Head Injury

By

Tony Suharsono

Introduction

Almost 2000 patients per 100.000

population attend an Casualty department

annually with head injury.

Of these, between 200 and 400 will require

admission

Male 70 %

Adult 60 %

Definition

Suatu injuri yang dapat melibatkan seluruh struktur kepala mulai dari lapisan kulit kepala atau tingkat yang paling ringan, tulang tengkorak, duramater, vaskuler otak sampai dengan jaringan otak sendiri baik berupa luka tertutup maupun tembus

Mechanism of head injury

Acceleration

Deceleration

Compression

Coup VS Contra coup

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Pathophysiology

Injury can occur to the scalp, scull and brain, independently or in combination

Damage to the brain can occur directly as a result of the original injury (primary brain damage) or indirectly as a result of other factors (secondary brain damage)

The principles cause of secondary brain damage are hypoxia, hypovolemia, and increases in intracranial pressure secondary to cerebral edema or haematoma formation, and cerebral infection.

Pathophysiology

Contact between the surface of the brain

and the interior skull causes bruising

(contusions).

Distortion of the brain caused by internal

shearing forces leads to stretching and

tearing of axonal tracts within the white

matter

Alcohol and head injury

The ingestion of alcohol can affect the conscious

state, and is also associated with an increased

change of sustaining head injury.

Alcohol can also alter conscious state by inducing

hypoglycemia

Therefore all patients with altered consciousness

must have stix testing of capillary blood

Type of head injury

Scalp Injury

Hemorrhage from scalp-wounds is often brisk,

and occasionally life threatening, particularly in

infant and small children, but adult are also at

risk if the wound is large or bleeding is

prolonged

Be careful with patient with bleeding

tendencies or those on anticoagulant teraphy

Scalp Injury

The scalp wound should be carefully inspected for

foreign bodies, underlying fractures, and

herniating brain

Scalp wounds can be probed gently with the finger

of a sterile gloved hand to determine the depth of

the wound

Hemorrhage from scalp wounds can be controlled

by covered wound with non adherent gauze and

secured with a dressing

Type of Head Injury

Scull fracture

Forces large enough to bruise the scalp may

fracture the scull beneath.

Type scull fracture

Scull fracture

Less common in children than in adult

The close relationship between scull fracture and intracranial hematoma in adult makes the detection of a fracture important

A compound depressed fracture result when a violent sharp blow lacerates the scalp, and drives bone fragment into the intracranial cavity, sometimes tearing the durameter

Compound depressed scull fracture

Type of Head Injury

Basilar Scull Fracture

A basilar scull fracture describe a fracture location, not a type

Most basilar scull fracture are linear

Anterior fossa fracture

Periorbital ecchimosis

Rhinnorrhea

Middle fossa fracture

Battle sign

Hemotympanum

Otorrhea

Basilar Scull Fracture

Posterior fossa fracture

The posterior fossa is formed of thick, smooth

bone that rarely is fracture

A small amount of bleeding into this fossa can

put fatal pressure on the brain stem

Check the presence of CSF with halo test

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Type of Head Injury

Brain injury

Primary brain damage occur as a result of the

initial injury

It can be due to direct impact damage from

blunt or penetrating injury and or a result of

rotation forces and contra coup injuries induced

by impact

Movement of the brain after impact causes

surface lesion, and produces contusion of the

brain matter

Brain injury

Intracerebral hematoma, subaracnoid hemorrhage

and brain laceration may occur as direct

consequence of the impact

The degree of primary brain damage correlated

with the period of altered consciousness and post

traumatic amnesia

A deteriorating conscious level with or without

localizing neurological sign is the hallmark of

progressive secondary brain injury

Brain injury

The commonest cause of secondary brain damage is hypoxia

Hypovolemia is also commonly lead to secondary brain injury

Alone or in combination, hypoxia, hypercapnia, poor cerebral perfusion and cerebral contusion are among the factors that may lead to raised intracranial pressure

Brain injury

Causes of raised intracranial pressure after

head injury

Haematoma

Focal cerebral oedema

Diffuse oedema

Obstruction of CSF pathway

Brain injury

Factors increasing intracranial pressure

Hypoxia

Hypercapnia

Hypotension

Intracranial hemorrhage

Intracranial infection

Brain injury

About 70% of patient persistently in coma

after severe head injury have raised intra

cranial pressure

As intracranial pressure rises cerebrospinal

fluid is driven out of the intracranial

compartment

Intracranial Haematoma

In the context of multiple injury, intracranial

haematoma must be suspected when coma persist

or develops in spite of adequate airway control,

oxygenation, and appropriate fluid replacement

from other injuries.

Classical sign of an expanding intracranial

haematoma (dilatated ipsilateral pupil and

contralateral hemiparesis) are late and inconsistent

signs and represent establish brain injury

Herniation

Herniation occurs whenever portions of the

brain extend beyond their normal location

and impinge on other areas of brain tissue

Herniation can result from an expanding

hematoma, cerebral edema, and a mass.

Herniation

Herniation

Early signs

Decreasing level of consciousness

Ipsilateral pupil dilatation

Cheyne stokes respiration

Contralateral hemiparesis

Positive babinski reflex

Elevated ICP

Late signs

Unconsciousness

Bilateral fixed and dilatated pupil

Central neurogenic breathing or other abnormal

respiratory pattern

Flexion or extension posturing

Elevated ICP unresponsive to therapy

Bradicardia

Herniation

Diagnostic examination techniques

and devices used in head injury

X ray

CT scan

MRI

Angiography

Intracranial pressure monitoring

CT scan

Immediate CT scan

Patient in coma GCS 8 or less

Patients with depression of concious level

GCS 9-13 associated with scull fracture

Patient who deteriorate with a progression to

coma

CT scan

Urgent CT Scan

Patient who are drowsy and/or disorientated

GCS 14-15 and have a scull fracture

Patient with abnormal neurological signs

together with a scull fracture

Patient with depression of conscious level

(GCS 9-13) together with focal neurological

deficit.

Guidelines for CT Scanning

Patient undergoing CT examination must

have

A secure airway

Adequate ventilation

Circulating blood vol devicit corrected

Further haemorrhage controlled

Intracranial pressure monitoring

Is indicated for any patient with severe head

injury (GCS70 mmHg

CPP=MAP-ICP

Assessment

Airway

Breathing

Circulation

Disability

Exposure and environment control

Full set of vital sign, Five interventions,

facilitation of family presence

Assessment

Give comfort measures

History (MIVT: mechanism, injuries

suspected, vital sign on scene, treatment

received) and head to toe examination

Inspect the posterior surfaces

Specific examination

GCS

The cranial nerve

Pupillary response

Reflexes

Sensation

Examination of nose and ears for blood,

CSF, Hemotympanum

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Pupillary response

Nursing Diagnose

Infective airway clearance

Risk of aspiration

Impaired cerebral perfusion

Ineffective breathing pattern

Risk of infection

Management of patient with head

injury

The to main aim of management patient

with head injury are

Firstly, to provide the best condition for

recovery from any brain damage already

sustained and

Secondly, to prevent or to treat complication

leading to secondary brain damage

Management of patient with head

injury

Airway

Orally intubate patients with a GCS less than or

equal to 8

Insert an oral gastric tube to decompress the

stomach. Avoid nasogastric tube

Breathing

Maintain PaO2 greater than 100 mmHg and

oxygen saturation greater then 95%

Avoid hiperventilation unless signs of

herniation are present

Consider neuromuscular blockade for patient

who are difficult to ventilate

Circulation

Establish normovolemia. Keep MAP 70-90

mmHg

Maintain CPP >70 mmHg

Restore volume as needed with isotonic

fluid and blood product

Insert indwelling urinary catheter. Maintain

an hourly urine output of 0,5-1 mL/Kg

Disability

Perform and document serial neurologic

examination

Facilitate Diagnosis and

Neurosurgical Consultation

Rapidly obtain appropriate diagnostic

studies

Monitor ICP in all patients with a GCS

score of 8 or lower

Facilitate surgical intervention

Admit to a neurologic critical care unit or

transfer to an appropriate facility

Reduce Intracranial pressure

Provide sedation and analgesia

Infuse mannitol 0,25-1 g/Kg in intermitten bolus

Maintain head on a neutral, midline position

Keep the patients head elevated 30 degrees

Minimize external stimulation

Consider ventriculostomy placement for CSF

drainage

Consider surgical decompression

General Care

Assess for and manage other injuries

Immobilize the spine and obtain cervical spine films

Perform toxicologic or alcohol screening as indicated

Regulate temperature to maintain normotermia

Treat seizure

Do not use IV dextrose infusion

Do not give dextrose 50% except in hypoglycemia

Do not give steroid

Consider organ donation in patient with a GCS of less than or equal to 4 who remain unresponsive to treatment

Thank Qiu

tony, psik 2007

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