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
 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
 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
 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.)
Sodium 127
Saline commenced
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.)
 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)
 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
 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

 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

 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
 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?
 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…