Transcript Hyponatraemia in primary care

Common electrolyte disorders
in primary care
Steve Hyer
ELECTROLYTES
Approach
History including
drugs
Examination
including fluid
status, blood
pressure
Screening tests
Confirmatory
tests
Thinking about electrolytes
Excess/
reduced
intake
Redistribution
Excess/
reduced
Loss
Is hyponatraemia important?
3 reasons……
1. The wrong
treatment can be
disastrous
2. Rapid correction
can be disastrous
3. Acute severe
hypoNa
associated with
increased
mortality
T1: Low density
T2: High density
Scope
Sodium
Potassium
Calcium
Case 1
69y F Na 121
Previously Na 139
Started bendro 10d
previously
Stopped bendro:
Na 134 10d later.
Diagnosis: Thiazideinduced hyponatraemia
Case 2
88y M
Acutely unwell with
sodium 120 mmol/l
and signs of pleural
effusion.
Chest CT scan showed
extensive inoperable
bronchial carcinoma. .
Diagnosis: SIADH
associated with carcinoma
bronchus
Case 3
83y F
Na 126–129 mmol/l
following AP resection
and ileostomy.
Urine: maximal
sodium conservation.
Na normalised by
reversal of ileostomy .
Diagnosis: Salt and water
loss through high flow stoma
Case 4
56y M
10d diarrhoea and
vomiting.
Na 108 mmol/l K 5.5
Subsequent
investigations
confirmed Addison’s
disease. .
Diagnosis: Hyponatraemia
due to adrenal insufficiency
2 important hormones….
No aldosterone!
(Adrenal insufficiency)
ACE-inhibitors effectively lead to low
aldosterone; can cause hypoNa
Diagnosis adrenal insufficiency
SYNACTHEN
TEST
Enhanced ADH release
Tumours releasing
ADH eg Ca bronchus
CNS disorders
affecting
hypothalamus eg SAH
Pain especially
thoracic
Nausea
Opiates, SSRIs, CBZP
Atypical pneumonia
Dilutional hyponatramia
V2 receptors
One important bit of the kidney….
Distal convoluted tubule
This is where the
aldosterone
works
Drugs
Renal tubular
acidosis
Chronic
pyelonephritis
Excess water intake with low solutes
Low solute intake: Fun runners
Drinking fluids
every mile
Gain weight after
run!
Drink 3 litres + in
a run of 1-2 hrs
 Severe
hyponatraemia
and even death
Non
elite
runner
Low solute intake: Beer potomania
Beer
Very low sodium/
potassium
Maximum 4-5 litres
of electrolye free
water excretable
per day
In absence of
solute, >5L beer;
Tea + toast
severe hypoNa
old ladies
Primary polydipsia
Low osmotic
threshold to feel
thirsty
Unable to suppress
thirst
Exaggerated thirst
Hyponatraemia +
polydipsia +
polyuria
Diagnosis……
Clinical symptoms
Plasma Na+
Symptoms
>125
Usually none.
Occasional headache,
nausea
Headache, nausea,
cramps, confusion
120 -125
Mortality
(%)
Not
reported
23
115-120
Agitation, drowsy,
stupor
30
<115
Seizures, coma
40
Step 1: Assess Volume status
Mucosal membranes,
tongue, skin turgor,
urine output
Step 2: CLASSIFY
Hyper-volaemic
Normo-volaemic
Hypo-volaemic
Weight: Down
OK
Up
Step 3:
Evaluate:
Clinical
Step 4:
Evaluate:
Laboratory
Losing
sodium in
urine
Conserving
sodium
Management SIADH
Underlying cause
Fluid restrict
(0.5-1L/d)
May take days to
come down
Maintain Na intake
(Demeclocyclinecauses NDI)
VAPTANS
(e.g.Tolvaptan)
V2 blocker
Tolvaptan
Oral agent
Currently only in
secondary care for
chronic SIADH
Expensive but could
reduce hospital stay
Especially where fluid
restriction poorly
tolerated
C/I Hypovolaemic
hypoNa
?long term
Secondary care
Special tests
Hypertonic saline
test
Water loading tests
Measurement of
AVP
Hypertonic saline
infusions –Na rise
not >10mmol/d
Scans, etc
DDI: Dipsogenic DI
Summary: Hyponatramia
Multitude of causes
Many patients with chronic mild
hyponatraemia have adapted and
apparently very well- may
decompensate in acute illness
First do no harm!
Hypernatraemia Na>145
History
Thirst/ Polyuria
No symptoms
Drugs
Examination
Dehydrated
Think diabetes
insipidus
Excessiv
e water
loss
Algorithm Na
Loss of
water
Loss of
water
Hypokalaemia
History
Diarrhoea, vomiting
No symptoms
Drugs eg Ventolin,
diuretics, insulin
Examination
Fluid status
Blood pressure
Think diuretics
Cola drink hypokalaemia
Sugar++++
Caffeine +++
At least 2
litres/day
Hypertension + low K+
Think Conn
(Hyperaldosteronism)
Think Cushing
Think renal artery
stenosis
Renin: Aldo ratio
Algorithm K
Gut
loss
Renal
loss
Hyperkalaemia K>5.0
History
Renal
No symptoms
Drugs eg ACE-I,
spiro, amiloride
Examination
Addisons
Renal
Think renal failure
Don’t forget haemolysed
samples, old samples
Algorithm
Input
Output
Don’t
forget
Addison
Hypercalcaemia Ca>2.6
Mild
hypercalcaemia
(Ca <3mmol)
Mostly due to
primary
hyperparathyroidis
m
Usually
asymptomatic
Diagnosis: Ca
blood/ urine + PTH
Recommending PTH-ectomy
 Patient fit for surgery
 Significantly reduced
BMD on DEXA scan
 Reduced renal
function (eGFR)
 Ca>2.85
 History of stones
 Increased Ca
excretion
Frail elderly: consider
bisphosphonate
infusion
Moderate-severe Ca
Consider
malignancy esp
older patient
Myeloma
Sarcoidosis
Thyrotoxicosis
FHH
Drugs
Bisphosphonates
Malignant hypercalcaemia
Tumour mets
Non-metastatic
(PTH-RP)
Algorithm
Low calcium Ca <2.2mmol
Usually Vitamin D
deficiency (30%
elderly, 90%
Asians?)
May be Chronic
renal failure
HypoPTH
PseudohypoPTH
(Low Mg)
Lack of sun
Phytate in chipatis
Housebound
Low Ca
High PTH
Low Ca
Low PTH
High Ca
High PTH
High Ca
Low PTH
Assessment Ca
History
Diet/ diarrhoea/
mal-absorption
Thyroid surgery
Drugs eg phenytoin
Examination
Tetany, Chvostek
Renal
Investigations
Ca/P/ Alk P’ase/
Vit D/ PTH
Treatment Vit D deficiency
Calciferol (D2)
Ex: Calcium & Vit D
400u bd
Colecalciferol (D3)
Ex: Adcal-D3 (400)
bd
Ergocalciferol
10,000 u (malabsorption)
Analogues
Ex: One –Alpha
0.25mcg (renal
failure)
Pure vitamin D (Boots, Tesco,
Holland & Barrets:
*25mcg (1000u) od (treat)
*10 mcg (400u) od (maintain)