Survival patients with acute cholestasis

Survival patients with acute cholestasis

524A AASLD ABSTRACTS HEPATOLOGYOctober 2001 1407 1408 SURVIVAL OF PATIENTS W I T H ACUTE CHOLESTASIS. Tarek I Hassa- DILATED BILE DUCTS IN NEONA...

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524A

AASLD ABSTRACTS

HEPATOLOGYOctober 2001

1407

1408

SURVIVAL OF PATIENTS W I T H ACUTE CHOLESTASIS. Tarek I Hassa-

DILATED BILE DUCTS IN NEONATAL LIVER DISEASE. Rebecca A Jar-

nein, Leia Mehlman, Ed Barber, Katherine Hall, Mahmoud E1-Tahawy, Christopher Mathews, University of California, San Diego, San Diego

dine, Luca Livio, Pat Farrant, John Karani, Mark Davenport, Giorgina MieliVergani, Alastair Baker, King's College Hospital, London United Kingdom

Background: Acute cholestasis is a clinical, laboratory and histopathologic presentation of different types of liver disease. It complicates acute viral infections, alcoholic hepatitis, drug induced hepatitis, TPN, and sepsis. Outcomes for patients with acute cholestasis are not clear. We conducted a retrospective analysis of patients admitted to our medical center between 1/1/99 and 3/1/01 with cholestasis and bilirubin > 10mg/dL. Methods: After excluding trauma and pediatric cases, we had a population of 369 patients. Patients were classified into one of three groups according to whether their serum bilirubin improved, continued to increase or remained stable over the analysis period. Mortality for each group was also tabulated. Results: Group 1, (regressive cholestasis) n = 197, Group 2 (stable cholestasis) n = 109 and Group 3 (progressive cholestasis) n=63. The mean age of the groups were 53, 55 and 51 years, respectively. The patient population was male 59%, and 67% Caucasian with 12% African American, 9 % Hispanic and 6% Asian. The etiology of cholestasis by diagnostic group were; Alcoholic Liver Disease n= 124, Viral Liver Disease n=45, Drug Induced Liver Disease n=25 and others n=175. Overall, the mortality rate was 38%. Mortality for Group 1 was 18% (n = 36), Group 2 was 52% (n= 58) and Group 3 mortality was 73% (n= 46). Predictors of mortality by diagnostic group were statistically significant (p= 0.0002). Predictors of mortality based on laboratory values include mean total serum bflirubin >21mg/dL, mean BUN > 58mg/dL, mean Creatinine > 2.4mg/dL and mean prothrombin time > 20 seconds. Summary: 1) Mortality rates in patients with progressive cholestasis are overwhelmingly high. 2) Renal failure is a predictor of poor outcome. Conclusion: Acute Cholestasis should be classified clinically according to its course. This classification can predict patient survival.

The aim was to define the aetiological features and prognostic significance of dilated bile ducts (DBD) on ultrasound (U/S) in infants less than 6 mo. old with neonatal liver conditions. The records of 97 infants with common bile duct (BD) -->l.0mm (our limit of normal in infants born at term up to 6 weeks otd) were reviewed and data on presentation, investigation, diagnosis, treatment and outcome were collected. Patients with follow-up were divided by BD at presentation intG Gp A = BD 1.0-1.4mm, (n=14), Gp B = BD 1.5-1.9mm (11=9), Gp C = BD 2.0-2.5mm (n=22), Gp D = BD >2.Smm (n=52). Median age at presentation was 40d (range 0-181), 4 with antenatal U/S diagnosis. 11 were born at <30 wks, 14 at 31-36 wks and 72 at term, 14 had intrauterine growth retardation. One mother had diabetes and one took olazepine during pregnancy. All but 2 were jaundiced, 43 with pale stools. 13 had necrotising enterocolitis, 24 had other sepsis and 16 received parenteral nutrition. 15 had birth asphyxia, 4 with fits. 4 had cardiac anomalies and/or failure. 13 other congenital anomalies in 16 infants were found. Causes of neonatal cholestasis were found in 30, 6 metabolic, 5 congenital infections, 3 biliary atresia (BA), 3 endocrine and 2 neonatal sclerosing cholangitis (NSC), 8 had haemolytic conditions and 3 acute liver failure. Investigations included MethylbromIDA scan in 22, percutaneous transhepatic cholangiogram (PTC) in 27 (1 failed), endoscopic retrograde cholangiopancreatogram in 7 (2 failed), liver biopsy in 29. BD diagnoses were normal in 10, choledochal cyst (CDCy) in 13, inspissated bile syndrome (IBS) in 40, stricture, either inflammatory or secondary to perforation in 4, unexplained dilatation or minor anomaly including common pancreatico-biliary channel in 25, BA 3 and NSC 2.49 underwent surgery, 3 of them Kasai porto-enterostomy. 44 received ursodeoxycholic acid. Median follow-up was 6 too. (< 1-101 too.) with 6 lost and 4 died. Final BD outcome was normal ill 52, BD remained dilated in 30 (3 CDCy), chronic liver disease was present in 5. In Gp A 91% and in Gp B 50% resolved spontaneously without any having biliary pathology.In Gp C, 40% resolved spontaneously, 7 BD remained dilated despite surgery and 3 had biliary pathology. In Gp D 24% resolved spontaneously, 6 BD remained dilated without intervention, 20 BD were normal after intervention and 6 remained dilated after intervention. Conclusions: Factors known to be associated with IBSwere confirmed. All causes of neonatal liver disease can be associated with DBD. No intrinsic biliary pathology was found in BD< 2.0ram suggesting this as the cut-off size for normal in this group. 29% of DBD will settle spontaneously with the likelihood of doing so inversely proportional to the degree of dilatation and related to the presence of pathology. 30% of DBD will remain dilated even after cholangiography or surgery despite absence of evidence of liver disease. Follow-up is required to determine if this represents a variant of normal or a mild choledochal malformation.

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PRIMARY SCLEROSING CHOLANGITIS PRESENTING AS A PANCREATIC MASS. Mohssen Nassiri Toosi, Jenny Heathcote, University Health Net-

ERCP ASSOCIATED COMPLICATIONS IN PATIENTS W I T H PRIMARY SCLEROSING CHOLANGITIS. Sue C Eng, Scott D Lee, Michael B Kimmey,

work, Toronto, ON Canada

Bruce Y Tung, Michael D Saunders, Kris V Kowdley, University of Washington, Seattle, WA

Introduction & Method: Primary Sclerosing Cholangitis (PSC) is likely a systemic disease which predominantly affect the biliary tree, although the ancreatic and salivary duels may also be affected. A revlaw of the natural hiatory of all patients given a diagnosis o~PSC at a single center was conducted. The aim was to ciari~ the presentation of pancreatitis in the PSC patients 2opula tion. Results: 72 patients were confirmed to have PSC (mate to femala ratio = 1.7/ 1). Diagnosis of PSC was confirmed by imaging alone(71%), imaging and liver biopsy(17%) or by liver biopsy alone(13%). The diagnosis of PSC was made following referal for abnormal liver tests (67%), jaundice (17%), acute cholangitis(5%) abdominal pain(3%), and hepatosplenomegaly(2%). Inflammatory bowel disease(60%), non-insulin dependent diabetes mellitus(13%), thyroid disease(S%), pancreatic disease(7%), "dtiligo(3%), rheumatoid arthritis(1%), and hypereosinophilia (1%) were other co-existent extrahepatic diseases. Three patients, whopresented with abdominal complaints (Jaundice abdominal pain and malabsorption) with marked weight toss, were found to have a pancreatic mass. They were suspected both on clinical and radiological findings to have a pancreatic mall nancy and only later were found to have PSC using further imaging techniques. Two patients despite therapy wit~ thainage procedures had recurrent jaundice and underwent open biopsy of the pancreas. Only chronic ancreatitis was identified. The long term follow-up and good clinical response to medical therapy suggested the lace of a pancreatic malignancy. Treatment was with biliary drainage, pancreas enzyme supplements and ursodeoxycholic acid (UDCA). Discussion: The presence of significant weight fuss and imaging findings suggested pancreatic malignancy, hut open biopsy showing chronic pancreasitis and further imaging techniques confirmed clinically the possibility that pancreatitis may develop in relation to sclerosing cholangitis. Therapy with supplementaI pancreatic enzymes was accompanied with dramatic improvement of signs and symptoms of maiabsorption. The 2-4 years follow-up was accompanied with weight gain and improvement in liver biochemistry tests. PSC Cases u a j~aacrea~lamass

Age Gen pre~

Case I

(Yr.)

tier

45

M~

Case2

4i

Case 3

78

Clisical W ~ h

Ab.

Auioirn

floss

tests

disease

Yes (65

Yes

~ave~' Dis.

o Ja~r~di ce

y~

Lb,)

Pa~cre~

Other

Surge~ NIDDM, PUD

Fern Abd~a inal a~e Pair~

Yes

Yes

Y~

Ne~

Hyp~sio Ol~a~i~ n,UT~,PID ~/opsy

~c ~.~,te ias~fiC

Yes

Yes

Yes

NO

NIDDM, Opet~ve Mgralvalve r~u~it~,on ~lOpSy

NIDDM ( ~ ~ s ) , PUD (pepi~ u~,erdisease),Lrf] {u~-y tract infection),PIO ~ v ~ i n f l ~ r ~ r ~ disease)

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No

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Background: Endoscopic retrograde cholangiopancreatography (ERCP) is the gold standard for the diagnosis of primary sclerosing cholangitis (PSC). Complications of ERCP include cholangitis, pancreatitis, biliary or intestinal perforation, bacteremia, and hemobilia, which occur in approximately 8% of cases. Some have suggested that therapeutic ERCP should be avoided in PSC because of increased risk of infection or bile duct perforation. The goal of this study was to examine complication rate after diagnostic or therapeutic ERCP among PSC patients under a protocol using pre- and postprocedure antibiotics. Methods: The endoscopic database at a single institution was retrospectively reviewed and all ERCP done betweenJannary 1998 and March 2000 in patients with PSC were examined. Medical records were reviewed for all postprocedure complications that occurred within one week after the ERCP. Results: 85 out of 753 ERCPs (11.3%) in this time period were performed on 27 patients with PSC and 3 patients with suspected PSC. Antibiotics were given prior to 84/85 ERCPs (99%), and at least one dose of antibiotics following 76/85 ERCPs (93%). Cholangiography was successful in 83/85 ERCPs; 2 patients required percutaneous transhepatic cholangiographic drainage. Of the remaining ERCPs, 67 were therapeutic, requiring the placement of biliary stents and/or balloon dilation, and 16 were diagnostic. There were a total of 9 complications: cholangitis (n= 5), pancreatitis (n=2), bile duct perforation (n = 1), and liver abscess (n = 1). The liver abscess occurred in a patient requiring percutaneous drainage after failed ERCP. Infection or bile duct perforation occurred in 8.2%. All were managed conservatively and there was no mortality. Seven complications occurred in the therapeutic group while 2 occurred in the diagnostic group. There was no difference in complication rate between therapeutic and diagnostic ERCP (RR = 0.84; 95% CI 0.19-3.65). Conclusions: (1) The comphcation rate after ERCP in PSC is acceptable. (2) The risk of complications is not increased in PSC patients requiring therapeutic intervention at ERCP. (3) Infection or bile duct perforation is relatively infrequent. (4) We speculate that use of pre- and postprocedure antibiotics may have decreased the risk of infectious complications after therapeutic ERCP among our PSC patients.