head injury outline of management c

7/31/2019 Head Injury Outline of Management c

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Head injuryout line of management

Professor Panna Lal SahaProfessor of Surgery & Head

Department of Surgery


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Introduction 500,000 cases of head injury occur in

the USA each year 10 % of these die prior reaching a

hospital

Of These 80% mild 10% moderate 10% severe

> 20% of the head injury patientssuffer varying degrees of disability


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Anatomy


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Anatomy The head can be divided

into the following layers:1) Scalp.

2) Skull.3) Meninges.4) Brain.

5) Cerebrospinal fluid.6) Tentorium.


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Scalp

1. S : skin2. C : connective tissue3. A: aponeurosis (galea)4. L: loose areolar tissue5. P: pericranium

Bleeding from scalp laceration can result inmajor blood loss especially in children


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SkullIt is composed of Cranial vaultand base.

The floor of the cranial cavity

is divided into 3 parts:- Anterior fossa frontal lobe - Middle fossa temporallobe

- posterior fossa brain stemand cerebellum


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Meninges

1. Dura2. Arachnoid

3. pia

Subdural space is a potetial space exist in whichhemorrhage can occur

Cerebrospinal fluid circulate between thearachnoid and pia matter in the subarachnoid space


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Brain

Consist of:1) Cerebrum:

Frontal Parietal Temporal occipital

2) Cerebellum.3) Brain stem:

Midbrain Pons medulla

frontal

temporal

parietal

occipital


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Cerebrospinal Fluid It is produced at a rate of 30 ml / hour.


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Tentorium

Divide the head into : Supratentorial :

Anterior fossa Middle fossa

Infratentorial :

Posterior fossa


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Cerebral blood flow

Normal CBF is approximately 50ml/100 g of brain/min

If CBF < 20 ml/min the EEG activity willgradually disappear, and at CBF of 5ml/min cell death

In normal person the Autoregulation maintain a

constant CBF between MAP of 50 and 160 (mmHg). In head injured patient its severely disturbed. MAP < 50 mm Hg CBF declines steeply MAP > 160 mm Hg passive dilation of the cerebral

vessels increase in CBF


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Intracranial pressure Several pathological processes that affect the brain

can cause elevation of the intracranial pressure. ICP can have consequences that adversely affect brain

function and hence the patient outcome. So elevated ICP not only indicate the presence of aproblem but can often contribute to the problem 10 mm Hg - normal ICP

20 mm Hg abnormal 40 mm Hg sever elevation


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Cerebral Perfusion Pressure

It can be calculated by:CPP = MAP ICP

Perfusion pressure of less than 70 mm Hg isgenerally associated with poor outcome followinga head injury. This indicate the priority of

maintaining the cerebral perfusion in themanagement of severe head injury patient.


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Classification

of head injuries


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Head injuries are classified according to:

1) Mechanism of injury.2) severity of the injury.3) Morphology of the injury.


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1) Mechanism

This can be :1) Blunt injury which is divided

into:- High velocity(automobile).- Low velocity (fall, assult).


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1) Mechanism

Penetrating injury e.ggunshot wounds or otherpenetrating wounds.


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2) Severity

This classified according to Glasgow coma Scale into:

1) Mild (GCS score 14-15).2) Moderate (GCS score 9-13).3) Severe (GCS score 3-8).


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Type Stimulus Type of Response Points

Eyes Open Spontaneously

To verbal commandTo painNo response

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Best MotorResponse

To verbal commandTo painful stimulus

ObeysLocalized painFlexion-withdrawalFlexion-abnormalExtensionNo response

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Best VerbalResponse

Oriented and conversesDisoriented and conversesInappropriate wordsIncomprehensible soundsNo response

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Lowest score = 3, Highest score = 15


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3) MorphologySkull

Fracture

Vault

Basilar

Linear vs stellate Depressed / nondepresed Open / closed

With/without CSF leakage With/without nerve palsy

Intracraniallesions

Focal

Diffuse

Epidural Subdural Intracerebral

Mild concussion Classic concussion Diffuse axonal injury


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Skull fractures


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1) Skull fractures

The significance of skull fracture should not beunderestimated since it takes considerable forceto fracture the skull.

linear vault fracture increase the risk of anintracranial heamatoma by about 400 times in aconscious patient and by 20 in comatose patient.

Fragment depressed more than the thickness of

the skull require surgical elevation Open or compound skull fracture require earlysurgical repair


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Cont

Basal skull fractures usually require CT scan withbone window

The presence of clinical signs of basal skull fractureshould increase the index of suspicion and help in itsidentification: Periorbital ecchymosis ( Raccoon eye) Retroauicular ecchymosis ( Battles sign )

CSF leakage 7 th nerve palsy times in comatose one.


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Management


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Scalp wounds

They are usually tolerated well and cause fewcomplications.

Shave the hair around the wound and clean thewound before suturing.

Bleeding from a deep scalp wound usually can becontrolled by applying direct pressure cauterizingor ligating large vesseles.


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Depressed skull fractures

Need to be elevated if the degree of depression isgreater than the thickness of the adjacent skull.

Less significant depressed fracture can safely bemanaged with closure of the overlying scalplaceration.


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Intracranial lesions


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2) Intracranial lesions

These lesions may be classified as focal or diffuse,although the two forms frequently coexist.

Diffuse brain injury is the most common type of head injury . It represent a continuum of braindamage produced by increasing amounts of acceleration-deceleration forces

In general they have a normal CT scan butdemonstrate altered sensorium or even deep coma.


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2) Intracranial lesions

Based on the depth and duration of coma , diffuseinjuries may be classified as mild concussion

,classic concussion and diffuse axonal damage.


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Mild concussion Consciousness is preserved but

there is a noticeable degree of temporary neurologicaldysfunction .

These injuries are common and,because of their mild degree,often go unnoticed .

The mildest form of concussionresults in confusion anddisorientation without amnesia(loss of memory ) .


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Classic Cerebral Concussion

There is a loss of consciousness which is transientand reversible.

This condition always is accompanied by somedegree of severity of posttraumatic amnesia.

The length of amnesia is a good measure of theseverity of the injury.

Many patients with classic cerebral concussionhave no sequale other than amnesia for the eventsrelating to the injury, but some patients may havemore long-lasting neurological deficits e.g.

memory difficulties and depression.


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Diffuse axonal injury Term used to define prolonged post traumatic coma

that is not due to mass lesion or ischemic insult These patients are rendered deeply comatose and

remain so for prolonged periods They often demonstrate evidence of decortications or

decerbration and often remain severely disabled , if they survive

These patients often exhibit autonomic dysfunctionsuch as Hypertension, Hyperhydrosis, andHyperpyrexia .


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Focal intracranial lesions

Intracranial bleeding Venous bleeding

Slow, insidious onset Arterial bleeding

Signs and symptoms will be apparent within a

few hours


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Epidural hematoma


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Epidural hematoma Occurs in the potential space

between the dura and thecranium. Also referred to asextradual.

Caused by a blow to the headcauses an interruption to thedura vesseles includingbranches of the middle

meningeal arteries, veins,dura venous sinuses and skullvesseles.


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Epidural hematoma Non traumatic causes of EDH

includes infectious disease of the skull- Vascular malformation of the

dura matter, Metastasis to the skull, Spontaneous EDH in patient with

couaglopathy. 10-20% of patient with head

trauma and 17% of previouslyconscious patient followinghead trauma have EDH.


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Epidural hematoma

In traumatic EDH Hematoma forms extremely fastWithin 10 20 minutes after injury.

patient may present with external evidence of headinjury such as scalp laceration, cephal hematoma,or contusions. Systemic injuries may also bepresent.

Most often the head injury is in the temporal or

temporoparietal region. Patient with epidural hematoma may present withthe classical lucid interval (20-50% of cases) ortalk and die .


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Epidural hematoma

Initially, the concussive force that caused the headinjury results in an alteration of consciousness.After recovering consciousness, the EDH

continues to expand until the mass effect of thehemorrhage itself results in increased intracranialpressure, a decreased level of consciousness, and apossible herniation of the brain.

With severe intracranial hypertension, thecerebral perfusion is compromised resulting in aCushing response .


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Epidural hematoma

The classic Cushing triad involves systemichypertension, bradycardia, and respiratory

depression. This response will be elevated bythe evacuation of the mass


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Investigations


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Lab studies

Hematocrit level, chemistries, and coagulationprofile are essential in the assessment of a patientwith intracranial bleeding.

Severe head injury can cause release of tissuethromboplastins, which can result in DIC.

In adults, EDH rarely causes a significant drop inthe hematocrit level within the rigid skull cavity.

In infants, whose blood volume is already limited,EDH within an expansile cranium with opensutures can result in significant blood loss.


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Imaging Skull X-Ray may reveal afracture crossing the

vascular shadow of themiddle meningeal artery

branches.An occipital,frontal, or vertex fracturealso might be observed.

> 90% of EDH cases areassociated with skullfractures. In children, thisrate is less because of greater skull deformability.


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CT scanning CT scanning is the most

accurate and sensitivemethod of diagnosing.

Itll appear Biconvex or lenticular in shapeas its limited by theadherence of the dura to

the inner table of theskull, especially at thesuture lines.


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CT scanning

The signal density of the hematoma comparedwith the brain parenchyma changes over timeafter the injury. The acute phase is hyperdense (bright signal on CT scan).The hematoma then

becomes isodense at 2-4 weeks, and then itbecomes hypodense (dark signal) thereafter.

Hyper acute blood may be observed as isodenseor low-density areas, possibly indicating ongoinghemorrhage or a low serum hemoglobin level.


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CT scanning

Hydrocephalus may be present in patients with alarge posterior fossa EDH exerting a mass effectand obstructing the fourth ventricle.

Approximately 10-50% of EDH cases areassociated with other intracranial lesions. Theselesions include subdural hematomas, cerebral

contusions, and intracerebral hematomas


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MRI Acute blood on MRI is isointense, making this modality less

suited to detection of hemorrhage in acute trauma. However,

mass effect can be observed when its extant.


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Therapy


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1.Conservative Therapy

Not all cases of acute EDH require immediatesurgical evacuation. However, If treated early , theprognosis is usually excellent because the directdamage to the underlying brain is usually limited

Outcome is directly related to the neurological statusof the patient before surgery.

If a lesion is small and the patient is in good

neurological condition, observing the patient withfrequent neurological examinations is reasonable.


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Conservative therapy

Early follow-up scanning can be used to assess forfurther increase in hematoma size prior todeterioration

If a rapid size increase is noted, then surgery isindicated

When treating patients with spontaneous EDH, theunderlying primary disease process must beaddressed in addition to the fundamentalprinciples discussed above


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2.Surgical management

Criteria for immediate surgical intervention is anEDH with:

1) Volume greater than 30 ml.2) Thickness of 15 mm.3) A midline shift beyond 5 mm.

as most patients with such an EDH experience aworsening of the conscious state and/or exhibitlateralizing signs.


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Surgical management

Location is also an important factor in the surgicaldecision. Temporal hematomas, if they are large or expanding,

may lead to uncal herniation and more rapiddeterioration.

While, EDH in the posterior fossa, which is oftenrelated to interruption of the lateral venous sinus, oftenrequires prompt evacuation because of the limited spaceavailable compared with the supratentorialcompartment.


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Surgical management In the pre CT scan era, drilling exploratory burr

holes was common especially when the patientdemonstrated lateralizing signs or rapid deterioration.

Now with fast-scan techniques, this type of exploration is rarely required. Its only reserved forpatients with definitive localizing signs and clinicalevidence of intracranial hypertension who are unable

to tolerate a CT scan because of severe hemodynamicinstability and/or for patients who require immediatesurgical intervention for systemic injuries.


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Position of emergency burr holes


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Surgical management

Surgical treatment of epidural hematomas involve:1. opening the skull over the site of hemorrhage.The

EDH is readily apparent after elevating the boneflap, and it is removed.

2. Coagulation of bleeding dural vessels is usuallyperformed.

3. Epidural tack-up sutures are placed from the durato the craniotomy bone edge and to the center of the craniotomy flap to tamponade epiduralbleeding from areas beyond the craniotomy edgesand to prevent recurrence


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Surgical management

If the patient presents with a dilated pupil orclinical signs of intracranial hypertension, a smallincision is first made in an area considered to beover the hematoma. Then a rapid burr hole ismade, and the epidural is partially evacuated. Thismaneuver often allows for some initial pressurerelief until the entire epidural blood clot can be

evacuated. Follow-up CT scans are performed to determine

the extent of clot evacuation. These scans can alsohelp evaluate for delayed hematomas.


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Subdural hematoma


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Subdural Hematoma Much more common

than epidural Occur most frequently

from tearing of a

bridging vein betweenthe cerebral cortex and adraining venous sinus

Also can be associatedwith arterial lacerationon the brain surface


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Sudural hematoma Normally cover the entire

surface of the hemisphere Prognosis is much worse

than epidural Hematoma forms slowly

signs and symptoms maynot be appear until hours

after injury.


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Subdural hematoma

A subdural hematoma (SDH) is classified by theamount of the time that has elapsed from the timeof the inciting event, if known, to the diagnosis.When the inciting event is unknown, theappearance of the hematoma on CT or MRI canhelp date the hematoma.

Its classified to:1) Acute SDH:


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Subdural hematoma

2) Subacute SDH: 3- 20 days and is isodense orhypodense compared to the bain.

3) Chronic SDH: older than 20 days and arehypodense compared to the brain.


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Acute subduralhematoma


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Pathophysiology

- The usual mechanism to produce an acute SDH ishigh-speed impact to the skull. This causes braintissue to accelerate relative to a fixed duralstructure, which, in turn, tears blood vessels.

- This mechanism also leads to associatedcontusions, brain edema, and diffuse axonalinjury

- The ruptured blood vessel often is a veinconnecting the cortical surface to the dural sinuses


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Pathophysiology

Alternatively, a cortical vessel can be damaged bydirect laceration.

An acute SDH due to a ruptured cortical arterymay be associated with only minor head injury,and no cerebral contusions may be associated


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Clinically

- Acute SDHs are most likely to occur after headinjury from a fall, motor vehicle accident, or anassault.

- SDH occurs in men more frequently than inwomen, with a ratio in the range of 3:1.- Patients found to have an acute SDH are on

average older than other trauma patients.

- In one study, the average age of a trauma patientwithout an acute SDH was 26 years, while theaverage age of patients with an acute SDH was 41years.


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Clinically

- Therefore, older patients appear to be at greaterrisk for developing an acute SDH after headinjury. This is believed to be due to older patientshaving more atrophy, which allows more sheerforce against bridging veins immediately afterimpact.

- The clinical presentation of an acute SDHdepends on the size of the hematoma and thedegree of any associated parenchymal braininjury. Common neurological findings include :


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Clinically

1) Altered level of consciousness2) A dilated pupil ipsilateral to the hematoma

3) Failure of the ipsilateral pupil to react to light.4) Hemiparesis contralateral to the hematoma.

The patient should be examined for relatedinjuries (using guidelines established by ATLSCommittee on Trauma) such as spinal cord injuryor long bone fractures


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Investigations

1) lab Studies :coagulation profile and platelet count should be

done to determine whether defective coagulationwas involved in the formation of the acute SDH.2) imaging :

CT scan needs to be performed on an emergentbasis when an acute SDH is suspected and shouldbe obtained immediately after stabilizing thepatient using standard advanced trauma lifesupport (ATLS) guidelines


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Acute SDH

Acute SDH appears onCT scan as a crescent-shaped hyperdense areabetween the inner tableof the skull and thesurface of the cerebral

hemisphere.


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Management

Conservative :- Small acute SDHs less than 5 mm thick on axial

CT images, without sufficient mass effect to causemidline shift or neurological signs, can befollowed clinically

- The patient with an acute SDH should betransfused with fresh frozen plasma (FFP) andplatelets to maintain the PT within the normalrange and the platelet count above 100,000.


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Management

Surgical :- Surgery for acute SDH consists of a large

craniotomy (centered over the thickest portion of the clot) to decompress the brain, stop any activesubdural bleeding, and evacuate anyintraparenchymal hematomas in the immediatevicinity of the acute SDH.

- The craniotomy exposure should include thesylvian fissure because this can be a likely source

of a ruptured cortical vessel.


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Chronic subduralhematoma


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Pathophysiology

Most chronic SDHs begin as SDG. An SDG begins as a separation in the dura-

arachnoid interface, which then is filled bycerebrospinal fluid (CSF).

Dural border cells proliferate around this CSFcollection to produce a new membrane. Then,fragile new vessels grow into the membrane.These vessels can bleed and become the source of blood into the space, which results in the growthof the chronic SDH.


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Pathophysiology

Chronic SDHs that form from acute SDHs havemembranes between the dura and hematoma at 1week and between the brain and hematoma at 3weeks.

The hematoma liquefies at 1-3 weeks of age andbecomes hypodense on CT scan. If not resorbed,

the vessels in the membranes surrounding thehematoma can hemorrhage repeatedly, resulting inthe enlargement of the hematoma.


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Clinically

A higher incidence of chronic SDH exists inmen.The male-to-female ratio is 2:1.

Most adults with chronic SDH are older than 50

years One quarter to one half of patients with chronic

SDH have no identifiable history of head trauma.If a patient does have a history of head trauma, itusually is mild.

The average time between head trauma andchronic SDH diagnosis is 4-5 weeks.


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Clinically

Risk factors for a chronic SDH includes chronicalcoholism, epilepsy, coagulopathy, arachnoidcysts, anticoagulant therapy (including aspirin),

cardiovascular disease, and thrombocytopenia, anddiabetes.

Clinical presentation often is insidious, with: symptoms of decreased level of consciousness

balance problems cognitive dysfunction and memory loss. Motor deficit.


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Clinically

Headache, or aphasia . Acute presentation also is possible, as in the case

of a patient who presents with a seizure. Neurologic examination may demonstratehemiparesis, papilledema, hemianopsia, or thirdcranial nerve dysfunction.

In patients aged 60 years or older, hemiparesis is acommon presenting sign. In patients younger than 60 years, headache is a

common presenting symptom.


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Investigation

Lab studies :This includes coagulation profile, CBC and

routine SU+E and LFTs test. Imaging:On a contrast-enhanced CT scan, the chronic SDHmembrane will enhance to varying degrees.Typical signs of mass effect may be observed,such as midline shift and ventricular compression.


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Management

Surgical:- Liquefied chronic SDHs commonly can be treated

with drainage through 1-2 burr holes. A closeddrainage system sometimes is left in the subduralspace for 24-72 hours postoperatively.

- A nonliquified chronic SDH cannot bedecompressed adequately by burr holes and mustbe removed by craniotomy.


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Contusions Almost always seen in

association with subduralhematomas.

Majority occur in the frontal andtemporal lobes , although it canoccur in any part of the brainincluding the cerebellum and

brainstem Contusions can in a period of hrs or days coalesce to form anintracerebral hematoma


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Intracerbral hematoma


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Intracerebral Hemorrhage Hemorrhage within the

substance of the brain is arelatively frequent occurrencein head injury.

Usually results due to acompressive force applied tothe brain.

It can occur acutely with Rapiddeterioration in neurologicalfunction or more commonly indelayed fashion.


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ICH After sever head injury ICH can be found in CT in:

- 20% initialy.- 35% after 24 h.- 80% after 72 h.

2 basic mechanism that produce traumaticintracerebral hematoma Coup or Countercoup injury.

Other mechanism includes Injury to vessel wall dueto hypoxia , CO2 accumulation and acidic PH.


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ICH

Management:Surgical evacuation should be done if there is:

- Deteriorating neurological status- Intracranial pressure elevations unresponsive to

medical treatment- Midline shift more than 1 cm- Temporal hematoma larger than 30 cc


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Effects of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASHTrial): randomised placebo-controlled trial. Lancet 2004; 364: 13211-1328.Ghajar J.

Traumatic brain injury. Lancet 2000; 356: 923-929.GentlemanD. Guidelines for the resuscitation and transfer of patients with serioushead injury. Br Med J 1993; 307: 547-542.Flannery T, Buxton N.

Modern management of head injuries. J R Coll Surg Ed 2001; 46: 150-153.McNaughton H, Harwood M. Traumatic braininjury: assessment and management. Hosp Med 2002; 63: 8-12.


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Thank you

head injury outline of management c

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