Cutaneous cytomegalovirus vasculitis: An unusual clinical presentation of a common opportunistic pathogen

HUMAN

PATHOLOGY--VOLUME

13, N U M B E R

12

DeceMber 1982

T h e m a j o r i t y o f l e s i o n s c o n t a i n i n g a r t h r o c o n i d i a occ u r r e d in p a t i e n t s in t h e t h i r d a n d f o u r t h d e c a d e s o f life, with t h e i n c i d e n c e steadily d e c r e a s i n g in t h e f o l l o w i n g two d e c a d e s . T h e o l d e s t p a t i e n t r e p o r t e d was a 6 1 - y e a r - o l d F i l i p i n o 2 n m n w i t h a scalp lesion; his case was u n u s u a l in t e r m o f lfis a g e a n d race a n d t h e site o f tlte lesion. W i t h t h e e x c e p t i o n o f two blacks r e p o r t e d by J o r e s s a n d Bt, s h u e f f s and Guilfoil, s the patient whose race was mentioned (25 cases) w e r e wlfite, as was o u r p a t i e n t . Inchtding the present report, only three reports describe e x t r a p n l m o n a r y a r t h r o c o n i d i n m f o r m a t i o n . T h e first was a report of injection grannloma by Levan and Huntington, 2 the second a report of a gastric sample by Joress and B n s h n e f f . 3 T h e e x t r a p u l m o n a r y f o r m a t i o n in t h e l a t t e r case m a y h a v e e m a n a t e d f r o m t h e h m g via a s p i r a t e d s p u t u m . As in o u r p a t i e n t ' s s e c o n d skin b i o p s y (1978), a r t h r o c o n i d i a m a y b e o v e r l o o k e d , T h e m o r p h o l o g i c r e c o g n i t i o n o f art h r o c o n i d i a m a y b e difficult. W l t e n b e g i n n i n g s p h e r u l e s and endospores are present, one can be confident of the d i a g n o s i s (fig. lc), I f o n l y isolated h y p h a l e l e m e n t s a r e seen, cuhure and complement fixation should be performed. T i r e c o n d i t i o n s r e q u i r e d f o r tissue mycelia! g r o w t h a r e n o t well k n o w n . O c c a s i o n a l r e p o r t s d e s c r i b i n g t h e mycelial f o r m in t h e l u n g n o t e c o n n e c t i o n s w i t h b r o n c l t i o l e s o r b r o n c h i . 9-12 It ltas b e e n s p e c u l a t e d tltat tiffs c o o l e r t e m p e r a t n r e a n d Itiglter o x y g e n t e n s i o n c r e a t e a n o p t i m a l c u l t u r e e n v i r o n m e n t t h a t a p p r o x i m a t e s tlte n a t u r a l l t a b i t a t f o r tim o r g a n i s m , lt't3"t4 S n c h c o n d i t i o n s m a y also e x p l a i n t h e f i n d ings in tire c u t a n e o u s lesions r e p o r t e d by L e v a n a n d H u n t i n g t o n 2 a n d in t h e m u l t i p l e sites o f skin, s n b c n t a n e o u s CSF r e s e r v o i r , a n d p n l m o n a r y g r a n u l o m a in o u r p a t i e n t . T i r e C S F l o c a t i o n o f C. immitis a r t h r o c o n i d i a is consist e n t with o t h e r r e p o r t s o f e x t r a p u h n o n a r y C. immitis art h r o c o n i d i a , T h e r e a s o n f o r t h e p r e d o m i n a n c e o f t h e art b r o c o n i d i n m f o r m a m o n g wlfite p a t i e n t s a n d m a l e p a t i e n t s remains unexplained. ACKNOWLEDGMENTS T i l e a u t h o r s t h a n k A r t h u r U n d e r m a n , MD, S n s a n B. Turkel, MD, Debbie Anderson, and Sue Evans, MT (ASCP). REFERENCES 1. Biddle M: Coccidioidomycosis: the diagnosis and epidemlology. USC Med Bull 5;12, 1953

2. Levan NE, [luntington RWJr: Primary cutaneous coccldioldomycosls in agricultural workers. Arch Dermatol 92:215, 1965 3. Joress MH, Buslmeff BP: Pulmonary coccidloidomycosis: clinical and roentgenological observations in residual leslous. Dis Chest 22:55, 1952 4. Forbus WD, Bestebreurtje AM: Coccidioidmnycosis: a study of 95 cases of the disseminated type with special reference to the pathogenesis of the disease. Milit Surg 99:653, 1946 5. ttuntingtou RW Jr, Waldmann WJ, Sargent JA, et al: Pathologic and clinical observations on 142 cases of fatal coccidioidom)'cosis with necropsy. In Ajello L (ed): Coccidioidomycosis. Tucson, University of Arizona Press, 1967, p 143 6. Ajello I.: Coccidioidomycosis: Current Clinical and Diagnostic Stains. Miami, Symposia Specialists, 1977 7. Drutz DJ, Catanzar OA: Coccidioldomycosis, part I (state of the art) and part il. Am Rev Respir Dis 117:559 aml 727, 1978 8. Guilfoil PII: Surgical therapy for pulmonary coccidioidomycosis. Am Surg 19:975, 1953 9. Alznauer RL, Rolle C, Pierce W: Analysis of focalized pulmonary granulomas due to Coccidioidesimmitis. Arch Pathol 59:6.tl, 1955 10. Deppisch LM, Donowho EM: Pulmonary coccidioidom)cosis. AmJ Clin Pathol 58:489, 1972 11. Medeiros AA, Mark EJ: A 51-year-old woman with chest pain aud a coin lesion. N EnglJ Med 302:218, 1980 12. Wiun WA: A long-term stud)' of 300 patients with cavitary abscess lesions of the hmg ofcoccidioidal origin: an analytical stud)" with special reference to treatment. Dis Chest 5.t(suppl 1):12, 1968 13, Fiese MJ, Cheu S, Sorensen RIt: Mycelial forms ofCoccMioidesimmitis in sputum and tissues of the human host. Ann Intern Med 43:255, 1955 14. Puckett TF: Ilyphae ofCoccidioidesimmitis in tissues of the human bost. Am Rev Tuber 70:320, 1954 15. Kruse RIt, Green TD, Leeder WD: Infection of control monkeys with CoccidioMesimmitisby caging with inoculated monkeys. In Ajello L (ed): Coccidioidom) costs. Tucson, University of Arizona Press, 1967, p 387 16. Sulkin SE, Pike RM: Survey of laboratory-acquired infections. Am J Public Ileahb 41:769, 1951 17. tluntington RW Jr: Coccidioldomycosis. In tlandbuch der Speziellun Pathologischen Anatomie und tlistologie (The Patbologic Anatomy of Mycoses). Berlin, Springer-Verlag, 1971, p 147 18. Bass tiE, Kooperstein SI, Friedman MM, et al: Pulmonary coccidioidomycosis. Dis Cbest 12:271, 1946 19. Smith CE, Beard RR, Saito MT: Pathogenesis ofcoccklioidomycosis with special reference to pulmonary cavitation. Ann Inter Med 29:623, 1948 20. Greer SJ, l-'orseeJH, Mahon tlW; The surgical management of pulmonary coccidioidomycosis in focalized lesions. J Thorac Surg 18:591, 19t9 21. Greer SJ, Grow JB: The surgical lesions of pulmonary coccidioidomycosis. Dis Chest 16:336, 1949 22. Weisel W, Owen GC: Pulmonary resection for coccidioidomycosis: report of a case. J Thorac Surg 18:674, 19-19 23. ForseeJH, Perkins RB: Localized pulmonary coccidioidomycosis: a surgical disease. JAMA 155:!223, 1954 24. Htmtington RW Jr: Diagnostic and biologic implication of the histopathology of coccidioidomycosis. In Proceedings of Symposium on Coccidioidomycosis, US Public lleahb Pnblication no. 575. Atlanta, US Communicable Disease Center, 1957, p 36

CUTANEOUS CYTOMEGALOVIRUS VASCULITIS: AN UNUSUAL CLINICAL PRESENTATION OF A C O M M O N OPPORTUNISTIC PATHOGEN JEFFRE'," L. CURTIS, MD,* A,XD BARBARA ~l. EGBERT, M D t

A case of cutaneous leukocytoclastic cytomegalovirus (CMV) vasculitis arising in a man with acute myelogenous leukemia is described. An antemortem biopsy specimen of ulcerated skin and an open lung biopsy specimen showed leukocytoclastic vasculitis and no,specific diffuse interstitial pneumonitis, respectively, neither Accepted for publication April 12, 1982. *Fellow, Surgical Pathology, Stanford University Medical Center, Stanford, California. "'~Staff Pathologist, Palo Alto Veterans Administration Hospital, Palo Alto, California; and Cli,tical Assistant Professor, Department of Pathology, Stanford University Medical Center. Address correspondence anti reprint requests to Dr. Curtis, Department of Surgical Pathology, Stanford University Medical Center, Stanford, CA 94305.

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tissue demonstrating viral infection. Autopsy material revealed CMV vasculitis with typical intmnuclear inclusions identified in enlarged endothelial cells associated with thrombus formation and luminal narrowing, in addition to florid CMV pneumovitis. This case represents an unusual although clinically relevant expression of a common opportunistic pathogen. Hum Pathol 13:11381141, 1982. C y t o m e g a l o v i r n s ( C M V ) is r e c o g n i z e d as a n i n f e c t i o n s a g e n t s l t o w i n g a p a r t i c u l a r proclivity f o r tim i l n m u n o c o m p r o m i s e d host. P a t i e n t s with m a l i g n a n c y o r c h r o n i c deb i l i t a t i n g disease a n d r e n a l a n d c a r d i a c a l l o g r a f t r e c i p i e n t s lmve b e e n d e m o n s t r a t e d to b e at h i g h - r i s k f o r d e v e l o p i n g clinically a p p a r e n t lesions. ' a Tiffs D N A virus is o f t e n f o u n d in c o m b i n a t i o ~ witlt t h e two o p p o r t u n i s t i c p r o t o z o a n p a r t -

0046-817718211200ll 138 $00.80 9 W. B. Saunders Co.

CASE STUDIES sites Toxoplasma gondii and Pneumocystis carinii 3-~ and may elicit a wide variety o f clinical symptoms. Pneumonitis, hepatitis, a form o f mononucleosis, chorioretinitis, central and peripheral nervous system abnormalities, gastrointestinal disturbances, renal impairment, and hemolytic anemia are some o f the clinical manifestations documented in the postnatal host. ~'2"6Despite this diversity o f presentation, cutaneous p.athologic features associated with acquired CMV infection are apparently uncommon and have been reported only rarely in the literature. Purpuric and petechial lesions as well as pruritic anti nonpruritic rashes, often following ampicillin therapy, have been associated with CMV mononucleosis but are not commonly biopsied. 7 We could find only three references to cutaneous CMV-induced vasculitis. 7-9 Two o f the patients were chronically ill, one with alcoholic hepatitis and the other as a renal transplant recipient. T h e other reported case, documented serologically, occurred in an adult wonmn with well-controlled insulindependent diabetes mellitus. A biopsy specimen showed subacute nonocclusive vasculitis without endothelial viral inclusions. We report an additional case o f CMV-induced vasculitis, in this instance occurring in an aduh man with acute myelogenous leukemia. REPORT OF A CASE Tile patient was a 58-year-old Caucasian man who was admitted to the Palo Alto Veterans Administration Medical Center for evahmtion and treatment of leukocytosis and anemia. A peripheral blood smear showed a predominance o f blast forms, and a bone marrow aspirate and biopsy specimen obtained shortly after admission revealed acute myelogenous leukemia. Clinical remission was successfldly induced via a D A T (doxorubicin cytosine arabinoside 6thioguanine) protocol regimen and persisted until the time o f death. T h e patient's clinical course during induction and the remainder of his hospital stay was marked by several separate episodes o f sepsis, with both coagulasepositive Staphylococcus aureus and Serratia marcescens grown from blood cuhures. Each episode o f sepsis resulted in the development o f acute adnlt respiratory distress syndrome, which seemed to resolve following administration o f appropriate antibiotics and steroids in all but the last instance. Tllrougllout most o f the second month following induction, the patient's puhnonary function continued to deteriorate, until total ventilatory support was required for the final few weeks o f life. An o p e n lung biopsy specimen showed nonspecific diffuse interstitial pneumonitis. No microorganisms were cuhured from the specimen, and viral studies were not performed. Antemortem serologic data showed elevated titers o f cold agglutinins but were otherwise negative. Legionella titers also were negative. Soon thereafter, the patient developed purple-black necrotic discolorations o f the nose, cheeks, toes, and fingers. These lesions were interpreted clinically to be consistent with purpura fulminans. A biopsy specimen showed leukocytoclastic vasculitis with thrombi in dermal vessels. The skin lesions persisted while tile patient's clinical course continued to deteriorate, and he died approximately two months following induction. At autopsy the patient's lungs were diffusely consolidated with areas o f hemorrhage and necrosis. Microscopic examination showed a fuhninant interstitial pneumonitis v)ith obvious intranuclear and intracytoplasmic inclusions, diagnostic o f CMV infection, present throughout both hmgs in m a n y ' e n l a r g e d alveolar lining cells. Cytomegalovirus inclusions were also seen in endothelial ceils of vessels associated with the necrotizing ecchymoses.

The bone marrow at autopsy showed no evidence o f residual leukemia. All cell lines showed normal morphologic features and maturation, with a mild increase in immature erythroid and myelold forms. P A T H O L O G I C FINDINGS Formaldehyde- and Zenker's-solution-fixed paraffinembedded sections o f skin were obtained both ante mortern, approximately one month before death, and post mortem, at autopsy. T h e s e were p r e p a r e d with hematoxylin-eosin, periodic acid-Schiff, and Gram stains and examined. T h e biopsy specimen o f skin from the right cheek (fig. 1) revealed a relatively normal epidermis; tile underlying dermis showed leukocytoclastic vasculitis that affected many o f the superficial and deep dermal vessels. Neutrophils were present within vessel walls and were associated with karyorrhectic debris and erythrocyte extravasation. Many o f the affected vessels contained thro0abi, Special stains for bacteria and fungi were negative, and no evidence o f septic embolization was present. Typical intranuclear inclusion bodies were not identified in the endothelial cells o f the vessels in this specimen. Sections o f some necrotizing skin lesions that had persisted over tile final months were taken at autopsy (fig. 2). These revealed focally ulcerated epidermis overlying derntis showing a subacute vasculitis, which was associated with thrombi showing varying degrees o f organization. Some vessel walls showed early sclerotic changes. T h e inflammatory infiltrate was predominantly mononnclear, with lymphocytes and occasional plasma cells. Many o f these small vessels contained typical CMV intranuclear inclusions within endothelial nuclei (fig. 2). T h e infected cells were markedly enlarged, and some had become detached from the vessel wall; these either floated freely in vascular lumens or became enmeshed in organizing thrombi. Microscopic evidence o f viral pneumonitis was also present in postmortem sections, which slmwed an interstitial pattern similar to that seen on the open h m g biopsy. Numerous sloughed and intact alveolar-lining cells containing intranuclear inclusions were identified. Although pulmonary vasculitis was not identified, many vessels contained organizing thrombi. Intranuclear inclusions were also identified within a glial nodule in the pons and in a hilar lymph node. DISCUSSION Cutaneous CMV-induced superficial and deep dermal vasculitis was documented in this patient by identification by typical CMV inclusions in endothelial cells from postmortem skin biopsy speciments; the inclusions were associated with a mononuclear inflammatory infiltrate, organizing thrombi, and early sclerotic changes in vessel walls. A previous biopsy had revealed a more active stage o f the lesion, with neutrophilic infiltration o f vessel walls and karyorrhectic debris but without viral inclusions. Tile changes in the skin were mirrored by those in tile lungs, with an antemortem open h m g biopsy specimen showing nonspecific interstitial pneumonitis and postmortem sections displaying florid CMV pneumonitis. It seems reasonable to implicate CMV as the etiologic agent in both instances, with the virus becoming histologically apparent only in tissues obtained post mortem. A review o f the literature revealed cutaneous CMV infection to be a rare clinical manifestation o f a common opportunistic pathogen, with only eight cases documented previously. 4,5'7,9-~3Although six o f these eight had inclusion bodies in capillary endothelial cells, only two o f the eight had concomitant vasculitis, r'~ In one o f the patients a mot1139

HUMAN PATHOLOGY--VOLUME

13, N U M B E R 12

December 1982

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Figure I (left). Antemortem biopsy specinten from right cheek, showing leukocytoclastic vasculitis of a superficial dermal vessel with neutrophilic infiltration of vessel wall, karyorrhectic debris, thrombus formation, and extravasation of er)'throcytes. No viral inclusions are present in endothelial cells. (x 192.) Figure 2 (right). Postmortem biopsy specimen of necrotizing ecchyntotic skin lesion front the foot, showing a deep dermal/subcutaneous fat border vessel with two enlarged endothelial cells that contain typical owl's-eye intranuclear inclusions of cytomegalovirus (aoowhead). Throntbi are seen within the lumen, and a ntild mononnclear intiltrate is present. (• Inset, dermal vessel showing narrowing of the vascular lumen and an enlarged endothelial cell with prominent inu'anuclear inclusion, (•

billiform rash developed following ampicillin therapy, whereas in the o t h e r necrotizing skin ulcers w e r e present, similar to those seen in o u r patient. T h e association o f C M V - i n d u c e d vasculitis with ulcer f o r m a t i o n is not without p r e c e d e n t , a l t h o u g h the two r e p o r t e d cases o c c u r r e d in the gastrointestinal tract and resulted in fatal p e r f o r a t i n g ulcers. 1 0 , 1 4 Clinically a p p a r e n t C M V infection in t h e adult may arise via d e novo acquisition, usually f r o m c o n t a m i n a t e d blood transfusion p r o d u c t s or, as is m o r e f r e q u e n t l y the case, by activation o f latent virus. Tixe virus m a y be harb o r e d , without clinical o r microscopic e x p r e s s i o n , by both debilitated a n d healthy patients, z't5 A l t h o u g h serologic evid e n c e o f infection exists in the majority o f adults e x p o s e d to the virus, antibody titers in i m m u n o s u p p r e s s e d p e r s o n s are u n p r e d i c t a b l e and thus not a reliable diagnostic feature. 2a5 O u r patient received n u m e r o u s transfusions o v e r the last few m o n t h s o f his illness. Serologic studies p e r f o r m e d on blood o b t a i n e d post m o r t e m w e r e n e g a t i v e for all antigens assayed and thus w e r e probably unsatisfactory. It is difficult, if not impossible, to d e l i n e a t e w h e t h e r this patient's infection arose f r o m reactivation o f latent virus o r f r o m an e x o g e n o u s source. T h e best and most reliable diagnostic criterion remains identification o f characteristic intranuclear a n d intracytoplasmic inclusions in a f f e c t e d tissues. Viral particles have been identified in b o t h fixed and wand e r i n g m a c r o p h a g e s , which m a k e u p the m a i n d e f e n s e

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m e c h a n i s m in tire n o r m a l itost? '2.G It is conceivable, therefore, tttat the virus nmy be passively t r a n s p o r t e d to previously i n f l a m e d tissues a n d so not r e p r e s e n t a p r i m a r y infectious agent. Nonetheless, the e x t e n t o f viral infection d o c u m e n t e d in p o s t n t o r t e m tissues f r o m the skin and lungs leads us to implicate C M V as the etiologic a g e n t o f the p n e u m o n i t i s and vasculitis in the case. C y t o m e g a l o v i r u s i n d u c e d vasculitis is a clinically relevant, albeit s o m e w h a t rare, manifestation o f this c o m m o n o p p o r t u n i s t i c p a t h o g e n a n d should be i n c l u d e d in the d i f f e r e n t i a l diagnosis o f ulc e r a t i n g skin lesions in i m m u n o c o m p r o n f i s e d persons.

REFERENCES 1. Nankervis GA, Kumar ML: Diseases produced by cytomegalovirus. Med Clin North Am 62:1021, 1978 2. Rose PP: C)tomegalovirus in cancer patients. Pathol Annu 13:175, 1978 3. Ryning FW, Mills J: Pneumocystis carinii, Toxoplasma gondii, cytomegalovirus and t he cornpromised host. West J Med 130:i 8, 1979 4. Symmers WS: Generalized cytomegalic inclusion-body disease associated with pneumocystis pneumonia in adults. J Clin Pathol 13:!, 1960 5. WilliamsG, Stretton TB, Leonard JC: C}tomegalic inclusion disease and Pneumocystis carinff infection in an adult. Lancet 2:951, 1960 6. Weller TIi: The cytomegalovirus: ubiquitous agents with protean clinical manifestations. N EnglJ Med 284:203, and 267, 1971 7. Lin CS, Penha PD, Krishnan MN, et al: Cytomegalic inclusion disease of the skin. Arch Dermatol 117:282, 1981 8. Banji A, Salisbuo" R: Cytomegalovirus and vasculitis. Br Med J 1:623, 1978

CASE STUDIES 9. MinarsN, SilvermanJF, Escobar MR, et al: Fatal cytomegalicinclusion disease: associated skin manifestationsin a renal transplant patient. Arch Dermatol 113:1569, 1977 10. NakonecznaI, Kay S: Fatal disseminatedcytomegallcinclusiondisease in an adult presentingwith a lesionof the gastrointestinaltract. Amj Clin Pathol 47:124, 1967 11. RobsonGS, MackayIR: Generalizedcytomegalovirusinfectionin a patient with lupoid hepatitis. Anat Ann Med 18:147, 1969

12. EvansDJ, WilliamsED: Cytomegalicinclusiondisease in an adult.J Clin Pathol 21:311, 1968 13. WongT, WarnerNE: Cytomegalovirusinclusiondiseasein adults. Arch Pathol 74:403, 1962 14. GoodmanMD, Porter DD: C)'tomegalovirusvasculitiswith fatal colonic hemorrhage. Arch Pathol 96:281, 1973 15. BusselJ, Danou F, Ferchal F, et ah Cytomegalovirusinfectionin malignant blood diseases: clinicaland laboratorydata in 29 patients. Nouv Rev Fr tlematol 20:67, 1978

CLINICALLY ASYMPTOMATIC PITUITARY ADENOMA MANIFESTING AS PITUITARY APOPLEXY AND FATAL THIRD-VENTRICULAR HEMORRHAGE UMA P. KALYANARAMAN,gIBBS, MSc*

A 56-year-old woman with an asymptomatk pituitary adenoma had a fatal third-ventricular hemorrhage of sudden onset. A suprasellar mass with hemorrhage and rupture into the third ventricle was found at autopsy. Histologically, the tumor cells from the suprasellar mass and the third-ventricular hemorrhage were diaguostic of a pituitary adenoma. The pathogenesis of the thirdveutricular hemorrhage from a pituitary adenoma and the need to consider pituitary apoplexy in the differential diagnosis of thirdventricular hemorrhage are discussed. On the basis of a review of the literature, it is felt that computerized tomographic scanning, although most helpful in diaguosis of sellar lesions, does not replace skull radiographs and sellar tomography in the htvestigation of saspected pituitary apoplexy. Hum Patho113 :1141-114 3 , 1982. Pituitary apoplexy is defined as a hemorrltage of sudden onset of infarction in a pituitary gland, t Rarely the gland may be normal, lint often it is enlarged owing to tumor, z Clasically, symptonas consist of sudden onset or worsening of pre-existing headache, sudden deterioration of vision, ocular palsies, confusion, drowsiness, and coma. Brougham et al. z and others 3"4 have reviewed tim condition in detail. A case of an asymptomatic pituitary a d e n o m a m a n i f e s t i n g as a fatal t h i r d - v e n t r i c u l a r h e m o r r h a g e is presented. Tiffs mode of clinical presentation of pituitary apoplexy has not been reported previously.

dead after clinical and electroencephalographic evalnations supported irreversible central nervous system damage. On admission, a computed tomographic (CT) scan with contrast e n h a n c e m e n t (fig. 1, left) revealed a Immorrhagic mass lesion occupying the anterior third ventricle, with dilatation of the ventricular system. T h e impression was of colloid cyst or another type of ueoplasm with lmmorrhage. Autopsy Findings. General autopsy findings were unrenmrkable. Gross examination of tim brain revealed severe brain edema with bilateral uncal herniation and minimal subaraclmoid hemorrlmge. A grossly necrotic suprasellar nmss approximately 2.5 cm in diameter was seen (fig. 1, right). Coronal sections of the brain after fixation showed a dilated third ventricle distended with lmmorrhage and extending slightly into the lateral ventricles. Microscopically, the suprasellar mass showed a papillary ttmmr composed of c o h u n n a r cells with eosinophilic cystoplasm and perivascular rosette fornmtion (fig. 2, left). Sections from the third-ventricular hemorrhage showed cells similar to those in the suprasellar mass, a r r a n g e d in similar perivascular rosettes (fig. 2, rigkt). T h e histologic appearance of the suprasellar t u m o r and of the cells from the hemorrhagic mass in the ttfird ventricle was characteristic of pituitary a d e n o m a with papillary features. DISCUSSION

REPORT OF A CASE A 54-year-okl white woman was admitted to St. Francis Hospital in coma. Prior to admission, a spinal tap at a n o t h e r hospital showed u n i f o r m l y blood-stained cerebrospinal fluid. T h e patient's medical history was sketchy and indicated tlmt she might have been unconscious for 24 hours. She had complained o f a "severe headache" the day prior to admission and was found unconscious the next morning. Her history was not significant except for atrial fibrillation and surgery for diverticulosis of the colon. She had no history of headache or visnal problem. On admission, the patient was comatose a n d on a respirator. Physical examination revealed generalized flaccidity, and no corneal, oculocephalic, or deep t e n d o n reflexes. T i m pupils were dilated and tixed. Respiratory support was discontintted, and tim patient was pronotmced * Assistant Professor of Pathology (Neuropathology), Universit)' of Illinois at Peoria; and Neurot)athologist, St. Francis Hospital, Peoria. Accepted for publication April 12, 1982. Slides fi-ont this case were presented at the diagnostic slide scnfinar of the American Association of Neuropathologists, hekl in New Orleans, June 1980. Address correspondence attd reprint requests to Dr. Kalyanaraman, Department of l'athology, Peoria School of Medicine, One Illini Drive, I'O Box 1649, Peoria, IL 61656.

T h e pituitary gland is an organ with complex functions and anatomic relationships. It is not unusual for a t u m o r arising from the pituitary to manifest in different ways, especially as "pituitary apoplexy." Rare cases or pituitary apoplexy m a n i f e s t i n g as acute p y o g e n i c m e n i n g i t i s with hemiparalysis) internal carotid artery occlusion,6 a n d middle cerebral artery thrombosis 7 emphasize the variations in clinical presentation. T h e outcome of pituitary apoplexy is usually death, but timely diagnosis and surgical intervention lmve significantly reduced tile mortality. 2 Henderson's review of 338 patients with pituitary adenomas from the Cushing series* revealed 21 largely cystic tumors with hemorrhage. T h a t series and Bakay's review of 300 cases of pituitary adenomas from tim Olivecrona series 9 failed to reveal any case nmnifesting as third-ventricular hemorrlmge. T h e pathogenesis of pituitary apoplexy is not well understood. Atheromatous emboli, ~~anticoagulant therapy, tt and roentgen therapy 12 have all been incriminated. With regard to its manifestation as third-ventricular hemorrlmge, I would postulate that when hemorrlmge occurs suddenly in a pituitary adenonm it results in an expansion the pituitary's size. T h e resulting increase in intracapsular pressure within the adenoma may produce acute compression of neighboring structures. T h e floor of the third ventricle may be already thinned by a long-standing pituitary

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