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MSC: Disease of major orgns > Hyponatraemia > Flashcards

Hyponatraemia Flashcards

1
Q

What are consequences of Hyponatraemia on the brain?

A

Acute

  • Rapid change in osmolality
  • Brain cannot adapt quickly enough
  • H2O moves into cell
  • Cell swells

Chronic

  • Progressive change in osmolality
  • Brain adapts
  • Decreases the osmotic contents of its cells
  • Limits degree of cell swelling
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2
Q

What are Symptoms of Hyponatraemia?

A
  • General malaise
  • GI disturbances: Anorexia, Nausea, Vomiting
  • Cramps
  • Weakness
  • Headache
  • Confusion
  • Disorientation
  • Agitation
  • Delirium
  • Lethargy
  • Seizures
  • Coma
  • Death
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3
Q

How do the symptoms present based on disease progression?

A
  • Symptoms correlate with degree of cerebral over-hydration
  • Therefore severity of symptoms correlates with the rate of sodium change.
  • Acute hyponatraemia leads to severe symptoms
  • Chronic Hyponatraemia leads to mild symptoms
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4
Q

What leads to hyperosmolar hyponatraemia?

A
  • Due to presence of an effective solute in the ECF which creates an osmotic gradient. H2O moves out of cell and into the ECF
  • This causes “Dilutional hyponatraemia”
  • H2O will move from an area of low Osmolality to an area of High Osmolality
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5
Q

What are causes of Hyperosmolar Hyperglycaemia?

A
  • HYPERGLYCAEMIA: DKA (diabetic ketoacidosis) and HHS (hyperglycaemic hyperosmolar state)

Other rarer causes:

  • MANNITOL
  • SORBITOL
  • MALTOSE
  • RADIOCONTRAST DYE
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6
Q

How is correcting for sodium measurement in the event of hyperglycaemia done?”

A
  • “16 for 6 rule” (other formulae exist)
  • For every 16 mmol/L increase in glucose, sodium will decrease by 6 mmol/L
  • This allows estimation of ‘true’ sodium assuming patient was normoglycaemic
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7
Q

What are causes of Iso-osmolar hyponatraemia (AKA “PSEUDOHYPONATRAEMIA”)?

A

1. HYPERTRIGLYCERIDAEMIA

  • Triglycerides >50 mmol/L e.g. Pancreatitis

2. HYPERPROTEINAEMIA

  • Total protein >150 g/L e.g. Multiple myeloma
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8
Q

Why does hyperosmolar hyponatraemic occur in hyperglycaemic states?

A

In a hyperglycaemic state dilutional hyponatremia occurs due to shift of water from the intracellular to the extracellular compartment secondary to hyperglycemia and increased plasma osmolality

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9
Q

Why is hyponatraemia not associated with increased concentrations of urea or ethanol?

A
  • Urea and ethanol are able to freely cross cell membranes and distribute themselves evenly between the ECF and ICF.
  • No osmotic gradient established.
  • These are not considered effective solutes.
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10
Q

How does electrolyte exclusion effect in pseudohyponatraemia?

A
  • Indirect ISEs measure Na+ concentration in the plasma H2O
  • Assumes plasma is 93% H2O
  • If increased lipid/increased protein, a fraction of the plasma H2O space is replaced
  • The Na+ concentration in the plasma H2O is normal but now each litre of plasma contains <93% H2O
  • So Na+ concentration per litre of total plasma is lower
  • Analytical phenomenon for indirect ISE’s
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11
Q

What is hypoosmolar hyponatraemia?

A
  • Most common type of hyponatraemia
  • Plasma osmolality is appropriately low (<275 mOsm/kg)
  • Usually associated with H2O retention. Excess H2O in relation to solute (Na+)
  • Termed “Dilutional hyponatraemia” as well
  • Generally cannot occur if there is no H2O intake
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12
Q

What are different volume statuses assessed in Hypoosmolalar Hyponatraemia?

A
  • Hypovolaemic: Dehydrated and Fluid Deplete
  • Euvolaemic: Normal Hydration
  • Hypervolaemic: Oedematous and Fluid overloaded
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13
Q

How is volume status assessed in hypo-osmolar hypovolaemia?

A

Can be difficult to assess. Clinical diagnosis (mainly)

Clues from:

  • Clinical history, e.g. vomiting, diarrhoea, fluid intake
  • Lab results, e.g. urea, creatinine
  • Physical examination: Blood pressure, Heart rate, Dry skin / mucus membranes, Skin turgor
    *
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14
Q

What are causes of Hypervolaemic Hyponatraemia?

A
  • HEART FAILURE
  • CIRRHOSIS
  • NEPHROTIC SYNDROME

Hyponatraemia in these patients is often secondary to diuretics but hyponatraemia can be secondary to severe defect in renal water excretion and salt handling

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15
Q

How does Hypervolaemic hyponatraemia occur?

A
  • Decrease in effective ECF volume
  • Activation of RAAS and ADH release
  • Leads to Sodium reabsorption and water retention
  • Retention of H2O is greater than retention of Na+
  • Urine Na+ and osmolality reflect Na+ and H2O retention.
  • Urine Na+ <10 mmol/L and Urine osmolality >200 mOsm/kg. if the patient is on diuretics then the Urine Na+ >20 mmol/L
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16
Q

How does Hypovolaemic Hyponataraemia occur?

A
  • Seen in hypovolaemia / dehydration. Loss of both Na+ and H2O but loss of Na+ is greater
  • Fluid loss leads to ADH release and stimulation of thirst.
  • This leads to water retention and repalcement of H2O with hypotonic fluid by drinking.
  • This leads to dilutional hyponatraemia
17
Q

What are causes of extra-renal fluid loss in Hypovolaemic Hyponatraemia?

A
  • GI losses: Vomiting, Diarrhoea
  • 3rd SPACE losses: Burns, Pancreatitis, Peritonitis
  • SKIN losses: Sweating, Cystic fibrosis
  • HAEMORRHAGE
18
Q

What are renal fluid loss causes of Hypovolaemic hyponatraemia?

A
  • SALT-WASING NEPHROPATHIES: Interstitial nephritis, Polycystic kidneys, Chronic pyelonephritis, Medullary cystic disease, Partial urinary tract obstruction
  • CEREBRAL SALT WASTING
  • DIURETICS: Loop diuretics, Thiazide diuretics
  • HYPOADOSTERONISM: Adrenal insufficiency, Congenital adrenal hyperplasia, Drugs (ACEIs ,A2RBs)
19
Q

What is Euvolaemic Hyponatraemia?

A
  • Most common cause of hyponatraemia in hospitalisedpatients
  • Normal total body Na+ therefore normal ECF volume but increased total body water
  • Acute/ chronic water overload plus inability of kidneys to excrete electrolyte-free H2O leads Dilutional hyponatraemia
20
Q

What are causes of Euvolaemic Hyponatraemia with low urine osmolality (<100 mOsm/kg)?

A
  • PRIMARY POLYDIPSIA (psychogenic)
  • RESET OSMOSTAT
  • BEER POTOMANIA
21
Q

What are causes of Euvolaemic Hyponatraemia with high urine osmolality (>100 mOsm/kg)?

A
  • SIADH
  • ADRENAL INSUFFICIENCY
  • DIURETICS
  • (HYPOTHYROIDISM)
22
Q

What is Syndrome of Inappropriate Antidiuretic Hormone(SIADH)?

A
  • Variety of disorders associated with inappropriately increased ADH for plasma osmolality
  • Leads to non-physiological release of ADH
  • H2O retention accompanies normal H2O intake which leads Dilutional hyponatraemia
23
Q

What is the criteria for SIADH?

A

Bartter & Schwartz Criteria – 1957

  • Hyponatraemia
  • Plasma hypo-osmolality (<280 mOsm/kg)
  • Inappropriately concentrated urine (>100 mOsm/kg)
  • Euvolaemic
  • Normal renal, adrenal and thyroid function
  • Urine Na+ >20 mmol/L
24
Q

What are causes of SIADH?

A
  • Increased Hypothalamic secretion
  • Ectopic ADH production
  • Potentiation of existing ADH
  • Exogenous ADH / ADH analogues
25
Q

What can lead to increased hypothalamic secretion of ADH?

A
  • NEUROPSYCHIATRIC: Infections, Trauma, Inflammation, Tumours, Vascular
  • DRUGS: SSRIs, MOIs, Tricyclics, Antipsychotics, Carbamazapine, Nicotine
  • PULMONARY: Infection, Ventilatory
  • POST-OP
  • SEVERE NAUSEA
  • IDIOPATHIC
26
Q

What can lead to Ectopic ADH production?

A
  • THORACIC TUMOURS (mainly): Small cell lung cancer, Bronchiogenic, Carcinoid, Mesothelioma, Thyoma
  • NON-THORACIC TUMOURS: Pancreas, Duodenal, Prostate, Bladder, Ureter, Lymphoma, Myeloproliferative
27
Q

What drugs can lead to potentiation of existing ADH?

A
  • Carbamazepine
  • Cyclophosphamide (iv)
  • Chlorpropamide
  • Tolbutamide
  • Prostaglandin synthase inhibitors
  • Indomethacin
28
Q

What are some exogenous ADH/AVP analogues?

A
  • dDAVP (Desmopressin)
  • Vasopressin
  • Oxytocin
29
Q

What are some risks with correcting hyponatraemia?

A

CENTRAL PONTINE MYELINOLYSIS

  • Severe neurological disorder
  • Patients with severe, chronic hyponatraemia at most risk
30
Q

What are characteristics of Central Pontine Myelinolysis?

A
  • Paraparesis
  • Quadriparesis
  • Mutism
  • Dysphagia
  • Delirium
  • Death

From rapid over-correction of hyponatraemia

31
Q

What is the mechanism for central pontine myelinolysis?

A
  • Acute increase in ECF Na+ concentration
  • H2O leave cells leading to osmotic shrinkage of axons
  • This severs connections with myelin sheath
32
Q

What are recommendations for correcting chronic hyponatraemia?

A

CHRONIC (Asymptomatic patients)

Correct hyponatraemia by:

  • <10-12 mmol/L in the first 24h
  • & by <18 mmol/L in the first 48h
33
Q

What are recommendations for correcting acute hyponatraemia?

A

Risk of cerebral oedema from not treating > risk of harm from over-correction

Give hypertonic saline to to increase Na+ quickly and correct hyponatraemia by:

  • 1-2 mmol/L per hour for 3-4h or until asymptomatic
  • <10-12 mmol/L in the first 24h

MSC: Disease of major orgns (23 decks)

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