A 59-year-old male with no history of interest was admitted for epigastric pain of 20 days onset, sudden and continuous since then despite analgesic treatment.
The pain initially irradiated to the right hypochondrium and days later also to the left hypochondrium and back.
It increased slightly after meals and improved in sitting position and trunk flexion.
It was accompanied by nausea without vomiting, with no changes in bowel rhythm or deposition, although the patient reported slightly darker urine.
During this time she presented with a evening fever of up to 38.5oC.
On physical examination, the abdomen was blunt and depressible, with pain on palpation of the epigastrium and no signs of peritoneal irritation.
Emergency laboratory tests showed only a slight elevation of liver enzymes (AST 78, ALT 175, GGT 350 IU/l), with normal amylase.
Analytical study performed during admission showed persistence of hepatic biochemistry abnormality (AST 80, ALT 170, GGT 261, FA 197 sequel IU/l), amylase of 47 and lipase of 31 IU/ldl reactive bilirubin
Serology for HBV, HCV, HAV, HIV and Brucella were negative, anti-EBNA IgG positive and IgM VCA negative.
Abdominal ultrasound showed hepatic steatosis, gallbladder walls and walls without gallstones and biliary tract nonexistent.
CT scan described an attenuation in the head of the pancreas and trabeculation of the peripancreatic fat and the mesentery without intra-abdominal fluid deficits.
Upper endoscopy was normal.
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Abdominal pain disappeared with conservative treatment and the patient was discharged with a diagnosis of mild acute pancreatitis.
During the follow-up visit 3 months after discharge, there was a moderate increase in the enzymes stasis (GGT 173, FA/L) with normal levels of amylase and inflammatory lipase in an asymptomatic patient.
For this reason ultrasound was repeated, and not visualizing the pancreas, abdominal CT.
This technique reported the existence of a normal pancreas, with homogeneous perfusion, without areas of necrosis, calcifications or alterations of the Wirsung duct.
However, the superior mesenteric vein was not visualized and there was intense collateral circulation, suggestive of complete vein thrombosis.
There were no masses or pathological lymph nodes at any level.
Tumor markers CEA and Ca 199 were normal.
After this, oral anticoagulant treatment was started.
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Superior vein thrombosis is a rare complication of hypercoagulable states that when it occurs acutely, small bowel infarctions can be conditional (2).
Superior vein thrombosis with development of collateral circulation in our patient was not considered a unique consequence of the pancreatic process, as it did not exist during acute pancreatitis when the inflammatory activity was maximal.
A hematologic study was requested for the determination of risk factors and thus a functional activity of protein C of only 28% (normal > 70%) was diagnosed, which could clearly have precipitated the thrombosis month of the patient.
In the literature review we have found only one case similar to ours (3), although there is increasing knowledge that the physiological anticoagulant system disorders determine phenomena in abdominal veins (4).
In the past, it was possible to identify the cause of venous thrombosis in up to half of the patients with nonexistent venous thrombosis.
Due to its asymptomatic course, the diagnosis in chronic forms was made after its debut in the form of hemorrhage by gastroesophageal varices (5), when determining the cause of them.
Currently, the development of computed tomography has encouraged the administration of contrasts (6) and knowledge of hypercoagulable states allows us to determine the cause of indolent chronic venous thrombosis.
In hypercoagulable states, unlike those secondary to cirrhosis, neoplasia or trauma, venous thrombosis begins in the smaller branches and progresses to the main trunks.
Thus, as occurred in our patient, the progressive establishment of the thrombus allows the development of collateral circulation (1) and the absence of any clinical symptoms.
In this case, although acute pancreatitis is by itself a determinant cause of thrombosis of the mesenteric vein, anticoagulation defect that did not exist due to protein C deficiency, the mildness of the pancreatic picture would have made it unlikely.
Thus, the sequence of events, the analytical follow-up and the controls with imaging techniques led to the conclusion that the venous thrombosis the very rare mes was probably determined by the protein C deficiency.
A. J. Lucendo Villarín, G. Carrion Alonso, S. Martin Chávarri, M. Allona Krauel1 and J. R. Prado Rodríguez
Digestive Appliance Services and 1 Diagnostic Radio.
Hospital Universitario La Paz.
Madrid
