ACUTE KIDNEY INJURY IN

CRITICALLY ILL PATIENTS

ARIEF MUNANDAR
INTENSIVIST
 BACKGROUND
• Acute kidney injury (AKI) is a common complication
among patients with critical illness in hospital.
• The incidence of AKI is now believed to be
significantly higher than previously believed with
over 50% of patients in criticall illness developing
AKI.
• Mortality among critical illnes patients with AKI and
multi organ failure has been reported to be more
than 50%.

Mohsenin Journal of Intensive Care (2017) 5:57

BACKGROUND....
• AKI is characterized by a sudden decrease in kidney
function over a periode hours to days, resulting in
accumulation of creatinin,urea, and other waste products.
• According to the 2012 Kidney Disease improvng Global
Outcome (KDIGO) consensus guidlines,AKI is defined by
an increase in the serum creatinine level 0,3 mg/dl (2,5
mikromol/L) or more within 48 h;a serum creatinine level
that has increased by at least 1,5 times the baseline value
within the previous 7 days;or urine volume of less than
0,5 ml/kgbw per hour for 6 h.
BACKGROUND....
• AKI is not a single disease but rather a
syndrome comprising multiple clinical
conditions.
• Outcomes from AKI depend on the underlying
disease, the severity and duration of renal
impairment, and the patients renal baseline
condition.

Kidney International (2012) 81,819-825.

BACKGROUND....
• Increasing serum creatinin level 0,3 from the
baseline will increase mortality rate by 4th
fold,induce mechanical ventilation
chance,and increasing LOS.
• The timing of RRT associated with the
evolution of AKI.
BACKGROUND....
• The development of AKI is the consequence
of complex interactions between the actual
insult and subsequent activation of
inflammation and coagulation.
• Loss of renal function can occur without
histological signs of tubular damage or even
necrosis.
BACKGROUND....
• The detrimental effects of AKI are not limited
to classical well-known symptoms such as
fluid overload and electrolyte abnormalities.
• AKI can also lead to problem that are not
readily appresiated at the bedside and can
extend well beyond the ICU stay, including
progression of CKD and impaired innate
immunity.→ HIGHER INFECTION RATES
BACKGROUND....
• Although some manifestations of AKI are
directly linked to impaired glomerular/tubular
function and easily recognized at the bedside
in the form of hyperkalemia,pulmonary
oedema, pericarditis, or encephalopathy,other
effects are less obvious or might not become
apparent until sometime after the patient
has left the hospital.
BACKGROUND....
• Surgery remains a leading cause of AKI in
hospitalized patients (the incidence ranges from
18% to 47%).
• The postoperative period study,mortality
ranges from 1% to 30%,and approaching to 80%
if RRT is required.
• In the ICU setting,investigator confirmed major
surgery as the second leading cause of AKI (in
34%),with overall hospital mortality of 60,3%.
BACKGROUND....
• AKI during a hospital admission and despite
significan developments in hospital care with
mortality associated with AKI remains high.
• Deficits in the recognition and subsequent
management of patients who have developed
AKI have been shown clearly especially in
rural hospital.
• A significan proportion of AKI develope in
hospital (hospital-acquired AKI, HA-AKI) and
systematically highlighting patients at the
highest risk of HA-AKI is of great
interest,because HA-AKI still be NEGLECTED.

BMJ Open 2017:7

 CAUSES OF AKI
• The pathogenesis of AKI is complex due to
multiple etiologies and risk factors.
• Risk factors include increasing age,presence of
heart failure (CRS),liver failure
(HRS),CKD,anemia,nephrotoxic agents
(antibiotic,NSAIDS,radiocontras),DM.
• Infection,shock,sepsis,DM,need for mechanical
ventilation,and surgery are well recognized as
high-risk setting for the development of AKI.
CAUSES OF....
• Etiologically,AKI is divided into pre-renal,
renal, and post-renal causes.
• Renal hypoperfusion is often the initial insult
in AKI especially in perioperative, which
importantly can lead to a reduction in
medullary blood flow.
• Pre-renal AKI including sepsis accounts for 60-
70% of all AKI cases in critically ill patients.
MANAGEMENT AND PREVENTION OF AKI

• The main management of AKI is preventing

insult episodes which could be trigerring
hypovolemia,hypotension and hypoperfusion.
• Primary prevention of AKI,including
identification of patients at risk;proper
management of acute illness;measure to
improve renal perfusion (MAP treshold 65-70
mmhg);awareness with nephrotoxic drugs.

Med Intensiva.2017;41(2):116-126
MANAGEMENT AND....
• Secondary prevention, the early detection of
the deteriorating of the disease is the most
important secondary prevention.
• The monitoring of diuresis,electrolyte,and
creatinin is recomended for identification of the
initial stages of AKI, in 48 h.
• Once an AKI diagnosis has been established,the
patient should be reassessed from an angle
more focused on renal function.
 RECOMMENDED TO BE TAKEN IN AKI
• Volume expansion to optimize systolic volume
and blood pressure in the case of shock,to
normalized the preload.
• Early onset of amines may have to improve BP
in combination with volume expansion.The
amine of choice is norepinephrine.
• Daily monitoring of water balance and measure
rapid creatinin clearence ( 2 or 4 h),as well as
general monitoring of every critical patient.
RECOMMENDED TO....
• Daily monitoring of AKI-related complications
such as hyperpotasemia,hypocalsemia and
hyperphosphatemia.
• Consistently high uremia values can produce
changes in platelet aggregation and increase
the bledding complications,that can partially
improve with the administration of
desmopresin.
RECOMMENDED TO....
• Discontinuation of nephrotoxic drugs,or dose
adjustment.
• Avoiding the use of Furosemide as it can worsen the
evolution of AKI,hinder the dayli assesment of renal
function and delay the start of dialytic techniques.
• Avoiding low dose of dopamine,it does not improve
the evolution of AKI,and it can worsen renal blood
flow and produce a higher frequency of SVT.
• Providing adequate nutrition.
 CONCLUSION
• AKI is prevalent in critically ill patients.
• The most cammon etiologies of AKI are due to fluid
volume deficit,or kidney hypoperfusion and ATN due to
shock,inflammatory state,nephrotoxic drugs and surgery.
• Early recognition of pathophysiology of AKI by careful
review of patients history and hospital course and
intravascular volume assesment,daily monitoring of fluid
balance,serum creatinin,elektrolyte,albumin,hb,urine
analysis should guide management strategy in order to
reduce further progression of AKI and mortality.
THANK YOU
 CASE ILLUSTRATION
• Pasen Tn.X 66TH,MRS UGD tgl 9-12-2021 pkl
10.10.
• Keluhan utama : lemas 2 hari
terakhir,mual/muntah tidak ada,bak dan bab
normal,nafsu makan turun.
• Px : TD 100/60,Nadi 102x/mnt,rr 20x,spor
99%.Kesadaran CM,GCS 15
• LAB : HB 13,9,AL 7,8, AT 70 RB, GDS 346
• TGL 10-12-2021, LAB : HB 13,6,AL 9,7,AT
50RB,Na 128,K 4,0,CL 99,1,gelisah.Dx
encephalitis,dm.
• TGL 13-12-2021,pasen penurunan
kesadaran,tensi turun,rr naik,spo2 turun.
• Pasen masuk icu,px gcs E2V2M3,TD 70/40,N
120,T 39,UO TURUN,hasil lab hb 10,8,al 30
rb,AT 70 RB,Ureum 201,Creatinin 4,67,gds
457,alb 2,8.