Intern Survival Guide - Acute and Chronic Renal Failure
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Transcript Intern Survival Guide - Acute and Chronic Renal Failure
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.