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Clinical reference

Complications

Four complications that a clinician looking after dialysis patients must be able to recognise without hesitating, and the principles behind managing them. The specific regimens are not here, and that is deliberate: they belong to your unit protocol and your local sensitivities.

Intradialytic hypotension

The definition of intradialytic hypotension varies between studies, which is precisely why the literature is so hard to compare. The commonly cited KDOQI definition is a fall in systolic blood pressure of 20 mmHg or more, or a fall in mean arterial pressure of 10 mmHg or more, associated with symptoms and requiring an intervention.

Nadir-based definitions, for example any intradialytic systolic blood pressure below 90 or 100 mmHg, correlate better with mortality in several analyses (CJASN review of intradialytic hypotension, 2018). If you are auditing IDH in your unit, decide which definition you are using and say so, because the rate you report is largely a function of that choice.

And note that IDH is often asymptomatic. A patient who is not complaining is not necessarily a patient who is not crashing.

What the evidence points at

The ultrafiltration rate is the modifiable lever with the strongest outcome signal. A UF rate above 10 mL/h/kg, and more so above 13 mL/h/kg, is strongly predictive of cardiovascular and all-cause mortality.

CJASN review of intradialytic hypotension, 2018

The mechanism implicated is repeated myocardial stunning: acute, reversible segmental hypoperfusion and contractile dysfunction, leading over time to permanent loss of contractility.

CJASN review of intradialytic hypotension, 2018

Prescribe an ultrafiltration rate that balances the risk of haemodynamic instability against the benefit of volume removal. KDOQI declined to set a hard numeric cap.

KDOQI Hemodialysis Adequacy, 2015

Management, in rough order of leverage

  • Reduce interdialytic weight gain. Dietary sodium is the primary lever, not fluid instruction: sodium drives thirst, thirst drives intake, intake drives the weight that has to come off.
  • Extend session time or increase frequency. This is the mechanistically clean fix, because it lowers the UF rate required to reach dry weight.
  • Reassess the dry weight, and raise it where that is appropriate. A patient repeatedly driven below their true dry weight will crash repeatedly, and the prescription, not the patient, is at fault.
  • Review antihypertensive timing on dialysis days. This is an individual decision by the treating team, and patients must never adjust it themselves.
  • Avoid eating during the session in susceptible patients: splanchnic vasodilatation after a meal can precipitate the drop.
  • Cool the dialysate, as an individualised measure. See the caveat below, which matters.
  • Acute management: lay the chair flat and raise the legs, reduce or stop ultrafiltration, give a small fluid bolus if needed, and give oxygen if required.
  • Midodrine and other pressors are used in refractory cases. The evidence is limited.
  • Dialysate sodium modelling: raising dialysate sodium reduces IDH but increases thirst, interdialytic weight gain and long-term volume load. The net benefit is uncertain and the practice is contested.

Dialysis disequilibrium syndrome

Dialysis disequilibrium syndrome is a neurological syndrome occurring during or shortly after dialysis, ranging from headache, nausea, restlessness and disorientation through to seizures, coma and death.

The final common pathway is cerebral oedema. The mechanism is debated between the reverse urea effect, in which urea is removed from the blood faster than it leaves the brain, exacerbated by reduced brain urea transporter expression in chronic uraemia, and the idiogenic osmole and intracerebral acidosis hypothesis (International Journal of Nephrology and Renovascular Disease review, 2019).

Risk factors: a first haemodialysis treatment, a very high pre-dialysis urea, extremes of age, and pre-existing neurological disease.

Prevention

  • Limit the rate of urea removal in the first sessions. That is the whole principle, and everything below is a way of achieving it.
  • A short initial session, around 2 hours.
  • A low blood flow rate.
  • A reduced dialysate flow rate, for example 200 mL/min.
  • A small surface-area dialyser.
  • A urea reduction target of only around 40% in at-risk patients.
  • Sodium modelling and intravenous osmotic agents (mannitol, hypertonic saline) are also used.

Reported measures from the published literature. The evidence base is weak: the 2022 Cochrane review of interventions to prevent dialysis disequilibrium found the evidence limited, and protocols vary substantially between units. Follow your own.

Access failure

Covered in full on the vascular access page. The recognition points that matter at the chair, and in the emergency department, are these.

  • A lost or weakened thrill is time-critical. A thrombosing access may still be salvageable if it is treated within hours, and the unit must be able to respond the same day.
  • Clinical monitoring is primary and surveillance is supplementary (KDOQI Vascular Access, 2019). Do not perform pre-emptive angioplasty on an imaged stenosis in the absence of clinical indicators: intervention requires both clinical signs or symptoms and a stenosis of 50% or more.
  • Watch the machine, not only the arm: rising venous pressure, falling arterial pressure, poor achievable blood flow, prolonged bleeding after needle removal, increasing recirculation, and an unexplained fall in Kt/V.
  • Steal syndrome: distal ischaemia in the access hand. A strong thrill does not exclude it. It is the combination of a strong thrill with distal ischaemic symptoms that supports the diagnosis.
  • Catheter-related bloodstream infection: fever or rigors in a patient with a catheter is a bloodstream infection until proven otherwise. KDOQI sets a facility performance goal below 1.5 infections per 1,000 catheter days.
  • Central venous stenosis: arm and facial swelling with new chest wall collaterals, classically after previous catheters.

PD peritonitis

Diagnosis requires at least 2 of 3: (1) clinical features consistent with peritonitis, that is abdominal pain and/or cloudy effluent; (2) dialysis effluent white cell count above 100 per microlitre (above 0.1 x 10^9/L) after a dwell of at least 2 hours, with more than 50% polymorphonuclear cells; (3) positive dialysis effluent culture.

ISPD Peritonitis Guideline Recommendations, 2022

Unit performance targets: an overall peritonitis rate of no more than 0.40 episodes per patient-year at risk, and more than 80% of patients peritonitis-free per year.

ISPD Peritonitis Guideline Recommendations, 2022

Empirical antibiotic cover must include both Gram-positive and Gram-negative organisms, with intraperitoneal administration preferred. The specific regimen must be selected against local organism and sensitivity patterns and the unit protocol.

ISPD Peritonitis Guideline Recommendations, 2022

Cloudy effluent is peritonitis until proven otherwise. Do not wait for the culture to start treatment, and send the effluent for cell count, differential and culture before the first dose goes in.

The 2022 update revised the definitions of refractory peritonitis, relapsing peritonitis, peritonitis-associated catheter removal, PD-associated haemodialysis transfer, peritonitis-associated death and peritonitis-associated hospitalisation, and introduced new categories: pre-PD peritonitis, enteric peritonitis, catheter-related peritonitis, and medical cure. If your unit is reporting against pre-2022 definitions, its numbers are not comparable with anyone else current numbers.

No regimen and no dose appears on this page. That is not squeamishness: it is the guideline instruction. ISPD is explicit that empirical therapy is chosen against local organism and sensitivity patterns, and a regimen published on a public website, read by a clinician in a different country with a different resistance profile, is a hazard rather than a help. Use your unit protocol.

Other complications worth flagging

  • Cardiovascular disease is the leading cause of death in dialysis, and it is not primarily atherosclerotic: sudden cardiac death, arrhythmia and heart failure dominate. The dialysis procedure itself, with its rapid electrolyte shifts, myocardial stunning and volume swings, is part of the problem rather than merely the setting for it.
  • Infection is the second leading cause of death, and catheters are the dominant modifiable risk.
  • Protein-energy wasting predicts mortality strongly. A falling albumin, a falling weight and a low nPCR should prompt urgent dietetic and clinical review, not further dietary restriction. This is the error that a well-meaning restriction culture makes most often.
  • Uraemic pruritus affects a large minority of dialysis patients, is associated with poor sleep, depression and mortality, and is substantially under-treated. Ask about it, because patients frequently do not raise it.
  • Calciphylaxis (calcific uraemic arteriolopathy): rare, devastating, with painful violaceous skin lesions progressing to necrotic ulceration, and a high mortality. Suspect it early. Do not dismiss painful skin lesions in a dialysis patient.
  • Beta-2 microglobulin amyloidosis in long-vintage patients: carpal tunnel syndrome, shoulder pain, destructive arthropathy.
  • Encapsulating peritoneal sclerosis in long-vintage PD patients: rare, serious, and a reason to discuss PD duration proactively rather than reactively.
  • Missed sessions are a complication, not an administrative event. In a European cohort study, in the 48 to 72 hours between a missed session and the next scheduled one, the mortality rate rose from 4.86 to 51.9 per 100 patient-years and hospitalisation from 0.58 to 2.1 per year. Missing the first session of the week, after the long interdialytic gap, was roughly twice as dangerous as missing a mid-week session (hazard ratio 2.04 for mortality, 1.78 for hospitalisation) (BMC Nephrology, 2020).

Sources

  1. Diagnosis and treatment of intradialytic hypotension in maintenance hemodialysis patients (Clinical Journal of the American Society of Nephrology, 2018)
  2. Dialysis disequilibrium syndrome: prevention and management (International Journal of Nephrology and Renovascular Disease, 2019)
  3. Interventions for preventing haemodialysis dysequilibrium syndrome (Cochrane review) (Cochrane Database of Systematic Reviews, 2022)
  4. ISPD Peritonitis Guideline Recommendations: 2022 Update on Prevention and Treatment (International Society for Peritoneal Dialysis, 2022)
  5. KDOQI Clinical Practice Guideline for Vascular Access: 2019 Update (the ESKD Life-Plan) (KDOQI, American Journal of Kidney Diseases, 2019)
  6. KDOQI Clinical Practice Guideline for Hemodialysis Adequacy: 2015 Update (KDOQI, American Journal of Kidney Diseases, 2015)
  7. Hospitalization and mortality following non-attendance for haemodialysis (BMC Nephrology, 2020)