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Hepatorenal Syndrome
SMF ILMU PENYAKIT DALAM
RSAY METRO/FK UNILA
JOHN ELFRAN SIHOMBING
Pembimbing: dr. Ronald David Martua Nababan, Sp.PD
Cirrhosis Evolves Clinically From Compensated to Decompensated Stage
• Compensated cirrhosis• Cirrhosis without complications• Median survival >12 years
• Decompensated cirrhosis• Cirrhosis with complications: ascites
(±HRS), variceal hemorrhage, jaundice, or encephalopathy
• Annual rate of decompensation of 4-5%• Median survival ~1.5 years
Pathogenesis of Ascites in Cirrhosis
↑ intrahepatic resistance
cirrhosis
Portal hypertension
Splanchnic vasodilatation
↓ Effective arterial blood volume
Activation of neurohumoral systems
Sodium retension
ascites
(Boyer, T.D.)
Common Pathogenesis in Refractory Ascites, Hyponatremia, and HRS
↑ ↑ intrahepatic resistance
cirrhosis
Portal hypertension
Splanchnic vasodilatation
↓ ↓ Effective arterial blood volume
Activation of neurohumoral systems
Sodium retension
ascites
Water retention Renal vasoconstriction
Refractory Ascites Hiponatremia HRS(Boyer, T.D.)
DefinisiSindrom hepatorenal (SHR)
adalah gangguan fungsi ginjal sekunder pada penyakit hati tingkat berat, baik akut maupun kronis, yang bersifat fungsional dan progresif (Setiawan dan Hernomo, 2006).
Hepatorenal syndrome
Kriteria Mayor berdasarkan International Ascites Club
• Hepatic insufficiency and portal hypertension
• Low GFR (< 40 ml/min) or creatinine > 1.5 mg/dl
• No shock, bacterial infection, fluid loss and current or recent treatment with nephrotoxic drugs
• No sustained improvement after withdrawal of diuretics and infusion of 1.5 liters of saline
• Proteinuria of < 500 mg/dl and negative renal ultrasound
Hepatorenal syndromeAdditional Criteria
Kriteria Minor berdasarkan International Ascites Club
• Urine volume < 500 ml/d• Urine sodium < 10 meq/L• Urine osmolality > plasma• Urine RBCs < 50/hpf• Serum sodium < 130 meq/L
*Semua kriteria mayor harus dijumpai dalam menegakkan diagnosa Sindroma Hepatorenal, sedangkan kriteria tambahan merupakan pendukung untuk diagnosa Sindroma Hepatorenal
Hepatorenal syndrome
• Type 1-Doubling of serum creatinine to > 2.5 mg/dl in less than 2 weeks.
• Type 2-Moderate but steady decrease in renal function to creatinine > 2.5 mg/dl.
Who Develops HRS?
Cirrhotic patients with ascites• May be preceded by precipitating factor
• Spontaneous bacterial peritonitis (SBP)
• Sepsis• Total paracentesis• Upper GI hemorrhage
Patients with acute alcoholic hepatitisPatients with acute liver failure
Treatment of HRS General Measures
• Stop all diuretics• Look for nephrotoxic drugs• Examine urine for white cells and casts• Perform renal ultrasound• Give 1.5 liters saline/albumin• Treat infection
Pharmacologic Therapy
Vasoconstrictors Plus Albumin for HRS
↑ intrahepatic resistance
cirrhosis
Portal hypertension
Splanchnic vasodilatation
↓ Effective arterial blood volume
Activation of neurohumoral systems
Renal vasoconstriction
HRS
vasoconstrictors
Albumin
+
(Boyer, T.D.)
Terlipressin
• Synthetic 12-aminoacid peptide• Pro-drug, with pharmacologic activityof its own• Constrictive activity via V1-receptors
• vascular & extravascular smooth muscle cells
• Splanchnic vasoconstriction • ↓portal flow • ↓portal pressure
• Systemic vasoconstriction • ↑effective blood volume • ↓renin and angiotensin
renal vasodilatation
improvement in serum creatinine
Non-pharmacologic Therapy
• Dialysis
• TIPS (Transjugular intrahepatic portosystemic shunt)
• Liver Transplantation
Patogenesis Sindrom Hepatorenal pada Sirosis, Berdasarkan Teori Vasodilatasi Arterial, dan Intervensi Terapi Efektif
(Glines, 2003)
DAFTAR PUSTAKA
Boyer, T.D. Hepatorenal Syndrome. University of Arizona. USA.
Glines, Pere. 2003. Hepatorenal Syndrome. Lancet 2003; 362: 1819-1826. Didapat dari www.med.upenn.edu/gastro/documents/LancetHRS.pdf
Setiawan, P. B, Hernomo K. Sindrom Hepatorenal. Dalam: ed. Sudoyo, Ari Wdkk. Buku Ajar Ilmu Penyakit Dalam Jilid I Edisi IV. Jakarta: Pusat Penerbitan Departemen Ilmu Penyakit Dalam Fakultas Kedokteran Universitas In-donesia; 2006. Hal 452 – 454
TERIMA KASIH