Data Interpretation Flashcards
Approach to Hyponatraemia
is it true hypoNa?
if reduced serum osmolality (<275 mOsm/kg) = true hypoNa
DDx normal or elevated serum osmolality
translocational hypoNa — due to hyperglycaemia, mannitol or glycine
pseudohypoNa — due to severe hyperlipidaemia or hyperproteinaemia
is hypoNa acute or are there any severe symptoms
(ie do u need to act before finding the aetiology)
if acute = can rapidly correct — but only if 100% sure (ie has a bloods from 48 hrs ago thats normal Na
if severe = can consider hypertonic saline immediately
what is the cause
low urine osmolality (<100 mOsm)
interpretation: kidneys excreting large vol of free water (appropriate response to low Na)
reset osmostat syndrome + recently drank water
low solute intake – malnourished alcoholic, low salt & protein diet
psychogenic polydipsia
high urine osmolality (>100) + low urine Na (<30)
interpretation: trying to keep water in due to low effective arterial blood vol
if hypovolaemic hypoNa = ?GI loss (vomiting, diarrhoea) or renal loss (diuretics that dont rlly lose Na)
if hypervolaemic hypoNa = ?organ failure (cardiac, renal) or protein lossing (cirrhosis, nephrotic syndrome)
high urine osmolality (>100) + high urine Na (>30)
interpretation: renal loss of Na
main DDx
active diuretic use that loses Na too (ie thiazides)
renal disease — CKD, AKI, RTA
adrenal insufficiency — reduced aldosterone release
severe hypothyroidism
if all r/o = SIADH
rare mimics of SIADH:
CSW cerebral salt wasting syndrome
reset osmostat syndrome
classification of hyponatraemia
biochemical
mild = 130-135
moderate = 125-130
severe = <125
symptoms
volume state: hypovolaemic vs euvolaemic vs hypervolaemic
onset: acute (<48 hrs) vs chronic (>48 hrs)
presentation of hyponatraemia
(least serious)
asymptomatic
N&V, confusion, headache
seizure, pulmonary oedema
coma, stroke, osmotic demyelination syndrome
cognitive dysfunction, falls, osteoporosis
(most serious)
Ix for hyponatraemia
Hx & Exam
Hx
meds
fluid intake
neuro symptoms
co-morbidities
exam — volume state
hypovolaemic: orthostatic hypotension, dry mucous membranes, reduced skin turgor, increased HR
hypervolaemic: oedema, ascites, SOB, increased weight
vitals
bedside glucose
bloods
U&E
Cr
tox screen
plasma & urine osmolality
TFTs
+/- cortisol
urinary Na
+/- CXR – if ?SIADH – find for pneumonia or malignancy
Tx of hyponatraemia
acute hyponatraemia
only if 100% sure hyponatraemia only happened in last 48 hrs
if severe (acc to symptoms) = 100 ml 3% NaCl given over 10 mins — repeat up to 3x
monitor Na+ hrly
aim: 4-6 mmol/K increase in 6 hrs
if mild-moderate hypoNa = 0.5-2.0 ml/kg/hr 3% NaCl
chronic hyponatraemia
max: 8 mmol/L per day increase in Na
if hypervolaemic hypoNa
fluid restrict
Tx underlying disorder
+/- loop diuretics
vasopressin receptor antagonist
if euvolaemic hypoNa
fluid restrict (1-1.5L/day) or aim -500ml I/O
Tx underlying disorder
+/- vasopressin antagonist
UNLESS reset osmostate syndrome = dont need to correct Na, just Tx underlying
if hypovolaemic hypoNa
fluid replacement w isotonic saline
if symptomatic = aim 3-6 mmol/L per day increased
monitor Na q8-12h + every 24 hr thereafter
always monitor Na levels!! — dont rise too fast!
complications of hyponatraemia
acute: seizures, coma —> death
chronic: falls + osteoporosis —> fractures
rapid correction = osmotic demyelination syndrome
irreversible nerve damage
risk factors:
Na <105
alcoholism, malnutrition
liver disease
hypoK
approach to hyperkalaemia
is it true hyperK?
haemolysed blood
severe thrombocytopenia
leucocytosis
severity of hyperK —- indicators of emergent correction
severe hyperK (hyperK >6.0)
rapid rate of rise
ECG changes
what is the cause
impaired excretion of K:
decreased glomerular filtration — AKI or CKD
hypoaldosteronism
adrenal insufficiency — primary (addison’s disease or congenital adrenal hypoplasia) vs secondary
hyperkalaemia (type 4) renal tubular acidosis
drugs — ACEI, ARBs, spironolactone
release of intracellular K+ into ECF:
cell lysis — rhabdomyolysis, tumour lysis syndrome, burns
insulin deficiency – DKA
inorganic acidosis
increase in serum osmolality — IV hypertonic mannitol, IV globulin, hyperglycaemia
drugs — succinylcholine, digoxin OD, fluoride poisoning
increased K+ intake:
large vol RBC transfusion
high dietary intake + CKD or impaired renal K+ excretion
approach to hypokalaemia
- is it apparent from the history?
K+ moving from ECF to ICF:
intensive insulin therapy — eg. DKA
increased beta adrenergic activity — bronchodilators (acute asthma), stress-induced catecholamine release (eg. MI)
poor K+ intake:
refeeding syndrome
chronic poor nutrition
GI K+ loss
diarrhoea, vomiting
ileostomylosses
- test urinary K+
urinary K+ low = appropriate kidney response — ie should be covered above
urinary K+ high = inappropriate kidney response = renal K+ wasting
- DDx renal K+ wasting
A. hypertension + hypervolaemia + metabolic alkalosis
interpretation = RAAS activation driving hypoK
renal A stenosis
primary hyperaldosteronism (Conn’s syndrome)
steroid excess
pseudohyperaldosteronism
B. normo/hypotension + eu/hypovolaemia + metabolic acidosis
RTA renal tubular acidosis
C. normo/hypotension + eu/hypovolaemia + metabolic alkalosis
if High urine Cl:
Mg deficiency
active diuretic therapy
if low urine Cl:
vomiting or NG tube suction
non-reabsorbable anions
check serum Mg —- hypoMg a/w refractory hypoK
approach to hyperCa
initial steps:
- check corrected Ca2+ = Ca + 0.02(40 - albumin)
- classify into 3 clinical pictures
hypercalcaemia + CKD
hypercalcaemia + no CKD + normal/increased PTH
hypercalcaemic + no CKD + low PTH
hypercalcaemia + CKD = CKD causing it — tetrtiary hyperparathroidism
hypercalcaemia + no CKD + normal/increased PTH
normal physio: hyperCa should suppress PTH — ie PTH is driving hyperCa
parathyroid adenoma
lithium therapy – stimuates PTH secretion
FHH familial hypercalciuric hypercalcaemia
hypercalcaemia + no CKD + reduced PTH
usually malignancy
bone invasion — osteoclast activity
paraneoplastic syndrome — production of PTHrP
high vit D levels — eg. lymphoma
if ca r/o = consider
vit D intoxication
granulomatous disease
high bone turnover
