FRACTURES OF THE VAULT OF THE SKULL

Fractures of the vault of the skull may be restricted to the vault or associated with a basic fracture. Evidence has been brought forward previously to show that many vault fractures may be regarded as mere upward extension from a primary basic lesion. The limitation of a fracture to the vault depends on the nature of the productive force, the degree of violence used, the site of application, and the direction of the force. Thus, the smaller the weapon, the greater the violence, the nearer the site of application to the vertex, the more direct the blow, the greater is the tendency to vault limitation. Again, compound fractures are much more liable to vault limitation than simple fractures, as is proved, for instance, by the reports of Sir Prescott Hewitt—20 compound fractures in which the fracture was restricted to the vault of the skull, and 56 simple fractures in which the base was involved in all but one.

Fractures of the vault may involve:—

(a) the external table only;
(b) the internal table alone;
(c) the whole thickness of the skull.

Fractures of the external table alone.

These fractures are excessively rare. Their existence was even doubted till the recent South African War, when Makins [23] saw one case of this nature. They appear to be due to the impact of a glancing bullet (see [p. 297]). A ‘gutter-shaped’ depression results, the comminuted fragments of the external table being carried away or distributed in the region of the lacerated scalp (see [Chapter IX]).

Fractures of the internal table alone.

Ambrose Paré drew attention to this class of fracture in 1652, but it remained for Teevan to investigate more fully the condition in 1865. Previous to Teevan’s investigations, it had been considered that the internal table of the skull was the more brittle, and that fractures confined to the internal table were to be explained on that hypothesis. Teevan, however, demonstrated the incorrectness of such a theory, for, on firing bullets through the skull, from without inwards and from within outwards, it was found that on all occasions the more distal table suffered the more severely. This was explained in the following manner:—the fracture of the proximal table was produced by the bullet, whilst that of the distal table resulted, not from the passage of the bullet alone, but also from various fragments of bone driven along with the bullet.

Teevan’s experiments also proved that a fracture of the internal table alone could be produced mechanically, this being in obedience to the law that ‘when a pressure is applied to a body the fracture commences on the line of extension, not that of compression’.

Fractures of the internal table are undoubtedly more common in those situations where diploic tissue is prevalent, e.g. in the frontal, parietal, and upper occipital regions. In the squamo-temporal and cerebellar regions fractures of the internal table are almost unknown.

Teevan also stated that ‘but little force is required to produce such a fracture, and that they are produced usually by some small body, such as a stone’.

Fractures involving the whole thickness of the skull.

Fractures which involve the whole thickness of the skull may be:—

(a) Simple or compound.

(b) With or without depression.

When depressed, the fragments of bone may be either loose or interlocked, forming in the latter case the so-called pond and gutter fractures.

(d) Fissured, stellate, comminuted, punctured, &c.

(e) Explosive.

Symptoms associated with fracture of the vault.

A diagnosis of fracture of the vault is made:—

On the evidence obtained by local examination.

On the evidence supplied by symptoms dependent on injury to the intracranial contents.

The various intracranial lesions are discussed elsewhere (see [Chapters III] and [IV]).

Evidence supplied by local examination.

A compound fracture will be most readily determined by digital examination, previous to which the scalp-wound must be carefully cleansed. Digital examination is greatly preferable to investigation with the aid of the probe. In any case care must be taken to avoid mistaking one of the sutures of the skull for a fissured fracture.

In simple fractures the diagnosis is frequently obscured by an extensive subaponeurotic or subpericranial hæmatoma. Irregularities of surface are more or less diagnostic of a solution in the surface of the bone, and a linear hæmatoma is of corresponding clinical value. In any case, the presence of an extensive hæmatoma must be regarded as of so suggestive a nature that exploration is called for, more especially when prolonged concussion or compression are co-existent. Such treatment is imperative when the hæmatoma—whether diffuse, localized, or linear—pulsates, such a condition implying a breach in the surface of both bone and dura with communication between the extra-cranial and some intra-cranial hæmorrhage.

Pringle [24] lays stress on the value of percussion as an aid to diagnosis.

‘The patient’s head must be supported beneath the occiput, the mouth either open or shut—it matters not, so long as it is the same throughout the examination—and the skull is struck sharply with the finger. When a fracture is present, two changes in note may be elicited. Either a note lowered in pitch over the fracture zone, or, in addition, a definite crack-pot sound. The note elicited is most typical when comminution is present, and some fragments loose. A fracture of a T or L or V-shape gives the best crack-pot sound, and the crack quality is always most pronounced when the percussing finger comes over the angular portion of the bone. Hæmorrhage into the subaponeurotic region blurs the note.’

Fig. 42. A Comminuted Fracture of the Skull.

If time and occasion permit, an X-ray photograph will clinch the matter.

When the fracture involves the internal table alone, the symptoms are less definite. Teevan stated that this class of fracture does not lead to the development of any symptoms unless:—

The middle meningeal artery be injured.

The dura mater and brain be irritated.

The brain be compressed.

He also adds that the existence of the following features suggests the nature of the injury:—

The history of a slight blow, probably with a small body.

The blow situated over the parietal region.

Fig. 43. An Explosive Fracture of the Vault of the Skull. A shows the right side of the skull and the site of entry of the bullet. B shows the extension of the fracture round the left half of the skull. In the left upper parietal region (Fig. B) a fissured fracture is seen where the bullet failed to perforate the skull.

Chronic fixed pain, some days or weeks afterwards, with symptoms of brain-irritation or encephalitis, and even suppuration, suggesting irritation of the meninges and brain by spicules of bone.

Compression and paralysis on the opposite side of the body some hours afterwards, as the result of injury to the middle meningeal artery.

Symptoms of compression early and slight, combined with partial paralysis of the opposite side of the body.

‘The less definite the symptoms of compression, the greater the reason to believe that they are caused by the internal table only.’

Before entering into the question of treatment of fractures of the skull, it is essential that allusion should be made to the temperature in its relation to head-injuries. The great importance of temperature changes in the consideration of operative treatment will be manifest when discussing the treatment of fractures of the base.

The temperature in its relation to head-injuries.

The various temperature changes observed in cases of head-injury have afforded a subject prolific in discussion. Broca, Battle, Guyon, Walsham, and others have endeavoured to deduce facts from the examination of head cases, but the results have been rather indefinite. In over 300 cases that have come under my observation, accurate records of the temperature charts were obtained, the patients were watched throughout their illness, and in the case of death, the autopsies were attended.

The following deductions were made:—

1. That, for a variable period of time after the injury, the temperature is always subnormal—sometimes so low that it cannot be registered. This is the period of shock.

2. That the patient may die in this state of shock, but that, if he lives, reaction takes place and the temperature rises.

3. That this rise in temperature is, in fatal cases, rapid and progressive. In one case the temperature rose 6° in seven hours, in another 8° in four hours. Death occurs when the temperature is at its highest—anything up to 106°, and even more when registered in the rectum.

4. That the temperature may rise to a moderate height, and there ‘mark time’. This is the ‘crisis’ of the case. A subsequent fall in temperature generally indicates recovery, a further rise usually points to a fatal termination.

5. That the rise of temperature is independent of any special osseous lesion, since similar changes are observed in fractures of the vault and in fractures of the base.

6. That laceration of the brain is present in the majority of cases in which marked temperature changes are observed, but that the changes in temperature are totally independent of any special regional brain-injury.

Richet arrives at the conclusion that two hypotheses present themselves, accounting for temperature changes in general: (1) that there are certain temperature regulators in the encephalon which, when excited, become stimulated in function; (2) that the cortical injury acts in a sort of reflex manner on the regulatory centres situated in the pons or bulb.

Attention was also drawn to the experiments of Lorin and van Benedin, who, after excising the two cerebral hemispheres of a pigeon, showed that the heat regulatory centre was preserved intact, proving that the corpus striatum is not necessarily the head-office for heat-regulation in general.

Till, therefore, more evidence comes to hand with respect to heat-regulation in general, one cannot go beyond the broad statement that, in severe head-injuries, definite temperature changes occur, that the changes are independent of any special lesion of bone or brain, that they are generally associated with some brain-injury, and that they are probably due to the influence exerted by the lesion on the heat-regulating centres in the region of the pons and bulb.

With regard to the value of the temperature, both with respect to prognosis and treatment, a very much more definite statement can be made.

First with respect to the prognosis. All cases of head-injury may be grouped into four classes, according to the changes of temperature present.

Group 1.

The temperature, at first subnormal, undergoes a rapid and progressive rise. Prognosis most unfavourable.

Group 2.

The temperature, at first subnormal, rises gradually to 101° or 102° and there ‘marks time’. This hesitancy marks the crisis of the case, further elevation indicating a fatal result, whilst a fall offers every hope of recovery.

Group 3.

The temperature, at first subnormal, rises to normal and remains at that level. Prognosis very favourable.

Group 4.

The temperature, at first subnormal, remains subnormal. The condition of shock persists, and the prognosis is most unfavourable.

Practically all cases of head-injury fall readily into one or other of these four groups, and the temperature chart presents so clear a picture that it must be regarded as of the greatest possible value in estimating the prognosis in any given case. In other words, the temperature chart affords an almost infallible guide both to prognosis and treatment.

With respect to alteration in temperature on the two sides of the body, the clinical value of such changes must, from my own observations, be regarded as of a very indefinite nature.

It now remains to discuss the value of temperature changes with respect to treatment.

Treatment of Fracture of the Base of the Skull.

In the earlier paragraphs of this chapter the special treatment of aural and nasal hæmorrhages and cerebro-spinal discharge was discussed, and some allusion was made to the necessity of exploring the middle fossa in cases of profuse arterial or venous aural bleeding. The general treatment of basic fractures now requires description, previous to which, however, space must be made for a short account of the routine treatment by Urotropin—as advised by Crowe and Cushing—as a prophylactic against the development of meningeal infection. The following is a summary of Crowe’s paper [25] on the ‘excretion of Urotropin in the cerebro-spinal fluid and its therapeutic value in meningitis’.

1. Urotropin, when given by the mouth, invariably appears in the cerebro-spinal fluid.

2. The largest amount of Urotropin is present in the cerebro-spinal fluid from thirty minutes to an hour after the ingestion of the drug.

3. After doses of Urotropin, within therapeutic limits, a sufficient amount of the drug appears in the cerebro-spinal fluid to exercise a decided inhibitory effect on the growth of organisms inoculated into this fluid after its removal from the body.

4. Following a subdural inoculation of dogs and rabbits with streptococcus, 60-80 grains of Urotropin a day, given under conditions which insure absorption, will markedly defer, and in some cases prevent, the onset of a fatal meningitis.

5. In view of these observations, the prompt administration of Urotropin is advised in all clinical cases in which meningitis is a possible or threatened complication, or even when meningeal infection has actually occurred.

Fig. 44. A Temperature Chart illustrating the Changes in Temperature observed in Head-injuries. (For description, see text.)

[Larger chart]

Acting on these suggestions, I am accustomed to treat all head cases with this drug, 10-20 grains three times a day by mouth. It may be given per rectum, though probably with less satisfactory results. Traumatic cases are treated as soon as possible, other cases receive their dose for two or three days previous to the operation, the drug being continued till all fear of possible meningeal infection has vanished.

In discussing the general treatment of basic fractures, it must be accepted that the basic fracture in itself requires no treatment. Danger or death is dependent on intracranial complications, and an uncomplicated basic fracture demands no active surgical treatment. The special treatment applicable to cases complicated by hæmorrhages, both external to and beneath the dura mater, is discussed in the next chapter. It is therefore only necessary to enter into those cases of fractured base which are associated with concussion, irritation, and compression of the brain—in other words, the average case of fracture of the base of the skull.

The surgeon must always be guided by the general condition of the patient—the blood-pressure, character of pulse, state of respiration, depth of unconsciousness, &c.—but, in my opinion, the temperature chart affords perhaps the most valuable basis on which rules can be formulated guiding the surgeon in his general line of treatment.

Thus (1) when the temperature remains subnormal the patient is in a condition of severe cerebral shock, due, in the majority of cases, to contusion or laceration of the brain, the grosser lesion being most commonly situated either at the apex of the temporo-sphenoidal lobe or at the anterior inferior part of the frontal lobe. The patient is, however, suffering from shock, and the treatment advocated for that condition in general is equally applicable to these cases in particular. The patient should be placed in the so-called head-down position, and the extremities firmly bandaged from below upwards. The vaso-motor depression should be combated by the administration of rectal or intra-venous infusions of saline solution, to each pint of which is added 1 drachm of a 1 in 1,000 solution of Adrenalin Chloride. It is at once obvious that, whilst combating the condition of shock, this mode of treatment may tend at the same time to encourage fresh bleeding if the brain should have been lacerated, or if intracranial vessels should have been torn. For this reason I regard rectal infusion as the more safe of the two methods, in spite of the fact that intra-venous infusion brings about a more rapid improvement in the patient’s condition. The effect of the infusion must be carefully observed, and as soon as the blood-pressure rises and the temperature shows a tendency to rise—say from the subnormal to the normal—the infusion process must be stopped, and the further progress of the case observed.

The risks attendant on this mode of treatment are obvious, but in their consideration, it must also be borne in mind that if the patient remains in the collapse stage, without evidencing any sign of reaction, he will inevitably die. If the treatment advocated should tide the patient over this stage and induce a definite reaction, as exemplified by rise of blood-pressure and elevation of temperature, the further treatment of the case can be considered under the next group.

(2) When the temperature rises progressively the patient evidences symptoms pointing to compression of the brain—coma, slow pulse, noisy and stertorous respiration, hot skin and turgid face. Later on, as a result of the increasing pressure, the medullary centres begin to show signs of exhaustion, the pulse-rate increasing, and the respiration becoming Cheyne-Stokes in character.

Whether these symptoms result primarily from the nature of the lesion, 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.

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.

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.

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.

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.