A Case Of Severe Hyponatraemia

Dazed and Confused

History      

Mrs AA, 66 yo ♀ from home w husband PHx hypertension, hyperlipidaemia 1/52 ago dx with UTI. Allergy: penicillin – given Bactrim by LMO 4/7 vomiting, diarrhoea, anorexia, increasing confusion 2/7 Na 110, asked to present to ED Presented to MMC ED with severe confusion, lethargy, anorexia. No seizures/fits/neurological symptoms.

Drugs Telmisartan (A2RB)  Atorvastatin 

Examination 

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General: Confused +++ Not oriented to time, place or person. GCS 14. Very dry mucous membranes, clinically volume deplete. Pink, perfused. Chest: JVP 0 cm, S1+S2+0, Scattered R basal crackles Abdo: Soft, tender palpable bladder, nil organomegaly Neuro: 5/5 power bilat, brisk reflexes, downgoing plantars, normal sensation. Nil seizure activity.

Investigations         

Urgent VBG: Na 98, K 3.7, Gluc 10.5 pH 7.50, pCO2 25, HCO3 20 Serum Osmolality: 211 (~twice serum Na + K ie 103) Urine Osmolality: 263 Urine Na: 51 Urine K: 28 eGFR >60 CXR: NAD MSU MC&S: Enterococcus spp sens amox, nitrofurantoin UEC in 11/2007: Na 139, K 4.7

Management    

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Admit ICU Monitor for seizures Hourly VBG After extensive discussion w. ICU consultantdecision to commence N Saline + 10mmol KCl for volume depletion and hypokalaemia Aim for 8mmol increase in serum sodium per day only – risk of central pontine myelinolysis H20 restriction – 500mL orally only per day

Progress      

Increase in serum sodium to 111 (13mmol) after 11 hrs! Saline ceased, H20 restriction continued Likely secondary to drop in ADH once hypovolaemia corrected Fortunately nil neurological changes, seizures, paralysis! Continuing hypokalaemia, hypocalcaemia, hypophosphataemia (replaced IV via CVC) Hypokalaemia spontaneously resolved. Calcium and phosphate remained low

Investigations (cont.) Saline commenced

Sodium 127 Saline Ceased

Investigations (cont.) Cortisol: 1022 (N)  TSH: 0.37 Subclinical Hyperthyroidism  FT4: 19.5  Vit D: 25  PTH: 3.9 (N)  MSU MC&S: Enterococcus spp sens amox, nitrofurantoin 

Progress (cont.)  

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Day 3: Discharge from ICU (Na 119) Day 4-8: Confusion and unsteady gait slowly resolved with increase in serum Na to 132 Day 8 (day of discharge): Patient stated she felt much better, had been confused ++ for 2 months with husband caring for her at home. Used to drink >3-4L/day at home because it was “a good thing for health” but understands fluid restriction and need for adherence. Patient discharged with follow up UEC CMP 1/9 and 4/9 with LMO – for FFIx if drop in sodium

Bad pun of the week

“Mrs AA and how she decided to stop drinking!!”

Differential Diagnosis 

Acute volume depletion only in setting of UTI, vomiting, diarrhoea  However:

Na 98!! CNS adaptation occurs over 2-3 days. Marked decrease in Na over 1-2 days assoc with cerebral oedema & seizures. Mrs AA relatively asymptomatic (exc confusion)

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Acute on chronic hyponatraemia  Perhaps

slow decrease in Na ?Primary Polydipsia ?SIADH acutely worsened by volume depletion during illness

Differential Diagnosis 

If chronic hyponatraemia  Primary

polydipsia- high water intake reported by patient, low urinary sodium when pt volume replete. However: normal renal function- to overwhelm kidney ability to clear H2O r/q intake >10L/day!!  SIADH- normal urinary osmolality even when serum sodium 127. However: borderline low urine sodium

Diagnosis Unclear

Salt and Water A potentially confusing topic!

Measuring the sodium Blood gas machine = direct measurement (new)  For UEC however, sample centrifuged, lipid and protein component removed  Thus if grossly raised lipids (severe hyperlipidaemia) or protein (myeloma) – Na appears low “pseudohyponatraemia”  Result should be verified 

Distribution of fluid

Control of Fluid Balance and Osmolality

Effective Volume   

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An idea about tissue perfusion and useful IV volume Indirect measures – MAP, JVP, renal artery pressure Detected by body in several places – carotid baroreceptors Low in hypovolaemia Low in CCF – poor CO Low in CLD – hyperdynamic circulation, ascites, AV fistulae Low in nephrotic sx – ascites

Urine Output 

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Effective Volume  R-A-A axis, sympathetic drive  Total salt & osmolar excretion/day LowADH  Urine osmolality OsmoleExcreted (mmol / hr ) UrineOutput ( L / hr ) = UrineOsmolality (mmol / L)

Hyponatraemia 

Inability to produce dilute urine

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Causes:  Interference

of renal ability to dilute urine  Low effective volume  SIADH  Endocrine: Addison’s, hypothyroidism, DKA

Causes of hyponatraemia          

Old age Post-surgical Diuretics – thiazides, spironolactone, lasix CCF, CLD, CRF, Nephrotic syndrome Volume depletion and H2O overload Drugs – anticonvulsants, chemo, Ecstasy Endo: DKA, Hypothyroidism, Addison’s Neuro – tumour, bleed, infection, psychosis Paraneoplastic SIADH – esp. Lung Exogenous vasopressin, iatrogenic ie fluids

Management - Investigation 

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Is this real?  Verify result – (done automatically at MMC) or with VBG (direct)  If VBG Na normal and/or high osmolar gap investigate for pseudohyponatraemia instead- lipids, myeloma screen! What other osmotes are there?  UEC, BSL, Plasma osmo • Check for urea, glucose as additional osmotes. • DKA should not be missed! • Posm ~ 2x Na – adjust if high urea, glucose. Work out osmolar gap Is the urine appropriate?  Measure urine output, urine osmo (this incl urea) and sodium. potassium now and post FR/sodium correction

Management – History History of fits/seizures!  Chronicity of symptoms, any major fluid losses, any oedema, water intake, comorbidities  Drugs  Comorbidities  GCS/MSE/Orientation 

Management – Examination Assess fluid state – hyper/hypo/normovolaemia  Neuro exam  Other examinations PRN 

Management – what next? 

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If there are fits/coma all bets are off- pt may require hypertonic saline and ICU admission Hypovolaemia:  N. Saline w. close monitoring of serum sodium  Restrict free water Fluid Overload:  Fluid and free water restriction ± diuresis (lasix) Normovolaemic:  Cease offending drugs  Fluid and free water restriction

Central Pontine Myelinolysis Fast correction of sodium/24-48hrs  Unclear aetiology  Poor relationship with speed of correction ?assoc with correction over 1-2 days rather than hourly  Destruction of myelin sheaths in pons  Severe paralysis, locked-in syndrome  Try to avoid correction >10mmol/day – close monitoring of UEC essential 

Further Investigation Repeat UEC – monitor Na, K, renal function  Cortisol, TSH  Repeat urine osmo, Na and K post FR/correction of serum Na to see if it corrects (and how quickly)  Consider: CT brain, CT chest/abdo/pelvis 

Between the ocean and the desert…