Update in the management of AKI Professor Harun-Ur-Rashid PhD, FCPS, FRCP Chief...
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Transcript of Update in the management of AKI Professor Harun-Ur-Rashid PhD, FCPS, FRCP Chief...
Update in the management of AKI
Professor Harun-Ur-Rashid PhD, FCPS, FRCP
Chief Consultant,Nephrology
and
Founder President
Kidney Foundation, Bangladsh
Introduction
• AKI is a global problem and occurs in the community and in the hospital
• It is a predictor of immediate and long term adverse outcomes.
• World wide incidence of AKI is poorly known
Incidence of AKI around the world
• USA - 24 cases /1000 discharge
• Kuwait - 4 per 100,000 cases / year
• Nigeria - 12 per year in children
• North India - 20 cases / 1000 discharge
• Bangladesh -24 cases /1000 discharge
in a tertiary care hospital
Definition of ARF
• AKI is defined by an abrupt decrease in kidney function that includes but not limited to ARF.
• It is a broad clinical syndrome with various aetiologies
KDIGO,2012
History of ARF
• Ischaemia Renalis -by William Heberden in 1802.
• Acute Bright’s disease-William oslears 1909.
• ARF- Homer W. Smith, 1951
• A 27 year male ,with severe diarrhoea for 2 days
• BP 90/60,develop oliguria
• Serum Cr 272 micromol,K-2.6,Na-123
• In next 2 days, S.Cr jumped to 450
What is the diagnosis ?
Rifle criteria for diagnosis and classification of AKI
Class Serum creatinine of GFR Urine output
Risk Increase in serum creatinine x 1.5 or GFR decrease >25%
Less than 0.5ml/kg/h for more than 6 hours
Injury Serum creatinine x 2 or GFR decreased >50%
Less than 0.5 ml/kg per hour for more than 12 hours
Failure Serum creatinine x 3, or serum creatinine >4mg/dl (>354 μmol/l) with an acute rise >0.5 mg/dl (>44 μmol/l) or GFR decreased >75%
Less than 0.3 ml/kg/h for 24 hours or anuria for 12 hours
Loss Persistent acute renal failure-complete loss of kidney function >4 weeks
End-stage kidney disease
ESRD>3 months
Criteria for diagnosis of AKI
• Increase in Scr. by ≥ 0.3 mg/dl (≥26.5 μmol/L) within 48 hours.
or
• Increase in Scr. to >1.5 times baseline which is known or presumed to have occurred within the prior 7 days
or
• Urine volume <0.5ml/kg/h for 6 hours.
AKIN,2007
Staging of AKI
Stages Sr Cr Urine Output
1 1.5-1.9 times baseline or
≥0.3mg/dl (26.5 (μmol/L)
<0.5ml/kg/h for 6-12 hours
2 2.0-2.9 times baseline <0.5ml/kg/h for >12 hours
3. 3.0 times baseline Or
Increasing in Sr Cr to ≥ 4.0 mg/dl (≥353.6 μmol/L
Or Initiation of RRT
<0.3ml/kg/h for ≥ 24 hours
Anuria for ≥12 hours
AKIN criteria,2007
Diagnosis of AKI, CKD and AKD
Functional criteria Structural criteria
AKI Increase in SCr by 50% within 7 days, OR No criteria
Increase in SCr by 0.3 mg/dl (26.5µmol/l)
within 2 days, OR Oliguria
CKD GFR <60 ml/min per 1.73m2 >3 months Kidney damage for
>3 months
AKD AKI, OR Kidney damage for
GFR <60ml/min per 1.73m2 for <3 months, OR <3 months
Decrease in GFR by ≥35% or increase in
SCr by >50% for <3 months
NKD GFR ≥60ml/min per 1.73 m2 Stable SCr No damage
Classification of AKI
• Pre-renal
• Renal
• Post-renal
Classification of AKI
Pre-renal Cause:
• Hypovolemic state i.e Gastroenteritis
• Low cardiac out-put state ie CCF
• Systemic vasodilatation ie sepsis
• D.I.C
• Renal vasoconstriction ie cyclosporine
• Impaired renal auto reguletory response ie ACE. ARB, COX
• Plants and toxin
Classification of AKI
Renal Cause:
• AGN/RPGN
• Interstitial nephropathy
Post renal :
• Renal Stone disease
• Other obstructive disease
Risk assessment of AKI
Factors that cause AKI:
• Sepsis
• Critical illness
• Circulatory shock
• Burns
• Trauma
• Cardiac and Non-cardiac Surgery
• Nephrotoxic drug
• Radio contrast agent
• Poisonous plants and animal
Factors that determine susceptibility of AKI
• De hydration or Volume Depletion
• Advanced age
• Presence of CKD
• Chronic Disease i.e. heart, lung, liver
• DM
• Cancer
• Anaemia
Biomarkers for early diagnosis of AKI
Biomarkers Associated Injury
• Cystatin –C Proximal tubular Injury
• KIM-1 Ischaemic and Nephrotoxin
• NGAL Ischaemic and Nephrotoxin
• Cytokine- Toxic and
IL6,8,18 Delayed graft function
• a-GST Proximal and distal T injury
&
n-GST
Evaluation and general management of patients with AKI
• Patients should evaluate promptly to determine the cause.
• Monitor the patients with Scr & urine output .
• Manage according to cause & stage of AKI
• Evaluate patients at 3 months for resolution or worsening of preexisting CKD.
Treatment and prevention of AKI
• Management of Specific cause
• Management of Hypotension and shock
• Treatment of infection
• Glycaemic control and nutrition support
• Use of diuretic
• Vasodilator therapy
• Growth factor intervention
• Role of Erythropoietin
• RRT
Management of Hypotenison and shock in AKI
Careful titration of fluid:
• ORS for children and infant
• IV isotonic Saline for adults
• 4% albumin Vs saline for ICU
• Hydroxyethyl Starch Vs Albumin for ICU
Bouchard J,MehtaRL,2010;Finfer et al, N Engl J Med,2004
Vasoachive medication:
• Non epinephrine, dopamine or vasopressin only after dehydration is corrected to maintain BP
-Useful in septic shock, burns, liver failure
-Not suitable for Cardiogenic shock
Marik,Intensive Care Med,2002;KellumJA,Decker J,2001
Management of Hypotension and shock in AKI
Glycaemic control and nutritional support in AKI
Tight glycaemic control :
• Pl. glucose -80-110 mg/dl• Total calorie intake -20-30 kcal/kg• Protein intake -0.8-1.0 g/ kg/day-
noncatabolic state -1.0-1.5 g/kg/day- Catabolic state
Van den Berghe et al,N Engl J Med,2001
Role of Diuretics in AKI
• No evidence to reduce incidence or severity of AKI
• Indicate only if patients are volume over loaded
• Diuretic only Convert oliguric to non oliguric
• It promote earlier diuresis but no effect on survival
Ho and Power;Anaesthesia,2010;Cantarovich et al,Am J Kid Dis,2004
Role of Vasodilator therapy in AKI
• Low dose dopamine – no benifit
• Fenoldopen – not useful
• Atrial natruretic peptide - not useful
Friedrich et al, Ann. Intern med,2005
Growth factor intervention in AKI
• Recombinant human IGF-1- Not useful
Hirscberg et al,Kid Int,1999
Role of EPO in the prevention of AKI
• Use of Erythropoetin in the Prevention of
AKI in ICU –Not Useful
Endre et al,Kid Int,2010
Role of RRT in AKI
• Indicated only if Acute and severe renal failure, volume over load, hyperkalema, acidosis & symptoms of uraemia
• Intermittent HD and CRRT- found equally effective
• SLED – combines both IHD and CRRT
Rabindranath et al,Syst. Review,2007;
Bagshaw et al,Crit Care Med,2008.
Role of PD Vs HD in AKI
• Optimum Treatment of AKI remain uncertain
• Studies looking at various therapeutic approach give different results
• Optimum dose of PD is uncertain
• Considered reasonable Treatment in Developing Countries
Karen Yeates,PDI,2012
Comparing PD and EBP for RRT
Variable Phu et al., 2002 (2) Reference Gabriel et al., 2009 (4)
George et al.,
2011 (12)
Country Vietnam Brazil India
Setting ICU Mostly ICU (77%) ICU
Patietns
Study group (n) 70 120 50
Mean age (years) 35.5 63.4 46.9
Sepsis (%) 31.4 44.5 38
PD technique
Exchanges Manual Cycler Manual
EBP technique
Type CVVH Daily intermittent HD CVVHDF
Mortality on PD [n/N(%)] 17/36 (47) 35/60 (58) 18/25 (72)
Mortality on EBP [n/N(%)] 5/34 (15) 32/60 (53) 21/25 (84)
AKI in ICU in a Tartiary Care Hospital
AKI in a ICU in a tartiary care hospital in Dhaka
• Study period = Jan 2010- Dec 2010
• Total No patients studied = 121
• No of AKI detected (RIFLE criteria) = 46(38%)
Mean age: 50±12 yrs.(Range 18-80 yrs;
M 72,F 49)
Alam B et al ,2011
Causes of AKI in ICU patients
Trauma
Surgical
Metabolic/poisoning
Hepatic
Gastrointestinal
Respiratory Neurological
Cardiac Sepsis/Septic Shock
4.3
28.3
0.0
4.3 4.3
10.9 26.1
28.3 45.7
Par cent
Severity of AKI as RIFLE criteria
no. %
• Risk - 23 19.0
• Injury -15 12.4
• Failure - 8 6.6
AKI following Coronary Angiography
AKI following Contrast during elective CAG and percutanious intervention
• Study period = January 2010- December 2010
Total No CAG = 111
Mean age =51.9± 9.6 yrs
• Non-ionic radio contrast agent used
• AKI detected in 13 (11.7%)
Alam M,et al,2011
Risk factors for contrast induced AKI:
• Diabetes mellitus• Pre-existing renal insufficiency • HTN• ACE/ARB/NSAIDs
• LVEF-40%• Dose of Contrast:
What are the precaution needed before doing CAG:
• Evaluate the risk : Baseline Sr Cr ≥115μmol in men and ≥88.4μmol in female
• Risk out weigh potential benefits – use contrast
• Use low –osmolar or iso-osmolor contrast and volume as low as possible
• Volume status be optimized before administration of contrast
Summary and Conclusion
• AKI is a global problem and is common, harmful and a treatable condition
• Etiological factors are rapidly changing all over the world
• Early diagnosis and appropriate management can improve the overall prognosis of AKI