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12. Crary MA, Baldwin BO. Surface electromyographic characteristics of swallowing in dysphagia secondary to brainstem stroke. Dysphagia 1997; 12(4): 180–187. 13. Donner MW. Swallowing mechanism and neuromuscular disorders. Seminars in Roentgenology 1974; 9(4): 273–282. 14. Horner J, Buoyer FG, Alberts MJ, Helms MJ. Dysphagia following brain-stem stroke: clinical correlates and outcome. Archives of Neurology 1991; 48(11): 1170–1173. 15. Logemann J, Kahrilas P, Kobara M, Vakil N. The benefit of head rotation on pharyngeal dysphagia. Archives of Physical Medicine and Rehabilitation 1989; 70(10): 767–771. 16. Logemann JA, Kahrilas PJ. Relearning to swallow after stroke – application of manuevres and indirect biofeedback: a case study. Neurology 1990; 40(7): 1136–1138. 17. Saltzman LS, Rosenberg CH, Wolf RH. Brainstem infarct with pharyngeal dysmotility and paralyzed vocal cord: management with a multidisciplinary approach. Archives of Physical Medicine and Rehabilitation 1993; 74(2): 214–216. 18. Silbiger ML, Pikielney R, Donner MW. Neuromuscular disorders affecting the pharynx: cineradiographic analysis. Investigative Radiology 1967; 2(6): 442–448. 19. Veis SL, Logemann JA. Swallowing disorders in persons with cerebrovascular accident. Archives of Physical Medicine and Rehabilitation 1985; 66(6): 372–375. 20. Hagen C, Malkmus D, Durham P. Levels of cognitive functioning. In: Rehabilitation of the Head Injured Adult: Comprehensive Physical Management. Professional Staff Association of Ranchos Los Amigos Hospital, Inc., Downey, CA 1979. 21. Hayden D, Square P. Verbal Motor Production Assessment for Children. Psychological Press, San Antonio, TX 1999. 22. Enderby P. Frenchay Dysarthria Assessment. College Hill Press, UK 1983. 23. Reilly S, Skuse D, Wolke D. Schedule for Oral Motor Assessment. Whurr Publishers, London 2000. 24. Westmead Hospital and Community Health Services (1998, ISBN 1-876109-60-2). Parramatta Hospitals’ Assessment of Dysphagia, third edn. Author, Westmead Hospital and Community Health Services, NSW. 25. Ward EC, Conroy A-L. Validity, reliability and responsivity of the Royal Brisbane Hospital Outcome Measure for Swallowing. Asia Pacific Journal of Speech, Language and Hearing 1999; 4: 109–129. 26. Morgan AT, Ward E, Murdoch B, Bilbie K. Acute characteristics of pediatric dysphagia subsequent to traumatic brain injury: videofluoroscopic assessment. Journal of Head Trauma Rehabilitation 2002; 17(3): 220–241. 27. Logemann JA (ed) Manual for the videofluorographic study of swallowing. Pro-Ed, Austin 1993. 28. Lazarus C, Logemann JA. Swallowing disorders in closed head trauma patients. Archives of Physical Medicine and Rehabilitation 1987; 68(2): 79–84. 29. O’Neil KH, Purdy M, Falk J, Gallo L. The dysphagia outcome and severity scale. Dysphagia 1999; 14(3): 139–145. 30. Rosenbek JC, Robbins JA, Roecker EB, Coyle JL, Wood JL. A penetration–aspiration scale. Dysphagia 1996; 11(2): 93–98. 31. Bastian RW. Videoendoscopic evaluation of patients with dysphagia: an adjunct to the modified barium swallow. Otolaryngology Head and Neck Surgery 1991; 104(3): 339–350. 32. Hoppers P, Holm SE. The role of fiberoptic endoscopy in dysphagia rehabilitation. Journal of Head Trauma Rehabilitation 1999; 14(5): 475–485. 33. Langmore SE, Terpenning MS, Schork A, Chen Y, Murray JT, Lopatin D et al. Predictors of aspiration pneumonia: how important is dysphagia. Dysphagia 1998; 13(2): 69–81. 34. Leder SB. Fiberoptic endoscopic evaluation of swallowing in patients with acute traumatic brain injury. Journal of Head Trauma Rehabilitation 1999; 14(5): 448–453. 35. Buchholz DW. Clinically probable brainstem stroke presenting primarily as dysphagia and nonvisualized by MRI. Dysphagia 1993; 8(3): 235–238. 36. Barnes MP. Rehabilitation after traumatic brain injury. British Medical Bulletin 1999; 55(4): 927–943. 37. Arvedson JC, Lefton-Greif MA. Pediatric Videofluoroscopic Swallow Studies. Communication Skill Builders, San Antonio, TX 1998.
Haemorrhagic brain metastasis from a thymic carcinoma Journal of Clinical Neuroscience (2004) 11(2)
Mohammed Al-Barbarawi MBBS CHAM (JORDAN), Sarah F. Smith MPH (HONS), Lali H.S. Sekhon MBBS (HONS) PHD (SYD) FRACS, Department of Neurosurgery, Royal North Shore Hospital and University of Sydney, St. Leonards, NSW 2065, Australia
Summary Brain metastasis from thymic carcinoma is extremely rare, and there is still no consensus regarding the best management of thymic metastasis to the central nervous system. Here, we report the first-known Australian case. A review of the current literature and the characteristics of thymic tumours with brain metastasis indicate that aggressive management may be able to improve long-term outcomes for these patients. A 49-year-old man presented 2 weeks after thoracotomy for thymic carcinoma resection with a 2-day history of headache, right-sided weakness and expressive dysphasia. CT and MR scans revealed two metastatic brain lesions, one within the left frontal lobe with cystic necrosis and haemorrhage, the other deep in the parietal lobe adjacent to the left ventricle with a lesser degree of haemorrhage. The patient underwent frameless stereotactic craniotomy for excision of the frontal lesion. Histopathology confirmed poorly differentiated thymic carcinoma. Post-operatively his weakness and speech improved dramatically, and he was discharged home within a week, with radiotherapy and chemotherapy to follow. However, he represented with rapidly worsening symptoms and died within a week. Thymic carcinoma is a rare tumour, displaying malignant features clinically and histopathologically with local invasion to adjacent organs. Metastasis is predominantly to lung, bone, liver and kidney, with less predilection for the central nervous system. Treatment for thymic carcinoma is multimodal, but outcome remains poor and life expectancy is very short when brain metastasis with haemorrhage is present. ª 2003 Elsevier Ltd. All rights reserved. Journal of Clinical Neuroscience (2004) 11(2), 190–194 0967-5868/$ - see front matter ª 2003 Elsevier Ltd. All rights reserved. doi:10.1016/j.jocn.2003.05.001
Keywords: brain metastasis, frameless stereotactic craniotomy, radiotherapy, thymic carcinoma, thymic epithelial tumours, TET Received 29 March 2003 Accepted 21 May 2003 Correspondence to: A/Prof. Lali Sekhon, Department of Neurosurgery, Level 7, Royal North Shore Hospital, St. Leonards, NSW 2065, Australia. Tel.: +61-2-99268703; Fax: +61-2-94375172; E-mail:
[email protected]
INTRODUCTION Thymic tumours are rare and comprise a wide spectrum of types, with thymoma and lymphoma occurring most frequently. Neoplasms arising from thymic epithelial cells are currently classified as thymoma, invasive thymoma and thymic carcinoma.1 Local invasion to adjacent organs is the usual means of spread, with metastasis, particularly to brain, seldom occurring.2;3 Because of this rarity we report a new case presenting with two haemorrhagic metastases to the brain from proven poorly differentiated thymic carcinoma, then discuss the aggressive behaviour of thymic carcinoma with brain metastases in a review of the literature. CASE REPORT A 49-year-old man presented in July 2002 with a brief history of chest pain, shortness of breath and fatigue. His general examiª 2003 Elsevier Ltd. All rights reserved.
Haemorrhagic brain metastasis from a thymic carcinoma 191
nation was unremarkable apart from being out of breath. Neurological examination was entirely normal. Chest X-ray revealed a right anterior mediastinal mass and massive right pleural effusion with lower lobe collapse (Fig. 1). CT scan confirmed the mass, measuring 10 8 7 cm, to extend from the top of the aortic arch inferiorly to the anterior margin of the heart, with evidence of superior vena caval compression and loss of the mediastinal fat plane, suggesting local invasion (Fig. 2). A chest drain was inserted for pleural effusion, and CT-guided biopsy revealed possible primary thymic carcinoma (WHO type C, Masaoka stage IVa4 ). As thymic carcinoma can be associated with other primary carcinoma, further investigations were carried out looking for other primary tumour or metastasis, which proved to be negative.
Fig. 3 Photomicrograph of thymic tumour biopsy. Areas of necrosis, mitosis, hypercellularity and pleomorphism are seen, consistent with poorly differentiated carcinoma (Haematoxylin & eosin, 400).
Fig. 1 Chest X-ray showing right anterior mediastinal mass with massive pleural effusion and lower lobe collapse.
Fig. 2 CT scan chest showing 10 8 7 cm mass occupying the anterior mediastinum and extending to adjacent structures.
ª 2003 Elsevier Ltd. All rights reserved.
Methotrexate/bleomycin/cisplatin chemotherapy was given for 5 months. Post-chemotherapy progress CT scan revealed a significant reduction in tumour size. However, at thoracotomy for resection on 12/12/2002, extensive tumour was found, invading the pleura, aorta and pericardium. A diagnosis of stage IVa according to the Masaoka system was confirmed and histopathology showed a poorly differentiated thymic carcinoma with involvement of the margins (Fig. 3). He was discharged home after an uneventful post-operative course and was planned to receive radiotherapy. A few days before starting radiotherapy to the mediastinum he presented with a two-day history of headache, progressive rightsided weakness, expressive dysphasia and confusion. CT scan of the brain revealed a 5 4.5-cm haemorrhagic lesion within the left frontal lobe surrounded by oedema and causing a significant mass effect. A further 2 2-cm lesion was seen deep in the left parietal region effacing the left lateral ventricle (Fig. 4). Preoperative MR scanning revealed two haemorrhagic lesions with cystic necrosis, a larger frontal and smaller deep parietal lobe (Fig. 5). The patient was offered resection of the frontal lesion, since it was readily amenable to surgery and the cause of his rapidly worsening symptoms. Radiotherapy was planned for management of the smaller deep posterior tumour. At frameless stereotactic craniotomy on 27/12/2002, the tumour appeared soft and haemorrhagic with necrosis in the core; gross tumour removal and evacuation of a 4 4-cm intracerebral haematoma were carried out. Pathological analysis confirmed thymic carcinoma (Fig. 6), and tumour staging was revised to Masaoka IVb. Postoperatively he was well. Speech improved significantly, power returned on the right side and he was able to walk unaided. The patient was discharged home on the 12th post-operative day with radiotherapy planned for the next week. Three days later the patient returned to the Emergency Department with rapidly progressing right sided weakness and further speech problems. A brain CT scan was repeated which showed enlarging left parietal tumour of 4 5 cm with increased mass effect and a new haemorrhagic lesion in the left cerebellar hemisphere. He was admitted for further assessment and management. CT chest showed a large complex mediastinal mass indicating recurrence with rapid growth. After discussion with the family further treatment was discontinued and he died five days later. Journal of Clinical Neuroscience (2004) 11(2)
192 Al-Barbarawi et al.
Fig. 4 Non-contrast CT brain scan showing 5 4.5 cm left frontal tumour with haemorrhagic necrosis. Another lesion can be seen behind it deep within the parietal lobe measuring 2 2 cm. Midline shift to the right and lateral ventricle effacement are also seen.
Fig. 5
Post-gadolinium T1-weighted MRI showing partly cystic and haemorrhagic metastases in the frontal and parietal lobes with oedema and mass effect.
DISCUSSION Thymoma and lymphoma are the commonest primary thymic neoplasms, but the differential diagnosis should also include germ cell tumours because of their sensitivity to modern therapy.5 Neuroendocrine tumours, also found in the thymus, arise from Kulchitsky cells and vary in malignant potential. The histopathological classification and anatomical staging of primary thymic tumours remain controversial.6;7 Initial classifications identified thymomas and lymphomas, based on the ratio of epithelial to lymphocytic cells,7 and included a lymphoepithelial mixed cell type identified by Masaoka et al.8 In 1977 Shimosato et al.9 proposed that some thymomas be classified as a thymic carcinoma type, and additional subtypes were added subsequently.10 LeGolvan and Abell11 found the 5-year survival of 65% of thymic epithelial tumour patients was related to local invasion rather than to cell type. In 1985 Marino and Muller-Hermelink introduced a Journal of Clinical Neuroscience (2004) 11(2)
classification of thymic epithelial tumours (TETs) according to histologic resemblance of the epithelial tumour cells to normal thymic cortical or medullary cells.12 Medullary and mixed thymomas were considered benign, cortical thymoma or well-differentiated thymic carcinoma were usually invasive and had a high frequency of intrathoracic metastasis. This system was not well accepted because of its poor prognostic ability and its confusing terminology.13;14 In 1999, the WHO published a scheme for thymoma using three categories based on prognosis, tumour epithelial cell morphology and the epithelial cell/lymphocyte ratio.1 Thymic carcinoma (type C) is more likely to metastasise than other types. In 1981 Masaoka developed a staging system for thymic tumours,4 which was subsequently modified15 as follows: Stage I. The tumour is encapsulated, still contained within the thymus and may invade into but not through the capsule.
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Haemorrhagic brain metastasis from a thymic carcinoma 193
Fig. 6 Photomicrograph showing large cell malignant tumour infiltrating cerebral tissue. Pleomorphic cells with vesicular nuclear chromatin and prominent nucleoli are present. A high mitotic rate, necrosis and haemorrhage are visible (Haematoxylin & eosin, 400).
Stage II. Tumour invades beyond the capsule into nearby fatty tissue; may be adherent to, but not breaking through, the pleura or pericardium. Stage III. Tumour extends into neighbouring tissues or organs, including pericardium, lungs, main blood vessels. Stage IVa. Tumour spreads widely throughout the pleura and /or pericardium. Stage IVb. Extrathoracic spread. Tumour spreads to distant organs via lymphatic or haematogenous systems. This staging system is considered to be the most important prognostic factor.14 TETs affect men and women nearly equally, with mean ages varying between 49 and 62.7 Thirty to fifty percent of patients are asymptomatic, where the mass is detected during a routine chest X-ray. About 30% of patients present with compression effects on adjacent structures such as lung, trachea or major blood vessels which may cause cough, chest pain, dyspnoea, dysphagia, hoarseness or recurrent chest infection.7;16 One-third present with paraneoplastic syndromes, 5% with red cell aplasia and 5–12% with hypogammaglobulinaemia. Thirty to fifty percent may present with myasthenia gravis, but 15% of patients with myasthenia gravis would have thymoma. Seventeen to twenty eight percent patients with thymoma have other malignancy.17 Thymic carcinoma is an invasive tumour accounting for 6% of all thymic tumours16 Metastases are not uncommon to the regional lymph nodes and/or through haematogenous pathways to distant organs, particularly bone, lung and liver18–21 but rarely to the central nervous system.21–23 Most brain metastases are parenchymal. Extra-axial metastasis is extremely unusual.18 Yamamura et al.22 found 27 documented cases in 1993 of intracranial metastasis from thymic carcinoma. The overall 5-year survival rate for high-grade thymic carcinoma is 15–19%.7;16 Surgery, radiotherapy and chemotherapy are recommended as the most effective treatment for thymic carcinoma.2;3;24 . Hanna et al.5 report that thymic carcinoma are chemotherapy-sensitive tumours with a 30–50 % 5-year survival. Review of the literature reveals the importance of resection of a cerebral lesion in patients with known thymic carcinoma to identify the histopathology. Irradiation of the lesion is then ª 2003 Elsevier Ltd. All rights reserved.
recommended for better quality of life.21;22;25 Our patient presented after a short symptomatic period and did not display myasthenia gravis or any other primary malignancy on full body screening. His biochemistry showed no abnormalities. Disease progression with the presence of two brain metastases having cystic necrosis and haemorrhagic components indicates the aggressive nature of this patient’s tumour, with only one metastasis amenable to resection. Despite craniotomy, his condition rapidly deteriorated even before radiotherapy could be started. This associates the histologic appearance of this tumour with very poor survival. CONCLUSION Thymic carcinoma is a rare tumour. Review of the literature shows this tumour’s lack of predilection for spread to the brain, and the potential for thymic brain metastases to haemorrhage. The prognosis for patients is grim with very short life expectancy. We believe that the presence of haemorrhage and cystic necrosis on imaging indicate the aggressive nature of tumour in a patient diagnosed with Type C TET. Intensive management is vital to improve quality of life and survival rate for these patients. In our opinion the best therapeutic option is surgical resection with radiotherapy and chemotherapy. Frameless stereotactic craniotomy is recommended for better localisation and safer resection. ACKNOWLEDGEMENTS The authors thank Dr. N. Pavlakis, Oncology Department, Royal North Shore Hospital, for support and Dr. C. McKenzie, Department of Anatomical Pathology, Royal North Shore Hospital, for provision of photomicrographs. Sarah Smith is supported by the Andrew Olle Memorial Trust.
REFERENCES 1. Rosai J. Histological typing of tumors of the thymus. In: World Health Organisation International Histological Classification of Tumors, Heidelberg; 1999. 2. Ritter JH, Wick MR. Primary carcinomas of the thymus gland. Semin Diagn Pathol 1999; 16: 18–31.
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3. Fletcher CD. Diagnostic Histopathology of Tumors, second edn. Churchill Livingstone, London; 2000: 1270–1307. 4. Masaoka A, Monden Y, Nakahara K, Tanioka T. Follow-up study of thymomas with special reference to their clinical stages. Cancer 1981; 48: 2485–2492. 5. Hanna N, Gharpure VS, Abonour R, Cornetta K, Loehrer Sr PJ. High-dose carboplatin with etoposide in patients with recurrent thymoma: the Indiana University experience. Bone Marrow Transplant 2001; 28: 435–438. 6. Wilkins KB, Sheikh E, Green R, Patel M, George S, Takano M, Diener-West M, Welsh J, Howard S, Askin F. Clinical and pathologic predictors of survival in patients with thymoma. Ann Surg 1999; 230: 562–572. 7. Chalabreysse L, Roy P, Cordier JF, Loire R, Gamondes JP, Thivolet-Bejui F. Correlation of the WHO schema for the classification of thymic epithelial neoplasms with prognosis: a retrospective study of 90 tumors. Am J Surg Pathol 2002; 26: 1605–1611. 8. Masaoka A, Yamakawa Y. TNM classification of thymic epithelial tumors. Gan To Kagaku Ryoho 1997; 24: 749–754. 9. Shimosato Y, Kameya T, Nagai K, Suemasu K. Squamous cell carcinoma of the thymus. An analysis of eight cases. Am J Surg Pathol 1977; 1: 109–121. 10. Levine GD, Rosai J. Thymic hyperplasia and neoplasia: a review of current concepts. Hum Pathol 1978; 9: 495–515. 11. Legolvan DP, Abell MR. Thymomas. Cancer 1977; 39: 2142–2157. 12. Marino M, Muller-Hermelink HK. Thymoma and thymic carcinoma. Relation of thymoma epithelial cells to the cortical and medullary differentiation of thymus. Virchows Arch A Pathol Anat Histopathol 1985; 407: 119–149. 13. Pan CC, Wu HP, Yang CF, Chen WY, Chiang H. The clinicopathological correlation of epithelial subtyping in thymoma: a study of 112 consecutive cases. Hum Pathol 1994; 25: 893–899. 14. Dawson A, Ibrahim NB, Gibbs AR. Observer variation in the histopathological classification of thymoma: correlation with prognosis. J Clin Pathol 1994; 47: 519–523. 15. Koga K, Matsuno Y, Noguchi M, Mukai K, Asamura H, Goya T, Shimosato Y. A review of 79 thymomas: modification of staging system and reappraisal of conventional division into invasive and non-invasive thymoma. Pathol Int 1994; 44: 359–367. 16. Regnard JF, Magdeleinat P, Dromer C, Dulmet E, De MV, Levi JF, Levasseur P. Prognostic factors and long-term results after thymoma resection: a series of 307 patients. J Thorac Cardiovasc Surg 1996; 112: 376–384. 17. Welsh JS, Wilkins KB, Green R, Bulkley G, Askin F, Diener-West M, Howard SP. Association between thymoma and second neoplasms. JAMA 2000; 283: 1142–1143. 18. Ahn JY, Kim NK, Oh D, Ahn HJ. Thymic carcinoma with brain metastasis mimicking meningioma. J Neurooncol 2002; 58: 193–199. 19. Zhang Z, Cui Y, Li B, Wang F, Li Z, Sun C, Xu L. Thymic carcinoma (report of 14 cases). Chin Med Sci J 1997; 12: 252–255. 20. Thomas CR, Wright CD, Loehrer PJ. Thymoma: state of the art. J Clin Oncol 1999; 17: 2280–2289. 21. Nagakawa K, Sakaki S, Oka Y, Matsuoka K. Malignant thymoma with intracranial metastases. No Shinkei Geka – Neurol Surg 1988; 16(Suppl 5): 589–595. 22. Yamamura K, Kubo O, Aoki N, Kagawa M. Falx metastasis of thymic carcinoma: a case report and review of literature. No Shinkei Geka 1993; 21: 921–924. 23. Mizushima H, Matsumoto K, Ryu H, Usami S, Doi H, Kuwasawa J, Matsui S. Cerebral metastasis from malignant thymoma. No To Shinkei 1988; 40: 1157–1162. 24. Geffen DB, Benharroch D, Yellin A, Ariad S, Or R, Cohen Y. Multimodal treatment of metastatic thymic carcinoma including high-dose chemotherapy with autologous stem cell transplantation: report of a case with more than 4-year disease-free survival. Am J Clin Oncol 2001; 24: 566–569. 25. Dewes W, Chandler WF, Gormanns R, Ebhardt G. Brain metastasis of an invasive thymoma. Neurosurgery 1987; 20: 484–486.
Paradoxical embolism secondary to ovarian carcinoma resulting in stroke D.J. Holthouse MBBS HON, P. Robbins P. Watson MBBS FRACS
MBBS FACP,
Departments of Neurosurgery, Sir Charles Gairdner Hospital and Pathcentre, QE II Medical Centre, Australia
Journal of Clinical Neuroscience (2004) 11(2)
Summary A middle aged woman presented with a posterior fossa stroke after an elective ear nose and throat procedure. The occurrence of a paradoxical embolism was suspected. The evidence for this and a discussion about this condition are presented. ª 2003 Elsevier Ltd. All rights reserved. Journal of Clinical Neuroscience (2004) 11(2), 194–196 0967-5868/$ - see front matter ª 2003 Elsevier Ltd. All rights reserved. doi:10.1016/S0967-5868(03)00194-2
Keywords: stoke, paradoxical embolism, ovary Received 9 May 2003 Accepted 23 May 2003 Correspondence to: Dr. David J. Holthouse, MBBSHON, 39 Doney Street, Alfred Cove, WA 6154, Australia. Tel.: +08-9346-2865; E-mail:
[email protected]
CASE REPORT A 51-year-old Asian woman presented 3 days after rhinoplasty surgery with drowsiness (GCS 11). The procedure had been uneventful with no periods of hypoxia or hypotension, and she was discharged the following day. According to her relatives, she was relatively withdrawn, drowsy and progressively deteriorating on the morning of presentation. When initially seen she was moving all limbs to command, but she then deteriorated rapidly (GCS 9). A CT head revealed a large cerebellar infarct with secondary hydrocephalus (Fig. 1). She had no significant medical history. The patient was taken to theatre and an external ventricular drain was placed. The patient’s condition improved but she remained at a GCS of 13 and it was apparent that she had bilateral abducens nerve palsies. During her stay in the intensive care unit she demonstrated a tendency to desaturate and an echocardiogram was ordered. There was no evidence of vegetations, but the right ventricle was severly dyskinetic, and a high resolution CT chest was ordered to exclude a significant pulmonary embolus. A large embolus involving the right pulmonary artery (Fig. 2) was identified. There was no evidence of DVT on calf Dopplers. In addition, it was noted on the echocardiogram that there was a patent foramen ovale. As a result of the haemodynamic changes there was significant right to left shunting. The right atrial pressure was 50 mm Hg. The possibility of a paradoxical embolism was raised. It was noted that there was a pelvic mass on examination of the abdomen. CT abdomen revealed a large ovarian mass which was thought to represent an ovarian cancer (Fig. 3). The patient was heparinized and maintained with an APTT of 60–70. A CT angiogram of the head revealed evidence of an infarct in the left PICA region with obstruction of this vessel distally. She remained in the intensive care unit for 2 weeks and required a tracheostomy because she was failing to adequately guard her airway. The patient was transferred to a high dependency unit where she continued to improve. She developed severe per-rectal bleeding which was investigated by colonoscopy. The cause was attributed to haemorrhoids. Anticoagulation was ceased and a caval umbrella was inserted. One month after presentation the right ovarian mass was removed and a modified radical hysterectomy performed. The ovarian malignancy was an adenosquamous carcinoma with no signs of dissemination (grade 1). Histopathologically, there was a question as to whether it has arisen in an area of old scarring secondary to endometriosis. Post operatively the patient had problems with ileus and a prolonged gastric stasis. She required long periods of total parental nutrition and subsequently nasojejª 2003 Elsevier Ltd. All rights reserved.
