0703083

83Volume 7, Number 3 ■ may/JuNe 2009 www.SupportiveOncology.net

J Support Oncol 2009;7:83–87, 90 © 2009 Elsevier Inc. All rights reserved.

r e v i e w

Manuscript submitted December 15, 2008; accepted April 17, 2009.

Correspondence to: Doug G. Adler, MD, University of Utah School of Medicine, Department of internal Medicine, Divi-sion of Gastroenterology and Hepatology, 30N. 1900e 4r118, Salt Lake City, UT 84132; telephone: (801) 587-3574; fax: (801) 581-8007; e-mail: [email protected]

Celiac Plexus Neurolysis for Pain Relief in Pancreatic CancerJill C. Moore, MD, and Douglas G. Adler, MD, FACG, FASGE

Dr. Moore is a Fellow in Gastroenterology at the University of Utah School of Medicine, Department of internal Medicine, Division of Gastroenterology and Hepatology, Huntsman Cancer Center, Salt Lake City, Utah. Dr. Adler is Associate Professor at the University of Utah School of Medicine, Department of internal Medicine, Division of Gastroenterology and Hepatology, Huntsman Cancer Center, Salt Lake City, Utah.

inflammatory drugs (NSAiDs), acetaminophen, opioids, radiation therapy, chemotherapy, and ce-liac plexus neurolysis (CPN).

CPN is a technique whereby alcohol or phenol, alone or in combination with a local anesthetic, is injected directly into or near the celiac ganglia to de-stroy the visceral afferent nociceptors to ameliorate or alleviate chronic abdominal pain.10 Afferent nerve fibers for nociception pass diffusely through the celiac plexus. These fibers extend from organs within the abdominal viscera up to the splenic flexure.11 CPN is an alternative or additive tool in the management of pain due to pancreatic cancer.

Pancreatic Cancer PainAbdominal pain due to pancreatic cancer can

be severe and is usually epigastric with radiation to the back. in a large prospective study by Brescia and colleagues, 44% of patients with pancreatic cancer had severe pain.12 Although only 30%–40% of patients with pancreatic cancer report moderate to severe pain at the time of diagnosis, more than 80% of patients with advanced cancer experience severe pain.13,14 Pain due to pancreatic cancer may be difficult to treat and may require high-dose opioids for relief; however, patients may have a disappointing response to opioids.15,16

The cause of pain in patients with pancreatic cancer is not well understood. One theory attri-butes the severe pain to neuropathy, with damage to intrapancreatic nerves and tumor invasion into the extrapancreatic nerves leading to abdominal

Abstract Palliation of pain in pancreatic cancer often requires a mul-tidisciplinary approach, with options including oral analgesics, chemo-radiotherapy, and celiac plexus neurolysis (CPN). Although CPN may be performed endoscopically, percutaneously, or surgically, endoscopic ul-trasonography (EUS)-guided CPN is becoming more commonplace, giv-en the overall improved real-time visualization and reduced risk of major (neurologic) complications. Regardless of the technique used, CPN may have a long-lasting benefit in between 70% and 90% of patients with pancreatic cancer.

P ancreatic cancer is the second most com-mon gastrointestinal malignancy, ac-counting for approximately 30,000 cases each year, and is the fourth leading cause

of cancer deaths in the United States annually.1 Pancreatic cancer is a disease of the elderly, with most patients presenting in the sixth and seventh decades of life.2 Patients with pancreatic cancer typically present with epigastric abdominal pain, jaundice, and associated weight loss; the majority of cases are due to adenocarcinoma.3

Despite advances in diagnosis and treatment, pa-tients with pancreatic cancer often have a poor prog-nosis. This is primarily because a significant portion of patients present with advanced disease, which pre-cludes operative and potentially curative treatment.4 Advanced disease is typically associated with arterial involvement and/or metastatic disease. Less than 5% of patients diagnosed with pancreatic cancer are still alive 5 years after diagnosis, and complete remission is rare.5 A small percentage of patients with pancre-atic malignancies have favorable prognosis, including other tumors of the exocrine pancreas such as serous cystadenomas, acinar cell tumors, and pancreatic neuroendocrine tumors.5 risk factors associated with the development of pancreatic adenocarcinoma in-clude chronic inflammatory conditions of the pan-creas (chronic pancreatitis), advanced age, and to-bacco use.6 Less than 5% of pancreatic cancers are due to genetic factors.7

in many patients, management of pancreatic cancer is directed toward treatment of biliary and/or gastric outlet obstruction and pain.8,9 The pain due to pancreatic cancer is often severe and difficult to treat. Options for pain management include medications such as nonsteroidal anti-

84 www.SupportiveOncology.net The JourNal of SupporTiVe oNcology

CPN for Pain Relief in Pancreatic Cancer

pain.15 Others hypothesize that the pain may be due to the prox-imity of critical structures such as the stomach, duodenum, liver, and transverse colon as well as destruction of pancreatic tissue, which may cause ischemia, inflammation, and pain.17

recommendations for pain management from the world Health Organization include an analgesic ladder, with medica-tion titration progressing from NSAiDs to opioids.18 Opioids have many side effects, including but not limited to nausea, vom-iting, dry mouth, anorexia, pruritus, constipation, sedation, and delirium.19 These side effects may limit adequate drug titration for pain and may hinder quality of life (QOL). Oral analgesics remain the mainstay of therapy and may provide relief to 50%–90% of patients with cancer.20,21 Patients often seek alternative methods to control pain to reduce or avoid opioid analgesic use or to reduce opioid use to minimize side effects. Cancer patients often fear pain, especially if it is chronic and unrelieved, but it can be one of the most manageable symptoms when compared with other complications of cancer, such as fatigue, anorexia, weight loss, constipation, depression, and anxiety.22,23

CPN TechniquesThe celiac plexus is located below the diaphragm in an

antecrural position and abuts and/or surrounds the origin of the celiac artery, which is the first major artery to arise from the aorta below the diaphragm. The celiac plexus contains a network of ganglia and interconnecting fibers primarily from the upper abdominal viscera and includes fibers that transmit nociception from the pancreas. This plexus contains both vis-ceral afferent and efferent sympathetic fibers and parasympa-thetic fibers. The ganglia vary in number (1–5), size (diameter 0.5 cm–4.5 cm), and location (T12–L2).24

The terms celiac plexus block (CPB) and CPN are often used interchangeably in the literature, although these terms refer to two distinct procedures with different indications and risks. CPB (also referred to as celiac plexus blockade) generally refers to the injection of steroids with or without a local anes-thetic to temporarily inhibit celiac plexus function and reduce inflammation and pain thought to be of pancreatic origin. CPB is typically reserved for patients with benign pancreatic condi-tions, most commonly painful chronic pancreatitis. CPN refers to the use of a neurolytic agent, such as ethanol or phenol, in combination with a local anesthetic agent to permanently de-stroy nerve fibers and produce lasting pain relief. CPN is gener-ally reserved for patients with pancreatic malignancies. (CPB will not be discussed further in this article.)

The CPN technique was first described by Kappis in 1914.25 The technique described a posterior, retrocrural approach. Af-ter the celiac trunk has been localized, a needle is placed in this location, and a local anesthetic is injected at the site. This step is followed by injection of a neurolytic agent such as alco-hol. The aim is to destroy the visceral afferent nociceptors to alleviate chronic abdominal pain.10

Since that time, different approaches were developed to im-prove the accuracy of needle placement, increase efficacy, and decrease complications. Different techniques utilize different routes to reach the celiac plexus, diverse imaging modalities,

and varying agents to perform the neurolysis.26 Methods to ad-minister such agents to the celiac ganglion include surgery, CT-guided injection, percutaneous ultrasonography, fluoroscopy, or endoscopic ultrasonography-guided (eUS) approaches.

SurgiCal CPN

Often performed when unresectable disease was identified dur-ing surgery, CPN can be accomplished during laparotomy or lap-aroscopy and in combination with gastrojejunostomy and biliary bypass. The major advantage of the surgical approach is the abil-ity to combine adequate long-term palliation for all three primary symptoms of pancreatic cancer (pain, jaundice, and gastric outlet obstruction) in a single procedure.27 As an alternative to direct surgical lysis, chemical splanchnicectomy can be performed during surgery.28,29 with this technique, 20 mL of 50% alcohol is injected on each side of the aorta at the level of the celiac axis, although volumes and concentrations of alcohol can vary.

in a study of surgical CPN by Lillemoe and colleagues,14 pain relief was reported in more than 80% of patients, and the development of pain was prevented for up to 6 months post-operatively. They also found a survival benefit in patients who received chemical splanchnicectomy. Other surgical tech-niques include a thoracoscopic approach,30 cryoablation with ultrasonographic guidance,31 and ganglionectomy (excision or transaction of the ganglia).26

in the past, surgical treatment was the primary method for palliating the symptoms of pancreatic cancer. Due to better initial tumor staging, a desire to avoid unnecessary surgery, and decreased invasiveness, CT-based approaches or eUS-guided CPN have largely replaced surgery as a means of per-forming CPN.27

PerCuTaNeouS CPN

The celiac axis can be accessed using a posterior or anterior percutaneous approach. CPN via the percutaneous approach is typically performed by anesthesiologists or interventional ra-diologists, with or without radiologic guidance.

The posterior approach is sometimes referred to as the ret-rocrural, posterolateral, transcrural, or antecrural technique, depending on the direction of needle placement. Percutaneous neurolysis using the posterior technique involves introducing a needle posterolateral to the L1 vertebra, alongside the ver-tebral body, and then adjusting the approach (eg, transaortic, retrocrural, and transcrural) to reach the presumed area of the celiac plexus32,33 (Figure 1).

The anterior approach was developed to improve visualiza-tion of the celiac plexus and partly to reduce the risk of spinal cord injury (as a result of the needle entering a spinal artery or piercing the dura mater) associated with the posterior ap-proach.34,35 in addition, the anterior approach can obviate the need for transcrural placement of the needle and thus avoid crossing the aorta. The anterior approach is typically performed with radiologic guidance via transcutaneous ultrasonography or CT. A needle is advanced by the anterior route to the area above the celiac plexus, and a local anesthetic is injected, fol-lowed by 30 mL to 40 mL of 50% alcohol.


Moore, Adler

euS-guided CPN

in 1996, wiersema and wiersema published the first report of eUS-guided CPN.36 Thirty patients with inoperable pancreatic (n = 25) or other intra-abdominal malignancies underwent CPN during eUS for staging and fine-needle aspiration (FNA). After staging and/or FNA, those patients with malignancy believed to be inoperable and patients referred for neurolysis underwent eUS-guided CPN. The region of the celiac ganglia was identified via the location of the origin of the celiac artery. At the time of this publi-cation it was not known how to identify the ganglia itself via eUS. The technique has been widely adopted by the eUS community.

in 2006, by which time eUS-guided CPN had become relatively commonplace, Levy et al and Gerke et al simultane-ously reported the appearance of the celiac ganglia on eUS.37,38 Levy and colleagues localized the gastrointestinal ganglia with eUS and used FNA to obtain neural tissue, thus confirming the identification of the ganglia. The celiac ganglia were retro-spectively identified on prior CT imaging in the patients who underwent eUS. The ganglia were visualized best with linear, as opposed to radial, echoendoscopes (although in practice they can be seen with either echoendoscope). They described the ganglia as discrete hypoechoic structures with hyperechoic focus or strands, which they thought were the neural rami.

The modern technique for eUS-guided CPN utilizes a linear echoendoscope with Doppler imaging. The standard approach is transesophageal (in the distal esophagus) or transgastric (in the proximal stomach) and antecrural. The needle is directed into the area of the celiac plexus and a local anesthetic is injected, fol-lowed by a neurolytic agent (Figure 2). exact doses and volumes of agents vary by institution, but 10 cc to 20 cc of 0.25% bupiva-caine followed by 10 cc to 20 cc of 98% ethanol is a representative formulation. eUS-guided CPB and CPN appear to be as effective and safe as other techniques while being more cost-effective, be-cause tumor staging, tissue acquisition for a pathologic diagnosis, and CPN can be performed in one procedure.13

efficacy of CPN for Pain relief in Pancreatic CancerSeveral studies have largely demonstrated the efficacy of

CPN and subjective improvement in pain. wong et al com-pared CPN via the posterior percutaneous approach with opi-oids alone in a double-blinded, randomized, controlled trial.39 The primary outcomes were pain control, QOL, and survival. Patients were allowed additional opioids as needed for pain re-lief, as prescribed by blinded providers.

The first week after randomization, pain intensity and QOL scores were improved (pain intensity, P ≤ 0.01 for both groups; QOL, P < 0.001 for both groups), with a larger decrease in pain for the neurolysis group (P = 0.005). From repeated mea-sures analysis, pain in the neurolysis group was also lower over time (P = 0.01). Opioid consumption, frequency of opioid adverse effects, and QOL were not significantly different be-tween groups. in the first 6 weeks, fewer patients in the CPN group reported moderate or severe pain (pain intensity rating of at least 5 of 10) versus the opioid-only patients (14% vs 40%; P = 0.005). At 1 year, 16% of CPN patients and 6% of

opioid-only patients were alive, without a significant survival difference (P = 0.26, proportional hazards regression).

in another study, Kawamata and colleagues compared CPN and morphine treatment with regard to pain and QOL in pa-tients with pancreatic cancer pain.20 This prospective, nonran-domized study of 21 patients with pancreatic cancer pain evalu-ated the effectiveness of CPN (n = 10) on pain relief and QOL, compared with the traditional NSAiD-morphine treatment (n = 11). They monitored morphine requirements and used a visual analog scale (vAS), performance status (PS) as deter-mined by medical staff, and answers to QOL questionnaires.

vAS scores in the CPN group were statistically lower for the first 4 weeks after the procedure than in the NSAiD-morphine group. Opioid use was significantly lower in the CPN group at 4 to 7 weeks. At 10 weeks, opioid use was lower, but not sig-nificantly, in the CPN group. A statistically significant improve-

Figure 1 CT-Guided Celiac Plexus Neurolysis, Posterior Approach

Two 22-gauge needles were inserted from a posterior approach, with the tips positioned in the region of the celiac ganglion. Image courtesy of Allene Burdette, MD.

Figure 2 Perineuronal EUS-guided Celiac Plexus Neurolysis

A 22-gauge needle is introduced into the region of the celiac ganglia, just above the origin of the celiac artery (CA). The superior mesenteric artery (SMA) is seen originating just below the CA.



ment in PS, as well as QOL, was found in patients undergoing neurolysis. There were fewer side effects after CPN. They sum-marized that CPN does not directly improve QOL in patients with pancreatic cancer pain but may reduce deterioration of QOL attributed to the long-lasting analgesic effect, limitation of side effects, and the reduction of morphine consumption, com-pared with treatment with NSAiD-morphine analgesics alone.

A systematic review examined the efficacy and safety of CPN compared with standard treatment in five randomized controlled trials involving 302 patients with unresectable pan-creatic cancer.40 The primary outcome was pain measured on a 10-point vAS. The secondary outcomes included opioid usage, adverse effects, QOL, and survival. A total of 147 patients un-derwent CPN, and the control group included 155 patients.

CPN was associated with lower vAS scores for pain at 2, 4, and 8 weeks (weighted mean difference [wMD], 0.60; 95% con-fidence interval [Ci], –0.82 to –0.37). Opioid usage (in mg/d oral morphine) was also reduced at 2, 4, and 8 weeks (wMD, 85.9; 95% Ci, –144.0 to –27.9). CPN was associated with a reduction in constipation (relative risk 0.67; 95% Ci, 0.49 to 0.91) but no other adverse events. No differences in survival were observed. QOL could not be adequately analyzed. in patients with unresectable pancreatic cancer, CPN is associated with improved pain control, reduced use of opioids, and less constipation compared with stan-dard treatment, although with minimal clinical significance.

Stefaniak and colleagues compared the effectiveness of CPN and videothoracoscopic splanchnicectomy (vSPL), a lysis of the splanchnic nerve performed thoracoscopically, in a conser-vatively treated control group.41 Fifty-nine patients with pain due to inoperable pancreatic cancer were treated with CPN (n = 35) or vSPL (n = 24) in two nonrandomized, prospec-tive, case-controlled protocols. intensity of pain (vAS-pain), QOL, and opioid usage were compared between the groups and to a control group of patients treated conservatively before the procedure and after 2 and 8 weeks of follow-up.

Both methods of neurolysis resulted in a major reduction of pain and fatigue. A significant improvement in physical, emo-tional, and social well-being was found only in the CPN group. Mean daily opioid consumption was decreased substantially after both procedures. The authors concluded that although both CPN and vSPL provided significant reduction of pain and improvement of QOL in inoperable pancreatic cancer pa-tients, CPN is preferred due to the similar efficacy, less inva-siveness, and more positive effect on QOL.

An older meta-analysis reviewed the efficacy and safety of CPN for cancer pain from 24 published studies.42 A total of 63% of included patients had pancreatic cancer. A bilateral posterior approach with 15–50 mL 50%–100% alcohol was the most com-mon technique. Nonradiologically guided CPN was performed in 246 patients (32%); CT-guided CPN, in 214 patients (28%); radiography-guided CPN, in 271 (34%); fluoroscopy-guided CPN, in 36 (5%); or ultrasonography-guided CPN, in 7 (< 1%). eUS-guided CPN was likely performed in the minority of pa-tients due to the relative paucity of eUS hardware and practitio-ners at the time the study was published (over a decade ago).

Good to excellent pain relief was reported in 878 of 989

patients (89%) during the first 2 weeks after CPN. Long-term follow-up (more than 3 months) revealed persistent benefit. Partial to complete pain relief continued in approximately 90% of patients 3 months after CPN and in 70% to 90% until death, even if survival was beyond 3 months post procedure. Patients with pancreatic cancer responded similarly to those with other intra-abdominal malignancies. Common adverse effects were transient, including local pain (96%), diarrhea (44%), and hy-potension (38%); complications occurred in 2%. Overall, CPN provided long-lasting pain relief for 70%–90% of patients with pancreatic cancer pain, regardless of the technique used, with mild adverse side effects and uncommon severe adverse events.

A small retrospective study by Levy et al evaluated the safety and efficacy of intraneuronal injection.43 CPN was performed at 2–4 weeks in patients with moderate to severe pain due to unresectable pancreatic carcinoma (CPN = 17; CPB = 1) or chronic pancreatitis (CPN = 5; CPB = 13). Thir-ty-three patients underwent a total of 36 injections. Pain relief was reported in 94% of patients with pancreatic cancer. Of pa-tients with chronic pancreatitis, 80% reported pain relief with CPN. Thirteen patients (39%) reported initial exacerbation of pain, which correlated with improved therapeutic response (P < 0.05). Transient hypotension and diarrhea developed in 12 (36%) and 6 (18%) patients, respectively.

in a small, prospective, randomized study, Adler et al evalu-ated direct intraneuronal injection of lidocaine and triamcino-lone compared with perineuronal injection near or around the celiac plexus in 14 patients with pancreatic cancer.44 Neuro-lytic agents were not used, as there were limited safety data on eUS-guided injection into the ganglia at the time of the study. The celiac plexus could be identified in all patients. intraneu-ronal injection was thought to be as simple and safe to perform as perineuronal injection. This small study did not detect a difference in pain relief between injections into the two differ-ent locations, but larger studies may be needed to determine whether one location is superior to the other for CPN.

Safety and Complications of CPNComplications associated with CPN tend to be minor, and

serious complications are infrequent. Local pain, diarrhea, and transient hypotension are often seen. A meta-analysis of more than 1000 patients with intra-abdominal cancer (the majority with pancreatic cancer) reported the following complications associated with percutaneous CPN: local pain (96%), diarrhea (44%), and hypotension (38%).42 Serious neurologic complica-tions occurred in 1% of patients and included lower extrem-ity weakness and paresthesia, epidural anesthesia, and lumbar puncture. Significant non-neurologic complications occurred in an additional 1% and included pneumothorax; shoulder, chest, and pleuritic pain; hiccoughing; and hematuria. The posterior approach was also associated with retroperitoneal fibrosis, which may interfere with surgery.32 There are case re-ports of gastroparesis45 and gastric perforation with CPN.46

A randomized, prospective study of 22 patients with chronic pancreatitis pain compared eUS- and CT-guided CPN via the an-terior approach.13 There were no serious complications reported


Moore, Adler

with either technique. They commented on the benefit of real-time imaging with eUS-guided CPN and the ability to perform FNA during the same procedure. The eUS approach was pre-ferred by patients who had experienced both procedures due to the lack of back pain and more sedation during eUS. in addition, eUS-guided CPN was found to be more cost-effective. The ante-rior approach had a decreased risk of neurologic complications but is reported to cause retroperitoneal abscess formation.47

The American Society of Gastrointestinal endoscopy (ASGe) reviewed the complications associated with eUS-guided CPN in a clinical guideline published in 2005.48 The perforation rate with eUS-guided CPN (for any indication) is 0.03% to 0.07%. Based on limited data, the eUS approach probably has a rate of perforation similar to that of standard esophagogastroduodenoscopy (eGD; 0.03%). Use of FNA did not increase complication rates. The risk of infection is reported as similar to that of standard eGD, which ranges from 0% to 8%. reports of fever after eUS with FNA (us-ing the same technology as eUS-guided CPN) range from 0.4% to 1%. There are reported cases of retroperitoneal abscess, but this is a rare complication. The risk of pancreatitis is 0% to 2%. Mild intraluminal hemorrhage occurs in 1.3% to 4% of cases, and severe hemorrhage is infrequently reported.49

reported risks specific to eUS with neurolysis include transient diarrhea (4%–15%), orthostasis (1%), transiently increased pain (9%), and abscess, which is rarely reported. To date, no paralysis has been reported via the eUS route. in a prospective study of eUS-guided CPN for pancreatic cancer pain by Gunaratnam et al,

transient pain of less than 48 hours’ duration was found in 9% of patients.50 Gastroparesis has been reported after CPN as well.45

ConclusionManagement of patients with pancreatic cancer is often di-

rected toward palliation of symptoms such as pain, malignant biliary obstruction, and gastric outlet obstruction. Pain is one of the most-feared symptoms in patients with cancer, yet it can be the most treatable when compared with other complica-tions of cancer. Palliation of pain in pancreatic cancer often requires a multidisciplinary approach, with options including oral analgesics, chemoradiotherapy, and CPN.

regardless of the technique used, CPN has a long-lasting benefit in up to 70% to 90% of patients with pancreatic can-cer.42 CPN is safe, with common mild side effects and uncom-mon severe adverse effects. it is an alternative to opioid an-algesics, both for improving pain control and for avoiding or reducing the side effects of high-dose opioids, which can signifi-cantly hinder QOL. Most investigators do not think that CPN prolongs the lives of patients with pancreatic cancer. CPN may be performed via endoscopic, percutaneous, or surgical routes. None of these procedures represents a gold standard for per-forming CPN, although eUS-guided CPN is becoming more commonplace, given the overall improved real-time visualiza-tion and reduced risk of major (neurologic) complications.

Acknowledgment: The authors wish to thank Dr. Allene Burdette for her assistance in the preparation of this article.

references PubMed ID in brackets

Cancer Facts and Figures 2004. Atlanta, GA: 1. American Cancer Society; 2004.

Brennan MF. Pancreatic cancer. J Gastroenterol 2. Hepatol 2000;15(suppl):G13–G16.[11100987]

Li D, Xie K, Wolff R, Abbruzzese JL. Pancreatic 3. cancer. Lancet 2004;363:1049–1057.[15051286]

Poston GJ, Williamson RC. Causes, diagnosis, 4. and management of exocrine pancreatic cancer. Compr Ther 1990;16:36–42.[1689234]

Ghaneh P, Costello E, Neoptolemos JP. 5. Biology and management of pancreatic cancer. Gut 2007;56:1134–1152.[17625148]

Thirumurthi S, Adler DG. Pancreatic adenocar-6. cinoma. Hospital Physician 2006;42:38–49.

Chappuis PO, Ghadirian P, Foulkes WD. The role 7. of genetic factors in the etiology of pancreatic adeno-carcinoma: an update. Cancer Invest 2001;19:65–75.[11291558]

von Wichert G, Seufferlein T, Adler G. Palliative 8. treatment of pancreatic cancer. J Dig Dis 2008;9:1–7.[18251787]

Christo PJ, Mazloomdoost D. Cancer pain and 9. analgesia. Ann N Y Acad Sci 2008;1138:278–298.[18837907]

Levy MJ, Wiersema MJ. EUS-guided celiac 10. plexus neurolysis and celiac plexus block. Gastrointest Endosc 2003;57:923–930.[12776048]

Day M. Sympathetic blocks: the evidence. Pain 11. Pract 2008;8:98–109.[18366465]

Brescia FJ, Portenoy RK, Ryan M, Krasnoff L, 12. Gray G. Pain, opioid use, and survival in hospital-ized patients with advanced cancer. J Clin Oncol 1992;10:149–155.[1345797]

Gress F, Schmitt C, Sherman S, Ikenberry S, 13.

Lehman G. A prospective randomized comparison of endoscopic ultrasound- and computed tomography-guided celiac plexus block for managing chronic pan-creatitis pain. Am J Gastroenterol 1999;94:900–905.[10201454]

Lillemoe KD, Cameron JL, Kaufman HS, Yeo CJ, Pitt 14. HA, Sauter PK. Chemical splanchnicectomy in patients with unresectable pancreatic cancer: a prospective ran-domized trial. Ann Surg 1993;217:447–455.[7683868]

Ceyhan GO, Michalski CW, Demir IE, Müller 15. MW, Friess H. Pancreatic pain. Best Pract Res Clin Gastroenterol 2008;22:31–44.[18206811]

Cruciani RA, Jain S. Pancreatic pain: a mini 16. review. Pancreatology 2008;8:230–235.[18509251]

Brescia FJ. Palliative care in pancreatic cancer. 17. Cancer Control 2004;11:39–45.[14749622]

Cancer Pain Relief and Palliative Care. Geneva, 18. Switzerland: World Health Organization; 1990.

Harris JD. Management of expected and 19. unexpected opioid-related side effects. Clin J Pain 2008;24(suppl 10):S8–S13.[18418226]

Kawamata M, Ishitani K, Ishikawa K, et al. 20. Comparison between celiac plexus block and morphine treatment on quality of life in patients with pancreatic cancer pain. Pain 1996;64:597–602.[8783327]

Saunders C. Appropriate treatment, appropri-21. ate death. In: Saunders DC, ed. The Management of Terminal Malignant Disease. Baltimore, Md: Edward Arnold; 1984.

Strang P. Existential consequences of unre-22. lieved cancer pain. Palliat Med 1997;11:299–305.[9373581]

Holland JC. Anxiety and cancer: the patient 23. and the family. J Clin Psychiatry 1989;50(suppl):20–25.

[2681170]Ward EM, Rorie DK, Nauss LA, Bahn RC. The 24.

celiac ganglia in man: normal anatomic variations. Anesth Analg 1979;58:461–465.[574729]

Kappis M. Erfahrungen mit local anasthesie bie 25. bauchoperationen [German]. Vehr Dtsch Gesellsch Chir 1914;43:87–89.

Noble M, Gress FG. Techniques and results of 26. neurolysis for chronic pancreatitis and pancreatic cancer pain. Curr Gastroenterol Rep 2006;8:99–103.[16533471]

House MG, Choti MA. Palliative therapy 27. for pancreatic/biliary cancer. Surg Clin North Am 2005;85:359–371.[15833477]

Boas RA. Sympathetic blocks in clinical prac-28. tice. Int Anesthesiol Clin 1978;16:149–182.[84795]

Andtbacka RH, Evans DB, Pisters PW. Surgical 29. and endoscopic palliation for pancreatic cancer. Minerva Chir 2004;59:123–136.[15238887]

Pietrabissa A, Vistoli F, Carobbi A, Boggi U, Bisà 30. M, Mosca F. Thoracoscopic splanchnicectomy for pain relief in unresectable pancreatic cancer. Arch Surg 2000;135:332–335.[10722037]

Kovach SJ, Hendrickson RJ, Cappadona CR, et 31. al. Cryoablation of unresectable pancreatic cancer. Surgery 2002;131:463–464.[11935137]

Michaels AJ, Draganov PV. Endoscopic ul-32. trasonography guided celiac plexus neurolysis and celiac plexus block in the management of pain due to pancreatic cancer and chronic pancreatitis. World J Gastroenterol 2007;13:3575–3580.[17659707]

Kitoh T, Tanaka S, Ono K, Ohfusa Y, Ina H, 33. Otagiri T. Combined neurolytic block of celiac, inferior mesenteric, and superior hypogastric plexuses for continued on page 90


mesenteric, and superior hypogastric plexuses for incapacitating abdominal and/or pelvic cancer pain. J Anesth 2005;19:328–332.[16261474]

Giménez A, Martínez-Noguera A, Donoso L, 34. Catalá E, Serra R. Percutaneous neurolysis of the celiac plexus via the anterior approach with sonographic guidance. Am J Roentgenol 1993;161:1061–1063.[8273610]

Buy JN, Moss AA, Singler RC. CT guided celiac 35. plexus and splanchnic nerve neurolysis. J Comput Assist Tomogr 1982;6:315–319.[7076925]

Wiersema MJ, Wiersema LM. Endosonography-36. guided celiac plexus neurolysis. Gastrointest Endosc 1996;44:656–662.[8979053]

Levy M, Rajan E, Keeney G, Fletcher JG, Topazian 37. M. Neural ganglia visualized by endoscopic ultrasound. Am J Gastroenterol. 2006;101:1787–1791.[16780554]

Gerke H, Silva RG Jr, Shamoun D, Johnson CJ, 38. Jensen CS. EUS characteristics of celiac ganglia with cytologic and histologic confirmation. Gastrointest Endosc 2006;64:35–39.[16813800]

Wong GY, Schroeder DR, Carns PE, et al. Effect 39. of neurolytic celiac plexus block on pain relief, qual-ity of life, and survival in patients with unresectable

pancreatic cancer: a randomized controlled trial. JAMA 2004;291:1092–1099.[14996778]

Yan BM, Myers RP. Neurolytic celiac plexus block 40. for pain control in unresectable pancreatic cancer. Am J Gastroenterol 2007;102:430–438.[17100960]

Stefaniak T, Basinski A, Vingerhoets A, et al. 41. A comparison of two invasive techniques in the management of intractable pain due to inoperable pancreatic cancer: neurolytic celiac plexus block and videothoracoscopic splanchnicectomy. Eur J Surg Oncol 2005;31:768–773.[15923103]

Eisenberg E, Carr DB, Chalmers TC. Neurolytic 42. celiac plexus block for treatment of cancer pain: a meta-analysis. Anesth Analg 1995;80:290–295.[7818115]

Levy MJ, Topazian MD, Wiersema MJ, et al. 43. Initial evaluation of the efficacy and safety of endo-scopic ultrasound-guided direct ganglia neurolysis and block. Am J Gastroenterol 2008;103:98–103.[17970834]

Adler DG, Hilden K, Thomas K, Wills J, Wong R. 44. Endoscopic celiac plexus blockade via direct intraneu-ronal injection versus perineuronal injection: results of a pilot study. Am J Gastroenterol 2008;103:2958–

2959.[19032487]Iftikhar S, Loftus EV Jr. Gastroparesis after ce-45.

liac plexus block. Am J Gastroenterol 1998;93:2223–2225.[9820401]

Takahashi M, Yoshida A, Ohara T, et al. Silent 46. gastric perforation in a pancreatic cancer patient treated with neurolytic celiac plexus block. J Anesth 2003;17:196–198.[12911209]

Navarro-Martinez J, Montes A, Comps O, 47. Sitges-Serra A. Retroperitoneal abscess after neuro-lytic celiac plexus block from the anterior approach. Reg Anesth Pain Med 2003;28:528–530.[14634943]

Adler DG, Jacobson BC, Davila RE, et al. ASGE 48. guideline: complications of EUS. Gastrointest Endosc 2005;61:8–12.[15672049]

Gress F, Ciaccia D, Kiel J, Sherman S, Lehman 49. G. Endoscopic ultrasound (EUS) guided celiac plexus block (CB) for management of pain due to chronic pancreatitis (CP): a large single center experience. Gastrointest Endosc 1997;45:AB173.

Gunaratnam NT, Sarma AV, Norton ID, 50. Wiersema MJ. A prospective study of EUS-guided celiac plexus neurolysis for pancreatic cancer pain. Gastrointest Endosc 2001;54:316–324.[11522971]

continued from page 87


0703083

Documents

Transcript of 0703083