Renal Medicine - Electrolytes and Fluid Balance Flashcards
Give the criteria for the WHO performance status:
0
1
2
3
4
5
0: fully active without restriction
1: restricted in physically strenuous activity, but ambulatory and able to carry out light work
2: ambulatory and capable of self-care, but unable to carry out light work
3: capable of limited self-care, confined to bed or chair >50% of the time
4: completed disabled and confined to bed or chair; cannot self care
5: dead
Interpret the following VBG result:
PaO2: 14 (11 – 13 kPa)
pH: 7.33 (7.35 – 7.45)
PaCO2: 3.0 (4.7 – 6.0 kPa)
HCO3–: 17 (22 – 26 mEq/L)
Metabolic acidosis - partially compensated by respiratory alkalosis.
Interpret the following VBG result:
PaO2: 12.7 kPa (11 - 13 kPa)
pH: 7.50 (7.35 - 7.45)
PaCO2: 5.5 kPa (4.7 - 6.0 kPa)
HCO3-: 29 (22 - 26 mEq/L)
BE: +3
Metabolic acidosis - not compensated
Give some causes of metabolic alkalosis.
GI losses (e.g. diarrhoea / vomiting)
Renal losses (e.g. primary hyperaldosteronism, diuretics)
Intracellular shift (e.g. hypokalaemia)
What is the anion gap?
A calculation that is useful to work out what is the cause of metabolic acidosis?
Anion gap = sodium - (chloride + bicarbonate)
Normal anion gap 8-12
Give some causes of a metabolic acidosis, with anion gap >12.
Acidosis due to increased acid, for example:
- lactic acidosis in anaerobic exercise, sepsis and organ ischaemia
- ketoacidosis (e.g. diabetic, alcohol abuse)
- toxins (e.g. isoniazid, aspirin, methanol)
- renal failure
Give some causes of a metabolic acidosis, with anion gap <8.
Acidosis due to reduced alkali, for example:
- GI losses of HCO3 in vomiting and diarrhoea
- renal losses of HCO3 in renal tubular acidosis and Addison’s
- toxins (e.g. ammonium chloride, acetazolamide)
What are the causes of hypernatraemia?
Hypovolaemic hypernatraemia due to dehydration (e.g. diuretics, excess sweating, burns, diarrhoea).
Euvolaemic hypernatraemia due to renal losses (e.g. diabetes insipidus) and extra-renal losses (e.g. insensible and respiratory losses).
Hypervolaemic hypernatraemia due to sodium gains (e.g. primary hyperaldosteronism, Cushing’s syndrome, sodium chloride tablets)
What are the symptoms of hypernatraemia?
- thirst
- apathy
- irritability
- weakness
- seizures
- hyperreflexia
- coma
What is diabetes insipidus?
The lack of ADH, preventing the kidneys from being able to concentrate the urine, leading to polyuria.
How is hypernatraemia usually treated?
Free water
What are the causes of hyponatraemia?
Hypovolaemic hyponatraemia (e.g. diuretics, Addison’s, diarrhoea, vomiting).
Euvolaemic hyponatraemia (e.g. hypothyroidism, SIADH, adrenal insufficiency).
Hypervolaemic hyponatraemia (e.g. congestive heart failure, nephrotic syndrome, liver cirrhosis).
What is SIADH?
An excessive release of ADH causing excessive water reabsorption, causing a euvolaemic hyponatraemia.
How is hyponatraemia managed?
Acute - IV 3% saline solution + furosemide
Chronic - IV 0.9% saline + furosemide
Why is is dangerous to correct chronic hyponatraemia too quickly?
A rapid correction of chronic hyponatraemia can cause osmotic demyelination syndrome, whereby the myelin sheath within the pons is destroyed.
What is the main complication of hyperkalaemia?
Cardiac arrhythmias such as ventricular fibrillation.
Give some disease states that can cause hyperkalaemia.
- acute kidney injury
- chronic kidney disease
- rhabdomyolysis
- adrenal insufficiency
- tumour lysis syndrome
Give some medications that can cause hyperkalaemia.
- aldosterone antagonists (e.g. aldosterone)
- ACE inhibitors (e.g. ramipril)
- ARBs (e.g. candesartan)
- NSAIDs (e.g. ibuprofen)
- potassium supplements
What are the ECG changes associated with hyperkalaemia?
An ECG is required in all patients with a serum potassium > 6mmol/L.
- tall peaked T waves
- flattening or absence of P waves
- broad QRS complexes
Extreme hyperkalaemia may cause sine wave pattern, which is a dangerous arrhythmia likely to progress into ventricular fibrillation.
How should hyperkalaemia ≤6mmol/L be managed?
No urgent treatment required, however consider changes to diet and medications (e.g. stopping spironolactone or ramipril).
When does hyperkalaemia warrant urgent treatment?
- serum potassium ≥6mmol/L with ECG changes
- serum potassium ≥6.5mmol/L regardless of ECG changes
How is severe hyperkalaemia managed?
- insulin and dextrose drives carbohydrates into cells and takes potassium with it, reducing the blood potassium
- calcium gluconate stabilises the cardiac muscle cells and reduces the risk of arrhythmias
What is rhabdomyolysis?
The condition by which myocytes undergo apoptosis, resulting in skeletal muscle cells releasing:
- myoglobin (myoglobinurea and AKI)
- potassium (hyperkalaemia and arrhythmias)
- phosphate
- creatine kinase
What are the signs and symptoms of rhabdomyolysis?
- muscle aches and pains
- oedema
- fatigue
- confusion
- red-brown urine
What are the causes of rhabdomyolysis?
- prolonged immobility (e.g. following a fall)
- extremely rigorous exercise beyond the person’s fitness level
- crush injuries
- seizures
Following admission of a frail patient following a fall, for which the ambulance service inform you they were on the floor for 5 hours, how should they be investigated for rhabdomyolysis?
Urine dipstick (++ blood, myoglobinuria)
Creatine Kinase (CK ++)
U&Es (AKI and hyperkalaemia)
ECG to assess response to hyperkalaemia
How is rhabdomyolysis treated?
IV fluids to rehydrate the patient and encourage filtration of the breakdown products.
IV sodium bicarbonate makes the urine more alkaline, reducing toxicity of myoglobin on the kidneys.
IV mannitol increases GFR to help flush breakdown products and reduce oedema.
Treat complications, particularly hyperkalaemia.
What is renal tubular acidosis?
Metabolic acidosis due to pathology in the tubules of the kidney.
What is Type 1 renal tubular acidosis?
Pathology in the distal convuluted tubule means the kidney is unable to excrete hydrogen ions in urine.
What are the causes of Type 1 renal tubular acidosis?
- hyperthyroidism
- sickle cell anaemia
- SLE
- genetic
How does type 1 renal tubular acidosis present?
Failure to thrive in children
Hyperventilation to compensate for the metabolic acidosis
Chronic kidney disease
Bone disease (osteomalacia)
What are the complications of type 1 renal tubular acidosis?
- metabolic acidosis
- high urinary pH
- hypokalaemia
How is type 1 renal tubular acidosis treated?
Oral bicarbonate
What is Type 4 renal tubular acidosis?
Reduced aldostone increases expression of ENaC, increasing reabsorption of Na+ and thus the electrochemical gradient by which K+ is excreted into the lumen.
Resultant hyperkalaemia causes proton shift out of cells, causing a metabolic acidosis.
Causes of type 4 renal tubular acidosis.
- adrenal insufficiency
- ACEi
- spironolactone
- SLE
- diabetes
- HIV
What are the complications of type 4 renal tubular acidosis?
- hyperkalaemia
- high chloride
- metabolic acidosis
- low urinary pH
How is type 4 renal tubular acidosis managed?
- fludrocortisone
- sodium bicarbonate for hyperkalaemia
What are the features of hypokalaemia?
- fatigue
- constipation
- paralysis
- cardiac arrhythmias
- worsened glucose control in diabetes
- hypertension
Give some causes of hypokalaemia.
- vomiting
- diarrhoea
- caffeine
- alpha-blockers (e.g. doxazosin)
- refeeding syndrome
- primary hyperaldosteronism
- renal tubular acidosis
Which ECG changes are associated with hypokalaemia?
- small T waves
- U waves
- increased PR interval
How is hypokalaemia treated?
- replace magnesium
- oral potassium replacement
- IV potassium replacement
