Fluid and Electrolyte Balance Disorders
Dehydration
Clinical features:
↓JVP
Tachycardia
Weak pulse
↓Blood pressure and pulse pressure
↓Urine output
Investigations will show:
↑Urea - In dehydrated patients, the urea is much higher in comparison to creatinine
↑Sodium
↑Albumin
↑Haematocrit
Fluid Overload
Clinical features:
↑JVP
S3 and/or S4 heart sounds
Signs of pulmonary oedema
Peripheral oedema
Investigations will show:
↓Sodium
Hypernatraemia
Defined as Na > 145 mmol/L.
Clinical features:
Lethargy
Weakness
Confusion
Agitation
Seizures
Coma
Causes:
Excess water loss - DI, Diuretics, DKA, Diarrhoea, Vomiting, Sweating, Burns
Excessive hypertonic fluid - IV fluids, Enteral feeds
Decreased thirst - Acute illness, Old age
Management - Fluids
Hyponatraemia
Defined as Na < 135 mmol/L.
Causes:
Hypovolaemic - Burns, Sweating, Diarrhoea, Vomiting, Addison’s disease
Euvolaemic - SIADH, Hypothyroidism
Hypervolaemic - Heart failure, Renal failure, Liver failure, Nephrotic syndrome
Management:
Hypovolaemic - IV 0.9% Saline, Treat underlying cause
Euvoleamic
SIADH - Fluid restriction, ADH receptor antagonists (e.g. tolvaptan), Furosemide
Hypothyroidism - Levothyroxine
Hypervolaemic - Fluid restriction, Treat underlying cause
Complication to be aware of if Na is corrected to quickly is Central pontine myelinolysis.
N.B. In a state of hyponatraemia, water shifts into brain cells. If this Na is corrected to quickly, it causes a huge osmotic shift of that water out of the brain cells, leading to shrinkage and lysis = Central pontine myelinolysis.
Hyperkalaemia
Defined as K > 5.5 mmol/L.
Causes:
Impaired excretion - AKI, CKD, ACEi/ARBs, Spironolactone, NSAIDs, LMWH (inhibits ald. release), Addison’s disease
Increased release - Lactic acidosis, Insulin deficiency, Rhabdomyolysis, Tumour lysis syndrome, Massive haemolysis, Digoxin toxicity, B-blockers
All patients with this need cardiac monitoring with regular ECG's. The ECG changes that may be seen include:
Flattened P-waves
Tall tented T-waves
Widened QRS complexes
Prolonged PR interval (1st degree block)
Management:
If K > 6.5 or ECG changes - Give Calcium gluconate (or chloride) over 10 mins for cardioprotection
Insulin + Glucose - Insulin to push K into cells, and glucose to prevent hypoglycaemia
Nebulised Salbutamol - Helps push K into cells
N.B. Calcium carbonate reduces excitability of cardiac myocytes. It works by stabilises the resting potential of cardiac cell membranes and reduces depolarisation, therefore preventing cardiac arrest and dysrhythmias.
Hypokalaemia
Defined as K < 3.5 mmol/L.
Causes:
Renal - Diuretics, Conn’s syndrome, Cushing’s, Hypomagnesaemia
Extra renal - Inadequate oral intake, Gut losses (e.g. diarrhoea, vomiting), Redistribution into cells (e.g. b-agonists, insulin, theophylline, alkalosis)
The ECG changes that may be seen include - U have no Pot or no T but a long PR and a long QT’
N.B. U waves are positive deflections seen immediately after a T wave.
Management:
Asymptomatic:
Oral slow release Potassium chloride or Sando-K
Treat underlying cause
Symptomatic or ECG changes:
IV infusion of 1L 0.9% Saline containing 40mmol Potassium chloride
Avoid glucose solutions
Check for and treat concomitant hypomagnesaemia as it increases the risk of arrhythmia
Treat underlying cause
N.B. Glucose solutions should be avoided as it will cause insulin release, therefore more K to be pushed into cells and a worsening of the hypokalaemia.

