Nutrition and perioperative critical care in the hepatopancreatobiliary surgery patient

Sarcopenia

Body mass index (BMI) is widely used in patient risk models but fails to account for the diversity of body composition. A relative dearth of lean muscle mass, called sarcopenia, is associated with functional impairments, physical disability, perioperative complications, prolonged hospital length of stay, and poorer long-term outcomes in cancer patients. Unlike cachexia, sarcopenia develops over a long period of time and is not necessarily associated with weight loss. Thus many patients who fall into a normal range for weight and BMI may have unrecognized sarcopenia. Patients who are both obese by BMI calculation and sarcopenic are categorized as having “sarcopenic obesity.” Sarcopenic obesity has been reported as one of the most powerful independent predictors of poor survival for patients with cancer and is associated with impaired functional status and decreased ability to tolerate chemotherapy, surgery, and other invasive therapies. ^,

The most clinically applicable method used to identify sarcopenia uses computed tomography (CT) imaging to estimate lean muscle mass of the psoas muscle of a single CT image at the L3 level normalized for height (total psoas area in mm ² / height in m ² ). ^, Patients are sarcopenic if these values are less than 385 mm ² /m ² in women or less than 545 mm ² /m ² in men. In retrospective studies, sarcopenic patients who underwent liver transplantation, liver resection, and pancreatic resection had increased perioperative complications, increased postoperative mortality, and worse overall and recurrence-free survival. ^{, ,}

The pathophysiology of sarcopenia is not well understood but poor nutrition, alterations in hormonal and other signaling pathways, and inflammatory factors and cytokines are thought to be the principal mechanisms behind the development of sarcopenia in the chronically ill. ^, Investigations seeking to mitigate the effects of sarcopenia have reported that exercise combined with supplemental protein or amino acids can reverse sarcopenia in the elderly. ^, These observations support the practice of prescribing exercise and supplemental protein to sarcopenic patients before hepatopancreatobiliary (HPB) surgery.

Frailty

Whereas sarcopenia describes a specific and quantifiable finding, frailty comprises a more global assessment of physiology and resilience. Initially considered to be synonymous with age, frailty describes a depletion of physiologic reserves culminating in both a higher degree of vulnerability to physiologic stressors and a simultaneous decrement in the ability to recover from these physiologic challenges. Considering the physiologic challenges of HPB diseases and major abdominal surgery, the assessment of frailty and incorporation into perioperative planning and patient selection is gaining interest. With an aging population, a surgeon can expect to encounter more elderly and potentially more frail patients.

Frailty is a risk factor for multiple adverse outcomes such as surgical complications, mortality, and loss of functional independence. In regards to postsurgical complications, the idea of diminished physiologic resilience contributes to increases in failure-to-rescue events, suggesting that these patients are less likely to recover from postsurgical complications even if they are managed appropriately. ^, With increased postoperative complications, length of stay, disposition care requirements, and healthcare-associated costs due to frailty, modifying frailty could potentially alter costs associated with healthcare.

Assessment and quantification of frailty is based on comorbidity and functional capability. Tools such as the 11-variable modified Frailty Index (mFI) are used to identify patients at higher risk for postoperative complications, disposition to facilities rather than home, and longer lengths of stay in oncologic surgical. A 5-factor modified frailty index has also been derived from American College of Surgeons National Quality Improvement Project (ACS-NSQIP) data. Comparing the 5- and 11-factor frailty indices across surgical subspecialties supports the predictive ability of the shorter 5-factor frailty index for the prediction of mortality, postoperative complications, and 30-day readmission in general surgery procedures. This study did not specifically parse out HPB or surgical oncology patients ( Table 26.1 ).

Identifying frail patients allows for their enrollment in programs designed to improve modifiable risk factors when a surgery is planned or a period of observation, such as during or following neoadjuvant therapy, is included in a treatment plan. Degree of medical optimization, nutritional goals, and exercise prescription would be tailored to a patient’s specific needs. ^, Prehabilitation of frail patients has not been studied extensively in a HPB surgery population. Prehabilitation efforts performed in non-HPB abdominal surgery population focus on smoking cessation, improving exercise tolerance, stress elimination, and nutritional improvement.

Obstructive jaundice

Approximately 45% to 70% of patients with obstructive jaundice present with malnutrition because of anorexia resulting in diminished oral intake. The primary nutritional deficit resulting from obstructive jaundice is malabsorption of fat and fat-soluble vitamins in addition to trace minerals. Biliary sepsis in patients with obstructive jaundice contributes to malnutrition by shifting protein synthesis from anabolic protein synthesis to acute-phase protein synthesis. Although some authors have advocated preoperative biliary drainage (PBD) in patients undergoing HPB surgery, multicenter trials and Cochrane analysis have demonstrated no evidence to support or refute routine biliary drainage and stenting in patients with malignant HPB diseases awaiting surgery. ^, Conversely, PBD should probably be performed in patients undergoing extended hepatectomy to improve the health of the planned remnant. To reverse the catabolic effects of chronic endotoxemia and restore hepatic protein synthesis, patients with cholangitis should be treated with biliary decompression for at least 4 weeks before major HPB surgery (see Chapter 43 ).

For patients with pancreatic disease presenting with recent-onset obstructive jaundice, PBD may not be required in the absence of profound malnourishment or deconditioning. Although routine PBD is discouraged in such patients because of substantial increases in the incidence of postoperative infectious complications, patients with long-standing obstructive jaundice, cholangitis, and those who are planned to receive neoadjuvant therapy before resection benefit from biliary decompression during this period.

Such patients are best managed with internal biliary drainage as part of a comprehensive nutritional repletion program. Internal drainage can be accomplished by endoscopic drainage, percutaneous biliary access with internal stenting, or rendezvous procedure (see Chapters 30 and 31 ). For patients managed with external biliary drainage, bile refeeding may be a consideration: prolonged external drainage and discarding of bile occurring in the setting of biliary obstruction or disconnection culminates in dehydration, metabolic acidosis, progressive loss of biliary protein, and nutrient malabsorption. Most patients can tolerate bolus infusion of bile into their small bowel of 150 mL or less every 4 hours. If a patient has percutaneous jejunal feeding access, it is preferable to provide bile refeeding in a continuous manner. An alternative to enteric bile refeeding is to provide oral bile salts (ursodeoxycholic acid, 300 mg QID) to form micelles for fat absorption.

Hepatic steatosis

The presence, degree, and evolution of hepatic steatosis may all be considerations in the operative assessment and planning for patients undergoing hepatic resection (see Chapter 69 ). Classically defined by the presence of 5% or greater of triglycerides in hepatic parenchyma based on biopsy, many studies characterize the degree of steatosis based on severity. Although the most common etiology of steatosis is because of nonalcoholic fatty liver disease (NAFLD), chemotherapy-associated steatosis (CAS) describes a change in intrahepatic fat (IHF) composition over time during chemotherapy administration. The degree of steatosis and presence of inflammation may alter the detection and tracking of hepatic lesions and size of the planned remnant when hepatectomy is planned.

Cytotoxic chemotherapy administered in the treatment of colorectal liver metastases (CRCLM) may also contribute to hepatic steatosis or steatohepatitis. CAS has been described as a result of many current regimens used in the treatment of colorectal cancer and CRCLM including irinotecan and fluorouracil. An additional description of etiologic factors of steatosis and chemotherapy-associated changes is provided in Chapter 69 .

The degree of steatosis can contribute to the development of postoperative complications. Retrospective studies have found that patients undergoing hepatic resection were at significantly higher risk for infectious, wound-related, GI, and hepatobiliary complications when the background liver was characterized by at least 30% steatosis. Severe steatosis can also increase operative time and increase transfusion requirements. The degree of steatosis, with potential correlation to remnant function, also correlates with increasing overall postoperative morbidity, post-hepatectomy liver failure (PHLF), increased intensive care unit (ICU) stay, and increased hospital length of stay.

Liver parenchymal modification has been described in bariatric literature via low-calorie diets (800–1000 kCal/day for 4 weeks). ^, Further dietary studies focusing on intrahepatic fat burden demonstrate that drastic changes in intrahepatic fat can be achieved in short periods of time. ^, Pharmacologic interventions have also been investigated as measures to decrease intrahepatic fact and mitigate the inflammatory changes of steatohepatitis, ^, but the duration of medication use in these studies may limit their practical use in the prior liver resection.

Cirrhosis and liver failure

Cirrhosis causes multiple hormonal and metabolic alterations, yielding loss of fat and muscle mass, glucose intolerance, insulin resistance, increased plasma glucagon and catecholamines, elevated serum free fatty acids, hypoproteinemia, and hyperammonemia. These metabolic aberrations eventually lead to increased skeletal muscle proteolysis with muscle wasting and increased peripheral lipolysis, leading to hyperglycemia and hyperlipidemia. Added risk factors for malnutrition include protein-restricted diets used in an effort to prevent encephalopathy. The practice of routine protein restriction should be abandoned in an already malnourished patient because it exacerbates the problems inherently associated with malnutrition (see Chapters 77 and 78 ).

Pancreatic cancer

Pancreatic cancer (PC) is associated with a severe metabolic derangement referred to as “cancer anorexia-cachexia syndrome” ^, (see Chapter 62 ). This syndrome is associated with anorexia, tissue wasting, malnutrition, weight loss, and a loss of compensatory increase in feeding. The pathogenesis is dependent on disorders of carbohydrate, protein, lipid, and energy metabolism mediated by proinflammatory cytokine elaboration and an overall increase in leptin. ^, PC patients have the highest incidence of cachexia among patients with cancer; up to 80% of such patients have cachexia at the time of initial diagnosis. Increasing severity of anorexia-cachexia in PC patients interferes with therapy and correlates with short survival. ^, For this reason, patients with PC are perhaps the most likely of all patients undergoing HPB surgery to benefit from nutritional support strategies.

Pancreatic exocrine insufficiency

Benign and malignant conditions of the pancreas can produce biliary and/or pancreatic duct obstruction resulting in maldigestion and malabsorption. The majority of patients with PC present with malnutrition and weight loss, with 75% found to have pancreatic exocrine insufficiency (PEI) at presentation. The etiology of PEI in patients with PC is incompletely understood but likely related to main pancreatic duct obstruction, glandular atrophy, age- or cancer-related pancreatic exocrine senescence, and potentially reduced exocrine function because of previous pancreatitis. Because PEI is so common in patients with pancreatic cancer, an argument can be made to provide pancreatic enzymes to all symptomatic patients at the time of diagnosis. Asymptomatic patients, on the other hand, should be evaluated for PEI by fecal elastase 1 assay. The nutritional consequences of untreated or unrecognized steatorrhea can lead to significant weight loss, malnutrition, vitamin deficiencies, poor quality of life, and delays in therapy. ^,