Sodium disorders Flashcards
What is the significance of plasma sodium in critical illness
Alterations in sodium are associated with worse outcomes
What are the broad causes of hypernatraemia
- Free water deficit (most common)
- inadequate water intake
- excessive water loss - . Sodium excess
when might hypernatraemia be due to inadequate water intake
- denied access to water for extended periods.
- hypodipsic hyponatraemia (associated with neurologic disease eg GME or as a breed condition in mini schnauzers)
when might hypernatraemia be due to excessive water loss
- Renal loss, especially osmotic dieuresis
- GI losses
- Diabetes inspidius (inability to concentrate urine)
When might hypernatraemia be due to excessive sodium intake
- sodium containing drugs and fluids
- ingestion of saltwater and playdoh
- Hyperaldosteronism
What are the effects of hypernatraemia on the CNS and how are they compensated
- water moves out of the relatively hypoosmolar cells into the now hyperosmolar ECF.
- leading to cell shrinkage
- cells develop idiogenic osmoles in response - to increase the cell osmolarity and limit the fluid shift.
- This starts within hours but needs 24hr for full compensation.
What are the clinical signs of hypernatraemia
- Often none if chronic due to cell adaptation.
- if acute then neuro signs relating to CNS cell shrinkage
- depressed mentation, head pressing, seizure, coma.
State the equation for calculating free water deficit
FWD = ((patient NA/Normal Na)-1) x (0.6 x BW)
How quickly is the free water deficit replaced and why?
- replaced by the number of hours calculated to return NA to normal by 0.5mmol/l to 1mmol/l per hour
- slow to stop the water rushing into the now hyperosmolar cells (due to idiogenic osmole development) and cause cell swelling
How is Na corrected in a symptomatic patient?
- More rapid correcting at 2mmol/l/hr until reaches high end normal.
- Use FWD equation changing normal NA for the top of reference range target and then return quickly
How would correction differ in a patient with known Na intoxication
- If known that the hypernatraemia is acute due to ingestion the FWD can be replaced very quickly.
What consideration is given to the oral intake of water in the hypernatraemic patient
- oral intake can help normalise a sodium, offered in hourly intervals or via NG tube.
- oral water intake has to be accounted for when considering how fast the NA will change.
- should not offer unlimited access to water in the hypernatraemic patient incase of sudden large volume intake.
Can D5W be used to correct fluid deficit
- NO it rapidly moves intracellularly.
- Extracellular volume replacement requires sodium containing fluids.
- patient should be resuscitated with fluids within 6mmol/l of its plasma sodium.
- May need to add some 7.2% saline to isotonic crystalloids to make a custom fluid for this purpose (1.2mmol/ml)
What is the main complication of treating hypernatraemia and how is it managed
- CNS cell swelling due to rapid correction = cerebral oedema and neuro signs.
- Stop fluids and oral water
- reassess NA and check if the speed of the drop is apprpropriate.
- 0.5g/kg mannitol over 20-30 minutes can counteract cerebral oedema.
- reinstate sodium correction at a slower rate or using a fluid with less free water
another differential for neuro signs is worsening hypernatraemia, check
What is the effect of hyponatraemia on cells and how do they compensate
- free water mores from the relatively hyposmolar ECF to the cells, resulting in CNS cell swelling.
- Cells expel electrolytes and organic osmoles to reduce their osmolarity and limit further cell swelling.
What rae the clinical signs of hyponatraemia
- often none if chronic and compensated
- neuro if severe: depressed mentation, seizure, coma and death from brain herniation
What effect might hypontaremia have on USG
May cause a low USG as it reduces renal concentrating ability (medullary washout)
What are the differentials for hyponatraemia
- Decreased circulating volume = ADH secretion = water rentention and increased thirst (common) (can happen in CHF, third spacing, GI and renal dx)
- hypoadrenocorticism
- Dieuretic usuage
- renal tubular dysfunction
- Syndrome of inappropraiate ADH
-GI parasites - Pscycogenic polydipsia
How can diuretic usuage lead to hyponatraemia
- secondary to hypovolaemia (which leads to water rentention)
- hypokalaemia causes sodium ions to move into the cell in exchange for potassium.
What complication can occur if hyponatraemia is treated too rapidly
- Myelinolysis resulting from Neuronal shrinking
- typically delayed by a couple of days (ataxia, paresis, obtundation and dysphagia)
- can be permanent
NB most have starting Na <110mmol/l
What is the significance of hyponatraemia in CHF
- Caused by volume retention
- Usually mild
- May persist due to ongoing dieuretic usage
How is mild hyponatraemia >130mmol/l managed
- usually from a decrease in effective circulating volume and doesnt require specific therapy.
- treat the underlying disease and monitor sodium
What is the initial therapy for a symptomatic patient with profound (120mmol/l) hyponatraemia
- Administer 2ml/kg of 3% NaCL over 20min, which should aim to increase sodium by 5mmol/l
- This can be repeated until the patient is no longer symptomatic
- 0.5g/kg mannitol can be given to reduce brain oedema and prevent herniation in an emergency
After rescue treatment for the symptomatic patient, what would be the ongoing treatment where the hypernatraemia was known to be acute
- continue to correct to the lower end of the reference range.
- should not have to relower if the sodium rises more quickly than expected
After rescue treatement for the symptomatic patient, what would be the ongoing treatment when the duration of hyponatraemia was unknown or chronic
- must be cautious due to myelinolysis risk
- raise by 10mmol/l in the 1st 24hr then 8mmol/l in subsequent 24hr periods.
- could concurrently give loops dieuretics to eliminate excess free water if the urine is concentrated.
many think 0.5mmol/l per hr is too fast to increase hyponatraemia
What is the sodium deficit equation to target a controlled increase in sodium
sodium deficit = (target NA - patient NA) x (0.6 x BW)
What would be your approach if, on rechecking the sodium, it had corrected too quickly
- relower with oral or D5W to reduce the myelinolysis risk.
- use the FWD equation but replace the normal NA with target NA
-Giving loop dieuretics at the same time may help lowering the sodium in an already hyponatraemic patient
What is the effect of hyperglycaemia on sodium
causes pseudohyperntraemia. Glucose draws water into the extracellular fluid, diluting the sodium
State the equation for correctiong sodium in a hypernatraemic animal
- each 3.5mmol/l increase in BG will drop the sodim value by 1mmol/l
- to correct divide the glucose value but 3.5 and add this to the sodium
how would you treat the hyponatraemic patient presenting with shock
if sodium is ,130mmol/l you may need to creat a custom fluid (within 6mmol/l of patient) for bolusing
