Dr Zaw Myint16 . 7 . 2014

Trauma Vs total admission , 2013

Trauma Vs total admission , Jan – Jun 2014

RELEVANT ANATOMYRELEVANT ANATOMY

Scalp - skin - subcutaneous - aponeuonerosis

- loose areolar layer - periosteumSkull boneMeninges - dura mater - arachnoid mater - pia materBrain tissue

AETIOLOGYAETIOLOGY

RTA >50%

MECHANISMMECHANISMMobility of brain in relation to skull & membranes

because of firm attachment to skull by dura mater, falx cerebri & tentorium, if the brain moves against them , there is damage to brain.

Configuration of interior of the skullrough surface in ant: fossa, sphenoidal ridge , and also at falx & tentorium with sharp edges

Preexisting state of the brainaging brain has less reserve than the younger brain

Deceleration & accelerationCoup & counter coup

CLASSIFICATIONCLASSIFICATION

* Scalp injury -contusion -abrasion -haematoma - subcutaneous -

subaponeurotic/subgaleal - subperiosteal -laceration / incised -avulsion

* Skull injury ( fracture ) - open / closed - vault # / basal # - linear / depressed / comminuted

- Basal # -ant: cranial fossa …. Panda bear , CSF

rhino -mid: cranial fossa…. Battle, CSF oto

* Meningeal injury ( haematoma ) - extradural - subdural - subarachnoid

- intracerebral

* Brain injury - primary - cerebral concussion - cerebral contusion - cerebral laceration - diffuse axonal injury (DAI ) - secondary

Causes of secondary brain injury

■ Hypoxia: PO2 < 8 kPa■ Hypotension: systolic blood pressure (SBP)

< 90 mmHg■ Raised ICP > 20 mmHg■ Low CPP < 65 mmHg■ Pyrexia■ Seizures■ Metabolic disturbance

Brain metabolismBrain oxygen consumption is about 3.5 ml/ 100 g/min.

Cerebral blood flow and autoregulationapproximately 55 ml/ 100 g/minmaintained at a constant level via cerebral

autoregulation, in MAP of between 50 and 150 mmHg.

In TBI,autoregulation become disordered.Cerebral blood flow then fluctuates with MAP and the brain is mor e vulnerable to hypotension.

PATHOPHYSIOLOGYPATHOPHYSIOLOGY

* Rigid box* Content about 1400 - 1600 ml brain cellular space 65 - 70 % interstitial space 10 - 15 % blood 5 % CSF 5 %* Intracranial volume is relatively constant.* Any increase in vol: in one space leads to

decrease in others.

Monro-Kellie doctrine

Kellie, George Monro, secundus, Alexander

A doctrine stating that any increase in the volume of the cranial will elevate intracranial pressure and that an increase in one element must occur at the expense of the others.

Description In 1783 Alexander Monro deduced that the cranium was a "rigid box" filled

with a "nearly incompressible brain" and that its total volume tends to remain constant. The doctrine states that any increase in the volume of the cranial contents (e.g. brain, blood or cerebrospinal fluid), will elevate intracranial pressure. Further, if one of these three elements increase in volume, it must occur at the expense of volume of the other two elements. In 1824 George Kellie confirmed many of Monro's early observations.

Bibliography A. Monro:

Observations on the structure and function of the nervous system. Edinburgh, Creech & Johnson 1823, page 5.

G. Kellie:An account of the appearances observed in the dissection of two of the three individuals presumed to have perished in the storm of the 3rd, and whose bodie were discovered in the vicinity of Leith on the morning of the 4th November 1821 with some reflections on the pathology of the brain. The Transactions of the Medico-Chirurgical Society of Edinburgh, 1824, 1: 84-169

CPP = MAP - ICP( 70 – 80 ) = ( 80 – 90 ) - ( 5 – 15 ) mmHg

CPP < 50 mmHg cerebral ischaemia

CPP < 30 mmHg death

ICP CPP Brain herniation As EDH enlarges , it pushes the temporal lobe medially causing herniation of uncus & hipocampal gyrus into tentorial opening . ( Tentorial or uncal herniation ) If Pr: increases further, medulla & cerebellum are forced downwards into the foramen magnum.( coning )

Uncal herniation syndrome

- decreasing level of consciousness - early dilatation of ipsilateral pupil - contralateral hemiparesis due to decussation of decending pyramidal tract with deep tendon hyperreflexia & Babinski’s sign.

With severe intracranial hypertension, Cushing’s response may occur –

- systolic hypertension - sinus bradycardia - respiratory depression

situation deteriorates further if ventilation is impaired, as hypoxia produces additional cerebral swelling. Hypercarbia results in vasodilatation of the blood vessels in the uninjured parts of the brain, thereby increasing intracranial pressure.

Hypotension & hypovolemia

Eliminate hypoxia and hypovolaemia; each can

alone induce coma. If they are coupled with head trauma, mortality increases.

Features of increased ICP symptoms - headache

- nausea, projectile vomiting- drowsiness- blurring of vision- fit

signs - Cushing’ triad- papilloedema- fall in GCS- uncal herniation syndrome

Focal neurological deficit

MANAGEMENTMANAGEMENTPrimary survey with resuscitation

A - clear & protect AIRWAY , control cervical spine B - assess & maintain adequate BREATHING C - assess & maintain adequate CIRCULATION D - briefly assess neurological function, DISABILITY E - EXPOSE the whole body, check the

ENVIROMENT

Multidisplinary team approach

Q. At the scene of an accident tracheal intubation may have been carried out. What evidence is there that this benefits head injury patients?

A. Clear evidence is elusive. A widely accepted view is that intubation should be carried out ‘as soon as safely possible’ in selected patients. When transport times are long and trained personnel are available such management seems logical. In this context the adverse effects of transporting a severely head-injured patient with a compromised airway outweigh the possible complications of intubation in the field.Scoop and run Versus Stay and play

Q. Will intubation and ventilation in these circumstances require the patient to be anaesthetised? If so, what techniques and drugs would you use and why?

A. The patient will require to be anaesthetised, even when consciousness is already impaired, to minimise the risk of secondary brain damage due to induced raised ICP (intracranial pressure). Rapid sequence induction and intubation is the recommended technique using a combination of sedative with low cardiopressant effects (e.g. midazolam, ketamine), analgesic (fentanyl) and muscle relaxant (e.g.succinylcholine) agents.

Q. What pathophysiological process makes it unlikely that isolated intracranial injury would cause hypotension?

A. It takes only 100 to 150 mL of intracranial blood loss to cause brain death by herniation. Thus hypotension normally signifies extracranial injury.

Q. Do you know of the commonly quoted exception to the above rule?

A . Only in newborn infants and babies can intracranial haemorrhage result in significant hypotension.

Disability

AVPU, GCSpupillary size and reactionLateralising signmotor functionScalp bleedinghypoglycaemia, alcohol and drug abuse

Adjuncts to the primary survey

■ Blood – FBC, urea and electrolytes, clotting screen,

glucose, toxicology, cross-match■ ECG, pulse oxymetry■ Two wide-bore cannulae for intravenous fluids■ Urinary and gastric catheters■ Radiographs of the cervical spine and chest

Secondary survey

H/O - from pt or witness - mechanism of injury

- Use of airbags, seat-belts, crash-helmets - Neurological state and vital parameters

at the scene and during transport - Estimated blood loss

- past medical history - use of alcohol, drugs

P/E - scalp - face … eye, ear, nose - vital signs - motor status - GCS

AMPLE

Paediatric GCS for children under five years of age

Feature Scale ScoreResponses Notation

Eye opening Spontaneous 4To voice 3To pain 2None 1

Verbal response Orientated/interacts/follows objects/smiles/alert/coos/babbles words to usual ability 5Confused/consolable 4Inappropriate words/moaning 3Incomprehensible sounds/irritable/inconsolable 2None 1

Best motor response Obey commands/normal movement 6

Localise pain/withdraw to touch 5Withdraw to pain 4Flexion to pain 3Extension to pain 2None 1

TOTAL COMA ‘SCORE’ 3/15 – 15/15

GCS 13 - 15 …….. Mild 9 - 12 …….. Moderate 3 - 8 …….. Severe ( < 8 - coma )

To consider - treat the pt as OPD / In pt

- need investigation / stable for it / X ray or CT

- consult neurosurgeon / transfer- urgent OT

It depends on- severity- local facilities

Criteria for admission- GCS < 15

- GCS 15, additional risk factors

- N,V

- persisting post-traumatic amnesia- fit after injury- focal neurological signs in limbs & pupils- irritability or abnormal behavior- recent skull #- abnormal CT

- significant medical co-morbidity or social problems

Investigations

1. Skull X ray

Indications – mechanism of injury is not trivial - unconsciousness

- vomiting, amnesia - full thickness laceration of scalp or

boggy haematoma - medico legal evidence

Linear Linear FractureFracture

Vessel Vessel groovegroove

Suture Suture lineline

DensityDensity Dark Dark blackblack

GrayGray GrayGray

CourseCourse StraightStraight CurvingCurving Along Along suture suture lineslines

BranchingBranching Usually Usually nonenone

Often Often branchingbranching

Join with Join with other other suture suture lineslines

WidthWidth Very thinVery thin Thicker Thicker than than fracturefracture

Jagged Jagged and wideand wide

Risk of intracranial haematoma in head injury

GCS Skull fracture Risk

15 _ 1 in 31300

+ 1 in 81

9 - 14 _ 1 in 180

+ 1 in 5

3 - 8 _ 1 in 27

+ 1 in 4

2. CT scan

NICE guidelines for CT in head injury■ GCS < 13 at any point

■ GCS 13 or 14 at 2 hours

■ Focal neurological deficit

■ Suspected open, depressed or basal skull fracture

■ Seizure

■ Vomiting > one episode

Urgent CT head scan if none of the above but:

■ Age > 65

■ Coagulopathy (e.g. on warfarin)

■ Dangerous mechanism of injury (CT within 8 hours)

■ Antegrade amnesia > 30 min (CT within 8 hours)

TREATMENT PLANNING Mild ( GCS 13 - 15 )

- GCS 15, no criteria for investigations D/C with information

- criteria for X ray (+) skull x rayno # observation # CT & admit - if

criteria for CT (+), no need for X raynormal CT observe for at least

one night abnormal CT discuss with neurosurgical unit

Moderate ( GCS 9 – 12 )- urgent CT

abnormal CT urgent transfer

normal CT exclude other causes of GCS if (- ), discuss with neurosurgeon

transfer / observation at A&E

if GCS still decreases

transfer

Severe ( GCS 3 – 8 )- immediate discussion with neuro: unit & transfer

- if motor response 5 or 6 no need ventilation maintain SaO2>95%,Pco2<6kPa,Po2>12kPa at FiO2 40%- if motor response 4 or less

ETT & ventilation, maintain Pco2 4 – 4.5kPa, MAP at least 90 mmHg

- if transfer is inappropriate ( eg. d/t severe co-morbidity ),

keep pt at local ICU & continue neuro: consultation.

Medical management

Head up 300 if spinal clearance allows .Ensure that the cervical collar doe not

obstruct venous return from the head.Maintain normocapnia : PCO2 4.5–5.0 kPa.Hyperventilation ??Avoid hypotensionSedation +/– muscle relaxantDiuretics: furosemide, mannitolBarbiturte, thiopentone

NormothermiaSeizure controlSteroids - associated with increased

mortality and should not be used.Antibiotics, ATT, ranitidineCare of unconscious pt

Sedation & analgesia

-decrease the reaction of the brain to stimulation-reduce the incidence of seizures-blunt autonomic responses to TBI-propofol and remifentanil, or fentanyl-midazolam or diazepam with fentanyl

Mannitol

-it stays in the vascular compartment and creates a temporary osmotic gradient-serum osmolarity exceeds 320 mOsmol-0.3 g/kg intravenously, in 15 to 20 min

Hyperventilation

-causes cerebral vasoconstriction thereby lowering CBF and consequently ICP-may result in hypoperfusion-PaCO2 between 30 and 35 mmHg is usually safe

Barbiturates

-thiopentone and methohexital-reduce cerebral metabolism and lower ICP-S.E - hypotension, hypothermia, immunodepression and infection-Continuous EEG-recording is suggested

Q. What particular type of infection is associated with the use of barbiturates in head-injured patients?A. Respiratory infection.

Q. Give two reasons why this might occur with barbiturates.A. Reduced respiratory ciliary activity and immune function.

Q. What other class of drug which has been used in the management of severe head injury has been reported to have a similar side effect?A. Steroids.

Hypothermia

Moderate hypothermia reduces cerebral metabolismthree phases- induction -temperature down to 34 °C quickly- maintenance phase- rewarming phase- slow and controlled warming

Anticonvulsant

-phenytoin and carbamazepine-reduce the liability to early seizures-A seizure in the comatose patient is a lifethreatening emergency

Q. A head-injured patient, several hours after evacuation of a large extradural haematoma, has his sedation reduced to allow neurological assessment prior to extubation. He is observed to start having a generalised seizure. Presuming ABCs are addressed, outline your pharmacological approach.A. An intravenous bolus dose (10 mg or more) of diazepam will probably abort the seizure. An intravenous infusion of phenytoin should then be commenced.

Q. Outline your ongoing management of the phenytoin therapy?A. Phenytoin should be given no faster than 25 mg/min (as it is cardiotoxic) until the loading dose (usually 1000 mg in an adult) is given. Then start a maintenance adult dose of 250–300 mg per day as guided by clinical response and the plasma level of the drug.

Q. If the patient’s convulsions do not stop within 30 minutes, outline further pharmacological steps.A. Consider thiopentone (thiopental) (a 200 mg bolus followed by an infusion of 5–15 mg/min). Clonazepam can be used if the seizures are mainly focal.

Other pharmacological agents

-agents are tested e.g. blockade of glutamate receptors, scavenging of free radicals, and blockade of calcium channels

-More recent research has moved toward the test of drugs, hormones, and other endogenous substances for multiple neuroprotective mechanisms.

Monitor- level of consciousness by GCS

- pupils - size, symmetry & light response- motor power – symmetry & pattern of limb movement- vital signs - BP, PR, RR, T-Pulse oximetry-3-lead-ECG-Capnography (ventilated patients)

Q. How frequently should such monitoring be performed?

A. As frequently as indicated by the patient’s condition. In a recently admitted or unstable patient, recordings every 15 minutes (or more frequently) are desirable.

ICP monitoring

should be placed in GCS less than 8T (after resuscitation)

EVD, intraparenchymal fibreoptic catheter, epidural

may be discontinued when the ICP remains in the normal range within 48-72 hours of withdrawal of ICP therapy or if the pt is following commands.

Surgical treatment- for scalp injury

- for # e.g.. depressed- for intracranial h’age

exploratory Burr holecraniectomy

- for increased ICPCSF drainage via ventriculostmyDelayed evacuation of swelling contusionDecompressive craniectomy

Exploratory Burr hole

Without CT, exploratory Burr holes are made under GA at following sites – - first should be placed over skull # site - if EDH (-), repeat in temporal, frontal & parietal regions starting on site of first dilated pupil - if (-), same procedure should be repeated in opposite site

COMPLICATIONSCOMPLICATIONS

Immediate- extradural haematoma

- subdural haematoma- intracerebral haematoma - cerebral contusion with

oedema & ICP

Intermediate - infections ….. meningitis

abscesses - - post traumatic fits

Late- aerocele- CSF fistula

- hydrocephalus- persisting neurological deficit

- psychiatric sequelae- post traumatic syndrome

nausea, giddiness, lethargy, etc

Glasgow Outcome scores (GOS)

Good recovery 5Moderate disability 4Severe disability 3Persistent vegetative state 2Dead 1

Q. What factors are most likely to affect outcome?

A.-the nature and extent of intracranial and extracranial damage-the depth and duration of post-traumatic coma-the patient’s age-general medical health and previous state of function-the quality of available clinical care.

PREVENTIONPREVENTION

Primary prevent of accidentsSecondary reduce the effect of collisionTertiary improve the medical care