Periodic migrainous neuralgia associated with an arteriovenous malformation.

The likeliest explanation for these fatty lesions is that they are produced by pancreatic enzymes which have entered the circulation either directly or via lymphatics. The latter is thought to be the more important route. Abdominal peritoneal lymphatic drainage and transdiaphragmatic lymphatic absorption of abdominal fluid are probably prime factors in the ingress of pancreatic enzymes to the thoracic duct and hence into general circulation (Scarpelli, 1956; Perry, 1947). Circulatory trypsin may break down vessel wall integrity and allow lipase to hydrolyse neutral fat in fat cells to glycerol and fatty acid. It has also been suggested (Hodson-Walker and Woods, 1970) that the lesions are secondary to vascular spasm or necrosis, which leads to local areas of fat necrosis. The primary insult on the vessel being from pancreatic enzymes or due to intravascular thrombosis sometimes seen in acute pancreatitis. A further but unlikely factor is that the lesions are caused by emboli of necrotic pancreatic tissue (Blauvelt, 1946). Peripheral fat necrosis has been described in acute pancreatitis and as a marker of pancreatic neoplasm. This case and the others described should serve as a reminder that pancreatic disease may present with bizarre and obscure symptoms and signs.