PATHOGENESIS AND MANAGEMENT SEPSIS - AKI

FAJAR YUWANTO
RSUD ABDUL MOELOEK
BANDAR LAMPUNG
Acute kidney injury is the new consensus term for acute renal failure.
It refers to a clinical syndrome characterised by :
a rapid (hours to days) decrease in renal excretory function
the accumulation of products of nitrogen metabolism such as creatinine and urea
Other common clinical and laboratory manifestations include decreased urine output
(not always present), accumulation of metabolic acids, and increased potassium
and phosphat

(Bellomo R,2012)
Acute kidney injury is a common and important diagnostic and therapeutic challenge for
clinicians.

Incidence varies :
More than 5000 cases per million people per year for non-dialysis-requiring.
295 cases per million people per year for dialysis-requiring disease.
The disorder has a frequency of 1·9% in hospital inpatients
Especially common in critically ill patients :
AKI is greater than 40% at admission to the intensive-care unit if sepsis is present.
more than 36% on the day after admission to an intensive-care unit,
and prevalence is greater than 60% during intensive care unit admission
HUBUNGAN AKI DENGAN CKD

(KDIGO 2014)
STAGING AKI : RIFLE

GFR Criteria * Urine Output Criteria

Risk Increased Screat x 1.5 or
GFR decrease > 25% UO < 5 ml/kg/h x 6 hr

High Sensitivity
Injury Increased Screat x 2or
GFR decrease > 50% UO < 5 ml/kg/h x 12 hr

UO < 5 ml/kg/h x 24 hr
Increased Screat x 3or
Failure GFR decrease > 75%
or Anuria x 12 hrs

High Specificity
Persistent ARF = Complete loss
Loss Of Kidney Function > 4 weeks

End Stage Kidney Disease

ESKD ( > 3 moths )
ETIOLOGI AKI :
Biomarker AKI Early detection
Plasma Neutrophil gelatinase-
associated lipocalin (NGAL)
Cystatin C
Urine panel NGAL
Interleukin 18 (IL-18)
Kidney injury molecule 1 (KIM-1)

(Majumdar , 2010)
 SEPSIS AKI
(SEPSIS-INDUCED ACUTE KIDNEY INJURY)
Acute kidney injury (AKI) occurs in :
19% patients with moderate sepsis
23% with severe sepsis
51% with septic shock
The beginning and ending supportive therapy (BEST) kidney
investigators highlighted the fact that sepsis is the most common
cause of AKI in critically ill patients (47.5%), after evaluating a varied
population, in 54 hospitals spread over 23 countries.
 SEPTIC AKI VS NON-SEPTIC AKI

Septic AKI was associated with :

 Greater derangement in hemodynamic and laboratory parameters
 Greater severity of illness and higher need for mechanical ventilation and
 Vasopressor therapy.
 Oliguria was found to be more common in septic AKI (67 vs. 57%; P < 0.001).
 Septic AKI had a higher in-hospital mortality rate, compared with nonseptic
AKI (70.2 vs. 51.8%; p < 0.001).
 Median duration of ICU and hospital stay for survivors (37 vs. 21d; P < 0.0001), was
longer for septic AKI.
Moreover, new evidence indicates that the biomarkers may even be able
to differentiate septic from non-septic AKI. In a study of 83 patients (43
with sepsis) in Melbourne, septic.
AKI was associated with significantly higher plasma (293 vs. 166 μg/ml)
and urine (204 vs. 39 μg/mg creatinine) NGAL compared with non-
septic AKI (P < 0.001).[11]

(Majumdaar,2010)
Key pathogenic pathways involved in the clinical course of sepsis
that also have implications in the pathophysiology of sepsis-induced acute kidney injury.

(Zarjou,2011)
(Doi, 2016)
(Allobaidi,2015)
 AKI Stage

High Risk 1 2 3
Discontinue all nephrotoxic agents when posible
Ensure volume status and perfusion pressure
Consider functional hemodynamic monitoring
Monitor Serum creatinine and urine output
Avoid hyperglycemia
Consider alternatives to radiocontrast procedures
Non-invasive diagnostic workup
Consider Invasive diagnostic workup
Check for changes in drugs dosing
Consider Renal Replacement Therapy
Consider ICU admission
Avoid subclavian catheters if possible

(KDIGO 2012)
PREVENTION AND MANAGEMENT
1. Antibiotic for Sepsis
2. Fluid managemen and vasopressor :
- Rehidration.
- Isotonic fluid managemen .
- Colloid Hydroxyethylstarch (HES )  worsening renal function.
- Vasopressor if neseccary.
2. Nutrisi dan Glycemic control
- Total Energi intake : 20 – 30 kcal/kg/day
- Protein : 0,8 – 1,0 g/kg/day AKI non dialysis.
1,0- 1,5 g/kg/day AKI dialysis.
> 1,5 – 1,7 g/kg/day : CRRT.
-Glucose target 110- 149 mg/dl.
3. Diuretik.
- Not recommended. Indication : overhidrasi.
4. Avoid Nefrotoxic agent.
Renal
Replacement
Terapi ( Dialysis )

When ?
Which?
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