Sodium Flashcards

1
Q

Match the following

  1. Mild hyponatraemia
  2. 127-134mmol/L
  3. <135mmol/L

A. Hyponatraemia
B. Self corrects
C. Elevated risk of morbidity and mortality

A
  1. B
  2. C
  3. A
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2
Q

Why do acute cases experience more severe symptoms? (hyponatraemia)

A

Acute cases cause rapid change in osmolality the brain cells cant adapt to. Water moves into the cells causing oedema.

Chronic setting the cells need to re-establish themselves.

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3
Q

What are symptoms of hyponatreamia?

A

They are non-specific and tend to correlate to the degree of cerebral oedema.

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4
Q

What test is done following a serum sodium of <135mmol/L?

A

Follow up testing requires freezing point depression to determine the plasma osmolality. The determination of plasma osmolality will tell the clinician the first indications of causality to the hyponatraemia

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5
Q

Describe the 3 plasma osmolalities causing hyponatraemia

A

Hyper-osmolar hyponatraemia

  • Known as dilutional hyponatraemia
  • Movement of water into the ECF occurs due to the increase in another osmotically active electrolyte, causing the dilution of plasma sodium concentration
  • Main cause hyperglycaemia

Iso-osmolar hyponatraemia

  • Aka pseudonatraemia
  • Occurs because the assumption by indirect ISE that 93% of plasma is water is not true
  • Hypertriglyceridaemia or proteinuria replace water causing the assumption to be false

Hypo-osmolar hyponatraemia

  • Can be due to 3 different volume states: euvolaemic, hypervolaemic, hypovolaemic
  • low plasma osmolality is measured together with a low sodium
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6
Q

What is the 16 for 6 rule?

A

Used to estimate sodium when glucose is abnormally high (works for dilutional hyponatraemia); where for every 16mmol/L increase in glucose will cause sodium to decrease (after glucose has fallen to normal) by 6mmol/L

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7
Q

How can you limit electrolyte exclusion effect causing pseudonatraemia?

A

Use a direct ISE where no dilution step is involved.

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8
Q

If the patient is hypo-osmolar hyponatraemic, what should be done next?

A

Examine volume status to determine if they are: euvolaemic, hypervolaemic, hypovolaemic

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9
Q

Describe how hypervolaemic hyponatraemia can occur?

A

This state can be seen in heart failure, cirrhosis or nephrotic syndrome. The plasma and ECF volumes are increased in heart failure and cirrhosis, but there is a ADH stimulation.

Retention of water is greater than sodium
- Urine Na+ and osmolality reflect Na+ and H2O retention

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10
Q

Describe how hypovolaemic hyponatraemia can occur?

A

Here loss of sodium is greater than water. Can be caused by renal or non-renal causes. This state is often seen in patients on diuretics.
Patient experiences fluid loss stimulating ADH release and thirst. Results in water retention, by drinking hypotonic fluid - causes dilutional hyponatraemia.

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11
Q

How is the cause for hypovolaemic hyponatraemia caused?

A

Investigated by measuring the urine sodium, where a renal sodium of <20 is extra renal fluid loss (G losses, skin lossses) and >20 is renal fluid loss (diuretics, salt-wasting nephropathy, cerebral salt wasting, hypoaldosteronism).

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12
Q

How does euvolaemic hyponatraemia occur?

A

This is a condition where the water content is normal but the sodium conc is low. Most common hyponatraemia in hospitalised patients. What happens is that a normal Na conc will be diluted during a acute/chronic overload.
The cause can be further investigated using urine osmolality. A urine osmolality of <100 is due to primary polydipsia, reset osmostat, beer potomania
A urine osmolality of >100 can be due to SIADH, adrenal insufficiency, diuretics, and hypothyroidism.

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13
Q

What is a common syndrom of ADH?

A

syndrome of inappropriate ADH (SIADH)

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14
Q

What is SIADH?

A

A non-physiological release of ADH, which can be diagnosed by meeting a criterion of associated biochemical effects

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15
Q

How is SIADH diagnosed?

A

Using a criteria of biochemical effects. This criteria differs between places, but commonly include: hyponatraemia, plasma hypo-osmolality, inappropriate concentration of urine, euvolemic, normal renal, adrenal, and thyroid function, and lastly urine Na>20mmol/L

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16
Q

Describe SIADH interms of sodium?

A

Dilutional hyponatraemia as there is normal water, but abnormal retention causing sodium to dilute.

17
Q

What is the cause of SIADH?

A

Due to increased hypothalamic secretion, ectopic ADH production, potentiation of existing ADH (kidney), or exogenous analogues of ADH

18
Q

What causes the increased hypothalamic secretions (SIADH)?

A

Neuropsychiatric (infections, trauma, inflammation), drugs (SSRI, tricyclins), pulmonary (infection), post-op, severe nausea or idiopathic

19
Q

What causes the increased ectopic ADH (SIADH)?

A

Associated with thoracic tumours (small cell lung cancer, carcinoid, thyoma, bronchiogenic), non-thoracic tumours (pancreas, duodenal, prostate, bladder).

20
Q

How is hyponatraemia treated?

A

The clinician can choose to treat it using fluid replacement or fluid restrictions.
Acute: 1-2mmol/L per hour for 3-4h or until asymptomatic, but still <10-12mmol/L in the first 24h

Chronic: <10-12mmol/L in the first 24hrs and by <18mmol/L in the first 48hrs

21
Q

What is the main risk to correcting hyponatraemia?

A

The main risk of correcting hyponatraemia is central pontine myelinolysis, a severe neurological disorder, due to rapid over correction of hyponatraemia. Central pontine myelinolysis is characterised by paraparesis, quadriparesis, mutism, dysphagia. Patients with severe chronic hyponatraemia are at the most risk

22
Q

What does hypernatraemia imply?

A

There is a negative water balance relative to sodium

23
Q

What are the causes to hypernatraemia

A

pure water loss, hypotonic fluid loss, salt gain

24
Q

How is pure water intake deficit causing hypernatraemia?

A

It is a combination of inadequate water intake together with normal fluid losses, commonly seen in elderly, babies, decreased sense of thirst, or patients with oesophageal obstruction, or diabetes insipidus

25
Q

What are some causes of sodium overload causin hypernatraemia?

A

Salt gain is very uncommon but can be caused iatrogenic using IV hypertonic saline or IV sodium bicarbonate. Also includes when mineralocorticoid is in excess

26
Q

How should hypernatraemia be treated?

A

Treatment of hypernatraemia will require the administration of fluid replacement using a 0.9% saline with 5% glucose at a rate of <10-12mmol/L per day to help restore hydration.

27
Q

What are the differences between the types of IV?

A

They are administered as fluid replacment as crystalloid or colloid solutions.
The crystalloid solutions contain low molecular weight salt and sugars that dissolve in water and can pass freely between intravascular and interstitial space. Whereas the colloid solutions have large molecular weight substances that do not dissolve in water and remains in the vascular space for a longer time. Colloids expand circulating blood volume to minimal risk of oedema

28
Q

What 3 crystalloids are available in care?

A

Isotonic, hypertonic and hypotonic crystalloid

29
Q

When are hypotonic crystalloids administered?

A

act to cause fluid shift from ECF to ICF, e.g. half-normal saline to treat dehydration from hypernatraemia, metabolic acidosis, DKA

30
Q

When are hypertonic crystalloids administered?

A

contain large amounts of solutes used to move fluid from cells into intravascular spaces incl bloodstream

31
Q

When are hypertonic crystalloids administered?

A

Are the most common, e.g. normal saline, and are used in dehydration caused by electrolyte imbalances and fluid losses