Head Injury

IntroductionHead injury include any trauma to the scalp, skull or brain .the term head trauma used primarily to signify craniocerebral trauma, which includes an alteration in consciousness, no matter how brief. Head trauma has a high potential for poor outcomes. Death from head trauma occur at three time points after injury : immediately after injury, within 2 hours after injury ,and approximately 3 weeks after injury. The majority of deaths after a head injury occur immediately after the injury, either by direct head trauma or from massive haemorrhage and shock. Deaths occurring within few hours of the trauma are caused by progressive worsening of head injury or internal bleeding. immediate recognizing changes in neurologic status and rapid surgical intervention are critical in the prevention of deaths at this point. Deaths occurring 3 weeks or more after injury result from multisystem failure

Key words-

DefinitionIt is disruption of normal brain function due to trauma related injury resulted in compromised neurological function resulting in focal or diffuse symptoms. or it is an insult to the brain that is capable of producing physical ,intellectual, emotional ,social and vocation changes.

Etiology and risk factors1.motor vehicle accident 2.younger male below 30 year 3.alcohol or substance abuse 4.sports injury,fall,assult 5.peak incidence during evening nights, weekend

Mechanism of injuryhead injury are caused by a sudden impact force to the head or inertial forces within the skull. 1.penetrating injuryIt is the form of primary injury and include head wounds made by foreign bodies(eg-knives or bullet) or those made by bone fragments from a skull fracture.Bone fragments from a skull fracture may cause local brain injury and damaging other structure(eg-nerves, blood vessels ).if major blood vessels severed or ruptured,a large clot(hematoma) may form, which resultant damage to adjacent or remote structure(eg- brain compression as in a herniation syndrome) thus hematoma itself can cause extensive brain tissue damage.eg- skull fracture 2.coup-contrecoups injuries-(coup – French word means blow)-(counter-blow)This injury indicate that clients has sustained a combined injury at the point of impact and an injury on the side of brain opposite from the movement of the brain within the skull 3.diffuse injuryit occur when a blow is received that does not result in fracture but causes the brain to move enough to shear or tear some of the veins going from the cortical surface of the brain to the skull. Because the brain is able is able to move within the skull ,movement of brain can result in injuries at different location eg –head hits the steering wheel.

Types of injury1.scalp injury2.skull injury 3.brain injury4.focal injury-

1.scalp injuryScalp injury can cause lacerations ,hematomas ,and contusions or abrasions to the skin. these injury may unsightly and may bleed profusely.

2.skull fractureSkull fracture present with the brain injury.depressed skull fractures injury the brain by bruising it(resulting in a contusion) or by driving bone fragments’ into it(causing lacerations.) Types1.linear skull fractures2. depressed skull fracture3. basilar skull fracture-

thin line appear in radiography and do not require treatment. may be palpated and are seen radiographically. occur in bones over the base of the frontal and temporal lobes.

These are not observable on pain radiographs but may be manifested as ecchymosis around the eyes or behind the ear or by blood or CSF leakage from the ear.

3.Brain injuries1. open-caused by penetrating injury. 2. closed -these are from blunt injury 3.concussionit is result in loss of consciousness for 5 min or less and retrograde amnesia. There is no break in the skull or dura or no visible damage on a CT or MRI. 4.contusions – These are associated with more extensive damage than that from concussion. With contusion the brain itself is damaged,often with multiple areas of petechail and punctuate hemorrhage and bruised areas in brain tissue. In serious contusion ,diffuse axonal injury occur due to anatomical disruption of the white matter. Microscopic nerve fibre lesion also occur. 5.diffuse axonal injuryit involve the tissue of the entire brain and occurs at microscopic level. It is the most severe form of head injury because there is no focal lesion to remove.

Classification1.mild diffuse axonal injuryIn this loss of consciousness lasting 6 to 24 hours is characteristic, and short term disability may be occur. 2. moderate diffuse axonal injuryComa lasting less than 24 hours is the predominant feature ,with incomplete recovery on awakening . 3. severe diffuse axonal injuryin this injury to brain stem .other features like immediate loss of consciousness, prolonged coma, abnormal flexion or extensor posturing ,hypertension, and fever.

4.Focal injury ( hematoma )1.Epidural hematoma(extra dural hematoma)it occurs from injury to the cerebral blood vessels ,most often the middle meningeal artery bleeding is usually continuous, and large clot forms,which separate the dura from the skull. Manifestations(classic symptoms)with an epidural hematoma, the following sequence of events may occur1.The client is unconscious immediately after head trauma. 2.the client awakens and is quite lucid. 3.loss of consciousness occurs and pupil dilation response rapidly deteriorated, with onset of eye movement paralysis, on the same side that of the hematoma. 4.the client lapses into a coma. Although these manifestation are often described as “classic’’ for an epidural hematoma, few client present with such classic manifestations ,and astute assessment is necessary to prevent death.

2.sub dural hematoma it is the collection of blood in the subdural space(between the durameter and arachnoid mater).Tearing of the bridging veins over the brain causes most subdural hematomas. a.) acute and sub acute subdural hematoma-it is usually results from brain or blood vessel laceration. it occur within 24-48 hours of injury b.)chronic subdural hematoma-it develops several weeks or even months after injury because of a slow accumulation of fluid in a larger -than-normal space. 3.intracerebral hematoma-

it is caused by bleeding directly into the brain tissue and deep within the brain associated with edema.

Classification of head injuryGlasgow coma scalePARAMETER

FINDING

SCORE

Eye opening

Spontaneously

4

To speech

3

To pain

2

Do not open

1

Oriented

5

Confusion

4

Inappropriate speech

3

Incomprehensive sound

2

No verbalization

1

Obeys command

6

Localizes pain

5

Withdraws from pain

4

Abnormal flexion

3

Abnormal extension

2

No motor response

1

Best verbal response

Best motor response

1. Mild head injury-

(GCS 13-15,with loss of consciousness to 15 minutes)

2. Moderate head injury-

(GCS 9-12,with loss of consciousness for up to 6 hours)

3.

(GCS 3-8,with loss of consciousness greater than 6 hours)

Severe head injury-

Associated injuries; extracranial trauma1. facial trauma and skull fracture-orbital, mandible, zygoma, maxillary, nasal fracture 2. vascular injuries-vertebral or carotid artery dissection 3. spine fracture with or without SCI 4. soft tissue injuries

Clinical manifestationsWith the history and careful assessment, it is easy to identify the clinical picture related to head injury. Examination of features are as follows: Skull fracture

CSF or other fluid draining from the ear or nose.



Evidence of various cranial nerve injuries



Blood behind the tympanic membrane



Periorbital ecchymoses(bruises around the eyes)



Later , a bruise over the mastoid process(battle’s sign)

Cranial nerve injuryIndications of cranial nerve and inner ear damage may be noted at the time of the initial injury or may not appear till later. They include following

Vision change -optic nerve damage



Hearing loss - auditory nerve damage



Loss of sense of smell - olfactory nerve damage



Squint or fixed, dilated pupil and loss of some eye movement - oculomotor nerve damage



Facial paresis or paralysis(unilateral) - facial nerve damage



Vertigo caused- damage otoliths in the inner ear



Nystagmus - damage to the vestibular system

Concussion

Loss of consciousness for 5 min or less



Retrograde amnesia, post traumatic amnesia or both



Headache, dizziness, nausea ,vomiting



No break in skull or dura and visible damage is seen in CT or MRI scans.

Contusions-

Contusion are often associated





Cerebral contusions-manifestation of cerebral contusion vary, depending on which area of cerebral hemispheres are damaged Agitated ,confused head injury ->

temporal lobe contusion

Hemiparesis

->

frontal contusion

An aphasic head injury

-> frontotemporal contusion

Brain stem contusionTypically an altered LOC continues for at least several hours and usually days, or weeks. Damage to the reticular activating system may render the client permanently comatose. Other neurologic abnormalities are present symmetrical.

In addition to the altered LOC that is always present with brain stem contusion, respiratory ,papillary ,eye movement and motor abnormalities may occur.  Respiration may be normal ,periodic ,very rapid, or ataxic  Pupils are usually small, equal, and reactive. Damage to the upper brain stem(third cranial nerve) may cause papillary abnormalities.  Loss of normal eye movement may occur because pathways controlling eye movements transverse the midbrain and pons.  The client may respond to light or noxious stimuli by purposeful movements, such as pushing the stimulus away or the client may have response

Caused of raised intra cranial pressure after injury

Haematoma



Focal cerebral oedema related to a contusion or hematoma



Diffuse oedema after ischaemia(cytotoxic)



Diffuse brain swelling( “brain engorgement” )



Obstruction of cerebrospinal fluid pathway( rare condition)

Diagnostic evaluation-

1 .CT scan to identify and localize lesion ,edema, bleeding. 2. MRI to identify and diagnosis DIA. 3 .lumber puncture to assess bleeding within the subarachnoid space ,to rule out increased ICP

4 .skull and cervical spine film films to identify fracture, displacement. 5.CBC,coagulation profile, electrolyte levels, serum osmolarity, ABG values and other laboratory values to monitor for complication and guide treatment. 6. neuropsychological test during rehabilitation phase to determine cognitive deficits. 7. Glasgow Coma Scale-

Management of head injury patientGeneral management Maintain A,B,C,D,E A-airway with cervical spine control

- assess and maintain airway

-intubate for GCS less than 8(comatose) -placement of NG tube with intubation to prevent aspiration B-breathing – provide ventilator support -O2 as needed to maintain pao2 greater than 100 mmHg -maintain paco2 35 to 45 mmHg C-circulation – prevent hypotension -maintain SBP above 90 mmHg through use of vasopressors (dopamine,adrenaline,salbutamol) and albumin -maintain normovolemia -treat symptomatic arrhythmias(quinidine,propranolol,verapamil) D-dysfunction of central nervous system-to assess the nervous system involvement -check response to coma scale, pupil, limb movement E-exposure and radiography-remove all the cloths -perform physical examination -obtain radiography of chest, pelvis ,cervical spine

-CT scan of brain and spine  Management of sympathetic storming with medication such as oxycodone (opiate) ,propranolol (beta-adrenergic antagonist), clonidine (alpha-adrenergic antagonist) dantrolene(muscle relaxant),gabapentin(antiepileptic), and bromocriptine (dopamine receptor antagonist)  Supportive care-nutritional support(initiate within 3 to 5 days) rehabilitation services, skin care  Antibiotic to prevent infection with skull fracture or penetrating wound  Treatment of hyponatremia (due to DI, dehydration, diaphoresis) with fluid replacement, pitressin therapy.  Treatment of hypernatremia (due to cerebral salt wasting or SIADH) by monitoring daily fluid status, fluid restriction, oral salt replacement, IV saline 0.9% or 0.3%(250-500 cc over 3 to 5 hours)

Medical managementSedative and analgesic-paracetamol,dihydrocodeine preparation,cocodamol Nausea-metoclopramide 10 mg Antibiotics-benzylpenicillin or phenoxymethylpenicillin,if patient have allergy with penicillin give oral co-trimoxazole Mannitol(osmitrol)-to reduce cerebral edema and decreaseICP It is a powerful diuretic and may be life saving but it carries danger. A catheter should be inserted into the bladder. Seizure –phenytoin if persist use with clonazepam.

Surgical Management – Management of head injury patient-Swelling in the brain is monitored and treated aggressively, as brain edema (swelling) can have dire consequences. If swelling increases intracranial pressure, or ICP, the brain will be compressed against the immovable skull, preventing blood from circulating adequately and causing brain damage. An ICP monitor can be inserted through the skull to provide a constant pressure reading, which can help to determine when surgery becomes necessary. 1. CraniotomyA craniotomy is a surgical procedure to open the skull in order to access the brain for surgical repair. The following describes the general steps undertaken during a craniotomy:  The patient is placed under general anesthesia  The hair on the patient’s scalp is shaved (this may only involve a portion)  The neurosurgeon incises through the scalp over the area where the brain injury is believed to be

 

A hole is cut in the skull in order to access the brain The neurosurgeon repairs any damaged blood vessels, removes any blood clots, or removes foreign objects or bone fragments  After the repair is done, the piece of bone that was removed is replaced and muscle and skin are stitched up  Drains may be placed in the brain to allow drainage of any blood that collects After surgery, the patient will be moved to an ICU bed. The patient may be on a ventilator and may remain on one for some time after surgery. 2. Burr Hole SurgeryA Burr Hole surgery is done to remove blood clots that are present around the surface of the brain. When the clots are found beneath the firm covering of the brain, known as Dura Mater, it is called as Subdural Hematoma. Usually when the hemorrhage is about moderately old, like about 2 – 3 weeks, the clot can be punctured and drained out by making a small hole in the skull, this avoiding opening of the skull. Procedure-The patient will be administered with general anesthesia and the head would be partly shaven to expose the operative area of the skull. Then surgeon then makes an incision on the scalp over the area of the Hematoma. The surgeon then uses an air powered drill to make a hole in the skull. The tough covering of the brain, Dura Mater, is now opened. The clot which is now visible to the surgeon is then removed and the surgeon may pass a drain around the brain to provide post operative drainage. The scalp is then closed

Nursing Management1 .assess for ABC 2. open the airway using the jaw-thurst technique without head tilt .oral suction equipment should be at hand. make sure that you donot stimulate the gag reflex as this can increase in ICP 3. administer high flow oxygen- the most common cause of death from head injury is cerebral anoxia. 4.assist inadequate respiration with a bag –valve mask as necessary 5.control bleeding- do not apply pressure to the injury site. apply a bulky, loose dressing .Do not attempt to stop the blood flow of blood or cerebrospinal fluid (CSF) from the nose or ear,apply a loose dressing if needed. 6.initiate two IV lines. the rate of flow should be determined by the patient’s hemodynamic status. 7.keep the neck in a neutral position with the cervical spine immobilised 8.be prepare to manage seizure 9. provide immunization with tetanus toxide. 10.monitor sign of increased ICP-altered LOC, abnormal pupil response ,increased pulse pressure, bradycardia, hyperthermia.

11.monitor for sign of sympathetic storming-altered LOC, diaphoresis, tachycardia, tachypnea, hypertention ,hyperthermia,agitation,dystonia. 12.monitor for hypotension,arrhythmias 13.monitor for laboratory finding and report abnormal value. 14.perform cranial nerve ,motor ,sensory, and reflex assessment 15.maintain normothermia

PrognosisPrecise predictions are difficult with TBI, but some generalizations can be made:    

The more severe the injury, the longer the recovery period, and the more impairment a survivor will have once recovery has plateaued. Recovery from diffuse axonal injury takes longer than recovery from focal contusions. Recovery from TBI with hypoxic injury is less complete than without significant hypoxic injury. The need for surgery does not necessarily indicate a worse outcome. For example, a patient requiring the removal of a blood clot may recover as completely as one who never needs surgery.

Cognitive and behavioral processes are controlled by specific areas of the brain, so the location of the injury determines the type of impairment. There are several mechanisms of recovery after brain injury. Initial improvement may be due to the reduction of swelling (edema) of brain tissue occurring over days, weeks or months, depending on the severity of the injury. Next, damaged brain cells begin functioning again, usually over a period weeks to months. Finally, undamaged areas of the brain may, to a certain extent, take over the functions of areas that suffer permanent damage.

Complications – 1. infection-systmic(respiratory, urinary ), neurologic (meningitis, ventriculitis) 2. increased ICP, hydrocepha,brain herniation 3. seizure-post traumatic seizure disorder 4. permanent neurologic deficits-cognitive, motor, sensory, speech 5. neurobehavioral alteration -impulsivity, uninhibited aggression and emotional lability 6. persistent sympathetic storming 7.DIC(disseminated intravascular coagulation), horomone)

SIADH(syndrome of inappropriate antidiuretic

8. neurological behavioural alteration9.Death

MASTER- PLAN

Name of the subject

:- Medical surgical nursing

Name of the topic

:- Head injury

Unit

:- 4

A .V.Aids

:- Black board ,chart, transparencies

Name of supervisor

:- Mrs. Sija Binoy (vice –principal)

Date and time

:-01/04/2011

Duration

:- 45 min

venue

:- M.sc(N) Lecturer Hall

SEMINAR ON HEAD - INJURY

SUBMITTED TO-

SUBMITTED BY-

MRS.SIJA BINOY

MR.PRADEEP KUMAR

VICE-PRINCIPAL

MSC (N) 1 ST YEAR

SUBMITTED ON-01/04/2011

AREAS OF HEAD INJURY