Liver Resection

As the liver is a tremendously vascular organ, intraoperative or postoperative complications are often related to excessive blood loss (16); thus a number of techniques have been developed to achieve preresection vascular control and decreased bleeding. While liver resection can often be performed without the need for interruption of blood flow to the liver, in many cases some degree of reduction of flow is required to prevent excessive blood loss.

Selective inflow control can be established by division or occlusion of the vascular structures supplying the segment(s) of liver to be removed. The right or left portal pedicle containing the respective portal vein, hepatic artery, and bile duct are controlled with a vascular clamp. This technique has the advantage of preserving blood flow to the segment of the liver being preserved but is generally only useful in smaller resections.

Total inflow occlusion (Pringle maneuver) results from clamping the entire inflow of the liver at the hepatoduodenal ligament; this has been shown to reduce blood loss during the parenchymal transection phase of the resection (17). While there is some concern regarding warm ischemic injury, abundant data shows that the normal liver can tolerate inflow occlusion for up to 1 hour, and there are reports suggesting that some cirrhotic livers can safely tolerate 60 minutes of inflow occlusion as well (18). We use total inflow occlusion when selective occlusion provides insufficient control. Clamp times are expected to be less than 30 minutes for formal hepatectomies, but may be higher for more complex parenchymal transections. In such cases, total occlusion is carried out in 15-minute increments with 5-minute reperfusion intervals. An alternative to the intermittent clamping technique is to use ischemic preconditioning, during which the liver inflow is occluded for 10 minutes, after which it is allowed to reperfuse for 15 minutes prior to clamping again for a sustained time period up to 1 hour. Intermittent clamping is associated with more blood loss than ischemic preconditioning; however, the protective results of ischemic preconditioning in ischemia reperfusion injury have not been uniform across age groups and may not be as effective in livers that have been exposed to preoperative chemotherapy (19).

Total vascular isolation of the liver, with both inflow occlusion and occlusion of the supra- and infrahepatic vena cava, can be useful for technically demanding cases where the vena cava or proximal hepatic veins are involved with tumor (Fig. 60.3). Total isolation has been shown to be safe for up to 60 minutes in normal liver, but can be accompanied by varying degrees of hemodynamic instability (20). In cases where this is required, we carry out as much of the operation as possible prior to isolation of the liver to reduce the ischemic time and the period of hemodynamic instability.

Hemodynamic Monitoring during Liver Resection

Central venous pressure (CVP) monitoring has traditionally been used to minimize blood loss during hepatectomy. During liver resection, hepatic vein pressure and blood loss are linearly related to CVP, with a CVP of 2 to 3 mmHg optimal for hepatic resections (21,22). The most troublesome bleeding during liver resection is usually from branches of the hepatic vein; this can be minimized by maintaining the CVP of 5 mmHg or less during the period of hepatic transection. Cooperation of the anesthesiologist in minimizing volume loading, and occasionally using pharmacologic agents to reduce CVP is essential. However, if total vascular isolation is to be used, volume loading prior to caval clamping is required to avoid an acute decrease in cardiac output at the time the clamps are applied. Low CVP anesthesia can result in significant volume depletion postoperatively and needs to be considered as part of the differential of hypotension and low urine output in the ICU after liver resection.

Knowledge of the details of intraoperative conduct of the operation is, therefore, important to the physicians that are to manage the postoperative care of the liver resection patient in the ICU setting. Was inflow occlusion or vascular isolation required and for how long? Prolonged clamp times are associated with greater liver dysfunction. Was the patient maintained with a low CVP throughout the course of the surgery? If so then the patient may need volume expansion on arrival to the ICU. How much liver remains and is it normal? If the percentage of liver is less than 25% in normal livers, or less than 40% in cirrhotic livers or livers with bile duct obstruction, the chance of liver failure and the need for its management is higher. Was there significant blood or fluid requirements? Patients may need a period of ventilation while fluid shifts and equilibrates.

Pancreatic and Bile Duct Surgery

The majority of patients undergoing pancreatic or bile duct surgeries do not require admission to an ICU setting immediately postoperatively because of issues specific to the pancreaticobiliary surgery itself. In general, procedures on the pancreas or biliary tree should not be associated with major intraoperative hemodynamic changes or alterations in physiology. Tumors of the head of the pancreas or bile duct may involve the portal vein or cause extensive fibrotic reaction in the area. Technical difficulties can arise in which damage occurs to, or resection is required of, the portal vein (Fig. 60.4). If portal vein resection or repair is required, it is more likely that the patient will require ICU care. Portal vein resection, when planned, requires variable durations of portal venous outflow obstruction from the gut, which are usually short and well tolerated, but can increase the amount of fluid third spaced in the bowel wall. Portal vein injury, however, can lead to massive transfusion requirements and hypotension that can require postoperative ICU care. The more common indications for admission to the ICU after pancreatic or biliary surgery are either an underlying medical condition or the development of a complication postoperatively. Pancreatic or bile leaks can lead to sepsis but will be discussed later in the chapter.

Portal Decompressive Procedures

Surgical portal decompressive procedures are becoming a rarity since the introduction of transjugular intrahepatic portosystemic shunt (TIPS) procedures. Decompressive procedures do, however, remain indicated in select patients with variceal bleeding with preserved liver function that have failed medical management and who are not transplant candidates. The myriad technical variations of surgical portosystemic shunts are beyond the scope of this chapter but certain commonalities exist.

Whether total or partial shunts, selective or nonselective patients will have had the high-pressure portal system surgically connected to the low-pressure caval circulation to lower the pressure in the portal venous system and stop variceal bleeding. Reduction of portal flow in patients that have borderline liver function can precipitate liver dysfunction or failure. Additionally, the fraction of portal flow diverted into the systemic circulation through the shunt is not cleared by the liver until it returns to the liver via the arterial circulation. This may induce encephalopathy, and shunts that divert most or all of the portal flow into the systemic circulation are more likely to induce encephalopathy than do those shunts that are selective or partial. One special case scenario is Budd–Chiari syndrome in which the hepatic venous outflow is obstructed, usually due to thrombosis secondary to a hypercoagulable state. In this disorder, blood flow perfuses the hepatic sinusoids from both hepatic artery and portal vein, but cannot exit through the blocked hepatic veins. A functional side-to-side shunt is performed (portacaval, mesocaval) that allows hepatic arterial blood to flow into the sinusoids and then exit via the portal vein, and through the shunt into the systemic circulation. It is not uncommon for liver function to deteriorate initially after the shunt is performed with subsequent gradual improvement and liver regeneration. Support of liver function may be required immediately after the shunt while liver function stabilizes. In some cases the shunt may precipitate acute liver failure making urgent liver transplantation the only option.

Immediate Postoperative Management

Postoperative fluid management is important in the care of patients after major hepatobiliary surgery. In particular, fluid shifts in patients who have had major liver resection can be difficult to manage after surgery. Intraoperatively, most liver resections are performed with low CVP and low intravascular volume. This practice minimizes bleeding during the hepatic parenchymal transection phase of the procedure, but may pose some difficulty in postoperative management. Postoperatively, patients that have had a major liver resection may have signs of hypovolemia with low urine output and low blood pressure. Volume re-expansion should be gentle, as partial liver resection leads to hypoalbuminemia, and pulmonary edema and ascites can develop with aggressive resuscitation. Although the use of albumin infusions is generally frowned upon in critical care medicine, albumin and fresh frozen plasma (FFP) may be useful in the resuscitation of patients after liver resection as the physiology is similar to patients with cirrhosis. We will use albumin containing fluids for volume expansion if the serum albumin is less than 2.9 mg/dL. FFP can be used for volume expansion; however, it is generally reserved for abnormalities in coagulation. Serial lactate levels are helpful in the postoperative management of patients after liver resection. Elevated lactic acid levels may be a sign of hypovolemia, but the lack of response to volume can indicate liver dysfunction.

After liver resections, glucose metabolism is altered, due to both a reduction in functional liver mass and relative dysfunction of the remaining liver secondary to ischemia reperfusion injury, especially if vascular control has been used during the procedure. As glycogen stores are depleted, the liver uses gluconeogenesis to provide glucose. As a result, patients may become hypoglycemic, although lethal hypoglycemia is rare. It has become standard practice in most critical care units to tightly control blood glucose levels. While the advantages of this approach, particularly regarding reduced risk of sepsis, remains for patients after major liver resection, aggressive blood glucose control with insulin infusions requires closer monitoring and may require reduced insulin dosing to prevent hypoglycemia.

Patients who have undergone shunt surgery need a different approach than patients undergoing other hepatobiliary surgery. Patients need more aggressive fluid management immediately postoperatively to maintain circulating intravascular volume and reduce the risk of shunt thrombosis. Maintenance fluid should be D5 0.45% saline solution to provide the liver with carbohydrate. After the immediate postoperative period, patients are also at risk for ascites formation, hence excessive sodium should be minimized. Additional volume expansion should be with albumin or FFP. Diuretics can be reinstituted after the immediate postoperative period. A general rule is to use furosemide and spironolactone in combination with 100 mg of spironolactone for every 40 mg of furosemide. Antibiotics should be administered for 24 hours postoperatively to minimize infection.

While encephalopathy is rare in patients after liver resection, unless they present in liver failure or have pre-existing liver disease, the presence of asterixis can be an early sign of encephalopathy. Encephalopathy is treated with lactulose and dietary protein restriction, as in other patients with end-stage liver disease. Infection, dehydration, and bleeding, as well as narcotic use, must be evaluated as they can trigger encephalopathy.

Hypophosphatemia

After liver resection, care must be taken to aggressively replace low serum phosphate.

The exact mechanism of the hypophosphatemia remains unclear, as both increased utilization during liver regeneration and renal wasting mechanism have been proposed (23).

Regardless of the etiology, the clinical consequences of hypophosphatemia are well established, and include respiratory depression, diaphragmatic insufficiency, seizures, and cardiac irritability. Additionally, hepatocellular regeneration is dependent on ATP and, after liver resection, regeneration may be impaired if phosphate is not repleted (24). In a series of 35 liver resections, 21% had significant postoperative hypophosphatemia (less than 2.5 mg/dL). This group had a significant increase in complications (80%) compared with the normophosphatemic group (28%) (25). Phosphate should be replaced with potassium or sodium phosphate preparations, or added to parenteral nutrition solutions. Recent studies in living donor right hepatic lobectomies suggest that replacement up to two times the recommended daily allowance (60 mmol) is necessary to replete severe hypophosphatemia and prevent its complications (26).

Liver Function: Assessment and Support

Liver function should be carefully monitored after major liver resections and shunt surgery, as liver failure is a risk in any major hepatobiliary surgery. The risk of liver failure increases with the extent of hepatectomy and in patients with preoperative liver disease or cirrhosis (27,28). Although standard liver function tests are helpful after major liver resection or shunt surgery, they may not show elevation until the patient has significant liver failure. Transaminases are frequently elevated in the 200 to 300 units/dL range postresection due to the direct effect of mechanical injury to the liver during transection, as well as to partial devascularization of areas of the liver. Measurements of liver function, including the prothrombin time and lactate, are more helpful in evaluating for early postoperative liver dysfunction.

Elevated total and indirect bilirubin are also useful indicators of postoperative liver dysfunction; however, isolated elevation of total bilirubin in the presence of normal liver function can have other etiologies. Perioperative blood transfusions can lead to hemolysis and hyperbilirubinemia with a predominance of direct hyperbilirubinemia, and can be diagnosed with a standard hemolytic workup. Bile leaks or obstruction can also lead to an elevated serum bilirubin. The diagnosis and treatment of bile leaks are covered later in this chapter. Many popular anesthetics, antibiotics, and other drugs can cause hepatotoxicity and elevation of the serum bilirubin, and need to be reduced or stopped if liver failure occurs.

When postoperative liver dysfunction does develop, it is important to exclude sepsis and anatomic causes of liver failure. A postoperative ultrasound can evaluate for portal vein, hepatic arterial, or hepatic vein thrombosis or obstruction, which may be amenable to surgical intervention. If the patient does not have sepsis, drug toxicity, biliary obstruction or leak, or vascular occlusion, the liver failure is likely related to a pre-existing liver disease and/or the extent of resection. Treatment is then supportive, with correction of coagulopathy, encephalopathy, and ascites, as above. Systemic antibiotics, or gut decontamination may be beneficial since the liver Kupffer cells play a role in decreasing bacterial translocation from the portal blood flow, and patients with liver failure or biliary leak or obstruction, may have an increased risk of bacteremia and sepsis. In some patients postoperative liver failure is fatal.

N-acetylcysteine has been shown to decrease liver injury after acetaminophen overdose (29) and lessen hepatic ischemia reperfusion injury (30). Intravenous infusions of prostaglandin have also been linked to improvement of ischemia reperfusion injury and liver damage (31). Although definitive clinical data are lacking, both N-acetylcysteine and PGE1 have been used to ameliorate postoperative damage in both liver resection and transplant patients. N-acetylcysteine is given over 16 hours as a continuous infusion of 40 mL of 10% solution mixed in 250 mL of D5W. Prostaglandin is also given as a continuous intravenous infusion, starting at 0.15 mcg/kg/hr. It is titrated up to 1 mcg/kg/hr based on systemic hypotension.

Coagulation Disorders

The liver synthesizes both procoagulant and anticoagulant proteins and, with liver dysfunction after liver resection, patients may be hypercoaguable, hypocoagulable, or both. Coagulopathy is more commonly associated with liver resection and dysfunction and can be particularly significant in the immediate postoperative period when excessive coagulopathy can lead to surgical bleeding and reoperation. Several studies have demonstrated and increase in prothrombin time directly proportional to the extent of liver resection (32,33). This coagulopathy has been attributed to impaired synthesis and clearance of clotting factors, inhibitors, and regulatory proteins (34,35). Patients with underlying liver disease and cirrhosis also often have thrombocytopenia and qualitative platelet defects. In addition, intraoperative hypothermia and perioperative transfusions, which, while not routine, are not uncommon during major hepatobiliary surgery, and can contribute to postoperative coagulopathy.

Serial hemoglobin and prothrombin levels should be measured. Because of the vascular nature of hepatobiliary surgery combined with postoperative coagulopathy from decreased liver function, as well as the frequent need for intravascular volume expansion, serial hemoglobin levels should be followed to watch for postoperative bleeding. In general, we would obtain a hematocrit and international normalized ratio (INR) on ICU arrival and then repeat about 6 hours later. The surgeon should be notified of excessive bloody output from the drains, increasing abdominal distention, or hemodynamic instability. In the immediate postoperative period or if bleeding is suspected, the INR should be corrected if it goes above 2.0, unless specified otherwise by the surgeon (36). Vitamin K should be given in addition to FFP. Any patient who is bleeding should have their coagulopathy completely corrected. For severe bleeding, both aprotinin and activated factor VII or 4-factor prothrombin complex are safe in patients during and after liver resection (35,37). A thromboelastogram may be helpful in these situations to determine the exact cause of the coagulopathy and is now routinely used in liver transplantation and hepatobiliary surgery. Patients who fail to stop bleeding after correction of their coagulopathy require return to the operating room. The surgical team should be made aware of any patient immediately postsurgery that requires transfusion.

There is a common perception that patients post liver resection have some degree of auto-anticoagulation from physiologic liver dysfunction that is protective against venous thromboembolism (VTE) (38). In reality, patients undergoing major liver resection are considered at moderate to high risk for thromboembolic complications according to 2012 American College of Chest Physician (ACCP) guideline (39). It is imperative to start prophylaxis for VTE once the acute risk of hemorrhage has passed, especially in patients with malignancies. At our institution, we prefer low–molecular-weight heparin unless the patient has renal insufficiency or another contraindication to VTE prophylaxis. There are data suggesting VTE rate actually is increased in proportion to the extent of hepatectomy. Additionally, advanced age, higher BMI, male gender, high ASA classification (3 or higher), postoperative organ space infection, longer procedure times, as well as higher postoperative INR (1.5 or higher vs. less than 1.5), all increase the risk of postoperative VTE (38,40).

Pain Management and Sedation

The large subcostal incision needed for major hepatobiliary surgery can result in significant pain after surgery. However, altered pharmacokinetics and coagulopathy in particular after partial liver resection or shunt surgery can make postoperative pain management challenging. Patients with liver failure or compromised liver function secondary to hepatectomy have altered metabolism of many common medications, in particular, narcotics and sedatives that require clearance via the liver.

One of the more common problems that arises in the ICU after liver resection is oversedation of patients. A standard dose of narcotics given to a patient who has had 80% of the liver resected may well cause prolonged respiratory depression and signs and symptoms of encephalopathy. Narcotics and benzodiazepines should be used at the minimum dose required to achieve pain control/sedation. After liver resection, it is recommended that basal rates on patient-controlled anesthesia pumps be avoided, as metabolism of narcotics is difficult to forecast. Benzodiazepines also have altered clearance after liver resection, and thus should be dosed at lower levels or avoided altogether, if possible. In patients who require ongoing intubation we have found it useful to use sedative agents such as propofol, rather than narcotics, since the level of sedation can be more easily titrated and reversed.

Epidural pain management may be optimal after liver resection; however, it is contraindicated in many patients because of postoperative coagulopathy. Unfortunately, that includes many hepatic resections and shunt surgery. Recent literature has examined the use of epidural catheters in patients undergoing living donor partial hepatic resection. In one review of eight patients, good pain control was achieved with only one case of oversedation requiring naloxone. Although postoperative coagulopathy did occur, it was not to the extent that factor transfusion was needed prior to catheter removal, and there were no cases of hemorrhage (41). Epidural analgesia may be useful in select patients who do not have underlying liver disease and who are not undergoing extended resections.

Nutrition

Although nutrition plays an important role in the care of any critically ill patient, the role of the liver in protein and carbohydrate metabolism makes proper postoperative nutrition imperative in the management of patients after major hepatobiliary surgery, in particular, after partial liver resection when liver function is temporarily reduced. Patients with preoperative biliary obstruction, malignancy, and cirrhosis are at higher risk for nutrition-related complications after major liver or bile duct surgery. Preoperative nutritional risk factors that are associated with postoperative complications in hepatobiliary surgery include weight loss of over 14% lean body mass over 6 months, serum albumin less than 3 g/dL, hematocrit less than 30%, total body potassium less than 85% normal, less than 25th percentile for mid-arm circumference, and skin test anergy (42). Preoperative bilirubin, albumin, prealbumin, prothrombin time, transferring, and vitamin and trace mineral deficits may also be important preoperatively.

As with most critically ill patients, early enteral nutrition has been associated with improved outcomes. In hepatobiliary surgery, both enteral and parenteral nutrition have been associated with improved outcomes, especially in high-risk patients (42,43). However, parenteral nutrition has been clearly associated with an increased risk of infection (44). Enteral nutrition has been shown to improve gut flora, preventing gastrointestinal atrophy and loss of immunocompetence. A review of five prospective randomized trials on enteral and parenteral nutrition in patients after liver resection found a decrease in wound infection and line sepsis in patients on enteral nutrition (45). There were no differences in mortality.

In patients who have undergone routine liver resection or shunt surgery, low-volume enteral feeds can be started almost immediately postoperatively. In patients who have had hepaticojejunostomies or pancreatic surgery, return of bowel function is necessary prior to starting feeds, unless the feeding tube is placed distal to the anastomosis. It is best to consult with the operating surgeon before starting enteral feeds in any patient, in particular those with enteric reconstruction. Patients with major pancreatic surgery (pancreaticoduodenectomy [PD], subtotal or total pancreatectomy) may require pancreatic enzyme supplementation with enteral feeds or when resuming oral intake.

Patients with chronic liver disease or cirrhosis often have severe metabolic derangements that make nutritional management difficult. The depletion of the fat-soluble vitamins, in particular a loss of vitamin K, leads to coagulopathy and diminished antioxidant response. Chronic liver disease also stimulates a catabolic state with proteolysis and cachexia; protein loss can be exacerbated by dietary restriction to help decrease encephalopathy. Branched-chain amino acids, initially thought to reduce the development of encephalopathy in catabolic patients with advanced liver failure, have not borne out in clinical trials. Patients with cirrhosis also have abnormal glucose tolerance and insulin levels, along with elevated ammonia levels, hypophosphatemia, and hypoalbuminemia, all of which influence perioperative nutrition. All Child’s B or C cirrhotic patients should be fed enterally when hospitalized. Caloric needs of the patients are increased to a goal of 25 to 25 kcal/kg/d; protein requirements are 1 to 1.5 g/kg dry weight in those not encephalopathic, with a minimum of 0.5 g/kg dry weight if encephalopathy has ensued (45). Patients with ascites require sodium restriction of 2 g/d and a fluid restriction of 1 to 1.5 L/d, in combination with diuretics, if tolerated.

Patients with preoperative obstructive jaundice often have chronic, low-grade endotoxemia and sepsis. This can lead to weight loss and anorexia, often due to malabsorption of fat and fat-soluble vitamins related to the obstruction, which itself leads to coagulopathy and a diminished antioxidant response. Endotoxemia also results in decreased hepatic protein synthesis and catabolism (46). Patients with biliary obstruction require a low-fat diet, as absorption is impaired, as well as replacement of the fat-soluble vitamins. Medium-chain triglycerides may be helpful, because their absorption is not bile salt dependent and these may avoid diarrhea until bile flow is re-established.

Partial liver resections also cause metabolic abnormalities secondary to the regenerating liver. Hepatic mitochondria switch to fat from glucose as their preferred energy source in hepatic regeneration (47). As a result, hypertonic glucose and insulin infusions should be avoided immediately after resection, as hyperglycemia and insulinemia suppress fatty acid release and decrease ketone body production by the liver. Some investigators have advocated administering fat and/or ketone bodies after liver resection to accelerate regeneration; conclusive evidence that this is beneficial is lacking. Similarly, infusions of glucose and insulin directly into the portal vein have also been looked at to improve regeneration although, again, conclusive evidence is lacking. Adequate liver regeneration is dependent on protein and calories; postoperative parenteral nutrition should be protein and fat supplemented, but low on glucose, to improve hepatic regeneration. General goals are 30 kcal/kg/d, with 1.0 to 1.5 g protein, glucose not to exceed 5 mg/kg/min, and fat making up 30% of the calories. Patients with cancer may need an increase of up to 35 kcal/kg/d and 2 g protein.

Well-nourished patients need no postoperative support, while malnourished patients will benefit from early enteral nutrition when possible, or parenteral nutrition until they are capable of taking enteral nutrition.

Renal Failure

Acute renal failure occurs after major hepatobiliary surgery in 10% of patients (48) and, similar to other critically ill patients, significantly increases postoperative mortality (49). Risk factors for perioperative renal failure include postoperative sepsis, preoperative uremia, preoperative anemia, malignant disease, and preoperative jaundice (48,50,51). In particular, preoperative obstructive jaundice appears to be a significant risk factor, with an estimated 10% of patients developing postoperative renal failure (52). Both dehydration and endotoxin production from bile duct obstruction have been postulated to cause renal failure in these patients (53). Many studies have been performed trying to decrease this risk, including using mannitol, bile salts, hydration, and lactulose (52–55).

In all patients with acute renal failure, adequate hydration, treatment of sepsis, and avoidance of nephrotoxic drugs are mandatory. However, in patients with obstructive jaundice, lactulose and bile salts may decrease endotoxin absorption, and have been shown in some studies to be beneficial in the prevention of renal failure (51,52). Preoperative biliary drainage to help lessen the perioperative inflammatory response is also an important adjunct to prevent postoperative renal failure. Once acute renal failure does occur, supportive care and dialysis are needed until renal function returns.

Patients with advanced cirrhosis or postoperative liver failure may develop hepatorenal syndrome (HRS). This is more significant in the acute care of patients with liver failure or after liver transplantation. HRS is a diagnosis of exclusion, based on urine sodium less than 10 mEq/L combined with a urine osmolality greater than that of plasma osmolality that does not respond to volume. The cause of HRS is likely multifactorial, but is primarily related to circulatory disturbances in patients with advanced liver disease, reduced liver function, and portal hypertension. Systemic vasodilatation and low mean arterial pressure results in afferent renal arterial vasoconstriction and a reduction in glomerular filtration rate (56). Although liver transplantation remains the only cure for HRS, vasoconstrictors, albumin infusions, and transhepatic portosystemic shunts are able to reduce HRS, and may prevent its development in patients with spontaneous bacterial peritonitis (57).

Postoperative Complications

Complications Following Bile Duct Resection/Reconstruction

Perhaps the most extensive hepatobiliary operations are performed for proximal extrahepatic CCCs. With mounting evidence demonstrating significantly improved survival following extended liver and bile duct resections and reconstructions versus local bile duct resections, centers with experienced hepatobiliary surgeons are presenting series with improved outcomes (100–103). Nonetheless, significant complications remain associated with these procedures.

Perioperative mortality following extended liver and biliary resections ranges from 1.3% to 16% (102,104–106). Complications following these procedures occur in 51% to 81%, and many patients have multiple complications (100,102,105,106). Complications include bile duct leaks, bleeding, liver failure, pleural effusions, wound infection, and sepsis (104,106–108). Each of these complications can also be found in liver resections alone and share the same risk factors. In addition, each complication can be approached with the same preventative strategy and treatment.

Liver failure following extended resections for obstructive CCC may have a unique pathophysiology and hence preventative strategy. Prolonged biliary obstruction causes significant hepatocellular dysfunction, and liver failure occurs in up to 27.6% of patients who undergo extended liver and biliary resections and reconstructions for CCC and is frequently fatal (106,108). Resection of up to 75% of the liver along with possible vascular reconstruction that requires an increased duration of ischemic injury to the liver is often necessary to resect hilar CCC and in the setting of pre-existing liver dysfunction liver failure can be problematic. Strategies to optimized functional liver volume prior to extended liver resections for hilar CCCs are essential to preventing postoperative liver failure. One strategy is to promote hepatocellular functional recovery by preoperatively decompressing the biliary tree using percutaneous transhepatic cholangiocatheterization. This practice is somewhat controversial as it may introduce infection into an otherwise sterile biliary tree, and so may be avoided in patients who can undergo surgery within 2 to 3 weeks after the onset of jaundice. Another strategy is to perform contralateral PVE to increase the remnant liver volume prior to resection. A number of centers have demonstrated decreased liver failure rates when these strategies are employed (103,104,109).

Complications Following Pancreatic Surgery

The mortality rate following PD ranges between 2.7% and 6.9% (109–114). Risk factors for perioperative mortality include elevated serum bilirubin, diameter of pancreatic duct, increased intraoperative blood loss, pancreatic fistulas, and older age (113).

Complications occur in between 22.1% and 30.2% of PDs, and include pancreatic fistulae, delayed gastric emptying, bleeding, abdominal abscesses, and wound infections (112,113).

Pancreatic fistulae are a dreaded complication of PD, occurring in 12% to 18% of patients (110–112,115–118). Pancreatic fistulae are associated with a mortality rate of 0% to 19% (104,111,112). These patients often die secondary to massive erosive bleeding from sepsis and pancreatic enzyme accumulation. These bleeding episodes occur in 1% to 8.8% of PD patients and carry a mortality rate of 47% to 50% (114,119,120).

Risk factors for pancreatic fistulae include small duct size, soft pancreas texture, duration of surgery greater than 8 hours, diabetes, lower creatinine clearance, preoperative jaundice, and increased intraoperative blood loss (112,116,118,121).

Despite numerous studies evaluating potential strategies to prevent pancreatic fistulae following PD, including the use of octreotide, fibrin sealants, pancreatic stents, different methods, and sites of pancreatic anastomosis, none have proven effective (117,122–125). Pancreatic fistulae are initially detected on postoperative day 6, presenting with abdominal pain, fever, nausea/vomiting, and leukocytosis. Fistulae are then confirmed by CT scan which often demonstrates a fluid collection behind the pancreatic anastomosis, elevated serum amylase, drain output greater than 50 mL/d, and drain amylase 10-fold greater than serum amylase (117,122). Management is initially conservative with bowel rest, total parenteral nutrition, antibiotics, and monitoring of clinical signs and symptoms and drain output. If repeat imaging demonstrates increased accumulation of fluid and the patient does not respond to conservative measures, another drain may be placed percutaneously to prevent progression of abdominal sepsis. Eighty percent to 90% of patients seal pancreatic fistulae with these measures (110,115). However, those patients who develop uncontrolled leaks and abdominal sepsis may require surgery, usually for completion pancreatectomy. In addition, a smaller group of patients with fistulae will suffer life-threatening erosive intra-abdominal bleeding, usually from the stump of the gastroduodenal artery, small arterial branches to the pancreas, or rarely from the portal vein. These patients will present with signs and symptoms of sepsis and hypovolemia, such as fever, abdominal pain, hypotension, anemia, and bloody drain output; they are treated by rapid resuscitation and angiography for potential embolization of the bleeding arterial branch. If arterial bleeding cannot be controlled in this manner, or if the bleeding is venous, the patient is surgically explored for hemostasis and completion pancreatectomy. Surgery in this setting is associated with a high mortality: up to 36% of patients requiring surgery after PD for bleeding will not survive (114,120,123).