---

Complications in Hemodialysis - Complete Classification

---

Overview

---

I. INTRADIALYTIC (ACUTE) COMPLICATIONS

1. Hypotension (Most Common Acute Complication)

• Excessive ultrafiltration (UF rate >10-13 mL/kg/hr) overwhelms vascular refilling
• Heat transfer from dialysate causes vasodilation, counteracting compensatory vasoconstriction
• Solute diffusion reduces intravascular osmolality, reducing osmotic drive for vascular refilling
• High-risk patients: diabetics, older age, female sex, longer dialysis vintage, underlying heart disease

• Cardiac dysfunction: LVH, ischemia, hypoxia, arrhythmia, pericardial tamponade
• Medications: antihypertensives, opiates
• Decreased vascular tone: sepsis, eating before/during dialysis, dialysate temperature >37°C
• Intradialytic blood loss: tubing or dialyzer filter leaks

• Halt ultrafiltration; Trendelenburg positioning
• Oral salt (broth) or normal saline 100-500 mL IV
• If refractory: vasopressors, invasive hemodynamic monitoring in ICU

---

2. Dialysis Disequilibrium Syndrome (DDS)

• Timing: End of dialysis, most common during first dialysis or hypercatabolic states
• Pathophysiology: Rapid large solute clearance causes a transient osmolar gradient - blood osmolality falls faster than brain osmolality, water moves into the brain causing cerebral edema
• Symptoms (mild to severe):
  • Mild: Nausea, vomiting, headache, hypertension, restlessness
  • Severe: Seizures, coma, death
• Prevention: Limit solute clearance when initiating HD (slow, short first sessions)
• Treatment: Stop dialysis; IV hypertonic saline (5 mL of 10-23% NaCl) or mannitol 0.25 g/kg IV to raise serum osmolality

---

3. Muscle Cramps

• Very common, particularly at end of session
• Cause: Rapid fluid/electrolyte shifts, excessive UF relative to patient's dry weight, low dialysate sodium
• Management: Hypertonic saline, hypertonic dextrose, or stretching; review dry weight

---

4. Air Embolism

• Mechanism: Air enters extracorporeal circuit through tubing disconnection or pressure errors
• Clinical presentation (position-dependent):
  • Sitting: Air travels retrograde through internal jugular vein → cerebral circulation → raised ICP, neurologic symptoms
  • Recumbent: Air enters right ventricle/pulmonary circulation → pulmonary hypertension + systemic hypotension
  • Patent foramen ovale (right-to-left shunt): Arterial air embolism → MI or stroke
• Symptoms: Acute dyspnea, chest tightness, loss of consciousness, cardiac arrest; cyanosis; churning sound in heart
• Treatment: Clamp venous blood line immediately; supine positioning; 100% O2; percutaneous aspiration of air from right ventricle; IV steroids; full heparinization; hyperbaric oxygen

---

5. Electrolyte Disturbances

• Hyperkalemia: Most common electrolyte emergency requiring intervention
• Hyponatremia/Hypernatremia: Errors in dialysate concentrate mixing → rapid osmolar shifts, hemolysis
• Hypoglycemia: In diabetic and non-diabetic ESRD patients (drugs, malnutrition, sepsis)
• Hypo/Hypercalcemia, Hypo/Hypermagnesemia: Related to dialysate composition errors

---

6. Arrhythmias

• Risk factors: LVH, coronary artery disease, disordered Ca/phosphate metabolism, calcification of conduction system
• Key triggers during HD: Rapid potassium removal (low K dialysate baths <2 mEq/L most implicated), rapid changes in Ca, Mg, and pH
• Pattern: Cardiac arrest clusters around the long interdialytic interval (Monday/Tuesday after weekend gap)
• Types: Ventricular tachycardia/fibrillation (most common arrest rhythm), atrial fibrillation (prevalence >20% in HD patients)
• Cardiac arrest: 1-year survival only ~15%; ICD may be considered in high-risk patients (leadless/subcutaneous ICDs preferred to avoid central venous stenosis)

---

7. Chest Pain and Back Pain ("First Use Syndrome" / Dialyzer Reactions)

• Onset: within first few minutes of dialysis
• Symptoms: Burning, pruritus, urticaria, severe dyspnea, chest/back pain, hypotension, angioedema, cardiac arrest
• Cause: Complement activation by cuprophane membrane or hypersensitivity to ethylene oxide sterilant
• Treatment: Stop dialysis; do NOT return blood; epinephrine/antihistamines/steroids; switch to synthetic membrane

• Onset: later in session (~20-40 min)
• Symptoms: Chest and back pain only, without systemic signs
• Cause: Complement activation → transient pulmonary leukostasis → hypoxemia
• Treatment: Supplemental oxygen; supportive care; session can often continue

---

8. Hemolysis

• Causes: Kinked blood lines, dialysate errors (low osmolality, overheated dialysate, contamination with chloramine, formaldehyde, or copper), mechanical pump trauma
• Symptoms: Back/chest pain, port-wine or pink-tinged blood returning from dialyzer, nausea
• Consequences: Acute hyperkalemia (from lysed RBC potassium release), anemia
• Treatment: Clamp blood lines; do NOT return blood; urgent hyperkalemia management

---

9. Fever and Chills / Bacteremia

• Causes: Contaminated dialysate, access infection (AV fistula, graft, or catheter-related bloodstream infection)
• Most common organisms: Staphylococcus aureus, coagulase-negative staphylococci, gram-negatives
• Management: Blood cultures; empiric antibiotics; catheter exchange or removal if catheter-related

---

10. Hypoxemia

• Mechanism: Complement-mediated pulmonary leukostasis (leukocyte aggregation in pulmonary capillaries), bioincompatibility of dialyzer membrane
• Also: Removal of CO2 by acetate-based dialysate → hypocapnia → decreased respiratory drive
• Clinically: Mild, often subclinical; more significant in patients with pre-existing lung disease

---

II. CHRONIC / LONG-TERM COMPLICATIONS

1. Cardiovascular Disease (Leading Cause of Death)

• Accounts for ~40% of identifiable deaths in ESKD
• Manifestations: LVH (most common cardiac abnormality), coronary artery disease, heart failure, sudden cardiac death
• High-output cardiac failure: Can occur when >20% of cardiac output is diverted through AV access
  • Branham sign (heart rate fall on temporary access occlusion) is diagnostic
  • Doppler US measures access flow; surgical banding is treatment of choice
• Myocardial stunning: HD procedure itself contributes to cardiac mortality via repeated ischemia (troponin release, regional LV dysfunction, reduced myocardial blood flow on PET)

---

2. Pericardial Disease

• Uremic pericarditis: Occurs in CKD stage 5 before or after starting dialysis; presents with fever, pleuritic chest pain worse when supine, pericardial rub
• Dialysis-related pericarditis: Inadequate dialysis or fluid overload
• Complications: Pericardial effusion, cardiac tamponade (requires urgent pericardiocentesis)
• Treatment: Intensify dialysis; NSAIDs; pericardiocentesis if tamponade

---

3. Hypertension

• Persistent hypertension (despite dialysis) common from volume overload, activation of renin-angiotensin-aldosterone system
• Paradoxically, hypertension during HD can indicate DDS
• Management: Salt and fluid restriction; dry weight optimization; antihypertensives; more frequent/longer HD sessions improve BP control

---

4. Anemia

• Erythropoietin deficiency (reduced renal production)
• Iron deficiency (dialysis-related blood loss ~2-3 g Fe/year)
• Chronic inflammation, malnutrition, aluminum toxicity (historical)
• Treatment: Erythropoiesis-stimulating agents (ESAs), IV iron supplementation, target Hb 10-11 g/dL

---

5. Mineral and Bone Disorder (CKD-MBD)

• Hyperphosphatemia: Requires dietary restriction + phosphate binders (calcium carbonate, sevelamer, lanthanum)
• Hypocalcemia / Hypercalcemia
• Secondary Hyperparathyroidism: High PTH → osteitis fibrosa cystica
• Renal Osteodystrophy: Spectrum includes osteitis fibrosa cystica, adynamic bone disease, osteomalacia, mixed
• Vascular calcification: Calcification of arterial walls and cardiac valves (major contributor to CV mortality)
• Calciphylaxis (Calcific uremic arteriolopathy): Medial calcification of small arteries → ischemic skin necrosis; life-threatening

---

6. Beta-2 Microglobulin Amyloidosis (Dialysis-Related Amyloidosis)

• Mechanism: β2-microglobulin (MW 11,800 Da) is not cleared by most dialysis membranes → accumulates → forms amyloid fibrils
• Manifestations: Carpal tunnel syndrome (most common), destructive arthropathy, shoulder periarthritis, cystic bone lesions ("dialysis cysts"), pathologic fractures, spondyloarthropathy of cervical/lumbar spine
• Timing: Usually after >5-7 years on dialysis; almost universal after 15+ years
• Treatment: High-flux membranes (better but incomplete clearance); hemodiafiltration; renal transplant (reverses progression)

---

7. Neurological Complications

• Uremic encephalopathy: Inadequate dialysis → confusion, asterixis, myoclonus, seizures, coma
• Peripheral neuropathy: Uremic neuropathy; "restless legs syndrome"
• Dialysis encephalopathy (aluminum toxicity - historical): Progressive aphasia, myoclonus, dementia, seizures; caused by aluminum in dialysate water; now rare with reverse osmosis water treatment
• Autonomic neuropathy: Contributes to intradialytic hypotension, gastroparesis, erectile dysfunction

---

8. Nutritional and Metabolic Complications

• Protein-energy wasting (PEW): Loss of amino acids across dialyzer (~6-8 g/session); dietary restriction compounds this; increased mortality
• Hypoalbuminemia: Powerful predictor of mortality in HD patients
• Vitamin deficiencies: Water-soluble vitamins (C, B complex, folate) removed during dialysis
• Hyperlipidemia: Elevated triglycerides; low HDL (accelerates atherosclerosis)
• Carbohydrate metabolism: Glucose gain from dialysate; hypoglycemia in diabetics

---

9. Infection

• Second most common cause of death in HD patients (after cardiovascular disease)
• Vascular access infections most common (see Access Complications below)
• Peritonitis (for PD patients)
• Impaired immune function (uremia suppresses T-cell and neutrophil function)
• Prevention: AV fistula preferred over catheters; strict sterile technique; vaccination (hepatitis B, influenza, pneumococcal)

---

10. Hematologic Complications

• Bleeding tendency: Uremic platelet dysfunction (abnormal GPIb-vWF interaction); treated with DDAVP, conjugated estrogens, cryoprecipitate
• Thrombosis: Paradoxically, HD patients also have elevated thrombotic risk
• Anticoagulation during HD: Systemic heparin (standard); low-molecular-weight heparin; regional citrate anticoagulation (for high-bleeding-risk patients); heparin-free HD

---

11. Psychosocial Complications

• Depression: Serious, underrecognized; strongly correlates with mortality and morbidity; HD patients are ~3 times more likely to commit suicide than controls
• Anxiety, fatigue, poor quality of life
• Sleep disorders, restless legs syndrome: Common; worsen fatigue and depression
• Sexual dysfunction: Erectile dysfunction in men; menstrual irregularities in women

---

12. Malignancy

• Increased risk of renal cell carcinoma (acquired cystic kidney disease), urothelial carcinoma
• General increase in cancer risk due to immune dysfunction
• Routine cancer screening should be individualized based on expected survival and transplant candidacy

---

III. VASCULAR ACCESS COMPLICATIONS

A. Arteriovenous Fistula (AVF) Complications

---

B. Arteriovenous Graft Complications

• Similar to AVF but with higher rates of thrombosis and infection
• Pseudoaneurysm formation from repeated needle sites
• Graft infection (often S. aureus) - frequently requires graft excision

---

C. Tunneled Central Venous Catheter (CVC) Complications

---

IV. TECHNICAL / MACHINE ERRORS

---

Quick Reference Summary Table

---