s Submitted for the 68th Annual Scientific Meeting of the American College of Gastroenterology October 10-15, 2003, Baltimore, Maryland: LIVER: PDF Only
Background: Surveillance rates for HCC remain limited in patients with cirrhosis. We evaluated whether opt-out mailed outreach increased uptake with or without a $20 unconditional incentive. Methods: This was a pragmatic randomized controlled trial in an urban academic health system including adult patients with cirrhosis or advanced fibrosis, at least 1 visit to a specialty practice in the past 2 years and no surveillance in the last 7 months. Patients were randomized in a 1:2:2 ratio to (1) usual care, (2) a mailed letter with a signed order for an ultrasound, or (3) a mailed letter with an order and a $20 unconditional incentive. The main outcome was the proportion with completion of ultrasound within 6 months. Results: Among the 562 patients included, the mean age was 62.1 (SD 11.1); 56.8% were male, 51.1% had Medicare, and 40.6% were Black. At 6 months, 27.6% (95% CI: 19.5–35.7) completed ultrasound in the Usual care arm, 54.5% (95% CI: 47.9–61.0) in the Letter + Order arm, and 54.1% (95% CI: 47.5–60.6) in the Letter + Order + Incentive arm. There was a significant increase in the Letter + Order arm compared to Usual care (absolute difference of 26.9%; 95% CI: 16.5–37.3; p <0.001), but no significant increase in the Letter + Order + Incentive arm compared to Letter + Order (absolute difference of −0.4; 95% CI: −9.7 to 8.8; p =0.93). Conclusions: There was an increase in HCC surveillance from mailed outreach with opt-out framing and a signed order slip, but no increase in response to the financial incentive.
The critical shortage of transplantable organs necessitates utilization of unconventional donors. We describe a successful experience of controlled non-heart-beating donor (NHBD) liver transplantation.Controlled NHBDs had catastrophic head injury, prognosis for no meaningful recovery, decision to withdraw life support, and subsequent consent for donation. After stopping mechanical ventilation in the operating room, death determination by a nontransplant caregiver, and rapid aortic cannulation, liver and kidneys were recovered.Controlled NHBDs contributed 5% of hepatic allografts (8/164) from August 1996 through June 1999 (9% in 1998). Sixteen NHBDs afforded 8 livers and 24 kidneys. Liver donors (n=8) were 11-66 years old; half were >50 years old. Premortem alanine aminotransferase was 25-157 U/L. Arrest occurred 3-27 min after stopping ventilation. Perfusion started 3-5 min after incision, and <22 min after hypotension (mean arterial pressure: <50 mmHg). Patient and graft survivals are 100% at 18+/-12 months follow-up. There was no intraoperative complication, reperfusion syndrome, poor graft function, primary nonfunction, arterial thrombosis, biliary complication, or serious infection. Postoperative day 2 prothrombin time was 13+/-1 sec. Peak alanine aminotransferase was 980+/-601 U/L. Intensive care unit and posttransplant lengths of stay were 2+/-2 and 10+/-7 days, respectively. Soon after transplantation there was frequent temporary hyperbilirubinemia (five of eight recipients; bilirubin peak: 7-29 mg/dl, 2-3 weeks after transplantation) and rejection (4/8 recipients, <3 weeks after transplantation).NHBDs significantly and safely expanded our donor pool. NHBD surgeons must be capable of rapid procurement. Cautious liberalization of criteria for accepting livers from NHBDs with confounding risk factors is justified. Refined ethics guidelines would broaden approval of NHBDs.
Purpose: Case Report: A 62 year old male with a history of Hepatitis C related cirrhosis and hepatocellular carcinoma, s/p prior transarterial chemoembolization underwent an orthotopic liver transplant (OLT) at our institution. The 52 year old deceased donor liver was procured by another team. Cold ischemia time was 9.3 hours. Intraoperative hemodynamics were uncomplicated. On the first post-operative day (POD#1) an abdominal ultrasound confirmed a normal echo texture of the liver allograft and patent hepatic and portal vessels. Soon thereafter the patient spiked high grade fevers, cultures were obtained and the patient was commenced on broad spectrum antibiotics. There was no hemodynamic instability Laboratory studies revealed marked transaminitis (AST 3146 U/L, ALT 1348 U/L). A repeat abdominal ultrasound on POD#2 showed two wedge shaped low attenuation densities in segments 5 and 6 of the liver. The hepatic and portal vasculature was again patent with normal waveforms and resistive indices. A CT scan confirmed the ultrasound findings and the presence of hepatic infarction. The patient had no prior history of a hypercoaguable state. He continued to spike fevers despite antibiotics, and cultures remained negative. A repeat abdominal ultrasound after 2 weeks showed that the hepatic infarcts had resolved. His liver enzymes had trended down to the normal range. A diagnosis was made of hepatic infarcts of unclear etiology, leading to post-OLT fever. This patient is six months post OLT and has not had any other complications. Discussion: Hepatic infarcts are an important cause of post OLT allograft failure and are usually due to stenosis or thrombosis of the hepatic and/or portal vasculature. In addition to stenosis/thrombosis of the major hepatic vessels, other contributing factors to post OLT hepatic infarcts may include: prolonged duration of cold and warm ischemic time, manual handling of the liver during surgery, spasm of the hepatic artery, intra-operative hypotension, reperfusion injury and post op systemic hypotension. In donors with significant atherosclerotic burden, cannulation of the aorta can cause dissection and/or embolization leading to hepatic infarcts. Post-OLT hepatic infarction can present clinically as acute allograft rejection, transaminitis and fever of unknown origin. It can also lead to non-anastomotic biliary strictures, cholangitis and bile duct stenosis. Most importantly hepatic infarcts should be monitored for abscess development and prophylactic broad spectrum antibiotics should be initiated.
Introduction: We observed severe hyponatremia (SevHy) with increasing frequency in our patients with cirrhosis leading to repeated hospitalizations and a perception of associated high mortality. The aim is to evaluate causes, management modalities, prognosis and outcomes of SevHy in cirrhosis. Methods: 40 cirrhotics with SevHy (Na<125) were compared to 41 cirrhotic controls matched for age, gender, bilirubin, creatinine and INR. Data was collected on mode of presentation, ascites, edema, diuretic regimen during the week prior to episode of SevHy, MELD before/after correction of SevHy, body weight, treatment regimens for the SevHy, time to correction of SevHy, and mortality. Results: Demographics between groups were similar. Serum sodium was 122±3.1 mEq/l (113-125) and 134±3.8 (129-147) in cirrhotics with and without SevHy respect (p < 0.05). MELD was 22±6.7 (MELD-Na 29±5.1) and 23±6.9 (MELD-Na 25±6.3) respectively (p < 0.05). Frequency of ascites and edema in both groups30% and 22% respectively. Prior to SevHy, most patients were on combinations diuretics of spironolactone (S) and furosemide (F) but 69% hyponatremic patients had a ratio of S to F of 1.0 or less. Both groups had significant renal dysfunction with Cr of 2.3±2.0 vs. 2.00±1.7 respectively (p < 0.05). Therapy of SevHy: 55% of patients received multiple treatment modalities: SevHy was perceived to be of hypovolemic type in 64%; 48% of patients had diuretics stopped or markedly decreased. 35% received IV fluids resuscitation; 68% were treated with water restriction; 11% received salt tablets; and 8.3% required vaptans. Correction of SevHy was achieved over 3.5±2.8 days. Admission mortality was higher in the patients with severe hyponatremia (OR, 3.88, 95% CI, 1.24-12.1, p < 0.05). Although MELD-Na was higher, no listed patient received a liver transplant during the admission due to severity of the hyponatremia. Conclusion: Severe hyponatremia is an ominous complication of cirrhosis linked with high inpatient mortality. Inappropriate combination of diuretics may be associated with SevHy. Correction of serum sodium requires multiple treatment modalities. Review of use of diuretics in cirrhosis could be a useful topic for quality improvement initiatives for hepatology providers caring for patients with ascites and/or edema. Lastly, the impact of SevHy on transplantation was limited to patient inactivation rather than enhancement of liver allocation.
Introduction: Spontaneous bacterial peritonitis (SBP) is an ascitic fluid infection caused by bacteria in patients with cirrhosis. It is the most common infection amongst cirrhotics, occurring in 10%-30% of hospitalized patients, with an in-hospital mortality rate of ˜20%. Methods: Medical records of 89 patients aged ≥18 years diagnosed with SBP during their hospitalization within the past 10 years were obtained. 73 of them met criteria of having established cirrhosis. Data was compiled including medications on admission, initial studies including serum sodium (Na), creatinine (Cr), blood urea nitrogen (BUN), total bilirubin, and Child-Pugh score (CPT). Indications for patients requiring SBP prophylactic treatment were defined based on 2012 AASLD guidelines: 1) History of SBP, 2) Presenting with an upper GI bleed, 3) initial biochemical studies including ascitic fluid total protein Results: Data was compiled and analyzed via SPSS. The most common indication warranting SBP prophylaxis was biochemical (47.5%); then a history of SBP (32.8%), upper GI bleed (14.8%), and low ascitic fluid protein (4.9%). 32.8% (95% CI: 0.22-0.45) of those with an indication for prophylactic treatment did not receive it. 80% of those with a history of SBP were on antibiotic prophylaxis upon hospital admission, and 78% of those with an upper GI bleed received antibiotics. 59% of patients with biochemical indications were treated, and 33% of those with a low ascitic fluid protein were started on antibiotics. Conclusion: Our study at a university tertiary care medical center showed about one-third of patients with indications for SBP prophylaxis did not receive antibiotics. This study is one of only a few to look at how frequently patients receive SBP prophylactic treatment according to AASLD guidelines. The most common missed indication was a low ascitic fluid protein. Multiple clinical trials have shown a reduction in SBP occurrence and mortality in cirrhotics with low ascitic protein who receive prophylaxis. Our study brings up an important question as to why these patients were not placed on prophylaxis. Increased recognition of the guidelines for SBP prophylaxis is of paramount importance to prevent initial and recurrent infections, thereby reducing mortality in such a critically ill population.
