Another dreaded topic for internal medicine residents is managing low sodiums. The key to understanding sodium balance in the body is to realise that blood sodium is simply a measure of 2 things: the amount of water, and the amount of sodium in the body. If any one of these is affected, the sodium concentration in the blood is affected - the question is which one? Once you know which of the two is causing the problem - the treatment becomes a lot simpler.
In this article however, we will discuss what to do in the immediate management for someone with severe symptomatic sodium - an endocrine emergency.
When to suspect hyponatraemia
Hyponatraemia often has non-specific symptoms and can present in a variety of ways. These include fatigue, nausea, vomiting, headaches, drowsiness, confusion and in the most severe cases, even seizures. Often enough though, hyponatraemia is an incidental finding discovered when the first set of lab tests sent from the Emergency Department come back.
Once you've made the initial diagnosis, the key is to assess the patient, the severity of the hyponatraemia, institute any measures to stabilise the patient and appropriately site the patient.
Some caveats
When you see a severely abnormal test result, always remember to consider a few things - haemolysis or a diluted sample, molecules that can cause hypertonicity such as glucose/mannitol or ethanol and pseudohyponatraemia.
Look at the other blood test results - is the potassium grossly elevated, is the bilirubin extremely high? If so, consider haemolysis and assess whether the sample results are accurate for use.
If the glucose is significantly elevated, or the patient has been on a mannitol infusion (in cases of raised intracranial pressure after a head injury or neurosurgery for example), the hyponatraemia may be due to this. Hypertonicity induced by the elevated glucose draws water into the circulation from the interstitium leading to dilution of the existing sodium i.e. hyponatraemia.
If the glucose level is elevated, correct the sodium for the glucose level. Personally, I use the following formula, but you can also use a calculator such as MdCalc easily available online.
c. If the sample appears lipaemic (milky looking blood sample) or the patient has a history of multiple myeloma/Waldenstrom macroglobulinaemia, consider pseudohyponatraemia causing a falsely lowered sodium level.
When time is at a premium, using a point of care iSTAT machine to check electrolytes along with an arterial blood gas can be very helpful as these machines use a technique that does not involve dilution of the sample (the amount of dilution used in regular lab test processing is based on an assumption of the proportion of blood components being within a normal range). Direct ion-specific assays allow iSTAT machines to give you a rapid and accurate sodium level without being altered due to dilution.
How to assess a patient with hyponatraemia
There are 4 main steps in approaching a patient with hyponatraemia as outlined below:
1) Assess the patient:
Fluid status - this is key in determining the underlying cause though clinical examination is not in any way particularly reliable. That said someone who's been vomiting, hasn't eaten in a week and looks bone dry, is probably dry. It's still important to hone these examination skills because lab tests will take an hour or two at the least to come back and you will need some idea of what the cause is to institute your initial treatment
Consciousness level - someone who is drowsy or having active seizures is clearly very unwell and has symptomatic hyponatraemia. This patient is going to need close monitoring and urgent treatment.
Thyroid status/evidence of adrenal insufficiency - both hypothyroidism and hypocortisolism can cause hyponatraemia (though it can be difficult to assess this in the acute setting, looking for a thyroidectomy scar or a medical alert bracelet can give you a hint)
A brief history if possible - often a history of recent gastrointestinal losses, or new medications could be a major clue in the underlying cause. Recent blood test results may also be helpful.
2) Determine the severity:
If the sodium level is <120mmol/L, the patient has severe hyponatraemia
Another way to assess severity is looking at symptoms - if the patient is drowsy, vomiting, or having seizures, then again, this is severe symptomatic hyponatraemia
Another key aspect to decide severity and urgency to raise the sodium is the chronicity of hyponatraemia. If a patient has a documented normal sodium within the last 48 hours, the patient is more likely to be symptomatic. In addition, rapid normalisation of the sodium levels is less likely to cause complications such as Osmotic Demyelination Syndrome (ODS, more of this later)
3) Stabilise the patient:
Assess the usual ABCs and stabilise the patient as necessary. For example, if they are drowsy and unable to protect their airway, consider preemptive intubation.
If they are in shock and hypotensive, do not fret about what fluids to give - use standard resuscitation fluids such as normal saline, lactated Ringer's or Hartmann's solution as per your local guidelines. They are much more likely to die from shock than from hyponatraemia at that point.
4) Appropriately site the patient:
Although a resident may not often have to think about this since these decisions may be left to the Medical Registrar or the Emergency Department team,. putting this on your checklist ensures you are not left to deal with a sick patient with severe symptomatic hyponatraemia on a general ward without the appropriate staff and support to closely monitor and treat this patient.
Anyone with a sodium < 115mmol/L should arguably be in a high dependency or ICU setting and likewise for anyone receiving 3% hypertonic saline unless the patient is clinically well and being managed by an Endocrinology team.
Immediate management
Assuming we are dealing with an unwell patient with severe symptomatic hyponatraemia, the patient should be in either the high priority assessment area of ED, high dependency or ICU,
The key decision is whether or not the patient requires hypertonic saline. If a patient has severe symptomatic hyponatraemia, then the answer is usually yes.
Start with 100ml* of 3% hypertonic saline over 10-20 minutes and recheck the sodium after 30 minutes aiming for a rise of 3-5mmol/L to raise the patient's seizure threshold and reduce the risk of seizures
Keep IV lorazepam 2mg on standby for the treatment of seizures
If the sodium does not correct sufficiently and the patient continues to have a reduced GCS or ongoing seizures, repeat the bolus of hypertonic saline once more and recheck the sodium after another 30mins-1hour
After the initial 3-5mmol/L correction, aim for sodium correction of not more than 8mmol/24h (including the original 3-5mmol/L rise) and not more than 18mmol/48 hours to prevent osmotic demyelination syndrome monitoring every 2-4 hourly
Initiate GCS charting and strict intake and output monitoring with insertion of an indwelling urinary catheter for accuracy.
Subsequent management would depend on the aetiology of the hyponatraemia as revealed by further investigations.
*The European Society of Endocrinology guidelines 2014 suggest using 150ml aliquots instead and rechecking within 20mins. The American 2013 guidelines by Verbalis and team suggest using 100ml repeated up to 3 times as necessary to bring up the sodium by 5mmol/L. The above regimen is my personal preference as giving 100mls at each bolus reduces the risk of overcorrection beyond the intended initial rise of 5mmol/L.
Bolus vs slow infusion of hypertonic saline
Interestingly, evidence shows that bolus doses allow for more rapid correction of sodium and GCS. Additionally there is some non-significant evidence that the risk of overcorrection with rapid bolus doses is slightly lower. See articles 3 and 4 below in the references for further details.
Workup for underlying causes
Investigations to consider include:
Renal function tests (urea, electrolytes and bicarbonate)
Capillary blood glucose (as discussed above under caveats)
Lipids and total protein levels if there is concern regarding pseudohyponatraemia
TFT, cortisol (deficiencies can cause hyponatraemia)
Urine sodium, serum osmolality and urine osmolality (paired samples)
CT Brain (especially if the patient's GCS does not improve after the sodium has increased by at least 5mmol/L as you may need to consider other causes of a low GCS
Plain chest radiograph
Urine drug screen (ecstasy can present with water intoxication, SIADH and seizures secondary to hyponatraemia)
Differentials to consider based on the patient's fluid status:
Dry - look for a history of gastrointestinal losses, weight loss drugs, diuretics etc
Overloaded - cardiac, liver or renal failure history
Euvolaemic - Assess for any hypocortisolism, hypothyroidism, review medication charts, fluid intake, solute intake (consider tea and toast diet or beer drinker's potomania), SIADH
The subsequent management is really dependent on the underlying cause and is beyond the scope of this post but we can discuss these in subsequent posts.
Resources:
Clinical practice guideline on diagnosis and treatment of hyponatraemia, European Journal of Endocrinology, Volume 170, Issue 3, Mar 2014, Pages G1–G47, https://doi.org/10.1530/EJE-13-1020
Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Verbalis JG, Goldsmith SR, Greenberg A, Korzelius C, Schrier RW, Sterns RH, et al. Am J Med. 2013 Oct. 126 (10 Suppl 1):S1-42.
Garrahy A, Dineen R, Hannon AM, et al. Continuous Versus Bolus Infusion of Hypertonic Saline in the Treatment of Symptomatic Hyponatremia Caused by SIAD. J Clin Endocrinol Metab. 2019;104(9):3595-3602. doi:10.1210/jc.2019-00044
Baek SH, Jo YH, Ahn S, et al. Risk of Overcorrection in Rapid Intermittent Bolus vs Slow Continuous Infusion Therapies of Hypertonic Saline for Patients With Symptomatic Hyponatremia: The SALSA Randomized Clinical Trial. JAMA Intern Med. 2021;181(1):81–92. doi:10.1001/jamainternmed.2020.5519
Comentarios