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Flashcards in Sodium Deck (10):



Hyponatraemia may be caused by water excess or sodium depletion. Causes of pseudohyponatraemia include hyperlipidaemia (increase in serum volume) or a taking blood from a drip arm. Urinary sodium and osmolarity levels aid making a diagnosis

Urinary sodium > 20 mmol/l

Sodium depletion, renal loss (patient often hypovolaemic)
diuretic stage of renal failure
cerebral salt wasting syndrome

Patient often euvolaemic
SIADH (urine osmolality > 500 mmol/kg)

Urinary sodium < 20 mmol/l

Patient hypovolaemic:
Sodium depletion, extra-renal loss
diarrhoea, vomiting, sweating
burns, adenoma of rectum

Water excess (patient often hypervolaemic and oedematous)
secondary hyperaldosteronism: heart failure, cirrhosis
reduced GFR: renal failure
IV dextrose, psychogenic polydipsia


Cerebral Salt Wasting Syndrome - Example Question

A 72-year-old woman is recovering on the neurosurgical unit following a subdural haemorrhage. Four days earlier she underwent Burr hole surgery. You are asked to see her due to a persistently low sodium for the past three days. You note the following investigations:

Day 2 post-surgery
Serum Na+ 116 mmol/l

Day 3 post-surgery
Serum Na+ 117 mmol/l

Day 4 post-surgery
Serum Na+ 115 mmol/l
Urinary Na+ 25 mmol/l
Serum osmolality 280 mmol/l

Examination of the patient demonstrates dry mucous membranes and delayed capillary refill time.

What is the most likely diagnosis?

Diabetes insipidus
> Cerebral salt wasting syndrome
Renal tubular acidosis type IV
Sheehan's syndrome

Diabetes insipidus is classically associated with hypernatraemia. Sheehan's syndrome refers to the specific situation of pituitary necrosis following childbirth. The cardinal feature of renal tubular acidosis type IV is hyperkalaemia.

This leaves SIADH and cerebral salt wasting syndrome. The hydration status in this patient can be considered hypovolaemic making SIADH unlikely (typically euvolaemic). Additionally, this diagnosis should only be made in the absence of hypothyroidism and adrenal dysfunction.

Cerebral salt wasting syndrome can occur following neurosurgery. It occurs due to sodium wasting in the urine. Comparatively, it is treated with replacing fluid and sodium losses.


Hyponatraemia - Correction

Hyponatraemia: correction

Central pontine myelinolysis
demyelination syndrome caused by rapid correction of chronic hyponatraemia
may lead to quadriparesis and bulbar palsy
diagnosis: MRI brain


Hypernatraemia - Causes


Causes of hypernatraemia
osmotic diuresis e.g. hyperosmolar non-ketotic diabetic coma
diabetes insipidus
excess IV saline

Hypernatraemia should be corrected with great caution. Although brain tissue can lose sodium and potassium rapidly, lowering of other osmolytes (and importantly water) occurs at a slower rate, predisposing to cerebral oedema, resulting in seizures, coma and death1. Although there are no clinical guidelines by NICE or Royal College of Physicians at present, it is generally accepted that a rate of no greater than 0.5 mmol/hour correction is appropriate1.

1. Reynolds RM, Padfield PL, Seckl JR; Disorders of sodium balance. BMJ. 2006 Mar 25;332(7543):702-5.


Reducing Hypernatraemia - Example Question

A frail 82 year old gentleman was brought in by his daughter, who found him on the floor in his flat. He had tripped in a mechanical and had been unable to get back up, lying on the floor for the past 3 days. On examination, he appears extremely dehydrated but has no specific focal weakness, systemic examination is unremarkable. He has sustained no musculoskeletal injuries. His blood tests are as follows:

Na+ 168 mmol/l
K+ 6.0 mmol/l
Urea 24 mmol/l
Creatinine 260 µmol/l (baseline 107 three months ago)
Creatinine kinase 11,000 mmol/l

ECG shows normal sinus rhythm at 99/ minute.

You diagnose him with rhabdomyolysis and an acute kidney injury, likely of pre-renal cause. Intravenous fluid rehydration is initiated with intravenous 5% dextrose. You ask your colleague to check the patients blood tests in 12 hours.

What is the aim in correcting the patients hypernatraemia?

Reduce blood sodium to under 145 mmol/l as quickly as possible
> Reduce blood sodium by 0.5mmol/hr. The drop in 12 hours should be no greater than 6 mmol/l
Reduce blood sodium by 1mmol/hr. The drop in 12 hours should be no greater than 12 mmol/l
Aim for blood sodium above 145 mmol/l
Blood sodium does not require monitoring if intravenous fluids is running, CK falling and renal function improving


Acute Hyponatraemia

Definition = occurs within a duration of 48h

- over consumption of fluids
- prolonged race duration eg marathon, inadequate training

When hyponatraemia develops over a short duration, the ability of the brain to adapt is exceeded and cerebral oedema can result > can lead to CONFUSION, SEIZURES, COMA

Patients may die from brain herniation

Mx of Hyponatraemia in this situation:
- HYPERTONIC SALINE - A Small quick increase in the serum sodium is required in order to decrease intracranial pressure. Hypertonic saline 3% boluses (w senior advice) are the most appropriate treatment to improve neurological status in such patients


Mx of Hyponatraemia

Always ascertain volume status in Hyponatraemia

- Rehydration with NaCl 0.9% or a balanced crystalloid (Hartmann's)
- Avoid rapid correction of Na+ in order to reduce risk of osmotic Cx such as Central Pontine Myelinolysis

- Check urine and serum osmolality:
> Does patient meet criteria for SIADH?
> Treat underlying cause where possible
- Fluid restriction (500-750mL/d)
- Monitor fluid balance and perform daily weights
- Consider Demeclocycline or Tolvaptan (under specialist supervision) - Both inhibit action of ADH

- Fluid and Salt Restriction
- Consider diuretics
- Treat underlying cause (e.g. Cardiac F)


Pseudohyponatraemia - Causes

Hyperlipidaemia - high serum concentrations of triglycerides, cholesterol
Taking blood from drip arm
Immunoglobulin therapy
Patients with high serum protein such as myeloma patients.


Hypernatraemia - Causes

Hypernatraemia is usually caused by:

excess of hypertonic fluids (IV saline, enteral or parenteral nutrition);
excessive free water loss - renal (diabetes insipidus, diuretics, osmotic diuresis as with hyperglycaemia), GI (diarrhoea, vomiting), skin (sweating, burns)
reduced thirst - seen in very old and very young patients.


Mx of Hyponatraemia in Liver Disease

The management of hyponatraemia in liver cirrhosis is a difficult area and a consensus hasn't been reached in all areas of management. However in patients with mild hyponatraemia (126-135 mmol/L) the recommendations are consistent. The British Society of Gastroenterology recommendations are as follows:

Sodium 126-135 mmol/L with normal creatinine - Continue normal diuretic regimen and observe, do not fluid restrict the patient.

Sodium 121-125 mmol/L with normal creatinine - International opinion is to continue diuretics, however, the British Society of Gastroenterology recommend a more cautious approach, and suggest either stopping diuretics or reducing the dose.

Sodium 121-125 mmol/L with raised creatinine (>150 mmol/L or >120 mmol/L and rising) - Stop diuretics and volume expand with human albumin solution 4.5%, gelofusine, or haemaccel

Sodium <121 mmol/L - Incredibly controversial, but the British society of gastroenterology suggest stopping diuretics and volume expanding with human albumin solution 4.5%, gelofusine, or haemaccel (which all contain sodium concentrations similar to that of normal saline).

They do, however, recognise that the level of evidence for this recommendation is 5 (or D) i.e. expert opinion, and further work needs to be done into the role of volume expansion and fluid restriction in cirrhosis.