206
Gynaecology Case Reports
J Obstet Gynaecol Downloaded from informahealthcare.com by Gazi Univ. on 05/04/15 For personal use only.
Case report A 32-year-old parous woman presented with acute lower pelvic pain. The onset was sudden, the pain was steady and radiating to the back. She had a levonorgestrel-releasing coil (Mirena® Bayer HealthCare Pharmaceuticals) inserted for contraception 2 years previously. A pregnancy test was negative. Transvaginal ultrasound examination revealed a cyst measuring 8 cm in diameter on the right ovary. The sonographic appearance was that of a cyst with a thin wall, smooth surface and hyperechogenic content. Doppler showed high-velocity, low-impedance peripheral vascularisation of the ovary. Initial diagnosis was torsion of a corpus luteum cyst. She was operated on laparoscopically and a pedunculated benign ovarian cystic mass, originating from the right ovary, was recognised (Figure 1). The procedure was aspiration of the cystic fluid, and removal of the pathological tissue by coagulation and cutting at the level of the pedicle, leaving the rest of the ovary intact. Intact removal of the cyst prior to aspiration could not be performed due to technical issues. Her postoperative course was uneventful. The pathology report was that of a corpus luteum cyst. At 30 days postoperatively, and 5 days after menstruation, she presented, with no abnormal clinical signs or symptoms. A pelvic examination suspected an enlarged right adnexa. An ultrasound examination was performed and it revealed a cystic mass on the right ovary measuring 8 cm, similar to the one extracted. Conservative management was decided upon. She received combined oral contraceptives (COP) (oestradiol valerate/dienogest – Qlaira®) and was re-examined 1 month later. Transvaginal ultrasound evaluation did not reveal any pathology. She was advised to continue with COP and the coil was removed.
Discussion Corpus luteum may have an abnormal development and instead of degeneration, it might persist or even form a cystic mass known as a corpus luteum cyst or luteal cyst. The excess of progesterone production may result in abnormal uterine bleeding (Barbuscia et al. 2010) or the cyst might even be ruptured or twisted causing internal haemorrhage and acute abdominal pain. In our case, the patient presented with symptoms of ovarian torsion. Sonographic appearance varies and the content of these cysts may appear as hyperechogenic or as a greatly enlarged fine trabecular (‘jelly-like’) echostructure, due to the presence of fibrin strands, and mimic other causes of gynaecological pathology, such as ectopic pregnancy, tubo-ovarian abscesses, endometriomas, fibroids and neoplasms (Swire et al. 2004). Treatment of a corpus luteum cyst depends on its clinical complications. They usually disappear spontaneously or decrease in volume after the subsequent menstrual flow or within 5 weeks from diagnosis. In our case, because of the acute symptomatology and due to the large size of the cyst, it was decided that surgical laparoscopic treatment should be applied. There was a rapid recurrence of the cyst
within 1 month. The recurrence, the lack of any acute symptoms and the pathology report from the laparoscopy, suggested conservative treatment for the second cyst. The cyst regressed after the administration of only one course of oral contraceptives, which is quite usual in everyday practice in Greece, although the mechanism is not clear. In these cases, the use of COP is mostly empirical and not evidencebased. Although there was no evidence that the coil was the causal factor for the recurrence of the cyst, it was removed upon the patient’s request. It is well known that, after insertion of the coil, plasma levels of levonorgestrel stabilise at 100–200 pg/ml after a few weeks, which is thought to be a significantly low concentration to be considered aversively effective for ovarian function (Jensen 2005). A levonorgestrel coil could lead to a cystic formation of ⬎ 3 cm in diameter, at 6–12 months after insertion, for 17.5–21.5% of women, respectively (Varma et al. 2006). The vast majority of them are asymptomatic and a high rate (94%) of spontaneous resolution of the cysts is exhibited within 6 months (Varma et al. 2006). In the reported case herein, the formation of the cyst, the first as well as the recurrent, could not be undoubtedly attributed to the levonorgestrel-releasing coil. Benign cysts in reproductive age sometimes can be difficult to manage and treatment requires consideration of the woman’s age, parity and clinical presentation. Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References Barbuscia M, DE Luca M, Ilaqua A et al. 2010. [Etiopathogenetic and clinical considerations of corpus luteum cysts]. Giornale di Chirurgia 31:103–107. Jensen JT. 2005. Contraceptive and therapeutic effects of the levonorgestrel intrauterine system: an overview. Obstetrical and Gynecological Survey 60: 604–612. Muzii L, Panici PB. 2001. Surgery for functional cysts: is it unnecessary? Journal of the American Association of Gynecologic Laparoscopists 8:616–618. Swire MN, Castro-Aragon I, Levine D. 2004. Various sonographic appearances of the hemorrhagic corpus luteum cyst. Ultrasound Quarterly 20:45–58. Varma R, Sinha D, Gupta JK. 2006. Non-contraceptive uses of levonorgestrelreleasing hormone system (LNG-IUS) – a systematic enquiry and overview. European Journal of Obstetrics, Gynecology, and Reproductive Biology 125:9–28.
Sudden sensorineural hearing loss after laparoscopic cystectomy under general anaesthesia N. Aydin1, Y. Aydin2 & S. Uludag2 1Kanuni Sultan Suleyman Training and Research Hospital and 2Istanbul University, Istanbul, Turkey
DOI: 10.3109/01443615.2014.935722 Correspondence: Y. Aydin, Atakent mah, Soyakolimpiakent sit, D 12 Blok No: 53. Postal Code:34303, Halkali, Istanbul, Turkey. E-mail: [email protected]
Introduction
Figure 1. Rapid recurrence of a corpus luteum cyst after laparoscopic surgery in a young woman with a levonorgestrel releasing coil.
Few cases of hearing loss following non-otological surgical procedures have been reported, and the majority of these cases have been associated with cardiopulmonary surgery (Walsted et al. 2000). Hearing loss after other types of surgery, especially laparoscopic surgery performed under general anaesthesia, is extremely rare (Warltier et al. 2003). This report describes one such case. Screening to detect perioperatory hearing alterations is not consistently performed. Surgical procedures can simulate such alterations, which may go unnoticed because of their subclinical nature if audiometry is not performed. Hearing loss in association with epidural anaesthesia and lumbar puncture has been reported frequently (Schaffartzik et al. 2000). Its occurrence in association with local
Gynaecology Case Reports 207 anaesthesia, such as blocking of plexes or odontological anaesthsia with nerve blocking, has also been reported (Rosemberg et al. 1995). A 43-year-old woman at surgical risk of ASAI underwent laparoscopic cystectomy under anaesthesia (tiyopental, tracrium, sevoflurene and alfentanil) due to endometriosis. The findings of a complete preoperative evaluation were normal. The patient showed no evidence of abnormal alteration in vital signs during the induction of anaesthesia, surgery or post-anaesthesic recovery. Several hours after the operation, she complained of severe tinnitus, vertigo and bilateral hearing loss. An otorhinolaryngologist examined the patient and diagnosed bilateral sensorineural hearing loss. Biometric examination and computed tomography of the ear yielded normal findings. The patient was treated with prednisol (40 mg/day parenterally) for 4 days, followed by oral steroids (20 mg/day) for 1 week. She was discharged from the hospital on the 5th day. Audiometry performed after the discontinuation of steroid treatment showed no improvement in her condition. Thus, hyperbaric oxygen therapy (HBOT) was applied for 6 weeks. Control audiometry performed after this treatment showed moderate improvement (Figure 1).
Discussion
Sudden sensorineural hearing loss is defined as hearing loss ⱖ 30 db in three consecutive frequencies, ocurring within 72 h. Its aetiology is known in only 10% of affected patients, and it is considered to be ideopathic in the remainder of cases; common causes include accidents, cranioencephalic trauma, infection and metabolic disease (Warltier et al. 2003). Hearing loss has been reported to occur more frequently in association with spinal anaesthesia (Schaffartzik et al. 2000), but its incidence is unknown due to a lack of research. Hearing deficits usually affect the ability to detect sounds at low frequencies (125–1,000 Hz). Measurable low-frequency deficits have been reported in 10–50% of patients receiving epidural anaesthesia, therefore less than one-fourth is clinically known (Michel et al. 1990). Most reported cases of sudden sensorineural hypoacusis following non-otological surgery under general anaesthesia have occurred in association with cardiopulmonary bypass surgery (Walsted et al. 2000). In the case described here, sudden hearing loss occurred in association with laparoscopic cystectomy performed under general
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J Obstet Gynaecol Downloaded from informahealthcare.com by Gazi Univ. on 05/04/15 For personal use only.
Case report
anaesthesia. A literature search revealed very few descriptions of the occurrence of this condition in association with laparoscopic surgery. The aetiology of hearing loss is not clearly understood, although several hypotheses have been proposed. One hypothesis involves changes in body pressure that affect pressure in arteries feeding neuronal structures. General and (especially) spinal anaesthesia can cause sudden hypotension, leading to decreased oxygenation of intracranial sensory neurons (Chao 2004). Some authors have argued that increased intraabdominal pressure due to carbon dioxide insufflation may reduce venous return to the heart, thereby decreasing the blood supply to brain. If this were the case, however, the incidence of sudden hearing loss after laparoscopic procedures would presumably be much higher than observed. Anaesthesic agents that readily dissolve (e.g. nitrous oxide) and penetrate tissues can cause pressure changes on the labyrinthic membrane that may lead to its rupture (Segal et al. 1984). Sevoflurane was the only anaesthesic gas used in the case described here, and its effect on hearing loss is not clear. Ventilation with an oxygen mask may damage the ossicular chain or create a fistula in the oval window, which may lead to hearing loss (Schaffartzik et al. 2000). Another mechanism proposed to underlie this condition is epithelial damage to internal ear microcirculation, which disturbs cochlear functions. Such damage could be caused by decreased blood flow or thrombosis of the microcirculation (Warltier et al. 2003; Chao 2004). Steroids, antihistamines, vasodilators and carbon dioxide inhalation have been used to treat sensorineural hearing loss. Given the high spontaneous resolution rate (up to 65% of cases) of this condition, however, randomised studies are necessary to evaluate the effectiveness of any treatment modality. Severe hearing loss, the presence of vertigo, young or very old patient age and delayed diagnosis are poor prognostic factors (Eisenman and Arts 2000). The findings of a review by Bennett et al. (2012) suggested that HBOT improves oxygen supply to the inner ear, thereby improving hearing in people with acute hearing loss. However, the authors noted that this result should be interpreted cautiously because of the modest number of patients included, methodological shortcomings and poor reporting in studies reveiwed. Our case supports the review findings, as 1 week of steriod treatment did not improve the patient’s hearing loss, but 6 weeks of HBOT resulted in moderate improvement. Only prospective trials could document a clear benefit of HBOT for sudden hearing loss. No evidence indicates that HBOT has a beneficial effect on chronic ISSHL or tinnitus (Bennett et al. 2012).
0.25
0.5
1
SISI 1dB R
L kHz %
2
Frequenz in kHz 3 4 6 8
0 10 20 30 40 50 60 70 80 90 100
Figure 1. Audiogram of the patient showing bilateral sensorineural hearing loss just after the operation on the left, and after HBO treatment on the right.
208
Gynaecology Case Reports
We have reported a case of persistent bilateral sudden sensorineural hearing loss following laparoscopic surgical treatment of an endometriotic cyst. This complication is rare and poorly understood, as it is related to diverse, complex physiopathological mechanisms. The ability to prevent and treat this condition is thus limited. Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
J Obstet Gynaecol Downloaded from informahealthcare.com by Gazi Univ. on 05/04/15 For personal use only.
References Bennett MH, Kertesz T, Perleth M et al. 2012. Hyperbaric oxygen for idiopathic sudden sensorineural hearing loss and tinnitus. Cochrane Database of Systematic Reviews (10):CD004739. Chao T. 2004. Sudden sensorineural hearing loss after rapid reduction of blood pressure in malignant hypertension. Annals of Otology, Rhinology and Laryngology 113:73–75. Eisenman D, Arts A. 2000. Effectiveness of treatment for sudden sensorineural hearing loss. Archives of Otolaryngology – Head and Neck Surgery 126: 1161–1164. Michel O, Brusis T, Loennecken I et al. 1990. Inner ear hearing loss following cerebrospinal fluid puncture: a too little appreciated complication? HNO 38:71–76. Rosemberg P, Lamberg T, Tarkkila P et al. 1995. Auditory disturbance associated with interscalene brachial plexus block. British Journal of Anaesthesia 74:89–91. Schaffartzik W, Hirsch J, Frickmann F et al. 2000. Hearing loss after spinal and general anesthesia: A comparative study. Anesthesia and Analgesia 91:1466–1472. Segal S, Man A, Winerman I. 1984. Labyrinthine membrane rupture caused by elevated intratympanic pressure during general anesthesia. American Journal of Otology 5:308–310. Walsted A, Andreassen K, Berthelsen P, et al. 2000. Hearing loss after cardiopulmonary bypass surgery. European Archives of Oto-Rhino-Laryngology 257:124–127. Warltier D, Sprung J, Bourke D et al. 2003. Perioperative hearing impairment. Anesthesiology 98:241–257.
Bilateral catamenial pneumothorax and pulmonary emboli J. M. Geynisman1, J. P. Lekovic1 & T. Tsai2 1Department of Obstetrics and Gynecology, New York Presbyterian
Hospital Weill Cornell Medical College, New York and 2Reproductive Endocrinology, New York Hospital Queens, Flushing, NY, USA DOI: 10.3109/01443615.2014.935725 Correspondence: J. M. Geynisman, New York Presbyterian Weill Cornell Medical Center, 505 E 70th Street, 5HT, NY, NY 10065, USA. E-mail: [email protected]
Introduction A 41-year-old woman presented with unstable vital signs and was found to have bilateral haemopneumothoraces and concern for bilateral pulmonary emboli. The patient had a history of endometriosis and after stabilisation and video-assisted thoracoscopic surgery, it was confirmed that this was a misdiagnosis of catamenial pneumothorax.
Case report A 41-year-old G0 woman presented to the emergency room with 1 week of dyspnoea. As a physician herself, she had treated herself with albuterol, prednisone, levofloxacin and oseltamivir, with no improvement in her symptoms. On presentation, she was tachypnoeic to 36, tachycardic to 135, with an oxygen saturation of 85% on room air. A chest X-ray was performed, which demonstrated bilateral haemopneumothoraces. A CT angiogram of the chest demonstrated bilateral subsegmental pulmonary emboli. She underwent
placement of a chest tube on the right side only, as this side had a significantly larger pneumothorax. The chest tube immediately drained 900 cc of bloody fluid. She was started on a heparin drip for her pulmonary emboli and was admitted to the medical intensive care unit for workup. Her general medical history was only significant for migraines, however her gynaecological history was significant for stage 3 endometriosis confirmed by laparoscopy 5 years previously. Her symptoms presented shortly after menarche with dysmenorrhoea and she had used oral contraceptives and anti-inflammatory medications in the past with adequate control of her pain and bleeding. Her history was also significant for leiomyomas and she reports that she underwent a laparoscopic myomectomy with removal of 20 myomas 2 years previously. Her last menstrual period began on the day of her presentation to the emergency room. The patient reported that she had recently begun to take a number of herbs to treat her pelvic pain but did not believe any of them were thrombogenic. She did not use tobacco but had a family history of lung and prostate cancer. She reported that all three of her sisters had endometriosis. The patient had only abdominal and pelvic endometriosis in the past and denied any haemoptysis, chest pain or dyspnoea with her menses. The differential diagnosis at this time was pulmonary embolism, with a possible underlying malignancy vs catamenial pneumothorax. Her chest tube continued to drain serosanguinous fluid over the next week, so a plan was made to perform video-assisted thoracic surgery with talc pleurodesis. On visualisation of the pleural space, there were no endometriomas noted but the cardiothoracic surgeon did encounter and biopsied multiple small endometriotic implants, which had haemorrhaged into the pleural space. It was deemed that the CT angiogram had been falsely-positive and that the emboli which were noted were more likely parenchymal haemorrhages. Following pleurodesis, the patient gradually stabilised and the chest tube was removed. The patient was counselled that her best chances of preventing a recurrence were to undergo hysterectomy and bilateral salpingo-oophorectomy (BSO). However, she wanted to maintain the possibility of fertility and elected to try leuprolide acetate therapy. Endometriosis was first described by Rokitansky in 1861. It is defined as the presence of endometrial glands and stroma outside of the uterine cavity. It is present in approximately 1–2% of all reproductive age women, but it is more prevalent among infertile women (15–25%) (Bulletti et al. 2010). Pathogenesis of endometriosis remains controversial, and there are several accepted theories: vascular/lymphatic dissemination, retrograde menstruation and coelomic metaplasia. Direct transplantation has also been proposed as a mechanism in abdominal scar endometriosis (Akbulut et al. 2010; Hensen et al. 2006). Catamenial pneumothorax is the most common clinical expression of thoracic endometriosis syndrome, or the ‘porous diaphragm syndrome’ proposed by Kirchner (1998) and it includes four separate entities: catamenial haemothorax, catamenial haemoptysis, endometriosis lung nodules and catamenial chest pain. Its recognition has improved in the past decade and it now comprises almost onethird of all unexplained pneumothorax is reproductive age women (Alifano et al. 2006; Shiraishi 1991). While there are numerous case reports of catamenial pneumothorax (Ciriaco et al. 2009; Alifano et al. 2003; Rousset-Jablonski et al. 2011; Bagan et al. 2003), our case is unique in that the initial presentation was mistaken for pulmonary embolism, a condition with significant morbidity and mortality, whose treatment (therapeutic anticoagulation) also carries a risk of significant morbidity. A retrospective analysis of 110 cases, as well as other case reports and series, showed that histological confirmation of endometriosis during surgery is rare, and possibly depending on when in the menstrual cycle the surgery/biopsy was performed (Joseph and Sahn 1996; Bobbio et al. 2007; Triponez et al. 2010; Pryshchepau et al. 2010). Suppression of the ectopic endometrium can be attempted with oral contraceptives, progestins, danazol or gonadotropin-releasing hormone analogues. Unfortunately, pneumothorax and haemotho-
Gynaecology Case Reports
J Obstet Gynaecol Downloaded from informahealthcare.com by Gazi Univ. on 05/04/15 For personal use only.
Case report A 32-year-old parous woman presented with acute lower pelvic pain. The onset was sudden, the pain was steady and radiating to the back. She had a levonorgestrel-releasing coil (Mirena® Bayer HealthCare Pharmaceuticals) inserted for contraception 2 years previously. A pregnancy test was negative. Transvaginal ultrasound examination revealed a cyst measuring 8 cm in diameter on the right ovary. The sonographic appearance was that of a cyst with a thin wall, smooth surface and hyperechogenic content. Doppler showed high-velocity, low-impedance peripheral vascularisation of the ovary. Initial diagnosis was torsion of a corpus luteum cyst. She was operated on laparoscopically and a pedunculated benign ovarian cystic mass, originating from the right ovary, was recognised (Figure 1). The procedure was aspiration of the cystic fluid, and removal of the pathological tissue by coagulation and cutting at the level of the pedicle, leaving the rest of the ovary intact. Intact removal of the cyst prior to aspiration could not be performed due to technical issues. Her postoperative course was uneventful. The pathology report was that of a corpus luteum cyst. At 30 days postoperatively, and 5 days after menstruation, she presented, with no abnormal clinical signs or symptoms. A pelvic examination suspected an enlarged right adnexa. An ultrasound examination was performed and it revealed a cystic mass on the right ovary measuring 8 cm, similar to the one extracted. Conservative management was decided upon. She received combined oral contraceptives (COP) (oestradiol valerate/dienogest – Qlaira®) and was re-examined 1 month later. Transvaginal ultrasound evaluation did not reveal any pathology. She was advised to continue with COP and the coil was removed.
Discussion Corpus luteum may have an abnormal development and instead of degeneration, it might persist or even form a cystic mass known as a corpus luteum cyst or luteal cyst. The excess of progesterone production may result in abnormal uterine bleeding (Barbuscia et al. 2010) or the cyst might even be ruptured or twisted causing internal haemorrhage and acute abdominal pain. In our case, the patient presented with symptoms of ovarian torsion. Sonographic appearance varies and the content of these cysts may appear as hyperechogenic or as a greatly enlarged fine trabecular (‘jelly-like’) echostructure, due to the presence of fibrin strands, and mimic other causes of gynaecological pathology, such as ectopic pregnancy, tubo-ovarian abscesses, endometriomas, fibroids and neoplasms (Swire et al. 2004). Treatment of a corpus luteum cyst depends on its clinical complications. They usually disappear spontaneously or decrease in volume after the subsequent menstrual flow or within 5 weeks from diagnosis. In our case, because of the acute symptomatology and due to the large size of the cyst, it was decided that surgical laparoscopic treatment should be applied. There was a rapid recurrence of the cyst
within 1 month. The recurrence, the lack of any acute symptoms and the pathology report from the laparoscopy, suggested conservative treatment for the second cyst. The cyst regressed after the administration of only one course of oral contraceptives, which is quite usual in everyday practice in Greece, although the mechanism is not clear. In these cases, the use of COP is mostly empirical and not evidencebased. Although there was no evidence that the coil was the causal factor for the recurrence of the cyst, it was removed upon the patient’s request. It is well known that, after insertion of the coil, plasma levels of levonorgestrel stabilise at 100–200 pg/ml after a few weeks, which is thought to be a significantly low concentration to be considered aversively effective for ovarian function (Jensen 2005). A levonorgestrel coil could lead to a cystic formation of ⬎ 3 cm in diameter, at 6–12 months after insertion, for 17.5–21.5% of women, respectively (Varma et al. 2006). The vast majority of them are asymptomatic and a high rate (94%) of spontaneous resolution of the cysts is exhibited within 6 months (Varma et al. 2006). In the reported case herein, the formation of the cyst, the first as well as the recurrent, could not be undoubtedly attributed to the levonorgestrel-releasing coil. Benign cysts in reproductive age sometimes can be difficult to manage and treatment requires consideration of the woman’s age, parity and clinical presentation. Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References Barbuscia M, DE Luca M, Ilaqua A et al. 2010. [Etiopathogenetic and clinical considerations of corpus luteum cysts]. Giornale di Chirurgia 31:103–107. Jensen JT. 2005. Contraceptive and therapeutic effects of the levonorgestrel intrauterine system: an overview. Obstetrical and Gynecological Survey 60: 604–612. Muzii L, Panici PB. 2001. Surgery for functional cysts: is it unnecessary? Journal of the American Association of Gynecologic Laparoscopists 8:616–618. Swire MN, Castro-Aragon I, Levine D. 2004. Various sonographic appearances of the hemorrhagic corpus luteum cyst. Ultrasound Quarterly 20:45–58. Varma R, Sinha D, Gupta JK. 2006. Non-contraceptive uses of levonorgestrelreleasing hormone system (LNG-IUS) – a systematic enquiry and overview. European Journal of Obstetrics, Gynecology, and Reproductive Biology 125:9–28.
Sudden sensorineural hearing loss after laparoscopic cystectomy under general anaesthesia N. Aydin1, Y. Aydin2 & S. Uludag2 1Kanuni Sultan Suleyman Training and Research Hospital and 2Istanbul University, Istanbul, Turkey
DOI: 10.3109/01443615.2014.935722 Correspondence: Y. Aydin, Atakent mah, Soyakolimpiakent sit, D 12 Blok No: 53. Postal Code:34303, Halkali, Istanbul, Turkey. E-mail: [email protected]
Introduction
Figure 1. Rapid recurrence of a corpus luteum cyst after laparoscopic surgery in a young woman with a levonorgestrel releasing coil.
Few cases of hearing loss following non-otological surgical procedures have been reported, and the majority of these cases have been associated with cardiopulmonary surgery (Walsted et al. 2000). Hearing loss after other types of surgery, especially laparoscopic surgery performed under general anaesthesia, is extremely rare (Warltier et al. 2003). This report describes one such case. Screening to detect perioperatory hearing alterations is not consistently performed. Surgical procedures can simulate such alterations, which may go unnoticed because of their subclinical nature if audiometry is not performed. Hearing loss in association with epidural anaesthesia and lumbar puncture has been reported frequently (Schaffartzik et al. 2000). Its occurrence in association with local
Gynaecology Case Reports 207 anaesthesia, such as blocking of plexes or odontological anaesthsia with nerve blocking, has also been reported (Rosemberg et al. 1995). A 43-year-old woman at surgical risk of ASAI underwent laparoscopic cystectomy under anaesthesia (tiyopental, tracrium, sevoflurene and alfentanil) due to endometriosis. The findings of a complete preoperative evaluation were normal. The patient showed no evidence of abnormal alteration in vital signs during the induction of anaesthesia, surgery or post-anaesthesic recovery. Several hours after the operation, she complained of severe tinnitus, vertigo and bilateral hearing loss. An otorhinolaryngologist examined the patient and diagnosed bilateral sensorineural hearing loss. Biometric examination and computed tomography of the ear yielded normal findings. The patient was treated with prednisol (40 mg/day parenterally) for 4 days, followed by oral steroids (20 mg/day) for 1 week. She was discharged from the hospital on the 5th day. Audiometry performed after the discontinuation of steroid treatment showed no improvement in her condition. Thus, hyperbaric oxygen therapy (HBOT) was applied for 6 weeks. Control audiometry performed after this treatment showed moderate improvement (Figure 1).
Discussion
Sudden sensorineural hearing loss is defined as hearing loss ⱖ 30 db in three consecutive frequencies, ocurring within 72 h. Its aetiology is known in only 10% of affected patients, and it is considered to be ideopathic in the remainder of cases; common causes include accidents, cranioencephalic trauma, infection and metabolic disease (Warltier et al. 2003). Hearing loss has been reported to occur more frequently in association with spinal anaesthesia (Schaffartzik et al. 2000), but its incidence is unknown due to a lack of research. Hearing deficits usually affect the ability to detect sounds at low frequencies (125–1,000 Hz). Measurable low-frequency deficits have been reported in 10–50% of patients receiving epidural anaesthesia, therefore less than one-fourth is clinically known (Michel et al. 1990). Most reported cases of sudden sensorineural hypoacusis following non-otological surgery under general anaesthesia have occurred in association with cardiopulmonary bypass surgery (Walsted et al. 2000). In the case described here, sudden hearing loss occurred in association with laparoscopic cystectomy performed under general
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Frequenz in kHz 3 4 6 8
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Hörpegel in dB
Hearing level. Perte auditive. Perdida auditiva
Pure tone adiogram Audiogramme tonal Audiograma tonal
SISI 1dB
Hearing level. Perte auditive. Perdida auditiva
Tonaudiogramm
Hörpegel in dB
J Obstet Gynaecol Downloaded from informahealthcare.com by Gazi Univ. on 05/04/15 For personal use only.
Case report
anaesthesia. A literature search revealed very few descriptions of the occurrence of this condition in association with laparoscopic surgery. The aetiology of hearing loss is not clearly understood, although several hypotheses have been proposed. One hypothesis involves changes in body pressure that affect pressure in arteries feeding neuronal structures. General and (especially) spinal anaesthesia can cause sudden hypotension, leading to decreased oxygenation of intracranial sensory neurons (Chao 2004). Some authors have argued that increased intraabdominal pressure due to carbon dioxide insufflation may reduce venous return to the heart, thereby decreasing the blood supply to brain. If this were the case, however, the incidence of sudden hearing loss after laparoscopic procedures would presumably be much higher than observed. Anaesthesic agents that readily dissolve (e.g. nitrous oxide) and penetrate tissues can cause pressure changes on the labyrinthic membrane that may lead to its rupture (Segal et al. 1984). Sevoflurane was the only anaesthesic gas used in the case described here, and its effect on hearing loss is not clear. Ventilation with an oxygen mask may damage the ossicular chain or create a fistula in the oval window, which may lead to hearing loss (Schaffartzik et al. 2000). Another mechanism proposed to underlie this condition is epithelial damage to internal ear microcirculation, which disturbs cochlear functions. Such damage could be caused by decreased blood flow or thrombosis of the microcirculation (Warltier et al. 2003; Chao 2004). Steroids, antihistamines, vasodilators and carbon dioxide inhalation have been used to treat sensorineural hearing loss. Given the high spontaneous resolution rate (up to 65% of cases) of this condition, however, randomised studies are necessary to evaluate the effectiveness of any treatment modality. Severe hearing loss, the presence of vertigo, young or very old patient age and delayed diagnosis are poor prognostic factors (Eisenman and Arts 2000). The findings of a review by Bennett et al. (2012) suggested that HBOT improves oxygen supply to the inner ear, thereby improving hearing in people with acute hearing loss. However, the authors noted that this result should be interpreted cautiously because of the modest number of patients included, methodological shortcomings and poor reporting in studies reveiwed. Our case supports the review findings, as 1 week of steriod treatment did not improve the patient’s hearing loss, but 6 weeks of HBOT resulted in moderate improvement. Only prospective trials could document a clear benefit of HBOT for sudden hearing loss. No evidence indicates that HBOT has a beneficial effect on chronic ISSHL or tinnitus (Bennett et al. 2012).
0.25
0.5
1
SISI 1dB R
L kHz %
2
Frequenz in kHz 3 4 6 8
0 10 20 30 40 50 60 70 80 90 100
Figure 1. Audiogram of the patient showing bilateral sensorineural hearing loss just after the operation on the left, and after HBO treatment on the right.
208
Gynaecology Case Reports
We have reported a case of persistent bilateral sudden sensorineural hearing loss following laparoscopic surgical treatment of an endometriotic cyst. This complication is rare and poorly understood, as it is related to diverse, complex physiopathological mechanisms. The ability to prevent and treat this condition is thus limited. Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
J Obstet Gynaecol Downloaded from informahealthcare.com by Gazi Univ. on 05/04/15 For personal use only.
References Bennett MH, Kertesz T, Perleth M et al. 2012. Hyperbaric oxygen for idiopathic sudden sensorineural hearing loss and tinnitus. Cochrane Database of Systematic Reviews (10):CD004739. Chao T. 2004. Sudden sensorineural hearing loss after rapid reduction of blood pressure in malignant hypertension. Annals of Otology, Rhinology and Laryngology 113:73–75. Eisenman D, Arts A. 2000. Effectiveness of treatment for sudden sensorineural hearing loss. Archives of Otolaryngology – Head and Neck Surgery 126: 1161–1164. Michel O, Brusis T, Loennecken I et al. 1990. Inner ear hearing loss following cerebrospinal fluid puncture: a too little appreciated complication? HNO 38:71–76. Rosemberg P, Lamberg T, Tarkkila P et al. 1995. Auditory disturbance associated with interscalene brachial plexus block. British Journal of Anaesthesia 74:89–91. Schaffartzik W, Hirsch J, Frickmann F et al. 2000. Hearing loss after spinal and general anesthesia: A comparative study. Anesthesia and Analgesia 91:1466–1472. Segal S, Man A, Winerman I. 1984. Labyrinthine membrane rupture caused by elevated intratympanic pressure during general anesthesia. American Journal of Otology 5:308–310. Walsted A, Andreassen K, Berthelsen P, et al. 2000. Hearing loss after cardiopulmonary bypass surgery. European Archives of Oto-Rhino-Laryngology 257:124–127. Warltier D, Sprung J, Bourke D et al. 2003. Perioperative hearing impairment. Anesthesiology 98:241–257.
Bilateral catamenial pneumothorax and pulmonary emboli J. M. Geynisman1, J. P. Lekovic1 & T. Tsai2 1Department of Obstetrics and Gynecology, New York Presbyterian
Hospital Weill Cornell Medical College, New York and 2Reproductive Endocrinology, New York Hospital Queens, Flushing, NY, USA DOI: 10.3109/01443615.2014.935725 Correspondence: J. M. Geynisman, New York Presbyterian Weill Cornell Medical Center, 505 E 70th Street, 5HT, NY, NY 10065, USA. E-mail: [email protected]
Introduction A 41-year-old woman presented with unstable vital signs and was found to have bilateral haemopneumothoraces and concern for bilateral pulmonary emboli. The patient had a history of endometriosis and after stabilisation and video-assisted thoracoscopic surgery, it was confirmed that this was a misdiagnosis of catamenial pneumothorax.
Case report A 41-year-old G0 woman presented to the emergency room with 1 week of dyspnoea. As a physician herself, she had treated herself with albuterol, prednisone, levofloxacin and oseltamivir, with no improvement in her symptoms. On presentation, she was tachypnoeic to 36, tachycardic to 135, with an oxygen saturation of 85% on room air. A chest X-ray was performed, which demonstrated bilateral haemopneumothoraces. A CT angiogram of the chest demonstrated bilateral subsegmental pulmonary emboli. She underwent
placement of a chest tube on the right side only, as this side had a significantly larger pneumothorax. The chest tube immediately drained 900 cc of bloody fluid. She was started on a heparin drip for her pulmonary emboli and was admitted to the medical intensive care unit for workup. Her general medical history was only significant for migraines, however her gynaecological history was significant for stage 3 endometriosis confirmed by laparoscopy 5 years previously. Her symptoms presented shortly after menarche with dysmenorrhoea and she had used oral contraceptives and anti-inflammatory medications in the past with adequate control of her pain and bleeding. Her history was also significant for leiomyomas and she reports that she underwent a laparoscopic myomectomy with removal of 20 myomas 2 years previously. Her last menstrual period began on the day of her presentation to the emergency room. The patient reported that she had recently begun to take a number of herbs to treat her pelvic pain but did not believe any of them were thrombogenic. She did not use tobacco but had a family history of lung and prostate cancer. She reported that all three of her sisters had endometriosis. The patient had only abdominal and pelvic endometriosis in the past and denied any haemoptysis, chest pain or dyspnoea with her menses. The differential diagnosis at this time was pulmonary embolism, with a possible underlying malignancy vs catamenial pneumothorax. Her chest tube continued to drain serosanguinous fluid over the next week, so a plan was made to perform video-assisted thoracic surgery with talc pleurodesis. On visualisation of the pleural space, there were no endometriomas noted but the cardiothoracic surgeon did encounter and biopsied multiple small endometriotic implants, which had haemorrhaged into the pleural space. It was deemed that the CT angiogram had been falsely-positive and that the emboli which were noted were more likely parenchymal haemorrhages. Following pleurodesis, the patient gradually stabilised and the chest tube was removed. The patient was counselled that her best chances of preventing a recurrence were to undergo hysterectomy and bilateral salpingo-oophorectomy (BSO). However, she wanted to maintain the possibility of fertility and elected to try leuprolide acetate therapy. Endometriosis was first described by Rokitansky in 1861. It is defined as the presence of endometrial glands and stroma outside of the uterine cavity. It is present in approximately 1–2% of all reproductive age women, but it is more prevalent among infertile women (15–25%) (Bulletti et al. 2010). Pathogenesis of endometriosis remains controversial, and there are several accepted theories: vascular/lymphatic dissemination, retrograde menstruation and coelomic metaplasia. Direct transplantation has also been proposed as a mechanism in abdominal scar endometriosis (Akbulut et al. 2010; Hensen et al. 2006). Catamenial pneumothorax is the most common clinical expression of thoracic endometriosis syndrome, or the ‘porous diaphragm syndrome’ proposed by Kirchner (1998) and it includes four separate entities: catamenial haemothorax, catamenial haemoptysis, endometriosis lung nodules and catamenial chest pain. Its recognition has improved in the past decade and it now comprises almost onethird of all unexplained pneumothorax is reproductive age women (Alifano et al. 2006; Shiraishi 1991). While there are numerous case reports of catamenial pneumothorax (Ciriaco et al. 2009; Alifano et al. 2003; Rousset-Jablonski et al. 2011; Bagan et al. 2003), our case is unique in that the initial presentation was mistaken for pulmonary embolism, a condition with significant morbidity and mortality, whose treatment (therapeutic anticoagulation) also carries a risk of significant morbidity. A retrospective analysis of 110 cases, as well as other case reports and series, showed that histological confirmation of endometriosis during surgery is rare, and possibly depending on when in the menstrual cycle the surgery/biopsy was performed (Joseph and Sahn 1996; Bobbio et al. 2007; Triponez et al. 2010; Pryshchepau et al. 2010). Suppression of the ectopic endometrium can be attempted with oral contraceptives, progestins, danazol or gonadotropin-releasing hormone analogues. Unfortunately, pneumothorax and haemotho-
