Neurol Med Chir (Tokyo) 50, 990¿994, 2010

Acute Epidural-Like Appearance of an Encapsulated
Solid Non-organized Chronic Subdural Hematoma
—Case Report—
Ruth PRIETO, Jos áe M. PASCUAL*, Issa SUBHI-ISSA**, and Miguel YUS***
Departments of Neurosurgery, **Pathology, and ***Radiology,
Cláƒnico San Carlos University Hospital, Madrid, Spain;
*Department of Neurosurgery, La Princesa University Hospital, Madrid, Spain

Abstract
We report the exceptional case of an encapsulated solid non-organized chronic subdural hematoma
(SDH) in a 67-year-old woman that was admitted with acute hemiplegia followed by rapid deterioration
in consciousness 5 months after a minor head trauma. Computed tomography (CT) showed an extracerebral biconvex shaped hyperdense mass that led to the misdiagnosis of an acute epidural hematoma. Urgent craniotomy revealed an encapsulated mass filled with solid fresh clot in the subdural space.
Complete evacuation of this SDH, including both its inner and outer membranes, was achieved, and the
patient recovered successfully. Histological analysis confirmed that the content of the hematoma corresponded to a newly formed clot that was enclosed between an inner membrane, composed of two collagen layers, and an outer membrane with a three layered structure. Chronic SDH may seldom present
as an encapsulated solid non-organized lesion that consists of a fibrous capsule enclosing a fresh clot
and lacking the thick fibrous septations that typically connect the inner and outer membranes of organized chronic SDH. This entity mimics the clinical course and radiological appearance of acute
epidural hematomas and should be considered in the differential diagnosis of extracerebral hyperdense
biconvex shaped lesions.
Key words: acute epidural hematoma, biconvex hematoma,
encapsulated hematoma, organized subdural hematoma

Introduction

contrast medium.5)
We report on the rare case of an extracerebral hyperdense hematoma with a biconvex shape on CT that was diagnosed in an aged person who had suffered a rapid neurological deterioration and had no history of a recent head
trauma. The lesion was thought to correspond to an acute
epidural hematoma but an encapsulated solid non-organized chronic SDH was actually found during the surgical exploration of the mass. The diagnosis of an encapsulated and solid non-organized chronic SDH that mimics
the radiological appearance of an acute epidural hematoma is exceptional with only one similar case previously
reported. Here we provide the neuroradiological and surgical findings of this atypical epidural-like chronic SDH as
well as a detailed histological analysis of the lesion.

Chronic subdural hematoma (SDH) is a common type of
intracranial hemorrhage characterized by an insidious onset that usually involves elderly people with a history of
minor head trauma.12,20,31) Chronic SDH consists of a fibrous capsule filled, in the majority of cases, with bloody
fluid.7) The fibrous capsule is composed of an outer membrane under the dura mater and an inner membrane over
the arachnoid. Generally, these typical or liquid chronic
SDHs are successfully evacuated through burr holes.
Nevertheless, about 0.5–2% of them develop thick membranes and/or multiple septations turning into encapsulated masses of predominantly solid consistency that require
a craniotomy to be successfully removed.1,9,12,13,17,21,23,25)
This latter uncommon SDH subtype is known as organized chronic SDH. A crescent shape and a density usually similar or lower to that of the adjacent cerebral parenchyma are the usual computed tomography (CT) features
of both liquid and organized chronic SDHs.6,19) In contrast, acute epidural hematomas are biconvex or lentiform
shaped lesions with high-density content on CT without
Received

January 8, 2010;

Accepted

chronic subdural hematoma,

Case Report
A 67-year-old woman presented at the emergency room
with acute onset of left hemiplegia and slurred speech.
The patient had no indication of recent head trauma. On
admission, she was confused and disoriented to time and
space, opened her eyes to voice stimulation, and obeyed
simple orders. The patient scored 13 points on the Glas-

March 2, 2010

990

Encapsulated Solid Non-organized Chronic SDH

Fig. 1 Preoperative axial computed tomography scans at
different levels showing a right extracerebral biconvex-shaped
subdural hematoma, hyperdense relative to the adjacent brain
parenchyma that mimics the appearance of an acute epidural
hematoma (upper row), and 3 months after the surgery showing
a laminar hyperdense area under the craniotomy flap suggestive of calcification of the dura mater (lower row).

gow Coma Scale (GCS; eye: 3, verbal: 4, motor: 6). Neurological examination revealed left hemiplegia and facial
weakness. The patient was receiving anticoagulation
medication (acenocoumarol) because of a history of paroxysmal atrial fibrillation. She had also a history of arterial
hypertension, chronic renal insufficiency, and protein-caloric malnutrition. Relatives of the patient indicated that
she had suffered a minor head trauma 5 months before the
admission, caused by an accidental fall in which she fractured her hip. CT performed at that time was unremarkable and the patient was operated on for the hip fracture.
Blood tests performed at the emergency room showed
that her international normalized ratio was 1.6 (normal
values: 0.8–1.2) and her creatinine level was 2.8 mg/dl
(normal values: 0.6–1 mg/dl). Emergent head CT revealed
an extracerebral and mostly hyperdense right frontoparietal mass with a biconvex morphology (Fig. 1 upper
row). These signs led us to the wrong diagnosis of an acute
epidural hematoma. The low density areas observed within the hematoma were considered a swirl phenomenon
caused by unclotted blood secondary to active bleeding, a
phenomenon typically observed in acute epidural hematomas.38)
An urgent large right fronto-temporo-parietal craniotomy was performed on the day of admission. Contrary to
our expectations no epidural hematoma was found (Fig.
2). Once the dura mater was opened, an encapsulated solid
lesion was observed. The dura mater was easily dissected
from the encapsulated lesion that had a glistening blue-yellowish appearance. After opening the fibrous membrane
under the dura mater (outer membrane), a fresh solid darkred clot containing scattered xanthochromic fluid spots
was disclosed. The clot was totally evacuated allowing inspection of a thin transparent fibrous membrane over the
brain surface (inner membrane). Then, this inner mem-

Neurol Med Chir (Tokyo) 50, November, 2010

991

Fig. 2 Intraoperative photographs showing the skin incision
for a large fronto-temporo-parietal craniotomy (A, inset),
removal of the frontoparietotemporal craniotomy flap and exposure of the dura mater with absence of epidural lesions (A),
opening of the dura mater and reflection toward the sagittal sinus disclosing a subdural encapsulated lesion (B), opening of
the fibrous capsule exposing a fresh dark-red clot with some
yellowish spots (asterisk) (C), and after removal of the capsule
demonstrating absence of vascular anomalies on the brain surface under the hematoma (D).

brane was separated from the underlying arachnoid layer
using water jet dissection. Complete removal of the hematoma and its surrounding membranes demonstrated the
absence of vascular anomalies on the brain surface.
Surgical specimens, that included separately fresh clots
and fragments of the outer and inner membranes, were
fixed in 10% formalin, embedded in paraffin, stained with
hematoxylin and eosin, and prepared for routine light
microscopy. Histological examination evidenced that the
hematoma consisted of a fresh or newly formed clot enclosed by two thin membranes (Fig. 3). The inner membrane of the hematoma was thinner than the outer and was
composed of two layers, a dense collagenous layer right
over the hematoma and a loose collagenous layer next to
the arachnoid. In the sections corresponding to the outer
membrane of the hematoma, three layers could be identified, with a middle dense collagenous layer bounded by
two loose collagenous layers (one just behind the dura
mater and the other over the hematoma). The loose collagenous layer on the side of the dura mater showed abundant sinusoidal thin-walled blood vessels with a large lumen. In the vicinity of blood vessels within the loose collagenous tissue of both the inner and outer membranes,
abundant eosinophils, macrophages, and deposits of iron
pigment were observed. In addition, scattered areas of recent hemorrhage were observed within the outer membrane.
Immediately after the surgery, the GCS score of the
patient improved to 15 and neurological examination
showed mild left-side weakness. The patient completed rehabilitation therapy and eventually recovered from left-

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992

Fig. 3 Representative photomicrographs of the operative
specimens. A: Fresh or newly formed clot (FC) and fibrin
meshwork (asterisk). Hematoxylin and eosin (HE) stain, original magnification ×20. B: The outer membrane has a threelayer structure: a middle dense collagenous layer (DC) bounded
by two loose collagenous layers (LCs), the most superficial
beneath the dura mater (D-LC) and the deepest adjacent to the
FC (FC-LC). HE stain, original magnification ×10. C: The inner membrane had a two-layer structure, with a DC adjacent to
the FC and LC over the arachnoid. HE stain, original magnification ×20. D: The D-LC contains thin-wall large sinusoidal
vessels, and was infiltrated by hemosiderin-laden macrophages
(white arrows) and eosinophils (black arrows). HE stain, original magnification ×40. E: The FC-LC enclosed newly formed
blood vessels and hemosiderin-laden macrophages (white arrows). HE stain, original magnification ×40. F: The LC within the outer membrane contained abundant infiltration of eosinophils (black arrows) and hemosiderin-laden macrophages
(white arrows). HE stain, original magnification ×40.

side weakness. Three months after the surgery, the patient
was healthy and had no neurological deficits. Follow-up
CT showed expansion of the right cerebral hemisphere
(Fig. 1 lower row).

Discussion
The present case of atypical chronic SDH occurred in an
aged patient with sudden and rapid neurological derangement, and appeared as an extracerebral hyperdense biconvex shaped lesion on CT. These features led us to the
radiological misdiagnosis of an acute epidural hematoma.
However, a fibrous capsule filled with a fresh-solid clot between the dura mater and arachnoid space was the unexpected lesion found at the surgical intervention. This case

was also unusual for the absence of recent head trauma or
significant coagulopathy in a patient presenting with such
important acute bleeding. Given the striking surgical finding, we thought that histological analysis of both the capsule and the content of this hematoma could provide some
insight into the pathological mechanisms involved in its
development.
Most chronic SDHs consist of a fibrous capsule
enclosing bloody fluid. After undergoing encapsulation,
chronic SDHs usually experience gradual enlargement
through repetitive episodes of bleeding from the outer
membrane.16,28) Thickness and composition of the neomembranes varies greatly from case to case depending
on the age of the hematoma, although complete formation
of the fibrous capsule usually requires 3 to 4 weeks.7,30) A
majority of chronic SDHs are liquid when diagnosed and
can be treated by evacuation-aspiration through burr
holes. However, a few cases develop a solid structure due
to the penetration of fibroblasts that replace the fibrin
meshwork of the hematoma by collagen fibrils. Whole organization of a chronic SDH occurs when the outer and
inner membranes fuse completely, a process that takes a
period of 6 to 12 months. These solid or organized chronic
SDHs usually require a craniotomy to be adequately
evacuated.17,25)
The two major structural features of the present hematoma were the presence of mature thin fibrous outer and inner neomembranes, usually observed in encapsulated liquid chronic SDH, in addition to the solid fresh-clot content. Histological features of the membranes were similar
to those of typical chronic SDHs27,30,34) (Fig. 3). This hematoma lacked the thick membranes or fibrous septations
present in organized chronic SDHs. Consequently, the
term encapsulated solid non-organized chronic SDH was
the chosen to define this particular lesion. Histological
analysis of the surgical specimen suggested that acute
massive bleeding had occurred within an unnoticed preexisting encapsulated chronic SDH. The outer membrane
had a three-layered structure, with a middle layer of compact or dense collagenous tissue bounded by two layers of
loose collagenous tissue. This arrangement corresponded
to the type III membrane described in the histological classification of the structure of the outer membrane of chronic SDHs according to the time of maturation since the
traumatic event.22) Hence, the period of maturation of the
fibrous capsule in this case was probably several months.
Besides, rich infiltration by hemosiderin-laden macrophages and eosinophils was observed in the loose collagenous tissue of both the inner and outer membranes.
Eosinophilic infiltration occurs in up to 80% of the neomembranes of chronic SDHs with a duration of more
than 3 months,10,26,34,35) but is almost absent in both fresh
hemorrhages and completely organized hematomas.10)
Presence of hemosiderin-laden macrophages within the
neomembranes supported previous and repeated bleeding
episodes.4) Therefore, the three-layered structure of the
outer membrane and the abundant infiltration of
hemosiderin-laden macrophages and eosinophils within
the fibrous capsule are the fundamental findings supporting the long evolution of the chronic SDH in the present

Neurol Med Chir (Tokyo) 50, November, 2010

Encapsulated Solid Non-organized Chronic SDH
case.
Fresh clotted blood secondary to recent bleeding within
a chronic SDH usually undergoes a rapid liquefaction. In
contrast, the present case harbored a recently formed clot
which remained solid and filled the cavity of the fibrous
capsule. Only one case of a chronic SDH with a septated
compartment containing an organized solid clot has been
reported.37) Biochemical conditions that determined the
absence of clot liquefaction in both the previous and our
own cases are unknown. Bloody fluid of chronic SDHs
usually remains liquid because its chemical composition
prevents the function of hemostatic mechanisms. Failure
of coagulation is due to the consumption of clotting factors within the chronic SDH, secondary to over-activation
of both the intrinsic and extrinsic clotting pathways.15,33,34)
Moreover, the hematoma fluid has an anticoagulant effect
when added to normal blood due to its high content of
fibrinogen degradation products that inhibit the fibrin
polymerization.18,32,34) No measures of coagulation proteins and inhibitors were performed in the hematoma
contents of our case, but we believe that an imbalance of
the normal relationships between coagulant/anticoagulant
factors could explain the absence of liquefaction of the
subdural clot within the chronic SDH.
Regardless of the consistency of the hematoma, whether
solid or liquid, both acute and chronic SDHs that expanded at the virtual subdural space generally show a crescent
shape on CT. Only a few cases of biconvex-shaped subdural blood collections mimicking the morphology of
acute epidural hematomas have been reported, and most
of them corresponded to acute SDHs diagnosed in patients
with hemorrhagic diathesis.3,11,14,24) Only one previous
case of a chronic SDH displaying the same epidural-like
biconvex shape has been reported, in which acute bleeding had presumably superimposed on earlier chronic encapsulated content.24) The epidural-like appearance of our
chronic SDH was likely related to the acute bleeding into
the cavity of a previously encapsulated chronic SDH. Expansion of the clot against the wall of the capsule offering
the least resistance, which is the inner membrane, may
have caused stretching and ballooning of this wall, and so
resulted in the biconvex epidural-like appearance of the
hematoma.3,29)
This solid non-organized chronic SDH appeared mostly
as hyperdense indicative of a recent bleeding. Definite
causes of the acute massive bleeding in this case remain
elusive, but the sinusoidal fragile vessels identified within
the loose collagenous layer of the outer membrane may
represent the original source (Fig. 3D). Blood vessels of
this type are a constant finding within the neomembranes
of mature chronic SDHs and are considered to be the main
source of repetitive bleedings into these hematomas.8,16,36)
The elevated amount of eosinophils in the neomembranes
of this hematoma could also have been involved, because
degranulation of these cells releases angiogenic and
fibrinolytic factors involved in both the formation of
fragile sinusoidal vessels and their tendency to spontaneous bleeding.2) Finally, the patient's history of hypertension could have favored the bleeding tendency of these
fragile vessels.

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993

In conclusion, an encapsulated solid non-organized
chronic SDH consists of a fibrous capsule enclosing a
fresh clot and lacking the thick membranes and fibrous
septations that typically connect the inner and outer membranes of organized chronic SDHs. Such hematomas may
appear as a hyperdense biconvex-shaped mass on CT
without contrast medium, mimicking the morphology of
an acute epidural hematoma. These hematomas may cause
abrupt and severe neurological derangement as result of
acute bleeding within the previously developed chronic
SDH. History of hypertension and coagulopathy may be
factors contributing to such massive bleeding within a
chronic SDH in the absence of a recent head trauma.

Acknowledgments
We express our deep appreciation to Manuel Espantale áon,
director of the Clinico San Carlos Library, for assisting
with the references and to Larry Gavan for his linguistic
assistance and throughout review of the scientific style of
the manuscript.

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Address reprint requests to: Ruth Prieto, M.D., Department of
Neurosurgery Cláƒnico San Carlos University Hospital, c/
Profesor Martin Lagos s/n 28040 Madrid, Spain.
e-mail: rprieto＠iib.uam.es

Neurol Med Chir (Tokyo) 50, November, 2010