Electrolyte abnormalities Flashcards
What are the 2 most common mechanisms for hyponatraemia in ICU
Dilutional from excess total body water
Excess sodium loss - usually GI or renal
What are the clinical features of hyponatraemia and why do they occur?
Result from fluid shift and consequent tissue oedema.
Lethargy, confusion and nausea occur at Na < 125
Seizures and decreased conscious level can occur due to cerebral oedema and occur at Na < 115
What are the causes of hyponatraemia?
Salt and water loss e.g. diarrhoea, vomiting and diuretics.
Syndrome of inappropriate anti-diuretic hormone secretion (SIADH)
Drugs - NSAIDs, ACEIs, diuretics, PPIs, anti-depressants, anti-psychotics, carbamazepine
Excess administration of hypotonic fluids
Organ failure resulting in fluid overload e.g. heart failure, MODS, liver failure
Adrenal insufficiency
Severe hypothyroidism
What is SIADH?
State of water retention and urinary sodium loss.
Causes include paraneoplastic, severe pneumonia, drugs e.g. anti-psychotics. Its are
Clinically euvolaemic or mild oedematous
Characterised by inappropriately high urine sodium, may have low serum osmolality and high urine osmlolity
How should you assess a patient with low sodium?
Attention to fluid status and medications
Measure paired serum/urine osmolality and sodium - although results confounded by many factors in the critically unwell
How do you manage low sodium?
Depends on clinical severity and underlying aetiology
Salty/water loss - rehydrate with IV 0.9% saline
SIADH - fluid restrict, stop offending drugs, demeclocycline may be considered in severe cases - induces a temporary nephrogenic diabetes insipidus
Drug-related - stop drugs, supportive therapy
Organ dysfunction - treat underlying condition
How do you manage severe hyponatraemia?
If the patient is comatose or seizing then hypertonic saline should be considered.
The European society of endocrinology suggest a 150ml bolus of 3% sodium chloride until an increase in sodium of 5mmol/l is achieved
After the initial corrections eh rate of increase should remain within 10mmol/l/24hours for the first 24 hours and then 8/24 hours following this.
What are the clinical features of hypernatraemia?
Agitation and lethargy
Coma
Pts can be Hypovolaemic - in situation of fluid loss e.g. diuretics, GI loss
Euvolaemic - may be seen in diabetes insidious
Hypervolaemia - hypertonic saline administration
What are the causes of high sodium?
Excess loss of free water - dehydration, diuretics, Conns syndrome, nephrogenic diabetes insipidus - e.g. drug induced by lithium, neurogenic diabetes insidious - TBI, brain tumour, phenytoin
How is hypernatraemia managed?
If hypovolaemic - treat underlying cause and replace fluid. Once haemodynamically stable replace half the total body water deficit in the first 24 hours
If hypervolaemic - then high sodium is normally due to iatrogenic hypertonic sodium solutions - stop offending agent, consider diuresis
Nephrogenic diabetes insipidus - stop causative drug, fluid resus as needed
Craniogenic DI - treat underlying cause as able, fluid resus as needed, demopressin or vasopressin if severe
Conns - spironolactone
How can you calculate free water deficit?
FWD (litres) = 0.6 x weight (kg) x ((current NA/target NA)-1)
Target Na normally taken to be 140
What causes hypokalaemia?
Decreased Intake - malnutrition, cancer, chronic disease
Increased loss - GI - D/V, Renal - diuretics, RTA, osmotic diuresis, excess mineralocorticoid e.g. conns, bushings, liquorice toxicity
Movement of K into cells - alkalosis, salbutamol, insulin, refeeding
What are the consequences of hypokalaemia?
Muscle weakness and cardiac arrhythmias
Normally occur at K < 2.5
How is hypokalaemia managed?
Treat underlying cause
Consider stopping offending medication
Potassium replacement - 10-20mmol/hr if mild
Faster replacement may be needed if pt unstable - with ECG monitoring via a CVC
Magnesium replacement if needed
Continuous ECG monitoring if K <3
What are the consequences of hyperkalaemia?
Muscle weakness
ECG changes - T waves peaked, widened QRS, sinusoidal pattern, ventricular arryhtmias, cardiac arrest
Normally develop at K > 6
What causes hyperkalaemia?
AKI
CKD
Iatrogenic
Drugs - spironolactone, ACEI, A2RBs, suxamethonium, digoxin toxicity
Cell lysis - Tumour lysis syndrome, rhabdo, haemolysis, blood transfusion
Hypoadrenalism
How is hyperkalaemia managed?
Identify and treat cause
12 lead ECG - if no changes and K < 6 monitor
If ECG changes or K >6 - continuous ECG monitoring, 10mls 10% calcium gluconate, nebuliser salbutamol, 10 units actrapid + glucose
RRT if AKI/CKD is the cause or its refractory tp the above measures
What is the main clinical symptom of low phosphate and at what level does it occur?
Muscle weakness
Doesn’t normally occur until < 0.3
What are the causes of low phosphate?
Critical illness
Drugs - diuretics, catecholamines
Refeeding syndrome
RRT
How is low phosphate normally managed?
Replacement - enterally or IV
What are the causes of high phosphate?
Iatrogenic - IV or enemas, vitamin D toxicity
Acute illnesses - AKI, tumour lysis, metabolic acidosis, trauma, rhabdo
Endo - hypoparathyroidism
What are the clinical features of high phosphate
Low calcium and its consequences
Ectopic calcification
AKI
How is high phosphate managed?
Stop exogenous replacement
Phosphate binders if chronic
Hypertonic dextrose can be considered
RRT if severe or refractory
What are the causes of a low magnesium?
Critical illness
GI or renal losses
Drugs - diuretics, amoniglycosides, tacrolimus
