235

Clinical Neurology and Neurosurgery, 94 (1992) 23.5-240 Q 1992 Elsevier Science Publishers B.V. All rights reserved 0303-8467/92/S 05.00

CLINEU 00190

Case report

Subdural hematoma due to dural metastasis: case report and review of the literature M. Bergmanna, Z. Puskasb and K, Kuchelmeister” Departments of “Neuropathology, and bNeurosurgery, University of Miinstev, Miinster, Germany (Received 19 November, 199If (Revised, received 27 January, 1992) (Accepted 27 January, 1992) Key words:

Subdural hematoma; Dural metastasis

Sununary A case of chronic subdural hematoma associated with dural metastasis from gastric cancer is reported. It is compatible with the concept that subdural bleeding may result from obstruction of dural vessels by neoplastic cells. Other possible pathogenetic mechanisms of this rare comphcation are discussed and a literature review is given. For proper diagnosis of this condition histologic investigation of the subdural membrane is mandatory.

Introduction

Case report

Subdural hematomas occur mostly in the shape of acute subdural hemorrhage resulting from severe craniocerebral trauma with rupture of the bridging veins and subsequent bleeding into the subdural space [l]. Mortality from this lesion is high and few patients achieve complete recovery [2]_Conversely a history of trauma is lacking in more than 50% of chronic subdural hematomas, which are found most often in young children and elder patients. Clinical symptoms include headache, lethargy and personality change [3,4]. Non-traumatic subdural hematomas are caused by vascular disorders, coagulopathies, intracranial hypotension and meningitis [5]. Subdural hematoma secondary to dural metastasis is unusual. We report on one patient with metastatic adenocarcinoma of the stomach, who developed nontraumatic subdural hematoma.

G.-H.W., a 35-year-old man, was hospitalized on September 24, 1990, with a IO-month history of recurring gastric disturbances and dysphagia of 5 weeks duration. A tubular adenocarcinoma in the cardiac region was diagnosed. The tumor was only partially resected because of widespread local infiltration (p T3 N2). Three courses of palliative cytostatic therapy - leucovorin (530 mg), vepesid (210 mg) and 5-fluorouracil (890 mg) - were given with a drug-free interval of 1 month. Under this regimen hemoglobin declined from 14.2 to 11.9 mg/dl and thrombocytes from 2.8 to 1 x 105/mm3. On January 20, 1991 the patient was admitted to our hospital complaining of increasing headaches since several days. There was no history of head trauma. Except for somnolence the neurological status was unremarkable. Blood chemistry revealed anemia with 3.37 x 106/mm3 erythrocytes, 9.3 mg/dl hemoglobin and nearly normal coagulation parameters with 105/mm3 thrombocytes (normal: > 1.3 x lo’), prothrombin time of 58% (normal: 70-lOO%),

Correspondence to: Dr. M. Bergmann, Institut ftir Neuropathologie der Universitiit Monster, Domagkstr. 17, D-4400 Miinster, Germany.

Fig. 1. a: preoperative CT scan showing a hypodense right hemispheric subdural effusion and a considerable midline shift to the left. b: on the postoperative CT scan the subdural fluid collection is slightly reduced in size, the shift of the ventricular system is still present due to a right hemispheric edema.

partial thrombin time 36.7 s (normal: 2840 s), thrombin time of 17 s (normal: l&20), 253 mg/dl fibrinogen (normal: 170410 mg/dl) and 121% antithrombin III (normal: 80-120%). Chest x-ray showed evidence of pleural carcinosis. CT scan of the head disclosed a hypodense

General

autopsy

revealed

remaining

tumor

tissue at

the anastomosis and widespread metastatic disease with pleural and peritoneal carcinomatosis, lymphangiosis carcinomatosa of the lung and metastases in both adrenals. The right-sided dura was covered with fresh hemorrhages of up to 0.5 cm thickness. The underlying hemisphere was markedly edematous with a right-to-left midline shift under the falx cerebri. Signs of increased intracranial pressure and a rightsided posterior infarct

right hemispheric fluid collection with a marked midline shift to the left side (Fig. la). When the patient suddenly slipped into coma and developed respiratory insufficiency a large subdural hematoma was evacuated by emergency craniotomy. Postoperatively, the patient was alert oriented for only

were present. Microscopically

1 day, then the mental status deteriorated again. On the CT scan the subdural effusion had slightly diminished in size, but an edema of the right hemisphere with right-to-

were detected in the vessels of the outer dura mater with venous congestion and a granulation tissue showing numerous fresh hemorrhages (Fig. 2). Disseminated tumor

left shift of the ventricular system and a right-sided terior infarct was present (Fig. lb). Jacksonian major fits appeared in the last 2 days and the patient 8 days after admission.

emboli in smaller meningeal and intracerebral vessles had led to recent cortical microinfarcts in both cerebral

posand died

emboli

of a tubular

adenocarcinoma

hemispheres.

Fig. 2. a: low power view demonstrating intravascular tumor cell aggregates within dural vessels of the outer and inner dural layer containing fresh hemorrhages (hematoxylineosin, magnification x 80). b: intravascular tumor cells in outer dural layer in higher magnification (hematoxylineosin, magnification x 400).

237 TABLE 1 SUBDURAL

HEMATOMA

WITH DURAL METASTASIS;

SUMMARY OF DATA IN 35 CASE REPORTS

Ca = carcinoma, SH = subdural hematoma, CSH = chronic or subacute hematoma, ASH = acute SH, PHI = pachymeningeosis hemorrhagica interna- subdural membrane without hematoma, CT = cranial computed tomography, Bio = bioptical, Aut = autoptical diagnosis, + = present, - = absent, * = acute clinical presentation, ** = without clinical symptoms, ( ) = No. of cases [g-31]. Age/sex

Author

Primary tumor

SH type

Coagulopathy

Metastases

Diagnosis

Skull

CT

Brain

Bio

Aut

Westenhoefer, 1904

29/F

Ca stomach

PHI**

+

Wohlwill, 1913

68/F

Ca breast

PHI**

+

Puerckhauer,

76/M

Ca prostate

PHI**

+

64/M 65/F 64/M 41/M 52iF

unknown Ca stomach Ca lung Ewing sarcoma unknown

PHI** CSH PHI** PHI CSH

+ + +

neuroblastoma, Ca breast (2) Ca stomach

PHI (4)

+ (4)

+

1929

Russel & Cairns, 1934

Meyer & Reah, 1953

Braun, 1963

47/F

Ca stomach

CSH

McDonald & Burton, 1966

43/M

M. Hodgkin

CSH

Krempien,

56/F

Ca breast

CSH

Castleman et al., 1972

71/M

Ca stomach

CSH

Braun, 1973

56/M

anaplastic Ca

CSH*

Leech et al.. 1974

62/M

Ca prostate

CSH

+

Ambiavagar 1978

54/F

Ca cervix

CSH*

75/M

Ca prostate

CSH**

Vonofakos et al., 1980

57/M 55/M

Ca esophagus Ca prostate

Kurzaj et al., 1980

36/M

Turner & Graf, 1982

1970

_ -

-

+ t k + + +

+

-

+

_

_

-

_

+ -

_

+

_

+

+

-

-

_

-

_

_

_

CSH CSH*

+ +

-

+ +

+ +

Ca pancreas

CSH

_

-

_

-

83/F

Ca endometrium

ASH

-

+

-

+

+

Furui et al., 1943

64/F

Ca stomach

CSH

+

-

_

+

-

Cave, 1983

29/F

chorioncarcinoma

ASH

-

_

+

-

& Sher,

238 TABLE 1 continued Author

Agelsex

Primary tumor

SH type

Coagulopathy

Metastases

Diagnosis

Skull

Brain

CT

Bio

Aut

Rouah et al., 1986

42/M

testicular seminoma

CSH*

+

+

_

+

+

_

Bucci et al., 1986

62/M 63/M

Ca prostate Ca prostate

CSH CSH

_ _

_ _

_ _

+ +

+ +

_ _

Villette et al., 1987

61/M

Ca lung

CSH

+

+

+

_

D’Angelo et al., 1988

70/F

Ca breast

CSH

f

+

+

_

Cheng et al., 1988

64/M

Ca prostate

CSH’

McKenzie et al., 1990

66/M 67lM

hepatocellular Ca ASH Ca lung CSH

Kamada et al., 1991

63lM

Ca rectum

_

_ _

CSH’

+

_

+

+

_

+ _

+ _

+ +

+ +

+ _

+

_

+

+

_

Discussion

prostate years.

According to the literature, about 24% of patients with cancer develop intracranial metastases, the most com-

Diagnosis of SH is nowadays usually made by CT scan, which is, however, usually an insensitive method of

mon primary sites being lung, breast and skin (melanoma). Whereas carcinomatous infiltration of the dura is

demonstrating malignant meningeal Therefore ante mortem demonstration

present in up to 9% of autopsied cases with primary extraneural malignancies, especially in cancer of the prostate [6] and breast [7], only 35 histologically confirmed

ses depends on biopsy and histological evaluation of the subdural membrane. Although the prognosis is usually poor, recognition and emergency evacuation of the hematoma can be life saving. Radiation therapy should be

cases of subdural hematoma (SH) due to dural carcinomatous infiltration have been reported in the literature so far (Table 1). Most of them were chronic SH with formation of a subdural membrane. In some cases, which are listed under the term pachymeningitis hemorrhagica interna in Table 1, only this membrane without grossly evident

and

lung

cancer.

Age ranged

from

29 to 83

neoplasms [32]. of dural metasta-

applied. Cancer cells commonly reach the brain by the arterial circulation. Spreading by the valveless vertebral venous system (Batson’s for dissemination

plexus) seems an important pathway of prostatic cancer to the skull and

hemorrhage was present. Three cases developed an acute SH. Dural invasion usually developed after widespread metastases. It was accompanied by skull deposits in 14

perhaps the dura and could explain the proclivity of this cancer for skull and the dural metastases [6]. The combination of subdural hematoma and dural metastasis can be explained by venous tumor emboli in the outer dural

reported cases, which, however, did not encroach directly on the underlying dura. Clinically the patients usually presented with headache, lethargy and personality change of chronic or subacute progression. Sometimes they deteriorated acutely with development of coma due to complicating acute hemorrhage. There was a slight male predominance, possibly related to the underlying neoplasias like stomach,

layer leading to congestion and subsequent rupture of the thin-walled vessels in the inner dural layer [I 11. These vascular tumor emboli were present in most reported cases. On the other hand, coagulation disorders, which have been reported in 60-92% of patients with cancer, predispose to bleeding into the subdural space [33,34]. The rich vascular capillary bed of the reactive granulation tissue increases the potential for secondary deposi-

239

tion of cancer cells [30]. Coagulopathy was present in 5 cases in Table 1 and could not be excluded in 14 further cases since data regarding coagulation parameters could not be obtained leaving only 9 cases, in which coagulopathy almost certainly played no role in the pathogenesis of SH. Our case represents an example of subacute SH in combination with carcinomatous infiltration of the dura. Pathogenetically relevant to the formation of the SH were the tumor emboli in the outer parts of the dura, but an existing minor thrombocytopenia presumably had no bearing on pathogenesis. The case shows that biopsy and histological examination of a subdural membrane in every patient with cancer and SH are indispensable for a proper diagnosis of the condition.

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I

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9 10

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Subdural hematoma due to dural metastasis: case report and review of the literature.

A case of chronic subdural hematoma associated with dural metastasis from gastric cancer is reported. It is compatible with the concept that subdural ...
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