Hyponatraemia Flashcards
What is mild/moderate/severe hyponatraemia
- 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.
What is acute/chronic hyponatraemia
• 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
What is another way to classify hyponatraemia
- Hypertonic or hyperosmolar hyponatraemia (high serum osmolality).
- Pseudo-hyponatraemia or isotonic hyponatraemia (normal serum osmolality).
- Hypotonic or true hyponatraemia (low serum osmolality)
How is hypotonic/true hyponatraemia classified?
Hypovolemic hyponatraemia (volume depletion). Hypervolemic hyponatraemia (volume overload). Euvolemic hyponatraemia (normal volume status).
What is pseudohyponatraemia?
artifactually (falsely) low serum sodium concentration due to hyperproteinaemia (multiple myeloma is the most common cause) or hypertriglyceridemia
AKA normal serum osmolality
What is hypertonic or hyperosmolar hyponatraemia?
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)
What is hypovolemic hypotonic hyponatraemia caused by
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
What is hypervolemia hypotonic hyponatraemia caused by?
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 )
What is euvolemia hypotonic hyponatraemia caused by?
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)
How can you diagnose SIADH?
• 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!)
Drugs associated with hyponatraemia? What increase ADH secretion
○ Anticonvulsants: carbamazepine ○ Anti neoplastics: cyclophosphamide ○ Hypoglycaemics: sulphonylureas ○ Narcotics: morphine ○ Antipsychotics (such as haloperidol and phenothiazines).
Drugs associated with hyponatraemia? What potentiate ADH
○ Tricyclic
○ SSRIs: prozacs
○ Paracetamol
Indomethacin
Drugs associated with hyponatraemia? Diuretics which prevent sodium reabsorption
○ Thiazides
○ Frusemide
○ K+ sparing (amiloride, spironolactone)
What is the clinical presentation of hyponatraemia?
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
What does ADH do?
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