Hyponatraemia Dr Andy Lewington Consultant Nephrologist/Honorary Clinical Associate Professor Leeds Teaching Hospitals A.J.P.Lewington@leeds.ac.uk
Disclosures of Interest Associate Clinical Director NIHR Leeds In-Vitro Diagnostic Co-operative NICE AKI and CKD Guideline Update Committee Member 2018 NICE Diagnostic Assessment Programme Committee for Point of Care Creatinine Testing before Contrast BMJ Best Practice Editor
Outline Physiology Causes Complications Clinical assessment Treatment Case presentation
Physiology Sodium Extracellular ion Normal > 135 meq/l Responsible for osmolality Osmolality Total no. of moles of solute/ kg of slovent 275-290 mosmol/kg Determines transcellular distribution of water
Physiology Sodium concentration/osmolality maintained by Urinary excretion of sodium and water ADH secretion Water load ingestion Suppression of ADH Excretion of dilute urine
Physiology Max daily urine output 10 L Min urine osmolality 50-100 mosmol/kg Max urine osmolality 1000 mosmol/kg (age based)
Clinical Features Symptoms depend on severity and rate of sodium reduction gradual decreases in sodium usually result in minimal symptoms rapid decreases can result in severe symptoms (cerebral oedema) Polydipsia muscle cramps Headaches Confusion altered mental status Coma status epilepticus
Causes Pseudohyponatraemia Hyperlipideamia Hyperglyceamia Myeloma - hyperproteinaemia Hypovolaemic hyponatraemia Diuretics Thiazides GI losses Adrenal insufficiency Osmotic diuresis Mannitol Salt wasting nephropathies
Causes Hypervolaemic hyponatraemia Heart failure reduced cardiac output Unsuppressed ADH Liver cirrhosis arterial vasodilatation Unsuppressed ADH CKD egfr<15 Min urine osmolality 200-250 mosmol/kg
Causes Euvolaemic hyponatraemia Malnourishment Exercise excessive water ingestion Reset osmostat Pregnancy Primary polydipsia Prostate surgery Sorbitol irrigation - absorption SIADH
Causes of SIADH CNS disease Malignancy Drugs Carbamazepine Fluoxetine Serotonin inhibitors Hypothyroidism Adrenal insufficiency Pulmonary disease Recent surgery
Clinical Assessment Comprehensive clinical evaluation Mental status Identify potential cause Recent surgery, medication etc Volume status Hypovolaemic Renal or GI fluid losses Euvolaemia SIADH Hypervolaemia (oedema) Heart failure Liver cirrhosis
Investigations U&Es Bicarbonate Glucose Serum osmolality Urine Na Urine osmolality
Assessment of Hyponatreamia
Assessment of Hypo-osmolar hyponatraemia Na < 135 meq/l Urine Osm < 100 Urine Osm > 100 Psychogenic Polydipsia Assess kidney function Normal Kidney disease Volume status? Primary kidney disease Euvolaemic Hypervolaemic Hypovolaemic SIADH e.g. Drugs UNa > 20 UNa < 20 UNa > 20 UNa < 20 Kidney Dx Cirrhosis Heart failure Kidney losses e.g. duiretics Extra-renal losses e.g. Vomiting Diarrhoea, Burns
Treatment Key considerations Duration of hyponataemia? Acute < 48hrs Chronic > 48hrs Severity?
Treatment Rate of correction of sodium Severe hyponatraemia ( Na < 120 meq/l) with neurological symptoms Rapid initial correction 4-6 meq/l in first 4-6 hrs Identify cause (Avoid correcting by > 8 meq/l in 24 hr period if > 48hrs duration)
Treatment
Treatment Risk of overly rapid correction Osmotic demyelination Occurs a few days afterwards Results from rapid movement of water out of cells pontine and extra-pontine regions seizures disturbed consciousness gait changes MRI changes
Indian J Crit Care Med. 2013 Jul-Aug; 17(4): 231 233.
Treatment Mild to moderate hyponatraemia (120-129 meq/l) Less severe symptoms Identify reversible cause Fluid restrict < 800 mls/day Oral salts 9g ~ 154mEq sodium
Treatment Role of ADH antagonist? Tolvaptan oral Used in patients with hyponatraemia secondary to SIADH Risks of Overly rapid correction Hepato-toxicity limit use < 30 days
Treatment Renal Replacement Therapy Acute onset < 48hrs In setting of AKI Volume overload Oliguric Rapid correction recommended Intermittent HD CRRT
Treatment Renal Replacement Therapy Chronic onset > 48hrs In setting of AKI Volume overload Oliguric Gradual correction recommended CRRT Monitor Na + on ABG Adjust dose of CRRT
Case Presentation
Case Presentation 65 year old male End stage kidney failure Membranous GN Kidney transplant 2006 Biventricular heart failure Bronchiectasis
Case Presentation Admitted 20/11/17 Felt generally unwell for a month Lethargy Reduced appetite Wt 52Kg Fevers Increasingly breathless for last 3 months reduced exercise tolerance
Case Presentations Mycophenolate Mofetil Tacrolimus Paracetamol Fluoxetine Lansoprazole Atorvastatin Ramipril Furosemide
Case Presentation On examination Alert, not confused Normovolaemic on examination BP 80/50 Crackles at lung bases O 2 Saturations 95%
Case Presentation Investigations Hyponatraemia Hypercalcaemia Elevated CRP
Case Presentation
20/11/17
20/11/17
Heart size is at the upper limits of normal. There is perihilar interstitial oedema
Case Presentation Initial treatment IV 0.9% sodium chloride fluid resucitation caution Oral fluid restriction Fluoxetine stopped Pamidronate Dietician input
20/11/17
20/11/17 Hypo-osmolar hyponatraemia
20/11/17
23/11/19
CT 23/11/19 CT Thorax Abdomen Pelvis with contrast : Comparison is made with previous CTs up to including 14/11/2008. There are progressive lung changes with quite extensive groundglass type inflammatory change predominantly in the upper lobes. Bronchiectasis at the bases and plugging of the left lower lobe bronchus with low density material. Comment: Progressive lung changes with new groundglass change
Case Presentation Respiratory referral Bronchoscopy abnormal left lower lobe with extensive secretions
25/11/17
27/11/17
BAL Result Patient allergic to Trimethoprim Commenced on Primaquine (G6pd normal) and clindamycin for 21days
Patient discharged Case Presentation
Summary Chronic hypo-osmolar hyponatraemia Euvoleamic Multiple causes Malnourished Fluoxetine PCP Urine osmolality 146 mosmol/kg SIADH
Conclusions Comprehensive clinical evaluation Duration Severity Investigations Cause Treatment Acute rapid correction possible Chronic gradual correction
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