hepatorenal syndrome john

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