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Anesthesia for Transjugular Intrahepatic Portosystemic Shunt

Corey Scher, MD
The Mount Sinai Medical Center New York, New York

Anesthesiologists have always felt the challenge, if not the dilemma, of providing a service and being a doctor at the same time. The days that we have practiced anesthesiology as physicians are the most rewarding and are very much related to our clinical assignments. It may come as a surprise to the anesthesiologist that the dreaded transjugular intrahepatic portosystemic shunt (TIPS) assignment will challenge the intellect and brings the rewards of self-esteem if the clinician fully understands the complexities of the patient, procedure, and anesthetic. The TIPS procedure involves a percutaneously created connection between the hepatic portal and systemic circulation that is placed to reduce portal pressure as cirrhosis in the liver obstructs normal portalsystemic blood ow. The goal of the TIPS is to divert portal ow into a hepatic vein and thus return it to the right atrium. This will reduce the gradient between the portal and systemic circulation. Shunt patency is maintained by an expandable metal stent or other synthetic stent across the intrahepatic tract. Accepted indications for TIPS include variceal bleeding that cannot be controlled with medical treatment refractory ascite portal decompression in hepatic venous outow obstruction (Budd Chiari), hepatic hydrothorax, or hepatorenal syndrome. The technical aspects of TIPS have progressively improved since the inception of the procedure by Colopinto et al in 1983.1 Although many patients undergoing TIPS have low Model for End Stage Liver Disease scores (a numerical function of bilirubin,

REPRINTS: COREY SCHER, MD, DEPARTMENT OF ANESTHESIA, THE MOUNT SINAI MEDICAL CENTER, NEW YORK, NY 10029, E-MAIL: COREY.SCHER@MOUNTSINAI.ORG
INTERNATIONAL ANESTHESIOLOGY CLINICS Volume 47, Number 2, 2128 r 2009, Lippincott Williams & Wilkins

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international normalized ratio, and creatinine) and are not considered to have end stage liver disease (ESLD), they usually suffer from multiorgan disease as a result of loss of hepatic synthetic and metabolic function. The anesthesiologist must understand the multiple organ systems that are involved in such patients to provide a safe anesthetic and not further compromise the tenuous state.

Preoperative Anesthetic Evaluation of the Patient Presenting for TIPS

The current clinical paradigm for the patient with ESLD focuses on medical optimization in preparation for liver transplantation. It is important to understand that the patient is not cured after transplantation, and faces a lifetime of immunosuppressive therapy and its potential complications including infection, rejection, and lymphoproliferative disorders. Severe liver disease may cause cirrhotic cardiomyopathy, pulmonary hypertension, portopulmonary syndrome, hepatorenal syndrome, hepatic encephalopathy, anemia from variceal bleeding, bone marrow suppression, and electrolyte abnormalities. In addition, patients are on a whole host of medications that are often unfamiliar to the anesthesiologist. The preanesthetic assessment must include an understanding of each of these end organ effects.
Cardiac Evaluation

Cirrhotic cardiomyopathy is the term applied to a host of cardiac problems as a result of liver cirrhosis.2 Although a pulmonary artery catheter may reveal a cardiac output of 12 L/min; it goes without saying that the heart is not twice as healthy as a patient with a cardiac output of 6 L/min. Angiogenesis and the creation of varices as a mechanism to bring blood back to the heart results in a large preload. While resting left ventricular ejection fraction may be normal in a patient with cirrhotic cardiomyopathy, the heart does not respond to loading conditions like a normal heart. In the cirrhotic patient, ventricular performance may not be characterized by a normal starling curve, in which an increase in preload produces an increase in pressure. Rather, the heart may not generate pressure with loading like a normal heart. Of extreme importance, the Q-T interval adjusted to heart rate (QTc) is commonly prolonged in cirrhotic cardiomyopathy. This prolongation may make the patient arrhythmias such as Toursades de Pointes, which is a rapid, polymorphic ventricular tachycardia with a characteristic twist of the QRS complex around the isoelectric baseline.3 This rhythm disturbance may degenerate into ventricular tachycardia or ventricular brillation. If a prolonged QTc interval is determined,

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it may be wise to apply transcutaneous pacing pads before initiating an anesthetic.


Pulmonary Evaluation

Three particular areas should be investigated that are particular to the ESLD patient and should be evaluated before TIPS. First, extensive ascites and pleural effusions may produce compressive atelectasis and impair ventilation and oxygenation. Second, of greater signicance but of lesser incidence is hypoxemia associated with portopulmonary syndrome.46 Although the exact mechanism of the hypoxemia is unclear, simply stated, blue blood stays blue and passes through varices within the lung rather than pulmonary capillaries that participate in gas exchange. Although this is a simplistic explanation, it serves the clinician well until science proves something better. Interestingly, the incidence of portopulmonary syndrome and level of hypoxemia correlate poorly with the severity of liver disease. The third area to be addressed is the signicant problem of pulmonary hypertension. The exact mechanism of pulmonary hypertension remains to be elucidated. There is a general consensus that patients with a pulmonary artery systolic pressure in excess of 60 mm Hg are poor candidates for hepatic transplantation. In the setting of a newly placed TIPS, the previously under lled right ventricle receives additional new ow from the new hepatic vein and may fail in the face of preexisting pulmonary hypertension, which increases afterload, and the additional preload from increased venous return.4 A resting echocardiogram can screen for pulmonary hypertension.
Neurologic Evaluation

Encephalopathy has been well described in ESLD. Although the etiology is complex, ammonia is most often cited as a leading factor. Ammonia, which is metabolized by the normally functioning liver, is not in the patient with ESLD. Ammonia is broken down to glutamine, which accumulates in the astrocytes and produces cellular swelling. Other substances that are normally metabolized by the liver also accumulate in the central nervous system and likely enhance hepatic encephalopathy. Although standard treatment includes lactulose as a means of increasing bowel motility to decrease protein/ammonia absorption, numerous trials of other medications are ongoing, including a bioarticial liver that removes ammonia from the blood. It is important to note that the bioarticial liver in clinical use in Europe only removes noxious substances and does not have any synthetic function. It is important to perform a neurologic examination before proceeding with the TIPS procedure as encephalopathy may be exacerbated by the TIPS procedure. In patients without cirrhosis,

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venous blood from the gastrointestinal tract is transported to the portal vein and thus to hepatic veins for metabolic and synthetic functions by the hepatocytes. In the cirrhotic patient, blood in the portal vein cannot enter the scarred liver. The TIPS procedure reestablishes the portalhepatic vein-caval ow. The onset of clinically apparent encephalopathy or increase in its severity is explained by the direct conduit from the portal vein for ammonia and other substances normally metabolized by the liver that seems to bypass hepatocyte function.7 Delayed awakening or a marked decrease in mental status after an anesthetic for TIPS is usually addressed conservatively by instituting those routine measures that lower the ammonia load from the gastrointestinal tract. Return to baseline is common within a few days. Coagulation Disorders There are several hemorrhagic complications of the procedure. Severe bleeding may occur at multiple sites. Capsular tears, hepatic vein tears, and disruption of the portal vein have been reported.8 Coagulation disorders may be complex. The activity of liver-dependent coagulation factors, factors X, IX, VII, and II, may be decreased. Circulating plasminogen may lead to brinolysis. Thrombocytopenia is common because of platelet trapping secondary to portal hypertension. The liver also synthesizes thrombopoetin, which is vital to stimulate the bone marrow to produce platelets.8 What challenges our intuition is that we often see abnormal results of standardized coagulation tests like the prothrombin time, partial thromboplastin time, and international normalized ratio that suggest the patient is extremely coagulopathic, whereas at the same time there is identiable clot in the portal or hepatic veins. This clinical picture is referred to Budd-Chiari syndrome and may ultimately lead to ESLD that may actually extend from the portal vein to the vena cava and right ventricle. In this setting, use of the thromboelastogram may suggest a specic evidence-based treatment plan so that fresh frozen plasma and platelets are not reexly ordered on call to the interventional suite. Recurrent TIPS stent stenosis has been reported in a patient with resistance to activated protein C. Combination therapy with low-dose enoxaparin and clopidogrel could not prevent recurrent stent occlusion.9 Finally, therapy with high-dose enoxaparin was sufcient to prevent further shunt complications. Sufce it to say that the coagulation disorders of TIPS patient may and usually is more complex than giving liver-based factors and platelets.
Renal Evaluation

The patient with liver disease often has concomitant renal dysfunction. The commonly applied term for this is hepatorenal syndrome. Our understanding of this syndrome is incomplete. Mechanistically, the cirrhotic liver generates an increase in portal pressure, which produces

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splanchnic blood pooling.10 This splanchnic blood pooling results in relative hypovolemia in the central and arterial system, initiating activation of the renin-angiotensin-aldosterone axis and the sympathetic nervous system. These compensatory mechanisms induce renal vasoconstriction, followed by hypoperfusion of the kidneys and development of hepatorenal syndrome. Histologically, the kidney is usually normal, but clinically the syndrome has a wide range of signs and symptoms, with the extreme cases resulting in renal failure that requires hemodialysis. Anesthetic techniques may need to be adjusted to account for the degree of patients renal failure. Methods to lower serum potassium by hyperventilation, glucose-insulin, calcium, and sodium bicarbonate may be needed, particularly if multiple units of packed red blood cells, which may increase serum potassium levels, are required. Although there are clinical trials of vasopressors to force splanchnic blood to the kidney, these are not yet employed routinely as part of the management of hepatorenal syndrome. A common presentation of hepatorenal syndrome is a dilutional hyponatremia due to a limitation in free water excretion.11 This may occur in the setting of ascites. The treatment consists of water and sodium restriction. The level of hyponatremia should be evaluated, and hyponatremia was corrected carefully before initiation of this relatively elective procedure. Worsening of hyponatremia during the TIPS procedure may contribute to postprocedure encephalopathy. Anesthetics that rely on renal metabolism should not be used.
Venous Access Evaluation

Venous access to administer an anesthetic may be challenging in the chronically ill patient. Specialized visualization techniques, including ultrasound and uoroscopy, and the assistance of the interventional radiology team, may be useful in gaining venous access. Many interventionalists are trained to gain venous access at locations, such as the lumbar veins, that are outside the routine practice of the anesthesiologist. A bedside consult with one of the interventionalists before initiating venous access attempts may save the clinician and patient emotional, if not physical, discomfort when many scars are noted on the patients skin.
Consent

The TIPS procedure ranges from a 45-minute uncomplicated event to a case requiring invasive monitoring and postprocedure an admission to the intensive care unit. It is vital that the patient, if not encephalopathic, or surrogate understands the wide range of possibilities that may occur during this difcult interventional procedure. If a separate consent for anesthesia is not used, a preprocedure note that clearly

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documents that the patient or surrogate understands the potential interventions and complications related to anesthesia should be written.

Indications and Contraindications for TIPS

Although the indications are discussed above, there is a wide array of unproven or, better stated, unproven but promising indications. These include reduction of intraoperative morbidity during liver transplantation, and initial therapy to prevent an initial variceal bleed. As the both technology surrounding TIPS improves and as more types of patients become candidates for transplantation, it is likely that TIPS will be employed more frequently for these other indications. Absolute contraindications to this procedure include right-sided heart failure, polycystic liver disease, and severe hepatic failure. Although the rst and last contraindications seem obvious, polycystic liver disease needs further explanation. This inherited disorder often includes polycystic kidneys. Over time, the liver may develop multiple uid-lled cysts and grow in size to ll much of the abdominal cavity. The liver is often not cirrhotic and poses enormous technical challenges that do not serve the best interests of the patient. Relative contraindications include systemic infection (colonization of the stent), severe hepatic encephalopathy that is poorly controlled medically, hypervascular hepatic tumors, and portal vein thrombosis.

TIPS: the Procedure and the Anesthetic

The patients neck is examined with an ultrasound probe to determine the patency of the right and left internal jugular veins. After the site for cannulation (usually the right internal jugular vein) is selected, the vein is accessed under ultrasound guidance and a wire is placed via the Seldinger technique into the right hepatic vein. A 5.0-Fr catheter is then inserted and wedged into the vein. CO2 (50 mL) is injected to opacify the portal venous system. If this fails, an occlusion balloon catheter is employed to obtain biplane CO2 wedged hepatic venograms and biplane uoroscopy is used to obtain an optimal portogram.12 The wedged venograms serve as a guide for the Colopinto needle that is inserted through the right hepatic vein and directed in an anterior-inferior path to access the right portal vein. Contrast material then is injected to verify the point of the Colopinto needle entry. A guidewire and catheter then are inserted into the portal vein, followed by portal venography. Pressure measurements are made between the right atrium and portal vein. If the pressure gradient exceeds 12 mm Hg (portal higher then atrial), the denitive shunt is placed. If the gradient is not elevated, it is often assumed that spontaneous

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shunts (splenorenal) may have formed. Several models of stents are commercially available and are often dilated by angioplasty to the optimal lumen desired.13 This simple explanation does not elucidate the fact that this procedure may be relatively uneventful at times and performed quickly, or it may be technically challenging and last for hours. There is rarely a case that one can predict accurately both duration and complications. It is our custom and practice, unless otherwise contraindicated, to perform general endotracheal anesthesia. With limited access to the patient, once prepped and draped and with frequent movements of the head to facilitate vascular cannulation, we favor intubation as opposed to placement of a laryngeal mask airway. Medications with limited hepatic metabolism (eg, desurane, cis-atracurium) are used. As the procedure is not painful, opioids are used sparingly. In addition, minimal volumes of crystalloid solutions are administered, as the patient has a decreased ability to excrete free water. Excessive uid administration may compound preexisting hyponatremia. Invasive monitoring is determined on a case-by-case basis and with the consensus of the interventionalists. It is essential that all personnel use proper shielding, including eye protection (to prevent lens opacities and cataracts), to minimize exposure to ionizing radiation.14 It is our practice not to assign these cases to pregnant anesthesiologists to avoid any exposure to the developing fetus.

References

1. Colopinto RF, Stronell RD, Gildiner M. Formation of intrahepatic portosystemic shunts using a balloon dilatation catheter: preliminary clinical experience. AJR Am J Roentgenol. 1983;140:709714. 2. Mandell LS, Lindenfeld J, Tsou MY, et al. Cardiac Evaluation of liver transplant candidates. World J Gastroenterol. 2008;14:34453451. 3. Moller S, Henriksen JH. Cardiovascular complications of cirrhosis. Gut. 2008;57: 268278. 4. Schenk P, Fuhrmann V, Madl C, et al. Hepatopulmonary Syndrome: prevalence and predictive value of various cut offs for arterial oxygenation and their clinical consequences. Gut. 2002;51:853859. 5. Swanson KL, Wiesner RH, Nyberg SL, et al. Survival in portopulmonary hypertension: Mayo clinic experience categorized by treatment subgroups. Am J Transplant. 2008;8:24452453. 6. Krug S, Seyfarth HJ, Hagendorff A, et al. Inhaled Iloprost for hepatopulmonary syndrome: improvement of hypoxemia. Eur J Gastroenterol Hepatol. 2007;19: 11401143. 7. Kavitt RT, Yang VL, Jensen DM. Cerebral edema and hyperammonemia after transjugular intrahepatic portosystemic shunt placement in a cirrhotic patient. Clin Gastroenterol Hepatol. 2008;6:10541056. 8. Peck-Radosavljevic M. Review article: coagulation disorders in chronic liver disease. Ailment Pharmacol Ther. 2007;26(suppl 1):2128.

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9. Siewert E, Salzmann J, Purucker E, et al. Recurrent throbotic occlusion of a transjugular intrahepatic portosystemic stent-shunt due to activated protein C resistance. World J Gastroenterol. 2005;11:50645067. 10. Moreau R, Lebrec D. Acute kidney injury: new concepts hepatorenal syndrome: the role of vasopressors. Nephron Physiol. 2008;109:7379. 11. Martin-Llahi M, Guevara M, Gines P. Hyponatremia in cirrhosis: clinical features and management. Gastroenterol Clin Biol. 2006;30:11441151. 12. LaBerge JM, Ring EJ, Gordon RL. Creation of transjugular intrahepatic portosystemic shunts with the wallstent endoprosthesis: results in 100 patients. Radiology. 1993;187:413420. 13. Otal P, Smayra T, Bureau C. Preliminary results of a new expanded-polytetrauoroethylene-covered stent-graft for transjugular intrahepatic portosystemic shunt procedures. AJR Am J Roentgenol. 2002;178:141147. 14. Vano E, Gonzalez L, Fernandez JM, et al. Eye lens exposure to radiation in interventional suites: caution is warranted. Radiology. 2008;248:945953.