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Management of Patients with Injuries of the Skull and Brain
Management of Patients with Injuries of the Skull and Brain JOHN E. ADAMS, M.D., F.A.C.S. * HOWARD C. NAFFZIGER, M.D., F.A.C.S. **
OF PRIMARY importance in the treatment of the patient with an acute head injury is proper diagnosis. The physician is responsible for minimizing the effects of damage done and for selection of the patient who will require surgical treatment because of either intracranial bleeding or, less often, intracranial infection. Approximately 25 per cent of patients sustaining a craniocerebral injury will require some type of surgical care. An estimated 10 per cent will have received fatal injury and will succumb despite all efforts. The remaining 65 per cent will recover provided they are treated upon sound physiological principles. Proper diagnosis and adequate treatment of craniocerebral injuries depend upon a thorough understanding of the resultant basic pathology and abnormal physiology. The lowering of mortality and morbidity in the past decade has been largely due to increasing knowledge of the altered physiology of the brain following injury, and it is significant that cerebral physiopathologic alterations from trauma have received more attention than our earlier concern with intracranial pressure and its relief. It has been clearly shown1 that, in closed head injuries, the important injuring force is the rate of either acceleration or deceleration of the brain within the cranium. Upon impact, the brain undergoes rotary and linear movements within the cranium. The basal portions of the brain, particularly the frontal and temporal lobes, are so housed in the middle and frontal fossae that they cannot share in this movement and may be severely injured and conFrom the Department of Neurological Surgery, Univer sity of California School of Medicine, San Francisco, California. *Assistant Professor of Neurological Surgery, University of California School of Medicine; Assistant Visiting Neurological Surgeon, San Francisco County Hospital; Consultant in Neurological Surgery, Oakland Naval Hospital and Children' s Hospital, San Francisco. **Professor of Neurological Surgery, Emeritus, University of California School of Medicine.
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tused. It is this mechanism "hich explains the former concept of "contrecoup" injury. As a result of this injuring force and the subsequent contusion, the cerebral tissue undergoes a process which has been termed "cerebral swelling." This happens to be a good term, since it is not clearly understood whether the accumulation of fluid with the subsequent increase in size of the brain is in the extra- or intracellular fluid space. The exact cause and location of the fluid accumulation, however, are not important. The net result is the same, namely, an actual increase in size of the affected protions which, as noted above, are most frequently the basal areas of -the frontal and temporal lobes. If this process continues unabated, the hippocampal portions of the temporal lobes, in particular, expand and herniate through the incisura of the tentorium cerebelli, thus compressing the brain stem and obstructing the venous return from the midbrain. The end result of this mechanism is the fatal hemorrhage in the pons familiar to anyone who has examined a brain at post mortem following injury. What practical application in the treatment of patients with craniocerebral injuries can be gained from this concept of the disordered physiology? Although the initiating cause of the swelling is not fully understood, it is certainly true that any degree of cerebral hypoxia will augment the changes, since it will increase the permeability of blood vessels. It is therefore mandatory and a first principle in treatment to maintain adequate oxygenation of tissues. This in turn implies a free airway and free respiratory exchange. Secondly, venous drainage from the brain should be aided, since any increase in the venous pressure will in turn be transmitted to the capillary bed, thus causing an increased transudation of fluid into the extracellular fluid spaces. Thirdly, any factors which augment the demand of the tissues for oxygen should be minimized. Thus, every effort should be made to avoid hyperpyrexia, which will naturally cause an increased metabolic rate. CEREBRAL COMPRESSION
Traumatic cerebral compression is almost invariably due to an expanding intracranial hemorrhage. When the wound has been compounded, pathogenic organisms may gain access to the intracranial contents and produce subsequent cerebral compression with the development of a subdural or cerebral abscess. The diagnosis is usually not difficult, since there will be signs of cranial or meningeal infection associated with increasing intracranial pressure and evidence of a focal expanding mass. Intracranial hemorrhage of surgical significance is extradural, subdural or intracerebral. The source of the first is usually a torn middle meningeal artery following a fracture through the temporal fossa. Less often, laceration of one of the major dural venous sinuses can cause an extradural
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hemorrhage. Since venous pressure is lower than arterial, the process is less rapid than when the middle meningeal artery is the source of bleeding. The usual source of subdural bleeding is the bridging veins which pass from the cortex into the superior sagittal sinus at the convexity. These vessels are unsupported and easily ruptured. A frequent and often overlooked source of subdural bleeding is subcortical vessels which may be contused and bleed into the substance of the brain. The hemorrhage then may gradually extrude into the subdural space. The obvious result of an expanding hemorrhage is to augment the process of cerebral swelling which is already taking place. It is essential, therefore, that early diagnosis be made and surgical exploration and evacuation of the clot be carried out. DIAGNOSIS
There are several immediate requirements which must be met by the physician when first confronted by the patient with craniocerebral trauma. Evidence of injury to other areas of the body, particularly the cervical spine, must be sought for and properly evaluated. Shock, if present, must be treated. However, shock is an infrequent accompaniment of head injuries per se. 2 Arterial hypotension persisting more than 2 to 3 hours following an acute injury to the head may be due to a profound brain injury, or less commonly to extensive loss of blood from the wound, or finally to an injury elsewhere in the body. A careful evaluation of the patient's neurological status should be made. It is by establishing this base line that one can differentiate the primary damage from the trauma and recognize signs which may be developing from hemorrhage and which may necessitate surgical exploration. The single most important feature of this examination is a careful estimation of the patient's state of consciousness. If the patient is conscious, the degree of retrograde amnesia should be determined. The patient's orientation as to time and place will give a rough estimation as to the degree of immediate injury to the brain. If the patient is comatose or semicomatose, his response to various types of painful stimuli can be used as a reference point. A useful stimulus is strong supraorbital pressure. Ordinarily, it is a deeply comatose patient who will not respond in some way to this stimulus. Evidence of focal injury or compression of the brain should be carefully looked for. It may be manifested by either irritative or paralytic phenomena. Focal seizures are not uncommon immediately following acute injuries to the brain. Reflex changes, a progressive hemiparesis, and unilateral dilatation of the pupils also indicate focal injury, compression of the brain, or progressive swelling of the temporal lobe. The patient should be placed on a chart of the vital signs, although in our experience, blood pressure, pulse and respiratory alterations are a less reliable guide to complicating intracranial hemorrhage than the more significant increasing stupor, associated with the development of focal
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signs. Certainly, if the clinical status of the patient indicates increasing coma plus the development of lateralizing neurological signs, the decision as to exploration should never be delayed until alterations in blood pressure and pulse indicate increasing intracranial pressure. In summary, it may be stated that when a patient, following an injury to the head, demonstrates a progressive loss of consciousness, particularly if associated with the development of focal neurological signs, surgical exploration becomes mandatory. TREATMENT Roentgen Examination
After the initial neurological evaluation of the patient, the question will arise as to whether roentgen examination of the skull should be made. This is rarely necessary immediately, particularly if the patient is in critical condition or extremely restless. In the first place, moving the patient to the x-ray room may be extremely deleterious, whereas in the second instance, satisfactory films would probably not be obtained. If absolutely necessary, it may be better to move a portable x-ray machine to the patient rather than move him unnecessarily. When the films are taken, it is essential to obtain accurate anterior. and posterior views as well as a stereoscopic lateral projection. Roentgen examination should be carried out as soon as possible in the following instances: 1. When the possibility that a depressed fracture of the skull exists, x-ray examination is essential in order to determine the extent of the depression and to aid in the decision as to whether the depression should be elevated. 2. In instances where there is bleeding or loss of cerebrospinal fluid from either the nose or the ear, films will help to determine the extent of the fracture into the accessory air sinuses and will occasionally reveal the presence of air in the subarachnoid space or ventricles as a cause of increased intracranial pressure. 3. Where there are signs of a progressive deterioration indicative of intracranial hemorrhage, and particularly where no localizing signs are present, roentgen examination may be extremely valuable if a fracture line can be demonstrated crossing the middle meningeal groove or the course of a major dural sinus. In addition, if there is a calcified pineal gland which is displaced, this finding may be invaluable in lateralizing the disturbance and in simplifying the subsequent operative procedure. Additional x-rays of the chest and spine may be indicated by such signs as deformity, cervical rigidity, marked cervical tenderness, paraplegia, respiratory distress and so forth. The medicolegal importance of such examination is great. Should immediate films not be taken, it is essential tha(before the patient leaves the hospital a complete roentgen examination of the skull be made, since so many of these cases frequently result in litigation.
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Lumbar Puncture
From the practical standpoint, a lumbar puncture is not often a necessity. It has been stated that this procedure is not hazardous in patients with intracranial injuries. The authors have seen occasional instances where the performance of a lumbar puncture was followed by almost immediate death. Occasions present themselves, however, where the information to be gained from a careful lumbar puncture outweighs the risk. The intracranial pressure, if measured carefully, and the appearance of the cerebrospinal fluid may in some instances be deciding factors in the decision as to whether an exploratory trepanation is necessary. (In most instances, however, this decision is based purely on clinical findings.) If meningeal infection is suspected, naturally, examination of the cerebrospinal fluid is essential. When a lumbar puncture is performed, the technique should be meticulous. A fine lumbar puncture needle (No. 22) should be used. When the needle is felt penetrating the interspinous ligament, the stilette should be withdrawn and a water manometer attached to the needle, so that when the dura is penetrated the fluid immediately enters the manometer. Sufficient time should be taken to allow adequate relaxation of the patient and to obtain an accurate pressure recording. (If the patient is restless, there is less to be gained from a lumbar puncture.) The fluid within the manometer is then used for a cell count, so that in all only 2 or 3 cu. mm. of fluid are withdrawn. Under these circumstances, a lumbar puncture can be done with little risk. If there is doubt as to whether a complicating intracranial hemorrhage is taking place, further observation is warranted if a lumbar puncture reveals bloody fluid and pressure which is not greatly increased, since the clinical course then can probably be accounted for by intrinsic brain injury rather than an expanding clot. Occasionally, lumbar puncture will provide some relief for the patient who has signs of severe meningismus and headache, due to blood in the cerebrospinal fluid. At the present time, most authorities do not feel that repeated therapeutic lumbar punctures have any value other than for symptomatic relief of headache. Care of the Patient
The therapeutic measures used in the treatment of a patient with brain damage are based upon the physiological principles enumerated above. Excellent nursing care is a necessity. The objectives to be met are as follows: 1. M aihtenance of Circulation. Since proper oxygenation of tissues, we feel, is a critical factor, the circulation to the brain must be maintained. If present, shock must be combated vigorously, and the systemic blood pressure must be maintained. 2. Provision for an Adequate Airway. This is of extreme importance.
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In the unconscious patient, the position of choice in bed is with the head lowered and the patient on his side so as to provide adequate drainage of secretions from the upper respiratory pathways. In craniocerebral injuries, however, this position mitigates against free venous drainage from the head. It is usually necessary, therefore, to compromise and keep the patient's head slightly elevated with intermittent lowering for postural drainage. The upper respiratory passages are kept open by meticulous attention to the posterior pharynx and an oral airway by means of which the tongue is held forward. Nasopharyngeal secretions must be given constant attention and removed when necessary by general suction with a rubber catheter. The use of oxygen by either a nasal tube or an oxygen tent is usually an essential. If in spite of the above measures, the patient appears to have labored respiration or if there is unrelieved cyanosis, * then either an indwelling endotracheal tube should be placed or an immediate tracheotomy should be done. The latter procedure offers the advantage of insuring an excellent exchange, and at the same time it permits the early placement of a stomach tube and the institution of an adequate caloric and protein intake, free of the danger of aspiration of vomitus. 3 3. Control of Temperature. A rise in temperature above 102° F. should be combated vigorously by discarding bedclothes and garments. Ice packs should be applied to the groin, axillae and neck. If these measures fail, a fan should blow upon the patient's body continuously. Acetylsalicylic acid in dosages of 10 to 15 grains can be administered by rectum. Rectal temperatures should be used invariably. 4. Fluid Balance. It is our firm opinion that programs of either dehydration or excessive fluid intake above physiological requirements are not warranted. The physiological needs of the patient are best served by maintaining an adequate fluid intake so as to permit a urine excretion of approximately 1000 cc. per day. An indwelling catheter may be necessary for accurate measurement. In order to reduce the degree of cerebral edema, where the fluid intake is being maintained by parenteral fluids, only 1000 cc. of the daily intake of fluid should contain sodium. In general, unless excessive temperature or sweating is present, a fluid intake of from 2000 to 3000 cc. of fluid per day is adequate. 5. Nutrition. As soon as feasible, a Levin tube should be passed and a caloric intake of 2500 to 3000 calories per day should be instilled by some type of formula. The protein requirements should be met, as a protein deficiency occurs early and rapidly in the unconscious patient. 6. Sedation. The hyperactive, restless, semiconscious patient may become a problem in control. His hyperactivity may be due to severe head pain or an overdistended bladder and in the latter instance, catheteriza*It should be remembered that cerebral hypoxia may be present in the absence of peripheral cyanosis since the oxygen requirements of the brain are so much greater than those of peripheral tissues.
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tion may be all that is necessary. It is important to quiet such a patient in order to prevent further injury and to decrease metabolic requirements. Restraints usually only add to restlessness and should be used only as a last resort. Sedation, therefore, may be necessary but should be used cautiously. In the alcoholic patient, paraldehyde per rectum is the drug of choice. Phenobarbital sodium injected subcutaneously can add to restlessness. The drug and dosage, therefore, have to be determined by individual requirements. Morphine and other respiratory depressants should not be used. It goes without saying that meticulous attention to the skin with frequent turning, prevention of bladder distention, and care of the bowel are common features indispensable to the management of any unconscious patient. Surgical Treatment of Acute Craniocerebral Trauma
The Scalp Wound. The principles of wound healing apply to the scalp as much as to wounds of any other part of the body. Immediate hemorrhage is usually controlled by a pressure dressing. If the wound consists only of a scalp laceration, a closure can be effected after thorough shaving of the surrounding scalp and preparation of the skin. If a compound fracture is present, and particularly if there is evidence of underlying brain injury, these measures should be delayed until full neurosurgical facilities are available. No probing or inspection of the wound should be made until the definitive care is undertaken. Local anesthesia is preferred if the patient is sufficiently cooperative. If a general anesthetic agent is necessary owing to the restlessness of the patient, intravenous barbiturates should be used only when administered by a competent anesthetist. If there is any question as to the presence of intracranial bleeding, the entire head should be shaved. After preliminary preparation of the head and wound, it is wise to change gloves and gown and redrape. Specific Surgical Measures. 1. A depressed fracture, if compounded, requires early debridement, elevation and repair. When the injury is not compounded and roentgen examination clearly indicates that the depression is slight, it is sometimes justifiable not to operate if the patient's neurological examination is entirely negative. However, it must be remembered that the x-ray examination cannot always accurately portray the degree of depression. Furthermore, there is no certain way to ascertain whether the dura has been torn by the depressed fragment of inner table without surgical exploration, and this information is extremely important since the incidence of post-traumatic seizures will be extremely high if a meningeal-cortical laceration has occurred. Elevation of the depressed fragments, repair of the lacerated dura, and gentle debridement of the contused cortex will minimize the resultant
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cortical meningeal cicatrix and thereby reduce the likelihood of subsequent seizures. The great majority of depressed fractures will therefore require exploration and elevation. The latter procedure can be difficult if the fragments are impacted, and it is sometimes necessary to fashion a free bone flap and remove the fracture en bloc (Fig. 321). When the fracture overlies a dural sinus, attempts to elevate it may be accompanied by profuse hemorrhage and the operating surgeon should be prepared for this eventuality. Experience gained in W orld War II and in the Korean conflict sub-
Fig. 321. Method of removing depressed fracture as a free bone flap by placement of burr holes and connecting Gigli saw cuts. (Ficarra: Emergency Surgery, published by F. A. Davis Company.)
stantiate the time-honored surgical precept that foreign bodies cannot be left in contaminated wounds. Attempts were made to cover fresh traumatic defects with a plate of tantalum or other foreign material even when the wound was compounded. Reliance was placed upon prophylactic antibiotic therapy to avoid infection. However, most of the plates put in under these circumstances had to be removed subsequently. Similarly, a cranial~defect which involves the frontal sinus should never be plated until the sinus has been exenterated and sufficient time has elapsed (6 months) to insure against the development of infection. 2. As stated above, where there is any suspicion that a craniocerebral injury is being complicated by a progressive hemorrhage, immediate exploration is indicated. It is far better to carry out a negative exploration than to overlook an expanding intracranial clot with the subsequent
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loss of the patient. Such exploration is best carried out by burr holes placed one each in the frontal, temporal and parietal regions of the skull (Fig. 322). Exploration should be bilateral, as the bleeding is frequently so. Preparation should be made so that either a small bone flap can be turned or the burr opening enlarged into a subtemporal craniectomy so
Fig. 322. Position of head for exploratory trepanation. Any of the burr openings can be connected as shown by the dotted lines so as to fashion a small bone flap. (Ficarra: Emergency Surgery, published by F. A. Davis Company.)
as properly to control bleeding should it arise from the middle meningeal artery. If a subdural hematoma is solid, it is frequently impossible to wash it out through several burr openings. In such cases, a small bone flap hinged on the temporal muscle usually provides adequate exposure. With prompt and adequate evacuation of an intracranial hematoma, there should be early improvement in the patient's condition. Not infrequently, however, and in particular when there has been delay in surgical treatment, removal of the clot alone may be insufficient to halt herniation of the inferior portion of the temporal lobe through the incisura of the tentorium. When this is the case, the depressed cortex lying beneath the clot does not expand to its former position adjacent to
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the dura and there is a lack of pulsation of the brain. The incisura becomes blocked and cerebrospinal circulation through the subarachnoid channels and basal cisterns is obstructed. Under these circumstances, not only will the patient fail to improve, but his condition will progressively deteriorate until a fatal outcome results from secondary brain stem hemorrhage. For this reason, if the patient's condition does not immediately improve, or if the brain fails to expand following evacuation of the clot, there is much to be gained by elevating the temporal lobe and dividing the tentorium to the incisura. This relieves the incisural block and reestablishes cerebrospinal fluid circulation. Should the basal portions of the temporal lobe be found swollen and contused, resection of this pulpified brain is often warranted. Other Surgical Indications. The occurrence of rhinorrhea or otorrhea indicates a basal skull fracture through the middle or frontal cranial fossa. This naturally represents a compounding of the wound and formerly was considered to be a surgical emergency in order to prevent subsequent intracranial infection. With the advent of modern chemotherapeutic and antibiotic therapy, this situation no longer represents as great a threat as formerly. It now is quite justifiable to temporize in the hope that the spinal fluid leak will seal over spontaneously, during which time vigorous prophylactic therapy can be carried out. The patient should be cautioned to avoid excess straining, blowing his nose, and so forth. If drainage persists, surgical correction of the rent in the dura should be carried out. SUMMARY
The prime requisite for lowering mortality and morbidity from craniocerebral trauma is early diagnosis and appropriate surgical treatment of complicating intracranial hemorrhage, and treatment of injury to the cerebral tissues based upon sound physiological principles. In essence, these measures consist of maintaining adequate circulation to the brain, free respiratory exchange, and proper oxygenation of the blood, avoiding excessive temperature rises, insuring a physiologically sufficient but not excessive fluid intake, and providing meticulous nursing care. REFERENCES 1. Pudenz, R. H. and Shelden, C. H.: The Lucite Calvarium: A Method for Direct Observation of the Brain. J. Neurosurg. 3: 487-505,1946. 2. Campbell, E. H. and Whitfield, R. D.: The Incidence and Significance of Shock in Head Injury. In Symposium on Shock, Army Medical Service Graduate School, Washington, D. C., P. XX-1 to XX-15, May 7-9,1951. 3. Echols, D. H., Llewellyn, R., Kirgis, H. D., Rehfeldt, F. C. and Garcia-Bengochea, F.: Tracheotomy in the Management of Severe Head Injuries. Surgery 28: 801-811 (Nov.) 1950. University of California Hospital Sa.n Francisco 22, California
OF PRIMARY importance in the treatment of the patient with an acute head injury is proper diagnosis. The physician is responsible for minimizing the effects of damage done and for selection of the patient who will require surgical treatment because of either intracranial bleeding or, less often, intracranial infection. Approximately 25 per cent of patients sustaining a craniocerebral injury will require some type of surgical care. An estimated 10 per cent will have received fatal injury and will succumb despite all efforts. The remaining 65 per cent will recover provided they are treated upon sound physiological principles. Proper diagnosis and adequate treatment of craniocerebral injuries depend upon a thorough understanding of the resultant basic pathology and abnormal physiology. The lowering of mortality and morbidity in the past decade has been largely due to increasing knowledge of the altered physiology of the brain following injury, and it is significant that cerebral physiopathologic alterations from trauma have received more attention than our earlier concern with intracranial pressure and its relief. It has been clearly shown1 that, in closed head injuries, the important injuring force is the rate of either acceleration or deceleration of the brain within the cranium. Upon impact, the brain undergoes rotary and linear movements within the cranium. The basal portions of the brain, particularly the frontal and temporal lobes, are so housed in the middle and frontal fossae that they cannot share in this movement and may be severely injured and conFrom the Department of Neurological Surgery, Univer sity of California School of Medicine, San Francisco, California. *Assistant Professor of Neurological Surgery, University of California School of Medicine; Assistant Visiting Neurological Surgeon, San Francisco County Hospital; Consultant in Neurological Surgery, Oakland Naval Hospital and Children' s Hospital, San Francisco. **Professor of Neurological Surgery, Emeritus, University of California School of Medicine.
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tused. It is this mechanism "hich explains the former concept of "contrecoup" injury. As a result of this injuring force and the subsequent contusion, the cerebral tissue undergoes a process which has been termed "cerebral swelling." This happens to be a good term, since it is not clearly understood whether the accumulation of fluid with the subsequent increase in size of the brain is in the extra- or intracellular fluid space. The exact cause and location of the fluid accumulation, however, are not important. The net result is the same, namely, an actual increase in size of the affected protions which, as noted above, are most frequently the basal areas of -the frontal and temporal lobes. If this process continues unabated, the hippocampal portions of the temporal lobes, in particular, expand and herniate through the incisura of the tentorium cerebelli, thus compressing the brain stem and obstructing the venous return from the midbrain. The end result of this mechanism is the fatal hemorrhage in the pons familiar to anyone who has examined a brain at post mortem following injury. What practical application in the treatment of patients with craniocerebral injuries can be gained from this concept of the disordered physiology? Although the initiating cause of the swelling is not fully understood, it is certainly true that any degree of cerebral hypoxia will augment the changes, since it will increase the permeability of blood vessels. It is therefore mandatory and a first principle in treatment to maintain adequate oxygenation of tissues. This in turn implies a free airway and free respiratory exchange. Secondly, venous drainage from the brain should be aided, since any increase in the venous pressure will in turn be transmitted to the capillary bed, thus causing an increased transudation of fluid into the extracellular fluid spaces. Thirdly, any factors which augment the demand of the tissues for oxygen should be minimized. Thus, every effort should be made to avoid hyperpyrexia, which will naturally cause an increased metabolic rate. CEREBRAL COMPRESSION
Traumatic cerebral compression is almost invariably due to an expanding intracranial hemorrhage. When the wound has been compounded, pathogenic organisms may gain access to the intracranial contents and produce subsequent cerebral compression with the development of a subdural or cerebral abscess. The diagnosis is usually not difficult, since there will be signs of cranial or meningeal infection associated with increasing intracranial pressure and evidence of a focal expanding mass. Intracranial hemorrhage of surgical significance is extradural, subdural or intracerebral. The source of the first is usually a torn middle meningeal artery following a fracture through the temporal fossa. Less often, laceration of one of the major dural venous sinuses can cause an extradural
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hemorrhage. Since venous pressure is lower than arterial, the process is less rapid than when the middle meningeal artery is the source of bleeding. The usual source of subdural bleeding is the bridging veins which pass from the cortex into the superior sagittal sinus at the convexity. These vessels are unsupported and easily ruptured. A frequent and often overlooked source of subdural bleeding is subcortical vessels which may be contused and bleed into the substance of the brain. The hemorrhage then may gradually extrude into the subdural space. The obvious result of an expanding hemorrhage is to augment the process of cerebral swelling which is already taking place. It is essential, therefore, that early diagnosis be made and surgical exploration and evacuation of the clot be carried out. DIAGNOSIS
There are several immediate requirements which must be met by the physician when first confronted by the patient with craniocerebral trauma. Evidence of injury to other areas of the body, particularly the cervical spine, must be sought for and properly evaluated. Shock, if present, must be treated. However, shock is an infrequent accompaniment of head injuries per se. 2 Arterial hypotension persisting more than 2 to 3 hours following an acute injury to the head may be due to a profound brain injury, or less commonly to extensive loss of blood from the wound, or finally to an injury elsewhere in the body. A careful evaluation of the patient's neurological status should be made. It is by establishing this base line that one can differentiate the primary damage from the trauma and recognize signs which may be developing from hemorrhage and which may necessitate surgical exploration. The single most important feature of this examination is a careful estimation of the patient's state of consciousness. If the patient is conscious, the degree of retrograde amnesia should be determined. The patient's orientation as to time and place will give a rough estimation as to the degree of immediate injury to the brain. If the patient is comatose or semicomatose, his response to various types of painful stimuli can be used as a reference point. A useful stimulus is strong supraorbital pressure. Ordinarily, it is a deeply comatose patient who will not respond in some way to this stimulus. Evidence of focal injury or compression of the brain should be carefully looked for. It may be manifested by either irritative or paralytic phenomena. Focal seizures are not uncommon immediately following acute injuries to the brain. Reflex changes, a progressive hemiparesis, and unilateral dilatation of the pupils also indicate focal injury, compression of the brain, or progressive swelling of the temporal lobe. The patient should be placed on a chart of the vital signs, although in our experience, blood pressure, pulse and respiratory alterations are a less reliable guide to complicating intracranial hemorrhage than the more significant increasing stupor, associated with the development of focal
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signs. Certainly, if the clinical status of the patient indicates increasing coma plus the development of lateralizing neurological signs, the decision as to exploration should never be delayed until alterations in blood pressure and pulse indicate increasing intracranial pressure. In summary, it may be stated that when a patient, following an injury to the head, demonstrates a progressive loss of consciousness, particularly if associated with the development of focal neurological signs, surgical exploration becomes mandatory. TREATMENT Roentgen Examination
After the initial neurological evaluation of the patient, the question will arise as to whether roentgen examination of the skull should be made. This is rarely necessary immediately, particularly if the patient is in critical condition or extremely restless. In the first place, moving the patient to the x-ray room may be extremely deleterious, whereas in the second instance, satisfactory films would probably not be obtained. If absolutely necessary, it may be better to move a portable x-ray machine to the patient rather than move him unnecessarily. When the films are taken, it is essential to obtain accurate anterior. and posterior views as well as a stereoscopic lateral projection. Roentgen examination should be carried out as soon as possible in the following instances: 1. When the possibility that a depressed fracture of the skull exists, x-ray examination is essential in order to determine the extent of the depression and to aid in the decision as to whether the depression should be elevated. 2. In instances where there is bleeding or loss of cerebrospinal fluid from either the nose or the ear, films will help to determine the extent of the fracture into the accessory air sinuses and will occasionally reveal the presence of air in the subarachnoid space or ventricles as a cause of increased intracranial pressure. 3. Where there are signs of a progressive deterioration indicative of intracranial hemorrhage, and particularly where no localizing signs are present, roentgen examination may be extremely valuable if a fracture line can be demonstrated crossing the middle meningeal groove or the course of a major dural sinus. In addition, if there is a calcified pineal gland which is displaced, this finding may be invaluable in lateralizing the disturbance and in simplifying the subsequent operative procedure. Additional x-rays of the chest and spine may be indicated by such signs as deformity, cervical rigidity, marked cervical tenderness, paraplegia, respiratory distress and so forth. The medicolegal importance of such examination is great. Should immediate films not be taken, it is essential tha(before the patient leaves the hospital a complete roentgen examination of the skull be made, since so many of these cases frequently result in litigation.
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Lumbar Puncture
From the practical standpoint, a lumbar puncture is not often a necessity. It has been stated that this procedure is not hazardous in patients with intracranial injuries. The authors have seen occasional instances where the performance of a lumbar puncture was followed by almost immediate death. Occasions present themselves, however, where the information to be gained from a careful lumbar puncture outweighs the risk. The intracranial pressure, if measured carefully, and the appearance of the cerebrospinal fluid may in some instances be deciding factors in the decision as to whether an exploratory trepanation is necessary. (In most instances, however, this decision is based purely on clinical findings.) If meningeal infection is suspected, naturally, examination of the cerebrospinal fluid is essential. When a lumbar puncture is performed, the technique should be meticulous. A fine lumbar puncture needle (No. 22) should be used. When the needle is felt penetrating the interspinous ligament, the stilette should be withdrawn and a water manometer attached to the needle, so that when the dura is penetrated the fluid immediately enters the manometer. Sufficient time should be taken to allow adequate relaxation of the patient and to obtain an accurate pressure recording. (If the patient is restless, there is less to be gained from a lumbar puncture.) The fluid within the manometer is then used for a cell count, so that in all only 2 or 3 cu. mm. of fluid are withdrawn. Under these circumstances, a lumbar puncture can be done with little risk. If there is doubt as to whether a complicating intracranial hemorrhage is taking place, further observation is warranted if a lumbar puncture reveals bloody fluid and pressure which is not greatly increased, since the clinical course then can probably be accounted for by intrinsic brain injury rather than an expanding clot. Occasionally, lumbar puncture will provide some relief for the patient who has signs of severe meningismus and headache, due to blood in the cerebrospinal fluid. At the present time, most authorities do not feel that repeated therapeutic lumbar punctures have any value other than for symptomatic relief of headache. Care of the Patient
The therapeutic measures used in the treatment of a patient with brain damage are based upon the physiological principles enumerated above. Excellent nursing care is a necessity. The objectives to be met are as follows: 1. M aihtenance of Circulation. Since proper oxygenation of tissues, we feel, is a critical factor, the circulation to the brain must be maintained. If present, shock must be combated vigorously, and the systemic blood pressure must be maintained. 2. Provision for an Adequate Airway. This is of extreme importance.
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In the unconscious patient, the position of choice in bed is with the head lowered and the patient on his side so as to provide adequate drainage of secretions from the upper respiratory pathways. In craniocerebral injuries, however, this position mitigates against free venous drainage from the head. It is usually necessary, therefore, to compromise and keep the patient's head slightly elevated with intermittent lowering for postural drainage. The upper respiratory passages are kept open by meticulous attention to the posterior pharynx and an oral airway by means of which the tongue is held forward. Nasopharyngeal secretions must be given constant attention and removed when necessary by general suction with a rubber catheter. The use of oxygen by either a nasal tube or an oxygen tent is usually an essential. If in spite of the above measures, the patient appears to have labored respiration or if there is unrelieved cyanosis, * then either an indwelling endotracheal tube should be placed or an immediate tracheotomy should be done. The latter procedure offers the advantage of insuring an excellent exchange, and at the same time it permits the early placement of a stomach tube and the institution of an adequate caloric and protein intake, free of the danger of aspiration of vomitus. 3 3. Control of Temperature. A rise in temperature above 102° F. should be combated vigorously by discarding bedclothes and garments. Ice packs should be applied to the groin, axillae and neck. If these measures fail, a fan should blow upon the patient's body continuously. Acetylsalicylic acid in dosages of 10 to 15 grains can be administered by rectum. Rectal temperatures should be used invariably. 4. Fluid Balance. It is our firm opinion that programs of either dehydration or excessive fluid intake above physiological requirements are not warranted. The physiological needs of the patient are best served by maintaining an adequate fluid intake so as to permit a urine excretion of approximately 1000 cc. per day. An indwelling catheter may be necessary for accurate measurement. In order to reduce the degree of cerebral edema, where the fluid intake is being maintained by parenteral fluids, only 1000 cc. of the daily intake of fluid should contain sodium. In general, unless excessive temperature or sweating is present, a fluid intake of from 2000 to 3000 cc. of fluid per day is adequate. 5. Nutrition. As soon as feasible, a Levin tube should be passed and a caloric intake of 2500 to 3000 calories per day should be instilled by some type of formula. The protein requirements should be met, as a protein deficiency occurs early and rapidly in the unconscious patient. 6. Sedation. The hyperactive, restless, semiconscious patient may become a problem in control. His hyperactivity may be due to severe head pain or an overdistended bladder and in the latter instance, catheteriza*It should be remembered that cerebral hypoxia may be present in the absence of peripheral cyanosis since the oxygen requirements of the brain are so much greater than those of peripheral tissues.
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tion may be all that is necessary. It is important to quiet such a patient in order to prevent further injury and to decrease metabolic requirements. Restraints usually only add to restlessness and should be used only as a last resort. Sedation, therefore, may be necessary but should be used cautiously. In the alcoholic patient, paraldehyde per rectum is the drug of choice. Phenobarbital sodium injected subcutaneously can add to restlessness. The drug and dosage, therefore, have to be determined by individual requirements. Morphine and other respiratory depressants should not be used. It goes without saying that meticulous attention to the skin with frequent turning, prevention of bladder distention, and care of the bowel are common features indispensable to the management of any unconscious patient. Surgical Treatment of Acute Craniocerebral Trauma
The Scalp Wound. The principles of wound healing apply to the scalp as much as to wounds of any other part of the body. Immediate hemorrhage is usually controlled by a pressure dressing. If the wound consists only of a scalp laceration, a closure can be effected after thorough shaving of the surrounding scalp and preparation of the skin. If a compound fracture is present, and particularly if there is evidence of underlying brain injury, these measures should be delayed until full neurosurgical facilities are available. No probing or inspection of the wound should be made until the definitive care is undertaken. Local anesthesia is preferred if the patient is sufficiently cooperative. If a general anesthetic agent is necessary owing to the restlessness of the patient, intravenous barbiturates should be used only when administered by a competent anesthetist. If there is any question as to the presence of intracranial bleeding, the entire head should be shaved. After preliminary preparation of the head and wound, it is wise to change gloves and gown and redrape. Specific Surgical Measures. 1. A depressed fracture, if compounded, requires early debridement, elevation and repair. When the injury is not compounded and roentgen examination clearly indicates that the depression is slight, it is sometimes justifiable not to operate if the patient's neurological examination is entirely negative. However, it must be remembered that the x-ray examination cannot always accurately portray the degree of depression. Furthermore, there is no certain way to ascertain whether the dura has been torn by the depressed fragment of inner table without surgical exploration, and this information is extremely important since the incidence of post-traumatic seizures will be extremely high if a meningeal-cortical laceration has occurred. Elevation of the depressed fragments, repair of the lacerated dura, and gentle debridement of the contused cortex will minimize the resultant
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cortical meningeal cicatrix and thereby reduce the likelihood of subsequent seizures. The great majority of depressed fractures will therefore require exploration and elevation. The latter procedure can be difficult if the fragments are impacted, and it is sometimes necessary to fashion a free bone flap and remove the fracture en bloc (Fig. 321). When the fracture overlies a dural sinus, attempts to elevate it may be accompanied by profuse hemorrhage and the operating surgeon should be prepared for this eventuality. Experience gained in W orld War II and in the Korean conflict sub-
Fig. 321. Method of removing depressed fracture as a free bone flap by placement of burr holes and connecting Gigli saw cuts. (Ficarra: Emergency Surgery, published by F. A. Davis Company.)
stantiate the time-honored surgical precept that foreign bodies cannot be left in contaminated wounds. Attempts were made to cover fresh traumatic defects with a plate of tantalum or other foreign material even when the wound was compounded. Reliance was placed upon prophylactic antibiotic therapy to avoid infection. However, most of the plates put in under these circumstances had to be removed subsequently. Similarly, a cranial~defect which involves the frontal sinus should never be plated until the sinus has been exenterated and sufficient time has elapsed (6 months) to insure against the development of infection. 2. As stated above, where there is any suspicion that a craniocerebral injury is being complicated by a progressive hemorrhage, immediate exploration is indicated. It is far better to carry out a negative exploration than to overlook an expanding intracranial clot with the subsequent
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loss of the patient. Such exploration is best carried out by burr holes placed one each in the frontal, temporal and parietal regions of the skull (Fig. 322). Exploration should be bilateral, as the bleeding is frequently so. Preparation should be made so that either a small bone flap can be turned or the burr opening enlarged into a subtemporal craniectomy so
Fig. 322. Position of head for exploratory trepanation. Any of the burr openings can be connected as shown by the dotted lines so as to fashion a small bone flap. (Ficarra: Emergency Surgery, published by F. A. Davis Company.)
as properly to control bleeding should it arise from the middle meningeal artery. If a subdural hematoma is solid, it is frequently impossible to wash it out through several burr openings. In such cases, a small bone flap hinged on the temporal muscle usually provides adequate exposure. With prompt and adequate evacuation of an intracranial hematoma, there should be early improvement in the patient's condition. Not infrequently, however, and in particular when there has been delay in surgical treatment, removal of the clot alone may be insufficient to halt herniation of the inferior portion of the temporal lobe through the incisura of the tentorium. When this is the case, the depressed cortex lying beneath the clot does not expand to its former position adjacent to
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the dura and there is a lack of pulsation of the brain. The incisura becomes blocked and cerebrospinal circulation through the subarachnoid channels and basal cisterns is obstructed. Under these circumstances, not only will the patient fail to improve, but his condition will progressively deteriorate until a fatal outcome results from secondary brain stem hemorrhage. For this reason, if the patient's condition does not immediately improve, or if the brain fails to expand following evacuation of the clot, there is much to be gained by elevating the temporal lobe and dividing the tentorium to the incisura. This relieves the incisural block and reestablishes cerebrospinal fluid circulation. Should the basal portions of the temporal lobe be found swollen and contused, resection of this pulpified brain is often warranted. Other Surgical Indications. The occurrence of rhinorrhea or otorrhea indicates a basal skull fracture through the middle or frontal cranial fossa. This naturally represents a compounding of the wound and formerly was considered to be a surgical emergency in order to prevent subsequent intracranial infection. With the advent of modern chemotherapeutic and antibiotic therapy, this situation no longer represents as great a threat as formerly. It now is quite justifiable to temporize in the hope that the spinal fluid leak will seal over spontaneously, during which time vigorous prophylactic therapy can be carried out. The patient should be cautioned to avoid excess straining, blowing his nose, and so forth. If drainage persists, surgical correction of the rent in the dura should be carried out. SUMMARY
The prime requisite for lowering mortality and morbidity from craniocerebral trauma is early diagnosis and appropriate surgical treatment of complicating intracranial hemorrhage, and treatment of injury to the cerebral tissues based upon sound physiological principles. In essence, these measures consist of maintaining adequate circulation to the brain, free respiratory exchange, and proper oxygenation of the blood, avoiding excessive temperature rises, insuring a physiologically sufficient but not excessive fluid intake, and providing meticulous nursing care. REFERENCES 1. Pudenz, R. H. and Shelden, C. H.: The Lucite Calvarium: A Method for Direct Observation of the Brain. J. Neurosurg. 3: 487-505,1946. 2. Campbell, E. H. and Whitfield, R. D.: The Incidence and Significance of Shock in Head Injury. In Symposium on Shock, Army Medical Service Graduate School, Washington, D. C., P. XX-1 to XX-15, May 7-9,1951. 3. Echols, D. H., Llewellyn, R., Kirgis, H. D., Rehfeldt, F. C. and Garcia-Bengochea, F.: Tracheotomy in the Management of Severe Head Injuries. Surgery 28: 801-811 (Nov.) 1950. University of California Hospital Sa.n Francisco 22, California