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Electrolyte abnormalities > Electrolyte abnormalities > Flashcards

Electrolyte abnormalities Flashcards

1
Q

What are the 2 most common mechanisms for hyponatraemia in ICU

A

Dilutional from excess total body water

Excess sodium loss - usually GI or renal

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2
Q

What are the clinical features of hyponatraemia and why do they occur?

A

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

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3
Q

What are the causes of hyponatraemia?

A

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

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4
Q

What is SIADH?

A

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

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5
Q

How should you assess a patient with low sodium?

A

Attention to fluid status and medications

Measure paired serum/urine osmolality and sodium - although results confounded by many factors in the critically unwell

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6
Q

How do you manage low sodium?

A

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

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7
Q

How do you manage severe hyponatraemia?

A

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.

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8
Q

What are the clinical features of hypernatraemia?

A

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

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9
Q

What are the causes of high sodium?

A

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

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10
Q

How is hypernatraemia managed?

A

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

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11
Q

How can you calculate free water deficit?

A

FWD (litres) = 0.6 x weight (kg) x ((current NA/target NA)-1)
Target Na normally taken to be 140

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12
Q

What causes hypokalaemia?

A

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

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13
Q

What are the consequences of hypokalaemia?

A

Muscle weakness and cardiac arrhythmias

Normally occur at K < 2.5

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14
Q

How is hypokalaemia managed?

A

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

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15
Q

What are the consequences of hyperkalaemia?

A

Muscle weakness
ECG changes - T waves peaked, widened QRS, sinusoidal pattern, ventricular arryhtmias, cardiac arrest
Normally develop at K > 6

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16
Q

What causes hyperkalaemia?

A

AKI
CKD
Iatrogenic
Drugs - spironolactone, ACEI, A2RBs, suxamethonium, digoxin toxicity
Cell lysis - Tumour lysis syndrome, rhabdo, haemolysis, blood transfusion
Hypoadrenalism

17
Q

How is hyperkalaemia managed?

A

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

18
Q

What is the main clinical symptom of low phosphate and at what level does it occur?

A

Muscle weakness

Doesn’t normally occur until < 0.3

19
Q

What are the causes of low phosphate?

A

Critical illness
Drugs - diuretics, catecholamines
Refeeding syndrome
RRT

20
Q

How is low phosphate normally managed?

A

Replacement - enterally or IV

21
Q

What are the causes of high phosphate?

A

Iatrogenic - IV or enemas, vitamin D toxicity
Acute illnesses - AKI, tumour lysis, metabolic acidosis, trauma, rhabdo
Endo - hypoparathyroidism

22
Q

What are the clinical features of high phosphate

A

Low calcium and its consequences
Ectopic calcification
AKI

23
Q

How is high phosphate managed?

A

Stop exogenous replacement
Phosphate binders if chronic
Hypertonic dextrose can be considered
RRT if severe or refractory

24
Q

What are the causes of a low magnesium?

A

Critical illness
GI or renal losses
Drugs - diuretics, amoniglycosides, tacrolimus

25
Q

What are the clinical features of low magnesium?

A

Cardiac arrhythmia incl torsades
Seizures and coma
Hypokalaemia and its consequences

26
Q

How is low magnesium managed?

A

Replacement

Continuous ECG monitoring if unstable

27
Q

At what level do adverse features of hypermagnesaemia normally occur?

A

> 3.5

28
Q

What causes high magnesium?

A

Excess magnesium administration esp in the context of AKI

29
Q

What are the clinical features of high magnesium levels?

A

Muscle weakness with the potential for respiratory arrest
Coma
Cardiac conduction defects and cardiac arrest

30
Q

How is hypermagnesaemia managed?

A

Continous ECG monitoring
Stop infusion
Calcium gluconate (for cardiac stabilisation)
Consider RRT

31
Q

What causes low calcium?

A 
Critical illness
Hypoparathyroidism
Vitamin D deficiency
High phosphate
Low magnesium
Resp alkalosis/hyperventilation
Drugs - xs phosphate, propofol, heparin, diuretics
Citrate toxicity - massive transfusion or citrate anti-coagulation
32
Q

What are the clinical features of low calcium?

A

Tetany, coma and seizures, impaired cardiac function, coagulation defect

33
Q

How is low calcium managed?

A

Treat and underlying causes as able
Consider checking PTH and Vit D
10mls 10% calcium gluconate if symptomatic, may need to be followed by an infusion

34
Q

What level of calcium in hypercalcaemia?

A

> 2.65 total serum calcium, > 1.3 ionised

35
Q

What are the causes of high calcium?

A 
Malignancy
Hyperparathyroidism, renal dysfunction, drugs - vit D toxicity, thiazides, lithium, tamoxifen
Immobility
Pagets
Sarcoidosis
TB
36
Q

What are the clinical features of high calcium?

A

Lethargy, fatigue, abdo pain, constipation, nephrocalcinosis, pancreatitis
Severe toxicity > 3.5 coma, bradycardia

37
Q

How is high calcium managed?

A

Identify and treat underlying cause
Remove precipitants as able
Rehydration alone may be sufficient
Bisphosphonates if fluid is not sufficient- esp in malignancy
Steroids may be of use if the cause is sarcoidosis
Diuretics promote urinary calcium loss - ensure pt not hypovolaemic

Electrolyte abnormalities (2 decks)

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