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GANGGUAN PANKREATOBILIER Dr Willy B Uwan, MARS, SpPD, K-GEH, FINASIM SMF Penyakit Dalam Klinik Penyakit Hati dan Saluran Cerna Unit Endoskopi Diagnostik.

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Presentasi berjudul: "GANGGUAN PANKREATOBILIER Dr Willy B Uwan, MARS, SpPD, K-GEH, FINASIM SMF Penyakit Dalam Klinik Penyakit Hati dan Saluran Cerna Unit Endoskopi Diagnostik."— Transcript presentasi:

1 GANGGUAN PANKREATOBILIER Dr Willy B Uwan, MARS, SpPD, K-GEH, FINASIM SMF Penyakit Dalam Klinik Penyakit Hati dan Saluran Cerna Unit Endoskopi Diagnostik dan Terapeutik RSU St Antonius Pontianak

2 Pankreatitis Akut Definisi Peradangan akut, non-bakterial pada organ pankreas. Patofisiologis Terjadinya pankreatitis akut diawali karena adanya jejas di sel asini pankreas akibat: Obstruksi duktus pankreatikus (terutama oleh migrasi batu empedu) Stimulasi hormon cholecystokinin (CCK) sehingga akan mengaktifasi enzim pankreas (misalnya karena pengaruh hipertrigliseridemia dan alkohol) Iskemia (misalnya pada pankreatitis akut paska prosedur endoscopic retrograde cholangiopancreatography / ERCP atau atherosklerosis)

3 Etiologi Beberapa penyebab pankreatitis akut adalah: Obstruksi batu di duktus koledokus (38%) Alkohol (36%) Pankreas divisium (7%) Komplikasi paska tindakan ERCP (5,4%) Hipertrigliseridemia (1-4 %) Obat-obatan (1-4 %) Hiperkalsemia Pankreatitis akut idiopatik (10-15 %)

4 ETIOLOGY  Gallstones, microlithiasis, biliary sludge  Ethanol (5 years, > 50g/day), ERCP  Toxins, tumors, trauma  Steroids and ulcers  Mumps and other infections  Autoimmune  Stenosis (sphincter of Oddi dysfunction, papillary stenosis)  Hypertriglyceridemia, hypercalcemia, hypothermia  Genetic (<30 years old, family history)  Drugs (Azathioprine, estrogen, HIV drugs, tetracycline, sulfa

5 Fase Pankreatitis Akut Pada umumnya perjalanan klinis pankreatitis akut dapat dibagi: 1.Fase awal Fase awal terjadi pada minggu pertama, ditandai dengan adanya systemic inflammatory response syndrome / SIRS 2.Fase lambat Fase lambat berlangsung beberapa minggu sampai bulan dan ditandai dengan adanya SIRS yang persisten atau oleh karena komplikasi lokal dari pankreatitis akut.

6 Diagnosis Diagnosis pankreatitis akut ditegakkan berdasarkan: Anamnesis Pemeriksaan fisik Laboratorium Pemeriksaan imaging Menurut klasifikasi Atlanta (2012), diagnosa pankreatitis akut tegak bila memenuhi 2 dari 3 kriteria berikut: Nyeri perut bagian atas Peningkatan amilase atau lipase > 3x nilai batas atas normal Pemeriksaan imaging (USG / CT scan atau MRI)

7 Sistem skor Marshall untuk menilai gagal disfungsi organ Sistem organSkor Respirasi (Pa02/Fi02) > – – – 200≤101 Ginjal (serum kreatinin; mg/dl) <1,41,4 – 1,81,9 – 3,63,6 – 4,9>4,9 Kardiovaskular (mm Hg) >90<90, respon(+) dengan cairan <90, respon(-) dengan cairan <90, pH<7,3 <90, pH<7,2

8 Definisi pankreatitis akut berat: perbandingan kriteria Atlanta 1992 dan 2012 Kriteria Atlanta (1992)Kriteria Atlanta (2012) Pankreatitis akut ringan Tidak adanya gagal organ Tidak adanya komplikasi lokal Pankreatitis akut ringan Tidak adanya gagal organ Tidak adanya komplikasi lokal Pankreatitis akut berat 1.Komplikasi lokal dan atau 2.Gagal organ Perdarahan gastrointestinal >500 cc /24 jam Syok – tekanan darah sistolik ≤90 mmHg Pa02 ≤ 60% Kreatinin ≥ 2 mg/dl Pankreatitis akut sedang – berat 1.Komplikasi lokal atau sistemik tanpa gagal organ persisten 2.Gagal organ sementara (<48 jam) Pankreatitis akut berat Gagal organ persisten (>48 jam) (memakai kriteria skor Marshall) Gagal organ tunggal Gagal organ multiple

9 Klasifikasi Pankreatitis Akut Berdasarkan Klasifikasi Atlanta 2012, tingkat keparahan pankreatitis akut dibagi: 1.Pankreatitis akut ringan 2.Pankreatitis akut sedang 3.Pankreatitis akut berat



12 Tatalaksana Terapi supportif: resusitasi cairan, koreksi gangguan elektrolit dan koagulasi, pemberian oksigen Antibiotik: diberikan pada infeksi ekstra pankreas seperti kolangitis Analgetik: pilihan narkotik injeksi Terapi nutrisi Terapi pembedahan


14 EPIDEMIOLOGY  AP was responsible for approximately 300,000 hospital admissions in the United States in  Recent studies show the incidence of AP varies between 4.9 and 73.4 cases per 100,000 worldwide.  Although the case fatality rate for AP has decreased over time, the overall population mortality rate for AP has remained unchanged.


16 DIAGNOSIS (REVISED ATLANTA CONSENSUS 2012) 2 of the 3 criteria: 1. Abdominal pain consistent with the disease 2. Serum amylase and or lipase greater than three times the upper limit of normal, and or 3. Characteristic findings from abdominal imaging Contrast-enhanced computed tomography (CECT) and or magnetic resonance imaging (MRI) should be reserved for patients in whom:  the diagnosis is unclear or  who fail to improve clinically within the first 48 – 72h after hospital admission or to evaluate complications

17 CLINICAL PRESENTATION  Sudden-onset abdominal pain and persists for hours to days  Nausea and vomiting  Delirium, hemodynamic instability, extreme respiratory distress

18 PHYSICAL EXAMINATION  Abdominal tenderness with guarding especially in the epigastric region  Bowel sounds are diminished

19 LABORATORY STUDIES  Elevated serum amylase and or lipase ≥ 3xULN  > 5xULN and lipase is more specific

20 IMAGING STUDIES  Ultrasound:  Most sensitive noninvasive for detecting gallstone and biliary tract dilation  CT scanning:  Superior to ultrasound for detecting the changes associated with pancreatitis and its complications

21 IMAGING STUDIES  ERCP:  Primarily a therapeutic tool in acute biliary pancreatitis (no role in diagnosing)  EUS:  A sensitive test for detecting persistent biliary stones for further ERCP procedure

22 SYSTEMIC COMPLICATIONS  Pulmonary processes (hypoxemia, pleural effusions, ARDS)  Renal failure  Coagulopathy  Delirium  Shock



25 INITIAL ASSESSMENT AND RISK STRATIFICATION  Hemodynamic status and resuscitative measures  Stratify patients into higher and lower risk categories (admission setting)  Evaluate organs failure Tenner et al, American College of Gastroenterology Guideline: Management of Acute Pancreatitis, Am J Gastroenterol

26 DEFINITIONS OF SEVERITY  The onset of acute pancreatitis is defined as the time of onset of abdominal pain Early discharge No need imaging Very rare mortality SIRS Mortality 36-50% Infected necrosis

27 DEFINITIONS OF SEVERITY  A score of ≥ 2 in any system define the presence of organ failure

28 PROGNOSTIC SCORING SYSTEM (SEVERITY OF AP)  Ranson’s criteria; Glasgow prognostic criteria; APACHE II; Balthazar CT severity index;  BISAP:  is applicable within the first 24h presentation  ≥ 3 had a mortality rate of approx. 15% CRITERIAPOINTS BUN > 25mg/dL1 Impaired mental status1 Presence of SIRS (≥ 2 criteria)1 Age > 60yo1 Presence of pleural effusion1

29 TREATMENT  Supportive (first 24h is golden hours):  Massive volume repletion  Parenteral/enteral feeding  NGT?  No rule for the use prophylactic antibiotics  No evidence to support routine use of somatostatin  ERCP

30 INITIAL MANAGEMENT  Obtain vital signs at frequent intervals (such as every 4-6 h)  Supplemental oxygen be administered during the first 24–48 h, especially if narcotic agents are used to control pain.  BGA should be performed when oxygen saturation is ≤95%, hypoxemia or hypotension refractory to a bolus of IV fluids.

31 INITIAL MANAGEMENT  Aggressive hydration using isotonic crystalloid solution should be provided to all patients, unless cardiovascular, renal or other related comorbid factors exist (most beneficial during the first 12 – 24 h).  Lactate Ringer solution may be the preferred.  Large volume normo-saline may lead to a non- anion gap, hyperchloremic metabolic acidosis.

32 AGGRESSIVE HYDRATION Bolus 1 to 2 L of crystalloids (approx. 20 mL/kg) Continuous infusion of 150 to 300 cc/hour (approx. 3 mL/kg/h), first 24 hours Fluid requirements assessment (intervals 6 h of admission and for h)  Decrease hematocrit and BUN  Maintain a normal creatinine

33 ICU? Severe Need aggressive fluid resuscitation (elderly and cardiovascular disease) Deteriorating respiration (no hypoxemia)

34 NUTRITION IN AP  Mild acute pancreatitis:  Oral feedings can be started immediately if there is no nausea and vomiting and the abdominal pain has resolved.  Initiation of feeding with a low-fat solid diet appears as safe as a clear liquid diet.  Severe acute pancreatitis:  Enteral nutrition is recommended (nasogastric and nasojejunal).  Parenteral nutrition should be avoided, unless the enteral route is not available/not tolerated/not meeting caloric requirements.

35 NUTRITION IN AP  Oral intake of limited amounts of calories is usually initiated when:  Abdominal pain has subsided  Parenteral narcotics are no longer required  Nausea and vomiting have ceased  Abdominal tenderness has markedly decreased  Bowel sounds are present  Overall assessment of the patient has improved

36 ANTIBIOTICS IN AP Should be given for:  Infection included extra-pancreatic  Necrosis who deteriorate or fail to improve after 7-10 days of hospitalization → infected Is not recommended:  Prophylactic antibiotics  No source of infection is identified

37 ERCP IN AP  Concurrent acute cholangitis should undergo ERCP within 24 h  Progressive bilirubin increasing (CBD obstruction/biliary pancreatitis)  In the absence of cholangitis and or jaundice, MRCP or EUS rather than diagnostic ERCP should be used to screen for choledocholithiasis if highly suspected.

38 Autoimmune Pancreatitis (Ig G4– Associated Cholangitis) Stricturing of the pancreatic duct, focal or generalized pancreatic enlargement, IgG4 > 140 mg/dL Lymphoplasmacytic infiltrate on biopsy Response to corticosteroid therapy

39 P rimary S clerosing C holangitis

40 Epidemiology Prevalence: 6-16 cases/ Incidence: 1 case/ Geographical variation Men > Women Median age: 40 years Concomitant (60-80%) with UC

41 Pathophysiology Immune-mediated process Genes: HLA-DRB1*1501-DQB1*602, HLA- DRB1*1301-DQB1*0603, HLA-A1-B8-DRB1*0301- DQB1*0201 ‘Second Hit’ – environmental trigger, toxin or infectious exposure Innate and adaptive immune system Lymphocyte migration, cholangiocyte damage, fibrosis

42 Clinical Presentations Asymptomatic Non-specific: fatigue, pruritus, jaundice, weight loss Less common: fever, chill, night sweat, abdominal pain Jaundice, Hepato-splenomegaly, Excoriations Cirrhosis

43 Clinical Presentations Elevated alkaline phosphatase and bilirubin Aminotransferase normal or mildly elevated Synthetic function altered in advanced disease

44 Clinical Presentations US: ductal wall thickening and focal bile duct dilations, gallbladder wall thickening, distention, gallstones and mass CT: thickened and inflamed bile ducts, saccular dilation intra-hepatic ducts and mass in gallbladder MRCP: “beaded” appearance – multifocal short annular strictures alternate between normal and dilated

45 Diagnosis Gold standard: MRCP with sensitivity and specificity of 86% and 94%, and ERCP Multifocal annular strictures alternating with segments of normal or dilated bile ducts of intrahepatic and/or extrahepaticbile ducts – ‘bead on a string apperance’ Rule out IgG-4 Liver biopsy rarely helpful – “onion skin” (25%), small duct PSC, PSC-AIH overlap syndrome


47 Onion Skin Apperance NEJM 1995

48 Diagnosis Classic PSC: biliary strictures with normal intervening segments or diffusely involved long segments. Radio-occult: strictures not present, shallow ulcerations bile duct Small duct PSC more difficult to diagnosis Antibodies are non-specific

49 Serum Autoantibodies in PSC

50 Differential Diagnosis Clinical Liver Disease, Vol 3, No 3, March 2014

51 Treatments No proven medical therapy Ursodeoxycholic acid (UDCA): 15 mg/kg/day – improve biochemical markers and inflammation Endoscopic treatment - dominant bile-duct stenosis Liver transplantation (LTx) – end stage liver disease, portal hypertension refractory therapy, intractable pruritus, reccurent cholangitis LTx: 5 and 10 year survival rates of 87.4% and 83.2 %

52 Major RCT of UDCA in the Treatment of PSC PSC Management and Surveillance Clinical Liver Disease, Vol 3, No 3, March 2014

53 Complications Obstructive Colorectal Cancer, Cholangiocarcinoma, HCC, Gallbladder Cancer Cirrhosis Cholelithiasis, Fat-soluble vitamin deficiencies, Osteoporosis

54 The risk of developing PSC-associated cancers Dtsch Arztebl Int 2013

55 Clinical surveillance of PSC Dtsch Arztebl Int 2013

56 Cholangiocarcinoma surveillance in PSC Clinical Liver Disease, Vol 3, No 3, March 2014

57 Prognosis Median time to death or transplantation: years for asymptomatic and no IBD 9 years for symptomatic Mayo Risk Score: R = 0.03 (age [years]) loge (bilirubin [mg/ dL]) loge (AST [UIL]) (variceal bleeding [0/1]) − 0.84 (albumin [g/dL])

58 Gallbladder cancer surveillance in PSC Clinical Liver Disease, Vol 3, No 3, March 2014

59 Subclassification of PSC

60 Relationships between subphenotypes of PSC


62 Diagnostic Algorithm for the Overlap Syndromes

63 Diagnostic Features of the Overlap Syndromes

64 Treatment Options for the Overlap Syndromes

65 Simplified Criteria for the Diagnosis of AIH

66 Kolangiokarsinoma Tumor primer dari epitel duktus biliaris Kanker hepatobilier terbanyak kedua setelah karsinoma hepatoseluler 95% adalah adenokasinoma Lokasi 20% intra hepatik /perifer, 80% ekstra hepatik (70-80% perihilar dan 20-30% distal duktus biliaris) Faktor risiko: kolangitis sklerosing primer, kista duktus biliaris, sirosis hepatis, hepatitis B dan C, infeksi clonorchis sinensis




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