Covered most common Complications in Haemodialysis.

1. CME
Nephrology
By
Farah Adibah Kasmin
Supervisor
Dr Gan Chye Chung
C o m m o n P r o b l e m s
d u r i n g H a e m o d i a l y s i s
P P U M | 4 . 1 0 . 2 3

2. The most type of Renal Replacement Therapy (RRT) in
Malaysia is Haemodialysis.
In 2016, the prevalence of Haemodialysis is 1059
patients in per million population.
Despite alot of technological advancements have been
made, there are still a lot of acute complications of
haemodialysis are encountered during clinical practice.
Introduction

3. Intradialytic Hypotension / Hypertension
Dialysis Disequilibrium syndrome
Fever
Dialyser reaction
Bleeding
Air embolism
Muscle cramps
Access dysfunction
Acute complications

4. Decrease in SBP (mmHg) Decrease in MAP (mmHg)
KDOQI clinical practice guidelines (2005) ≥20 ≥10
European Best practice (2007) ≥20 ≥20
Intradialytic Hypotension
Intradialytic hypotension (IDH) is the most frequent complication of hemodialysis.
It occurs in about 10–40% of dialysis treatment.
Intradialytic hypotension has been associated with a range of clinical consequences including
inadequate dialysis dose, myocardial ischemia, brain atrophy, vascular access thrombosis and
increased mortality .
Different definitions of intradialytic hypotension.

5. Intradialytic Hypotension

6. Intradialytic Hypotension
Reeves and McCausland, cJASN 2018

7. Intradialytic Hypertension
It occurs in 8% to 30% of treatments, during or after haemodialysis.
Defined as a rise of SBP >10 mmHg during HD, a rise of MAP > 15 mmHg during or immediately
post-HD and/or any rise of blood pressure during HD.
In a number of patients, blood pressure remains elevated despite fluid removal is a condition
called as dialysis-refractoryhypertension.

8. Management of Intradialytic Hypertension
Accurate determination of the patient’s dry weight.
Optimization of antihypertensive after achieve dry weight.
-Gradual ultrafiltration.
- Use of minimally dialyzable or nondialyzable medications: ARB, CCB, Clonidine or Carvedilol.

9. Dialysis Disequilibrium Syndrome
It is a clinical diagnosis characterized by neurologic deterioration, restlessness, mental confusion,
headache, occasional muscle twitching, and coma.
Usually develops toward the end of dialysis but may be delayed for up to 24 hours.
Observed sporadically in patients who are initiated on haemodialysis using high-flux dialyzers
with large surface areas and short dialysis time.

10. Pathogenesis of DDS
Reverse osmotic shift –> Urea removal by dialysis = lowered plasma osmolality = osmotic gradient
that promotes water movement into brain cells > cerebral edema.
Intracerebral acidosis –> An uncertain mechanism causes a drop in cerebral intracellular pH =
leads to accumulation of excess hydrogen ions and increased production of organic acids =
increased intracellular osmolality = water movement into brain cells = cerebral edema.

11. Risk factors of DDS
First hemodialysis treatment.
Markedly elevated blood urea nitrogen (BUN) concentration prior to a dialysis session (eg:> 60
mmol/L).
Extremes of age.
Pre-existing neurologic diseases: Head trauma, stroke, seizure.
Concomitant presence of other conditions that could be associated with cerebral edema (such as
hyponatremia, hepatic encephalopathy, or hypertensive emergency).
Concomitant presence of another condition associated with increased permeability of the blood-
brain barrier (such as sepsis, vasculitis, thrombotic thrombocytopenic purpura, hemolytic uremic
syndrome, encephalitis, or meningitis).

12. Treatment of DDS
Main target is reduce brain edema and prevent complications.
If DDS is suspected, discontine the haemodialysis.
For mild symptoms, reduce the blood flow rate to reduce the urea clearance rate.
In cerebral edema, mannitol or hypertonic solution can be administered to reduce the osmotic
gradient between blood and brain.
Prevention of DDS
The target reduction in blood urea should initially be limited to 30%.
Limit the duration of the first HD to 2 - 2.5 hours.
Limit the blood flow to 200 - 250 ml / minute.
Use dialysate with high sodium levels (144-145 mmol / L) to reduce the osmotic effect
Consider continuous renal replacement therapy (CRRT) in patients at high risk for DDS, such as
cerebral injury, intracerebral hemorrhage, intracranial mass.

13. Intradialytic Fever and CRBSI
Development of fever during / after initiation of HD - high suspicions of vascular access infection.
Central-line-associated bloodstream infection (CLABSI) is defined as a bloodstream infection in a
patient with a central line in situ or removed in the last 48 hours, with no other obvious cause of
infection.
Catheter-related bloodstream infection (CRBSI) requires a pathological diagnosis through positive
blood cultures.

14. Common Organisms
Gram-positive organisms Coagulase-negative staphylococci and S. aureus together account for 40
to 80%.
Gram-negative organisms for 20 to 40%.
Polymicrobial infections for 10 to 20%.

17. Removal of Catheter

18. Retention of Catheter

19. Antibiotic Duration for Retained Catheters

20. Choice of Antibiotics for CRBSI

21. Choice of Antifungal for CRBSI

23. Exit Site Infection

24. Inability to achieve Qb of ≥300 ml/min during the first 60 minutes of HD despite at least one
attempt to improve flow.
Types of Complications:
-Thrombosis.
-Fibrin sheath formation.
-Infection.
-Vascular thrombosis or stricture.
-AV fistula.
Access Dysfunction

25. For thrombus within or outside the lumen, prevention with catheter lock:
-Heparin instillation (1000 to 10,000 U/ml) into the lumens in a volume sufficient to fill to the lumen
tip.
-Alternative, trisodium citrate 4%.
Manangement of Access Dysfunction
For catheter thrombosis:
-Forceful flushing.
-Urokinase or tPA.

26. Muscle Cramps
Occur in 5% to 20% of patients late during dialysis, leads to 15% of premature discontinuations of treatment.
Frequently involve the legs.
Pathogenesis unknown.
Largely attributed to decreased muscle perfusion and contraction of intravascular volume that occurs in
response to excessive ultrafltration.
Acute management
Increasing plasma osmolality by infusion of hypertonic saline, dextrose saline or manniltol.
Prevention
Resassess dry weight.
Adjust IDWG.
Increase Na dialysate.
Drugs- oral Quinine sulphate/ benzodiazepine/ Vit E/ carnitine.

27. Air embolism
It is rare but a fatal comlplication.
Symptoms:
-Sitting upright: Air will enter the central nervous system causing fits.
-Recumbent: Air enters the heart causing decreased cardiac output and sudden onset of dyspnoea, cough and
central cyanosis.

28. Acute management
Clamping the venous blood line.
Stopping the blood pump.
Place he patient in Trendelenburg position.
Oxygen therapy.
CRP if required.
Prevention
Check air detecting alarm system prior to initiating haemodialysis.
Flushing dialysis catheter prior to dialysis
Dialyzer rinsing before use.

29. Bleeding
Platelet dysfunction / impaired platelet-endothelium interaction
Use of anticoagulation during haemodialysis
Platelet-dialyser membrane interaction leading to thrombocytopenia
Management
Heparin-free haemodialysis- this requires increased blood flow rate and frequent flushing with isotonic
saline.
Blood product transfusion.
Protamine when haemostasis is poor in heparinised patients.
Avoid catheter removal within 4-6 hours after dialysis.

30. Type A: Anaphylactic type.
Due to hypersensitivity to ethylene oxide used to sterilize dialyzers.
Type B: Non Anaphylactic type
Attributable to complement activation.
Mild: Itching, urticaria, cough, sneezing, coryza, watery eyes, abdominal pain
and diarrhoea.
Severe: Anaphylactic reaction.
Chest pain/ back pain.
Need to exclude cardiac ischemia.
Management: Stop dialysis (without returning blood) and clamp the
extracorporeal circuit, antihistamines. Management: Supportive
Dialyzer Reaction
Dialyzer reactions refer to all of the abnormal sequelae resulting from the interaction between blood
constituents and the hemodialysis membrane.

31. Thank You