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.