Acute Kidney Injury in Children: Azilah Sulaiman

Acute Kidney Injury in Children
Azilah Sulaiman
Case scenario..
2
Discussion
Introduction
Abrupt decrease in kidney function that include, but is not limited to acute renal
failure
Reversible increase in blood concentration of creatinine and nitrogenous waste
products & inability of kidney to regulate fluid and electrolyte homeostasis
appropriately
Broad clinical syndrome: encompasses various etiologies

Specific kidney diseases
Non-specific conditions e.g. ischemia, toxic injury
Extra-renal pathology
More than one etiologies may coexist at the same time
Epidemiological evidence supporting the notion that even mild, reversible AKI
has important clinical consequences including risk of death
4
1. Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney inter., Suppl. 2012; 2: 1138
2. Acute kidney injury in children, S. Phillips Andreoli, Pediatr Nephrol (2009) 24:253263
5
Acute kidney injury in children,S. Phillips Andreoli, Pediatr Nephrol (2009) 24:253263
Concerns: suboptimal care contributes to development of acute kidney injury
2009 NCEPOD reports the results of an enquiry into deaths of a large group of adult patients
with acute kidney injury that described systemic deficiencies in the care of patient who died of
AKI
ONLY 50% of these patient received GOOD care. Other deficiencies in the care of patient
who died of AKI included failure in AKI prevention, recognition, therapy and timely access
to specialist services
NICE develops its first guideline in AKI in adults, children and young people in 2013
AIMS:
Early intervention
Importance of risk assessment and prevention
Early recognition and treatment
6
Prevention, detection and management of acute kidney injury up to the point of renal replacement therapy; NICE clinical guideline 2013
Risk Assessment
Kidney usually able to withstand several insults without causing significant structural or
functional change
If present: indicate severe systemic derangement and predicts poor prognosis
Risk of AKI: by exposure to factors that cause AKI, by presence of factors that
increased susceptibility to AKI
Risk assessment:
Hospital acquired AKI
Community- acquired AKI
7
Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney inter., Suppl. 2012; 2: 1138
8
How to.
Prevent AKI:
Consider pediatric early warning score (PEWS) to identify children and young
people who are at risk of developing AKI
Best: PEWS with multiparameter or aggregate weighted scoring systems that measure
HR/RR/SBP/ GCS/ O2 saturation/ temperature/ capillary refill time
Measure urine output
To record weight twice daily to determine fluid balance
Measure renal profile lactate, blood glucose and blood gas
9
Detecting AKI:
Serum creatinine (sCr) still remains the cornerstone of clinical diagnosis of AKI
Criteria that may be used:
RIFLE
pRIFLE
the slow rate of rise in sCr might prohibit accurate classification of AKI. Consequently, the criteria emphasizes
estimated creatinine clearance (using the Schwartz formula) over fold increase in sCr
Application of pRIFLE definitions has, however, been inconsistent between studies and consequently associated
with differing risk between studies
AKIN
KDIGO
Adult and pediatric AKI definitions have been harmonized to emphasize fold change in sCr in adults and children
10
Acute kidney injury: an intensivists perspective, John R. Prowle, Pediatr Nephrol (2014) 29:1321
11
AKI in the ICU: definition, epidemiology, risk stratification, and outcomes,Kai Singbartl and John A Kellum, Kidney International 81, 819-825 (May (1) 2012)
12
KDIGO staging system for severity of AKI
Defines AKI as any of the following:

serum creatinine by 0.3mg.dL (
26mol.L) within 48Hrs
OR
serum creatinine to 1.5 times
baseline, which is known or presumed to
have occurred within prior 7 days
OR
Urine volume <0.5ml/kg/H for 6 Hrs
13
14
Management of AKI
Stage-based management of AKI
Stage predictor of the

risk of mortality and
decreased kidney
function
All actions listed provide
overall starting point for
stage-based evaluation
and management but
neither complete nor
mandatory for individual
patient
Shading of boxes indicate priorities of action

- Solid shading indicate actions that are equally appropriate at all stages
- Graded shading indicates increasing priority as intensity increases
16
Fluid Management
Fluid overload
Associated with increased morbidity and mortality in adult and children developing AKI
Degree of fluid overload has been suggested as an Index of AKI severity in pediatric
population
Associated with impaired recovery of renal function in patient surviving critical illness
Children have smaller window of appropriate treatment as they are more at risk of harm from
inadequate cardiac preload & more sensitive to adverse effects of fluid overload
17
18
Acute kidney injury: an intensivists perspective, John R. Prowle, Pediatr Nephrol (2014) 29:1321
Protocolized hemodynamic management
Suggested for use to prevent development or worsening of AKI in high risk patient in
perioperative settings or in patient with sepsis induced tissue hypoperfusion
(defined as hypotension persisting after initial fluid challenge or blood lactate >4mmolL)
Should be started as soon as hypoperfusion is recognized Early goal directed therapy

During 1st 6 hours of resuscitation to achieve specific physiologic end-points: GOALS of
initial resuscitation
1. CVP 8-12mmHg or 12-15mmHg in ventilated patients
2. MAP 65mmHg
3. Urine output 0.5ml/kg/hr
4. Superior vena cava oxygenation or mixed venous oxygen saturation 70% or 65% respectively
Suggest targeting resuscitation to normalize lactate in patients with elevated lactate level
Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2012 19
Diuretics and dopamine receptor agonist
Diuretics and renal dose dopamine commonly used to prevent or limit AKI
Diuretics:
Observational studies: 59-70% of patient with AKI were given diuretics at the time of
nephrology consultation or before the start of RRT
Stimulation of urine output eases management of AKI but conversion of oliguric to
non-oliguric AKI not proven to alter the course of renal failure
Retrospective study does actually demonstrated the use of diuretics in AKI was
associated with adverse outcome
High dose of frusemide can cause ototoxicity, continued use in individual patients
with AKI need to take into consideration the risk and potential benefits or lack of
benefits
Using diuretics is not recommended to prevent AKI or treat AKI except in the
management of fluid overload
21
Renal dose dopamine
0.5g/kg/min to 3-5g/kg/min
To improve renal perfusion following ischemic insult common in intensive
units
Action: increased renal blood flow by promoting vasodilatation
May improve urine output by promoting natriuresis
No definitive studies to demonstrate low dose dopamine are effective in
decreasing need for dialysis or improve survival times in patient with AKI
Some study showed that renal dose dopamine is not effective in therapy of
AKI and one study demonstrated that low doses worsened renal perfusion
and renal function
Lauschke A, Teichgraber UKM, Frei U, Eckardt KU (2006) Low-dose dopamine worsens renal perfusion in patients with acute renal failure. Kidney Int 69:16691674
22
General supportive management
Glycemic control
Tight glycemic control frequently used in patient at risk of AKI or developed AKI
Help reduce severity of AKI
Intensive Insulin Therapy (IIT glucose 4.44-6.11mmol/L) vs. Conventional Insulin therapy (CIT-
glucose 9.99-11.1mmol/L) in critically ill patient
Risk of hypoglycemia is higher in IIT (NICE-SUGAR trial in adult)
Work group suggestion: using insulin to prevent hyperglycemia

Aim glucose control between 6.11mmol/L to 8.33mmol/L
23
Nutritional aspect:
Protein-calorie malnutrition is an important independent predictor of in-hospital mortality in
patients with AKI
Must consider metabolic derangement and proinflammatory state associated with renal failure and
derangement of nutritional balance due to RRT
Suggest achieving total energy intake of 20-30kcal/kg/day in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Protein administration:
0.8-1.0g/kg/day in noncatabolic AKI
1.0-1.5g/kg/day in patient with AKI on dialysis
Up to maximum 1.7g/kg/day in patient on continuous renal replacement therapy (CRRT) and in
hypercatabolic patient
Suggest enteral feeding help maintain gut integrity, reduce gut atrophy & bacterial or endotoxin
translocation
24
Referring to Nephrologist:
Discuss the management of acute kidney injury with nephrologist as soon as possible
and within 24hours of detection when 1 of the following present:
1. When patients meet the criteria for renal replacement therapy

2. Possible diagnosis that may need specialist treatment (e.g. vasculitis,
glomerulonephritis, tubulointerstitial nephritis or myeloma)
3. Acute kidney injury with no clear cause
4. Inadequate response to treatment
5. Complications associated with AKI
6. Stage 3 AKI according to pRIFLE, AKIN or KDIGO criteria
7. Renal transplant patient
8. Chronic kidney disease stage 4 or 5
25
Timing
for
Renal
Replacement
Therapy
26
27
Discontinue RRT when it is no longer required, either because intrinsic kidney
function has recovered to the point that it is adequate to meet patient needs, or
because RRT is no longer consistent with the goals of care
28
Prognosis of AKI
Highly dependent on etiology of AKI
Those developing AKI as a part of multiorgan failure has higher mortality rate than
children with intrinsic cause of AKI e.g. HUS, or RPGN.
Recovery: depends on etiology
Nephrotoxic AKI and hypoxic/ischemic AKI usually recover normal renal function
Some still can have CKD
Children that suffer substantial loss of nephrons as in HUS/ RPGN at risk of renal failure
long after initial insult
Follow up:
1. Adult- 2-3years
2. Children and young people: longer follow up beyond puberty
3. Important complications for children hypertension, proteinuria, reduced renal
function
29
2. Prevention, detection and management of acute kidney injury up to the point of renal replacement therapy; NICE clinical guideline 2013
TAKE HOME MESSAGES:
30
REFERENCES:
1. Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical
Practice Guideline for Acute Kidney Injury. Kidney inter., Suppl. 2012; 2: 1138.
2. Acute kidney injury: an intensivists perspective, John R. Prowle, Pediatr Nephrol (2014) 29:1321
3. AKI in the ICU: definition, epidemiology, risk stratification, and outcomes, Kai Singbartl and John A Kellum,
Kidney International 81, 819-825 (May (1) 2012
4. Prevention, detection and management of acute kidney injury up to the point of renal replacement therapy;
NICE clinical guideline 2013
5. Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock:
2012

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Acute Kidney Injury in Children

Broad clinical syndrome: encompasses various etiologies

Importance of risk assessment and prevention

Early recognition and treatment

Measure urine output

To record weight twice daily to determine fluid balance

Measure renal profile lactate, blood glucose and blood gas

Defines AKI as any of the following:

Stage predictor of the

Shading of boxes indicate priorities of action

Should be started as soon as hypoperfusion is recognized Early goal directed therapy

Work group suggestion: using insulin to prevent hyperglycemia

1. When patients meet the criteria for renal replacement therapy

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