Epilepsy, collapse… NOT a seizure!

Labs and Lytes 032

Author: Christiaan Yu
Reviewer: Sarah Yong, Chris Nickson

A 50-year-old gentleman presented following an unwitnessed collapse at home in the bathroom. He has a background of epilepsy treated with phenytoin, oxcarbazepine, and levetiracetam.

His laboratory results on admission show:

Sodium (mmol/L) 118 (135-145)
Potassium (mmol/L) 4.0 (3.5-5.2)
Chloride (mmol/L) 107 (95-110)
Bicarbonate (mmol/L) 32 (22-32)
Urea (mmol/L) 6.0 (4-9)
Creatinine (umol/L) 52 (60-110)
Glucose (mmol/L) 5.5 (3.5-7.7)
Osmolality (mOsmol/L) 257 (275-300)

NB. reference ranges also shown in brackets in the right-hand column.

Q1. Describe and interpret the laboratory findings.

Severe hypotonic hyponatremia.

Hyponatraemia is classified as follows:

Acuity

  • Acute: <48 hours
  • Chronic: >48 hours or duration unknown

Biochemistry

  • Mild: Na 130-135 mmol/L
  • Moderate: Na 125-129 mmol/L
  • Severe: Na <125 mmol/L

Symptoms

  • Moderately symptomatic: any of
    • Nausea without vomiting
    • Confusion
    • Headache
  • Severely symptomatic: any of
    • Vomiting
    • Cardiorespiratory distress
    • Abnormal and deep somnolence
    • Seizures
    • Coma (GCS ≤8)

Osmolarity

  • Hypotonic: <275 mOsm/kg
  • Isotonic: 270-300 mOsm/kg
  • Hypertonic: >300 mOsm/kg

Note that biochemical severity does not necessarily correlate with the severity of symptoms. Chronicity, in particular the rate at which a given severity of hyponatraemia developed, often determines how symptomatic the patient is.

You telephone the patient’s family doctor, and discover that he had a blood test 3 days earlier and his serum sodium was 135 mmol/L. It sounds acute!

Q2. Matched urine results have come back as follows. What is your likely diagnosis?

Urine Sodium (mmol/L) 44
Urine Osmolality (mOsmol/L) 441


Findings are consistent with syndrome of inappropriate ADH secretion (SIADH).

SIADH is a diagnosis of exclusion, characterised by the following:

  1. Hyponatremia
  2. Euvolemia
  3. High urinary sodium (>20-30mmol/L)
  4. Urine osmolality > plasma osmolality

The syndrome is inappropriate because you would expect the urine osmolality to be low as the patient attempts to pass dilute urine, if serum sodium is low. Therefore, in this case it is inappropriately concentrated.

This diagnostic algorithm published by Spasovski et al (2014) is a useful guide, click here to open in a new window.

Q3. What is the most likely cause of this syndrome on this patient?

Anti-epileptics are a common cause of SIADH. In this patient, either (or both) the oxcarbazepine or levetiracetam are likely to be the culprit drug.

Other important causes include major surgery, ADH production, drugs (anti-depressant, anti-psychotics, anaesthetics drugs), CNS disorders, hypothyroidism, hypoadrenalism, HIV and pulmonary disorders…. and a whole lot more!

Remember that SIADH is not really a diagnosis, we need to find the underlying cause!

Q4. What are the key aspects of management of this patient’s condition?

Other than attending to the ABCs, the key aspects of management are the treatment of severe hyponatraemia:

  1. Treat reversible causes
    Including cessation of culprit drugs, treating pulmonary pathology or concomitant endocrine disorders.
  2. Correct biochemistry
    The rate of correction of hyponatremia is based on chronicity and severity.
    In acute severe hyponatremia, aim for 1-2 mmol/hour correction.
    In chronic severe hyponatraemia, aim for 0.5-1mmol/hour correction.
    Correct sodium by 4-6mmol in the first 24 hours, and less than 10mmol/L over any given 24 hour period.
    In the acute setting, or if there are severe symptoms, hypertonic saline is useful for urgent initial (partial!) correction. IV infusion of 150 ml 3% hypertonic saline (or 20 mL 23.4% hypertonic saline) over 20 min then recheck sodium on a venous blood gas. Stop if symptoms resolve or there a 5 mmol/L increase in sodium occurs. Hypertonic saline can cause phlebitis so is best given via central access.
    Most cases of hyponatraemia, and SIADH, can be treated without hypertonic saline if the underlying cause is addressed.
  3. Avoid complications
    Do not correct Na any faster than 10-12 mmol/L over 24 hour period. Any quicker bears the serious risk of osmotic demyelination syndrome, which usually presents 3-5 days post treatment!
    The frequency of sodium monitoring required means that most patients with severe hyponatraemia need high dependency unit (HDU)-level care.
  4. Specific treatment
    SIADH is best treated by fluid restriction, typically 1 to 1.5L/24h, guided by the rate of Na correction.
    Vasopressin receptor antagonists (i.e Tolvaptan) can be considered for SIADH, but are rarely used in our setting. These drugs produce an aquaresis without affecting electrolyte excretion.

References

All case-based scenarios on INTENSIVE are fictional. They may include realistic non-identifiable clinical data and are derived from learning points taken from clinical practice. Clinical details are not those of any particular person; they are created to add educational value to the scenarios.

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