Mortality during Transjugular Intrahepatic Portosystemic Shunt Placement

A 70-yr-old, 81-kg man with alcoholic cirrhosis was scheduled to undergo an emergent TIPS procedure. Thirty-six hours before admission, while awaiting cardiac catheterization for new onset chest pain, gastroesophageal bleeding developed, requiring a 6-unit packed erythrocyte infusion. He underwent two endoscopies with sclerotherapy but continued to have slow blood loss. While awaiting scheduled TIPS procedure, frank hematemesis and hypotension developed. The patient underwent emergent endoscopy, but the site was not amenable to banding or sclerotherapy. He was scheduled for emergent TIPS procedure. His medical history was significant for the incidental finding of a 5-cm abdominal aortic aneurysm and the recent development of atypical chest pain, with further diagnostic therapy delayed secondary to his gastroesophageal bleeding. His chest pain was relieved with nitroglycerin patch. He had no episodes of heart failure or arrhythmias. Electrocardiography showed normal sinus rhythm without signs of ischemic changes or prior infarction. There was no history of encephalopathy or renal dysfunction. Current medications included sucralfate, nitroglycerin patch, and furosemide. Physical examination was unremarkable with the exception of the presence of abdominal ascites and pedal edema. Laboratory values were as follows: hematocrit 33% after receiving 2 units of packed erythrocytes, platelet count 110,000 mm sup -3, prothrombin time 15.7 s, partial thromboplastin time 29.9 s, Na 139 mmol/l, K sup + 3.9 mmol/l, Cl 107 mmol/l, HCO³23 mmol/l, blood urea nitrogen 9 mg/dl, Cr 0.7 mg/dl, glucose 93 mg dl sup -1, and NH⁴60 micro mol/l.

Two 18-G peripheral intravenous catheters and a 20-G right radial arterial catheter were placed, and standard ASA monitoring was performed in the angiography suite. Further invasive monitoring was not necessary because of the stability of the patient's chest pain with nitroglycerin patch, normal electrocardiography results, no history of congestive heart failure or arrhythmia, and the relatively hemodynamic stability of the TIPS procedure. Sedation was achieved with 50 micro gram *symbol* kg sup -1 *symbol* min sup -1 propofol, 2 mg midazolam in 0.5-mg increments, and 100 micro gram fentanyl in 25-micro gram boluses intravenously. Two hours after the start of the procedure, the patient's systolic blood pressure decreased from 110 to 60 mmHg with an increase in heart rate to 110 beats/min. No ST-T changes were noted on electrocardiogram monitoring. This coincided with dilation of the Wallstent device. As the patient lost consciousness, ventilation was supported with 100% Oxygen²via mask followed immediately by direct laryngoscopy and intubation of the trachea. Hypotension was treated with a total of 200 micro gram phenylephrine without effect, at which time 100-micro gram incremental boluses of epinephrine (total 400 micro gram) were titrated to achieve a systolic blood pressure in the range of 90 mmHg. Massive extravasation of contrast at the junction of the inferior vena cava and right hepatic vein was confirmed by fluoroscopy and was determined to have been caused by a tear made during the dilation of the Wallstent device. Blood flow distal to the laceration was intermittently occluded while attempts to bypass the laceration with a balloon stent were performed. The patient's blood pressure was maintained using crystalloid and blood products, including packed erythrocytes, whole blood, and fresh frozen plasma, as well as a dopamine infusion (10–15 micro gram *symbol* kg sup -1 *symbol* min sup -1) and 100-micro gram boluses of epinephrine (total 800 micro gram over 55 min). Small doses of midazolam and fentanyl were given during this period. A surgical consultation obtained immediately determined that surgical repair was technically impossible because of the site of the laceration. Attempts to repair the laceration with multiple balloon stents failed. Sixty minutes after initiating resuscitative measures, the patients family opted to withdraw support, and the patient died of irreversible hypovolemic shock.

The most common cause of portal hypertension in the United States remains alcohol-induced cirrhosis of the liver. [9]The incidence of initial variceal bleeding in patients with liver disease is between 27% and 48%. [10]Mortality is approximately 50% after each episode of bleeding [11]with an initial 6-month mortality risk of 40–60%. [12,13]Because of this high early mortality, attention has been focused on prompt intervention and prophylaxis. Therapy has included the use of nonselective beta blockers, endoscopic sclerotherapy, shunt surgery, and more recently, TIPS. Endoscopic sclerotherapy can control active bleeding in 90% of the patients, [14,15]and recurrent gastroesophageal bleeding is usually amenable to repeat sclerotherapy. The small percentage of patients who do not respond to sclerotherapy become candidates for the placement of shunts.

Van Buuren et al. found that the incidence of long-term complications was comparable between TIPS and surgical shunting, but TIPS was associated with a lower morbidity and mortality. [16,17]TIPS has the advantage of being performed under local anesthesia with sedation, is nonoperative with procedural trauma limited to a puncture wound, and can be performed safely in patients awaiting liver transplantation. [5]The presence of a surgical shunt has been associated with a longer duration of surgery during liver transplants, greater procedural difficulty, and greater transfusion requirements compared to patients with TIPS. [6,8]In addition, the success rate of TIPS procedures appears to be about 90%, suggesting the procedure is technically feasible. [4].

Multiple complications from TIPS have been reported, with the incidence of hepatic encephalopathy and shunt occlusion the most common. [8]Hepatic encephalopathy has been reported in 10–20% of patients within 1 month of the procedure. [8]Shunt occlusion occurs in 5–10% of patients but rarely in the immediate postprocedural period. [8]Bleeding, including intraperitoneal hemorrhage, biliary hemorrhage, or liver capsule hematomas, was reported by Haag et al. in 15 patients; however, all but two resolved spontaneously. Of the two affected, one died from disseminated intravascular coagulopathy, and the other improved after therapy for coagulopathy was instituted. [4].

Currently, mortality has not been associated with the technical aspects of performing a TIPS procedure. The role of the anesthesiologist is to provide the necessary support should inadvertent complications occur, remembering that most angiography suites are not well equipped for the management of an actively bleeding patient in hypovolemic shock. Advocating invasive monitoring in otherwise stable patients is not encouraged, but full pharmacologic and airway support should be available in angiography suites even when a stable course is expected in these otherwise complicated patients. The placement of TIPS appears to be a breakthrough that will be increasingly introduced in most hospitals that require active participation of the anesthesia team.