Hyponatraemia. Dr Andy Lewington Consultant Nephrologist/Honorary Clinical Associate Professor Leeds Teaching Hospitals

Transcription

1 Hyponatraemia Dr Andy Lewington Consultant Nephrologist/Honorary Clinical Associate Professor Leeds Teaching Hospitals

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3 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

4 Outline Physiology Causes Complications Clinical assessment Treatment Case presentation

5 Physiology Sodium Extracellular ion Normal > 135 meq/l Responsible for osmolality Osmolality Total no. of moles of solute/ kg of slovent mosmol/kg Determines transcellular distribution of water

6 Physiology Sodium concentration/osmolality maintained by Urinary excretion of sodium and water ADH secretion Water load ingestion Suppression of ADH Excretion of dilute urine

7 Physiology Max daily urine output 10 L Min urine osmolality mosmol/kg Max urine osmolality 1000 mosmol/kg (age based)

8 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

9 Causes Pseudohyponatraemia Hyperlipideamia Hyperglyceamia Myeloma - hyperproteinaemia Hypovolaemic hyponatraemia Diuretics Thiazides GI losses Adrenal insufficiency Osmotic diuresis Mannitol Salt wasting nephropathies

10 Causes Hypervolaemic hyponatraemia Heart failure reduced cardiac output Unsuppressed ADH Liver cirrhosis arterial vasodilatation Unsuppressed ADH CKD egfr<15 Min urine osmolality mosmol/kg

11 Causes Euvolaemic hyponatraemia Malnourishment Exercise excessive water ingestion Reset osmostat Pregnancy Primary polydipsia Prostate surgery Sorbitol irrigation - absorption SIADH

12 Causes of SIADH CNS disease Malignancy Drugs Carbamazepine Fluoxetine Serotonin inhibitors Hypothyroidism Adrenal insufficiency Pulmonary disease Recent surgery

13 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

14 Investigations U&Es Bicarbonate Glucose Serum osmolality Urine Na Urine osmolality

15 Assessment of Hyponatreamia

16 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

17 Treatment Key considerations Duration of hyponataemia? Acute < 48hrs Chronic > 48hrs Severity?

18 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)

19 Treatment

20 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

21 Indian J Crit Care Med Jul-Aug; 17(4):

22 Treatment Mild to moderate hyponatraemia ( meq/l) Less severe symptoms Identify reversible cause Fluid restrict < 800 mls/day Oral salts 9g ~ 154mEq sodium

23 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

24 Treatment Renal Replacement Therapy Acute onset < 48hrs In setting of AKI Volume overload Oliguric Rapid correction recommended Intermittent HD CRRT

25 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

26 Case Presentation

27 Case Presentation 65 year old male End stage kidney failure Membranous GN Kidney transplant 2006 Biventricular heart failure Bronchiectasis

28 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

29 Case Presentations Mycophenolate Mofetil Tacrolimus Paracetamol Fluoxetine Lansoprazole Atorvastatin Ramipril Furosemide

30 Case Presentation On examination Alert, not confused Normovolaemic on examination BP 80/50 Crackles at lung bases O 2 Saturations 95%

31 Case Presentation Investigations Hyponatraemia Hypercalcaemia Elevated CRP

32 Case Presentation

33 20/11/17

34 20/11/17

35 Heart size is at the upper limits of normal. There is perihilar interstitial oedema

36 Case Presentation Initial treatment IV 0.9% sodium chloride fluid resucitation caution Oral fluid restriction Fluoxetine stopped Pamidronate Dietician input

37 20/11/17

38 20/11/17 Hypo-osmolar hyponatraemia

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40 23/11/19

41 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

42 Case Presentation Respiratory referral Bronchoscopy abnormal left lower lobe with extensive secretions

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44 27/11/17

45 BAL Result Patient allergic to Trimethoprim Commenced on Primaquine (G6pd normal) and clindamycin for 21days

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47 Patient discharged Case Presentation

48 Summary Chronic hypo-osmolar hyponatraemia Euvoleamic Multiple causes Malnourished Fluoxetine PCP Urine osmolality 146 mosmol/kg SIADH

49 Conclusions Comprehensive clinical evaluation Duration Severity Investigations Cause Treatment Acute rapid correction possible Chronic gradual correction

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