Chronic Kidney Disease in the ICU

Quick Answer

Chronic Kidney Disease (CKD) in the ICU refers to the management of critically ill patients with pre-existing reduced kidney function (eGFR <60 mL/min/1.73m^2 for ≥3 months). CKD affects 10-15% of the adult population and these patients are 2-3 times more likely to require ICU admission compared to the general population. ESKD patients on maintenance dialysis have ICU mortality rates of 20-40%, significantly higher than non-CKD patients with similar illness severity.

Key Clinical Features:

• Altered pharmacokinetics requiring dose adjustments for renally-cleared drugs
• Baseline electrolyte abnormalities (hyperkalaemia, hyperphosphataemia)
• Cardiovascular disease burden (accelerated atherosclerosis, LVH, pericarditis)
• Anaemia (normochromic normocytic, EPO deficiency)
• CKD-Mineral and Bone Disorder (CKD-MBD)

Emergency Management:

1. Assess dialysis access patency and recent dialysis schedule
2. Correct life-threatening hyperkalaemia (calcium gluconate, insulin-dextrose, RRT)
3. Manage volume status carefully (may be fluid-overloaded or depleted)
4. Adjust all medication doses for CKD stage
5. Coordinate with nephrology for dialysis timing and modality

ICU Mortality: 20-40% in ESKD patients, compared to 15-25% in general ICU population

Must-Know Facts:

• Use CKD-EPI equation for GFR estimation (not Cockcroft-Gault)
• Dialysis patients require vascular access preservation (avoid AV fistula arm for blood draws, lines)
• Contrast-induced AKI risk is markedly increased in CKD G4-5
• Standard APACHE II/III scoring underestimates mortality in ESKD patients

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CICM Exam Focus

What Examiners Expect

Second Part Written (SAQ):

Common SAQ stems:

• "A 58yo male on maintenance haemodialysis is admitted to ICU with septic shock. Outline your approach to antimicrobial dosing and dialysis management."
• "A 72yo female with CKD G4 (eGFR 22) requires emergency surgery. List the preoperative considerations and perioperative management strategies."
• "Discuss the pathophysiology and ICU implications of CKD-Mineral and Bone Disorder."
• "A dialysis patient develops severe hyperkalaemia post-cardiac surgery. Outline your management approach."

Expected depth:

• KDIGO CKD staging and implications for drug dosing
• Distinction between maintenance dialysis patients and non-dialysis CKD
• Cardiovascular complications of CKD (LVH, accelerated atherosclerosis, pericarditis)
• Drug dosing tables for common ICU medications
• Transition from intermittent HD to CRRT when haemodynamically unstable
• Understanding of uraemic toxin accumulation and clearance

Second Part Hot Case:

Typical presentations:

• Day 3 post-CABG in ESKD patient with oliguria and hypotension
• Septic shock in peritoneal dialysis patient with peritonitis
• Hyperkalaemia and acidosis in CKD patient with diarrhoea
• AKI on CKD requiring new dialysis initiation

Examiners assess:

• Systematic A-E examination approach
• Recognition of dialysis access (fistula examination, tunnelled catheter inspection)
• Fluid status assessment (JVP, peripheral oedema, lung auscultation)
• Medication review and dose adjustment capability
• Communication with nephrology team
• Family discussion regarding prognosis and goals of care

Second Part Viva:

Expected discussion areas:

• GFR estimation methods and limitations in critical illness
• Drug dosing adjustments across CKD stages
• Dialysis prescription in haemodynamically unstable patients
• Anaemia management in CKD (EPO, iron, transfusion thresholds)
• Cardiovascular risk stratification in CKD
• Withdrawal of dialysis and end-of-life considerations
• Indigenous health disparities in CKD prevalence and outcomes

Examiner expectations:

• Safe, consultant-level decision-making
• Evidence-based practice (KDIGO guidelines, major trials)
• Ethical considerations around dialysis withdrawal
• Resource stewardship
• Indigenous health awareness

Common Mistakes

• Using Cockcroft-Gault instead of CKD-EPI for GFR estimation
• Failing to adjust drug doses for CKD stage
• Attempting blood draw or cannulation from AV fistula arm
• Overlooking baseline hyperkalaemia when interpreting potassium levels
• Assuming all dialysis patients are anuric (some have residual renal function)
• Underestimating cardiovascular disease burden
• Not considering uraemic bleeding tendency when planning procedures
• Forgetting contrast-induced AKI prevention in non-dialysis CKD patients

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Key Points

Must-Know Facts

1. KDIGO CKD Staging: G1-5 classification based on eGFR (G1 ≥90, G2 60-89, G3a 45-59, G3b 30-44, G4 15-29, G5 <15 mL/min/1.73m^2); albuminuria staging A1-3 provides additional prognostic information.

2. GFR Estimation: CKD-EPI equation is preferred over MDRD and Cockcroft-Gault; all equations are inaccurate in acute illness, obesity, extremes of muscle mass, and non-steady-state creatinine.

3. Drug Dosing: Most renally-cleared drugs require dose reduction in CKD G4-5; notable exceptions include drugs with hepatic metabolism (propofol, fentanyl) and those with large therapeutic windows.

4. Uraemic Toxins: Accumulation of middle molecules (beta-2 microglobulin), protein-bound solutes (p-cresyl sulfate, indoxyl sulfate), and small water-soluble solutes contributes to uraemic syndrome.

5. Cardiovascular Disease: CKD patients have 10-20x higher cardiovascular mortality than age-matched controls; LVH affects 70-80% of ESKD patients; accelerated atherosclerosis with medial calcification is characteristic.

6. Anaemia: Normochromic normocytic anaemia due to EPO deficiency; target Hb 100-115 g/L (not normalisation); iron supplementation essential before ESA therapy.

7. CKD-MBD: Hyperphosphataemia, hypocalcaemia, elevated PTH, vitamin D deficiency lead to renal osteodystrophy, vascular calcification, and increased fracture risk.

8. Dialysis Access Preservation: Never use AV fistula/graft arm for blood draws, cannulation, or blood pressure measurement; tunnelled dialysis catheters should only be accessed by trained personnel.

9. RRT Transition: Haemodynamically unstable maintenance HD patients should transition to CRRT; PD patients may require temporary HD or CRRT during critical illness.

10. Indigenous Health Disparity: Aboriginal and Torres Strait Islander peoples have 5-10x higher rates of ESKD compared to non-Indigenous Australians; often younger at dialysis initiation with higher complication rates.

Memory Aids

CKDMBD - CKD Metabolic Bone Disease Components:

• C: Calcium abnormalities (hypocalcaemia, occasionally hypercalcaemia)
• K: Klotho deficiency (accelerated ageing)
• D: D vitamin deficiency (calcitriol)
• M: Mineral imbalance (phosphorus retention)
• B: Bone disease (osteodystrophy, adynamic bone disease)
• D: Dialysis-related (aluminium toxicity historical, beta-2 microglobulin amyloidosis)

ADJUST - Drug Dosing Mnemonic:

• A: Assess GFR using CKD-EPI
• D: Determine if drug is renally cleared
• J: Judge appropriate interval extension vs dose reduction
• U: Use loading dose if needed (unchanged in CKD)
• S: Supplement dialysed drugs post-dialysis
• T: Therapeutic drug monitoring when available

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Definition and Epidemiology

Definition

Chronic Kidney Disease (CKD) is defined by KDIGO 2012 as abnormalities of kidney structure or function present for >3 months with implications for health. The diagnosis requires either:

1. Markers of kidney damage (one or more):

   • Albuminuria (ACR ≥30 mg/g or ≥3 mg/mmol)
   • Urine sediment abnormalities
   • Electrolyte abnormalities due to tubular disorders
   • Abnormalities detected by histology
   • Structural abnormalities on imaging
   • History of kidney transplantation

2. Reduced GFR: eGFR <60 mL/min/1.73m^2

CKD Staging (KDIGO 2012):

Albuminuria Categories:

End-Stage Kidney Disease (ESKD): CKD G5 requiring renal replacement therapy (haemodialysis, peritoneal dialysis, or kidney transplantation) for survival. In Australia, patients are classified as ESKD when they commence RRT or have eGFR <15 with symptoms requiring dialysis initiation.

Epidemiology

International Data:

• Global CKD prevalence: 8-16% of adult population (approximately 850 million people worldwide)
• CKD G3-5 prevalence: 10-13% in developed countries
• ESKD on RRT: 2.0-3.0 million globally, growing at 6-7% annually
• ICU admission rate in CKD patients: 2-3x higher than general population
• CKD patients represent 10-15% of all ICU admissions

Australian/New Zealand Data (ANZDATA Registry 2023):

• Prevalent dialysis population: Approximately 14,000 patients in Australia
• Incident ESKD: 3,200 new patients commencing RRT annually in Australia
• Haemodialysis: 65-70% of dialysis patients
• Peritoneal dialysis: 15-20% of dialysis patients
• Kidney transplantation: 50% of prevalent ESKD population with functioning graft
• Median age at RRT commencement: 63 years (Australia), 57 years (New Zealand)
• Leading causes: Diabetic nephropathy (40%), glomerulonephritis (15%), hypertensive nephropathy (12%)

Risk Factors for ICU Admission in CKD:

• Non-modifiable: Age >65 years, male sex, longer dialysis vintage
• Modifiable: Diabetes mellitus, cardiovascular disease, inadequate dialysis, malnutrition, infections (vascular access-related)
• Dialysis-specific: Haemodialysis (higher ICU admission than PD), catheter access (vs fistula), missed dialysis sessions

High-Risk Populations:

• Aboriginal and Torres Strait Islander peoples: 5-10x higher ESKD rates, younger age at onset (median 48 years), diabetes and glomerulonephritis as leading causes
• Māori: 3-4x higher ESKD rates than non-Māori New Zealanders
• Pacific Islander populations: 4-5x higher rates
• Remote/rural populations: Significant access challenges for regular dialysis

Outcomes:

• ICU mortality CKD G3-4: 15-25%
• ICU mortality ESKD on dialysis: 20-40%
• Hospital mortality ESKD: 25-50%
• 1-year mortality after ICU admission in ESKD: 50-60%
• 5-year survival on dialysis: 35-50%
• Post-ICU RRT dependence in AKI on CKD: 30-50% require chronic dialysis

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Applied Basic Sciences

This section bridges First Part basic sciences with Second Part clinical practice

Renal Physiology and GFR Estimation

Normal Kidney Function:

• Glomerular filtration rate (GFR): 90-120 mL/min/1.73m^2 in healthy adults
• Declines approximately 1 mL/min/year after age 40
• Nephron endowment varies (600,000 to 1.2 million per kidney)

GFR Estimation Equations:

CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration) 2021:

• Current gold standard for GFR estimation
• Uses serum creatinine, age, and sex
• Race coefficient removed in 2021 update
• More accurate than MDRD at higher GFR values (>60 mL/min/1.73m^2)
• Formula: GFR = 142 × min(Scr/κ, 1)^α × max(Scr/κ, 1)^-1.200 × 0.9938^Age × 1.012 [if female]
  • κ = 0.7 (female), 0.9 (male); α = -0.241 (female), -0.302 (male)

MDRD (Modification of Diet in Renal Disease):

• Older equation, still widely used
• Underestimates GFR at higher values
• Less accurate in elderly, obese, and non-Caucasian populations

Cockcroft-Gault:

• Estimates creatinine clearance (not GFR)
• Historically used for drug dosing
• Requires actual body weight (problematic in obesity, oedema)
• Formula: CrCl = [(140-age) × weight × (0.85 if female)] / (72 × Scr)

Limitations of GFR Estimation in ICU:

• Non-steady-state creatinine (AKI, recovering AKI, acute on chronic)
• Altered creatinine generation (muscle wasting, decreased hepatic production)
• Dilutional effects from fluid resuscitation
• Drug interference with creatinine assays (trimethoprim, cimetidine)
• Extremes of body habitus (sarcopenia, morbid obesity)

Measured GFR: 24-hour creatinine clearance or nuclear medicine studies (Cr-51 EDTA, Tc-99m DTPA) provide more accurate GFR but impractical in critical illness.

Uraemic Toxin Accumulation

Classification of Uraemic Toxins (European Uremic Toxin Work Group):

Clinically Significant Uraemic Toxins:

Urea (MW 60 Da):

• Surrogate marker for small water-soluble toxins
• BUN >35 mmol/L associated with uraemic symptoms
• Contributes to nausea, anorexia, cognitive impairment
• Carbamylation of proteins leads to structural modifications

Indoxyl Sulfate and p-Cresyl Sulfate:

• Protein-bound uraemic toxins (>90% albumin-bound)
• Generated from gut bacterial metabolism of tryptophan and tyrosine
• Cause endothelial dysfunction, cardiovascular toxicity
• Associated with CKD progression, mortality
• Poorly cleared by dialysis due to protein binding

Beta-2 Microglobulin (MW 11,800 Da):

• Middle molecule; component of MHC Class I
• Accumulates in ESKD (concentrations 20-60x normal)
• Causes dialysis-related amyloidosis (carpal tunnel, arthropathy, bone cysts)
• Better cleared by high-flux dialysis, haemodiafiltration

Fibroblast Growth Factor-23 (FGF-23) (MW 22,000 Da):

• Phosphaturic hormone elevated very early in CKD
• Suppresses calcitriol production
• Associated with LVH, cardiovascular mortality
• Levels correlate with CKD progression and mortality

CKD-Mineral and Bone Disorder (CKD-MBD)

Pathophysiology:

Early CKD (G2-3):

1. Phosphorus retention begins (even with normal serum levels)
2. FGF-23 increases (phosphaturic, suppresses 1-alpha-hydroxylase)
3. Calcitriol (1,25-dihydroxyvitamin D) decreases
4. PTH begins to rise

Progressive CKD (G4-5):

1. Overt hyperphosphataemia
2. Hypocalcaemia (reduced intestinal absorption, calcitriol deficiency)
3. Secondary hyperparathyroidism (PTH 2-10x normal)
4. Klotho deficiency (FGF-23 co-receptor)
5. Vascular and soft tissue calcification

Bone Disease Subtypes:

• High-turnover disease: Osteitis fibrosa (excess PTH), increased bone resorption
• Low-turnover disease: Adynamic bone disease (over-suppressed PTH), increased fracture risk
• Osteomalacia: Vitamin D deficiency, historical aluminium toxicity
• Mixed uraemic osteodystrophy: Combined features

ICU Implications:

• Hypocalcaemia: Symptomatic with tetany, seizures, QT prolongation
• Hypercalcaemia: From tertiary hyperparathyroidism or calcimimetics
• Hyperphosphataemia: Contributes to vascular calcification, arrhythmias
• Fracture risk: Increased vertebral and hip fractures in CKD
• Metastatic calcification: Cardiac valves, vasculature, soft tissues

Anaemia of CKD

Pathophysiology:

Erythropoietin (EPO) Deficiency (Primary cause):

• Peritubular fibroblasts in renal cortex produce EPO
• Progressive loss of EPO-producing cells with nephron loss
• Relative deficiency: EPO levels inappropriately low for degree of anaemia
• EPO production begins to decline at eGFR <60 mL/min/1.73m^2
• Severe deficiency in CKD G5 (EPO levels 10-20% of normal)

Iron Deficiency:

• Absolute: Blood loss (dialysis, GI losses), inadequate intake
• Functional: Iron sequestration despite adequate stores (hepcidin excess)
• Hepcidin upregulated by inflammation, prevents iron release from stores

Other Contributing Factors:

• Reduced RBC lifespan (uraemic toxins, 60-80 days vs normal 120 days)
• Chronic inflammation (anaemia of chronic disease)
• Blood loss (dialysis circuit, occult GI bleeding)
• Vitamin deficiencies (B12, folate)
• Aluminium toxicity (historical)
• Bone marrow suppression by uraemic toxins

Target Haemoglobin (KDIGO 2012):

• Avoid Hb >130 g/L (increased cardiovascular events, mortality)
• Individualised targets 100-115 g/L for most patients
• Consider transfusion threshold 70-80 g/L in stable patients
• CREATE Trial (PMID: 17108343) and TREAT Trial (PMID: 19880844): Normalisation of Hb with ESAs associated with increased stroke, thrombotic events

Cardiovascular Disease in CKD

Accelerated Atherosclerosis:

• Traditional risk factors (diabetes, hypertension, dyslipidaemia) highly prevalent
• Non-traditional risk factors (uraemic toxins, oxidative stress, inflammation, hyperphosphataemia)
• Medial arterial calcification (Mönckeberg's sclerosis) characteristic of CKD
• Arterial stiffness and increased pulse wave velocity
• CAD prevalence: 40-50% in ESKD patients

Left Ventricular Hypertrophy (LVH):

• Present in 70-80% of ESKD patients at dialysis initiation
• Concentric (pressure overload: hypertension) and eccentric (volume overload)
• Contributes to diastolic dysfunction, arrhythmias, sudden death
• Regression possible with BP control, anaemia correction, adequate dialysis

Uraemic Pericarditis:

• Occurs with severe uraemia (BUN >35-45 mmol/L)
• Haemorrhagic pericardial fluid (uraemic platelet dysfunction)
• Risk of tamponade higher than non-uraemic pericarditis
• Treatment: Intensive dialysis (daily HD for 1-2 weeks)
• Pericardiocentesis if tamponade; surgical drainage if recurrent

Sudden Cardiac Death:

• Leading cause of death in dialysis patients (25-30%)
• Electrolyte shifts during dialysis (potassium, calcium)
• QT prolongation, ventricular arrhythmias
• Highest risk in first 6-12 hours after dialysis session

Pharmacology in CKD

Pharmacokinetic Alterations:

Protein Binding Changes:

• Hypoalbuminaemia: Increased free fraction of acidic drugs (phenytoin, valproate)
• Uraemic toxins compete for binding sites
• Altered drug distribution (free fraction crosses membranes)

Key ICU Drug Dosing Principles:

1. Loading dose: Generally unchanged (determines initial concentration)
2. Maintenance dose: Reduce dose and/or extend interval
3. Supplemental dosing: Required after dialysis for significantly dialysed drugs
4. TDM: Essential for drugs with narrow therapeutic index (vancomycin, aminoglycosides)

Drug Removal by Dialysis:

• Factors favouring removal: Low MW (<500 Da), low protein binding (<80%), low Vd (<1 L/kg), water solubility
• CRRT removes drugs more slowly but continuously
• High-flux HD and haemodiafiltration remove larger molecules

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Clinical Presentation

ICU Admission Scenarios

Typical Presentations:

Scenario 1: Septic Shock in Maintenance Haemodialysis Patient

• History: 65yo male, ESKD from diabetic nephropathy, HD via tunnelled catheter, missed 2 dialysis sessions
• Presentation: Fever, hypotension, confusion, catheter erythema
• Examination: Febrile 38.8°C, HR 120, BP 80/50, lactate 5.2, oliguria (baseline anuric)
• Key issues: Line sepsis, volume overload, hyperkalaemia, drug dosing

Scenario 2: Post-Cardiac Surgery AKI on CKD

• History: 72yo female, CKD G4 (eGFR 22), post-CABG x3
• Presentation: Day 2 post-op with oliguria, rising creatinine, pulmonary oedema
• Examination: JVP elevated, bilateral crackles, trace pedal oedema, poor urine output despite furosemide
• Key issues: Distinguish AKI from CKD progression, RRT timing, volume management

Scenario 3: Peritoneal Dialysis Patient with Peritonitis

• History: 58yo male, ESKD, CAPD for 3 years, cloudy PD effluent
• Presentation: Abdominal pain, fever, nausea, cloudy dialysate
• Examination: Diffuse abdominal tenderness, no peritonism, PD catheter exit site clean
• Key issues: Empiric antibiotic selection (IP vs IV), need for catheter removal, temporary HD

Scenario 4: Hyperkalaemia with Cardiac Toxicity

• History: 45yo male, CKD G5 (eGFR 8, pre-dialysis), missed nephrology follow-up
• Presentation: Weakness, palpitations, peaked T waves on ECG
• Examination: Bradycardia, hypotension, K+ 8.2 mmol/L, widened QRS
• Key issues: Immediate cardioprotection, temporising measures, urgent RRT

Symptoms and Signs

History:

• Chief complaint: Often non-specific (fatigue, nausea, confusion)
• Dialysis history: Modality, schedule, recent sessions, vascular access
• Medications: EPO, phosphate binders, antihypertensives
• Recent illness: Infection, bleeding, dietary indiscretion

Examination:

General:

• Appearance: Sallow complexion, uraemic fetor, asterixis
• Vital signs: Hypertension common; hypotension suggests sepsis/volume depletion

A - Airway:

• Usually patent
• Uraemic odour (ammoniacal breath)

B - Breathing:

• Respiratory rate: May be elevated (metabolic acidosis compensation, pulmonary oedema)
• Kussmaul breathing in severe metabolic acidosis
• Auscultation: Crackles suggest fluid overload; pleural effusion common

C - Circulation:

• Heart rate: Variable; bradycardia with hyperkalaemia
• Blood pressure: Usually hypertensive; hypotension concerning for sepsis
• JVP: Elevated in volume overload; low in true volume depletion
• Heart sounds: Pericardial rub (uraemic pericarditis); murmurs (valvular calcification)
• Dialysis access examination:
  • "AVF: Thrill (continuous), bruit, warmth, aneurysmal dilation"
  • "AVG: Palpable conduit, thrill, bruit"
  • "Tunnelled catheter: Exit site erythema, discharge, tunnel tenderness"

D - Disability/Neurology:

• GCS: May be reduced with uraemic encephalopathy
• Asterixis: Metabolic flap (hepatic, uraemic, CO2 narcosis)
• Peripheral neuropathy: Stocking-glove sensory loss, weakness

E - Exposure/Everything Else:

• Temperature: Fever suggests infection; hypothermia in severe sepsis/uraemia
• Skin: Excoriations (pruritus), calciphylaxis (painful necrotic skin lesions)
• Oedema: Peripheral, sacral, pulmonary
• PD catheter: Exit site appearance, tunnel assessment

Severity Scoring

KDIGO CKD Stage (baseline):

• Important for prognosis and drug dosing
• Does not indicate acute illness severity

APACHE II/III Limitations in ESKD:

• Chronic physiological derangements (elevated creatinine, low serum albumin) contribute to score
• APACHE II underestimates mortality in ESKD by 10-15%
• Disease-specific mortality higher than APACHE-predicted

SOFA Score:

• Renal component based on creatinine or UOP
• Chronic dialysis patients score maximally on renal component regardless of acute status
• Serial SOFA more useful for trajectory assessment

Differential Diagnosis

Key Differentials for Acute Deterioration in CKD Patient:

1. AKI on CKD: Acute decline superimposed on chronic disease; distinguish from expected trajectory

   • Causes: Sepsis, nephrotoxins, hypovolaemia, obstruction
   • May require acute RRT initiation or intensification

2. Uraemic Crisis: Severe symptomatic uraemia

   • BUN >35-45 mmol/L with encephalopathy, pericarditis, bleeding
   • Emergency indication for RRT

3. Dialysis Adequacy Issue: Inadequate solute clearance

   • Missed sessions, access dysfunction, underdialysis
   • Check Kt/V, urea reduction ratio

4. Volume Overload vs Depletion: Often difficult to assess

   • CKD patients may be total body fluid overloaded but intravascularly depleted
   • Post-dialysis hypotension common

5. Electrolyte Emergency: Hyperkalaemia, severe acidosis, hypocalcaemia

   • Life-threatening; requires immediate intervention

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Investigations

Laboratory Investigations

Bedside Tests:

Arterial Blood Gas:

• Typical findings: Metabolic acidosis (non-anion gap or mixed)
• pH: Often 7.25-7.35 (chronic compensation)
• HCO3: Typically 18-22 mmol/L in stable CKD G4-5
• PaCO2: Compensatory respiratory alkalosis
• Lactate: Elevated suggests sepsis, hypoperfusion, or metformin accumulation
• Ionised calcium: May be low despite normal total calcium

Blood Tests:

Full Blood Count:

• Hb: Typically 90-110 g/L (anaemia of CKD)
• WCC: Elevated with infection; may be blunted in uraemia
• Platelets: Usually normal; function impaired (uraemic platelet dysfunction)

Urea, Electrolytes, Creatinine:

• Urea: Elevated (>25 mmol/L in ESKD); >35 mmol/L suggests inadequate dialysis
• Creatinine: Baseline elevated; acute rise suggests AKI on CKD
• eGFR: For baseline staging (inaccurate in non-steady state)
• Sodium: Variable; pseudo-hyponatraemia if severe hyperglycaemia
• Potassium: Typically 5.0-6.0 mmol/L; >6.5 mmol/L dangerous
• Bicarbonate: Low (metabolic acidosis)
• Phosphorus: Typically 1.5-2.5 mmol/L (elevated)
• Calcium (corrected): Variable; adjust for albumin
• Magnesium: Often elevated in CKD

Liver Function Tests:

• Albumin: Often low (inflammation, malnutrition, proteinuria)
• Bilirubin: Usually normal unless concomitant liver disease
• Transaminases: May be elevated with hepatorenal involvement

Coagulation:

• INR, APTT: Usually normal
• Platelet function: Impaired (prolonged bleeding time)
• Fibrinogen: May be elevated (acute phase reactant)

Cardiac Biomarkers:

• Troponin: Baseline elevation in ESKD (troponin T > troponin I)
• Interpret with trend rather than absolute value
• BNP/NT-proBNP: Chronically elevated in ESKD (cleared by kidney); interpret cautiously

Inflammatory Markers:

• CRP: Useful for infection/inflammation; chronically elevated in CKD
• Procalcitonin: Accumulates in CKD; cut-offs need adjustment (use >1.0-1.5 ng/mL)

Specific CKD Tests:

• PTH: Typically 2-9x upper limit of normal in ESKD
• Vitamin D: 25-OH-D (storage form) and 1,25-OH2-D (active) often low
• Iron studies: Ferritin, transferrin saturation (TSAT)
  • "Target: Ferritin >200 ng/mL, TSAT >20%"

Dialysis Adequacy Assessment

Haemodialysis:

• Kt/V: Target ≥1.2 per session (urea kinetic modelling)
• Urea Reduction Ratio (URR): Target ≥65%
• Formula: URR = (Pre-dialysis urea - Post-dialysis urea) / Pre-dialysis urea × 100
• Access flow: Fistula/graft patency assessment

Peritoneal Dialysis:

• Weekly Kt/V urea: Target ≥1.7
• Creatinine clearance: Target ≥50 L/week/1.73m^2
• PD effluent: Cell count and differential if peritonitis suspected
  • WBC >100/mm^3 with >50% polymorphonuclear cells = peritonitis

Imaging

Chest X-Ray:

• Cardiomegaly (LVH, pericardial effusion)
• Pulmonary oedema (perihilar distribution, Kerley B lines)
• Pleural effusions (often bilateral)
• Vascular calcification (visible in large vessels)

Echocardiography:

• LV hypertrophy (concentric or eccentric)
• Diastolic dysfunction (Grade I-III)
• Valvular calcification and dysfunction
• Pericardial effusion (uraemic pericarditis)
• Assess fluid status (IVC collapsibility, E/e' ratio)

Renal Ultrasound:

• Small kidneys (<9 cm) suggest chronic disease
• Large kidneys: Diabetes, polycystic kidney disease, amyloid, obstruction
• Cortical thickness: Reduced in CKD
• Hydronephrosis: Exclude obstruction

Vascular Access Imaging:

• Duplex ultrasound for fistula/graft assessment
• Venogram if central stenosis suspected
• Fistulogram for access salvage planning

Physiological Monitoring

Non-Invasive Monitoring:

• Continuous ECG: Monitor for hyperkalaemia (peaked T waves, widened QRS), arrhythmias
• SpO2: Target 92-96%
• NIBP: Avoid fistula arm
• Temperature: Continuous in sepsis
• Fluid balance: Strict I/O charting; daily weights

Invasive Monitoring:

• Arterial line: Radial artery in non-fistula arm preferred
• Central venous catheter: Consider femoral if upper body access limited by fistula/catheter
• CVP interpretation: Altered by chronic volume state, LVH, diastolic dysfunction

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ICU Management

This is the core clinical section - most detailed

Initial Assessment (First Hour)

A - Airway:

• Assessment: Usually patent unless uraemic encephalopathy
• Intervention: Intubation if GCS <8 or severe pulmonary oedema
• RSI considerations: Succinylcholine relatively contraindicated if K+ >5.5 mmol/L
• Alternative: Rocuronium (dose unchanged in CKD; sugammadex safe)

B - Breathing:

• Oxygen therapy: Target SpO2 92-96%
• Ventilatory support:
  • "NIV: First-line for pulmonary oedema (if no contraindications)"
  • "Invasive ventilation: If failing NIV, severe acidosis, encephalopathy"
• Lung-protective ventilation if intubated

C - Circulation:

Fluid Resuscitation:

• Assess volume status carefully (clinical examination + echocardiography)
• ESKD patients often total body fluid overloaded but intravascularly depleted
• Initial bolus: 250-500 mL crystalloid if hypotensive with evidence of hypovolaemia
• Reassess after each bolus (clinical and echocardiographic)
• Avoid excessive fluid in anuric patients

Vasopressors/Inotropes:

• First-line: Noradrenaline (weight-based dosing unchanged in CKD)
• Second-line: Vasopressin (renally cleared but safe at standard doses)
• Inotropes: Dobutamine, adrenaline if cardiogenic component
• Targets: MAP ≥65 mmHg (may need higher in chronic hypertensive patients)

Hyperkalaemia Management (if K+ >6.0 mmol/L or ECG changes):

1. Cardiac membrane stabilisation: Calcium gluconate 10% 10 mL IV over 2-3 min (repeat if ECG unchanged)
2. Intracellular shift:
   • Insulin 10 units + 50 mL 50% dextrose IV
   • Salbutamol 10-20 mg nebulised
   • Sodium bicarbonate 8.4% 50 mmol (if acidotic)
3. Potassium removal: Urgent RRT (definitive in ESKD)
4. Avoid: Succinylcholine, potassium-containing fluids

D - Disability:

• GCS monitoring: Uraemic encephalopathy responsive to dialysis
• Sedation: Reduced doses for renally-cleared agents
• Analgesia: Morphine accumulates (use fentanyl or hydromorphone); paracetamol safe
• Glucose control: Target 6-10 mmol/L; insulin half-life prolonged in CKD

E - Everything Else:

• Temperature management: Target normothermia
• Source control: Remove infected dialysis catheters if line sepsis suspected
• Dialysis access assessment: Examine fistula/graft/catheter

Dialysis Considerations

Maintenance Haemodialysis Patients:

Vascular Access Preservation:

• NEVER use AV fistula/graft arm for:
  • Blood draws (damages endothelium, promotes thrombosis)
  • IV cannulation (vein sacrifice)
  • Blood pressure measurement (cuff damages fistula)
  • Central line insertion (subclavian stenosis affects arm access)
• Tunnelled dialysis catheter:
  • Access only by trained dialysis/ICU nursing staff
  • Lock with heparin or citrate when not in use
  • Do not use for non-dialysis purposes (unless emergency and no other access)

Dialysis Schedule:

• Continue regular dialysis schedule if haemodynamically stable
• Liaise with renal unit for timing and access transport
• If hospitalised: Coordinate with in-patient dialysis team
• Document: Last dialysis date, usual schedule, access type

Haemodynamic Instability - Transition to CRRT:

• Indication: Hypotension (requiring vasopressors), septic shock, cardiogenic shock
• CRRT provides:
  • Gradual solute clearance (less osmotic shifts)
  • Continuous fluid removal (less haemodynamic instability)
  • Temperature control
• Modality: CVVHDF (most common) or CVVH
• Prescription: 20-25 mL/kg/h effluent dose
• Anticoagulation: Regional citrate preferred (PMID: 19114892)

Peritoneal Dialysis Patients:

Continue PD if Possible:

• Advantages: Maintains peritoneal function, no vascular access needed, less haemodynamic instability
• If stable: Continue automated PD (APD) or continuous ambulatory PD (CAPD)
• Dose may need increase in critical illness

Suspend PD and Convert to HD/CRRT if:

• Peritonitis (relative contraindication to continue PD)
• Severe volume overload requiring rapid ultrafiltration
• Abdominal surgery (ileus, peritoneal contamination)
• Respiratory failure (abdominal distension impairs ventilation)
• Haemodynamic instability requiring precise fluid control

PD Peritonitis Management:

• Diagnosis: Cloudy effluent + WBC >100/mm^3 (>50% PMNs) ± abdominal pain
• Empiric antibiotics: IP vancomycin + gentamicin (or ceftazidime)
• Most common organisms: Coagulase-negative staphylococci, S. aureus, gram-negative bacilli
• Catheter removal indications: Fungal peritonitis, refractory bacterial peritonitis (>5 days), tunnel infection
• ISPD Guidelines 2022 (PMID: 35264029)

Glucose Absorption from PD:

• PD dialysate contains dextrose (1.5%, 2.5%, or 4.25%)
• Significant glucose absorption: 100-200 g/day
• Causes: Hyperglycaemia, weight gain, hypertriglyceridaemia
• Management: Adjust insulin doses; use icodextrin for long dwells

Drug Dosing in CKD

Comprehensive Drug Dosing Table for ICU Medications:

Antimicrobials

Sedatives and Analgesics

Cardiovascular Drugs

Anticoagulants

Neuromuscular Blockers

Electrolyte Management

Baseline Abnormalities in CKD:

• Potassium: Chronically 5.0-6.0 mmol/L (tolerated)
• Bicarbonate: 18-22 mmol/L (chronic metabolic acidosis)
• Phosphorus: 1.5-2.5 mmol/L (hyperphosphataemia)
• Calcium: Often low-normal (after albumin correction)
• Magnesium: Often elevated (reduced excretion)

Hyperkalaemia Management:

• Acute rise >1 mmol/L or >6.5 mmol/L: Treat urgently
• Chronic K+ 5.5-6.0: Tolerated; dietary counselling
• Definitive treatment in ESKD: Dialysis

Metabolic Acidosis:

• Chronic: Well-compensated, pH 7.32-7.38
• Acute deterioration: Consider sepsis, lactic acidosis, AKI on CKD
• Bicarbonate therapy: Reserved for pH <7.1 or severe hyperkalaemia
• Dialysis: Corrects acidosis with bicarbonate-based dialysate

Phosphorus Management:

• Hyperphosphataemia contributes to vascular calcification, pruritus
• Acute management: Dietary restriction, phosphate binders with meals
• Dialysis: Removes phosphorus (HD more effective than PD)

Surgical and Procedural Considerations

Preoperative Assessment:

• Volume status optimisation (dialysis timing: 12-24h pre-op for HD patients)
• Potassium: Target <5.5 mmol/L
• Bleeding risk: Consider DDAVP 0.3 mcg/kg if uraemic bleeding anticipated
• Transfusion: Hb target 80-100 g/L pre-operatively

Contrast-Induced AKI Prevention (Non-dialysis CKD G3-5):

• High risk: eGFR <30, diabetes, heart failure, multiple myeloma
• Prevention:
  • IV saline 1 mL/kg/h for 6-12h pre- and post-procedure
  • Minimise contrast volume (<100 mL or <3 mL/kg)
  • Use iso-osmolar or low-osmolar contrast
  • Hold metformin (risk of lactic acidosis if AKI develops)
  • Avoid concurrent nephrotoxins
• N-acetylcysteine: No proven benefit (PRESERVE trial, PMID: 29192710)

Dialysis Patients and Contrast:

• CIN risk is less relevant (already on dialysis)
• Consider prophylactic dialysis session post-contrast if large volume
• No routine post-contrast dialysis required

AKI on CKD - Surgical Considerations:

• Higher risk of further renal deterioration
• May precipitate dialysis requirement in CKD G4-5
• Involve nephrology early for pre-operative optimisation
• Consider surgery timing around dialysis schedule

Anaemia Management

Transfusion Thresholds:

• Stable CKD/ESKD: Hb <70 g/L (restrictive strategy)
• Acute bleeding, symptomatic anaemia, cardiac ischaemia: Hb <80-90 g/L
• Risks of transfusion in CKD:
  • Allosensitisation (reduces transplant options)
  • Volume overload
  • Hyperkalaemia (stored blood K+ 20-30 mmol/L)
  • Iron overload with repeated transfusions

Erythropoiesis-Stimulating Agents (ESAs):

• Not routinely started in ICU
• Continue outpatient ESA at reduced dose if already prescribed
• Withhold if hypertension uncontrolled, active bleeding, malignancy
• Resume when stable

Iron Supplementation:

• Check iron studies before ESA initiation
• IV iron preferred in ICU (poor GI absorption, inflammation)
• Target: Ferritin >200 ng/mL, TSAT >20%

Australian-Specific Protocols

ANZDATA Registry:

• National registry of ESKD patients in Australia and New Zealand
• Tracks outcomes, modality distribution, complications
• 2023 Report: Dialysis mortality 15-20% annually; improving over time

Indigenous Health Considerations:

Aboriginal and Torres Strait Islander Peoples:

• 5-10x higher rates of ESKD compared to non-Indigenous Australians
• Younger age at dialysis initiation (median 48 years vs 63 years)
• Higher rates of diabetic nephropathy
• Significant geographic barriers to dialysis access in remote communities
• Cultural factors affecting dialysis modality choice and adherence

Specific Considerations:

• Involve Aboriginal Hospital Liaison Officer (AHLO) early
• Family-centred decision-making (extended family involvement)
• Consider patient's connection to Country (dialysis location preferences)
• Remote dialysis access: Purple House (Central Australia), satellite units
• Telehealth for nephrology follow-up in remote areas
• Cultural considerations for end-of-life discussions

Māori (New Zealand):

• 3-4x higher ESKD rates than non-Māori
• Whānau (extended family) involvement in care decisions
• Tikanga (cultural protocols) considerations
• Māori Health Workers as cultural liaison

Remote Dialysis Access Challenges:

• Limited satellite dialysis units in remote Australia
• Patients often relocate for dialysis (away from Country)
• Peritoneal dialysis may be preferred for remote living
• RFDS (Royal Flying Doctor Service) transport for emergencies

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Monitoring and Complications

ICU-Specific Monitoring

Daily Parameters:

• Vital signs: Continuous (note BP target may be higher if chronic hypertension)
• Fluid balance: Strict I/O charting; daily weights
• Laboratory: Daily UEC, FBC; ABG as indicated
• Dialysis adequacy: Pre/post urea if on HD; Kt/V weekly

Trend Monitoring:

• Potassium trajectory: Assess accumulation rate
• Acidosis: Monitor for improvement with dialysis
• Lactate clearance: Serial measurements in sepsis
• Inflammatory markers: CRP trend

Access Monitoring:

• Fistula/graft: Daily assessment for thrill, bruit, signs of thrombosis
• Tunnelled catheter: Exit site inspection, flow rates, lock integrity
• Temporary vascath: Insertion site, position confirmation

Complications

Cardiovascular Complications:

Intradialytic Hypotension:

• Incidence: 20-30% of HD sessions
• Causes: Excessive ultrafiltration, autonomic dysfunction, acetate dialysate, eating during dialysis
• Prevention: Sodium modelling, cool dialysate, midodrine pre-HD
• Management: Fluid bolus, reduce UFR, shorten session, consider CRRT in ICU

Arrhythmias:

• Electrolyte shifts (K+, Ca2+) during and after dialysis
• Highest risk 6-12 hours post-HD (intracellular K+ redistribution)
• AF common (volume shifts, structural heart disease)
• VT/VF: Leading cause of sudden death in ESKD

Pericarditis/Pericardial Effusion:

• Uraemic pericarditis: Haemorrhagic (uraemic platelet dysfunction)
• May progress to tamponade
• Treatment: Intensive daily dialysis (not NSAIDs - contraindicated in CKD)
• Pericardiocentesis if tamponade; surgical drainage if recurrent

Infectious Complications:

Vascular Access Infection:

• Catheter-related bloodstream infection (CRBSI): 2-5 per 1,000 catheter-days
• Organisms: S. aureus (30-40%), coagulase-negative staphylococci (30%), gram-negatives (15%)
• Management: Blood cultures, empiric vancomycin + gram-negative cover, consider catheter removal
• Fistula/graft infection: Less common but may require surgical drainage

PD Peritonitis:

• Most common cause of technique failure
• Organisms: Gram-positive (60%), gram-negative (20%), culture-negative (15%), fungal (5%)
• Fungal peritonitis: Catheter removal mandatory

Bleeding Complications:

Uraemic Platelet Dysfunction:

• Prolonged bleeding time despite normal platelet count
• Mechanism: Impaired platelet adhesion (von Willebrand factor dysfunction)
• Risk: GI bleeding, access site bleeding, post-procedural bleeding
• Treatment:
  • DDAVP 0.3 mcg/kg IV (tachyphylaxis with repeated doses)
  • Cryoprecipitate (contains vWF)
  • Conjugated oestrogens (0.6 mg/kg/day × 5 days - prolonged effect)
  • Adequate dialysis

Metabolic Complications:

Hyperkalaemia:

• Most common life-threatening complication
• Accumulation rate: 0.5-1 mmol/L/day in anuric patients
• Prevention: Low-K+ diet, avoid K+-sparing drugs, timely dialysis
• Emergency: Calcium, insulin-dextrose, salbutamol, urgent RRT

Severe Acidosis:

• pH <7.2 may impair cardiovascular function
• Bicarbonate therapy: Controversial; consider if pH <7.1
• Dialysis: Corrects acidosis with bicarbonate-based dialysate

Hypoglycaemia:

• Reduced insulin clearance prolongs half-life
• Reduced gluconeogenesis (renal source of gluconeogenesis)
• Higher risk in dialysis patients on insulin
• Glucose monitoring: More frequent in CKD

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Prognosis and Outcome Measures

Mortality

Short-Term Outcomes:

• ICU mortality in CKD G3-4: 15-25%
• ICU mortality in ESKD on dialysis: 20-40%
• Hospital mortality in ESKD: 25-50%
• 28-day mortality post-ICU in ESKD: 30-45%

Long-Term Outcomes:

• 90-day mortality post-ICU in ESKD: 40-55%
• 1-year mortality post-ICU in ESKD: 50-65%
• 5-year survival on dialysis: 35-50%

Factors Affecting Mortality:

• Age: Strongest predictor
• Dialysis vintage: Longer duration associated with higher mortality
• Comorbidities: Diabetes, CVD, peripheral vascular disease
• Dialysis modality: HD vs PD similar; in-centre HD may be higher risk
• Access type: Catheter-dependent patients have higher mortality
• Acute illness severity: APACHE, SOFA scores

Morbidity

Functional Recovery:

• Return to baseline function: 40-60% of ICU survivors
• Prolonged rehabilitation common
• ICU-acquired weakness: Higher rates in CKD (protein catabolism, uraemia)

Dialysis Dependence:

• AKI on CKD: 30-50% become permanently dialysis-dependent
• Loss of residual renal function: Common after ICU admission

Quality of Life:

• Significantly impaired in dialysis patients
• Post-ICU: Further deterioration in physical and psychological domains
• PICS (Post-Intensive Care Syndrome): Common but understudied in CKD

Prognostic Scores

APACHE II/III Limitations:

• Chronic elevated creatinine contributes to score
• Underestimates mortality in ESKD by 10-20%
• Calibration poor for dialysis population

Surprise Question:

• "Would you be surprised if this patient died in the next 12 months?"
• Useful for identifying patients who may benefit from palliative care discussion

Withdrawal of Dialysis

Epidemiology:

• Withdrawal of dialysis accounts for 15-25% of ESKD deaths in Australia/NZ
• Increasing as population ages and comorbidity burden increases
• ANZDATA 2023: Second most common cause of death after cardiovascular disease

Indications for Discussion:

• Poor functional status (bedbound, severe dementia)
• High symptom burden despite optimal dialysis
• Progressive comorbidities (malignancy, severe heart failure)
• Patient request
• Family consensus after prolonged ICU admission without recovery

Process:

1. Multidisciplinary team meeting: ICU, nephrology, palliative care, nursing
2. Family meeting: Explain prognosis, explore goals of care, cultural considerations
3. Palliative care involvement: Symptom management, family support
4. Documentation: Advance care directive, medical treatment decision form
5. Location of death: ICU, ward, home, hospice (patient/family preference)

Time to Death After Dialysis Withdrawal:

• Median: 7-10 days (range 1-30+ days)
• Depends on residual renal function, fluid status
• Symptom management: Uraemia → drowsiness (often comfortable)

Indigenous Cultural Considerations:

• "Sorry business" (Aboriginal mourning protocols)
• Connection to Country (dying on traditional lands)
• Extended family involvement in decision-making
• Whānau (Māori extended family) involvement
• Cultural liaison and interpreter services essential

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SAQ Practice

SAQ 1: Drug Dosing in CKD Patient with Septic Shock

Time Allocation: 10 minutes
Total Marks: 15

Stem: A 62-year-old male with ESKD on maintenance haemodialysis (thrice weekly via left arm AV fistula) is admitted to ICU with septic shock secondary to a left lower lobe pneumonia. He weighs 85 kg. His last haemodialysis session was 48 hours ago.

Observations on arrival:

• HR: 115 bpm
• BP: 78/45 mmHg (MAP 56)
• RR: 28/min
• SpO2: 91% on 10 L/min
• Temperature: 38.9°C
• GCS: 14 (E4V4M6)

Investigations:

• K+: 6.2 mmol/L
• Urea: 32 mmol/L
• pH: 7.28, HCO3: 16, Lactate: 4.8 mmol/L
• CXR: Left lower lobe consolidation

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Question 1.1 (5 marks)

Outline your approach to antimicrobial selection and dosing in this patient.

Model Answer:

Empiric Antibiotic Selection (2 marks):

• Community-acquired pneumonia with septic shock: Broad-spectrum coverage required
• Options:
  • Piperacillin-tazobactam + azithromycin (atypical cover) OR
  • Ceftriaxone + azithromycin OR
  • Meropenem (if risk factors for resistant organisms)
• Add oseltamivir if influenza season/suspected

Dose Adjustments for ESKD (2 marks):

Loading Dose Consideration (1 mark):

• Loading dose unchanged for beta-lactams to achieve therapeutic concentration rapidly
• Piperacillin-tazobactam: Give full 4.5 g loading dose, then adjust maintenance

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Question 1.2 (5 marks)

This patient requires vasopressor support and ongoing renal replacement therapy. Discuss your approach to dialysis management.

Model Answer:

Modality Selection (2 marks):

• Haemodynamically unstable (septic shock requiring vasopressors)
• Convert from intermittent HD to CRRT (CVVHDF preferred)
• Rationale:
  • Continuous solute removal (avoids rapid osmotic shifts)
  • Gradual fluid removal (less intradialytic hypotension)
  • Continuous temperature control

CRRT Prescription (2 marks):

• Modality: CVVHDF (combination convection and diffusion)
• Dose: 20-25 mL/kg/h effluent (85 kg = 1,700-2,125 mL/h)
• Dialysate: Bicarbonate-based (corrects acidosis)
• Blood flow: 150-200 mL/min
• Ultrafiltration: Titrate to achieve negative fluid balance (target 100-200 mL/h if tolerated)

Anticoagulation (1 mark):

• Regional citrate anticoagulation preferred (50% reduction in bleeding risk vs heparin)
• Alternative: Systemic heparin if citrate contraindicated (severe liver dysfunction)
• Monitor: Ionised calcium, total:ionised calcium ratio (citrate toxicity if ratio >2.5)

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Question 1.3 (5 marks)

Outline your management of the hyperkalaemia (K+ 6.2 mmol/L) in this patient.

Model Answer:

Immediate Assessment (1 mark):

• ECG: Assess for peaked T waves, widened QRS, sine wave pattern
• Severity: K+ 6.2 with acidosis increases risk of cardiac toxicity
• Context: ESKD patient 48h since last dialysis - expected accumulation

Cardiac Membrane Stabilisation (1 mark):

• Calcium gluconate 10% 10 mL IV over 2-3 minutes
• Repeat if ECG changes persist
• Mechanism: Stabilises cardiac membrane, does not lower K+

Intracellular Shift (2 marks):

• Insulin-dextrose: 10 units Actrapid + 50 mL 50% dextrose IV
  • Onset 15-30 min, duration 4-6 hours
  • Monitor BSL hourly
• Salbutamol: 10-20 mg nebulised
  • Additive effect to insulin-dextrose
  • "Caution: May cause tachycardia (already present)"
• Sodium bicarbonate: 50 mmol 8.4% IV
  • Useful if acidotic (pH 7.28)
  • Shifts K+ intracellularly

Definitive Removal (1 mark):

• Urgent CRRT initiation (dialysis removes K+)
• K+ removal rate: ~15-30 mmol/hour with CRRT
• Target: K+ <5.5 mmol/L

---

Common Mistakes:

• Using standard antibiotic doses without CKD adjustment
• Forgetting loading doses in renally-impaired patients
• Ordering intermittent HD in haemodynamically unstable patient
• Relying solely on medical management for hyperkalaemia in ESKD (dialysis is definitive)

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SAQ 2: Dialysis Management in Critically Ill Patient

Time Allocation: 10 minutes
Total Marks: 15

Stem: A 58-year-old female with ESKD secondary to polycystic kidney disease, on automated peritoneal dialysis (APD) for 4 years, presents to ED with abdominal pain, fever, and cloudy peritoneal dialysate. She is admitted to ICU with septic shock.

Observations:

• HR: 108 bpm
• BP: 85/55 mmHg (MAP 65 on noradrenaline 0.15 mcg/kg/min)
• RR: 22/min
• SpO2: 96% on 4 L/min
• Temperature: 38.5°C

PD effluent analysis: WBC 850/mm^3 (85% neutrophils), protein 2.4 g/dL

Investigations:

• K+: 5.8 mmol/L, Urea: 28 mmol/L
• pH: 7.31, Lactate: 3.2 mmol/L

---

Question 2.1 (5 marks)

What is the diagnosis and how would you manage the PD-related infection?

Model Answer:

Diagnosis (2 marks):

• PD peritonitis - confirmed by:
  • Cloudy PD effluent
  • WBC >100/mm^3 with >50% polymorphonuclear cells (850/mm^3, 85% PMNs)
  • Abdominal pain and fever
• Severity: Septic shock requiring ICU admission

Empiric Antibiotic Therapy (2 marks):

• Intraperitoneal (IP) antibiotics are first-line for PD peritonitis
• Empiric regimen (ISPD Guidelines 2022):
  • Vancomycin IP 25 mg/kg (single loading dose) + Gentamicin IP 0.6 mg/kg (each exchange)
  • OR Vancomycin IP + Ceftazidime IP 1 g (each exchange)
• Given septic shock: Add IV coverage:
  • IV vancomycin 15-20 mg/kg loading + IV piperacillin-tazobactam (empiric gram-negative)
• Await PD effluent gram stain and culture to guide de-escalation

Catheter Management (1 mark):

• Continue PD for antibiotic delivery if possible
• Indications for catheter removal:
  • Fungal peritonitis (mandates removal)
  • Refractory bacterial peritonitis (>5 days of appropriate antibiotics)
  • Tunnel infection or exit site abscess
  • Enteric organisms (high risk of failure)

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Question 2.2 (5 marks)

Given her haemodynamic instability, outline your approach to renal replacement therapy in this patient.

Model Answer:

Suspend Peritoneal Dialysis (1 mark):

• Peritonitis is relative contraindication to continuing PD
• Abdominal distension impairs ventilation in critically ill
• Cannot guarantee consistent dwell times/drain in ICU setting

Convert to Temporary Haemodialysis/CRRT (2 marks):

• Modality: CRRT (CVVHDF) due to haemodynamic instability
• Vascular access:
  • Insert temporary dialysis catheter (vascath)
  • "Preferred site: Right internal jugular vein (US-guided)"
  • Avoid subclavian (central stenosis affects future AVF creation)
  • "Catheter: 11-13.5 Fr, 15-20 cm length"

CRRT Prescription (1 mark):

• Dose: 20-25 mL/kg/h effluent
• Dialysate: Bicarbonate-based
• Anticoagulation: Regional citrate preferred
• Ultrafiltration: Gentle (100-150 mL/h) given septic shock

Long-Term Planning (1 mark):

• If catheter removed for peritonitis: Temporary HD until PD catheter reinsertion (minimum 2-3 weeks after peritonitis resolution)
• If peritonitis resolved with catheter in situ: Resume PD when stable
• Consider modality switch to HD if recurrent peritonitis

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Question 2.3 (5 marks)

Discuss the considerations for glucose management in this peritoneal dialysis patient.

Model Answer:

Glucose Absorption from PD Dialysate (2 marks):

• PD dialysate contains dextrose (1.5%, 2.5%, or 4.25%)
• Glucose absorption: 60-80% of dialysate glucose absorbed
• Daily glucose load: 100-200 g/day (400-800 kcal)
• Consequences:
  • Hyperglycaemia
  • Weight gain
  • Hypertriglyceridaemia
  • Poor glycaemic control in diabetics

ICU Glucose Management (2 marks):

• Target: 6-10 mmol/L (NICE-SUGAR guidance)
• Challenges:
  • Variable glucose absorption depending on dwell time, concentration
  • "If PD suspended: Sudden reduction in glucose load → hypoglycaemia risk"
  • "If on IV insulin infusion: Adjust for PD status"
• Monitoring: BSL every 1-2 hours initially; more frequent if unstable

When PD Suspended (1 mark):

• Reduce insulin infusion rate (no longer absorbing PD glucose)
• Monitor for hypoglycaemia
• Restart PD glucose absorption calculations when PD resumed
• Consider: Reduced gluconeogenesis in ESKD increases hypoglycaemia risk

---

Common Mistakes:

• Treating PD peritonitis with IV antibiotics alone (IP antibiotics are first-line)
• Continuing PD in septic shock (transition to CRRT)
• Not anticipating glucose management challenges when suspending PD
• Using subclavian vein for dialysis access (central stenosis risk)

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Viva Scenarios

Viva 1: Haemodialysis Patient with Septic Shock

Stem: "A 65-year-old male on maintenance haemodialysis via a tunnelled right internal jugular vein catheter presents with septic shock. He had dialysis yesterday. Blood cultures are positive for Staphylococcus aureus."

Duration: 12 minutes (2 min reading + 10 min discussion)

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Opening Question:

"What are your immediate concerns and priorities in managing this patient?"

Expected Answer (2-3 minutes):

Immediate Concerns:

1. Life-threatening sepsis: Septic shock requiring resuscitation per SSC guidelines
2. Catheter-related bloodstream infection (CRBSI): High suspicion given S. aureus and catheter
3. Metastatic complications: S. aureus bacteraemia → endocarditis, osteomyelitis, septic emboli
4. Dialysis management: May need transition to CRRT if haemodynamically unstable

Priorities:

1. Resuscitation: Fluid bolus (judicious in ESKD), vasopressors to MAP ≥65
2. Source control: Consider catheter removal (S. aureus CRBSI high treatment failure rate with catheter retention)
3. Antimicrobials: IV vancomycin (or flucloxacillin if MSSA) - dose for ESKD
4. Alternative access: Femoral temporary catheter or urgent AV fistula/graft use if matured

---

Follow-up Question 1 (2-3 minutes):

"The patient is requiring noradrenaline 0.3 mcg/kg/min. His dialysis catheter is the suspected source. How do you approach dialysis access management?"

Expected Answer:

Catheter Management:

• Strong indication for removal given:
  • S. aureus (vs coagulase-negative staphylococci which may be treated with catheter retention)
  • Septic shock
  • High treatment failure rate (40-60%) if catheter retained
• Attempt catheter exchange over guidewire is NOT recommended for S. aureus infection
• Complete removal with new catheter at different site

Alternative Access Options:

1. Temporary vascath in femoral vein (while treating current infection)
2. Contralateral IJ placement (after 48-72h of appropriate antibiotics, if improving)
3. Existing AV fistula/graft: If matured, can be used for dialysis immediately

CRRT for Haemodynamic Instability:

• Given vasopressor requirement, CRRT preferred over intermittent HD
• Can use temporary femoral vascath for CRRT

---

Follow-up Question 2 (2-3 minutes):

"Blood cultures remain positive at 72 hours despite appropriate antibiotics and catheter removal. What additional investigations and management would you consider?"

Expected Answer:

Persistent Bacteraemia Concerns:

• S. aureus bacteraemia >72h despite source control = complicated bacteraemia
• Must exclude metastatic infection

Investigations:

1. Transthoracic ± Transoesophageal Echocardiography: Infective endocarditis (15-25% of S. aureus bacteraemia in dialysis patients)
2. Spinal imaging (MRI): Vertebral osteomyelitis/discitis if back pain
3. CT scan: Metastatic abscesses (splenic, renal, pulmonary)
4. Repeat blood cultures: Confirm ongoing bacteraemia

Management of Complicated S. aureus Bacteraemia:

• Prolonged antibiotic course: Minimum 4-6 weeks IV therapy
• ID consultation for antibiotic management
• Serial echocardiography if endocarditis confirmed
• Surgical referral if large vegetation, heart failure, uncontrolled infection

Antibiotic Considerations in ESKD:

• Vancomycin: TDM essential (AUC/MIC-guided or trough 15-20 mg/L)
• Flucloxacillin (if MSSA): Standard dosing (hepatic elimination)
• Daptomycin: Alternative; adjust dose for CrCl <30

---

Follow-up Question 3 (2-3 minutes):

"The patient stabilises and is ready for ICU discharge. What are the key considerations for long-term dialysis access?"

Expected Answer:

Immediate Access (During Hospitalisation):

• Temporary femoral or IJ catheter for ongoing dialysis
• Not suitable for long-term use (infection risk)

Long-Term Access Planning:

1. Preferred: AV fistula creation (lowest infection rate, best patency)
   • Refer to vascular surgery
   • Maturation time: 6-12 weeks
   • Preferred sites: Radiocephalic → brachiocephalic → brachiobasilic
2. Alternative: AV graft (if poor native vessels)
   • Can be used earlier (2-4 weeks)
   • Higher infection and thrombosis rates
3. Temporary/Bridging: Tunnelled catheter (new site)
   • Only after infection cleared
   • Transition to fistula/graft when ready

Vascular Preservation:

• Avoid peripheral IV cannulation in non-dominant arm veins
• Avoid blood draws from antecubital veins (future AVF sites)
• Avoid subclavian catheter placement (central vein stenosis)

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Viva 2: End-of-Life Considerations in ESKD

Stem: "A 78-year-old Aboriginal woman with ESKD from diabetic nephropathy has been on haemodialysis for 5 years. She was admitted with aspiration pneumonia, now Day 14 in ICU with ventilator-dependent respiratory failure, vasopressor requirement, and no improvement. Her baseline function was poor (nursing home resident, dependent for ADLs)."

Duration: 12 minutes (2 min reading + 10 min discussion)

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Opening Question:

"How would you approach goals of care discussions with this patient's family?"

Expected Answer (2-3 minutes):

Preparation:

1. Gather information:
   • Prognosis: Poor trajectory, multi-organ failure, no improvement over 14 days
   • Baseline function: Nursing home, ADL-dependent
   • Patient's previously expressed wishes (advance care directive?)
   • Family dynamics: Identify decision-makers
2. Involve cultural liaison:
   • Aboriginal Hospital Liaison Officer (AHLO) essential
   • May need Aboriginal interpreter
   • Understand family structure (extended family involvement)
3. Team meeting: ICU, nephrology, palliative care, nursing, AHLO

Family Meeting Approach:

1. Setting: Private room, adequate time, all key family present
2. Introductions: Who everyone is, their role
3. Explore understanding: "What have you been told about [patient's] condition?"
4. Provide information: Clear language, avoid jargon, check understanding
5. Acknowledge emotions: Allow silence, validate grief
6. Discuss goals: What would [patient] have wanted?
7. Make recommendation: Provide medical recommendation if appropriate
8. Document: Medical treatment decision form, family meeting summary

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Follow-up Question 1 (2-3 minutes):

"The family is considering withdrawal of dialysis. What are the specific considerations for dialysis withdrawal?"

Expected Answer:

Medical Considerations:

• Time to death: Median 7-10 days after dialysis withdrawal (range 1-30+ days)
• Depends on: Residual renal function, volume status, comorbidities
• Symptoms at end-of-life:
  • Uraemia → progressive drowsiness, confusion (often comfortable)
  • Fluid overload → dyspnoea (may need morphine, diuretics if some response)
  • Hyperkalaemia → arrhythmia (usually painless)

Palliative Care Involvement:

• Essential for symptom management
• Morphine/hydromorphone for dyspnoea
• Midazolam for agitation
• Glycopyrrolate for secretions
• Avoid unnecessary interventions

Process:

1. Clear documentation of decision
2. Discontinue dialysis sessions
3. Discontinue other active treatments (vasopressors, antibiotics)
4. Continue comfort measures
5. Allow family presence (flexible visiting)

Ethical Framework:

• Withdrawal of dialysis = withdrawal of life-sustaining treatment (not euthanasia)
• Patient autonomy (through family if patient lacks capacity)
• ANZICS Statement on End-of-Life Care

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Follow-up Question 2 (2-3 minutes):

"The family mentions that the patient would want to return to Country before dying. How do you approach this request?"

Expected Answer:

Cultural Significance:

• Connection to Country is profoundly important in Aboriginal culture
• Dying on traditional lands has deep spiritual meaning
• May affect family's grief and healing process

Practical Considerations:

1. Feasibility assessment:
   • Is patient stable enough for transfer?
   • Distance and transport requirements (RFDS, road)
   • Available care at destination (health clinic, family capacity)
2. Medical retrieval:
   • Contact RFDS or state retrieval service
   • Plan for symptom management during transfer
   • Anticipatory medications (morphine, midazolam)
3. Receiving facility coordination:
   • Remote health clinic notification
   • Telehealth support from palliative care
   • Local community support

If Return Not Possible:

• Explore alternatives (bringing Country elements to patient)
• Ensure cultural practices can be observed in hospital
• Involve Elders, AHLO, family in creating culturally safe space

Documentation:

• Clear plan for transfer or death in ICU
• Cultural considerations documented
• Family consensus recorded

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Follow-up Question 3 (2 minutes):

"What are the specific cultural protocols if the patient dies in the ICU?"

Expected Answer:

Aboriginal Cultural Protocols:

• Sorry business: Mourning period with specific cultural practices
• Naming: Some communities avoid saying deceased's name
• Viewing: Specific protocols about who can view/touch the body
• Timing: Family may need time for extended family to arrive
• Location: Preference for body to return to community quickly

ICU Actions:

1. Allow adequate family time with body
2. Consult AHLO before any post-mortem procedures
3. Coronial considerations (discuss sensitively)
4. Cultural practices in mortuary (smoking ceremonies may be requested)
5. Family may have specific washing/dressing protocols

Communication:

• Express condolences appropriately
• Provide support resources
• Debriefing for staff if needed