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Computed Tomography of Lethal Midline Granuloma

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Computed Tomography of Lethal Midline Granuloma 대 한방사선 의 학회 지 1991; 27(4) : 513~517 Journal of Korean Radiological Society, July, 1991 Computed Tomography of Lethal Midline Granuloma Ho Suk Lee, M.D., Tae Ho Kim, M.D., Kyung Jin Sub, M.D., Tae Hun Kim, M.D. Yong Joo Kirn, M.D., Dul‘ Sik Kang, M.D. Department of Diagnostic Radiology, CoJ1ege of Medicine, Kyungpook National University - Ab8tract- In order to clarify the CT findings oflethal midline granuloma (LMG) diagnosed clinically or histopathologically, the authors retrospectively analyzed 12 patients who were seen at Kyungpook National University Hospital from February 1985 to August 1989. CT showed nasal mucosal thickening and/or soft tissue mass (9 cases), spreading of the lesions along the facial subcutaneous fat plane (8 cases), invasion into the paranasal sinuses (5 cases), bone destruction (5 cases), nasopharyngeal mass lesion (2 cases), and extension of the lesion into the infratemporal fossa (1 case). In spite of the fact that CT does not make definitive diagnosis of LMG, it permits evaluation of the extent of the lesion, detection of the combined lesion, differential diagnosis, and close monitoring of its evolution under treatment. Index Word8: Nose , Lethal Midline Granuloma 261.622 Paranasal sinuses. Computed Tomography 23.1211 Nose. Computed Tomography 261. 1211 Recent research on the condition historically Introduction known as lethal midline granuloma concludes that it is a form of T-cell lymphoma.(2) Since the first report ofMcBride (1897)(1). the tenn The prominent histological features ofLMG are in­ lethal midline granuloma (LMG) and it8 various f1ammation, necrosis, and thrombosis with infiltra­ synonyms-progressive lethal granulomatous 비cera­ tion of the atypical histiocytes into the perivascular tion (Stewart. 1933).lethal granulomatous ulceration connective tissue of midline facial tissue (Williams. 1949). idiopathic The purpose of this retrospectlve study was to lethal granulomatous ulceration (Woodburn & Har­ clarify the CT findings of LMG. ris. 1951), nonhealing granuloma (Waltone, 1959), polymorphic reticulosis (Eichel et a 1., 1966), midline Materials and Methods malignant reticulosis (Kassel et al., 1969), midline granuloma (Dellon, 1977), and lymphomatoid Our study included 12 patients with LMG who granulomatosis (DeRemee et a 1., 1978)-have been were seen at Kyungpook National University Hospital used to describe a rare lesion of a nonhealing from February 1985 to August 1989. They were 9 granuloma that ultimately causes necrosis and men and 3 women with an age range of 17 to 71 years destruction of the nose and midface. According to (mean: 40 yrs). WHO (1978), LMG is defined as a progressively Four cases were pathologically proved and 8 cases destructive nontuberculoid granulomatous lesion had nonspecific pathologic findings, but their clinical localized in the nasal cavity, paranasal sinuses, or findings and courses were identical to LMG. palate and infiltrating the soft and hard tissue All patients were examined with a CT/T 8800 이 논문은 1 99 1 년 l 월 4 일 접수하여 1 9 91 년 5 월 17 일 에 채택되었음 Received January 4. accepted May 17. 1991 - 513- Journal of Korean Radiological Society 1991; 27(4): 513-517 scanner (GE, Milwaukee, Wl, U.S.A.) using con­ Table 1. Clinical Features tiguous 5 or 10-mm-thick sections from the frontal Symptoms/Signs No. of cases s inus to the hyoid bone after 50cc bolus and 100cc 8 Nasal stuffiness dripping of contrast (RayvistR 300) administration. 5 Facial swelling and pain 4 Axial or axial with coronal images were obtained. Mucocutaneous u lceration 3 Nasal discharge 2 Results Swallowing difficulty 2 Sore throat 2 The most common clinical features of LMG was Foulodor nasal stuffiness. Other symptoms and signs includ­ ed facial swelling and pain, mucocutaneous ulcera­ nose (1 case). tion, nasal discharge, and fo ul odor (Table 1). The The main histologicaI findings were acute or primary lesion sites were the nasal cavity (8 casesJ, chronic infIammation (12 cases) and focal or massive nasopharynx (2 casesl, palate (1 casesJ, and external necorsis (7 cases). Atypical histiocyte infiltrations ‘ ',J# 1... .. ""-효l‘ “ - 홈 훌. la lb 2 Fig. 1. a , b. A soft tissue mass lesion is seen in posterior portion ofthe left nasal cavity ‘ Nasal septum is perforated The mucosa of the anterior nasal septum is mildly thickened, and the lesion spreads along the left facial fat plane Soft tissue of slightly lower density in Ieft maxillary sinus suggests infIammation secondary to obstruction of max. illary sinus ostium. Fig.2, Section through the midantrum shows soft tissue mass filling both sides ofthe nasal cavity. Bone destruc­ tions are present involving both medial walls of the maxillary antra. &나"""" k *‘ 3a 3b 4 • Fig.3. a. b. There is a soft tissue mass occupying nasal cavity with mucosal thickening. Irregular bone destruc. tions are present in the medial wall of the right maxillary antrum Chronic sinusitis is present in the right maxillary antrum ‘ Fig. 4. A soft tissue mass lesion is involving the anterior portion of the right nasal cavity and nares - 514- Ho Suk Lee, et al: Computed Tomography of Lethal Midline Granuloma Fig. 5. Midantral scan shows thicken­ ing of the right nares with spreading of the lesion into the soft tissue of the cheek overlying the right antrum. Fig. 6. An axial section through the junction of the nasopharynx and oropharynx shows soft tissue mass n the right nasopharynx with partial obliteration of the right parapharyngeal space. 5 6 were seen in 4 cases, but fibroid necrosis, granuloma, midline d estructive disease , Wegener's and giant cells were not observed granulomatosis, polymorphic reticulosis, and Prominent CT findings included nasal mucosal nonHodgkin's lymphoma.(3) thickening and/or a soft tissue m ass (9 cases) (Fig. The etiology of LMG has been controversial, and 1.2 ,3 ,4). Spreading ofthe lesions aIong the facial sub­ the proposed pathogeneses have been immunologic cutaneous fat plane was noted frequently (8 cases) disorder(4,5), neoplastic process(6), or close relation (Fig. 1.5). Invasion into the paranasal sinuses was with lymphoma(7). But recent research concludes observed in 5 cases‘ the maxillary sinus (5/5), that it is a form of T-celllymphoma(2), and the ap­ ethmoid sinus (5/5) , and sphenoid sinus (4/5) (Fig. 2) ‘ plication ofimmunological studies with monoclonal but frontal sinus invasion was not seen. antibody panels is now a standard procedure and Bone destruction (5 cases) and nasopharyngeal sho 비 d help in avoiding misdiagnosis. Kataura et mass lesion (2 cases) were also observed (Fig. 2 , 3 .6). a l.(8) studied 3 patients with lethal midline Extension of the lesion into the infratemporal fossa granuloma using monoclonal antibodies against T was seen in 1 case (Table 2) cell subsets, clearly demonstrating that the tumor cells in each case were probably T-cell, not from Table 2. CT Findings histiocytes, reticulum cells, or B-cells. CT findings No. of cases The prominent histologicaI features ofLMG are in­ flammation, necrosis, and thrombosis, a 1l 3 ofwhich Nasal mucosal thickening and/or 9 suggest a similarity to Wegener’ s granulomatosis, soft tissue mass Spreading of the lesions along the 8 but differentiate the lesion from lymphosarcoma(9). facial subcutaneous fat plane True vasculitis is a typical finding in Wegener’s ζ 니 Invasion into paranasal sinuses granulomatosis but does not appear in the LMG ‘ DF Bone destruction It p이 ymorphic 끼 a hough cells may infiltrate the Mass in nasopharynx ι perivascular connective tissue mimicking vasculitis. Histologically, the lesions ofLMG are separable from Discussion Wegener’ s granulomatosis by the absence of necrotizing epithelioid granulomas, a tendency The term ‘'lethal midline granuloma" does not toward a necrotizing angioinfiltrativegrowth pattern, properly reflect the current observation that several and abundant atypical lymphoproliferative cellular different diseases can produce noninfectious mid- components( lO). ln LMG cases, only ulceration ofthe facial destruction. In many cases‘ this is neither lethal upper respiratory tract occurs, whereas the lungs and nor midline, and granuloma may be a bsen t. Recent. kidneys are never affected. This specific organ in- ly. the disorders producing erosion of the upper volvement is a lso a significant point in differential aerodigestive passage are more accurately classified diagnosis from Wegener‘ s granulomatosis by clinical and histological criteria as idiopathic A recen t study on the CT findings of LMG show - 515- Journal of Korean Radiolog ical Society 1991 ; 27(4): 513-517 ed a more or less complete filling of the air cavities granuloma. Otolaryng Clinics North America 1982: ofthe face by an abnormal soft tissue mass reaching 15:685-692 the nasal cavity and the nasopharynx. the ethmoidal 2. Platt J C. Tomich CE. Campbell S. Malignant lym­ cells. the sphenoidal sinus. the maxillary sinus. and phoma presenting as a midline lethal granuloma. J Oral Maxillofac Surg 1989; 47:511-513 the frontal sinus( 11). These findings are identical to 3. Pickens JP. Modica L. Current concepts of the lethal the results of our study. except for the frontal sinus midline granuloma syndrome. Otolaryngol Head involvement. CT permits the precise evaluation of the Neck Surg 1989; 100:623-630 extent of the lesions. It is known that the lesions can 4. Friedmann I. Sando 1, Balkany T. Clinical records. extend to the intracranium. to the infratemporal Idiopathic pleomorphic midfacial granuloma fossa. and to the orbit and can infiltrate the sub­ (Stewart’s type). J Laryngol Otol 1978; 92:610 cutaneous tissue ofthe face(II). In this study. cranial 5. Fau ci AS. Johnson RE. WolffSM. Radiation therapy or orbital invasion was not observed. but the of midline granuloma. Annals of Internal Medicine spreading ofthe lesion along the facial subcutaneous 1976; 84:140-147 fat plane was frequently seen. Paranasal sinus inva­ 6. Eichel BS. Maeberg TE.
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