Acute Hemodialysis & Dialysis

The contract between this chapter and the reader.

1. 1. Identify the urgent indications for dialysis in acute kidney injury.
2. 2. Apply the timing evidence — start for an indication, not preemptively.
3. 3. Choose between intermittent HD, CRRT, and SLED in AKI.
4. 4. Explain dialysis disequilibrium syndrome and who is at risk.
5. 5. Prescribe a safe, gentle first dialysis session.
6. 6. Anticipate first-session hazards beyond disequilibrium.
7. 7. Choose acute access and anticoagulation.
8. 8. Manage hyperkalemia and electrolyte shifts during acute dialysis.
9. 9. Reassess the ongoing need for dialysis as AKI evolves.

A sixty-second reading. Each bullet stands alone.

• Urgent indications for dialysis in AKI are refractory hyperkalemia, acidosis, and fluid overload, severe uremia, and certain intoxications (AEIOU).
• In the absence of an urgent indication, randomised trials show no benefit to starting dialysis early rather than waiting.
• Early initiation exposes patients who might recover to dialysis and its harms, so watchful waiting is appropriate without an indication.
• Intermittent HD suits stable patients and rapid correction; CRRT suits instability and cerebral edema; SLED is a hybrid.
• Dialysis disequilibrium syndrome is a neurological syndrome caused by too-rapid urea removal in a very uremic patient.
• It arises because plasma urea falls faster than brain urea, creating an osmotic gradient that shifts water into the brain (cerebral edema).
• Highest risk is the first-ever session with a very high urea, the elderly, the young, and pre-existing CNS disease.
• Prevent it with a gentle first session: short time, low blood flow, a smaller dialyzer, and a modest urea reduction.
• Other first-session hazards include hypotension, arrhythmia from rapid electrolyte shifts, and bleeding.
• Acute access is usually a non-tunneled temporary catheter in the right internal jugular; avoid the subclavian.
• Use heparin-free or citrate anticoagulation when bleeding risk is high.
• Dialysis treats hyperkalemia definitively, but watch for rebound and avoid very low-potassium baths.
• Many AKI patients recover, so reassess the need for dialysis as kidney function evolves.

The medical core. An expert should agree acute HD in AKI is fully covered here.

Why it matters at the bedside

Acute dialysis answers two questions in order: should this patient be dialysed at all, and — if so — how do you give the first treatment without harming them? The evidence has made the first question one of restraint, and the first session one of gentleness, because the very uremic brain does not tolerate being cleared quickly.

Urgent indications

• Some situations mandate dialysis now, summarised as AEIOU: refractory metabolic acidosis, refractory hyperkalemia (electrolytes), certain dialyzable intoxications, diuretic-resistant fluid overload, and severe uremia (encephalopathy, pericarditis, or uremic bleeding). When one of these is present and not correctable medically, dialysis is started without delay.

When to start: the timing evidence

• In the absence of an urgent indication, the temptation is to start ‘early’ to get ahead of trouble — but randomised trials comparing early or pre-emptive initiation with waiting for an indication found no survival benefit to starting early. Worse, an early-start policy dialyses patients who would have recovered without it, exposing them to the line, the procedure, and its complications. The discipline is watchful waiting until an indication appears.

Choosing the modality

• Intermittent HD suits the haemodynamically stable patient and situations needing rapid correction — severe hyperkalemia, some intoxications — and it frees the patient for procedures and mobilisation. CRRT is preferred in instability and cerebral edema (its own chapter), and SLED is the hybrid between them. Overall survival does not clearly differ by modality, so the choice follows haemodynamics, goals, and resources.

Dialysis disequilibrium syndrome

• The signature hazard of acute dialysis is disequilibrium: headache, nausea, confusion, and in severe cases seizures or coma, from cerebral edema. The mechanism is osmotic. In a very uremic patient, dialysis lowers plasma urea rapidly, but urea leaves the brain more slowly (a ‘reverse urea effect’), so the brain is briefly hyperosmolar relative to plasma; water follows the gradient into brain tissue, and it swells. The greater the pre-dialysis urea and the faster its removal, the greater the risk.

The gentle first session

• Prevention is entirely in the prescription. For a first-ever session with a very high urea, dialyse gently: a short time (around two hours), a low blood-flow rate, a smaller dialyzer, and a lower dialysate flow, aiming only for a modest urea reduction rather than a large drop. The dose is then increased over subsequent sessions as the urea comes down safely. In the highest-risk patients, a higher dialysate sodium or an osmotic agent such as mannitol can blunt the gradient.

Other first-session hazards

• Beyond disequilibrium, the unstable, uremic patient is vulnerable to hypotension from fluid removal, arrhythmia from rapid electrolyte shifts (a too-fast potassium drop), and bleeding from uremic platelet dysfunction compounded by anticoagulation. Each is anticipated rather than discovered.

Access and anticoagulation

• Acute dialysis usually runs through a non-tunneled temporary catheter, placed in the right internal jugular; the subclavian is avoided because central stenosis would jeopardise future access. When bleeding risk is high — as it often is in the acutely ill, uremic, or peri-procedural patient — anticoagulation is heparin-free or regional citrate.

Hyperkalemia and electrolyte shifts

• Dialysis is the definitive treatment for refractory hyperkalemia, but two cautions apply: potassium rebounds after the session as it redistributes from cells, and a very low-potassium dialysate can itself provoke arrhythmia by dropping the level too fast. A moderate bath with post-dialysis monitoring is safer than an aggressive one.

Reassessing the need as AKI evolves

• Unlike chronic dialysis, acute dialysis is a bridge: many AKI patients recover kidney function. So the need is reassessed continually — rising urine output, falling solute and fluid requirements, and improving biochemistry signal recovery — and dialysis is stopped when it is no longer needed rather than continued by inertia.

Evidence base

• The lack of benefit from early initiation rests on several large randomised trials; the urgent indications and the gentle-first-session approach rest on consensus and mechanism; and the modality comparisons rest on randomised and observational data showing no clear survival difference.

Five fully-built tables.

Table A — Urgent indications (AEIOU)

Table B — Modality selection in AKI

Table C — Disequilibrium: risk and prevention

Table D — The gentle first session

Table E — Acute hazards and mitigation

Visualise & Map

Numbered rules. These numbers are the cross-reference handle for the cases and flowcharts.

Clinical Reasoning

Five cases. Each stops you at a decision before it answers it.

Exhaustive. Every threshold and rule in the chapter is here.

Safety & Evidence

Panel A — Red flags

Panel B — NEVER DO

Anti-patterns clinicians fall into. Each becomes a Level 22 distractor.

The grade reflects strength of evidence, not importance.

Patient Decisions

Outcomes as natural frequencies. Figures are representative; the direction of effect is given where precise numbers are uncertain.

Apply & Test

Copy-paste chart notes that map to the real decisions in this chapter.

Template 1 — Acute dialysis initiation note

• Indication (AEIOU) / or watchful waiting rationale: ___.
• Modality: IHD / CRRT / SLED; rationale (haemodynamics, goals): ___.
• DDS risk: first session? urea ___; gentle-session parameters (time, Qb, dialyzer): ___.
• Access: right IJ temporary catheter (subclavian avoided).
• Anticoagulation: heparin / heparin-free / citrate; bleeding risk: ___.

Template 2 — Daily acute dialysis review

• Indication still present? potassium / acid-base / volume / uremia: ___.
• Urine output and trend: ___ (recovering?).
• Tolerance: hypotension / disequilibrium symptoms / bleeding: ___.
• Electrolytes and rebound: ___.
• Plan: continue / space out / stop dialysis; drug-dose review: ___.

Pre-rounds compression. Rules only.

Active recall. At least one card per objective.

Micro-teaching for rounds. Two scenarios, five steps each.

Metacognition anchored to this chapter's tensions. No answers provided.

1. 1. Waiting feels passive when a number is climbing; how do you hold to watchful waiting against the urge to ‘do something’?
2. 2. The safest first session is the one that clears the least; how do you reconcile the instinct to fix severe uremia fast with the harm of doing so?
3. 3. Acute dialysis is a bridge, yet stopping it takes more confidence than starting it; what evidence of recovery would make you comfortable to stop?
4. 4. A temporary catheter placed in a hurry can cost a future fistula; how does the long view change the choices you make in an acute crisis?
5. 5. Disequilibrium is rare, so it is easy to forget; how do you keep a rare but catastrophic hazard alive in your routine for first sessions?

Nine items, each anchored in this chapter. At least one per objective.