SHOULD WE SCREEN FOR HEPATOCELLULAR CARCINOMA? G. Roehrig 1 ; 1 UCSF Primary Care Internal Medicine Program, San Francisco, CA LEARNING OBJECTIVES: 1)Recognize screening methods for Hepatocellular carcinoma (HCC) and the evidence for or against them. 2)Identify who should be screened for HCC. CASE INFORMATION: A 46 year old woman with a history of injection (IV) drug use and alcoholism presents for establishment of primary care, without specific medical complaints. Her last IV drug use was over 10 years ago, is recently HIV negative, and doesn't recall hepatitis testing. She reports 15 yrs of intermittent heavy drinking. Her past medical history is also significant for Diabetes mellitus Type 2 and obesity. Her medications include methadone and metformin. Reveiw of systems: negative history of jaundice, ascities, bruising, or gastroentestinal bleeding. Exam: Obese woman with normal vital signs and no scleral icterus. She had normal cardiac and pulmonary exams and her abdomen was obese few spider angiomata. Initial lab values: Hepatitis C antibody positive, B negative, Hct: 35.8, Platelets: 109, INR 1.1, Albumin 3.0, AST: 94 (Normal < 40), ALT: 87 (Normal < 40), Total Bili 1.1, Alk Phos 174 (Normal < 130). Given the lab results and spider angiomata, an abdominal ultrasound (U/S) was ordered which showed signs of cirrhosis as well as a 1.4 cm liver``hemangioma''. An alpha-fetoprotein (AFP) subsequently obtained was 42.0 (normal < 20). The patient was referred to Hepatology, but then lost to follow-up. Repeat AFP 6 monts later was 316. An abdominal CT was obtained to better characterize the lesion showed growth to 2.7cm. A biopsy of the lesion was not done due to its location but a routine liver biopsy confirmed cirrhosis. The patient underwent transarterial chemoembolization for presumed HCC, her AFP at this time was 551. DISCUSSION: The major risk factor for development of HCC is cirrhosis, at a rate of 1 ± 7% per year. The most common etiologies of cirrhosis are viral Hepatitis (B or C) and alcohol. Data for time to development of HCC range from 15 ± 25 years. Survival rates are 50% at 3 years for resectable lesions and 20% at one year for non-resectable HCC. Screening tools: AFP > 20 sensitivity of 39 ± 70%, U/S = 58 ± 85%, CT = 46 ± 84%, AFP and U/S combined = 79 ± 90%. Unofficial screening guidelines, followed by many surveyed by Chalasani et al, aren't necessarily supported through evidence-based medicine (EBM). The 6 month screening periods initially arose from data on tumor doubling time. Currently, most hepatologits do every 6 month AFP or U/S in patients with documented cirrhosis, with CT imaging alternatively being used. A recent cost-effective analysis by Sarasin et al concluded that screening offered minimal survivial benefits for the majority. The most significant benefits were found in well-compensated Child's A cirrhosis, especially with resectable tumors. There is a logical argument for screening liver transplant candidates. In summary, there is currently no EBM to support screening beyond the select group of patients mentioned above. There is a need for more research to better establish the mortality benefit and cost-effectiveness of HCC screening. A 52 year old man with a history of low back pain and alcoholism presented to his PMD with severe low back pain. He was given Vicodin, but returned to clinic 5 days later with worsening pain, constipation, difficulty walking, and a fever. Pt was sent to a local hospital where he was found to be confused and febrile with bilateral chest infiltrates; last drink had been 2 days prior. He was treated for pneumonia and presumed alcohol withdrawal. 4/4 blood cultures grew out S. aureus, but TTE showed no valvular vegetations. 4 days later, pt was transferred to our hospital where he was febrile to 103, agitated, disoriented, unable to follow commands, but spontaneously moving all extremities. To the extent testable, neurologic exam was nonfocal except for marked low back pain on neck flexion and possible nucchal rigidity. He had no spinal tenderness. He was pan-cultured and a head CT showed no acute event. MRI and TEE were planned for the following morning to rule out SEA and endocarditis, respectively. Lumbar puncture was initially deferred because of concerns for possible SEA and because pt was already on meningitis-dose Nafcillin. The following morning (5 hrs after admission) the patient no longer spontaneously moved his lower extremities and his toes were upgoing bilaterally. Emergent MRI showed a large T9 epidural abscess with posterior and anterior extension. Patient underwent emergent neurosurgical evacuation and had slow but progressive improvement in lower extremity function over the next 2 weeks. One week after transfer to rehabilitation, he expired in the middle of the night. Autopsy showed reaccumulation of the epidural abscess with infarction of nearly half of his spinal cord. IMPLICATIONS/DISCUSSION: Spinal epidural abscess is a rare but serious infection with potentially disasterous consequences, as highlighted in this case. Entertaining the diagnosis early is the key to prompt discovery and treatment. Severe back pain in a febrile patient, particularly with other risk factors for SEA (IVDU, past back surgeries, bacteremia), warrants rapid workup. Spinal MRI should be done as soon as the diagnosis is entertained, ideally before any neurologic deficits develop. In most cases, spinal cord damage occurs suddenly secondary to cord infarction from thrombosis or interruption of the local venous or arterial supply rather than via cord compression. Management requires neurosurgical evacuation and antibiotics (etiology is S. aureus in > 60% of cases). Early surgical intervention ( < 24hrs) is associated with markedly better prognosis.