Core concept1 exam ›
- Dialysis removes a drug only if the molecule can reach the membrane and most of it is in the blood
- Four properties, all must be favourable
| Property | Dialysable |
|---|---|
| Molecular weight | <500 Da (haemodialysis); high-flux membranes extend to ~10-15 kDa |
| Protein binding | <60-80% - only free drug crosses |
| Volume of distribution | <1-2 L/kg - a large Vd means the drug is in tissue, not blood |
| Water solubility | Hydrophilic |
- The single most useful discriminator is Vd - a drug with Vd 20 L/kg cannot be cleared, however small the molecule
- Dialysis clears the plasma compartment, and redistribution from tissue is slow -> rebound after the session
Key detail
- Dialysable - mnemonic I-STUMBLED
- Isopropanol, Salicylate, Theophylline, Uraemia/Urea, Methanol, Barbiturates (phenobarbital), Lithium, Ethylene glycol, Depakote (valproate at high level)
- Also metformin (lactic acidosis), dabigatran, aciclovir, atenolol, sotalol, potassium, carbamazepine (with high-flux/haemoperfusion)
- NOT dialysable
- Digoxin (Vd ~7 L/kg), TCAs (Vd ~20), amiodarone (Vd ~60), benzodiazepines (protein bound), phenytoin (>90% bound), warfarin, opioids, beta-blockers with high lipid solubility (propranolol, metoprolol), verapamil, paracetamol at therapeutic dose (though dialysable in massive overdose)
- Lithium is the exemplar: MW 7 Da, zero protein binding, Vd 0.7-1 L/kg -> highly dialysable
- Indications: severe neurotoxicity (seizure, dec GCS), level >4 mmol/L acute or >2.5 with symptoms, renal impairment, inability to tolerate volume resuscitation
- Rebound rise after the session from slow tissue redistribution -> recheck level at 6-8 h and often re-dialyse
- Other techniques
- Haemoperfusion (charcoal) - removes protein-bound and lipophilic drugs (theophylline, carbamazepine, phenytoin); largely superseded
- CRRT clears more slowly but continuously; less rebound
- Multiple-dose activated charcoal ("gut dialysis") - carbamazepine, dapsone, phenobarbital, quinine, theophylline
- Urinary alkalinisation - salicylate, phenobarbital, methotrexate
- Lipid emulsion - local anaesthetic and lipophilic drug toxicity
Clinical relevance
- Salicylate poisoning - dialyse for level >7 mmol/L (or >5 with renal impairment), altered mental state, pulmonary oedema, acidosis refractory to bicarbonate
- Intubation is hazardous - loss of the compensatory hyperventilation causes rapid deterioration
- Metformin-associated lactic acidosis - dialysis for pH <7.1, lactate >15, or renal failure
- Toxic alcohols - dialysis alongside fomepizole for high level, acidosis, visual symptoms or renal failure
- Do not dialyse for a drug you cannot remove - digoxin toxicity is treated with Fab, TCA toxicity with bicarbonate
- Renal replacement in a poisoned patient also corrects acidosis, hyperkalaemia and volume overload, which may itself be the indication
Correlations
- Determinants of steady-state concentration - Vd and protein binding
- Specific antidotes in poisoning; toxidrome recognition
- TCA overdose - why dialysis has no role
- Digoxin mechanism of action
- Arterial blood gas interpretation - mixed acid-base in salicylate toxicity
4 of 4 sections written · drafted 2026-09-04