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Overview of SIADH and management

Overview of SIADH and management

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SIADH SIADH Presentation Transcript

  • SIADH By Hiren Divecha FY2 Hairmyres Hospital 1/5/2007
  • Sodium• Needed for: 1. Nerve conduction 2. Co-transport of metabolites• 135-146 mmol/L• Regulation – Thirst – ADH – RAAS – ANP & BNP
  • Euvolaemic HyponatraemiaHypervolaemic Hypovolaemic
  • Hypovolaemic Euvolaemic HypervolaemicExtracellular Na ↓ N ↑TBW Slightly ↓ Slightly ↑ ↑↑Causes Renal Thiazides CCF •Diuretics •Osmotic diuresis SIADH Liver failure (glucose, urea, mannitol) Glucocorticoid def Renal failure •Addison’s •Salt-wasting neph Hypothyroidism Nephrotic syndrome Gut Primary polydipsia •Vomiting Pregnancy •Diarrhoea iv dextrose Other Sodium-free irrigant •Haemorrhage •3rd space loss (BO, burns, peritonitis, pancreatitis)
  • Causes of SIADHNeoplastic Pulmonary CNS Drugs OtherLung Infection Infection AVP analogues Idiopathic•Small cell •Pneumonia •Abscess •Desmopressin•Mesothelioma •Abscess •Meningitis •Oxytocin Hereditary •TB •AIDS •Vasopressin (V2 receptor)GI •Aspergillosis•Stomach Bleeds Stimulate AVP•Pancreas Asthma •Subdural release/action •SAH •SSRIsGU Cystic Fibrosis •Antipsychotics•Bladder CVA •Anti-epileptics•Prostate PPV •NSAIDs•Endometrium Head trauma •MDMAThymoma MS, GBSLeukaemiaLymphoma Shy-DragerSarcoma
  • Clinical Features<120 mmol/l <110 mmol/l– Dysgeusia • Drowsiness– Lethargy • Confusion– Anorexia • Depressed reflexes– Nausea, vomiting • Extensor plantar responses– Irritability • Seizures– Headache • Coma– Cramps • Death– Muscle weakness
  • Criteria for SIADH• Bartter and Schwartz (1967) – Hyponatraemia – Clinically euvolaemic – No diuretic use – Serum osmolality <275mOsm/kg – Urine osmolality >100 mOsm/kg – Urine sodium >40mmol/L – Normal thyroid, adrenal and renal function
  • Management - acute• Benzodiapines• Aim for 1-2mmol/L/hr initially – Resolution of neurology – Slow replacement (10 mmol/L/day)• Frusemide (free water excretion)• Find and treat cause
  • TBW = weight * 0.5 (girls) = weight * 0.6 (guys)Na+ to replace = desired change in Na+ * TBWRate of Na+ replacement = rate of desired change * TBWRate infusion = Rate of Na+ replacement / (conc of infusate)
  • As a rough guide• To increase Na+ by 1mmol/L/hr – 1 ml/kg/hr of 3% saline – 1.7 ml/kg/hr of 1.8% saline• Max. rate = 70 mmol of Na+/hr• Monitor U&E 2 – 3 hourly
  • Management - Chronic• Risk of osmotic demyelination if change is >12mmol/L/day• Symptomatic – Aim for lower rate of correction (0.5mmol/L/hr)• Asymptomatic – Fluid restrict – Demeclocycline – Oral urea
  • Fluid restriction (Urinary Na + Urinary K) / Plasma Na• >1 – <500ml/day• 1 – 500-700ml/day• <1 – <1L/day
  • Vasopressin Receptor Antagonists• RCTs showed sustained increase in plasma Na compared to placebo• Risk of hypotension with non-selective antagonists• V2 selective antagonists in trials• No reports of osmotic demyelination
  • Osmotic Demyelination Syndrome• Central pontine + extrapontine• Over-enthusiastic correction of Na+• In chronic hyponatraemia – Brain tissue losses inorganic and organic solutes – Takes few days• Predisposing factors – Alcoholism – Malnourishment
  • Osmotic Demyelination Syndrome• Demyelination• Pontine symptoms – Dysarthria, dysphagia, pseudobulbar palsy – Flaccid quaraparesis• Extra-pontine – Tremor, ataxia, mutism – Parkinsonism, dystonia• Reversible ? – 5% dextrose and desmopressin
  • References1. “The syndrome of inappropriate antidiuresis”, Ellison et al, NEJM, 2007;356(20):2064-722. “Hyponatraemia”, Adrogue & Madias, NEJM, 2000;342(21):1581-89