Head Injury for Medical Finals (based on Newcastle university learning outcomes)

8/14/2019 Head Injury for Medical Finals (based on Newcastle university learning outcomes)

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Hospital Based Practice Head injury.

Presentation varies from transient stunning for a few seconds, to prolonged coma.

A fraction of patients who attend A&E with head injury need to be admitted for observation.

Admit patients who have.

Confusion Abnormal CT

Decreased GCS

Clinical or radiological evidence of skull fracture.

Neurological signs.

Severe headache and vomiting

Difficult assessment.

Alcohol or drugs

Very young or old

Concurrent medical conditions.

Eg. Clotting disorders

Diabetes.

Poor social circumstances/ lives alone.

If you do discharge a patient from A&E, they should be sent home with.

A responsible adult who will remain with them for the next 24 hours.

A head injury card that describes possible signs and symptoms.

In the alert patient, assess the following.

Circumstances surrounding injury.

Endogenous factors.

Eg. Loss of conciousnes causing a fall

Exogenous factors.

Eg. Being knocked down. Any extracranial trauma.

Period of loss of consciousness

Reflects severity of diffuse brain injury.

Period of post traumatic amnesia.

Period of antegrade amnesia reflects degree of brain damage

Period of retrograde amnesia doesnt accurately reflect severity of brain injury.

Headache or vomiting.

Common after head injury.

Persistant head injury and vomiting suggests raised ICP.

GCS

Any evidence of skull fracture. Neurology.

Any focal neurological signs.

Extracranial injury.

Any evidence of occult blood loss.


2/10

Drowsy or unconscious patient needs.

Urgent assistance from senior A&E and anaesthetic staff.

Protect airway.

Intubate patients with deteriorating levels of consciousness

Over breathing patient to induce hypocapnia can reduce ICP.

This is controversial, consult an intensivist.

Patients with no neurological deficit who are able to protect their airway dont

require intubating.

Assume there is a C spine fracture until an X ray has been performed that shows

all 7 cervical vertebrae are intact.

Hyperventilation.

Note pattern of breathing.

Central neurogenic respiration.

Regular, rapid deep and continuous breathings.

Rate of about 25 bpm.

No acidosis or hypoxia on blood gases.

Increasing regularity signifies progression of coma and worsening

prognosis

Due to diffuse damage to central areas of the brain.

Apneustic breathing..

Prolonged inspiration, followed by period of apnoea.

Implies damage to pons.

Cluster breathing.

Closely grouped respirations, followed by periods of apnoea.

Implies damage to pons.

Ataxic breathing.

Chaotic and irregular mix of breathing and apnoea.

Implies damage to medullary respiratory centres.

Normally progresses to respiratory arrest quite quickly.


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Biots respiration (gasping breathing)

Gasps for air, followed by apnoeic periods.

Implies damage to medullary respiratory centres.

Normally progresses to respiratory arrest quite quickly.

Cheyne Stoke respiration.

Periods of rapid, deep breathing followed by periods of apnoea.

Due to.

Bilateral, deep hemisphere and basal ganglia damage.

Cardiovascular dysfunction

Respiratory dysfunction

Slow, shallow breathing.

Due to medullary depression

Often due to opiates or benzodiazepine.

Long tract signs.

Due to structural brainstem damage.

|Causes dysfunction of descending tracts.

Complex picture can occur due to decussation of pathways within

the brainstem.

Support circulation.

Initially treat hypotension with colloids.

If persistent or severe, exclude cardiac cause with ECG and occult haemorrhage (eg.

Intra abdominal).

Treat seizures

Diazepam IV or PR.

If continuing to fit give IV phenytoin. Rapid survey of chest, abdomen and limbs.

Flail chest

Haemo/pneumothorax

Intra abdominal bleeding

Limb lacerations

Long bone fractures.

Brief history.

Obtain from ambulance crew or relatives.

Establish if patient lost consciousness before or after the head injury.

Faints or SAH can cause loss of consciousness, and so cause a fall and head

injury, rather than the head injury causing the loss of consciousness. Gain a feel for the tempo of neurological deterioration.


4/10

Symptoms of minor head injury.

Headache

Dizzines

Fatigue

Reduced concentration

Memory deficit

Irritability

Anxiety

Insomnia

Hyperacusis

Photophobia

Depression

Generally slowed information processing.

Symptoms of a major head injury.

Any symptoms of minor head injury.

Behavioural problems.

Irritability

Impulsivity

Egocentricity

Emotional lability

Impaired judgement

Impatience

Anxiety

Depression

Hyper or hyposexuality

Dependency

Euphoria Aggressiveness

Apathy

|Childishness

Disinhibition.

Cognitive impairment.

Memory deficits

Difficulty in abstract thinking

Generally slowed information processing.

Poor concentration

Slowed reaction time

Impaired auditory comprehension

Reduced verbal fluency

Anomia


5/10

Difficulty planning or organising.

Examination.

Rapid neurological examination should only take a few minutes.

GCS

Pupil.

Size

Shape

Reaction to light

Resting eye position.

Spontaneous eye movements.

If reduced and patient unresponsive, look for oculocephalic and

oculovestibular reflexes.

Dont do Dolls head manoeuvre until C spine fracture has been exclude.

Assess motor function.

Note any asymmetry.

Look for features suggesting brain shift or herniation.

Head and spine assessment.

Examine skull for fractures

1% will have fractures.

Fracture increases the risk of intercranial haematoma from

1:1000 to 1:30 in alert patients.

1:00 to 1:4 in confused or comatose patients.

Absence of skull fracture does not rule out potentially fatal injuries.

Basal skull fractures are suggested by.

Extensive periorbital haematoma

Bruising behind the ear.

Battles sign.

Bleeding from the ear.

Leaking of CSF from nose or ear.

Check for facial fractures

Maxillary

Mandibular.

Consider possibility of spinal cord trauma.

Log roll patient.

Examine for.

Tenderness over spinous processes

Paraspinal swelling

Gap between spinous processes Flaccid and anaesthetised limbs


6/10

Painless urinary retention.

Investigations.

Indications for skull x ray.

History of high impact injury

Decreased level of consciousness

Amnesia

Nausea or vomiting Neurological signs or symptoms

CSF/ blood from nose/ear

Scalp bruising or swelling

Suspected penetrating injury

Difficulty in clinical assessment.

Elderly

Young

Alcohol

Drugs

Seizures

Things to look for on skull x ray. Linear skull fractures

Depressed skull fracture.

Requires elevation if depressed by more than the thickness of the vault.

> 3 mm shift of a calcified pineal (if present).

Integrity of craniocervical junction.

Fluid level in sphenoid sinus.

Things to look for on C spine film.

Check all 7 cervical vertebrae.

Check integrity of C7 T1 junction.

Check alignment.

Anterior and posterior vertebral bodies

Posterior margin of spinal canal

Spinous processes

Step of 25% of vertebral body suggests facet joint dislocation.

Check contours.

Outlines of vertebral bodies

Outlines of spinous processes

Avulsion fractures

Wedge fractures

Difference of > 3 mm between anterior and posterior body heights.

Check odontoid.


7/10

Should be < 3 mm between anterior arch of C1 and odontoid.

Disc spaces.

Space > 5 mm between anterior C3 and back pharyngeal shadow suggests

retropharyngeal mass.

Abscess

Haematoma from fracture of C2.

Indications for urgent CT.

GCS < 12

Skull fracture and persistent neurological dysfunction

Neurological dysfunction, eg. Seizures.

Coma after resuscitation

Suspected compound fracture of vault or base of skull, eg. CSF leak.

Persistent confusion of neurological disturbances at 12 hours.

Significant head injury requiring general anaesthesia.

Indication for neurosurgical referral.

Recent intracranial lesion seen on CT

Persisting coma after initial resuscitation

Confusion the persists at 4 hours.

Progressive focal neurological signs

Seizure without full recovery

Depressed skull fracture

Suspected penetrating injury

Signs of basal skull fracture

Need for urgent CT, but facilities not available.

Management.

Resuscitate.

Take bloods for.

FBC

U&E

Group & Save

ABGs

Toxicology screen.

If appropriate.

Subsequent management depends on pace of development. 40% of comatose head injury patients have intracranial haemorrhage.

Not possible to distinguish clinically between diffuse brain injury and intracranial

haemorrhage.

CT scan.

Most patients who need resuscitation will need CT.

Urgency depends on rate of deterioration.

Treat raised ICP.

If present.

Very severe injuries may require simultaneous surgical decompression and

resuscitation.

May need to reduce ICP while waiting for CT scan.

Mannitol


8/10

Hyperventialtion to cause hypocapnia

Frusemide.

Surgery.

May be indicated for.

Extradural haemorrhage

Subdural haemorrhage

Intracranial haemorrhage.

Rarely. Complex head wounds.

Eg. Compound depressed skull fractures.

Generally, urgent evacuation is required if an extradural haematoma.

Causes midline shift of > 5 mm

Volume of > 25 ml.

If haematoma too small to evacuate on original CT scan, rescan at 9 12 hours

regardless of any improvement or deterioration of condition.

Non operative management.

Brain contusions may be seen as areas of low density on CT.

CT is a very poor way of detecting primary diffuse brain injury.

Raised ICP may be seen as effacement of

Cavity of 3rd ventricle

Perimesencephalic cisterns.

Further management.

Aim is to reduce and minimise secondary brain injury.

Causes of secondary brain injury.

Systemic

Hypoxaemia

Hypotension

Hypercarbia

Severe hypocapnoea Pyrexia

Hyponatraemia

Anaemia

DIC

Intracranial.

Haematoma.

Extradural

Subdural

Intracerebral.

Brain swelling/ oedema

Raised ICP Cerebral vasospasm


9/10

Epilepsy

Intracranial infection.

Management may be better undertaken at a neurosurgical centre.

Principles of management are.

Regular monitoring.

If there is deterioration, consider a secondary brain injury.

Intubate if.

New signs of raised ICP

Declining levels of consciousness

Signs of transtentorial herniation

Consider over breathing and mannitol

Close monitoring of BP, ABG, electrolytes and urine output.

Pre emptive treatment may prevent neurological decline.

Hypotension is common due to.

Sedatives

Hypovolaemia

Replace fluids carefully so as to not aggravate raised ICP.

Prompt treatment of seizure.

Insert NG tube.

Nutrition

Drugs.

Ranitidine for peptic ulcer prophylaxis.

Stool softeners.

Straining can aggravate raised ICP.

Before transfer to Neurosurgical unit.

Assess for.

Respiratory insufficiency

Shock

Internal injury.

Perform.

CXR

ABG

C spine X ray

Consider appropriate treatment, which may include.

Intubation

If airway threatened or obstructed.

Ventilate.

Cyanosis

PaCO2 > 5.9 kPa


10/10

PaO2 < 7.9 kPa

IV fluids.

Commence carefully.

Mannitol

Discuss with neurosurgeon first

Cervical collar or traction. Transfer with staff who are able to intubate, ventilate, cannulate and suction.

Documents

Head Injury for Medical Finals (based on Newcastle university learning outcomes)