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ACUTE KIDNEY INJURY
• Dr. NARAYANA L.
• Asst. Prof Paediatrics
• ESIC Medical College, Hyderabad
Diagnostic Criteria For Acute Kidney Injury
• An abrupt (within 48 hours) reduction in kidney
function
– An absolute increase in serum creatinine of more than
or equal to 0.3 mg/dl
– A percentage increase in serum creatinine of more than
or equal to 50% (1.5-fold from baseline)
– A decreased urine output (less than 0.5 ml/kg/hr for 6
hours)
Pathophysiology of AKI
2012
AKI Epidemiology & Incidence
• AKI is quite common in critically ill children
• Incidence ranging from 1% to 82% of all ICU
or postoperative CPB admissions
• Cardiopulmonary bypass (CPB) to be
associated with a 20% to 40% AKI rate
• Nephrotoxic medications are a commonly
reported cause of AKI
• Effects of AKI are long lasting in survivors
But INDIA Differs -
• Incidence of AKI was 5.2 % in the pediatric
wards and 25.1 % in the PICU
• Etiologies being –
– Infections - 55.4 %
– Acute glomerulonephritis -16.9 %
– Cardiac disease - 4.8 %
– Envenomation's - 4.2 %
– Hemolytic uremic syndrome - 3.6 %
The Indian Journal of Pediatrics 2013
AKI & Associated Conditions
• Sepsis-Associated AKI
– Criteria for AKI
– Consensus criteria for sepsis
– Absence of other clear and established
non-sepsis related causes
• Incidence of pediatric sepsis-associated
AKI has ranged from 9% to 34%.
• Sepsis-associated AKI is also associated with
lower survival
• Pathogenic mechanisms of AKI in sepsis are
complex and multifactorial
• Combination of blood flow alterations and
cytokine-mediated injury
• “Peak Concentration Hypothesis”
• Deficiency of ADAMTS-13 is found in septic AKI
patient
• Associated with increased mortality
• Specific cytokine gene promoter
polymorphisms
– To predispose some patients with sepsis to
develop AKI
– To increase likelihood of mortality in sepsis-
Septic AKI contd..
AKI and Other Organ Involvement
• AKI manifests most commonly as single organ
failure
• AKI is a synergistic contributor to mortality with
multiple organ system failure
• Cardio-renal syndrome (CRS)
• Hepato-renal syndrome
AKI and Fluid Overload (FO)
• AKI contribute to FO
• FO itself may contribute to AKI
• Fluid balance is an independent risk factor for
mortality
• Early institution of renal replacement therapy is
associated with better outcome
When To Suspect Renal Failure?
• Non specific sign and symptoms suggestive of
uremia nausea, anorexia, drowsiness or
convulsions
• Oliguria or anemia especially in children with
predisposing illness such as diarrhea
• Hyperventilation due to acidosis , dehydration
• History of nephrotoxic drugs.
• Edema
• Hypertension
• Hematuria or proteinuria
• Sign of urinary obstruction such as poor stream,
dribbling and abdominal mass
Management Principles In Acute Renal
Failure
• Identify and correct pre-renal and post-renal factors
• Optimize cardiac output and renal blood flow
• Review drugs
• Accurately monitor fluid balance and daily body
weight
• Optimize nutritional support
• Identify and aggressively treat infection
• Initiate dialysis before uremic complications
Treatment Of AKI In Children
• Medical Therapies :
– Numerous medical approaches have been
attempted for prevention and treatment of
AKI.
– Prevention trials suggests –
• Detection of an early biomarker of injury
to allow for early and optimized directed
AKI Prevention Trials
• 2 settings most conducive
– Radio-contrast administration
– Cardio-Pulmonary Bypass
• Medications tested in this setting
– N-Acetyl cysteine (NAC)
– Fenoldopam
– Fluid administration
– Sodium bicarbonate
– Diuretics
– Low dose dopamine
– Theophylline
– Non-reliance of serum creatinine as the
marker of AKI
– Furosemide trials - no benefit in outcomes.
– “Renal dose” dopamine is ineffective
– Maintenance of appropriate arterial blood
pressure should be considered essential to
optimize renal perfusion
Treatment Trials
Metabolic Control
• Reduced mortality in surgical patients
with tight glycemic control
• Insulin’s anti-inflammatory and anti-
apoptotic effects
• Tight glycemic control a/w -
– Reduction in numbers of patients with
severe acute renal failure requiring dialysis
or CRRT
– Reduction in numbers of patients with
elevated creatinine
Renal Replacement Therapy
• Indications
– Renal failure
– Severe acidosis
– Hyperkalemia
– Other electrolyte abnormalities
– Toxin/poisonings
– Fluid overload >10% in the Critically ill
patient
Organogenesis 2011
Modalities
• Peritoneal dialysis (PD)
• Intermittent hemodialysis (IHD)
• Sustained low-efficiency dialysis (SLED)
• Extended daily dialysis (EDD)
• Continuous renal replacement therapy
(CRRT)
Organogenesis 2011
Continuous Renal Replacement
Therapy
• Preferred modality for severe AKI with FO
• Timing of CRRT initiation is still not clear
• CRRT v/s intermittent hemodialysis & peritoneal
dialysis
– Gradual & constant removal of solutes
– Independent adjustment of composition and volume
of extracellular fluid
– Minimum hemodynamic impact
Types of CRRT
• Slow continuous ultrafiltration (SCUF)
• Continuous veno-venous hemofiltration (CVVH)
• Continuous veno-venous hemodialysis
(CVVHD)
• Continuous veno-venous hemo-diafiltration
(CVVHDF)
Plasma Exchange in AKI and MOSF
• Beneficial in setting of –
Sepsis, thrombocytopenia & multi-organ
failure
• A more rapid reduction in organ dysfunction
scores
• Decreased mortality
Extracorporeal Life Support Organization
(ELSO) GUIDELINES
• Goal “To return the extracellular fluid volume to normal
(dry weight) and maintain it there.”
• Institution of diuretics once the patient is hemo-
dynamically stable
• “ If this is not sufficient to achieve negative fluid
balance or if the patient is in overt renal failure, then
continuous hemofiltration is added to the
extracorporeal circuit to maintain fluid and electrolyte
balance.”
Points To Remember
• Definition of AKI is evolving
• KDIGO guidelines to be followed at present
• Reliance on serum creatinine alone is not sufficient
• Gene probes & urinary biomarkers represents the
future tools
• Association of AKI with sepsis, multiple organ
involvement, FO carries heightened risk
• Further studies are needed to guide prevention and
treatment of AKI

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Acute Kidney Injury in children p[t.pptx

  • 1. ACUTE KIDNEY INJURY • Dr. NARAYANA L. • Asst. Prof Paediatrics • ESIC Medical College, Hyderabad
  • 2. Diagnostic Criteria For Acute Kidney Injury • An abrupt (within 48 hours) reduction in kidney function – An absolute increase in serum creatinine of more than or equal to 0.3 mg/dl – A percentage increase in serum creatinine of more than or equal to 50% (1.5-fold from baseline) – A decreased urine output (less than 0.5 ml/kg/hr for 6 hours)
  • 4.
  • 5.
  • 6.
  • 7.
  • 8.
  • 10.
  • 11. AKI Epidemiology & Incidence • AKI is quite common in critically ill children • Incidence ranging from 1% to 82% of all ICU or postoperative CPB admissions • Cardiopulmonary bypass (CPB) to be associated with a 20% to 40% AKI rate • Nephrotoxic medications are a commonly reported cause of AKI • Effects of AKI are long lasting in survivors
  • 12. But INDIA Differs - • Incidence of AKI was 5.2 % in the pediatric wards and 25.1 % in the PICU • Etiologies being – – Infections - 55.4 % – Acute glomerulonephritis -16.9 % – Cardiac disease - 4.8 % – Envenomation's - 4.2 % – Hemolytic uremic syndrome - 3.6 % The Indian Journal of Pediatrics 2013
  • 13. AKI & Associated Conditions • Sepsis-Associated AKI – Criteria for AKI – Consensus criteria for sepsis – Absence of other clear and established non-sepsis related causes • Incidence of pediatric sepsis-associated AKI has ranged from 9% to 34%.
  • 14. • Sepsis-associated AKI is also associated with lower survival • Pathogenic mechanisms of AKI in sepsis are complex and multifactorial • Combination of blood flow alterations and cytokine-mediated injury • “Peak Concentration Hypothesis”
  • 15.
  • 16. • Deficiency of ADAMTS-13 is found in septic AKI patient • Associated with increased mortality • Specific cytokine gene promoter polymorphisms – To predispose some patients with sepsis to develop AKI – To increase likelihood of mortality in sepsis- Septic AKI contd..
  • 17. AKI and Other Organ Involvement • AKI manifests most commonly as single organ failure • AKI is a synergistic contributor to mortality with multiple organ system failure • Cardio-renal syndrome (CRS) • Hepato-renal syndrome
  • 18. AKI and Fluid Overload (FO) • AKI contribute to FO • FO itself may contribute to AKI • Fluid balance is an independent risk factor for mortality • Early institution of renal replacement therapy is associated with better outcome
  • 19. When To Suspect Renal Failure? • Non specific sign and symptoms suggestive of uremia nausea, anorexia, drowsiness or convulsions • Oliguria or anemia especially in children with predisposing illness such as diarrhea • Hyperventilation due to acidosis , dehydration • History of nephrotoxic drugs. • Edema • Hypertension • Hematuria or proteinuria • Sign of urinary obstruction such as poor stream, dribbling and abdominal mass
  • 20. Management Principles In Acute Renal Failure • Identify and correct pre-renal and post-renal factors • Optimize cardiac output and renal blood flow • Review drugs • Accurately monitor fluid balance and daily body weight • Optimize nutritional support • Identify and aggressively treat infection • Initiate dialysis before uremic complications
  • 21. Treatment Of AKI In Children • Medical Therapies : – Numerous medical approaches have been attempted for prevention and treatment of AKI. – Prevention trials suggests – • Detection of an early biomarker of injury to allow for early and optimized directed
  • 22. AKI Prevention Trials • 2 settings most conducive – Radio-contrast administration – Cardio-Pulmonary Bypass • Medications tested in this setting – N-Acetyl cysteine (NAC) – Fenoldopam – Fluid administration – Sodium bicarbonate – Diuretics – Low dose dopamine – Theophylline
  • 23. – Non-reliance of serum creatinine as the marker of AKI – Furosemide trials - no benefit in outcomes. – “Renal dose” dopamine is ineffective – Maintenance of appropriate arterial blood pressure should be considered essential to optimize renal perfusion Treatment Trials
  • 24. Metabolic Control • Reduced mortality in surgical patients with tight glycemic control • Insulin’s anti-inflammatory and anti- apoptotic effects
  • 25. • Tight glycemic control a/w - – Reduction in numbers of patients with severe acute renal failure requiring dialysis or CRRT – Reduction in numbers of patients with elevated creatinine
  • 26. Renal Replacement Therapy • Indications – Renal failure – Severe acidosis – Hyperkalemia – Other electrolyte abnormalities – Toxin/poisonings – Fluid overload >10% in the Critically ill patient Organogenesis 2011
  • 27. Modalities • Peritoneal dialysis (PD) • Intermittent hemodialysis (IHD) • Sustained low-efficiency dialysis (SLED) • Extended daily dialysis (EDD) • Continuous renal replacement therapy (CRRT) Organogenesis 2011
  • 28. Continuous Renal Replacement Therapy • Preferred modality for severe AKI with FO • Timing of CRRT initiation is still not clear • CRRT v/s intermittent hemodialysis & peritoneal dialysis – Gradual & constant removal of solutes – Independent adjustment of composition and volume of extracellular fluid – Minimum hemodynamic impact
  • 29. Types of CRRT • Slow continuous ultrafiltration (SCUF) • Continuous veno-venous hemofiltration (CVVH) • Continuous veno-venous hemodialysis (CVVHD) • Continuous veno-venous hemo-diafiltration (CVVHDF)
  • 30. Plasma Exchange in AKI and MOSF • Beneficial in setting of – Sepsis, thrombocytopenia & multi-organ failure • A more rapid reduction in organ dysfunction scores • Decreased mortality
  • 31. Extracorporeal Life Support Organization (ELSO) GUIDELINES • Goal “To return the extracellular fluid volume to normal (dry weight) and maintain it there.” • Institution of diuretics once the patient is hemo- dynamically stable • “ If this is not sufficient to achieve negative fluid balance or if the patient is in overt renal failure, then continuous hemofiltration is added to the extracorporeal circuit to maintain fluid and electrolyte balance.”
  • 32. Points To Remember • Definition of AKI is evolving • KDIGO guidelines to be followed at present • Reliance on serum creatinine alone is not sufficient • Gene probes & urinary biomarkers represents the future tools • Association of AKI with sepsis, multiple organ involvement, FO carries heightened risk • Further studies are needed to guide prevention and treatment of AKI