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Acta Neurochir (Wien) (1990) 102:149-151

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9 by Springer-Verlag 1990

Symptomatic Subacute Subdural Haematoma
Following Spontaneous Acute Subdural Haematoma
N . A o k i a n d K. Tsutsumi
Department of Neurosurgery, Tokyo Metropolitan Fuchu Hospital, Tokyo, Japan

Summary
Two patients with non-traumatic acute subdural haematoma
were observed, initially without surgical intervention. Eleven days
after the onset, each patient developed hemiparesis and an increase
in severity of headache. Serial computed tomography scans demonstrated that the initial hyperdense haematomas became hypodense
with a definite increase in volume. The term "symptomatic subacute
subdural haematoma" was proposed to properly define this pathological process, which necessitated removal of the haematoma in
the subacute stage. The mechanism of increase in the volume of the
haematoma is discussed.
Keywords: Acute subdural haematoma; subacute subdural haematoma; chronic subdural haematoma.

Introduction
Subacute

subdural

haematoma

(SDH)

itself has

rarely received attention, and has merely been recogn i z e d as a p a t h o l o g i c a l c o n d i t i o n e i t h e r t r a n s f o r m i n g
into chronic SDH or occurring at a subacute stage after
a c u t e S D H 2, 4. R e c e n t l y t h e a u t h o r s h a v e e n c o u n t e r e d
two patients who developed new symptomatology
the subacute stage after spontaneous

in

acute SDH; this

pathological process was considered to be properly def i n e d as s y m p t o m a t i c

subacute SDH.

Details of this

lesion are described, and the mechanism of the increase
in the volume of the haematoma

is d i s c u s s e d .

Case Reports
Case 1. This 72-year-old man who had a ten-year history of hypertension developed sudden onset of headache and vomiting during
dinner on April 22, 1987. His recent medical history was unremarkable with neither cerebrovascular disease, head trauma nor alcohol
intake. Although no disturbance of consciousness or other associated
neurologicaI symptoms were present, he attended the Department
of Neurosurgery, Tokyo Metropolitan Fuchu Hospital, in the early
morning on August 23, complaining of persistent headache.

E x a m i n a t i o n : On arrival physical examination showed no
abnormal findings apart from a moderate degree of hypertension.
Although the patient complained of pain all over his head, neurological evaluation including funduscopic examination failed to reveal
any abnormalities. Computed tomography (CT) scans without intravenous injection of contrast medium (Fig. 1) revealed a high density lesion covering the entire cerebral hemisphere on the left side,
indicating acute SDH. A mild degree of mass effect was noted.
Cerebral angiography did not show any aneurysm, arteriovenous
malformation or other findings. Results of laboratory examinations
including blood routine, b!ood chemistry and coagulation studies
were all within normal limits.
C linic al c o u r s e : Because of the lack of objective neurological
findings, he was initially treated conservatively. His headache was
gradually alleviated after the use of intravenous administration of
glycerol and peroral analgesics. On May 3, eleven days after the
onset of symptoms, however, he was found to have an unsteady gait,
urinary incontinence and disorientation. Hemiparesis on the right
side was evident. CT scans (Fig. 2) showed an increase in the volume
of the subdural haematoma on the left side, of lower density than
the cerebral parenchyma. Distortion of the midline structures was
also increased. On the following day, upon percutaneous subdural
tapping a dark-brown, liquid haematoma gushed out. The subdural
space was irrigated with saline. His subsequent clinical course was
uneventful. Although a small volume of subdural fluid still was visible
on CT scans, he was discharged from this hospital without neurological deficits on May 18. His final follow-up examination three
months later confirmed complete resolution of symptoms. No further
CT evaluation was performed.
Case 2. This 36-year-old man with an unremarkable past history
developed pain on the occipital region when he awoke at 7.30 a.m.
on July 3 I, 1987. He did not have any recent episode of head trauma.
Since no relief of pain followed, he visited a nearby hospital on
August 3, and was diagnosed as having acute SDH. On that day,
he was referred to this hospital.
E x a m i n a t i o n : Physical and neurological examination showed
him to be alert and oriented. No retinal haemorrhages were present.
CT scans without contrast injection (Fig. 3) demonstrated a small
volume of a high density lesion over the left cerebral hemisphere,
indicating acute SDH. Cerebral angiography failed to reveal any
abnormal features. No abnormalities in routine blood counts, blood
chemistry and coagulation studies were discovered.

150

N. Aoki and K. Tsutsumi: Symptomatic Subacute Subdural Haematoma

Fig. 1. Computed tomography scans at the time of admission in case
1, showing a high density lesion covering the entire cerebral hemisphere on the left side (arrows)

Fig. 2. Computed tomography scans eleven days after the onset in
case 1, disclosing enlargement of subdural haematoma with low
density (arrows). Note the midline shift

Fig. 3. Computed tomography scans 3 days following the onset in
case 2, revealing a thin, high density mass over the right cerebral
cortex (arrows)

Fig. 4. Computed tomography eleven days after the onset in case 2,
demonstrating an increase in the volume of the haematoma associated with decreased attenuation (arrows)

C l i n i c a l course : He was admitted for neurological observation. The headache was alleviated by administration of peroral analgesics, and, though without complete resolution of the headache,
he left this hospital on August 6. Eleven days after the onset of the
headache (on Augst 11), however, he suffered an acute increase in
the severity of his headache, and was readmitted to this hospital.
Although there were no objective findings on neurological examination, CT scans (Fig. 4) disclosed an increase in the volume of
subdural haematoma, which had a lower density than that on the
initial scans. A midline shift was also shown. Percutaneous subdural
tapping yielded liquid haematoma with chocolate-like colour, which
was irrigated with saline. He was discharged from this hospital on
August 30, without reaccumulation of subdural fluid on CT. The
further follow-up with CT scans on September 12 revealed minimal
fluid collection over the left frontal region. At that time, no symptoms
were noted.

Discussion
C l i n i c a l c h a r a c t e r i s t i c s in t h e p r e s e n t t w o p a t i e n t s
i n c l u d e d e v e l o p m e n t o f n e w s y m p t o m s e l e v e n d a y s after the o n s e t o f n o n t r a u m a t i c a c u t e s u b d u r a l h a e m a tomas. The progressive enlargement of SDH on CT
scans in t h e s u b a c u t e stage was r e s p o n s i b l e f o r these
s y m p t o m s . T h i s p a t h o l o g i c a l p r o c e s s m a y be r e f e r r e d
to as s y m p t o m a t i c s u b a c u t e S D H . S u b a c t u e S D H has
n o t b e e n fully r e c o g n i z e d as b e i n g a d e f i n i t e clinical
e n t i t y 2, 5; t h e m e c h a n i s m o f i n c r e a s e in the v o l u m e o f
t h e h a e m a t o m a is w o r t h discussing. B a s e d o n serial C T
scans, the p r o g r e s s i v e e n l a r g e m e n t o f S D H in the prese n t p a t i e n t s is a c c o m p a n i e d by d e c r e a s e d a t t e n u a t i o n

N. Aoki and K. Tsutsumi: Symptomatic Subacute Subdural Haematoma
o f the h a e m a t o m a . A l t h o u g h analysis o f the h a e m a t o m a c o n t e n t o r investigation o f the capsule was n o t
o b t a i n e d , u p o n p e r c u t a n e o u s s u b d u r a l t a p p i n g 1, the
m a c r o s c o p i c a p p e a r a n c e o f the h a e m a t o m a c o n t e n t did
n o t suggest s u b s e q u e n t bleeding. It has been k n o w n
t h a t c e r e b r o s p i n a l fluid (CSP) c o n t r i b u t e s m i n i m a l l y
to an increase in the v o l u m e o f c h r o n i c S D H 11. HOWever, in the s u b a c u t e stage d u r i n g the h a e m o l y t i c p r o cess, C S F influx into the s u b d u r a l space m a y be caused
by the c o l l o i d - o s m o t i c pressure difference between the
liquid h a e m a t o m a a n d C S F 13, or t h r o u g h the residual
tearing o f the a r a c h n o i d m e m b r a n e . I n a d d i t i o n , o p a cification o f the s u b d u r a l space b y m e t r i z a m i d e C T
c i s t e r n o g r a p h y d u r i n g the early stage o f c h r o n i c S D H
has been d o c u m e n t e d a. S u b d u r a l fluid collection compresses the u n d e r l y i n g brain, p o s s i b l y followed b y ven o u s o b s t r u c t i o n or shifts o f the brain. This could be
p r o p o s e d as a n o t h e r m e c h a n i s m , by which b r a i n swelling a n d further collection o f fluid are f o r m e d , causing
a d d i t i o n a l s y m p t o m s at the s u b a c u t e stage.
A f t e r the a d v e n t o f C T scans, p o s t - t r a u m a t i c subd u r a l fluid collection has been k n o w n to c o n t r i b u t e to
the d e v e l o p m e n t o f c h r o n i c S D H 12 T h e r e has been,
however, only a few r e p o r t s d o c u m e n t i n g the occurrence o f c h r o n i c S D H o r i g i n a t i n g f r o m acute S D H 6,
7, ~0, ~4. I n the p r e s e n t two patients, the S D H resolved
after s u b d u r a l t a p p i n g in the s u b a c u t e stage w h e n new
s y m p t o m s developed; however, if they were n o t t r e a t e d
at the time b e c a u s e o f m i n i m a l s y m p t o m s , the transf o r m a t i o n into c h r o n i c S D H c o u l d ensue f r o m the subacute S D H . This d e v e l o p m e n t a l process o f chronic
S D H can be facilitated b y p a r t i c i p a t i o n o f C S F 9 which
is d r a w n into the h a e m a t o m a cavity d u r i n g the subacute stage.
To s u m m a r i z e , acute S D H w i t h o u t surgical treatm e n t is liquified a n d m a y progressively enlarge, so t h a t
new s y m p t o m s d e v e l o p in the s u b a c u t e stage. F u r t h e r m o r e , this p a t h o l o g i c a l process m a y c o n t r i b u t e to
the s u b s e q u e n t d e v e l o p m e n t o f c h r o n i c S D H .

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Addendum. Since acceptance of this paper another publication reporting on 4 cases of subacute subdural haematoma has been published: (Morinaga K, Matsumoto Y, Omiya N, Mikami J, Ueda M,
Sato H, Inoue Y, Okawara S, Takahashi Y, Fujisawa Y [1990]
Subacute subdural hematoma. Report of 4 cases and a review of the
literature. Brain Nerve 42:131-136 [in Japanese])
Correspondence and Reprints: Nobuhiko Aoki, Department of
Neurosurgery, Tokyo Metropolitan Fuchu Hospital, 2-9-2 Musashidai, Fuchu-Shi, Tokyo 183, Japan.