D-dimer levels in the blood may be elevated as a result of fibrin breakdown.On duplex ultrasound, demonstration of echogenic material within the portal vein, complete or partial absence of colour flow in the portal vein, presence of collateral vessels around the portal vein or gall bladder that bypass the portal vein. Treatment
Treatment is aimed at opening the blocked veins to minimize complications; the duration of clot (acute versus chronic) affects treatment. Unless there are underlying reasons why it would be harmful, anticoagulation (low molecular weight heparin, followed by warfarin) is often initiated and maintained in patients who do not have cirrhosis. Anticoagulation for patients with cirrhosis who experience portal vein thrombosis is usually not advised unless they have chronic PVT 1) with thrombophilia, 2) with clot burden in the mesenteric veins, or 3) inadequate blood supply to the bowels. In more severe instances, shunts or a liver transplant may be considered. If blood flow to the gastrointestinal tract has been compromised chronically, surgery may be required to remove dead intestine.Different considerations are made in the management of PVT in pediatric patients or those who have already received a liver transplant. See also
Pylephlebitis
Budd–Chiari syndrome

References
External links

Merck
The onset of back and leg pain is characterized by severe pain and stiffness in back and thighs followed by loss of tendon reflexes and paralysis. Psychiatric symptoms are present, such as paranoid schizophrenia-like features but rarely psychosis and hallucinations. The acute attacks classically present with dark-red photosensitive urine (often called port-wine urine), but this is a nonspecific symptom. Physical examination often shows no abnormalities.Hyponatremia is the most common electrolyte abnormality during acute attacks, occurring in 40% of patients and presenting as SIADH. Hypomagnesemia is also common. There are no pathognomonic signs or symptoms.The most common identified triggers for acute attacks are medications, weight loss diets, and surgery. Many medications have been associated with AIP including antibiotics, hormonal contraceptives, seizure medications, anesthetics, and HIV treatment drugs. Cause
Porphyrias are caused by mutations in genes that encode enzymes in heme synthesis. In normal physiology, heme synthesis begins in the mitochondrion, proceeds into the cytoplasm, and finishes back in the mitochondrion. Heme is produced in all cells, but 80% of all heme is produced in erythropoietic cells in bone marrow and 15% in parenchymal cells in the liver, where turnover of hemoproteins is high. In AIP, over 100 mutations have been identified on the long arm of chromosome 11 at the HMBS gene, which codes for the cytoplasmic enzyme porphobilinogen deaminase. This deficiency prevents heme synthesis, which can not be completed and the metabolite porphobilinogen accumulates in the cytoplasm.AIP is an autosomal dominant porphyria resulting in about 50% normal activity of the affected enzyme.