by sadek al rokh

1. Hyponatremia
According to NICE Guidelines
By/Sadek Al-Rokh
 Consultant Acute medicine & Endocrinology and Diabetes
(East Sussex trust UK).
 MRCP (UK).
 SCE Acute medicine of the royal college of physicians .
 SCE Endocrine and diabetes of the royal college of
physicians.
 European board in Endocrine and diabetes.

2. Hyponatremia Defined
 Hyponatremia is defined as a serum sodium level of less than 135 mEq/L.
 Hyponatremia may be further classified as mild (135-130 mEq/L), moderate(125-129)
or severe (less than 125 mEq/L).
 Severity of the symptoms is dependent both on the serum sodium concentration as
well as the rapidity of change.
 Hyponatremia is a common electrolyte disorder affecting 15- 30% of hospital
admissions. It is common in older patients with multiple co-morbidities.
 Overall hyponatraemia is associated with increased morbidity and mortality.
 Acute and severe hyponatremia may result in cerebral edema, seizures, coma, and
cardiopulmonary arrest.
 But even chronic mild hyponatremia is associated with poor outcomes. These
patients may have subtle neurocognitive deficits that are difficult to detect, and
resolve with correction of the hyponatremia.
 These deficits put individuals at risk for falls and traumatic injury.
 Patients with even mild hyponatremia have a 30% higher risk of death and are
hospitalized 14% longer than those with a normal serum sodium.

3. Causes of Hyponatremia
 Hypovolemic Hyponatremia:
 Both total body sodium and water are decreased but sodium to
a greater extent
 Fluid loss: vomiting, diarrhea, sweating, GI suction
 Renal causes: salt-wasting nephropathies, renal tubular acidosis,
mineralocroticoid deficiency, diuretics, osmotic diuresis
 Third spacing fluids: burns, rhabdomyolysis, bowel obstruction
 Hypervolemic Hyponatremia:
 Total body sodium increased with a relatively larger increase in
total body water
 Chronic renal failure
 Cirrhosis
 Heart failure.

4. Causes of Hyponatremia
 Euvolemic Hyponatremia:
 Total body sodium normal but increased total body water
 SIADH (2nd to atypical lung infection, malignancy, drug induced)
 Psychogenic polydipsia
 Hypothyroidism
 Adrenal insufficiency
 Water intoxication
 Dilutional Hyponatremia:
 Hyperglycemia (i.e. in DKA, Hyperosmolar hyperglycemic states).
 Pseudohyponatremia:
 hyperlipidemia, hyperproteinemia.

5. Corrected Sodium in hyperglycemia
 Sodium Correction in hyperglycemia =
measured Na + [(glucose level - 100) x 0.016]

6. Clinical Manifestations
 The clinical manifestations define the severity of the hyponatremia (i.e. the serum level
does not define severity). Symptoms and signs are dependent on both the serum level
as well as the rapidity of change in the serum sodium.
 Mild/moderate Hyponatremia:
 Headache
 Nausea/vomiting
 Muscle cramps
 Lethargy
 Restlessness
 Severe Hyponatemia:
 Disorientation
 Focal neurologic deficits
 Seizures (Status epilepticus common)
 Coma

7. Management of Hyponatremia with mild
symptoms :
Broad recommendations:
 Assessment of volume status and establishing the cause and duration of hyponatremia
are essential to guide emergency management.
 In patients with asymptomatic, chronic mild hyponatremia 125-135mmol/L no further
investigation or treatment may be required. These patients do not usually require
admission and should be referred back to their GP +/- conside endocrine/renal referral.
 These guidelines refer to patients with symptoms and a serum sodium <130mmol/L, or
asymptomatic patients with marked hyponatremia <125mmol/L.
 Patients with severe hyponatremia <120mmol/L and rapid onset hyponatreamia with
neurological impairment are at very high risk and should be considered for HDU
admission.
 Rehydration should be the mainstay of people with hypovolaemia and hyponatreamia.
 Fluid restriction should be the main stay of treatment for all other causes of hyponatremia.
 The rate of correction of hyponatremia should generally be a rise of 8- 10 mmol/L/24
hours but never exceed 12mmol/L/24 hours due to the risk of sudden osmotic shift and
pontine demyelination.

8. Management of acute or chronic
hyponatremia with mild symptoms :
 Indication for possible ICU admission if :
 Reduced level of consciousness
 Fits
 Need for treatment with Hypertonic Saline
 [Na+] is <115 mmol/l, where it is not apparent that this is chronic. These patients
may not have serious neurological symptoms as above but it may still be
desirable to raise [Na] by initially by 0.5 mmol/hr, but no more than 10 mmol/24
hours.
 Rates of correction:
 Safe limit – 10 mmol/L in first 24 hours, 8 mmol/L in subsequent 24 hours
 Groups at more risk of osmotic demyelination are elderly patients, children < 16,
malnourished, alcoholics, CNS disease and post operative patients.
 May need to consider slow lowering limits for correction in these groups of
patients.

9. Management of Hyponatremia with
mild symptoms :
DANGER of Rapid Overcorrection:
 Rapid overcorrection of serum sodium can cause osmotic demyelination
syndrome (ODS)
 ODS can manifest as ataxia, quadraplegia, CN palsies or “locked-in” syndrome
 Can occur up to 7 days after rapid correction
 Preventing overcorrection
 Do not increase serum sodium by more than 6-8 mEqL in the 1st 24 hours
 Fluid restrict patient after relief of neurologic emergency
 Monitor urine output (UO): If UO > 100 ml/hr, send urine osmolarity + urine sodium
 Urine osmolarity < 100, give DDAVP 1 mcg
 Correct Hypokalemia
 Often will see hypokalemia in patients with severe hyponatremia
 Correction of hypokalemia can improve hyponatremia
 Oral repletion safe and efficacious if patient tolerating oral intake

10. STEP 1: EVALUATE
 Assess for symptoms & signs of hyponatraemia.
 Is patient on drugs that can cause hyponatraemia?
 RV fluid balance especially post op.
 History of or symptoms/signs suggesting : endocrine dx,
cardiac/lung/liver/renal disease, SIADH or its causes.
 Perform Investigations:
 U&Es, Mg, bicarbonate, LFTs, glucose
 Paired serum & urine osmolality (but unhelpful if diuretics have been given)
 Urine Spot Na+
 TSH, FT4
 Random Cortisol (if Adrenal insufficiency is suspected • LFTs

11. STEP 2: ASSESS VOLUME STATUS
(Hypovolaemic Hyponatraemia)
 Clinically : The patient will be dehydrated
 Investigations:
 Extrarenal Causes of Na loss : Vomiting ,Diarrhoea , Third Spacing (Pancreatitis, Bowel Obstruction,
Burns)
 Urine Na < 20 mmol/l , Urine Osmol > 100 mOsmol/Kg
 Renal Causes of Na loss : Diuretics, Addisons disease ,Salt wasting nephropathy , Proximal RTA .
 Urine Na > 20 mmol/l , Urine Osmol > 100 mOsmol/Kg
 Treatment:
 Treat cause (e.g. stop diuretics, steroid replacement in Addisons)
 Restore intravascular volume with IV crystalloids.
 If symptomatic, e.g give fluid challenge of 1 L 0.9% N Saline over 2-4 hours. Monitor Na 1-2 hourly.
 If asymptomatic, restore volume with 0.9% Saline more gradually.

12. STEP 2: ASSESS VOLUME STATUS
(Euvolemic Hyponatremia)
 Clinically : The patient looks euvolemic.
 Investigations :
 SIADH
 Drugs (e.g. antidepressants, antipsychotics, anti hypertensive like ACE inhibitor and ARBS, carbamazepine,
chlorpropamide, opiods, vincristine, NSAIDs)
 Glucocorticoid deficiency
 Hypothyroidism
 Urine Na > 20 mmol/l , Urine Osmol > 100 mOsmol/Kg , TSH, Am cortisone.
 Treatment:
 Stop offending drugs and hypotonic fluids.
 If significant symptoms, or rapid onset (< 24-48 hours) causing significant hyponatraemia, consider use of
Hypertonic Saline +/- Frusemide.
 If asymptomatic or mild symptoms → Water Restrict to < Urine Output (usually 750-1000 ml/day)
 Treat the underlying cause of SIADH, and in resistant cases , consider Demeclocycline or ADH Receptor
Antagonists (Tovaptan).

13. SIADH GUIDELINES
 Diagnosis of SIADH :
 Clinically euvolaemic.
 Excluded renal failure
 Excluded adrenal insufficiency
 Excluded severe hypothyroidism
 Urine Na+ > 20
 Urine Osmolality > 100
 Serum Osmolality < 275
 Consider and treat underlying cause e.g.
 Malignancy.
 Atypical lung infection (Legionella, mycoplasma).
 Drug induced

14. SIADH GUIDELINES
 Treating SIADAH:
1- Stop any drugs that can cause hyponatraemia. If thought to be drug induced this may be all that is
required. Monitor Na+ levels after stopping medications but there is no need to do fluid restriction unless Na+
not improving.
2- If serum NA is not improving do fluid restriction to <750 ml per day.
3- After fluid restriction if Na is not improving start Tovaptan :
Tolvaptan advice
If using Tolvaptan (ADH antagonist) the following is advised:
 Discuss with endocrinology team before administration. Prescription must be authorised by a consultant
 Remove any fluid restriction
 Allow patient to drink to thirst response
 Initiate at a dose of 15mg stat.
 Repeat Na+ 6 hours later
 Repeat dose if no improvement after 24 hours (and if no improvement after second dose – reconsider
diagnosis)
 May only need one or two doses to correct sodium levels back to normal so do not prescribe on the
regular side of the chart
4- Demeclocycline (150 - 300 mg 6 hourly) may be indicated in cases of SIADH resistant to fluid restriction – it
induces a nephrogenic diabetes insipidus reversing ADH effects but expert advice should be sought before
initiation

15. Drug induced SIADH
Antihypertensives ACE Inhibitor, ARBS, Amlodipine
Diuretics Thiazides, Indapamide, Amiloride, loop
diuretics.
Anti-Psychotics TCA, SSRI, , Quatipane , Halopridol ,
Phenothiazines, Butyrophenones
Anti-Diabetics Sulphonylures
Anti-epileptics Carbamazepine, sodium valproate,
barbiturates.
Proton pump inhibitors Proton pump inhibitors
Anticancer agents Vinca alkaloids (e.g. Vincristine), platinum
compounds (e.g. Cisplatin), Alkylating agents
(e.g. Cyclophosphamide)

16. STEP 2: ASSESS VOLUME STATUS
(Hypervolaemic Hyponatraemia)
 Clinically: The patient looks hypervolemia.
 Investigations:
 Urine Na < 20 mmol/l
 Urine Osmol > 100 mOsmol/Kg
 Cardiac Failure
 Cirrhosis
 Nephrotic Syndrome
 Urine Na > 20 mmol/l
 Urine Osmol > 100 mOsmol/Kg
• Chronic Renal Failure
 Treatment
 Treat the underlying disease.
 Water and Salt Restriction.
 If severe water overload, co-administer loop diuretic (Furosemide).

17. Management of acute or chronic hyponatremia with
severe CNS symptoms : (Hyponatremic
encephalopathy)
 Symptoms of hyponatremic encephalopathy (Acute symptomatic
hyponatraemia) : (CNS disturbance)
 Coma
 Confusion
 Drowsiness
 Reduced GCS
 Seizures
 Encephalopathic

18. Management of acute or chronic hyponatremia with
severe CNS symptoms : ( Hyponatremic
encephalopathy)
 Discuss with ICU and if appropriate, ideally move to a Level 2 monitored
environment
 Hypertonic saline :
 Administer 1.8% hypertonic saline* 300m IV over 30 minutes Aim is to
improve symptoms NOT correct Na+ back to normal
 Or 150 ml of hypertonic saline 3% over 15 min is given according to other
guidelines.
 Repeat VBG after 20 minutes if no clinical improvement. If Na+ remains the
same, a repeat bolus dose of hypertonic saline can be given.
 Target: Serum sodium must be raised urgently (but by no more than 1-2
mmol/L per hour in first 2-3 hours) until serious symptoms resolve.
 To increase Na 5 mmol, then shift to isotonic saline or fluid restriction
according to the case.

19. Management of hyponatremia in special
cases :
 The Patient with Cirrhosis and Hyponatraemia
 Water and salt restriction are the mainstay of treatment, with use of aldosterone
antagonists as required. Diuretics should be withheld if severely hyponatraemic.
 Treatment is often difficult and special expertise should be sought.
 Primary Adrenal deficiency
 This should be suspected if hyponatraemia is associated with postural
hypotension and significant volume depletion (without an obvious alternative
cause of sodium loss). Hyperkalaemia and hypoglycaemia can also be present.
 If the patient is hemodynamicaly unstable start Hydrocortisone 100 mg iv at
once since you suspected adrenal insufficiency.
 Try to take blood sample for ransom cortisone and short synactin test before
starting hydrocortisone.