Management of Acute Head Trauma

Management of Acute Head Trauma

Management of Acute Head Trauma HENRY G. SCHWARTZ, M.D., F.A.C.S. * IN THE management of acute head trauma, multiple elements have to be borne in min...

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Management of Acute Head Trauma HENRY G. SCHWARTZ, M.D., F.A.C.S. *

IN THE management of acute head trauma, multiple elements have to be borne in mind. The injury may involve scalp, bone, meninges, brain, intracranial blood vessels, and cerebrospinal fluid. These areas may be affected singly or in any combination. Peak damage may involve these elements immediately and concurrently, or there may be delayed manifestations of pressure or infection which must be watched for. Whatever the presenting clinical picture may be when the patient is first seen and whatever the apparent injuries are, the head injured patient should be looked upon as a potential continuum of pathological entities, which may require specific therapy as time goes on. For these reasons, it is difficult to lay down a rigid plan of management which will apply to all cases. Careful evaluation of the patient's general condition, physical and neurological findings, and the history of the injury are essential. This evaluation should be carried out with reasonable dispatch. The general atmosphere of panicky concern which frequently surrounds the admission of a patient with a major injury to the hospital emergency room should not be allowed to pressure the physician into headlong activity at the expense of over-all evaluation of the patient. This should not be interpreted as an excuse for desultoriness or lack of diligence. HISTORY

Whenever possible it is of importance to obtain an accurate history of the injury. The mechanics of head trauma may help considerably in evaluating the likely site or sites of major brain damage. The injury may be the result of a direct blow (a blunt instrument or a rapidly moving missile) against or into the relatively stationary head. On the other hand, the head itself may have been moving rapidly until suddenly arrested by a fixed or slowly moving object. In the case of the former mechanism local deformation of the skull may occur, inflicting gross damage upon the immediately underlying blood vessels or brain; or lines of force may extend to adjacent or distant parts of the skull such as the squamous

* Professor of Neurological S'urgery, Washington University School of Medicine. Chief of Neurosurgical Service, Barnes and Allied Hospitals, St. Louis, Missouri. 1475

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portion of the temporal bone, the posterior walls of the frontal sinuses, or the thin roof of the orbit. The mechanism of injuries sustained by a rapidly moving head, such as might occur in a head-on collision, consists of rapid acceleration of the skull and contained brain followed by sudden deceleration as the head strikes the dashboard or pavement. With sudden arrest of the skull, the more slowly moving brain in its pool of cerebrospinal fluid continues to advance and strikes the inner table of the bone, the roof of the orbit, the sharp wings of the sphenoid bone, or the edges of the falx or tentorial margin. In addition to more or less direct lines of force thus affecting the undersurface of the frontal lobes, the tips of the temporal lobes, and the tearing of blood vessels running to the longitudinal sinus, rotational or shearing forces may occur in some instances, resulting in twisting and tearing of the upper part of the midbrain. Finally, bone or missiles driven into the brain may give rise to force transmitted in such a way that the medial portion of the temporal lobe may herniate into the incisura of the tentorium, resulting in midbrain and pontine hemorrhage. Inquiry should be made into the question of loss of consciousness, its duration and whether or not there has been alteration of consciousness between the moment of injury and the time seen by the examining physician. Progressive stupor or drowsiness is an indication of pressure or brain swelling. Along with the inquiry about state of consciousness, the patient or his companions should be quizzed concerning vomiting, ability to move the extremities, presence or absence of convulsive seizures, and escape of blood and cerebrospinal fluid from the nose or ears. The answers to these questions can contribute to evaluation of generalized or localized damage to the brain. EXAMINATION

General physical examination in addition to neurological examination is of course essential in every case. Shock is rarely encountered in head injuries, unless there has been considerable loss of blood. If shock is present, appropriate treatment including blood transfusion must be instituted promptly, and a diligent search made for injury to the long bones, abdominal and thoracic viscera. Proper measures must be taken in dealing with associated injuries. Vital signs consisting of blood pressure, pulse, respirations and temperature are recorded and checked at frequent intervals. The head is examined for lacerations, subgaleal hematomas, palpable bone defects and evidence of spinal fluid leakage from the nose or ears. Neurological examination is necessarily limited in the unconscious patient, but some pertinent observations can always be made, to be used as a baseline against which later abnormal findings may be accurately interpreted. Pupillary size, equality and reaction should be carefully noted. Eye movements can usually be tested. Even in the comatose

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patient, symmetry of facial innervation can be judged by exerting pressure over the mastoid process or supraorbital nerve; at times, paralysis of one side of the face is made evident by the slackness of one cheek when the patient exhales. Gross function of the extremities can be estimated by the reaction of withdrawal to painful stimuli. Activity of the tendon and abdominal reflexes should be noted, as well as the presence or absence of pathological toe signs. Of utmost importance in acute head injury is respiratory function. Any obstruction of the airway will reflect back through the jugular veins and major intracranial venous sinuses, causing increased intracranial pressure. This is aggravated further by the vasodilating effects of accumulated carbon dioxide. Therefore, early attention must be focused on the patient's airway, Proper posturing.with the patient turned on his side, will prevent the tongue and lower jaw from sagging back and will improve patency of the upper airway. Clearing the pharynx and trachea of secretions or of blood and vomitus can usually be achieved by suction. Suction should be carried out gently, trying to avoid trauma to the posterior pharynx and trachea. In some cases where these simple measures fail, tracheotomy may prove invaluable in combating anoxia due to respiratory tract obstruction. In addition to these measures, we have found that placing the patient in a cool oxygen tent serves the dual purpose of combating hypoxia and hyperthermia. After the foregoing evaluation of the patient has been made, roentgenograms are taken. In addition to skull fracture, it is also "vise to exclude fracture or dislocation of the cervical spine. FRACTURE OF THE SKULL

It is axiomatic that morbidity. and mortality in .head Injuries are primarily the result of brain damage and that fracture of the skull is of secondary importance. At the same time, there are some fractures which demand surgical intervention and others which, by their presence, arouse a high index of suspicion of a potential underlying lesion which may require operation. It is customary to classify. skull fractures as .simple .and .compound. Under the first category are (1) linear fractures and (2) comminuted fractures, with ·or without depression. Under compound fractures are included (1) abrasions of the skull, (2) linear, (3) comminuted, with or without depression and (4) fractures communicating with the ear .or accessory nasal sinuses. Simple Fractures

Simple linear fractures require no treatment so far as the bone defect is concerned. However, the presence of a fracture crossing the squamous portion of the temporal bone should serve to increase our alertness to detect a possible extradural hematoma due to a tear of the middle menin-

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Fig. 376. A, Roentgenogram of a large depressed fracture of the right parietal bone in a newborn infant. B, Reduction was achieved by introduction of a blunt elevator through a small perforator opening made adjacent to the posterior margin of the fracture.

geal artery. Similarly, a linear fracture of the occipital bone makes us more aware of the relatively uncommon extradural or subdural hematoma of the posterior fossa due to bleeding from the lateral sinus. These possible complications may occur especially rapidly in young children in whom dura is readily separable from the inner table of the skull. Simple comminuted fractures may require operation if there is significant depression, and particularly if the depression overlies important areas of the brain such as the left inferior frontal or temporal lobes (speech centers in right-handed individuals), the motor-sensory areas adjacent to the frontoparietal fissure, or the occipital poles (visual centers). A word of caution should be injected at this point, with the recommendation that a diagnosis of depressed fracture should be withheld until roentgenographic evidence is available; for even experienced hands may erroneously interpret the firm margins of a subgaleal or pericranial hematoma as the edges of a fracture. At times, depressed fracture may occur in the newborn as a result of forceps delivery. Ordinarily these are small and are immediately reduced by the obstetrician who applies gentle pressure at the margins, not unlike the method used to spring a dent in a ping-pong ball. One of these fractures which failed to respond to this method was being prepared for surgery when the baby howled vigorously. The effect of this Valsalva maneuver resulted in a visible and audible spontaneous "popping out" of the depression! Occasionally, a forceps-induced fracture may be of considerable size and its very bulk demands surgical interference. Figure 376 illustrates such a fracture of the right parietal bone. Correction is achieved by placing a small perforator opening adjacent to the fracture

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Fig. 377. A, B, Simple, comminuted, depressed fracture of the left parietal bone, overlying the sensorimotor area. C, Exposure of the fracture. D, After opening lacerated dura, an intracerebral hematoma was encountered and evacuated under direct vision.

edge. Through this opening a blunt, curved elevator is introduced and the bone is molded back to normal shape and position. In Figure 377 is illustrated a simple, comminuted, depressed fracture overlying the frontoparietal sulcus in a two year old child. At operation, after the depressed fragments were lifted out, a laceration of the dura and a small intracerebral hematoma were found. Evacuation of the hematoma and repair of the dura resulted in excellent recovery and decreased the chances of formation of a dense scar in an "epileptogenic" area. If the fracture is depressed only minimally, it is probably best left alone. As a rule of thumb, it is our opinion that depressions over 1 em. should be elevated, and those between 5 and 10 mm overlying important areas also benefit from surgery. At operation, even if the dura is found intact, we have found it wise to open that membrane; at times this will reveal a subdural clot or an area of pulpified brain which should be removed.

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Fig. 378. A, Elevation of massively infected laceration of scalp, revealing underlying bone almost entirely denuded of periosteum. B, The posterior part of the infected scalp was necrotic and had to be sacrificed, The remainder was loosely approximated over gauze and rubber drains. Because of infection no attempt could be made to swing a skin flap over residual denuded parieto-occipital bone. This defect was later covered by skin graft.

Enthusiasm for surgery in this type of fracture must be tempered with judgment and trepidation if the depressed bone overlies the posterior half of the longitudinal sinus or the torcular Herophili. In such instances it may be wiser to leave at least the immediately adjacent fragment alone rather than risk laceration and thrombosis of a major channel of venous drainage from the brain. Lacerations of the Scalp

Before proceeding with a discussion of compound fractures, mention should be made concerning the general tendency to minimize the complications of the less formidable lacerations of the scalp. The scalp is extremely vascular and healing is usually quite rapid. Thus there has developed an attitude somewhat less careful than that which is maintained in dealing with laceration of the skin in other parts of the body. Carelessness has been enhanced, if not condoned, by the ready availability of antimicrobial drugs. Although it is true that in most cases the natural resistance of the scalp plus the use of antibiotics may permit healing, the importance of meticulous handling of these lesions is emphasized by the following case. A 9 year old boy was struck by a car and incurred a laceration of the vertex of the scalp. He was admitted to a hospital where the laceration was sutured. Antitetanus serum was administered and he received 600,000 units of penicillin twice a day. The day after the accident he had a convulsion, became progressively drowsy, and 2 days later he was transferred to our hospital, suspected of having a subdural hematoma. On admission, the boy was in deep coma and in shock. Blood pressure could not be obtained. Temperature was 40.6° C. (106.9 F.). Foul purulent drainage exuded from between the scalp sutures, and there was extensive swelling of the scalp, face and neck. He was treated for shock, following

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which the head was shaved, sutures were removed, and a large quantity of pus was evacuated from the scalp. Drainage was instituted and wet dressings were applied. He was given penicillin (400,000 units every 6 hours) and streptomycin (0.5 gram twice daily). By the second day, edema of the scalp and face began to subside and the patient became alert and oriented. Under general anesthesia, debridement of the infected scalp wound was performed. Most of the hemicranium was found to be denuded of periosteum (Fig. 378). All necrotic tissue beneath the elevated scalp was removed and several pockets of pus in the temporal region were evacuted. The posterior portion of the scalp was necrotic and had to be sacrificed. The residual portion of the scalp flap was loosely approximated. It was necessary to leave an extensive area of denuded parietal and occipital bone uncovered by skin, since the presence of infection precluded any possibility of swinging a flap. As infection was overcome, the outer table of the denuded area sloughed off, leaving a clean bed of granulation tissue. Subsequently, this was covered with a split thickness skin graft from the thigh. Healing proceeded without any further difficulty and the boy was discharged, 2 months after admission, with neurological examination entirely normal.

Happily, the end result in this youngster was good. Yet we cannot forebear saying that, had the scalp laceration been adequately treated in the beginning, weeks of anxiety and hospitalization could have been avoided. It was fortunate, indeed, that the suspicion of a subdural hematoma was not borne out, since attempted evacuation of such a lesion through the pool of subcutaneous pus would have been virtually hopeless.

COlllpound Fractures of the Skull The general principles which apply to compound fractures of the extremities are equally applicable to the skull. The primary goals are (1) the prevention or eradication of infection which may take the form of a fatal abscess or meningitis and (2) the improvement of physiologic defects resulting from the injury. Nowhere else is precise, meticulous surgery so important, and the technique of thorough debridement will be reviewed. It goes without saying that prompt intervention is desirable. However, if the patient is in shock or in a condition otherwise unsatisfactory to tolerate operation, delay may be necessary. It used to be held that the golden period for definitive surgery was about 12 hours. It was believed that, after this lapse of time, closure was too hazardous and that radical surgery should give way to acceptance of inevitable infection, with complicating meningitis, cerebral fungus or abscess formation-all resulting in high morbidity and mortality rates. Out of the nettle of World War II blossomed the realization that even wounds which were seen late could be attacked with the same precise surgical methods that applied in early cases. Subsequently, the addition of antibiotics has served to decrease (but not obviate) the risk of infection. It cannot be too strongly emphasized that,

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Fig. 379. A, B, After minimal excision of skin margins, the underlying compound depressed fracture is visualized. C, Bone fragments have been removed and openings in the dura have been sutured. D, Galea and skin are closed in layers with interrupted silk sutures.

if facilities for complete debridement are not available, it is wiser to delay rather than subject the patient to inadequate surgery which serves only to hide infection temporarily. Patients with head wounds, who may be expected to survive, tolerate transportation quite well. If transportation to a distant hospital is contemplated, immediate treatment should consist of clipping or shaving the hair surrounding the wound and the application of a snug, dry dressing. Penicillin S-R (400,000 units) should be given. As noted earlier, patients with limited head wounds are not usually in shock but, if this is present, treatment for shock should be instituted. Morphine should not be given. The only exceptions to this rule are some patients with associated fractures of the extremities. After the patient's arrival at the hospital where complete facilities are available, surgical debridement is done along the following lines (Fig. 379): Under general endotracheal anesthesia, the scalp is shaved. The skin is prepared with soap (preferably Septisol or pHisohex) and water. Copious saline irrigation of the lacerated wound is then carried out and appropriate drapes are applied around the field. Skin margins and galea

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should be excised minimally. If enlargement of the wound is needed, incision should be planned so that both exposure of the underlying fracture and closure of the scalp may be facilitated. Linear or slightly curved extensions are best. Superficial dirt, gravel and foreign material are removed, aided by frequent flushing of the wound with saline. Abrasions of the skull and fine linear fractures are best handled with a gouge, removing a portion of the outer table; if there then appear to be spreading lines of fracture beneath the narrowly debrided outer table, the full thickness of bone is removed. This will prevent the likelihood of later extradural abscess. Depressed bone fragments are lifted out, exposing the dura. Even if the dura is not lacerated, we have found it desirable to make a small opening which permits detection of a subdural clot or evidence of contused or macerated brain. If the dura is penetrated by indriven bone fragments or a missile, the opening should be enlarged and the cerebral lesion attacked under direct vision. Flat, malleable retractors are inserted through the mouth of the brain tract and macerated brain, clot and indriven material are removed with suction and cup forceps. In removing deep-lying bone fragments in a narrow tract, due care must be taken to free the fragment from any large vessels that may be in the vicinity before lifting it out; at times a main cerebral vascular trunk may be almost inextricably bound up in a nest of fragments, and considerable patience is required to free the vessel. Every effort is made to remove all indriven bone fragments, since their retention has been found to be responsible for the development of serious infection later on. We believe this to be so important that postoperative roentgenograms are made routinely; if any fragments are still seen in the brain, reoperation is performed. As debridement of the brain tract is carried out with a small suction tip, customary control· of bleeding with the electrocautery or silver clips is necessary. At times the tract may extend into or through the ventricle, in which case the importance of complete hemostasis is vital. In gunshot wounds, the course of the missile may extend a great distance. The stream of indriven bone chips will usually end at a considerable distance proximally and, beyond this point, the missile tract will become difficult to follow. When this stage of debridement is reached, further extended search for a metallic foreign body along a dwindling tract is not indicated. Unless the bullet is readily accessible, heroic efforts to remove it are not essential, since metallic objects do not commonly act as a nidus for infection. After complete hemostasis and debridement of the brain, the dura is carefully sutured with interrupted silk sutures. If a dural defect is present, closure with a piece of temporal fascia or pericranium is indicated. Closure of the galea and skin is then carried out in layers. Repair of the bone defect with acrylic resin or other material is deferred to a later date.

Henry G. Schwartz Fractures Cornrrrurricatfng with the Ear, Nose or Accessory Nasal Sinuses

Cerebrospinal otorrhea and rhinorrhea constitute potential pathways for infection of the meninges. They are usually due to linear fractures of the petrous portion of the temporal bone or the cribriform plate. It is important that these patients are not subjected to any manipulations which may lead to the introduction of bacteria into the subarachnoid space. In cases with otorrhea, instrumentation of the auditory meatus must be avoided. Only the pinna of the ear should be cleaned. A sterile cotton pad is then loosely applied to the external auditory orifice, and the whole ear is then covered by loose-meshed gauze. The patient is encouraged to lie on the side of the draining ear and the loose outer dressing is changed when it becomes saturated. In most cases, drainage ceases in from 24 to 48 hours and the fistula closes. In rhinorrhea the situation is similar. The head of the bed is elevated to enhance outward flow of fluid and every effort is made to keep the patient from blowing his nose which may force bacteria or air into the subarachnoid space. In the unconscious patient, aspiration of fluid entering the pharynx from the posterior nares may be prevented by use of a suction tube through the mouth. Spontaneous cessation of rhinorrhea is the rule, but, if it persists longer than six or seven days, frontal craniotomy is carried out; the dural margins caught in the fracture site are freed and the dural defect is sutured. Penicillin and streptomycin are given routinely in cases of cerebrospinal fistula to minimize the chance of meningitis. INTRACRANIAL INJURY

Damage to the intracranial contents is of primary importance in all head injuries whether or not there is a fracture of the skull. This damage may involve nervous tissue itself, the intracranial vascular system, or the cerebrospinal fluid. Concussion

Concussion is a physiologic rather than a demonstrably pathologic state, which results from rapid deceleration of movement of the skull and continued acceleration of movement of the contained brain. Within the terms of strict definition, there is no evidence of anatomic damage (although it is possible that some changes may be demonstrable with more refined microscopic techniques). The loss of consciousness is believed to be due to an interruption or abnormal discharge of nerve impulses and is ordinarily spontaneously reversible. In more severe injuries, an anatomic substrate may be found consisting of rupture of capillaries or actual tearing of brain tissue. With contusion or laceration of the brain, loss of consciousness is more prolonged and may not be

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reversible. This is particularly true where the lesion lies in the brain stem. Most head injuries resulting in concussion require no special treatment other than a brief period of rest. In this connection, it is of interest to recall that, during the London blitz, early ambulation was practiced of necessity and the incidence of post-traumatic headache was negligible. It is of further interest to note that, after the emergency passed, the usual incidence of post-traumatic headache occurred. Contusion and laceration of the brain may be accompanied or followed by cerebral swelling, The exact mechanism of this swelling is not known. In some cases there is true edema as well as vasodilatation and increased venous pressure. The vast majority of cases improve with maintenance of good respiratory exchange and moderate limitation of fluids (1500 to 2000 cc. daily). If, however, extravasation and edema are too great to permit of accommodation of increased brain bulk in the skull, intracranial pressure rises to the point where decompensation results, with hypoxia of the brain and medullary centers. The clinical manifestations of decompensation are coma, restlessness, fever, slowing of the pulse and respirations, and vomiting. It is important that these signs are frequently looked for and recorded in all patients. The administration of hypertonic solutions to reduce intracranial pressure is indicated under these circumstances and we have found the slow intravenous administration of 100 cc. of 50 per cent sucrose helpful. Recently, 30 per cent urea has been advocated. Indiscriminate and too frequent use of hypertonic solutions may be harmful and continued overdehydration may result in impaired fluid balance and deterioration of consciousness. In patients with obviously severe brain damage, manifested by deep coma, thready pulse, Cheyne-Stokes respiration, or decerebrate rigidity (usually due to midbrain contusion or compression), reduction of metabolic needs of the embarrassed brain would appear to be a reasonable goal. To this end, hypothermia may be of value in these patients. Maintenance of temperature ranging between 33° and 35° C. (91.4° and 95° F.) for as long as three to four days has been beneficial in a few cases. All patients must be carefully observed not only by the physician but also by nurses and attendants for the development of general or localizing signs which indicate need for surgical intervention. Extradural Hematoma

This lesion is usually due to hemorrhage from the middle meningeal artery. However, it may also occur from tears adjacent to venous sinuses or rarely from emissary diploic vessels. The classical syndrome consists of an initial, brief period of unconsciousness, followed by a lucid interval. At this stage, usually six to 24 hours after injury (earlier in young children) the patient becomes drowsy, manifests progressive signs of increasing intracranial pressure, with bradycardia, slowed respirations, steplike rise in blood pressure, and progressive paresis or Jacksonian convulsions

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of one side of the body. The atypical case is recognized with some difficulty; the lucid interval may not appear because of coincident diffuse brain damage, and the classical rise in blood pressure may appear very late or not at all. Particular attention should be paid to restlessness, increasing stupor, gradual onset of hemiplegia or patholgic reflexes which were not obtained on admission, and inequality of the pupils. Dilatation of the pupil may appear on the side of the lesion, rarely on the opposite side, as a result of compression of the third nerve at the level of the incisura. Treatment consists of immediate surgery with evacuation of the clot and control of the bleeding point. Subdural Hem.atom.a

Subdural hematomas may be classified as acute and subacute or chronic. Acute subdural hernorrhage is usually associated with tearing of cortical veins and gives rise to symptoms within 24 to 48 hours. The difficulty of distinguishing this from an extradural hematoma is exemplified by the following case: A 4 year old child struck her head on a concrete'floor after falling down a flight of eight steps. She was momentarily stunned, and then roused up. About 20 minutes later she became stuporous. On admission to the hospital, within an hour after the fall, she had a dilated, fixed left pupil and spasticity of all extremities, more marked on the right. The child was deeply comatose and the pulse rate was 60. Immediate operation was performed. A perforator opening in the left temporal region was made without disclosing an anticipated extradural clot. The dura was opened and the temporal lobe bulged prominently. Needle exploration yielded no evidence of an intracerebral hematoma. Another burr hole was then made in the left frontal region. Here a thick, currant-jelly type of subdural clot, about 80 cc. in volume, was found and removed after enlarging the opening in the skull. No specific bleeding point was visualized. On completion of the operation, which was done under local anesthesia, the child became conscious, moved all extremities well and the previously fixed dilated pupil was of normal size and reacted promptly to light. Her subsequent course was uncomplicated.

Subacute or chronic subdural hematomas are usually the result of oozing from a bridging vein running from the cotrex to the longitudinal sinus, and appear to develop more commonly following relatively mild head injury than as a sequel to severe brain trauma. Although a few authorities believe that subdural hematomas arise from splitting of the dura with hemorrhage between the layers, most neurosurgeons and neuropathologists suspect that the lesion begins with venous oozing into the subdural space. Since this potential space lies superficial to the arachnoid, blood or fluid trapped here cannot be absorbed through ordinary subarachnoid channels. The clot is subsequently surrounded by a fibroblastic membrane. Progressive enlargement of the hematoma is believed to be due to additional small hemorrhage from the capillaries of the

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outer membrane or to the entry of blood serum or cerebrospinal fluid into the sac filled with fluid of high osmotic pressure. Symptoms may develop from afew days to several months after:the injury. In the subacute cases, suspicion is directed to the patientwho, after apparently convalescing wen for five or six days after a head injury, begins to lose a little ground, becomes somewhat obtunded or restless, develops minimal hemiparesis, or shows inequality of the pupils or other evidence of oculomotor nerve weakness. In the more chronic lesions, neurologic signs may be very minimal and confusing. The patient may complain of headache, drowsiness, and there may be a personality change. Neurological examination may reveal slight weakness of an extremity, less commonly is there full-blown hemiplegia. Jacksonian convulsions may appear. The most significant finding may be a dilated pupil, and, if present, this is of considerable localizing value. Roentgenograms of the skull may reveal a displaced calcified pineal body. Electroencephalography may show lateralizing slow activity and depression of amplitude. If subdural hematoma is suspected, exploratory burr holes are made. Since the majority of these lesions lie in the frontoparietal region, we usually elect to make the first opening at the level of insertion of the temporal muscle. If no hematoma is found, additional openings are made in the frontal and parieto-occipital areas. In the usual case, after incision of blue-colored dura, the outer membrane of the hematoma is opened widely and the contents of the sac are evacuated. In most cases simple drainage through an enlarged burr hole is adequate. However, when the membranes are fairly thick in older lesions, the brain frequently fails to expand and obliterate the dead space. In such patients a formal craniotomy is recommended to permit wide removal of both inner and outer membranes. Since subdural hematomas are frequently bilateral, it is good policy to make perforator openings on both sides. Although we believe that exploratory burr holes constitute a harmless procedure in suspected cases, increased skill in performance and interpretation has led us to adopt angiography as a valuable diagnostic method which permits accurate localization. Figure 380, B, illustrates the angiographic appearance of a patient whose month-old subdural hematoma was then removed by formal osteoplastic craniotomy (Fig. 380, C, D).

Subdural Hydrorrra Subdural hydroma is a rare complication of head injury, and its differential diagnosis from extradural or subacute subdural hematoma cannot be made before operation. The symptoms are due to accumulation of cerebrospinal fluid in the subdural space. On one occasion we have visualized the tiny opening in the arachnoid membrane through which fluid

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fig. 380. A, Normal angiogram showing superficial branches of middle cerebral artery close to inner table of skull, and central position of anterior cerebral artery. B, The middle cerebral artery separated by 2 em. from the inner table of the skull and the anterior cerebral is shifted across the midline, by a large subdural hematoma. C, Hematoma exposed at craniotomy. D, After removal of hematoma, the underlying brain shows residual concave depression.

spouted with each pulsation of the brain. Because of presumed ball-valve action, the escaping fluid cannot return to the subarachnoid space through the small rent in the arachnoid. As more and more fluid is expressed into the subdural space, the collection of fluid compresses the underlying brain. Treatment consists of making an enlarged perforator opening; in addition to stellate incision of the dura, the arachnoid should also be opened widely to permit free communication with the subarachnoid space. SUMMARY

Trauma to the head may involve scalp, skull and intracranial contents singly or in combination. The effects of injury may be immediate or there may be delay in the development of complicating signs. Therefore, careful evaluation and recording of history and findings are essential in all cases.

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Brain damage is of primary importance and every effort should be made to maintain an adequate airway to minimize cerebral hypoxia. As a rule, skull fracture may be considered as of secondary importance. There are some fractures, however, which demand surgical intervention. Operation is indicated in (1) large simple depressed fractures which serve to decrease intracranial space appreciably and (2) limited simple depressed fractures which overlie important brain areas. In compound fractures, the necessity of complete and precise surgery is vital, and the orderly steps to be followed have been described. If facilities for adequate operation are not available, these patients are better managed by application of a dry dressing and transportation to a hospital equipped for this type of surgery. Lacerations of the scalp should command the same respect and meticulous handling of traumatized tissue as do the more imposing compound fractures. Reliance upon antimicrobial agents cannot compensate for careless management. The majority of patients with cerebral concussion will recover with conservative management. The development of increased deterioration of consciousness, progressive neurologic signs and evidence of increasing intracranial pressure may indicate the presence of an extradural or suhdural hematoma. Exploratory burr holes are indicated in such cases. Chronic subdural hematomas may manifest very minimal or confusing neurologic signs. Cerebral angiography is of considerable value in making the diagnosis. 600 S. Kingshighway St. Louis 10, Missouri