Hyponatraemia GIM SpRTraining Day September 2016

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Hyponatraemia GIM SpRTraining Day September 2016 Jenny Clayton Consultant Diabetes and Endocrinology Nottingham University Hospitals

Transcript of Hyponatraemia GIM SpRTraining Day September 2016

Page 1: Hyponatraemia GIM SpRTraining Day September 2016

Hyponatraemia

GIM SpR Training Day

September 2016

Jenny Clayton

Consultant Diabetes and Endocrinology

Nottingham University Hospitals

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Plan of action- hyponatraemia

• Why is it important?

• Classification of hyponatraemia

• Case history

• Diagnostic work up

• Emergency treatment acute severe hyponatraemia

• Treatment non severe hyponatraemia

Hyponatraemia guideline

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Why is it important?

• Common – present in 15-20% emergency admissions to

hospital.

• Spectrum mild/subtle symptoms to severe/life-threatening

symptoms.

• Associated increased mortality and morbidity.

• Associated increased length of stay.

• Presents to all specialities: medical, oncology, intensivists,

surgeons, neurosurgeons.

• Potential to do harm- risk of osmotic demyelination.

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How can it be classified?

• Symptoms?

– Mild/asymptomatic

– Moderate

– Severe

• Sodium concentration?

– Mild

– Moderate

– Severe

• Onset?

– Acute

– Chronic

• Volume status?

– Hypovolaemic

– Euvolaemic

– Hypervolaemic

• Aetiology?

– Usually multifactorial in

medical in-patients (75%)

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• Symptoms relate to the sodium concentration and

time scale of the drop (acute vs chronic).

0 24 48 72 96 120 144 168120

125

130

135

140

145

Patient 2

Patient 1

Time (hours)

So

diu

m c

on

cen

trati

on

(mM

ol/

l).

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• Causes according to volume status.

• Accurate diagnosis essential to guide appropriate treatment.

Hypovolaemic Euvolaemic Hypervolaemic

Renal sodium loss Thiazide diuretics CCF

Osmotic diuresis Hypothyroidism Cirrhosis

Diuretic agents 2º Adrenal insufficiency Nephrotic syndrome

1º Adrenal insufficiency SIADH Renal failure

Salt-wasting nephropathy CNS disorders Pregnancy

Cerebral salt wasting Cancer

Extrarenal sodium loss Drugs

D & V Pulmonary disease

Blood loss Miscellaneous e.g.post op

Fluid sequestration (3rd space) Decreased solute intake

Excess sweating

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Case History

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Case History – day 1, admission 1

• 39 year old male.

• MOPED accident 16/3/16, alcohol related.

• Admission under trauma team

• Subdural haematoma

• Pneumocephalus

• Basal skull fracture

• Complex facial fracture

• Sesamoid fracture left thumb

• CT CAP: adrenal incidentaloma

Na 138

K 4.1

Urea 4.1

Creatinine 77

LFTs normal

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Case history- day 2, admission 1

• Discharged home

• FU orthopaedic hand clinic

• FU ENT

• FU ophthalmology

• Endocrine referral re adrenal incidentaloma.

Bloods that day

• Na 126

• Random cortisol 619

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Case history – 4 days later…

• Seen at orthopaedic pre-op clinic

• Feeling unwell, nauseus

• Na 116

• K 4.7

• Urea 2.5

• Creat 54

Emergency admission to medical ward arranged

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Case history- day 1, admission 2

• Further history?

• Further assessment?

• Investigations?

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Results

• Na 116

• K 4.7

• Urea 2.5

• Creat 54

• Random cortisol 407

• Calcium 2.23

• TSH 3.8

• Serum osmolality 236

• Urine osmolality 634

• Urine Na 138

• Urine K 62

• CXR Right basal atelectesis

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Diagnosis- cause of hyponatraemia?

Management?

Fluid restriction?

Frequency of electrolyte checks?

Sodium rise targets?

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Case history - progress

• Fluid restriction 1.5 L • Day 1: sodium 116 mmol/l

• Day 2: sodium 117 mmol/l

• Day 3: sodium 120 mmol/l

• Day 4: sodium 118 mmol/l

• Day 5: sodium 118 mmol/l

• Day 6: sodium 118 mmol/l

• Day 7: sodium 121 mmol/l

• Day 8: sodium 122 mmol/l

• Day 9: sodium 131 mmol/l �discharged

• 2 weeks later @ GPs: sodium 136 mmol/l

Was the fluid restriction

effective?

Alternative management

strategies?

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What is the latest guidance for the work up

and management of hyponatraemia?

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Management of hyponatraemia

• Joint guidance European

endocrine society, European

Renal society, European

Society Intensive care.

• First published consensus

guideline on management.

• Published 2014, European

Journal of Endocrinology, 47

pages long!

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UK

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Work up/investigations

Careful history/drug history

Assessment of volume status/examination

Drug category Examples

Anticancer agents Vinca alkaloids (vincristine, vinblastine)

Platinum compounds (cisplatin, carboplatin)

Alkylating agents (IV cyclophosphamide, melphalan)

Antidepressants SSRI, Tricyclics, MAOIs

Anti-epileptic drugs Carbamazepine, Oxycarbazepine, Sodium valproate

Anti-hypertensive agents ACE inhibitors

Diuretics Thiazides, Indapamide, Amiloride, Loop diuretics

Antipsychotic drugs Phenothiazines, Butyrophenones (haloperidol)

Proton pump inhibitors Omeprazole

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Work up/investigations

Careful history/drug history

Assessment of volume status

Screening blood/urine panel

• U&Es

• Glucose

• Lipids

• Thyroid function

• Liver function

• Cortisol

• Plasma osmolality

• Urine osmolality

• Urine sodium

• Urine potassium

Is it hypotonic hyponatraemia?Could it be pseudo hyponatraemia?

Is the patient hyperglycaemic?Could it be a drip arm sample?

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Work up/investigations

Careful history/drug history

Assessment of volume status

Further investigations

• CXR

• CT head

• Short synacthen test

• CT CAP

Screening blood/urine panel

• U&Es

• Glucose

• Lipids

• Thyroid function

• Liver function

• Cortisol

• Plasma osmolality

• Urine osmolality

• Urine sodium

• Urine potassium

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Aetiology according to volume status and

urinary sodium

HYPOVOLAEMICHYPOVOLAEMICHYPOVOLAEMICHYPOVOLAEMIC EUVOLAEMICEUVOLAEMICEUVOLAEMICEUVOLAEMIC HYPERVOLAEMICHYPERVOLAEMICHYPERVOLAEMICHYPERVOLAEMICUrinary Na >20mmol/L

Urinary Na <20mmol/L

Urinary Na>20mmol/L

Urinary Na >20mmol/L

Urinary Na <20mmol/L

Renal losses• Osmotic diuresis• Diuretic therapy• Addison’s disease• Salt-losing nephropathy•Cerebral salt wasting

Extra-renal losses• Diarrhoea• Vomiting• Burns• Fistulae• Pancreatitis

• SIADH• Glucocorticoiddeficiency• Hypothyroidism• Diuretic therapy• Drugs

• Acute or chronic renal failure• Diuretic therapy

• Nephroticsyndrome• Cirrhosis• Cardiac failure

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Management of hyponatraemia

Balance of risk

• Risk of cerebral oedema greatest if drop in sodium is severe and

acute (<48hrs).

• Risk of osmotic demyelination is greater with more chronic

hyponatraemia (>48hrs), severe hyponatraemia and rapid

correction.

Untreated severe hyponatraemia.

Risk of neurological sequelae from cerebral oedema

Treatment of severe hyponatraemia.

Risk of neurological sequelae from osmotic demyelination syndrome

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Osmotic demyelination

• Develops one to several days after treatment of hyponatraemia.

• Demyelination of pontine and extrapontine (thalamus, basal

nuclei, cerebellum) neurons.

• Flaccid quadriplegia, pseudobulbar palsy, seizures, coma, death.

• At risk groups: elderly, children, malnourished, alcoholics, CNS

disease, hypoxaemia.

MRI appearances:T2 images show hyperintense areas of demyelination.

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Management of severe hyponatraemia

Guidance same in European and UK papers.

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* If low body weight give 3% saline at 2mls/kg body weight over 20 minutes

Previous approach: Adrogue

Formula

Change in serum Na

= Infusate Na (513)-serum Na

Total body water+1

Total body water = Body weight x 0.6/0.5/0.45

(young male/young female,old male/old female)

Hyponatraemia with severe symptoms(somnolence, seizures, coma)

First hour management

• 150 mls 3% (hypertonic)

saline over 20 mins*.

• Check sodium

concentration.

• Further 150 mls 3% saline

and repeat until sodium

risen by 5 mmol/L.

• Manage in level 2/3 bed.

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Hyponatraemia with severe symptoms(Vomiting, somnolence, seizures, coma)

First hour management

• 150 mls 3% (hypertonic)

saline over 20 mins*.

• Check sodium concentration.

• Further 150 mls 3% saline

and repeat until sodium risen

by 5 mmol/L.

• Manage in level 2/3 bed.

Subsequent management

• Stop hypertonic saline.

• Slow infusion 0.9% saline.

• Diagnosis specific treatment.

• Limit rise in sodium in first 24

hours to ≤ 10mmol/l and

8mmol/l each following 24

hours.

• Check sodium at least 6

hourly.

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– If sodium rise is excessive then IV dextrose or

desmopressin may be required.

– Small increase in sodium often gives major clinical

improvements.

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Hyponatraemia with moderately severe

symptoms (nausea, confusion, headache)

• Cause specific treatment.

• Stop contributing/provoking

medications if possible.

• Immediate treatment with single

infusion of 150 mls 3% hypertonic

saline over 20 minutes.

• Aim 5 mmol/l increase in 24 hours.

• Limit sodium rise to ≤ 10mmol/l in first

24 hrs and 8mmol/l in each following

24 hours.

• Check sodium at 1,6 & 12 hours.

Alarm bells………

European

guideline

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Management of non severe hyponatraemia

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General hyponatraemia management

• Stop non-essential fluids, medications that can

contribute/provoke.

• Cause specific treatment.

• Avoid increase in sodium concentration >10mmol/l in first 24

hours and >8 mmol/l in each subsequent 24 hours.

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Hyponatraemia with hypovolaemia*

• Restore extracellular volume with IV 0.9% saline or a balanced

crystalloid solution at 0.5-1 ml/kg/hour.

• If haemodynamic compromise the need for rapid fluid

resuscitation overrides the risk of an overly rapid increase in

sodium.

• Close biochemical and clinical monitoring, may need level 2

bed.

* If unclear if hypovolaemic or euvolaemic can give 1 litre 0.9% saline over

12 hours and review response at 6 and 12 hours.

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Hyponatraemia with hypervolaemia

• Treat underlying condition.

• Fluid restriction to prevent further fluid overload.

• OK to use loop diuretics (fluid loss>urine sodium losses)

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Euvolaemic hyponatraemia

• Confirm it is hypotonic

hyponatraemia

– Plasma osmolality <275

mOsm/kg.

• Check urine osmolality

– Urine osmolality

<100mOsm/Kg suggests

primary polydipsia or

beer potomania.

• Confirm diagnosis of SIADH

– Hypotonic plasma (<270

mOsm/kg).

– Inappropriate urine

osmolality (>100 mOsm/kg);

usually > plasma osmolality.

– Excessive renal sodium loss

(>20mmol/l).

– Normal renal, adrenal and

thyroid function.

– Interpret with caution if

patient on diuretics.

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Treatment of SIADH

• Treat underlying cause

• Fluid restriction

– Use estimate of

electrolyte-free water

clearance to predict

response

– Furst formula:

urine/plasma

electrolyte ratio (U/P)

Furst formula

U/P electrolyte ratio=

Urine [Na] +Urine [K] mmol/l

Serum [Na] mmol/l

U/P < 0.5 :Fluid restrict to 1000mls

U/P 0.5-1.0 :Fluid restrict to 500mls

U/P >1.0 : Fluid restriction unlikely to

be beneficial

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Treatment of SIADH

UK consensus

• Fluid restrict as first line:

Furst formula (24-48 hours)

• Second line (consult

endocrinologist)

– Demeclocycline 150-

300mg tds

– Tolvaptan 15mg OD: 6

hourly Na checks.

Prescribe as single doses.

Allow free fluids.

European guide

• Fluid restrict as first line:

Furst formula

• Second line

– Increased solute with 0.25-

0.5g/kg per day of urea or

– Low dose loop diuretic and

oral sodium chloride

• Vasopressin receptor

antagonists are not

recommended.

• Demeclocycline or lithium is

not recommended.

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Black triangle

alerts for

tolvaptan

Use with caution

and very careful

monitoring

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UK consensus

algorithm

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Summary

• Hyponatraemia is very common. Careful clinical

assessment, investigation and interpretation of the

biochemistry essential.

• Severe hyponatraemia is a medical emergency and

needs cautious management. Primum non nocere.

• New algorithms offer practical guidance.

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Thank you!