Electrolyte abnormalities Flashcards
Become confident with the management of common electrolyte abnormalities
Causes of nephrogenic diabetes insipidus
Lithium
Head injury
Things to consider with a hypernatremia patient (broadly speaking)
1) Dehydration/ impaired thirst mechanism/ impaired access to water e.g., cognitive impairment, learning difficulty
2) Check a glucose ? diabetic with HHS !
Causes of hypernatraemia
Not reabsorbing water
No ADH: Central diabetes insipidus
ADH produced, but not working on the kidneys: Nephrogenic diabetes insipidus
ADH produced, but impaired thirst mechanism/ no access to water
Loosing water via
GI tract: Vomiting, diarrhoea, stoma, laxatives
Renal: Diuretics (loop) high glucose (osmotic diuresis) Insensible losses (sweat, increased RR)
Too much sodium
- Hypertonic saline, hypertonic dialysis
- Increase in aldosterone (Conn’s, cushing’s)
Consequences/ risks of hypernatraemia
High blood osmolality, get fluid shift from cells to the blood, causes cell shrinkage
In the brain, can cause tearing of the arteries -> cause ICH
Shrinking of brain cells = death of brain cells
Osmotic demyelination syndrome (shrink of cells in the pons, where corticobulbar (speech), spinothalamic(paralysis), VI, run through (palsy) reticular formation (consciousness reduced)
Symptoms of hypernatremia
Nausea and vomiting
Thirsty, loss of appetite
Lethargy and weakness
Confusion (brain cells dying)
Severe: Seizure, myoclonic jerks, coma, ICH, coma, death
Approach to hypernatraemia patient
Why - think of the causes
ADH working = urine osmolality low
- Losing water, ADH, not drinking (GI loss, renal loss)
- low urinary sodium, as RAAS is working
- Given extra sodium, ADH working, losing sodium in urine as so much in blood!
ADH not working = urine osmolality high
- Diabetes insipidus (central, nephrogenic)
NEWS & BM
Fluid balance
Blood-type - electrolytes (U&E, bone profile, magnesium) glucose
Urine and serum osmolality and sodium
Management of hypernatraemia
Fluids, calculate free water deficit, monitor sodium, > 160 ? ITU, fluid balance
Hypotensive: NaCL until BP normal
Non-diabetic: IV dextrose e.g. bag over 6 hours, check sodium 4-6 hours after start to ensure rate falling is okay (12 mmol in 24 hrs, 0.5 an hour)
Diabetic: Saline dex, monitor BMs - dex can make worse as cause osmotic diuresis, ? HHS if high glucose before starting!
Approach to hyponatraemia
exclude spurious result
1) Severity
2) Onset - acute VS chronic
3) Symptoms - unlikely with mild
4) Serum osmolality
5) Fluid balance - hypovolemic, euvolemic, hypervolemic
6) Review meications
Think SOS
Serum osmolality, fluid status, review medications
Causes of hyponatraemia
Hypovolemic - ADH activated as low blood volume
Renal: Diuretics (thiazide! loop) low aldosterone (Addinson’s)
cerebral and renal salt wasting
GI loss - vom, diarrhoea, stoma
Insensible loss - sweat, burn, ventilation
Third spacing
Blood loss
Euvolemic - ADH not activated
Tea & toast
Beer potomania
Primary polydipsia
SIADH
Low cortisol, hypothyroidism
Drugs
Hypervolemic - third spacing, ADH activation
CCF, nephrotic syndrome, cirrhosis
Non ADH dependant causes of hyponatraemia
Tea and toast
Beer potomania
Primary polydipsia - anticholinergic medications, psych
SIADH
Medications - thiazide and loop diuretics, SSRI, AED, antipsychotic drugs
Low cortisol
Hypothyroid - bad!
Causes of SIADH
Malignancy -> GI, lung
Pulmonary disease -> COPD, pneumonia
Medications - SSRIs, AED, AP
Intracranial pathology e.g., SAH, stroke
What is SIADH
No trigger for the release of ADH (blood volume fine, perfusion of kidneys okay)
ADH released w/o a cause!
RAAS not activated, so no sodium reabsorption from aldosterone! Higher sodium in urine!
Symptoms of hyponatraemia
Mild, can be asymptomatic!
Due to cerebral oedema
- nausea, vomiting
- headaches
- drowsy
severe: seizures, reduced GCS, cardio-rsp arrest, coma
Chronic: Gait instability, altered mental status, reduced concentration
Investigations for hyponatraemia
- Serum and urine osmolality and sodium (ADH working or not)
- Urine dipstick (nephrotic syndrome)
- Bloods: U&E albumin (indicated dehydration, nephrotic syndrome), LFTs (cirrhosis) pro BNP (CCF) TFTs (? low), 9am cortisol (? low)
- CXR - ? CCF
What requires emergency treatment with hyponatraemia
Severity - severe
Onset - acute
Symptoms - severe YES
What makes person more at risk of seizures in hyponatraemia?
Epilepsy! (more at risk of seizures)
Brain injury e.g., previous stroke, mass (more at risk of herniation)
Consequences of hyponatraemia
Cerebral oedema
- Brain herniation
- Increase neurone irritability = seizures
Emergency treatment for hyponatraemia
IV 3% NaCl over 20 minutes
Check sodium after
Not reduce more than 8-10 mmol/ ml in 24 hours - risk ODS
Find cause
Give fluids
Regular monitoring of sodium
Complications/ to think about when correcting hyponatraemia
1) ODS
2) Chronic = ODS risk higher
3) Low K+ -> chucks Na out of cells when going into cell, increase osmolality even more
Osmotic demyelination syndrome
Over correction of hyponatraemia, increase osmolality of blood, fluid shift out from cells = shrink = die
astrocyte responsible for myelination, these die = demyelination
In pons have tracts running through
Corticobulbar = speech lost
spinothalamic = paralysis
VI = palsy
reticular formation = consciousness
symptoms develop 2 days after, dysphagia, dysarthria, paraparesis, quadriparesis
max correction 4-6 mmol in 24 hours!
Management of non-emergency hyponatraemia hypovolemic
work out cause
mild and mod, no symptoms, fluid status assessment, review medications
- Hypovolemic: NaCl replace fluids, if sodium improves supports diagnosis,
if falls - alternative diagnosis ? SIADH
monitor sodium and fluid balance
Sudden acute drop to think
Taken from a drip arm?
Yes = repeat (VBG)
No = treat as appropriate ?emergency
Management of non-emergency SIADH hyponatraemia
- SIADH: FR 500-1000ml a day -> vaptans can be used (ADH antagonist)
Monitor sodium! Fluid balance!
Management of non-emergency hypervolemic hypernatraemia
Fluid restrict 500-1000ml a day
monitor sodium and fluid balance
consider loop diuretics
ADH antagonist/ vaptans
Who not to give?
Hypovolemic - worsens
Hepatoxic - don’t give to liver disease
stimulate thirst receptors
Causes of hypercalcaemia
Hyperparathyroidism
Primary - benign hyperplasia, adenoma (most common), malignancy (MEN1, 2a)
Tertiary - secondary to chronic kidney disease, chronic low vit D - parathyroid gland increase PTH production and hypertrophy
Malignancy
- PTHrP released - 1000x more potent than PTH
- Bone lysis/ lytic lesions - mets to bone
- myeloma - cytokine increase OC activity
Increased in vitamin D
- Oral/ OTC
- Granuloma e.g., sarcoidosis, make own vitamin D
FHH - sensors need a higher level of calcium before -ve feedback
Medications; thiazide diuretics (increase calcium reabsorption DCT) and lithium (increase PTH)
Endocrine: Acromegaly, Addison’s, thyrotoxicosis, phaeochromocytoma
Prolonged immobolisation = high bone turnover
PTH dependant and independant causes of hypercalcaemia
PTH dependant: Hyperparathyroidism,FHH, lithium
PTH independant:
Malignancy, vitamin D, thiazides, endocrine stuff, immobility
Presentation of hypercalcaemia
High calcium = stabilise voltage-gated sodium channels, reduced excitability
- Slower or absent reflexes
- Slow muscles: Myalgia, weakness
- Slow GI muscles: Constipation, nausea, vomiting, bloating
- Confusion, psychosis
More calcium exreted in urine, osmotic diuresis
- polyuria, polydipsia, dehydration
- Renal stones (high calcium oxalate, and dehydrated)
- Bone breakdown
Bone pain
- Calcium mediated gastric acid release
Dyspepsis
severe - arrythmia
chronic more likely hyperparathyroidism, is more gradual
acute - think more malignancy
Investigations for hypercalcaemia
Calcium levels
Phosphate
PTH
Magnesium (high calcium, reduce magnesium)
Vitamin D
Albumin
LFTs - ALP rise in bone lysis
U&E - renal function
FBC
ECG
ECG finding in hypercalcaemia
- Bradycardic
- Short QTc interval
- PR, QRS prolonged
risk of AV node branch blocks - Osbourne wave - +ve deflection @ J point between QRS and ST segment
Lab findings in hyperparathyroidism
Calcium high
Phosphate low
PTH high
Lab findings in malignancy
Calcium high
Phosphate high
PTH low (calcium -vely feeds back)
Acute management of hypercalcaemia
Mild: encourage oral, review meds, repeat
> 3.5 or > 3 with symptoms
Aggressive IV NaCl 3-4 litres for 2-3 days, increases filtration and excretion of calcium, careful in overload
Loop diuretics, inhibit calcium reabsorption in DCT, give after fluids or if cannot have,
deranged electrolytes (K+, Na+)
Bisphosphonates: Take 2-3 days to work, inhibit OC of bone, indicated in hypercalcaemia of malignancy!
Steroids - Inhibit vitamin D conversion to active vitamin D, vit D excess, granuloma, haematological malignancy -
How do steroids work in hypercalcaemia management?
Steroids inhibit the conversion of vitamin D to active vitamin D - reduce GI absorption of calcium
Cause of hypokalaemia
1) Drip arm with no K+ in
2) Reduced intake
Oral, IV, TPN
Malabsorption
Low magnesium
(lose K+ in urine, body can alter reabsorption!)
2) Extracellular to intracellular
Alkalosis (e.g. loss HCL in vomiting), insulin, adrenaline, beta-2-agonist
3) Increased losses
GI: Vom, diarrhoea, laxative abuse, stoma
Renal: Loop & thiazide diuretics, high aldosterone (conn’s, cushings) (Na+ high, K+ low), renal tubular acidosis
Insensible losses
Investigations for hypokalaemia
U&E, Mg, Bone profile
ECG
Digoxin level if on!
ECG in hypokalaemia
PR prolonged
T wave inverted
ST depression
Q waves
QTc can be prolonged - risk of VF and torsade de pointes
when to be cautious in potassium replacement?
When giving K+ to a person with renal impairment/ medications that affect kidney (NSAIDs, ACEI, ARB)
ECG changes in hypercalcaemia
Bradycardic
PR prolonged, QRS prolonged - risk of bundle branch block
QTc shortened
Osbourne waves
Acute onset of symptoms in hypercalcaemia - what to think about
? malignancy causing symptoms??
More chronic - think primary hyperparathyroidism
What to think about in low K+
Digoxin toxicity - do they take it? If yes, then can increase risk of toxicity
Mg?
Causes,
Review medications
ECG, U&E, Mg
