1._Acute_Kidney_Injury_(AKI)

Report
Acute kidney Injury(AKI)
Dr Dana Ahmed Sharif
Renal Physician
MRCP UK/ MRCP London
Resource materials
•
•
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•
Davidson’s Principles & Practice of Medicine
Kumar & Clark Clinical Medicine
Oxford textbook of Clinical Nephrology
Oxford handbook of Nephrology and
hypertension
• Renal Association website( www.renal.org)
• K/DOQI guideline (www.kidney.org)
• AKI network ( www.akinet.org)
Renal function
• Kidney has many roles:
Renal function
• Kidney has many roles:
- Excretory function
Renal function
• Kidney has many roles:
- Excretory function
- Osmolality regulation
Renal function
• Kidney has many roles:
- Excretory function
- Osmolality regulation
- Acid base balance
Renal function
• Kidney has many roles:
- Excretory function
- Osmolality regulation
- Acid base balance
- BP regulation through
salt and water balance
Renal function
• Kidney has many roles:
- Excretory function
- Osmolality regulation
- Acid base balance
- BP regulation through
Salt and water balance
- Hormone secretion ( Erythropoietin, Vit D3)
Definition of Acute Kidney Injury
Acute usually reversible decline in renal function*
• Rapid time course( < 48 hrs)
• Reduction of kidney function:
A- Rise in serum creatinine, defined by either:
1- absolute increase in serum creatinine of >0.3mg/dl( >26µmol/l)
2- % increase in serum creatinine of > 50%
B- Reduction in urine output, defined as < 0.5ml/kg/hr for more than
6 hrs
* Acute kidney injury network
Incidence of AKI*
• 500 ppm/year – UK ( up to 38,000/yr)
• Incidence of AKI needing dialysis 200 ppm/year
• Pre renal and acute tubular necrosis (ATN) accounts for 75% of the
cases of AKI
• 7% of all hospital admissions( 65% of intensive care admission)
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•
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Mortality:
5-10% in uncomplicated AKI
50-70% in AKI secondary to other organ failure( intensive care)
> 50% in dialysis requiring AKI
*Xue JL, Daniels F, Star RA et al. Incidence and mortality of acute renal failure in Medicare beneficiaries, 1992 to 2001. J Am Soc
Nephrol 2006; 17: 1135–1142.
Acute kidney
injury
Pre renal
- ↓ Effective renal
blood flow:
1- Haemorrhage
2- Volume depletion
3- Low cardiac
output
4- Sepsis
5- CCF
6- Cirrhosis
- Arterial
stenosis/Occlusion
- Vasomotor:
1- NSAID
2- ACEI/ ARBs
Intrinsic
Post renal
Diagnosing pre-renal AKI
• Is the patient volume depleted?
Diagnosing pre-renal AKI
• Is the patient volume depleted?
• Is cardiac function good?
Diagnosing pre-renal AKI
• Is the patient volume depleted?
• Is cardiac function good?
• Is the patient septic?
Diagnosing pre-renal AKI
• Is the patient volume depleted?
• Is cardiac function good?
• Is the patient septic?
History
Examination
Investigation
Diagnosing pre renal AKI
• History
• Examination :
1- Signs of Hypovolaemia:
a- Low BP( and reduced pulse pressure)
b- Postural BP drop ( a fall in systolic BP > 10mmHg)
c- Sinus tachycardia and postural increase in heart
rate ( increase in HR > 10 beat/min).
d- Low JVP even when the patient is supine
e- Cool peripheries and vasoconstriction
f- Poor urine output
Diagnosing pre-renal AKI
2- Sings of hypervolaemia( high extracellular fluid):
a- Increased circulating volume:
- High BP
- Elevation of the JVP
b- Increased interstitial fluid:
- Peripheral or generalized oedema
- Pulmonary oedema (tachypnoea, tachycardia, third heart sound, basal
crackles)
- Pleural effusion
- Ascites
. Lab investigation:
- Blood tests
- urine: including urinary Na( low)
Case 1
• 67 yr man – IHD
• Admitted with D&V – O/E JVP not seen, BP
100/60 lying, 80/50 standing, pulse 105 bpm
• Creatinine 5.8 (0.7-1.2mg/dl)
• x2 IV access
• Given IV saline
• Catheterised and started on furosemide
• Function worsened and transferred to renal unit
What was the only helpful intervention
1- Inserting a urinary catheter
2- Inserting a CVP line
3- Administering IV fluids
4- Administering diuretics
What was the only helpful intervention
1- Inserting a urinary catheter
2- Inserting a CVP line
3- Administering IV fluids
4- Administering diuretics
Treatment of pre renal failure
• DO NOT put in a urinary catheter
• DO NOT GIVE DIURETICS – improving urine
volume does not mean an improvement in
renal function
• CVP line rarely needed – and certainly not
substitute for clinical examination
Treatment of pre-renal failure
• Volume replacement
• Improve cardiac function in congestive
cardiac failure
Treatment of pre-renal failure
Volume replacement: fluid, blood, plasma
expander…
A- Resuscitate:
- Hypotensive and tachycardic
B- Replacement
C- Maintenance
Treatment of pre-renal failure
Volume replacement: fluid, blood, plasma expander…
A- Resuscitate:
- 0.9% Normal saline
- be aware of fluid overload (high BP, RR, basal lung crackles and low
satO2)
- fluid challenge ( trial 200-300ml N saline IV in 10min, then re-assess,
repeat if necessary)
B- Replacement: depends on
a- Degree of hypovolaemia
b- Ongoing losses
c- Whether oligo-anuric
d- Cardiovascular status
Treatment of pre-renal failure
- A rough guide ( be aware of elderly and those with poor left
ventricular function):
- first litre over 2 hours, THEN REASSESS
- second litre over 4 hours, THEN REASSESS
- third litre over 6 hours, THEN REASSESS
*Remember to add insensible loss, if not sure or think you over
done it, stop all fluid and reassess the patient
C- Maintenance:
Once euvolaemic, and assume no other losses, match urine out put
plus 30mls/hour (insensible loss may be higher if febrile)
Acute kidney
injury
Pre renal
Intrinsic
Vascular
1- Vasculitis
2- Thrombotic
microangiopathy
3- Scleroderma
renal crisis
4- Renal vein
thrombosis
5- Cholesterol
emboli
Post renal
Acute GN
Acute TIN
ATN
Glomerluonephritis
tubulointestitial
nephritis
acute tubular
necrosis
Acute kidney
injury
Pre renal
Intrinsic
Vascular
1- Vasculitis
2- Thrombotic
microangiopathy
3- Scleroderma
renal crisis
4- Renal vein
thrombosis
5- Cholesterol
emboli
Post renal
Acute GN
Acute TIN
ATN
(Glomerluonephritis)
(tubulointestit
ial nephritis)
acute tubular
necrosis
Ischaemic
Nephrotoxic
Acute kidney
injury
Pre renal
Intrinsic
Vascular
1- Vasculitis
2- Thrombotic
microangiopathy
3- Scleroderma
renal crisis
Post renal
Acute GN
Acute TIN
ATN
(Glomerluonephritis)
(tubulointestit
ial nephritis)
acute tubular
necrosis
Ischaemic
Nephrotoxic
4- Renal vein
thrombosis
5- Cholesterol
emboli
Endogenous
1- Haemoglobinuria
2- Myoglobinuria
3- Casts and Crystals
Exogenous
1- Nephrotoxic
drugs
2- Radiocontrast
Diagnosing Intrinsic Renal AKI
•
Has pre-renal and post renal been excluded?
•
History
- Drug, Rash, joints, nose bleed, haemoptysis, hearing loss, claudication, IHD,
diabetes, fever or night sweat, Recent infection
•
Examination
- Oedema, rash, mouth ulcer, hearing loss, uveitis, AF, ischaemic toe, bruits,
evidence of scleroderma, prosthetic valve or stigmata of Endocarditis
•
Laboratory investigations
- Urine including microscopy for dysmorphic RBC, Protein, Bence Jones protein,
protein/creatinine ratio or 24hr protein excretion
- Blood – nephritic screen – ANA, dsDNA, ANCA, antiGBM, Immunoglobulines
protein electrophoresis, Rh-factor, HBV, HCV, HIV, cryoglobulins, blood film, CK,
C3,C4, ASO-titre , ESR and CRP
.
US kidneys
.
Renal biopsy
Criteria for distinction between prerenal and intrinsic causes of renal
dysfunction
Pre renal
Intrinsic
Urine specific gravity
> 1.020
< 1.010
Urine osmolality(mOsm/Kg)
> 500
< 500
Urine Na+ (mmol/l)
< 20*
> 40
Fractional excretion of Na+
< 1%
> 1%**
* Except in diuretics or dopamine
** remains low in contrast nephropathy and myoglobinuria
Case 2
What did they do right?
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•
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56 years old man
Cough, haemoptysis and joint pain
O/E JVP +6cm
Creatinine 7.5mg/dl( 0.7-1.2) on admission
IV access, started on IV fluid and diureticsSOB worsened
• Transferred to renal unit after 1 week when
renal function failed to improve
What was done correctly
1. Omission of urine catheter
2. Administered IV fluids and diuretics
3. Transfer to renal unit after 1 week
What was done correctly
1. Omission of urine catheter
2. Administered IV fluids and diuretics
3. Transfer to renal unit after 1 week
Treatment of intrinsic renal AKI
• GN – autoimmune – immune suppression/
plasma exchange
• Infective Bacterial Endocarditis – antibiotics
• Interstitial nephritis
- Stop offending medication
- Corticosteroids
Treatment of intrinsic renal AKI
• ATN
- In-hospital mortality 19-37%*
- Recovery could take up to 6 weeks**
- Self correcting (full 60%, some 30%, dialysis 5-10%)
- Very severe – permanent cortical necrosis
* Oxford handbook of Nephrology and Hypertension 2009
** Kumar and Clark/ Clinical Medicine July 2012
Acute kidney injury
Pre renal
Intrinsic
Post renal
Obstruction
1- Bladder out-let
obstruction
2- Bilateral ureteral
obstruction
Nature of Obstruction
• Outside
- Tumours, prostate, retroperitoneal fibrosis, cervical Ca
• Within wall
- Tumours, strictures
• Within lumen
- Stones, tumours
Diagnosing post renal AKI
• History
- pain, anuria, haematuria, prostatism
• Examination
- palpable bladder, central abdo mass, PR, PV
• Observation
• Laboratory investigations
- Urine
- Blood
- Imaging – US, CT
Treatment of Post renal AKI
• Obtain drainage of Urine
- Bladder catheter – per urethra, suprapubic
- Retrograde drainage
- Antegrade drainage
Case 3
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82 years old man
Not passed urine for 20 hrs
O/E: large bladder and prostate on PR
Creatinine: 8.3 mg/dl
USS- dilated bladder
Urine catheter inserted, start to pass lots of urine
Following day creatinine – 4.2 but then over
subsequent days rises to 5.1 then 5.8 then 6.4.
still passing lots of urine
What is the right intervention
A- Restrict fluid to reduce urine output
B- Give IV normal saline
C- Remove catheter
D- Investigate for other causes of renal failure
What is the right intervention
A- Restrict fluid to reduce urine output
B- Give IV normal saline
C- Remove catheter
D- Investigate for other causes of renal failure
Post recovery diuresis
• Occurs post resolution of AKI
- Post relief of obstruction
- Post ATN
• Important to check fluid status
- Clinical exam
- BP and pulse
- Daily weight
- Input and output chart
• Treatment – IV fluids
replace electrolyte
Complication of AKI
• 64 years old man
admitted with:
Potassium 7.4
Urea: 90
Creatinine: 8.5
What is the first line treatment
A- Insulin and dextrose
B- IV calcium gluconate
C- Ca+2 resonium
D- Low potassium diet
E- Dialysis
What is the first line treatment
A- Insulin and dextrose
B- IV calcium gluconate
C- Ca+2 resonium
D- Low potassium diet
E- Dialysis
Other Complications of AKI
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•
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Pulmonary oedema
Acidosis
Uraemia
Other electrolyte disturbance such as
hyerphosphataemia and hypocalcaemia
Who is a risk?
Many cases of AKI should never occur in the first place
1- Elderly
2- Pre-existing renal disease
3- Surgery, trauma, sepsis or myoglobinuria
4- Diabetes
5- Volume depletion( Nil By Mouth, bowel obstruction,
burn)
6- LV dysfunction
7- Nephrotoxic drugs
8- Cirrhosis (reduce arterial volume)
Common nephrotoxins
• NSAID
• Diuretics, ACEI, ARB2 especially in volume
depleted patient
• Antibiotics, Aminoglycosides, Vancomycin
• Amphotericin B
• Immunosuppressant (ciclosporin, tacroliums)
and chemotherapy (Cisplatin)
• IV contrast
Reducing risk perioperatively
• Three principles:
1- Avoid dehydration
2- Avoid nephrotoxins
3- Review clinical status and renal function those
at risk
• Optimize volume status
1- No patient should go to theatre dehydrated
2- Review daily weight, input and output chart
3- Calculate losses especially those NBM ( use
0.9% N saline and NOT 5% Dextrose)
Reducing risk perioperatively
• Optimize blood sugar control in DM ( use
sliding scale
• Catheterize those with prostate disease
• Avoid surgery if possible immediately after a
contrast procedure
• Stop nephrotoxic drugs 24-48hrs
preoperatively
• Review the patient EARLY postoperatively
Have you..
• Have seen the result of K and acted appropriately?
• Assessed the patient’s volume status and treated pulmonary oedema or
corrected hypovolaemia?
• Taken full history and examined patient head to toe?
• Excluded palpable bladder?
• Seen the patient’s regular drugs? And stopped nephro-toxins?
• Arranged urgent ultrasound(within 24hr)*
• Performed urine test and send for microscopy and MSU
• Checked acid-base status and intervened appropriately?
• Checked for any previous tests of renal function?
• Checked Hb, Calcium and Phosphate?
• Send blood for full nephritic and myeloma screen if you are suspecting
intrinsic renal failure?
* NCEPOD recommendation/ National Confidential Enquiry in to patient outcome and death.
www.ncepod.org.uk
Acute kidney injury
Pre renal
- ↓ Effective circulatory
volume:
1- Haemorrhage
2- Volume depletion
3- Low cardiac output
4- Sepsis
5- CCF
6- Cirrhosis
Intrinsic
Vascular:
1- vasculitis
2- Thrombotic
microangiopathies
Post renal
Acute GN
Acute TIN
ATN
( Glomerluonephritis)
(tubulo-intestitial
nephritis)
(acute tubular
necrosis)
Obstruction
1- Bladder out-let
obstruction
2- Bilateral ureteral
obstruction
3- hypertensive
emergencies
Ischaemic
Nephrotoxic
- Arterial
stenosis/Occlusion
Endogenous
- Vasomotor:
1- Haemoglobinuria
1- NSAID
2- ACEI/ ARBs
2- Myoglobinuria
3- Myoglobin casts
4- Intratubular crystals
Exogenous
1- Nephrotoxic
drugs
2- Radiocontrast
Summary
• 3 categories of AKI
• Simple clinical assessment will define which
• Be aware of life threatening complications and
emergency treatment
• Recognise those at risk

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