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Bagian Ilmu Penyakit DalamFKU UNISBA

Acute Kidney Injury(AKI)


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Epidemiology of AKI: A Common,

Serious Problem

AKI is present in 5% of all hospitalizedpatients, and up to 50% of patients in ICUs

The incidence is increasing -globally

Mortality rate 50 - 80% in dialyzed ICUpatients 4 Million die each year of AKI

AKI requiring dialysis is one of the mostimportant independent predictors of death

in ICU patients 25% of ICU dialysis survivors progress to

ESRD within 3 years


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Epidemiology AKI

5% of hospital patients

Up to 30% of ICU admissions

Isolated AKI requiring renal replacement

therapy; survival = 90%AKI with multi-organ failure; survival =

10%


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Definition of AKI

(functional derangement)

Sudden and severe decrease in the

glomerular filtration rate

Increase in plasma BUN and Creat Retention of salt and water

Development of acidosis and

hyperkalemia

N Engl Med 1998;338:671- 675


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The need for Defining ARF

Acute renal occurs in 5-20% of critically ill

patients with a mortality of 28-90%

Conclusion :

- We have no idea what ARF is!

At least 30 definitions of ARF are in use


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Issues in Design of Clinical

Trials in ARF

Heterogeneity of patient population

Effect of co-morbidty and illness on outcome Large variations in clinical practice

Lack of a standarddized definition of ARF

Metha et al, J Am Soc Nephrol 2002


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AKI: Common Causes

Ischemia (60%): cardiovascular disease,

cardiac surgery, abdominal surgery, shock,

sepsis

Nephrotoxins(30%): antibiotics, contrast,chemotherapy, anti-rejection, NSAIDs

These causes also frequently lead to

sub-clinical renal injury,a vastly

underestimated problem


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Diagnosis of AKI is Often

Delayed

Elevation in serum creatinine is the current gold

standard, but this is problematic

Normal serum creatinine varies widely with age,gender, diet, muscle mass, muscle metabolism,

medications, hydration status

In AKI, serum creatinine can take several days

to reach a new steady state


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Kr iter ia Kenaikan kreatinin

ser um & penurunanLFG

Penurunan produksi urin

(Ur in Output=UO)

Risk Kenaikan kreatinin 1.5

kali atau penurunan LFG

> 25%

UO < 0.5 ml/kg/jam

selama 6 jam Sensitivitas

Tinggi

Injury Kenaikan kreatinin 2 kali

atau penurunan LFG >50%

UO < 0.5 ml/kg/jam

selama 12 jam

Failure Kenaikan kreatinin 3 kali

atau penurunan LFG >75% / kreatinin 4 mg/dl

(peningkatan akut 0.5

mg/dl)

UO < 0.3 ml/kg/jam selama 24

jam atau anuria selama 12 jam

Loss GGA menetap = penurunan fungsi ginjal lebih dari 4

minggu

Spesifitas

tinggi

ESRD Gagal ginjal terminal (> 3 bulan)= ESRD

RIFLE criteria for AKI

Lamaire et al, The Lancet 2005, 365: 417-430


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Definition of Acute

oliguria Definition: < 400 ml of urine / day

Often the earliest sign of renaldysfunction

Crucial to identify reversible causesearly associated with high morbidityand mortality and the therapeuticwindow is narrow

N Engl Med 1998; 338:671-675


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Oliguria

Urine < 500 ml day-1 or< 20 ml h-1

In > 80% of cases caused by

hypovolaemia and:

nephrotoxic drugs

hypertensiondiabetes mellitus


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Causes of AKI

Pre-renal (35-40%)

Intrarenal (55-60%)

ATN accounts for 85% interstitial nephritis

glomerulonephritis

renal vascular disease Post-renal (2-5%)

Singri N. JAMA 2003;289:747-51


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Causes of AKI

Three categories

Pre renal

Renal (intrinsic)

Post renal (obstructive uropathy)

Prompt identification and treatment of

pre renal and post renal causes may

prevent the development of protractedAKI

N Engl Med 1998;338:671- 675


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Pre renal failure

Hypovolemia

Hemorrhage, GI fluid loss (diarrhea,

vomiting, NG suction), 3rd spacing

(pancreatitis, bowel disease), renal loses(diuretics, glycosuria), trauma, surgery,

burns

Relative hypovolemia (effective volume)

Sepsis, hepatic failure, anaphylaxis,

vasodilator drugs, nephrotic syndrome,

anesthetic agentsN Engl Med 1998;338:671- 675


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Pre renal failure

Myocardial failure

Myocardial infarction, pulmonary embolism,

congestive heart failure, tamponade,

mechanical ventilation Disruption of renal autoregulation

Angiotensin-converting-enzyme

Renal artery or vein occlusion Thrombosis, thromboembolism, severe

stenosis, dissecting aneurysm

N Engl Med 1998;338:671- 675


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Intrinsic Renal Failure

Small vessel vasculitis or acute

glomerulonephritis

Connective tissue disease (SLE,

scleroderma) Malignant hypertension

Toxemia of pregnancy

Microscopic polyarteritis Poststreptococcal glomerulonephritis

Rapidly progressive glomerulonephritis

N Engl Med 1998;338:671- 675


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Interstitial nephritis

Drugs (e.g methicillin)

infection

Cancer (lymphoma, leukemia, sarcoidosis)

N Engl Med 1998;338:671- 675


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Acute tubular necrosis

Ischemia (secondary to pre renal events)

Nephrotoxic antibiotics (gentamicin,

kanamycin) Heavy metals (mercury, cisplatin)

Solvents (carbon tetrachloride, ethylene,glycol)

Radiographic contrast agents Intratubular crystals (uric acid or oxalate)

Intratubular pigments (myoglobinuria)


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Post renal Failure

Upper urinary tract obstruction

Ureteral obstruction of one or both kidneys

Lower urinary tract obstruction

Bladder outlet obstruction (more common)

N Engl Med 1998;338:671- 675


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Thadhani, R. et al. N Engl J Med 1996;334:1448-1460

Main Categories of Acute Renal Failure


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Acute Tubular Necrosis

Renal hypoperfusion +/- nephrotoxins

Leucocyte adhesion to vascular endothelial

cells Tubular cell damage

necrosis

apoptosis

sublethal injury -disruption of cell adhesion

ATN not a good term


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Tubular epithelial cell

damage

Little obvious histological damage in ARFfocal only

Straight (S3) segment of proximal tubule ismost commonly injured (not TAL)

Sublethal injury disrupts epithelial adhesionloss of barrier function and shedding of cells

into lumen


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Abuelo JG. NEJM 2007;357:797-805


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Acute Kidney Injurypotential life threatening

complications Hyperkalemia

Muscle weakness and paralysis

ECG changes

Metabolic acidosis

Kussmauls respiration, hypotension,

hyperreflexia Salt and water retention

Pulmonary edema, ascites, pleural effusion

N Engl Med 1998;338:671- 675


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Complications of acute

oliguria

Cardiovascular

Congestive heart failure, pulmonary

oedema, hypertension (25%), arrhytmia,

pericarditis Infections

Occur in 30 70% of patients

A leading cause of morbidity and mortality

N Engl Med 1994;331:1416 20


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Complications of acute

oliguria

Neurological

Confusion, somnolence, seizures

Gastrointestinal

Anorexia, nausea, vomiting, ileus

Gastrointestinal bleed in 10 30% of

patients

Anemia (decreased erythropoiesis, GI bleedand frequent blood sample)

N Engl Med 1994;331:1416 20


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Management of AKI

DO search for a cause

DO NOT give furosemide or dopamine

unless definite fluid overload


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Diagnostic evaluation

History

Examination

Urine

Blood tests

Radiological investigations

Renal biopsy


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Identifying the cause of

oliguria

Pre renal (common)

Has the patient got an aduquate

BP and cardiac output?

Renal (less common) Have we poisoned the kidney?

Is there a primary renal cause?

Post renal (common)

Is there obstruction to the urine

flow?


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Post renal - ultrasound

Renal pelvis calculi, tumours, blood clot

Ureter stones, accidental ligation

Bladder prostatic enlargement, bladder

tumour

Urethra - stricture


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Rules for the management of oliguria

(1)

Maximize treatment before referral to

ICU

Close observation of vital signs

Regular serum U&E

Dont let out of less than 0.5 mls/kg/hour

continue for more than 2 hours


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Rules for the management of oliguria

(2)

Exclude obstruction to urine outflow

(particularly if absolute anuria)

Bladder washout to exclude blocked

catheter Renal ultrasound scan

Fluid resuscitation

Consider central line If appropriate Close monitoring of vital signs


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Vital signs assessment

(observations)

Monitor vital signs appropriately

RR, oxygen requirement, and chest

auscultation during fluid resuscitation

Use CVP line for trend information

Parameter for review

Use Early Warning Score

Monitor urea and electrolytes


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Prerenal

Hypovolaemia (haemorrhage, sepsis, GIloss, burns)

Hypotension (hypovolaemia, cardiac

failure, vasodilatation) Functional acute renal failure (NSAIDs,

hepatorenal syndrome)

Abdominal compartment syndrome


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Factors increasing susceptibility

to renal hypoperfusion

Failure to decrease afferentarteriolar resistance

Structural changes

Old age Hypertension

Reduced PGs NSAIDs & COX-2 inhibitors

Afferent arteriolar

constriction Sepsis

Hepatorenal syndrome

Radiocontrast agents

Failure to increaseefferent arteriolarresistance

ACE-inhibitors Angiotensin-receptor

blockers

Renal artery stenosis

Abuelo JG. NEJM 2007;357:797-805


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Renal rescue - avoid risk factors

Nephrotoxic drugs

NSAIDs inhibit synthesis of renal

prostaglandins - needed for afferent

arteriolar dilatation during low statesACE inhibitors - reduce production of

angiotensin II (normally constricts efferent

arterioles) Gentamicin - once daily dosing safer


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Abdominal compartment

syndrome

Several causes: acute pancreatitis, peritonitis,

retroperitoneal haematoma, intestinal

obstruction, major trauma Mechanism: reduced renal blood flow, direct

compression of renal parenchyma

Transduce urinary catheter: > 25-30 mmHg -consider decompression

R l l h


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Renal replacement therapy -

indications

Oliguria

Anuria

Urea > 30 mmol l-1

Creatinine > 400

mmol l-1

Hyperkalaemia

Pulmonary oedema

Metabolic acidosis

(pH < 7.1)

Uraemia causing:

encephalopathy

pericarditis

neuropathy

P i i l f di l i d


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Principles of dialysis and

filtration

Dialysis: diffusion of solute across a semi-

permeable membrane and down a

concentration gradientFiltration: movement of solute by

convection across a semi-permeable

membrane

M d f l l t


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Continuous arteriovenous haemofiltration (CAVH)

Continuous venovenous haemofiltration (CVVH)

Continuous venovenous haemodialysis (CVVHD)

Continuous venovenous haemodiafiltration(CVVHDF)

Modes of renal replacement

therapy


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blood in blood out

filtrate

Haemofiltratio

n replacement fluid

Controlled output:Gate-clamp controller

or pump

H di filt ti


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blood in blood out

Filtrate Dialysate

Replacement

fluid

Haemodiafiltration


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Renal replacement therapy


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Thank You

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