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Chapter30:CT-guided neurolysis for cancer-related abdominal and pelvic pain
A B
C D
Figure 30.5 (A) Celiac plexus neurolysis, retrocrural technique. The tip of the needle (arrowhead) is in the right retrocrural space with ipsilateral-only contrast
spread (arrow). (B) Technique was repeated on the contralateral side with needle placement (arrowhead) and contrast spread (arrow) in the left retrocrural space. (C) Postprocedure computed tomography demonstrates ethanol spread (arrows) extending cranially in the right and left retrocrural space. The greatest, greater, and lesser splanchnic nerves course through this space. (D) Transdiscal trajectory of needle (long arrow) with tip in the contralateral retrocural space (arrowhead). Contrast in the ipsilateral retrocural space (short arrow) was deposited from previous (not shown) paravertebral needle placement.
inadvertent spinal artery injection with neurolytic. During the procedure, it is important to aspirate prior to every injection to help assess vascular intrusion.
Some patients may not have signicant pain relief aer CPN. If a procedure is unsuccessful, repeat CPN may be con­sidered. First, images from a prior procedure are reviewed to ascertain previous needle placement, spread of contrast, and volume of neurolytic injected; the procedure may be repeated using the same technique if one or more of these variables is found to be suboptimal. However, modication of approach
Figure 30.6 Celiac plexus neurolysis, retroaortic retrocrural technique. A 22G
Chiba needle (arrowhead) is advanced through a retroaortic plane (long arrow) to the contralateral retrocural space (short arrow). Unilateral contrast spread is seen. After ethanol deposition and needle flush, the needle is retracted to the ipsilateral retrocrural space and injection repeated (not shown).
may be considered, i.e., opting for a retrocrural neurolysis if prior antecrural neurolysis was unsuccessful.

Superior hypogastric neurolysis

Over 50% of patients with lower abdominal/pelvic primary or secondary malignancy may suer from pelvic pain. Opioid anlagesics are again the mainstay of therapy. Because nociceptive information from the bladder, prostate, gonads,
30,31,32,33
uterus, upper vagina, and bowel from the descending colon to the upper rectum travel with sympathetic aerents via the supe­rior hypogastric plexus, superior hypogastric neurolysis can be
319
Section X:Specialized interventional techniques in cancercare
Figure 30.7 Superior hypogastric
neurolysis, transdiscal approach. Needle is advanced through the L5–S1 disc. Neurolytic is instilled anterior to the disc.
an important adjunctive tool in the treatment of cancer-related pelvicpain.
Anatomy
Nociceptive stimuli from pelvic organs travel along sympa­thetic aerents to the lumbar sympathetic chain. ese bers form a network that lies anterior to the L5–S1 vertebral levels and is an extension of the aortic plexus over the aortic bifurca-
30,34
tion. transdiscal approach (Figure30.7).
It is generally accessed by needle via a paravertebral or
35
Technique
Although many reports in the literature describe uoroscopic guidance for superior hypogastric neurolysis, CT guidance may be performed eectively. As with CPN, CT guidance oers the advantage of excellent anatomic delineation and helps guide needle placement in a retroperitoneal location anterior to the L5–S1 levels, while avoiding aorta, common iliac vessels, and exiting spinal nerves.
Positioning and approach
e superior hypogastric plexus is typically accessed using a posterior approach. In general, a paravertebral or a transdis­cal approach may be used. If a transdiscal approach is selected, prophylactic antibiotics (e.g., 1gram cefazolin intravenously) are administered. e patient is placed in the prone position with pillow placed underneath the abdomen to facilitate right­and/or le-sided access to the superior hypogastric nerve; however, a lateral decubitus position may be considered if the patient is unable to lieprone.
Preliminary CT images are obtained for access planning. e CT gantry is angulated such that CT images are parallel to the L5–S1 disc. Aneedle path is planned which ideally termi­nates near midline and anterior to the L5–S1 disc (Figure30.8). Exiting spinal nerve roots may be visualized on CT; a needle trajectory is chosen that avoids traversal of these roots so as
Figure 30.8 Superior hypogastric neurolysis. Needle (arrowhead) is advanced
via transdiscal trajectory with tip advanced just anterior to the L5–S1 disc. Contrast spread (arrow) is seen anterior to the disc.
to reduce the risk of intraprocedural pain. However, a para­vertebral approach may be hampered by iliac crest, lumbar transverse process, or other intervening structures. If a purely paravertebral route is unavailable on either side, a transdiscal approach is chosen. e use of a transdiscal approach may also shorten procedure time.
35
A 20–22G needle (e.g., Chiba) is advanced using CT, CT uoroscopy, or cone-beam CT guidance just past the ante­rior margin of the disc, where there is typically a sense of loss of resistance, but no more than 1cm anterior to the disc.35 Aspiration is performed to ensure no return of blood products; this is performed prior to every needle injection. Subsequently, 2mL dilute contrast is administered (Figure30.8) in similar fashion to CPN. Ideally, contrast spread is observed anteriorly on both sides of the L5–S1 disc, and may be seen over the upper sacrum as well as along the common iliac vessels. In this sce­nario, 2mL local anesthetic (e.g., 1% lidocaine) is administered followed by 20mL 95–100% ethanol. e needle is ushed with
320
Chapter30:CT-guided neurolysis for cancer-related abdominal and pelvic pain
saline or local anesthetic and removed. However, if contrast spread is seen only unilaterally, the volume of ethanol injected is halved and indwelling needle tip adjustment toward the con­tralateral side or new needle placement on the contralateral side may be performed.
Outcomes
A number of reports have described reduction in pain scores as well as opioid requirements aer superior hypogastric neu-
19,30,36
rolysis.
Plancarte etal., for example, reported a reduction in pain score of 50% in 51% of patients undergoing the pro­cedure.36 Erdek etal. also found a strong correlation between positive outcome and CT guidance.
19,30
Complications
As with other CT-guided procedures, bleeding is a possible complication. Some authors using uoroscopic technique suggest the risk of injury to the ureter as well as lumbosacral nerves.30 However, the use of CT guidance may help reduce this risk, as intervening structures are better delineated. If a trans­discal approach is used, there may be a small risk of discitis or disc herniation/rupture.
30,35,37
Figure 30.9 Ganglion impar neurolysis. Needle is advanced through the
sacrococcygeal junction (arrow). Contrast spread (arrowhead) is noted in the precoccygeal space.
and caudad within the precoccygeal space. Ideally, contrast encompasses the ganglion if visible on CT.
39,40
is is followed with 2mL local anesthetic (e.g., 1% lidocaine) and 5–10mL 95–100% ethanol. e needle is ushed with local anesthetic or normal saline and removed.

Ganglion impar neurolysis

Although superior hypogastric neurolysis may be a useful adjunct in the treatment of cancer-related pelvic pain, it may be less eective for low pelvic/perineal pain. e termination of the paravertebral sympathetic chains known as the ganglion impar or ganglion of Walther is another target for neurolysis.38 It may be performed in conjunction with superior hypogastric
Outcomes
Only a few reports exist in the literature summarizing the experience with ganglion impar blockade/neurolysis in cancer-related pain. In a series of 16 patients with cancer-related rectal, vaginal, and/or perineal pain, 50% had complete relief, whereas the remaining patients had 60–90% pain relief, with follow-up ranging from 4months to death.
38,41
neurolysis.
Anatomy
e ganglion impar lies anterior to the sacrum/coccyx, at approximately the level of the sacrococcygeal ligament.38 It is involved in mediating sympathetic and nociceptive informa­tion from the lower rectum/anus, distal vagina and urethra, vulva, and perineum.38 It can sometimes be visible on CT as an oval-shaped structure measuring about 2–3mm in longest dimension anterior to the sacrococcygeal joint or coccyx.
39,40
Technique
Various techniques using uoroscopic, CT, and ultrasound guid­ance have been described. suggested as enabling more accurate needle placement with lower risk of complication, such as traversal of pelvic viscera or vessels.
38,39
Typically, the patient is placed in prone position with pillow placed below the abdomen and lower extremities internally rotated.39 CT gantry angulation may be performed to
38,39,41,42,43,44,45
CTguidance has been
obtain images parallel to the sacrococcygeal junction; sagittal reformations may be helpful to identify the junction.
A single 22G needle is advanced through the sacrococ­cygeal joint, with tip advanced just anterior to the junction. Approximately 2mL dilute contrast as with CPN is injected (Figure 30.9); contrast spread is typically seen cephalad
Complications
Although signicant complications have not been reported in the literature, potential complications include perforation of pelvic viscera or bleeding.39 In addition, traversal or injection of the sciatic nerve is a possibility.39 Use of CT guidance, emp­tying the bladder prior to the procedure, and use of contrast injection through the needle to predict neurolytic spread may help minimize these complications.
39

References

1. Kambadakone A, abet A, Gervais DA, Mueller PR, Arellano RS. CT-guided celiac plexus neurolysis:a review of anatomy, indications, technique, and tips for successful treatment. Radiographics 2011; 31:1599–1621.
2. de Oliveira R, dos Reis MP, Prado WA. e eects of early or late neurolytic sympathetic plexus block on the management of abdominal or pelvic cancer pain. Pain 2004:110:400–408.
3. Staats PS, Hekmat H, Sauter P, Lillemoe K. e eects of alcohol celiac plexus block, pain, and mood on longevity in patients with unresectable pancreatic cancer:a double-blind, randomized, placebo-controlled study. Pain Med 2001; 2:28–34.
4. Wong GY, Schroeder DR, Carns PE, etal. Eect of neurolytic celiac plexus block on pain relief, quality of life, and survival in patients with unresectable pancreatic cancer:a randomized controlled trial. JAMA 2004; 291:1092–1099.
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5. Wyse JM, Chen Y-I, Sahai AV. Celiac plexus neurolysis in the management of unresectable pancreatic cancer:when and how? World J Gastroenterol 2014; 20:2186–2192.
6. Yan BM, Myers RP. Neurolytic celiac plexus block for pain control in unresectable pancreatic cancer. Am J Gastroenterol 2007; 102:430–438.
7. Miguel R. Interventional treatment of cancer pain:the fourth step in the World Health Organization analgesic ladder? Cancer Control 2000; 7:1490156.
8. Shulman M, Harris JE, Lubenow TR, Nath HA, Ivankovich AD. Comparison of epidural butamben to celiac plexus neurolytic block for the treatment of pain of pancreatic cancer. Clin J Pain 2000; 16:304–309.
9. Arcidiacono PG, Calori G, Carrara S, McNicol ED, Testoni PA. Celiac plexus block for pancreatic cancer pain in adults. Cochrane Database Syst Rev 2011; 16:CD007519.
10. Tam A, Ahrar K. Palliative interventions for pain in cancer patients. Semin Intervent Radiol 2007; 24:419–429.
11. Rathmell JP. Atlas of Image-Guided Intervention in Regional Anesthesia and Pain Medicine. 2nd edn. Philadelphia, PA:Lippincott Williams and Wilkins,2012.
12. Eisenberg E, Carr DB, Chalmers TC. Neurolytic celiac plexus block for treatment of cancer pain:a meta-analysis. Anesth Analg 1995; 80:290–295.
13. Penman D. Celiac plexus neurolysis. Best Pract Res Clin Gastroenterol 2009; 23:761–766.
14. Noble M, Gress FG. Techniques and results of neurolysis for chronic pancreatitis and pancreatic cancer. Curr Gastroenterol Rep 2006; 8:99–103.
15. Soweid AM, Azar C. Endoscopic ultrasound-guided celiac plexus neurolysis. World J Gastroenterol Endosc 2010; 2:228–231.
16. Mercadante S,Nicosia F. Celiac plexus block:a reappraisal. Reg Anesth Pain Med 1998; 23:37–48.
17. Wang PJ, Shang MY, Qian Z, etal. CT-guided percutaneous neurolytic celiac plexus block technique. Abdom Imaging 2006; 31:710–718.
18. Titton RL, Lucey BC, Gervais DA, Boland GW, Mueller PR. Celiac plexus block:a palliative tool underutilized by radiologists. Am J Roentgenol 2002; 179:633–636.
19. Erdek MA, Halpert DE, Gonzalez-Fernandez M, Cohen SP. Assessment of celiac plexus block and neurolysis outcomes and technique in the management of refractory visceral cancer pain. Pain Med 2010; 11:92–100.
20. Loukas M, Klaassen Z, Merbs W, etal. A review of the thoracic splanchnic nerves and celiac ganglia. Clin Anat 2010; 23:512–522.
21. Bonica JJ. e role of the anaesthetist in the management of intractable pain. Proc R Soc Med 1954; 47:1029–1032.
22. Erdine S. Celiac ganglion block. Agri 2005; 17:14–22.
23. de Cicco M, Matovic M, Fracasso A, etal. Single-needle celiac plexus block:is needle tip position critical in patients with no regional anatomic distortions? Anesthesiology 1997; 87:1301–1308.
24. Zhang XM, Zhao QH, Zeng NL, etal. e celiac ganglia:anatomic study using MRI in cadavers. Am J Roentgenol 2006; 186:1520–1523.
25. de Cicco M, Matovic M, Bortolussi R, etal. Celiac plexus block:injectate spread and pain relief in patients with regional anatomic distortions. Anesthesiology 2001; 94:561–565.
26. Penman ID, Gilbert D. Basic technique for celiac plexus block/ neurolysis. Gastroenterol Endosc 2009; 69:S163–S165.
27. Wang ZJ, Webb EM, Westphalen AC, Coakley FV, Yeh BM. Multi-detector row computed tomography appearance of celiac ganglia. J Comput Assist Tomogr 2010; 34:343–347.
28. Rykowski JJ, Higler M. Ecacy of neurolytic celiac plexus block in varying locations of pancreatic cancer. Anesthesiology 2000; 92:347–354.
29. Ina H, Kitoh T, Kobayashi M, etal. New technique for the celiac plexus block:the transintervertebral disc approach. Anesthesiology 1996; 85:212–217.
30. Kroll CE, Schartz B, Gonzalez-Fernandez M, etal. Factors associated with outcome aer superior hypogastric plexus neurolysis in cancer patients. Clin J Pain 2014; 30:55–62.
31. van der Beuken-van Everdingen MH, de Rijke JM, Kessels AG, etal. Prevalence of pain in patients with cancer:a systematic review of the past 40years. Ann Oncol 2007; 18:1437–1449.
32. van der Beuken-van Everdingen MH, de Rijke JM, Kessels AG, etal. High prevalence of pain in patients with cancer in a large population-based study in e Netherlands. Pain 2007; 132:312–320.
33. Breivik H, Cherney N, Collett B, etal. Cancer-related pain:a pan-European survey of prevalence, treatment, and patient attitudes. Ann Oncol 2009; 20:1420–1433.
34. Bosscher H. Blockade of the superior hypogastric plexus block for visceral pelvic pain. Pain Pract 2001; 2:162–170.
35. Gamal G, Helaly M, Labib YM. Superior hypogastric block:transdiscal versus classic posterior approach in pelvic cancer pain. Clin J Pain 2006; 22:544–547.
36. Plancarte R, de Leon-Casasola OA, El-Helaly M, Allende S, Lema MJ. Neurolytic superior hypogastric plexus block for chronic pelvic pain associated with cancer. Reg Anesth 1997; 22:562–568.
37. Erdine S, Yucel A, Celik M, Talu GK. Transdiscal approach for hypogastric plexus block. Reg Anesth Pain Med 2003; 28:304–308.
38. Scott-Warren JT, Hill V, Rajasekaran A. Ganglion impar blockade:a review. Curr Pain Headache Rep 2013; 17:306.
39. Datir A, Connell D. CT-guided injection for ganglion impar blockade:a radiologic approach to the management of coccydynia. Clin Radiol 2010; 65:21–25.
40. Chang-Seok O, In-Hyuk C, Hyun-Ju J, etal. Clinical implications of topographic anatomy on the ganglion impar. Anesthesiology 2004; 101:249–250.
41. Plancarte R, Amescua C, Patt RB, etal. Presacral blockade of the ganglion of Walther (ganglion impar). Anesthesiology 1990; 73:A751.
42. Foye PM. New approaches to ganglion impar blocks via coccygeal joints. Reg Anesth Pain Med 2007; 32:269.
43. Ho KY, Nagi PA, Gray L, etal. An alternative approach to ganglion impar neurolysis under computed tomography guidance for recurrent vulvar cancer. Anesthesiology 2006; 105:861–862.
44. Foye PM. Ganglion impar injection techniques for coccydynia (coccyx pain) and pelvic pain. Anesthesiology 2007; 106:1062–1063.
45. Lin CS, Cheng JK, Hsu YW, etal. Ultrasound-guided ganglion impar block:a technical report. Pain Med 2010; 11:390–394.
322
Chapter
Palliative procedures for ascites and eusion
31
Hooman Yarmohammadi and George I. Getrajdman

Introduction

e denition of ascites is the pathological accumulation of uid in the peritoneal cavity. Malignant ascites is accumulation of uid in the peritoneal cavity as a consequence of cancer.1 Refractory ascites is when ascites fail to respond to:(1) bed rest; (2)uid restriction to 1500mL/day and salt restriction to 80 mmol/day; (3) 400 mg/day spironolactone or 300mg/ day triamterene plus 120mg/day furosemide for 4 weeks; or (4) when patients are intolerant to medical therapy because of azotemia.
2,3
e most common cause of benign and malignant ascites, accounting for nearly 80% of cases, is liver cirrhosis.4 Malignant ascites is present in approximately 10% of all patients with ascites.5 e cancers most commonly associated with ascites can be divided into two groups of intra-abdominal (i.e., ovary, stomach, pancreas, and colon) and extra-abdominal (i.e., breast, lung, and lymphoma) malignancies.6 In approximately 20% of all patients with malignant ascites the primary origin of the tumor is unknown.
7
e pathophysiology of malignant ascites is multifacto­rial and not completely clear.8 e cause of ascites in cancer patients diers from that in patients with cirrhosis. e most common recognized pathophysiology is alteration in vascular permeability of the parietal peritoneum and metastatic spread to the peritoneum or peritoneal carcinomatosis (50%). Vascular endothelial growth factor (VEGF) increases vascu­lar permeability. Multiple reviews have demonstrated high levels of VEGF in patients with malignant ascites, particu­larly in patients with ovarian, gastric, and colorectal cancers.10 Other mentioned causes are obstruction of draining lymphat­ics due to lymphatic invasion (20%; most commonly seen in lymphoma and breast cancer), liver metastasis, resulting in portal vein hypertension (15%), and hormonal mechanisms.11 Depleted or reduced circulatory blood volume activates the renin–angiotensin–aldosterone system, leading to sodium retention in patients with ascites, including patients with malignant ascites.
12
Diagnostictests
A basic metabolic panel, including serum electrolytes, blood urea nitrogen and creatinine, hepatic function panel, including
serum albumin, and urinary sodium levels, provides measures of liver function, volume, and nutritional depletion, and helps to guide initial therapy. A diagnostic paracentesis should be performed for cell count with dierential, Gram stain with cul­ture, albumin level, and cytology. Cytology is 97% sensitive for carcinomatosis. Aserum-ascites albumin gradient >1.1gram/ dL is 97% accurate for the diagnosis of portal hypertension.

Management of ascites

Ascites causes discomfort and signicant reduction in the patient’s quality of life. Except for breast, lymphoma, and ovar­ian cancer, once cancer patients develop ascites, the 1-year sur­vival is less than 10% and the median survival time ranges from 1 to 4months. erefore, palliative therapies play a vital role in the management of these patients. Treatment options include dietary restriction, diuretics, repeated large-volume paracen­tesis, permanent indwelling catheters, implantable abdominal ports/drains, peritoneovenous shunts, and transjugular intra­hepatic portosystemic shunt (TIPS).
Diuretics and sodium restriction
Reduction in sodium intake to 1–2grams of salt per day, uid restriction to 1–2L/day, and diuretics are oen used as the rst line of therapy. However, there are no controlled trials assessing
6,9
their ecacy in malignant ascites.13 Nevertheless, diuretic ther­apy seems to be successful in 40–44% of patients with malig­nant ascites. with malignant ascites secondary to liver metastases and portal hypertension with low serum albumin levels,14 and usually do not work in the setting of carcinomatosis. ese are the patients who have high plasma renin activity and serum-ascites albu­min gradient >1.1g/dL and negative uid cytology.14 Even in this group of patients, diuretics and sodium restriction appear to be eective at the beginning of the disease and the ecacy decreases with progression of the disease.
Spironolactone is the most commonly used diuretic in malignant ascites and the dose ranges from 100 to 450mg/day. Other drugs, such as furosemide, may be added to this regi­men, particularly if urine sodium is <30mEq/L or the patient develops hyperkalemia on spironolactone. In general, the maximum ascitic reabsorption expected from ecient diuretic
5,8,12
Diuretics are more eective in treating patients
Interventional Oncology, Second Edition, ed. Jean-François H. Geschwind and Michael C. Soulen. Published by Cambridge University Press. ©Cambridge University Press2016
323
Section X:Specialized interventional techniques in cancercare
therapy is about 800mL, a weight loss of <1kg/day.15 Typical starting doses are 100mg spironolactone taken in the morn­ing, with or without 40mg furosemide. Daily weights should be recorded for 1week and basic metabolic panel rechecked. If the initial dose is not eective and the basic metabolic panel remains acceptable, the dose(s) can be doubled. is is con­tinued weekly until ascites becomes controlled or the patient reaches an intolerable dose, with a maximum dose of 160mg furosemide and 400mg spironolactone.
Medical therapy has the advantage of being non-invasive. e disadvantages are limited eectiveness in malignant ascites and the risks associated with medical treatment and diuretics, such as hyponatremia, hyperkalemia, dehydration, cramp­ing, renal insuciency (20%), and hepatorenal syndrome. erefore, these patients need continuous check of clinical parameters and electrolytes.
Large-volume paracentesis
Large-volume paracentesis is the most common method of managing malignant refractory ascites.12 Large-volume para­centesis provides temporary symptomatic relief in approxi­mately 90% of patients.
5,8,16
e drainage volume should be
Figure 31.1 Pigtail or Cope-type loop catheter (Cook Medical Inc.,
Bloomington, IN, USA).
adjusted depending on the patient’s condition and severity of ascites. Up to 4–6liters per session has been generally accepted to be safe, but patients with larger volumes can be tapped dry to maximize duration of benet.
17,18
Although there is no consen­sus on the speed of uid drainage, reports show that 30–90min­utes is generally well tolerated.19 Drainage can be accomplished with no image guidance. However, ultrasound guidance is fast, simple, and decreases the risks. Ultrasoundguidance is also important in patients with loculated ascites.
Some authors recommend simultaneous infusion of 5% dextrose during paracentesis to prevent hypotension.20 If the patient is hypotensive, dehydrated, or known to have severe renal impairment, simultaneous intravenous hydration should be considered. Concurrent albumin infusion has been shown to be beneciary in patients with cirrhotic-related ascites; how­ever, there is no evidence that its infusion is helpful in patients with malignant ascites.
21,22
e main advantage of large-volume paracentesis is that it provides rapid temporary symptomatic relief in approximately 90% of patients.
8,16
However, palliation is brief, with symptoms returning aer a few days, and repeated treatment is required at a mean interval of 10.4days.8 ere is risk of visceral injury, uid leak, peritonitis/sepsis, bowel perforation, hypotension, renal failure, or uid loculation. Chronic depletion of uid, electrolytes, and proteins leads to rapid deterioration in quality of life over 1–2months.
23
Permanent indwelling catheters
A permanent catheter should be oered to patients requiring frequent large-volume paracentesis. e patient will be able to easily drain ascites from home, eliminating the need for hos­pital visits. Options include non-tunneled pigtail or Cope-type loop catheters (Figure 31.1), tunneled catheters such as Tenckho (Figure31.2), PleurX (Denver Biomedical, Denver, CO) (Figure31.3), and the Asept Peritoneal Drainage System
Figure 31.2 Tenckhoff peritoneal dialysis catheters; straight and coiled (Cook
Medical Inc. Bloomington, IN, USA).
(pfmmedical, Cologne, Germany), and peritoneal Port-A­Caths (Smiths Medical, St. Paul, MN) (Figure31.4).
28,29,30,31,32
12,24,25,26,27,
ese catheters are placed with ultrasound or uoroscopy as guidance using intravenous conscious sedation. ey are usually placed as an outpatient procedure or during hospital admission. Asingle dose of prophylactic antibiotic is recom­mended prior to placement.
5,24
Risk of infection is multifactorial and depends on type of catheter, tunneling, operator’s experience, and sterility of the
324
Chapter31:Palliative procedures for ascites and eusion
AB
procedure.24 Tunneled catheters are associated with lower rate of infection and greater stability compared to non-tunneled catheters.
27,33
ey have a long-term success rate of 96%.34 Potential complications are leakage from the insertion site, catheter occlusion, catheter dislodgment, and cellulitis.34 Catheters may remain in place for many months. However, it has been recommended to remove them once daily drainage is less than 100mL in order to prevent infection.
35
Pigtail or Cope-type loop catheter
ese catheters are typically placed using ultrasound or uor­oscopy as guidance. Ascites is drained intermittently or con-
Figure 31.3 PleurX catheter (Denver Biomedical, Golden, CO, USA).
tinuously through gravity and capped. Complications occur in 24–35% of patients and include peritonitis, leakage, occlusion, and dislodgment.
26,29,36
Infection rates in these types of cath­eters are most likely related to the duration of catheter place­ment. erefore, non-tunneled catheters should be used only when the life expectancy is only a fewweeks.
Tenckho catheter
ese catheters have one or two Dacron cus that reside in the subcutaneous tissue. e tip may be straight or coiled (Figure 31.2). Scar tissue forms around the cu and lowers infection rate and dislodgment. ese catheters are placed under ultrasound and uoroscopy guidance to minimize com­plications, i.e., bowel perforation or bleeding.
5,29,33
e catheter is inserted either midline or in the lower quadrants (le or right, lateral to the course of inferior epigastric vessels) depending on where the largest area of ascites is observed on ultrasound (Figure31.5). e catheter is tunneled in the subcutaneous tis­sue. e tunnel is created in a lateral and inferior or lateral and superior direction. e cu should lie at least 2cm distal to the incision in the subcutaneous tissue. e tube should exit in a way that the site is visible to the patient for daily care and the tube is easily accessible to the patient for drainage. e proce­dure is performed as an outpatient procedure. In patients with
Figure 31.4 Peritoneal Port-A-Cath (Bard Medical, C. R. Bard Inc., Covington,
GA, USA).
dicult anatomy, CT guidance may beused.
Complications are catheter occlusion, leakage, cellulitis,
and peritonitis. Barnett and Rubins performed a literature
Figure 31.5 (A) Tenckhoff catheter
(white dotted lines) placed in midline and tunneled lateral and superior. (B) Tenckhoff catheter placed in the right lower quadrant; the subcutaneous tunnel is directed lateral and superior.
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Section X:Specialized interventional techniques in cancercare
Peritoneal Port-A-Catheters
ese ports are placed using the same technique that is used for placing venous or chest ports (i.e., mediport) and the port is placed in the subcutaneous pocket.
Two dierent types of abdominal ports have been reported
in the literature for management of malignant ascites.
31,32,37
e rst group used 6F or 8F vascular access ports.37 Ahigh com­plication rate was reported with this group, including occlu­sion, wound dehiscence, and high rate of bacterial peritonitis.37 e second group used 16F ports specially designed for perito­neal access.
31,32
e larger catheter size allowed faster drainage
of ascites.
ese ports can be accessed only using special non-coring needles, i.e., Huber needle. erefore, the main disadvantages of these ports are that health care professionals are required
Figure 31.6 PleurX catheter (white arrows) placed in the most dependent
area of the pelvis; the tunnel is directed superior and medial, forming a C loop.
for each drainage attempt. Additionally, drainage speed is very slow compared to other catheters.
Peritoneovenousshunts
Peritoneovenous shunt was introduced by Harry H. Leveen in 1974.38 Lund and Newkirk modied it in 1979 by adding a unidirectional pump that could be manually compressed. is variant was associated with a lower rate of occlusion. e most recent shunt is a modication known as the Denver shunt (CareFusion Corporation, San Diego, CA) (Figure31.7).
review and stated that peritonitis occurred in 4.4% of cancer patients who received a Tenckho catheter.33 In order to mini­mize leakage, the ascites should be well drained. erefore, it is recommended to drain the ascites, at the time of procedure, as much as can be safely achieved. Additionally, applying topi­cal surgical glue to the access incision may further minimize leakage.
Depending on the rate of ascites reaccumulation, each patient is instructed to drain the ascites frequently enough to avoid developing tense ascites. is usually results in draining every other day. Catheters are drained using intermittent-gravity drainage.
e shunt transmits the ascites uid from the peritoneal cavity back into the central venous circulation. e Denver shunt is made of two Silastic limbs connected by a pump cham­ber. is pump chamber contains either one or two one-way valves that open at a pressure of 1cm H2O. ese unidirec­tional valves prevent the reux of blood into the venous limb of the shunt. e two-valve model is more commonly used and is more eective in preventing reux.39 e one-valve type is used when the ascites uid is very viscous or the amount of daily production of ascites is very high.
39
e Denver shunt is available with two venous limb sizes of
11.5F and 15.5F. e smaller sizes should be used when access­ing the saphenous vein or subclavian vein. Most authors prefer
PleurX and Asept catheters
ese catheters are 15.5F Silastic, single-cu, tunneled cath­eters. ey are Food and Drug Administration-approved for draining both malignant pleural eusion and ascites. ese catheters have a one-way valve, making it a closed system, therefore the catheter will not drain unless connected to cus­tomized vacuum bottles. e PleurX catheter is placed using similar technique for Tenckho catheter placement, with minor dierences. e access site is superior and lateral to the umbilicus and the subcutaneous tunnel is made medially and superior. is method creates a C-shape tunnel and helps pre­vent uid leakage (Figure31.6).
Patients are instructed to drain their ascites every day for 2 weeks to allow the tunnel tract to heal. Aerwards, they are instructed to perform drainage as needed to prevent tight ascites.
Complications are similar to Tenckho catheter and include infection, occlusion, leakage, and peritonitis.
23,26,27
internal jugular vein for access. Both 11.5F and 15F calibers can be used in the internal jugular vein. e larger-size shunt occludes less commonly compared to the smaller-caliber catheter.
Since there is no external drainage catheter, there is no lifestyle limitation. Furthermore, there is no loss of uid or protein-rich ascites. erefore, this shunt is especially bene­cial in patients with chylous ascites.
e procedure is relatively simple and can be performed with moderate sedation, although some anesthesiologists will use deep sedation or general anesthesia. Some authors perform it as an outpatient procedure and some admit the patient for overnight observation.
40,41,42,43
Patients receiving Denver shunts are oen cachectic, and vulnerable to hypothermia due to the large exposed area of prepped surgical eld, so a warming device is recommended. e pump chamber should be placed over the lower ribs to permit manual compression of the pump. e distance from the pump chamber to the rst peritoneal
326
Chapter31:Palliative procedures for ascites and eusion
A BC
Figure 31.7 Denver shunt. (A) The internal jugular vein limb with the tip of the shunt at the level of the cavoatrial junction (arrows). (B) The Denver shunt pump
along the lower right chest wall (arrows). (C) The peritoneal limb of the shunt ending in the pelvis (arrows).
side hole is shorter than on tunneled catheters, so the distance from the planned pump pocket to the peritoneal entry site must be measured carefully to assure that the side holes will be well within the peritoneal cavity.
Since the longest part of the procedure is draining the patient’s ascites, the rst step is to place a large-bore drainage catheter at the planned peritoneal entry site. All ascites should be drained in order to minimize the risk of disseminated intra­vascular coagulopathy (DIC).44 While the ascites is draining, lidocaine with epinephrine is inltrated generously in the pump pocket. A2-cm incision is made cephalad to the planned location of the pocket, so that it is well away from the location that the patient will be pumping. e peritoneal end and pump are then tunneled down to the peritoneal entry site, taking care not to torque the tubing.
Once the peritoneal end of the device is in place, access to the internal jugular vein is obtained, and the long tunnel from the pump pocket incision to the jugular access site is anes­thetized. Along malleable metal tunneler comes with the kit. Using surgical glue to attach the venous limb to the tunneler is a useful trick to prevent dislodgment of the catheter while pull­ing through the long tunnel, especially in cachectic patients.
Once all the ascites is drained, high-ow tubing is used to instill 1liter of warm saline into the peritoneal cavity. e large-bore drain is then exchanged for the peritoneal end of the shunt via an included peel-away sheath, and the pump used to prime saline through the venous limb of tubing. e venous limb is then placed, and the incisions sutured andglued.
All patients should receive a prophylactic intravenous anti­biotic (rst-generation cephalosporin). Some authors con­tinue the antibiotic for 7–10 days postprocedure.39 Patients are instructed to pump the shunt 20 times twice a day, while recumbent in the morning and evening. e manual pumping should be performed while the patient is in the supine position, because the maximum ow occurs when the patient is supine.
e overall complication rate of peritoneovenous shunts is
25–40%.
16,41,45
Complications of peritoneovenous shunting are occlusion (most common at 24–31%), infection (4.5%), transi­ent fever (5%), thrombosis of central veins, pulmonary edema (10–16%), pulmonary embolism (6.7%), leak, congestive heart failure, dissemination of tumor, variceal bleeding, and DIC (2.4–9.3%).
6,46,47,48
Most patients develop a dilutional coagu­lopathy, and some authors use the term “subclinical” DIC. e maximum change in coagulation factors occurs immedi­ately postprocedure. ese changes gradually normalize from day 3 to 2weeks aer the shunt placement.
49,50
Transient fever happens in 5% of patients and should be dierentiated from infection.
e shunt drains ascites uid that may contain malignant cells into the central venous system, particularly the pulmon­ary vasculature. is complication has been described in mul­tiple case reports.
51,52,53
However, there is no clear evidence of clinically important hematogenous dissemination of tumor cells. Tarin etal. evaluated 14 patients with inoperable can­cer who were treated with peritoneovenous shunts for malig­nant ascites.54 ey concluded that clinical observations and ndings at necropsy indicated that peritoneovenous shunting does not result in the establishment of clinically important hematogenous metastases and that metastases do not neces­sarily develop even when large numbers of viable tumor cells regularly enter the blood.54 High protein content in the ascitic uid (>4.5g/L) was considered a contraindication to shunting because of higher risk of shunt occlusion; however, this can be prevented by using the 15.5F Denvershunt.
Patient selection is the most important step in treating patients with shunt. In general, complications are more frequent in patients with highly cellular ascites uid. Contraindications for placing Denver shunt include:congestive heart failure, his­tory of variceal bleeding, grossly bloody ascites, coagulation disorder (high international normalized ratio of > 2.0, low
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Section X:Specialized interventional techniques in cancercare
platelet counts <50×109), peritonitis, loculated ascites, liver failure (total bilirubin level >6mg/dL), and renal failure (if the patient is not on dialysis).
6,8,55
Massive pleural eusion, varices with no history of bleeding, and portal hypertension are rela­tive contraindications.
56,57
e shunt is eective in symptomatic relief in 70% of patients.6 e best response rate is seen in patients with ovarian or breast cancer (≥50%) and the worst response rate has been reported in patients with gastrointestinal cancers (10–15%).6 erefore, some authors classify gastrointestinal cancer as a contraindication for shunt placement.
6,16
e Denver shunt has the advantage of no external drain and no loss of uid or nutrients, therefore it provides excel­lent palliation and higher quality of life. As a result, the shunt should be used in patients with no contraindication and in whom life expectancy is long enough to derive benet. ere is no consensus on the time span; some authors advocate an expected survival of more than 1month and others more than 3months.
6,58,59,60
Overall, the mean functional survival time for peritoneovenous shunt is 12weeks, with 75% of patients eec­tively palliated until death.
8,50
beta-interferon was eective in 40% of patients with malig­nant ascites.72 e mechanism by which OK-432, a penicillin heat-treated powder of Su-strain Streptococcus pyogenes A3, acts is by activation of the cytotoxic T cell.
69,73
Intraperitoneal OK-432, alone or in combination with interleukin-2, demon­strated 60% response rate in 77 patients with gastrointestinal malignant ascites and 82% in 22 gastric cancer patients.
73,74
Side eects of immunotherapy include fever, chills, nausea, and bowel distension.
Intraperitoneal radioisotopes, like AU-198 or 32P chro­mic phosphate, have been used in the treatment of malignant ascites. However, they have been gradually abandoned because of the complex logistics involved.
75,76
An increased level of activity of VEGF has been reported in dierent cancers, including ovarian, gastric, pancreatic, colorectal, and sarcoma.77 erefore, a new concept of targeted therapy with the goal of reducing the production of ascites by inhibition of neovascularization of the tumor via inhibition of VEGF has been reported.77 Anti-VEGF drugs that have been investigated include anti-VEGF antibodies, anti-VEGF recep­tor antibodies, and metalloproteinase inhibitors. Bevacizumab, an anti-VEGF molecule, has been injected intraperitoneally in
Transjugular intrahepatic portosystemicshunts
TIPS creation is an eective treatment for refractory ascites.61 However, TIPS in regard to malignant ascites is only useful in cancer patients who have portal hypertension as the underly­ing mechanism of ascites formation.62 TIPS is contraindicated in patients with extensive liver metastasis, congestive heart fail­ure, liver failure, and hepatic encephalopathy. Complications of TIPS are hepatic encephalopathy, occlusion, and liver failure.
patients with malignant ascites of gastrointestinal, gynecologi­cal, and breast cancer origin, and was successful in decreasing ascites.77 Matrix metalloproteinases (MMP) increases vas­cular permeability similarly to VEGF. MMPs are utilized by cancer cells in the process of metastasis.78 MMP inhibitors were given intraperitoneally in mice with ovarian and colon cancer-induced ascites and the eusion resolved.
79
Intraperitoneal chemotherapy, immunotherapy, and targeted therapy all are promising medical options for the treatment of
Other suggested methods for treatment of
malignant ascites; however, their clinical application is not yet completely elucidated and further investigations are needed.
malignant ascites
Intraperitoneal chemotherapy has been studied with dif­ferent drugs and in various cancers. Most common drugs used are cisplatin, mitomycin, Adriamycin, bleomycin, and 5-uorouracil.
63,64,65
e outcomes are not encouraging, par­ticularly when used in patients with gastrointestinal malignan­cies. Ovarian cancer seems to be the most sensitive cancer to intraperitoneal chemotherapy.15 Since the chemotherapy drug needs to be evenly distributed in the peritoneal cavity, presence of loculated ascites is a contraindication for this technique. Overall, a temporary partial response is detected in less than half of the patients (<47%), and these results are based on isolated experiences with small numbers of patients. e com­plications include fever, abdominal pain, and adhesions in the longterm.
Immunotherapy with intraperitoneal injection has been reported with dierent success rates and dates back to the 1980s. ese include intraperitoneal injection of alpha- or beta-interferon,66 tumor necrosis factor(TNF),67 non-pathogenic forms of infectious agents like Corynebacterium parvum,68 and OK-432.
69,70
TNF inhibits the interaction between VEGF and its receptor, F1k-1. However, the ecacy of intraperitoneal TNF treatment has not been well documented in humans with malignant ascites.71 Gebbia etal. reported that intraperitoneal
Management of malignant eusions
Malignant pleural eusions are more commonly seen with breast and lung cancer, as well as lymphoma. Similarly to malignant ascites, the presence of malignant eusions indicates poor prognosis, with expected survival of a few months.
Malignant eusions may cause dyspnea, shortness of breath, cough and pleuritic chest pain, impairing the quality of life of cancer patients. e treatment options are thoracentesis or drainage catheter insertion.
Computed tomography (CT) of the chest within 1 week (or more recently if there has been an intervention) should be performed prior to performing the procedure.17 is CT scan provides important procedure-planning information and may also detect any loculations.
Thoracentesis
e initial thoracentesis is used for diagnostic purposes. e aspirate is sent for culture, cell count, cytology, pH level, and lactate dehydrogenase. It may also be useful to identify non-malignant eusions in patients with known malignancy.
Malignant eusions in patient with lymphoma or small cell lung cancer may resolve aer chemotherapy. In these patients
328