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Anesthetic evaluation and management of a patient with thoracic endometriosis syndrome presenting for elective surgery
Journal of Clinical Anesthesia 25 (2013) 220–223
Contents lists available at SciVerse ScienceDirect
Journal of Clinical Anesthesia journal homepage: www.JCAfulltextonline.com
Case Report
Anesthetic evaluation and management of a patient with thoracic endometriosis syndrome presenting for elective surgery Christopher A.J. Webb MD (Resident, Postdoctoral Fellow) a, Garret M. Weber MD (Resident, Postdoctoral Fellow) a, Richard K. Raker MD (Associate Clinical Professor) a,⁎ a
Department of Anesthesiology, College of Physicians & Surgeons/Columbia University Medical Center, New York, NY 10032, USA
a r t i c l e
i n f o
Article history: Received 12 December 2011 Received in revised form 11 September 2012 Accepted 3 October 2012 Keywords: Catamenial pneumothorax Endometriosis Pneumothorax Thoracic endometriosis Thoracic endometriosis syndrome
a b s t r a c t Thoracic endometriosis syndrome is a relatively uncommon disorder characterized by recurrent pneumothoraces, hemothorax, chest pain, dyspnea, and hemoptysis within 48 to 72 hours of menstruation. A 34 year old, ASA physical status 2 woman with recurrent catamenial pneumothoraces due to thoracic endometriosis syndrome is presented. After treatment with video-assisted thoracoscopic surgery, she underwent successful elective diagnostic abdominal laparoscopy without incident. The presence of parenchymal injury and damage predisposes these patients to ventilator-induced lung injury. Postponement of surgery until the intermenstrual period, with lung protective ventilation, allows patients with this disease to successfully undergo general anesthesia and surgery. © 2013 Elsevier Inc. All rights reserved.
1. Introduction Endometriosis is an estrogen-mediated, chronic inflammatory disease that is characterized by the presence of extrauterine endometrial tissue [1]. Clinically, endometriosis occurs in 5% to 10% of reproductive women and is defined by dyspareunia, dysmenorrhea, menorrhagia, and infertility [1,2]. While endometriosis is normally confined to the pelvic cavity, reports of thoracic endometriosis and associated pneumothoraces have been described [3,4]. Since the initial description by Barnes in 1953, numerous case reports have described the pathogenesis of thoracic endometriosis and catamenial pneumothoraces. The anesthetic management of a young woman undergoing elective laparoscopic surgery after video-assisted thoracoscopic surgery (VATS) with mechanical pleurodesis for recurrent pneumothoraces is presented. 2. Case report A 34 year old, ASA physical status 2 woman presented for diagnostic abdominal laparoscopic surgery for confirmation of endometriosis. She was previously being managed by thoracic surgery for recurrent right-sided pneumothoraces. Computed tomographic ⁎ Correspondence: Richard K. Raker, MD, Department of Anesthesiology, Columbia University College of Physicians & Surgeons/Columbia University Medical Center, 630 West 168th St., PH 527C, New York, NY 10032, USA. E-mail address: [email protected] (R.K. Raker). 0952-8180/$ – see front matter © 2013 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jclinane.2012.10.011
(CT) scan showed multiple blebs involving both the left and right pleura. Management of her second pneumothorax involved VATS with mechanical pleurodesis and patch repair of diaphragmatic defects. Multiple diaphragmatic defects, pleural blebs, and abnormal inflammatory tissue that were concerning for thoracic endometriosis were observed. However, tissue biopsies at that time were inconclusive for endometriosis. At the completion of the procedure, two-lung ventilation was resumed and a new right-sided chest tube was placed. The operative course was uneventful, and the patient was discharged home after a few days with plans for diagnostic abdominal laparoscopy with gynecological surgery. Because of the thoracic endometriosis, the gynecology team decided to postpone surgery until her current menstrual cycle had completed. She returned two weeks later for the elective abdominal laparoscopic procedure. Her previous anesthetic records were reviewed; preoperative chest radiographs confirmed resolution of her previous right-sided pneumothorax. On arrival at the operating room (OR), a peripheral intravenous (IV) catheter was placed and standard ASA monitors (four) were attached. The surgical team was present for induction, and emergency placement of a chest tube was readily available. While the patient had previously tolerated one-lung ventilation, the decision was made to attempt two-lung ventilation due to placement in the Trendelenburg position, the surgical technique, which included abdominal insufflation with carbon dioxide, and body habitus. As there are no clear guidelines regarding positive-pressure ventilation (PPV) after VATS and mechanical pleurodesis for pneumothoraces, the decision was
C.A.J. Webb et al. / Journal of Clinical Anesthesia 25 (2013) 220–223
made to proceed with two-lung ventilation with double-lumen tubes (DLTs) available for lung isolation. The patient was preoxygenated and denitrogenated with 100% oxygen for 5 minutes. Given the concern for trauma with mask ventilation, the airway was secured by rapid-sequence intubation. The patient underwent a smooth IV induction with fentanyl 150 μg, midazolam 2 mg, lidocaine 100 mg, rocuronium 60 mg, and propofol 150 mg. She was intubated without difficulty. General anesthesia was maintained with sevoflurane without nitrous oxide (N2O). To minimize ventilator-induced lung injury from high tidal volumes (VTs) and barotrauma [5], the ventilator mode was changed to pressure-controlled ventilation-volume guarantee (PCV-VG) using the Aisys Carestation [(previously Datex Ohmeda) GE Healthcare, Madison, WI, USA] anesthesia machine. Using lungprotective ventilation, VTs were set at 330 mL based on her ideal body weight of 55 kg, and peak inspiratory pressure (PIP) was set to 20 cm H2O [6,7]. The surgical team was advised to minimize abdominal insufflation pressures to 10 - 12 mmHg. The patient was placed in steep Trendelenburg position until PIP values reached a maximum of 20 cm H2O. Adequate ventilation was guided by capnography with end-tidal carbon dioxide less than 40 mmHg. The patient was fully paralyzed to maximize abdominal wall compliance. Operative findings showed severe retrograde menstruation with visualization of lesions suggestive of stage IV endometriosis. She had endometrial implants along the bladder surface, pelvic sidewalls, cecum, appendix, paracolic gutters, and diaphragm. Multiple biopsies were obtained and sent for diagnostic studies. Neuromuscular relaxation was reversed and the trachea was extubated with the patient deeply anesthetized to avoid any airway reactivity or impeded expiration. She was placed on nasal cannula oxygen and brought to the recovery room. Postoperative chest radiograph was negative for pneumothoraces. She was observed overnight and discharged home the following day. Pathology reports confirmed the diagnosis of endometriosis. One month later, the patient returned to the Thoracic Surgery Clinic with similar complaints of dyspnea and chest pain. Repeat chest imaging showed a recurrent, large, right-sided pneumothorax. She urgently underwent a second VATS with mechanical pleurodesis of both the pleura and diaphragm. Given the concern for development of a tension pneumothorax, a right-sided chest tube was placed in the OR before induction of anesthesia. A left 35-French DLT was placed and the left lung was ventilated with VTs of 200 - 250 mL of O2 and air. Large diaphragmatic defects were noted and repaired with a pericardial patch. Two-lung ventilation was resumed and the surgeon requested an increase in positive end-expiratory pressure to 15 cm H2O. With the right lung fully inflated, the surgical team attempted to identify areas of air leaks and potential sites for rupture. Overall, her perioperative course was again uneventful and she was discharged home. She is currently being followed by the thoracic surgery team for catamenial pneumothoraces and she continues to be symptom-free. 3. Discussion Thoracic endometriosis syndrome is a relatively uncommon disorder, with only a few hundred cases reported in the literature [8]. Characterized by recurrent pneumothoraces, hemothorax, chest pain, dyspnea, and hemoptysis 48 to 72 hours either before or after onset of menstruation, thoracic endometriosis syndrome presents the clinical challenge of a potential pneumothorax [8–11]. While the incidence of thoracic endometriosis syndrome is unknown, it is one of the most common extrapelvic manifestations of endometriosis [12]. Thoracic endometriosis syndrome was first described by Barnes in 1953 in a woman who suffered from endometriosis-induced hemothorax [13]. Subsequently, in 1958, Maurer et al documented the first pneumothoraces associated with thoracic endometriosis syndrome, termed catamenial pneu-
221
mothoraces [3]. In 1996, Joseph and Sahn performed a case series of over 100 women with thoracic endometriosis and found that 73% of women presented with a pneumothorax, 14% with a hemothorax, 7% with hemoptysis, and 6% with lung nodules only [8]. A recent retrospective study by Rousset-Jablonski et al looked at risk factors characterizing thoracic endometriosis and catamenial pneumothorax as compared with women who had noncatamenial and nonendometriosis-related pneumothorax. They showed that women with thoracic endometriosis presenting with catamenial pneumothoraces were more likely to have recurrent thoracic and/or scapular pain, infertility, and a history of pelvic surgery/uterine scrapings [14]. Three parallel mechanisms involving either a hormonal, metastatic, or anatomical model for the development of thoracic endometriosis have been described. The hormonal model, as described by Rossi and Goplerud in 1974, focuses on elevated levels of prostaglandin F2α during ovulation [15]. During menses, the sloughing endometrial tissue releases the potent vasoconstrictor prostaglandin F2α , producing vasospasm and bronchial constriction leading to rupture of pleural blebs [15]. However, this hypothesis alone cannot explain the pathogenesis of thoracic endometriosis syndrome since prophylactic therapy with nonsteroidal anti-inflammatory drugs does not decrease the incidence of recurrent pneumothoraces [11]. Second, if this hypothesis were true, one would expect both lungs to be equally involved rather than the clinical dominance for right-sided disease [8]. The second mechanism suggests a metastatic model for transplantation of endometrial tissue. Through right-sided congenital diaphragmatic fenestrations, transdiaphragmatic lymphatic channels, hematogenous embolization via pelvic veins, or direct invasion of the diaphragm, the pleural tissue becomes exposed to endometriotic cells [11,16,17]. During menstruation, the endometrial cells engorge and eventually slough, causing localized areas of inflammation and parietal irritation [18]. The latter results in chest pain and ultimately pulmonary air leaks, leading to the development of a pneumothorax [18]. Finally, the anatomical model is centered around the concept of entrainment of air into the peritoneal cavity through the vaginal canal. During menstruation, the cervical mucus plug is lost and creates a direct communication between the environment and the peritoneum via patent fallopian tubes [11,15]. This is evidenced by the fact that subdiaphragmatic air has been found on chest radiographs in women with catamenial pneumothoraces [19]. The influx of air into the peritoneum communicates with the pleural space through predominantly right-sided diaphragmatic defects and fenestrations [20,21]. These right-sided fenestrations/defects are similarly found in other obstetric complications such as Meigs’ syndrome, in which right-sided pleural effusions predominate [22]. However, if this model were true, one would expect more women to suffer from catamenial pneumothoraces, or at least demonstrate radiographic evidence of subdiaphragmatic air during menstruation. There is growing evidence that perhaps the pathogenesis of thoracic endometriosis syndrome incorporates aspects of all three models and is based on retrograde regurgitation of endometriotic cells [23,24]. In one of the largest case series involving over 100 patients, Joseph and Sahn discovered that more than 55% of women with thoracic endometriosis syndrome had evidence of pelvic endometriosis found during diagnostic laparoscopy or laparotomy [8]. Once in the peritoneum, these endometriotic cells follow the clockwise peristaltic movement of the peritoneal fluid from the left peritoneal gutter, across the pelvic floor toward the right peritoneal gutter, ultimately reaching the peritoneal surface of the right diaphragm [25,26]. It is this migration toward the right diaphragm that most likely accounts for the 90% incidence of right-sided pneumothoraces in woman with thoracic endometriosis syndrome [8]. Endometrial tissue exhibits increased proteolytic activity, unlike nonendometrial tissue [27]. This upregulated proteolytic activity combined with the
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enhanced invasiveness of endometrial tissue by heat-stable proteins found in the peritoneal fluid enables the implanted tissue to invade the diaphragm and adhere to the lung parenchyma [24,28]. During menses, the sloughing endometrial tissue releases the potent vasoconstrictor, prostaglandin F2α. This vasoconstrictor causes vasospasm and bronchial constriction, leading to localized ischemia and pleural blebs, respectively [15]. Both damaged alveolar tissue and pleural blebs/bullae are susceptible to rupture during bronchospasm, impeded expiration, or PPV [20,29]. As described by Ting et al [30], 4 primary mechanisms cause ventilator-induced lung injury, leading to a pneumothorax. The first mechanism occurs in bullae that either fail to communicate or poorly communicate with the bronchial tree. In this situation, the use of N2O will cause expansion and ultimately rupture of overdistended bullae. The second pathway occurs in overly compliant bullae with good bronchial tree communication. In this situation, the overly compliant bullae will receive a larger portion of the VT as compared with normal or noncompliant bullae. Again, overdistension leads to bullae rupture. The third pathway involves the ball-valve mechanism that traps air during inspiration such that progressive expansion leads to rupture. The final mechanism involves bullae with varying degrees of wall thickness or unevenly distributed pleural pressure that results in rupture during forced or impeded expiration [30,31]. Treatment of endometriosis traditionally has included either a medically induced oophorectomy with gonadotropin-releasing hormone (GnRH) agonists, Danazol, or oral contraceptives. Surgical management includes removal of extrapelvic endometrial tissue along with a hysterectomy/salpingoopherectomy [1]. Management of thoracic endometriosis syndrome is similar but combines VATS with mechanical or chemical pleurodesis for treatment of associated catamenial pneumothoraces [11,29]. Presurgical treatment of endometriosis remains controversial. To date, there are no clear guidelines regarding preoperative medical management of endometriosis. A few studies have shown a reduction in size of endometriosis and thus improvement in Retrospective American Fertility Society scores (rAFS) but no improvement in outcomes [32,33]. Preoperative hormonal therapy also increases the amount of intrapelvic fibrosis, which complicates differentiation of normal tissue from endometrial tissue during dissection [32,33]. Our patient presented with recurrent, right-sided pneumothoraces, although initial pleural biopsies were inconclusive of endometrial tissue. Of note, multiple pleural blebs were observed on gross examination. This was consistent with previous findings in which nearly 25% of patients with thoracic endometriosis syndrome exhibited bullae or blebs as the sole pleural lesions, while roughly 10% of patients have absolutely no pathologic pleural findings [10]. While multiple diaphragmatic defects and fenestrations were noted during VATS, diaphragmatic biopsies were not obtained. Owing to the clinical diagnosis of thoracic endometriosis syndrome, the decision was made to postpone diagnostic laparoscopy to ensure resolution of her concurrent menstrual cycle and decrease the risk of intraoperative pneumothoraces. As there are no clear guidelines for delaying surgery or PPV after VATS with mechanical pleurodesis and patch repair, the patient was cleared by the Thoracic Surgery service for her laparoscopic procedure. Gamaleldin et al reported their anesthetic management of a patient with a known catamenial pneumothorax treated with presurgical placement of a chest tube after induction of anesthesia [34]. While our case was similar, our patient’s pneumothorax had resorbed during the interval time. However, she still presented significant risk for development of intraoperative pneumothoraces due to her presumed diagnosis of thoracic endometriosis and preoperative CT scan showing bilateral pleural blebs and bullae. Our primary anesthetic concern for the case was the development of an intraoperative pneumothorax and subsequent conversion to a
tension pneumothorax during PPV. While the recurrence rates for pneumothoraces managed with either open thoracotomy with pleurectomy or VATS with mechanical pleurodesis is 1% and 5%, respectively, the recurrence rates in patients with thoracic endometriosis and surgical management are unknown [35]. During the VATS cases, the concern for intraoperative pneumothorax was less likely as a chest tube had been placed prior to induction of general anesthesia. In addition, placement of a DLT allowed for deflation of the affected lung and ventilation of the dependent lung with low VTs. To minimize further lung injury and risk of intraoperative pneumothorax, surgery was postponed until the intermenstrual period, during which hormonal levels are normal and pleural bleb/ bullae are least susceptible to rupture. During this period, women with thoracic endometriosis syndrome are least likely to develop signs and symptoms of the syndrome [8–10]. Neuraxial anesthesia for thoracic endometriosis syndrome, as described by Yokoyama et al, was considered but deferred owing to both the surgical position and laparoscopic technique required. General anesthesia and placement of an endotracheal tube using rapid-sequence intubation was determined to be the most optimal technique, since even low airway pressures generated during bag-mask ventilation may lead to hyperinflation and injury [31]. To minimize barotrauma, PIP values were limited to less than 25 cm H2O, while lung protective ventilator settings with low VTs based on ideal body weight and a high respiratory rate enabled adequate ventilation [36,37]. While PCV-VG was utilized, it should be noted that studies comparing modes of ventilation in patients with known lung injury have only demonstrated lower PIP values with no difference in outcomes [38,39]. Abdominal wall relaxation with muscle relaxants allowed for adequate abdominal insufflation requiring minimal pressures. Finally, tracheal extubation while the patient was deeply anesthetized further prevented barotrauma associated with impeded expiration. In summary, the anesthetic management of a patient with thoracic endometriosis after recent VATS with mechanical pleurodesis, who presented for elective diagnostic abdominal laparoscopic surgery, is reported. Preoperative evaluation should involve collaboration with the patient’s gynecologist, thoracic surgeon, and primary surgical team to ensure that elective surgery is delayed until the intermenstrual period. Complications associated with thoracic endometriosis syndrome are least likely to occur during that time. If PPV is necessary, strategies such as optimizing patient position, using lung-protective ventilation, limiting abdominal insufflation pressures during pneumoperitoneum, and maintaining a deep level of anesthesia will aid the anesthesiologist in safely managing these patients. Options for converting to one-lung ventilation in addition to emergency management of a tension pneumothorax should be readily available.
References [1] Giudice LC, Kao LC. Endometriosis. Lancet 2004;364(9447):1789–99. [2] Bulun SE. Endometriosis. N Engl J Med 2009;360:268–79. [3] Maurer ER, Schaal JA, Mendez FL Jr. Chronic recurring spontaneous pneumothorax due to endometriosis of the diaphragm. J Am Med Assoc 1958;168:2013–4. [4] Channabasavaiah AD, Joseph JV. Thoracic endometriosis: revisiting the association between clinical presentation and thoracic pathology based on thoracoscopic findings in 110 patients. Medicine 2010;89:183–8. [5] Fernández-Pérez ER, Keegan MT, Brown DR, Hubmayr RD, Gajic O. Intraoperative tidal volume as a risk factor for respiratory failure after pneumonectomy. Anesthesiology 2006;105:14–8. [6] Amato MB, Barbas CS, Medeiros DM, et al. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med 1998;338:347–54. [7] Parsons PE, Eisner MD, Thompson BT. et al; NHLBI Acute Respiratory Distress Syndrome Clinical Trials Network. Lower tidal volume ventilation and plasma cytokine markers of inflammation in patients with acute lung injury. Crit Care Med 2005;33:1–6 [discussion 230-2]. [8] Joseph J, Sahn SA. Thoracic endometriosis syndrome: new observations from an analysis of 110 cases. Am J Med 1996;100:164–70.
C.A.J. Webb et al. / Journal of Clinical Anesthesia 25 (2013) 220–223 [9] Joseph J, Reed CE, Sahn SA. Thoracic endometriosis. Recurrence following hysterectomy with bilateral salpingo-oophorectomy and successful treatment with talc pleurodesis. Chest 1994;106:1894–6. [10] Korom S, Canyurt H, Missbach A, et al. Catamenial pneumothorax revisited: clinical approach and systematic review of the literature. J Thorac Cardiovasc Surg 2004;128:502–8. [11] Peikert T, Gillespie DJ, Cassivi SD. Catamenial pneumothorax. Mayo Clin Proc 2005;80:677–80. [12] Jubanyik KJ, Comite F. Extrapelvic endometriosis. Obstet Gynecol Clin North Am 1997;24:411–40. [13] Barnes J. Endometriosis of the pleura and ovaries. J Obstet Gynaecol Br Emp 1953;60:823–4. [14] Rousset-Jablonski C, Alifano M, Plu-Bureau G, et al. Catamenial pneumothorax and endometriosis-related pneumothorax: clinical features and risk factors. Hum Reprod 2011;26:2322–9. [15] Rossi NP, Goplerud CP. Recurrent catamenial pneumothorax. Arch Surg 1974;109: 173–6. [16] Slasky BS, Siewers RD, Lecky JW, Zajko A, Burkholder JA. Catamenial pneumothorax: the roles of diaphragmatic defects and endometriosis. AJR Am J Roentgenol 1982;138:639–43. [17] Shearin RP, Hepper NG, Payne WS. Recurrent spontaneous pneumothorax concurrent with menses. Mayo Clin Proc 1974;49:98–101. [18] Van Schil PE, Vercauteren SR, Vermeire PA, Nackaerts YH, Van Marck EA. Catamenial pneumothorax caused by thoracic endometriosis. Ann Thorac Surg 1996;62:585–6. [19] Roth T, Alifano M, Schussler O, Magdaleinat P, Regnard JF. Catamenial pneumothorax: chest X-ray sign and thoracoscopic treatment. Ann Thorac Surg 2002;74:563–5. [20] Lillington GA, Mitchell SP, Wood GA. Catamenial pneumothorax. JAMA 1972;219: 1328–32. [21] Cowl CT, Dunn WF, Deschamps C. Visualization of diaphragmatic fenestration associated with catamenial pneumothorax. Ann Thorac Surg 1999;68:1413–4. [22] Majzlin G, Stevens FL. Meigs' syndrome. Case report and review of literature. J Int Coll Surg 1964;42:625–30. [23] Sampson JA. Peritoneal endometriosis due to the menstrual dissemination of endometrial tissue into the peritoneal cavity. Am J Obstet Gynecol 1927;14: 422–69. [24] Gaetje R, Kotzian S, Herrmann G, Baumann R, Starzinski-Powitz A. Invasiveness of endometriotic cells in vitro. Lancet 1995;346(8988):1463–4.
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[25] Suginami H. A reappraisal of the coelomic metaplasia theory by reviewing endometriosis occurring in unusual sites and instances. Am J Obstet Gynecol 1991;165:214–8. [26] Kruitwagen RF, Thomas C, Poels LG, Koster AM, Willemsen WN, Rolland R. High CA-125 concentrations in peritoneal fluid of normal cyclic women with various infertility-related factors as demonstrated with two-step immunoradiometric assay. Fertil Steril 1991;56:863–9. [27] Sillem M, Prifti S, Neher M, Runnebaum B. Extracellular matrix remodelling in the endometrium and its possible relevance to the pathogenesis of endometriosis. Hum Reprod Update 1998;4:730–5. [28] Starzinski-Powitz A, Gaetje R, Zeitvogel A, et al. Tracing cellular and molecular mechanisms involved in endometriosis. Hum Reprod Update 1998;4:724–9. [29] Alifano M. Catamenial pneumothorax. Curr Opin Pulm Med 2010;16:381–6. [30] Ting EY, Klopstock R, Lyons HA. Mechanical properties of pulmonary cysts and bullae. Am Rev Respir Dis 1963;87:538–44. [31] Yokoyama T, Tomoda M, Kanbara T, Nishiyama T, Manabe M. Epidural anesthesia for a patient with catamenial pneumothorax. Masui 2001;50:290–2. [32] Tsujioka H, Inoue Y, Emoto M, et al. The efficacy of preoperative hormonal therapy before laparoscopic cystectomy of ovarian endometriomas. J Obstet Gynaecol Res 2009;35:782–6. [33] Yap C, Furness S, Farquhar C. Pre and post operative medical therapy for endometriosis surgery.Cochrane Database Syst Rev 2004(3):CD003678. [34] Gamaleldin H, Tetzlaff JE, Whalley D. Anesthetic implications of thoracic endometriosis. J Clin Anesth 2002;14:36–8. [35] MacDuff A, Arnold A, Harvey J; BTS Pleural Disease Guideline Group. Management of spontaneous pneumothorax: British Thoracic Society Pleural Disease Guideline 2010. Thorax 2010;65(Suppl 2):ii18–31. [36] Slinger P. Perioperative lung injury. Best Pract Res Clin Anaesthesiol 2008;22: 177–91. [37] Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med 2000;342:1301–8. [38] Guldager H, Nielsen SL, Carl P, Soerensen MB. A comparison of volume control and pressure-regulated volume control ventilation in acute respiratory failure. Crit Care 1997;1:75–7. [39] Riverso P, Bernardi PL, Corsa D, Morra MG, Paganini G, Parigi F. A comparison of ventilation techniques in ARDS. Volume controlled vs pressure regulated volume control. Minerva Anestesiol 1998;64:339–43.
Contents lists available at SciVerse ScienceDirect
Journal of Clinical Anesthesia journal homepage: www.JCAfulltextonline.com
Case Report
Anesthetic evaluation and management of a patient with thoracic endometriosis syndrome presenting for elective surgery Christopher A.J. Webb MD (Resident, Postdoctoral Fellow) a, Garret M. Weber MD (Resident, Postdoctoral Fellow) a, Richard K. Raker MD (Associate Clinical Professor) a,⁎ a
Department of Anesthesiology, College of Physicians & Surgeons/Columbia University Medical Center, New York, NY 10032, USA
a r t i c l e
i n f o
Article history: Received 12 December 2011 Received in revised form 11 September 2012 Accepted 3 October 2012 Keywords: Catamenial pneumothorax Endometriosis Pneumothorax Thoracic endometriosis Thoracic endometriosis syndrome
a b s t r a c t Thoracic endometriosis syndrome is a relatively uncommon disorder characterized by recurrent pneumothoraces, hemothorax, chest pain, dyspnea, and hemoptysis within 48 to 72 hours of menstruation. A 34 year old, ASA physical status 2 woman with recurrent catamenial pneumothoraces due to thoracic endometriosis syndrome is presented. After treatment with video-assisted thoracoscopic surgery, she underwent successful elective diagnostic abdominal laparoscopy without incident. The presence of parenchymal injury and damage predisposes these patients to ventilator-induced lung injury. Postponement of surgery until the intermenstrual period, with lung protective ventilation, allows patients with this disease to successfully undergo general anesthesia and surgery. © 2013 Elsevier Inc. All rights reserved.
1. Introduction Endometriosis is an estrogen-mediated, chronic inflammatory disease that is characterized by the presence of extrauterine endometrial tissue [1]. Clinically, endometriosis occurs in 5% to 10% of reproductive women and is defined by dyspareunia, dysmenorrhea, menorrhagia, and infertility [1,2]. While endometriosis is normally confined to the pelvic cavity, reports of thoracic endometriosis and associated pneumothoraces have been described [3,4]. Since the initial description by Barnes in 1953, numerous case reports have described the pathogenesis of thoracic endometriosis and catamenial pneumothoraces. The anesthetic management of a young woman undergoing elective laparoscopic surgery after video-assisted thoracoscopic surgery (VATS) with mechanical pleurodesis for recurrent pneumothoraces is presented. 2. Case report A 34 year old, ASA physical status 2 woman presented for diagnostic abdominal laparoscopic surgery for confirmation of endometriosis. She was previously being managed by thoracic surgery for recurrent right-sided pneumothoraces. Computed tomographic ⁎ Correspondence: Richard K. Raker, MD, Department of Anesthesiology, Columbia University College of Physicians & Surgeons/Columbia University Medical Center, 630 West 168th St., PH 527C, New York, NY 10032, USA. E-mail address: [email protected] (R.K. Raker). 0952-8180/$ – see front matter © 2013 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jclinane.2012.10.011
(CT) scan showed multiple blebs involving both the left and right pleura. Management of her second pneumothorax involved VATS with mechanical pleurodesis and patch repair of diaphragmatic defects. Multiple diaphragmatic defects, pleural blebs, and abnormal inflammatory tissue that were concerning for thoracic endometriosis were observed. However, tissue biopsies at that time were inconclusive for endometriosis. At the completion of the procedure, two-lung ventilation was resumed and a new right-sided chest tube was placed. The operative course was uneventful, and the patient was discharged home after a few days with plans for diagnostic abdominal laparoscopy with gynecological surgery. Because of the thoracic endometriosis, the gynecology team decided to postpone surgery until her current menstrual cycle had completed. She returned two weeks later for the elective abdominal laparoscopic procedure. Her previous anesthetic records were reviewed; preoperative chest radiographs confirmed resolution of her previous right-sided pneumothorax. On arrival at the operating room (OR), a peripheral intravenous (IV) catheter was placed and standard ASA monitors (four) were attached. The surgical team was present for induction, and emergency placement of a chest tube was readily available. While the patient had previously tolerated one-lung ventilation, the decision was made to attempt two-lung ventilation due to placement in the Trendelenburg position, the surgical technique, which included abdominal insufflation with carbon dioxide, and body habitus. As there are no clear guidelines regarding positive-pressure ventilation (PPV) after VATS and mechanical pleurodesis for pneumothoraces, the decision was
C.A.J. Webb et al. / Journal of Clinical Anesthesia 25 (2013) 220–223
made to proceed with two-lung ventilation with double-lumen tubes (DLTs) available for lung isolation. The patient was preoxygenated and denitrogenated with 100% oxygen for 5 minutes. Given the concern for trauma with mask ventilation, the airway was secured by rapid-sequence intubation. The patient underwent a smooth IV induction with fentanyl 150 μg, midazolam 2 mg, lidocaine 100 mg, rocuronium 60 mg, and propofol 150 mg. She was intubated without difficulty. General anesthesia was maintained with sevoflurane without nitrous oxide (N2O). To minimize ventilator-induced lung injury from high tidal volumes (VTs) and barotrauma [5], the ventilator mode was changed to pressure-controlled ventilation-volume guarantee (PCV-VG) using the Aisys Carestation [(previously Datex Ohmeda) GE Healthcare, Madison, WI, USA] anesthesia machine. Using lungprotective ventilation, VTs were set at 330 mL based on her ideal body weight of 55 kg, and peak inspiratory pressure (PIP) was set to 20 cm H2O [6,7]. The surgical team was advised to minimize abdominal insufflation pressures to 10 - 12 mmHg. The patient was placed in steep Trendelenburg position until PIP values reached a maximum of 20 cm H2O. Adequate ventilation was guided by capnography with end-tidal carbon dioxide less than 40 mmHg. The patient was fully paralyzed to maximize abdominal wall compliance. Operative findings showed severe retrograde menstruation with visualization of lesions suggestive of stage IV endometriosis. She had endometrial implants along the bladder surface, pelvic sidewalls, cecum, appendix, paracolic gutters, and diaphragm. Multiple biopsies were obtained and sent for diagnostic studies. Neuromuscular relaxation was reversed and the trachea was extubated with the patient deeply anesthetized to avoid any airway reactivity or impeded expiration. She was placed on nasal cannula oxygen and brought to the recovery room. Postoperative chest radiograph was negative for pneumothoraces. She was observed overnight and discharged home the following day. Pathology reports confirmed the diagnosis of endometriosis. One month later, the patient returned to the Thoracic Surgery Clinic with similar complaints of dyspnea and chest pain. Repeat chest imaging showed a recurrent, large, right-sided pneumothorax. She urgently underwent a second VATS with mechanical pleurodesis of both the pleura and diaphragm. Given the concern for development of a tension pneumothorax, a right-sided chest tube was placed in the OR before induction of anesthesia. A left 35-French DLT was placed and the left lung was ventilated with VTs of 200 - 250 mL of O2 and air. Large diaphragmatic defects were noted and repaired with a pericardial patch. Two-lung ventilation was resumed and the surgeon requested an increase in positive end-expiratory pressure to 15 cm H2O. With the right lung fully inflated, the surgical team attempted to identify areas of air leaks and potential sites for rupture. Overall, her perioperative course was again uneventful and she was discharged home. She is currently being followed by the thoracic surgery team for catamenial pneumothoraces and she continues to be symptom-free. 3. Discussion Thoracic endometriosis syndrome is a relatively uncommon disorder, with only a few hundred cases reported in the literature [8]. Characterized by recurrent pneumothoraces, hemothorax, chest pain, dyspnea, and hemoptysis 48 to 72 hours either before or after onset of menstruation, thoracic endometriosis syndrome presents the clinical challenge of a potential pneumothorax [8–11]. While the incidence of thoracic endometriosis syndrome is unknown, it is one of the most common extrapelvic manifestations of endometriosis [12]. Thoracic endometriosis syndrome was first described by Barnes in 1953 in a woman who suffered from endometriosis-induced hemothorax [13]. Subsequently, in 1958, Maurer et al documented the first pneumothoraces associated with thoracic endometriosis syndrome, termed catamenial pneu-
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mothoraces [3]. In 1996, Joseph and Sahn performed a case series of over 100 women with thoracic endometriosis and found that 73% of women presented with a pneumothorax, 14% with a hemothorax, 7% with hemoptysis, and 6% with lung nodules only [8]. A recent retrospective study by Rousset-Jablonski et al looked at risk factors characterizing thoracic endometriosis and catamenial pneumothorax as compared with women who had noncatamenial and nonendometriosis-related pneumothorax. They showed that women with thoracic endometriosis presenting with catamenial pneumothoraces were more likely to have recurrent thoracic and/or scapular pain, infertility, and a history of pelvic surgery/uterine scrapings [14]. Three parallel mechanisms involving either a hormonal, metastatic, or anatomical model for the development of thoracic endometriosis have been described. The hormonal model, as described by Rossi and Goplerud in 1974, focuses on elevated levels of prostaglandin F2α during ovulation [15]. During menses, the sloughing endometrial tissue releases the potent vasoconstrictor prostaglandin F2α , producing vasospasm and bronchial constriction leading to rupture of pleural blebs [15]. However, this hypothesis alone cannot explain the pathogenesis of thoracic endometriosis syndrome since prophylactic therapy with nonsteroidal anti-inflammatory drugs does not decrease the incidence of recurrent pneumothoraces [11]. Second, if this hypothesis were true, one would expect both lungs to be equally involved rather than the clinical dominance for right-sided disease [8]. The second mechanism suggests a metastatic model for transplantation of endometrial tissue. Through right-sided congenital diaphragmatic fenestrations, transdiaphragmatic lymphatic channels, hematogenous embolization via pelvic veins, or direct invasion of the diaphragm, the pleural tissue becomes exposed to endometriotic cells [11,16,17]. During menstruation, the endometrial cells engorge and eventually slough, causing localized areas of inflammation and parietal irritation [18]. The latter results in chest pain and ultimately pulmonary air leaks, leading to the development of a pneumothorax [18]. Finally, the anatomical model is centered around the concept of entrainment of air into the peritoneal cavity through the vaginal canal. During menstruation, the cervical mucus plug is lost and creates a direct communication between the environment and the peritoneum via patent fallopian tubes [11,15]. This is evidenced by the fact that subdiaphragmatic air has been found on chest radiographs in women with catamenial pneumothoraces [19]. The influx of air into the peritoneum communicates with the pleural space through predominantly right-sided diaphragmatic defects and fenestrations [20,21]. These right-sided fenestrations/defects are similarly found in other obstetric complications such as Meigs’ syndrome, in which right-sided pleural effusions predominate [22]. However, if this model were true, one would expect more women to suffer from catamenial pneumothoraces, or at least demonstrate radiographic evidence of subdiaphragmatic air during menstruation. There is growing evidence that perhaps the pathogenesis of thoracic endometriosis syndrome incorporates aspects of all three models and is based on retrograde regurgitation of endometriotic cells [23,24]. In one of the largest case series involving over 100 patients, Joseph and Sahn discovered that more than 55% of women with thoracic endometriosis syndrome had evidence of pelvic endometriosis found during diagnostic laparoscopy or laparotomy [8]. Once in the peritoneum, these endometriotic cells follow the clockwise peristaltic movement of the peritoneal fluid from the left peritoneal gutter, across the pelvic floor toward the right peritoneal gutter, ultimately reaching the peritoneal surface of the right diaphragm [25,26]. It is this migration toward the right diaphragm that most likely accounts for the 90% incidence of right-sided pneumothoraces in woman with thoracic endometriosis syndrome [8]. Endometrial tissue exhibits increased proteolytic activity, unlike nonendometrial tissue [27]. This upregulated proteolytic activity combined with the
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enhanced invasiveness of endometrial tissue by heat-stable proteins found in the peritoneal fluid enables the implanted tissue to invade the diaphragm and adhere to the lung parenchyma [24,28]. During menses, the sloughing endometrial tissue releases the potent vasoconstrictor, prostaglandin F2α. This vasoconstrictor causes vasospasm and bronchial constriction, leading to localized ischemia and pleural blebs, respectively [15]. Both damaged alveolar tissue and pleural blebs/bullae are susceptible to rupture during bronchospasm, impeded expiration, or PPV [20,29]. As described by Ting et al [30], 4 primary mechanisms cause ventilator-induced lung injury, leading to a pneumothorax. The first mechanism occurs in bullae that either fail to communicate or poorly communicate with the bronchial tree. In this situation, the use of N2O will cause expansion and ultimately rupture of overdistended bullae. The second pathway occurs in overly compliant bullae with good bronchial tree communication. In this situation, the overly compliant bullae will receive a larger portion of the VT as compared with normal or noncompliant bullae. Again, overdistension leads to bullae rupture. The third pathway involves the ball-valve mechanism that traps air during inspiration such that progressive expansion leads to rupture. The final mechanism involves bullae with varying degrees of wall thickness or unevenly distributed pleural pressure that results in rupture during forced or impeded expiration [30,31]. Treatment of endometriosis traditionally has included either a medically induced oophorectomy with gonadotropin-releasing hormone (GnRH) agonists, Danazol, or oral contraceptives. Surgical management includes removal of extrapelvic endometrial tissue along with a hysterectomy/salpingoopherectomy [1]. Management of thoracic endometriosis syndrome is similar but combines VATS with mechanical or chemical pleurodesis for treatment of associated catamenial pneumothoraces [11,29]. Presurgical treatment of endometriosis remains controversial. To date, there are no clear guidelines regarding preoperative medical management of endometriosis. A few studies have shown a reduction in size of endometriosis and thus improvement in Retrospective American Fertility Society scores (rAFS) but no improvement in outcomes [32,33]. Preoperative hormonal therapy also increases the amount of intrapelvic fibrosis, which complicates differentiation of normal tissue from endometrial tissue during dissection [32,33]. Our patient presented with recurrent, right-sided pneumothoraces, although initial pleural biopsies were inconclusive of endometrial tissue. Of note, multiple pleural blebs were observed on gross examination. This was consistent with previous findings in which nearly 25% of patients with thoracic endometriosis syndrome exhibited bullae or blebs as the sole pleural lesions, while roughly 10% of patients have absolutely no pathologic pleural findings [10]. While multiple diaphragmatic defects and fenestrations were noted during VATS, diaphragmatic biopsies were not obtained. Owing to the clinical diagnosis of thoracic endometriosis syndrome, the decision was made to postpone diagnostic laparoscopy to ensure resolution of her concurrent menstrual cycle and decrease the risk of intraoperative pneumothoraces. As there are no clear guidelines for delaying surgery or PPV after VATS with mechanical pleurodesis and patch repair, the patient was cleared by the Thoracic Surgery service for her laparoscopic procedure. Gamaleldin et al reported their anesthetic management of a patient with a known catamenial pneumothorax treated with presurgical placement of a chest tube after induction of anesthesia [34]. While our case was similar, our patient’s pneumothorax had resorbed during the interval time. However, she still presented significant risk for development of intraoperative pneumothoraces due to her presumed diagnosis of thoracic endometriosis and preoperative CT scan showing bilateral pleural blebs and bullae. Our primary anesthetic concern for the case was the development of an intraoperative pneumothorax and subsequent conversion to a
tension pneumothorax during PPV. While the recurrence rates for pneumothoraces managed with either open thoracotomy with pleurectomy or VATS with mechanical pleurodesis is 1% and 5%, respectively, the recurrence rates in patients with thoracic endometriosis and surgical management are unknown [35]. During the VATS cases, the concern for intraoperative pneumothorax was less likely as a chest tube had been placed prior to induction of general anesthesia. In addition, placement of a DLT allowed for deflation of the affected lung and ventilation of the dependent lung with low VTs. To minimize further lung injury and risk of intraoperative pneumothorax, surgery was postponed until the intermenstrual period, during which hormonal levels are normal and pleural bleb/ bullae are least susceptible to rupture. During this period, women with thoracic endometriosis syndrome are least likely to develop signs and symptoms of the syndrome [8–10]. Neuraxial anesthesia for thoracic endometriosis syndrome, as described by Yokoyama et al, was considered but deferred owing to both the surgical position and laparoscopic technique required. General anesthesia and placement of an endotracheal tube using rapid-sequence intubation was determined to be the most optimal technique, since even low airway pressures generated during bag-mask ventilation may lead to hyperinflation and injury [31]. To minimize barotrauma, PIP values were limited to less than 25 cm H2O, while lung protective ventilator settings with low VTs based on ideal body weight and a high respiratory rate enabled adequate ventilation [36,37]. While PCV-VG was utilized, it should be noted that studies comparing modes of ventilation in patients with known lung injury have only demonstrated lower PIP values with no difference in outcomes [38,39]. Abdominal wall relaxation with muscle relaxants allowed for adequate abdominal insufflation requiring minimal pressures. Finally, tracheal extubation while the patient was deeply anesthetized further prevented barotrauma associated with impeded expiration. In summary, the anesthetic management of a patient with thoracic endometriosis after recent VATS with mechanical pleurodesis, who presented for elective diagnostic abdominal laparoscopic surgery, is reported. Preoperative evaluation should involve collaboration with the patient’s gynecologist, thoracic surgeon, and primary surgical team to ensure that elective surgery is delayed until the intermenstrual period. Complications associated with thoracic endometriosis syndrome are least likely to occur during that time. If PPV is necessary, strategies such as optimizing patient position, using lung-protective ventilation, limiting abdominal insufflation pressures during pneumoperitoneum, and maintaining a deep level of anesthesia will aid the anesthesiologist in safely managing these patients. Options for converting to one-lung ventilation in addition to emergency management of a tension pneumothorax should be readily available.
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