Can an occluded Transjugular Intrahepatic Portosystemic Shunt (TIPS) cause hyperammonemia?

Occluded TIPS and Ammonia Levels

No, an occluded TIPS will not cause elevation in ammonia levels; rather, TIPS occlusion would be expected to reduce or normalize ammonia levels by eliminating the portosystemic shunt that bypasses hepatic ammonia clearance.

Understanding the Relationship Between TIPS and Hyperammonemia

TIPS Creates Hyperammonemia Through Shunting

• A functioning TIPS causes hyperammonemia by diverting portal blood away from the liver, preventing hepatic ammonia metabolism and allowing ammonia to reach the systemic circulation directly 1
• Research demonstrates that hyperammonemia in patients with cirrhosis and a TIPS results from portosystemic shunting, where ammonia produced by the portal drained viscera and kidneys bypasses hepatic clearance 1
• Low ammonia levels before TIPS placement predict higher risk of post-TIPS hepatic encephalopathy, as these patients experience greater increases in blood ammonia after the shunt is created 2

Physiologic Mechanism

• In patients with a functioning TIPS, skeletal muscle removes more ammonia from circulation than the cirrhotic liver, demonstrating the critical role of portosystemic shunting in maintaining hyperammonemia 1
• The portal drained viscera produce the highest amount of ammonia, and when this blood bypasses the liver through a TIPS, systemic ammonia levels rise 1
• Hepatic encephalopathy occurs in up to 50% of patients after TIPS creation, directly related to the hyperammonemia caused by the shunt 2

Clinical Implications of TIPS Occlusion

Expected Ammonia Response

• When a TIPS becomes occluded, portal blood flow is restored through the liver, allowing hepatic ammonia metabolism to resume and ammonia levels to decrease
• The EASL guidelines recommend TIPS reduction or occlusion for chronic symptoms of over-shunting, including severe recurrent hepatic encephalopathy (more than three episodes), which is driven by hyperammonemia 2
• Therapeutic TIPS occlusion is performed specifically to reduce ammonia levels and treat refractory hepatic encephalopathy 2

Clinical Monitoring After TIPS Dysfunction

• If TIPS dysfunction is suspected based on clinical findings (such as recurrent varices or ascites), endoscopic screening should be performed to check for varices needing treatment 2
• Doppler ultrasound should be conducted to evaluate TIPS patency, though it has low specificity (33-95%) and high false positive rates (50%) for detecting dysfunction 2
• Laboratory evaluation including assessment for bleeding and hepatic dysfunction should be performed, but ammonia elevation would not be expected with TIPS occlusion 2

Common Pitfalls and Caveats

Distinguishing TIPS Dysfunction from Other Causes

• Do not attribute new hepatic encephalopathy to TIPS occlusion—the opposite is true, as occlusion should improve encephalopathy by reducing ammonia 2
• If a patient with an occluded TIPS develops encephalopathy, look for other precipitants such as infection, hyponatremia, gastrointestinal bleeding, or renal dysfunction 2
• Remember that competing collaterals (spontaneous portosystemic shunts) can maintain hyperammonemia even with a non-functioning TIPS, and these may require embolization 2

Clinical Decision-Making

• In cases of refractory hepatic encephalopathy with a patent TIPS, embolization of competing collaterals should be attempted before TIPS reduction or occlusion 2
• The presence of hepatofugal flow through collaterals despite a functioning TIPS indicates significant competing shunts that may be the primary cause of hyperammonemia 2