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Depending on severity and duration of the renal dysfunction, this accumulation is accompanied by metabolic dysturbance, such as metabolic acidosis and hyperkalaemia, changes in body fluid balance, and effects on many other organ systems.
TABEL 2 : RIFLE criteria ADQI Bellomo et al, Curr Opin Crit Care 2002;6:505-8
Category GFR Criteria Risk Increased creatinin x1.5 or GFR decrease > 25% Increased creatinine x2 or GFR decrease > 50% Increase creatinine x3 or GFR decrease > 75%
Injury
Failure
High Specivity
Loss ESKD
Persistent ARF = complete loss of kidney function > 4 weeks End Stage Kidney Disease (> 3 months)
GFR=Glomerular Filtration Rate ARF; Acute Renal Failure UO = Urine Output ESKD; End Stage Kidney Disease References : Bellomo R, Kellum JA, Mehta R, Palevsky PM, Ronco C. Curr Opin Crit Care. 2002 Dec; 8(6):505-8.
EPIDEMIOLOGY
1% of hospitalized patients
20% of patients treated in ICU 4-15% of patients after cardiovascular surgery Cause of mortality 1. (75%) : Sepsis/multy organ dysfuntion syndrome 2. Cardiopulomonal( 50%)
Time / days
Prerenal
35 %
Renal
50 %
Postrenal
10 %
PRERENAL
Relative decrease in blood volume (ineffective arterial volume) Congestive heart failure Decompensated liver cirrhosis
Arterial occlusion or stenosis of renal artery
Haemodynamic form NSAIDs ACE-inhibitors or angiotensin-II receptor antagonists in renal-artery stenosis or congestive heart failure
Hypovolemia
Baroreceptor activation
Respons neurohormonal
Vasopressin
INTRINSIC RENAL
Glomerulonephritis
Ischaemic (50%)
Nephrotoxic (35%)
Endogenous Intratubular pigments (haemoglobinuria, myoglobinuria) Intratubular proteins (myeloma) Intratubular crystals (uric acid, oxalate)
POSTRENAL
RENAL ANAEMIA
Information Sought
Clues to the cause of acute renal failure Indicators of severity of metabolis disturbance Estimate of volume status (hydration) Markers of glomerular or tubulointerstitial inflammation, urinary tract infection or crystal uropathy To assess extent of GFR reduction and metabolic consequences To differentiate prerenal from established renal failure To determine presence of anemia, leucocytosis, and platelet consumption
Plasma biochemistry
Urine biochemistry
Findings that suggest prerenal causes Volume depletion Congestive heart failure Severe liver disease or other edematous state Findings that suggest postrenal causes Palpable bladder or hydronephrotic kidneys Enlarge prostat Abnormal pelvic examination Large residual bladder urine volume History of renal calculi (perform USG to screen obstruction) Findings that suggest intrinsic renal disease Hypotension, exposure to nephrotoxic drugs Recent radiographic procedure with contrast
Information Sought
To determine kidney size, presence of obstruction, abnormal renal parenchymal texture
WHEN ?
Reverse An-/Oliguria to Normouria -volume replacement -osmotic diuresis (mannitol 12.5-25 g in 30m) -forceed diuresis (furosemide 40-300mg/4-6h) -correct acidosis & hyperkalemia) -reverse hypercatabolism)
Increase metabolism
Avoid persistent Causative of decrease RF
Expert nursing care (management catheter care and skin in general; physicological support).
Initiate dialysis before uraemic complication emerge. Give drugs in doses appropriate for their clearance.
Characteristics
Asterixis, seizures, nausea & vomiting, pericarditis
Hyperkalemia
K+ >6.5 mmol/L; K+ 5.5-6.5 mmol/L if ECG changes Fluid overload resistant to diuretics, especially pulmonary edema
Fluid overload
Metabolic acidosis
pH < 7.2 despite sodium bicarbonate therapy; sodium bicarbonate not tolerated because of fluid overload
Proposed criteria for the initiation of renal replacement therapy in adult 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 enchepalopathy Uremic pericarditis Uremic neuropathy/myopathy Severe dysnatremia ([Na] > 160 or < 15 mmol/liter) Hyperthermia/Hypothermia Drug overdose with dialysable toxin
WHEN ?
The presence of : - one of the above criteria is sufficient to initiate renal replacement therapy in a critically ill patients - two of these criteria makes renal replacement urgent and mandatory. - combined derangements suggest initiation of renal replacement therapy even before the above mentioned limits have been reached.
CAVH
Willem KOLF 1943-1944 Dialysis in 15 pts (1 survived)l
KRAMER 1977
IHD
HD
Renal Replacement
Belding SCRIBNER 1960, begin chronic dialysis
HYBRID DIALYSIS
PD
SELLIGMENT & FINE 1945
APD
Adapted from Mehta RL. Supportive therapies; intermittent hemodialysis, continuous renal replacement therapies and peritoneal dialysis. In : Schrier RW, editor. Atlas of diseases of the kidney, Current Medicine, Philadelphia: Blackwell Science; 1998: with permission.
WHICH ?
# Proses difusi ( Perpindahan molekul melalui membran semi permeable Dengan cara difusi) # Dipengaruhi oleh : - berat molekul - perbedaan konsentrasi - Resistensi/ jenis membran # Proses Filtrasi (Perpindahan cairan dengan cara convective) # Dipengaruhi oleh : - Perbedaan tekanan (transmembrane) - Koefisien ultrafiltrasi
Dengan dialisis darah dibersihkan dengan proses difusi dan filtrasi Melalui membran semi-permeable dalam Ginjal Buatan Darah kotor masuk dialisat
Darah bersih
Proses difusi
GINJAL BUATAN
a. Modifikasi proses dialysis, dengan - Qb = 150 cc/menit - Qd = 300 cc/menit - tD = 6 12 jam / hari b. Dimulai Juli, 1998 di University of Arkansas, Amerika
c. Indikasi untuk ARF dengen hemodinamik tidak stabil d. Merupakan alternatif terapi dari CAVHD atau CVVHD e. Biasanya menggunakan Mesin Fresenius 4008, dengan ginjal BUKAN Cellulosa Acetate
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