Hyponatraemia Flashcards

1
Q

What is normal serum sodium?

A

135-145mmol/l

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2
Q

What is hyponatraemia?

A

Low serum sodium

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3
Q

What are three important facts about hyponatraemia?

A
  1. It is the commonest electrolyte abnormality you will see (20-30% hospital admissions)
  2. It can kill
  3. It is usually caused by an excess of water and is therefore dilutional
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4
Q

What is the total body water percentage?

A

Men: 60% water, 42 litres
Women: 55% water, 38 litres

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5
Q

What are the compartments in which fluids will spread into?

A

-Intracellular (30L)
=locked in by cell membranes
-Interstitial (9L)
=water that bathes cells and peritoneal space (pericardial sac)
-Vascular (3L)
=in vessels/ free water in blood
=Kidneys, guts, (skin, lungs= insensible losses can be up to half a litre of fluid)

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6
Q

How does water move between compartments?

A
  • Ions so water moves to keep osmolality equal on both sides

- Sodium-potassium ATPases= potassium intracellular cation and sodium is extracellular cation

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7
Q

What forces contribute to water movement?

A
  • Internal hydrostatic pressure (out of compartment)
  • External hydrostatic pressure in
  • Internal and external osmotic pressures (pulling into compartments)
  • sodium= external osmotic pressure
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8
Q

How does cerebral oedema occur?

A
  • Dilute sodium-containing fluids (4% dextrose, 0.18% saline)
  • Dilutes extracellular space= hyponatraemia
  • Fluid moves to hypertonic cellular space (osmotic and hydrostatic forces)
  • Cerebral oedema occurs (=confusion)
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9
Q

What is the volume status of hyponatraemia?

A
  • Most people are normal with 55-60% total body water= euvolaemic/ normovolaemic
  • Some people are volume deplete= hypovolaemic
  • Some people are volume overloaded= hypervolaemic
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10
Q

What are the types of hyponatraemia?

A

-Normovolaemic
-Hypovolaemic
-Hypervolaemic
=Clinical signs are generated when there is a difference in the relative size of fluid compartments from normal (extracellular compartment)

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11
Q

What are the clinical signs of hypovolaemia?

A
  • Postural hypotension (dizzy as less perfusion to head)
  • Tachycardia (to maintain cardiac output)
  • Absence of jugular venous pulse at 45 degrees
  • Reduced skin turgor/ dry mucosae (pinch test)
  • Supine hypotension
  • Oliguria (passing smaller volumes of urine)
  • Organ failure
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12
Q

What are the clinical signs of hypervolaemia?

A
  • Hypertension
  • Tachycardia
  • Raised jugular venous pulse at 45 degrees
  • Gallop rhythm (between the two normal)
  • Peripheral and pulmonary oedema
  • Third space gains= peritoneal, pleural and joint spaces
  • Organ failure
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13
Q

What happens during gastroenteritis to blood volume?

A

-Salt-rich diarrhoea
=water loss cannot compensate for Na+ loss so hyponatraemia
-Hydrostatic forces favour water movement from cells to the extracellular space
-Osmotic forces favour the reverse
-Vascular depletion causes hypotension
-Standing up causes postural hypotension and collapse
-Hypovolaemic hyponatraemia

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14
Q

Why does hypovolaemic hyponatraemia occur?

A
  • Common conditions
  • Excessive sodium losses; water losses are insufficient to concentrate sodium back up
  • Depends of volume of water lost and concentration of sodium therein
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15
Q

What are the causes of hypovolaemic hyponatraemia?

A

-Haemorrhage
-Vomiting
-Diarrhoea
-Burns (more evaporation of water)
-Diuretic states (kidneys losing lots of water like diabetes mellites, hypercalcaemia)
-Sequestration (inflammation in compartment draws water in, pneumonia)
-Misc. renal disease
-Heat exposure
-Addison’s disease
-Iatrogenic
=Diuretics
=Stromas/ fistulae
=Gastric aspiration

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16
Q

What are the causes of euvolaemic hyponatraemia?

A

-Water being evenly distributed across all compartments
-Hyponatraemia is dilutional
-Causes:
=Hypotonic intravenous fluids
=hypothyroidism?
=SIADH

17
Q

What are the causes of hypervolaemic hyponatraemia?

A

-Water gains exceed sodium gains
=Heart failure
=Liver failure
=Nephrotic syndrome

18
Q

How does heart failure lead to hypervolaemic hyponatraemia?

A

-Enlarged, pleural effusions
-A reduced cardiac output
=Reduced effective circulating volume
=Reduced organ perfusion
=Physiological correcting mechanism kicks in
=Hypovolaemia wins over tonicity
=Renin/ angiotensin/ aldosterone stimulation
=ADH stimulation
-

19
Q

What do the correcting mechanisms in heart failure result in?

A
  • Sodium retention (aldosterone)
  • Water retention (aldosterone and ADH)
  • Hyponatraemia (from dilution)
  • Fluid overload worsens LV function
  • Hypovolaemia continues to win over hyponatraemia
  • Maladaptive response (cycle worsens)
20
Q

What is SIADH?

A

-Syndrome of inappropriate ADH secretion
-ADH secretion is excessive
=Not suppressed by reduced tonicity (anti-diuretic)
=water reabsorption is excessive
=sodium diluted
-hyponatraemia
-Clinically euvolaemic

21
Q

What is the aetiology of SIADH?

A

-Pituitary hypersecretion/ direct effect:
=Neurological (meningitis, encephalitis, head injury, stroke)
-Ectopic secretion (malignancy):
=SCLC, pancreas, bladder, prostate
=Pulmonary (non-malignant)= TB, pneumonia
-Potentiation of action
=Drugs (thiazide diuretic, carbamazepine, amitriptyline)

22
Q

What is the treatment for hypovolaemia?

A
-Restoration of volume state
=Blood if necessary
=crystalloid (0.9% saline)
-Cessation of diuretics
-Steroids for Addison's
23
Q

What is the treatment for hypervolaemia?

A
-Diuretics
=usually loop diuretics (furosemide/ bumetanide)
-Fluid restriction
-Treatment of underlying cause
=heart attack
24
Q

What is the treatment for euvolaemic hyponatraemia?

A
-Treat underlying cause
=stop IV fluids
-thyroxine replacement
-Fluid restriction
=down to 500ml/day
-Rarely
=demeclocycline (decreases sensitivity to ADH)