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1656 CASE REPORT HIRANO ET AL Ann Thorac SurgFREE JEJUNAL FLAP WITH VENOUS OCCLUSION 2010;89:1656–9
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ntra-ventricular septum is forced to bulge towards theeft ventricle reducing its compliance. At the sameime, the negative intrathoracic pressure during inspi-ation reduces left ventricular venous return as pulmo-ary vessels dilate. The combination results in a reduc-
ion in LV end diastolic volume, stroke volume andherefore systemic systolic pressure. Pulsus paradoxuss a clinical sign is not limited to cardiac tamponade,ut can be found in asthma or chronic obstructiveulmonary disease (COPD) requiring high inspiratoryressures, pulmonary embolus, tension pneumothoraxnd right ventricular infarction via differing physiolog-cal means.
There are a variety of anatomical sites in the dia-hragm through which abdominal contents can herni-te; anteriorly the foramen of Morgagni, posteriorlyhe foramen of Bochdalek, the dome in traumaticupture and most commonly the esophageal hiatus.he latter can manifest as two distinct types of hernia,ost commonly the sliding type or more significantly,
he rolling or paraoesophageal type. The hernia mayontain the gastric cardia, abdominal fat, small or largeowel. In normal circumstances these do not cause anyxtrinsic cardiac compression unless they involve in-rapericardial herniation or the hernial sac is large andhe hernia acute.
Un-repaired diaphragmatic herniae are well known toave potential sequelae for cardiovascular stability [5–13]articularly in intrapericardial hernia. Tamponade fol-
owing hiatus hernia repair is either seen early due toericardial haemo-effusion bleeding from surgical inju-ies to epicardial vessels and myocardium [2, 3] butecurrence causing tamponade has only been reported inhe late postoperative phase [4]. We believe that this ishe first reported case of cardiac tamponade due toernia recurrence occurring in the immediate postoper-tive period after hernia repair.Given that the immediate postoperative period is a
eriod of potential cardiorespiratory instability dueo altered consciousness, multi-factorial respiratoryompromise and cardiovascular stress due to anaes-hetic agents, pneumoperitoneum and fluid shifts, theonsequences of cardiac compression are potentiallyife-threatening.
The management of cardiac tamponade is two-fold: med-cal and definitive. Medical therapy is not sufficient alonend only provides time for intervention to occur. Theodality of the medical therapy is controversial and theo-
etically comprises fluid resuscitation, inotropy and after-oad reduction [1] although many clinicians would use aasopressor agent. Acute tamponade requires urgent inter-ention, typically pericardiocentesis for pericardial fluid orir and in the instance of hernia – urgent decompression byeduction. Without intervention, the condition is highlyikely to progress with the patient developing worseninghock, pulseless electrical activity and death.
Therefore, we conclude that the presence of shockymptoms and signs after diaphragmatic hernia repairequires the exclusion of cardiac tamponade as the un-
erlying cause and that the development of pulsus para-AY
2010 by The Society of Thoracic Surgeonsublished by Elsevier Inc
oxus in these patients heralds a medical emergencyecessitating swift surgical intervention. Furthermore,e propose that the definition of cardiac tamponade
hould be expanded to include causes which are extrap-ricardial but produce compression of the chamber of theeart and the characteristic clinical and pathophysiolog-
cal features of traditionally defined cardiac tamponade.
eferences
1. Spodick DH. Acute cardiac tamponade. N Engl J Med2003;349:684–90.
2. Kemppainen E, Kiviluoto T. Fatal cardiac tamponade afteremergency tension-free repair of a large paraesophagealhernia. Surg Endosc 2000;14:593.
3. Puchakayala MR, Abbey K, Haft J, Orringer MB. Delayedpericardial tamponade following transthoracic hiatal herniarepair. J Cardiothorac Vasc Anesth 2006;20:245–6.
4. Kovacich JC, Boyle EM Jr, Needle D, Maier RV. Iatrogenicintrapericardial diaphragmatic hernia associated with car-diac tamponade. J Trauma 2001;50:136–9.
5. Devbhandari MP, Khan MA, Hooper TL. Cardiac compres-sion following cardiac surgery due to unrecognised hiatushernia. Eur J Cardiothorac Surg 2007;32:813–5.
6. Wolfgang R, Lee JG. Endoscopic treatment of acute gastricvolvulus causing cardiac tamponade. J Clin Gastroenterol2001;32:336–9.
7. Kalra PR, Frymann R, Allen DR. Strangulated gastricvolvulus: an unusual cause of cardiac compressionresulting in electromechanical dissociation. Heart 2000;83:550.
8. Handley DV, Havill JH. Diaphragmatic rupture with cardiactamponade. Aust N Z J Surg 1975;45:155–7.
9. Fleyfel M, Ferreira JF, Gonzalez de Linares H, Merlier O,Harchaoui A. Cardiac tamponade after intrapericardial dia-phragmatic hernia. Br J Anaesth 1994;73:249–51.
0. Beddingfield GW. Cardiac tamponade due to traumatichernia of the diaphragm and pericardium. Ann Thorac Surg1968;6:178–80.
1. Adamthwaite DN, Snyders DC, Mirwis J. Traumatic pericar-diophrenic hernia: a report of 3 cases. Br J Surg 1983;70:117–9.
2. Loehning RW, Takaori M, Safar P. Circulatory collapsefrom anesthesia for diaphragmatic hernia. Arch Surg1965;90:109 –14.
3. Girzadas DV Jr, Fligner DJ. Delayed traumatic intrapericar-dial diaphragmatic hernia associated with cardiac tampon-ade. Ann Emerg Med 1991;20:1246–7.
urvival of a Free Jejunal Flapith Venous Occlusion
akashi Hirano, MD, PhD, Keigo Fujita, MD,atoru Kodama, MD, PhD, Shinsuke Takeno, MD, PhD,nd Masashi Suzuki, MD, PhD
epartments of Otolaryngology and Surgery II, Faculty ofedicine, Oita University, Oita, Japan
he jejunum offers numerous advantages for reconstruc-ion compared with other methods, despite transplanta-ion; however, total necrosis occasionally occurs in a
ccepted for publication Oct 9, 2009.
ddress correspondence to Dr Suzuki, 1-1 Idaigaoka, Hasama-machi,ufu, Oita, 8795593, Japan; e-mail: [email protected].
0003-4975/10/$36.00doi:10.1016/j.athoracsur.2009.10.020
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1657Ann Thorac Surg CASE REPORT HIRANO ET AL2010;89:1656–9 FREE JEJUNAL FLAP WITH VENOUS OCCLUSION
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ejunal flap caused by vascular thrombosis and loss ofxial blood supply. Survival of a free jejunal flap afternterruption of the vascular pedicle is rare. We report theurvival of a free jejunal flap, despite venous occlusion,t 5 weeks after the procedure. This may indicate thatenous neovascularization of a free jejunal flap is com-lete within 5 weeks after the operation.
(Ann Thorac Surg 2010;89:1656–9)© 2010 by The Society of Thoracic Surgeons
he jejunum offers numerous advantages for recon-struction over other methods despite transplanta-
ion, including good vascularity, natural mucus lubrica-ion, and maintenance of peristalsis [1]. Furthermore,onor-site morbidity is low and harvesting is relativelyimple. The overall mortality rate remains relatively lowbelow 5%), and the overall success rate exceeds 94% [2].espite the high success rates that have been reported,
otal necrosis occasionally occurs in a jejunal flap causedy vascular thrombosis and loss of axial blood supply.Survival of a free jejunal flap after interruption of the
ascular pedicle is rare, and only three reports exist inhe recent literature. They describe partial to nearly totalap survival after early loss of the axial blood supply at 10
o 19 days [3–5]. We report the survival of a free jejunalap, despite venous occlusion, at 5 weeks after therocedure. This may indicate that venous neovascular-
zation of a free jejunal flap is complete within 5 weeksfter the operation.
70-year-old man presented with dyspnea and hoarse-ess from rapid enlargement of the neck that had devel-ped during a 3-month period. Nasopharyngoscopyemonstrated a raised lesion in the pyriform sinus of theypopharynx. A computed tomography (CT) scan re-ealed an isodense 5- � 4-cm mass in the region of theeft lobe of the thyroid. Fine-needle aspiration cytology ofhe neck mass resulted in a diagnosis of squamous cellarcinoma of the thyroid (T4 N2c M0). He received 4000Gy to the primary tumor and the neck 4 weeks beforeurgical intervention.
He underwent a total laryngopharyngectomy and bi-ateral neck dissection. A free jejunal transfer was per-ormed to reconstitute the pharynx and cervical esopha-us. Revascularization was performed by anastomoses ofhe facial artery and left external jugular vein (Fig 1).
Surgical site infection arose 4 days after the operations a complication of diabetes mellitus and radiotherapy.he left internal jugular vein ruptured at 2 weeks, and
he internal jugular vein was ligated under general an-sthesia. Anastomosis to the external jugular vein re-ained intact. After the ligation of the internal jugular
ein, the neck skin showed wound disruption with necknfection, and the external jugular vein was exposed.
ealing by granulation occurred gradually. Blood circu-ation to the external jugular vein was completely oc-luded at 5 weeks after the operation; however, theejunal flap did not become congested and survived
otally. rHe began oral intake at 6 weeks after the procedure.igure 2 shows an enhanced CT scan and a 3-dimen-ional CT angiogram (3-D CTA) of the neck at 4 days andweeks after the operation. At 4 days postoperatively,
he venous circulation of the internal jugular vein andxternal jugular vein was intact. However, the venousirculation of both the internal and external jugular veinad disappeared by 5 weeks.
omment
arly survival of the free jejunal flap after transfer de-ends on the integrity of its vascular pedicle. Skin anduscle flaps have been shown to survive after disrup-
ions of their axial blood supplies at 10 days [6–8].urvival of transferred intestinal segments after early
nterruption of the vascular pedicle is rare, and only threeeports exist in the recent literature:
● Fisher [3] reported 2 patients with partial flapsurvival after pedicle disruption at days 10 and 14.For both cases, the anterior wall was necrotic, andsurvival of the posterior wall was ascribed tocollateral circulation that developed between theflap and neck tissues.
● Keen [4] reported a patient with entire flap sur-vival after pedicle disruption at 19 days.
● Chen and colleagues [5] reported that 3 freejejunal flaps lost their axial blood supplies duringthe early postoperative period. Neovasculariza-tion from the recipient bed was adequate to main-tain viability at 17 days postoperatively.
These reports demonstrated the viability of jejunalaps after early disruption of arterial blood supply andescribed partial to nearly total flap survival after pedicleisruption at 10 to 19 days. Here we report survival of a
ree jejunal flap after the early to late disruption of bloodow due to venous occlusion. Bertino and colleagues [9]
ig 1. A free jejunal transfer was performed by anastomoses of theacial artery and left external jugular vein (arrows). Internal jugularein was also exposed (arrowheads).
eported 5 patients with of free jejunal flap failures, of
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1658 CASE REPORT HIRANO ET AL Ann Thorac SurgFREE JEJUNAL FLAP WITH VENOUS OCCLUSION 2010;89:1656–9
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hich 3 resulted in venous thrombosis accompanied byleeding from the mouth at the onset of flap failure fromto 30 days after the operation. Their report indicated
hat 30 days after the procedure might not be sufficient tostablish venous neovascularization in a free jejunal flap.We investigated the timing of neovascularization of
ejunal flaps by reviewing several experimental studies.ordeiro and colleagues [10] investigated the timing ofeovascularization after pedicle ligation of jejunal flaps
n a dog model. A minimum of 4 weeks before ligation ofhe pedicle was necessary for flap survival. When inter-uption of the vascular pedicle was performed afterejunal transfer in a rat model, Yano and colleagues [11]eported that the survival rate of jejunal flaps in anrtery-ligated group was higher than that in a vein-igated group. Complete survival of the jejunal transfersn both the artery-ligated and vein-ligated groups re-uired 2 weeks after the jejunal transfers. This report
ndicated that venous occlusion was more dangeroushan arterial occlusion for successful transfer of intestinen a rat model, and that at least 2 weeks after theperation may be required to establish neovasculariza-ion of a free jejunal flap.
For our patient, the external jugular vein was the onlyoute of venous return from the jejunal flap because itad no collateral circulation. Survival of this free jejunalap without external jugular vein blood circulation indi-ated synthesis of venous vascularization in the flap. CT
ig 2. Enhanced postsurgical (bottom) com-uted tomography (CT) imaging and (top)-dimensional CT angiograms show the neckt (a) 4 days and (b) 5 weeks. (a) At 4 days,he venous circulation of the internal jugularein and external jugular vein (arrow) wasntact. (b) At 5 weeks, however, the venousirculation of both the internal and externalugular vein had disappeared.
maging and 3-D CTA confirmed the disappearance of
enous return of the external jugular vein at 5 weeks afterhe operation. Based on this case, we suggest that venouseovascularization of a free jejunal flap may be completeithin 5 weeks. Thus, for flap salvage, a conservative aproach is recommended for patients with venous disrup-
ion until 5 weeks or later.
eferences
1. Nakatsuka T, Harii K, Takushima A, at al. Prefabricated freejejunal transfer: a new reconstructive technique for highpharyngeal defects. Plast Reconstr Surg 1999;103:458–64.
2. Reece GP, Bengtson BP, Schusterman MA. Reconstruction ofthe pharynx and cervical esophagus using free jejunal trans-fer. Clin Plast Surg 1994;21:125–36.
3. Fisher J. Survival of transferred intestinal segments aftervascular pedicle interruption. Plast Reconstr Surg 1987;79:616–7.
4. Keen M. Survival of transferred intestine after interruptionof blood supply. Plast Reconstr Surg 1987;80:750–1.
5. Chen HC, Tan BK, Cheng MH, et al. Behavior of free jejunalflaps after early disruption of blood supply. Ann Thora Surg2002;73:987–9.
6. Khoo CTK, Bailey BN. The behaviour of free muscle andmusculocutaneous flaps after early loss of axial blood sup-ply. Br J Plast Surg 1982;35:43–6.
7. Tsur H, Daniller A, Strauch B. Neovascularization of skinflaps: route and timing. Plast Reconstr Surg 1980;66:85–90.
8. Black MJM, Chait L, McC.O’Brien B, et al. How soon may theaxial vessels of a surviving free flap be safely ligated: a study
in pigs. Br J Plast Surg 1978:31;295–9.
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1659Ann Thorac Surg CASE REPORT CHOW ET AL2010;89:1659–61 PULMONARY IMT INVADING GEJ
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9. Bertino G, Benazzo M, Occhini A, et al. Reconstruction of thehypopharynx after free jejunal flap failure: Is a second freejejunum transfer feasible? Oral Oncol 2008;44:61–4.
0. Cordeiro PG, Santamaria E, Hu QY, et al. The timing andnature of neovascularization of jejunal free flaps: an exper-imental study in a large animal model. Plast Reconstr Surg1999;103:1893–901.
1. Yano K, Hata Y, Matsuka K, et al. An experimental study ofischemia following subcutaneous heterotopic intestinalgraft: influence of arterial or venous occlusion. J ReconstrMicrosurg 1992;8:385–9.
ulmonary Inflammatoryyofibroblastic Tumor Invading
he Gastroesophageal Junctionimon C. Chow, MD, Ayoub Nahal, MD,erge Mayrand, MD, and Lorenzo E. Ferri, MD, PhD
ivision of Thoracic Surgery, Department of Pathology, andivision of Gastroenterology, McGill University, Montreal,uebec, Canada
ulmonary inflammatory myofibroblastic tumors are rareeoplasms of intermediate malignant potential. Mostatients are asymptomatic and present with incidentalndings on imaging. Dysphagia due to direct invasion
nto the esophagus is an extremely rare presentation ofhis uncommon tumor. The diagnosis is difficult to makereoperatively. Complete surgical resection offers theest chance of cure. We describe a 27-year-old man whoresented with progressive dysphagia and the diagnosisas only revealed after en bloc resection of the esopha-
us, cardia, and left lower lobe.(Ann Thorac Surg 2010;89:1659–61)
© 2010 by The Society of Thoracic Surgeons
ulmonary inflammatory myofibroblastic tumors arerare mesenchymal tumors of uncertain origin.
ence, they are also referred to as inflammatory pseudo-umors, plasma cell granulomas, xanthogranulomas, orbrous histiocytomas. This reflects their debatable iden-
ity of neoplasm vs inflammation. We present a casenvolving a symptomatic 27-year-old man with extremelyare invasion into the esophagus and describe the man-gement and outcome. These tumors are difficult toiagnose preoperatively; however, complete surgical re-ection offers definitive diagnosis and excellent treat-ent. The literature on the characteristics of these tu-ors will also be reviewed.
27-year-old man presented with a 6-month history ofague retrosternal pain and progressive dysphagia toolids without weight loss. An upper endoscopy demon-trated a tight gastroesophageal junction. Upon retroflex-on, a firm submucosal mass in the cardia was noted, with
ccepted for publication Sept 8, 2009.
ddress correspondence to Dr Ferri, McGill University Health Centre,
ontreal General Hospital, Rm L9-112, 1650 Cedar Ave, Montreal,uebec, H3G1A4, Canada; e-mail: [email protected]. v2010 by The Society of Thoracic Surgeonsublished by Elsevier Inc
small area of central mucosal ulceration. Multipleiopsy specimens of this area demonstrated only mildhronic inflammation, with focal areas of early goblet celletaplasia. A chest computed tomography image
howed a large 7- � 4-cm mass intricately involving theastroesophageal junction and left lower lobe, withoutvidence of regional lymphadenopathy or metastasesFig 1). This prompted several repeat upper endoscopiesnd an endoscopic ultrasound, biopsy specimens fromhich again revealed nonmalignant squamous or colum-ar epithelium with unremarkable smooth muscleundles.Given the persistence of symptoms and the failure to
erive a definitive diagnosis, the patient was referred forurgical resection. Because of the location and bulkyature of the tumor, a left thoracoabdominal approachas used. The mass was observed to be approximately� 5 cm, intimately involving the wall of the distal
sophagus, proximal cardia, and medial basal segment ofhe left lower lobe. An en bloc resection of the distalsophagus, gastric cardia, and a portion of the left lowerobe was performed with a 1-cm rim of diaphragm.
The surgical specimen consisted of large, irregular,ubbery to firm tumor showing a white fibrous appear-nce on cut section. The tumor was partially encapsu-ated at the pleuropulmonary aspect, while appearing
ore infiltrative at the esophagogastric end (Fig 2). Theumor epicenter was localized at the periphery of theesected lung from which it most likely originated andxtensively penetrated downward into the wall of thesophagus and stomach. It involved the pleura, theeriesophageal space, the gastric serosa, muscularis pro-ria, and submucosa of the esophagus, and stomach,ith no obvious ulceration into the mucosal surface.Histologically, the pulmonary margin, proximal esoph-
geal, and distal gastric mucosal margins were free ofumor. Focally, the tumor involved a surgical margin
icroscopically at the level of the diaphragm. Most of the
ig 1. A computed tomography scan demonstrates a large tumor in-
olving the left lower lobe, esophagus, and gastric cardia0003-4975/10/$36.00doi:10.1016/j.athoracsur.2009.09.082
