Nuclear receptor subfamily 1, group H, member 4 (Nr1h4, FXR) is a bile acid activated nuclear receptor mainly expressed in the liver, intestine, kidney and adrenal glands. Upon activation, the primary function is to suppress cholesterol 7 alpha-hydroxylase (Cyp7a1), the rate-limiting enzyme in the classic or neutral bile acid synthesis pathway. In the present study, a novel Fxr deficient mouse line was created and studied with respect to metabolism and liver function in ageing mice fed chow diet. The Fxr deficient mice were similar to wild type mice in terms of body weight, body composition, energy intake and expenditure as well as behaviours at a young age. However, from 15 weeks of age and onwards, the Fxr deficient mice had almost no body weight increase up to 39 weeks of age mainly because of lower body fat mass. The lower body weight gain was associated with increased energy expenditure that was not compensated by increased food intake. Fasting levels of glucose and insulin were lower and glucose tolerance was improved in old and lean Fxr deficient mice. However, the Fxr deficient mice displayed significantly increased liver weight, steatosis, hepatocyte ballooning degeneration and lobular inflammation together with elevated plasma levels of ALT, bilirubin and bile acids, findings compatible with non-alcoholic steatohepatitis (NASH) and cholestasis. In conclusion, ageing Fxr deficient mice display late onset leanness associated with elevated energy expenditure and improved glucose control but develop severe NASH-like liver pathology.

BACKGROUND:

PON1 is an HDL-associated enzyme having antioxidant activity. PON1 is synthesized in the liver, and there is decreased synthesis of PON1 with increased lipid peroxidation. The study was carried with the aim of establishing whether chronic liver disease (CLD) produced any significant changes in serum arylesterase (AE) and lactonase activities of PON. The second objective was to determine whether there was any correlation between serum AE and lactonase activities and the various routine liver function tests. The usefulness of adding serum lactonase and AE activity to standard liver function tests was analyzed by multiple logistic regression analysis. Finally, the diagnostic efficacy or analytical performance of AE and lactonase in assessing patients with CLD was determined using 'receiver operating characteristic' (ROC) plot.

METHODS:

The study group consisted of 120 subjects; 60 were patients with liver disease out of which 40 were having chronic alcoholic liver disease and 20, acute viral hepatitis B, and 60 were healthy controls. Serum PON1 lactonase activity was measured manually using dihydrocoumarin, and AE activity was measured using phenylacetate as substrate. Liver function tests (bilirubin, albumin, AST, ALT, alkaline phosphatise) were done by standard technique.

RESULT:

The serum lactonase and AE activities were decreased significantly in patients with chronic alcoholic liver disease (p < 0.001, p < 0.001) and acute viral hepatitis B (p < 0.001, p < 0.001). Both measurements showed higher efficiency in testing liver dysfunction in multivariate regression analysis. Model 1 consisted of bilirubin, albumin, AST, ALT, and alkaline phosphatase, R2 = 0.912. Model 2 consisted of model 1+arylesterase having higher R2 = 0.0.954, and model 3 consisted of model 1+lactonase having R2 = 0.962. ROC plots demonstrated a high diagnostic accuracy for serum PON1 lactonase (area under ROC curve = 0.982) and serum PON1 arylesterase (area under ROC curve = 0.986).

CONCLUSION:

Low PON1 lactonase and AE activity were found in acute viral hepatitis B and in chronic alcoholic hepatitis.

SESSION TYPE: Miscellaneous Cases IIPRESENTED ON: Tuesday, October 23, 2012 at 11:15 AM - 12:30 PM

INTRODUCTION:

The short-term prognosis of pulmonary embolism (PE) depends on haemodynamic status of the patient. Risk stratification becomes very critical especially for normotensive patients. We present a case of submassive PE with concomitant right ventricle (RV) thrombus.

CASE PRESENTATION:

43 year-old male without any significant medical history who presented with two-week history of progressive dyspnea on exertion, chest tightness and right calf pain. Risk factors were obesity (BMI=42.4) and driving 416 miles days before symptom onset. Physical examination revealed an obese male with increased work of breathing. He was normotensive with a heart rate of 128, respiratory rate of 22 and oxygen saturation of 95% on 2 Liters of oxygen. His lungs were clear to auscultation bilaterally in all fields and cardiac exam was pertinent for a loud S3 gallop. He had a non-erythematous, swollen and tender right calf. Chest computed tomography with intravenous contrast revealed extensive emboli in the proximal branches of his pulmonary artery (Figure 1). Doppler ultrasound of his right lower extremity showed a deep vein thrombosis. Surface echocardiogram showed RV strain and free-wall hypokinesis, RV systolic pressure of 78mmHg, right atrium pressure of 20mmHg and a large RV thrombus (Figure 2). EKG pattern confirmed sinus tachycardia with an S1, Q3, T3 morphology and right-axis deviation. Admission labs were remarkable for troponin 0.37, BNP 629pg/mL, D-dimer 8934ng/mL, alkaline phosphatase 95unit/L, ALT 76unit/L and AST 51unit/L. He was immediately bolused with unfractionated heparin and continued on an infusion prior to being transferred to the medical ICU. Given his significant clot burden in both the pulmonary circulation and RV, pulmonary embolectomy was considered, however we elected to administer 24-hour continuous systemic thrombolytic therapy through a pulmonary artery catheter. He developed mild epistaxis which did not require interruption of thrombolytic infusion. He remained hemodynamically stable with improvement of his tachycardia and dyspnea. His troponin, liver transaminases and BNP improved suggesting improvement of RV strain. Maximum D-dimer value was &gt;15,000ng/mL after thrombolytic infusion which was attributed to clot dissolution.

DISCUSSION:

Our case illustrates the complex decision making regarding aggressive medical versus surgical treatment strategies in managing a normotensive patient with submassive PE and large RV thrombus. It also highlights the need for risk stratification of confirmed acute PE.

CONCLUSIONS:

Prompt administration of continuous systemic thrombolytics resulted in improved morbidity and mortality in our patient.1) Sanchez O, Trinquart L, Colombet I, et al. Prognostic value of right ventricular dysfunction in patients with haemodynamically stable pulmonary embolism: a systematic review. European heart journal 2008; 29:1569-1577DISCLOSURE: The following authors have nothing to disclose: Milan Patel, Timothy Udoji, Kenneth LeeperNo Product/Research Disclosure InformationEmory University, Atlanta, GA.

SESSION TYPE: Critical Care Cases IIPRESENTED ON: Wednesday, October 24, 2012 at 11:15 AM - 12:30 PM

INTRODUCTION:

Hemophagocytic Lymphohistiocytosis (HLH) also termed as hemophagocytosis has been associated with a variety of viral, bacterial, fungal, and parasitic infections, as well as collagen-vascular diseases and malignancies. HLH in association with Ehrlichia Chaffeensis has been reported in children but not in adults1. We present a case of Ehrlichiosis in an adult complicated with Hemophagocytosis.

CASE PRESENTATION:

A 74 year old Caucasian male presents to emergency room with 1 week history of gradually worsening dyspnea, high fever, nausea and lethargy. Initial laboratory data apart from acute kidney injury (BUN:74 mg/dl, Creatinine: 3.4 mg/dl) was significant for coagulopathy (INR:7.8, PTT: 50, D dimer: 2.63 ug/ml, fibrinogen: 263 mg/dl), thrombocytopenia (Platelets:16,000), elevated liver enzymes (AST:261 U/L, ALT:78 U/L, ALP: 60 U/L, total bilirubin: 1.8 mg/dl, LDH: 1398 mg/dl) and anemia with leucopenia (Hb: 10 mg/dl, Hct: 30%, WBC:4100/uL). Further history revealed that he had a tick bite while camping 1 week prior to the symptom onset and hence, was started on doxycycline. Clinical suspicion of HLH was made based on very high levels of ferritin (12000 U) and high triglycerides (387 mg/dl). A bone marrow aspirate was obtained which showed the presence of reactive marrow along with hemophagocytosis (presence of macrophage with engulfed nucleated red blood cell) as shown in the Fig 1a. Fig 1b reveals a hemosiderrin laden macrophage. Tick borne serologies were reported positive for Ehrlichia PCR (Ehrlichia chaffeensis DNA. The patient's combination of clinical features and laboratory evaluation fulfilled the revised diagnostic criteria for HLH2. His clinical condition improved with supportive management and doxycycline with no other proven therapies for HLH.

DISCUSSION:

Hemophagocytic lymphohistiocytosis (HLH) is a rare complication of infectious diseases and has not been reported in adults with Ehrlichia Chaffeensis to best of our knowledge. (HLH) is a disease with major diagnostic and therapeutic difficulties.

CONCLUSIONS:

The most typical features of HLH are fever, hepatosplenomegaly, lymphadenopathy, skin rash, jaundice, cytopenias, as well as hypertriglyceridemia, coagulopathy with low fibrinogen levels, liver dysfunction, and elevated levels of ferritin and serum transaminases. Pathologic finding of hemophagocytosis (phagocytosis by macrophages of erythrocytes, leucocytes, platelets and their precursors) is a distinct clinical feature.1) Hemophagocytic lymphohistiocytosis secondary to Ehrlichia chaffeensis infection: a case report. Burns S, Saylors R, Mian A ; J Pediatr Hematol Oncol 20102) Henter JI, Horne A, Arico M, et al. HLH-2004: diagnostic and therapeutic guidelines for hemophagocytic lymphohistiocytosis. Pediatr Blood Cancer. 2007DISCLOSURE: The following authors have nothing to disclose: Sridhar Badireddi, Manish JoshiNo Product/Research Disclosure Information, Little Rock, AR.

SESSION TYPE: Critical Care Student/Resident Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Intensive care patients often have multiple comorbidities and very complex treatment plans. Pinpointing an exact precipitating factor responsible for a patient's rapid health decline is difficult. Late or inappropriate identification can further complicate the picture. Swift action and maintaining a broad differential is paramount in order to correctly identify the cause and treat appropriately.

CASE PRESENTATION:

We present a 40-year-old African American female who developed multiorgan system dysfunction secondary to sepsis and complications of antiretroviral therapy. She has a history of CKD on dialysis, NSTEMI s/p MVR, and HIV on antiretroviral therapy. She presented with acute lower back pain radiating to right upper thigh associated with 10-day history of progressive weakness, pain, and anorexia. On the second day of admission she became lethargic. Severe bradycardia (HR 30's), hypotension (BP 80/40), hypoglycemia (glucose 19), low oxygen saturation (O2 sat 80's) and metabolic acidosis with pH 7.11, HCO3 14, and lactate level of 11.9 mmol/L were noted. She failed to respond to narcan and D50. Upon admission she had blood cultures drawn and Vancomycin was started. Blood cultures grew staphylococcus epidermidis and septic shock was considered. However, this was not an exact fit given absence of fever, no elevated WBC, severe bradycardia, and no strong evidence of infection. Cardiogenic shock, endocarditis, meningitis, and encephalitis were excluded. Elevated cardiac enzymes were thought to be secondary to underlying kidney failure. The patient had hepatomegaly and elevated liver enzymes (ALT 508, AST 992), which were most likely secondary to hypoperfusion, underlying liver disease, or complications of antiretroviral therapy. For the past year she was on Efavirenz and Tenofovir, which has a blackbox warning for lactic acidosis and severe hepatomegaly. Her liver function prior to admission was normal. The antiretroviral therapy was held and liver function and lactate levels subsequently returned to baseline.

DISCUSSION:

As seen in this case, the exact cause of the patient's decline was unclear but rather confounded by multiple comorbidities. Lactic acidosis secondary to antiretroviral therapy presents with nonspecific symptoms making the diagnosis difficult. Our patient was subject to an extensive workup and evaluation.

CONCLUSIONS:

The immediate recognition of antiretroviral therapy as a culprit was important in preventing further decline. This case highlights the importance of thorough evaluation and proper identification of medications and their potential side effects especially in intensive care patients whose health is very precarious to subtle alterations.1) Vired package insert. Foster City, CA: Gilead Sciences, 2001.DISCLOSURE: The following authors have nothing to disclose: Shiayin Yang, Youngsook YoonNo Product/Research Disclosure InformationUniversity of Toledo, Holland, OH.

SESSION TYPE: Cardiovascular Student/Resident Case Report Posters IPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

This case describes a patient who was initially diagnosed with a cardiomyopathy of unknown etiology. Subsequent testing several years later revealed an underlying celiac disease as the primary etiology.

CASE PRESENTATION:

A 37 year old male who emigrated to the United States from Albania in 2000 with past medical history significant for mild elevation in liver function studies as well as non-ischemic cardiomyopathy diagnosed in 2006 presented to our internal medicine clinic in 2009 to establish care. At that time, the patient had complaints of abdominal distension, weight loss, as well as prior elevated liver function tests of unknown etiology. Initial laboratory studies showed an alkaline phosphatase of 142, ALT of 100, and AST of 75. Abdominal ultrasound and outside CT scan results were unremarkable for any pathology. A hepatitis panel as well as alpha-1-antitrypsin level were normal. The patient was subsequently referred to the gastroenterology department, who performed a colonoscopy with biopsies. Biopsy results showed likely celiac disease, which was confirmed with positive tissue transglutaminase studies. The patient was started on a gluten-free diet. His transaminase levels were noted to decrease. In addition, the patient's cardiac function began to improve as well, without changes in medication. Initial cardiac MRI results from 2009 when the patient first established care showed global left ventricular hypokinesis with a left ventricular ejection fraction of 33%. Subsequent echocardiograms after the initiation of a gluten-free diet showed improvement of function, with the latest left ventricular ejection fraction of 45% in August 2010. The patient was subsequently diagnosed with cardiomyopathy secondary to celiac disease. As the patient modified his diet, his cardiac function began to improve while his tissue transglutaminase antibodies declined.

DISCUSSION:

This case is interesting in the fact that a patient's diet change after moving to the United States from Albania caused an exacerbation of an underlying celiac disease, which attributed to the patient developing a non-ischemic cardiomyopathy. Studies have shown a loose relationship between autoimmune conditions, such as celiac disease and non-ischemic cardiomyopathy. Our case provides additional evidence to this relationship.

CONCLUSIONS:

Although rare, Celiac Diseaes is a known cause of cardiomyopathy. The vast majority of patients improve significantly solely with the implementation of a gluten-free diet and, therefore, physicians should be aware of this disease relationship.1) Goel, et al.. Cardiomyopathy Associated with Celiac Disease. Mayo Clinic Proceedings. 2005;80:674-6.2) Curione, et al.. Carnitine deficiency in patients with coeliac disease and idiopathic dilated cardiomyopathy. Nutrition, Metabolism & Cardiovascular Diseases. 2005;15:279-83.DISCLOSURE: The following authors have nothing to disclose: David Snipelisky, Keels JornNo Product/Research Disclosure InformationMayo Clinic, Jacksonville, FL.

SESSION TYPE: Infectious Disease Student/Resident Case Report Posters IIIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Klebsiella pneumoniae liver abscess syndrome (KLAS) is a distinctive clinical condition that was first described in Taiwan and is rarely reported in the United States (US).

CASE PRESENTATION:

A 37 year-old Hispanic male from Guatemala who immigrated to the US one year ago, complained of 5 days of generalized abdominal and right-sided chest pain associated with fever, chills and shortness of breath. He denied any significant past medical history. He presented with tachycardia, tachypnea, fever of 102 F, blood pressure of 93/51mmHg and was hypoxic. Remarkable findings on physical examination included bilateral rales, abdominal right upper quadrant tenderness and hepatomegaly. Laboratory studies showed platelets of 15,000 mcL, a total bilirubin of 2,3 mg/dl , direct bilirubin of 1 mg/dl, AST 219 IU/L and ALT 235IU/L. His clinical condition rapidly deteriorated requiring intubation and vasopressors. A CT of the thorax showed bilateral multifocal pneumonia and a 6cm fluid collection on the right hemithorax consistent with empyema. An abdominal CT showed a 15cm x 17cm cystic mass with multiple septations on the right hepatic lobe. Blood, bronchial wash and liver cyst aspirate grew Klebsiella pneumoniae which was sensitive to cephalosporins. Appropriate antibiotics were started and a percutaneous drainage was initially placed. Given his persistent fever, laparoscopic drainage of the liver abscess was ultimately required. Subsequently, the patient remained afebrile and complete functional recovery was observed after 4 weeks of oral antibiotics.

DISCUSSION:

Klebsiella pneumoniae liver abscess syndrome is a community-acquired infection. Typical presentation includes fever, abdominal pain and pleuritic chest pain. Distant metastasis, the salient feature of the disease, can occur in 7-12 % of patients, with meningeal and ophthalmic involvement yielding poor prognosis. Diabetes mellitus and Asian descent are known risk factors. Majority of cases occur in Asia, and in the US most patients are of Asian descent. Most KLAS cases are caused by the K1 serotype, whose hallmark is the mucoviscosity-associated gene A that confers virulence by the production of a thick polysaccharide capsule which prevents phagocytosis. Percutaneous drainage and appropriate antibiotics are the mainstream treatment. Surgical intervention may be required if the patient fails to respond in 4-7 days, as occurred in our case.

CONCLUSIONS:

Due to the emergence of KLAS in the US, raising awareness of this distinctive syndrome is of utmost importance to achieve the best care for these patients.1) McIver C, Janda J. Pathophysiology and laboratory identifi cation of emerging hepatovirulent Klebsiella pneumoniae. Clin Microbiol Newsl. 2008;30:127-31.DISCLOSURE: The following authors have nothing to disclose: Julie Lai, Rene FrancoNo Product/Research Disclosure InformationEinstein Medical Center, Philadelphia, PA.

SESSION TYPE: Critical Care Student/Resident Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Liver transplantation (LT) for acute liver failure (ALF) is an uncommon occurrence in the setting of pregnancy, and carries a high risk of fetal demise in the first and second trimesters. Furthermore, maternal hyperthyroidism increases fetal risk in the setting of LT, and the medical literature contains a single case report in this context that reported fetal demise (1). We report a case of a hyperthyroid pregnant patient who underwent successful LT at 19 weeks gestation for ALF due to propylthiouracil hepatotoxicity, followed by a subsequent delivery of a healthy infant at 38 weeks gestation.

CASE PRESENTATION:

The patient was a 36-year-old pregnant woman with a past medical history of Graves disease, who was initiated on PTU therapy 3 months prior. Her initial presentation was characterized by complaints of fatigue, pruritis and jaundice. Her initial serum workup revealed a total billirubin 19.6 mg/dl (direct billirubin 17.5) , INR 2.99, AST 2549 U/l, ALT 1427 U/l. An extensive serum workup for potential etiologies for her hepatic dysfunction was unrevealing. Her initial mental status was normal, but over the next 24 hours, she rapidly progressed to advanced hepatic encephalopathy, which necessitated elective intubation for airway protection. Intracranial pressure (ICP) monitoring revealed normal ICP levels. Given her worsening coagulopathy and encephalopathy, a decision was made to list her for transplantation with a presumptive diagnosis of PTU induced ALF. In preparation for surgery, cold iodine therapy was administered to minimize the risk of an intraoperative thyroid storm. She subsequently underwent a successful LT within the next 36 hours; specific intraoperative interventions included the use of an esmolol intravenous drip for thyroid storm prophylaxis, and continuous fetal monitoring. Two weeks after her LT, the patient underwent a total thryoidectomy. Eventually, the patient had a successful full term pregnancy.

DISCUSSION:

This case highlights a multi-organ system based approach to maternal and fetal management in the setting of maternal acute liver failure and hyperthyroidism. In addition, it demonstrates the issues that need to be addressed in preparation for liver transplantation in this setting, with specific focus on the peri-operative endocrine management of hyperthyroidism.

CONCLUSIONS:

In summary, this case illustrates the successful multi-disciplinary intensive care management of a complex case involving liver transplantation for acute liver failure of a hyperthyroid pregnant patient in her second trimester, with favorable outcomes for the patient and her infant.1) Morris CV, Goldstein RM, Cofer JB, Solomon H, Klintmalm GB. An unusual presentation of fulminant hepatic failure secondary to propylthiouracil therapy. Clin Transplants. 1989 : 311.DISCLOSURE: The following authors have nothing to disclose: Milan Patel, Ram SubramanianNo Product/Research Disclosure InformationEmory University, Atlanta, GA.

SESSION TYPE: Critical Care Student/Resident CasesPRESENTED ON: Monday, October 22, 2012 at 01:45 PM - 03:00 PM

INTRODUCTION:

Hemophagocytic lymphohistiocytosis (HLH) is a rare disease marked by overactive histiocytes and lymphocytes and is associated with a high mortality(1). We present a case of HLH in an otherwise healthy young adult female who presented with recurrent fevers and multi-organ failure.

CASE PRESENTATION:

A 20 year old previously healthy female presented to a community hospital with fevers to 105 F, body aches, and generalized weakness. The patient had a leukocytosis to 19.3 and a mild transaminitis. Chest radiography, blood, CSF and urine cultures were negative. Serologies and PCR studies for mycoplasma, syphilis, CMV, EBV, HSV, HIV and acetominophen level were negative. The patient was given broad spectrum antibiotics. She had persistent fevers and was transferred after one week to our institution. Multiple laboratory and imaging studies did not reveal an occult infection. The patient developed a worsening transaminitis with AST/ALT peaking at 8766/1115, a coagulopathy (INR of 1.9) and a lactic acidosis of 12.9. She was anemic at 6.5 and thrombocytopenic at 63. An abdominal MRI revealed splenomegaly. The patient developed cardiorespiratory failure requiring intubation and vasopressors. Ferritin was elevated at 28,000. The patient underwent a bone marrow biopsy which revealed hemophagocytosis. She was started on dexamethasone and etoposide. Over two weeks the patient's liver failure and hypotension resolved and she was extubated.

DISCUSSION:

Secondary HLH may be associated with various infectious, inflammatory and malignant triggers(2). HLH is marked by inappropriate overstimulation of cytotoxic lymphocytes that lead to macrophage activation and high levels of cytokines(1,2). Characteristic features include fever, hepatosplenomegaly, CNS disease, cytopenias, transaminitis, hypofibrinogemia, high tryglyceride levels, hemophagoctyosis in bone marrow or CSF fluid, and elevated markers of T-cell activity(3). Treatment requires immunosuppresion with steroids, etoposide and CSA per the HLH 94 protocol with frequently HSCT(1,2). With current treatment 5-year survival is approximately 50%(2). This case displayed many characteristic features of HLH but given the relative rarity of the disease other infectious syndromes were considered first and the diagnosis delayed.

CONCLUSIONS:

Hemophagocytic lymphohistiocytosis is a rare disorder that is marked by immune dysregulation that can lead to multi-organ failure and death. Early diagnosis is essential.1) Fischer A. Primary Immune Deficiency Diseases. In: Kasper et al. Harrison's Principles of Internal Medicine. 18th ed New York, NY: MCGraw-Hill 2011:27042) Trottestam H et al. Chemoimmunotherapy for hemophagocytic lymphohistiocytosis: long-term results of the HLH-94 treatment protocol. Blood 2011;118(17):4577-843) Henter JI et al. HLH-2004: Diagnostic and therapeutic guidelines for hemophagocytic lymphohistiocytosis. Pediatr Blood Cancer 2007;48(2):124-31DISCLOSURE: The following authors have nothing to disclose: Ryan Dunn, Maggie Davis HovdaNo Product/Research Disclosure InformationUniversity of Chicago, Chicago, IL.

SESSION TYPE: Non Pulmonary Critical Care PostersPRESENTED ON: Wednesday, October 24, 2012 at 01:30 PM - 02:30 PM

PURPOSE:

Complications of primary non-function after orthotopic liver transplant (OLT) can be managed by total hepatectomy to avoid toxic liver syndrome as bridge therapy to re-transplantation. Postoperative critical care of these patients is challenging. We present the largest case series of critically ill anhepatic patients awaiting re-transplantation. Continuous venovenous hemofiltration (CVVH) was utilized to control volume status and maintain metabolic homeostasis.

METHODS:

A retrospective chart review was completed on eight patients admitted to the surgical ICU after unsuccessful OLT in an anhepatic state to await re-transplantation between 2006 and 2010. Upon admission to the ICU, patients were on mechanical ventilation and placed on CVVH using a polysulfone filter. Lab tests were repeated every six hours and changes to CVVH replacement fluid and balance were adjusted accordingly. The retrospective data was recorded prior to the start of CVVH and before re-transplantation to examine changes in lab values during the anhepatic phase. Data is reported as mean±SD and was analyzed using a Student's paired t-Test with a two-tailed distribution. A p-value &lt;0.05 was considered significant.

RESULTS:

As expected, ALT decreased by an average of 607±588 (p=0.02), and AST by 1781±2130 (p=0.05). The pH increased from 7.17±0.08 to 7.32±0.14 (p=0.02). Serum lactate remained constant (14.4±7.6 mmol/L pre-CVVH, and 14.4±8.4 mmol/ L prior to re-transplant). There were no significant changes in INR (3.2±1.3, 2.2±0.6), glucose (124±39, 145±45 mg/dL), Na (146±4, 139±9 mEq/L), K (4.6±0.7, 4.4±0.6 mEq/L), and iCa (1.1±0.1, 1.17±0.4 mmol/L).

CONCLUSIONS:

Seven of the eight patients were successfully bridged to re-transplantation. The mean time to re-transplantation was 39.1±17.4 hours. The longest anhepatic period was 65.7 hours. Patients can be successfully managed using CVVH in the anhepatic state until a new donor liver is available.

CLINICAL IMPLICATIONS:

Without the use of liver support systems, anhepatic patients were kept metabolically stable utilizing CVVH.DISCLOSURE: The following authors have nothing to disclose: Roozehra Khan, Ronaldo Go, Sumit Kapoor, Ananda Dharshan, Marjan Rahmanian, Anthony Manasia, Adel Bassily-Marcus, Roopa Kohli-Seth, John Oropello, Ernest BenjaminNo Product/Research Disclosure InformationMount Sinai Hospital, New York, NY.