fwd: head injury bambury

Head Injury

Niamh Bambury

Lecturer in Surgery

18/09/08

Introduction

• Head trauma results in approximately 70,000 deaths, 80,000 long-term disabilities, and 60,000 new seizure disorders each year

• These injuries most often occur in individuals who are 15-24 years old and are twice as common in men

• Causality is bimodal– vehicular accidents being most common in those

under 25 years– falls in those over 75 years

• Nearly half involve intoxication with drugs or alcohol

Anatomy

• Scalp

• Structure of the brain

• Meninges

• Blood supply

• Venous drainage

• CSF

Scalp

• Skin• Connective tissue layer• Aponeurotic layer-frontalis, occipitalis and

temporalis merge• Pericranium• Blood supply

– ECA and ICA– Vessels run in dense connective tissue so bleed

profusely when cut(can’t retract)

Structure of the brain

• Forebrain– Cerebrum

• 2 cerebral hemispheres connected by corpus callosum

• Cerebral hemispheres have central cavities called the lateral ventricles

• Gyri and sulci

– Diencephalon• Thalamus• Hypothalamus• Third ventricle (communicates with the lateral ventricles through the

interventricular foramina)

Structure of the brain

• Midbrain– Cerebral peduncles

(consists of descendingtracts from the cerebrum

to the spinal cord)• Crus cerebri• Substantia nigra• tegmentum

– Tectum• 4 colliculi• Pineal body

Structure of the brain

• Hindbrain– Pons– Medulla oblongata– Cerebellum

Meninges

• Dura mater– Falx cerebri– Tentorium cerebelli– Extradural space-

• seperates dura from the skull• meningeal vessels run in this• contains venous sinuses

– Subdural space• seperates arachnoid from dura

Meninges

• Arachnoid mater– Arachnoid villi project into dural sinuses– Subarachnoid space-contains CSF-is traversed

by cranial nerves,arteries and veins

• Pia Mater– Invests brain and SC tissue

Blood supply

CSF

• Produced in the choroid plexus of the lateral 3rd and 4th ventricles

• Flow is from the lateral to the 3rd to the 4th ventricle via cerebral aqueduct

• Then flows into sunarachnoid space via 2 foramen of Luschka and the single foramen of magendie

• Absorbed back into the blood stream via the arachnoid villi which project into the sagittal sinus

• 140mls contained in adult• 500ml/day produced

Neurophysiology

• Blood brain barrier– Selectively controls entry of substances into the

ECF of the CNS– Consists of endothelial cells with tight junctions– Active mechanisms exist to transport substances– May be compromised in cases of severely raised

intracranial pressure

Intracranial pressure

• Normal ICP=10mmHg• Abnormal>20 mmHg• Monroe Kellie doctrine states

– the cranial compartment is incompressible– the volume inside the cranium is a fixed volume– its constituents namely blood, CSF, and brain tissue

create a state of volume equilibrium– any increase in volume of one of the cranial

constituents must be compensated by a decrease in volume of another.

Monroe-Kellie doctrine

CSF

Brain

Blood

Compensation occurs upto a value of 100mls.eg. an increase in lesion volume (e.g. extradural hematoma) will be compensated by thedownward displacement ofCSF and venous blood.

Why is ICP important

• Cerebral perfusion pressure(CPP)= mean arterial pressure(MAP)-ICP

• MAP=1/3 pulse pressure+diastolic blood pressure• Thus decreasing ICP or increasing MAP leads to

an increase in CPP• CPP is normally controlled by auto regulation

with arteriolor vasoconstriction keeping a constant value between 50 and 1500mmHg.

• If this fails as in pathological states this can lead to a significant drop in CPP

Causes of raised ICP

-Surgical• Haematoma• Oedema due to contusion/haematoma• Oedema due to ischaemia• Infection-empyema

-Medical• Electrolyte imbalance• Ischaemia-CVA• Infection-meningitis

ICP cont’d

Effects of raised ICP– Tentorial herniation– Pupillary dilatation due to compression of 3rd CN– Motor weakness due to compression of corticospinal

tract– Coning-brainstem is being squeezed through the

foramen magnum compressing cardiorespiratory centres

Raised ICP

• Symptoms– Decreased conscious level– Headache– Nausea and vomiting

• Signs – Fall in GCS– Dilated pupil– Papilloedema

Neurological assessment in A&E

• Always commence with– Airway– Breathing – Circulation– Disability

• Neurological status

• Pupils

Disability

• Brief assessment• Pupils

– Size– Symmetry– Response to light

• AVPU score– Alert– Verbal stimuli– Pain– Responsive

Secondary Survey of the head

• Neurological state– GCS– Pupils– Eyes

• Examination of the face– Facial bones– Teeth

• Examination of the scalp

Secondary survey of the head

• Examination of the scalp– Battle’s sign-fracture of the base of the skull– CSF/blood from ears– Presence of scalp wound/haematoma

Glasgow coma scale

Classification of head injury

• GCS– Minor-GCS>8– Major-GCS<8

• Mechanism– Blunt– Penetrating

• Pathology– Focal/Diffuse– Primary/Secondary

Intracranial haemorrhage

• Classification– Contusion– Extradural haematoma– Subdural haematoma– Subarachnoid haemorrhage– Intracerebral haemorrhage– Diffuse axonal injury

Contusions

• Classed under focal brain injury• Due to rapid deceleration injuries• The brain hits off the rigid skull causing

coup and contre coup bruising• Coup injury occurs under the site of

impact with an object• Contrecoup injury occurs on the side

opposite the area that was impacted

Contusions

• Frontal and temporal contusions are common

• Also cause mass effect as a result of blood and oedema which leads to midline shift

Extradural haematoma

• Due to trauma-blow to temporal or parietal bone

• Causes rupture of underlying middle meningeal artery

• Presents as initial concussion followed by lucid interval due to accommodation of expanding haematoma.

Extradural haematoma

• Followed by rapid decompensation as ICP raises when the temporal lobe is pushed into the tentorial opening.

• This is called coning.

• Carries a 5% to 20% mortality rate.

Extradural haematoma

Respects the suture lines.Seen on CT Brain as lens-shaped blood collectionwith a convex medialborder .

Acute Subdural haematoma

• Severe head injury-Sudden deceleration injuries --leads to a more rapid deterioration in patient’s condition.

• Due to– rupture of a bridging vein due to shearing

forces– laceration of brain substance

• Thin layer of blood in the subdural space (between the dura and arachnoid mater)

Acute Subdural haematoma

Appear on Ct Brainas crescent-shapedblood collectionswith a concave medial border. This does not resect the suture lines.Note also midline shift.

Subarachnoid haemorrhage

• Trauma is the most common cause of Subarachnoid haemorrhage

• Bleeding occurs between the arachnoid and pia mater.. SAH may be complicated by hydrocephalus.

• Confusion can sometimes arise between SAH due to trauma and due to a ruptured aneurysm or arteriovenous malformation (AVM); the patient may collapse and hit their head as a result of a bleed and the history (from the patient or a witness) is important.

Subarachnoid haemorrhage

Increased attenuationis seen in the CSF spacesover the cerebralhemispheres (look closely at the Sylvian fissure), in the basal cisterns orin the ventricular system.It may be complicatedfurther by Hydrocephalus

Intracerebral haematoma

• Injury of the brain substance itself

• Associated with cerebral laceration, contusion, oedema and necrosis

• Evacuation of the clots can have poor results

• Not as easy to remedy.

Diffuse axonal injury

• Occurs due to shearing forces between grey and white matter.

• Generalized cerebral oedema results due to parenchymal disruption leadsing to an increase in ICP

• Ranges from – mild form-concussion – severe form- persistent vegetative state

Monitoring of ICP

• Invasive– External ventricular drain(EVD)- inserted via frontal

Burr hole into lateral ventricles. This allows drainage of CSF if necessary

– Brain parenchymal ICP transducer- catheter is introduced through Burr hole and placed in contact with parenchyma and linked to pressure transducer

• Non- invasive– Transcranial pressure-estimates flow in middle

meningeal artery.

Medical management of raised ICP

• Sedate and intubate• Nurse patient at 30 degree angle-aids

venous drainage• Mild hyperventilation- keep pCO2 approx

4.5kPa- if allowed to fall lower this leads to vasoconstriction and subsequent ischaemia

• Mild hypothermia

Medical management of raised ICP

• Maintain ICP at 10 mmHg– Mannitol(0.5g/kg)- transient mild reduction in ICP

– Hyperventilation

– Hypothermia

– Thiopentone infusion(5mg/kg)

• Aim to maintain CPP at 60-70mmHg– Fluid management

– Use of inotropes(this increases MAP)

Surgical management

• External ventricular drainage-drain CSF to transiently reduce ICP

• Burr holes

• Evacuation of mass lesion +/- craniectomy

• Decompressive craniectomy

Surgical management

• Burr Holes– Small holes through the skull over the site of an

intracranial haematoma

– Aim is for partial evacuation and reduction in ICP

– Must be placed directly over haematoma

– Temporary measure only whilst awaiting definitive neurosurgical intervention

– Also used for insertion of invasive monitoring equipment

Surgical management

• Decompressive craniectomy– part of the skull is removed to allow the brain

room to expand– some evidence suggests that it does improve

outcome by lowering ICP– The part of the skull that is removed is known

as a bone flap