1. An epidural haematoma (EDH) is a collection of blood between the skull and the dura mater that is usually caused by an injury to the middle meningeal artery from a head trauma. 2. Symptoms of an EDH can include confusion, loss of consciousness, headaches, vomiting and neurological deficits. Patients may experience an initial lucid interval followed by deterioration in their mental status. 3. A CT scan is the primary method used to diagnose an EDH, which appears as a hyperdense, biconvex lesion between the skull and dura. Surgical evacuation is usually required for symptomatic EDHs, while small, asymptomatic EDHs may be monitored conservatively.

1. EPIDURAL
HAEMATOMA
DR.KARAN R RAWAT
GUIDE
DR.PANKAJ GUPTA
DR.JITENDRA SINGH
DR.ARVIND SHARMA

2. SKULL ANATOMY

6. HEAD INJURY
• DEFINITION –a history of a blow to the head or the presence
of a scalp wound or those with evidence of altered
consciousness after a relevant injury’.
• The level of consciousness as assessed by the Glasgow Coma
Scale

10. • The person may have varying degrees of symptoms associated with the severity of
the head injury. The following are the most common symptoms of a head injury.
However, each individual may experience symptoms differently. With this type of
moderate to severe head injury, immediate medical attention is required.
Symptoms may include:
• confusion
• loss of consciousness
• blurred vision
• severe headache
• vomiting
• loss of short-term memory, such as difficulty remembering the events that lead
right up to and through the traumatic event
• slurred speech
• difficult walking
• dizziness
• weakness in one side or area of the body
• sweating
• pale skin color
• seizures
• behavior changes including irritability
• blood or clear fluid draining from the ears or nose
• one pupil (dark area in the center of the eye) looks larger than the other eye
• deep cut or laceration in the scalp
• open wound in the head
• foreign object penetrating the head

14. EPIDURAL HAEMATOMA
• It is a collection of blood between the
potential space that exists between the inner
table of skull and the dura (periosteal layer).
Extension of hematoma usually is limited by
the suture lines owing to the light attachment
of the dura at these locations (continuation of
periosteal layer of the dura with the
pericranium at the sutures)

17. EPIDEMIOLOGY
• EDH approx. 2% of all patients with head injuries and 5 %- 15 % of
patients with fatal head injuries .
• EDH –
1.ACUTE 58%
2.SUBACUTE 31%
3.CHRONIC 11%
• Occurs in young adults and is rare in children below 2 years of age
<due to plasticity of immature calvarium > or after the age of 60
years <dura is adherent to overlying bone >
• The incidence of delayed extradural haematoma (DEDH) following
initially negative CT scan is reported to 10% - 30 %

18. Pathophysiology
It results from brief linear contact force to the calvarium
that causes seperation of the periosteal dura from the
bone and disruption of interposed vessels due to
sheering stress
Skull # are found in 85% - 95 % of adult cases
Chronic or delayed manifestation may occur when the
venous sources are involved
The haematoma arises from injury to the middle
meningeal artery in over half of the patients ,from the
middle meningeal vein in one third and from diploic
veins or torn dural venous sinus from the remainder .

19. • The temporoparietal region and middle
menigeal artery are most commonly involved
66%
• Anterior ethemoidal arteries may be involved
in frontal injuries ,the transverse or sigmoid
sinus in occipital injuries and superior saggital
sinus in trauma to the vertex .
• Posterior fossa EDH occur in 5 % of all cases of
EDH

20. Clinical presentation
• Kristiansen and tandon in 1960 described that the patients
with EDH may have the following five clinical presentations
:-
• Concious throughout 8 % - 24 %
• Unconcious throughout 23 %- 24 %
• Initially concious and subsequently unconcious 20 %- 28 %
• Initially unconcious and subsequently lucid 14 % - 21 %
• The “textbook” presentation of brief traumatic loss of
conciousness LOC followed by lucid interval for several
hours and then obtundation,contralateral hemiparesis and
ipsilateral pupilliary dilatation occurs in less than 10 – 27 %
of the patient

21. Lucid interval
• An epidural hemorrhage is often characterized by the
following sequence of events:
– Blunt trauma/ a blow to the head, followed by:
– 1) Initial confusion, decreased consciousness, or loss of
consciousness
– 2) A “lucid interval” (20-50%):
• a brief period of full conciousness/restored mental status. The
patient seems back to his/her “normal self.”
– 3) Change in mental status +/- unstable vital signs (blood
pressure, heart rate):
• the patient becomes confused, somnolent (sleepy), may have
neurologic signs such as hemiparesis, one dilated pupil, may
become comatose.

22. • The lucid interval is not pathognomic for EDH
,other post traumatic mass lesions can also
present in a similar manner
• There is no definitive symptom for EDHs ,
• The triad of head injury
• 1.lucid interval
• 2.mydriasis on the side of the haematoma
• 3.contralateral hemiparesis
• Occurs in 18 % of the cases and mainly when
EDH is localised to temporoparietal region

23. • The dilated and non reactve pupil can be
associated with ipsilateral hemiplegia <due to the
indentation of the contralateral cerebral
peduncle by the edge of the tentorium cerebelli
(kernohan’s notch )
• Initially,the pupil on the side of the EDH contracts
due to the irritation of the occulomotor nerve
and opposite pupil will be normal in size
• In the next stage,ipsilateral pupil dilates due to
paralysis of the oculomotor nerve .
• Finally ,pupil of both the sides become dilated
and fixed (hutchinson’s pupil )

24. • Patients may also complain of headache
nausea and vomitting
• A post traumatic disorder (a form of vagal
syncope ) described by danny brown
consisting of lucid interval followed by
bradycardia ,brief episodes of restlessness and
vomitting without intracranial hypertension or
mass must be considered in differential
diagnosis

25. Diagnosis
• The diagnosis of EDH must be considered when the plain
skull xrays show a fracture and it must be clinically
corelated
• If the clinical condition of the patient permits and a non
contrast computed tomogram is possible,it must be done
urgently
• The classic CT appearance is seen in 84 % of the cases and
shows hyperdense ,biconvex
• The derivation of the ABC/2 formula is as follows: The
volume of an ellipsoid is 4/3π(A/2)(B/2)(C/2), where A, B,
and C are the three diameters. If π is estimated to be 3,
then the volume of an ellipsoid becomes ABC/2.

26. • Generally EDH is confined within the sutures but this
may not be the case everytime ,occasionally ,air may
be seen within the haematoma due to an associated
internal or external compound fracture of the skull.
• MRI can also be done but it is in no way superior to CT
and also time consuming .
• INFRARED SPECTROSCOPY which can be used with
reasonable sensitivity and specificity for detection of
intracranial lesions in a short time .and could be
informative when the patient is herniating and urgent
surgical intervention is required
• Cervical spine evaluation is usually necessary because
of the risk of neck injury associated with EDH .

32. 1.Chronic ossified EDH
2.EDH stopped at the coronal sutures

39. Posterior fossa EDH
• Extradural posttraumatic posterior fossa hematoma is a
rare condition estimated to complicate about 0.3% of
all craniocerebral injuries, and represents 4% to 12.9%
of the entire group of extradural hematomas.1 Due to
the small volume of the posterior fossa and contained
important structures mortality can be high if the
haematoma is missed. A high index of suspicion is
needed for timely intervention to prevent death. We
had three mortalities during our early study period
where we were less aggressive and since then our
indication has changed based on our protocol. Since
then there

40. • Presence of occipital haematoma, swelling, site of impact and often Battles sign
are clue to its diagnosis. Fracture of the occipital bone is and important sign that
mandates observation and repeat san later to diagnose these haematomas.
Change in GCS or severe headache with vomiting and new onset cerebellar signs
are associated features that help to clinch the diagnosis
• stiffness and drowsiness were the commonest clinical signs. CT scan remains the
choice of investigation to detect these haematomas. The presence of haematoma
more than 10 ml, hydrocephalus and displacement of the IV ventricle are all
indications for surgery
• Conservative management is another option if the patient is symptomless and he
is under close monitoring in the neurosurgical ICU. There have also been case
reports of these haematomas resolving spontaneously without any intervention
• supratentorial pathologies associated with PFEDH have been reported in as high as
50%-87.5%.6 This may be in the form of haematoma or contusion. A contre coup
mechanism may be the explanation for such injuries
• Surgery remains the gold standard for the treatment of symptomatic PFEDH. This
may be in the form of suboccipital craniectomy or craniotomy or both depending
on the size of the haematoma

41. Post.fossa saggital c+ arterial phase

43. MANAGEMENT
• LAB INVESTIGATIONS
• 1. CBC with platelets :to monitor for infection and asseses haematocrit and
platelets for furthur haemorrhagic risk
• 2.PROTHROMBIN TIME /ACTIVATED PARTIAL THROMBOPLASTIN TIME (aPTT) :to
identify bleeding diasthesis
• 3. SERUM CHEMISTRY including electrolytes,blood urea nitrogen ,creatinine and
glucose :to characterize metabolic deaarangement that may complicate the clinical
course
• Toxicology screen and serum alcohol level :to identify associated cause of head
trauma and establish need for survelliance with regard to withdrawl symptoms
• Type and hold an appropriate amount of blood : to prepare for necessary
transfusion needed due to blood loss or anaemia

44. • Management of EDH is most of the time surgical
but in few selected patients ,non surgical
management may be attempted ,these are :
• A. Small EDH less than equal to 1 cm
• B. subacute or chronic EDH
• C.minimal neurological signs and symptoms
these patients are closely observed and surgery is
undertaken if no evidence of progressive
improvement is noted. In 50 % of the cases ,there
is transient increase in size between day5 – 16 and
it is that time where non surgical patients need
special attention .surgery should be done for most
posterior fossa EDHs

45. In a rapidly deteriorating patient with suspected EDH ,a CT scan
is inapropriate .the clinical triad of :
Altered mental
status
Unilateral pupillary
dilatation with loss
of light reflex
Contralateral
hemiparesis
Is often due to upper brainstem compression by uncal herniation which in majority of
the trauma cases is due to EDH .in such patients exploratory burr holes are indicated

46. MRI
• MRI can clearly demonstrate the displaced dura
which appears as a hypointense line on T1 and T2
sequences which is helpful in distinguishing it
from subdural haematoma.
• Acute EDH appears isointense on T1 and shows
variable intensities from hypo- to hyperintense
on a T2 sequence. Early subacute EDH appears
hypointense on T2 while late subacute and
chronic EDH are hyperintense on both T1 and T2
sequences.
• Intravenous contrast may demonstrate displaced
or occluded venous sinus in case of venous origin
of EDH.

47. Angiography
• It can be used to evaluate nontraumatic cause
(i.e. AVM) of EDH. Rarely angiography can
demonstrate middle meningeal artery
laceration and contrast extravasation from
middle meningeal artery into paired middle
meningeal veins known as "tram track sign".

48. • Differential diagnosis
• With large haematomas, there is rarely significant confusion as to the correct diagnosis.
In smaller lesions, especially when there is associated parenchymal injury (e.g. cerebral
contusions, traumatic subarachnoid blood, concurrent subdural haematoma) the
diagnosis can be more challenging.
• Differential considerations include:
• subdural haemorrhage (SDH)
– can cross sutures
– usually sickle shaped
– limited by dural reflections
– usually in older patients or in young patients with significant other closed head
injuries
• meningioma
– may be hyperdense
– enhances with contrast
– usually remote from fracture (e.g. parafalcine)
•

51. MANNITOL IS
CONTRAINDICATED
IN EDH

54. Mechanism of action
• Mannitol exerts its ICP-lowering effects via two
mechanisms—an immediate effect because of plasma
expansion and a slightly delayed effect related to its
osmotic action. The early plasma expansion reduces
blood viscosity and this in turn improves regional
cerebral microvascular flow and oxygenation. It also
increases intravascular volume and therefore cardiac
output. Together, these effects result in an increase in
regional cerebral blood flow and compensatory
cerebral vasoconstriction in brain regions where
autoregulation is intact, resulting in a reduction in ICP.

63. MORBIDITY AND MORTALITY
• DELAY IN THE DIAGNOSIS AND TREATMENT IS
THE MOST COMMON PREVENTABLE CAUSE OF
MORBIDITY AND MORTALITY .
• RECURRENT OR RESIDUAL HAEMATOMA MAY
RESULT FROM THE FAILURE TO GAIN FULL ACCESS
TO HAEMATOMA AND TO THE LACERATED
MENINGEAL VESSELS OR MULTIPLE SMALL
BLEEDERS ON THE DURA WHERE IT HAS BEEN
STRIPPED OFF THE INNER TABLE OF THE SKULL

64. • MORTALITY FOLLOWING TREATMENT OF EDH
VARIES FROM 5% TO 43 %.
• IN CHILDREN 5%- 10 %
• INCREASES SHARPLY IN THOSE OVER 40 YEARS
35% - 50 %
• OLDER AGE,POOR PREOPERATIVE
NEUROLOGICAL CONDITION ,LARGE
HAEMATOMA VOLUME ,DELAY IN OPERATIVE
EVACUATION ,LARGE MIDLINE SHIFT AND
POST OPERATIVE ELEVATION IN ICP ARE ALL
ASSOCIATED WITH POOR PROGNOSIS