Suf m-emrg~ servingaEO-i

ABC of Major Trauma

HEAD INJURIES-I Ross

Grah

ulo

Characteristis of patients with head ijurnes attendg accident and emr gency deartmaret in Scotland Numbers are percentages of

patients 70

Male Adult

60

Recenty drunk alcohol Type

of

scalp

suffded

injury:

40

iaceraton

Skull fracture Conscio

people cma ezprc a hed iry-

250000

25

2 eaCh

Neer unconsciu

e

3-5

14 16

Sport

12

Work

8~

i.bcof

all

(le

sfihixm

admit

the

only 1% of the

into a

is;-lcid O cnm docrors can

United wswitciusdwiked

18

Role of cident and em ge.ydepartment in aagemnt e of head * Resuscitate, diagnose, and record * Detecto exclude other- injries * Request, supervise, an interwet r-esult of radiography and oh

investj

num

A

life dLa 5%Y)j who

m diuy a

an

yearwhorhave

arm

MOsr

&r being

m _ § oe a c~1 C8befif hhmu T

nou

each

2

ti theus

enlfr-q

15 at'

Fall Assaul Road traffc acckden Domesm

but

yea

5

oftheirwork.

injured,but head

s

Recovered from amnesia Impaired Cause of injury:

ab

to

'~~~~~~~~~~x emd

inital

I

_hfd

asb

m

i

the dcdpmn ciagt dF vvWfKKS C r na a y=WSif~~~~~~~~~~~~m Fiji ai rF,, 1stx kwled ofte lf.2 iif

s

* Decide ifadmission is needed and i so, where * Laise with oher speciaies-for exame, neurosrgy-aboutserou cases

* Ensure adequae rangemet for observing and maintaining patients condition during transferto other deparument or hospis * Observe progress of patients with ninor inquris, who should be ated to short stay beds

* Ensure adequate arrangenentsforfollow up

Mechanisms of brain damage Thifuse

dmagie

The brainiS pjOfiy ancfred reners

it lable to

nwe

within

within the skull and its the skull

Contact between the surf-ace of the bi

bruising

Causes of btrain damage aftersevere head injury.

(COUtusl),

at

in

and the nuciersku

frotal and

Distotion ofth brain caued by and

tearing of axonal

inory

manfestsisefasmi

fibr

tx

;

are

widhin

widesprea

soff

imsianal

rcp

sewc

seI

resjomsto,

Is to s white

nmtter.

rracto s,

Smceh &fhue

basatlathesieof bum

IorespOsibeforthe

ikI

s;echnO

ury

-s ZBof

bb_s be _ momlafi

mnwb*".

BMJ

vourir

30()

9 JuE 1990

1515

M-~

Focal

iw~~.adwg

Skafifmcum-At the point of impac *./::

:; ?

s

Rmay oocur

Such

ahuls because of A

m

compound depressed

aceraes

A

I

linear

a

a

elastic skulls.

fiacur

results when

sharp blow

vioent

a

dfactue is also a

nli

fractur

cranw

ek-vat and

pmmX PK

an-

the riOf this

inr

the skull deforms inwards and kss comon in dchkhe than in

anal cviy, scalp and drives bone frMts to the tarin te hdma maer This ijury is an impornt source of

ri wnal

mosedsomllf,

are

the

d6e_6dementL A

Cbmapooltdidep

fiactures

is

n

cause of

epilpsy, but

by surcal treamtmt.

inu

chiefy

is

poweu

as an

wondary

indicar of

iedk

Ib-The inbending of the create a sace in which an extraduralhxoa develos. This can be asKiated withFitte brain dmg,and optimal m off underying dura and

kul may

_tolity and morbidity due to

shou

-cndr cenrdal __ trea

LJWt pmonotmcd

with co

vn

I

um

peso.Delayed sibecerebral

nt can cause

dama

eMKh^

midlin

shiftad

aci

n4

maSubdural and erebral common

bleeding are four times

than

tore

exuraduria

They

tearing of cerebral veins or from laeainof the braini's surface, or both. An

result from

associatio

common,

brain

wth

damage

is

be

but the outcome may

good if an opetio

is

perored prompty.

nUSK1 1caused by a a on to the 'contra-xpt W*.y).

NMIowoI----M,mmm

occipt (.a

Hypoia

Tuhe

and

ischaaemia

brain requirs

cotiuous

perfusion with wel oxygenated blood.

Fle atic neuroihl dmage ocrs if this is reduced below critcal thrshold for more tn afew minutes. Nmally the brain regulates a

in consunt perfusion desite wide varions its own blod supply to blood pressure; when injured, the brain loses thi capacityandis

in sys

thus particury vunrable to hypoxia occur.

ic dama

w

hypotension or

A reduction in mean arterial blood pressue to belkw 60-80 mm Hg, particularly when

kmad i

d}I sdty isd

neIunes

patients t);,

artyjxDia

sten,

(1it3.

d

y

ause

ut

may become severey shocked mafter

ic

Muliply injured injury.

C When a head injury is sever enough to produce respiratr disder and badycardia occur and are a potent cause of

Sishaemic

iury

1516

, pressure is for more than a few

l

int

neuronal damag if

owing

g.

to

The

-m

aiway is often

mobstrution

or loss

immediatey after

of protective rflexes.

BMJ vOLumE 300

9 JUN 199

Causes of raised intracranial pressure after head injury * Haematoma * Focal cerebral oedema related to a contusion or haematoma * Diffuse oedema after ischaemia

(cytotoxic) * Diffuse brain swelling ("brain engorgement") * Obstruction of cerebrospinal fluid pathway (this is rare)

Raised intracranial pressure About 70% of patients persistently in coma after severe head injury have raised intracranial pressure. This jeopardises cerebral perfusion because cerebral perfusion pressure is equal to mean arterial blood pressure minus intracranial pressure. As intracranial pressure rises cerebrospinal fluid is driven out of the intracranial compartment-the first stage in compensation. As the pressure continues to rise brain shifts occur within the cranial cavity. The most important of these brain shifts is uncal transtentorial herniation or "coning." This causes impairment of conscious level, development of a fixed dilated pupil, and brain stem compression with cardiovascular and respiratory abnormalities.

Midbrain sectioned at level of third cranial nerves shows uncal transtentorial herniation or "coning." Note bilateral "notching" of third nerves due to compression against tentorium.

Tonsillar ' herniation

Consequences of unrelieved brainstem compression: "flame shaped" brainstem haemorrhage with irreversible damage to vital centres.

tentonal herniation

Intracranial contents within closed skull show shifts in response to haematoma.

Management of head injuries For patients with a depressed conscious level the first priority is to stabilise circulation and respiration and prevent further secondary cerebral damage. The risks of secondary complications then need to be assessed and a decision made regarding transfer to a neurosurgical centre. Glasgow coma chart.

Additional factors In addition to the factors recorded on the Glasgow coma chart the following should be recorded: * Pupil diameter and reaction to light * Pulse and blood pressure * Temperature and respiration * Movement of all limbs

BMJ

VOLUME 300

9 JUNE 1990

All patients require ongoing recording of conscious level (by the Glasgow coma scale)-the best motor response should be used.

To exclude traumatic

tetraplegia the response to painful stimuli should be tested by supraorbital nerve compression if limb responses are absent. Patients observed may be either in hospital or, in certain cases, at home, provided that the patient can be discharged into the care of a responsible adult.

1517

Management of patients who cannot talk Airway with cervical spine controlDefinitive control of airway; keep a rigid cervical collar on * Breathing-Analysis of blood gas tensioins (Po2>13 kPa (100 mm Hg) and Pco2