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Chapter29:Palliative care and symptom management
Table 29.15 Commonly used antidepressants
Class Common dosing Comments
Tricyclic (and related) Cardiac conduction delays and anticholinergic
Amitriptyline 25–150 mg at night
10 mg is starting dose in elderly
Nortryptiline 25–150 mg at night
10 mg is starting dose in elderly
Desipramine 25–200 mg a day. May divide bid. 10 mg is
starting dose in elderly
Selective serotonin reuptake inhibitors
Paroxetine 20–50 mg daily
10 mg is starting dose in elderly
Fluoxetine 20–60 mg each morning Activating. Long half-life
Sertraline 25–200 mg daily
Citalopram 20–60 mg daily
Escitalopram 10–20 mg daily
Start with 5 mg in elderly
Selective serotonin and norepinephrine
reuptake inhibitors
Buproprion 100 mg bid to150 mg tid Available in sustained-release form
Venlafaxine 37.5–75 mg bid to tid Available in sustained-release form
Mirtazapine 15–45 mg qhs Associated with sedation and weight gain
Duloxetine 20–60 mg daily or bid Effective for neuropathic pain
Psychostimulants
Methylphenidate Start 2.5–5 mg in morning and at noon Available in sustained-release form. Unclear what
Dextroamphetamine Start 2.5–5 mg in morning
side effects often limit their use. Sedating. Some
efficacy for neuropathic pain. Start with low
doses and increase slowly, particularly in elderly
May have particular benefit in anxiety disorders
May have particular benefit in anxiety disorders
and neuropathic pain
the maximum effective dose is in depression
in patients with concomitant neuropathic or chronic pain.
Mirtazapine can cause weight gain, improve nausea, promote
sleep, and has relatively fewer drug interactions than other
antidepressants; thereby it may be of particular use in cancer
patients.
160
Psychostimulants such as methylphenidate and dextroamphetamine may be useful in patients with prominent symptoms
of psychomotor retardation.
161
ey usually begin alleviating
depressive symptoms within 2days and so can be particularly
helpful in patients with short life expectancies.
144
they are dosed twice daily, in the early morning and again at
noon, to avoid nocturnal insomnia. Dose adjustments can be
made every 2–3days.
Anxiety
Anxiety occurs commonly in cancer patients; estimates of
prevalence are between 30% and 50%.
portion of cancer patients, perhaps around 10%, will have a
primary anxiety disorder (panic disorder, phobias, or generalized anxiety disorder).
142
Temporary anxiety around specic
events (e.g., awaiting test results, before clinic visits or procedures) is common and not pathologic. However, when anxiety
becomes pervasive, or limits a patient’s ability to participate in
daily activities or necessary medical care, it should be treated.
162,163,164
An unclear pro-
158,159
Generally
Anxiety may be secondary to a variety of conditions, including drug eects (especially glucocorticoids and antidopaminergic agents), drug or alcohol withdrawal, uncontrolled pain or
dyspnea, and depression.
Anxiety responds well to cognitive or psychotherapeutic
interventions,
153
and prompt referral for more challenging
situations is important. Complementary interventions such
as aromatherapy, massage, progressive muscle relaxation, and
guided imagery therapy can be helpful.
165,166
Pharmacologic
treatment of anxiety is used for temporary, incidental anxiety and for chronic, pervasive symptoms. Incidental anxiety– such as before a procedure– best responds to cognitive
interventions; however, pretreatment with short-acting benzodiazepines is the pharmacologic mainstay. Longer-term
treatment of anxiety is more complicated and best performed
in conjunction with a patient’s primary provider or a mental
health professional. Scheduled, low-dose long-acting benzodiazepines (such as clonazepam or sustained-release alprazolam)
are eective but run the risk of excessive sedation, tolerance,
and abuse. Buspirone is a non-benzodiazepine anxiolytic that
has minimal abuse potential but, like SSRIs, takes several
weeks to be eective.
anxiety disorder as well.
167
SSRIs may be eective for generalized
168
SSRI dosing is similar for anxiety as
for depression.
309
Section X:Specialized interventional techniques in cancercare
Coordinating care in patients with
advancedcancer
Patients with advanced cancer and multiple cancer-related
symptoms require coordinated multidisciplinary management
to optimize care. As one of the many specialists who will be
involved in the care of these patients, interventional oncologists have an opportunity and responsibility to help coordinate
care. Many dierent practice models exist and the specialists
involved will vary from patient to patient. In some patients,
such as those with end-stage hepatocellular carcinoma, the
interventional oncologist may be the patient’s primary physician coordinating care. In others, the palliative care physician, medical oncologist, surgical oncologist, or hepatologist
may be coordinating care, with the interventional oncologist
in a consultant role. Whatever the role assumed in a particular
patient, communication amongst the managing physicians is
critical.
Summary
As stated earlier, palliative care is focused on symptom relief
and maximizing patient function, without necessarily impacting the natural history of the underlying disease. As the eld
of interventional oncology matures, interventional radiologists
caring for patients with advanced cancer will need to be comfortable with the management of common clinical problems
encountered in this patient population. ey will need to feel
comfortable with communicating prognosis and other critical
information to patients and their families. Working in concert with colleagues in other clinical cancer specialties, interventional oncologists will be able to oer therapeutic options
which will maximize quantity and quality of life and help to
optimally manage the many common symptoms in this challenging and rewarding patient population.
References
1. World Health Organization. WHO denition of palliative care.
Available at:www.who.int/cancer/palliative/denition/en.
Accessed April 1,2006.
2. Mosenthal AC, Murphy PA. Trauma care and palliative
care:time to integrate the two? J Am Coll Surg. 2003;
197:509–516.
3. Curtis JR, Rubenfeld GD. Improving palliative care for patients
in the intensive care unit. J Palliat Med. 2005; 8:840–854.
4. von Gunten, CF. Secondary and tertiary palliative care in US
hospitals. JAMA. 2002; 287:875–888.
5. Himelstein BP, Hilden JM, Boldt AM, Weissman DE. Pediatric
palliative care. NEJM. 2004; 350:1752–1762.
6. www.capc.org/capc-growth-analysis-snapshot-2011.pdf.
Accessed 18 Sept2014.
7. Temel JS, Greer JA, Muzikansky A, etal. Early palliative care
for patients with metastatic non-small-cell lung cancer. N Engl J
Med. 2010; 363(8):733–742
8. Casarett D, Pickard A, Bailey FA, etal. Do palliative
consultations improve patient outcomes? J Am Geriatr Soc.
2008; 56(4):593–599.
9. Norton SA, Hogan LA, Holloway RG, et al. Proactive palliative
care in the medical intensive care unit:eects on length of stay
for selected high-risk patients. Critical Care Medicine. 2007;
35:1530–1535
10. Bendaly EA, Groves J, Juliar B, Gramelspacher GP. Financial
impact of palliative care consultation in a public hospital. J
Palliat Med 2008; 11(10):1304–1408.
11. Morrison RS, Penrod JD, Cassel JB, etal. Palliative Care
Leadership Centers' Outcomes Group. Cost savings associated
with US hospital palliative care consultation programs. Arch
Intern Med. 2008; 168(16):1783–1790.
12. Ranganathan A, Dougherty M, Waite D, Casarett D. Can
palliative home care reduce 30-day readmissions? results of
a propensity score matched cohort study. J Palliat Med. 2013;
16(10):1290–1293
13. Brumley R, Enguidanos S, Jamison P, et al. Increased
satisfaction with care and lower costs:results of a
randomized trial of in-home palliative care. J Am Geriatr Soc.
2007; 55:993–1000.
14. Morrison RS, Meier D. Palliative care. NEJM. 2004;
350:2582–2590.
15. Weeks JC, Catalano PJ, Cronin A, etal. Patients’ expectations
about eects of chemotherapy for advanced cancer. N Engl J
Med. 2012; 367(17):1616–1625.
16. Schag CC, Heinrich RL, Ganz PA. Karnofsky performance
status revisited:reliability, validity, and guidelines. J Clin Oncol.
1984; 2:187–193.
17. Vigano A, Dorgan M, Jeanette B, Bruera E, Suarez-Almazor
ME. Survival prediction interminal cancer patients:a systematic
review of the medical literature. Palliat Med. 2000; 14: 363–374.
18. den Daas N. Estimating length of survival in end-stage
cancer:a review of the literature. J Pain Symptom Manage. 1995;
10:548–555.
19. Lamont EB, Christakis NA. Complexities in prognostication in
advancer cancer. “To help them live their lives the way they want
to.” JAMA. 2003; 290:98–104.
20. Maltoni M, Pirovano M, Scarpi E, etal. Prediction of survival
of patients terminally ill with cancer. Results of an Italian
prospective multicentric study. Cancer. 1995; 75:2613–2622.
21. Reuben DB, Mor V, Hiris J. Clinical symptoms and length of
survival in patients with terminal cancer. Arch Int Med. 1988;
148:1586–1591.
22. Janisch L, Mick R, Schilsky RL, etal. Prognostic factors for
survival in patients treated in phase Iclinical trials. Cancer.
1994; 74:1965–1973.
23. Maltoni M, Caraceni A, Brunelli C, etal. Prognostic factors
in advanced cancer patients:evidence-based clinical
recommendations– a study for the steering committee of the
European Association for Palliative Care. J Clin Oncol. 2005;
23:6240–6248.
24. Ralson SH, Gallacher SJ, Patel U, Campbell J, Boyle IT.
Cancer-associated hypercalcemia:morbidity and mortality.
Clinical experience in 126 treated patients. Ann Intern Med.
1990; 112:499–504.
25. Iwase M, Kurachi Y, Kakuta S, et al. Clin Oral Investig. 2001;
5:194–198.
26. Siddiqui F, Weissman DE. Fast facts and concepts #151;
Hypercalcemia of malignancy. February 2006. End-of-Life
Physician Education Resource Center. www.eperc.mcw.edu.
310
Chapter29:Palliative care and symptom management
27. Khuntia D, Brown P, Li J, Mehta MP. Whole-brian radiotherapy
in the management of brain metastasis. J Clin Onc. 2006;
24:1295–1304.
28. McMillan DC. e systemic inammation-based glasgow
prognostic score:adecade of experience in patients with cancer.
Cancer Treat Rev. 2013; 39(5):534–540.
29. Gripp S, Moeller S, Bolke E, etal. Survival prediction in
terminally ill cancer patients by clinical estimates, laboratory
tests, and self-rated anxiety and depression. J Clin Oncol. 2007;
25(22):3313–3320.
30. Christakis NA, Lamont EB. Extent and determinants of error
in physicians’ prognoses in terminally ill patients:prospective
cohort study. West J Med. 2000; 172(5):310–313.
31. Glare P, Virik K, Jones M, etal. A systematic review of
physicians’ survival predictions in terminally ill cancer patients.
BMJ. 2003; 327:195–201.
32. Christakis NA, Lamont EB. Extent and determinants of error in
doctors’ prognoses in terminally ill patients:prospective cohort
study. BMJ. 2000; 320:469–473.
33. Lamont EB, Christakis NA. Prognostic disclosure to
patients with cancer near the end of life. Ann Int Med. 2001;
134:1096–1105.
34. Hagerty RG, Butow PN, Ellis PM, Dimitry S, Tattersall MH.
Communicating prognosis in cancer care:a systematic review of
the literature. Ann Oncol. 2005; 16:1005–1053.
35. Randall TC, Wearn AM. Receiving bad news:patients with
haematological cancer reect upon their experience. Palliat
Med. 2005; 19:594–601.
36. Weissman DE. Fast facts and concepts #13; Determining
prognosis in advanced cancer. 2nd Edition, July 2005. End-ofLife Palliative Education Resource Center. www.eperc.mcw.edu.
37. Ambuel B, Weissman DE. Fast facts and concepts #6; Delivering
bad news:part1. 2nd Edition, July 2005. End-of-Life Palliative
Education Resource Center. www.eperc.mcw.edu.
38. Ambuel B, Weissman DE. Fast facts and concepts #11;
Delivering bad news; part2. 2nd Edition, September 2005.
End-of-Life Palliative Education Resource Center. www.eperc.
mc w.edu.
39. Weissman DE. Decision making at a time of crisis near the end
of life. JAMA. 2004; 292:1738–1743.
40. Lussier D, Huskey AF, Portenoy RK. Adjuvant analgesics in
cancer pain management. e Oncol. 2004; 9:571–591.
41. Mercadante S, Portenoy RK. Opioid poorly-responsive cancer
pain. Part1:clinical considerations. J Pain Symptom Manage.
2001; 21:144–150.
42. omas JR, von Gunten CF. Pain in terminally ill patients.
Guidelines for pharmacological management. CNS Drugs. 2003;
17:621–631.
43. Cherny NI. Cancer pain:principles of assessment and
syndromes. In:Berger AM, Portenoy RK, Weissman DE,
eds. Principles and Practice of Palliative Care and Supportive
Oncology, 2nd edition. NewYork, NY:Lippincott Williams and
Wilkins; 2002:3–52.
44. Menefee LA, Monti DA. Nonpharmacologic and
complementary approaches to cancer pain management. J Am
Osteopath Assoc. 2005; 105:S15–20.
45. Hillard RE. Music therapy in hospice and palliative care:a
review of the empirical data. eCAM. 2005; 2:173–178.
46. Mercadante S, Casuccio A, Agnello A, Pumo S, etal. Analgesic
eects of nonsteroidal anti-inammatory drugs in cancer pain
due to somatic or visceral mechanisms. J Pain Symptom Manage.
1999; 17:351–356.
47. Mercadante S, Fulfaro F, Casuccio A. A randomized controlled
study on the use of anti-inammatory drugs in patients with
cancer pain on morphine therapy:eects on dose-escalation
and a pharmacoeconomic analysis. Eu J Cancer. 2002;
38:1358–1363.
48. Davis MP, Walsh D, Lagman R, LeGrand SB. Controversies in
pharmacotherapy of pain management. Lancet Oncol. 2005;
6:696–704.
49. Leppert W, Luczak J. e role of tramadol in cancer pain
treatment– a review. Supp Care Cancer. 2005; 13:5–17
50. Hanks GW, de Conno F, Cherny N, etal. Morphine and
alternative opioids in cancer pain:the EAPC recommendations.
Br J Cancer. 2001; 84:587–593
51. Gutstein, HB, Akil H. Opioid analgesics. In:Hardman JG,
Limbird LE, eds. Goodman and Gilman's:the Pharmacological
Basis of erapeutics, 10th Ed. NewYork, NY:McGraw-Hill;
2001:569–619.
52. Weissman DE. Fast facts and concepts #71:Meperidine for
pain:What’s all the fuss? June 2002. End-of-Life Physician
Education Resource Center. www.eperc.mcw.edu.
53. Arano GM, Brennan MJ, Douglas PD, Ginsberg B.
Evidence-based oral transmucosal fentanyl citrate (OTFC)
dosing guidelines. Pain Med. 2005; 6:305–314.
54. Bruera E, Sweeney C. Methadone use in cancer patients with
pain:a review. J Palliative Med. 2002; 5:127–138.
55. Gordon DB, Weissman DE. Fast facts and concepts #70:PRN
range analgesic orders. June 2002. End-of-Life Physician
Education Resource Center. www.eperc.mcw.edu.
56. Quigley C. e role of opioids in cancer pain. BMJ. 2005;
331:825–829.
57. Dean M. Opioids in renal failure and dialysis patients. J Pain
Symptom Manage. 2004; 28:497–504.
58. Paice JA, Toy C, Shott S. Barriers to cancer pain relief:fear
of tolerance and addiction. J Pain Symptom Manage. 1998;
16:1–9.
59. Sloan P, Melzack R. Long-term patterns of morphine dose and
pain intensity among cancer patients. Hosp J. 1999; 14:35–47.
60. Collin E, Poulain P, Gauvain-Piquard A, etal. Is disease
progression the major factor in morphine ‘tolerance’ in cancer
pain treatment? Pain. 1993; 55:319–326.
61. National Cancer Institute. Substance Abuse Issues In Cancer
(PDQ). Available at:www.cancer.gov/cancertopics/pdq/
supportivecare/substanceabuse/healthprofessional. Accessed
April 1,2006.
62. Passik SD, Kirsh KL, Caspar D. Addiction-related assessment
tools and pain management:instruments for screening,
treatment planning, and monitoring compliance. Pain Med
2008; 9:S145–166
63. Chou R, Fanciullo GJ, Fine PG, Miaskowski C, Passik SD,
Portenoy RK. Opioids for chronic noncancer pain:prediction
and identication of aberrant drug-related behaviors:areview
of the evidence for an American Pain Society and American
Academy of Pain Medicine Clinical Practice Guideline. J Pain.
2009; 10(2):131–146
311
Section X:Specialized interventional techniques in cancercare
64. Claxton R, Arnold R. Screening for opioid misuse and abuse.
Fast Facts and Concepts. August 2011; 244. www.eperc.mcw.edu/
EPERC/FastFactsIndex/_244.htm
65. [Anonymous]. Management of chronic pain syndromes:issues
and interventions. Pain Med. 2005; 6:S1–S21.
66. Caraceni A, Zecca E, Bonezzi C, etal. Gabapentin for
neuropathic cancer pain:a randomized controlled trial from
the gabapentin cancer pain study group. J Clin Oncol. 2004;
22:2909–2917.
67. McDonald AA, Portenoy RK. How to use antidepressants and
anticonvulsants as adjuvant analgesics in the treatment of
neuropathic cancer pain. J Supp Oncol. 2006; 4:43–52.
68. Smith EM, Pang H, Cirrincione C, etal. Eect of duloxetine
on pain, function, and quality of life among patients with
chemotherapy-induced painful peripheral neuropathy:
arandomized clinical trial. JAMA. 2013; 309(13):1359–1367.
69. Hanks GW. e pharmacological treatment of bone pain.
Cancer Surv. 1988; 7:87–101.
70. Hamouda WE, Roshdy W, Teema M. Single versus conventional
fractionated radiotherapy in the palliation of painful bone
metastases. Gulf J Oncolog. 2007; 1(1):35–41.
71. Hayashi S, Tanaka H, Hoshi H. External beam radiotherapy
for painful bone metastases from hepatocellular
carcinoma:multiple fractions compared with an 8-gy single
fraction. Nagoya J Med Sci. 2014; 76(1–2):91–99.
72. Wu JS, Wong R, Johnston M, Bezjak A, Whelan T, Cancer Care
Ontario Practice Guidelines Initiative Supportive Care Group.
Meta-analysis of dose-fractionation radiotherapy trials for the
palliation of painful bone metastases. Int J Radiat Oncol Biol
Phys. 2003; 55(3):594–605.
73. Callstrom MR, Charboneau JW. Percutaneous ablation:safe,
eective treatment of bone tumors. Oncology (Williston Park).
2005; 19(11 Suppl 4):22–26.
74. Posteraro AF, Dupuy DE, Mayo-Smith WW. Radiofrequency
ablation of bony metastatic disease. Clin Radiol. 2004;
59(9):803–811.
75. Finlay IG, Mason MD, Shelley M. Radioisotopes for the
palliation of metastatic bone cancer:a systematic review. Lancet
Oncol. 2005; 6:392–400.
76. Posteraro AF, Dupuy DE, Mayo-Smith WW. Radiofrequency
ablation of bony metastatic disease. Clin Radiol. 2004; 59:803–811.
77. Hacein-Bey L, Baisden JL, Lemke DM, etal. Treating
osteoporotic and neoplastic vertebral compression fractures with
vertebroplasty and kyphoplasty. J Palliat Med. 2005; 8:931–938.
78. Elkersh MA, Simopoulos TT, Bajwa ZH. Fundamentals of
interventional pain medicine. e Neurol. 2005; 11:285–293.
79. Wong GY, Schroeder DR, Carns PE. Eect of neurolytic celiac
plexus block on pain relief, quality of life, and survival in
patients with unresectable pancreatic cancer. Arandomized
controlled trial. JAMA. 2004; 291:1092–1099.
80. Davis MP, Walsh D. Treatment of nausea and vomiting in
advanced cancer. Support Care Cancer. 2000; 8:444–452.
81. de Boer-Dennert M, de Wit R, Schmitz PI, etal. Patient
perceptions of the side-eects of chemotherapy:the inuence of
5HT3 antagonists. Br J Cancer. 1997; 76:1055–61.
82. Aapro M. 5-HT3-receptor antagonists in the management of
nausea and vomiting in cancer and cancer treatment. Oncology.
2005; 69:97–109.
83. Olver IN. Update on anti-emetics for chemotherapy-induced
emesis. Intern Med J. 2005; 35:478–481.
84. Hesketh PJ, Grunberg SM, Gralla RJ, etal. e oral
neurokinin-1 antagonist aprepitant for the prevention of
chemotherapy-induced nausea and vomiting:a multinational,
randomized, double-blind, placebo-controlled trial in patients
receiving high-dose cisplatin– the Aprepitant Protocol 052
Study Group. J Clin Oncol. 2003; 21:4077–4080.
85. Herrstedt J, Muss HB, Warr DG, etal. Ecacy and tolerability of
aprepitant for the prevention of chemotherapy-induced nausea
and emesis over multiple cycles of moderately emetogenic
chemotherapy. Cancer. 2005; 104:1548–1555.
86. Hocking CM, Kichenadasse G. Olanzapine for
chemotherapy-induced nausea and vomiting:asystematic
review. Support Care Cancer. 2014; 22(4):1143–1151
87. Chung F, Lane R, Spraggs C, etal. Ondansetron is more
eective than metoclopramide for the tratement of
opioid-induced emesis in post-surgical adult patients.
Ondansetron OIE Post-Surgical Study Group. Eur J
Anaesthesiol. 1999; 16:669–677.
88. Glare P, Pereira G, Kristjanson LJ, Stocker M, Tattersall M.
Systematic review of the ecacy of antiemetics in the treatment
of nausea in patients with far-advanced cancer. Supp Care
Cancer. 2004; 12:432–440.
89. Bruera E, Seifert L, Watanabe S, etal. Chronic nausea in
advancer cancer patients:a retrospective assessment of a
metoclopramide-based antiemetic regimen. J Pain Symptom
Manage. 1996; 11:147–153.
90. Mystakidou K, Befon S, Liossi C, Vlachos L. Comparison of
the ecacy and safety of tropisetron, metoclopramide, and
chlorpromazine in the treatment of emesis associated with far
advanced cancer. Cancer. 1998; 83:1214–1243.
91. Critchley P, Plach N, Grantham M, etal. Ecacy of haloperidol in
the treatment of nausea and vomiting in the palliative patient:a
systematic review. J Pain Symptom Manage. 2001; 22:631–634.
92. Passik SD, Lundbert J, Kirsh KL. A pilot exploration of the
antiemetic activity of olanzapine for the relief of nausea in
patients with advanced cancer and pain. J Pain Symptom
Manage. 2002; 23:526–532.
93. Passik SD, Kirsh KL, eobald DE, etal. A retrospective chart
review of the use of olanzapine for the prevention of delayed emesis
in cancer patients. J Pain Symptom Manage. 2003; 25:485–488.
94. Navari RM, Einhorn LH, Passik SD, etal. A phase II trial of
olanzapine for the prevention of chemotherapy-induced nausea
and vomiting:a Hoosier Oncology Group study. Supp Care
Cancer. 2005; 13:529–534.
95. Mizukami N, Yamauchi M, Koike K, etal. Olanzapine for the
prevention of chemotherapy-induced nausea and vomiting
in patients receiving highly or moderately emetogenic
chemotherapy:arandomized, double-blind, placebo-controlled
study. J Pain Symptom Manage. 2014; 47(3):542–550.
96. Basch E, Prestrud AA, Hesketh PJ, etal. Antiemetics:American
Society of Clinical Oncology clinical practice guideline update. J
Clin Oncol. 2011; 29(31):4189–4198.
97. Navari RM, Nagy CK, Gray SE. e use of olanzapine
versus metoclopramide for the treatment of breakthrough
chemotherapy-induced nausea and vomiting in patients
receiving highly emetogenic chemotherapy. Supp Care Cancer.
2013; 21(6):1655–1663.
312
Chapter29:Palliative care and symptom management
98. Tramer MR, Carroll D, Campbell FA, Reynolds DJ, Moore
RA, McQuay HJ. Cannabinoids for control of chemotherapy
induced nausea and vomiting:quantitative systematic review.
BMJ. 2001; 323:1–8.
99. Walsh D, Nelson KA, Mahmoud FA. Established and potential
therapeutic applications of cannabinoids in oncology. Supp
Care Cancer. 2003; 11:137–143.
100. www.ncsl.org/research/health/state-medical-marijuana-laws.
aspx. Accessed June 23, 2014.
101. Swi W, Gates P, Dillon P. Survey of Australians using cannabis
for medical purposes. Harm Reduct J. 2005; 2:18.
102. Walsh Z, Callaway R, Belle-Isle L, etal. Cannabis
for therapeutic purposes:patient characteristics,
access, and reasons for use. Int J Drug Policy. 2013;
24(6):511–516.
103. Bowles DW, O'Bryant CL, Camidge DR, Jimeno A. e
intersection between cannabis and cancer in the United States.
Crit Rev Oncol Hematol. 2012; 83(1):1–10.
104. Malik IA, Khan WA, Qazilbash M, Ata E, Butt A,
Khan MA. Clinical ecacy of lorazepam in prophylaxis
of anticipatory, acute, and delayed nausea and vomiting
induced by high doses of cisplatin. Aprospective
randomized trial. Am J Clin Oncol. 1995;
18:170–175.
105. Ezzo J, Vickers A, Richardson MA, etal. Acupuncture-point
stimulation for chemotherapy-induced nausea and vomiting. J
Clin Onc. 2005; 23:7188–7198.
106. Roscoe JA, Morrow GR, Hickok JT, etal. e ecacy of
acupressure and acustimulation wrist bands for the relief of
chemotherapy-induced nausea and vomiting. AUniversity
of Rochester Cancer Center Community Clinical Oncology
Program multicenter study. J Pain Symptom Manage. 2003;
26:731–742.
107. I, Bruera E. Constipation in advanced cancer patients. Supp
Care Cancer. 1998; 6:356–364.
108. Homsi J, Walsh D, Rivera N, etal. Symptom evaluation in
palliative medicine:patients report vs systematic assessment.
Supp Care Cancer. 2006; 14:444–453.
109. Fallon M, O’Neill B. ABC of palliative care:constipation and
diarrhoea. BMJ. 1997; 315:1293–1296.
110. Tamayo AC, Diaz-Zuluaga PA. Management of opioid-induced
bowel dysfunction in cancer patients. Supp Care Cancer. 2004;
12:613–618.
111. Allan L, Richarz U, Simpson K, Slappendel R. Transdermal
fentanyl versus sustained release oral morphine in
strong-opioid naïve patients with chronic low back pain. Spine.
2005; 30:2484–2490.
112. Meissner W, Schmidt U, Hartmann M, Kath R, Reinhart K.
Oral naloxone reverses opioid-associated constipation. Pain.
2000; 84:105–109.
113. Sykes NP. An investigation of the ability of oral naloxone to
correct opioid-related constipation in patients with advanced
cancer. Palliat Med. 1996; 10:135–44.
114. Clemens KE, Faust M, Jaspers B, Mikus G. Pharmacological
treatment of constipation in palliative care. Curr Opin Support
Palliat Care. 2013; 7(2):183–191.
115. omas J, Karver S, Cooney GA, etal. Methylnaltrexone for
opioid-induced constipation in advanced illness. N Engl J Med.
2008; 358(22):2332–2343.
116. Portenoy RK, omas J, Moehl Boatwright ML, etal.
Subcutaneous methylnaltrexone for the treatment of
opioid-induced constipation in patients with advanced
illness:adouble-blind, randomized, parallel group,
dose-ranging study. J Pain Symptom Manage. 2008;
35(5):458–468.
117. Yavuzsen T, Davis MP, Walsh D, LeGrand S, Lagman R.
Systematic review of the treatment of cancer–associated
anorexia and weight loss. J Clin Oncol. 2005; 23:8500–8511.
118. Body JJ. e syndrome of anorexia–cachexia. Curr Opin Oncol.
1999; 11:225–260.
119. MacDonald N. Is there evidence for earlier intervention in
cancer-associated weight loss? J Supp Oncol. 2003; 1:279–286.
120. Wilcock A. Anorexia:a taste of things to come? Palliat Med.
2006; 20:43–45.
121. Simons JP, Schols AM, Hoefnagels JM, Westerterp KR,
ten Velde GP, Wouters EF. Eects of medroxyprogesterone
acetate on food intake, body composition, and resting energy
expenditure in patients with advanced, nonhormone-sensitive
cancer:a randomized, placebo-controlled trial. Cancer. 1998;
82:553–560.
122. Desport JC, Gory-Delabaere G, Blanc-Vincent MP, etal.
Standards, options, and recommendations for the use of
appetite stimulants in oncology (2000). Br J Cancer. 2003;
89:S98–S100.
123. Sood A, Moynihan TJ. Cancer-related fatigue:an update. Curr
Oncol Rep. 2005; 7:277–282.
124. Raison CL, Miller AH. Depression in cancer:new
developments regarding diagnosis and treatment. Biol Psychiat.
2003; 54:283–294.
125. Hickok JT, Roscoe JA, Morrow GR, Mustian K, Okunie P,
Bole CW. Frequency, severity, clinical course, and correlates
of fatigue in 372 patients during 5 weeks of radiotherapy for
cancer. Cancer. 2005; 104:1772–1778.
126. Ahlberg K, Ekman T, Gaston-Johansson F, Mock V. Assessment
and management of cancer-related fatigue in adults. Lancet.
2003; 362:640–650.
127. Adamsen L. Midtgaard J, Andersen C, Quist M, Moeller
T, Roerth M. Transforming the nature of fatigue through
exercise:qualitative ndings from a multidimensional exercise
programme in cancer patients undergoing chemotherapy. Eur J
Cancer Care. 2004; 13:362–370.
128. Patrick D, Gagnon DD, Zagari MJ, etal. Assessing the
clinical signicance of health-related quality of life (HRQoL)
improvements in anaemic cancer patients receiving epoetin
alfa. Eur J Cancer 2003; 39:335–345.
129. Mock V. Evidence-based treatment for cancer-related fatigue.
J Natl Cancer Inst Monograph. 2004; 32:112–118.
130. Smith RE. Erythropoietic agents in the management of cancer
patients. Part1:Anemia, quality of life, and possible eects on
survival. J Supp Oncol. 2003; 1:249–258.
131. Munch TN, Zhang T, Wiley J, Palmer JL, Bruera E. e
association between anemia and fatigue in patients with
advanced cancer receiving palliative care. J Palliat Med. 2005;
8:1144–1149.
132. Monti M, Castellani L, Berlusconi A, Cunietti E. Use of
red blood cell transfusions in terminally ill cancer patients
admitted to a palliative care unit. J Pain Symptom Manage.
1996; 12:18–22.
313
Section X:Specialized interventional techniques in cancercare
133. Bruera E, Driver L, Barnes EA. Patient-controlled
methylphenidate for the management of fatigue in patients
with advancer cancer:a preliminary report. J Clin Oncol. 2003;
21:4439–4443.
134. Schwartz AL, Mori M, Gao R, Nail LM, King ME. Exercise
reduces daily fatigue in women with breast cancer receiving
chemotherapy. Med Sci Sports Exerc. 2001; 33:718–723.
135. Dimeo FC, Stieglitz RD, Novelli-Fischer U, Fetscher S, Keul
J. Eects of physicial activity on the fatigue and psychologic
status of cancer patients during chemotherapy. Cancer. 1999;
85:2273–2277.
136. Iop A, Manfredi AM, Bonura S. Fatigue in cancer patients
receiving chemotherapy:an analysis of published studies. Ann
Oncol. 2004; 15:712–720.
137. Covey AM. Management of malignant pleural eusions and
ascites. J Supp Oncol. 2005; 3:169–176.
138. Garrison RN, Kaelin LD, Galloway RH, Heuser LS. Malignant
ascites. Clinical and experimental observations. Ann Surg.
1986; 203:644–651.
139. Runyon BA, Hoefs JC, Morgan TR. Ascitic uid analysis in
malignancy-related ascites. Hepatol. 1988; 8:1104–1109.
140. Lee CW, Bociek G, Faught W. A survey of practice in
management of malignant ascites. J Pain Symptom Manage.
1998; 16:96–101.
141. Marrero J, Martinez FJ, Hyzy R. Advances in critical care
hepatology. Am J Respir Crit Care Med. 2003; 168:1421–1426.
142. Aass N, Fossa SD, Dahl AA, Moe TJ. Prevalence of anxiety and
depression in cancer patients seen at the Norwegian Radium
Hospital. Eur J Cancer. 1997; 33:1597–604.
143. Pirl WF. Evidence report on the occurrence, assessment, and
treatment of depression in cancer patients. J Natl Cancer Inst
Monograph. 2004; 32:32–39.
144. Stiefel F, Trill MD, Berney A, Olarte JM, Razavi D. Depression
in palliative care:a pragmatic report from the Expert Working
Group of the European Association for Palliative Care. Supp
Care Cancer. 2001; 9:477–488.
145. Ebmeier KP, Donaghey C, Steel JD. Recent developments and
current controversies in depression. Lancet. 2006; 367:153–167.
146. Goodwin JS, Zhang DD, Ostir GV. Eect of depression on
diagnosis, treatment, and survival of older women with breast
cancer. J Am Geri Soc. 2004; 52:106–111.
147. Hjerl K, Andersen EW, Keiding N, Mouridsen HT, Mortensen
PB, Jorgensen T. Depression as a prognostic factor for breast
cancer mortality. Psychosomat. 2003; 44:24–30.
148. Passik SD, Dugan W, McDonald MV, Rosenfeld B, eobald
DE, Edgerton S. Oncologists’ recognition of depression in their
patients with cancer. J Clin Oncol. 1998; 16:1594–1600.
149. Periyakoil VJ. Fast facts and concepts #43:Is it grief or
depression? August 2005. 2nd edition. End-of-Life Physician
Education Resource Center. www.eperc.mcw.edu
150. Chochinov HM, Wilson KG, Enns M, Lander S. “Are you
depressed?” Screening for depression in the terminally ill. Am J
Psychiat. 1997; 154:674–676.
151. Arnold RA. Fast fact and concept #146:Screening for
depression in palliative care. December 2005. End-of-Life
Physician Education Resource Center. www.eperc.mcw.edu.
152. Holland JC, Morrow GR, Schmale A, etal. A randomized
clinical trial of alprazolam versus progressive muscle relaxation
in cancer patients with anxiety and depressive symptoms. J Clin
Oncol. 1991; 9:1004–1011.
153. Sheard T, Maguire P. e eect of psychological interventions
on anxiety and depression in cancer patients:results of two
meta-analyses. Br J Cancer. 1999; 80:1770–1780.
154. ase ME, Greenhouse JB, Frank E, etal. Treatment
of major depression with psychotherapy or
psychotherapy–pharmacotherapy combinations. Arch Gen
Psychiatry. 1997; 54:1009–15.
155. Temel JS, Greer JA, Muzikansky A, etal. Early palliative care
for patients with metastatic non-small-cell lung cancer. N Engl J
Med. 2010; 363(8):733–742.
156. Clark DB, Andrus MR, Byrd DC. Drug interactions between
linezolid and selective serotonin reuptake inhibitors:case
report involving sertraline and review of the literature.
Pharmacother. 2006; 25:269–276.
157. Weinrieb RM, Auriacombe M, Lynch KG, Lewis JD. Selective
serotonin re-uptake inhibitors and the risk of bleeding. Expert
Opin Drug Safety. 2005; 4:337–344.
158. Kroenke K, Messina N, Benattia I, Graepel J, Musgnung J.
Vanlafaxine extended release in the short-term treatment
of depressed and anxious primary care patients with
multisomatoform disorder. J Clin Psychiat. 2006; 67:72–80.
159. Raskin J, Pritchett YL, Wang F, etal. A double-blind,
randomized multicenter trial comparing duloxetine with
placebo in the management of diabetic peripheral neuropathic
pain. Pain Med. 2005; 6:346–356.
160. eobald DE, Kirsh KL, Holtsclaw E, Donaghy K, Passik SD.
An open-label, crossover trial of mirtazapine (15 and 30 mg)
in cancer patients with pain and other distressing symptoms. J
Pain Symptom Manage. 2002; 23:442–447.
161. Pereira J, Bruera E. Depression with psychomotor
retardation:diagnostic challenges and the use of
psychostimulants. J Palliat Med. 2001; 4:15–21.
162. Burgess C, Cornelius V, Love S, Graham J, Richards M,
Ramierez A. Depression and anxiety in women with early breast
cancer:ve year observational cohort study. BMJ. 2005; 330:702.
163. Hipkins J, Whitworth M, Tarrier N, Jayson G. Social support,
anxiety and depression aer chemotherapy for ovarian
cancer:a prospective study. Br J Health Psychol. 2004;
9:569–581.
164. Fowler JM, Carpenter KM, Gupta P, Golden-Kreutz DM,
Andersen BL. e gynecologic oncology consult:symptom
presentation and concurrent symptoms of depression and
anxiety. Obstet Gynecol. 2004; 103:1211–1217.
165. Fellowes D, Barnes K, Wilkinson S. Aromatherapy and massage
for symptom relief in patients with cancer. Cochrane Database
of Systematic Reviews. (2):CD002287,2004.
166. Sloman R. Relaxation and imagery for anxiety and depression
control in community patients with advanced cancer. Cancer
Nurs. 2002; 25:432–435.
167. Bottomley A. Anxiety and the adult cancer patient. Eur J
Cancer Care. 1998; 7:217–224.
168. Goodman WK. Selecting pharmacotherapy for generalized
anxiety disorder. J Clin Psychiat. 2004; 65:S8–S13.
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Chapter
CT-guided neurolysis for cancer-related abdominal
and pelvicpain
30
Ashrafabet
Introduction
Cancer-related abdominal and pelvic pain is unfortunately
common.
pancreatic cancer suer from substantial pain.
ment of cancer-related pain is challenging, with systemic analgesic therapy being, in general, the rst-line treatment.
atic cancer, pain is not well controlled by such analgesics.
Compounding this challenge is the side-eect prole of
1,2,3,4,5,6
For instance, up to 70–80% of patients with
2,4,5,6
e treat-
7,8,9
Unfortunately, for up to one-third of patients with pancre-
opiates– including nausea, vomiting, constipation, and sedation– that can paradoxically degrade quality of life. Managing
cancer-related pain refractory to such analgesic therapy
requires additional strategies that demand a multidisciplinary
approach, including surgery, radiation oncology, pain medicine, and interventional radiology.
Image-guided neurolysis represents an important strategy
in battling cancer-related abdominal and pelvic pain.
7,10
Celiac
plexus neurolysis (CPN) is the most common type and can be
a very eective adjunctive therapy; it may have a lasting eect
in 70–90% of patients with pain related to abdominal malig-
1,11,12
nancy.
e keys to treatment success with image-guided
neurolysis are to: (1) review cross-sectional imaging, usually computed tomography (CT); (2)understand the relevant
anatomy; (3)inject sucient volume of neurolytic agent; and
(4)ensure adequate spread of neurolytic agent.
1
Although the terms have been used interchangeably, a
neurolysis procedure should be distinguished from a “block.”1
Neurolysis refers to permanent disruption of neural pathways
that mediate pain, usually with agents such as ethanol or phenol, whereas a block refers to temporary disruption with local
anesthetics or steroids.
1,13,14,15
Neurolytic eects, however, may
last no more than 3–6months due to neural regeneration and
tumor growth.
Ethanol at a 95–100% concentration is a commonly used
neurolytic agent.1 One disadvantage is transient pain experienced during instillation; lidocaine or bupivacaine may
be instilled rst or mixed with ethanol to reduce intraprocedural pain. Alternatively, phenol may be used as a neurolytic
agent. It has a local anesthetic eect and so intraprocedural
pain is less common. However, it is a less potent neurolytic
and is more viscous than ethanol, which limits mixing with
contrast material.
monly usedagent.
Various modalities for imaging guidance have been
described, including uoroscopy, CT, and endoscopic ultrasound. CPN may be performed using CT guidance or CT uoroscopy given the excellent delineation of anatomic structures
as well as spread of contrast agent aorded by CT at the time
of neurolysis.
7,8,9
Celiac plexus neurolysis
e celiac plexus is a complex network of neural bers and ganglia that mediate aerent as well as sympathetic and parasympathetic eerent information for the upper abdominal viscera.
It does not mediate nociceptive stimuli from the musculoskeletal system or abdominal wall.1 Hence, neurolysis of the celiac
plexus may be performed for cancer-related upper abdominal
1,11
pain.
Longer-lasting pain relief may be achieved when per-
forming the procedure earlier in the disease process.
Contraindications to CPN include uncorrectable coagulopathy and/or thrombocytopenia, and intra-abdominal infection
or sepsis. Bowel obstruction is also a contraindication, as neurolysis of the sympathetic eerents mediated by the plexus may
transiently impact bowel motility.
Anatomy
e celiac plexus is situated along the anterolateral surface
of the aorta extending from the origin of the celiac artery
to that of the superior mesenteric artery.
work is comprised of aerent bers from abdominal viscera
that carry nociceptive information, sympathetic eerent bers that travel via the greatest, greater, and lesser splanchnic
nerves from the T5–T12 sympathetic ganglia along the vertebral column to the celiac ganglia, as well as parasympathetic
eerent bers from the vagus nerve.
tion includes bowel extending from the distal esophagus to
transverse colon, pancreas, liver, biliary tract, kidneys, adrenal glands, proximal ureters, and mesentery.
relief and side eects of CPN– the latter including transient
orthostatic hypotension and diarrhea– can be understood by
knowledge of the types of neural information transmitted via
this network.
1,16,17,18
As such, ethanol is the more com-
1
1,2,19
1
1,11,16,17,20,21
1,11,18,22
Visceral innerva-
is net-
1,11,16,18,20,21,22
Pain
Interventional Oncology, Second Edition, ed. Jean-François H. Geschwind and Michael C.Soulen. Published by Cambridge University Press.
©Cambridge University Press2016
315
Section X:Specialized interventional techniques in cancercare
e celiac ganglia may be visualized on CT, and may
mimic a limb of an adrenal gland (Figure30.1).
4,25,26
e right and le ganglia are positioned anterolateral
to diaphragmatic crus.
1,17,27
Hence, neurolysis is performed
1,13,18,20,22,23,2
by instilling a neurolytic agent into the antecrural space
(Figure30.2), with spread extending between the celiac and
superior mesenteric artery origins. Alternatively, neurolytic
may be deposited into the retrocrural space (Figure30.2),
where the greatest, greater, and lesser splanchnic nerves
course between the sympathetic ganglia along the vertebral
column and the celiac ganglia.
1,11
Technique
Coagulation and platelet parameters are checked and corrected.
Patients receive intravenous hydration, as transient hypotension is a potential complication. Prior CT imaging is reviewed
to ascertain location of tumor, determine whether antecrural or retrocrural deposition of neurolytic is appropriate, and
determine overall needle approach and patient positioning.
A transcrural approach in which a needle is advanced
through the diaphragmatic crus into the antecrural space
(Figure30.3) is suitable in many patients who do not have gross
tumor inltration in the region of the celiac plexus. Otherwise,
a retrocrural technique (Figure30.3) is generally considered
when tumor inltrates the antecrural space as this may inhibit
neurolytic spread. In addition, masses located within the pancreatic tail appear to respond more successfully if a retrocrural
neurolysis is performed.
28
Positioning and approach
Placing the patient prone facilitates bilateral posterior paravertebral access to either the antecrural or retrocrural space.
One disadvantage is the possibility of transgression of pleura/
lung, risking pneumothorax. CT gantry angulation may help
exclude lung. Alateral decubitus position may help reduce ipsilateral lung volume. Some patients are unable to lie prone, e.g.,
because of respiratory diculty, morbid obesity, or severe pain,
and a lateral decubitus or oblique position is preferred.
Although an anterior approach with the patient supine is
possible, this is rarely needed and considered somewhat riskier
Figure 30.1 Computed tomography appearance of the celiac ganglia.
The right (arrow) and left (arrowhead) ganglia are anterolateral to the
diaphragmatic crus and may mimic a limb of the adrenal gland.
given the chance of visceral transgression when advancing a
needle through the peritoneal cavity.
1
Other maneuvers may be necessary to facilitate a safe needle
path. If a needle path that avoids pleura and lung is not obtainable, the needle may be advanced into the extrapleural fat along
Figure 30.2 Antecrural and retrocural
approaches to celiac plexus neurolysis.
Retrocrural
Antecrural
Splanchnic Nerves
Sympathetic ganglia
In the antecrural approach, the needle is
directed toward the celiac plexus. In the
retrocrural approach, the needle is directed
toward the splanchnic nerves.
T12
Aorta
Celiac Plexus
Diaphragm
316
Chapter30:CT-guided neurolysis for cancer-related abdominal and pelvic pain
A
Kidney
Aorta
B
Diaphragmatic
Crus
Figure 30.3 (A) Celiac plexus neurolysis,
antecrural technique. Right and left
paravertebral approach is illustrated,
with neurolytic instilled anterior to aorta
between origins of the celiac and superior
mesenteric arteries. (B) Retrocrural
technique. Neurolytic is instilled
posterior to the diaphragmatic crus
and posterolateral to the aorta.
Kidney
Diaphragmatic
Crus
the vertebral column. Normal saline may be injected, hydrodissecting pleura and lung laterally. Occasionally, a paravertebral
approach may require a needle path that passes through liver
or retroperitoneal organs such as kidney. In such a scenario,
it is important to minimize the number of needle punctures
through the organ, and in the case of kidney traversal, select a
needle path that avoids the renal sinus.
Antecrural
e antecrural site for neurolytic deposition may be selected
in patients without gross tumor inltration into the celiac
plexus and who do not have masses located within the pancreatic body/tail.28 Aposterior approach is oen the most direct,
and typically bilateral needle placement along the paravertebral space is performed. Preliminary CT images are obtained
and needle path is selected, targeting the space anterior to the
aorta between the origins of the celiac and superior mesenteric
Aorta
1
arteries. Once needle site, depth, and angulation are determined on review of preliminary CT images, local anesthesia
(e.g., 1% lidocaine) is administered.
CT, CT-uoroscopy, or cone-beam CT may be used for
imaging guidance. A20–22G needle (e.g., Chiba) is typically
advanced through either the right or le paravertebral space
until the tip lies within 1cm anterior to the aorta. Aspiration is
performed prior to every injection to ensure no return of blood
products that may suggest vascular intrusion. Subsequently, no
more than 5mL dilute contrast (e.g., 1:25–1:40 iopamidol in
normal saline) is injected and CT performed to assess contrast spread (Figure30.4). Adequate positioning is achieved if
contrast spread is seen around the anterior aorta and propagates in craniocaudal fashion toward the origins of the celiac
and superior mesenteric arteries. Contrast spread may also be
seen along the celiac and superior mesenteric arteries. Needle
adjustment may be necessary if spread is seen predominantly
317
Section X:Specialized interventional techniques in cancercare
space. In general, a 20–22G needle is advanced into the retrocrural space via the paravertebral approach. Aspiration is
performed prior to every injection to make sure there is no
vascular intrusion; the major concern is penetration of the
aorta or a spinal artery. Approximately 2mL dilute contrast is
injected to conrm spread anterior and lateral to the thoracic
and lumbar vertebral bodies.1 is is followed with 2mL local
anesthetic and 5–10mL 95–100% ethanol.
Smaller volumes of ethanol are used in very small retrocrural spaces or if the bulk of contrast spreads predominantly
posteriorly toward the neuroforamina. Rarely, contrast spread
is seen to extend to the contralateral retrocrural space, in which
case the volume of local anesthetic and ethanol used may be
Figure 30.4 Celiac plexus neurolysis, antecrural technique. The tip of the
needle (short arrow) is anterior to the aorta. Contrast spread along the right
(arrowhead) and left (long arrow) aspect of the aorta is seen.
doubled and contralateral procedure avoided. Otherwise, bilateral needle placement is required. Care is taken not to inject
within the diaphragmatic crus– this may result in pain and
may expand the crus in a manner that can narrow or attenuate
the retrocrural space, making further needle positioning more
too anteriorly or if contrast predominantly ows backward
along the paravertebral space. Ideally, contrast will spread to
encompass the celiac ganglia if identiableonCT.
If contrast spread is seen along the ipsilateral aspect of
the aorta only, 2mL local anesthetic such as 1% lidocaine is
instilled through the needle, followed aer a few minutes with
20 mL 95–100% ethanol. e needle is ushed with either
1–2mL local anesthetic or saline, removed, and the procedure is repeated on the contralateral side. If, however, contrast
spread is seen to extend unequivocally to the contralateral side
(Figure 30.4), the local anesthetic and ethanol volumes are
challenging.
Occasionally, a retroaortic fat plane exists between the vertebral disc or body and the posterior wall of the aorta that will
enable safe passage of a needle. If this is the case, a needle path
from the skin to the contralateral retrocrural space may exist
that would enable a single-needle retroaortic retrocrural technique (Figure30.6). In this scenario, the needle is advanced
from a paravertebral approach toward the contralateral retrocrural space, traveling posterior to the aorta. Once neurolysis
is performed, the needle is ushed and withdrawn into the ipsilateral retrocrural space for repeat neurolysis.
doubled and a contralateral procedure may not be required.
Alternative approaches to the antecrural space are available.
Atransdiscal approach may be considered in the absence of
severe degenerative disc disease; in this scenario, antibiotics
(e.g., cefazolin 1gram) are administered at the start of the procedure. A22G needle is advanced through the T12–L1 or L1–L2
disc and along the aorta until the antecrural space is reached at
the approximate level of the celiac artery origin.
1,17,18,29
CT gan-
try angulation may help to image along the axis of thedisc.
A transaortic approach to the antecrural space may also
be considered in the absence of aortic aneurysm. e primary advantage of this approach is that only a single needle
placement is required. e needle is advanced through the
aorta into the antecrural space; aspiration is performed prior
to every injection to ensure no blood products are seen that
may indicate needle tip within vascular lumen. Subsequently,
4mL dilute contrast is injected and CT performed to conrm
contrast spread in the antecrural space. is is followed with
2–4mL local anesthetic and 40mL ethanol; the needle is again
ushed prior to removal.
Retrocrural
In the setting of pancreatic tail mass and/or gross tumor inltration of the antecrural space at the celiac origin on CT, the
retrocrural site (Figure 30.5) is selected for neurolysis. e
technique is similar to the posterior paravertebral or transdiscal approaches described previously, with the exception that
smaller volumes of injectant are used as it is a more constricted
Outcomes
In one meta-analysis of over 1,100 patients with pain due to
one of a number of abdominal malignancies, approximately
90% of patients achieved partial or complete pain relief at
3months and 70–90% had partial or complete pain relief at the
time of death.12 One of the key benets of CPN is the reduction
of postprocedure opiate dependence, which reduces the risk of
opiate-related side eects. In a meta-analysis of six randomized
controlled trials, patients who underwent CPN experienced
statistically signicant pain relief that correlated with reduction in both opiate use as well as associated constipation and
no major complications.
9
Complications
Although some patients are referred for CPN as inpatients, the
procedure may be performed safely in the outpatient setting.
In addition to pain relief, some eects of CPN may be seen
postinjection; this may be attributable to the types of neural
information carried by the celiac network. is includes orthostatic hypotension that is most oen transient (<12hours) and
is likely related to neurolytic eect on sympathetic eerents;
adequate periprocedure intravenous hydration is hence important.1 Transient diarrhea may also occur; the mechanism is
not completely understood but is presumably related to unopposed parasympathetic innervation.1 Exceedingly rare reports
of paraplegia are found in the literature, probably related to
318