SimFridays - Hyponatraemia

February is endocrine-themed, and I’ve tried to pick out cases that I have had difficulties with or reflected upon. We see patients with hyponatraemia all the time, but not so often are they severely deficient or symptomatic. 

The simulated case: 
A woman in her 60s presenting after a minor fall in her shower, reported to be acting strangely by her family. She has come through START and initial investigations have shown a sodium level of 113. She has been moved to resus.

What happened?
The ACP looked at her previous blood tests and her recent GP consultation record, which showed her sodium had been normal 4 months ago and that she had consulted about a long-term cough but had been lost to follow-up. 

After examination there was no suspicion of traumatic injuries from the fall. She had formal bloods taken, an ECG (sinus tachycardia), and a second cannula. Additional blood tests like bone profile, magnesium, osmolality calculation were added on, and a urine sample was planned to test osmolality and urinary electrolytes. A chest x-ray showed a large unilateral pleural effusion.

As per the guideline a plan was made to give 150mL of 2.7% sodium chloride IV.

What did we think? 
In debrief we discussed:

Immediate management considerations:
Severe hyponatraemia puts the patient at risk of seizures, coma and arrest. In this simulation they had the symptom of confusion. The guideline (see the ‘to do’ section for its location) recommends 150mL of 2.7% hypertonic saline over 20 minutes followed by a sodium check, aiming for 5mmol/L increase over 1 hour. Overall we’re aiming for no more than 10mmol/L increase in the first 24 hours to reduce risks of demyelination. It was difficult to find the hypertonic saline at the time of the sim - this will be looked into.

Although we may not see the results in ED, it’s helpful to have paired serum and urine osmolalities, urinary electrolytes and TFTs as well as the standard bloods. After initial management the subsequent steps will rely on this information. A random cortisol is less helpful than a 9am one, but may be helpful if Addisonian crisis is suspected as the cause. 

Note if starting fluid restriction this should be at about 500mL less than the patient’s usual intake, but otherwise interestingly the restriction amount can actually be estimated using the urinary electrolyte results - have a look at the guideline.

Causes of hyponatraemia:
It’s worth considering potential causes of pseudohyponatraemia: having high triglycerides, high serum protein levels or taking blood during an infusion can falsely alter the reported sodium level. 

Otherwise, for hyponatraemia, as per the guideline the causes can be organised by whether they cause a hypovolaemic, euvolaemic or hypervolaemic state. So it's really critical to consider the patient's fluid status.

You can then consider some of the causes:
Fluid overload state: all the “failures” - cardiac failure, renal failure/nephrotic syndrome.
Euvolaemia: low intake of salt, SIADH, hypothyroidism, medications, surgery.
Dehydrated: vomiting, diarrhoea, Addison’s, nephritis, salt wasting syndrome.

In terms of SIADH which caused this patient’s hyponatraemia, there are further causes to consider. The patient has potentially had a head injury which can cause low sodium, but they have also had a cough and abnormal chest x-ray. This could represent pneumonia which can cause hyponatraemia. However their history of several months cough and weight-loss on a background of COPD and smoking, with pleural effusion on x-ray, may represent a small cell lung cancer producing ectopic ADH. 

The part of the guideline for asymptomatic or chronic hyponatraemia takes you through the different investigation depending on fluid status and urine osmolality. 

Mechanism of hyponatraemia:
I’ve always found it tricky to think through why in SIADH patients can be euvolaemic with hyponatraemia and why this isn’t corrected. I found this video resource great for working through it. In essence, the excess ADH increases aquaporin expression in the nephron, more water is reabsorbed through these and blood volume increases. But then, in response to the increased fluid volume in the body, the renin-angiotensin-aldosterone axis is downregulated, there is reduced aldosterone action, overall causing loss of sodium WITH water. Eventually there is some adaptation and the kidneys become less sensitive to ADH. Overall the net effect is euvolaemia but with loss of sodium. 

Decision whether to request a CT head:
It was decided that the patient would benefit from a CT head scan, but this was judged to be currently lower priority than the other management steps. In this case it would have been normal. 

To do:

Have a watch of this video explaining SIADH  [  ]

Ensure you know where to find hypertonic saline in ED  [  ]

Refresh yourself on the acute hyponatraemia guideline, go into the G: drive, clinical guidelines, then click to search for hyponatraemia  [  ]

If you took part in the sim or watched on the livestream, you can use this blog as a starter to reflect on your own experience of it   [  ]

Thank you to Laura for being our simulated patient today.
Blog by: James Keitley - ED sim fellow - on behalf of the ED sim team.

---------------
For clinical decisions please refer directly to primary sources. This blog may not be updated. All images copyright- and attribution-free in the public domain or taken by the author.