SUBDURAL HEMATOMA

By- Muskan Ahuja

SUBMITTED BY – MUSKAN AHUJA

A1106618136
SEMSTER 6A

SUBMITTED TO-DR. MEENA GUPTA

TABLE OF CONTENTS
S.No TOPIC Page No
Keywords 3
Abbreviations
Method
Background

1. Introduction 4

2. Etiology 4

3. Pathophysiology 5
4. Types of subdural hematoma 6
5. Clinical Presentation of patient 7
6. Risk Factors 7
7. Diagnosis 8
8. Imaging 9
9. Treatment 10
10. Review of Literature 11
11. References 12
  Key words
1. Angiogenesis
2. Subdural hematoma
3. Corticosteroids
4. Head trauma
5. Inflammation
6. Pathophysiology

 Abbreviations and Acronyms

1. ACE: Angiotensin-converting enzyme
2. BHC: Burr-hole craniostomy
3. SDH: Chronic subdural hematoma
4. COX-2: Cyclooxoygenase 2
5. CSF: Cerebrospinal fluid
6. CT: Computed tomography
7. IL: Interleukin
8. PGE2: Prostaglandin E2
9. VEGF: Vascular endothelial growth factor

 Method
Performed a thorough literature search in PubMed , CINAHL, and Google scholar,
focusing on any aspect of the patho-physiology and nonsurgical treatment of SDH.
 Background
Subdural hematoma (SDH) is one of the more frequent pathologic entities in daily
neurosurgical practice. Historically, SDH was considered progressive recurrent
bleeding with a traumatic cause. How-ever, recent evidence has suggested a complex
pathway of inflammation, angiogenesis, local coagulopathy, recurrent microbleeds.
1. INTRODUCTION
Subdural hematoma is characterized under the Extra- axial haemorrhage which is
defined as bleeding which occurs inside the skull but outside the brain tissue. A
subdural hematoma occurs when a blood vessel near the surface of the brain bursts.
Blood builds up between the brain and the brain's tough outer lining. The condition is
also called a subdural haemorrhage. In a subdural hematoma, blood collects
immediately beneath the dura mater. The dura mater is the outermost layer of the
meninges. The meninges is the three-layer protective covering of the brain.
.
1.1 Meninges of the Brain

Meninges of brain diagmmatic reprsenation ( red area where subdural

hematoma happens) Figure 1

2. ETIOLOGY
Etiology Although majority of the CSDHs are due to trauma, intracranial hypotension and
defective coagulations could also be responsible.
2.1 Post traumatic
Post-traumatic Definite history of trauma could be obtained in majority of the cases.
Majority of these cases have mild head injury, although moderate to severe injury could
be the causative factor in some cases. This injury could be trivial and may go unnoticed.
Some cases could occur after neurosurgical operations. The thin walls of bridging veins,
circumferential arrangement of collagen fibers, contribute to the more fragile nature of
bridging vein in the subdural portion as compared to the subarachnoid portion. Repeated
injury on the head during play may be the cause of SDH in children.
 2.2 Intracranial hypotension
The cerebrospinal fluid (CSF) leakage could cause intracranial hypotension which could
lead to SDH formation. Spontaneous intracranial hypotension Spontaneous intracranial
hypotension could be the cause of SDH, especially in young to middle-aged patients,
without preceding trauma or hematological disorders. MRI scans of the spine useful in
the evaluation of intracranial hypotension.[1] The presence of an underlying spontaneous
spinal CSF leak should be considered in SDH, even among the elderly taking
anticoagulants.
2.2.1 CSF rhinorrhea
It could be the cause of the intracranial hypotension leading to SDH.[2]
2.3 Other factors -
Causes of acute subdural hematoma include the following
 Coagulopathy or medical anticoagulation
 Nontraumatic intracranial hemorrhage due to cerebral aneurysm,
 Postsurgical (craniotomy, CSF shunting)
 Child abuse or shaken baby syndrome (in the pediatric age group)

Causes of chronic subdural hematoma include the following:

 Acute subdural hematoma, with or without surgical intervention

 Spontaneous or idiopathic

3. PATHOPHYSIOLOGY
Pathology SDH consists of an outer membrane, hematoma cavity, and an inner membrane.
Hematoma fluid is usually liquid that does not clot. Usually hematomas are liquefied, but
mixed lesions with solid components are also seen. The fibrinolytic factors appear to be
associated with evolution in SDHs with heterogeneous density.[3] Usually there is no
infection in these hematomas, but the SDH is a potential site for bacterial infection. The
possibility of infected SDH should be considered when a patient has features of infection.[4]
The developing hematoma capsule shows gradual changes in cellular and vascular
organization with progression in hematoma age. Initial changes include angiogenic and
aseptic inflammatory reactions. It is followed by fibroblasts-proliferation and development
of collagen fibrils. Young hematomas (15-21 days after trauma) show numerous capillaries,
suggesting formation of new blood vessels. Older hematomas (40 days after trauma) usually
show numerous capillaries and thin-walled sinusoids accompanied by patent, larger diameter
blood vessels. Blood vessels are frequently occluded by clots in the fibrotic outer membrane
of 60 or more days old hematoma. (refer to the figure 2)
 CSF interposed
Cleavage of the beween broken cell
Minor head trauma
dural border cell layer and rest of the
dura

Immature capillaries Increase fibrolast -

allow extravasion of Injured cells
vascular contentsinto on dural slide of released cytokines
hematoma cavity outer membrane

Hematoma enlarges Fibrin clots

Eosinphils recuited disintegrates
Leads more cell injury
Plasminogen and platetes don not
thrombin cavity aggreagate

Pathophysiology of subdural hematoma ( Figure 2)

4. TYPES OF SUBDURAL HEMATOMA

Subdural hematomas are usually characterized on the basis of their size and location and the
amount of time elapsed since the inciting event age (ie, whether they are acute, subacute, or
chronic).
4.1 Acute subdural hematoma
Acute subdural hematomas are less than 72 hours old and are hyperdense
compared with the brain on computed tomography scans. The subacute phase
begins 3-7 days after acute injury.

3.2 Chronic subdural hematoma

Chronic subdural hematomas develop over the course of weeks and are hypodense
compared with the brain.
 5. CLINICAL PRESENATION OF PATIENT

Balance and
walking problem Dizziness

Headache Seizures

Slurred Vision
speech problem

Nausea Weakness
6. RISK FACTORS
 Head injury, such as from car crashes, falls, or sudden changes in speed
 Playing high-impact sports
 Advanced age. This makes it more likely that the brain has shrunk, putting the blood
vessels at risk for damage.
 Alcohol abuse
 Previous brain injury
 Using blood-thinning medicine
 Violence, such as shaken baby syndrome
 Cerebrospinal fluid leak (rare)
 Blood vessel rupture at a weak or bulging spot (cerebral aneurysm) (rare)
 Tumor (rare)
 Bleeding disorders such as hemophilia
7. DIAGONSIS
Clinical diagnosis
The diagnosis of a chronic subdural haematoma can present many difficulties taking into
account the fact that it frequently appears in elders, who anyway have a higher or a lower
degree of psychical disorders due to brain involution. Moreover, in the context of a usual
brain injury, which can pass unobserved and may frequently be ignored, the chronic subdural
haematoma has a latent period until the appearance of the clinical symptoms, the diagnosis
presenting many errors.
Therefore, the main element that can lead to the diagnosis of chronic subdural haematoma is
the minor brain injury; however, it should not be forgotten that it is seriously taken into
account only by some of the patients or their families. Besides the trauma, there are 3
elements that can contribute to the clinical diagnosis of a chronic subdural haematoma the
signs of hemispheric brain damage or the foci (mainly the motor deficits and the speech
disorders), psychical disorders which are most often met (chronic subdural haematoma being
one of the causes of evolutive dementia in elders) and the symptomatic fluctuation. Besides
these 3 elements, other relevant clinical signs have also been described in cases of
haematoma: headache, drowsiness, signs of intracranial hypertension
Generally, the clinical stage of chronic subdural haematoma orients towards an injury at the
level of the brain hemisphere but does not help in the differential diagnosis of other brain
injuries.
Usually, a progressive slow expansive intracranial process or an ischemic stroke is
suspected. The suspicion of expansive intracranial injury makes us perform a paraclinical
investigation (CT or MRI), which makes the diagnosis clearer by evidencing the iso- or
hypodense subdural collection.
If the CT examination is currently very easily accessible, the diagnosis of chronic subdural
haematoma has become quite simple, the main condition being that you only have to think
about such a diagnosis. This is valid mostly in cases of elders, who progressively develop
psychic disorders, representing the group of patients with chronic subdural haematoma.
Regarding the differential diagnosis, it should not be forgotten that the clinical signs of a
haematoma mimic an intracranial neoformation or an ischemic stroke. In youngsters, chronic
subdural haematomas often manifest with epilepsy crises and behavior disorders, which are
due to alcohol consumption.
8. IMAGING
 Computed tomography (CT)
Preferred examination CT scanning is usually the first evaluation in patients with suspected
acute subdural hematoma because CT scans depict acute hemorrhage and skull fractures
well, they are relatively fast to obtain, and CT scanning is more readily available than
MRI.

Computed tomography (CT) scan Late sub acute subdural hematoma has
demonstrating a patient with subdural decreased attenuation compared with
hematomas of varying ages. This patient had a adjacent brain tissue. Attenuation of the
CT scan 1 week prior that demonstrated a hematoma remains higher than that of
chronic subdural hematoma (represented by cerebrospinal fluid.
the low density fluid on this study). Over the
next week, his clinical condition progressively
declined, then he collapsed shortly before this
image was obtained. The gray blood represents
subacute hemorrhage, whereas the white blood
represents acute

 Magnetic Resonance Imaging

Axial T1-weighted magnetic resonance imaging

demonstrates bilateral subacute subdural hematomas with
increased signal intensity. Areas of intermediate intensity
represent more acute hemorrhage into the subacute
collections
9. TREATMENT
Nonsurgical Treatment
 Angiotensin-Converting Enzyme Inhibitors Angiotensin-converting enzyme
(ACE) inhibitors decrease VEGF production ,possibly resulting in a reduction
of new and immature vascularization, a decreased extra vasation of fluid into the
subdural space, and a reduction of recurrence ofCSDH.108In a prospective
randomized controlled trial,109the ACE inhibitor perindopril was tested against
there was no statistically significant effect on recurrence rate. Retrospective
case-control study in which they found higher hematoma volumes and a higher
frequency of recurrences in patients treated with ACE inhibitors as an addition to
surgery. These investigators hypothesize that this situation could be caused by an
increase inbradykinin levels, causing increased vascular permeability of the
neo-membranes in SDH.
 Dexamethasone Steroids might be an option in the nonsurgical treatment of SDH.
Dexamethasone is known to be anti inflammatory and has anti angiogenic effects.
Moreover, it is able to inhibit the formation of new blood vessels. Over the past
decades, dexamethasone has been assessed in multiple studies as mono-
therapy .Dexamethasone is a non invasive treatment and might significantly
reducemortality and lead to a better outcome
 Post surgery role of physical therapist
 Speech therapy
 Regaining strength
 Helps in the proper circulation of blood after surgery, thus preventing blood clots.
 Helps in improving the muscle strength, posture and balance of the body.
 Physiotherapy also proves beneficial in helping a person get back on their feet.
 Physiotherapy also provides effective self – care training to the patient like safely
getting out of bed, bathing, climbing stairs, etc.
 Physiotherapy reduces pain and equips you with pain control and manual therapy
techniques.
 Finally, physiotherapy reduces the risk of post – operative pulmonary complications
(PCCs)/
10. REVIEW OF LITERATURE
S.N Author Name Title Methodology Study Result Conclusion
o
1. Patrick A retrospectively There was a Surgical
Mulligan, Bethwe Neurological reviewed data on 45 significant managemen
and functional patients above 70
l Raore, improvement t of SDH in
outcomes of years who
and Jeffrey underwent in the patients
(2013) subdural craniotomy or burr neurological over 70
hematoma holes for acute, status of years of age
evacuation in chronic or mixed patients from provides
patients over subdural hematomas. admission to significant
70 years of We analyzed both
follow up as improvemen
age neurological and
functional status assessed using t in
before and after Markwalder neurological
surgery. grading scale status, but
(1.98 vs. does not
1.39; P =0.005) change
, yet no functional
improvement status.
in functional
outcome was
observed as
assessed by
Glasgow
Outcome Score
2. José Pedro Acute Eighty-nine medical Sixty-nine They were
Lavrador, Joaqui Subdural records of patients were associated
consecutive patients
m Cruz Hematoma included; 52% with the
with age ≥18 years
Teixeira, Edson Evacuation: old who were were male; worst
Oliveira, Diogo Predictive submitted to aSDH 74% were outcome.
Simão, Maria Factors of evacuation were older than 65 Age and
Manuel Santos Outcome reviewed. years; 41% OAT were
(2018) Demographic were under oral not
characteristics,
antithrombotic predictive
neurological status
on admission, therapy (OAT); factors in
anticoagulant or at admission, this series.
antiplatelet therapy, 54% presented Caution
and outcome on with Glasgow should be
discharge were coma scale taken when
collected. Patients
(GCS) ≤8; 23% considering
with insufficient data
concerning these were submitted these factors
variables were to a in the
excluded from the craniectomy surgical
study. decision.
12. REFRENCES
1. Poonnoose SI, Manjooran RP, Mathew J, Ramachandran P. Chronic subdural haematoma
associated with nontraumatic CSF rhinorrhea: A management challenge. J Clin Neurosci
2007;14:281-3.
2. Park SH, Kang DH, Park J, Hwang JH, Hwang SK, Sung JK, et al. Fibrinogen and
D-dimer analysis of chronic subdural hematomas and computed tomography findings: A
prospective study. Clin Neurol Neurosurg 2011;113:272-6.
3. Iimura Y, Tsutsumi S, Mitome Y, Nonaka Y, Abe Y, Yasumoto Y, et al. Infantile chronic
subdural hematoma infected by Escherichia coli: Case report. Neurol Med Chir (Tokyo)
2010;50:482-4.
4. Moskala M, Goscinski I, Kaluza J, Polak J, Krupa M, Adamek D, et al. Morphological
aspects of the traumatic chronic subdural hematoma capsule: SEM studies. Microsc
Microanal 2007;13:211-9.
5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6159091/
6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3821407/
7. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4556906/
8. https://www.portea.com/physiotherapy/post-surgical-
rehab/#:~:text=Post%20surgery%20physical%20therapy%20plays,prior%20level%20of%20p
hysical%20function.
9. https://emedicine.medscape.com/article/344482-overview#a3
10. https://www.webmd.com/brain/subdural-hematoma-symptoms-causes-treatments
11. https://emedicine.medscape.com/article/1137207-overview#a5