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CKD Comprehensive MRCP/FCPS Part 2 Notes

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TOPIC 1: CKD ANEMIA - DIAGNOSIS, STAGING & MANAGEMENT

Definition (KDIGO 2026)

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Pathophysiology Mnemonic: "RAISE"

• Reduced EPO production (loss of functioning renal mass)
• Anemia of chronic inflammation (hepcidin-mediated iron block)
• Iron deficiency (absolute or functional/iron-restricted erythropoiesis)
• Shortened RBC survival (uremic toxins)
• Extra losses (dialysis membrane, GI blood loss, frequent blood tests)

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Evaluation / Workup

• OLD: "Absolute iron deficiency" → NEW: "Systemic iron deficiency" (ferritin low, TSAT low)
• OLD: "Functional iron deficiency" → NEW: "Iron-restricted erythropoiesis" (ferritin normal/high but TSAT low, reflects hepcidin-mediated block)

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Haemoglobin Targets (KDIGO 2026)

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Iron Therapy

When to Give Iron?

• Treat if symptomatic anemia AND (ferritin <100 ng/mL OR TSAT <20%)
• Consider IV iron trial if ferritin 100-500 ng/mL + TSAT <30% (anticipate ESA need)
• Withhold routine iron if ferritin >700 ng/mL OR TSAT >40%

• Most patients require IV iron routinely (losses from dialysis ~1-2g/year)
• IV iron preferred over oral (poor oral absorption due to high hepcidin, GI intolerance)
• Give proactively to maintain TSAT 20-40% and ferritin 200-500 ng/mL

Oral vs Intravenous Iron

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Blood Transfusion in CKD

• Threshold: Hb <7 g/dL acutely symptomatic (or <8 with cardiac disease)
• Acute bleeding / surgical requirement
• Bone marrow failure / ESA hyporesponsiveness
• Symptoms refractory to other therapy (angina, breathlessness at rest)

1. Iron overload
2. HLA sensitisation (blocks future transplantation - most important in CKD)
3. Transfusion-transmitted infection risk
4. Alloantibody formation

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TOPIC 2: ERYTHROPOIESIS-STIMULATING AGENTS (ESAs)

Types of ESAs

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When to Start ESA

1. Hb persistently <10 g/dL despite correction of reversible causes
2. Patient is symptomatic (fatigue, dyspnoea, palpitations)
3. Iron replete (ferritin and TSAT adequate - give iron FIRST)
4. Other causes excluded (B12/folate deficiency, haemolysis, blood loss)

• Active malignancy (except palliative)
• Recent stroke or MI (increased thrombosis risk)
• Uncontrolled hypertension
• Pure red cell aplasia (PRCA - due to anti-EPO antibodies)

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ESA Dosage

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How to Give ESA

• Non-dialysis CKD: SC route preferred (bioavailability better, lower doses needed)
• Haemodialysis: IV route at end of dialysis session is convenient (avoids needle stick)
• Peritoneal dialysis: SC preferred
• Do NOT give IV in non-HD patients (IV has shorter half-life, less efficient)

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Monitoring ESA

• Haemoglobin: Check every 2-4 weeks until stable, then monthly
• Anti-EPO antibodies: If sudden Hb drop + reticulocytopenia → suspect PRCA
• Blood pressure: Hypertension is a key side effect (EPO increases peripheral resistance)
• Iron status: TSAT + ferritin every 3 months; replete before/during ESA
• Thrombosis: Check platelets; avoid Hb >13 g/dL

• Defined as requiring >2x standard dose with suboptimal response
• Causes mnemonic: "IRIC"
  • Iron deficiency (commonest)
  • Read: Infections, inflammatory states (CRP high - hepcidin blocks iron)
  • Inadequate dialysis
  • Causes: Blood loss, B12/folate, hyperparathyroidism, PRCA, aluminium toxicity, haematologic malignancy

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New Class: HIF-PHI (Hypoxia-Inducible Factor Prolyl Hydroxylase Inhibitors)

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TOPIC 3: ARTERIOVENOUS FISTULA (AVF) IN CKD

Why AVF?

1. AVF (autologous) - preferred
2. AV Graft (prosthetic, e.g. PTFE)
3. Tunnelled central venous catheter (last resort)

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When to Refer for AVF Creation

• Refer to vascular surgery when eGFR <30 mL/min (or eGFR 15-29 to plan)
• Create AVF 6 months before expected dialysis start (maturation time needed)
• For elderly/diabetics with slow progression: refer earlier at eGFR <30

• Vein mapping (duplex ultrasound) - vein diameter ≥2.5 mm needed
• Allen's test (check radial/ulnar dominance)
• Dominant vs non-dominant arm (prefer non-dominant)

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Types of AVF

A. By Location (Distal to Proximal - ALWAYS start distally)

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B. High-Flow vs Low-Flow AVF

• High-flow fistula "steals" blood from hand
• Presents as: pain, coldness, paraesthesia in hand, tissue loss
• Management: DRIL procedure (distal revascularization-interval ligation) or banding

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Fistula Maturation

• Minimum 6 weeks to mature (ideally 3-6 months)
• Diameter ≥6 mm when tourniquet applied
• Depth ≤6 mm from skin surface (for needling)
• Flow ≥600 mL/min

• Commonest cause: stenosis at anastomosis or outflow
• Investigation: Fistulogram / Doppler USS
• Management: Percutaneous transluminal angioplasty (PTA) or surgical revision

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AV Graft vs AVF

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Patient Counselling for AVF

• Surgery: Minor day-case procedure under local anaesthetic. Small incision. Takes 1-2 hours.
• Protect the arm: Never allow blood pressure measurement, blood tests, IV cannulas in the fistula arm. No tight clothing or watches.
• Arterial thrill/bruit: Normal. They should feel a buzzing sensation - report if it stops.
• Care and monitoring: Check thrill daily. Report redness, swelling, pus, loss of thrill, or pain.
• Exercise the arm: Squeeze a stress ball or soft rubber ball 30 min/day to promote maturation.

• Non-dominant arm preferred
• Keep arm warm to dilate vessels
• Avoid sleeping on the fistula arm
• Emergency: if bleeding, apply firm pressure and seek help immediately
• Timeline: Usually 6-12 weeks before use; some up to 6 months
• Failure rate: ~40% fail to mature (more in elderly, diabetics, women with small veins)
• Regular monitoring: Monthly physical examination; annual duplex if stable

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TOPIC 4: CKD-MINERAL BONE DISEASE (CKD-MBD)

Definition

1. Abnormal calcium, phosphate, PTH, FGF23, vitamin D metabolism
2. Bone abnormalities (renal osteodystrophy)
3. Vascular/soft tissue calcification

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Pathogenesis Mnemonic: "FGF-PCP Loop"

1. Phosphate retention → hyperphosphatemia
2. Reduced 1,25(OH)₂D (calcitriol) production → hypocalcaemia
3. Hypocalcaemia → PTH↑ (secondary hyperparathyroidism)
4. FGF23↑ (earliest marker - rises before Ca/PO4/PTH change) → inhibits 1-alpha hydroxylase → worsens calcitriol deficiency → further PTH stimulus
5. Calcitriol deficiency → reduced GI Ca/P absorption
6. Chronic PTH elevation → bone resorption → renal osteodystrophy

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Types of Renal Osteodystrophy

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Diagnosis (KDIGO 2017 + 2024 CKD Guideline)

Biochemical Monitoring - Start at G3a-G5

Imaging

• X-ray: Subperiosteal resorption (radial border of middle phalanges - classic HPT), "rugger jersey spine," "salt and pepper skull," brown tumours, looser zones (osteomalacia)
• Bone mineral density (DXA): Recommended in CKD G3a-G5D if results change management
• Vascular calcification assessment: Lateral abdominal X-ray or echocardiogram

Bone Biopsy (Gold standard for renal osteodystrophy type)

• Indications: Unexplained fractures, persistent hypercalcaemia, suspected Al toxicity, before parathyroidectomy
• Technique: Tetracycline double-labelling before biopsy (marks mineralisation front)

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Management

Step 1: Phosphate Control (most important)

• Reduce processed foods (high bioavailable phosphate as additives)
• Prefer plant-based proteins (lower phosphate bioavailability)

Step 2: Vitamin D Therapy

• Can cause hypercalcaemia, hyperphosphataemia, raised FGF23
• Contraindicated if Ca >2.54 mmol/L or Ca × PO₄ product >4.4 mmol²/L²
• Monitor Ca + PO₄ monthly when starting

Step 3: PTH Management

• Non-dialysis CKD: Maintain in the normal range
• Dialysis (G5D): PTH 2-9x upper limit of normal (accounts for skeletal resistance to PTH)
  • Too low PTH → adynamic bone disease
  • Too high PTH → osteitis fibrosa

• Mechanism: Allosteric activators of calcium-sensing receptor (CaSR) → reduce PTH secretion
• Indication: Secondary hyperparathyroidism in dialysis patients when PTH persistently elevated despite VitD and phosphate control
• Cinacalcet (Mimpara): Oral; 30-180 mg/day; risk of hypocalcaemia
• Etelcalcetide (Parsabiv): IV at end of HD; avoids GI side effects; newer
• Monitor: Ca (risk of hypocalcaemia), PTH, QTc prolongation with cinacalcet
• EVOLVE trial: Cinacalcet reduced parathyroidectomy and fractures but did not reduce CV mortality significantly

Step 4: Parathyroidectomy

• PTH persistently >800-1000 pg/mL with symptoms
• Severe hypercalcaemia (Ca >2.85 mmol/L) unresponsive to medical therapy
• Pathological fractures
• Calciphylaxis (calcinosis cutis)
• Failed calcimimetic/VitD therapy

• Subtotal parathyroidectomy (3.5 glands) - preferred
• Total parathyroidectomy + autotransplantation (forearm)
• Post-op: Watch for "Hungry Bone Syndrome" - severe hypocalcaemia (avid Ca uptake by demineralised bone)

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Surveillance / Monitoring Summary

• Ca: 2.1-2.4 mmol/L (avoid high-normal)
• PO4: 1.1-1.76 mmol/L (aim normal)
• PTH: 2-9x ULN = 130-600 pg/mL approx
• Ca × PO4 product: <4.4 mmol²/L²

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TOPIC 5: CKD ATHEROSCLEROSIS AND PAD

CKD as a CVD Risk State

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Atherosclerosis in CKD

• Hyperhomocysteinaemia
• Inflammation (CRP, IL-6, TNF-alpha)
• Proteinuria / endothelial dysfunction
• Phosphate load + vascular calcification
• Oxidative stress
• Carbamylation of LDL
• Renin-angiotensin system activation
• Anaemia (cardiac hypertrophy/remodelling)
• Thrombin / prothrombotic state
• Endotoxaemia (gut bacterial translocation)
• Sympathetic overactivation

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Peripheral Arterial Disease (PAD) in CKD

Why CKD Worsens PAD?

• Increased atherosclerotic burden (accelerated)
• Medial vascular calcification (Monckeberg's sclerosis) - makes arteries stiff, non-compressible
• Impaired wound healing (uraemia, anaemia, malnutrition)
• Autonomic neuropathy in diabetic CKD
• Higher rates of amputation

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Diagnosis of PAD in CKD (2024 ACC/AHA + 2025 ACC Guidelines)

Clinical Presentation

• Asymptomatic (most common - 50%)
• Intermittent claudication: Calf pain/cramp on walking, relieved by rest
• Chronic Limb-Threatening Ischaemia (CLTI): Rest pain, tissue loss, gangrene
• Fontaine Classification:

Ankle-Brachial Index (ABI) - Cornerstone Diagnostic Test

Additional Investigations

• Duplex USS: First-line imaging for anatomy
• CT angiography (CTA): Preferred for revascularisation planning (contrast risk in CKD - use lowest dose, ensure hydration)
• MRA: Good for CKD (no nephrotoxic contrast with gadolinium; caveat - avoid gadolinium if eGFR <30 due to nephrogenic systemic fibrosis risk)
• Digital subtraction angiography: Gold standard; only if intervention planned
• Exercise treadmill ABI: To unmask borderline resting ABI

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Management of PAD in CKD

Antiplatelet/Anticoagulation

• Aspirin 75 mg for all symptomatic PAD in CKD
• Clopidogrel 75 mg - alternative or add-on after revascularisation
• Low-dose rivaroxaban (2.5 mg BD) + aspirin 100 mg: COMPASS trial - reduces MACE and MALE (major adverse limb events) in PAD - applicable in CKD but use cautiously if eGFR <30
• Vorapaxar: PAR-1 antagonist; some benefit in PAD but avoid in CKD (haemorrhagic risk)

Statins

• All CKD patients ≥50 years: Statin or statin + ezetimibe (KDIGO 2013 lipid guideline)
• 4D and AURORA trials: Statins did NOT reduce CV mortality in dialysis patients specifically - start before dialysis but do not initiate de novo in dialysis
• SHARP trial (CKD, not dialysis): Simvastatin + ezetimibe → 17% reduction in atherosclerotic events

Smoking Cessation - most effective single intervention for PAD

Revascularisation in PAD

• Indications: CLTI (rest pain, tissue loss), debilitating claudication not responding to exercise
• Options:
  • Endovascular (PTA ± stent): Preferred for iliac/femoral short occlusions; faster recovery
  • Surgical bypass: Longer occlusions, CLTI in fit patients
• CKD-specific consideration: Higher peri-operative mortality; contrast nephropathy risk; poor wound healing; higher re-stenosis rate

Wound Care and Foot Care

• Regular podiatry review
• Daily foot inspection
• Diabetic foot teams for CKD-diabetic patients
• Orthopaedic/vascular MDT for tissue loss

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Key Differences: Atherosclerosis vs Arteriosclerosis in CKD

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RAPID-FIRE EXAM MNEMONICS SUMMARY

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MRCP/FCPS HIGH-YIELD EXAM POINTS

1. Hb target NEVER >13 g/dL in CKD on ESA - increased stroke/thrombosis above this
2. Withhold iron if ferritin >700 OR TSAT >40% (KDIGO 2026)
3. Transfusion sensitises - reduces transplant options (allosensitisation)
4. CERA (Mircera) = monthly dosing - longest acting ESA
5. PRCA - sudden reticulocytopenia + Hb drop on ESA → test for anti-EPO antibodies → stop ESA, switch class
6. AVF created 6 months before anticipated dialysis start
7. High-flow fistula → risk of steal syndrome (HAIDI) and high-output cardiac failure
8. FGF23 is the EARLIEST abnormal biomarker in CKD-MBD
9. PTH target in dialysis: 2-9x ULN (not normal - need some PTH activity for bone turnover)
10. Low PTH = adynamic bone disease - often from over-treatment with calcium/VitD
11. Calciphylaxis = ischaemic skin necrosis from vascular calcification - indication for parathyroidectomy ± sodium thiosulfate
12. ABI >1.40 = non-compressible arteries (Monckeberg's in CKD/DM) → use Toe-Brachial Index instead
13. Gadolinium MRI contraindicated if eGFR <30 (nephrogenic systemic fibrosis)
14. Statins NOT started de novo in dialysis (4D, AURORA trials negative) - but continue if already on them
15. COMPASS trial: Low-dose rivaroxaban + aspirin reduces limb events in PAD (use cautiously in CKD <30)
16. SHARP trial confirmed lipid lowering reduces CV events in non-dialysis CKD
17. Sevelamer (non-calcium binder) also reduces LDL and CRP - preferred in dialysis patients with vascular calcification

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Dialysis Disequilibrium Syndrome & Complications of Dialysis

MRCP/FCPS Part 2 - Complete Notes

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PART 1: DIALYSIS DISEQUILIBRIUM SYNDROME (DDS)

Definition

• First few dialysis sessions (especially acute initiation)
• Severely uraemic patients (BUN >100 mg/dL)
• Paediatric patients and elderly
• High-efficiency dialysis in hypercatabolic states

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Pathophysiology - Two Competing Theories

Theory 1: Urea Osmole Hypothesis (Reverse Osmosis / "Reverse Urea Effect") - Most Accepted

1. Rapid dialysis removes urea from the blood quickly
2. Urea crosses the blood-brain barrier slowly (ineffective osmole)
3. Brain retains high urea = brain osmolality > plasma osmolality
4. Water shifts into brain down osmotic gradient → cerebral oedema → raised ICP

Theory 2: Idiogenic Osmoles + CNS Acidosis

• Rapid urea removal → intracellular brain pH falls (paradoxical CNS acidosis)
• CO₂ (produced by bicarbonate buffering) crosses BBB faster than HCO₃⁻
• Brain becomes paradoxically more acidotic → intracellular osmoles generated → water influx
• Both mechanisms likely contribute simultaneously

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Mnemonic for Risk Factors: "BUN-SCAN"

• BUN >100 mg/dL (severe uraemia at dialysis initiation)
• Uraemic encephalopathy pre-existing
• Neonates and children (high brain water content, immature BBB)
• Sodium abnormalities (hyponatraemia)
• Cerebral pathology (prior stroke, head injury, brain tumour)
• Acid-base: severe acidosis
• Newly initiated dialysis patients (first treatment)

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Clinical Features

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Differential Diagnosis of Neurological Symptoms During Dialysis

• DDS (dialysis disequilibrium)
• Air embolism (cerebral)
• Subdural haematoma (3-4% of dialysis patients historically; reduced now)
• Hypo/hypernatraemia (dialysate error)
• Septic encephalopathy
• Epilepsy / pre-existing seizure disorder
• Low glucose (hypoglycaemia - especially diabetics)
• First use syndrome (anaphylactic - Type A dialyser reaction)

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Management of DDS

Immediate (Acute Episode):

Prevention (Most Important):

• Short initial sessions: 2 hours, blood flow rate 150-200 mL/min (not standard 300-400 mL/min)
• Low-efficiency dialysis initially (low flux membranes for first sessions)
• Osmolality augmentation: Add mannitol 1 g/kg or glucose to dialysate
• Watch BUN: Aim for no more than 30-40% BUN reduction per session initially
• Sodium: Use higher dialysate sodium (140-145 mEq/L) in first sessions
• Avoid high blood/dialysate flow rates initially
• Frequent shorter sessions better than one long aggressive session
• Escalate gradually over days

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PART 2: COMPLETE COMPLICATIONS OF DIALYSIS

Overview Classification

• Cardiovascular (hypotension, hypertension, arrhythmia, cardiac tamponade)
• Haematological (haemolysis, bleeding, air embolism, clotting)
• Access-related (infection, thrombosis, steal syndrome, aneurysm)
• Syndrome-specific (DDS, first-use, pyrogen reaction)
• Electrolyte/metabolic (hypokalaemia, hypocalcaemia, hypoglycaemia)
• Dialysis-specific chronic (amyloidosis, malnutrition, aluminium toxicity)

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COMPLICATION 1: INTRADIALYTIC HYPOTENSION (IDH)

Definition

Causes - "VAMPIRE"

• Volume excess removed too fast (excessive ultrafiltration rate - commonest)
• Antihypertensives taken pre-dialysis
• Myocardial dysfunction (LVH, ischaemia, stunning)
• Pericardial disease (effusion/tamponade - always consider recurrent IDH)
• Infection/Sepsis
• Reduced vascular tone (warm dialysate, post-meal blood shift, autonomic neuropathy)
• Extra fluid loss (bleeding, GI loss pre-dialysis)

Immediate Management

1. Trendelenburg position (supine, legs elevated) - first manoeuvre
2. Reduce or stop ultrafiltration immediately
3. Normal saline 100-250 mL IV bolus (repeat PRN) - isotonic saline is as effective as albumin
4. Reduce blood pump speed only if severe (compromises Kt/V)
5. Supplemental O₂
6. If persistent despite above → stop dialysis, send to ward/ED

• ECG + troponin (rule out MI/ischaemia)
• Bedside echo (rule out tamponade)
• Consider vasopressors (noradrenaline) if ICU transfer required
• Check for sepsis (blood cultures)

Prevention Strategies

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COMPLICATION 2: INTRADIALYTIC HYPERTENSION (IDHtn)

Definition

Causes

• Volume overload (commonest - inadequate fluid removal despite dialysis)
• Activation of RAAS during fluid removal
• Sympathetic overactivation
• Endothelin release
• Erythropoietin administration (increases peripheral vascular resistance)
• Fluid shift from dialysate (high sodium dialysate)
• Anxiety/pain

Management

1. Address volume overload - more aggressive ultrafiltration in subsequent sessions
2. Reassess dry weight (patient may be volume overloaded overall)
3. Increase dialysis intensity/frequency
4. Review ESA dose (if ESA-induced)
5. Do not give antihypertensives intradialytically unless hypertensive emergency
6. Hypertensive emergency (SBP >180 + symptoms): IV labetalol 20 mg or oral amlodipine/hydralazine; target gradual reduction, not more than 25% in first hour

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COMPLICATION 3: CARDIAC ARRHYTHMIAS

Causes

• Electrolyte shifts: rapid changes in K⁺, Ca²⁺, Mg²⁺ during dialysis
• Myocardial ischaemia / stunning (demand ischaemia from hypotension)
• LVH (extremely common in dialysis patients)
• Autonomic instability
• Low-potassium dialysate → risk of VT/VF
• Digitalis toxicity (dialysis reduces K⁺ → enhances digitalis effects)

Management

• Avoid dialysate potassium <2 mEq/L
• Do not use dialysate K <1 mEq/L even for severe hyperkalaemia
• Monitor QTc (avoid QT-prolonging drugs)
• Maintain Mg²⁺ in dialysate

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COMPLICATION 4: AIR EMBOLISM

Mechanism

Clinical Presentation - Position-Dependent

Immediate Management - Mnemonic: "CLOT-OH"

1. Clamp venous blood line immediately + turn off blood pump
2. Left lateral decubitus (Durant's manoeuvre) + head-down (Trendelenburg)
   • Traps air in right atrium/ventricle apex, away from pulmonary outflow
3. Oxygen: 100% O₂ via non-rebreather mask
   • Replaces nitrogen in bubbles, promotes reabsorption
4. Transoesophageal echocardiography (TEE) - most sensitive diagnostic tool
5. Other measures: Aspiration of air via percutaneous needle into right heart or cardiac catheter (ICU)
6. Hyperbaric oxygen therapy (if available + cerebral embolism confirmed)

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COMPLICATION 5: DIALYSER REACTIONS (FIRST USE SYNDROME)

Classification

• ACE inhibitor + AN69 polyacrylonitrile membrane = dangerous combination → Type A reaction via bradykinin accumulation
• Always use biocompatible membranes (polysulfone, polyethersulfone) in modern practice
• Rinse new dialysers with saline before use (reduces retained sterilant)

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COMPLICATION 6: MUSCLE CRAMPS

Causes

• Hyponatraemia (most common) or low dialysate sodium
• Plasma volume contraction (excessive UF rate)
• Over-removal below dry weight
• Poor vascular refilling (autonomic dysfunction, cardiomyopathy)
• Low magnesium

Immediate Management

1. Reduce or stop ultrafiltration
2. Saline 100 mL IV bolus (or 50 mL 50% dextrose)
3. Hypertonic saline (or hypertonic glucose 50%) if refractory
4. Stretch and massage the affected muscle
5. Apply warm or cold compress
6. Sodium profiling in subsequent sessions (higher early, tapers down)

Prevention

• Reassess dry weight
• Quinine sulfate 200-300 mg nocte (limited evidence; FDA caution for this use)
• Carnitine supplementation (meta-analysis: reduces HD-related cramps)
• Vitamin E 400 IU/day (some benefit)
• Adequate dialysate magnesium

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COMPLICATION 7: HAEMOLYSIS DURING DIALYSIS

Causes - "FOLD"

• Formaldehyde / bleach residual in dialyser (inadequate rinsing)
• Overheated dialysate (>42°C - denatures RBCs)
• Low osmolality dialysate (hypotonic → osmotic RBC lysis)
• Dialysate contaminants: chloramine, copper, nitrates

Recognition

• Dialysis lines appear port-wine red/pink (haemolysed blood looks different from fresh blood)
• Patient: chest pain, dyspnoea, back pain, rapidly falling Hb

Immediate Management

1. STOP dialysis immediately
2. DO NOT return blood (contains free Hb, K⁺, LDH - life-threatening hyperkalaemia)
3. Supplemental O₂
4. Send blood for: FBC, LDH, bilirubin, haptoglobin, K⁺, blood film
5. Treat hyperkalaemia (this is the life-threatening emergency - K⁺ released from lysed cells)
6. Investigate dialysate: send sample for temperature, osmolality, chloramine levels
7. Subsequent dialysis: use fresh dialyser, check water treatment system

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COMPLICATION 8: PYREXIA AND RIGORS (PYROGEN REACTION / BACTERAEMIA)

Two Types

Management of Fever During Dialysis

1. Vital signs + clinical assessment
2. Blood cultures (peripheral + from dialysis access before antibiotics)
3. Antipyretics (paracetamol)
4. If stable and low suspicion of bacteraemia: continue dialysis, monitor closely
5. If haemodynamically unstable / high fever + rigors: stop dialysis; do not return blood; empirical IV vancomycin 15-20 mg/kg (covers MRSA, common cause via CVC)
6. Assess for source: access site (CVC exit site, tunnel, port), foot ulcer, urinary tract
7. If access infection confirmed: consider lock therapy (antibiotic lock for CVCs) or access removal if severe

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COMPLICATION 9: HYPOGLYCAEMIA

Why it happens

• Glucose-free dialysate used in some centres → glucose diffuses out of blood into dialysate during session
• Common in: insulin-dependent diabetics, malnourished patients, those who skip pre-dialysis meal

Management

1. Check blood glucose during session (standard for diabetics)
2. Symptomatic hypoglycaemia: IV 50 mL 50% dextrose (dextrose 50 g)
3. IM/SC glucagon 1 mg if IV access unavailable
4. Adjust insulin dose (hold morning dose or reduce on dialysis days)
5. Use glucose-containing dialysate (1g/L glucose) for at-risk patients

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COMPLICATION 10: CARDIAC TAMPONADE

Why occurs in dialysis patients

• Uraemic pericarditis → haemorrhagic effusion (heparin used in dialysis → bleeding into pericardial space)
• Should be suspected in recurrent intradialytic hypotension without clear cause

Clinical Features

Management

1. Bedside echo (urgent) - confirms effusion + tamponade physiology
2. Heparin-free dialysis (or regional heparin) immediately
3. Pericardiocentesis (echo-guided) - both diagnostic and therapeutic
4. Avoid NSAIDs (increase bleeding risk)
5. Colchicine or prednisolone for recurrent uraemic pericarditis
6. If recurrent: pericardial window (surgical)

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COMPLICATION 11: VASCULAR ACCESS COMPLICATIONS

Summary Table

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COMPLICATION 12: ELECTROLYTE DISTURBANCES

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ICU MANAGEMENT FRAMEWORK FOR DIALYSIS COMPLICATIONS

When to Transfer to ICU

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RAPID-FIRE MRCP/FCPS EXAM POINTS

1. DDS = cerebral oedema - cause: rapid urea removal → osmotic gradient (brain > blood) → water into brain
2. Treatment of DDS = mannitol 0.25-0.5 g/kg IV or hypertonic saline to raise plasma osmolality
3. Prevention of DDS = slow initial sessions (2h, blood flow 150-200 mL/min), target ≤40% BUN reduction per session
4. IDH = most common acute dialysis complication (15-50%)
5. IDH treatment sequence: Trendelenburg → stop UF → normal saline bolus → stop dialysis if persistent
6. Midodrine 5-10 mg pre-dialysis = only oral agent with evidence for IDH prevention
7. Intradialytic hypertension = usually volume overload (not underload) - reassess dry weight
8. Cool dialysate (35-36°C) prevents IDH by inducing vasoconstriction
9. Air embolism: left lateral decubitus + head-down (Durant's manoeuvre) + 100% O₂ + DO NOT return blood
10. Millwheel murmur = churning sound on auscultation = pathognomonic of significant air embolism in heart
11. Type A dialyser reaction = within first 5 minutes; anaphylaxis; do NOT return blood; adrenaline
12. AN69 membrane + ACE inhibitor = Type A reaction (bradykinin accumulation)
13. Haemolysis during dialysis = port-wine coloured blood + back pain + hyperkalaemia → STOP, do NOT return blood
14. Recurrent unexplained IDH → always rule out cardiac tamponade with echo
15. Post-dialysis subdural haematoma can mimic DDS - always perform CT head if neurological signs persist after stopping dialysis
16. Hypoglycaemia in dialysis = glucose-free dialysate + fasted diabetic; treat with IV 50% dextrose
17. Pyrogen reaction = endotoxin in dialysate = fever within 1 hour + rigors; check water cultures
18. Cardiac arrest VT/VF during dialysis = defibrillate; amiodarone; suspect hyperkalaemia or ischaemia

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Summary: Complications and Mnemonic Overview