Chronic kidney disease and the dialysis patient

Why examiners ask this

The dialysis patient appears as the host for an AV fistula creation, a hip fracture or an emergency laparotomy, and the stem hides a potassium, a missed dialysis session or a fistula on the arm you want to use. Examiners test whether you understand the multisystem disease, not just the kidney: coronary disease, anemia, platelet dysfunction, delayed gastric emptying and altered drug handling. It stresses application of knowledge and judgment about timing.

The 60-second answer

Decision points and the "why"

• Dialysis timing — within 24 hours before elective surgery normalizes potassium, volume and acidosis; dialysis the same morning can leave the patient hypovolemic and hypokalemic with residual heparin, so I check a post-dialysis potassium and confirm the heparin dose.
• Potassium threshold — I proceed with elective surgery at a potassium up to about 5.5 mEq/L in a chronic patient with a normal ECG; above 6 or with ECG changes I delay and dialyze.
• Succinylcholine — it raises potassium by about 0.5 mEq/L, and renal failure itself does not exaggerate the rise; it is acceptable with a potassium below about 5 mEq/L, and contraindicated when the potassium is already high.¹
• Relaxant and reversal — cisatracurium undergoes Hofmann elimination and is my first choice; rocuronium is prolonged. Sugammadex is not recommended below a creatinine clearance of 30 mL/min because the complex is renally cleared; only high-flux hemodialysis removes it, lowering levels by about 70% over 3–6 hours.² Neostigmine and glycopyrrolate are also renally cleared and both last longer.
• Opioids — fentanyl, hydromorphone in reduced doses, and remifentanil are reasonable; morphine's glucuronides accumulate, with sedation from the 6-glucuronide and neurotoxicity from the 3-glucuronide,³ and normeperidine causes seizures.
• Uremic bleeding — platelet dysfunction from uremic toxins; desmopressin 0.3 mcg/kg IV improves platelet function within an hour,⁴ and dialysis and correcting anemia above 10 g/dL also help. I weigh this before neuraxial blocks.
• Regional for fistula creation — a brachial plexus block causes sympathectomy and vasodilation; in a randomized trial it raised 12-month primary patency from 59% with local infiltration to 79%,⁵ and it avoids a general anesthetic in a sick patient.

The complication they will inject

The patient missed dialysis for an urgent bowel obstruction. Preoperative potassium is 6.8, with peaked T waves, pH 7.22, and the patient is volume overloaded on 4 L of oxygen. The surgeon wants to go now. I tell the surgeon that if there is time, a 2–3 hour session of urgent dialysis makes the anesthetic safer, and the obstruction rarely kills in that interval. If ischemia means we cannot wait, I treat the potassium first: calcium chloride 1 g to stabilize the membrane, insulin 10 units with 25 g dextrose, albuterol, and bicarbonate for the acidosis. I do a modified rapid sequence with rocuronium, not succinylcholine, use an arterial line, hyperventilate mildly to keep the pH from falling, and avoid potassium-containing transfusion where possible by using fresh or washed cells. I arrange continuous renal replacement in the ICU.

Pitfalls that cost points

• Forgetting the fistula arm.
• Assuming hypotension after induction means deep anesthesia rather than a dry, autonomically neuropathic patient.
• Using morphine for postoperative analgesia.
• Proceeding with succinylcholine without knowing the potassium.
• Avoiding lactated Ringer's out of fear of its potassium; saline's acidosis raises potassium more.

Rapid-why

Q: Why are these patients anemic and does it matter? A: Low erythropoietin; they tolerate chronic anemia well, but it lowers oxygen-carrying reserve and worsens uremic bleeding.

Q: Why do they have delayed gastric emptying? A: Diabetic and uremic autonomic neuropathy; I give aspiration prophylaxis and use rapid sequence when symptomatic.

Q: Why is the response to induction drugs exaggerated? A: Hypoalbuminemia raises the free fraction of highly bound drugs, and the blood–brain barrier is more permeable; I reduce and titrate doses.

Q: What happens to dexmedetomidine and ketamine? A: Both are hepatically metabolized and reasonable choices, though active metabolites of ketamine accumulate modestly.

Numbers to know

Links

• hyperkalemia, Acute kidney injury (coming), succinylcholine, Neuromuscular blockade, monitoring and reversal, Preoperative cardiac evaluation for non-cardiac surgery
• KDIGO Clinical Practice Guideline for CKD Evaluation and Management (2024); ACC/AHA Guideline for Perioperative Cardiovascular Evaluation (2024)