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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)

ree
Hyperkalaemia ECG changes - LITFL https://litfl.com/hyperkalaemia-ecg-library/

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

ree
Hypokalaemia ECG changes - LITFL https://litfl.com/hypokalaemia-ecg-library/

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.



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