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Chapter 11 / Cirrhosis and Portal Hypertension 131

conditions. However, HRS is distinct from acute intrinsic renal failure, with

low urine sodium, a high urine/plasma creatinine ratio, high urine osmo-

lality, and normal urine sediment. In an attempt to distinguish HRS from

other etiologies, diagnostic criteria for HRS were developed (Table 11.4).

Pulmonary

Although some causes of cirrhosis can also cause pulmonary complications,

cirrhosis itself can have eects on the pulmonary system. As ascites devel-

ops, lymphatic transdiaphragmatic communication can result in hepatic

hydrothorax. e resultant eusion can directly compress pulmonary

parenchyma, which impairs gas exchange and may result in hypoxemia.

Hepatopulmonary syndrome (HPS) is diagnosed with hepatic dysfunc-

tion, oxygen tension less than 70mm Hg or diusion gradient greater than

20mm Hg, and pulmonary vascular dilation in structurally normal lungs.

Patients present with shortness of breath when moving from supine to

upright position (platypnea) and dyspnea in the absence of primary pulmo-

nary disease. On physical exam, patients may have clubbing and cyanosis of

nail beds. Portopulmonary hypertension is dened by a mean pulmonary

arterial pressure of greater than 25mm Hg in the presence of liver disease.

is rare entity has a signicant risk of mortality and is a relative contra-

indication to liver transplant. e exact mechanism of HPS is not known;

interestingly, portal hypertension is not required for its development.

e goal of treating and preventing pulmonary complications of cir-

rhosis and portal hypertension centers around uid management. With the

previously discussed uid derangements, extracellular uid increases and

intravascular volume decreases. Increasing ascitic uid can impair respira-

tion due to increased intra-abdominal pressure, so therapeutic paracente-

sis can help relieve this pressure and improve air exchange. Prevention of

Major Criteria

1. Low glomerular ltration rate, as indicated by serum creatinine >1.5mg/dL or

24-hour creatinine clearance 40mL/min

2. Absence of shock, ongoing bacterial infection, uid losses, and current

treatment with nephrotoxic drugs

3. No sustained improvement in renal function (decrease in serum creatinine to

≤1.5mg/dL or increase in creatinine clearance to 340mL/min) following diuretic

withdrawal and expansion of plasma volume with 1.5L of a plasma expander

4. Proteinuria <500 mg/d and no ultrasonographic evidence of obstructive

uropathy or parenchymal renal disease

Additional Criteria

1. Urine volume <500mL/d

2. Urine sodium <10mEq/L

3. Urine osmolality greater than plasma osmolality

4. Urine red blood cells <50 per high-power eld

5. Serum sodium concentration <130mEq/L

All major criteria must be present for the diagnosis of HRS. Additional criteria are not necessary for

the diagnosis but provide supportive evidence.

From Arroyo V, Ginés P, Gerbes A, et al. Denition and diagnostic criteria of refractory ascites

and hepatorenal syndrome in cirrhosis. Hepatology 1996;23:164, Mulholland MW, Lillemoe KD,

DohertyGM, et al. Greeneld’s surgery: scientic principles & practice. 5th ed. Philadelphia, PA:

Lippincott Williams & Wilkins, 2010.

Diagnostic Criteria for Hepatorenal Syndrome

TABLE

11.4

Section II / Liver132

uid accumulation is done through sodium restriction. e more complex

treatment of HPS and portopulmonary hypertension is beyond the scope

of this chapter.

Hepatic Encephalopathy

Hepatic encephalopathy is manifested by mental status alterations.

Although a debated topic, the pathophysiology of hepatic encephalopathy

is related to ammonia. Interestingly, the serum concentration of ammonia

does not correlate with the severity of encephalopathy. Normally, after bac-

terial digestion of proteins, ammonia is absorbed through the gut and then

undergoes degradation in the liver. With impaired hepatic function, ammo-

nia reaches the peripheral circulation, permeates the blood–brain barrier,

and causes alterations in mental status. Evidence exists both in favor of and

against elevated serum ammonia as the cause of hepatic encephalopathy.

Serum ammonia levels are elevated in up to 90% of patients with hepatic

encephalopathy, and treatments that reduce ammonia levels improve or

resolve this condition. Alternatively, there is poor correlation of ammonia

level with severity of encephalopathy; direct administration of ammonia to

patients with cirrhosis does not cause encephalopathy; and the same treat-

ments that reduce ammonia levels also reduce other toxin levels. Signs and

symptoms of hepatic encephalopathy include early ndings of memory

loss, mood disturbances, and sleep pattern alteration. As the condition pro-

gresses, confusion, lethargy, obtundation, and coma can occur. Asterixis,

elevated ammonia levels, and altered mental status are strongly suggestive

of hepatic encephalopathy.

Treating hepatic encephalopathy involves dietary modications and

medications that reduce ammonia production and/or neutralize its eects.

Initially, any precipitating factors need to be identied including infectious

source, electrolyte abnormalities, and medications. ese factors should be

treated if possible. Secondly, intravenous uids are administered to expand

intravascular volume and dilute the concentration of the toxins. In addi-

tion to marked dietary restriction of proteins, nitrogenous compounds

should be removed from the gut. is is done via medications that inhibit

the metabolism of such compounds in the gut, thereby reducing ammonia

levels. e preferred medication is lactulose, which can be administered

orally, through a nasogastric tube, or per rectum. Lactulose is administered

three to four times daily, with the goal of producing two to three soft bowel

movements per day. Dosing ranges from 45 to 90 g/d. Its mechanism has

been debated, but is possibly through alteration of bacterial metabolism

to increase bacterial uptake of ammonia. Other medications include neo-

mycin and metronidazole, which work to decrease the concentration of

ammonia-forming bacteria in the gut.

Ascites

Ascites is present when free uid within the peritoneal cavity reaches over

150 mL. In addition to cirrhosis and portal hypertension, the dierential

diagnosis for ascites is broad. Congestive heart failure and renal insuciency

both commonly cause ascites. Other causes of ascites include hypoalbumin-

emia; bile, chylous, or pancreatic urinary ascites; ovarian disease; perito-

neal dissemination of carcinoma; and myxedema. In the setting of cirrhosis,

increased sinusoidal pressure results in leaking of protein-rich uid directly

from the liver into the peritoneal cavity. Ascites is of prognostic signicance

in a patient with portal hypertension. One-year mortality with new-onset

ascites in a cirrhotic patient is estimated at 50%, compared to 10% in cir-

rhotic patients without ascites. is uid cannot be absorbed secondary to

the increased hydrostatic pressure and accumulates in the peritoneal cavity.

Chapter 11 / Cirrhosis and Portal Hypertension 133

Physical exam ndings include shifting dullness, bulging anks, increased

abdominal girth, and uid waves. With enough ascites accumulation,

increased intra-abdominal pressure can cause respiratory distress. Increased

intra-abdominal pressure in combination with muscle wasting can result in

abdominal wall and inguinal hernias, which are dicult to manage.

Management of renal sodium and water retention, dietary sodium

restriction, and bed rest are the initial steps in the treatment of ascites.

Sodium retention is exacerbated in the upright position secondary to

venous pooling and relative hypovolemia; therefore, bed rest is recom-

mended; up to 15% of patients respond with this therapy alone. In addi-

tion, dietary salt restriction is implemented; however, compliance with

this recommendation is generally poor. If these lifestyle modications are

ineective, diuretics are the mainstay of treatment. Furosemide and spi-

ronolactone are generally prescribed in combination to maximize eec-

tiveness. Intermittent large-volume paracentesis can be performed for

patients with large volumes of uid that are not responding to lifestyle or

medication interventions. Up to 30 L of uid can be removed with infusion

of concentrated albumin repletion. Ascites can also be treated with shunts,

either peritoneovenous (surgical) or portosystemic (i.e., TIPS), which are

discussed later in this chapter. Surgical portovenous shunts that are associ-

ated with signicant complications are rarely used. Table 11.5 lists treat-

ments of ascites, including doses for antibiotic prophylaxis for spontaneous

bacterial peritonitis (SBP) (see below).

Bed rest

Sodium restriction

1–2g/d (45–90mEq/d)

Fluid restriction

1–1.5L/d

Diuretics

Spironolactone

50mg PO q8h

Maximum of 100mg q6h

Furosemide

40–370mg/d

Antibiotics

Cefotaxime

2g IV q12h

Ooxacin

400mg PO q12h

Prophylaxis

Noroxacin

400mg/d while hospitalized

Ciprooxacin

750mg PO weekly

Noroxacin

400mg/d for 6 mo

Trimethoprim/sulfamethoxazole

One double-strength tablet ve times a week

Mulholland MW, Lillemoe KD, Doherty GM, et al. Greeneld’s surgery: scientic principles & practice.

5th ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2010.

Treatment of Ascites

TABLE

11.5

Section II / Liver134

Spontaneous Bacterial Peritonitis

Up to 10% of patients with portal hypertension and ascites will develop

SBP. e etiology of SBP is unclear, but often patients have had preceding

gastrointestinal hemorrhage. Ten to twenty percent of cases are detected

by evaluating routine paracentesis uid, but most patients present with

clinical symptoms of abdominal pain, fever, progressive encephalopathy,

and impaired renal function. Specic criteria for SBP include a serum–

scites–albumin gradient of ≥1.1g/dL, a polymorphonuclear count of ≥250

cells/mm

, and a single organism (usually G+) on culture. e presence of

more than one organism cultured from peritoneal uid raises suspicion for

secondary bacterial peritonitis and mandates evaluation for sources such

as a perforated viscus and appendicitis.

Antibiotic prophylaxis against SBP is given to patients with a low

protein count in their ascitic uid or patients with gastrointestinal hemor-

rhage, as those patients are at high risk for development of SBP. Patients with

hemorrhage are given ooxacin alone or neomycin, colistin, and nystatin in

combination. ese medications can reduce the incidence of SBP from up

to 20% to about 9% with few side eects. Patients with diagnosed SBP are

treated with intravenous cefotaxime or oral ooxacin.

Esophageal Varices

Esophageal varices are a life-threatening complication of portal hyperten-

sion and can be quite dicult to manage. Esophageal varices are the most

common site for life-threatening variceal bleeding. Typically, they are located

in the distal esophagus, in the submucosal venous plexus. As these vessels

dilate, they become more supercial and they erode into the lamina propria.

Variceal development is dependent upon the pressure in the portal system.

In general, a hepatic vein–portal vein gradient of about 12mm Hg is present

in patients with varices, although not all patients with this gradient or higher

will develop varices. Incidence varies widely in the literature, ranging from

8% to 90% of patients with cirrhosis. Nevertheless, once varices develop, the

risk of bleeding is 25% to 35%. Predictors of bleeding include a combination

of CTP class, variceal size, and specic markings present on endoscopy.

e mainstay of therapy for esophageal varices is medical, the goal being

decreased splanchnic blood ow and prevention of rst bleeding episode.

Beta-blockade is the rst-line treatment, with nadolol and propranolol being

the agents of choice. e mechanism of nonspecic beta-blockade includes

decreasing cardiac output as well as increasing splanchnic vasoconstriction;

combined, they result in decreased portal blood ow and decreased hepatic

portal venous gradient. Beta-blockers are eective regardless of the etiology

of portal hypertension, even in the absence of ascites. ey can also reduce

mortality from subsequent bleeding episodes in patients with large varices.

Organic nitrates are also eective in primary and secondary prevention of

bleeding. ese medications cause splanchnic vasoconstriction and arterial

vasodilation, thereby decreasing collateral resistance. Nitrates also decrease

hepatic resistance, likely a result of stellate cell contractility inhibition . Patients

with a contraindication to beta-blocker treatment receive nitrates as the rst-

line therapy. e combination of nitrates with beta-blockers decreases in the

incidence of variceal bleeding to a greater degree than either alone.

MANAGEMENT OF ACUTE VARICEAL BLEEDING

Medical Treatment

Acute variceal bleeding requires prompt attention. Basic management

includes securing a protected airway, establishing intravenous access with

large-bore catheters, close hemodynamic monitoring, thorough laboratory

Chapter 11 / Cirrhosis and Portal Hypertension 135

evaluation, intensive care monitoring, and blood product administration

as needed. Medications used in the situation of acute bleeding include

continuous intravenous administration of vasopressin and/or octreotide.

Octreotide infusion is very eective. It is the rst-line therapy in acute

variceal bleed, as it results in splanchnic vasoconstriction without any

unintended consequences. Its mechanism is indirect, by reducing the lev-

els of other gut hormones that normally cause vasodilation. Vasopressin

decreases portal venous ow to reduce portal pressure by splanchnic vaso-

constriction. Its vasoconstrictive eects on the coronary circulation can

lead to cardiac complications, so it is often used in combination with a

vasodilator such as nitroglycerin.

Endoscopic Treatment

Endoscopy has been established as a denitive intervention to stop vari-

ceal bleeding through interventions such as sclerotherapy or band liga-

tion. Sclerotherapy involves visualization of the varices through a exible

endoscope and injection of sclerosing agent in close proximity to the vari-

ces. Sclerotherapy has largely been replaced by band ligation secondary

to its complication rate of 10% to 30%, including esophageal perforation

due to ulceration caused by the sclerosing agent. Success rates for initial

control of esophageal variceal bleed range from 60% to 90%; often more

than one session is required to completely stop bleeding. Band ligation

is performed by insertion of an endoscope over a sheath, suctioning each

individual varix into the lumen of a channel, and placement of a rubber

band around the tissue to ligate it. In a few days, the tissue is sloughed

o, leaving only a small ulcer. Multiple bands can be placed during each

procedure; the exact number is dependent upon the equipment used.

Ligation has a success rate of 80% to 100% in the rst session. A signi-

cant reduction in the incidence of rebleeding, death from bleeding, and

overall mortality has been found with band ligation in comparison to

sclerotherapy.

Balloon Tamponade

Balloon tamponade represents a third-line treatment for patients who

fail medical and endoscopic management for acute variceal bleed. In

the 10% to 25% who fail first-line treatment strategies, balloon tampon-

ade has a high success rate. The Sengstaken-Blakemore and Minnesota

tubes are most commonly used. The concept is similar for both. The

tube has an esophageal balloon and a gastric balloon that sits at the

gastroesophageal junction in the cardia of the stomach. After insertion

via nasogastric route and radiographic evidence of proper position is

demonstrated, the two balloons are inflated, resulting in tamponade

of any gastric or esophageal varices. The esophageal balloon is inflated

between 15 and 40mm Hg of pressure and the gastric balloon initially

inflated with 30 mL of air and then with a total of 300 to 400mL. It is

imperative to secure the tube in place, using a facemask or helmet to

prevent inadvertent removal. About 10% to 20% of patients suffer from

significant complications including aspiration, perforation, and necro-

sis; however, 70% to 80% are treated successfully. These severe complica-

tions limit the use of balloon tamponade to 24 hours. Up to half of these

patients rebleed when the balloons are deflated. Balloon tamponade

can be very effective in the initial control of bleeding, but is merely a

temporizing measure until a more definitive procedure such as TIPS or

transplant can be performed. Figure 11.3 shows the algorithm for man-

agement of a patient with variceal bleeding when medical and endo-

scopic treatment fails.

Section II / Liver136

Transjugular Intrahepatic Portosystemic Shunt

Unsuccessful treatment of esophageal variceal bleeding by medication,

endoscopy, or balloon tamponade results in 90% mortality. erefore,

a more denitive procedure is required that can temporize until LT can be

performed. Traditionally, surgically created portosystemic shunts were the

mainstay of treatment. However, the signicant morbidity and mortality

associated with these procedures has led to the development of the less

invasive and lower-risk TIPS procedure. When medical, endoscopic, and

balloon tamponade fail, TIPS is the next line in therapy. is stent eec-

tively shunts blood from the portal vein into the hepatic vein, bypassing

the hepatic parenchyma and avoiding the area of increased resistance.

e goal hepatic portal venous pressure gradient to stop bleeding is less

than 12mm Hg. However, a gradient of less than 5mm Hg results in liver

ischemia secondary to decreased hepatic ow. Care needs to be taken

to achieve an adequate pressure to resolve varices, but maintain hepatic

perfusion.

Surgical Shunt Creation

Surgical shunt creation is the most eective method of reducing portal

venous pressure and preventing recurrent variceal bleeding. TIPS is pref-

erential, as the surgical creation of a shunt is associated with signicant

morbidity and mortality. Portosystemic shunts are divided into three types

depending on their diversion of ow: nonselective, selective, and partially

diverting.

Nonselective shunts involve anastomosis of the portal vein or SMV

to the IVC or the portal vein to the proximal renal vein. “Hepatofugal

ow” is the reversal of blood ow out of the liver and into the systemic

circulation. It is achieved by the large diameter of these anastomoses and

allows for decompression of the high-pressure portal venous system into

the low-pressure systemic circulation. A portacaval shunt can be done in

an end-to-side or side-to-side fashion. Mesocaval shunts are created via

a prosthetic or vein interposition graft. To create a central splenorenal

Variceal Bleeding with

Endoscopic/Pharmacologic Failure

Childs A

Emergency

Mesocaval

Portacaval

TIPS

Elective

Distal splenorenal

Mesocaval

Portacaval

? TIPS

Childs C

Emergency

TIPS

Liver Transplant

Elective

Liver Tr

ansplant

Childs B

Emergency

TIPS

? Liver Transplant

Elective

TIPS

Mesocaval

Portacaval

FIGURE 11.3 Suggested treatment options for patients who fail to undergo medical

management for variceal bleeding. (From Mulholland MW

, Lillemoe KD, Doherty GM, etal.

Greeneld’s surgery: scientic principles & practice, 5th ed. Philadelphia, PA: Lippincott

Williams & Wilkins, 2010.)

Chapter 11 / Cirrhosis and Portal Hypertension 137

shunt, a splenectomy is performed and the proximal splenic vein is

nastomosed to the left renal vein. Remember that ascites is caused by

leaking of protein-rich uid from the liver secondary to high pressure at

the level of the sinusoids. erefore, these nonselective shunts, by reduc-

tion of portal venous pressure, allow for a decrease in ascites in addition

to resolving varices.

e goal of a selective shunt is to create two distinct drainage path-

ways for the portal circulation. By diverting ow from the esophagogastric

circulation into the systemic circulation, a low-pressure system is created

and maintains a high pressure in the mesenteric system. is is done by

creating a distal splenorenal shunt. Unlike the proximal splenorenal shunt,

the very distal aspect of the splenic vein is anastomosed to the left renal

vein in an end-to-side fashion. is allows decompression of the short gas-

tric veins through the systemic circulation and relieves varices. It is impor-

tant to note that portal venous pressure is not reduced in this procedure.

erefore, ascites may persist or even worsen after a splenorenal shunt is

created. Another selective shunt involves anastomosis of the left gastric

vein to the IVC and works in the same way as a distal splenorenal shunt.

Partial shunts use small-diameter interposition polytetrauoroeth-

ylene or Dacron grafts to create mesocaval or portacaval shunts. ese

shunts allow for a decrease in the hepatic venous–portal pressure gradient

to less than 12mm Hg and maintain hepatopetal ow, thereby reducing the

risk of hepatic encephalopathy and accelerated hepatic dysfunction due to

lack of trophic hormones from the gut.

Complications and Outcomes with TIPS and Surgical Shunts

e major complication of TIPS is in-shunt stenosis, via either neointimal

hyperplasia or thrombosis. At 1 year, approximately 50% of shunts will be

occluded, but these results have improved dramatically with newer tech-

nology. Intervention is possible with thrombolysis, balloon dilation of the

stent, or placement of a second stent. About 15% of patients sustain nonre-

versible shunt occlusion. Ultrasonography to assess shunt patency should

be performed every 3 months. Given the relatively short duration of ecacy

of TIPS, it is ideal as a bridge to LT or for those that have severe enough

hepatic decompensation that they are unlikely to live long enough to expe-

rience TIPS failure. TIPS is not only eective in treatment of uncontrolled

variceal bleeding, it also reduces the rate of rebleeding episodes.

Both TIPS and surgically created shunts may be complicated by accel-

erated hepatic dysfunction and hepatic encephalopathy. With diversion of

blood ow from the liver, important trophic hormones present in the portal

circulation bypass the liver. Shunts that involve dissection near the porta

hepatis result in adhesions that make future LT dicult, another reason

that TIPS is preferred over the surgical portosystemic shunts. When it

comes to control of variceal hemorrhage, both nonselective and selective

shunts are successful in greater than 90% of cases.

LIVER TRANSPLANTATION: MANAGEMENT OF PORTAL

HYPERTENSION

e ideal management in selected patients with cirrhosis and at least one

clinical manifestation of portal hypertension is LT. ere are currently close

to three times the number of patients listed compared to available organs

in the United States. Due to the shortage of donors and the complexity of

the surgery, donor and recipient selection is key to successful treatment.

Patients typically undergo an exhaustive pretransplant workup to be consid-

ered candidates. Current 1-year survival rate after LT is 85%. Perioperative

Section II / Liver138

mortality is roughly 5%. Graft failure commonly results from sepsis. Other

common complications include hepatic artery thrombosis (5%), biliary

stricture (10%), biliary leak (<5%), and primary nonfunction (1%).

PREOPERATIVE CONSIDERATIONS

Cirrhosis portends a high risk for surgical and anesthetic complications,

including death. Careful assessment of the status of a patient’s liver dis-

ease is warranted prior to any elective procedure. Even with preoperative

risk stratication, cirrhosis may not be discovered until the time of sur-

gery. Most studies evaluating surgical risk in cirrhosis exclude Child class

Cpatients, and the majority of included cases are Child class A. is hetero-

geneity leads to poor generalizability of study results and, often, a misclas-

sication of surgical risk. As with any disease process, emergency surgery is

extremely high risk, with a high mortality rate. Estimates of mortality rates

for surgery in cirrhotics range from 11% to 25% versus 1.1% in noncirrhotic

patients. In general, the postsurgical 30-day mortality rate in Child class A

is 10% to 15%, Child class B is 30% to 40%, and Child class C is 75% to 80%.

Despite advances in surgical and anesthetic technique, these numbers are

largely unchanged over several decades.

e cause of these high mortality rates in cirrhosis is related to four

main organ systems: circulatory, pulmonary, immune, and hematologic.

Cirrhotics have a hyperdynamic circulation, and decreased hepatic perfu-

sion and anesthetic administration can exacerbate this, causing increased

hypotension and hypoxemia. Hypoxia may be exacerbated by previously

mentioned pulmonary complications due to ascites, hepatic hydrothorax,

portopulmonary hypertension, or HPS. Cirrhotic patients are more suscep-

tible to bacterial infection and subsequent sepsis, as well as wound healing

complications. Additionally, thrombocytopenia and coagulopathy lead to

bleeding complications. Malnutrition is prevalent among cirrhotic patients

and can exacerbate the aforementioned complications. Given the baseline

uid derangements in these patients, uid management intra- and postop-

eratively may be quite challenging.

e CTP class is used most widely in the literature to classify severity of

liver disease and surgical risk. It is easy to calculate, but it can have interob-

server variability, as the category of ascites and encephalopathy is subjective in

nature. e MELD score is more objective and gives weights to each variable. It

has been proven to be a good predictor of 30-day postoperative mortality, dem-

onstrating a linear relationship to mortality. Both CTP and MELD score may

be used in practice when determining surgical risk and guiding clinical man-

agement of a cirrhotic patient. Certainly, risk is optimized when a cirrhotic

patient is treated at a transplant center with an intensive care unit available.

CONCLUSION

Cirrhosis and subsequent portal hypertension are serious, life-threatening

diseases that may go undetected for years and may eventually lead to HCC.

Eventually, patients will succumb to the disease without a liver transplant,

although there are various ways to optimize medical management as a

bridge to transplant. Portal hypertension can result from cirrhosis, hepatic

vein obstruction, or portal vein thrombosis, all of which have many poten-

tial causes and may not be related to liver dysfunction. Variceal bleeding

is a life-threatening complication of portal hypertension and may be the

presenting symptom of end-stage liver disease. Detection of the subtle signs

and symptoms on history and physical, as well as careful interpretation of

laboratory and diagnostic imaging, can lead to early identication of cir-

rhosis cessation of the inciting factors of liver damage.

Chapter 11 / Cirrhosis and Portal Hypertension 139

EDITORIAL NOTE

e profound clinical importance of hepatic cirrhosis is impossible to under-

state. For example, contemporary 1-year mortality of cirrhotic patients after

a rst episode of esophageal variceal hemorrhage or new onset of ascites

is 50%!

Many surgeons have experienced the disastrous consequences of oper-

ating on cirrhotic patients (even those with seemingly well-

ompensated

cirrhosis)—intraoperative and occasionally delayed postoperative bleeding,

development of postoperative ascites (often leaking through abdominal

incisions) with secondary bacterial peritonitis; hepatic insuciency;

encephalopathy (commonly accompanied by aspiration/pneumonia); and

almost astonishingly high mortality, even after simple procedures. Cirrhotic

patients have no physiologic reserve and little margin for error. ese

patients should be approached by an experienced surgical team.