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Hyponatraemia

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Hyponatraemia: A sudden drop in serum sodium (Na) can cause cerebral oedema, leading to cell swelling and dysfunction. This can progress to brain herniation and neurological damage. A gradual decline in Na is generally better tolerated and requires less aggressive correction. Aim to increase Na by less than 12 mmol/L per day, with correction spread over 2-3 days if necessary to avoid complications.

Comatose Management Summary for Severe Hyponatraemia (Na < 115 mmol/L)
ABC and resuscitation if the patient is in coma or has seizures (Na typically < 115 mmol/L). Exclude opiate overdose and hypoglycaemia. Consider glucose and naloxone. Arrange HDU/ITU admission. Obtain IV access and measure cortisol, glucose, urine/serum Na, and TFTs. Assess volume status: is this due to water overload or salt loss? Review any recent water overload, drug history, and consider SIADH. Consider CT head if GCS is low to exclude SAH, SDH, ICH, tumour, pituitary apoplexy, or CNS infection. For hypovolaemic hyponatraemia: administer 0.5-1 L of IV normal saline (N-Saline) and reassess. For euvolaemic hyponatraemia (e.g., SIADH) with seizures or coma: Restrict fluids to 1L/day. Consider 3% hypertonic saline 150 ml over 15-30 mins if needed. Target an initial Na rise of 6 mmol/L to improve neurological status. Consider adding Demeclocycline or Tolvaptan for SIADH. Monitor Na levels every 2-4 hours to avoid rapid changes. Always check U&E regularly to ensure Na rise does not exceed 12 mmol/L per 24 hours. Involve senior help early if CNS symptoms are present, as hyponatraemia management can be complex.

Comatose Management Summary for Severe Hyponatraemia (Na < 115 mmol/L)

ABC and resuscitation if the patient is in coma or has seizures (Na typically < 115 mmol/L).
Exclude opiate overdose and hypoglycaemia. Consider glucose and naloxone. Arrange HDU/ITU admission.
Obtain IV access and measure cortisol, glucose, urine/serum Na, and TFTs.
Assess volume status: is this due to water overload or salt loss?
Review any recent water overload, drug history, and consider SIADH.
Consider CT head if GCS is low to exclude SAH, SDH, ICH, tumour, pituitary apoplexy, or CNS infection.
For hypovolaemic hyponatraemia: administer 0.5-1 L of IV normal saline (N-Saline) and reassess.
For euvolaemic hyponatraemia (e.g., SIADH) with seizures or coma:
- Restrict fluids to 1L/day. Consider 3% hypertonic saline 150 ml over 15-30 mins if needed.
- Target an initial Na rise of 6 mmol/L to improve neurological status.
- Consider adding Demeclocycline or Tolvaptan for SIADH.
- Monitor Na levels every 2-4 hours to avoid rapid changes.
Always check U&E regularly to ensure Na rise does not exceed 12 mmol/L per 24 hours.
Involve senior help early if CNS symptoms are present, as hyponatraemia management can be complex.

Physiology of Hyponatraemia

In response to low sodium, ADH is typically reduced, allowing for free water excretion.
Inappropriate ADH secretion (e.g., in SIADH) retains water and increases urine osmolality (often > 100 mOsm/kg), whereas other causes should have lower osmolalities.
Hypovolaemia triggers ADH release, thirst, and aldosterone-mediated sodium retention, with decreased urinary Na levels.
Hyponatraemia and low serum osmolality can cause water to enter cells, leading to cellular swelling, particularly in the brain, resulting in cerebral oedema.

Clinical Evaluation

Review drug chart, fluid balance, and assess the patient’s hydration status.
Classification of volume status:
- Hypovolaemic: Dry (dehydrated) appearance, reduced skin turgor, low BP, tachycardia, postural drop, dry mucous membranes, concentrated urine. Causes may include post-op, Addison’s, and salt-wasting nephropathy.
- Euvolaemic: No signs of oedema, normal BP, HR; consider SIADH.
- Hypervolaemic: Signs of fluid overload (e.g., ascites, oedema) due to heart, renal, or liver failure.

Types and Causes of Hyponatraemia

Hypovolaemic: Vomiting, diarrhoea, diuretics, cerebral salt wasting, Addison’s, burns, salt-losing nephropathy, drugs (e.g., thiazides).
Euvolaemic: SIADH, post-operative pain, stress, medications (e.g., opiates, NSAIDs, SSRIs), psychogenic polydipsia.
Hypervolaemic: Heart failure, chronic liver disease, renal failure, excessive hypotonic fluids or water intake (e.g., post-TURP, potomania).

Post-Operative Causes of Hyponatraemia

Use of 5% dextrose alone, leading to free water retention.
Post-surgical ADH release due to pain and stress.
Post-TURP syndrome due to excessive free water absorption.

Medical Causes of Hyponatraemia

Diuretics leading to salt and water loss.
Heart, liver, or renal failure causing water retention.
SIADH with excess water reabsorption in the kidneys.
Pseudohyponatraemia due to high lipids or proteins in plasma.

Severity of Hyponatraemia

Rapid Na drop or levels < 120 mmol/L are more likely to cause symptoms.
Na 110-115 mmol/L: Headache, irritability, delirium, weakness.
Na < 110 mmol/L: Coma, seizures, ataxia, tremor (emergency).

Investigations

U&E: Categorize as mild (Na 135-130), moderate (125-129), or severe (< 125 mmol/L).
Serum osmolality: < 275 mOsm/kg in SIADH.
Urine osmolality: > 100 mOsm/kg H₂O suggests SIADH with hypotonic plasma.
Urine Na⁺: Low (< 20) in hypovolaemia, high (> 30) in SIADH.
TFTs: High TSH suggests hypothyroidism.
Cortisol: Low cortisol (Addison's disease) may need confirmation with synacthen test.
CXR: To identify possible tumour or infection.
CT head: For suspected neurological changes or SAH.
Lipids: High lipids may indicate pseudohyponatraemia.

Central Pontine Myelinosis (CPM)

CPM is a serious consequence of rapid Na correction. It involves demyelination of the pons, leading to neurological deficits. This risk emphasizes the importance of correcting Na gradually, aiming for no more than a 12 mmol/L increase per 24 hours.

Algorithm

Differential Diagnosis

Pseudohyponatraemia: Caused by high lipids or proteins, which expand plasma volume. Na appears low, but plasma osmolality remains normal or high.

Management Principles

ABC: Stabilize airway, breathing, and circulation; consider HDU/ITU for severe cases.
Monitor U&E, NEWS score, and CNS status regularly.
Identify the cause (hypovolaemia, euvolaemia, or hypervolaemia) and tailor management based on clinical assessment.
Avoid rapid Na correction: Gradual correction helps prevent CPM. Aim for Na > 120 mmol/L initially to reduce CNS risk.
For hypovolaemic patients, cautiously replete with N-Saline. Frequent monitoring and gradual correction are essential.
For SIADH (euvolaemic), restrict fluids to 800-1000 ml/day. In symptomatic cases, consider a 3% saline bolus to raise Na by 5 mmol/L initially, followed by fluid restriction and, if needed, Tolvaptan or Demeclocycline.
In Addison's disease, perform a short synacthen test and administer IV hydrocortisone as required.
Post-TURP syndrome or sudden hypotonic fluid excess may require diuretics.
For hypervolaemic hyponatraemia, use fluid and salt restriction; consider diuretics as needed.

References

PLEASE NOTE LEGAL ADVICE: The contents are under continuing development and improvements and may contain errors of omission or fact. Feedback vital and always welcome at drokane at gmail.com. This is not to be used for the assessment, diagnosis or management of patients. It should not be regarded as medical advice. It is only for educational purposes. Please adhere to your local protocols. If you are unwell please seek healthcare advice from your doctor. This does not replace senior or specialist advice. If you do not accept this then please do not use the website. If you need medical advice, please consult a doctor or other appropriate medical professional. If you are a medical professional and you need advice then speak to your senior or colleagues.

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