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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