- Email: [email protected]
Perioperative Strategy for Severe Nutritional Risk-Related Frail Patients
Vol. 220, No. 5, May 2015
disease. Considering the important implications of this association, we would like to add some information that can help clarify the message in their article. Autosomal recessive polycystic kidney disease (ARPKD) is a rare, inherited form of renal disease that tends to be evident early in life, and can have important associated liver abnormalities, most notably congenital hepatic fibrosis. The underlying abnormality, a mutation in the polycystic kidney and hepatic disease 1 gene, leads to disruption in expression of fibrocystin/polyductin, a protein that plays a key role in the development of collecting and intrahepatic duct tubular architecture.2 Autosomal dominant polycystic kidney disease (ADPKD), a relatively more common disorder responsible for 5% to 10% of patients who enter end-stage renal disease, is caused by mutations in genes that encode mechanosensory ion channels (PKD1 or 2; disrupting polycystin 1 and 2, respectively). These patients commonly present later in life, with multiple large cysts in the kidneys and other organs, most notably liver and pancreas. Liver cysts are particularly prevalent in this patient population, and can sometimes trigger symptoms by compression or infection.3 Liver cysts tend to be isolated in ADPKD. In contrast, in ARPKD, the saccular ectasias can be seen to communicate directly with the intrahepatic biliary system, a fact that might allow imaging modalities to distinguish between the two forms.4 Soares and colleagues5 correctly indicate the presence of an association between ductal plate malformation during embryogenesis and ARPKD, however, they state this is due to a mutation in the PKD1 gene and quote a reference dealing with ADPKD. Although seemingly a minor mistake, based on dramatic differences in patterns of presentation, management, and inheritance for the two types of PKD, the information provided is confusing. Caroli disease has been reported in up to 30% of ARPKD patients.2,6 In contrast, <10 cases of Caroli disease in association with ADPKD have been reported in the literature,7 including that referenced by Soares and colleagues. We propose that a more in-depth analysis of the literature and clarification of the association between congenital hepatic fibrosis, Caroli disease, and Caroli syndrome with renal tubular ectasia and renal cystic diseases, along with an accurate description of the affected genes and modes of inheritance, would significantly strengthen their publication.
REFERENCES 1. Soares KC, Arnaoutakis DJ, Kamel I, et al. Choledochal cysts: presentation, clinical differentiation, and management. J Am Coll Surg 2014;219:1167e1180.
Letters
977
2. Sweeney WE Jr, Avner ED. Pathophysiology of childhood polycystic kidney diseases: new insights into disease-specific therapy. Pediatr Res 2014;75:148e157. 3. Ars E, Bernis C, Fraga G, et al. Spanish guidelines for the management of autosomal dominant polycystic kidney disease. Nephrol Dialysis Transplant 2014;29:iv95eiv105. 4. Gunay-Aygun M, Turkbey BI, Bryant J, et al. Hepatorenal findings in obligate heterozygotes for autosomal recessive polycystic kidney disease. Mol Genet Metab 2011;104:677e681. 5. Torra R, Badenas C, Darnell A, et al. Autosomal dominant polycystic kidney disease with anticipation and Caroli’s disease associated with a PKD1 mutation. Rapid communication. Kidney Int 1997;52:33e38. 6. Buscher R, Buscher AK, Weber S, et al. Clinical manifestations of autosomal recessive polycystic kidney disease (ARPKD): kidneyrelated and non-kidney-related phenotypes. Pediatr Nephrol 2014;29:1915e1925. 7. Aguilar M, Meterissian S, Levesque S, Andonian S. Nephrectomy in patients with Caroli’s and ADPKD may be associated with increased morbidity. Can Urol Assoc J 2011;5:E19eE22.
Disclosure Information: Nothing to disclose.
Perioperative Strategy for Severe Nutritional Risk-Related Frail Patients Tetsuji Fujita, Tokyo, Japan
MD
In an important study by Dr Sanford and colleagues,1 severe nutritional risk, as defined by the presence of at least one of the following criteria: BMI <18.5 kg/m2, serum albumin <3.0 g/dL, and unintentional weight loss >10% within 6 months before surgery, adversely affected longterm survival for geriatric patients (aged 65 years or older) after pancreaticoduodenectomy for benign pancreatic disease. When compared with those without severe nutritional risk, there were surprising differences in 5-year survival (64.8% vs 92.5%) and 10-year survival rates (23.2% vs 68.9%). Multivariate analysis was performed for adjusting confounders, which identified severe nutritional risk as an independent predictor for poor survival. Dr Sanford and colleagues mentioned that additional studies are needed to determine whether optimizing preoperative nutrition and functioning capacity improves long-term outcomes, meaning that long-term risk of death after surgery might be attenuated by preoperative nutritional support and exercise. Because Dr Sanford and colleagues do not explain the potential mechanism by which severe nutritional risk could predict long-term outcomes of geriatric patients, I would like to discuss whether nutritional status itself or nutrition-related factors
978
Letters
influenced outcomes, and whether pre- and/or postoperative intervention could improve operative outcomes or not. In the study by Dr Sanford and colleagues,1 there were no differences in BMI and serum albumin levels between patients who were judged to have severe nutritional risk and those judged not have risk (Table 2 in the article1), suggesting that these factors might not be independently associated with worse survival. The criteria for “severe” nutritional risk were defined by the European Society for Parenteral and Enteral Nutrition working group in 2006.2 In the 2006 European Society for Parenteral and Enteral Nutrition guidelines for patients undergoing surgery including organ transplantation, 10 to 14 days of enteral nutrition before major surgery is advocated as recommendation A even if surgery has to be delayed.2 In the 2012 European Society for Parenteral and Enteral Nutrition guidelines for perioperative care for pancreaticoduodenectomy, severe nutritional risk is replaced with “significantly malnourished,” and “significantly malnourished” is not defined there.3 Also in the 2012 guidelines, preoperative enteral nutrition is recommended for significantly malnourished patients, but evidence level is very low and recommendation grade is weak.3 The criteria for severe nutritional risk are accepted for preoperative evaluation of geriatric patients by the American College of Surgeons NSQIP and the American Geriatric Society. Noteworthy, in the ACS NSQIP/American Geriatric Society Best Practices guidelines, unintentional weight loss is an important component of frailty and low serum albumin level is a surrogate marker of frailty.4 Although a universally accepted definition of frailty is lacking, frailty is characterized by low physical activity due to muscle weakness and exhaustion and resultant increased susceptibility to disability. Frailty has been reported to be more associated with increased risks of postoperative morbidity and mortality than conventional preoperative assessment tools, such as the American Society of Anesthesiology score and Physiologic and Operative Severity Score for the Enumeration of Mortality and Morbidity.5 Among patients admitted to the ICU, frail patients were more likely than nonfrail patients to be living with help for walking, taking a bath, taking medication, and managing own finances, and to have received less than a high school education.6 Given such backgrounds, it is likely difficult to ameliorate frailty with exercise and nutrition supplementation for a short period before surgery. Sarcopenia is defined as depletion of muscle mass and is thought to be an objective measure of frailty. In addition to negative impacts of sarcopenia on short-term operative outcomes,7,8 long-term risk of adverse events is associated with sarcopenia. In 557 patients with a mean age of 65.7 years who underwent pancreatic
J Am Coll Surg
resection for pancreatic adenocarcinoma, sarcopenia was associated with increased risk of 3-year mortality after adjusting for tumor-specific risk factors (hazard ratio ¼ 1.63; 95% CI, 1.282.07).9 After liver transplantation, there was a 3-fold increase in mortality risk at 3 years in patients with sarcopenia compared with those without sarcopenia.10 Also, in patients who underwent resection of colorectal cancer liver metastasis, there was a significant difference in adjusted 3-year overall survival (hazard ratio ¼ 2.53; 95% CI, 1.604.01) between those with sarcopenia and those without sarcopenia.11 Frailty due to sarcopenia disturbs effective early mobilization and rehabilitation, which are in the forefront of prevention of additional muscle wasting and pulmonary complication after surgery. Accelerated skeletal muscle proteolysis is vital for survival during surgical stress. Amino acids such as glutamine and alanine released from skeletal muscle serve as a primary substrate for immune cells and enterocytes, are used for gluconeogenesis as nutrients of central nervous system and red blood cells, serve as a precursor for glutathione, and participate in acidbase homeostasis.12 In addition, amino acids can be translocated from skeletal muscle to the visceral organs, such as the liver and spleen.12 Nutrition supplementation alone is not able to prevent muscle catabolism.13,14 Skeletal muscle protein is the critical reserve for combating surgical stress. Between ages 20 and 80 years, the total muscle crosssectional area is decreased by about 40%.15 These findings might explain why geriatric patients are vulnerable to postoperative complications. Besides increased risks of disability and mortality due to nonmalignant diseases in geriatric patients, there might be a link between muscle wasting and susceptibility to cancer initiation and progression through declined function of natural killer cells.16 This might explain the poor oncologic outcomes of frail patients. If the data on sarcopenia and/or frailty are available in the study by Dr Sanford and colleagues,1 analysis of the correlation between severe nutritional risk and sarcopenia/frailty would be helpful for better understandings of their findings. Although sufficient data are lacking, it is supposed that complete self-recovery of skeletal muscle loss and weakness during hospitalization is difficult, particularly in geriatric patients undergoing major abdominal surgery. There is an additional reduction in lean body mass up to 90 days after liver transplantation for cirrhosis, and thereafter the post-transplantation recovery of lean body mass will not reach the premorbid levels.17 The Hospital Elder Life Program, which includes postoperative early ambulation, nutritional support, and cognitive enhancement, could attenuate frailty at discharge,18 but the benefit of the Hospital Elder Life Program was diminished at 3 months after surgery.19 A combined intervention of exercise and dietary
Vol. 220, No. 5, May 2015
counseling on an outpatient basis improved exercise capacity and muscle strength, and increased lean body mass at 12 months after liver transplantation in a randomized trial.20 Postoperative intervention would be more practical and effective than short-term preoperative intervention for geriatric frail patients to improve long-term operative outcomes. REFERENCES 1. Sanford ED, Sanford MA, Fields CR, et al. Severe nutritional risk predicts decreased long-term survival in geriatric patients undergoing pancreaticoduodenectomy for benign disease. J Am Coll Surg 2014;219:1149e1156. 2. Weimann A, Braga M, Harsanyi L, et al. ESPEN guidelines on enteral nutrition: surgery including organ transplantation. Clin Nutr 2006;25:224e244. 3. Lassen K, Coolsen MM, Slim K, et al. Guidelines for perioperative care for pancreaticoduodenectomy: Enhanced Recovery after Surgery (ERASÒ) Society recommendations. Clin Nutr 2012;31:817e830. 4. Chow WB, Cho CY, Rosenthal RA, Esnaola NF. ACS NSQIP/ AGS Best Practice Guidelines: Optimal Preoperative Assessment of the Geriatric Surgical Patient 2012. Available at: http://site.acsnsqip.org/wp-content/uploads/2011/12/ACSNSQIP-AGS-Geriatric-2012-Guidelines.pdf. Accessed February 24, 2015. 5. Joseph B, Pandit V, Sadoun M, et al. Frailty in surgery. J Trauma Acute Care Surg 2014;76:1151e1156. 6. Bagshaw SM, Stelfox HT, McDermid RC, et al. Association between frailty and short- and long-term outcomes among critically ill patients: a multicentre prospective cohort study. CMAJ 2014;186:E95eE102. 7. Peng PD, van Vledder MG, Tsai S, et al. Sarcopenia negatively impacts short-term outcomes in patients undergoing hepatic resection for colorectal liver metastasis. HPB (Oxford) 2011; 13:439e446. 8. Lieffers JR, Bathe OF, Fassbender K, et al. Sarcopenia is associated with postoperative infection and delayed recovery from colorectal cancer resection surgery. Br J Cancer 2012;107: 931e936. 9. Peng P, Hyder O, Firoozmand A, et al. Impact of sarcopenia on outcomes following resection of pancreatic adenocarcinoma. J Gastrointest Surg 2012;16:1478e1486. 10. Englesbe MJ, Patel SP, He K, et al. Sarcopenia and mortality after liver transplantation. J Am Coll Surg 2010;211: 271e278. 11. van Vledder MG, Levolger S, Ayez N, et al. Body composition and outcome in patients undergoing resection of colorectal liver metastases. Br J Surg 2012;99:550e557. 12. Wilmore DW. Metabolic response to severe surgical illness: overview. World J Surg 2000;24:705e711. 13. Finnerty CC, Mabvuure NT, Ali A, et al. The surgically induced stress response. JPEN J Parenter Enteral Nutr 2013; 37[Suppl]:21Se29S. 14. Plank LD, Connolly AB, Hill GL. Sequential changes in severely septic patients during the first 23 days after the onset of peritonitis. Ann Surg 1998;228:146e158. 15. Lexell J, Taylor CC, Sjo¨stro¨m M. What is the cause of the ageing atrophy? Total number, size and proportion of
Letters
16.
17. 18. 19.
20.
979
different fiber types studied in whole vastus lateralis muscle from 15- to 83-year-old men. J Neurol Sci 1988;84: 275e294. Lutz CT, Quinn LS. Sarcopenia, obesity, and natural killer cell immune senescence in aging: altered cytokine levels as a common mechanism. Aging (Albany NY) 2012;4: 535e546. Dasarathy S. Posttransplant sarcopenia: an underrecognized early consequence of liver transplantation. Dig Dis Sci 2013; 58:3103e3111. Chen CC, Lin MT, Tien YW, et al. Modified Hospital Elder Life Program: effects on abdominal surgery patients. J Am Coll Surg 2011;213:245e252. Chen CC, Chen CN, Lai IR, et al. Effects of a modified Hospital Elder Life Program on frailty in individuals undergoing major elective abdominal surgery. J Am Geriatr Soc 2014; 62:261e268. Krasnoff JB, Vintro AQ, Ascher NL, et al. A randomized trial of exercise and dietary counseling after liver transplantation. Am J Transplant 2006;6:1896e1905.
Disclosure Information: Nothing to disclose.
Patient Safety Sophia E de Rooij, MD, PhD, Barbara C van Munster, MD, PhD, Annemarieke de Jonghe, MD, PhD Groningen, Netherlands We read the recently presented best practices guideline for postoperative delirium in older adults with great interest.1 We think this guideline is properly equipping the health care professional caring for older adults in the perioperative setting with a set of evidence-based recommendation statements about the optimal care of older adults with delirium. Evidence-based nonpharmacological measures are the cornerstone of prevention and treatment for the frequent problem of delirium in perioperative patients. We strongly emphasize the advice of the group against preoperative prophylactic application of antipsychotics. We are surprised, however, that the use of melatonin in vulnerable patient groups is not mentioned in the guideline. Recently, 3 randomized controlled trials have been published that compared melatonin with placebo. Two of these studies found a clear reduction in the incidence of delirium.2,3 The third study, by our group, included hipfracture patients with a mean age of 84 years.4 In this highly vulnerable population, we failed to confirm an influence on the incidence of postoperative delirium, but in the melatonin arm, significantly fewer patients experienced longerlasting delirium (ie, 3 or more days). We miss a role for melatonin in the recommendation statements within the
disease. Considering the important implications of this association, we would like to add some information that can help clarify the message in their article. Autosomal recessive polycystic kidney disease (ARPKD) is a rare, inherited form of renal disease that tends to be evident early in life, and can have important associated liver abnormalities, most notably congenital hepatic fibrosis. The underlying abnormality, a mutation in the polycystic kidney and hepatic disease 1 gene, leads to disruption in expression of fibrocystin/polyductin, a protein that plays a key role in the development of collecting and intrahepatic duct tubular architecture.2 Autosomal dominant polycystic kidney disease (ADPKD), a relatively more common disorder responsible for 5% to 10% of patients who enter end-stage renal disease, is caused by mutations in genes that encode mechanosensory ion channels (PKD1 or 2; disrupting polycystin 1 and 2, respectively). These patients commonly present later in life, with multiple large cysts in the kidneys and other organs, most notably liver and pancreas. Liver cysts are particularly prevalent in this patient population, and can sometimes trigger symptoms by compression or infection.3 Liver cysts tend to be isolated in ADPKD. In contrast, in ARPKD, the saccular ectasias can be seen to communicate directly with the intrahepatic biliary system, a fact that might allow imaging modalities to distinguish between the two forms.4 Soares and colleagues5 correctly indicate the presence of an association between ductal plate malformation during embryogenesis and ARPKD, however, they state this is due to a mutation in the PKD1 gene and quote a reference dealing with ADPKD. Although seemingly a minor mistake, based on dramatic differences in patterns of presentation, management, and inheritance for the two types of PKD, the information provided is confusing. Caroli disease has been reported in up to 30% of ARPKD patients.2,6 In contrast, <10 cases of Caroli disease in association with ADPKD have been reported in the literature,7 including that referenced by Soares and colleagues. We propose that a more in-depth analysis of the literature and clarification of the association between congenital hepatic fibrosis, Caroli disease, and Caroli syndrome with renal tubular ectasia and renal cystic diseases, along with an accurate description of the affected genes and modes of inheritance, would significantly strengthen their publication.
REFERENCES 1. Soares KC, Arnaoutakis DJ, Kamel I, et al. Choledochal cysts: presentation, clinical differentiation, and management. J Am Coll Surg 2014;219:1167e1180.
Letters
977
2. Sweeney WE Jr, Avner ED. Pathophysiology of childhood polycystic kidney diseases: new insights into disease-specific therapy. Pediatr Res 2014;75:148e157. 3. Ars E, Bernis C, Fraga G, et al. Spanish guidelines for the management of autosomal dominant polycystic kidney disease. Nephrol Dialysis Transplant 2014;29:iv95eiv105. 4. Gunay-Aygun M, Turkbey BI, Bryant J, et al. Hepatorenal findings in obligate heterozygotes for autosomal recessive polycystic kidney disease. Mol Genet Metab 2011;104:677e681. 5. Torra R, Badenas C, Darnell A, et al. Autosomal dominant polycystic kidney disease with anticipation and Caroli’s disease associated with a PKD1 mutation. Rapid communication. Kidney Int 1997;52:33e38. 6. Buscher R, Buscher AK, Weber S, et al. Clinical manifestations of autosomal recessive polycystic kidney disease (ARPKD): kidneyrelated and non-kidney-related phenotypes. Pediatr Nephrol 2014;29:1915e1925. 7. Aguilar M, Meterissian S, Levesque S, Andonian S. Nephrectomy in patients with Caroli’s and ADPKD may be associated with increased morbidity. Can Urol Assoc J 2011;5:E19eE22.
Disclosure Information: Nothing to disclose.
Perioperative Strategy for Severe Nutritional Risk-Related Frail Patients Tetsuji Fujita, Tokyo, Japan
MD
In an important study by Dr Sanford and colleagues,1 severe nutritional risk, as defined by the presence of at least one of the following criteria: BMI <18.5 kg/m2, serum albumin <3.0 g/dL, and unintentional weight loss >10% within 6 months before surgery, adversely affected longterm survival for geriatric patients (aged 65 years or older) after pancreaticoduodenectomy for benign pancreatic disease. When compared with those without severe nutritional risk, there were surprising differences in 5-year survival (64.8% vs 92.5%) and 10-year survival rates (23.2% vs 68.9%). Multivariate analysis was performed for adjusting confounders, which identified severe nutritional risk as an independent predictor for poor survival. Dr Sanford and colleagues mentioned that additional studies are needed to determine whether optimizing preoperative nutrition and functioning capacity improves long-term outcomes, meaning that long-term risk of death after surgery might be attenuated by preoperative nutritional support and exercise. Because Dr Sanford and colleagues do not explain the potential mechanism by which severe nutritional risk could predict long-term outcomes of geriatric patients, I would like to discuss whether nutritional status itself or nutrition-related factors
978
Letters
influenced outcomes, and whether pre- and/or postoperative intervention could improve operative outcomes or not. In the study by Dr Sanford and colleagues,1 there were no differences in BMI and serum albumin levels between patients who were judged to have severe nutritional risk and those judged not have risk (Table 2 in the article1), suggesting that these factors might not be independently associated with worse survival. The criteria for “severe” nutritional risk were defined by the European Society for Parenteral and Enteral Nutrition working group in 2006.2 In the 2006 European Society for Parenteral and Enteral Nutrition guidelines for patients undergoing surgery including organ transplantation, 10 to 14 days of enteral nutrition before major surgery is advocated as recommendation A even if surgery has to be delayed.2 In the 2012 European Society for Parenteral and Enteral Nutrition guidelines for perioperative care for pancreaticoduodenectomy, severe nutritional risk is replaced with “significantly malnourished,” and “significantly malnourished” is not defined there.3 Also in the 2012 guidelines, preoperative enteral nutrition is recommended for significantly malnourished patients, but evidence level is very low and recommendation grade is weak.3 The criteria for severe nutritional risk are accepted for preoperative evaluation of geriatric patients by the American College of Surgeons NSQIP and the American Geriatric Society. Noteworthy, in the ACS NSQIP/American Geriatric Society Best Practices guidelines, unintentional weight loss is an important component of frailty and low serum albumin level is a surrogate marker of frailty.4 Although a universally accepted definition of frailty is lacking, frailty is characterized by low physical activity due to muscle weakness and exhaustion and resultant increased susceptibility to disability. Frailty has been reported to be more associated with increased risks of postoperative morbidity and mortality than conventional preoperative assessment tools, such as the American Society of Anesthesiology score and Physiologic and Operative Severity Score for the Enumeration of Mortality and Morbidity.5 Among patients admitted to the ICU, frail patients were more likely than nonfrail patients to be living with help for walking, taking a bath, taking medication, and managing own finances, and to have received less than a high school education.6 Given such backgrounds, it is likely difficult to ameliorate frailty with exercise and nutrition supplementation for a short period before surgery. Sarcopenia is defined as depletion of muscle mass and is thought to be an objective measure of frailty. In addition to negative impacts of sarcopenia on short-term operative outcomes,7,8 long-term risk of adverse events is associated with sarcopenia. In 557 patients with a mean age of 65.7 years who underwent pancreatic
J Am Coll Surg
resection for pancreatic adenocarcinoma, sarcopenia was associated with increased risk of 3-year mortality after adjusting for tumor-specific risk factors (hazard ratio ¼ 1.63; 95% CI, 1.282.07).9 After liver transplantation, there was a 3-fold increase in mortality risk at 3 years in patients with sarcopenia compared with those without sarcopenia.10 Also, in patients who underwent resection of colorectal cancer liver metastasis, there was a significant difference in adjusted 3-year overall survival (hazard ratio ¼ 2.53; 95% CI, 1.604.01) between those with sarcopenia and those without sarcopenia.11 Frailty due to sarcopenia disturbs effective early mobilization and rehabilitation, which are in the forefront of prevention of additional muscle wasting and pulmonary complication after surgery. Accelerated skeletal muscle proteolysis is vital for survival during surgical stress. Amino acids such as glutamine and alanine released from skeletal muscle serve as a primary substrate for immune cells and enterocytes, are used for gluconeogenesis as nutrients of central nervous system and red blood cells, serve as a precursor for glutathione, and participate in acidbase homeostasis.12 In addition, amino acids can be translocated from skeletal muscle to the visceral organs, such as the liver and spleen.12 Nutrition supplementation alone is not able to prevent muscle catabolism.13,14 Skeletal muscle protein is the critical reserve for combating surgical stress. Between ages 20 and 80 years, the total muscle crosssectional area is decreased by about 40%.15 These findings might explain why geriatric patients are vulnerable to postoperative complications. Besides increased risks of disability and mortality due to nonmalignant diseases in geriatric patients, there might be a link between muscle wasting and susceptibility to cancer initiation and progression through declined function of natural killer cells.16 This might explain the poor oncologic outcomes of frail patients. If the data on sarcopenia and/or frailty are available in the study by Dr Sanford and colleagues,1 analysis of the correlation between severe nutritional risk and sarcopenia/frailty would be helpful for better understandings of their findings. Although sufficient data are lacking, it is supposed that complete self-recovery of skeletal muscle loss and weakness during hospitalization is difficult, particularly in geriatric patients undergoing major abdominal surgery. There is an additional reduction in lean body mass up to 90 days after liver transplantation for cirrhosis, and thereafter the post-transplantation recovery of lean body mass will not reach the premorbid levels.17 The Hospital Elder Life Program, which includes postoperative early ambulation, nutritional support, and cognitive enhancement, could attenuate frailty at discharge,18 but the benefit of the Hospital Elder Life Program was diminished at 3 months after surgery.19 A combined intervention of exercise and dietary
Vol. 220, No. 5, May 2015
counseling on an outpatient basis improved exercise capacity and muscle strength, and increased lean body mass at 12 months after liver transplantation in a randomized trial.20 Postoperative intervention would be more practical and effective than short-term preoperative intervention for geriatric frail patients to improve long-term operative outcomes. REFERENCES 1. Sanford ED, Sanford MA, Fields CR, et al. Severe nutritional risk predicts decreased long-term survival in geriatric patients undergoing pancreaticoduodenectomy for benign disease. J Am Coll Surg 2014;219:1149e1156. 2. Weimann A, Braga M, Harsanyi L, et al. ESPEN guidelines on enteral nutrition: surgery including organ transplantation. Clin Nutr 2006;25:224e244. 3. Lassen K, Coolsen MM, Slim K, et al. Guidelines for perioperative care for pancreaticoduodenectomy: Enhanced Recovery after Surgery (ERASÒ) Society recommendations. Clin Nutr 2012;31:817e830. 4. Chow WB, Cho CY, Rosenthal RA, Esnaola NF. ACS NSQIP/ AGS Best Practice Guidelines: Optimal Preoperative Assessment of the Geriatric Surgical Patient 2012. Available at: http://site.acsnsqip.org/wp-content/uploads/2011/12/ACSNSQIP-AGS-Geriatric-2012-Guidelines.pdf. Accessed February 24, 2015. 5. Joseph B, Pandit V, Sadoun M, et al. Frailty in surgery. J Trauma Acute Care Surg 2014;76:1151e1156. 6. Bagshaw SM, Stelfox HT, McDermid RC, et al. Association between frailty and short- and long-term outcomes among critically ill patients: a multicentre prospective cohort study. CMAJ 2014;186:E95eE102. 7. Peng PD, van Vledder MG, Tsai S, et al. Sarcopenia negatively impacts short-term outcomes in patients undergoing hepatic resection for colorectal liver metastasis. HPB (Oxford) 2011; 13:439e446. 8. Lieffers JR, Bathe OF, Fassbender K, et al. Sarcopenia is associated with postoperative infection and delayed recovery from colorectal cancer resection surgery. Br J Cancer 2012;107: 931e936. 9. Peng P, Hyder O, Firoozmand A, et al. Impact of sarcopenia on outcomes following resection of pancreatic adenocarcinoma. J Gastrointest Surg 2012;16:1478e1486. 10. Englesbe MJ, Patel SP, He K, et al. Sarcopenia and mortality after liver transplantation. J Am Coll Surg 2010;211: 271e278. 11. van Vledder MG, Levolger S, Ayez N, et al. Body composition and outcome in patients undergoing resection of colorectal liver metastases. Br J Surg 2012;99:550e557. 12. Wilmore DW. Metabolic response to severe surgical illness: overview. World J Surg 2000;24:705e711. 13. Finnerty CC, Mabvuure NT, Ali A, et al. The surgically induced stress response. JPEN J Parenter Enteral Nutr 2013; 37[Suppl]:21Se29S. 14. Plank LD, Connolly AB, Hill GL. Sequential changes in severely septic patients during the first 23 days after the onset of peritonitis. Ann Surg 1998;228:146e158. 15. Lexell J, Taylor CC, Sjo¨stro¨m M. What is the cause of the ageing atrophy? Total number, size and proportion of
Letters
16.
17. 18. 19.
20.
979
different fiber types studied in whole vastus lateralis muscle from 15- to 83-year-old men. J Neurol Sci 1988;84: 275e294. Lutz CT, Quinn LS. Sarcopenia, obesity, and natural killer cell immune senescence in aging: altered cytokine levels as a common mechanism. Aging (Albany NY) 2012;4: 535e546. Dasarathy S. Posttransplant sarcopenia: an underrecognized early consequence of liver transplantation. Dig Dis Sci 2013; 58:3103e3111. Chen CC, Lin MT, Tien YW, et al. Modified Hospital Elder Life Program: effects on abdominal surgery patients. J Am Coll Surg 2011;213:245e252. Chen CC, Chen CN, Lai IR, et al. Effects of a modified Hospital Elder Life Program on frailty in individuals undergoing major elective abdominal surgery. J Am Geriatr Soc 2014; 62:261e268. Krasnoff JB, Vintro AQ, Ascher NL, et al. A randomized trial of exercise and dietary counseling after liver transplantation. Am J Transplant 2006;6:1896e1905.
Disclosure Information: Nothing to disclose.
Patient Safety Sophia E de Rooij, MD, PhD, Barbara C van Munster, MD, PhD, Annemarieke de Jonghe, MD, PhD Groningen, Netherlands We read the recently presented best practices guideline for postoperative delirium in older adults with great interest.1 We think this guideline is properly equipping the health care professional caring for older adults in the perioperative setting with a set of evidence-based recommendation statements about the optimal care of older adults with delirium. Evidence-based nonpharmacological measures are the cornerstone of prevention and treatment for the frequent problem of delirium in perioperative patients. We strongly emphasize the advice of the group against preoperative prophylactic application of antipsychotics. We are surprised, however, that the use of melatonin in vulnerable patient groups is not mentioned in the guideline. Recently, 3 randomized controlled trials have been published that compared melatonin with placebo. Two of these studies found a clear reduction in the incidence of delirium.2,3 The third study, by our group, included hipfracture patients with a mean age of 84 years.4 In this highly vulnerable population, we failed to confirm an influence on the incidence of postoperative delirium, but in the melatonin arm, significantly fewer patients experienced longerlasting delirium (ie, 3 or more days). We miss a role for melatonin in the recommendation statements within the