Head injuries

Question 1

Define mild traumatic brain injury

Answer 1

Patient with a GCS of 13-15 who has had a traumatically induced physiological disruption of brain function as manifest by

1) any period of loss of consciousness less than 30 minutes ‘
2) any loss of memory for events immediately before or after the accident
3) any alteration in mental state at the time of the accident (e.g feelin dazed, disoriented or confused)
4) focal neurological deficits that may or may not be transient

Question 2

What is normal CSF pressure

Answer 2

5-15 mmhg

Question 3

Describe cerebral haemodynamics

Answer 3

Extremely high metabolic rate using approxiamtly 20% of the entire oxygen consumed by the body and requiring approximately 15% of the total cardiac output.

HTN, alkalosis and hypocarbia all promote cerebral vasoconstriction

Cerebral vasoactivity is very sensitive to changes in the parital pressures of Co2 and O2. THe response to chances in pco2 is nearly linear between pco2 of 20 and 60. In this range lowering pco2 by as little as 1mmhg decreases the diameter of cerebral vessels by 2-3%. THis was the rational for hyperventilation to acheive hypocapnia – low normal co2 is now recommended

Hypoxia also causes vasodilation
In brain injury increased CBGF, vascular dilation and a disrupted BBB promote vasogenic oedema and can further increase ICP.

CBF also depends on CCP which is eqaul to MAP-ICP.
If CCP falls below 40mghg autoregualtion is lost and CBF declines resulting in tissue ischaemia. Recommended target of CCP is 60-70mmhg

Question 4

Discuss increased ICP in traumatic brain injury

Answer 4

Initially as ICP increases as a resutl of a traumatic mass lesion or oedema CSF is displaced from the cranial vault to the spinal canal offsetting the increased blood or brain volume.

When this is overwhelmed the elastic properties of the brain subtance allow tissue compression to provide buffering for the increased pressure.

Depending on rate and location the vault can accommodate approximately 50-100mls

Beyond this even small change sin intracranial relation such as from vasodilation, csf obtruction or focal oedema may increase ICP. If ICP reduces CCP to a point in which autoregulation is lost massive cerebral vasodilation occurs and systemic pressure is transmitted to the capilleries leading to vasogenic oedema and further increase in CCP.

Question 5

Discuss simple techniques to reduce ICP

Answer 5

Head elevation to 30 degress and keeping neck in a neutral position. Therapeutic hyperventialtion is only used in a small subset of patient who are imminently conning.

Question 6

Discuss broad categories of head injury

Answer 6

Seperated into three categories broadly based on the GCS score following resuscitation

Severe GCS <8 post resus
Moderate GCS 9-12 post resus
Mild GCS >13 post resus

Question 7

Discuss direct and indirect head trauma

Answer 7

Direct trauma, occurs when the head is struck or its motion is suddenly arrested by an object.

The resulting damage to the skull and brain depends on the consistency, mass, surface area and velocity of the object striking the head.

Direct injury can also be caused by compression of the skull

Indirect injury is caused when the cranial contents are set into motion by forces other than the direct contact of the skull with an object. A common example is acceleration deceleration injury. No direct mechanical impact is sustained but the cranial contents are set into vigorous motion. As the bridging subdural vessels are strained subdural haematomas may result.

Differential acceleration of the cranial contents occurs depending on the physical characteristics of the brain region. As one brain region slides past another shear and strain can occur, resulting in diffuse injury such as concussion or TAI.
Contrecoup contusions can occur when the movement of the intracranial vault are abruptly arrested.

Question 8

Discuss scalp wounds

Answer 8

The large blood vessels of the scalp do not fully constrict if they are lacerated and can be the source of substantial blood loss.

Subgaleal haematomas can become large because blood easily dissects through the loose areolar tissue.

Haemostasis may be difficult to acheive and blood loss may be significant to the point of causing HD compromise

Question 9

Discuss linear skull fractures

Answer 9

Linear skull fracture are single fracutres taht go through the entire thickness of th skull. Linear fracture are clinically important if they cross the middle meningeal groove or major venous dural sinuses as they can disrupt vascular structures and cause the formation of epidural haematomas.

Question 10

Discuss depressed skull fractures

Answer 10

Usually caused by direct impact with small blunt objects such as a hammer or basebal bat. Most occur over the parietal or temporal region.

THey are clincally improtant as they predispose patient to significant underlying brain injury and complicnations of trauma such as seizure or infection.

Question 11

Discuss basilar fractures

Answer 11

Linear fracture at the base of the skull usually occuring through the temporal bone.

Patient with basilar fractures are at risk for extra-axial haematomas because of the proximity of the fracutre to the middle cerebral artery.

Dural tears resulting from base of skull fracture may produce a communication among the subarachnoid space, paranasal sinus and the middle ear. THis offers a rout for the introduction of infection into the cranial cavity and suggested by a CSF leak.

Question 12

Discuss epidural haematoma

Answer 12

An EDH is bleeding that occurs between the inner table of the skull and drua. Most are the result of forceful direct impact that occurs across the middle meningeal artery or vein or a dural sinus. THe temporoparietal region is the most likley site for an EDH.

High arterial pressure of the bleeding dissects the dura away from the skull permitting haematoma formation.

EDH is primarily a disease of the young and accounte for up to 5% of patient who ahve experienced TBI. They are rare in older adults and children younger than 2 due to the close adherance of the dura to the skull in these age groups.

Question 13

Discuss subdural haematoma

Answer 13

A haemorrhage that occurs between the dura and the brain usually due to acceleration decceleration injury.

SDH occurs most commonly in patients wit0h brain atrophy such as alcoholics or older patients due to bridiging vessels traveresing a greater distance than in patient with no atrophy.

Once ruptured blood fills the potentional space between the dura and the arachnoid.

Slow bleeding assocaited with SDH delays the onset of symptoms. As a result the haematoma compresses the undelrying brain tissues for prolonged periods and can cause significant tissue ischaemia and damage. The prognosis of SDH does not necessarily depend on the size of the haematoma but rather on the pressure it applies to underlying tissue.

Question 14

Discuss traumatic subarachnoid haemorrhage

Answer 14

Blood within the CSF and meningeal intima and probably results from tears of small subarachnoid vessels.

SAH is detected on the first CT for STBI in 30% of cases and 50% on subsequent

It is associated with a poorer prognosis if present (60%f unfavourable vs 30%) for early mortality

Question 15

Discuss subdraul hygroma

Answer 15

Collection of clear xanthocromic blood tinged fluid int eh dural space. Pathogenesis of an SDHG is not certain. It may result from a tear in the arachnoid that permits CSF to escape into the dural space or effusion from injured vessels through area of abnormal permeability in the meninges. They may accumulate immediately after trauma or in a delay manner

Question 16

Discuss DAI and TAI

Answer 16

Diffuse axonal injury is characterised by a prolonged trauamtic coma not cause by a mass lesion or ishcaemia.

DAI has been widely adopted however the distrubution seen in TAI is more commonly multifocal than diffuse, DAI is also used to describe conditions not caused by trauma. As such TAI is the preferred term particuarly in mild TAI

In TAI axons sustain a primary insult in which they are torn or stretched and secondary insults lead to axonal swelling and disconnection and eventual axonal death.

Clincal grade of diffuse TAI have been based on length of coma

1) grade 1 mild coma for 6-24 hours
2) grade 2 moderate coma for longer than 24 hours but not decerebrate
3) Severe coma for greater than 24 hours and decerebrate.

Question 17

Discuss cerebral contusions

Answer 17

Contusions are bruises on the surface of the rbain usually caused by impact injury.

Most commonly contusions occur at the poles and inferior surfaces of the frontal and temporal lobes., where the brain comes into contact with bone protuberances in the base of the skull.

Compression of underlying tissue can cause local areas of ischaemia and tissue infraction –> eventually if not releived these areas become necrotic and cystic cavities form within them.

Question 18

Discuss intracerebral haematoma

Answer 18

Haematomas are formed deep within the brain tissues and are usually caused by shearing or tensile forces that mechanically stretch and tear deep small caliber arterioles. Found in the frontal and temporal lobes 85% of the timel. Only isolated in 12% of cases

Question 19

Discuss primary brain injury

Answer 19

Mechanical damage that occurs at the time of head trauma and includes brain laceration, haemorrhages, contusions and tissue avulsions.

Question 20

Discuss secondary brain injury

Answer 20

Results from intracellular and extracellular derangements that lead to alterations in cell function and propogation of injury through processes such as depolarization, excitoxicity, disruption of CA homeostasis, free radiacl generation and BB disurption.

Question 21

Discuss secondary brain insults

Answer 21

Hypotension

• defined as SBP less than 90mmhg,
• severe negative impact on brain injury otucome.

Hypoxia

• Defined as Pao2 less than 60mmhg.
• Causes include
• –Transiet or prolonged apneoa caused by brainstem compression
• –Partial airway obstruction caused by blood vomtius or other debris
• –injury to the chest wall that interferes with normal respiraotry excursion
• –pulmonary injury that reduces effective oxygentation
• –ineffective airway mangement such as inability to BVM or intubate

Hypocarbia and hypercarbia

• paco2 <35 or >46 are associated with increased mortality following TBI.
• Hypercarbia causes cerebral vasodilation with a resultant increaase in cerebral oedema and ICP

Anaemia
– reduced circulating o2 increasing risk of ishcaemia

Hyperpyrexia

Question 22

Discuss uncal herniation

Answer 22

Most common significant traumatic herniation -
Often assocaited with traumatic extra-axial haematomas in the lateral middle fossa or the temporal lobe.

As compression of the uncus begins the third nerve is compressed: anisocoria, ptosis impaired EOM and a sluggish reaction to light deveople on the ipsilateral sign of the haematoma.

Contralateral haemiparesis develops as the ipsilateral peduncle is compressed against the tentorium. With continued herniation bilateral decerebrate posturing occurs

In a certain percentage of TBI the cerebral peduncele is forced against the opposite edge of the tentoral hiatus leading to ipsilateral hemipareiss. This is termed Kernohan’s notch syndrome and causes false localizing motor findings.

Question 23

Discuss subfalcine herniation

Answer 23

the innermost part of the frontal lobe is scraped under part of the falx cerebri,
Symptoms not well defined
Cingulate herniation is frequently believed to be a precursor to other types of herniation

Question 24

Discuss central trnastentorial herniation

Answer 24

Clinical deterioation occurs as bilateral central pressure is exerted on the brain from above.

The intiial clinical manigestation may be a subtke chagne in mental status or decreased GCS, bilatearl motor weakness and pinpoint pupils,

Increased muscle tone and bilatearl babinzkis

Question 25

Discuss tonsillar herniation

Answer 25

When the cerebella tonsils herniate downward through the foramen magnum. Usually the result of a cerebella mass or large central vertex mass causing rapid displacement of the entire brainstem.

Clinically patient demonstrate sudden respiratory and CVS collapse as the medulla is compressed.

Flaccid quadriplegia is the most common motor presentation because of bilateral compression of the corticospinal tracts.

Timely neurointensive care and surigcal intervention results in recovery with mild to moderate disability in 50% of pateints

Question 26

Discuss Upward transtentorial herniation

Answer 26

Occurs as a result of an expanding posterior foss lesions, The LOC declines rapidly. Downward conjugate gase accompanied by the bascence of vertical eye movements

Question 27

Discuss TRANSCALVARIAL HERNIATION

Answer 27

Displacement of brain through a defect in the skull, such as a fracture site or following craniectomy

Question 28

Discuss the clinical presentation of epidural haematoma

Answer 28

Classic presentation is described as head trauma producing a decreased LOOC followed by a so called lucid period.

If EDH is rapidly deteced and evacuated the funcitonal outcome is excellent. Due to rapid expansion they are usually diagnosed quickly specifically in children

Posterior fossa EDH is the result of direct occiptial trauma resulting ina skull frqacture taht disrupts a venous sinus. Most patient will have signs of direct occiptal truma. They become symtpomatic within 24 hours after injury with complaints of headache nausea and vomiting and nuchal rigiidty

Question 29

Discuss clinical presentation of SDH

Answer 29

If the patient was rendered unconscious at the time of trauma the prongsis is poor as this is often associated with TAI.

DHS are classified by time to presentation. ACute SDHs are symptomatic within 24 hours after trauma. Mortality for SDH requriing surgery is 40-60%

Chronic SDH become symptomtic after 2 weeks or more. Signs and symptoms may be very subtle or nonsepcific, many pateints will demonstrate unilateral limb weakness– this occurs more frequently in those presenting with unilateral subdurals than bilatearl

Question 30

Discuss physical examination in TBI

Answer 30

Head and neck should be examined for external signs of trauma. A scalp laceration contusion, abrasion or avulsion may overlie a depressed skull fracture. Due to the mobility of the scalp nonalignment with scalp laceration and the fracture can occur by several centremetres.

Basillar skull fracture are a clinical diagnosis- base of skull fracture place people at risk of EDH due to localitiy of the middle cerebral artery. Basilar fracturecan also compress and entrap the CNs that pass though the basal foramina. CNs 3,4nand 4

Fractures to the sphenoid can disrupt the intracavernous internal carotid artery creating the potention for the fomration of pseoduaneurysms or carotid venous fistualae.

Question 31

Discuss clinical signs of basilar skull fracture

Answer 31

Haemotympanum, 
CSF rhinorrheoa or ottohea
Battles sign 
Raccoon eys (sparing of the tarsal plate) 
CN deficit particuarly 3-5 
Dizziness 
Tinnitus and nystagmus

Question 32

Discuss GCS

Answer 32

EYE

1) no response
2) response to pain
3) response to voice
4) spont

Voice

1) nil
2) incomprehensible
3) inappropriate - random exlamatory words
4) confused
5) oriented

Motor

1) nil
2) decerebrate
3) decorticate - above midbrain injury
4) withdraw
5) localise
6) obeys commands

Question 33

Discuss CT finding in TBI

Answer 33

EDH– hyperdence biconvex ovoid and lenticular. Does not usually extend beyond dural attachements at the suture lines. THe margins are sharply defined and the haematoma usually buulges inward toward the brian. EDHS of mixed density may indicate active bleeding. Posterior EDH is the most common tramatic mass lesion of the posterior fossa.

SDH - Extend beyond suture lines and may follow the contous of the tentorium. On Ct chronic subdrual may appear iso or hypodense to brain tissue. Midline shift effacement of the ipsilateral cortical sulci and ventricualr compression may occur.

SAH- Blood seen within the interhemispheric fissures and sulci

Subdrual hygroma – crescent shaped in the extra-axial space with density the same as CSF. Bilateral SDHGs are common

TAI- in mild cases nil MRI or CT evidence

Cerebral contusions- Heterogenous and irregular due to mixed regions of haemorrhage necrosis and infarction. Often the surrounding oedematous tissues appears hypodense

Intracerebaral haematoma – Unlike contusions ICH are usually deep in the brain tissue and ogten become well demarcated over time

Cerebral oedema – diffuse oedema manifests as bilateral compression of the ventricles loss of defintiion of the cortical sulci or effacement of the basal cisterns

Question 34

Discuss Rotterdam Score

Answer 34

Initial noncontrast CT for predicting 6 month mortality follwoing traumatic brain injury

1) basal cistern effacement
-0 - none
-1 - partially effaced
2- completley effaced

2) midline shift
0 no midline shift or <5mm
1- >5mm of midline shift

3) EDH
0- EDH present
1- no EDH

4) IVH or SAH
0- neither present
1- either present
2- add 1 to score

Question 35

Discuss the Ottowa subarachnoid rule

Answer 35

Very specific inclusion and exclusion criteria

• only apply in alert patients > 15years of age, new atraumatic sever headache with maximum intensity within 1 hour
• do not use if neurological deficit, prior aneurysms, prior SAH, known brain tumor or chronic recurrent headache (> 3 headaches of the same character and intensity for >6 months

If -ve to all of the following can be ruled out of SAH with 100% sensitivity

1) over 40
02) neck pain o0r stiffness
3) witnessed LOC
4) onset during exertion
5) thunderclap headache (peaking pain within 1 second)
6) limited neck flexion

Question 36

Discuss hunt and hess classification of SAH

Answer 36

Grading system base on clinical findings to predict mortality with SAH

1) Mild headache and oriented, minimal if any nucal rigidity - grade 1 30%
2) Full nuchal rigidity, moderate to severe headache, alert and oreinted with out CN deficit 40%
3) Lethargy confusion, mild focal deficit 50%
4) Stuporous more severe deficit 80%
5) Comatose, showing signs of severe deficit (posturing) 90%

Question 37

Discuss prehospital treatment of TBI

Answer 37

1) airway - controversal if securing airway in the field is benificial –> failed attempts definitly bad
- ultimate goal is to prevent hypoxia
- if short way to ED and oxygenation can be achieved should not intubate
- should be skilled operator with quality assurance measures and ETCO2 to ensure tube placement

2) Hypotension – avoid, look for signs of bleeding

Question 38

Discuss managment of TBI in the ED (airway, hypotension, brain directed hyperosmolar agents and hyperventilation)

Answer 38

1) airway - can have both primary and secondary loss of airway (trauma, bleeding and vomiting) (loss of brainstem reflexes, agitation, severe systemic hypotension
-if possible rapid but detailed neuro exam should be performed prior to the patient being given sedative or blockers
-
Hypotnesion - avoid, single episode of hypotension doubles mortality risk. Fluids and blood products as needed

Brain directed hyperosmolar therapy
- if signs of impending herniation ie. deepening coma, unequal pupils di
minishing neuorlogcial parameters the use of osmotic diuretics, mannitol or HTS is indicated.
-HTS given as a bolus is more effective than mannitol in lowering cumulative daily ICP eleavations
-proposed benefits of HTS include reducing secondary injury through effect son cellular modulation, decreasing cerebral oedema, improving peripheral perfusion and decreasing ICP. 30mls 23.4%

Hyperventilation
- Under normal circumstances Paco2 is the most powerful determinant of CBF between a range of 20-80mmhg there is a linearly responsive relationship between CO2 and CBF. Previously hyperventilation was was implored however the reduction in ICP that was achieved with this is due to reduction in CBF which can reduce perfusion. Hyperventilation can be used as a temporising measure if patient is about to herniate

Question 39

Discuss management of TBI in the ED(Cranial decompression, haemostatic agents, induced hypothermia, seizure prophylaxis, Ab prophylaxis, GLucose)

Answer 39

Cranial decompression
-In patient with impending herniation who do not respond to osmotic therapy and hyperventilation emergency cranial decompression may temporarily reverse arrest or herniation. Emergency trephination may temporise a patient to allow formal craniotomy
Only used if EDH found on CT and with appropriate skilled people.

Haemostatic agents

• Those on warfarin may be managed with prothrominex, vitamin K and FFP
• Idarucizumab – reversal for dabi
• TXA is useful in haemorrhagic trauma in general if given within the first three hours. However for patient with isolated head injury without systemic injuyry nil benefit and can be harmful

Induced hypothermia

• • Hyperpyrexia worsens outcome after severe TBI and guidlines ephasize maintaining normothermia with antipyretic medications and cooling deviced
• Induced hypothermia shows nil superior outcome compared to strict temperature control

Seizure prophylaxis

• Post traumatic seizures are defined as early if they occur within 7 days of injury or late when they occur after 7 days
• Post traumatic epilepsy is defined as recurrent seizure more than 7 days following injury
• 12% of blunt and 50% of penetrating head injuries develop seizure
• Early seizure are not an indication of future epilepsy they do howvere cause hypoxia, hypercarbia, release of excitatory neurotransmitters and increased ICP
• Recommended to use for the first 7 days of TBI
• If actively seizing treat as per normal

Antibiotic prophylaxis

• Blunt doesnt need
• Penetrating , gent, vanc and metronidazole cover
• invasive devices also cover for good measure

GLucose

• hyperglycaemia and hypoglycaemia are both associated with worse outcomes in TBI
• Should start to feed these patients at least at day 5 via NJ tube

Question 40

Discuss management of scalp wounds

Answer 40

Blood loss can be brisk and if is haemostasis is prioity.
Stapler is a useful tool to rapidly control bleeding, if need the wound can be re-opened cleaned and explored once stasis is achieved.

The emissay vessels of the subgaleal layer of the scalp drain directly into the diploe veins of tghe skull and into into the venous sinus. Contamination or infected scalp wounds ahve the potential to cause serious intracranial infections. Clots and debri should be removed prior to closure.

It is relatively easy to confuse a disruption in the galea or tear in the periosteum with a skull fracture, As such the base of the laceration should be visualised directly

Staples are as effecacious as sutures for laceration that does not involve the galea. Staples cannot be used to close teh galea and may not be effecitve alone in achieving haemostasis. Usually one layer of horizontal or vertical mattress suture is sufficient for closure of scalp wounds involving the galea

Question 41

Discuss management of depressed skull fractures

Answer 41

Edge of adjecent bone of depressed skull fracture can become lodged under the adjacent intact bone and may not reduce to anatomical location

They are usually open fractures with disruption of the galeal layer. THis can be felt with palpation but should be cautious as cna worsen the depression.

Exam can be misleading due to mobility of the scalp laceration may be several centremetres from a potentional depressed fracture

All patient with depressed skull fracture are at risk for infection adn complications and should be admitted for observation

If depression greater than the thickness of the cranium should undergo surgery to prevent infeciton

Indications for nonoperative management

• no clinical or radiographic evidence of dural penetration
• nil significant intracranial haematoma,
• no depression greater than 1cm
• nil frontal sinus involvement
• nil gross cosmetic defect
• nil pneumocephaly
• nil gross wound infection

Abs to all open

Question 42

Discuss management of basillar skull fracture

Answer 42

Large force
should be suscipcious of EDH in temporal bone fracture
Dont need routine prophylaxis of ABs for BOSF whether or not there is CSF leal

Most CSF leaks resolve spontaneoulsy wihtin a week
If persist for more than a week risk of bacterial menigitis is much higher and ABs should be used

Question 43

Discuss management of extra axial lesions

Answer 43

EDH - surgical intervention for anyone with mass effect or deterioation in GCS

• Urgent surgical intervention include
• EDH larger tahn 30cm volum, comatose patient or those with aniscoria
• For those awake with nil focal defecit nonsurgical management is based on the size of the haematoma (<30cm3) thickeness of clot >15mm and degree of shift <5mm

SDH
-IF patient is deeply comatose at presentaitojn supportive care may be best option - discuss with family
-Small SDH is often amenable to serial observations and appearance of the SDH on CT
Indication for surgical indications include:
1)acute SDH with a thickness of more than 1cm or a midline shift of more than 5mm regardless of GCS. 2)Worsening GCS >2 points from admission, 3)assymetrical pupils
4) GCS <8
5)persistant elevation in ICP

SAH

• tSAH wihtout other brian injury itself does not carry that grave of a prognosis
• Most serious compications is vasospasm whihc may be severe enough to induce ischaemia
• Post-traumatic vasospasm is common occurring approximatly 48 hours after injjry and persisting for up to 2 weeks

Question 44

Discuss CNS complications of TBI

Answer 44

Seizure- as discussed above

Meningitis of BOS fracutre

Brain Abscess - missle to head and open depressed skull fractures - clinical manifestations include headaches, nausea and vomtiing, declining mental status, signs of increased ICP and new focal neruolgoical findings in patients who had been imprving after trauma

Cranial osteomyelitis
-Usually seen after penetrating injury to the ksull

Question 45

Discuss medical complications of TBI

Answer 45

DIC- The injured brain is a source of tissue thromboplastin that activates the extrinsic clotting system. Can develop within hours after any injury disrupting brain tissue

• Coagulation abnormalities including DIC are detected in over 50% of patient with traumatic brain injury
• DIC increases the risk fo delayed ICH if pattient with DIC suddenly deterioates a repeat CT should be obtained to rule out haemorrhage
• High risk of VTE in moderate to severe TBI and can be safley treated with LMWH

Neurogenic pulmonary oedema

• Can develop within minutes to hours after head trauma
• PAthogenesis theroies include
• -catecholamine surge or blast from the TBI increasing intravascular pressure, cap permeability and hydrostatic oedema
• -systemic inflammatory reacition leading to endothelial damage and vasogenic oedema
• difficult ot manage in TBI as permissive hypercapnia, fluid restirction and prone ventilation are contraindicated in TBI
• Can use high Peep if adequate intravascular volume and MAP
• Controlling ICP can control the stimulus for the developement of neurogenic pulmomary oedema

Cardiac dysfunction

• A variety of cardiac rythym rate and conduction abnormalities are detcted after TBI
• cardiac abnormalities have been reported in up to 70% of patient with tSAH and more than 50% fo all patient with traumatic intracrnail haemorrahage
• Most common is SVT
• ECG finding incluyde large uptright or inverted twaves,QT intervals prolonged, depressed ST segments and u waves

Question 46

Discuss indication for intubation of head injury

Answer 46

• Altered GCS and loss of airway reflexes
• Oxygenation
• Ventilation
• Control of agitated patient
• Facilitate investigation

Question 47

Discuss canadian CT head rule

Answer 47

Only applies to patient with GCS 13-15 and at least on of the following

• LOC
• Amnesia to head injury event
• witnessed disorientation

Exclusions

• Age <16
• blood thinners
• seizure after injury

High risk criteria rules out need for neurosurg intervention

• GCS <15 at 2 hours post injury
• Suspected open or depressed skull fracture
• any sings of basilar skull fracture
• > 2 episodes of vomiting
• Age >65 years

Medium risk -Rules out need for CT

• retrograde amnesia to the event >30 minutes
• dangerous mechanisms (struck by motor vehicle, occupant ejected, fall from>3 feet or >5 stairs)

100% sensitive for both clinically important brain injuries and injuries that required neurosurg intervention

Question 48

Compare and contrast CCT, neworleans and nexus 2 for CT of head

Answer 48

CCT sens 99%, spec 47%
New Orleans sens 99%, spec 33%
Nexus 2 97% sens, 47% spec