984
procedures. Given that the anterior wall of the aneurysmal aorta is in close proximity to, and often adherent to the posterior wall of the duodenum, the third and fourth segments of the duodenum are the most likely sites for the formation of aortoenteric fistulae, occurring in 83% of both primary and secondary AEF.1 Secondary AEF is an infrequent, although serious complication of aortic aneurysmal repair (both open and endovascular). The incidence of secondary aortoenteric fistulae varies between 0.36 and 1.6% of aortic repair patients.1–4 Incidences of arterial tree embolization coil and guidewire erosion into adjacent viscera, although rare, have been previously documented.5–7 Based on our findings on gastroscopy as well as intraoperatively, this is the likely responsible mechanism for AEF in our patient. It has been previously postulated that a shrinking AAA, in combination with continual transmission of pressure from the aorta on the duodenum could cause embolization coils to erode into the bowel lumen.5 This may have been the case in our patient, given the resolution of endoleak post-coil embolization and reduction in aneurysmal sac size. Embolization coil erosion into bowel is an uncommon cause of secondary AEF. Long-term follow-up of AAA repair patients with endoleaks and subsequent coil embolization is required to assess the risk of developing complications such as AEF. Removal of the embolization coils at the time of aortic repair following infected EVAR could have prevented AEF formation in this patient. This case identifies the importance of removing foreign bodies which have the potential to erode into the duodenum.
Images for surgeons
References 1. Cronenwett JL, Johnson W. Chapter 42. Rutherford’s Vascular Surgery. Philadelphia: Elsevier Saundaers, 2010; 663–74. 2. Ruby BJ, Cogbill TH. Aortoduodenal fistula 5 years after endovascular abdominal aortic aneurysm repair with the Ancure stent graft. J. Vasc. Surg. 2007; 45: 834–6. 3. Hallett JW, Marshall DM, Petterson TM et al. Graft-related complications after abdominal aortic aneurysm repair: reassurance from a 36 years population-based experience. J. Vasc. Surg. 1997; 25: 277–85. 4. Johnston KW. Nonruptured abdominal aortic aneurysm: six-year follow-up results from the multicentre prospective Canadian aneurysm study. J. Vasc. Surg. 1994; 20: 163–70. 5. Bertges DJ, Villella ER, Makaroun MS. Aortoenteric fistula due to endoleak coil embolisation after endovascular AAA repair. J. Endovasc. Ther. 2003; 10: 130–5. 6. Farres H, Gonzales AJ, Garrett HE. Aortoduodenal fistula after endograft repair of abdominal aneurysm secondary to a retained guidwire. J. Vasc. Surg. 2012; 56: 1413–5. 7. Onohara T, Okadome K, Mii S et al. Rupture of embolised coeliac artery aneurysm into the stomach: is coil embolisation an effective treatment for coeliac anastomotic pseudoaneurysm? Eur. J. Vasc. Surg. 1992; 6: 330–2.
Zacharia T. Bazzi, MBBS, GDAAD Raffi Qasabian, MBBS, BSc, FRACS (Vascular Surgery) Department of Vascular Surgery, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia doi: 10.1111/ans.12583
Rectal constriction secondary to metastatic micropapillary adenocarcinoma of the bladder In Australia, bladder cancer is one of the 10 most common cancers, responsible for 2217 new diagnosis of cancer as well as 925 deaths in 2007.1 While over 90% of bladder cancers are urothelial in origin, only 1–2% of them represent primary adenocarcinoma. They commonly metastasize to regional lymph nodes, liver, lung and bone.2 Although they may involve the distal gastrointestinal tract, this is usually through direct invasion and non-contiguous metastasis rarely happens.3 In the literature, rectal constriction secondary to transitional cell carcinoma of the bladder has been reported by different authors.4–6 We describe a case of metastatic micropapillary adenocarcinoma of the bladder resulting in rectal constriction. A 65-year-old man presents with an alteration of bowel habit on the background history of micropapillary adenocarcinoma of bladder. The patient’s bladder cancer was diagnosed 28 months earlier because of left flank pain. Ultrasound showed a large bladder mass causing left-sided ureteric obstruction. He subsequently underwent a radical cystoprostatectomy, bilateral pelvic lymph node dissection and ileal conduit formation. Histopathology from the operative specimen confirmed a pT3N0 micropapillary adenocarcinoma of bladder. The surgical margins were clear. Adjuvant chemotherapy with gemcitabine and cisplatin was given post-operatively. The patient recovered well from the operation.
Twenty-three months post-treatment, he described increasing constipation, faecal incontinence and tenesmus. Digital rectal examination found a fixed circumferential tumour. Magnetic resonance imaging scan (Fig. 1) confirmed extensive thickening of rectal submucosa extending through the lamina propria and muscularis mucosa, with extension beyond the wall from 1 o’clock to 6 o’clock. Several irregular lymph nodes were found in the mesorectal fascia. On colonoscopy (Fig. 2), there was circumferential rectal wall thickening with narrowing of the rectal and anal canal, while rectal mucosa appeared to be intact. The biopsy histopathology showed poorly differentiated infiltrative carcinoma of urothelial origin (positive for urothelial markers P53, CK34 and CK7). A defunctioning end colostomy was created prior to chemotherapy, from which he recovered quickly with relief of his presenting symptoms. He subsequently received pelvic radiotherapy for palliative management. In the literature, a 10% risk of rectal involvement by bladder cancer has been reported.5,7 In 1989, Stillwell et al. described two cases of rectal constriction secondary to direct invasion of transitional cell carcinoma (TCC) of the bladder.5 Although the mechanism of spread is different to our patient (non-contiguous metastasis), normal mucosa was observed on colonoscopy/proctoscopy in both studies. © 2014 Royal Australasian College of Surgeons
Images for surgeons
985
(a)
(b)
Fig. 1. Rectal magnetic resonance imaging (MRI), there is extensive thickening of the submucosa through lamina propria and muscularis mucosa with extension beyond the wall from 1 to 6 o’clock. The tumour extends down to within 0.7 cm of internal sphincter. Extension of tumour laterally to levator ani bilaterally, and extending forward anteriorly to reach mesorectal fascia. (a) T2 weighted coronal view of rectal MRI; (b) T2 weighted axial view of rectal MRI.
This is in keeping with the extrinsic pathological process underlying these tumours.8 Similar in presentation to our patient, Langenstroer et al. identified a case of non-contiguous rectal metastasis of TCC following cystectomy.6 In their study, the patient had a stage T3a TCC who developed rectal metastases 34 months after radical cystoprostatectomy.6 This raised the possibility of surgical seeding as the underlying mechanism of metastasis.6 However, a 2010 report has described concurrent finding of non-contiguous rectal metastasis and primary bladder cancer without surgical intervention, which suggested other mechanisms rather than surgical spread.3 Previous studies have suggested that recurrence after cystectomy usually happens within the first 2 years; however, Ferguson et al. has reported a case of metastasis with 4 years of disease-free survival.4,6 © 2014 Royal Australasian College of Surgeons
Fig. 2. Colonoscopy photos. There is circumferencial extrarectal thickening of lower rectum, which is fixed and extensive. No mucosal disease was shown.
In 1999, Slaton et al. recommended a stage-specific surveillance protocol post-cystectomy, for which computed tomography follow-up was recommended for up to 24 months for stage pT3 or above.9 However, this approach to surveillance will miss some rectal recurrences. The prognosis of metastatic bladder cancer has been universally poor, with a mean survival rate of 4.7 months.6 In both studies of Langenstroer et al. and Stillwell et al., the patients died within 1 year of diagnosis.5,6 Both adjuvant radiotherapy and chemotherapy has been attempted by Stillwell et al. for local control of rectal obstruction, but the response was poor.5 Therefore, the technique of diverting colostomy was employed by both Langenstroer et al. and for our patient for relief of obstructive symptoms.6 Adenocarcinoma of the bladder can rarely cause rectal metastasis and obstruction. Close tumour surveillance post-radical cystectomy may be the most effective measure in detecting early signs of rectal metastasis prior to development of constriction. This phenomenon is associated with very poor prognosis and the majority of patients die within a year.5,6 Diverting colostomy may be the most effective therapy for symptomatic control of rectal obstruction, however, no treatment has been shown to vastly improve overall prognosis.6
References 1. Australia CC. Bladder Cancer. Cancer Types June 2012 [Cited 7 Nov 2012.] Available from URL: http://www.cancer.org.au/about-cancer/ types-of-cancer/bladder-cancer.html 2. Tabbara WS, Mehio AR. Metastatic patterns of bladder carcinoma. Prog. Clin. Biol. Res. 1984; 162A: 145–60. 3. Ying-Yue J, Shen SH, Wang JH. Unusual presentation of urothelial carcinoma of the bladder with noncontiguous rectal and diffuse muscular skeletal metastases. J. Urol. 2010; 184: 1163–4. 4. Ferguson JL, Smart JM, Geldart TR, Mead GM, Tung KT. Bladder carcinoma recurrence post-cystectomy simulating rectal carcinoma. Clin. Radiol. 2007; 62: 177–80. 5. Stillwell TJ, Rife CC, Lieber MM. Bladder carcinoma presenting with rectal obstruction. Urology 1989; 34: 238–40.
986
Images for surgeons
6. Langenstroer P, Zacharias A, Almagro U, Dewire D. Annular constriction of the rectum secondary to transitional cell carcinoma of the bladder. Urology 1996; 47: 442–4. 7. Saitoh H, Hida M, Wakabayashi T, Lida T, Satoh T. Metastasis of urothelial tumors of the bladder: correlation between sites and number of organs involved. Tokai J. Exp. Clin. Med. 1982; 7: 517–26. 8. Fry DE, Amin M, Harbrecht PJ. Rectal obstruction secondary to carcinoma of the prostate. Ann. Surg. 1979; 189: 488–92. 9. Slaton JW, Swanson DA, Grossman HB, Dinney CP. A stage specific approach to tumor surveillance after radical cystectomy for transitional cell carcinoma of the bladder. J. Urol. 1999; 162 (3 Pt 1): 710–4.
Yi Ma,* MBBS, BMedSci Hamish Shilton,† MBBS Paul Strauss,‡ MBBCh, FCS (SA) *Department of Surgery, Alfred Health, The Alfred, †Department of General Surgery, Monash Health, Melbourne, and ‡Department of General Surgery, Central Gippland Health Service, Sale, Victoria, Australia doi: 10.1111/ans.12587
Fishbone perforation causing duodenocaval fistula and caval thrombus Duodenocaval fistula (DCF) following duodenal perforation by a foreign body is extremely rare and potentially life-threatening. We describe a 56-year-old woman who presented with several weeks of non-specific colicky abdominal pain, rigors and vomiting. On examination, she was hypotensive (systolic blood pressure 70 mmHg) and febrile (38.1°C). Her abdomen was soft but tender to palpation, particularly in the epigastrium and right upper quadrants. Bilateral pitting oedema to the mid-shin was also elicited. Initial investigations demonstrated a significantly elevated C-reactive protein (240.6 mg/L) and a leucocytosis (13.9/nL). Her haemoglobin, and chest and abdominal radiographs were within normal limits. An abdominal computerised tomography (CT) scan was performed which demonstrated a linear foreign body (4.3 cm long, 2 mm wide) bridging the lumen of the inferior vena cava (IVC) from the second part of the duodenum (Fig. 1). This finding suggested perforation of the fishbone from the duodenum into the vena cava resulting in a DCF. Additionally, a 3-cm floating caval thrombus was identified surrounding the intraluminal tip of the fishbone, causing partial caval obstruction (Fig. 1). The patient was promptly commenced on intravenous piperacillin and tazobactam to treat sepsis which was presumed to be secondary
(a)
(b)
to bacterial seeding from the DCF. An intravenous heparin infusion was also commenced. Her blood cultures later returned positive for Streptococcus constellatus. Furthermore, a suprarenal retrievable vena caval filter (Cook Celect VC filter, Cook Medical, Bloomington, IN, USA) was placed via a right sided transjugular access to minimize thromboembolic complications following and/or during fishbone extraction. Under endoscopic visualization, the fishbone was retrieved successfully with a snare without related haemorrhage (Fig. 2). Repeat contrast enhanced CT scan demonstrated complete removal of the fishbone with unchanged thrombotic filling defect within the IVC (Fig. 1). The filter was subsequently removed using continuous suction on the introducer sheath. The presence of the thrombus within the tip of the IVC filter was confirmed (Fig. 3). The patient made an expedient recovery, and was discharged home with a 3-month course of oral Warfarin therapy. A follow-up CT scan performed 3 months after hospital discharge demonstrated complete resolution of the caval thrombus. Pleasingly, the patient did not describe any symptoms consistent with pulmonary embolism. This case illustrates a rare presentation of foreign body penetrating the IVC via the duodenum. There have been several case reports describing duodenal and caval perforation by toothpicks and
(c)
Fig. 1. Computed tomography (CT) scan images (Somatom Definition AS + with 128 × 0.6-mm slice thickness and Omnipaque 300 contrast) demonstrating: (a) Horizontal view prepresentation CT scan (performed for surveillance post-rectal cancer surgery 1 year prior) revealing retrospectively identified calcified 43-mm long linear foreign body within the lumen of the duodenum segment 3. (b) Coronal view of the fistula and the associated intracaval thrombus. (c) Residual thrombus (post-fishbone endoscopic retrieval) located just below the right renal vein origin with regular position and expansion of the suprarenal inferior vena cave filter. A 14-mm filling defect was identified within the filter struts.
© 2014 Royal Australasian College of Surgeons
procedures. Given that the anterior wall of the aneurysmal aorta is in close proximity to, and often adherent to the posterior wall of the duodenum, the third and fourth segments of the duodenum are the most likely sites for the formation of aortoenteric fistulae, occurring in 83% of both primary and secondary AEF.1 Secondary AEF is an infrequent, although serious complication of aortic aneurysmal repair (both open and endovascular). The incidence of secondary aortoenteric fistulae varies between 0.36 and 1.6% of aortic repair patients.1–4 Incidences of arterial tree embolization coil and guidewire erosion into adjacent viscera, although rare, have been previously documented.5–7 Based on our findings on gastroscopy as well as intraoperatively, this is the likely responsible mechanism for AEF in our patient. It has been previously postulated that a shrinking AAA, in combination with continual transmission of pressure from the aorta on the duodenum could cause embolization coils to erode into the bowel lumen.5 This may have been the case in our patient, given the resolution of endoleak post-coil embolization and reduction in aneurysmal sac size. Embolization coil erosion into bowel is an uncommon cause of secondary AEF. Long-term follow-up of AAA repair patients with endoleaks and subsequent coil embolization is required to assess the risk of developing complications such as AEF. Removal of the embolization coils at the time of aortic repair following infected EVAR could have prevented AEF formation in this patient. This case identifies the importance of removing foreign bodies which have the potential to erode into the duodenum.
Images for surgeons
References 1. Cronenwett JL, Johnson W. Chapter 42. Rutherford’s Vascular Surgery. Philadelphia: Elsevier Saundaers, 2010; 663–74. 2. Ruby BJ, Cogbill TH. Aortoduodenal fistula 5 years after endovascular abdominal aortic aneurysm repair with the Ancure stent graft. J. Vasc. Surg. 2007; 45: 834–6. 3. Hallett JW, Marshall DM, Petterson TM et al. Graft-related complications after abdominal aortic aneurysm repair: reassurance from a 36 years population-based experience. J. Vasc. Surg. 1997; 25: 277–85. 4. Johnston KW. Nonruptured abdominal aortic aneurysm: six-year follow-up results from the multicentre prospective Canadian aneurysm study. J. Vasc. Surg. 1994; 20: 163–70. 5. Bertges DJ, Villella ER, Makaroun MS. Aortoenteric fistula due to endoleak coil embolisation after endovascular AAA repair. J. Endovasc. Ther. 2003; 10: 130–5. 6. Farres H, Gonzales AJ, Garrett HE. Aortoduodenal fistula after endograft repair of abdominal aneurysm secondary to a retained guidwire. J. Vasc. Surg. 2012; 56: 1413–5. 7. Onohara T, Okadome K, Mii S et al. Rupture of embolised coeliac artery aneurysm into the stomach: is coil embolisation an effective treatment for coeliac anastomotic pseudoaneurysm? Eur. J. Vasc. Surg. 1992; 6: 330–2.
Zacharia T. Bazzi, MBBS, GDAAD Raffi Qasabian, MBBS, BSc, FRACS (Vascular Surgery) Department of Vascular Surgery, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia doi: 10.1111/ans.12583
Rectal constriction secondary to metastatic micropapillary adenocarcinoma of the bladder In Australia, bladder cancer is one of the 10 most common cancers, responsible for 2217 new diagnosis of cancer as well as 925 deaths in 2007.1 While over 90% of bladder cancers are urothelial in origin, only 1–2% of them represent primary adenocarcinoma. They commonly metastasize to regional lymph nodes, liver, lung and bone.2 Although they may involve the distal gastrointestinal tract, this is usually through direct invasion and non-contiguous metastasis rarely happens.3 In the literature, rectal constriction secondary to transitional cell carcinoma of the bladder has been reported by different authors.4–6 We describe a case of metastatic micropapillary adenocarcinoma of the bladder resulting in rectal constriction. A 65-year-old man presents with an alteration of bowel habit on the background history of micropapillary adenocarcinoma of bladder. The patient’s bladder cancer was diagnosed 28 months earlier because of left flank pain. Ultrasound showed a large bladder mass causing left-sided ureteric obstruction. He subsequently underwent a radical cystoprostatectomy, bilateral pelvic lymph node dissection and ileal conduit formation. Histopathology from the operative specimen confirmed a pT3N0 micropapillary adenocarcinoma of bladder. The surgical margins were clear. Adjuvant chemotherapy with gemcitabine and cisplatin was given post-operatively. The patient recovered well from the operation.
Twenty-three months post-treatment, he described increasing constipation, faecal incontinence and tenesmus. Digital rectal examination found a fixed circumferential tumour. Magnetic resonance imaging scan (Fig. 1) confirmed extensive thickening of rectal submucosa extending through the lamina propria and muscularis mucosa, with extension beyond the wall from 1 o’clock to 6 o’clock. Several irregular lymph nodes were found in the mesorectal fascia. On colonoscopy (Fig. 2), there was circumferential rectal wall thickening with narrowing of the rectal and anal canal, while rectal mucosa appeared to be intact. The biopsy histopathology showed poorly differentiated infiltrative carcinoma of urothelial origin (positive for urothelial markers P53, CK34 and CK7). A defunctioning end colostomy was created prior to chemotherapy, from which he recovered quickly with relief of his presenting symptoms. He subsequently received pelvic radiotherapy for palliative management. In the literature, a 10% risk of rectal involvement by bladder cancer has been reported.5,7 In 1989, Stillwell et al. described two cases of rectal constriction secondary to direct invasion of transitional cell carcinoma (TCC) of the bladder.5 Although the mechanism of spread is different to our patient (non-contiguous metastasis), normal mucosa was observed on colonoscopy/proctoscopy in both studies. © 2014 Royal Australasian College of Surgeons
Images for surgeons
985
(a)
(b)
Fig. 1. Rectal magnetic resonance imaging (MRI), there is extensive thickening of the submucosa through lamina propria and muscularis mucosa with extension beyond the wall from 1 to 6 o’clock. The tumour extends down to within 0.7 cm of internal sphincter. Extension of tumour laterally to levator ani bilaterally, and extending forward anteriorly to reach mesorectal fascia. (a) T2 weighted coronal view of rectal MRI; (b) T2 weighted axial view of rectal MRI.
This is in keeping with the extrinsic pathological process underlying these tumours.8 Similar in presentation to our patient, Langenstroer et al. identified a case of non-contiguous rectal metastasis of TCC following cystectomy.6 In their study, the patient had a stage T3a TCC who developed rectal metastases 34 months after radical cystoprostatectomy.6 This raised the possibility of surgical seeding as the underlying mechanism of metastasis.6 However, a 2010 report has described concurrent finding of non-contiguous rectal metastasis and primary bladder cancer without surgical intervention, which suggested other mechanisms rather than surgical spread.3 Previous studies have suggested that recurrence after cystectomy usually happens within the first 2 years; however, Ferguson et al. has reported a case of metastasis with 4 years of disease-free survival.4,6 © 2014 Royal Australasian College of Surgeons
Fig. 2. Colonoscopy photos. There is circumferencial extrarectal thickening of lower rectum, which is fixed and extensive. No mucosal disease was shown.
In 1999, Slaton et al. recommended a stage-specific surveillance protocol post-cystectomy, for which computed tomography follow-up was recommended for up to 24 months for stage pT3 or above.9 However, this approach to surveillance will miss some rectal recurrences. The prognosis of metastatic bladder cancer has been universally poor, with a mean survival rate of 4.7 months.6 In both studies of Langenstroer et al. and Stillwell et al., the patients died within 1 year of diagnosis.5,6 Both adjuvant radiotherapy and chemotherapy has been attempted by Stillwell et al. for local control of rectal obstruction, but the response was poor.5 Therefore, the technique of diverting colostomy was employed by both Langenstroer et al. and for our patient for relief of obstructive symptoms.6 Adenocarcinoma of the bladder can rarely cause rectal metastasis and obstruction. Close tumour surveillance post-radical cystectomy may be the most effective measure in detecting early signs of rectal metastasis prior to development of constriction. This phenomenon is associated with very poor prognosis and the majority of patients die within a year.5,6 Diverting colostomy may be the most effective therapy for symptomatic control of rectal obstruction, however, no treatment has been shown to vastly improve overall prognosis.6
References 1. Australia CC. Bladder Cancer. Cancer Types June 2012 [Cited 7 Nov 2012.] Available from URL: http://www.cancer.org.au/about-cancer/ types-of-cancer/bladder-cancer.html 2. Tabbara WS, Mehio AR. Metastatic patterns of bladder carcinoma. Prog. Clin. Biol. Res. 1984; 162A: 145–60. 3. Ying-Yue J, Shen SH, Wang JH. Unusual presentation of urothelial carcinoma of the bladder with noncontiguous rectal and diffuse muscular skeletal metastases. J. Urol. 2010; 184: 1163–4. 4. Ferguson JL, Smart JM, Geldart TR, Mead GM, Tung KT. Bladder carcinoma recurrence post-cystectomy simulating rectal carcinoma. Clin. Radiol. 2007; 62: 177–80. 5. Stillwell TJ, Rife CC, Lieber MM. Bladder carcinoma presenting with rectal obstruction. Urology 1989; 34: 238–40.
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Images for surgeons
6. Langenstroer P, Zacharias A, Almagro U, Dewire D. Annular constriction of the rectum secondary to transitional cell carcinoma of the bladder. Urology 1996; 47: 442–4. 7. Saitoh H, Hida M, Wakabayashi T, Lida T, Satoh T. Metastasis of urothelial tumors of the bladder: correlation between sites and number of organs involved. Tokai J. Exp. Clin. Med. 1982; 7: 517–26. 8. Fry DE, Amin M, Harbrecht PJ. Rectal obstruction secondary to carcinoma of the prostate. Ann. Surg. 1979; 189: 488–92. 9. Slaton JW, Swanson DA, Grossman HB, Dinney CP. A stage specific approach to tumor surveillance after radical cystectomy for transitional cell carcinoma of the bladder. J. Urol. 1999; 162 (3 Pt 1): 710–4.
Yi Ma,* MBBS, BMedSci Hamish Shilton,† MBBS Paul Strauss,‡ MBBCh, FCS (SA) *Department of Surgery, Alfred Health, The Alfred, †Department of General Surgery, Monash Health, Melbourne, and ‡Department of General Surgery, Central Gippland Health Service, Sale, Victoria, Australia doi: 10.1111/ans.12587
Fishbone perforation causing duodenocaval fistula and caval thrombus Duodenocaval fistula (DCF) following duodenal perforation by a foreign body is extremely rare and potentially life-threatening. We describe a 56-year-old woman who presented with several weeks of non-specific colicky abdominal pain, rigors and vomiting. On examination, she was hypotensive (systolic blood pressure 70 mmHg) and febrile (38.1°C). Her abdomen was soft but tender to palpation, particularly in the epigastrium and right upper quadrants. Bilateral pitting oedema to the mid-shin was also elicited. Initial investigations demonstrated a significantly elevated C-reactive protein (240.6 mg/L) and a leucocytosis (13.9/nL). Her haemoglobin, and chest and abdominal radiographs were within normal limits. An abdominal computerised tomography (CT) scan was performed which demonstrated a linear foreign body (4.3 cm long, 2 mm wide) bridging the lumen of the inferior vena cava (IVC) from the second part of the duodenum (Fig. 1). This finding suggested perforation of the fishbone from the duodenum into the vena cava resulting in a DCF. Additionally, a 3-cm floating caval thrombus was identified surrounding the intraluminal tip of the fishbone, causing partial caval obstruction (Fig. 1). The patient was promptly commenced on intravenous piperacillin and tazobactam to treat sepsis which was presumed to be secondary
(a)
(b)
to bacterial seeding from the DCF. An intravenous heparin infusion was also commenced. Her blood cultures later returned positive for Streptococcus constellatus. Furthermore, a suprarenal retrievable vena caval filter (Cook Celect VC filter, Cook Medical, Bloomington, IN, USA) was placed via a right sided transjugular access to minimize thromboembolic complications following and/or during fishbone extraction. Under endoscopic visualization, the fishbone was retrieved successfully with a snare without related haemorrhage (Fig. 2). Repeat contrast enhanced CT scan demonstrated complete removal of the fishbone with unchanged thrombotic filling defect within the IVC (Fig. 1). The filter was subsequently removed using continuous suction on the introducer sheath. The presence of the thrombus within the tip of the IVC filter was confirmed (Fig. 3). The patient made an expedient recovery, and was discharged home with a 3-month course of oral Warfarin therapy. A follow-up CT scan performed 3 months after hospital discharge demonstrated complete resolution of the caval thrombus. Pleasingly, the patient did not describe any symptoms consistent with pulmonary embolism. This case illustrates a rare presentation of foreign body penetrating the IVC via the duodenum. There have been several case reports describing duodenal and caval perforation by toothpicks and
(c)
Fig. 1. Computed tomography (CT) scan images (Somatom Definition AS + with 128 × 0.6-mm slice thickness and Omnipaque 300 contrast) demonstrating: (a) Horizontal view prepresentation CT scan (performed for surveillance post-rectal cancer surgery 1 year prior) revealing retrospectively identified calcified 43-mm long linear foreign body within the lumen of the duodenum segment 3. (b) Coronal view of the fistula and the associated intracaval thrombus. (c) Residual thrombus (post-fishbone endoscopic retrieval) located just below the right renal vein origin with regular position and expansion of the suprarenal inferior vena cave filter. A 14-mm filling defect was identified within the filter struts.
© 2014 Royal Australasian College of Surgeons
