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Chronic Renal Failure, peri-operative management of patients for
renal transplantation including CRRT
Dr. Devika Agarwal
University College of Medical Science & GTB Hospital, Delhi
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Scope of this presentationChronic Renal Failure• Definition of chronic renal failure• Causes and patho-physiology• Key peri-operative issues• Effect on anaesthetic drugs• Peri-operative managementAnaesthetic management of renal transplantCRRT
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Definition of CRFChronic renal failure is a decline in the glomerular filteration rate secondary to various diseases such as diabetes, glomerulonephritis and PCKD
Stages of CRF (National Kidney foundation Staging System):Stage 1 kidney damage with normal or increased GFR (>90
ml/min/1.73 m2 Stage 2 Mild (GFR of 60-89 ml/min/1.73 m2 )Stage 3 Moderate (GFR of 30-59 ml/min/1.73 m2 )Stage 4 Severe (GFR of 15-29 ml/min/1.73 m2 )Stage 5 ESRD (GFR of <15 ml/min/1.73 m2 ) or on dialysis
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Causes of chronic renal failure
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Common causes of CRF
• Diabetes Mellitus (40%)• Hypertension (27%)• Chronic Glomerulonephritis (13%)• Cystic Kidney Disease (3.5%)• Interstitial nephritis (4%)• Others (obstructive uropathy, lupus
nephritis, HIV)
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Pathophysiology of CRF And its implications for
anaesthetist
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Perpetuating triad of chronic kidney disease, anaemia, and cardiovascular disease
Parmar M S BMJ 2002;325:85-90
©2002 by British Medical Journal Publishing Group
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Patho-physiological manifestations of CRF
Electrolytes Volume expansion, hyponatremia, hyperkalemia, metabolic acidosis, hyperurecemia,hyperphosphatemia, hypocalcemia
Cardiovascular HTN, LVH, CHF, pulmonary edema, cardiomyopathy,pericarditis, hyperdynamic circulation
Hematological Anaemia,B & T cell dysfunction, qualitative platelet dysfunction, bleeding diathesis
Musculoskeletal Muscle weakness
Neurological Encephalopathy, memory loss, seizures, peripheral neuropathy, myoclonus
Gastrointestinal Gastroperesis, uremic gastroenteritis, peptic ulcers,pancreatitis, nausea & vomitting
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Strategies for active management of chronic renal disease
Parmar M S BMJ 2002;325:85-90©2002 by British Medical Journal Publishing Group
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Key peri-operative issues
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Remember in Peri-operative work-up
Anaemia
Platelet dysfunction
Coronary artery disease
Metabolic acidosisHypervolemia/CHF
Electrolyte imbalance
Immunosupression
Neuropathy
Gastroparesis
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Hematologic issues in CRFANAEMIA
CAUSES:• Chronic blood loss• Hemolysis• Marrow supression by
uremic factors• Reduced erythropoetin
production• Aluminium toxicity• Chronic infection• Bone marrow fibrosis due
to hyperparathyroidism
Anaesthetic Implications:• Decreased oxygen delivery • Increased cardiac output• Cardiac enlargement• Angina• CHF• Impaired mental acquity• Impaired host defence against
infection
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• Increased 2,3 DPG levels (chronic adaptation). Oxy-Hb dissociation curve shifted to right
• Routine transfusions- sensitisation to HLA antigens• Erythropoetin therapy – target hematocrit 36 –40%• Intraoperative transfusion – packed cells, washed RBCs (irradiated
and CMV negetive) for hypotension, hcrit < 15%
Patients with ESRD on hemodialysis require Hb levels 11-12 g/dl
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Hematologic issues in CRFCoagulation abnormality
CAUSES:• Decreased platelet factor
III• Abnormal platelet
aggregation and adhesion• Impaired prothrombin
consumption
Anaesthetic Implications:• Regional anaesthesia:Weigh the risk vs benefit of epidural placement in uremia patients
Thromboembolic complicationsCAUSES:• Urinary loss of antithrombin• Decreased levels of protein C
and S• Hyperfibrinogenemia• Impaired fibrinolysis• Increased platelet aggregability
Seen in patients with nephrotic syndrome
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Hyperkalemia• Serum potassium > 5.5 mEq/L• Impaired renal excretion in CRF• Peri-operative aggrevating factors:
- Hemolysis- Hemorrhage- Massive blood transfusion- Metabolic acidosis (every 0.1 unit change in blood pH
increase K+ by 0.6 mEq/L- Rhabdomyolysis- Succinylcholine- Beta blockers, ACE inhibitors
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ECG findings in hyperkalemia
Serum Potassium
ECG changes
•6-7 mEq/L
•7-8 mEq/L
•8-10 mEq/L
• >9 mEq/L
Tall T waves
loss of P waveWide QRSQRS merges T (sine waves)AV dissociation , VT,VF, cardiac arrest
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Treatment of hyperkalemia
• Antagonism of membrane effects of hyperkalemia Calcium gluconate – - 10 ml of 10% solution over 5-10 min- Dose can be repeated if no change in ECG after 5-10 min- decreases membrane excitability- Can exacerbate digitalis induced arrythmia calcium
gluconate given in 100 ml D5% over 20-30 min.
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Treatment of hyperkalemia
• Potassium movement into the cells Insulin and glucose – - 25 to 50 gram glucose with 10-20 units of regular insulin @
100 ml/hr- Insulin shifts potassium into the cells- Onset in 15 min,peak in 60 min,duration 4-6 hr.- Decreases potassium levels by 0.5 to 1.5mEq/LSodium bicarbonate infusion-- Most useful in metabolic acidosis with hyperkalemia- Watch for sodium overload and volume expansion in CRF
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Treatment of hyperkalemia
• Potassium movement into the cells Beta adrenergic agonists - 20 mg in 4ml saline nebulisation over 10 min / 0.5 mg iv- shifts potassium into the cells- Onset in 30-60 min, duration 2-4 hr.- Decreases potassium levels by 0.5 to 1.5mEq/LLoop diuretics- Furosemide 20-40 mg iv
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Metabolic Acidosis
• Mild to moderate acidosis - GFR less than 20-25% of normal
• pH> 7.2 with plasma bicarbonate 12- 22 mEq/L• bicarbonate correction - based on space of distribution of
bicarbonate 70% lean body weight with target bicarbonate level of 24 mEq/L
Bicarbonate replacement = 0.7 x wt(kg) x (24 – serum bicarbonate) half corrected
• If pH<7.2 dialysis
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Effect on commonly used anaesthetic drugs
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Effect of ESRD on anaesthetic drug metabolism
PharmacokineticsAbsorption - affecting by delayed gastric
emptyingDistribution – volume of distribution is
increased or decreased depending on total body water, protein binding and time since last dialysis
Elimination – prolonged half life for drugs with renal elimination. Eg. Vecuronium
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Inhalational anaestheticsInhalational anaesthetic
fluoride levels Nephrotoxic potential
Halothane 1-2 μM/L No
Isoflurane 3-5 μM/L No
Desflurane <1 μM/L after 1MAC-hr No
Sevoflurane 50 μM/L prolonged use Toxic in animal studies
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Intravenous induction agentsIntravenous induction
agentRenal effects Clinical implication
Thiopentone •Modest decrease in RBF and GFR•Increased unbound fraction
Induction and maintenance dose reduced
Propofol •Cloudy urine due to urates•Green urine due to phenols
•Does not adversely affect renal function
Etomidate •Metabolised by hydrolysis to inactive compounds
-
Ketamine •Does not alter renal function
•Does not alter renal function, not to be used in HTN
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Neuromuscular BlockersNMB Renal effects Clinical implications
Scholine Hyperkalemia Avoid RSI if K+ > 5.5 mEq/L
Rocuronium 30% renal excretion
Modified RSI
Atracurium No renal metabolism
Laudanosine epileptogenic – prolonged surgery
Vecuronium 30% Renal excretion
Avoid in CRF
Pancuronium 50% Renal excretion
Avoid in CRF
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Neuromuscular Blockers
CLINICAL IMPLICATIONS IN CRF PATIENTS
Increased Volumeof distribution
Larger initial dose to produce NM blockade
Reduced metabolism and
Excretion of drugs
reduced maintainence dose
Avoid long acting NMBs
Neuro-muscularmonitoring
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Opioid Analgesics
Opioid Renal effects Clinical implications
Morphine M-6-G renal excretion Delayed respiratory depression
Fentanyl 7% renal metabolism Safe in CRF
Alfentanyl No renal metabolism Safe in CRF
Remifentanyl No renal metabolism Safe in CRF
Meperidine Normeperidine causes seizures, myoclonus, altered sensorium
Avoid in CRF
Tramadol O-demethyl tramadol, 30% renal excretion
Best avoided, dosing interval increased
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Non opioid analgesics
• NSAIDS contraindicated- Hyperkalemia- Platelet dysfunction- Inhibit production of PGE2 and PGI2• Acetaminophen – safe perioperatively
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Local Anaesthetics
• Shortened duration due to altered protein binding
• Dose reduced by 25%• Risk of epidural hematoma
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Preoperative evaluation
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Clinical history
History related to present surgical conditionHistory related to kidney disease:• Cause• Duration• Treatment• Dialysis/ICU or hospital admission
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Symptoms of CRF
• Malaise• Weakness• Fatigue• Neuropathy• CHF • Anorexia• Nausea• Vomiting
• Seizure• Constipation• Peptic
ulceration• Diverticulosis• Anemia• Pruritus• Jaundice• Abnormal
hemostasis
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• Past history-H/O comorbid conditions -Htn , Diabetes, HIV, Polycyctic kidney disease, obstructive uropathy
OnsetProgessionTreatment – drugs, compliance,
controlcomplications
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History of dialysis
1. Dementia2. Cerebral edema3. Hypovolemia (hypotension after
anaesthesia induction)4. Peritonitis (peritoneal dialysis)5. Systemic anticoagulation
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History of dialysis
• Time since last dialysis – last dialysis should finish atleast 4-6 hrs prior to allow fluid shifts and elimination of heparinwithin 24 hrs of surgery
• Post dialysis status - Full blood counts- BUN, S.Cr, electrolytes- Coagulation- Patient’s weight• Dialysis related complications -
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• Family h/o kidney disease, HT, DM• Personal history-
– Smoker– Alcohol– Drug abuse
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Examination
• Blood pressure• Flow murmurs• Pericadial rub• Ankle/ sacral
edema• Pulmonary edema• Fistula
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Investigations• Full blood counts – normocytic normochromic anaemiaRaised TLC• Coagulation profile• KFT – BUN, S.Cr, S.E• ECG – ischemia, arrythmia, LVH• CXR • ABG – metabolic acidosis• LFT – if major surgery
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Chest X-rayPulmonary edema
Cardiomegaly
Pericardial effusion
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Anaesthetic management
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Anaesthetic management
Pre-op preparation- optimize BP, B.sugar- Correct serum potassium- ABG- Aspiration prophylaxis – metoclopramide
and H2 antagonist
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Intraoperative management
• Preoxygenation• Premedication – opioid (fentanyl)• Iv induction gradual and titrated• RSI – Sch if K+ < 5.5 mEq/L- modified RSI with rocuronium- Intubate controlled ventilation- Regional anaesthesia – risk of epidural
hematoma
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Maintenance of anesthesia• O2 + N2O + isoflurane + Atracurium / cis-
atracurium• Controlled ventilation
Monitors:• ECG• NIBP / IABP• Capnography• Pulse oxymery
• Temp• Neuromuscular monitoring • CVP• Urine output
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• Restricted fluids• Forced air warming and fluid warming• Emergency preparedness
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Post operative care
• Analgesia- NSAIDS avoided- Paracetamol safe• Oxygenation• Monitoring – ECG, BP, SPO2, Urine output• Early mobilisation and chest physiotherapy
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Perioperative management of patient with
renal transplantation
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• Kidney donors• Contraindication for kidney donation• Donor matching• Preservation and transport• Surgical aspects• Peri-operative management• Post-operative oligouria
Kidney transplant
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• Ideal donor- Age: 5 to 49 years- non hypertensive- Cause of death was not cerebrovascular accident- S. creatinine < 1.5 mg/dl
• Expanded criteria donor– Age: >60 years or 50-59 yr – additional risk factors (h/o HTN, death from cerebrovascular
accident or S.creatinine>1.5 mg/dl)70% risk of renal failure within 2 years
Criteria for kidney donation
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Contraindications to receiving kidney transplant
Absolute• Recent or metastatic
malignancy• Untreated current infection• Severe irreversible non renal
disease• Psychiatric illness• Recreational drug abuse• Limited irreversible
rehabilitative potential• Infection: hetatitis B,C, HIV
Relative• Vesical or urethral
abnormalities• Aortoiliac occlusive disease• Morbid obesity• smoking
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Donor matching
• ABO blood group: Ideal match: donor and recipient same phenotypeCompatible match: person with grp A may donate to A or AB
• Tissue typing: – HLA compatibility- Kidney with least number of
mismatches is prefered– With immunosupressive drugs recipients can receive an
organ with less than perfect match
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• Cross matching: – Recipient’s antibody response to donor HLA
antigens– Antibody produced after pregnancy or blood
transfusion(positive cross-match - relative contraindication
to transplant)
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Preservation and transport
• Temperature: 4*C – metabolic rate slowed 12 fold
• Cold storage solutions: - electrolyte composition similar to intracellular environment (low sodium, high potassium)
• Cold ischemia time: <36 to 40 hours
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Cadaver kidney:– Donor kidney flushed with cold storage
solution + packed in sterile container with ice– In a machine that pumps preservation solution
through organLiving donor kidney
– Preservation solution/ iced Ringer lactate with heparin and mannitol (ischemia time: 20 – 30 min)
Method of transport
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Surgical aspects
• Heterotopic position• Retroperitoneal – preferred- percutaneous
biopsy• Right or left ileac fossa• Inflow vessel - internal/ external ileac
artery • Outflow vessel -external ileac vein• Urinary continuity - to prevent reflux• Intraarterial injection of verapamil/
papaverine to prevent vasospasm (cadaveric donor)• Furosemide(200mg) frequently after
revascularisation
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• Dual kidney transplant-– More blood loss /
third space loss– Longer duration
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Preoperative preparation
• Preop work up for comorbidities
• Workup for chronic renal failure+ Urine analysis and urine culture
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Intraoperative management
GA preferred – longer operative time, blood loss, good muscle relaxation
RA – not preferred• Uremic bleeding tendency• Residual effect of heparin post dialysis
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Intra-operative monitoring
Routine monitoring-Heart rate-Blood pressure-ECG-pulse oximetry-capnograph-Neuromuscular monitoring
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CVP monitoring- Rationale- adequate hydration , prevent ATN- CVP guided fluid therapy – 12- 14 cm H2O - Post dialysis patients have intravascular fluid
depletion
Invasive monitoring
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Reasons for decline of CVP after revascularization :
1. Redistribution of fluids2. Changes in vascular permiability3. Increased nitric oxide levels
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Invasive blood pressure monitoring:- Indicated in patient with advanced co-morbidities- Hypotension may occur after unclamping of iliac
vessels and/or partial systemic absorption of vasodilators (verapamil or papaverine)
- Hypotension can cause delayed graft function
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Induction of anaesthesia
• Induction of immuno-suppression started before entering operating room
• Standard anaesthesia monitors• Central line and arterial-line placed
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• IV induction with reduced dose of thiopentone /propofol /etomidate:
1. Lower plasma protein levels 2. Post dialysis hypovolemia
Some studies have suggested increased dose requirement of propofol due to hyperdynamic circulation in uremic patients
Ketamine undesirable in patients due to underlying hypertension.
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• Blunt laryngoscopic response - fentanyl 5mc/kg iv – metabolised in liver with only
7% renal excretionRemifentanyl (metabolized by plasma esterase) and
alfentanyl (metabolized by liver) can also be used- Esmolol 0.5 – 1.0 mg/kg
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• Rapid sequence induction using succinylcoline/rocuronium
- increase in serum potassium by 0.5 to 1.0 mEq/l within 3-5min and lasting 10-15 minSuccinylcoline can be safely used in renal failure if serum potassium is < 5.5 mEq/l and repeated doses avoidedPlasma cholinesterase levels are 20% less – rarely causes prolonged block
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Maintenance of anaesthesia
• Volatile anaesthetic- sevoflurane – renal toxicity due to production of fluoride and compound Aisoflurane and desflurane- can be used safely
• Muscle relaxant – atracurium, cisatracurium – hoffman eliminationmivacurium – decreased activity of pseudocolinesterasePancuronium- dependant on renal clearance
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Intraoperative fluids
• Avoidance of potassium containing fluids• Normal saline and albumin 5% preferred• CVP 12-14 cm H2O• Furosemide/ mannitol to improve urine
output• Estimated blood loss – 200 – 500 ml
Larger losses replaced with RCC that is CMV negetive
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Intra-operative effect of polyclonal and monoclonal antibodies
Anaphylaxis 1. Stop ATG administration2. Continue mechanical ventilation with 100%
oxygen3. antihistamines,steroids and epinephrine
Patients on beta blockers or ACE inhibitors may not respond to therapy
Prevention: antihistamines, acetaminophen and steroids before injection
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Perioperative oligouria
Oligouria is urine output of less than 0.3mg/kg/hrLow urine output indicates dramatic reduction in glomerular filteration rate or mechanical obstruction
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Peri-operative renal dysfunctionType Cause Management
Pre-renal •Low intravascular volume•Relative decrease in blood volume (volatile anaesthetics
•Responds to fluid challenge
Renal •Structural- renal art. thr. , renal vein thr.•ATN -antibiotics, contrast dyes
Post-renal mechanical obstruction surgical wound closure impinging on graft vessels or ureter
-flush the foley’s catheter-Intraoperative ultrasound to examine flow at vascular anastomosis
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Continuous renal replacement therapy
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Indications of renal replacement therapy
Classical indications1. Volume overload leading to heart failure, pulmonary
edema or severe hypertension2. Anuria3. Hyperkalemia (> 6.5 mEq/L)4. Metabolic acidosis (pH < 7.1)5. Symptomatic uremia (encephalopathy, pericarditis, blood
dyscrasias)6. Dialysable intoxicants
– Lithium - Aspirin– Ethylene glycol - Theophylline– Methanol
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Indications of renal replacement therapy
Alternative indications• Endotoxic shock• Hypothermia (rewarming)• Nutritional support• Delibrate hypothermia• Traumatic rhabdomyolysis• Plasmapheresis (Gullian Barre syndrome,
myasthenia gravis, TTP
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Modes of renal replacement therapies
1. Intermittent (<24 hrs)• Intermittent hemodialysis (IHD)• Sustained low-efficiency dialysis (SELD)• Extended daily dialysis (EDD)2. Intermittent and continuous• Peritoneal dialysis (PD)3. Continuous• Continuous ambulatory peritoneal dialysis (CAPD)• Continuous renal replacement therapy
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Continuous renal replacement therapy
• Slow continuous hemofiltration (SCHF)• Continuous venovenous hemofiltration (CVVH)• Continuous venovenous hemodialysis (CVVHD)• Continous venovenous hemodiafiltration
(CVVHDF)
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Processes of renal replacement therapies
1. Ultrafiltration: • Blood is pumped to a
filtering membrane• Hydrostatic pressure
is higher on the blood side of the filter
• Leaves cellular material behind
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2. Convection:• “solute drag”-
solute molecules swept through membrane by moving stream of ultrafiltrate
• Positive pressure - blood compartment
• negetive pressure -dialysate compartment
• Driving force = trans-membrane pressure
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2. Convection:• Independent of any solute
gradient• Dependent on porosity
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3. Diffusion:• Movement of solutes from
higher to lower concentration across an electrochemical gradient
• In hemodialysis dialysate is pumped countercurrent to blood flowing on other side of semi-permeable membrane
• Particle size (<20 KDa)
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3. Diffusion:• Rate of diffusion
depends on – Solute (size, charge,
pr.binding)– Dialysis membrane
(porosity,thickness,surface area)
– Rate of delivery of solute– Conc. of dialysate
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4. Membrane adsorption:• Adsorption on artificial
membranes• Determined by pore size
and surface area• Membrane’s adsorptive
capacity gets saturated in first hours of RRT
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• Hemodialysis = Diffusion• Hemofiltration = Convection• Hemodiafiltration = diffusion + convection
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Type of CRRT Principle Application
SCUF fluid load CHF
CVVH fluid and middle sized molecules
CVVHD mostly small molecules
CVVHDF Small and medium sized molecules
Intensive careMost efficient approach
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Advantages of CRRT in critically ill patients
• Hemodynamically unstable patients• Precise volume control• Effective control of uremia, hyperkalemia and
hypophosphatemia• Rapid control of metabolic acidosis• Available 24 hours a day• Safe in patients with brain injury and cardiovascular disorders• Adjuvant therapy in sepsis
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Dialysate and replacement fluid
• Initially dialysate low in intracellular ions (potassium, magnesium and phosphate is used)
• Normokalemic solution when serum potassium is < 4.5 mEq/L
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(a) A pressure sensor todetects any decrease in pressure (e.g. vascular catheter blockage).
(b) A post-filter sensordetects reduced flow to the drip chamber,
(c) distal to the drip chamber Detects reduced flow if the return catheter port is blocked.
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Further reading
• Miller’s anaesthesia , 7th edition• Clinical anaesthesia, Barash• Yao and artusio’s anaesthesiology, 6th edition• Harrison’s principles of internal medicine, 16th
edition• Parmar MS. Chronic renal disease BMJ 2002;
826: 86-90
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Thank you