Head Injuries

Remember - Regard every patient with a head injury as having potential spinal cord injury.

Types of head injury

Type 1. Blunt, accelleration/decelleration injuries Type 2. Crush or compression

Scalp - often bleed a lot

Skull - fractures may occur

Brain - injuries tend to be diffuse and may lead to concussion, ie disturbance or loss of consciousness, associated with variable periods of amnesia.

Type 3. Sharp or penetrating Type 4 High velocity penetrating

Scalp - May be small puncture wounds with larger underlying injuries

Skull - often depressed skull fractures

Brain - usually focal damage

- little or no concussion

- effects depend on location and extent

- in high velocity injuries the shock wave leads to more widespread injury

Neurological observations

To look for changes in patients condition, Used after;

head injury, especially if patient was knocked out

intracranial disease

neuro-surgical procedures

other conditions effecting the brain, eg. overdose, ketoacidosis

10 - 15 minute frequency at first

Reduced to 2 - 4 hourly depending on patients condition

Performed by same nurse, together during handovers

Level of consciousness is a reliable indicator of cerebral function

Changes in conscious level occurs before pupil changes or changes in vital singns

Glasgow coma scale

A tool to objectively measure neurological condition

Uses eye opening, best verbal response and best motor response

Each response is given a score

Eye opening

spontaneous 4 to speech 3 to pain 2 none 1

Best verbal response

orientated 5 confused 4

inappropriate words 3 incomprehensible sounds 2

none 1

Best motor response

obeys commands 6 localises to pain 5

flexion to pain, (withdrawal) 4 flexion to pain, (abnormal) 3

extension to pain 2 none 1

The 3 modes of behaviour are then summated to give an overall score.

Normal would be Glasgow coma scale 15.

Any deterioration must be reported to medical staff at once as it may signify the development of an intracranial lesion.

If changes are noted during the assessment, again they must be reported at once.

Vital signs

Blood pressure, pulse, respiration and temperature.

To check ABC are adequate to prevent secondary brain damage secondary to cerebral hypoxia.

Blood pressure may rise in increased intracranial pressure. Pulse rate may fall.

Pupillary response

Normal pupils are equal is size and respond to light

+ means the pupil has contracted - means the pupil has not contracted

c means the eye is closed

A pupil will not react to light and may dilate due to pressure on the occulomotor, (third) cranial nerve.

Motor strength

Limb power is measured on both sides to respond to both cerebral hemispheres

/ means normal power on both sides

R means right L means left

Nursing management in head injuries

Assessment

Has patient been knocked out? Level of consciousness

Headache Vertigo

Temperature Shock

Management

Airway and breathing - hypoxia and excess CO₂ cause cerebral oedema.

Suction, humidified oxygen, semiprone position, intubation.

Observations, bleeding, loss of CSF from nose and ears may indicate base of skull fracture.

Keep safe during periods of agitation, look out for causes of distress.

Convulsions may occur.

Fluid balance, patients may be kept slightly dehydrated to reduce cerebral oedema.

Control temperature.

Aid in treatment of cerebral oedema, hyperosmolar solutions, (eg mannitol) and give steroids.

Keep head slightly elevated to reduce cerebral oedema, about 15` or 30` if there is a CSF leak.

Prophylactic antibiotics for open skull fractures.

Care of unconscious patient

Prevention of effects of immobility

Possible complications following a head injury

Amnesia personality and behavioural change

inability to formulate words – dysphasia inability to concentrate

impaired intelligence haemorrhage hydrocephalus

raised intracranial pressure cerebral infarction infection

meningitis convulsions visual disturbance

diabetes insipidus deafness damage to any of the cranial nerves hemiparesis or other paralysis death

Causes of unconsciousness

Poisons and drugs

Alcohol

General anaesthetics

Overdose eg. opiates

Gases, eg Carbon Monoxide

Heavy metals eg. Lead, Mercury

Vascular causes

Ischaemia

Haemorrhage

Infections

Encephalitis (Viral)

Meningitis (Bacterial)

Abscess

Endocrine causes

Diabetes

Myxoedema

Fits

Epilepsy

Eclampsia

Metabolic causes

Diabetes mellitus

Uraemia

Hepatic Coma

Mechanical causes

Trauma

Hypothermia, Hyperthermia

Dehydration

Tumours

Description of brain injury

Contusions

“Bruising” of cerebral tissue

Most commonly affects frontal, occipital and under-surface of temporal lobes

“Coup” - indicating haemorrhage and oedema immediately under injury site

“Contre-coup” - damage occurs directly opposite the injury site due to rapid acceleration/deceleration injury.

Laceration

eg. due to skull fracture

Haematoma

Localised collection of blood

Extradural - situated or occurring outside the dura mater

Subdural - between the dura mater and arachnoid mater

Intracerebral - within the brain substance

Diffuse brain injury

No localised brain pathology

Shearing of white matter - causing disruption and tearing of neuronal axon fibres

Features may therefore be focal or global

Intracranal Pressure

The pressure exerted within the cerebral ventricular system.

Adult skull is a rigid box, containing non-compressible components:

Brain (80%) Cerebrospinal fluid Blood

Normal value: 5 - 12 mmHg.

Transient rises occur with coughing sneezing.

A correlation exists between ICP and conscious level.

ICP increases ------- conscious level decreases.

Initial rise in ICP - compensatory mechanisms

1) Downward displacement of CSF to distendable spinal dural sac.

2) Reduction in blood flow.

As ICP rises, compensation overcome ------- Small rises in volume lead to dramatic rises in ICP.

Causes of RICP

Head injury Cerebral oedema

Abscess or inflammation Haemorrhage

Tumour Cranial surgery

Hydrocephalus SOL = Space occupying lesion

Pathophysiology is explained by modified Monro-Kellie hypothesis, which states: "the skull, a rigid compartment, is filled to capacity with essentially non-compressible contents - brain tissue, intra-vascular blood and cerebrospinal fluid. if any of these three increases in volume, another must decrease or else intracranial pressure will rise." (Hickey, 1986).

Signs and symptoms of raised ICP

Headache - early morning, associated with vomiting

Deterioration in conscious level, changes in GCS

Sudden change eg. quietness or restlessness

Contralateral Hemiparesis/Hemiplegia

Deterioration in respiratory pattern

Alteration in pupil size, light reaction.

Blurring of vision, ocular muscle paresis/ paralysis.

Increase in systolic BP, widening of pulse pressure.

Bradycardia, or pulse changes

Problems with speech, comprehension.

Localising signs, eg Grand Mal, Focal Seizure activity.

Moderately elevated temperature

Vomiting

Pupil change

Sleeping

Papilloedema

Herniation

Process by which tissues in a high pressure compartment is compressed and forced through an available opening into an adjoining low-pressure compartment.

Skull - 2 compartments

Supratentorial Infratentorial

Suppratentorial Herniation - Tentorial Notch

Infratentorial Herniation - Foramen Magnum.

Classic pre-coneing triad;

B.P. increase

Widening of pulse pressure

Bradycardia

Care and Management of Client with Closed Head Injury

Aims

Preservation of brain homeostasis

Prevention of secondary brain injury

Maintenance of cardiovascular and respiratory function to maintain cerebral perfusion

Collect information

What time did the accident occur? What caused the injury?

What was the direction and force of the blow? Was there loss of consciousness?

What was the duration of unconsciousness? Any related post-traumatic amnesia?

Any neurological deficits noted?

Difficulty in maintaining airway due to lowered level of consciousness

CO₂ retention ------- cerebral vasodilation -------- increase in ICP

Semi-prone position

Head of bed elevated 30 degrees ------- reduces intracranial venous pressure

Pulmonary secretions - suction no longer than 15 seconds, pre-oxygenate 100% 0₂

Hyperventilation - reduce pCO₂ to encourage cerebral vasoconstriction.

Alteration of conscious level and neurological function due to Head Injury

Establish base-line neurological status

Monitor Glasgow Coma Scale, limb and pupil size and reaction, vital signs as indicated.

Report any deterioration immediately.

Increased ICP with risk of brain herniation

Tentorial herniation

The protrusion of brain tissue into the tentorial notch, caused by increased intracranial pressure.

Nurse with head of bed elevated 30 degrees

Maintain head and neck position in neutral position - prevents cerebral venous drainage obstruction.

Avoid valsalva manoeuvre - increases intraabdominal pressure - intrathoracic pressure - ICP

Avoid extreme hip flexion

Control body temperature - 1 degrees centigrade increases metabolic demand of the brain by 10%

Assist in fluid restriction if indicated

Administer cerebral diuretics (hyperosmolar agent) eg. mannitol 20% 100 mls if indicated.

Controlled ventilation, avoid hypoxia

? Steroids (Dexamethesone)

? Hypothermia

? Removal of CSF

Pre-op care

Potential seizure activity

Seizure activity increases metabolic rate, causes hypercapnoea and increases ICP

Potential fluid and electrolyte imbalance

Maintain accurate fluid balance recording

Monitor urine for SG (diabetes insipidus may develop due to hypothalamic/adjacent structural damage)

Potential for altered nutrition due to decreased conscious level

Potential for injury due to altered consciousness, restlessness and confusion

Sedation contra-indicated: may mask deterioration in neurological condition

Need to consider:

Hygiene needs, prevent complications of bed rest eg. pressure sore development, muscle wasting and contractures.

Complications of Head Injury

Cerebro-spinal fluid leakage, CSF rhinorrhoea, otorrhoea due to basal skull fracture

? possibility of meningitis, cerebral abscess.

Post-traumatic epilepsy

Hydrocephalus

Diabetes insipidus.

Intracranial haemorrhage

Subdural haemorrhage

More common than extradural

Signs may be delayed after injury by weeks - blood oozes from veins

Headache, apathy, gradual deterioration in consciousness level - often with lucid periods, localising signs

Craniotomy is required

Subarachnoid haemorrhage (SAH)

Often hard to differentiate from intracerebral - both are usually spontaneous

Clinical features

Headache - often abrupt onset Loss of senses

Feelings of ill-ease in the head Increasing headache

Neck stiffness Vomiting

Coma

Caused by trauma and congenital lesions.

Blood in CSF is irritant therefore headache, neck stiffness, photophobia and irritability.

Extradural haemorrhage

Between the Dura and the Skull

70% rupture of middle meningeal vessels

Often a history of being unconscious followed by recovery, followed by changes

Check using CT/MRI

Local signs may present

Always account for after a skull fracture

Pre-op care

Signs of increased intracranial pressure (ICP) in infants and children

Infants

Tense, bulging fontanel : lack of normal pulsations Separated cranial sutures

Irritability High-pitched cry

Increased occipito-frontal circumference Distended scalp veins

Changes in feeding Cries when held or rocked

“Setting-sun” sign

Children

Headache Nausea

Vomiting often without nausea Diplopia - blurred vision

Seizures

Personality and Behaviour Signs

Irritability, restlessness

Indifference, drowsiness or lack of interest

Decline in school performance

Diminished physical activity and motor performance

Increased complaints of fatigue, tiredness, increased time devoted to sleep

Significant weight loss possible from anorexia and vomiting

Memory loss if pressure is greatly increased

Inability to follow simple commands

Progression to lethargy and drowsiness

Late Signs

Lowered level of consciousness

Decreased motor response to command

Decreased sensory response to painful stimuli

Alterations in pupil size and reactivity

Sometimes decerebrate or decorticate posturing

Cheyne-Stokes respirations

Papilloedema

HEAD INJURIES

Every Head Injury regarded as potential spinal cord injury.

Head injuries can arise due to:-

Road traffic accident

Industrial accident

Domestic accidents

Assault

Birth

Types of Head Injury

Type 1 - BLUNT - acceleration/deceleration injuries

Type 2 - CRUSH or COMPRESSION

Scalp - often bleed profusely

Skull - Fractures may occur

Brain - Injuries tend to be diffuse and may lead to concussion

Type 3 - Sharp or Penetrating

Type 4 - High velocity penetrating

Scalp - May be small puncture wounds with larger underlying injuries

Skull - often depressed fractures

Brain - Usually focal damage

little or no concussion

effects depend on location and extent

high velocity injuries lead to more widespread injuries

A. SCALP WOUNDS

Scalp is very vascular therefore severe bleeding

B. SKULL WOUNDS

Fractures may be:-

a. SIMPLE - usually of vault

b. COMPOUND - # of base very often compound

c. DEPRESSED - much force needed.

May affect Vault or Base Skull

Can cause:-

a. infection leading to meningitis

b. leakage of CSF from base of skull

c. extradural haematoma when # crosses branches of middle meningeal artery.

d. damage to cranial nerves especially - OLFACTORY/FACIAL

Damage to the temporal region dangerous because:-

a. middle meningeal artery from external carotid in this region

b. bone here thin compared to other parts of the skull

Fracture of BASE of skull dangerous because:-

1. Often compound # with leakage of CSF (via nose and ear) and infection producing meningitis, cerebral abscess.

2. Often due to severe violence eg falling from a height onto the feet, impact is transmitted up vertebrae to base of skull.

3. Vital Sub-tentorial area and cranial nerves may be involved.

4. Brain stem (medulla oblongata) passes near foramen magnum, therefore damage to base of skull often causes brain stem injuries.

C. BRAIN INJURY

1. Concussion

Swelling of brain tissue.

Functions disturbed due to brain being shaken producing loss of consciousness at time of injury with quick spontaneous recovery.

2. Contusion

Bruising or laceration of brain tissue. Immediate loss of consciousness - may have adverse effects depending on the situation eg. hemiparieses.

3. Compression

Usually due to haemorrhage

a. Extradural - due to bleeding from meningeal artery or vein from an overlying fracture.

b. Subdural - usually venous bleeding

I. Acute

II. Chronic - commonest in older age groups often following a trivial injury

Signs/Symptoms:- Headache, mental deterioration, drowsiness, apathy, confusion.

c. Subarachnoid and intracerebral

Signs and Symptoms

Sudden onset, severe headache, vomiting, visual disturbances, blood stained CSF, kernigs sign positive (unable to straighten leg at the knee joint when the thigh is flexed at right angles to the trunk. Sign of meningeal irritiation.

As haematoma increases the brain becomes compressed and displacement of the cerebral hemispheres distorts and damages the brain stem by displacing it downwards through the foramen magnum.

The Compression causes raised intracranial pressure

Signs and Symptoms

a. deterioration of consciousness

b. failure to respond to painful stimuli

c. increasing restlessness

d. blood pressure rises to force blood through compressed brain, also due to cerebral hypoxia

e. pulse and respirations fall - pressure on medulla

f. spasticity of opposite side of body - damage to motor cortex/pathway

g. initially constriction of pupil on same side then pupil becomes dilated and fixed.

Later both pupils dilate and fail to react to light - due to compression of the 3rd cranial nerve as the haematoma spreads.

h. respirations become laboured and noisy - may lead to cheyne stokes respirations

i. temperature rises - interference with heart regulating centre in hypothalamus

DECREBRATE RIGIDITY - (Without Cerebral Function) - due to damage to brain stem.

All limbs spastic, indicates severe damage to brain.

UNCONSCIOUSNESS

The complete awareness of self and environment with appropriate responsiveness to stimuli.

Full consciousness depends on interaction between the cerebral cortex and the reticular activating system located throughout the central portion of the brain stem.

Causes

1. Processes which interfere with metabolism of the brain stem and cerebral cortex

a. hypoglycaemia, diabetic ketoacidosis - glucose essential for cerebral neuronal functioning

b. cardiac failure

c. severe blood loss, anaemia, shock, respiratory failure, produce cerebral hypoxia

d. drug overdose

2. Supratentorial space occupying lesions

a. cerebral haemorrhage

b. tumours

c. abscess

d. haematoma

3. Infratentorial lesions

a. cerebral haemorrhage

b. brain stem infarction

c. tumours

d. abscesses

e. trauma

4. Psychogenic causes

stress, shock.