Electrolyte Imbalances and Biochemistry Flashcards
Causes of hypernatraemia?
-
Fluid Loss
- Diarrhoea, burns, fever, glycosuria (DM, DI)
-
Inadequate Intake
- Impaired thirst response in elderly or hypothalamic disease
-
Excess Na+
- Iatrogenic (excess crystalloids or Na+ containing drugs – IV Ben Pen), Conn’s syndrome
Presentation of hypernatraemia?
Anorexia, thirst, nausea, weakness, hyperreflexia, confusion, ↓GCS
Assess volume status
Investigations in hypernatraemia?
Daily serum Na+ concentrations
Renal function and electrolytes
Management of hypernatraemia?
Mild/Euvolaemic
- Encourage patient to drink water
- Slow infusion 5% dextrose
Severe/Hypovolaemic
- Slow infusion of 0.9% NaCl
- Glucose 5% thereafter to correct water deficit
Severe/Hypervolaemic
- Slow infusion of 5% glucose
Caution in treatment of hypernatraemia?
- If extracellular Na+ rapidly corrected, osmotic forces will drive fluid into cells, causing lysis resulting in neurological damage and death –> CENTRAL PONTINE DEMYELINATION
Aim for slow correction of Na+ - 10mmol/L/24h at very most. Treatment guided by volume status.
Causes of hyponatraemia?
Usually Dilutional
- Diuretics, Addison’s disease, DKA, D+V, burns
- SIADH
- Malignancy (lung, pancreas, lymphoma)
- Lung infections
- CNS infections or vascular events
- Drugs (SSRIs, tricyclics, carbamazepine, antipsychotics)
- Idiopathic
Pseudohyponatraemia = taking blood from arm with IV fluids running, a lipaemic sample or osmotically active substances in blood (e.g. hyperglycaemia).
Causes of hyponatraeima if HYPOvolaemic?

Causes of hyponatraeima if EUvolaemic?
(ADH leads to more concentrated urine)

Causes of hyponatraemia if oedematous?
Like SIADH but because of oedema

Presentation of hyponatraemia?
Headache, confusion, drowsiness, seizures, coma, death
Investigations in hyponatraemia?
Daily serum sodium concentrations, electrolytes and renal function
Blood/Urine Osmolalities
- In SIADH…
- Urine = high Na+ and high osmolality (concentrated)
- Blood = low Na+ and low osmolality (concentrated)
Daily weights (1 litre = 1kg)
Management of hyponatraemia?
Depends on volume status and underlying cause. If mild and asymptomatic, no treatment usually required.
Treat cause!
Overloaded
- Fluid restrict
Hypovolaemic
- Slow 0.9% NaCl – to replace lost fluid
Euvolaemic (SIADH)
- Correct cause + slow 0.9% NaCl
- Fluid restrict to 1 L/day. If resistant to fluid restriction, inhibition of ADH may be required –> demeclocycline.
Seizures/Coma
- Hypertonic saline - SENIOR SUPPORT
Causes of hyperkalaemia?
-
Reduced Renal Excretion
- AKI/CKD, drugs (potassium-sparing diuretics, ACEi, NSAIDs), Addison’s
-
Excess K+ Load
- Iatrogenic, massive blood transfusion
-
Increased Cellular Release
- Acidosis, tissue breakdown (rhabdomyolysis, haemolysis)
-
Pseudo-Hyperkalaemia
- Haemolysis, EDTA-contaminated sample
Investigations in hyperkalaemia?
- ECG – low flat P-wave, wide bizarre QRS complex becoming sinusoidal, tall tented T-waves, VF.
- Bloods – urgent repeat U+E; if K+ <7mmol/L with no new ECG changes or sample is haemolysed, repeat sample, otherwise follow treatment plan. Digoxin levels – toxicity will worsen hyperkalaemia.
- ABG – for acidosis if acute renal failure
What is this?

Sine wave - pre-terminal rhythm of hyperkalaemia

When does hyperkalaemia require management?
Serum K+ of >6.5 or hyperkalaemia with ECG changes requires immediate treatment
Management of Hyperkalaemia?
-
Calcium Gluconate 10% - 10ml IV over 5 mins
- Repeat every 10 min up to 50ml until K+/ECG corrected
-
Insulin/Dextrose - 10 units actrapid in 100ml 20% glucose
- Check CBG before, during and after
- Check K+ decreasing at 30 mins and overall result at 2 hours
- Salbutamol - 5mg neb
-
Calcium Resonium 15g TDS/QDS PO
- Takes 24h to work
- Constipates (give with lactulose)
-
Furosemide
- With IV fluids if necessary – enhances K+ excretion
Treatment of refractory hyperkalaemia?
Haemodialysis
Causes of hypokalaemia?
-
↑Renal Excretion
- Diuretics (except K+ sparing)
- Endocrine (steroids, Cushing’s, Conn’s)
- Renal tubular acidosis
- Hypomagnasaemia
-
Other K+ loss
- D+V
-
↑Cellular Uptake
- Salbutamol, insulin, alkalosis
What is renal tubular acidosis?
Failure of kidneys to acidify urine (normal anion gap)
Either…
- Not enough bicarb absorption (proximal)
- Not enough H+ excretion (distal)
Presentation and complication of hypokalaemia?
Symptoms
- Weakness, cramps, tetany, palpitations, nausea, paraesthesia
Signs
- Muscle weakness, hypotonia, arrhythmias, hyporeflexia
Complications
- Hypokalaemia increases risk of digoxin toxicity
Investigations in hypokalaemia?
- ECG – prolonged PR interval, depressed ST segment, small/inverted T waves, prominent U-wave
- Bloods – U+E (check for other imbalances, especially ↓Mg2+
- ABG – if alkalosis suspected
No pot and no T - long PR and a long QT
What is this?

U wave
Management of hypokalaemia?
>2.5, No ECG Changes
- Sando-K – 2 tablets TDS for 3/7 OR
- Add 20-40 mmol/L KCl to IV fluids
- Monitor U+E –> replace any concurrent ↓Mg2+ (8mmol MgSO4 in 100ml 0.9% saline IV over 1h)
<2.5 or ECG Changes
- 40mmol/L KCl in 1L 0.9% saline IV over 6 hours (unless oliguric)
Do not replace K+ faster than 10mmol/h outside of HDU/ICU
Definition of hypo/hypercalcaemia?
Hyper = >2.60 (treat at 3.0)
Hypo = <2.20
Causes of hypercalcaemia?
-
↓Renal Excretion
- Drugs (thiazide diuretics)
-
↑Release from Bone
- Bony mets (↑ALP) – PB KTL
- Myeloma (ALP normal)
- Sarcoidosis
- Thyrotoxicosis
-
Excess PTH
- Primary hyperparathyroidism (↑PTH) or tertiary hyperparathyroidism (↑↑↑PTH)
-
Excess Vitamin D
- Excess vitamin D intake
-
Dehydration
- Urea and albumin raised
Causes of hypercalcaemia? (mnemonic)
RHINOS
- *R**enal insufficiency (2o/3o hyperparathyroidism)
- *H**yperparathyroidism
- *I**atrogenic (overuse of vitamin D, Ca2+, thiazides)
- *N**eoplasms
- *O**ther endocrinopathies (hyperT, Addison’s)
- *S**arcoidosis
Presentation of hypercalcaemia?
If mild - asymptomatic
Severe - bone pain, renal colic, N+V, polyuria, altered consciousness, shortened QT interval
BONES, STONES, GROANS, PSYCHIATRIC OVERTONES
Investigations in hypercalcaemia?
Investigate for cause if not clear
- U+Es, ALP, PTH, phosphate
- Myeloma screen/Bence-Jones protein
- Serum ACE (if sarcoid suspected)
- Isotope bone scan (if bony mets suspected)
ECG - shortened QT. Continuous cardiac monitoring if severe hypercalcaemia
Management of hypercalcaemia?
Remove any underlying cause
Restrict dietary calcium
Rehydration
- NaCl 0.9% –> 1L 4-6 hourly for 24 hours; then 6 hourly for 48-72 hours with adequate K+
- Add loop diuretics once hydrated to enhance calcium excretion and prevent fluid overload (furosemide 80-100 mg OD)
Bisphosphonates
- Pamidronate infusion (can be started during rehydration)
- Dilute with NaCl 0.9%/glucose 5%
- Takes 2-4 days to have effect – max effect after 1 week
Causes of hypocalcaemia?
-
↑Renal Excretion
- Loop diuretics, CKD (↑PO43-), hypomagnasaemia
-
↑Deposition in Bone
- Bisphosphonates
-
↓/Ineffective PTH
- Hypoparathyroidism (surgical/congenital)
- Pseudohypoparathyroidism (resistance to PTH)
-
↓Vitamin D
- Deficiency (osteomalacia, rickets)
Presentation of hypocalcaemia?
Symptoms
- Tetany, paraesthesia, cramps, anxiety, seizures
Signs
- Chovstek’s sign
- Trousseau’s sign

Investigations in hypocalcaemia?
Bloods
- U+E
- PTH
- Phosphate, magnesium
ECG –> long QT (continuous cardiac monitoring if severe)
Management of mild hypocalcaemia?
Treat cause –> vitamin D deficiency
- Load with 100,000 units colecalciferol STAT and give adcal-D3 maintenance
- Monitor patients on digoxin – IV calcium can increase digoxin toxicity
Mild
- Oral calcium
- Calcichew tablets – up to 40 mmol per day (12.6 mmol per tablet)
Management of severe hypocalcaemia?
Calcium gluconate 10% 10 ml IV slowly over 10-30 mins
- Dilute in 40ml NaCl or 5% dextrose
- Repeat until asymptomatic
- Follow with infusion if required
- 40ml 10% calcium gluconate in 1L dextrose/NaCl over 4-8 hours
- ECG monitoring required
Biochemical profile of dehydration?
- Raised urea disproportionate to a smaller increase in creatinine
- Raised haematocrit (PCV)
- Low urine volume
- Decreased skin turgor
Dehydration affects urea more than creatinine because in dehydration a greater amount of urea is reabsorbed by the kidney - creatinine is hardly reabsorbed at all.
Biochemical profile of abnormal kidney function? (2 types)

Comparison of low GFR and tubular dysfunction?

Biochemical profile of thiazide and loop diuretics?
↓Na+
↓K+
↑HCO3-
↑urea
Comparison of serum biomarkers in bone disease?


Biochemical profile of hepatocellular disease?
- ↑Bilirubin
- ↑↑AST
- ↑ALT
- ↓Albumin (slightly)
- ↑Clotting times
Biochemical profile of cholestasis?
↑Bilirubin
↑↑yGT
↑↑ALP
↑AST
Biochemical profile of excess alcohol?
Evidence of hepatocellular disease
↑yGT
↑MCV
Biochemical profile of Addison’s?
↑K+
↓Na+
↑urea
Biochemical profile of Cushing’s?
↓K+
↑HCO3-
↑Na+
Biochemical profile of Conn’s syndrome?
↓K+
↑HCO3-
Na+ normal or ↑
HTN
Biochemical profile of diabetes insipidus?
↑Na+
↑Plasma osmolality
↓urine osmolality
(Hypercalcaemia and hypokalaemia may cause nephrogenic diabetes insipidus)
Biochemical profile of SIADH?
↓Na+
↓ or normal urea and creatinine
↓plasma osmolality
↑urine osmolality
↑urine Na+ (20 mmol/L)