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Acute Kidney Injury (aki)
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tarix | 26.03.2018 | ölçüsü | 26,27 Kb. | | #33463 |
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Acute Kidney Injury (AKI) |
Epidemiology of acute kidney injury (AKI)
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STAGE |
SERUM CREATININE
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URINE OUTPUT
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1
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1.5–1.9 times baseline
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≥0.3 mg/dl (≥26.5 mmol/l) increase
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<0.5 ml/kg/h for 6–12 hours
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2
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2.0–2.9 times baseline
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<0.5 ml/kg/h for ≥12 hours
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3
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3.0 times baseline
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Increase in serum creatinine to ≥4.0 mg/dl (≥353.6 mmol/l)
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Initiation of renal replacement therapy
OR, In patients <18 years, decrease in eGFR to <35 ml/min per 1.73 m2
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<0.3 ml/kg/h for ≥24 hours
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Anuria for ≥12 hours
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Grading of AKI directly is proportional to mortality
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Chertow, Glenn M., et al. "Acute kidney injury, mortality, length of stay, and costs in hospitalized patients." Journal of the American Society of Nephrology 16.11 (2005): 3365-3370.
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Costs approximately 1.2 billion pounds per year in the UK, not including those who go on to CRF
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http://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline.pdf
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Causes of acute kidney injury (AKI)
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AKI is NOT a diagnosis – it is a reflection of an unwell patient
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Nearly always signifies a systemically unwell patient rather than a primary renal injury- the history is very important!
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Classically broken into pre-renal, renal and post-renal
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There can often be a mixture of all aetiologies
| Pre-renal causes of acute kidney injury (AKI) -
Renal blood flow is compromised causing a reduced glomerular filtration rate
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Fluid
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Hypovolaemia (bleeding, dehydration, burns, pancreatitis)
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Hypotension (e.g. septic shock)
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Heart failure – low cardiac output
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Liver cirrhosis causing low volume
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Vascular
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Impairment of renal blood flow autoregulation
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Liver disease (hepatorenal syndrome - rare)
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ACE inhibitors and NSAIDs
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Renal causes of acute kidney injury (AKI)
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Acute tubular necrosis
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Ischaemia
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Hypovolaemia, CCF, renal artery stenosis, hepatorenal syndrome
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Basically all the causes of pre-renal failure, hence why intrinsic and pre-renal disease overlap.
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Nephrotoxic
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Endogenous
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Haemoglobinaemia
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DIC and other causes of haemolysis
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Myoglobinuria: Rhabdomyolysis (NB have low ca in these and very high cr>ur)
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Myeloma kidney disease – light chain nephropathy and tubular cast damage
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Tubular crystal formation
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Exogenous
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Imaging contrast
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Nephrotoxic medication
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Drugs
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Aminoglycosides, Amphoteracin
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Contrast agents
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NSAIDs, Platinum drugs
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Acute tubulointerstitial nephritis
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Drugs: NSAIDS, penicillins, diuretics, antiretrovirals and many more
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Infections: TB, legionella, leptospirosis
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Autoimmune: Sarcoid and Sjorgen’s
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Acute glomerulonephritis
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Vascular
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Thrombotic micorangiopathies: Haemolytic Uraemic Syndrome, Thrombotic Trombocytopaenic Purpura, Pre-eclampsia, Malignant hypertension
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Vasculitis
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Post-renal causes of acute kidney injury (AKI)
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These are all some form of obstruction either intraluminal, intramural or extrinsic obstruction
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Intraluminal
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Nephrolithiasis
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Tumours
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Sloughed papilla (post ATN, DM, sickle, analgesic nephropathy, amyloid and acute pyelonephritis)
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Clot retention
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Intramural
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Reflux
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Adynamic urethral segments
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Neurological disorder(MS, spinal cord injury, DM, PD, post-stroke
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Drugs: Anti-cholinergics and levodopa
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Tumours
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Strictures (worldwide post Schistomsomosa haematobium)
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Extrinsic
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Gravid uterus
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Benign and malignant masses
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Iatorgenic ureteric ligation
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Benign prostatic hypertrophy/prostate cancer
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Retroperitoneal pathology
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Retroperitoneal fibrosis – idiopathic, post inflammatory AAA, drugs (beta blockers and ergots)
| Treatment of acute kidney injury (AKI) -
Avoidance of AKI
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Identify high risk patients: Elderly, CKD, cardia failure, liver disease, diabetes, vascular disease, on nephrotoxic medications
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Monitor patients appropriately: fluid balance, bloods tests
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Maintain circulation: Hydration, resuscitation and oxygenation
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Minimise renal insult: nephrotoxics, contrast hospital acquired infection
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Manage acute illness
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Optimise volume status
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BP, CRT, pulse, oedema, sats, urine output
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Should have iv fluid protocol
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If fluid deplete: Crystalloid (500ml) stat bolus THEN REASSESS
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Maintenance: Hartmanns
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Need 25-30ml/kg water, 1mmol salt and 50-100g glucose per day
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Evidence of crystalloid or colloid
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Volume needed to resuscitate someone is comparable between crystalloid and colloid - SAFE study (2007) showed only 1.3x more crystalloid than colloid needed
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No evidence from RCTs that colloid is better at all and may cause harm. They are also more expensive.
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NB. CRISTAL study actually found that colloids (inc HES) improved mortality at 90 days post-ITU admission relative to crystalloid. So a confusing area.
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Saline or Hartmanns
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Plasma-lyte better outcomes than saline
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Stop nephrotoxics
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ACE-I, diuretics, metformin, allopurinol etc.
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Also consider stopping antihypertensives
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Avoid contrast if possible
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Dialysis or haemofiltration
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Further treatment
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Treat sepsis – antibiotics should be given within 1 hour of suspicion of sepsis
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Steroids (in AIN)
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Cyclophosphamide (vasculitis)
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Plasma exchange (HUS/TTP)
| Complications of acute kidney injury (AKI) -
Hyperkalaemia
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Calcium gluconate 10mls of 10% if ECG changes
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Insulin and dextrose 10units of actarapid in 50ml of 50% dextrose over 15 minutes (if potassium >6.5 mmol/L or ECG changes)
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Salbutamol 5mg nebulised (caution in tachycardia or heart disease)
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Insulin and salbutamol work for roughly 4 hours or less
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Furosemide is useful if the patient is passing good volumes of urine but ONLY IF THE PATIENT IS FLUID OVERLOADED
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Cation exchange resins are overused – moderate effect with high rates of constipation which might paradoxically make the situation worse – rectal route is preferable if must be used.
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Renal replacement therapy if refractory
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Longer term review diet, avoid potassium sparing diuretics/ACE-I, ARBS, NSAIDs.
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Be wary of the potassium load in blood transfusions
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Pulmonary oedema
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Sit patient up
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High-flow oxygen unless contraindicated – consider CPAP
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Opiates e.g. IV diamorphine 1.25-2.5 mg or morphine 2.5mg-5mg as both an anxiolytic and a venodilator – don’t give too often due to accumulation in renal failure
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If haemodynamically stable give 80mg furosemide IV and consider further boluses or infusion of 10mg/hour
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If haemodynamically stable GTN infusion titrating up from 1mg/hour as tolerated by blood pressure (systolic above 100mmHg)
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If unstable will need transfer to high dependency setting for urgent filtering
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If hyperkalaemic with bicarbonate <22mmol/L and not fluid overloaded then can consider 1.26% sodium bicarbonate over 1 hour (can be given via peripheral cannula but avoid in cannula that calcium gluconate was given through)
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Acidosis
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Bicarbonate use should be reserved for hyperkalaemia pending specialist help
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pH<7.15 will need immediate critical care input for filtration
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Uraemic encephalopathy
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Acute setting presents as coma
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Chronically: fatigue, weakness, anorexia, nausea, metallic taste, pruritis, impotence
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Will need emergency renal replacement therapy in the acute setting
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Uraemic pericarditis
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Hypertension (more of a problem in CRF – but acute renal failure can present with hypertensive emergency and needs aggressive treatment, e.g. nitroprusside, beta blockers, ACE-I slowly over 24-48h)
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Sepsis – avoid or adjust doses of nephrotoxic drugs (e.g. vanc and gent)
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Electrolyte derangement – fluid, sodium and potassium restriction, and RRT if it is still there.
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Questions concerning acute kidney injury (AKI)
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A 50 year old alcoholic male presents with sepsis secondary to klebsiella pneumonia. His background includes IHD, previous pneumonia, hypercholesterolaemia and hypertension. Medications include: furosemide, enalapril, aspirin, clopidogrel, co-amoxiclav (current) and simvastatin
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He is treated with IV antibiotics and is managed on an ITU setting for 1 week
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On step down to a medical ward routine bloods reveal:
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Sodium 132
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Potassium 5.0
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Urea 24 (from 8)
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Creatinine 390 (from 60)
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Clinically he is mildly dry, with a BP 135/83, HR 90, he is catheterised with a U/O 35ml/hr
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His management plan should include which of the following?
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Switch to high dose IV furosemide, stop enalapril, give IV fluids to maintain urine output, daily bloods
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Stop furosemide, stop enalapril, add in dopamine and maintain adequate hydration to maintain urine output, daily bloods
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Stop furosemide, stop enalapril, adequate fluids to maintain urine output, daily bloods
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Continue furosemide, stop enalapril, high dose corticosteroids and continue adequate fluids to maintain urine output, daily bloods
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None of the above
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