UNIVERSITY OF KHARTOUM

Faculty of Medicine
Postgraduate Medical Studies Board

Correlation between computerised tomography (CT)

findings, clinical presentation and immediate
postoperative results in subdural haematoma

By
Dr. Faiz A.S Kadhim
M.B. Ch.B. (University of Al Mustansiriyah, Iraq)

A thesis submitted in partial fulfillment for the requirements of the

Degree of Clinical MD in Radiology, October, 2004

Supervisor
Dr. Hago Mustafa Ali
Consultant Radiologist (MD)

Co-supervisor
Prof. Mohammed Abdel Rahman Arbab
Consultant Neurosurgeon
Faculty of Medicine
University of Khartoum
1

) (

- )(269

To the soul of my father.

To my mother for her patience.

To my wife "Nidhal" for her unlimited support.

To my family and all my teachers

Faiz

I would like to express my sincere thanks and gratitude to

my supervisor Dr. Hago Mustafa Ali, consultant radiologist,
Medical Corps for his meticulous supervision, continuous
guidance,

encouragement

and

much

valuable

advice

throughout all stages of the study.

I

am

greatly

indebted

to

my

co-supervisor

Prof.

Mohammad A. R. Arbab, professor of Neurosurgery, Faculty

of Medicine, University of Khartoum whose by his helpful
advice and discussion have permitted me to complete this
thesis.
A special thanks, to Mr. Al Hadi Bakhit, a consultant
Neurosurgeon in National Center of Neurological Sciences for
his unlimited help and advice on this project.
Also I would like to thanks Dr. Al Fadhil Osman and all
the

working

staff

in

Emergency

Department

of

Neurosurgery for their help.

I appreciate the help of Miss Khadiga Adam in analysis
of data and Miss. Widad A. Magsood for her tremendous
efforts in typing this work.
4

Faiz A.S. Kadhim

ABBREVIATIONS
SDH

Subdural hematoma

ASDH

Acute Subdural hematoma

SDHs

Subdural hematomas

CSDH

Chronic Subdural hematomas

ATSDH

Acute traumatic subdural haematoma

PCA

Posterior cerebral artery

CBF

Cerebral blood flow

CSF

Cerebrospinal fluid

GCS

Glasgow Coma Scale

TIA

Transient Ischemic Attack

CT

Computed Tomography

ICP

Intracranial Pressure

MRI

Magnetic Resonance Imaging

RBCs

Red blood cells

T1 -WIs

T1 weighted images

T2 -WIs

T2 weighted images

3D

Three dimension

IHD

Ischaemic heart disease

ABSTRACT
This prospective study was conducted between
January 2003 to January 2004 in National Center of
Neurological Sciences (Al Shaab Teaching Hospital), to deal
with postoperative immediate outcome of patients with
subdural hematoma in correlation with CT scan findings
and clinical presentation. One hundred randomly selected
patients with 116 subdural hematomas were operated on
depending upon CT scan findings.
The age range for the study group was 37-90 years
with a mean of 65 years.
Of the total (100 patients), male to female ratio was
9:1 (90:10). Thirty-six patients (36%) did not have any
history of trauma, 44 (44%) patients with history of a minor
trauma and 20 (20%) patients were sustained with a
relatively severe trauma.
Eighty-five (85%) patients had CT scan finding of
brain atrophy. Seventy-eight patients (78%) had unilateral
SDHs and 22 (22%) patients with bilateral SDHs.

Eighteen SDHs (15.5%) were purely hyperdense, 64

SDHs (55.2%) with mixed density and 29.3% (n= 39) were
purely hypodense. The mass effect of SDHs was seen clearly
as midline shift or compression on the ventricles.
This study showed no correlation between the
immediate outcome and CT scan findings like density,
number, mass effect or the midline shift. Also there is no
correlation with the time delay between start of complaint,
CT diagnosis and interventional management.
The

correlation

is

present

with

the

clinical

presentation at the time of admission especially for the dead

cases (6%). These results may be changed to a certain
degree if the sample size is larger or if any type of SDHs
studied separately.


2003 2004
) (
) (
.
100 116
: 65
%36 1:9 %44
%20 .
%85 :
%78 %20 %15.5
) 18( 64) %55.2 ( 34) %29.3(
.
.

 .%6
.

LIST OF FIGURES
Page No.
Fig. (1) Distribution of study population according to age

32

Fig. (2) Distribution of study population according to the sex

33

Fig. (3) Distribution of study population according to

the type of trauma

34

Fig.(4) Distribution of the time delay between the start

of complaint and intervention

35

Fig. (5) CT scan findings (Brain atrophy)

36

Fig. (6) CT scan findings (Number of SDHs)

37

Fig. (7) Distribution of SDHs according to their densities

38

10

LIST OF TABLES
Page No.
Table (1) Distribution of study populations according
to the mean age

39

Table (2) Relation between the midline shift and the

mass effects on lateral ventricle and /or sulci
Table (3)

Relation between thickness of an SDH and

the mass effects on lateral ventricle and /or sulci

Table (4)

40

41

Relation between the density of an SDH

and outcome 11

Table (5) Relation of CT findings (Number of SDH)

and outcome

43

Table (6) Relation between GCS and outcome

Table (7)

42

44

Distribution of patients according to the clinical

Presentation and surgical outcome

45

Table (8) The relation between the time delay (start of

Table (9)

complaints and intervention) and the outcome

46

Description of all data about the dead cases

47

11

CONTENTS
Page
Dedication .....................................................................................I
Acknowledgment............................................................................. II
Abbreviations............................................................................III
Abstract..............................................................................IV
Abstract (Arabic) .............................................................................VI
List of figures .........................................VII
List of tables..................................................................VIII

CHAPTER ONE
INTRODUCTION AND LITERATURE REVIEW .....................1
OBJECTIVES...........................................................................24

CHAPTER TWO
PATIENTS & METHODS .................................................25

CHAPTER THREE
RESULTS .............................................................27

CHAPTER FOUR
DISCUSSION...........................................................................48
CONCLUSION ...........................................................56
RECOMMENDATIONS ....................................57
REFERENCES...........................................................58
APPENDIX (Questionnaire)
12

INTRODUCTION AND LITERATURE REVIEW

1.1. Definition:
Subdural haematoma (SDH) is abnormal blood
collection or its breakdown between the inner layer of dura
and arachnoid membrane.(1)
The hyperacute phase of an SDH is within the first
day after injury.(1)
Acute SDHs are less than 3 days old. Subacute
SDHs are 3-20 days old. Chronic SDHs are older than 3
weeks.(2)
Clinically, SDHs behave as acute haematomas when
less than 1 week old and as chronic hematomas when they
are older than one week old.(3)

1.2. Relevant anatomy:

The brain and spinal cord are surrounded by three
membranes, or meninges, the dura mater, the arachnoid
mater and the pia mater.(4)
1.2.1. The dura mater:
The dura mater of the brain is conventionally
described as two layers:
13

The endosteal layer is nothing more than the

periosteum covering the inner surface of the skull bones.

The meningeal layer (dura mater proper); is a dense

strong fibrous membrane covering the brain.(4)
The falx cerebri, falx cerebelli and tentorium cerebelli
are folds of dura mater.
The superior sagittal sinus runs in its upper fixed
margin; the inferior sagittal sinus runs in its lower concave
free

margin;

and

the

straight

sinus

runs

along

its

attachment to the tentorium cerebelli.(4)

1.2.2. Dural venous sinuses:
They are situated between the layers of the dura
mater. Their main function is to receive blood from the brain
through cerebral veins and the CSF from he subarachnoid
space through the arachnoid villi.(4)

1.2.3. The arachnoid mater:

It is a delicate, impermeable membrane covering the
brain and lying between the pia matter internally and dura
mater externally.(4)

14

1.2.4. Subdural space:

It is a potential space separating the arachnoid
mater from the dura, filled by a film of lubricant.(4)
1.2.5. Subarachnoid space:
It is a space separating arachnid mater from the pia,
which is filled with CSF.(4)
1.2.6. Arachnoid villi:
They are the arachnoid projects into the venous
sinuses, which are most numerous along the superior
sagittal sinus. Aggregations of arachnoid villi are referred to
as arachnoid granulations.
Arachnoid villi serve as sites where the CSF diffuses
into the blood stream.(4)
1.2.7. Pia mater:
It is a vascular membrane covered by flattened
mesothelial cells. It closely invests the brain covering the
gyri and descending into the deepest sulci. It extends over
the cranial nerves and fuses with their epineurium.(4)

1.2.8. Development facts about the brain:

One of the many interesting things about the brain is
that, the cells that we are born with are all that we ever get
15

to work or play with. Actually, a newborn has more brain

than a fully matured adult. The brain doesn't reproduce
itself. And, as we are getting old, that brain we were born
with gradually shrinks.(5)
On the other hand, the skull, once fully grown, never
gets smaller. As the brain shrinks, it too pulls away from its
covering shell of bone. At the same time the blood vessels
which come from the brain and extend up into the skull
become stretched when they reach a certain limit, even a
miner pump to the skull can cause them to snap and bleed
into the subdural space, between the inner skull surface
and the brain.(4)

1.3. Pathophysiology:
ASDH usually develops by one of three mechanisms:

Bleeding from a damaged cortical artery (including

epidural hematoma).

Bleeding from underlying parenchymal injury.

And tearing of bridging veins from the cortex to one

of the draining venous sinuses. However, most SDHs are
thought to result from torn bridging veins as judged by
surgery or autopsy.(6)
16

The usual mechanism to produce an acute SDH is

high-speed impact to the skull. This causes brain tissue to
accelerate relative to a fixed dural structure, which, in turn,
tears blood vessels. This mechanism also leads to associated
contusions, brain edema, and diffuse axonal injury. An
acute SDH due to a ruptured cortical artery may be
associated with only minor head injury, or no cerebral
contusions may be associated. Patients experiencing this
kind of acute SDH were older, and some experienced lucid
interval before neurological deterioration.(6)
Chronic SDHs that form from acute SDHs have
membranes between the dura and hematoma at one week
and between the brain and hematoma at three weeks. The
hematoma liquefies at 1-3 weeks of age and become
hypodense on CT scan. If not resorbed, the vessels in the
membranes

surrounding

the

hematoma

can

bleed

repeatedly, resulting in the enlargement of the hematoma.(3)

CSDH commonly is associated with cerebral atrophy.
Cortical bridging veins are thought to be under greater
tension as the brain gradually shrinks from the skull; even
minor trauma may cause one of these veins to tear.(6)
17

However, as the hematoma (oedema from associated

parenchymal injury) expands, a limit is reached beyond
which compensatory mechanisms fail. The intracranial
compliance

begins

to

decrease;

small

increase

in

intracranial volume is associated with larger increases in

intracranial

pressure,

leading

to

decreased

cerebral

perfusion and global cerebral ischemia.(6)

In addition, the hematoma deforms and displaces the
brain. Eventually, transtentorial or subfalcine herniation
can develop as the brain is pushed past the dural folds of
the tentorial incisura or falx respectively. Although much
less common than supratentorial SDH, infratentorial SDH
can develop and causes tonsillar herniation and brainstem
compression.(6)
Characteristic herniation syndromes, may develop as
the brain shifts. As the medial temporal lobe or uncus,
herniates past the tentorium, it can compress the ipsilateral
posterior cerebral artery (PCA), oculomotor nerve, and
cerebral peduncle.
Subfalcine herniation caused by midline brain shift
may result in compression of the anterior cerebral artery
18

(ACA). Distribution of the cerebral blood flow (CBF) can

become markedly reduced as a result of a compressed
microcirculation,

which

was

caused

by

increased

intracranial pressure.(6)
The trauma is often less significant than that
required to produce an extradural hematoma. Fractures are
infrequently seen, and the bleeding may be venous and at a
lower pressure. Arterial bleeding, in severe trauma may
however, also produce a subdural collection.(7)

1.4. Incidence:
-

In the USA, incidence of SDH is related directly to the

incidence of blunt head trauma. SDH is the most
common type of intracranial mass lesion,, occurring in
about a third of these with severe head injuries (Glasgow
Coma Scale Score <9).(2)

Acute SDHs occur in 5-25% of patients with severe

head injuries. The occurrence of chronic SDH has been
reported 1-5.3 cases per 100.000 people per year. More
recent studies have shown a higher incidence, probably
because of better imaging techniques.(6)

19

The incidence of CSDH appears to be highest in the

5th through 7th decades of life. The highest incidence of
7.5 per 100.000 occurs in adults aged 70-79 years.(6)

1.5. Clinical presentation:

1.5.1 History:
A history of head injury was lacking in 25-50% of
patients in most series.(6)
Acute SDH has to be suspected, whenever, the
patient has experienced a mechanism of moderately severe
to severe blunt head trauma.(2)
Misdiagnosis of CSDH often is aided by its insidious
course. In-patients who have sustained head injury, 25%
have an interval of 1-4 weeks before symptoms develop.
Another 25% experience symptoms from 5 weeks to 3
months before their hospital admission. Only one third of
patients have no symptomatic period.(6)
Headache and confusion appear to be the most
common presenting features occurring in as many as 90%
and 56% of cases respectively, while hemiparesis and
decreased level of consciousness appear to be the most

20

common signs, occurring in approximately 56% and 40%

respectively.(6)
Misdiagnoses
tumor,

included:

subarachnoid

dementia,

hemorrhage,

stroke,

meningitis

TIA,
and

encephalitis.(6) Also malaria in endemic countries like Sudan

may lead to miss diagnosis.(5)
1.5.2. Physical examination:
The

initial

neurologic

examination

provides

an

important baseline that should be used to follow the

patient's clinical cause. When recorded in the form of the
GCS

score,

it

also

provides

important

prognostic

information.(6)
Signs of external trauma alert the physician to the
expected location of coup or countercoup injuries on CT
scan.(2)
GCS score less than 15 after blunt head trauma, in
patient with no intoxicating substance used for impaired
mental status baseline), warrant consideration of an urgent
CT scan.(2)

21

The presence of focal neurologic sign following blunt

head

trauma

is

ominous

and

requires

an

emergent

explanation.(2)

1.6. Work-up:
1.6.1 Lab studies:

Complete blood counts.

Coagulation profile.

Electrolytes.(2)
1.6.2 Imaging studies:
1.6.2.1 Plain radiographs:
A

chronic

extracerebral

hematoma

may

be

manifested by plain radiographs in several ways, depending

on the age at which the causative trauma occurred and its
effects on the underlying brain.(8)
In children, chronic bilateral effusions may simply
cause enlargement of the cranium, which will, however,
frequently

show

focal

expansion,

often

bilateral

and

involving predominantly middle cranial fossa.(8,9)

If

the

injury

has

occurred

early in

life,

and

interferred with brain growth, the cranial vault may be

thick, with an abnormal lack of conventional impression
22

and hypertrophy of the air cells and sinuses; one side

frequently more severely affected.(8,10)
Calcification, in the form of streaks or plaques,
resembling pleural calcification, but often parallel, is
occasionally seen in the capsule of the hematoma. Other
signs

of

old

trauma,

fractures,

burr

holes...etc

are

commonly present. In adult, the skull is frequently normal

or shows signs of raised intracranial pressure (ICP); the
pineal or choroid plexuses may be displaced.(8)
1.6.2.2 Angiography:
Angiography was carried out before the availability of
CT. The cardinal sign is the displacement of the cortical
arteries and veins, inwards from cranial vault, which is seen
as a diffuse, crescentic separation.(8,9)
Midline displacement and medial displacement of the
anterior choroidal artery, indicating herniation of the uncus
into the tentorial hiatus are often present.(8)
Angiogram is rarely employed nowadays in the
diagnosis of SDH.(11)
In any extracerebral collection, the absence of
commensurate midline displacement should suggest the
23

possibility of a contralateral lesion; traumatic lesions are

frequently multiple.(8)
1.6.2.3. Computerized tomography (CT):

Non contrast head CT scans are the primary means

of

making

management

diagnosis
purposes.(1)

and

suffice

Modern

CTs

for

immediate

can

produce

appropriate images in about 5 minutes and highly

sensitive to acute blood.(6)
Acute SDH appears on CT scan as a crescent shaped
hyperdense area, between the inner table of the skull and
the surface of the cerebral hemisphere. Acute SDHs usually
are unilateral.(7)
Rarely an acute SDH can appear isodense to the
brain in the following situations:
1.

If the hematocrit is low.(12)

2.

If the clot is a hyperacute (< 1 hour old),

and if active bleeding into the subdural space
occurs.(6)

3.

Disseminated

intravascular

coagulopathy.(13)

24

4.

Tears

in

the

arachnoid

membrane,

leading to dilution of the RBCs with CSF.(13)

The characteristic evolution of SDH appearance on
CT scan is as follows:

In the first week: the SDH is hyperdense to brain

tissue.(12)

In the second and third weeks: the SDH appears

isodense to brain tissue.(12)

After the third week, the SDH is hypodense to brain

tissue.(3)
Often chronic SDH appears as a heterogeneously
dense lesion, indicative of recurrent bleeding with fluid level
between the acute (hyperdense) and chronic (hypodense)
components of the hematoma.(3)
Typical signs of mass effect may be observed, such
as midline shift and ventricular compression.(3)
SDHs are relatively uncommon in the posterior
fossa, since the cerebellum undergoes little movement,
which is protective of its bridging cortical veins. SDHs that
do occur in this location are usually a result of parenchymal
cerebellar injury.(2)
25

Interhemispheric SDH causes the falx cerebri to

appear thickened, irregular and often associated with child
abuse.(2)
1.6.2.3 False negative CT scan:
High-convexity location, beam hardening artifact,
volume averaging with high density of calvarium obscuring
flat "en plaque" hematoma, too narrow window setting,
isodense hematoma due to delay in imaging 10-20 days
post-injury, due to low hemoglobin content of blood, lack of
clotting and CSF- dilution from associated arachnoid tear.(14)
1.6.2.5 Magnetic Resonance Imaging (MRI):

The multiple capability of MRI allows for significantly

better appreciation of the size and mass effect of an
SDH.(1)

In addition, small convex extra-axial collections may

be missed on CT.(1)

MRI is superior to CT for assessing the approximate

age of an SDH.(1)

However, CT remains the mainstay for evaluating

acute head injury and almost always provides enough
information for assessing and treating SDHs. When CT
26

findings are indeterminate or incongruent with the

clinical examination, MRI may be helpful.(8)
In

hyperacute

phase:

comprises

primarily

oxyhemoglobin and therefore, appears darker than brain on

T1-weighted images.(1)
The acute phase: the majority of acute SDHs are
homogeneous. They are imaged when the blood is in the
deoxyhemoglobin state, resulting in isointense to slightly
hypointense

gray

matter

on

T1-weighted

images

and

hypointense to gray matter on T2-weighted images.(1)

In some cases an acute SDH may be heterogenous.
The

reason

for

this

include

active

bleeding

with

oxyhaemoglobin contributing to the inhomogeneous signal,

admixture of CSF and rebleeding into pre-existing chronic
SDH. An acute SDH demonstrates the classic cresentic
shape in all planes.(1)
The

subacute

phase:

During

this

time

deoxyhaemoglobin is oxidized to methemoglobin and the

RBCs lyse. One change during this time is its subtle
increase in size due to an increase in osmotic pressure with
inward shift of waters. So subacute SDH may have
27

lenticular shape, especially on coronal plane. During this

stage the SDH appears hyperintense on T1-WIs, reflecting
the conversion of methemoglobin. The intensity on T2-WIs
reflects the integrity of RBC membranes. After haemolysis,
the extracellular methaemoglobin in the late subacute
phase results in increased T2-W signal intensity.(1)
During the late subacute stage: intra-axial and
extra-axial

hematoma

differs

in

appearance

on

MRI.

Specially methaemoglobin disappears faster from extra-axial

hematoma, which results in a more rapid loss of the bright
signals on T1-WIs.(1)
Another appearance sometimes seen with subacute
SDH, is the so called hematocrit effect, in which a
dependant component containing cellular elements forms a
straight line interface with a supernatant that contains
simple fluid. The hematocrit effect is appreciated on heavily
T2-WIs where the supernatant appears hyperitense and the
dependant portions appear hypointense.(1)
For an SDH that persists into the chronic phase, new
vessels, fibroblasts and macrophages migrate into the SDH
along its margin. In those SDHs that persist into chronic
28

stage, rebleeding is common, related to fragile nature of

new vessels in the capsule, lack a basement membrane and
thus are prone to rebleed with a trauma. These conditions
demonstrate decreased T1and T2 signal intensities which
represent

ferritin

and

hemosiderin

deposition

in

combination with decrease signal intensity of fibrous

tissue.(1)
The MRI appearance of intra-axial and extra-axial
hematoma differs in the chronic phase. The hemosiderin rim
that characterizes intra-axial hematoma is not seen in the
subdural space. Because of lack of blood brain barrier (BBB)
in the subdural space, the scavenger cells are not confined
to the extravascular space, and hence the accumulation of
hemosiderin at the periphery of a lesion doesn't occur. In
addition, the signal intensity of central portion of chronic
SDH

differs

from

that

seen

in

chronic

intra-axial

hematomas is hyperintense to gray matter on both T1- and

T2-WIs. This may be related to the protein content of the
fluid.(1)
Another feature that may be seen in a chronic SDH,
is the presence of a thin rim of fat signal intensity along the
29

inner margin of the collection. The exact cause of this

finding has not been determined, although it is likely that
this represents ossification of the dural pseudomembrane.(1)

1.7. Treatment:
The clinical status of the patient determines the type
of management. Small acute SDH less than 5 mm thick on
axial CT images, without sufficient mass effect to cause
midline

shift

or

neurological

signs,

can

be

followed

clinically.(3)
Emergent medical treatment of an acute SDH, that
causes impending transtentorial herniation, is the bolus
administration of mannitol therapy. Surgical evacuation of
the lesion is the definitive treatment and should not be
delayed.(3)
Chronic SDH without mass effect on imaging studies
and no neurological symptoms or signs except mild
headache, can be followed with serial scans and may
resolve. No medical therapy has been shown to be effective
in expediting rapid resolution of chronic SDHs.(3)
A thin layer under 1 cm may be reasonably tolerated
by the patient, but when the hematoma exceeds 1 cm it is
30

usually drained surgically, because of the mass effect, or if

the SDH is associated with midline shift greater than or
equal to 5 mm.(4,6)
Surgery

has

been

advocated

when

SDH

associated with compressed effaced basilar cisterns.(6)

1.8. Complications:
1.8.1. Postoperative complications:

Elevated ICP.

Brain edema.

New or recurrent bleeding / hematoma.

Infection.

Seizures.(2)

1.9.2 Chronic SDH:

Recurred hematoma (50%).

Infection (e.g. subdural empyema, wound).

Seizures (up to 10%).(2)

1.10. Prognosis:

Definitive prognosis is not possible at the time of

emergency

department

evaluation.

Ultimate

prognosis is related to the amount of associated

31

is

direct brain damage and the damage resulting from

the mass effect of the SDH.(2)

In ATSDH, poor outcome was correlated strongly

with the best sum GCS within the first 24 hours of
head

injury

pupillary

and

pupillary

reaction

to

light

inequality.
also

Age

correlate

and
with

outcome. Neurologic examination and postoperative

intracranial
prognostic

pressure
factors

monitoring

(elevated

ICP

are

important

postoperatively

indicates poor prognosis).(3)

No clear prognostic factors are associated with
CSDH. While some authors have found association
with preoperative level of neurological function and
outcome, other have not.(3) Eighty percent of patients
will resume their prehaematoma level of function.(3)

No

method

of

assessing

prognosis

is

100%

accurate.(6)

1.10. Computed tomography (CT):

1.10.1 Definition:

CT

is

an

x-ray

examination

characteristics.(15)
32

with

unique

The mechanism of operation involves passing a

collimated x-ray beam through a designed level of the

body in a circumferential (complete 360 or less) path,
with a set of detectors on the opposite side to record the
transmitted beam.(15)

The images contain a specific body thickness, which

is chosen by the radiologist to accomplish the required
diagnostic task.(16)
It is the digital images produced by the computer
from a large number of direct transmission measurement at
different angles through the patient.(16)
1.10.2. Advantages of CT over conventional radiographic
tomography are:

Better contrast resolution.

No superimposition of tissues.

Less scatter radiation.

Three-dimensional (3D) applications.

Bone mineral assay.(17)

Digital images, so variable window setting.(18)

1.10.3 CT number:

33

 The linear attenuation coefficient, , reflects the

degree to which the x-ray intensity is reduced by the
material.
values are scaled to that of water to give the:
CT number

tissue - water 100

water

e.g.

Material
water

CT valve
0

Air

- 1000

Bone

~ 1000(16)

1.10.4. CT number flexibility:

We can charge the appearance of the image by

varying the window width and level.(18)

This spreads a small range of CT numbers over a

large range of gray scale values.

This makes it easy to detect very small charge in CT

number.(15)

1.11. Scales:
1.11.1 Glasgow Coma Scale (GCS):(19)
Assessment of neurologic function based in these
determinants.
Response category

point value

Best motor response:

Obeys commands

6
34

Localizes stimuli

With draws (flexion)

Abnormal flexion

Extensor response

None

Verbal response :
Oriented

Confused conversation

Inappropriate words

Incomprehensible sounds

None

Eye opening:
Spontaneous

To speech

To noxious stimulation

None

Coma score = Score I + II III

1.11.2. Glasgow Outcome Scale:

(20)

The Glasgow outcome scale is often employed in

outcome assessment following head injuries.
Score

Meaning

Good recovery-resumption of normal life despite minor deficits

("return to work" not reliable)

Moderate disability (disabled but independent)-travel by public

transportation, can work in sheltered setting (exceeds mere
ability to perform "activities of daily living").

Severe disability (conscious but disabled)-dependent for daily

35

support ( may be institutionalized- but this is not a criteria).

2

Persistent vegetative state-unresponsive & speechless; after

2-3 weeks, may open eyes & have sleep/wake cycles.

Death-most deaths ascribable to primary head injury occur

within 48 hours.

OBJECTIVES

The aims of this study:

1.

To evaluate the association between the neurologic

presentation, as indicated by the clinical signs and
symptoms, Glasgow coma scale, its relation to CT
findings and the immediate outcome.

2.

To verify that, the admission CT findings as a

significant prognostic factor or not.

3.

To clarify the effect of the time between the accident

and the operative clot removal.

4.

To delineate the severity of trauma, age or gender of

the patients as a significant factors or not.

36

MATERIALS AND METHODS

2.1. Materials:
This prospective study was carried out during the
period from Jan. 2003 to Jan. 2004, at the National Centre
of Neurological Sciences (Al Shaab Teaching Hospital).
One
clinical

hundred

signs

hematomas

randomly

and

(SDHs)

symptoms
were

selected

patients

suggesting

admitted

to

the

with

subdural
Emergency

Department of Neurosurgery.
CT

was

introduced

as

an

integral

part

of

management of patients with suspected SDHs. CTs was

done in six radiologic centres. The CT was performed using
conventional and helical (spiral) CT machines, by welltrained technicians. The CT scan findings were assessed by
experienced radiologists.
Age, gender, history and type of trauma if present,
residence of the patients and the time interval between
37

trauma, CT performance and surgical intervention were

noted, as well as past history of diseases and associated
lesions.
Glasgow Coma Scale (GCS) was done routinely for all
patients

admitted

to

the

Neurosurgery

Emergency

Department.
Clinical data was classified as headache, side
weakness, headache and side weaknesses, and headache
with or without side weakness plus other neurologic signs.
CT findings like the number, site, size and age of
haematoma, through its density as well as its mass effects,
like midline shift, ventricular compression, displacement
and effaced sulci or cisterns are noted, as well as any
associated intracranial lesions.
Finally the surgical outcome was assessed at the
time of leaving hospital and was classified according to their
clinical improvement or not, the improvement with or
without neurologic deficit or the patient died.

2.3. Data analysis:

All data were entered and processed in personal
computer and calculated with a statistical program.
38

Categorical data were compared with proportion,

means, sensitivity, specificity, standard deviation, chisquared test and predictive value were computed.

RESULTS

There were one hundred patients, with one hundred

sixteen SDHs operated on. They were admitted to the study
in especially designated data sheet (see appendix).
The following variables were assessed with regards to
the age, sex, history of trauma and its severity, past history,
clinical presentation and GCS, time delay from injury
moment or start of complaint to CT scan diagnosis and
surgical treatment, and the immediate outcome at the time
of discharge from the hospital.
Fig. I and Table 1 showed that a mean age of 65
years, SD 11.5 (range from 37 to 90 years) and only 11% of
patients (n = 11) are within age group below the age of 50
years, 12% (n = 12) in age group 50 59 years and 77%
(n = 77) in the age of 60 years and over.
Fig. 2 shows that the overall male to female ratio
was 9 : 1, which means that males outnumber females.
39

Fig. 3 demonstrates that 36% of patient (n = 36) did

not give any history of trauma, 44% (n = 44) with history of
minor trauma, like falling during walking, praying or falling
from an animal, .. etc. Only 20% (n = 20) with history of a
rather severe or significant trauma, like kicked by stone,
rods or through motor vehicles accident.
Fig. 4 was related to time delay from start of
complaint to CT scan diagnosis and intervention. It showed
31% of patients (n= 31) with no time delay, 31% (n= 30)
within one month, 20% (n= 20) within 2 months and 18% (n
= 18) within 3 months or more.
Fig. 5 shows 85% of patients (n= 85) had CT scan
findings

of

brain

atrophy,

clearly

identifiable

in

supraventricular CT slices.
Fig. 6 demonstrates that 78% of patients (n = 78)
had an unilateral SDH and 22% (n= 22) with bilateral SDH
of different sizes.
Fig. 7 shows that 15.5% (n= 18) of SD collections
were purely hyperdense, 64 SD collections (55.2%) with
mixed density, isodensity or with layering and 29.3%
(n= 34) were purely hypodense.
40

Table 2 demonstrates with the mass effect on the

ventricles and/or sulci, in cases with unilateral SDH,
showing an increase in the mass effect and in midline shift.
While in cases with bilateral SDH, the mass effect is not
related to the degree of the midline shift.
Table 3 shows that the mass effects on the ventricles
and/or sulci is proportional to the thickness of the SDH,
especially when the thickness is more than 1 cm. This
relation was in the case of unilateral SDH, while there is no
such relation in cases of bilateral SDH and the mass effects
on ventricles were seen regardless of SDH thickness.
Table 4 shows no relation between the density of
SDH and the immediate outcome.
Table 5 demonstrates that 73% of patients (n= 73)
were

discharged

with

immediate

good

outcome

(improvement) regardless of the number of the SDHs. Six

patients (6%) died, three of them (3%) had a unilateral SDH
and the other three patients (3%) had bilateral SDHs.
Table 6 shows that 53% of patients (n= 53)
discharged with immediate good improvement with GCS
between 13-15, but cases with lower GCS are few in number
41

(n= 4) with GCS (9-12) and one case with GCS (< 8) and
they showed good or partial improvement at the time of
discharge from the hospital.
Table 7 in this table, the patients were classified into
4 subdivision groups of clinical presentation.
The first subdivision had headache only (n = 5; 5%).
The second one had hemiparesis only (n = 17; 17%). The
aforementioned groups showed good or partial immediate
improvement with no dead cases. The third groups included
patients with headache and hemiparesis. The last group had
neurologic

deficit

and

deterioration

in

the

level

of

consciousness too, five of the six dead cases were in that

clinical level.
Table 8 demonstrates that five of six dead cases
were with no time delay or less than one month between the
start of complaint and intervention.
Table 9 confined only to the dead cases. It shows the
following results:
i.

The fatality rate is 6% (n = 6).

ii.

All the dead cases were above age of 50

years.
42

iii. Four of six dead cases showed no

history of trauma with negative past
history of disease, or alcoholism, and
with unilateral SDH.
iv. 50% (n = 3) of dead cases demonstrated
mild to moderate decrease in GCS.
v. All the dead cases were within 3rd and
4th groups of clinical presentation.
vi. One of the dead cases, CT findings
showed I cm thickness of SDH, no
midline shift and with multiple cerebral
infarcts.

The

remaining

dead

cases

showed thickness of SDH of more than

1.5 cm with midline shift of I cm or more
than 1 cm.
vii. One case was found with hyperdense
SDH, 2 cases with mixed or isodense
SDH and 3 cases with pure hypodense
SDH.

43

Fig. (1) Distribution of study population according to the age groups

%
%

%
%
%

44

Fig. (2) Distribution of study population according to the sex

45

Femal
%

Male
%

Fig. (3) Distribution of study population according to

46

the type of trauma

%
%

Severe trauma

Minor trauma

NO trauma

Fig. (4) Distribution of the time delay between the start of

complaint and intervention

47

35
%

%
30
%

25
%

20
%

%
%

15
%

10
%

3 Months

Months

48

Month

Fig (5) CT findings (( Brain atrophy))

NO brain atrophy
15%

Brain atrophy
85%

49

Fig (6) CT scan findings (Number of SDHs)

Bilateral
22%

Unilateral
78%

50

Fig (7) Distribution of SDHs according to their densities

60.00
%

.%

50.00
%

40.00
%

.%
30.00
%

20.00
%

.%

10.00
%

0.00
%

Hypodensity

Mixed density

Hyperdensity

Table (1) Distribution of study populations according

to the mean age

51

Mi

Maximum

Mean

STD

90

65

11.5

nimum
100

37

52

Table (2) Relation between the midline shift and mass effects on
lateral ventricle and /or sulci
CT

Midline shift

No effect Compressed Obliterated

Total

Findings
Unilateral

<5mm

SDH

15

12

31

1 cm

36

38

>1cm

Bilateral

No shift

SDHs

<5 mm

65

100

1 cm
> 1cm
Total

53

26

Table (3) Relation between thickness of an SDH and the mass

effects on lateral ventricle and /or sulci
CT findings

Midline shift No effect Compressed Obliterated Total

Unilateral

1 cm

SDH

1.5 cm

10

33

38

2.5 cm

3.0 cm

10

12

22

10

25

65

100

2.0 cm

Bilateral

SDHs
Total

54

Table (4): Relation between the density of an SDH and outcome

CT findings

Improved

Partially improved

Died

Total

Hyperdensity

11 (11%)

3 (3%)

1 (1%)

15 (15%)

Mixed density

44 (44%)

12 (12%)

3 (3%)

59 (59%)

Hypodensity

18 (18%)

6 (6%)

2 (2%)

26 (26%)

73 (73%)

21 (21%)

6 (6%)

100 (100%)

Total
P. 0.05

55

Table (5) Relation of CT findings (Number of SDH)

and outcome
Nu Improvement
mber of

Partially

Deteriorated

Total

ied

Improvement

SDH

Unilateral

60 (60%)

15 (15%)

3 (3%)

78 (78%)

Bilateral

13 (13%)

6 (6%)

3 (3%)

22 (22%)

Total

73 (73%)

21 (21%)

6 (6%)

100 (100%)

P= 0.13

X2 = 4.0

df. = 2 (insignificant)

56

Table (6) Relation between GCS and outcome

Grad Improvement
e of GCS
Mild
GCS :13 - 15

53

10

53%

10%

GCS :9 - 12

4%

GCS :<8

1%

1%

Not done

15

10

15%

9%

73

21

73%

21%

P= 0.49

X2 = 2.3

64

1%

64%

2%

6%

2
2%

df. = 3 (insignificant)

57

Total
ied

Total

Deteriorated

Improvement

Moderate

Severe

Partially

28

3%

28%

100

6%

58

Table (8) The relation between the time delay (start of

complaints and intervention) and the outcome
Tim Improvement
e delay
< 1 month

Month

2 Months

3 Months
or more
Total

P= 0.021

Partially

Deteriorated
ied

Improvement
22

22%

6%

24

24%

4%

15

15%

5%

12

12%

6%

73

21

73%

21%

X2 = 9.6

31

3%

31%

30

2%

30%

21

1%

21%

18
18%

df. = 3 (significant)

59

Total

100

6%

100%

DISCUSSION
60

This prospective study included a randomly selected

one hundred patients with one hundred sixteen CT scan
diagnosed SHDs operated on at the National Center of
Neurological Sciences (Al-Shaab Teaching Hospital), during
the period from January 2003 to January 2004.
The study sample size was relatively similar to other
studies, Havenbergh, et al (1996) from Belgium studied 260
patients.(20) Massaro, et al (1996) from Italy studied 127
patients.(21) In all these studies, the number was dependent
on the duration of the study.
The studies done, correlated CT scan findings of
SDHs with outcome, followed the patients for certain time
and confined either to acute(20) or chronic SDHs only.(21) Our
study was related only to immediate outcome after recovery
and discharge. Second thing was that this study involved all
types of SDHs, third thing cross-sectional modalities (CT
and MRI) were present only in Khartoum and there was a
need for time for patient's arrival to the related hospital.
This study showed that the minimum age of patients
involved was 37 years and the maximum age was 90 years,
with a mean age of 65 years (Fig. 1). It was found that most
61

of the cases were above age of 50 (n= 89: 89%) and 77% of
patients (n=77) were above the age of 60 years (Table 1),
indicating that SDHs is mostly a disease of the aged
patients regardless the relation with other parameters.
In this study the overall male to female ratio was 9:1
(90:10)

indicating

that

males

outnumbered

females

(Fig. 2). This may be related to the fact that, in our

communities, old females restrict their movement to their
houses, while the males have no limited age for retirement.
Obajimi MO, et al (2002) from Ghana found that male to
female ratio in similar study was 2.6 :1, while the mean age
was 32.4 years.(22)
It was notable that 36% of patients (n=36) did not
give any history of trauma and 44% (n=44) gave a history
that classified as a minor trauma, like falling during
walking, praying or from an animals. Only 20% (n=20) gave
significant history of trauma, like kicked by hard stalk,
stone or fell from the car ((Fig. 3), suggesting that the
trauma was not necessary for the occurrence of SDH, and
the absence of the history of trauma didn't rule out the
possibility of the occurrence of SDH.
62

It was found that 31% of patients (n=31) with no

time delay between history of complaint and CT scan
diagnosis and surgical intervention, indicating that were
diagnosed within 72 hours (acute clinical phase of SDH),(2)
30% (n=30) within undetermined classification between
clinical subacute and chronic phase of SDH,(3) and 39%
within clinically chronic SDH (Fig. 4). According to CT scan
findings, the patients were divided into pure hyperdense
15.% (n= 18), mixed density 55.2% (n=64) and pure
hypodense 29.3% (n=34). The discrepancy between the
number of cases in clinical and radiological subdivisions
was mostly in cases with mixed density, may be attributed
to subacute and chronic cases, that undergone recurrent
bleeding, causing layering of the haematoma (haematocrit)
or a term of arachnoid membrane leading to dilution and so
the mixed density of an SDH. In comparison with other
study Lee KS, et al (1977) from Korea found that the density
of acute SDH was hyperdense in 98.6% of cases. In the
subacute group, it was hypodense in 45.7%, while in
chronic SDHs 86.7% were isodense, reaching the result that
absolute reliance on classification of haematomas as acute
63

or chronic based on CT density can lead to inaccuracies.(23)

For this reason, MRI is more sensitive for subdivision of
SDHs

depending

intensities

of

upon

its

blood

ability
from

to

visualize

signal

oxyhaemoglobin,

deoxyhaemoglobin to methaemoglobin and haemosiderin

formation in intracellular and extracellular compartments,
giving MRI ability to separate hyperacute from acute
collection.(1) But general limatations to MRI employment
should also be considered in the diagnosis of SDHs.(8)
From this study, we found that immediate good
improvement (n=73), partial improvement (n=21) or the dead
cases (n=6) had no significant relationship to the density of
the SDH (Table 4) and no relation to the duration of SDH.
It was also found that unilateral SDHs (n=78) out
numbered bilateral SDHs (n=22). Again the outcome had no
relation to the number of SDHs and the dead cases were
found in equal percentage in both unilateral and bilateral
SDHs (Table 5).
The midline shift was seen related to the mass effect
on the lateral ventricles in cases with unilateral collections,
and it was seen in all cases with a midline shift equal to or
64

more than 1 cm (Table 2). This is consistent with the

indications

for

surgical

management

based

on

CT

findings.(4,6).
In cases with bilateral SDHs, some of them (n=9)
showed a midline shift probably related to the asymmetry in
the sizes of SDH, causing a mass effect on ipsilateral lateral
ventricle (Table 2).
In this study, the mass effect on lateral ventricles
was strongly related to the thickness of an SDH, as there
were only 3 cases with a midline shift of 1 cm and showed
no effect on lateral ventricle. Only one case of 78 cases, with
thickness more than 1 cm, showed no midline shift. The
thickness rather than the size of an SDH has mass effect,
this depends on the anatomical fact that an SDH, unlike
epidural haematoma, is not limited by sutures,(4) so an
increase in thickness of SDH means that it is the last event
in the pathogenesis of SDH after complete expansion in all
directions. So any little increase in the thickness would lead
to more mass effect on the adjacent structures and results
in midline shift.

65

There was no relation between the density of the

SDH and outcome. Most of the cases (n=73) showed
immediate improvement of the patients with different SDH
density levels. This result may be changed if the sample size
is larger and the outcome of each subdivision studied
separately. Also the dead cases showed no relation to the
density of an SDH (Table 4).
This study showed that, 53% of the patients (n=53)
with mild decrease in GCS had good improvement or
recovery. In comparison with other studies, strongly related
outcome with GCS in cases of acute SDH was found.(21)
The study also showed that most of the cases with
good

or

partial

improvement

had

no

relation

with

subdivision of clinical presentation at the time of admission.

However, only the dead cases are related to clinical
presentation despite small the number of dead cases
(Table 7).
Also no relation was seen with time delay between
the

start

of

complaint,

CT

diagnosis

and

surgical

management. However, for the dead cases, they showed a

rather shorter time delay (Table 8), which may be related to
66

the severity of complaints, leading to early diagnosis and

management.
The fatality rate was 6% (n=6) and all cases showed
significant clinical presentation, suggesting that it could be
considered as a prognostic factor. The fatality rate showed
no relation to the density, number, thickness of an SDH or
midline shift, indicating CT scan findings had no relation to
the outcome. Van den Brink, et al from Netherlands showed
that the volume of haematoma did not correlate with the
preoperative neurological condition and consequently of no
additional prognostic value. (24) The same result was seen in
other studies.(20)
In an other comparative study (Robert H. Wilkins,
et al, 1996), showed that the outcome following treatment of
chronic SDH correlated most closely with the patient's
neurological state at the time of treatment.(25)
One of the dead cases showed CT findings of
conservative management.(4,6) A rather old age with a poor
general condition and cerebral infarcts responsible
neurological state, not due to the effect of
(Table 9).
67

for

a small SDH

In Similar studies, the outcome assessed after a

certain time, like six month outcome, which consequently
was not of additional prognostic value.(25) Others suggested
a need for postoperative follow-up during an interval up to 3
months.(26)
Pospiech J, et al from Essen-Germany (1993) said
that concomitant brain injuries were of greater importance
to the outcome rather than the effects of the haematoma
itself.(27)

CONCLUSION

68

CT is the mainstay for the presence, density,

number, size of SDHs and their mass effects.

CT is the modality of choice to exclude intracerebral

lesions, like CVA, that clinically may simulate an SDH.

CT can give an idea about the management of an

SDH, in other words, which one for conservative and
which one for surgical management.

CT scan findings were not correlated with immediate

outcome of an SDH.

Time delay between the start of the complaint, CT

employment and surgical intervention had no relation
with the immediate outcome.
The immediate outcome of SDH were correlated to the
clinical presentation at the time of admission.

RECOMMENDATION
69

CT scan examination should be performed to all

patients with neurological state suspicious of having an
SDH, in order to take accurate diagnosis and to select the
way of management, but should not be taken as a
prognostic factor.

Complementary use of other imaging modalities, like

MRI is suggested when CT scan is not conclusive.

REFERENCES
70

1-

David D. Stark, et al. Subdural haematoma. In:

Magnetic Resonance Imaging. 3rd ed. St. Louis: Mosby;
1999.

2-

P. 1351-52.

Tom Scaletta, et al. Subdural haematoma. EMedicine

Journal Aug. 2003; 2: 8. Available from

http://www.

Emedicine. Com/ Med /Topic 2885,hutm.

3-

Grant
eMedicine

P.

Sinson,
Journal

et

al.

2002;

Subdural
3(1).

haematoma,

Available

from

http://www. Emedicine. Com.

4-

Richard S Snell. The meninges of the brain and spinal

cord. In: Clinical neuroanatomy for medical students, 5th
ed. Baltimore, Maryland: Lippincott William and Wilkins;
2001. P. 427 - 441.

5-

John R. Mongiardi, et al. Subdural haematoma,

Atypical Scenario. Available from http://www.Brainsurgery.com/subdural. htm.

6-

Richard J. Meagher, et al. Subdural hematoma.

eMedicine Journal 2002. Available from http://www.
Emedicine. Com/

71

7-

Neil T, Specht, et al. Extra-axial collection. In:

Practical guideline to diagnostic imaging, 1st ed. St.
Louis: Mobsy; 1998. 533- 34.

8-

Grainger

and

Ellison.

Extra

axial

collection.

In:

Diagnostic radiology A textbook of medical imaging, 3rd ed.

London: Churchill Livingstone. 1997. P. 2395 -97.
9-

David Sutton. Head trauma. In: A textbook of radiology

and imaging, 4th ed. London: William Clowes Limited. 1987.
P. 1560.

10-

Ronald L. Eisenderg. Subdural haematoma. In: Clinical

imaging: An atlas of differential diagnosis. Baltimore,

Maryland: Lippincott Williams & Wilkins; 2003. P.

1056-

1057.
11-

David Sutton. Subdural haematoma. In: A textbook of

radiology, 6th ed. London: Churchill Livingstone; 1997. P.

1629.
12-

Robert I. Grossman, et al. Subdural hygroma. In:

Neuroradiology the requisites. St. Louis. Mosby; 1994.P. 152

-155.

72

13-

Assiff Saifuddin. Subdural haematoma. In: MCQs in

clinical imaging, 1sted. London: Chapmann & Hall Medical;

1994. Q.7. 22.D.
14-

Wolfgang Dahnert. Subdural haematoma. In: Radiology

Review Manual, 4th ed. Baltimore, Maryland: Lippincott

Williams & Wilkins; 2000. P. 269 -271.
15-

Rodney A. White, et al. Computed tomography. In:

Vascualr imaging: basic science and clinical correlation.

Philadelphia: J.B Lippincott Company; 2000. P. 449.
16-

Stewart C. Bushong. Special imaging technique. In:

Computed tomography; Essential of imaging series. New

York: McGraw-Hill; 2000. P. 101.
17-

Nick Keat. Principles of CT scanning; www./impact

scan.org.
18-

Hope RA. Glasgow coma scale. In: Oxford handbook of

clinical medicine, 3rd ed. Oxford: Oxford Press; 1994. P. 718.

19-

Mark

S.

Greenberg.

Glasgow

outcome

scale.

In:

Handbook of neurisurgery, 5th ed. Florida: Thieme; 2001. P.

861.

73

20-

T. Van Havenbergh, et al. Outcome of chronic subdural

hematomas: analysis of prognostic factors. Br. J Neurosurg

1996; 10(1): 35-39.
21-

F. Massaro, et al. One hundred and twenty-seven cases of

acute subdural haematoma operated on: correlation between

CT scan findings and outcome. Acta Neurochir (Wien) 1996;
138: 185-191.
22-

Obajimi MO, et al. CT evaluation of intracranial subdural

haematona: An Accra experience. Afr J Med Sci 2002 Dec;

31(4): 321 -4.
23-

Lee KS, et al. The computed tomographic attenuation

and the age of subdural haematoma. J Korean Med Sci 1997

Aug; 12(4): 353-9.
24-

Van den Brink, et al. The prognostic importance of the

volume of traumatic epidural and subdural haematoma.

Acta Neurochi (Wien) 1999; 141(5): 509 -14.
25-

Robert H. Wilkins, et al. Subdural haematoma. In:

Neurosurgery,

2nd

ed.

New

York:

McGraw-Hill

Professions Division, 1996. P. 2797 - 2802.

74

Health

26-

Asano Y, et al. Recurrent cases of chronic subdural

hematoma.-its clinical review and serial CT. No To Shinkei

1992 Sep; 44(9): 827 -31.
27-

Pospiech J, et al. Prognostic factors in acute traumatic

epi-and subdural hematoma; Aktuelle Traumatol 1993 Feb;

23(1): 1-6.

75


University of Khartoum
Faculty of Medicine
Postgraduate Medical Studies Board
Questionnaire:
Correlation between computerised tomography (CT) findings,
clinical presentation and immediate postoperative results in
subdural haematoma

Name:.......................................Age:..........................Sex:.............
.....

Residence:.......................................
...

Date of trauma:.............

Type of trauma: No

Date

of

Minor
CT

Severe

scan:........................

Rad.

center:..................................

Date

of

operation:.......................

Recurrence:..................................

Past history of:

Smoking

Yes

No

- Bleeding disorder
- Alcoholism
-

Diabetes mellitus

Hypertension

Others

GCS at the time of admission:.............

Clinical findings: ...

CT findings: ..
- Brain atrophy:

Yes

- Number of SDH:

Unilateral

No
Bilateral

- Site of SDH: .
76

Size

of

SDH:

.
- CT number of SDH or density: ..
- Mass effect: Obliterated

LV

Effaced sulci

Effaced basal cistern

- Midline shift:
-

Any

< 5 mm

associated

1 cm
intracranial

Patient's outcome:
Improvement with no neurologic deficit
- Improvement with neurologic deficit
- Deteriorated

Died

77

>1 cm
lesion:

78