Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:

Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1029_Библиотеки_им_академика_М_И_Перельмана

.pdf
Скачиваний:
0
Добавлен:
31.08.2026
Размер:
25 Мб
Скачать
178
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
E. Nisenbaum and E. A. Nicolli
22. Unal D, Orhan O, Eroglu C, Kaplan B.Prealbumin is a more sensitive marker than albumin to assess the nutritional status in patients undergoing radio­therapy for head and neck cancer. Contemp Oncol (Pozn). 2013;17:276–80.
23. Danan D, Shonka DC Jr, Selman Y, Chow Z, Smolkin ME, Jameson MJ. Prognostic value of albumin in patients with head and neck cancer. Laryngoscope. 2016;126:1567–71.
24. Yu J, Hong JP, Suh HP, etal. Prognostic nutritional index is a predictor of free ap failure in extremity reconstruction. Nutrients. 2020;12:562.
25. Jensen GL, Bistrian B, Roubenoff R, Heimburger DC. Malnutrition syndromes: a conundrum vs continuum. JPEN J Parenter Enteral Nutr. 2009;33:710–6.
26. Library ADAEA. Does serum albumin corre­late with weight loss in four models of prolonged protein-energy restriction: anorexia nervosa, non­malabsorptive gastric partitioning bariatric surgery, calorie-restricted diets, or starvation.
27. Detsky AS, McLaughlin JR, Baker JP, et al. What is subjective global assessment of nutritional status? JPEN J Parenter Enteral Nutr. 1987;11:8–13.
28. PG-SGA. https://pt- global.org/pt- global/.
29. Capuano G, Gentile PC, Bianciardi F, Tosti M, Palladino A, Di Palma M.Prevalence and inuence of malnutrition on quality of life and performance status in patients with locally advanced head and neck cancer before treatment. Support Care Cancer. 2010;18:433–7.
30. Souza MTP, Singer P, Ozorio GA, et al. Resting energy expenditure and body composition in patients with head and neck cancer: an observational study leading to a new predictive equation. Nutrition. 2018;51–52:60–5.
31. Bauer J, Capra S, Ferguson M.Use of the scored patient-generated subjective global assessment (PG-SGA) as a nutrition assessment tool in patients with cancer. Eur J Clin Nutr. 2002;56:779–85.
32. Nitichai N, Angkatavanich J, Somlaw N, Voravud N, Lertbutsayanukul C. Validation of the scored patient-generated subjective global assessment (PG-SGA) in Thai setting and association with nutritional parameters in cancer patients. Asian Pac J Cancer Prev. 2019;20:1249–55.
33. Cong M, Song C, Xu H, etal. The patient-generated subjective global assessment is a promising screen­ing tool for cancer cachexia. BMJ Support Palliat Care. 2020;12:e39.
34. Rodrigues CS, Lacerda MS, Chaves GV.Patient gen­erated subjective global assessment as a prognosis tool in women with gynecologic cancer. Nutrition. 2015;31:1372–8.
35. Härter J, Orlandi SP, Gonzalez MC.Nutritional and functional factors as prognostic of surgical cancer patients. Support Care Cancer. 2017;25:2525–30.
36. Jager-Wittenaar H, Ottery FD.Assessing nutritional status in cancer: role of the patient-generated sub-
jective global assessment. Curr Opinion Clin Nutr Metab Care. 2017;20:322–9.
37. Carriço M, Guerreiro CS, Parreira A. The valid­ity of the Patient-Generated Subjective Global Assessment Short-form©; in cancer patients under­going chemotherapy. Clinical Nutrition ESPEN. 2021;43:296–301.
38. De Groot LM, Lee G, Ackerie A, van der Meij BS. Malnutrition screening and assessment in the cancer care ambulatory setting: mortality predict­ability and validity of the patient-generated subjec­tive global assessment short form (PG-SGA SF) and the GLIM criteria. Nutrients. 2020;12:2287.
39. Jager-Wittenaar H, de Bats HF, Welink-Lamberts BJ, et al. Self-completion of the patient-generated subjective global assessment short form is feasible and is associated with increased awareness on mal­nutrition risk in patients with head and neck cancer. Nutr Clin Pract. 2020;35:353–62.
40. Kondrup J, Rasmussen HH, Hamberg O, Stanga Z. Nutritional risk screening (NRS 2002): a new method based on an analysis of controlled clinical trials. Clin Nutr. 2003;22:321–36.
41. Liu W, Gao L, Huang X, etal. Pretreatment nutri­tional risk as a prognostic factor in head and neck cancer patients receiving radiotherapy or chemora­diotherapy. Asia Pac J Clin Nutr. 2019;28:223–9.
42. Orell-Kotikangas H, Österlund P, Saarilahti K, Ravasco P, Schwab U, Mäkitie AA.NRS-2002 for pre-treatment nutritional risk screening and nutri­tional status assessment in head and neck cancer patients. Support Care Cancer. 2015;23:1495–502.
43. Hsueh SW, Lai CC, Hung CY, etal. A comparison of the MNA-SF, MUST, and NRS-2002 nutritional tools in predicting treatment incompletion of con­current chemoradiotherapy in patients with head and neck cancer. Support Care Cancer. 2021;29:5455–62.
44. Cederholm T, Jensen GL, Correia M, etal. GLIM cri­teria for the diagnosis of malnutrition—a consensus report from the global clinical nutrition community. J Cachexia Sarcopenia Muscle. 2019;10:207–17.
45. O'Neill JP, Shaha AR. Nutrition management of patients with malignancies of the head and neck. Surg Clin North Am. 2011;91:631–9.
46. Beeken L, Calman F. A return to “normal eating” after curative treatment for oral cancer. What are the long-term prospects? European journal of cancer part B.Oral Oncol. 1994;30:387–92.
47. Rettig EM, D'Souza G.Epidemiology of head and neck cancer. Surg Oncol Clin N Am. 2015;24:379–96.
48. Ross LJ, Wilson M, Banks M, Rezannah F, Daglish M. Prevalence of malnutrition and nutritional risk factors in patients undergoing alcohol and drug treat­ment. Nutrition. 2012;28:738–43.
49. Flannery AH, Adkins DA, Cook AM. Unpeeling the evidence for the Banana bag: evidence-based recommendations for the Management of Alcohol­Associated Vitamin and Electrolyte Deciencies in the ICU.Crit Care Med. 2016;44:1545–52.
12 Perioperative Nutrition inHead andNeck Free Flap Reconstruction
179
50. Jo YH, Talmage DA, Role LW.Nicotinic receptor­mediated effects on appetite and food intake. J Neurobiol. 2002;53:618–32.
51. Risso D, Drayna D, Morini G.Alteration, reduction and taste loss: Main causes and potential implica­tions on dietary habits. Nutrients. 2020;12:3284.
52. Cervenka BP, Rao S, Bewley AF. Head and neck cancer and the elderly patient. Otolaryngol Clin N Am. 2018;51:741–51.
53. Larsson L, Degens H, Li M, etal. Sarcopenia: aging­related loss of muscle mass and function. Physiol Rev. 2019;99:427–511.
54. Fearon K, Strasser F, Anker SD, etal. Denition and classication of cancer cachexia: an international consensus. Lancet Oncol. 2011;12:489–95.
55. Baracos VE, Martin L, Korc M, Guttridge DC, Fearon KC. Cancer-associated cachexia. Nat Rev Dis Primers. 2018;4:1–18.
56. Biswas AK, Acharyya S. Cancer-associated cachexia: a systemic consequence of cancer progres­sion. Annu Rev Cancer Biol. 2020;4:391–411.
57. George J, Cannon T, Lai V, etal. Cancer cachexia syndrome in head and neck cancer patients: part II.Pathophysiology Head Neck. 2007;29:497–507.
58. Lakananurak N, Gramlich L.The Role of preopera­tive parenteral nutrition. Nutrients. 2020;12:1320.
59. Weimann A, Braga M, Harsanyi L, et al. ESPEN guidelines on enteral nutrition: surgery including organ transplantation. Clin Nutr. 2006;25:224–44.
60. Parhar HS, Durham JS, Anderson DW, Rush B, Prisman E. The association between the nutrition­related index and morbidity following head and neck microsurgery. Laryngoscope. 2020;130:375–80.
61. Patel RS, McCluskey SA, Goldstein DP, et al. Clinicopathologic and therapeutic risk factors for perioperative complications and prolonged hospital stay in free ap reconstruction of the head and neck. Head Neck. 2010;32:1345–53.
62. Eskander A, Kang S, Tweel B, etal. Predictors of complications in patients receiving head and neck free ap reconstructive procedures. Otolaryngol Head Neck Surg. 2018;158:839–47.
63. Alwani MM, Jones AJ, Novinger LJ, etal. Impact of sarcopenia on outcomes of autologous head and neck free tissue reconstruction. J Reconstr Microsurg. 2020;36:369–78.
64. Anesthesiology AAoN. Enhanced recovery after surgery: considerations for pathway development and implementation. https://www.aana.com/docs/
default- source/practice- aana- com- web- documents­(all)/professional- practice- manual/enhanced­recovery- after- surgery.pdf?sfvrsn=6d184ab1_14.
65. Lassen K, Soop M, Nygren J, etal. Consensus review of optimal perioperative care in colorectal surgery: enhanced recovery after surgery (ERAS) group rec­ommendations. Arch Surg. 2009;144:961–9.
66. Dort JC, Farwell DG, Findlay M, etal. Optimal peri­operative care in major head and neck cancer surgery with free ap reconstruction: a consensus review and recommendations from the enhanced recovery
after surgery society. JAMA Otolaryngol Head Neck Surg. 2017;143:292–303.
67. Engelman DT, Ben Ali W, Williams JB, et al. Guidelines for perioperative care in cardiac surgery: enhanced recovery after surgery society recommen­dations. JAMA Surg. 2019;154:755–66.
68. Debono B, Wainwright TW, Wang MY, et al. Consensus statement for perioperative care in lum­bar spinal fusion: Enhanced Recovery After Surgery (ERAS®) Society recommendations. Spine J. 2021;21:729–52.
69. Chorath K, Go B, Shinn JR, etal. Enhanced recovery after surgery for head and neck free ap reconstruc­tion: a systematic review and meta-analysis. Oral Oncol. 2021;113:105117.
70. Network NCC.Head and neck cancers. https://www.
nccn.org/professionals/physician_gls/pdf/head- and­neck.pdf.
71. Talwar B, Donnelly R, Skelly R, Donaldson M.Nutritional management in head and neck can­cer: United Kingdom National Multidisciplinary Guidelines. J Laryngol Otol. 2016;130:S32–s40.
72. Victoria CCVaDoH.Optimal care pathway for peo­ple with head and neck cancer. Melbourne: Cancer Council Victoria; 2021.
73. Heyland DK, Montalvo M, MacDonald S, Keefe L, Su XY, Drover JW. Total parenteral nutrition in the surgical patient: a meta-analysis. Can J Surg. 2001;44:102–11.
74. Jie B, Jiang ZM, Nolan MT, Zhu SN, Yu K, Kondrup J.Impact of preoperative nutritional support on clini­cal outcome in abdominal surgical patients at nutri­tional risk. Nutrition. 2012;28:1022–7.
75. Von Meyenfeldt MF, Meijerink WJHJ, Rouart MMJ, Builmaassen MTHJ, Soeters PB.Perioperative nutritional support: a randomised clinical trial. Clin Nutr. 1992;11:180–6.
76. Van V B-d, der Schuer MA, Langendoen SI, Vondeling H, Kuik DJ, Quak JJ, Van Leeuwen PA. Perioperative enteral nutrition and quality of life of severely malnourished head and neck can­cer patients: a randomized clinical trial. Clin Nutr. 2000;19:437–44.
77. McClave SA, Kozar R, Martindale RG, et al. Summary points and consensus recommendations from the North American Surgical Nutrition Summit. JPEN J Parenter Enteral Nutr. 2013;37:99s–105s.
78. Huang AT, Georgolios A, Espino S, Kaplan B, Neifeld J, Reiter ER. Percutaneous endoscopic gastrostomy site metastasis from head and neck squamous cell carcinoma: case series and literature review. J Otolaryngol Head Neck Surg. 2013;42:20.
79. Nugent B, Lewis S, O'Sullivan JM.Enteral feeding methods for nutritional management in patients with head and neck cancers being treated with radiother­apy and/or chemotherapy. Cochrane Database Syst Rev. 2013;2013:Cd007904.
80. Corry J, Poon W, McPhee N, et al. Randomized study of percutaneous endoscopic gastrostomy ver­sus nasogastric tubes for enteral feeding in head and
180
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
E. Nisenbaum and E. A. Nicolli
neck cancer patients treated with (chemo)radiation. J Med Imaging Radiat Oncol. 2008;52:503–10.
81. Weimann A, Braga M, Carli F, et al. ESPEN guideline: clinical nutrition in surgery. Clin Nutr. 2017;36:623–50.
82. Worthington ML, Cresci G. Immune-modulating formulas: who wins the meta-analysis race? Nutr Clin Pract. 2011;26:650–5.
83. Morris SM Jr. Arginine: beyond protein. Am J Clin Nutr. 2006;83:508s–12s.
84. Tong BC, Barbul A. Cellular and physiologi­cal effects of arginine. Mini-Rev Med Chem. 2004;4:823–32.
85. Smith RJ. Glutamine metabolism and its physi­ologic importance. JPEN J Parenter Enteral Nutr. 1990;14:40s–4s.
86. Schloerb PR. Immune-enhancing diets: products, components, and their rationales. JPEN J Parenter Enteral Nutr. 2001;25:S3–7.
87. Calder PC. N-3 polyunsaturated fatty acids and inammation: from molecular biology to the clinic. Lipids. 2003;38:343–52.
88. Marimuthu K, Varadhan KK, Ljungqvist O, Lobo DN.A meta-analysis of the effect of combinations of immune modulating nutrients on outcome in patients undergoing major open gastrointestinal surgery. Ann Surg. 2012;255:1060–8.
89. Wong CS, Aly EH. The effects of enteral immu­nonutrition in upper gastrointestinal surgery: a systematic review and meta-analysis. Int J Surg. 2016;29:137–50.
90. Strickland A, Brogan A, Krauss J, Martindale R, Cresci G. Is the use of specialized nutritional for­mulations a cost-effective strategy? A national database evaluation. JPEN J Parenter Enteral Nutr. 2005;29:S81–91.
91. August DA, Huhmann MB. A.S.P.E.N. clini­cal guidelines: nutrition support therapy during adult anticancer treatment and in hematopoietic cell transplantation. JPEN J Parenter Enteral Nutr. 2009;33:472–500.
92. Arends J, Bachmann P, Baracos V, et al. ESPEN guidelines on nutrition in cancer patients. Clin Nutr. 2017;36:11–48.
93. Hegazi RA, Hustead DS, Evans DC.Preoperative standard Oral nutrition supplements vs Immunonutrition: results of a systematic review and meta-analysis. J Am Coll Surg. 2014;219:1078–87.
94. Howes N, Atkinson C, Thomas S, Lewis SJ.Immunonutrition for patients undergoing surgery for head and neck cancer. Cochrane Database Syst Rev. 2018;2018(8):CD010954.
95. Mueller SA, Mayer C, Bojaxhiu B, etal. Effect of preoperative immunonutrition on complications after salvage surgery in head and neck cancer. J Otolaryngol Head Neck Surg. 2019;48:25.
96. Brady M, Kinn S, Stuart P. Preoperative fasting for adults to prevent perioperative complications. Cochrane Database Syst Rev 2003;(4):Cd004423.
97. American Society of Anesthesiologists Task Force. Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: application to healthy patients undergoing elective procedures: an updated report by the American Society of Anesthesiologists Task Force on preoperative fasting and the use of pharma­cologic agents to reduce the risk of pulmonary aspi­ration. Anesthesiology. 2017;126:376–93.
98. Smith I, Kranke P, Murat I, etal. Perioperative fasting in adults and children: guidelines from the European Society of Anaesthesiology. Eur J Anaesthesiol. 2011;28:556–69.
99. Pogatschnik C, Steiger E.Review of preoperative car­bohydrate loading. Nutr Clin Pract. 2015;30:660–4.
100. Pimenta GP, de Aguilar-Nascimento JE.Prolonged preoperative fasting in elective surgical patients: why should we reduce it? Nutr Clin Pract. 2014;29:22–8.
101. Offodile AC 2nd, Chou HY, Lin JA, et al. Hyperglycemia and risk of adverse outcomes fol­lowing microvascular reconstruction of oncologic head and neck defects. Oral Oncol. 2018;79:15–9.
102. Viganò J, Cereda E, Caccialanza R, etal. Effects of preoperative oral carbohydrate supplementation on postoperative metabolic stress response of patients undergoing elective abdominal surgery. World J Surg. 2012;36:1738–43.
103. Zelić M, Stimac D, Mendrila D, etal. Inuence of preoperative oral feeding on stress response after resection for colon cancer. Hepato-Gastroenterology. 2012;59:1385–9.
104. Melis GC, van Leeuwen PA, von Blomberg-van der Flier BM, etal. A carbohydrate-rich beverage prior to surgery prevents surgery-induced immunodepres­sion: a randomized, controlled, clinical trial. JPEN J Parenter Enteral Nutr. 2006;30:21–6.
105. Helminen H, Viitanen H, Sajanti J.Effect of preop­erative intravenous carbohydrate loading on preop­erative discomfort in elective surgery patients. Eur J Anaesthesiol. 2009;26:123–7.
106. Smith MD, McCall J, Plank L, Herbison GP, Soop M, Nygren J. Preoperative carbohydrate treat­ment for enhancing recovery after elective surgery. Cochrane Database Syst Rev 2014;(8):Cd009161.
107. Noba L, Wakeeld A.Are carbohydrate drinks more effective than preoperative fasting: a systematic review of randomised controlled trials. J Clin Nurs. 2019;28:3096–116.
108. Amer MA, Smith MD, Herbison GP, Plank LD, McCall JL.Network meta-analysis of the effect of preoperative carbohydrate loading on recovery after elective surgery. Br J Surg. 2017;104:187–97.
109. Henriksen MG, Hessov I, Dela F, Hansen HV, Haraldsted V, Rodt SA.Effects of preoperative oral carbohydrates and peptides on postoperative endo­crine response, mobilization, nutrition and muscle function in abdominal surgery. Acta Anaesthesiol Scand. 2003;47:191–9.
110. Yi HC, Ibrahim Z, Abu Zaid Z, et al. Impact of enhanced recovery after surgery with preoperative
12 Perioperative Nutrition inHead andNeck Free Flap Reconstruction
181
whey protein-infused carbohydrate loading and post­operative early Oral feeding among surgical gyneco­logic cancer patients: an open-labelled randomized controlled trial. Nutrients. 2020;12:264.
111. Perrone F, da Silva Filho AC, Adôrno IF, et al. Effects of preoperative feeding with a whey protein plus carbohydrate drink on the acute phase response and insulin resistance. A randomized trial. Nutr J. 2011;10:66.
112. Pexe-Machado PA, de Oliveira BD, Dock­Nascimento DB, de Aguilar-Nascimento JE.Shrinking preoperative fast time with maltodex­trin and protein hydrolysate in gastrointestinal resec­tions due to cancer. Nutrition. 2013;29:1054–9.
113. de Carvalho CS, Silva TH, JCS A, etal. Preoperative fasting abbreviation with whey protein reduces the occurrence of postoperative complications in patients with head and neck cancer: a randomized clinical trial. Nutr Clin Pract. 2021;36:665–72.
114. Herbert G, Perry R, Andersen HK, etal. Early enteral nutrition within 24 hours of lower gastrointesti­nal surgery versus later commencement for length of hospital stay and postoperative complications. Cochrane Database Syst Rev. 2019;2019:CD004080.
115. Lewis SJ, Egger M, Sylvester PA, Thomas S.Early enteral feeding versus "nil by mouth" after gastro­intestinal surgery: systematic review and meta­analysis of controlled trials. BMJ. 2001;323:773–6.
116. Willcutts KF, Chung MC, Erenberg CL, Finn KL, Schirmer BD, Byham-Gray LD.Early Oral feeding as compared with traditional timing of Oral feeding after upper gastrointestinal surgery: a systematic review and meta-analysis. Ann Surg. 2016;264:264.
117. Milinis K, Gaskell P, Lau A, Lancaster J, Jones T.Early versus late oral feeding following total (pha­ryngo)laryngectomy: systematic review and meta­analysis. Head Neck. 2021;43:1359–68.
118. Grover S, Swisher-McClure S, Mitra N, etal. Total laryngectomy versus larynx preservation for T4a lar­ynx cancer: patterns of care and survival outcomes. Int J Radiat Oncol Biol Phys. 2015;92:594–601.
119. Hoffman HT, Porter K, Karnell LH, etal. Laryngeal cancer in the United States: changes in demograph­ics, patterns of care, and survival. Laryngoscope. 2006;116:1–13.
120. Singh R, Karantanis W, Fadhil M, et al. Meta­analysis on the rate of pharyngocutaneous stula in early oral feeding in laryngectomy patients. Am J Otolaryngol. 2021;42:102748.
121. Guidera AK, Kelly BN, Rigby P, MacKinnon CA, Tan ST.Early oral intake after reconstruction with a free ap for cancer of the oral cavity. Br J Oral Maxillofac Surg. 2013;51:224–7.
122. McAuley D, Barry T, McConnell K, Smith J, Stenhouse J. Early feeding after free ap recon­struction for oral cancer. Br J Oral Maxillofac Surg. 2015;53:618–20.
123. Brady G, Leigh-Doyle L, Riva F, Kerawala C, Roe J.Early post-operative feeding: an investigation of early functional outcomes for oral cancer patients treated with surgical resection and free ap recon­struction. Dysphagia. 2021;37:1008.
124. Kerawala CJ, Riva F, Paleri V.The impact of early oral feeding following head and neck free ap recon­struction on complications and length of stay. Oral Oncol. 2021;113:105094.
Pain Management
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
JoshuaIsaacReece, HeatherA.Edwards, andNicoleZ.Spence
13
Introduction
Head and neck cancers (HNCs) are a signicant public health problem, with over 350,000 new cases diagnosed yearly and 150,000 deaths annu­ally worldwide [1]. The disease process and mor­bidities of treatment have a profound effect on the quality of life. In addition to cosmetic changes and functional challenges, patients frequently suffer from acute and chronic pain. This chapter discusses pain management strategies for patients undergoing complex head and neck microvascu­lar reconstructive surgery.
Physicians strive to minimize psychological and physiologic stresses associated with surgery and pain. Furthermore, we seek to mitigate side effects and associated risks with opioid prescrip­tions. Adequate perioperative pain management is integral to patient care and outcomes. Each of the biological, psychological, and social dimen­sions of the pain experience should be considered and explored to provide optimal perioperative pain management [2]. Ensuring adequate analge-
J. I. Reece · N. Z. Spence (*) Department of Anesthesiology, Boston Medical Center, Boston University, Boston, MA, USA e-mail: Joshua.Reece@bmc.org;
Nicole.Spence@BMC.org
H. A. Edwards Department of Otolaryngology, Boston Medical Center, Boston University, Boston, MA, USA e-mail: Heather.Edwards@bmc.org
sia is crucial for patient comfort and enhances early ambulation, minimizes deconditioning, decreases length of stay, mitigates cardiac and pulmonary complications (i.e., reduces the risk of venous thromboembolism), improves recovery, reduces the likelihood of developing chronic pain, and reduces healthcare cost [3]. Providing adequate analgesia may be challenging as main­stay treatments like opioids have signicant side effects and addiction potential. The use of multi­modal analgesia has been studied in patients undergoing major head and neck surgeries and should be used as part of routine pain manage­ment. Multimodal techniques aim to reduce total opioid consumption and their associated side effects. Various pharmacologic and nonpharma­cologic options for analgesia are discussed in this chapter.
Factors Associated withPain
Pain is an unpleasant sensory and emotional experience associated with actual or potential tis­sue damage. The head and neck are richly inner­vated with many anatomical structures conned in a small space contributing to high sensitivity to pain [4]. Pain associated with head and neck reconstruction has characteristics of nociceptive and neuropathic pain types. Nociceptive pain is caused by tissue injury, whereas neuropathic pain
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Quimby et al. (eds.), Complex Head and Neck Microvascular Surgery,
https://doi.org/10.1007/978-3-031-38898-9_13
183
184
J. I. Reece et al.
is from nerve injury. Although seemingly similar, their descriptions and treatments may be unique.
Factors that correlate with the severity of post­operative pain include preoperative opioid use, increased body mass index, anxiety, depression, extensivity of surgery, and duration of surgical operation. Depression and anxiety are associated with increased perception of pain severity, whereas prolonged duration of acute pain leads to increased mood dysregulation [5]. In certain cases, consulting a psychiatrist preoperatively can aid in utilizing psychodynamic, behavioral, and pharmacologic modes of treatment [6]. Physicians should recognize that an individual’s perception, expression, and reaction to pain are inuenced by genetic, developmental, familial, psychological, social, and cultural variables. Each of these factors of the pain model can pro­foundly affect the experience of pain in each patient to varying degrees. Understanding these factors helps physicians individualize their approach to pain management within the frame­work of the biopsychosocial model. Physicians can identify and potentially intervene on these patient factors. With the help of case managers and social workers, clinical pathways can be developed to address sociocultural variables. Other independent factors that affect postopera­tive interpretation of pain include attention to pain and understanding, control, and expectation of pain. Data supports a correlation between higher cerebral function and perception of pain [7]. As personalized medicine grows, we may be able to offer patients more effective medications based on their underlying genetic factors.
Pain management considerations for patients undergoing head and neck free ap surgeries begin before the operation occurs. Physicians should set reasonable expectations for the degree of pain patients generally experience after free ap surgery. The initial postoperative period is the most painful, and pain normally reduces in subsequent days to weeks. Extended resection, ap coverage, nerve lesions, inammation, and high-dose opioid administration can lead to hyperalgesia and, at worst, chronic postoperative pain [8]. Causes of inadequate postoperative analgesia include lack of reasonable pain expec-
tations, complications, medication tolerance and side effects, and poor pain assessment [9]. Counseling should focus on minimizing opioid use, including instructions on how to safely taper off. The tapering process can take days to weeks or months, depending on the patient and his/her opioid use patterns. Follow-ups should be sched­uled to screen for opioid dependence, guide tapering, and assess for persistent pain. Clinical pathways developed at the departmental or insti­tutional level provide patients and physicians with appropriate preoperative planning and coun­seling centered around what to expect on the day of surgery and the postoperative course thereafter.
Opioids
Most opioids are synthetic derivatives of mor­phine, which was rst isolated from poppy plants in 1804 and is still used. Opioids play a vital role in analgesia as they are considered the treatment of choice for moderate-to-severe pain and recom­mended for patients who are unresponsive to other types of analgesic medications [10, 11]. Opioids vary based on their receptor afnity and agonist qualities. Opioids are classied as pure agonists, agonists-antagonists, or partial ago­nists. For acute postoperative analgesia, pure opi­oid agonists are most frequently chosen, whereas partial agonists and antagonists are utilized in the treatment of chronic pain and/or substance use disorders. Opioids are chosen and dosed based on their pharmacokinetics and pharmacodynamics within the context of each patient’s history. Opioid use is associated with side effects, includ­ing postoperative nausea and vomiting, constipa­tion, sedation, hypotension, and respiratory depression. These side effects, if present, create barriers to patients’ postoperative recovery.
Chronic opioid use is a global health problem, and surgery is often the point of initial exposure for many chronic opioid users [12]. A retrospec­tive study showed a considerable prevalence of chronic postoperative opioid use in patients who have undergone major resection with free ap reconstruction for head and neck cancers, with
13 Pain Management
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
185
52% of opioid-naïve patients continuing to use opioids at 3months and 41% at 12months post­operatively. In chronic opioid users, 82% contin­ued opioid use at 3months and 77% at 12months postoperatively [13]. Preoperative opioid use, prior tobacco use, and advanced pathologic T-stage were identiable risk factors for chronic opioid use in patients undergoing free ap recon­structive surgeries. Patient age may also factor into pain experience. One study showed that con­tinued opioid use was common in younger patients (under 60 years of age), whereas older patients had fewer opioid rells [14]. Growing evidence supports an association between opioid use in the acute postoperative period and subse­quent development of chronic opioid use [12,
1517]. State prescription monitoring programs
can be used to verify medication history to screen for patients at risk for potential use disorder.
Opioids can be rotated or converted based on their equianalgesic dose (Table 13.1); however, the side effect proles are the same at equianal­gesic doses. If patients are on opioids for a long term, they are at risk for withdrawal if abruptly discontinued. Withdrawal, while unpleasant, is not life-threatening. For patients who suffer from chronic pain or use opioids at baseline as outpatients, physicians should attempt to miti­gate these patients’ baseline pain. Perioperatively, patients should continue their basal analgesic medications. Some physicians may attempt to decrease baseline opioid use or encourage involvement in therapy or behavioral modica­tions to decrease patients’ pain prior to surgery. For patients on chronic opioid maintenance ther­apy (i.e., buprenorphine or methadone), physi­cians may consider consulting addiction
Table 13.1 Equianalgesic opioid dosages. When con­verting between opioids, the physician must decrease the dose offered (by 25–50%) to account for cross-tolerance or differences in opioid binding afnities. Failing to account for cross-tolerance puts a patient at risk of adverse events, such as respiratory depression. mg=milligram
Intravenous Oral Morphine 10mg 30mg Oxycodone 20mg Hydromorphone 1.5mg 7.5mg Fentanyl 0.15mg
specialists to participate in a multidisciplinary care team to assist with any necessary dose adjustments. Maintenance medications should be continued perioperatively, including buprenorphine- naloxone and methadone. Other medications, such as naltrexone, should be held. The timing and perioperative planning must be coordinated with an anesthesiologist or periop­erative physician in advance of surgery [18]. Patients with concomitant psychological pathol­ogies, including poorly controlled major depres­sive disorder, may meet indications to consult psychiatry to reduce postoperative complica­tions like worsening of preexisting psychiatric disorders. Multidisciplinary hospital pathways may be created to decrease a patient’s preopera­tive opioid use by 10–30% prior to their surgical admission, if able.
If complex HNC patients must be NPO post­operatively or must use a gastric tube, analgesic medication administration should be altered. If patients who are on chronic or long-acting oral opioid therapies are limited to using a gastric tube or parenteral administration postoperatively, their long-acting medications need to be con­verted into a regimen that would provide appro­priate, equianalgesic basal analgesia either enterally, intravenously, or transdermally. Long­acting opioids, such as MS Contin® or OxyContin®, cannot be crushed for administra­tion into a gastric tube. Consider consultation with the acute pain service or pharmacists for guidance. Parenteral opioids can be used postop­eratively, although currently there are no long­acting parenteral formulations available for use. However, when patients are able to tolerate an oral regimen, parenteral opioids should be con­verted to an oral (or per gastric tube) regimen as swiftly as possible as oral medications provide longer lasting analgesia.
Providing patients with patient-controlled analgesia (PCA) is safer than ordering nurse­administered intravenous opioid boluses. A PCA regimen consists of an infusion pump delivering a programmed dose of medication in response to the patient pushing a demand button. There are inherent safety facets when using a PCA, includ­ing that only the patient is to push the demand
186
J. I. Reece et al.
Table 13.2
are limited to pediatric patients or complex opioid-tolerant patients. If considering starting a continuous infusion, it is prudent to seek expertise from pain service physicians. mg=milligram; mcg=microgram
Demand dose 1mg 0.2mg 10mcg Lockout Every 6 or 10min Every 6 or 10min Every 6min Continuous infusion 0 0 0 1h limit 10mg or 6mg 2mg or 1.2mg 100mcg
button, and if the patient becomes sleepy, he/she will not be able to activate his/her demand. Consequently, PCAs decrease the risk of inadver­tent overdose. Furthermore, providing patients with an independent way to administer analge­sics as needed can be helpful for patients’ sense of control, eliminating administrative delays, and better approximating patients’ variable analgesic needs. Common PCA settings are listed in Table13.2. PCAs can help physicians understand a patient’s opioid consumption over 24h, and this data can help guide appropriate as-needed (PRN) opioid dosing. Some patients, however, such as those who are confused or delirious, may not be able to use a PCA effectively, and alternatives should be implemented.
Standard intravenous PCA starting settings for opioid-naïve patients [19]. Generally, continuous infusions
Morphine Hydromorphone Fentanyl
which is propagated by ascending sensory neu­rons. Local anesthetics target these rst-order sensory neurons. The synthesis of local inam­matory mediators, such as prostaglandins, can be inhibited by cyclooxygenase (COX) inhibitors. The initial sensory transmission from rst-order afferent nociceptive bers synapses in the dorsal horn of the central nervous system (CNS) using neurotransmitters, including substance P, prosta­glandins, adenosine, and glutamate. From the dorsal horn, the second-order neurons of the spi­nothalamic tract decussate and ascend the spinal cord to reach the thalamus. The trigeminotha­lamic tract supplies the head and face. Signals reaching the thalamus are processed by the ven­tral posterior nucleus (VPN) and transmitted to the cerebral cortex via the posterior limb of the internal capsule. This ascending pathway initi-
Multimodal Analgesia
ates conscious realization of pain. At the cerebral cortical level, pain is a subjective experience that
Multimodal analgesia is designed to reduce or eliminate opioid use [20]. Rather than relying solely on opioids, other analgesic modalities should be offered if and when appropriate. The mechanisms and pathways of pain signaling play a role in pharmacologic targets. As part of opti­mal perioperative care in head and neck recon­structive surgeries, effective pain management is an important goal of the Enhanced Recovery After Surgery (ERAS) protocol and includes multimodal analgesia [21]. Multimodal analgesia is the concurrent use of more than one modality of pain control to achieve effective analgesia, with opioids reserved for severe refractory pain [20]. An understanding of the physiologic basis of pain allows physicians to appropriately choose pharmacologic agents to target pain.
Pain occurs when mechanical energy of nox-
ious stimuli is converted into electrical energy,
varies in perception. A concomitant descending efferent pain pathway, originating within the hypothalamus, modulates the sensation of pain. This endogenous “pain-inhibiting” system is the target of some analgesic therapies, including opi­oids. Stimulation of the periaqueductal gray within the midbrain activates enkephalin­releasing neurons that descend to the raphe nucleus in the brain stem. Serotonergic neurons from the raphe synapse with inhibitory interneu­rons within the substantia gelatinosa, resulting in the release of enkephalin and dynorphin. Descending noradrenergic bers from the locus coeruleus of the brain stem modulate ascending pain signals. This explains some of the physio­logic hyperadrenergic manifestations of pain such as hypertension and tachycardia. These manifestations may be detrimental in microvas­cular surgeries intraoperatively and postopera-
13 Pain Management
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
187
tively. Many of the analgesic agents target receptors of the ascending and/or descending pain pathway; thus, understanding the neuro­physiologic basis of pain transmission and per­ception can help physicians provide superior analgesia.
Multimodal analgesia is successful because it targets different pain signaling molecules or directly affects receptors involved in the pain pathway. It is best clinical practice to use a multi­modal approach to manage patients’ pain during their hospital course [22]. A multimodal approach can be implemented preoperatively, intraopera­tively, and postoperatively. Preoperatively treat­ing patients with analgesic medications to reduce postoperative pain is known as preemptive anal­gesia and has become part of multimodal pain pathways that have been applied to many types of surgeries, including head and neck cancer sur­gery [23]. Preoperatively, patients can be admin­istered oral or intravenous medications. Preemptive analgesia has been shown to delay time to the rst analgesic request and reduce total analgesic use [24]. Timing of administration has not been shown to make a signicant difference in effect, thus giving preemptive analgesics immediately before surgery is acceptable. The most frequently used preemptive analgesics are acetaminophen and gabapentin [22]. Multimodal analgesia reduces opioid use intraoperatively and in the postanesthesia care unit (PACU) when patients are administered preoperative oral cele­coxib, gabapentin, and/or tramadol [25]. A large systematic review study showed that gabapenti­noids were the most commonly used non-opioid (72.9%) followed by nonsteroidal anti­inammatory drugs (NSAIDs) (44.6%), acet­aminophen (44.3%), corticosteroids (25.1%), ketamine (7.2%), and nerve block (3.4%) [22]. The use of multimodal analgesia is associated with signicant reductions in opioid use and con­comitantly decreases opioid-related adverse events (ORAEs) [26]. Patients who receive mul­timodal analgesia have lower pain scores in the postoperative period (POD 0–6) compared to opioid-only counterparts [20]. Of the multimodal analgesic regimens studied, none have demon­strated increased incidence of postoperative
hematomas or ap failure, even with the use of NSAIDs [27]. Topical applications, such as topi­cal capsaicin, lidocaine, or diclofenac, may be benecial for patients. These medications are well tolerated but should be limited in certain patient populations.
Lidocaine and ketamine infusions are viable options but depend on the expertise of intraopera­tive anesthesiologists or postoperative acute pain specialists and require investment from hospital systems to ensure safe and effective applications [8]. A multidisciplinary, dynamic approach to pain management for patients undergoing free ap surgery must be tailored to each patient. When possible, multimodal analgesic approaches should be implemented to decrease the risk of opioid dependence and ORAEs, provide better perioperative analgesia, and enhance recovery after surgery.
Acetaminophen
Most multimodal analgesic approaches include the use of acetaminophen. Acetaminophen, also known as paracetamol, was rst synthesized in 1877 and is widely used over the counter as an antipyretic and analgesic. Acetaminophen is inexpensive and has minimal side effects when used in appropriate doses. Acetaminophen has two mechanisms of analgesic action. First, pros­taglandin synthesis is inhibited through cycloox­ygenase- 1 (COX-1) and, mainly, COX-2. Second, the active paracetamol metabolite is formed in the CNS and acts as a weak agonist of cannabi­noid receptors CB1 and CB2 [28]. In addition to its role in preemptive analgesia, acetaminophen has been proven to provide effective analgesia in the postoperative phase of care [29]. Onset of action of oral acetaminophen can take up to 1h, whereas intravenous acetaminophen provides analgesic effect within 5–10min and peak anal­gesia within 1h. Studies have demonstrated that intravenous acetaminophen may play a role in reducing the total narcotic requirement in the rst 8h after surgical resection of head and neck can­cer surgery and contributes to alleviation of post­operative pain, decreased length of stay, and
188
J. I. Reece et al.
potentially decreased cost to the patient and hos­pital overall [30]. Current recommendations sug­gest a maximum of 3–4g administered in a 24-h period. In patients with hepatic dysfunction, a maximum of 2g should be administered in a 24-h period. Acetaminophen is known to be hepato­toxic; thus, caution should be used in patients with liver pathology. Otherwise, acetaminophen is well tolerated with minimal side effects and low addictive potential, making it essential to the multimodal analgesic approach.
Nonsteroidal Anti-inammatory Drugs (NSAIDs)
An important component of multimodal analge­sia is NSAIDs. Medications such as celecoxib, ibuprofen, and naproxen are within this class of drugs, most of which are widely used and easily accessible over the counter. Most conventional NSAIDs are nonselective competitive inhibitors of COX-1 and COX-2 and work by inhibiting the conversion of arachidonic acid to prostaglandins and thromboxane. Prostaglandins play a role in initiating the inammatory response, local vaso­dilation, and sensitization to pain and hyperalge­sia. Thromboxane induces vasoconstriction and platelet aggregation. Although celecoxib, unlike COX-1 inhibitors, has been shown to have mini­mal inhibitory effects on platelet aggregation, there have been case reports of associated surgi­cal bleeding [21]. While these medications are generally well tolerated, their manufacturers report considerable risk including gastric ulcer­ation/bleeding, renal failure, and increased risk of serious (and potentially fatal) adverse cardio­vascular thrombotic events, including myocardial infarction and stroke. Risk may occur early dur­ing treatment and may increase with duration of use. The use of NSAIDs should be avoided in patients with creatinine clearance (CrCl) less than 30 and/or on hemodialysis as NSAIDs may increase the risk of acute kidney injury and renal failure. It is recommended to use the lowest effective dose for the shortest duration of time, consistent with individual patient goals, to reduce the risk of adverse effects. Selective COX-2
inhibitors (i.e., celecoxib) were thought to be associated with increased risk of thrombosis by promoting an imbalance of prostacyclin and thromboxane; however, studies have demon­strated that the use of celecoxib does not have deleterious effects on free tissue transfer survival or healing [31]. The American Head and Neck Society showed that the use of celecoxib after head and neck free ap reconstructive surgery provides effective analgesia and reduces oral, intravenous, and total opioid consumption peri­operatively without increasing surgical ap­related complications [32]. NSAIDs are an effective adjuvant and should be considered as part of a multimodal analgesic regimen.
Gabapentinoids
Recent studies have shown that gabapentinoids do not have clinically signicant analgesic effects. Their use is not routinely recommended in the perioperative setting by the American Society of Anesthesiologists [33]. Despite these recommendations, some clinical pathways include gabapentin as part of their multimodal analgesic pathway. Though gabapentin is not routinely used for the management of postopera­tive pain, evidence supports use of gabapentin to improve pain control and signicantly decrease opioid use in the acute postoperative setting in head and neck free ap surgery [26]. In recon­struction surgeries involving the tongue, studies have shown that administration of a single preop­erative dose of gabapentin improves analgesia while decreasing opioid requirements (measured in morphine equivalents), sedation scales, and antiemetic usage without additional side effects or surgical complications [34].
Gabapentin, which acts on voltage-gated cal­cium channels, was initially marketed as an anti­convulsant and is currently used for neuropathic pain. Contrary to its name, it has no GABAergic action. Gabapentinoids exert their mechanism of action by reducing the activation of excitatory calcium channels and decreasing neuronal sig­naling within the pain signaling pathway. Gabapentinoids have the potential to be misused,