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SIADH

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Presentation about hyponatremia and SIADH

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SIADH

  1. 1. A case of Hyponatraemia Phyo Aung & Li-ni Lin
  2. 2. Ms JH <ul><li>56yo female referred from GP for bilateral lower leg cellulitis - unresponsive to Augmentin DF </li></ul><ul><li>Prior to presentation at Angliss hospital </li></ul><ul><ul><li>3 weeks of gross bilateral ankle oedema </li></ul></ul><ul><ul><li>2 weeks of bilateral lower limb cellulitis </li></ul></ul><ul><ul><li>4 days since commencing Moduretic </li></ul></ul><ul><li>Hyperactive behaviour at night </li></ul><ul><li>Recently noted to be unsteady on feet. </li></ul>
  3. 3. Other medical conditions <ul><li>Epilepsy </li></ul><ul><li>Intellectual disability secondary to SSPE measles </li></ul><ul><li>Depression </li></ul>
  4. 4. Medications <ul><li>Premarin 300mcg mane </li></ul><ul><li>Premia 1tab mane </li></ul><ul><li>Sodium valproate 1000mg TDS </li></ul><ul><li>Carbamazepine 400mg BD </li></ul><ul><li>Citalopram 20mg nocte </li></ul><ul><li>Olanzapine 10mg nocte </li></ul><ul><li>Augmentin Duo Forte </li></ul><ul><li>Amiloride 5mg/Hydrochlorothiazide 50mg mane </li></ul><ul><li>Haloperidol 0.5mg nocte PRN </li></ul><ul><li>Paracetamol 1g QID PRN </li></ul>
  5. 5. Social History <ul><li>lives in supported accommodation for mentally disabled </li></ul>
  6. 6. On examination <ul><li>HR 73, BP 120/70, RR 16, Temp 36.6 </li></ul><ul><li>SaO2 99% on RA </li></ul><ul><li>Patient alert but confused </li></ul><ul><li>Chest clear </li></ul><ul><li>JVPNE </li></ul><ul><li>S1 and S2 heard, no murmurs </li></ul><ul><li>Abdomen soft and non tender </li></ul>
  7. 7. <ul><li>Lower limbs </li></ul><ul><ul><li>Erythematous </li></ul></ul><ul><ul><li>Warm to touch </li></ul></ul><ul><ul><li>Pitting oedema up to knees </li></ul></ul><ul><ul><li>(left more than right) </li></ul></ul><ul><ul><li>No ulcers or breaks in skin </li></ul></ul>
  8. 8. Investigations <ul><li>Na 118 </li></ul><ul><li>K 3.7 </li></ul><ul><li>Cl 83 </li></ul><ul><li>Bicarbonate 27 </li></ul><ul><li>Urea 4.4 </li></ul><ul><li>Creatinine 34 </li></ul><ul><li>FBE 103 /5.7/384 </li></ul>
  9. 9. <ul><li>Bilirubin 3 </li></ul><ul><li>ALP 114 </li></ul><ul><li>GGT 54 </li></ul><ul><li>ALT 12 </li></ul><ul><li>TP 64 </li></ul><ul><li>Albumin 30 </li></ul><ul><li>Lipase 24 </li></ul><ul><li>Ca 2.27 </li></ul><ul><li>Mg 0.88 </li></ul><ul><li>Phos 1.26 </li></ul>
  10. 10. <ul><li>CRP 31 </li></ul><ul><li>BSL 6.3 </li></ul><ul><li>TSH 1.93 </li></ul><ul><li>Vitamin B12 737 </li></ul><ul><li>Folate 19 </li></ul><ul><li>Serum osmolality 260 (280-300) </li></ul>
  11. 11. <ul><li>Urine Na 49 </li></ul><ul><li>Urine K 37 </li></ul><ul><li>Urine osmolality 370 </li></ul><ul><li>Urine MCS </li></ul><ul><ul><li>no WBC </li></ul></ul><ul><ul><li>no RBC </li></ul></ul><ul><ul><li>no significant growth </li></ul></ul>
  12. 12. CXR
  13. 13. <ul><li>CXR </li></ul><ul><ul><li>The lungs are clear. </li></ul></ul><ul><ul><li>No consolidation is seen. </li></ul></ul><ul><ul><li>There is no pleural effusion. </li></ul></ul><ul><ul><li>Cardiomediastinal contour is within normal limits. </li></ul></ul><ul><li>CT Brain </li></ul><ul><ul><li>Unremarkable </li></ul></ul>
  14. 14. Assessment <ul><li>1. Bilateral lower limb cellulitis and oedema </li></ul><ul><li>2. Hyponatraemia </li></ul><ul><li>Differential diagnoses: </li></ul><ul><ul><li>Drug-induced hyponatraemia +/- SIADH </li></ul></ul>
  15. 15. Initial Management <ul><li>Free Water restriction </li></ul><ul><li>Daily body weights </li></ul><ul><li>Slow iv N/Saline 12/24 </li></ul><ul><li>Moduretic ceased, commenced on frusemide orally 20mg daily </li></ul><ul><li>iv cephazolin 2g TDS </li></ul>
  16. 16. iv N/Saline infusion started
  17. 17. iv N/Saline infusion ceased
  18. 18. <ul><li>After discussion with Neurology registrar: </li></ul><ul><ul><li>carbamazepine ceased and replaced with levetiracetam 500mg BD for 5days then 1g BD </li></ul></ul>
  19. 19. Carbamazepine ceased, commenced on levetiracetam
  20. 20. Sodium levels during admission iv N/Saline infusion started iv N/Saline infusion ceased carbamazepine ceased, levetiracetam started
  21. 21. Further investigations <ul><li>US Doppler of both legs: </li></ul><ul><ul><li>On both sides the deep venous system is patent and compressible with no evidence for a thrombus. </li></ul></ul><ul><ul><li>The great saphenous vein is also patent on both sides. </li></ul></ul>
  22. 22. <ul><li>Echocardiogram </li></ul><ul><ul><li>Possible left diastolic dysfunction and mildly elevated PA pressure </li></ul></ul><ul><ul><li>Left atrium mildly dilated </li></ul></ul><ul><ul><li>Right atrium mildly dilated </li></ul></ul><ul><ul><li>Trivial MR and TR </li></ul></ul>
  23. 23. On Discharge <ul><li>Discussion with GP, who agreed to frequent U&E monitoring </li></ul>
  24. 24. 1997 <ul><li>Commenced on carbamazepine 100mg BD </li></ul><ul><ul><li>Major seizure requiring iv diazepam </li></ul></ul><ul><ul><li>Several partial seizures requiring phenytoin infusion </li></ul></ul><ul><ul><li>Patient already on sodium valproate 1200mg BD </li></ul></ul>
  25. 25. Why Sodium disorder ? <ul><li>Important and most common electrolyte abnormality </li></ul><ul><li>Has potential for significant morbidity and mortality </li></ul><ul><li>Its homeostasis is vital to normal physiologic function of cells </li></ul><ul><li>Most dominant extracellular cation </li></ul><ul><li>Normal level is 135  145 mmol /L </li></ul><ul><li>Hyponatremia is defined as < 135 mmol/L </li></ul><ul><li>Severe hyponatremia < 125 mmol/L </li></ul>
  26. 28. Clinical Presentation <ul><li>Symptoms ranging from nausea and malaise (Mild Reduction) to confusion, seizures and coma (Severe Reduction) </li></ul><ul><li>Neurological symptoms =due to intracerebral osmotic fluid shift and cerebral edema </li></ul><ul><li>Neurological symptoms depends upon rapidity and severity of the serum sodium drops </li></ul><ul><li>Can also find symptoms of associated medical conditions eg.CCF, Liver Failure, Renal Failure </li></ul>
  27. 29. Assessing Fluid Status <ul><li>Features of fluid overload </li></ul><ul><li>Elevated JVP </li></ul><ul><li>Crackles over lung bases </li></ul><ul><li>Odema </li></ul><ul><li>Features of reduced extracellular fluid </li></ul><ul><li>dry mucous membrane </li></ul><ul><li>tachycardia </li></ul><ul><li>postural hypotension </li></ul><ul><li>oliguria </li></ul><ul><li>increased urine specific gravity </li></ul>
  28. 30. Investigations <ul><li>Urine Sodium and Osmolarity </li></ul><ul><li>Urine:Plasma osmolarity normal ( >1.3:1) </li></ul><ul><li>Serum Osmolarity and electrolytes </li></ul><ul><li>Thyroid Function tests </li></ul><ul><li>Liver function tests </li></ul><ul><li>Urea and Creatinine </li></ul><ul><li>Serum albumin,triglycerides,Serum cortisol levels </li></ul><ul><li>Imaging tests s/a CT Scan,Ultrasound,CXR </li></ul>
  29. 31. Treatment of Hyponatremia <ul><li>Acute </li></ul><ul><li>Onset < 3 days </li></ul><ul><li>Symptoms ++ </li></ul><ul><li>Tolerate rapid correction </li></ul><ul><li>Needs hypertonic solution </li></ul><ul><li>Chronic </li></ul><ul><li>Onset Longer period </li></ul><ul><li>Sometimes asymptomatic </li></ul><ul><li>Slow correction needs </li></ul><ul><li>rapid correction can damage brain by demyelination </li></ul><ul><li>Usually treated with free water restriction and treat underlying cause </li></ul>
  30. 32. Treatment of severe acute hyponatremia <ul><li>Use of hypertonic solutions depends upon </li></ul><ul><li>Duration and Magnitude of Hyponatremia </li></ul><ul><li>Degree and Severity of Clinical Symptoms </li></ul><ul><li>If Hypertonic saline is used, Na+ should be checked 2 to 4 hourly </li></ul><ul><li>The desired increase in Na+ is 0.5 to 1.0 mol/L per hour </li></ul><ul><li>Na+ deficit = 0.5 x Body Wt x (Desired – Current Na+ level) </li></ul><ul><li>0.5 x 60 kg x (125- 110) </li></ul><ul><li>0.5 x 60 x 15 = 450 mmol /L </li></ul><ul><li>Normal Saline 0.9 % contains 150 mmol /L </li></ul><ul><li>3% Saline contains 500 mmol / L </li></ul>
  31. 33. Danger of rapid correction <ul><li>Osmotic myelinosis ( Central Pontine Myelinosis) </li></ul><ul><li>rapid correction of Na in chronic hyponatremic patients  Increasing </li></ul><ul><li>extracellular tonicity  Brain Cells compensate by losing water  if hypertonic saline continue  drives water out of cells  myelinosis </li></ul><ul><li>Clinical Symptoms </li></ul><ul><li>Spastic quadriparesis </li></ul><ul><li>Difficulty in swallowing </li></ul><ul><li>Speech problems </li></ul><ul><li>Diplopia </li></ul><ul><li>Delirium+Coma </li></ul><ul><li>Deficits can be permanent. </li></ul>
  32. 35. Medical Treatments <ul><li>Frusemide </li></ul><ul><li>Increase free water excretion and sodium absorption. </li></ul><ul><li>Demelcocycline (Hypotonic Hyponatremia caused by SIADH) </li></ul><ul><li>cause insensitivity of distal renal tubules to the action of ADH and produce a nephrogenic diabetes insipidus. </li></ul><ul><li>Dose 600 – 900 mg/day Needs renal physician consult </li></ul><ul><li>Lithium </li></ul><ul><li>Arginine Vasopressin antagonists (for Hypervolemic Hyponatremia) </li></ul><ul><li>Aquaresis effect( increase urine output of mostly free water, with little electrolyte loss </li></ul>
  33. 36. Anti diuretic hormone
  34. 37. Syndrome of Inappropriate ADH Secretion Drugs Carcinoma Miscellaneous Pulmonary Diseases Neurological SIADH
  35. 38. Diagnosis Criteria for SIADH <ul><li>Hyponatremia (< 130 mmol/l) 118 mmol/l </li></ul><ul><li>Low plasma osmolarity(<270 mmol /kg) 260 mmol/kg </li></ul><ul><li>High urinary sodium(>30 mmol/l) 49 mmol/l </li></ul><ul><li>High urinary osmolarity(>150 mmol /kg) 370 mmol/kg </li></ul><ul><li>Low/Normal plasma urea+creatiine </li></ul><ul><li>Normal Cardiac, Liver , Thyroid functions </li></ul>
  36. 39. Drugs commonly associated with hyponatremia Class Drug Mechanism Diuretic Amiloride /Hydrochlorothiazide Indapamide Depletion total body sodium SSRI Sertraline Citalopram and others SIADH MAOI Moclobemide SIADH Anticonvulsant Carbamazepine SIADH Antipsychotic olanzipine SIADH
  37. 40. Summary <ul><li>Hyponatremia is a common medical condition </li></ul><ul><li>Management depends upon severity of clinical symptoms , duration and magnitude of sodium loss </li></ul><ul><li>Need to remember the danger of osmotic myelinosis </li></ul><ul><li>Drug induced hyponatremia is common </li></ul><ul><li>Polypharmacy make prevalence of drug induced hyponatremia likely to increase. </li></ul>
  38. 41. References <ul><li>Therapeutic Guidelines </li></ul><ul><li>Australia Prescriber Magazine Vol.26 No.5 2003 </li></ul><ul><li>Harrison’s 17 edition </li></ul><ul><li>MIMS Online </li></ul><ul><li>eMedicine </li></ul><ul><li>N Eng Journal Med 2000 , Hyponatremia </li></ul><ul><li>Dysnatremia management ,Acute Care Medicine Course </li></ul><ul><li>Clinical Physiology of electrolyte disorder </li></ul>

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