Salt Disorders in Neurosurgical Patients

What are the most common salt disorders in neurosurgical patients?

Various salt disorders can occur in neurosurgical patients including hormone disorders, medications-induced disorders and volume-related problems.

The most common are:

• hyponatraemia which is a low blood sodium concentration (<135 mmol/l) without any identifiable cause
• SIADH – syndrome of inappropriate anti-diuretic hormone (ADH) secretion
• Cerebral salt wasting syndrome (CSWS) – condition related to sodium wasting in your kidneys, often resulting from head trauma. Though its mechanism isn’t well understood, it’s thought to centre around decreased nerve input to, and natural steroid release from, the adrenal glands, alongside a release in proteins that promote sodium excretion
• Cranial diabetes insipidus – decreased levels of ADH being secreted from the pituitary mean you lose water from your kidneys

Despite being caused by different factors and exhibiting different mechanisms of pathology, all of them result in a low sodium blood concentration.

Neurosurgical patients with subarachnoid haemorrhage, traumatic brain injury or intracranial tumours have the highest risk for developing such complications.

Why are neurosurgical patients at risk of developing salt disorders?

Blood sodium levels are regulated by multiple mechanisms within the brain, including:

1. ADH – a hormone produced in pituitary gland responsible for sodium and water absorption in the kidney (in the distal convoluted tubule and the collecting duct)
2. Sympathetic nervous system – it stimulates the absorption of sodium in the kidneys (in the proximal tubule). What’s more, it’s believed to stimulate renin production.

In neurosurgical patients due to injury to the brain those mechanisms can be compromised leading to salt and water imbalance. This can result in hyponatraemia, or low blood sodium, or hpernatraemia – high blood sodium.

What are the symptoms of hyponatraemia?

Sodium is a key element in the functioning of our nervous system. Its flow in and out of your nerve cells dictates the movement of so many other molecules, such as water and sugars. When sodium drops therefore, it can have marked effects on your central nervous system.

Early hyponatraemia can be missed as the clinical features are rarely seen with serum sodium higher than 125mmol/l.

Such symptoms include:

• Tiredness
• Cramps
• Headache
• Nausea and vomiting

Advanced symptoms include:

• Delirium
• Decreased responsiveness to painful and verbal stimuli
• Lost control of urination and defecation

If not treated, hyponatraemia can lead to serious complications such as seizures, coma, respiratory arrest and death.

So what causes these symptoms?

For reference, mild hyponatraemia is classified as 130-135mEQ/l, moderate as 125 to 139mEQ/l and severe as anything less than 125.

Hyponatraemia can be chronic or acute. In chronic hyponatraemia, sodium levels drop gradually over 48 hours or longer. A fairly common example of this is when patients take carbamazepine for any condition involving seizures. Whilst our normal sodium normally runs at around 135-145 milliequivalents per litre (mEq/L), when taking carbamazepine long term, it is not unusual to see a sodium hovering around 130. In cases like this, it is very unlikely that the patient would become acutely symptomatic. Instead, if your sodium does drop for another reason, it is a reminder for your doctors to assess how big that drop is and how it compares to your baseline.

In acute hyponatraemia, sodium levels drop rapidly — resulting in potentially dangerous effects, such as rapid brain swelling, which can result in a coma and death. This means symptom recognition, as early as possible, is vital in prevention and treatment.

Some example conditions include SIADH, where excessive secretion of the anti-diuretic hormone ADH from your pituitary gland causes your kidneys to retain too much water. This dilutes sodium concentration in your blood and in the space around cells, but also means your cells themselves swell up.

Why is hyponatremia dangerous?

In hyponatremia, low blood sodium levels create an osmotic gradient between the brain and the plasma which promotes the movement of water from the plasma into brain cells. This in turn causes cerebral edema (brain swelling) and the neurological symptoms listed above.

Unless acute hyponatremia is corrected quickly, cerebral edema may manifest through elevated intracranial pressure and cerebral herniation which leads to the dying of the brain cells.

What about hypernatraemia?

This is usually more straightforward than hyponatraemia. It is defined as any sodium above 145mEq/L. Its mechanisms are such that either you lose water through dehydration (whether it be through inadequate water intake, diuretic medication, burns or diarrhoea), salt poisoning, aldosterone (an adrenal gland hormone that promotes sodium retention) excess, impairment with your usual neural mechanisms for thirst or, as previously mentioned, diabetes insipidus.

Neurosurgically relevant diabetes insipidus invariably occurs cranially, often due to head trauma, surgery on the pituitary gland or the presence of malignant or benign tumours of the brain or pituitary. Symptoms invariably include insatiable thirst, urination of 3-20L of water in 24 hours (consistent for each patient, but varying between patients), and waking up nightly to urinate. Due to consistently passing large volumes of diluted urine to try and preserve sodium, blood sodium can often increase.

Symptoms of high sodium tend to begin as above, but eventually, and especially after blood sodium exceeds 160, progress to lethargy, weakness, confusion, irritability and jerking in your muscles.

Diagnosis of the cause of hypernatremia is made through comparing blood and urine sodium values (or osmolality) alongside hormone testing.

What is the treatment?

The treatment of hyponatremia and hypernatremia depends on the cause. Management of the patient requires detecting an underlying mechanism responsible for clinical presentation.

Firstly, the root cause should be corrected if possible. For example, certain diuretic drugs should be stopped or in the case of diabetes insipidus the lacking hormone ADH should be replaced with the analog DDAVP.

Mineralocorticoids (e.g. aldosterone) deficiency and cerebral salt wasting can be treated with fludrocortisone.

If it’s not possible to identify the cause, hyponatremia is generally treated with:

• fluid restriction for euvolaemic patients (like in SIADH),
• isotonic saline for hypovolemic patients (like in CWS)
• diuretics for hypervolemic patients.

A combination of these therapies may be needed based on the presentation. In the case of severe symptomatic hyponatraemia hypertonic saline is used.

Hypernatremia meanwhile is typically treated using dilute fluids. If however there is a background of renal failure and the sodium is over 170, dialysis can become a legitimate option.

One final note is that for both hypo and hypernatremia, we need to be careful about the rate of correction of sodium. In hypernatremia and most cases of hyponatremia, if we know it’s chronic or the cause is unknown, we need to make sure that we don’t correct sodium too quickly. This can damage certain regions within the brain. However, once agin for hypernatremia, if we do know the cause and onset has been less than 24 hours, quick correction to normal values can actually preserve brain tissue.

References:

(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2912080/)
(https://litfl.com/cerebral-salt-wasting/)
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3381498/)
(https://www.aafp.org/afp/2015/0301/p299.html#:~:text=In%20general%2C%20hyponatremia%20is%20treated,to%20treat%20severe%20symptomatic%20hyponatremia)
(https://www.sciencedirect.com/science/article/pii/S0953711202903947)
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4470172/#:~:text=Neurosurgical%20patients%20almost%20always%20develop,such%20as%20hypoxia%20or%20hypercapnia)

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