Gagal Ginjal Akut

(GGA)

AKI
(ACUTE KIDNEY INJURY)

GANGGUAN GINJAL AKUT

(Gg GA)
 Pendahuluan

5 – 7% pasien rawat inap

Morbiditas ↑ mortalitas ↑ 20 – 70% (ICU)
Berkaitan dengan penyakit dasar,
pengobatan, prosedur diagnostik
Gagal ginjal akut  death risk ↑
Asimtomatik , reversibel
Kausa : prerenal, renal, postrenal
 GAGAL GINJAL AKUT
Batasan :
1. Konseptual
Penurunan laju filtrasi glomerulus (LFG),
dengan/tanpa oligouri pada ginjal yang
sebelumnya berfungsi normal.
2. Operasional
Kenaikan kreatinin darah :
a. Minimal 0,5 mg/dl bila awalnya < 3 mg/dl
b. Minimal 1 mg/dl bila awalnya > 3 mg/dl
setiap hari, pada minimal 2 X pemeriksaan
 Gagal Ginjal Akut
Definisi
Sindrom klinik akibat adanya gangguan fungsi
ginjal yang terjadi mendadak (beberapa jam –
minggu) yang menyebabkan retensi sisa
metabolisme nitrogen (Ur, Cr) dan non nitrogen,
dengan/ tanpa disertai oliguria
Berdasarkan pemeriksaan lab
– peningkatan mendadak kreatinin serum 0,5 mg% bila
kreatinin awal < 2,5 mg% atau
– peningkatan > 20% bila kreatinin awal > 2,5 mg%
Berat , outcome klinis  RIFLE
 Definition
Rapid (hours to weeks) decline in GFR and retention of
waste products
– “azotemia” (accumulation of nitrogenous wastes)
– elevated BUN and Creatinine levels
– decreased urine output (usually but not always)
Lack a uniform definition  Classic laboratory definition
– ↑ of creatinine of >0.5 mg/dl in <72hrs
– ↑ in more than 50% over baseline Cr.
– ↓ in calculated Cr Cl by more than 50%.
– Any ↓ in renal function that requires dialysis
– Cr > 1.5 x, urine output <0.5ml/kg/hr
– Cr ↑ ≥ 1.0 mg/dl/2d
 Definition
ADQI (the acute dialysis quality initiative)  RIFLE system
 classifies ARF into:
- 3 categories according to severity and
- 2 categories according to clinical outcomes
ARF also classified based on UO:
- anuric: < 100 mL/d
- oliguric: 100 – 399 mL/d
- nonoliguric: > 400 mL/d
Anuria usually reflects either complete urinary tract
obstruction or a vascular complicated by cortical necrosis
– RIFLE criteria/staging system
 Kriteria laju filtrasi glomerulus Kriteria jumlah urin

Risk Peningkatan kreatinin serum 1,5 kali <0,5 ml/kg/jam selama 6 jam

Injury Peningkatan kreatinin serum 2,0 kali <0,5 ml/kg/jam selama 12 jam

Failure Peningkatan kreatinin serum 3,0 kali <0,3 ml/kg/jam selama 24 jam
atau kreatinin ≥ 4 mg/dl atau atau anuria selama 12 jam
ada peningkatan akut ≥ 0,5mg/dl

Loss Gagal ginjal akut persisten,

hilangnya fungsi ginjal > 4 minggu

End Stage Gagal ginjal Terminal > 3 bulan

Renal Disease

Tabel 1 : klasifikasi RIFLE

 Perkiraan kadar normal kreatinin serum
berdasarkan kelompok usia dan ras
USIA LAKI-LAKI LAKI-LAKI WANITA WANITA
(tahun) (kulit hitam) (kulit putih) (kulit hitam) (kulit putih)
(mg/dl) (mg/dl) (mg/dl) (mg/dl)
20-24 1,5 1,3 1,2 1,0

25-29 1,5 1,2 1,1 1,0

30-39 1,4 1,2 1,1 0,9

40-54 1,3 1,1 1,0 0,8

55-65 1,3 1,1 1,0 0,8

> 65 1,2 1,0 0,9 0,8

 Perkiraan kadar normal kreatinin serum
(mg/dl) disesuaikan dengan kriteria RIFLE
Kadar 0.5 1.0 1.5 2.0 2.5 3.0
Awal (mg/dl) (mg/dl) (mg/dl) (mg/dl) (mg/dl) (mg/dl)

Risk 0,75 1,5 2,25 3,0 3,75 -

Injury 1,0 2,0 3,0 - - -

Failure 1,5 3,0 4,0 4,0 4,0 4,0

Kriteria RIFLE berdasarkan urine output (UO)
dan berat badan penderita (Roesli,2007)
Kriteria Berat badan pasien (kg)
RIFLE
40 50 60 70
RIFLE – R UO= < 120 cc UO= < 150 cc UO= < 180 cc UO= < 210 cc
(dalam 6 jam) (dalam 6 jam) (dalam 6 jam) (dalam 6 jam)

RIFLE - I UO= < 240 cc UO= < 300 cc UO= < 360 cc UO= < 420 cc
(dalam 12 jam) (dalam 12 jam) (dalam 12 jam) (dalam 12 jam)

RIFLE - F UO= < 288 cc UO= < 360 cc UO= < 432 cc UO= < 504 cc
(dalam 24 jam) (dalam 24 jam) (dalam 24 jam) (dalam 24 jam)
ANURI ANURI ANURI ANURI
(dalam 12 jam) (dalam 12 jam) (dalam 12 jam) (dalam 12 jam)
Acute Kidney Injury Network (AKIN- 2005)
Continuum of the renal injury

STAGE I STAGE II
STAGE III
STAGE IV STAGE V
LOSS ESRD
INJURY FAILURE
(L) (E)
RISK (I) (F)
(R)

Severity Outcome
 Pengaturan fungsi ginjal

Anatomical Mekanisme
Sirkulasi Intrarenal utk
Outflow ginjal
pathway Pembentukan
urin

Acute
Renal
failure
Fungsi ginjal
 Etiologi
Prerenal
Penurunan perfusi ginjal
– Deplesi volume intravaskuler
– Cardiac output ↓
– Vasokonstriksi/obst p.d renal
– Agen farmakologis gg autoregulasi
LFG
 Etiologi
Renal
Gangguan struktur nefron
– Gg pembuluh drh ginjal
– Peny. glomerulus dan mikrovaskular ginjal
– Peny. tubulus krn iskemia , toksin
endogen/exogen, obst
– Peny. tubulointerstitial akut
 Etiologi
Postrenal
 Obstruksi saluran kemih ( ‘urinary
collection system’ ) krn intrinsik /
ekstrinsik
– Obstruksi ureter bilateral
– Obstruksi bladder neck, urethra
 Patogenesis
Prerenal
Hipovolemia  autoregulasi : vasodilatasi
aferen konstriksi eferen  lama, berat
gg autoregulasi : konstriksi aferen
(hipovolemia  baroreseptor  RAA ,
simpatis, vasopresin release)
 Patogenesis
Renal
Hipoperfusi lama,memberat; obat/bhn
nefrotoksik  nekrosis: NTA

Postrenal
Obstruksi  awal: aliran drh↑ tek pelvis ginjal ↑
 1,5-2 jam: aliran drh ginjal↓  kronis: aliran
drh ↓↓ tek pelvis mjd normal  mediator
inflamasi, growth factor  fibrosis interstitial
 Diagnosis
Anamnesis
Pemeriksaan fisik
Laboratorium : serum kreatinin, vol. urin,
urinalisis, biomarker, DPL, kreatin
fosfokinase, hemostasis, FeNa , kimia urin
Pemeriksaan penunjang lain : USG , CT
abdomen, RPG , sistoskopi
Biopsi  pd dugaan kausa nefritik,SN,
unexplain
 Prerenal Renal

Sedimen urin Silinder hyalin Silinder granular

Na urin (mmol/L)* <20 >40
FeNa(%)* <1 >2
Rasio kreatinin urin:plasma* >40 <20
Ekskresi fraksional urea <35 >35
Osmolalitas urin >500 <250

ESTABLISHED

Rasio osmolalitas urin : plasma >1,5 < 1,1

Rasio ureum:kreatinin plasma >80 < 80
 Urinalysis
Urinalysis Pre-renal Intrinsic Postrenal

Sediment -- Casts, cellular Cellular debris

debris
WBC -- 2-4+ 1+
RBC -- 2-4+ Variable
Urine/Serum >1.5 <1.3 <1.5
Osmolality
Urine Na (mEq/L) <20 >40 >40
Fe Na (%) <1 >1-2 Variable
BUN/Scr >20 15 15
Ucr/Scr >40 <20 <20
 Tatalaksana
Pencegahan dan terapi non-dialisis
Perhatikan status volume , curah jantung , obat
nefrotoksik / yg mengganggu autoregulasi
Hidrasi  post op.,kontras, kemotherapi
Manitol, furosemide, low-dose dopamin pd
pencegahan & pemulihan NTA hsl tdk konsisten
Loop diuretic death risk↑, delay recovery
Low-dose dopamintdk ↓ mortalitas, tdk
↑recovery
Asetilsistein + hidrasi ↓ nefropati kontras
 Tatalaksana
Terapi suportif
mencegah/mengatasi komplikasi
prioritas :
Mencari,memperbaiki faktor pre dan
postrenal
Stop obat nefrotoksik
Optimalisasi curah jantung dan RBF
Perbaiki urine outflow
Monitoring balans cairan
 Tatalaksana
Mencari, mengatasi komplikasi akut
Nutrisi, asuhan keperawatan, dukungan
psikologis
Atasi infeksi
Inisiasi dialisis sebelum muncul komplikasi
uremik
Adjusting dose
 Tatalaksana
Hiperkalemia  biknat, insulin + glukosa
Asidosis  biknat
Nutrisi Na 2 gr/hr , karbohidrat > 100
gr/hr , protein 40 gr/hr , kontrol GD
 Tatalaksana
Terapi pengganti ginjal
Tujuan: mempertahankan hidup pasien
sampai terjadi perbaikan spontan fungsi
ginjal
Dimulai sebelum timbul komplikasi
(oliguria : ureum >100 mg%, kreatinin >
8 mg% , perbaikan klinik/biokimia (-))
 Tatalaksana
Indikasi terapi pengganti ginjal:
Oliguria (urin < 200cc/12 jam), anuria (urin <
50cc/12 jam)
Hiperkalemia (K>6,5 mmol/jam)
Asidemia berat (pH<7,0),asidosis metabolik
refrakter
Ensefalopati, perikarditis uremik
Na<120 mmol/L atau > 155 mmol/L
Overload
Overdosis obat yg dpt didialisis
 Tatalaksana
Pilihan modalitas : intermiten HD , CRRT
(e.c CVVH)  optimal : no EBM
Keuntungan vs kerugian , kondisi khusus
Dialisis harian lebih baik kontrol uremia,
resolusi cepat gagal ginjal, risiko
hipotensi <
Dialysis
 Dialysis

20% - 60% of ARF

Types:
– HD
– PD
– RRT
 RRT

Intermittent hemodialysis (IHD)

Continuous veno-venous hemofiltration
(CVVH)
CVV hemodialysis (CVVHD)
CVV hemodiafiltration (CVVHDF)
Slow low efficiency dialysis (SLED)
Peritoneal dialysis (PD)
Slow continuous ultrafiltration (SCUF)
Indications for RRT in critically ill ARF patients

Renal Replacement Renal Support

Life-threatening indications Nutrition

Hyperkalemia Fluid removal in CHF
Acidemia Cytokine manipulation in sepsis
Pulmonary edema Cancer chemotherapy
Uremic complications Treatment of respiratory acidosis
Solute control of ARDS
Fluid removal Fluid management in multiorgan
Regulation of acid-base and failure
electrolyte status
Proposed Criteria for the Initiation of RRT in
Critically ill Patients

Oliguria (urine output<200 ml/12 hr)

Anuria/extreme oliguria (urine output<50 ml/12 hr)
Hyperkalemia ([K+]>6.5 mmol/liter)
Severe acidemia (pH<7.1)
Azotemia ([urea]>30 mmol/liter)
Clinically significant organ (especially lung) edema
Uremic encephalopathy
Uremic pericarditis
Uremic neuropathy/myopathy
Severe dysnatremia ([Na]>160 or<115 mmol/liter)
Hyperthermia
Drug overdose with dialyzable toxin
( KI 1998, R. Belloma and C. Ronco)
CRRT

Blood filtered continuously by semi-permeable

membrane
AV: uses patient’s own BP
VV: pump-driven
Lower extracorporeal blood volume (compared to
HD) so better tolerated by hemodynamically
unstable patients
Types: hemofiltration (AVH, CAVH, SCUF),
continuous hemodialysis (CAVHD, CVVHD) and
continuous hemodiafiltration (CAVHDF or CVVHDF)
IHD in ARF and critically ill patients
 IHD vs. CRRT
Randomized trial, observational studies unclear
and limited because of patient populations and
significant cross-over to CRRT.
Meta-analysis unclear because of limitation of
original studies.
LEVEL 2B SUGGESTION of no difference
between the use of IHD vs. CRRT as therapy for
ARF (unclear)
 Simpulan
Gagal ginjal akut  Ganguan ginjal akut
(GgGA) ► kriteria RIFLE
Kausa : prerenal, renal, postrenal  sering
multipel
Diagnosis : anamnesa, pemeriksaan fisik,
pemeriksaan penunjang, biopsi
Tatalaksana : pencegahan, suportif, renal
replacement therapy