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Download Intern Survival Guide - Acute and Chronic Renal Failure
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Loss of renal function that results in Retention of waste products Reflected by urea levels Dysregulation of extracellular fluid Usually volume overload Dysregulation of electrolytes Usually potassium Dysregulation of acid/base balance Usually acidosis THIS OCCURS IN BOTH ACUTE AND CHRONIC RENAL FAILURE Acute Requires determination of cause(s) of renal failure Treatment of cause (to reverse renal failure) Management of the complications Volume status Electrolyte disturbance (hyperkalaemia) Toxin accumulation Acid/base disturbance Chronic Diagnosis (cause) usually known and management focus is that of complications Volume status Electrolyte disturbance (hyperkalaemia) Toxin accumulation Acid/base disturbance Should be treated the same as acute renal failure Determination of the cause of acute deterioration Management of the cause of the acute deterioration Management of the complications Acute renal failure Chronic renal failure Historic eGFR > current eGFR Historic eGFR = current eGFR Acute on chronic renal failure Historic eGFR abnormal BUT > current eGFR Melbourne Pathology Healthscope 1300 134 111 Dorevitch 9287 7700 9244 0444 St. Vincent’s Pathology 9288 2888 Pre-renal Renal Post-renal Easiest to exclude Males – usually secondary to prostatic obstruction History (male and females) Urinary urgency/frequency/poor stream/post void dribbling/incontinence Supra-pubic pain (severe if acute) Examination Large bladder Investigations Bladder scan – large residual bladder volume or large bladder with pain and inability to pass urine Investigations Bladder scan – large residual bladder volume or large bladder with pain and inability to pass urine IDC insertion – passage of large volume of urine Obstruction beyond the bladder usually not associated with acute renal failure unless Most people who obstruct 1 kidney still have a remaining normal kidney Pre-existing renal disease Solitary functioning kidney eGFR minimally affected in these cases Renal US hydronephrosis Relieve the obstruction Nephrology intervention infrequently required Urology opinion frequently required Dialysis rarely prior to alleviation of obstruction Monitoring for post-obstructive diuresis Massive urine output predisposing to dehydration (pre-renal failure) Electrolyte abnormalities (most often hypokalaemia) Renal hypoperfusion Multiple aetiologies Hypotension Cardiac Sepsis Intra-operative/Anaesthetic Dehydration GI losses Poor intake Diuretics Volume re-distribution (3rd space losses) CLD with ascites Drugs that affect GFR ACEi/ARB/spironolactone NSAIDS Renal hypoperfusion Beware – normotension in a patient on multiple antihypertensives that are being witheld indicates renal hypoperfusion Commonest cause in hospital is acute tubular necrosis (ATN) Progression of pre-renal causes Ischaemia for a period of time that leads to tubular cell death Toxins Drugs (Vancomycin/Gentamicin/amphoteracin) IV contrast (CT scans/angiography) Myeloma/immunoglobulins/paraproteins Glomerular disease Glomerulonephritis Rapidly progressive groups (characterised by microscopic haematuria) Pauci-immune GN (eg ANCA vasculitidies) Anti-GBM disease Lupus Nephritis Post-infectious GN Interstitial renal disease Acute interstitial nephritis (usually antibiotic related in hospitalised patients) History Aimed at identifying pre-renal insults History extends to medical records (anaesthetic notes in operative patients) Observation charts Dug charts Aimed at identifying renal insults Drug charts (nephrotoxins) Contrast studies IV/IA Examination Focuses upon volume status/hydration Pre-renal/3rd space sequestration Hypotension/postural hypotension tachycardia Investigations Bloods U/E, Cr Detection of renal failure ANA/ENA/dsDNA/c3 and 4/ANCA (MPO/PR3)/anti-GBM antibodies ASOT/anti-DNase B SPEP/serum free light chains Urine MSU M/C/S Bland urine sediment – no glomerular red cells Favous pre-renal/ATN/myeloma/interstitial renal disease Active urine sediment – glomerular red cells Seen in acute glomerulonephritis Hyaline/granular/tubular/epithelial casts Suggestive of ATN Pr/Cr Proteinuria > 1g/d (Pr/Cr > 0.1) suggestive of glomerular/intrinsic renal disease uBJP - immunoglobinopathy Renal Imaging US – to exclude renal tract obstruction (hydronephrosis) Renal Histology Renal biopsy If suspicion of intrinsic renal disease If disease not explicable by pre-renal/ATN 2 types Supportive (for all patients) Active – for treatable glomerulonephritidies Initiated and managed by renal services Pre-renal Resolves (improvement in renal function) quickly 24-48 hours with treatment/correction of the underlying insult ATN Does not resolve despite treatment/correction of the underlying insult Will recover but days to weeks for renal tubules to re- generate Dangers to avert resultant from renal failure Fluid accumulation Hyperkalaemia Acidosis Uraemia Correct renal hypoperfusion Mange sepsis Manage hypotension Manage dehydration/intravascular volume depletion Remove drugs that reduce GFR Remove nephrotoxins Prevent further noxious insults Pre-hydration/N-acetyl cysteine for IV/IA contrast studies ( and cessation of drugs the reduce GFR ) Volume management Euvolaemia JVP +3cm No peripheral oedema (provided no hypoalbuminaemia/right heart failure) Clear chest Normotension Stable body weight (often more accurate and easier than fluid balance charts) An IDC is not essential IV fluids to correct fluid deficiency Cease if patient euvolaemic Fluid restriction often required due to inadequate urine output (once euvolaemic) Avoid potassium in fluids in the setting of any type of renal failure Inability to excrete potassium Hartmann’s – contains potassium and lactacte (an acid that will compound potentially renal acidosis) In a post operative patient Only start potassium containing fluids after patient has an established urine output Diuretics for fluid overload May require high dose IV frusemide (up to 250mg) If no response – no benefit in repeat dose Can re-attempt on daily/2nd daily basis Can diuretics kick start a kidney? Should you adopt a push-pull (frusemide and fluid) technique No No Can diuretics prevent dialysis Possibly If kidneys are responsive diuretics can Remove fluid overload Remove hyperkalaemia via a kaluresis Reduce acidosis (induce a metabolic alkalosis) They do not impact upon uraemia Acidosis Renal failure associated with inability to excrete endogenous acids Na bicarbonate therapy (100ml 8.4%) vials may occasionally be necessary HCO3 < 10 At this point there usually exists an indication for dialysis therapy Hyperkalaemia Commonly seen in patients with renal impairment (acute and chronic) Causes Most commonly reduced excretion (renal handling most important) Renal impairment Deterioration in renal function Drugs (inhibitors of the Renin/Angiotensin/Aldosterone Axis) ACEi/ARB’s/Spironolactone Causes (cont) Excess intake Dietary Medications (slow K) Intravenous therapy Excess production Cell death (intracellular K >>> extracellular K) Rhabdomyolysis Tumour lysis Crush injuries Causes (cont) Shift from intracellular to extra cellular Acidosis (DKA) Insulin deficiency (drives K into intracellular compartments with co-transport of glucose) Symptoms/signs Most serious are cardiac conduction disturbances/arrhythmias Bradycardia Sinus arrest Idioventricular rhthyms VT/VF Asystole Muscle weakness/paralysis No set figure Best guide is 6.0 Toxic effects may be seen at lesser levels with rapid rise in K (unlikely if K < 5.0) Stabilise the heart Reduce serum potassium Increase removal Diuretics (if associated with fluid overload) K binding gut resins Dialysis/haemofiltration Reduce intake Dietary restriction Shift into intracellular compartment (re-distribution) Insulin/Dextrose Beta- agonists (salbutamol) Treat acidosis Hyperkalaemia identified (on blood test) ECG If changes of hyperkalaemia Stabilise the myocardial electrical system Ca Gluconate 10ml 10% IV Slow push (1 -2 minutes) In 100ml fluid (N/sal or D5W) over 5 mins Cardiac monitoring Repeat above again if ongoing ECG abnormalities (5 minutes) Confirm hyperkalaemia Venous ABG quickest and easiest (minutes) Start to lower serum potassium Rapidly acting measures Insulin therapy Dextrose 50%, 50mls IV Insulin (actrapid) 10 units IV BSL monitoring to monitor for hypoglycaemia Usually ~ 1 hour post intervention Benefit – rapid effect (within 15 minutes, maximum at 1 hour, total duration 4-6 hours) K improvement 0.5 – 1.2 mmol/L Rapidly acting Inhaled = intravenous Effects within 5 minutes Duration ~ 4 hours K lowering of 0.5 to 1.5 mmol/L Effects additive to insulin/glucose therapy 2nd line therapy Early (1 minute) paradoxical increase in K (0.5 mmol/L) Dose related effect 10mg < 20mg Adverse Promotes tachycardia Precipitate angina and angina related cardiac arrhythmias Animal study found induction of cardiac arrythmias in hyperkalaemic phase of salbutamol administration In the setting of acidosis (HCO3 < 15) Mixed reports regarding effectiveness Only used as an adjunct that MIGHT help in the management of hyperkalaemia Loop diuretics (frusemide) Known side effect of hypokalaemia Kaluretic properties Only effective if the patient has or can generate a significant urine output Used as adjunctive therapy and only in a patient with associated fluid overload Oral potassium binding resin Widely used in hospital (with minimal good evidence) 15 to 30g tds/qid if going to be effective Oral therapy if GUT working, otherwise PR Takes at least 24 hours to exert a benefit Studies previously examined preparation containing laxative sorbitol Laxatives alone can induce diarrhoea which promotes hypokalaemia Effectively removes potassium Most invasive Most difficult to organise Definitive therapy Acute renal failure Chronic renal failure Daily U/E, Cr Twice weekly U/E, Cr Acute on chronic renal failure Daily U/E, Cr Dialysis required Immediate Anuric Dialysis not predicted within 48 hours Basic investigations ordered U/E, Cr MSU M/C/S and Pr/Cr Renal US Clinical information that would be helpful Description of possible renal insults (pre-renal and renal) Do not sit on a patient with unexplained renal impairment especially if new They may have reversible rapidly progressive GN that needs to be acted upon within 1-2 days.
