Haemodialysis Complications
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Direct answer
Intradialytic hypotension — a symptomatic fall of more than about 20-30 mmHg systolic — accounts for the largest share of adverse events, in up to 20-30 per cent of sessions, followed by muscle cramps, nausea and headache; against these common troubles stand the rare killers: air embolism, acute haemolysis from chloramine-contaminated water, disequilibrium syndrome in the heavily uraemic first-dialysis patient, and type A anaphylactic first-use reactions. Long-term dialysis adds dialysis-related amyloidosis from beta-2 microglobulin and accelerated vascular disease. The diagnostic skill is timing and pattern: when in the session an event occurs, and in which patient, narrows the cause faster than any test.
What you must remember
- Hypotension: causes include excessive ultrafiltration, dry weight set too low, antihypertensives taken just before dialysis, autonomic neuropathy (especially diabetes), low dialysate sodium and a warm bath; treat with UF stopped, 100-250 mL saline, legs raised.
- Muscle cramps (5-20 per cent of sessions): typically late, after rapid fluid removal; manage with a saline bolus, hypertonic saline or 50 per cent dextrose; prevent with smaller interdialytic gains, sodium profiling and cooler baths.
- Disequilibrium syndrome: headache, nausea, restlessness, hypertension, seizures, even coma, classically in the first dialysis of a very uraemic patient — prevented by a short (about 2 hours), low-flow, smaller-dialyser first session capping urea reduction at roughly 40 per cent.
- First-use reactions: type A (anaphylactic, within minutes — ethylene oxide residue, or AN69 membrane with ACE inhibitors) needs dialysis stopped and the blood not returned, with adrenaline; type B (later, milder chest and back pain) is complement-related with cellulose membranes.
- Pyrogenic reaction: fever and rigours during dialysis with negative cultures, from endotoxin in water or dialysate — audit the water plant; it differs from access-related bacteraemia, which needs cultures and antibiotics.
- Acute haemolysis: chest tightness, breathlessness, dark plasma, falling haematocrit, rising potassium — from chloramine in water, an overheated bath, a kinked line or a faulty pump; stop dialysis and do not return the blood (it is hyperkalaemic).
- Air embolism: cough, chest pain, breathlessness, cyanosis, collapse; clamp the venous line, left lateral head-down position, 100 per cent oxygen, resuscitation.
- Long-term: dialysis-related amyloidosis (beta-2 microglobulin — carpal tunnel syndrome, arthropathy, cystic bone lesions) and accelerated atherosclerosis.
Three events on one timeline
Run the session timeline in your head, because complications sort by clock. At minute five of a first-ever dialysis, a uraemic man with blood urea 200 mg/dL becomes flushed, breathless and hypotensive after a new dialyser is connected: the type A first-use reaction — stop the pump, clamp the lines, do not return the blood, and treat anaphylaxis with intramuscular adrenaline, oxygen and fluids;
At hour three of a routine session, a diabetic woman yawns, feels sick, and cramps in her calves as her systolic pressure slides 40 mmHg: the commonest event, intradialytic hypotension with cramps, from ultrafiltration outpacing plasma refilling.
The rare events sit at the extremes: sudden breathlessness with dark serum drawn from the lines at any point means haemolysis — think chloramine breakthrough or an overheated bath, disconnect and discard the blood because lysed cells pour potassium back. Notice how each decision — return the blood or not, saline or adrenaline, water plant or antibiotics — falls out of the timing and the patient; that is what examiners mean by safe practice.
Where students slip
The most examined and most dangerous slip is returning the blood in type A reactions and in acute haemolysis — in both, the extracorporeal blood holds the culprit (allergen or lysed, hyperkalaemic cells) and must be discarded. The second is misreading disequilibrium syndrome as idiopathic epilepsy; the prevention question — short, low-efficiency first sessions capping urea reduction near 40 per cent — is asked more often than the treatment question. Finally, do not confuse pyrogenic reaction with infection: same fever, entirely different response — one goes to the water plant, the other to the blood-culture bottles.
Frequently asked questions
What is the commonest intradialytic complication and its immediate treatment?
Intradialytic hypotension, in up to 20-30 per cent of sessions. Reduce or stop ultrafiltration, give a 100-250 mL normal saline bolus, lay the patient flat with legs elevated, and give oxygen if required.
How is dialysis disequilibrium syndrome prevented in a very uraemic patient?
With a planned gentle first dialysis: about two hours, lower blood flow, a smaller dialyser, urea reduction capped near 40 per cent, then daily short sessions until uraemia stabilises.
What distinguishes a type A from a type B first-use reaction?
Type A begins within minutes with anaphylaxis — hypotension, bronchospasm, urticaria — classically from ethylene oxide residue or AN69 membranes with ACE inhibitors; the blood must not be returned. Type B appears later with milder chest and back pain from complement activation on cellulose membranes.
How is chloramine-induced haemolysis recognised and handled?
Chest pain, breathlessness and nausea during treatment with dark plasma, falling haematocrit and rising potassium. Dialysis is stopped, blood is not returned, and water chlorine testing is repeated urgently.