1. Ultrasound Evaluation of Visceral Veins
31ST annual congress

2. PORTAL VEINS
The portal vein waveform associated with a healthy liver demonstrates mild undulations. This is due to respiratory variation.

3. PORTAL VEINS
Increased pulsatility occurs due to the transmission of pressure across the hepatic sinusoids. Alternatively, an increased pulsatility index may occur with high right atrial pressure, which can be seen with right heart failure and tricuspid regurgitation.

4. PORTAL VEINS
In patients with cirrhosis, arterio-portal shunting is a major cause for pulsatility due to structural distortion in combination with a reversed portal venous flow.
Hepatocellular carcinoma, which is commonly seen in cirrhotic patients, may cause peri-lesion shunting via draining veins.
Liver biopsies performed on cirrhotic patients may also result in arterio-portal fistula formation.

5. PORTAL VEINS
Normal main portal vein (MPV) peak systolic velocities range between 20 cm/sec and 40 cm/sec. A low flow velocity of <16 cm/sec in addition to an increased diameter of the MPV (>13mm) are diagnostic features of portal hypertension.

6. PORTAL VEINS
With increasing portal venous pressure, there is a decrease in the portal venous flow velocities approaching stagnation. As this occurs, a to-and-fro flow can be seen which may lead to thrombosis or progress to flow reversal.

7. PORTAL VEINS
Porto-systemic collateral formation occurs with increasing portal pressure. Common collateral vessels include:
Coronary (left gastric) varices
Esophageal varices
Abdominal wall varices
Recanalized paraumbilical vein
Periportal varices
Gastrorenal varices
Splenorenal varices

8. PORTAL VEINS
Stagnation of portal flow is a function of advanced portal hypertension associated with severe liver fibrosis such that flow is absent. Absence of flow may also be seen with bland or tumor thrombus.
Approx. 11% of patients with cirrhosis will develop PVT. Periportal collaterals or cavernous transformation are seen with portal vein occlusion.

9. PORTAL VEINS
Portal vein thrombosis in patients with cirrhosis may be due to many factors, including reduced or stagnant blood flow and reduced levels of circulating anticoagulants (ie, protein C, protein S, and antithrombin III).

10. HEPATIC VEINS
The normal hepatic vein waveform reflects the pressure variations within the right atrium during the cardiac cycle producing a triphasic waveform.
Valsalva maneuver raises intrathoracic pressure and alters the hepatic venous waveform, often rendering it monophasic.

11. HEPATIC VEINS
Fibrotic or inflammatory changes of the liver may result in a monophasic flow pattern of the hepatic vein.
Hepatic venous pulsatility may disappear during pregnancy.
Distorted liver architecture due to cirrhosis can cause a reduction in hepatic vein caliber.

12. MESENTERIC VEINS
Venous drainage of the superior mesenteric vein parallels the arterial circulation and drains into the portal venous system.

13. MESENTERIC VEINS
Acute superior mesenteric vein thrombosis is uncommon, accounting for only 5-15% of all cases of acute mesenteric ischemia

14. MESENTERIC VEINS
The majority of cases are considered secondary to an identifiable underlying condition, including:
Hypercoagulable states
Malignancy
Polycythemia vera
Protein C deficiency
Protein S deficiency
Antithrombin III deficiency
Recent abdominal surgery
Intra-abdominal or systemic sepsis
Portal hypertension