/Kg
    • Hyper-tonic: > 295 mOsm/Kg

This must be measured and not calculated

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11
Q

What are the classifications of hyponatraemia by volume status?

A
  • Hypovolaemic
  • Euvolaemic
  • Hypervolaemic

There is in-consistency in the literature as to what exactly this refers to. Throughout, I reference this in relation to the effective circulating volume. Clinical tests of volume status in general have poor sensitivity, so this should no longer be used as the first part of your clinical assessment of hyponatraemia.

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12
Q

What are the classifications of hyponatraemia by rate of onset? What is the utility of this classification?

A
  • Acute: documented < 48 hours
  • Chronic: > 48 hours or undocumented and hence assumed.

Generally, it is safe to correct hyponatraemia at the rate at which it occurred. Chronic hyponatraemia should therefore be correctly more slowly. Without proof, one should always assume chronic, because it is more common, and safer to correct slowly if you are uncertain (to prevent osmotic demyelination)

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13
Q

Define calculated total osmolality

A

The concentration of all solutes in a given mass of water (mOsm/Kg)

Osmolality = 2([Na] + [K]) + [glucose] + [urea]

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14
Q

Define effective osmolality.

A

Effective osmolality is the concentration of all effective osmoles; solutes that contribute to an osmotic gradient.

Effective osmolality = 2([Na] + [K]) + [Glucose]

Urea is omitted, because it is not an effective osmole (it is free to cross semi-permeable membranes)

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15
Q

What are the main mechanisms responsible for water and sodium regulation?

A
  • Thirst
  • Vasopressin
  • Renin-Angiotensin-Aldosterone pathway
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16
Q

What is the vasopressin plasma osmotic threshold?

A

Around 280 mOsm/Kg; this is the osmolality at which vasopressin release is stimulated

17
Q

What is the osmotic thirst threshold?

A

Around 285 mOsm/Kg

Note, this is around 5 mOsm/Kg higher than the vasopressin osmotic threshold, ensuring that vasopressin is released before thirst is triggered. Otherwise one would feel thirsty most of the time

18
Q

Describe the relationship between urine osmolality and urine volume.

A

This is an inverse relationship; i.e. as urine osmolality is increased, its volume is decreased. This is largely achieved by the action of vasopressin to control the amount of free water present in the urine.

19
Q

Summarise the synthesis and release triggers for vasopressin.

A

The anterior hypothalamus is stimulated to increase vasopressin production by angiotensin II receptors (from low BP) and by a rise in plasma osmolality (lower free water, or raised solutes), detected by osmoreceptors that lie outside the blood brain barrier in the organum vasculosum of the lamina terminalis (OVLT) and the subfornical organ (SFO). Vasopressin is then transferred down neuronal axons and released from the posterior pituitary.

20
Q

Summarise the principle actions of vasopressin

A
  • Binds to V2 receptors in the principle cell of the collecting ducts
  • These are Gs protein coupled (GDP –> GTP, adenylate cyclase activation, ATP –> cAMP –> PKA –> Enzyme phosphorylation)
  • Nuclear transcription is enhanced to produce aquaporin-2 channels, which insert into the apical membrane
  • Free water is resorbed restoring plasma water and osmolality
  • A lesser effect is also to bind to V1 (Gq) receptors in vascular smooth muscle, causing some vasocontriction
21
Q

What is pseudohyponatraemia?
Which conditions might lead to this?

A

A falsely low serum sodium measurement caused by laboratory artefact.
Generally occurs when high lipid or protein content interfears with measurement, because serum is diluted by a fixed amount prior to measurement, and the measurement assumes a constant 7% solid phase of the sample (which is incorrect with excess lipid or protein)
This problem does not occur in a blood gas analyser, which uses a potentiometer on an undiluted sample.

22
Q

Will the measured osmolality be abnormal in pseudohyponatraemia?

A

Generally no (unless there is another co-existing pathology that would alter it).
This is because, unlike sodium measurement, the osmolality measurement is not diluted prior to analysis, and so the presence of excess lipid/protein does not impact the result.

23
Q

What is the most common tonicity of hyponatraemia

A

Hypotonic is the most common:
Sodium is low, and the serum osmolality is commensurately low. I.e. they are in agreement.

24
Q

How might you generate a hypertonic hyponatraemia?

A

The presence of effective osmoles may attract water, diluting the serum sample (causing the hyponatraemia) while exerting enough osmotic pressure on its own to raise the measured serum osmolality above normal.

25
Q

What are the causes of hypertonic/isotonic hyponatraemia?

A

Hypertonic:
- Glucose
- Mannitol
- Glycine
- Histodome-tryptophane-ketoglutarate (used in the preservation of transplant organs)
- Hyper-osmolar radiocontrast

Generally, these would also be a cause of isotonic hyponatraemia (just in lower concentration). Since Na is such a major contributor to osmolality, it has to be replaced by something osmotically active for the toniticy to even remain the same.

26
Q

What will the osmolar gap be in hypertonic hyponatraemia?

A

Unless caused by glucose, it will be raised.
Since the other causative agents are not included in the calculation of serum osmolality

27
Q

How should you further sub-classify hypotonic hyponatraemia?

A

By effective cirulatory volume:
- Low (reduced ECF)
- Normal (normal ECF)
- High (increased ECF)

28
Q

What are the main causes of hypotonic hyponatraemia with a reduced effective circulatory volume (reduced ECF)?

There are lots, so please structure your answer.

A
  • Non-renal sodium loss
    • Severe diarrhoea
    • Severe vomiting
    • Excessive sweating
    • Burns
    • Cystic fibrosis
  • Renal sodium loss
    • Diuretics (particularly thiazides)
    • Primary adrenal insufficiency
    • Cerebral salt wasting
    • The salt loosing nephropathies
  • Inflammatory losses
    • Sepsis
    • Bowel obstruction
    • Pancreatitis
    • Trauma
29
Q

What are the main causes of hypotonic hyponatraemia with a normal effective circulatory volume (normal ECF)?

A
  • SIADH
  • Secondary adrenal insufficiency
  • Hypothyroidism (this is always part of a hyponatraemia workup, but in practice, this is incredibly rare as a cause of hyponatraemia
  • High water, low solute intake: primary polydipsia, beer potomania, tea and toast hyponatraemia
30
Q

What are the main causes of hypotonic hyponatraemia with a increased effective circulatory volume (increased ECF)?

A

Advanced kidney disease
Heart failure
Liver failure
Nephrotic syndrome

31
Q

What are some “common” causes of an acute hyponatraemia?

A

TURP syndrome
Polydipsia
Excessive exercise
Drug induced:
- New thiazide prescription
- MDMA
- Colonoscopy prep
- Cyclophosphamide
- Oxytocin
- Desmopressin
- Terlipressin (or vasopressin)

32
Q

Does hyperglycaemia cause a pseudo-hyponatraemia?

A

No. This is a common misconception.
Hyperglycaemia will draw water into the extra-cellular space and cause a dilutional (isotonic/hypertonic) hyponatraemia.

However, you can predict what the sodium will be following correction of the hyperglycaemia, and if normal, the hyponatraemia will require no treatment beyond correction of the hyperglycaemia

33
Q

What is an appropriate formula to calculate the predicted sodium attributable to correction of hyperglycaemia?

A

Na (predicted) = Na (measured) + 2.4 x {(glucose - 5.5)/5.5}

All in mmol/L

34
Q

Which patients are at particular risk of osmotic demyelination syndrome?

A

Pre-menopausal women
Children

FFICM (3 decks)

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