Hyponatraemia (Case Presentation)

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Dazed and Confused

description

A case of severe hyponatraemia with a discussion of sodium and water balance

Transcript of Hyponatraemia (Case Presentation)

Page 1: Hyponatraemia (Case Presentation)

Dazed and Confused

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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.

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Drugs

Telmisartan (A2RB) Atorvastatin

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Examination

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.

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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

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Management

Admit ICU Monitor for seizures Hourly VBG After extensive discussion w. ICU consultant- decision 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

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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

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Investigations (cont.)

Saline CeasedSaline commenced

Sodium 127

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

Subclinical Hyperthyroidism

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Progress (cont.) 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

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Bad pun of the week

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

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Differential Diagnosis

Acute volume depletion only in setting of UTI, vomiting, diarrhoeaHowever: 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)

Acute on chronic hyponatraemiaPerhaps slow decrease in Na ?Primary Polydipsia ?SIADH acutely worsened by volume depletion during illness

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Differential Diagnosis

If chronic hyponatraemiaPrimary 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

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Salt and Water

A potentially confusing topic!

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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

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Distribution of fluid

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Control of Fluid Balance and Osmolality

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Effective Volume

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

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Urine Output

Effective Volume R-A-A axis, sympathetic drive Total salt & osmolar excretion/day

LowADH Urine osmolality

)/(

)/()/(

LmmolalityUrineOsmol

hrmmoletedOsmoleExcrhrLtUrineOutpu

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Hyponatraemia

Inability to produce dilute urine

Causes:Interference of renal ability to dilute urine

Low effective volumeSIADHEndocrine: Addison’s, hypothyroidism, DKA

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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

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Management - Investigation

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

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Management – History

History of fits/seizures! Chronicity of symptoms, any major fluid losses, any oedema, water intake, comorbidities

Drugs Comorbidities GCS/MSE/Orientation

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Management – Examination Assess fluid state – hyper/hypo/normovolaemia

Neuro exam Other examinations PRN

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Management – what next?

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

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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

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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

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Between the ocean and the desert…