Successful management of intra-abdominal hemorrhage in the presence of severe alcoholic liver disease with activated recombinant factor VII (rFVIIa; NovoSeven): a case report and review of the literature on approved and off-label use of rFVIIa.

A 37-year-old male with history of alcohol abuse presented to us with nausea, vomiting, and abdominal pain with ascites. He was diagnosed with alcoholic liver disease with coagulopathy and pancreatitis. During hospitalization, the patient developed intra-abdominal hemorrhage. He was treated with platelets, packed red blood cells and fresh frozen plasma without any improvement. Following this he was treated with activated recombinant factor VII (90 microg/kg), which resulted in normalization of the prothrombin time and the activated partial thromboplastin time and stabilization of hematocrit within a few hours. We review the current literature on the approved and off-label use of activated recombinant factor VII.     

Partial Portal Vein Ligation Plus Thioacetamide: A Method to Obtain a New Model of Cirrhosis and Chronic Portal Hypertension in the Rat

To obtain a new model of chronic portal hypertension in the rat, two classical methods to produce portal hypertension, partial portal vein ligation and the oral administration of thioacetamide (TAA), have been combined. Male Wistar rats were divided into four groups: 1 (control; n?=?10), 2 [triple partial portal vein ligation (TPVL); n?=?9], 3 (TAA; n?=?11), and 4 (TPVL plus TAA; n?=?9). After 3 months, portal pressure, types of portosystemic collateral circulation, laboratory hepatic function tests (aspartate aminotransferase, alanine aminotransferase, bilirubin, alkaline phosphatase, and gamma-glutamyl transpeptidase) and liver histology were studied. The animals belonging to group 2 (TPVL) developed extrahepatic portosystemic collateral circulation, associated with mesenteric venous vasculopathy without hepatic destructurization or portal hypertension. Animals from group 3 (TAA) developed cirrhosis and portal hypertension but not extrahepatic portosystemic collateral circulation, or mesenteric venous vasculopathy. Finally, the animals from group 4 (TPVL?+?TAA) developed cirrhosis, portal hypertension, portosystemic collateral circulation, and mesenteric venous vasculopathy. The association of TPVL and TAA can be used to obtain a model of chronic portal hypertension in the rat that includes all the alterations that patients with hepatic cirrhosis usually have. This could, therefore, prove to be a useful tool to study the pathophysiological mechanisms involved in these alterations.     

High-Risk Cutaneous Squamous Cell Carcinoma without Palpable Lymphadenopathy: Is There a Therapeutic Role for Elective Neck Dissection?

PURPOSE: The beneficial role of elective neck dissection (END) in the management of high-risk cutaneous squamous cell carcinoma (CSCC) of the head and neck remains unproven. Some surgical specialists suggest that END may be beneficial for patients with clinically node-negative (N0) high-risk CSCC, but there are few data to support this claim. We reviewed the available literature regarding the use of END in the management of both CSCC and head and neck SCC (HNSCC). METHODOLOGY: The available medical literature pertaining to END in both CSCC and HNSCC was reviewed using PubMed and Ovid Medline searches. RESULTS: Many surgical specialists recommend that END be routinely performed in patients with N0 HNSCC when the risk of occult metastases is estimated to exceed 20%; however, patients who undergo END have no proven survival benefit over those who are initially staged as N0 and undergo therapeutic neck dissection (TND) after the development of apparent regional disease. There is a lack of data regarding the proper management of regional nodal basins in patients with N0 CSCC. In the absence of evidence-based data, the cutaneous surgeon must rely on clinical judgment to guide the management of patients with N0 high-risk CSCC of the head and neck. CONCLUSIONS: Appropriate work-up for occult nodal disease may occasionally be warranted in patients with high-risk CSCC. END may play a role in only a very limited number of patients with high-risk CSCC.