or secondarily after the adoption of those measures advocated for the
collapse stage, it matters not. Our indications with respect to
treatment are clear. The increasing intracranial pressure must be
reduced. This desideratum is preferably carried out by the ligature of a
bleeding meningeal artery, or by the occlusion of a torn venous sinus,
but unfortunately, such a course is frequently out of the question. We
have, therefore, to deal with an increased and increasing intracranial
pressure, without definite localizing features. For this condition we
have at our disposal the following measures: venesection, lumbar
puncture, and ‘decompression’ operations.
=Venesection.= I regard venesection as a valuable means of reducing the
intracranial pressure. It is mainly of use in those cases that hover
between slight compression and the fully-developed condition.
Venesection may therefore be regarded as of special advantage in those
cases that show elevation of temperature to about 101° and there ‘mark
time’. The ‘bleeding’ should be carried out after exposure of the median
basilic, external jugular, or internal saphenous veins, preferably from
the first-named site. The amount of blood to be withdrawn varies
according to the individual circumstances of the case, but, in general,
the escape of blood should be encouraged till the pulse becomes soft,
frequent and compressible. On an average, the quantity of blood
withdrawn varies from 10-20 ounces. The operation not infrequently turns
the scale in favour of the patient. Venesection may also be carried out
in combination with ‘decompression’ operations.
When applied to suitable cases and carried out with discrimination,
venesection often tides the patient over the stage of ‘crisis’. The most
careful observation is needed in estimating the quantity of blood to be
withdrawn, the pulse, blood-pressure, respiration, and temperature
affording an adequate guide.
_Lumbar puncture._ In spite of the apparent advantages of this method,
it must, I think, be acknowledged that lumbar puncture is of but little
use in reducing the general intracranial pressure. Consequently, in
spite of the fact that this procedure has been strongly recommended,
experience shows that it is of little practical use. This statement,
based on personal experience, is at variance with the opinion of some
other surgeons. For instance, de Quènu reports 7 cases of fractured
skull which were ‘cured’ by this treatment, one of them requiring to be
punctured eight times. Lumbar puncture assists the diagnosis, but I am
doubtful whether it improves the prognosis.
_‘Decompression’ operations._ ‘Decompression’ operations may be carried
out over the cerebellar fossa or over the temporal region of the skull.
In =cerebellar decompression= a suitable scalp-flap is turned down and
the trephine applied over the centre of the exposed occipital bone.
After the removal of the disk the wall of the cerebellar fossa is cut
away with the craniectomy forceps, up to the line of the lateral sinus
above, to the mastoid process in front, to the vicinity of the foramen
magnum below, and almost up to the middle line on the inner side. The
bulging dura mater is incised in a crucial manner, right up to the
margins of the osseous gap, all meningeal vessels that cross the line
proposed for dural section being under-run with a fully-curved needle
threaded with catgut. A small drainage-tube is inserted between the dura
and the cerebellum and brought out through the most dependent part of
the scalp-flap. The flap is then sutured in position. The drainage-tube
should be stitched to the skin and withdrawn twenty-four to forty-eight
hours later, according to the progress of the case.
I have carried out this operation on several occasions, but in spite of
some immediate improvement in the condition of the patient, the remote
results have been so unsatisfactory that I have abandoned the operation
entirely. The effect of this cerebellar decompression is too radical,
the medullary centres strongly object to such heroic attempts at
pressure relief.
_Temporal_ decompression, more correctly known as the
=intermusculo-temporal decompression= operation of Harvey Cushing, leads
to very different results. Previous to dealing with the technique of the
operation, it will be convenient to enumerate the advantages claimed for
this method in general.
(1) The frequency with which the bony lesion occurs in the middle fossa
of the skull.
(2) The fact that cerebral contusions are especially liable to involve
the tip of the temporo-sphenoidal lobe.
(3) The exposure of the meningeal territory and the ease of determining
the presence of an extra-dural hæmorrhage.
(4) The possibility of draining through a split muscle rather than
directly through the scalp.
(5) The subsequent protective action of the muscle in case a hernia
tends to form in consequence of traumatic œdema.
(6) The subsequent absence of any deformities, the skin incision being
carried out for the most part through the hairy portion of the scalp.
=The operation.= The hair is shaved over the temporal region, with a
wide margin to the field of operation. In other respects, those
preliminary details should be adopted which are enumerated in Chapter
II. The skin incision commences well above and behind the external
angular frontal process, is directed along the line of, but below the
temporal crest, and curves downwards to terminate just anterior to
the tragus of the ear. Pressure is applied during the formation of the
incision so as to control bleeding from temporal arteries. The flap,
comprising skin, subcutaneous tissue, and superficial temporal artery,
is turned down to a zygomatic base, care being taken to avoid injury to
the temporal vessels at the base of the flap. The temporal fascia is
then incised, parallel to but immediately below the line of the skin
incision, and the fascia also turned down towards the zygoma. The
temporal muscle is split in the direction of its fibres, from the
temporal crest above to the zygoma below, stripped away from the bone
and well retracted in both forward and backward directions. In this
procedure care must be taken to avoid detachment of the muscle-fibres
from the temporal crest. The area of bone exposed, however, should be as
extensive as circumstances permit.
[Illustration: FIG. 45. INTERMUSCULO-TEMPORAL CEREBRAL DECOMPRESSION.
_First stage._ The scalp and temporal fascia have been turned down as
separate flaps. The temporal muscle is divided in the direction of its
fibres, and the exposed bone trephined.]
[Illustration: FIG. 46. INTERMUSCULO-TEMPORAL CEREBRAL DECOMPRESSION.
_Second Stage._ The temporal muscle is retracted on either side, the
bone has been freely cut away, and the bulging dura mater crucially
incised.]
[Illustration: FIG. 47. INTERMUSCULO-TEMPORAL CEREBRAL DECOMPRESSION.
_Third Stage._ The dural flaps are turned aside, exposing the lacerated
temporo-sphenoidal lobe. A rubber drainage-tube has been inserted
beneath the lacerated brain, lying on the floor of the middle fossa of
the skull and brought to the surface through the scalp-flap.]
[Illustration: FIG. 48. INTERMUSCULO-TEMPORAL CEREBRAL DECOMPRESSION.
_Fourth Stage._ The temporal muscle-fibres have been approximated, and
the temporal fascia reunited in part. The drainage tube is seen to
emerge through fascia and scalp.]
The trephine is applied to the bone, the surgeon aiming at the angle
between the anterior and posterior branches of the middle meningeal
artery. The disk is removed, the dura separated from the bone, and the
craniectomy forceps called into requisition, the bone entering into the
formation of the temporal fossa being freely cut away, more especially
in the _downward_, forward, and backward directions--in other words, in
the general line of the temporo-sphenoidal lobe. In the upward direction
the surgeon must be more guarded, more especially when the operation is
being conducted on the left side of the head. Broca’s area of motor
speech must be avoided, for fear of its inclusion in any hernial
protrusion that may ensue.
The bulging and probably discoloured dura mater is freely incised,
preferably in a crucial manner, though the exact line of such incision
is of little importance so long as it is free in character. Needless to
say, all meningeal vessels that cross the lines proposed for dural
section must first be ligatured (by underrunning with a fully curved
needle) on either side of those lines. The four dural flaps are turned
aside and the antero-external aspect of the temporo-sphenoidal pole
exposed. A small drainage--or drain of rubber tissue--can now be
inserted along the floor of the middle fossa skull in the immediate
vicinity of any lacerated brain or blood-clot, the drain lying between
the dura and the brain, and anchored to the dura mater or muscle by a
fine catgut suture.
The four dural flaps are allowed to remain loose over the surface of the
brain, whilst the temporal muscle is sewn across from side to side with
a few catgut sutures, room being allowed at the lower angle for the
emergence of the drain.
The temporal fascia is replaced and carefully united to its upper cut
margin, the drain being brought out through the fascia and through a
puncture hole made at the most convenient part of the scalp-flap. The
scalp-flap is approximated with numerous interrupted silk or salmon-gut
sutures.
The tube is allowed to remain for thirty-six hours or more, according to
the condition of the patient.
The operation may be carried out on one or on both sides of the skull;
if on the one side only, on that side at which laceration of the brain
is probably existent. In connexion with this it is necessary to state
that laceration by contre-coup is more common than direct brain-injury.
Thus, if the blow be inflicted on the right parieto-occipital region,
the operation should be conducted in the left temporal region.
In the absence of all localizing features the decompression should be
carried out on the _right_ side of the head, in order to avoid all
possibility of including, in the hernial protrusion that may result, the
motor speech area of Broca.
In cases of severe head-injury the surgeon must be prepared for many
disappointments, but, from my own experience, it would appear that
Cushing’s operation frequently brings about the most satisfactory
results.
It should, however, be clearly understood that indiscriminate
decompression operations only bring discredit on the method in general.
They should only be carried out in suitable cases.
TREATMENT OF FRACTURES OF THE VAULT OF THE SKULL
=Indications for operation.= It is the general custom to divide
fractures of the vault into two groups--those demanding operative
treatment and those in which an expectant attitude is advised--and
between these two groups a sharp line of demarcation is drawn. There is,
however, no such line of demarcation. In the event of the general
condition of the patient being compatible with operative interference,
such treatment is urgently called for under the following conditions:--
_All_ cases of punctured fracture.
_All_ cases of depressed fracture, whether diagnosed by palpation or by
inference, whether simple or compound, whether complicated or not.
_All_ cases of fracture complicated by extra-dural or localized subdural
extravasation of blood.
_All_ elevated fractures.
_All_ compound fractures.
In all these instances, from the presence of depressed fragments of
bone, from associated injury to the intracranial contents, or from other
causes, no mere expectant policy should be pursued. The surgeon has to
look into the future, to bear in mind the possibility of meningeal
infection, and the more remote results of head-injuries in general (see
Chapter VI). In other words, early and active surgical interference is
imperatively demanded, for not only is it necessary to strain every
endeavour to save the patient’s life, but the surgeon should also adopt
those procedures which guard most effectually against the more remote
possibilities of the case.
With regard to _simple_ fractures, if it can be determined that the
fracture, whether fissured, stellate, or comminuted, is simple and
uncomplicated by any serious intracranial lesion, no active surgical
treatment is required. The determination of such conditions is, however,
quite another matter, always difficult and sometimes, from the presence
of overlying hæmatomata, quite impossible.
In the general estimation of these cases it should be borne in mind that
simple uncomplicated vault fractures are decidedly rare. For instance,
Dwight, in 145 cases of fractured skull that came to autopsy, only found
six that evidenced a fissured fracture localized to the vault. It may,
of course, be urged that these statistics are fallacious, insomuch as
simple uncomplicated vault fractures would probably not come to the
post-mortem table. Clinical evidence, however, coincides with Dwight’s
statistics, and clinical evidence shows, furthermore, that a blow
sufficing to fracture the vault of the skull almost invariably results
in further injury.
In these doubtful cases the surgeon is greatly aided in his decision by
a general review of the patient’s condition, more especially by those
symptoms which are regarded as exemplifying the clinical conditions of
concussion, irritation, and compression.
_When the fracture is associated with mild concussion_ it may be
inferred that the brain is practically uninjured, and that operative
treatment is not required.
_When the fracture is associated with severe concussion_ it may be
inferred that the brain is damaged, to a degree proportionate to the
depth and duration of the stage of unconsciousness. The question of
operation depends to a very large extent on the general condition of the
patient, and more especially on the temperature and temperature changes
(see p. 114). With a persistent subnormal temperature it may be inferred
that the brain-injury is of a very severe nature, and that operative
measures are, for the time being, contra-indicated. In the event of the
temperature rising it may be accepted that the patient is passing from
the state of shock to that of reaction, operative measures again hinging
on the further progress of the case. If the temperature rises
progressively, the patient passing from the stage of reaction to that of
compression, operative measures are indicated. Under other circumstances
an expectant attitude can be adopted.
_When the fracture is associated with general cerebral irritation_ it
may be inferred that the brain is contused or slightly lacerated. Under
these circumstances operation is, for the time being, not required, and
an expectant attitude should be adopted.
_When the fracture is associated with compression_ it may be inferred
that the condition is dependent on depressed fragments of bone, or on
extra- or intra-dural bleeding. Operative measures are now urgently
indicated.
_When the fracture is confined to the internal table_ a diagnosis is
only possible when symptoms of localized irritation ensue, either due to
pressure exercised on the cortex by spicules of bone or resulting from
injury to some intracranial vessel, e. g. the middle meningeal artery.
In such cases operation is indicated. Under other circumstances the
surgeon must await the developments of the case.
=Treatment.= _When the fracture is associated with mild concussion._
During the stage of concussion no active treatment is required, beyond
putting the patient to bed--with the head low--enveloping him in hot
blankets, and applying hot bottles to the extremities. These bottles are
wrapped up in flannel: they should never be placed in contact with the
patient’s skin. As soon as the reaction stage _commences_, the bottles
and blankets should be removed, the patient covered with light clothing
only, and an ice-bag applied to the head, over the region at which the
injury was inflicted. Calomel, in suitable doses, should be given by
mouth, and a copious enema administered per rectum. Perhaps the most
essential point in the general consideration of the case is the
after-treatment. The patient should be kept in hospital or home for at
least one month, and for the next three months or more, according to the
urgency of the case, he should abstain from all mental and bodily work.
At the end of that period of time he may return to work, though still
kept under observation.
_When the fracture is associated with severe concussion._ In the event
of persistence of concussion symptoms of a severe type the prognosis is
decidedly unfavourable. This prolongation of cerebral shock is
undoubtedly dependent in its persistence on severe vaso-motor
depression, and in the majority of cases ending unfavourably it will be
found that the brain is generally œdematous and regionally contused or
lacerated. In cases of this nature the surgeon should confine his
attention, for the time being, to an endeavour at terminating this
vaso-motor depression, raising the blood-pressure and inducing a
definite reaction; the patient being treated after the manner indicated
on p. 118.
_When the fracture is associated with general cerebral irritation._ The
patient should be put to bed in a quiet and darkened room, under the
continuous attention of a trained nurse. An ice-bag or Leiter’s tubes
may be applied to the head, though the patient seldom tolerates such
attentions. I regard morphia as of the greatest service in this class of
cases. It should be given freely, subcutaneously, either by itself or in
combination with atropin. I generally order ¹⁄₄ gr. morphia with ¹⁄₁₀₀
gr. atropin every six hours, till the irritative symptoms subside.
Insomuch as all evidence tends to prove that general cerebral
irritation, as resulting from injury, implies a condition of contusion
or superficial laceration, a prolonged period of bodily and mental rest
is essential before the patient is discharged from treatment and allowed
to return to work--a period of not less than six months.
=The operative treatment of fractures of the vault.= The usual
preparatory treatment is carried out, the scalp-tourniquet applied, a
suitable scalp-flap framed and turned down, advantage being taken of all
existent scalp lacerations.
The subsequent details vary according to the circumstances of the
case:--
=Fissured fractures.= If, after thorough exposure of the parts, the
operator is satisfied that he has to deal with an uncomplicated fissured
fracture, the scalp-flap is accurately sewn into position (see p. 16).
On the other hand, if the symptoms point to the presence of an
extra-dural hæmorrhage, the bone is trephined where the fracture crosses
the line of the suspected vessel and the conditions treated as described
under middle meningeal hæmorrhage. In subdural extravasation the
trephine is applied over that part of the brain, in the immediate
vicinity of the fracture, from which the symptoms appear to emanate, and
the conditions treated as described under subdural hæmorrhage.
In a certain proportion of cases the symptoms point to a marked increase
of intracranial pressure without definite localizing features, a
condition pointing to diffuse subdural hæmorrhage, with or without brain
laceration. Under such circumstances much may be done to relieve the
increased intracranial pressure by carrying out the operation of
‘cerebral decompression’ (see p. 121).
=Depressed fractures.= The operative details vary according to the
nature of the osseous lesion:--
(_a_) If the depressed fragments of bone are so interlocked that
elevation is impossible (e. g. pond and gutter fractures), it will be
necessary to trephine in the immediate vicinity of the depression, in
order to lessen the mutual attachment of the fragments one to another,
so obtaining sufficient purchase for their elevation or removal.
The pericranium is stripped away from the region of the depression (see
Fig. 49), and a small trephine applied in such a manner that the
trephine circle includes the outer part of the depressed area. Care must
be taken to avoid more pressure over the depressed fragments than is
absolutely necessary, for fear of causing further damage to the
underlying structures. This advice is all the more important when it is
realized that the fracture of the internal table is almost invariably
more extensive than that which involves the visible external table of
the skull.
The disk of bone is removed and the conditions investigated with the
dural separator. When the degree of depression and the splintering of
the internal table are not excessive, the parts may be elevated into
position. In most cases, however, the uncertainty that exists with
regard to possible dural injury renders it necessary that the depressed
fragments should be elevated and removed, or so raised as to allow of
adequate inspection of the dura itself. For this purpose the craniectomy
forceps may be required. The dura can now be examined. If torn, the
opening may require enlargement, in order to determine whether any
osseous fragments have been driven into the brain-substance; all such
fragments are carefully removed. Hæmorrhage is arrested, the dura sewn
up, and the scalp-flap carefully sutured. Drainage should always be
avoided, the risk of infection is too great. As a prophylactic against
the development of meningeal infection, the patient should undergo the
routine treatment with urotropin (see p. 116).
(_b_) When the depression is of such a nature that the elevation of the
fragments can be carried out without preliminary trephining, the
fragments are raised with the periosteal separator, and the membranes
and brain examined as described above.
In =simple comminuted fractures= the larger fragments of bone are to be
replaced in the anticipation that they will live entire, in part, or
will act as scaffolding media for the formation of dense fibrous tissue.
After removal from the wound, and during the completion of the
operation, the vitality of all loose fragments may be preserved by
immersion in hot saline solution. All minute fragments of bone should be
discarded.
[Illustration: FIG. 49A. THE ELEVATION OF A DEPRESSED FRACTURE. _First
stage._ The trephine circle includes the outer portion of the depressed
area.]
[Illustration: FIG. 49B. THE ELEVATION OF A DEPRESSED FRACTURE. _Second
stage._ The trephine disk has been removed and the elevator is in
position.]
With respect to =compound= fractures, it is necessary that the bone
lesion should be fully exposed, all pockets of scalp-tissue being slit
up to their termination. Previous to any attempt at examination of the
injured bone, further precautions must be taken to avoid subsequent
infection, by reason of the bruised and soiled scalp. Such tags of
scalp-tissue as appear injured beyond repair should be cut away with the
scissors, and in order to avoid or diminish subsequent wound infection,
I have been accustomed to swab over the most suspicious parts with
pure carbolic acid, washing away the same with saline solution. Since
the advent of iodine sterilization, I have often utilized that solution
in preference to the carbolic, swabbing the whole surface exposed. I
think a combination of the two methods is advisable in more serious
cases, utilizing the carbolic for the margins of the wound and iodine
for the general surface. By means of this method the risk of meningeal
infection and scalp suppuration is greatly reduced. To aid in the
prophylaxis, the patient should again be placed under a course of
treatment by urotropin (see p. 116).
With regard to the bone, all loose fragments should be removed, only
those being preserved which retain their pericranial connexions. Even
these are thrown back so as to permit of the maximum inspection of the
dura mater. This membrane, if torn, is either sewn up at once or opened
up more freely in the investigation and removal of underlying blood-clot
or bone-débris. After removing such troubles the membrane is accurately
sutured. The bone-flaps are now replaced in position. Some surgeons
advocate the replacement of the smaller fragments of bone which have
previously been removed. These fragments may be sterilized by boiling,
but such a process destroys the bone-cells and, in consequence, they
become absorbed, merely acting as scaffolding media for the formation of
fibrous tissue. Added to that, in the event of suppuration, the presence
of such fragments not only leads to the persistence of a purulent
discharge, till the fragments are entirely removed, but also increases
considerably the risk of meningeal infection.
As a summary, therefore, it may be laid down that it is necessary to
remove all loose fragments of bone, the deficiency in the vault being
rectified, if necessary, at a later date by one of the methods
enumerated in Chapter VI.
The scalp-flap is accurately sewn up with interrupted salmon-gut
sutures, a gauze or cigarette drain being inserted at the most
convenient and dependent point, to be removed at the end of forty-eight
hours or more according to the progress of the case.
=Punctured fractures.= Here there is a special liability to dural
laceration and in-driving of comminuted fragments of bone. A full
exposure of the parts is therefore absolutely essential. The trephine
can be applied in the immediate vicinity of the puncture, or, as is
often advisable, in such a manner that the punctured area is included in
the trephine circle: this latter method may necessitate that the
trephining should be carried out without the aid of the guiding
fixation-pin, for which process some experience is needed.
After removal of the bone, the craniectomy forceps may be required, to
allow of adequate dural inspection. The dura mater is opened up with
blunt-pointed scissors, and the brain examined for in-driven fragments
of bone. These, when found, are removed. Deeply situated fragments of
bone and foreign bodies may be previously diagnosed by means of an X-ray
picture.
If possible, both membrane and scalp should be sutured without drainage,
but in the event of possible sepsis, a small cigarette drainage-tube
should be inserted so as to lie beneath the dura mater on the one hand
and emerge through the scalp wound at the other.
=Fractures limited to the external table.= For this class of fracture
the reader is referred to the section dealing with bullet-wounds of the
skull (see p. 296).
=Fractures limited to the internal table.= As previously indicated, the
diagnosis of this condition is only practicable when the depression of
the osseous fragments, or the hæmorrhage resulting from an injured
meningeal vessel, so irritate the dura mater and brain that localizing
symptoms ensue. For instance, epileptic fits of a Jacksonian type may
develop shortly after the accident, this condition demanding a full
exposure of the affected region. The operations required in the
treatment of traumatic epilepsy and intracranial hæmorrhages are
discussed in subsequent chapters.
THE MORTALITY FROM FRACTURE OF THE SKULL
Whatever the nature of the osseous lesion, the mortality is almost
entirely dependent on the question of associated injury to the
intracranial contents, more especially the brain.
In the case of fractures purely or mainly basic, of the cases that have
come under my care or observation, 116 recovered and 89 died--a
mortality of 44 per cent.
Battle, from an examination of 168 cases, puts the mortality at the low
figure of 32 per cent., whilst Crandon and Wilson, from an exhaustive
series of 530 cases, estimates it at 44 per cent.
The mortality varies according to the _age_ of the patient, the
death-rate being at its maximum at the two extremes of life--between 50
and 60 per cent. under the age of 5 years and over 60 per cent. after
the age of 70.
The mortality varies also according to the _fossa_ implicated. Thus, to
each fossa there are certain peculiar dangers--to the _anterior_ fossa,
meningeal infection from the nose, frontal and ethmoidal sinuses; to the
_middle_ fossa, meningeal infection from the naso-pharynx and ear, and
hæmorrhage from the middle meningeal and internal carotid arteries, and
from the cavernous venous sinus; and to the _posterior_ fossa,
laceration of the lateral and sigmoid venous sinuses.
After such consideration of local complications, it would appear that
the middle fossa of the skull presents the greatest dangers. Another
factor must, however, be taken into consideration--injury to the
brain--the commonest cause of death in all head injuries. The main vital
centres are grouped in the region of the fourth ventricle, and Leonard
Hill has proved that any increase in the intracranial pressure exerts
its influence most rapidly and most effectually when the lesion is
situated beneath the tentorium cerebelli.
One may assume, therefore, that fractures of the posterior fossa are the
most dangerous, and that those involving the anterior fossa hold out the
best prognosis.
In the case of pure or primary vault fractures the mortality may be
estimated by reference to the following table. It is composed from 88
cases admitted into St. Bartholomew’s Hospital between the years 1900
and 1906.
Under the age of 5 8 lived and 2 died. Mortality, 20 per cent.
„ „ 10 2 „ „ 3 „ „ 60 „
„ „ 15 6 „ „ 0 „ „ 0 „
„ „ 20 10 „ „ 3 „ „ 23 „
„ „ 30 9 „ „ 1 „ „ 10 „
„ „ 40 16 „ „ 9 „ „ 36 „
„ „ 50 3 „ „ 7 „ „ 70 „
„ „ 60 2 „ „ 1 „ „ 33 „
Over the age of 60 3 „ „ 3 „ „ 50 „
59 lived and 29 died. Mortality, 37 per cent.
=============================================
For the remote effects of skull fractures, see Chapter VI.
[17] _Brit. Med. Journ._, September 11, 1909, p. 645.
[18] Chassaignac, _Plans de la Tête_, 1842.
[19] _Milligan, Trans. of the Otolog. Soc._, vol. viii, p. 69.
[20] _Boston City Hosp. Reports_, 1894.
[21] Delfau and Günther narrate a case in which death occurred from
pressure on the tenth nerve. (_Deutsche Klinik_, Berlin, 1853.)
[22] _System of Surgery_, vol. i, p. 93.
[23] _Surgical Experiences in South Africa._
[24] _Edin. Med. Journ._, 1909, p. 526.
[25] _Johns Hopkins Hospital Bulletin_, April, 1909.
CHAPTER V
INTRACRANIAL INJURIES: EXTRA- AND SUB-DURAL HÆMORRHAGES. INJURY TO THE
BRAIN
HÆMORRHAGES
I. Extra-dural hæmorrhage.
Extra-dural hæmorrhage may be arterial or venous in origin. In the
former case the blood is derived almost exclusively from the middle
meningeal artery. When of venous origin the source is usually to be
found in a laceration of one of the sinuses of the brain. When blood is
poured out from a torn sinus it tends to occupy, and be widely diffused
in, the subdural space. A venous extra-dural extravasation is relatively
of infrequent occurrence, and the pressure exercised on the brain seldom
suffices to permit of the development of local or general symptoms of
cerebral compression. On these grounds extra-dural hæmorrhage may be
regarded as almost necessarily of arterial origin, and as derived from a
torn middle meningeal artery.
Middle meningeal hæmorrhage.
_General considerations._ The middle meningeal artery enters the middle
fossa of the skull through the foramen spinosum, and divides, after a
short intracranial course, into two main terminal divisions, anterior
and posterior. The _anterior_ branch passes forwards towards the
anterior inferior angle of the parietal bone, then changing direction
and turning upwards and backwards towards the vertex of the skull. The
_posterior_ branch passes horizontally backwards--grooving the squamous
portion of the temporal bone--towards the posterior inferior angle of
the parietal bone.
Throughout their intracranial course the main trunk and its terminal
branches are embedded in the outer wall of the dura mater, except in the
spheno-parietal region, where the anterior branch of the artery usually
occupies a channel in the bone--one between ¹⁄₂ and 1 inch in extent.
The anterior branch overlies the pre-Rolandic motor area, whilst the
posterior division is related to the temporo-sphenoidal and lower
parietal regions--‘silent’ areas of the brain.
Middle meningeal hæmorrhage occurs most commonly in connexion with a
fissured or comminuted fracture of the temporal region--the result of
direct violence. A fracture, however, is not necessarily present, the
hæmorrhage may take place on the side opposite to that at which the
injury was received (laceration by contre-coup), and both vessels may be
involved. Crisp English narrates three cases in which bilateral
extravasation resulted. These more rare examples of middle meningeal
hæmorrhage are more or less confined to patients suffering from marked
arterial degeneration.
Middle meningeal hæmorrhage, uncomplicated by brain injury, is of
infrequent occurrence, the associated injuries to bone and brain
confusing the diagnosis. Moreover, the special pressure effects are
dependent not only on the absence of serious brain lesion, but also on
the non-existence of a safety-valve, such, for instance, as is afforded
by a comminuted fracture of the bones entering into the formation of the
temporal fossa, or of the roof of the middle and external ears. In the
former case, blood will force its way into the temporal region, there
forming a temporal hæmatoma--one that may pulsate--whilst, in the latter
case, the blood escapes freely from the external auditory meatus. It
should be noted, however, that pressure applied to the temporal hæmatoma
may lead to the development of irritative or paralytic symptoms confined
to the muscles of the opposite side of the body, whilst the restriction
of aural bleeding, by means of plugs inserted into the ear, will lead to
the early development of compression symptoms.
The amount of blood extravasated varies--according to the calibre of the
vessel involved--from a drachm to several ounces. The largest coagulum
that has come under my observation was 4¹⁄₂ inches in the long diameter
and 1 inch in thickness. Krönlein narrates a case in which the clot
weighed 9 ounces.
[Illustration: FIG. 50A. THE INNER ASPECT OF THE SKULL.]
[Illustration: FIG. 50B. THE INNER ASPECT OF THE SKULL SEEN ON
TRANSILLUMINATION.]
In shape the clot is elliptical; in consistency it is either fluid or
jelly-like. During the early stages of its formation it can be readily
removed. Later on, it adheres to the dura mater, and, when removed,
leaves that membrane rough and discoloured.
Some uncertainty exists as to the relative frequency with which the
trunk and the two terminal branches are exposed to injury. There can be
no doubt that the majority of cases in which typical clinical symptoms
are present are such as evidence injury to the anterior terminal
division; this is due to the anatomical relation of the clot to the
motor cortex. Injury to the main trunk is of the rarest occurrence, for
the foramen spinosum lies immediately anterior to the petro-sphenoidal
suture, the course pursued by typical middle fossa fractures. I have
seen one case only, and have read the accounts of two others, in which
the foramen spinosum was directly implicated.
The attachment of the dura mater to the sides and base of the skull
exercises a most important influence on the direction in which the blood
spreads. Firmly adherent to the lesser wing of the sphenoid in front and
to the summit of the petrous bone behind, the membrane intervening
between these two regions is but loosely attached to, and readily
stripped away from, the floor of the middle fossa. As the clot increases
in size it exerts considerable mechanical pressure and tends to separate
still further the dura from the bone. The anterior and posterior
limitations compel the blood to extend first in the outward direction
and then upwards towards the vertex of the skull.
Krönlein divides middle meningeal extravasations, according to their
regional distribution, into three main groups:--
Temporo-parietal (the most common variety).
Parieto-occipital (rare).
Parieto-frontal (very rare).
Middle meningeal hæmorrhages yielding typical clinical symptoms are of
infrequent occurrence, yet such extravasations are very commonly present
in severe lesions of the skull. This is evidenced by the fact that
middle meningeal hæmorrhage--of a greater or lesser degree--was found in
20 per cent. of all cases of fractured skull, and in 45 per cent. of
those in which the middle fossa was involved. My experience is confirmed
by Dwight and Nichols. For example, Dwight, in 149 autopsies, notes that
middle meningeal hæmorrhage was existent in 49 cases (29 per cent.). He
maintains further that the artery is injured in nearly every case in
which the fracture, extending from vault to base or vice versa,
involves the middle fossa of the skull. Nichols reports 11 cases in 32
autopsies (34 per cent.).
=Symptomatology.= As the direct result of the blow the patient is
‘concussed’, remaining in that condition for a variable period of time,
a matter of seconds, minutes, or hours, according to the nature of the
associated damage to the bone and brain. In the most typical cases, the
patient, on regaining consciousness, should recover--again for a
variable period of time--complete control over mind and body, returning
to work, walking home or visiting hospital or doctor. More usually,
however, he remains slightly dazed, though recognizing his surroundings
and capable of answering questions. In any case--unless the hæmorrhage
is accompanied by grave cerebral lesion--there should be some attempt at
recovery, some return to consciousness. The importance of this ‘lucid
interval’ cannot be over-estimated. It should be noted, however, that
this interval of consciousness is not of itself absolutely diagnostic of
middle meningeal hæmorrhage--it ought to be associated with definite
localizing symptoms of brain compression (see below). I have encountered
several cases in which this lucid interval was present, and in which
operative procedures were carried out in the anticipation of finding an
extra-dural extravasation, only to find a subdural hæmorrhage. Such
subdural hæmorrhages are not infrequently associated with a similar
return to the conscious state, but are rarely--if ever--accompanied by
the early development of symptoms of localized brain compression. In the
event of doubt as to whether the surgeon has to deal with an extra or
subdural extravasation lumbar puncture will probably clear up the
diagnosis.
The duration of this ‘lucid’ interval is exceedingly variable. It is
usually a matter of minutes or hours, though both König and Wiesman
narrate cases in which eight days elapsed before the onset of definite
localized compression symptoms. I also have recollections of a case in
which the patient walked some miles across the moor to see his doctor,
and finding him away from home, walked home again, then becoming
unconscious and dying shortly afterwards.
All depends on the calibre of the vessel injured and on the existence of
a safety-valve, by means of which some of the extravasated blood can
escape externally (see p. 97).
No rule can be laid down as to the duration of this ‘lucid’ interval,
but all authorities are agreed as to its existence, even though it may
be of exceeding short duration. Its importance, from a clinical point of
view, cannot be overestimated. It was present in 43 out of 63 cases
reported by Jacobson, well marked in 32 (50 per cent.), less marked in
11 (18 per cent.). It was observed in 60 per cent. of cases that came
under my care.
During this period the blood is occupied in stripping away the dura from
the bone--the larger the vessel the easier the task and the shorter the
‘lucid’ interval.
The further progress of the case may be considered according to the
_general and local effects_ of the hæmorrhage.
=General effects.= As soon as the clot becomes of sufficient size as to
exert general pressure on the brain, symptoms of compression become
evident, the patient first entering on the stage of ‘slow cerebration’.
He is dull and apathetic, showing marked delay in responding to
questions. As the pressure increases, he gradually passes into a state
of unconsciousness.
The pulse becomes full and slow, the blood-pressure rises progressively
(to 200 or more mms. of Hg.), respiration is laboured and stertorous,
and the temperature raised (rising progressively). The skin is hot, the
face turgid and cyanosed. If the pressure is unrelieved, stimulation of
the medullary centres gives place to exhaustion, the pulse becoming
irregular and rapid, blood-pressure falls rapidly, and respiration is of
irregular rhythm and finally Cheyne-Stokes in character. Finally, the
patient becomes completely comatose, the pupils are widely dilated, and
the cornea insensitive. Both urine and fæces may be passed (through
paralysis of the sphincters), the extremities exhibit flaccid paralysis
and the reflexes are abolished. Death occurs primarily through paralysis
of the respiratory centre.
=Local effects.= In many cases considerable help to diagnosis may be
obtained by external examination--bruising and ecchymosis, or definite
hæmatomata, in the temporal or parietal regions. In some cases the
hæmatoma may pulsate, and in others the application of pressure to the
hæmatoma will lead to the development of fits involving the face and
extremities on the contra-lateral side. Copious hæmorrhage from the ear
should always arouse suspicion as to the probability of an extra-dural
hæmorrhage (see p. 97).
The _anterior_ branch of the artery, as it passes upwards towards the
vertex, overlies the pre-Rolandic or motor area. The pressure exercised
on that region of the brain leads--according to the site of
extravasation and the degree of pressure exercised--to the development
of twitchings, convulsions, spasticity, or paralysis of the muscles of
the face, upper and lower extremities on the contra-lateral side of the
body.
[Illustration: FIG. 51. TO ILLUSTRATE COMPRESSION OF THE BRAIN. As
produced by an extra-dural hæmorrhage from the posterior branch of the
middle meningeal artery.]
The late Professor von Bergmann[26] pointed out that the arm area is
most commonly affected, and that the leg area is never alone implicated.
Wiesmann[27] states ‘that isolated paralysis of the leg area is never
seen, but only paresis when the arm is paralysed, or both may be
similarly affected at once; convulsions may precede the affection’.
In discussing the frequency of local compression effects, Wiesmann
points out that some abnormal condition of the opposite extremities was
only absent in 16 out of a total of 257 cases. In 37 cases reported by
Jacobson,[28] hemiplegia, of a greater or lesser extent, was present in
19 (50 per cent.). The same authority explains that ‘with regard to the
onset of convulsions, if there be restlessness, spasmodic twitchings, or
movements of the limbs, it is only too probable that in addition to
middle meningeal hæmorrhage, contusion or laceration of the
brain-substance will be found at more places than one’.
In cases that have come under my observation twitchings of the muscles
of the face and upper extremities were observed in 37 per cent. of
cases, and paralysis in the same number. Some alteration in the
condition of the muscles on the contra-lateral side was present
therefore in 74 per cent. of cases.
If the hæmorrhage be situated on the left side of the brain, both motor
and sensory cortical speech areas may be involved, especially the
former.
With respect to _reflexes_, it has previously been stated that the
reflexes are abolished. This is true with respect to the later stages of
fully-developed compression. In the earlier state the reflexes on the
contra-lateral side may be increased, the difference between the two
sides affording some help in the differential diagnosis.
=Pupillary changes= are variable. According to Jonathan Hutchinson, the
pupil on the affected side becomes dilated, the blood extending inwards
towards the cavernous sinus and exercising direct compression of the
third nerve. The frequency with which a dilated pupil occurs in cases of
middle meningeal hæmorrhage, and the causation thereof, are, however,
matters of dispute. Phelps writes as follows: ‘Reference to cases cited
show that the so-called Hutchinson pupil may be observed as well in
hæmorrhages occurring in other situations than the middle fossa, and in
some cases of cerebral lesion without injury at all. There is no reason
to doubt that it is the result of cerebral contusion, but in what
relation they stand to specific cerebral injuries is undetermined.’
Walton states that ‘doubtless various factors play an important part in
producing the dilated pupil, but if disorders of any simple mechanism
are to be credited with the production of the Hutchinson pupil or other
pupillary changes, the only lesion worthy of the place is disturbance,
irritative or paralytic, of the intracranial fibres of the cilio-spinal
tract’.
The late Professor von Bergmann, from 70 cases, reports as follows:--
In 39 cases both pupils were markedly dilated (56 per cent.).
In 7 cases both pupils were markedly contracted (10 per cent.).
In 20 cases the pupil on the same side was dilated (30 per cent.).
In 4 cases the pupil on the opposite side was dilated (6 per cent.).
Parsons, in answering some queries in 1903, writes:--
‘I should anticipate from cortical irritation bilateral pupillary
dilatation, perhaps more marked on the opposite side: from pressure
the opposite effects, so far as mere cortical paralysis goes, but this
would be more liable to be vitiated by vascular changes--the complex
condition seen in coma. It is very difficult to elicit pupillary
constriction by cortical stimuli--very easy to elicit dilatation, but
always bilateral though often more marked on the opposite side.’
In cases examined by me the following conditions were found:--
Pupils equal 46 per cent. of cases
Pupils constricted on the affected side 36 per cent. of cases
Pupils dilated on the affected side 18 per cent. of cases
From my experience, therefore, and from that of the authorities quoted
above, it would appear that alterations in the size of the pupil are of
very doubtful significance in the diagnosis of middle meningeal
hæmorrhage, and that the ‘Hutchinson pupil’ is but rarely observed.
The results obtained by ophthalmoscopic examination are of much greater
value. Such investigations should be carried out as a routine procedure.
In the earlier stages of the hæmorrhage some œdema of the disk, together
with dilatation of retinal veins and diminution in the calibre of the
arteries, will be observed on the affected side. This affords a most
valuable aid in the differential diagnosis as to the side on which the
hæmorrhage is situated--not always such a simple matter as appears at
first sight.
=Treatment.= Operation is indicated in all cases of middle meningeal
hæmorrhage if the condition of the patient be compatible with such
treatment. The earlier the operation is carried out the better.
=Operation.= _For Hæmorrhage from the anterior branch._ After the usual
preparatory treatment, the ‘site of election’ for trephining is marked
out on the scalp by taking a point which lies 2 inches posterior to the
external angular frontal process, and the same distance above the
zygoma. A bradawl may be introduced so as to indent the external table
of the skull, thus aiding the subsequent accurate application of the
trephine.
[Illustration: FIG. 52A. EXPOSURE OF THE BRANCHES OF THE MIDDLE
MENINGEAL ARTERY. _First stage._ Suitable scalp-flaps have been turned
down, and the skull has been trephined over the ‘sites of election’ for
exposure of both anterior and posterior branches.]
[Illustration: FIG. 52B. EXPOSURE OF THE BRANCHES OF THE MIDDLE
MENINGEAL ARTERY. _Second stage._ The trephine-holes have been enlarged
with the craniectomy forceps in the required directions.]
The incision commences immediately posterior to the external angular
frontal process, curves upwards and backwards along the temporal crest,
and terminates in front of the tragus of the ear. The flap, comprising
skin, temporal fascia and muscle, and pericranium, is turned to its
zygomatic base and all bleeding-points secured.
The subsequent procedures vary according to the condition of the bone:--
_If there be no fracture of the bone_, the pin of the trephine is
applied to the indented spot and the disk of bone removed. After the
removal of the disk the clot will be exposed; but, in order to obtain
full exposure, the gap must be enlarged with the craniectomy forceps,
mainly in the upward and downward directions.
_If a fissured fracture be found_, the trephine is applied in close
relation to the intersection of the line of the artery and the line of
the fracture, the gap being enlarged in the required direction.
_When the fracture is comminuted_, the fragments of bone are either
elevated or removed until sufficient room has been obtained.
The greater part of the clot can be removed with a Volkmann spoon, or
with an ordinary teaspoon, and the region flushed out with hot saline
solution.
_To secure the bleeding-points._ When the artery is injured beyond the
limits of the gap, the bone must be nibbled away till the bleeding-point
is exposed. In some cases it may be necessary to remove a considerable
portion of the bone entering into the formation of the temporal fossa.
In the meantime, hæmorrhage may be controlled by plugging towards the
base of the skull with strips of gauze. Sufficient room having been
obtained, the gauze is withdrawn, when smart sponging should enable the
operator to determine the source of the hæmorrhage. At this stage of the
operation, a head-lamp is useful. After the exposure of the
bleeding-points, the following measures can be adopted whereby to arrest
the bleeding:--
(_a_) The application of a ligature or of silver ‘clips’ (see Fig. 6) on
either side of the bleeding-point.
(_b_) The vessel may be underrun on either side of the bleeding-point.
(_c_) The vessel may be seized with artery forceps and twisted.
(_d_) The hæmorrhage may be arrested by means of gauze plugs.
(_e_) The foramen spinosum may be occluded with bone or wooden pegs.
(_f_) The common or external carotid arteries may be ligatured.
Every effort should be made to control the hæmorrhage by means of
ligature, silver clip, underrunning, or torsion. Gauze plugs may usually
be relied on to stop the bleeding, but they possess the great
disadvantage of exercising pressure on the cortex and preventing
expansion of the brain.
Occlusion of the foramen spinosum and ligature of the carotid arteries
complicate and prolong the operation. The foramen spinosum is occluded
in the following manner: the dura mater is quickly stripped up with the
fingers away from the base of the skull, the soft parts gently but
firmly retracted and the foramen identified. Its occlusion may be
effected by means of a sterilized wooden match or bone peg, by a small
piece of bone derived from those osseous fragments which have been
removed during the operation, or with the aid of a piece of catgut; in
each case the occluding medium should be well driven into the foramen.
It is open to doubt whether ligature of the carotid arteries is ever
necessary, though several cases have been recorded in which such a
procedure was carried out. The external carotid should be tied in
preference to the common vessel, further interference with the
blood-supply of the brain increasing necessarily the risk of cerebral
œdema, &c.
The hæmorrhage having been arrested by one or other of these methods,
the cavity is thoroughly washed out with hot saline solution and
drained, a small rubber drainage-tube being brought out through the
scalp-flap. The tube should be removed after twenty-four to thirty-six
hours, according to the circumstances of the case.
_For hæmorrhage from the posterior branch._ The ‘site of election’ for
exposure of the posterior branch lies at the intersection of the two
following lines:--
A line drawn backwards from the upper border of the orbit parallel to
Reid’s base-line.
A line drawn vertically upwards from the posterior border of the mastoid
process.
The trephine is applied, the disk removed, and the gap enlarged with the
craniectomy forceps in the forward and backward directions. The hæmatoma
is evacuated and the bleeding arrested after the methods enumerated
above.
=Results.= The ultimate result of operation for middle meningeal
hæmorrhage depends on two factors--the time at which operation is
carried out, and the question of brain lesion. There is every reason to
believe that, when treated early and when uncomplicated by brain injury,
the prognosis, both immediate and remote, is wholly satisfactory.
Wiesman[29] collected 257 cases, of which 110 were submitted to
operation, with a mortality of 27 per cent. Of the cases in which no
operation was performed 88 per cent. died.
Duchaine[30] reports 27 cases in which operation was carried out, with
death in 6 cases only, a mortality of 22 per cent.
Von Bergmann collected 110 cases treated by operation, with 74
recoveries and 36 deaths, a mortality of 32·27 per cent.
Blake only lost 3 cases out of a total of 42 submitted to operation.
Even when every allowance is made for the fact that operative measures
were adopted in the more hopeful cases, the above statistics show
conclusively that early operation affords great hope of cure.
[Illustration: FIG. 53. A BASIC FRACTURE WITH LACERATION OF BOTH CAROTID
ARTERIES.]
Before passing on to =subdural hæmorrhage=, it will be convenient to
discuss briefly the question of injury to the =internal carotid artery=.
This vessel, during its forward passage in the outer wall of the
cavernous sinus, from the posterior to the anterior clinoid processes,
crosses the line of the typical middle fossa fracture (see p. 84). The
artery is loosely embedded in the sinus, it is protected by the third,
fourth, ophthalmic division of the fifth and sixth nerves, and it is
situated some distance above the level of the base of the skull. In
spite of this degree of protection from injury, the artery may be
lacerated in this part of its intracranial passage. The basic fracture
is necessarily of a very severe nature. Two cases have come under my own
care: one in which both arteries were torn across, the fracture passing
from one middle fossa to the other, with such wide separation of the
anterior and posterior segments of the skull that the two were freely
movable on one another (Fig. 53), whilst in the second case, the
fracture, originating in the left frontal region, passed backwards
across the anterior fossa, comminuting the base in the region of the
cavernous sinus, lacerating that sinus and tearing the artery (Fig. 54).
[Illustration: FIG. 54. A BASIC FRACTURE WITH LACERATION OF THE
CAVERNOUS SINUS. A, The optic nerve; B, The cavernous sinus; C, The
third nerve; D, The internal carotid artery.]
In both cases death was almost instantaneous, blood pouring from the
nose and mouth.
In some few cases the vascular lesion is confined to a minute tear in
the coats of the vessel, a fistulous communication being formed between
the artery and the cavernous sinus--arterio-venous aneurysm. This
condition is discussed on p. 204.
II. Subdural hæmorrhage.
Hæmorrhage into the subdural space may be (_a_) diffuse, or (_b_)
localized.
(_A_) =Diffuse subdural hæmorrhage.= The blood may be derived from one
of the great sinuses of the brain or from superficial cerebral vessels
(laceration of the brain).
The _superior longitudinal sinus_ may be torn by the in-driving of
fragments of bone in a comminuted depressed fracture of the vertex, or
by wide separation along the line of the sagittal suture. Blood is
diffused throughout the subdural space, on one or on both sides of the
falx cerebri, but always tending to gravitate towards the lower limits
of the supra-tentorial space.
In the event of the wound being compound, air may enter into the sinus.
Insomuch, however, as the sinus pressure is, under normal conditions,
positive, this complication is of rare occurrence, unless the patient is
in a state of profound shock, from loss of blood, or suffers from urgent
dyspnœa.
Allusion should also be made to the condition described by Stromeyer, as
‘sinus pericranii’, where a subpericranial hæmatoma communicates with a
venous sinus. Such hæmatomata may pulsate, are more or less reducible on
pressure, and are increased on straining or on the application of
pressure to the internal jugular vein.
The _lateral sinus_ may be laid open in any part of its course, more
especially at the angle of junction between the lateral and sigmoid
sinuses, in close relation to the occipito-mastoid suture, a region not
infrequently involved in basic fractures. The blood effused will occupy
the supra- or infra-tentorial spaces according to the situation of the
rent in the sinus-wall.
The _cavernous sinus_ is frequently involved in anterior and middle
fossa fractures. The blood effused usually escapes into the nose and
mouth.
[Illustration: FIG. 55. A COMMINUTED FRACTURE OF VAULT AND BASE, THE
BASIC FRACTURE INVOLVING BOTH MIDDLE AND POSTERIOR FOSSÆ. The middle
fossa fracture, on the left side, follows the usual course. The
posterior fossa fracture resulted in laceration of both lateral
sinuses--at the usual site, junction of sigmoid and lateral sinuses.
Probes are inserted at each site of laceration. The resultant hæmorrhage
was mainly intradural, but, as is seen in this figure, the dura mater of
the posterior fossa is stripped away from the bone by an extra-dural
extravasation.]
=Symptoms.= The rapid diffusion of blood throughout the subdural space,
and the usual coexistence of extensive injury to bone and brain, seldom
permit of the development of such definite symptoms as might accurately
define the localization of the hæmorrhage. The most important feature in
the diagnosis lies in the fact that compression symptoms are early in
onset and progressive in nature. The ‘lucid’ interval, so prominent a
feature in middle meningeal extravasations, is either absent or of such
short duration as to be difficult of recognition. The rapid development
of symptoms pointing to brain compression, and the nature of the injury
itself should enable the surgeon, in the majority of cases, to come to
the conclusion that the patient is suffering from diffuse subdural
hæmorrhage. In all cases of doubt, lumbar puncture should be carried
out, the presence of blood-corpuscles in the cerebro-spinal fluid
confirming the diagnosis.
=Indications for operation.= Whether one considers the case from the
point of view of the more immediate prognosis or from the more remote
aspect of the case, operation is indicated, if the condition of the
patient is compatible with such treatment. In considering the
advisability of adopting an active form of treatment, it must be taken
into account that, if the patient recovers without operation, the
presence of an extensive subdural blood-clot must necessarily interfere,
as an after-result, with the functions of the cortex, and that the
removal thereof affords considerable hope of permanent cure.
=Operation.= Operative measures may be considered as follows:--
The treatment of the fracture and of the dural rent.
The treatment of the subdural extravasation.
_The treatment of the fracture and of the dural rent._ A scalp-flap is
framed, suited to the occasion and formed with due regard to existent
scalp laceration. The fracture being fully exposed, depressed or
comminuted fragments of bone are elevated or removed. Complete exposure
of the sinus-wall, both in front and behind the site of laceration, is
required, and for this purpose the craniectomy forceps may be called
into requisition. In the event of copious bleeding during these
procedures, strips of gauze should be inserted on either side of the
sinus rent between the dura and the bone, thus compressing the sinus and
stopping the bleeding.
The sinus rent may be treated after one or other of the following
methods:--
1. It may be sewn up with mattress sutures of fine catgut, by which
means it may be possible to stop the hæmorrhage without interfering with
the sinus blood-stream.
2. The open mouth of the sinus may be puckered up by means of a
purse-string suture.
3. The needle may be passed right round the sinus on either side of the
rent, piercing the falx cerebri in the case of the superior
longitudinal sinus and the tentorium cerebelli in wounds of the lateral
sinus. The two ligatures are then tightened up and the bleeding
controlled.
4. The gauze plugs (see above) may be allowed to remain for twenty-four
hours or more, and then carefully withdrawn.
_The treatment of the subdural hæmorrhage._ Though the complete
evacuation of the clot is seldom practicable, much may be done to remedy
the condition. The tenseness of the dura mater, the absence of
pulsation, and the peculiar plum-colour imparted to that membrane by the
presence of underlying blood-clot point to the nature of the trouble.
The dura mater is incised and the presenting clot removed, as far as
circumstances permit, with the aid of a spoon and irrigation (hot saline
solution at a temperature between 110° and 115° Fahrenheit). Free
drainage must be supplied, and it is necessary, therefore, that a
counter incision should be made at the most dependent part of the clot.
A suitable region may present itself if the bone be extensively
comminuted. Under other circumstances, a narrow channel may be cut in
the bone, prolonged in the downward direction, till the lower limits of
the clot have been reached (see Fig. 56).
[Illustration: FIG. 56A. THE OPERATIVE TREATMENT OF SUBDURAL HÆMORRHAGE.
_First stage._ The skull has been trephined over the upper part of the
clot and the bone cut away in the downward direction in order to reach
the lower limits thereof. The dura mater has been incised, crucially in
the upper part and vertically in the lower part.]
[Illustration: FIG. 56B. THE OPERATIVE TREATMENT OF SUBDURAL HÆMORRHAGE.
_Second stage._ The clot has been removed and the dura mater sewn up. A
drainage tube has been inserted so as to drain the subdural region
through the lower part of the scalp-flap.]
A rubber drainage-tube may be inserted in the manner depicted in the
same figure. Except at the point of emergence of the tube, the dura
mater is sewn up (with fine interrupted catgut sutures).
(_B_) =Localized subdural hæmorrhage (subdural hæmatocele).= We are
greatly indebted to Bowen[31] for our knowledge of subdural hæmatomata.
That subdural hæmorrhage might take the form of a localized collection
was a recognized fact, but the condition was but little understood, the
typical clinical symptoms were not recognized, and surgeons hesitated to
adopt surgical remedies. All these facts impeded advance in both
diagnosis and treatment. Subdural hæmatoceles, even at this date, are
often regarded as rarities, but, in the light of present knowledge, it
would appear that wider recognition of the hæmorrhage in its clinical
aspect will show that such ideas are erroneous.
In the preceding section it was shown that subdural extravasation
resulting from sinus-injury tends to become diffused throughout the
subdural space. With respect to localized hæmorrhages our data are by no
means complete, but all available evidence tends to show that subdural
hæmatoceles are dependent on laceration of the pia-arachnoid vessels--a
condition practically synonymous with superficial laceration and
contusion of the cortex. The blood, derived from small cerebral veins
and minute cerebral arteries, exercises primarily but slight pressure
effect. Its force is expended on compressing and emptying the subjacent
and surrounding cerebral vessels, producing, in other words, a condition
of _local cerebral anæmia_. This pressure is insufficient to lead to the
development of general compression, but suffices to produce certain
rather indefinite symptoms. We have, therefore, before us a very
different picture to that depicted in cases of middle meningeal
hæmorrhage. In such extra-dural hæmorrhages some definite period of time
must elapse before the dura mater is sufficiently stripped from the bone
to allow of the formation of a clot of size sufficing to exercise both
local and general compression effects. Pressure effects then become very
manifest.
On the other hand, in localized subdural extravasations there is an
immediate effect, for the brain is contused or lacerated. On recovering
from the immediate effects of the injury--concussion of a greater or
lesser degree of intensity--the patient does not regain complete mental
and bodily convalescence. He suffers from symptoms suggestive of brain
irritation--headaches, photophobia, mental irritability, insomnia, loss
of appetite, the pulse accelerated, and the temperature slightly raised.
Later on, more definite symptoms arise, but, intervening between the day
of the accident and the time at which these more definite localizing
symptoms develop, there is an unmistakable _latent_ period--a period to
be sharply differentiated from the previously mentioned _lucid_ interval
(see p. 139).
This ‘latent’ period lasts for a variable period of time--seldom less
than a week or more than three months. At the end of that time the
picture changes, and the patient evidences symptoms obviously referable
to local brain compression. From a clinical point of view it is
fortunate that subdural hæmatoceles tend to involve the fronto-parietal
region with the consequent development of motor symptoms, especially
paresis or paralysis of the contra-lateral side. Hence the name
sometimes applied to the condition--traumatic late apoplexy. The speech
areas are implicated if the injury be situated on the left side.
Paralysis limited to the lower extremity is exceedingly suggestive, such
a palsy occurring only with the greatest rarity in extra-dural
hæmorrhages (from the middle meningeal artery).
If the pressure be unrelieved by operation the patient passes from the
excitatory to the paralytic stage of brain compression, gradually
falling into a condition of coma, the pulse increasing in frequency and
the respiration becoming more and more embarrassed.
In the study of this condition, the following are the points to which
special attention should be paid:--
1. The comparative want of severity with respect to the injury received.
2. The absence of any ‘lucid’ interval, such as is present, for example,
in middle meningeal hæmorrhage.
3. The presence of a definite ‘latent’ period.
4. The late development of symptoms pointing to general and local brain
compression.
Finally, it may be stated in general that the more indefinite and the
more deferred the pressure symptoms, the greater the probability that we
have to deal with a localized subdural hæmorrhage. Lumbar puncture may
materially aid in the differential diagnosis between extra-dural and
subdural hæmorrhages.
The following case affords a typical example of subdural hæmatocele:--
An elderly man fell down, striking the right side of the head against
the pavement. He lost his senses for a few minutes and was then
brought to the hospital, dazed and complaining of headache (note the
absence of any _lucid_ interval). He was sent home in a cab and was
assisted to bed by his wife. He kept to his bed during the next week,
complaining of constant headache, and was exceedingly irritable (this
is the ‘latent’ period). Towards the end of the third week his wife
noticed that he seldom used the left upper and lower extremities. This
paresis increased steadily, the face was drawn to the right side, and
his condition became so serious that the wife brought him again to the
hospital (this is the ‘manifest’ period).
When seen by me he was only partly conscious, the mental condition
varying, however, during the day. He was exceedingly irritable,
muttering to himself in a low tone, words being more or less
unintelligible. The left upper extremity was paralysed, the face drawn
to the right side, and the left lower extremity was but little used.
The pupils were equal, the disks normal. The temperature in the left
axilla was two degrees lower than on the opposite side.
The hæmatocele was exposed, cleared out, and the cavity drained.
Recovery was rapid and complete. Two years later all was well.
=Operation.= The lesion is usually of so gross a nature that little
difficulty will be experienced in determining the site for trephining.
The protective gauze and scalp-tourniquet are applied as usual (see p.
14), and a bradawl introduced through the scalp so as to indent the
external table and allow of the subsequent accurate application of the
trephine. A scalp-flap, suited to the occasion, is framed, the skull
trephined, and the disk of bone elevated and removed. The appearance of
the dura mater now allows the operator to verify his diagnosis--the
membrane is non-pulsatile, it bulges markedly outwards and presents a
blue-purple colour. The bone is then nibbled away in the downward
direction towards the lower limit of the clot, the scalp incision being
prolonged according to requirements.
In the region of the trephine-hole the dura is incised in a crucial
manner, and the four flaps held aside by catgut sutures passed through
the apex of each flap. A blunt director is introduced beneath the dura,
passing towards the lower limit of the clot, and the membrane slit up to
within a short distance of the lower margin of the gap. All meningeal
vessels that cross the line proposed for dural section must first be
underrun on either side of that line. Retraction of the dura will now
allow of adequate exposure of the underlying hæmatoma. Its removal can
be carried out with the aid of a spoon, and by means of gentle
irrigation (hot saline at a temperature between 110° and 115°
Fahrenheit). It is usually impossible to remove the whole of the
coagulum, but the greater portion can be got rid of in the manner
described.
The dura mater is approximated above by the cross-union of the four
apical sutures, whilst the downward prolongation is also sutured except
at the most dependent point, where a rubber drainage-tube is inserted
beneath the dura mater and brought out through the scalp-flap (see Fig.
56). This tube should be anchored to the dura mater with a single fine
catgut suture.
The tube should be allowed to remain in position for at least thirty-six
hours. In this the surgeon must be guided by the amount of discharge and
the general progress of the case.
=Results.= The most complete results obtained by operative treatment are
supplied by Bowen, who classifies a series of 72 cases as follows:--
Class A. Subdural hæmorrhage, apparently without other serious injury to
bone or brain.
36 cases. 22 recovered after operation.
14 died--11 without and 3 after operation.
Class B. With serious brain-injury.
36 cases. 6 recovered after operation.
30 died--10 without and 20 after operation.
In other words, every case died in which no operative measures were
adopted, whilst after operation 28 recovered and 23 died. My own
experience is limited to 4 cases, 3 of which recovered.
=Pia-arachnoid hæmorrhage.= From evidence obtained at post-mortem
examinations, it may be concluded that the great majority of cases of
severe head-injury--especially those in which ‘irritation’ of the brain
is a prominent feature--are associated with pia-arachnoid hæmorrhage.
This is evidenced by the presence of a film of blood and serum over
certain regions of the brain, not confined to the region subjacent to
the skull area primarily involved, but also present over the opposite
pole of the brain (injury by contre-coup).
Subpial hæmorrhage differs from the subarachnoid variety in that the
blood follows the invaginations of the pia mater, lining, therefore,
both major and minor cerebral sulci. Subpial and subarachnoid
hæmorrhages are, however, generally co-existent, and the
term--pia-arachnoid hæmorrhage--aptly describes the conditions commonly
found.
The =symptoms= resulting from such blood extravasations are such as are
described in the sections dealing with concussion and irritation of the
brain (see p. 166).
INJURY TO THE BRAIN
Injury to the brain must always be regarded as by far the most important
of the many complications associated with fracture of the skull. A
fracture is not necessarily accompanied by brain-injury, and laceration
of the brain may exist without a fracture. There can, however, be no
question that the more severe cases of head-injury are almost invariably
associated with some degree of brain-injury--varying from contusion to
extensive laceration, cortical or central.
No part of the brain is exempt from injury, but two regions, the
antero-inferior aspect of the frontal lobe and the antero-external
aspect of the temporo-sphenoidal lobe, show a special liability to
contusion and laceration.
The brain may be injured immediately subjacent to the site at which the
blow is delivered (direct injury), or at the pole directly opposite that
at which the blow was applied (indirect injury).
Direct injury results from the in-driving of comminuted and depressed
fragments of bone, from the passage of a foreign body, and from the
direct transmission and diffusion of forces through the subjacent
cerebral substance.
The indirect forms of injury are less readily explained. Their frequency
cannot be disputed. I drew attention to the subject in my Hunterian
Lectures in 1904, there stating that indirect injury to the brain was
more common than the direct form. My opinion is confirmed by Phelps,[32]
who states that injury by indirect violence is of almost constant
occurrence.
Three theories have been advanced in explanation:--
1. ‘Their production has been ascribed to the change in form that is
suffered by a skull in virtue of its elasticity when subjected to
violence which causes distortion of the brain to the point of bursting.’
2. ‘In the displacement of the cerebro-spinal fluid by the consecutive
depression and bulging that is believed to follow a blow on the head; a
momentary vacuum is formed at either axis of force, and the vessels of
the brain and meninges rupture from lack of support.’
Neither of these theories are tenable, insomuch as they are based on an
acceptance of the ‘bursting and compression’ theories (see p.
74)--theories which, in my opinion, it is impossible to accept.
3. The ‘contre-coup’ theory. According to this theory the injury is due
to sudden and violent displacement of the brain against the opposing
osseous barrier. This theory has been opposed by many--notably by
Helferich--on the ground that the brain is said to completely fill the
cranial cavity, and that ‘shaking’ from side to side is impossible.
This theory affords, however, the most satisfactory explanation of
contralateral laceration. The following points may be advanced in its
favour:--
(_a_) The frontal and temporo-sphenoidal lobes are more liable to
contusion and laceration than any other parts of the brain, both regions
possessing certain anatomical relations accounting for their ready
injury. The frontal pole is related to the angle of junction between
the horizontal and vertical plates of the frontal bone, the
temporo-sphenoidal lobe to the cul-de-sac, at the anterior part of the
middle fossa, that is overhung by the wings of the sphenoid bone.
(_b_) The lacerated area is almost invariably situated at that part of
the brain which lies opposite to the region struck in the line of the
transmitted force. Furthermore, brain lesions are most prevalent when
the accident results from a fall from a height, a class of accident in
which ‘shaking’ of the brain is most likely to occur, and least common
when the basal fracture is dependent on a bilateral compression force.
(_c_) The statements that ‘shaking’ cannot take place, and that the soft
cerebral substance cannot be driven forcibly and violently against the
opposing bony barrier, so as to be locally bruised and torn, are
incorrect.
That such violent displacement of the brain can and does occur is proved
by the following case:--
A prize-fighter was knocked out by a blow on the right side of the
head, dying a few hours later. The post-mortem revealed no fracture of
vault or base, but a linear laceration of the brain on the mesial
aspect of the right hemisphere which exactly corresponded to the free
margin of the falx cerebri. In this case, therefore, conclusive
evidence was obtained that the brain had been driven from right to
left against a firm and resisting barrier, corresponding laceration
resulting.
The lacerated area is usually cone-shaped, the base corresponding to the
surface of the brain, the apex facing towards the lateral ventricles. In
the most severe cases the anterior or lateral horns of the lateral
ventricles may be involved at the apex of the cone, and, in the event of
further cerebral softening, the horns of the ventricles may, as it were,
bulge outwards, thus assisting in the formation of those traumatic
cephaloceles that communicate between the lateral ventricle and the
surface of the brain.
On the other hand, if the degree of laceration be slight and the injury
compatible with life, organization and partial resolution takes place,
with the formation, in nearly all cases, of adhesions between the cortex
and the membranes, of false membranes, arachnoid cysts, and of blood
cysts. In the more serious cases cerebral fibrosis results, in direct
proportion to the degree of cerebral destruction, with corresponding
degeneration, both of the cerebral cortex and of the tracts that evolve
therefrom.
=Symptoms.= Certain regions of the brain may, when injured, give rise to
localizing symptoms. More generally, however, all localizing features
are obscured by an overpowering element--the presence of concussion,
irritation, or compression of the brain.
Still, in some cases, the localizing features are sufficiently marked,
at some period of the case, to allow of a more definite diagnosis. The
symptoms, therefore, must be considered under the two heads, (A)
_localizing_, and (B) _general_.
A. Localizing symptoms.
_Localizing to the frontal lobes._ Phelps,[33] from a series of 130
cases, arrived at the following conclusions--that, ‘in nearly every case
in which consciousness was retained or regained, and the mental
faculties not perverted by general delirium, laceration of the left
frontal lobe was attended by default in intellectual control, and that
the lesion was usually of the anterior region and implicated its
inferior surface.’ ‘Subcortical disintegration was characterized by
abrogation of mental power, and superficial laceration by aberration in
its manifestations.’ And secondly, that, ‘in nearly every instance in
which laceration was confined to the right side, the mental faculties
remained unaffected, except as they were obscured by delirium and stupor
occasioned by coincident general lesion.’
Although the above statements have not altogether been confirmed by
cases that have come under my observation, yet, coming from such a
source, they must be accepted unless refuted.
Bianchi states that, after extirpation of the frontal lobe of the ape,
the whole intellectual life of the animal is changed. Perception,
attention, inhibition, and in particular memory and association are
enfeebled. The psychical tone is lowered; the ape lacks initiative,
courage, and spirit.
Laceration of the under aspect of the lobe may, by direct involvement of
the olfactory region, interfere with the faculties of smell and taste.
_Localizing to those parts that minister to the function of speech._ The
condition of the patient usually prevents one from obtaining early
information as to the power of speech. Isolated lesions of the posterior
part of the third left frontal convolution result in _motor aphasia_, a
condition characterized by the inability on the part of the patient to
speak, in spite of the fact that comprehension is unimpaired. The
brain-injury is, however, seldom so defined as to be characterized by
loss of speech without other phenomena. In very close relation to the
area responsible for speech is the _writing_ centre, situated at the
posterior end of the middle frontal gyrus, near the centre for the
movements of the hands and fingers. Injury to this centre results in
_agraphia_ and _alexia_.
_Word-deafness_ results from lesions implicating the upper
temporo-sphenoidal lobe, and _word-blindness_ from injuries to the
supramarginal and angular gyri (see Fig. 57).
[Illustration: FIG. 57. THE AREAS CONCERNED IN SPEECH EXPRESSION.]
Phelps pointed out that the lesion must be an extensive one if the
symptoms included under the term _sensory aphasia_ (word-blindness,
word-deafness) are to be evolved. No localized injury to any small area
suffices, and the cortex must be deeply involved. Lacerations of the
brain are usually of so gross a nature that further differentiation is
seldom to be obtained. Here it might be noted that the cortical centres
responsible for speech and its accessories, word-seeing, word-writing,
and possibly word-hearing, are all situated on the left side in normal
right-handed individuals. The corresponding areas on the right side may
be regarded as ‘silent’ areas, and may be utilized, if desired, for
decompression purposes. No operation, with that purpose in view, should
be carried out, however, unless the surgeon is assured that the patient
is right-handed in his actions. A case has recently come to my
knowledge where a right-parietal decompression operation was carried out
with disastrous results.
_Localizing to the temporo-sphenoidal lobe._ The relation of sensory
aphasia to lesions of the temporo-sphenoidal lobe has already been
mentioned. The anterior poles of this portion of the brain, a region
frequently involved in head injuries, may lead to the development of
impaired smell and taste, especially if the lesion includes the uncinate
lobe and be situated on the left side. In other respects, the
temporo-sphenoidal lobe may be regarded as a ‘silent’ area of the brain.
_Localizing to the pre- and post-central convolutions._ Injury to the
pre-central or motor area usually leads to the development of definite
symptoms--twitchings, convulsions, or paralysis of the face and
extremities on the contra-lateral side. In the earlier stages reflexes
are abolished. Later on, as the result of degenerative changes in the
pyramidal tracts, spasticity, contractures, and rigidity, with increased
reflexes will be observed in the affected limbs. On the other hand, the
muscles do not show any reaction of degeneration. Babinski’s sign is
generally present.
Injury to the post-central convolutions might be expected to lead to
various alterations in tactile and muscle sense, in stereognosis, and in
sense of pain and temperature, but the general condition of the patient
seldom permits accurate demonstration. Such sensory disturbances are
more frequently observed as late results of head-injury.
_Localizing of the occipital lobes._ Laceration of the occipital lobes
may lead to homonymous hemianopia, for which defect it is probable that
the degree of laceration must be considerable, involving mainly the
mesial aspect of the occipital lobe (see Fig. 69). Schäfer has shown
that the greater portion of the occipital lobe may be removed in monkeys
without producing loss of vision, and it is only when the lesion
involves the parieto-occipital fissure and passes into the
occipito-temporal convolutions that loss of vision is permanent.
Slighter degrees of occipital injury may lead to subjective symptoms,
such as flashes of light, colour changes, &c.
_Localizing to the cerebellum._ Lesions of the cerebellum rarely permit
of the development of such localizing symptoms as are observed in
cerebellar tumours. Inco-ordination of movement, ataxia, and other
symptoms observed in cerebellar tumour formation are, from the general
condition of the patient, incapable of demonstration in cerebellar
laceration. It is necessary, however, to draw attention to the
significance of yawning and gaping. This symptom has been observed in
several recent cases, and, as far as my observation goes, is only
present in cerebellar lesions.
[Illustration: FIG. 58. THE CORTICAL MOTOR AND SENSORY AREAS.]
In the consideration of these localizing symptoms, it must be borne in
mind that brain lacerations are of an exceedingly gross nature, and that
there may be--as the late Professor von Bergmann[34] pointed
out--‘notwithstanding the severest brain symptoms, not the slightest
discoverable anatomical alteration in the brain. On the other hand,
notwithstanding the absence of all brain symptoms, extensive and
striking destruction of the brain substance.’
B. General symptoms.
Concussion or cerebral shock.
_Its pathology._ Concussion used to be regarded as implying a ‘molecular
disturbance’ of the brain--a definition so unsatisfactory that it may be
relegated to a desired obscurity. At the present day, though some
difference of opinion exists as to whether the condition is or is not
necessarily dependent in its development on associated cortical or
subcortical lesions, macroscopical or microscopical, concussion is
regarded as implying a condition of _acute cerebral anæmia_ through
sudden inhibition or paralysis of the vaso-motor centre.
With respect to the existence of visible lesions of the brain, Kocher
maintains that such lesions--hæmorrhages and the like--are necessarily
present, proposing that the term ‘brain concussion’ should be eliminated
in favour of ‘brain contusion’. On the other hand, the late Professor
von Bergmann pointed out that such a course was not possible, instancing
the many cases of concussion where contusion could not possibly have
existed.
There cannot, in my opinion, be any question as to which is the correct
view. It is unreasonable to ask one to believe that the milder cases of
concussion, cases in which the patient merely suffers from loss of
consciousness for a few minutes, from which he rapidly recovers and is
discharged from treatment within a few days, and from which he suffers
in the future from no remote ill effects whatsoever, it is unreasonable
to ask one to believe that such cases have experienced so severe a
lesion as brain contusion or laceration. Both these conditions would
require a long period of convalescence, and would tend to leave in their
train very serious after-results.
It is obvious, therefore, that there exists a degree of concussion from
which the patient can quickly and entirely recover. It is also clear
that in many cases the patient passes through a long and serious
illness, whilst, in some cases, a fatal termination may ensue--and that
too within a few hours. It is consequently clear that we have to deal
with varying grades of concussion, some of which are of so mild a nature
as to be clearly unassociated with definite cerebral lesion, whilst
others are of so serious a nature that death may take place within a
few hours, and in such cases the gravest cerebral lesions may be found
at the autopsy.
In other words, it would appear that concussion is more or less
dependent in its severity on the degree of associated cerebral change.
It is, however, to the milder type of case that we should turn in order
to determine what is exactly meant by concussion. In such cases the
patient merely suffers from a mild degree of _cerebral shock_, a
condition closely resembling shock in general. ‘Shock’ is defined as a
‘condition resulting from fall in blood-pressure, due to inhibition or
paralysis of the vaso-motor centre’. The afferent impulses that pass up
the various sensory paths inhibit or paralyse the vaso-motor centre, a
centre that has for its main function a tonic constricting influence on
the peripheral arteries. Hence, these vessels dilate atonically, the
blood collects in the great splanchnic area, and, insomuch as the
cerebral arteries possess no separate vaso-motor apparatus, they
passively follow the changes in the general circulation. The brain is
consequently in a state of arterial anæmia, the arteries relatively
emptied, the veins passively engorged.
Clinically, concussion or cerebral shock differs from ordinary shock in
one manifestation only--sudden loss of consciousness. This development
is readily explained on the ground that concussion results from a
violent blow applied in the near neighbourhood of the vaso-motor centre,
with consequent _sudden_ vaso-motor depression and _acute_ anæmia of the
cerebral cortex. This leads to immediate great fall of blood-pressure,
loss of consciousness, and lack of muscular control.
Statements have recently been brought forward to the effect that
concussion is in reality a mild type of compression. This view received
at first sight some confirmation from the experiments of Koch and
Filehne, who, from the application of consecutive slight blows to the
heads of dogs, showed that each blow resulted in bulbar stimulation
followed by bulbar depression. The blows being continued, the degree of
stimulation decreased and that of depression increased until exhaustion
and death resulted. During the periods of stimulation the pulse-rate
slowed, during those of depression it increased.
It should be noted, however, that concussion, as observed in the human
being, results from one sudden and violent blow. It may, I think,
safely be assumed that, in such cases, the stimulating effect of the
blow is entirely abolished in favour of an acute depression. And, as
Archibald[35] says, ‘their records of respiration, pulse, and
blood-pressure resemble far more closely the course of an increasing
compression, with its gradual slowing of pulse and respiration and
steady rise of blood-pressure, than that of concussion with its sudden
standstill of pulse and respiration and fall of blood-pressure.’
In _favourable cases_ the injury being of a comparatively mild nature,
the vaso-motor centre soon recovers tone, and, as the result of previous
depression, the vascular conditions are now reversed--_the stage of
depression_ giving place to the _stage of reaction_. The blood-pressure
rises, the carotids pulsate forcibly, the face is turgid and flushed,
the skin hot and moist, whilst the temperature rises, and the general
cerebral hyperæmia is evidenced by headache, restlessness, and perhaps
by delirium.
In the _more severe cases_ the vaso-motor depression is unduly
prolonged, or persists till death, the patient remaining concussed for a
considerable period of time, or dying in that condition. In these fatal
cases the post-mortem examination _usually_ reveals brain laceration,
but _always_ evidences considerable engorgement of superficial cerebral
veins, increase of cerebro-spinal fluid and œdema, both of the
pia-arachnoid region and of the brain substance itself. These latter
phenomena are accounted for by the fact that, insomuch as the venous
pressure and cerebro-spinal tension are equal, the greater the
engorgement of the cerebral veins the more extensive is the transudation
of fluid into the pia-arachnoid and cerebral systems. In a fatal case of
concussion--recently under my care--the surface of the cortex, when
exposed by operation, was obscured by a layer of œdematous pia-arachnoid
¹⁄₄ inch in depth.
Arguing from the presence of the very definite pathological changes
observed in all fatal cases--contusions, lacerations, hæmorrhages, and
œdema--one may arrive at the conclusions (1) that lesions of a similar
but less serious nature are existent in the serious but non-fatal cases,
and (2) that the prolongation of the stage of depression is directly
dependent on the presence of such lesions.
On investigating the numerous cases that come under the care of the
surgeon, certain features present themselves which are not always
readily explained on the definition of concussion as given above. Thus,
the variability of the symptoms evinced in cases of concussion admitted
into hospital are well exemplified by the following table, compiled from
a consecutive series of 50 cases admitted into St. Bartholomew’s,
diagnosed and treated as concussion:--
=12= _cases in the hospital for 7 days or less_ (_cerebral shock
only_).
_Temperature_ on admission: 8 subnormal.
2 normal.
2 slightly raised.
_Pulse_ on admission: 3 subnormal.
3 normal.
6 accelerated.
=26= _cases detained for 7 to 10 days_ (_probably cerebral shock
only_).
_Temperature_ on admission: 6 subnormal.
9 normal.
11 slightly raised.
_Pulse_ on admission: 4 subnormal.
12 normal.
10 accelerated.
=9= _cases detained for 14 to 21 days_ (_probably cerebral
contusion_).
_Temperature_ on admission: 2 subnormal.
3 normal.
4 slightly raised.
_Pulse_ on admission: 6 subnormal.
1 normal.
2 accelerated.
=3= _cases detained for 21 to 30 days_ (_certainly cerebral
contusion_).
_Temperature_ on admission: 1 normal.
2 slightly raised.
_Pulse_ on admission: 1 subnormal.
1 normal.
1 accelerated.
Still, when all is considered, concussion and compression are but
ill-defined from one another, both in their clinical and pathological
aspects. The more indefinite cases of concussion are probably such as
border on compression, the increasing œdema gradually carrying the
patient across the border line between the two conditions.
In the present state of our knowledge respecting concussion or cerebral
shock it may, I think, be accepted (1) that concussion is dependent on
an acute inhibition or paralysis of the vaso-motor centre; (2) that the
milder cases are unassociated with any pathological visible changes; (3)
that the prolongation and severity of the depression stage are directly
proportionate to the extent of the brain lesion, such lesions varying
from œdema and contusion to extensive hæmorrhages and lacerations.
Its symptomatology.
_The stage of depression._ The symptoms are evoked immediately on the
receipt of the blow, the patient falling to the ground from lack of
muscular control and loss of consciousness. The muscular system is
completely relaxed, the limbs, when raised, falling helplessly to the
ground. The face is deathly pale, the eyes usually open, fixed, and
expressionless, the pupils equal, commonly dilated and responsive to
light. The patient _may_ be aroused by strong stimuli--pinching,
shouting in the ear, pressure over the supra-orbital nerves, &c.
The pulse is small, slightly accelerated, and occasionally intermittent.
The respiration is weak, shallow, and often irregular. The temperature
is lowered, sometimes to such an extent that it cannot be registered on
the thermometer. The surface of the body is cold and clammy, beads of
sweat standing out on the brow. The deep reflexes are abolished. Some
attempts may be made at swallowing when fluids are placed in the mouth.
Urine is often expelled at the time of the accident, and, more rarely,
fæces may also be passed involuntarily.
The condition either gives place to that of reaction or the state of
unconsciousness and collapse becomes more profound, in which case the
prognosis is most unfavourable.
_The stage of reaction._ Weak, purposeless movements are observed and
the patient may sigh heavily, mutter, or groan. This is followed by
profuse vomiting, after which the temperature begins to rise, the body
becomes warmer, and the patient recovers his senses either entirely or
in part. The heart beats strongly, the pulse being full and slightly
accelerated in rate. The carotid arteries are seen to pulsate forcibly,
the face is flushed and moist. The patient is restless, and complains of
severe headache, due in all probability to intradural hypertension.
Under efficient treatment these symptoms of cerebral hyperæmia abate,
the patient recovering quickly or slowly, according to the severity of
the blow. Retrograde amnesia is often a conspicuous feature in the more
severe cases, varying greatly in depth and character, seldom permanent.
In the more serious cases--those associated with severe cerebral
injury--the pupils dilate fully and do not react to light. Corneal
reflex is absent. The medullary centres gradually become exhausted, the
pulse becoming smaller, increasing in rapidity, and finally
unrecognizable. Respiration becomes weaker and often Cheyne-Stokes in
character. Respiration ceases before the heart gives out.
Cerebral Irritation.
_Its pathology._ Sufficient evidence is supplied, both by clinical
symptoms and by post-mortem examination, to show that brain irritation
is dependent on definite brain lesions, these varying from ‘bruising’ to
minor degrees of laceration. Bruising or contusion of the
brain--evidenced by pia-arachnoid hæmorrhages and by cortical and
subcortical hæmorrhages--is most prevalent in the frontal and
temporo-sphenoidal regions. The same may be said with respect to
laceration.
_Its symptomatology._ From the initial stage of concussion the patient
passes into that of irritation, the reaction being of a rather violent
type and accompanied by considerable rise of blood-pressure.
The patient lies curled up in bed, the lower extremities flexed at the
hip and knee, the upper limbs bent across and partially covering the
forwardly flexed head. He is exceedingly restless. Restraint is usually
required. The eyes are tightly closed, and all attempts at pupillary
examination are strenuously resisted. The patient groans, mutters, and
uses language, perhaps suited to the occasion but not adaptable to
polite society. Headache is severe, often referred to the frontal
region. The skin is hot and dry--burning--the body temperature is raised
whilst the pulse is accelerated and its tension increased. Both urine
and fæces may be passed into the bed, not so much from loss of bladder
and rectal control as from transitory moral perversion.
The state of irritation subsides or merges into that of cerebral
compression.
Compression.
_Its pathology._ A compression force--whether foreign body, blood
extravasation, abscess or tumour--must act on the brain substance or on
the fluid constituents of the skull. The brain, however, is itself
incompressible. It may be squeezed like a sponge, but its actual
structure is unalterable. Consequently, the compressing force exercises
its main influence on the fluid contents, driving out the cerebro-spinal
fluid, depleting the cerebral veins and emptying the arterioles,
producing in other words a state of brain anæmia.
Experimentally, it has been ascertained that from 3 to 6 per cent. of
the cranial capacity can be taken up by a foreign body without producing
compression symptoms--probably owing to the escape of cerebro-spinal
fluid into the spinal canal, and the recession of the medulla and
cerebellum into the foramen magnum. Furthermore, it would appear that
the incidence of compression symptoms is associated with depletion of
those cerebral veins which are in closest relation to the compression
force. As this force increases--for example, in middle meningeal
hæmorrhage--the pressure exercised on the surrounding regions increases
proportionately, to the level of the capillary pressure, and even to
that of the smaller arteries. A state of cerebral anæmia results, first
localized to the region primarily involved, then invading more widely
and finally affecting both supra- and infra-tentorial spaces.
With regard to the continuity of pressure between these three spaces,
there is but little pressure discontinuity between the two
supra-tentorial spaces, whilst, between the supra- and infra-tentorial
regions, there is less ready communication.
A slight degree of compression in the supra-tentorial space will act on
the corresponding space only, greater degrees will involve all three.
On the other hand, a rise of infra-tentorial pressure is not of
necessity associated with a corresponding elevation in the other two
regions. For example, a cerebellar tumour readily affects the medullary
centres, whilst the higher cortical regions are for the time being
totally unaffected. Again, a tumour situated in the frontal pole does
not necessarily produce any of those symptoms of cerebral compression
which are regarded as referable to an increase of subtentorial
pressure--slow pulse, vaso-motor disturbances, subnormal pressure, and
deep rhythmical respiration.
Returning once more to the vascular effects of a localized compression,
it is obvious that whilst the compressing force is producing a
surrounding anæmia--depleted veins and arterioles--yet that the
neighbouring but more distant brain is venously engorged--from venous
retardation. Insomuch, moreover, as the venous tension and
cerebro-spinal pressure are equal, it is obvious that, as the result of
venous engorgement, there is some surrounding serous transudation into
the perivascular, pia-arachnoid, and cerebral regions. The brain
bordering on the anæmic area is therefore œdematous, the œdema
diminishing and fading away in direct proportion to the distance of the
area involved from the primary focus of compression.
If the compression force is of a progressive nature, the engorged area
becomes in turn anæmic, and still more distant regions become engorged
and œdematous. This state is known as that of _progressive œdema_. Its
complete development is largely dependent on brain infection--abscess of
the brain, &c.
The rapidity with which the symptoms of compression develop are largely
dependent on the producing cause. Thus, three examples may be cited:--
(1) Compression of slow development, requiring weeks or months before
typical symptoms are observable--e. g. tumour formation.
(2) Compression of medium development, requiring days only: e. g.
abscess, subdural hæmatocele, and some forms of middle meningeal
hæmorrhage.
(3) Compression of acute development, almost immediate: e. g. diffuse
subdural hæmorrhage, some cases of middle meningeal hæmorrhage,
depressed fractures, and intracranial foreign bodies.
The special symptoms of compression are, as Leonard Hill pointed out,
referable to the effects produced on the bulbar centres. That such is
the case is suggested by the following facts:--
(1) The same compression symptoms result wherever the compressing force
acts.
(2) Experimentally, an increased pressure in the posterior fossa
produces compression symptoms earlier than when the compressing force is
exercised in some more distant region of the brain.
(3) A fracture involving the posterior fossa gives rise to compression
symptoms earlier than a fracture in some more distant region.
(4) A far smaller body kills in the bulbar region than in the cerebral
chamber.
(5) The general pressure effects are in no way due to excitation of the
part of the brain pressed on, for, after division of the mesencephalon,
the pressure was just as active in calling forth changes in respiration
and circulation (Sir Victor Horsley).
Leonard Hill also pointed out that the first effect of anæmia of the
bulbar region was in the nature of stimulation, the vaso-motor centre
being influenced in such a manner as to produce a general rise of
blood-pressure. A further degree of compression may again produce the
same result, the arterial pressure rising considerably above the normal.
Later on, the medullary centres--and more especially the
vaso-motor--become exhausted, with consequent grave fall in
blood-pressure. The pulse, previously slow and full, becomes rapid,
small, readily compressible, and irregular in rhythm, whilst the
respiration, previously deep and regular, becomes gasping, irregular,
and Cheyne-Stokes in character.
The sequence of events may be depicted in another manner. In cerebral
compression, the battle--as pointed out by Schüster--largely resolves
itself into a life and death struggle between the attacking compression
force on the one hand and the defending vaso-motor centre on the other.
Up to a certain point the vaso-motor centre holds the whip-hand. The
capillary anæmia as produced by the compression force--cerebro-spinal
tension, &c.--brings about a condition which not only acts as a stimulus
to the vaso-motor centre but also exercises a marked effect on the
vagus and respiratory centres. The blood-pressure rises, the pulse is
slowed in rate, and its tension markedly increased, whilst the
respiration is slightly irregular both in depth and rhythm. The
vaso-motor centre thus attacked sends out further impulses so as to
raise the blood-pressure to slightly above requirements. The bulbar
centres are again flushed with blood, the vaso-motor centre ‘slacks
off’, and the blood-pressure falls again.
The compressing force is, however, still active and full of fight. A
further capillary anæmia results. The vaso-motor centre again responds
and the blood-pressure rises higher than ever, the pulse-rate is further
slowed, and the respiration is deeper, less regular, and even
stertorous.
This combat continues, and, in the presence of an active compression
force, there is that rhythmic activity of the vaso-motor centre which is
represented by the well-known Traube-Herring curves; again, the height
to which the vaso-motor centre drives the blood-pressure may be taken as
representing the activity of the compression force.
When the compressing force rises above a certain limit the _débâcle_
occurs--the vaso-motor centre retires from the fight, there is a rapid
fall in blood-pressure, the medulla is emptied of blood, and both
cardiac and respiratory centres share in the defeat (rapid pulse of poor
volume and Cheyne-Stokes respiration).
These being the effects as exercised by compression on the bulbar
centres, one must not omit to consider the results produced on the
higher cortical centres. Anæmia is the feature and unconsciousness is
the ultimate result, preceded by headache and drowsiness progressing on
to stupor and coma. Intermediate between the stages of sleepiness and
coma, one observes occasionally a stage of irritation--such as is
pictured in many cases of typical middle meningeal hæmorrhage.
In fatal cases the respiratory centre gives out first, the heart often
beating for some time after all attempts at respiration have ceased. In
a case recently under my care, respiration ceased during the process of
trephining. The patient was kept ‘alive’ for three hours by means of
artificial respiration, and under such mechanical breathing the patient
retained a good colour and the heart worked well. So soon, however, as
efforts were relaxed, the pulse became weaker and weaker until further
artificial respiration again restored the balance. This process was kept
up till it was realized that the respiratory centre was ‘dead’.
From these facts, it may be assumed that the special symptoms of
compression are dependent (_a_) on anæmia of the bulb--with
corresponding cardiac, respiratory, and vaso-motor changes; and (_b_) on
anæmia of the cortex--with unconsciousness.
=Its symptomatology.= According to Kocher, the following are the four
stages of compression:--
1. _The stage of compensation._ A mild degree insufficient to seriously
compromise the circulation. Cerebro-spinal fluid escapes into the spinal
canal and some of the venous radicles are compressed. Some venous
engorgement. Some headache, possibly some focal symptoms. Some mental
dullness.
2. _Stage of beginning compression._ Beginning failure of the
circulatory compensation. Headache pronounced, vertigo, restlessness,
excitement or delirium. Objective symptoms of venous stasis--dilatation
of the veins of the eye, both external and internal, œdema of the disk.
Affection of the medullary centres, shown by a slowed pulse and a slight
rise in temperature.
3. _Stage of fully-developed compression._ Widespread capillary anæmia.
Medulla affected markedly. The period of vaso-motor regulation has set
in with its high blood-pressure, and this, with its vagal quality, gives
the pulse its bounding character. The rise in blood-pressure shows a
definite rhythm. Also rhythmicities in respiration which may acquire the
Cheyne-Stokes character. Rhythmic alterations in the size of the pupils,
with alternate increase and decrease in the depth of stupor, so that the
‘up-wave’ causes the patient to moan, become irritable, and thrash
about, whilst the ‘down-wave’ sees him completely comatose. Pulse is
markedly slowed and the disks evidence pronounced ‘choking’. Reflexes
are abolished, cyanosis extreme, respiration snoring.
4. _Stage of paralysis._ Irregular cardiac and respiratory efforts,
pulse grows rapid, coma deepening, muscular relaxation, pupils widely
dilated, and permanent fall in blood-pressure. Respiratory paralysis.
Treatment.
(_a_) _Of concussion._ In considering the treatment of concussion, it
has to be remembered that we are treating a condition dependent on
vaso-motor depression, and that we are ignorant--at any rate for the
time being--as to the nature and extent of a possible cerebral lesion.
It is obvious, therefore, that although we are clear as to the general
lines on which treatment is to be carried out, yet that our earlier
methods must be expectant and our subsequent methods symptomatic. In
other words, we must be prepared, at any moment, to change the method of
treatment according as symptoms demand.
The more general treatment--applicable to all cases, of whatever
severity--consists in putting the patient to bed with the head low, in
the application of warmth to the body and extremities, and in the
administration of hypodermic injections of morphia, a drug of great
value in the more severe cases of concussion. It must, however, be
administered with caution, lest important symptoms be masked.
Strychnine and brandy are practically useless. They merely whip the
willing horse--the heart is doing full duty and cannot be further
stimulated by such measures.
In _mild and moderately severe cases_ this form of treatment will
suffice to tide the patient over the collapse stage and induce the stage
of reaction. So soon as this _commences_, the rising temperature and
vomiting heralding the change, the head of the bed should be lowered,
hot bottles and blankets removed--the patient being covered with a linen
sheet only--and all forms of stimulant avoided.
Calomel should be given by the mouth, 1 to 5 grains, according to the
age of the patient. Headache may be relieved by applying ice-bags to the
head, by tying round the forehead a handkerchief soaked in a weak
solution of eau-de-Cologne, and by the administration of various drugs,
more especially aspirin (10 grs.), antipyrin (10 grs.), and hyoscin (gr.
¹⁄₁₀₀).
In _more severe cases_ more radical measures must be adopted to combat
the severe vaso-motor depression, with its consequent splanchnic
congestion and cerebral anæmia. No method is more desirable than
infusion. This method, with its attendant advantages and disadvantages,
has been detailed on p. 118. It is merely necessary to add that infusion
must not be carried out in a haphazard manner. Its application is based
on scientific principles, and its results must be noted with the
greatest care. The surgeon must keep a watchful eye on the temperature
and blood-pressure, and he must be prepared at any moment to change his
plan of campaign.
(_b_) _Of irritation._ The patient should be kept in a darkened room and
should not be worried more than is absolutely necessary for diagnostic
purposes. An attendant is usually required, whose methods should be
persuasive rather than forcible. Great tact is required.
Morphia is of the greatest value in the treatment of this condition. It
relieves the headache, acts as a damper on the hyperæmic brain, and
keeps the patient from threshing about in bed and injuring himself.
Sleep is essential for an early recovery and cure.
In the _more severe cases_ venesection should be carried out, and
operative measures will be required if the rising temperature and slowed
high-tension pulse herald the advent or indicate the presence of
compression of the brain.
(_c_) _Of compression._ The various operations carried out for the
relief of compression of the brain are discussed elsewhere. They include
such operations as are conducted for localized hæmorrhages, whether
subdural or extra-dural (see Chap. V), and such also as are described as
‘decompression’ operations (see p. 121).