Metastatic Testicular Seminoma—A Case Report

Metastatic Testicular Seminoma—A Case Report

Auris Nasus Larynx 29 (2002) 219– 222 Case report Metastatic Testicular Seminoma —A Case Report Rajiv K. Bhalla a,*, Te...

152KB Sizes 0 Downloads 108 Views

Auris Nasus Larynx 29 (2002) 219– 222

Case report

Metastatic Testicular Seminoma —A Case Report Rajiv K. Bhalla a,*, Terence M. Jones a, Doug Errington b, Nicholas J. Roland a a

Department of Otolaryngology, Uni6ersity Hospital Aintree, Lower Lane, Li6erpool L9 7AL, UK b Clatterbridge Centre for Oncology, Li6erpool, UK

Received 15 January 2001; received in revised form 10 August 2001; accepted 21 September 2001

Abstract We present the case of a 42-year-old male who presented with a hot, tender swelling in the left supraclavicular fossa. He was pyrexial on presentation with a mildly elevated leucocyte count of 12.4 × 109/l. Clinical examination, including full ear, nose and throat assessment, proved unremarkable. The medical history revealed that 2 years earlier the patient had been diagnosed with a testicular seminoma for which he underwent a right inguinal orchidectomy and abdominal radiotherapy. CT scan highlighted a 6 cm para-laryngeal mass, of mixed attenuation, with an adjacent region of inflammation. Overall appearance was suggestive of an infective mass. Ultrasound-guided fine needle aspiration cytology revealed a metastatic seminomatous deposit. Imaging of the chest and abdomen revealed this as the only site of metastasis. He is currently undergoing chemotherapy, and is responding well. We review the pathology of testicular seminoma. This case highlights the myriad of pathologies that may present as a lump in the neck. © 2002 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Seminoma; Testicular tumour; Metastasis; Head and neck; Lymph nodes

1. Case report A 42-year-old man presented with a 7-day history of an inflamed mass in the left supraclavicular fossa. He had felt unwell with a viral-like illness for 48 h prior to the appearance of this mass. On presentation he was comfortable at rest, although pyrexial with a temperature of 38.3° C. Examination revealed an 8× 10 cm mass in the left supraclavicular fossa. The overlying tissue was oedematous and hot to the touch. There was marked distension of the overlying external jugular vein. He had markedly restricted neck movements, due largely to discomfort rather than steric hindrance. Full ear, nose and throat examination, including flexible nasendoscopy of the upper aerodigestive tract, was entirely normal. There was no clinical evidence of further lymphadenopathy, and his chest was clinically and  Bhalla R.K. and Jones T.M. jointly wrote the paper. The patient was under the joint care of Roland N.J. and Errington R.D.; both provided expert guidance and editorial advice during the writing of the report. Bhalla R.K. accepts full responsibility for the integrity of the paper. * Corresponding author. Tel.: + 44-151-529-5980; fax: + 44-151529-5263. E-mail address: [email protected] (R.K. Bhalla).

radiologically clear. Examination of his abdomen revealed no masses or organomegaly. Of note in his past medical history, he had a right inguinal orchidectomy with adjuvant para-aortic node radiotherapy (22× 9.5 cm fields, anterior/posterior opposed; radiation dose 30 Gy MPD/15F/21 days) for stage 1 testicular seminoma some 2 years prior. Check CT scans following radiotherapy were clear of disease, and tumour marker levels of alpha-fetoprotein (aFP), the b-subunit of human Chorionic Gonadotrophin (bhCG) and lactic dehydrogenase (LDH) had returned to normal. Routine blood investigations at this admission showed a mildly elevated white cell count at 12.4×109/ l. All other bloods, including tumour markers (aFP, bhCG and LDH), were within normal range. Urgent CT scanning over the bank holiday weekend showed a 6 cm para-laryngeal mass of mixed attenuation with adjacent inflammation. The mass was large enough to displace adjacent structures, most notably causing deviation of the trachea to the right and complete compression of the left internal jugular vein (Fig. 1). The differential diagnosis was of an infected mass, either a branchial cyst or an abscess associated with sternocleidomastoid, or a necrotic lymph node.

0385-8146/02/$ - see front matter © 2002 Elsevier Science Ireland Ltd. All rights reserved. PII: S 0 3 8 5 - 8 1 4 6 ( 0 1 ) 0 0 1 3 2 - 8


R.K. Bhalla et al. / Auris Nasus Larynx 29 (2002) 219–222

As the clinical evidence supported the diagnosis of an inflammatory or infective process, an initial treatment regime comprising intravenous Cefuroxime and Metronidazole, antipyretics and analgesia was implemented. On the 2nd day of admission an ultrasoundguided fine needle aspirate was performed to obtain a cytological specimen. Over the next 48 h, the pyrexia settled and the mass decreased in size, appearing less inflamed. Subsequent results from the cytological examination revealed the mass to be a metastatic seminomatous deposit (Fig. 2). Further abdominal and thoracic CT scans confirmed these sites to be free of disease. The patient has subsequently undergone a chemotherapeutic regime of VP-16 (Etoposide) and Cis-platin. Doses were calculated on the basis of a body surface area of 2 m2. VP-16 (ETP) 120 mg/m2 iv was given on days 1, 2 and 3. Cis-platin 50 mg/m2 iv was given on days 1 and 2. Four cycles at 21-day intervals were given [1]. The onset of cycle 2 was delayed as a result of a low blood count, thought to be due to reduced marrow tolerance following the previous radiotherapy. Subsequent use of Neupogen (recombinant human granulocyte-colony stimulating factor) alleviated the problems associated with a low peripheral blood count although profound marrow suppression complicated treatment following the final cycle of chemotherapy. Initial imaging showed PR (partial response) to therapy although the patient was clinically CR (complete response). Consolidation radiotherapy was not indicated [2]. The patient remains CR at 18month follow-up.

2. Discussion Tumours of the male gonad are classified into two broad categories, namely seminoma and nonseminomatous germ cell tumours (NSGCT). Whatever the cellular origin of the tumour, the most common presenting feature is a painless testicular enlargement. Although, the rate of progression differs depending on the histology, all germ cell tumours have the propensity to metastasize. Lymphatic spread is common to all testicular tumours. Sequential spread, initially involving the retroperitoneal, para-aortic and subsequently the mediastinal and supraclavicular lymph nodes, is typical. Haematogenous spread is also possible, primarily to the lungs, but also to the liver, brain and bony skeleton. Three clinical stages of tumour progression are defined. Stage 1 Stage 2 Stage 3

Tumour confined to the testis Distant spread, confined to infradiaphragmatic, retroperitoneal lymph nodes Distant spread, above the diaphragm and/ or not confined to retroperitoneal lymph nodes

Stages 2 and 3 are further subdivided into ‘early’ or ‘advanced’ depending on the tumour burden in the secondary deposits, as assessed radiologically.

Fig. 1. CT image identifying left para-laryngeal tumour (arrows). Note tracheal deviation to the right and complete compression of the ipsilateral internal jugular vein.

R.K. Bhalla et al. / Auris Nasus Larynx 29 (2002) 219–222


Fig. 2. Cytology of neck mass indicating metastatic seminoma.

Seminoma is the commonest of the testicular germ cell tumours, accounting for approximately 30% of all testicular neoplasms. Their peak incidence occurs in the fourth decade; they are virtually unheard of in infants. The tumours tend to grow rapidly but typically remain confined within the tunica albuginea of the testis. Should metastasis occur, lymphatic spread is more common with haematogenous spread occuring much later in the disease process. Consequently, approximately 70% of seminomas present at clinical stage 1 [3]. Testicular germ cell tumours secrete polypeptide hormones and enzymes that have proved extremely useful in the diagnosis and monitoring of therapeutic response of testicular tumours. Such tumour markers include alpha-fetoprotein (aFP), the b-subunit of human chorionic gonadotrophin (bhCG), placental alkaline phosphatase, placental lactogen and lactic dehydrogenase. aFP and bhCG are the most commonly used markers in clinical practice. Their measurement, however, has a very limited role in the management of patients with seminoma [4], as reflected by the normal values in our patient. Seminomas and their metastatic deposits are extremely radiosensitive. This, in addition to the delayed metastasis of seminomas, has resulted in a cure rate in excess of 90% of patients with stages 1 or 2 disease, when they are treated with orchidectomy and adjuvant para-aortic radiotherapy. Metastatic spread to other sites in the head and neck, although rare, have been reported [5– 9]. Most of these extra lymphatic deposits are assumed to have spread via the haematogenous route. In fact, several distinct routes of haematogenous spread have been described. Batson [10] proposed metastatic reflux via the vertebral

or the jugular venous systems. He suggested that the propulsive mechanism driving this mode of spread was transient increases in intra-abdominal and -thoracic pressure which could occur, for example, whilst straining at stool. Subsequent work [11–13] supported this theory. In addition, Nahum et al. [14] proposed that haematogenous spread of testicular tumour metastases to the head and neck could occur along the following route: sacral venous plexus veins to inferior vena cava, to heart, to pulmonary circulation, back to the heart and then ultimately, via the arterial system, to the head and neck. Supraclavicular deposition of metastatic seminoma is known to occur, typically as a late stage development following involvement of the more caudal lymph node groups [15]. However, the novelty of our case is the appearance of metastatic deposition in a solitary supraclavicular lymph node in the absence of any radiological evidence of concurrent lymphatic disease. Why this solitary deposit presented as an inflamed mass is a subject for some speculation. One possible mechanism could be a secondary bacterial infection following spontaneous haemorrhage into the substance of the tumour mass. Whatever the exact mechanism, this case serves to remind us of the myriad pathologies that may present as a solitary cervical mass.

Acknowledgements We would like to acknowledge the assistance of Dr John Sheard, Consultant Histopathologist and Cytologist, University Hospital Aintree, Liverpool, UK in producing the cytology images used in this report.


R.K. Bhalla et al. / Auris Nasus Larynx 29 (2002) 219–222

References [1] Horwich A, Oliver RT, Wilkinson PM, et al. A Medical Research Council randomized trial of single agent carboplatin versus etoposide and cisplatin for advanced metastatic seminoma. Eur J Cancer 1996;83(12):1623 – 9. [2] Duchesne GM, Senning SP, Aass N, et al. Radiotherapy after chemotherapy for metastatic seminoma — a diminishing role. Eur J Cancer 1997;33(6):829 –35. [3] Cotran RS, Kumar V, Robbins SL. Male genital system. In: Robbins Pathological Basis of Disease, 5th ed. Philadelphia, PA: W.B. Saunders Company, 1994:1015 – 22. [4] Bartlett NL, Freiha FS, Torti FM. Serum markers in germ cell neoplasms. Hematol Oncol Clin North Am 1991;5(6):1245 – 60. [5] Andaz C, Alsanjari N, Garth RJ, Dearnaley DP. Metastatic seminoma of the sphenoid sinus. J Laryngol Otol 1991;105:1075 – 8. [6] Ballinger WH, Wesley RE. Seminoma metastatic to the orbit. Ophthal Surg 1984;15(2):120 –1. [7] Kobayashi K, Igarashi M, Ohashi K, McBride RA. Metastatic seminoma of the temporal bone. Arch Otolaryngol Head Neck Surg 1986;112(1):102 –5.

[8] Lainson PA, Khowassah MA, Tewfik HH. Seminoma metastatic to the jaws. Report of a case. Oral Surg Oral Med Oral Pathol 1975;40(3):404 – 8. [9] Rush JA, Older JJ, Richman AV. Testicular seminoma metastatic to the orbit. Am J Ophthalmol 1981;91(2):258 –60. [10] Batson OV. The function of the vertebral veins and their role in the spread of metastases. Ann Surg 1940;112:138 – 49. [11] Bizon JG, Newman RK. Metastatic melanoma to the ethmoid sinus. Arch Otolaryngol 1986;112:664 – 7. [12] Kawai N, Asakura K, Sambe S, Kataura A, Enomoto K. Metastatic squamous cell carcinoma of the paranasal sinuses from a primary squamous cell carcinoma of the urinary bladder. J Laryngol Otol 1989;103(6):602 – 4. [13] McClatchey KD, Lloyd RV, Schaldenbrand JD. Metastatic carcinoma to the sphenoid sinus: case report and review of the literature. Arch Otolaryngol 1985;241(3):219 – 24. [14] Nahum AM, Bailey BJ. Malignant tumours metastatic to the paranasal sinuses, case report and review of literature. Laryngoscope 1963;73:942 – 53. [15] Wood A, Robson N, Tung K, Mead G. Patterns of supradiaphragmatic metastases in testicular germ cell tumours. Clin Radiol 1996;51(4):273 – 6.