EPIDURAL HAEMATOMA

DR.KARAN R RAWAT

GUIDEDR.PANKAJ GUPTA

DR.JITENDRA SINGHDR.ARVIND SHARMA

SKULL ANATOMY

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

• 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

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)

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 %

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 .

• 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

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

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.

• 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

• 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 )

• 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

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.

• 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 .

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

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

• 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

Post.fossa saggital c+ arterial phase

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

• 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

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

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.

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".

• 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)

MANNITOL IS CONTRAINDICATED

IN EDH

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.

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

• 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