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Neurosurgery: Some Diagnostic Problems
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Neurosurgery: Some Diagnostic Prohlems ROBERT A. GROFF, M.D. *
the numerous diagnostic problems in neurosurgery, there are two which seem appropriate for discussion in a symposium of general surgical interest. They are cranial trauma and subarachnoid hemorrhage. The former has a particular interest because of its frequency in this era, and the latter has come into prominence during the past two decades because of its common association with intracranial aneurysm, which has become a surgical lesion. These subjects will be discussed in brief and from a practical point of view in order to facilitate diagnosis, a plan of management and treatment for both problems. AMONG
CRANIAL TRAUMA
Patients with head injuries fall into three groups. The first comprises those in whom the injury is either mild or moderately severe; with bed rest, good nursing care and careful attention to fluid balance and nutrition, the patient gets well without surgery. The second group consists of those patients whose injury is so severe that no form of therapy will alter the outcome. The last group consists of those patients whose injury is such that careful observation and appropriate timing of surgical procedures will make the difference between recovery and death. It is this group that commands our interest. A thorough knowledge of the problem is essential. For this reason, it seems best to review briefly the pa.thology of closed brain injuries. No discussion of compound cranial injuries will be presented, since these injuries are clear-cut surgical problems. Pathology of Brain Injuries
The brain is subject to three types of injury when the head is struck by a force or the head strikes an object. The first of these is cerebral concussion. This term has come to mean a minor injury without specific pathology. It has never been seen hisFrom the Department of Neurosurgery, Graduate Hospital of the University of Pennsylvania, Philadelphia.
* Associate Professor of Neurosurgery, Graduate School of Medicine of the University of Pennsylvania, Philadelphia. 1585
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tologically and therefore is a physiologic state. By it is meant a general widespread disturbance of cell action with return of cell function within several minutes. Clinically, it is manifested by a dazed state or loss of consciousness for not more than three or four minutes. The patient recovers completely without sequelae. The second type of injury is cerebral contusion. This term refers to a "bruising" of the brain, which signifies destruction of brain tissue associated with hemorrhage. The degree of force to the head determines the extent of these changes. Clinically, it is recognized by periods of unconsciousness for five minutes up to several weeks. Various neurologic signs mayor may not be present, depending entirely upon whether a part of the brain is damaged which will produce a neurologic deficit. The cerebrospinal fluid in almost every instance contains blood. Because of this, meningeal signs may be present. The third type of injury is cerebral laceration. This is a pathologic diagnosis which can be made only at the operating table or at autopsy. From the clinical standpoint, it cannot be differentiated from a severe cerebral contusion. These injuries refer to those conditions which affect the brain only. There is another form of brain injury which is sometimes associated with a spot force to the skull, such as a glancing blow from a bullet causing a short, gutter-type fracture. Associated with this. may be a subcortical hemorrhage originating from one of the cortical vessels. The clinical picture is that of severe headache, signs of increasing intracranial pressure and usually focal convulsive seizures of the opposite side of the body. Two additional structures may be involved when the skull is injured. The first of these is rupture of the middle meningeal artery. The second is tearing of the veins which traverse the subdural space from the surface of the brain to the longitudinal sinus or dura. Bleeding occurs into the subdural space and causes a subdural hematoma. There are instances in which one of the large dural sinuses is torn, but bleeding is so profuse that death occurs in a matter of hours, preventing definitive surgery. Middle Meningeal Hemorrhage
Hemorrhage from the middle meningeal artery produces a rapid and characteristic syndrome. There are three important points about the syndrome which are essential in order to recognize it. The first is the fact that it is thought that the clinical picture requires about twelve hours to become manifest. This is incorrect, for in a series of 18 patients we have found that the average time was eight hours. It is, therefore, a rapidly developing clinical picture. The second point is that the injury to the head is invariably thought to be mild because the patient has been either dazed or rendered unconscious for a few minutes. The third fact is that during the succeeding few hours following the injury, there is increasing headache and a gradual seepage into an unconscious state with signs of increasing intracranial pressure.
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Because it is important to recognize this condition early, the following case is presented as an example of improper timing. CASE HISTORY. C. S., age 23, an attractive young lady who had been married for three months, was out motoring with her husband on a Sunday afternoon in early summer. Their car was struck by another, throwing the patient out of the car onto the dirt shoulder of the road. When her husband reached her side, she was dazed but able to get up and walk to another car, which took her to a hospital. Examination was essentially negative except for a fracture of the right clavicle. Because of this injury, she was admitted to a private room at 2 P.M., the accident having occurred about 1 :30 P.M. The pulse, respirations and temperature at the time of admission were normal. The patient was seen 2 hours later and complained bitterly of headache, but was otherwise comfortable. At 6 P.M. the nurse went hurriedly into the room because of a groaning noise and sounds of a disturbance. The patient was having a generalized convulsion which lasted about 5 minutes. After the convulsion she remained in coma. The pulse had slowed to 50 and the respirations were 14, displaying a Cheyne-Stokes character. By 6 :45 P.M. the patient, in Cheyne-Stokes respiration, was operated upon, and about 172: ounces of blood were removed from the right epidural space through a trephine opening, which was enlarged to a subtemporal decompression. The meningeal artery was actively bleeding, but was controlled by plugging the foramen spinosum with cotton. The patient never regained consciousness, and died 10 hours later. Autopsy failed to reveal the cause of death, since no postoperative bleeding had occurred and no other bleljding was found.
Comment. This case represents not so much a problem in diagnosis, but rather the failure to consider the likelihood of a middle meningeal hemorrhage as one of the diagnostic possibilities. The head injury was thought to be oflittle consequence, and all therapy was directed toward the fractured clavicle. It is true that no neurologic signs were present when the patient was examined in the Accident Ward, and this is to be expected. The complaint of headache, which was possibly as severe as or greater than the pain incident to the fractured clavicle, should have made the examiner suspicious of the head injury and stimulated the writing of orders to cover the potentiality. Had the regimen of taking pulse rate, respiratory rate and blood pressure at 15 or 30 minute intervals been inaugurated, signs of increasing intracranial pressure (slowing of pulse and respiratory rates and an increasing pulse pressure) would have been detected early. At the same time, the observations by the nurse that the patient was complaining of increasing headache and becoming duller would have added further evidence to the seriousness of the head injury and precipitated active therapy earlier. Diagnosis. The diagnosis of middle meningeal hemorrhage is made on clinical observation and the fact that it is regarded. as a possible sequela of head injuries. Lumbar puncture does not help in the diagnosis until late, when it reveals an increase in cerebrospinal fluid pressure which is already known by the clinical signs. The fluid is clear unless there is an alSs9ciated cerebral contusion, because the bleeding occurs between the dura and bone and therefore never has an opportunity to enter the sub-
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arachnoid space. Examination of the eyegrounds does not reveal papilledema or choked disks because it takes anywhere from twelve to sixteen hours for it to develop. X-ray films of the skull rarely if ever serve a useful purpose. They may show a fracture across the course of the middle meningeal artery, but this is not an assurance that the artery has been ruptured. Many cases are not associated with fracture. In the last analysis, therefore, it is the frequent observation of the patient over a period of four to six hours that will establish the diagnosis. It is the usual practice to assign a nurse to the duty of taking blood pressures, pulse and respiratory rates and recording them. Her understanding of the problem is just as important as her ability to make the necessary examinations. She should be instructed in the mechanism of increased intracranial pressure so that she knows what to expect and can make intelligent reports to the physician. This does not seem to be fully realized, or, if it is, sufficient attention is not paid to it. Her observations and timely reports are the only means by which the diagnosis is suspected and appropriate treatment instituted. Occasionally, the clinical picture of middle meningeal hemorrhage takes longer to develop than the time given. As Peet pointed out, this may be due to a dura which is tightly adherent to the skull, or one of the branches of the artery and not the main trunk is the source of bleeding. Thus the hemorrhage may be temporoparietal, temporo-occipital or frontal in relationship to the bones of the skull. The time interval between injury and clinical detection may be as long as forty-eight hours. Operation. As soon as the diagnosis is suspected, operation should be performed. Signs of localization do not occur until late. The reason for this is that the hemorrhage presses upon the temporal lobe, which is a "silent" area. In some instances the pupil is dilated on the side of the hemorrhage. Otherwise, it is rare to have a clue on which side the hemorrhage is located. The patient is prepared so that both temporal areas can be explored. A trephine is placed in the upper limits of a subtemporal decompression (Fig. 498); if no blood is recovered as soon as the skull is penetrated, the procedure is repeated in the same area on the opposite side. When the hemorrhage is found, the trephine opening is enlarged sufficiently to remove the clot and control the bleeding from the artery if necessary. Should the hemorrhage have been found with the first trephine, it would not be necessary to explore the opposite side, since bilateral middle meningeal hemorrhage, in my experience, never occurs. It is not necessary to open the dura unless it is tense. The wound should be drained for a period of forty-eight hours. Subdural Hematoma
Subdural hematoma, the result of the tearing of cortical veins which pass from the cortex of the brain to the longitudinal sinus or dura, is a much less rapid clinical syndrome. In the first place, it is caused by venous bleeding. In the second place, it is not the quantity of blood which causes the symptoms, but rather the mixture of the blood and cerebrospinal fluid which is continually being drawn into the encased
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blood, since, as soon as blood enters the subdural space, the dura forms a membrane about it in preparation for absorption. This membrane acts as a dialyzer, allowing cerebrospinal fluid to enter the disintegrating blood clot, as pointed out by Gardner, and accounts for the increase in size of the clot. More than 80 per cent of these clots are liquid by the time operation is performed. Two types are recognized because of the time interval required to produce symptoms. The subacute subdural hematoma manifests itself in five to ten days and is always associated with cerebral contusion. The chronic subdural hematoma is a condition which is an entity unto itself. Probably the most difficult decision to make in the management of
Fig. 498. Schematic drawing showing location of trephine at upper limits of a proposed sub temporal decompression for exploration in middle meningeal hemorrhage. Dotted area is amount of bone removed for a sub temporal decompression.
the patient with a cerebral contusion, especially when it is severe, is the differentiation between cerebral edema and a subacute subdural hematoma. Both conditions give rise to increased intracranial pressure. For example, the patient has been rendered unconscious and after the first twelve hours emerges into a state of reflex action. Purposeful movements occur. The arms and legs are withdrawn when painfully stimulated. The mental reaction consists in opening the eyes without recognition, or a fighting response to painful stimuli with a few "choice" words. The patient remains in this state for three or four days and then becomes less active, drifting into a state of coma. The pulse and respirations may become slow, but not necessarily. The pulse pressure-the difference between the systolic and diastolic pressures-may increase, but here again it does not always increase. Is this clinical picture cerebral edema or bleeding within the subdural space?
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A decision has to be made. The patient should be treated for the possibility of cerebral edema as the first step, unless the clinical course is rapid, when no time should be lost in performing exploratory trephines. A lumbar puncture should be made and after the pressure. has heen measured, 5 cc. of fluid should be removed. This is followed by an intravenous injection of 100 cc. of 50 per cent glucose solution. If a definite improvement in the clinical picture is not observed in the course of an hour or two, exploratory trephines under local anesthesia should be the next step. If, on the other hand, improvement is noted and is maintained for a number of hours and then regression observed, the conservative procedure should be repeated. The routine exploration in these patients by trephines should be similar to that for a chronic subdural hematoma, which will be given later. Should the exploratory trephines fail to disclose a subdural or intracerebral clot and the brain was found to be under definite tension in that it bulged through the dural opening, a right subtemporal decompression in a right-handed man should be done in order to control the increase in intracranial pressure. The opening in the skull under the temporal muscle should be at least 3 inches in diameter. Trephines which are no more than Yz to % inch in diameter do not relieve intracranial pressure. This cannot be stressed too strongly, for it is a mistaken idea which is still held, fortunately by only a very few. If the exploratory trephines revealed blood clots or liquid blood in the subdural space-a subacute subdural hematoma-a counter-trephine should be made and the space washed out as for chronic subdural hematoma. If a small amount of yellow or pinkish-yellow fluid is found and no increase in intracranial pressure, nothing further is indicated. In both instances the patients will show a definite improvement in their clinical course after the procedure. The patient who has a chron1·c subdural hematoma invariably presents a real diagnostic predicament. The patient enters the hospital in either stupor or a state of coma. The history is to the effect that a mild headache began two to three weeks previously and became increasingly more severe, so that during the several days before admission the patient was periodically difficult to arouse. Various diagnostic possibilities come into consideration: uremia, diabetic coma, cerebral thrombosis, bromide poisoning or even brain tumor. Blood and urine studies fail to substantiate diabetic coma or uremia, although the blood urea nitrogen may be elevated slightly. The blood bromide test is normal. On systemic and neurologic examination no abnormalities are found except for a slightly dilated pupil on one side, or maybe the pupils are equal. A lumbar puncture discloses clear fluid under normal pressure or a pressure slightly elevated or a pressure under 100 mm. of water. This patient should be considered to have a subdural hematoma until proved otherwise. An actual case will serve to emphasize this fact. CASE HISTORY. W. D., a man aged 52 years, was admitted to a hospital on the medical service with a history of having eaten a hamburger 3 weeks before
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and having had mild epigastric distress. The nauseated feeling left him by the next day, but headache developed and became increasingly more severe as the days went by. During the week prior to admission, he remained in the house and was in bed a good part of the time because of the headache. On admission, he was quite lethargic and complained bitterly of headache. His physical and neurologic examinations were within normal limits. Blood studies were all normal except for a positive test for trichinosis. A lumbar puncture was performed and a pressure of 180 mm. of water was obtained. The fluid was grossly clear. Because the tube containing the fluid was accidentally broken in the laboratory, the lumbar puncture was repeated the next day. The pressure was 170 mm. of water, and about 5 cc. of fluid were removed. The patient went into coma and Cheyne-Stokes respirations developed. A neurosurgical consultation was obtained, and a chronic subdural hematoma was evacuated through trephines from the right subdural space. There was no hematoma on the left side. The patient regained consciousness within 6 hours and made a complete recovery.
Comment. The misleading information in this man's history was the eating of a hamburger and the finding of trichinosis. After the patient had regained consciousness the history of striking his head against a steel beam and stunning himself for a few minutes just before the hamburger incident was disclosed. Had this bit of information been known prior to operation, the diagnosis would have been made earlier. Diagnosis. The obtaining of a history of trauma following the evacuation of a subdural hematoma is a common sequence. Yet it must be remembered that these lesions develop without trauma to the head. For this reason, it is important to consider the diagnosis in a patient who is unconscious, when an adequate explanation cannot be secured from the various tests, as well as historical data. The diagnosis of subdural hematoma is suspected clinically and made at the operating table. Headache of increasing intensity is the outstanding symptom. Usually, however, these patients are admitted to a hospital in a stuporous state, and historical information is difficult to obtain. From a neurologic standpoint, they do not, in the majority of instances, present definite neurologic signs. A dilated pupil should make one suspicious, and in the majority of cases this is found on the side of the hematoma. Rarely does a lumbar puncture give helpful information, but it does rule out the possibility of a subarachnoid hemorrhage. Many of these patients will show a slight elevation of the blood urea nitrogen, but urine examination makes this finding an unlikely cause for uremia, which is not an infrequent diagnosis made in these patients. A safe rule to follow is that when an unconscious state cannot be adequately explained by laboratory tests and examination, the diagnosis of subdural hematoma should be made and the patient subjected to exploratory trephines. Operation. Most subdural hematomas are liquid and occur over the front half of the cerebral hemisphere. The first two trephines, therefore, are made within the hairline and 3 cm. lateral to the midline (Fig. 499, A). They localize the hematoma, and another trephine is made in either the temporal or parieto-occipital area (Fig. 499, B) to permit washing
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out the dark brownish fluid with normal saline solution at body temperature. For this purpose, a catheter is inserted carefully between the dura and brain. An Asepto syringe filled with normal saline solution is attached to the free end of the catheter a~d fluid is injected firmly. Care should be exercised to prevent the fluid from becoming trapped in the subdural space. Washing should be continued until the fluid returns relatively clear. In some patients it will be noted that the brain does not expand after the hematoma has been washed out. Under normal conditions the brain should swell so that by the end of the procedure it will be a short distance from the dural opening. If the brain remains depressed, a lumbar puncture should be done and normal salt solution at body temperature in-
A
B
Fig. 499. A, Schematic drawing showing location of trephines for exploration in subdural hematoma. These two trephines are always made. B, Schematic drawing showing location of additional trephine at 2 or 3 to permit washing out subdural space containing subdural hematoma.
jected through the needle until the brain has reached a point close to the dural opening. It may require 100 cc. of fluid to accomplish this. Should it be impossible to do this during the operation, it can be done afterwards, provided a drain has been inserted into the subdural space through one of the trephine openings to permit the escape of air and fluid. Sufficient fluid should be injected to raise the cerebrospinal fluid pressure to about 180 mm. of water. This procedure prevents the complications of hyperthermia and death which may occur when the brain does not expand. Another point is that subdural hematomas are bilateral in 35 per cent of patients. Under no circumstances should a patient be trephined on only one side. if the first trephine has disclosed the hematoma, a trephine should always be made on the opposite side. This is a hard and fast rule, for there have been patients who were found to have a second hematoma on the unexplored side at autopsy.
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Indications for Operation
The indications for operation upon patients with severe cranial trauma are based entirely upon the clinical course of the patient. This excludes those instances in which the injury is associated with a compound or simple depressed fracture of the skull or a persistent cerebrospinal fluid leak from the ear or nose, which are clear-cut surgical problems. Although middle meningeal hemorrhage is not considered the result of a severe injury, its syndrome is a good example of a clinical course which demands operation. As soon as the syndrome is suspected, surgical intervention is indicated. The second example in which operation is necessary is the patient who is regressing and in whom the conservative measures of reducing intracranial pressure by the removal of cerebrospinal fluid and the use of dehydrating agents have not produced a favorable response. In this case, a subacute subdural hematoma is suspected, or cerebral edema which does not respond to the ordinary treatment. Exploratory trephines are made and a subtemporal decompression if the pathology is increased intracranial pressure. A linear, either simple or compound, fracture of the skull is not an indication for surgery of itself. The fact that a patient remains unconscious for several hours or even days or weeks does not mean that surgery is indicated. There are many examples of patients who have remained unconscious for a month or more and finally made an almost complete recovery without operation. The cause for this reaction is not clearly understood, but it is thought to be due to severe brain damage. Convulsive seizures of themselves are not indications for surgery. They are the result of irritation of the cortex of the brain. If, on the other hand, the clinical picture of the patient is that of increasing intracranial pressure--deepening of the stupor, slowing of the pulse and a rise of the pulse pressure-and it is associated with convulsions, there is a definite indication for surgery because of the progressive clinical signs and not the convulsive seizures per se. Care of the Unconscious Patient
It seems worthwhile to make a few remarks about the care of the unconscious patient. One of the greatest errors in the management of these patients is to place them on their backs. In this position the tongue drops back into the nasopharynx, partially obstructing the airway. There is no better way to produce increased intracranial pressure. Because the air exchange is reduced, cerebral anoxia is inevitable. At the same time there is an irritation of the structures in the throat and trachea, causing the production of mucus with all its potential complica. tions. An unconscious patient should never be placed on the back. This applies particularly to patients with brain injuries, but also includes those who are unconscious from other sources. The position of choice is on the side or on the abdomen with the head turned to the side. If mucus is a complicating factor, the foot of the bed should be elevated
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so that mucus will drain into the nasopharynx rather than the lungs. Aspiration should be done as often as necessary to maintain an unobstructed airway. If the color of the patient is poor or there is a suggestion of cyanosis, oxygen should be supplied by an intranasal catheter. The patient should be turned from one side to the other every two hours. Some unconscious patients, even in the optimum position for adequate air exchange, have a noisy, fighting, snorting type of breathing. A rubber airway will overcome this complication, Because the teeth are invariably held tightly together, it is difficult to insert the airway. If it is introduced upside down during a period of momentary relaxation for a distance of an inch or more and then quickly turned into the normal position, it will be possible to ease it all the way in during periods of relaxation. The procedure should not be hurried or force used. The airway will facilitate breathing, permit aspiration of mucus by a thin rubber catheter through it and, oddly enough, is not particularly annoying to the patient or a source of irritation. If it does not accomplish the purpose, a tracheotomy should be performed. For the first, twenty-four hours, fluids should be supplied by hypodermoclysis or intravenously. A total of 2000 cc. in this period should be given unless more should be necessary. At the end of the first day, with the patient still unconscious, feedings should be instituted by a nasal catheter. The schedule should be on a three-hour round-the-clock frequency. The quantity should be 250 cc. This provides a total of 2000 cc. in twenty-four hours. Of this quantity, half should be a gastrostomy mixture which has a caloric value of 1000. In other words, 1 cc. of the mixture equals 1 Calorie. The remainder may be either water or fruit juices plus a daily supply of vitamins. The tube also serves as a convenient way of introducing a cathartic in order that the bowel may be kept thoroughly cleansed. Since frequently the bladder is forgotten in these patients, it should be a routine to insert an indwelling catheter. It not only prevents restlessness in the stuporous patient, but also makes nursing care much easier. These details in the unconscious patient offer the maximum opportunity for recovery. They insure adequate oxygenation of blood, minimize pulmonary complications, provide adequate metabolic requirements, and maintain a fluid balance. Even though this is true, it is well to periodically check the blood chemistry in respect to chlorides, potassium, sugar and protein in order to correct any deficiency which may arise. Furthermore, it is much safer to use this regimen and use dehydration only if the clinical picture dictates its necessity. SUBARACHNOID HEMORRHAGE
Subarachnoid hemorrhage occurs spontaneously independent of trauma, and it is this type that offers a challenge in diagnosis. A patient enters the hospital with a history of having had a sudden severe headache several hours or more before and within a few minutes lapsed into unconsciousness or a dull mental state, adverse to talking because of the excruciating headache. A neurologic examination, except for the
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mental state, slowed pulse rate and an elevated blood pressure, fails to reveal any abnormal signs. A lumbar puncture reveals bloody cerebrospinal fluid under increased pressure. Ordinarily this would be considered a so-called stroke, but this is not an etiologic diagnosis. Spontaneous subarachnoid hemorrhage is in reality a syndrome and not a disease entity. Actually it is a series of symptoms which have come to be identified with blood in the cerebrospinal fluid. The causes for this syndrome are divided into two groups; spontaneous and secondary. The spontaneous group includes those which are the result of a leakage or rupture from a defect in a vessel wall such as aneurysm, arteriovenous anomaly or simply a congenitally weakened vessel wall. The secondary group comprises those incident to a general systemic disease process such as arteriosclerosis, blood dyscrasias, cardiorenal disease, diabetes, acute exanthema, brain tumor, epilepsy, syphilis, and so forth. Of these causes, the most common are cerebral aneurysm and cerebrovascular anomaly. Diagnosis and Management
When presented with the problem of spontaneous subarachnoid hemorrhage in a patient, what is the plan of management? The first step is to determine whether the patient is suffering from any of the systemic diseases whicll have been mentioned. This can be accomplished rapidly by a good history and a few well-directed laboratory tests such as blood sugar, blood urea nitrogen, complete blood count and bleeding and coagulation times. Serologic tests are important, but time should not be wasted in waiting for the report, since syphilis is a rare cause. Having failed to discover any systemic disease, the next step is to determine whether the patient has an aneurysm or brain tumor. These lesions are surgical lesions and in many instances can be treated suc~ cessfully. Time is the important factor, because patients with aneurysms, in their first hemorrhage, face the risk of a mortality ranging from 28 to 58 per cent. If they survive the first hemorrhage, the second will cause death in about 75 per cent. The gravity of the problem is apparent. For the purpose of establishing the diagnosis of an aneurysm or brain tumor under these circumstances, it is necessary to do arteriography. This procedure consists in introducing a needle into the common carotid artery either through the skin or by exposure of the artery. Either diodrast 35 per cent or thorotrast 25 per cent is injected into the artery, and at the exact moment an x-ray film of the skull is taken. The vascular pattern of the anterior two thirds of the cerebral hemisphere on the side of injection is visualized and any defect in connection with this pattern such as aneurysm or arteriovenous anomalies. Tumors are identified by either a staining of their blood supply or displacement of the normal vascular pattern, which applies to intracerebral hemorrhage or abscess as well . . There· are two complications to the procedure. One is the production of a hemiplegia on the side opposite the injection, caused by either vascu~ lar_spasm or thrombosis. The other is an increase in bleeding. The former
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is more likely to occur in the patient with arteriosclerosis or in one beyond the age of fifty years. Fortunately, both are rather uncommon, but the risk entailed with the test and the risk of the subarachnoid hemorrhage must be carefully weighed in order to evaluate the justification of the test. I~ When possible, arteriography should be performed when bleeding has subsided for two or three days. The condition of the patient, however, is the guide, for critical patients must be subjected to the procedure irrespective of possible complications if definitive treatment is to be successful. The important fact to determine is the presence of an aneurysm, where it is located and whether it is possible to treat it surgically. If the arteriogram reveals an aneurysm, the next step is ligation of the common carotid artery on the same side. For those aneurysms arising from the carotid syphon, the anterior cerebral artery near its origin and possibly the posterior communicating artery, this procedure is lifesaving. For those on other vessels, it is doubtful whether carotid ligation has any effect. In spite of this, the procedure should be done. The ligation of the common carotid artery is done under local anesthesia. The reason for this is to determine before ligation whether the artery can be occluded without causing a hemiplegia. Thus, after the vessel is exposed, it is occluded by a piece of rubber tissue or soft rubber catheter wound around the vessel and placing a clamp on the tissue or catheter to prevent slipping. The opposite arm and leg are tested every two or three minutes for fifteen minutes by the clock. At the end of this time, if no signs of weakness have developed, it is considered safe to ligate. In our Clinic, hernia silk is used and double ligations are performed about an inch apart. The upper ligature, or that one nearest the bifurcation of the common carotid into its internal and external branches, is placed no more than an inch below the "crotch" (Fig. 500). It is felt that little "dead space" in the carotid artery should be permitted, so that the reflex circulation from the external to the internal carotid artery will not eddy or stagnate. For this reason, clotting with subsequent emboli and/or propagating thrombus will be less likely to occur with the resulting sequelae of hemiplegia. If the patient, during the trial occlusion, exhibits weakness, it will be necessary to occlude the artery in stages. A broad (74: inch) metal clip cut from tantalum or other thin sheet metal is best suited for this purpose. Successive pinchings of the clip at three day intervals until the artery is occluded are satisfactory. An apparatus designed by Silverstone of Boston makes this procedure very simple. Should a delayed hemiplegia occur-that is, within the first twentyfour hours-the ligatures should be removed immediately. If this is accomplished within an hour of the complication, experience has shown: that the paralysis will usually disappear. At the same time the ligature is removed, a stellate ganglion block with 0.5 per cent procaine should be performed and repeated three 'or four times at four to six hour intervals. A better procedure is that suggested by Poppen. A thin polyethylene tube is placed underneath the fascia in close proximity to the stellate ganglion at the time of removing sutures from the artery and closing the wound. A slow drip of 0.5 per-cerit procaine is allowed to rilnthrough
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the tube. This is continued for two to three days, when the catheter is withdrawn. The example just presented is that of a patient without neurologic signs. If the patient was found to have a third nerve palsy-ptosis, complete internal ophthalmoplegia and paralysis of the superior, internal and inferior recti and inferior oblique eye muscles-the cause is probably an aneurysm arising from the syphon of the internal carotid or the posterior communicating artery. This sign localizes the lesion, and blood in the cerebrospinal fluid makes it a potential aneurysm. The patient should be taken to the operating room and the common carotid artery ligated on the side of the third nerve palsy.
Fig. 500. Schematic drawing showing position of ligatures for ligation of common carotid artery.
The procedure should be done under local anesthesia. By so doing, the possibility of further bleeding has been lessened, and some surgeons hold that the only additional therapy should be ligation of the internal carotid artery in a week or ten days following ligation of the common carotid artery. It is our opinion that the lesion should be verified by arteriography. If it can be approached surgically, an attack should be made upon it directly, either clipping the vessel on either side of the aneurysm or placing a clip upon the stalk. By this method, one can be certain that the lesion is under control. conclusion, it can be readily seen that when subarachnoid hemorrhage occurs in head injury, the cause is known and active treatment is instituted accordingly. On the other hand, when it occurs spontaneously, the etiology is not known. Because aneurysm and arteriovenous anomalies are responsible for a large percentage of the spontaneous variety, and because within recent years these lesions have been treated successfully by surgery, it is most important that active investigation be gotten underway as soon as possible.
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Neurosurgery: Some Diagnostic Prohlems ROBERT A. GROFF, M.D. *
the numerous diagnostic problems in neurosurgery, there are two which seem appropriate for discussion in a symposium of general surgical interest. They are cranial trauma and subarachnoid hemorrhage. The former has a particular interest because of its frequency in this era, and the latter has come into prominence during the past two decades because of its common association with intracranial aneurysm, which has become a surgical lesion. These subjects will be discussed in brief and from a practical point of view in order to facilitate diagnosis, a plan of management and treatment for both problems. AMONG
CRANIAL TRAUMA
Patients with head injuries fall into three groups. The first comprises those in whom the injury is either mild or moderately severe; with bed rest, good nursing care and careful attention to fluid balance and nutrition, the patient gets well without surgery. The second group consists of those patients whose injury is so severe that no form of therapy will alter the outcome. The last group consists of those patients whose injury is such that careful observation and appropriate timing of surgical procedures will make the difference between recovery and death. It is this group that commands our interest. A thorough knowledge of the problem is essential. For this reason, it seems best to review briefly the pa.thology of closed brain injuries. No discussion of compound cranial injuries will be presented, since these injuries are clear-cut surgical problems. Pathology of Brain Injuries
The brain is subject to three types of injury when the head is struck by a force or the head strikes an object. The first of these is cerebral concussion. This term has come to mean a minor injury without specific pathology. It has never been seen hisFrom the Department of Neurosurgery, Graduate Hospital of the University of Pennsylvania, Philadelphia.
* Associate Professor of Neurosurgery, Graduate School of Medicine of the University of Pennsylvania, Philadelphia. 1585
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tologically and therefore is a physiologic state. By it is meant a general widespread disturbance of cell action with return of cell function within several minutes. Clinically, it is manifested by a dazed state or loss of consciousness for not more than three or four minutes. The patient recovers completely without sequelae. The second type of injury is cerebral contusion. This term refers to a "bruising" of the brain, which signifies destruction of brain tissue associated with hemorrhage. The degree of force to the head determines the extent of these changes. Clinically, it is recognized by periods of unconsciousness for five minutes up to several weeks. Various neurologic signs mayor may not be present, depending entirely upon whether a part of the brain is damaged which will produce a neurologic deficit. The cerebrospinal fluid in almost every instance contains blood. Because of this, meningeal signs may be present. The third type of injury is cerebral laceration. This is a pathologic diagnosis which can be made only at the operating table or at autopsy. From the clinical standpoint, it cannot be differentiated from a severe cerebral contusion. These injuries refer to those conditions which affect the brain only. There is another form of brain injury which is sometimes associated with a spot force to the skull, such as a glancing blow from a bullet causing a short, gutter-type fracture. Associated with this. may be a subcortical hemorrhage originating from one of the cortical vessels. The clinical picture is that of severe headache, signs of increasing intracranial pressure and usually focal convulsive seizures of the opposite side of the body. Two additional structures may be involved when the skull is injured. The first of these is rupture of the middle meningeal artery. The second is tearing of the veins which traverse the subdural space from the surface of the brain to the longitudinal sinus or dura. Bleeding occurs into the subdural space and causes a subdural hematoma. There are instances in which one of the large dural sinuses is torn, but bleeding is so profuse that death occurs in a matter of hours, preventing definitive surgery. Middle Meningeal Hemorrhage
Hemorrhage from the middle meningeal artery produces a rapid and characteristic syndrome. There are three important points about the syndrome which are essential in order to recognize it. The first is the fact that it is thought that the clinical picture requires about twelve hours to become manifest. This is incorrect, for in a series of 18 patients we have found that the average time was eight hours. It is, therefore, a rapidly developing clinical picture. The second point is that the injury to the head is invariably thought to be mild because the patient has been either dazed or rendered unconscious for a few minutes. The third fact is that during the succeeding few hours following the injury, there is increasing headache and a gradual seepage into an unconscious state with signs of increasing intracranial pressure.
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Because it is important to recognize this condition early, the following case is presented as an example of improper timing. CASE HISTORY. C. S., age 23, an attractive young lady who had been married for three months, was out motoring with her husband on a Sunday afternoon in early summer. Their car was struck by another, throwing the patient out of the car onto the dirt shoulder of the road. When her husband reached her side, she was dazed but able to get up and walk to another car, which took her to a hospital. Examination was essentially negative except for a fracture of the right clavicle. Because of this injury, she was admitted to a private room at 2 P.M., the accident having occurred about 1 :30 P.M. The pulse, respirations and temperature at the time of admission were normal. The patient was seen 2 hours later and complained bitterly of headache, but was otherwise comfortable. At 6 P.M. the nurse went hurriedly into the room because of a groaning noise and sounds of a disturbance. The patient was having a generalized convulsion which lasted about 5 minutes. After the convulsion she remained in coma. The pulse had slowed to 50 and the respirations were 14, displaying a Cheyne-Stokes character. By 6 :45 P.M. the patient, in Cheyne-Stokes respiration, was operated upon, and about 172: ounces of blood were removed from the right epidural space through a trephine opening, which was enlarged to a subtemporal decompression. The meningeal artery was actively bleeding, but was controlled by plugging the foramen spinosum with cotton. The patient never regained consciousness, and died 10 hours later. Autopsy failed to reveal the cause of death, since no postoperative bleeding had occurred and no other bleljding was found.
Comment. This case represents not so much a problem in diagnosis, but rather the failure to consider the likelihood of a middle meningeal hemorrhage as one of the diagnostic possibilities. The head injury was thought to be oflittle consequence, and all therapy was directed toward the fractured clavicle. It is true that no neurologic signs were present when the patient was examined in the Accident Ward, and this is to be expected. The complaint of headache, which was possibly as severe as or greater than the pain incident to the fractured clavicle, should have made the examiner suspicious of the head injury and stimulated the writing of orders to cover the potentiality. Had the regimen of taking pulse rate, respiratory rate and blood pressure at 15 or 30 minute intervals been inaugurated, signs of increasing intracranial pressure (slowing of pulse and respiratory rates and an increasing pulse pressure) would have been detected early. At the same time, the observations by the nurse that the patient was complaining of increasing headache and becoming duller would have added further evidence to the seriousness of the head injury and precipitated active therapy earlier. Diagnosis. The diagnosis of middle meningeal hemorrhage is made on clinical observation and the fact that it is regarded. as a possible sequela of head injuries. Lumbar puncture does not help in the diagnosis until late, when it reveals an increase in cerebrospinal fluid pressure which is already known by the clinical signs. The fluid is clear unless there is an alSs9ciated cerebral contusion, because the bleeding occurs between the dura and bone and therefore never has an opportunity to enter the sub-
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Robert A. Groff
arachnoid space. Examination of the eyegrounds does not reveal papilledema or choked disks because it takes anywhere from twelve to sixteen hours for it to develop. X-ray films of the skull rarely if ever serve a useful purpose. They may show a fracture across the course of the middle meningeal artery, but this is not an assurance that the artery has been ruptured. Many cases are not associated with fracture. In the last analysis, therefore, it is the frequent observation of the patient over a period of four to six hours that will establish the diagnosis. It is the usual practice to assign a nurse to the duty of taking blood pressures, pulse and respiratory rates and recording them. Her understanding of the problem is just as important as her ability to make the necessary examinations. She should be instructed in the mechanism of increased intracranial pressure so that she knows what to expect and can make intelligent reports to the physician. This does not seem to be fully realized, or, if it is, sufficient attention is not paid to it. Her observations and timely reports are the only means by which the diagnosis is suspected and appropriate treatment instituted. Occasionally, the clinical picture of middle meningeal hemorrhage takes longer to develop than the time given. As Peet pointed out, this may be due to a dura which is tightly adherent to the skull, or one of the branches of the artery and not the main trunk is the source of bleeding. Thus the hemorrhage may be temporoparietal, temporo-occipital or frontal in relationship to the bones of the skull. The time interval between injury and clinical detection may be as long as forty-eight hours. Operation. As soon as the diagnosis is suspected, operation should be performed. Signs of localization do not occur until late. The reason for this is that the hemorrhage presses upon the temporal lobe, which is a "silent" area. In some instances the pupil is dilated on the side of the hemorrhage. Otherwise, it is rare to have a clue on which side the hemorrhage is located. The patient is prepared so that both temporal areas can be explored. A trephine is placed in the upper limits of a subtemporal decompression (Fig. 498); if no blood is recovered as soon as the skull is penetrated, the procedure is repeated in the same area on the opposite side. When the hemorrhage is found, the trephine opening is enlarged sufficiently to remove the clot and control the bleeding from the artery if necessary. Should the hemorrhage have been found with the first trephine, it would not be necessary to explore the opposite side, since bilateral middle meningeal hemorrhage, in my experience, never occurs. It is not necessary to open the dura unless it is tense. The wound should be drained for a period of forty-eight hours. Subdural Hematoma
Subdural hematoma, the result of the tearing of cortical veins which pass from the cortex of the brain to the longitudinal sinus or dura, is a much less rapid clinical syndrome. In the first place, it is caused by venous bleeding. In the second place, it is not the quantity of blood which causes the symptoms, but rather the mixture of the blood and cerebrospinal fluid which is continually being drawn into the encased
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blood, since, as soon as blood enters the subdural space, the dura forms a membrane about it in preparation for absorption. This membrane acts as a dialyzer, allowing cerebrospinal fluid to enter the disintegrating blood clot, as pointed out by Gardner, and accounts for the increase in size of the clot. More than 80 per cent of these clots are liquid by the time operation is performed. Two types are recognized because of the time interval required to produce symptoms. The subacute subdural hematoma manifests itself in five to ten days and is always associated with cerebral contusion. The chronic subdural hematoma is a condition which is an entity unto itself. Probably the most difficult decision to make in the management of
Fig. 498. Schematic drawing showing location of trephine at upper limits of a proposed sub temporal decompression for exploration in middle meningeal hemorrhage. Dotted area is amount of bone removed for a sub temporal decompression.
the patient with a cerebral contusion, especially when it is severe, is the differentiation between cerebral edema and a subacute subdural hematoma. Both conditions give rise to increased intracranial pressure. For example, the patient has been rendered unconscious and after the first twelve hours emerges into a state of reflex action. Purposeful movements occur. The arms and legs are withdrawn when painfully stimulated. The mental reaction consists in opening the eyes without recognition, or a fighting response to painful stimuli with a few "choice" words. The patient remains in this state for three or four days and then becomes less active, drifting into a state of coma. The pulse and respirations may become slow, but not necessarily. The pulse pressure-the difference between the systolic and diastolic pressures-may increase, but here again it does not always increase. Is this clinical picture cerebral edema or bleeding within the subdural space?
1590
Robert A. Groff
A decision has to be made. The patient should be treated for the possibility of cerebral edema as the first step, unless the clinical course is rapid, when no time should be lost in performing exploratory trephines. A lumbar puncture should be made and after the pressure. has heen measured, 5 cc. of fluid should be removed. This is followed by an intravenous injection of 100 cc. of 50 per cent glucose solution. If a definite improvement in the clinical picture is not observed in the course of an hour or two, exploratory trephines under local anesthesia should be the next step. If, on the other hand, improvement is noted and is maintained for a number of hours and then regression observed, the conservative procedure should be repeated. The routine exploration in these patients by trephines should be similar to that for a chronic subdural hematoma, which will be given later. Should the exploratory trephines fail to disclose a subdural or intracerebral clot and the brain was found to be under definite tension in that it bulged through the dural opening, a right subtemporal decompression in a right-handed man should be done in order to control the increase in intracranial pressure. The opening in the skull under the temporal muscle should be at least 3 inches in diameter. Trephines which are no more than Yz to % inch in diameter do not relieve intracranial pressure. This cannot be stressed too strongly, for it is a mistaken idea which is still held, fortunately by only a very few. If the exploratory trephines revealed blood clots or liquid blood in the subdural space-a subacute subdural hematoma-a counter-trephine should be made and the space washed out as for chronic subdural hematoma. If a small amount of yellow or pinkish-yellow fluid is found and no increase in intracranial pressure, nothing further is indicated. In both instances the patients will show a definite improvement in their clinical course after the procedure. The patient who has a chron1·c subdural hematoma invariably presents a real diagnostic predicament. The patient enters the hospital in either stupor or a state of coma. The history is to the effect that a mild headache began two to three weeks previously and became increasingly more severe, so that during the several days before admission the patient was periodically difficult to arouse. Various diagnostic possibilities come into consideration: uremia, diabetic coma, cerebral thrombosis, bromide poisoning or even brain tumor. Blood and urine studies fail to substantiate diabetic coma or uremia, although the blood urea nitrogen may be elevated slightly. The blood bromide test is normal. On systemic and neurologic examination no abnormalities are found except for a slightly dilated pupil on one side, or maybe the pupils are equal. A lumbar puncture discloses clear fluid under normal pressure or a pressure slightly elevated or a pressure under 100 mm. of water. This patient should be considered to have a subdural hematoma until proved otherwise. An actual case will serve to emphasize this fact. CASE HISTORY. W. D., a man aged 52 years, was admitted to a hospital on the medical service with a history of having eaten a hamburger 3 weeks before
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and having had mild epigastric distress. The nauseated feeling left him by the next day, but headache developed and became increasingly more severe as the days went by. During the week prior to admission, he remained in the house and was in bed a good part of the time because of the headache. On admission, he was quite lethargic and complained bitterly of headache. His physical and neurologic examinations were within normal limits. Blood studies were all normal except for a positive test for trichinosis. A lumbar puncture was performed and a pressure of 180 mm. of water was obtained. The fluid was grossly clear. Because the tube containing the fluid was accidentally broken in the laboratory, the lumbar puncture was repeated the next day. The pressure was 170 mm. of water, and about 5 cc. of fluid were removed. The patient went into coma and Cheyne-Stokes respirations developed. A neurosurgical consultation was obtained, and a chronic subdural hematoma was evacuated through trephines from the right subdural space. There was no hematoma on the left side. The patient regained consciousness within 6 hours and made a complete recovery.
Comment. The misleading information in this man's history was the eating of a hamburger and the finding of trichinosis. After the patient had regained consciousness the history of striking his head against a steel beam and stunning himself for a few minutes just before the hamburger incident was disclosed. Had this bit of information been known prior to operation, the diagnosis would have been made earlier. Diagnosis. The obtaining of a history of trauma following the evacuation of a subdural hematoma is a common sequence. Yet it must be remembered that these lesions develop without trauma to the head. For this reason, it is important to consider the diagnosis in a patient who is unconscious, when an adequate explanation cannot be secured from the various tests, as well as historical data. The diagnosis of subdural hematoma is suspected clinically and made at the operating table. Headache of increasing intensity is the outstanding symptom. Usually, however, these patients are admitted to a hospital in a stuporous state, and historical information is difficult to obtain. From a neurologic standpoint, they do not, in the majority of instances, present definite neurologic signs. A dilated pupil should make one suspicious, and in the majority of cases this is found on the side of the hematoma. Rarely does a lumbar puncture give helpful information, but it does rule out the possibility of a subarachnoid hemorrhage. Many of these patients will show a slight elevation of the blood urea nitrogen, but urine examination makes this finding an unlikely cause for uremia, which is not an infrequent diagnosis made in these patients. A safe rule to follow is that when an unconscious state cannot be adequately explained by laboratory tests and examination, the diagnosis of subdural hematoma should be made and the patient subjected to exploratory trephines. Operation. Most subdural hematomas are liquid and occur over the front half of the cerebral hemisphere. The first two trephines, therefore, are made within the hairline and 3 cm. lateral to the midline (Fig. 499, A). They localize the hematoma, and another trephine is made in either the temporal or parieto-occipital area (Fig. 499, B) to permit washing
Robert A. Groff
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out the dark brownish fluid with normal saline solution at body temperature. For this purpose, a catheter is inserted carefully between the dura and brain. An Asepto syringe filled with normal saline solution is attached to the free end of the catheter a~d fluid is injected firmly. Care should be exercised to prevent the fluid from becoming trapped in the subdural space. Washing should be continued until the fluid returns relatively clear. In some patients it will be noted that the brain does not expand after the hematoma has been washed out. Under normal conditions the brain should swell so that by the end of the procedure it will be a short distance from the dural opening. If the brain remains depressed, a lumbar puncture should be done and normal salt solution at body temperature in-
A
B
Fig. 499. A, Schematic drawing showing location of trephines for exploration in subdural hematoma. These two trephines are always made. B, Schematic drawing showing location of additional trephine at 2 or 3 to permit washing out subdural space containing subdural hematoma.
jected through the needle until the brain has reached a point close to the dural opening. It may require 100 cc. of fluid to accomplish this. Should it be impossible to do this during the operation, it can be done afterwards, provided a drain has been inserted into the subdural space through one of the trephine openings to permit the escape of air and fluid. Sufficient fluid should be injected to raise the cerebrospinal fluid pressure to about 180 mm. of water. This procedure prevents the complications of hyperthermia and death which may occur when the brain does not expand. Another point is that subdural hematomas are bilateral in 35 per cent of patients. Under no circumstances should a patient be trephined on only one side. if the first trephine has disclosed the hematoma, a trephine should always be made on the opposite side. This is a hard and fast rule, for there have been patients who were found to have a second hematoma on the unexplored side at autopsy.
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Indications for Operation
The indications for operation upon patients with severe cranial trauma are based entirely upon the clinical course of the patient. This excludes those instances in which the injury is associated with a compound or simple depressed fracture of the skull or a persistent cerebrospinal fluid leak from the ear or nose, which are clear-cut surgical problems. Although middle meningeal hemorrhage is not considered the result of a severe injury, its syndrome is a good example of a clinical course which demands operation. As soon as the syndrome is suspected, surgical intervention is indicated. The second example in which operation is necessary is the patient who is regressing and in whom the conservative measures of reducing intracranial pressure by the removal of cerebrospinal fluid and the use of dehydrating agents have not produced a favorable response. In this case, a subacute subdural hematoma is suspected, or cerebral edema which does not respond to the ordinary treatment. Exploratory trephines are made and a subtemporal decompression if the pathology is increased intracranial pressure. A linear, either simple or compound, fracture of the skull is not an indication for surgery of itself. The fact that a patient remains unconscious for several hours or even days or weeks does not mean that surgery is indicated. There are many examples of patients who have remained unconscious for a month or more and finally made an almost complete recovery without operation. The cause for this reaction is not clearly understood, but it is thought to be due to severe brain damage. Convulsive seizures of themselves are not indications for surgery. They are the result of irritation of the cortex of the brain. If, on the other hand, the clinical picture of the patient is that of increasing intracranial pressure--deepening of the stupor, slowing of the pulse and a rise of the pulse pressure-and it is associated with convulsions, there is a definite indication for surgery because of the progressive clinical signs and not the convulsive seizures per se. Care of the Unconscious Patient
It seems worthwhile to make a few remarks about the care of the unconscious patient. One of the greatest errors in the management of these patients is to place them on their backs. In this position the tongue drops back into the nasopharynx, partially obstructing the airway. There is no better way to produce increased intracranial pressure. Because the air exchange is reduced, cerebral anoxia is inevitable. At the same time there is an irritation of the structures in the throat and trachea, causing the production of mucus with all its potential complica. tions. An unconscious patient should never be placed on the back. This applies particularly to patients with brain injuries, but also includes those who are unconscious from other sources. The position of choice is on the side or on the abdomen with the head turned to the side. If mucus is a complicating factor, the foot of the bed should be elevated
Robert A. Groff
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so that mucus will drain into the nasopharynx rather than the lungs. Aspiration should be done as often as necessary to maintain an unobstructed airway. If the color of the patient is poor or there is a suggestion of cyanosis, oxygen should be supplied by an intranasal catheter. The patient should be turned from one side to the other every two hours. Some unconscious patients, even in the optimum position for adequate air exchange, have a noisy, fighting, snorting type of breathing. A rubber airway will overcome this complication, Because the teeth are invariably held tightly together, it is difficult to insert the airway. If it is introduced upside down during a period of momentary relaxation for a distance of an inch or more and then quickly turned into the normal position, it will be possible to ease it all the way in during periods of relaxation. The procedure should not be hurried or force used. The airway will facilitate breathing, permit aspiration of mucus by a thin rubber catheter through it and, oddly enough, is not particularly annoying to the patient or a source of irritation. If it does not accomplish the purpose, a tracheotomy should be performed. For the first, twenty-four hours, fluids should be supplied by hypodermoclysis or intravenously. A total of 2000 cc. in this period should be given unless more should be necessary. At the end of the first day, with the patient still unconscious, feedings should be instituted by a nasal catheter. The schedule should be on a three-hour round-the-clock frequency. The quantity should be 250 cc. This provides a total of 2000 cc. in twenty-four hours. Of this quantity, half should be a gastrostomy mixture which has a caloric value of 1000. In other words, 1 cc. of the mixture equals 1 Calorie. The remainder may be either water or fruit juices plus a daily supply of vitamins. The tube also serves as a convenient way of introducing a cathartic in order that the bowel may be kept thoroughly cleansed. Since frequently the bladder is forgotten in these patients, it should be a routine to insert an indwelling catheter. It not only prevents restlessness in the stuporous patient, but also makes nursing care much easier. These details in the unconscious patient offer the maximum opportunity for recovery. They insure adequate oxygenation of blood, minimize pulmonary complications, provide adequate metabolic requirements, and maintain a fluid balance. Even though this is true, it is well to periodically check the blood chemistry in respect to chlorides, potassium, sugar and protein in order to correct any deficiency which may arise. Furthermore, it is much safer to use this regimen and use dehydration only if the clinical picture dictates its necessity. SUBARACHNOID HEMORRHAGE
Subarachnoid hemorrhage occurs spontaneously independent of trauma, and it is this type that offers a challenge in diagnosis. A patient enters the hospital with a history of having had a sudden severe headache several hours or more before and within a few minutes lapsed into unconsciousness or a dull mental state, adverse to talking because of the excruciating headache. A neurologic examination, except for the
l'feurosurgery:
Diagnostic Problems
1595
mental state, slowed pulse rate and an elevated blood pressure, fails to reveal any abnormal signs. A lumbar puncture reveals bloody cerebrospinal fluid under increased pressure. Ordinarily this would be considered a so-called stroke, but this is not an etiologic diagnosis. Spontaneous subarachnoid hemorrhage is in reality a syndrome and not a disease entity. Actually it is a series of symptoms which have come to be identified with blood in the cerebrospinal fluid. The causes for this syndrome are divided into two groups; spontaneous and secondary. The spontaneous group includes those which are the result of a leakage or rupture from a defect in a vessel wall such as aneurysm, arteriovenous anomaly or simply a congenitally weakened vessel wall. The secondary group comprises those incident to a general systemic disease process such as arteriosclerosis, blood dyscrasias, cardiorenal disease, diabetes, acute exanthema, brain tumor, epilepsy, syphilis, and so forth. Of these causes, the most common are cerebral aneurysm and cerebrovascular anomaly. Diagnosis and Management
When presented with the problem of spontaneous subarachnoid hemorrhage in a patient, what is the plan of management? The first step is to determine whether the patient is suffering from any of the systemic diseases whicll have been mentioned. This can be accomplished rapidly by a good history and a few well-directed laboratory tests such as blood sugar, blood urea nitrogen, complete blood count and bleeding and coagulation times. Serologic tests are important, but time should not be wasted in waiting for the report, since syphilis is a rare cause. Having failed to discover any systemic disease, the next step is to determine whether the patient has an aneurysm or brain tumor. These lesions are surgical lesions and in many instances can be treated suc~ cessfully. Time is the important factor, because patients with aneurysms, in their first hemorrhage, face the risk of a mortality ranging from 28 to 58 per cent. If they survive the first hemorrhage, the second will cause death in about 75 per cent. The gravity of the problem is apparent. For the purpose of establishing the diagnosis of an aneurysm or brain tumor under these circumstances, it is necessary to do arteriography. This procedure consists in introducing a needle into the common carotid artery either through the skin or by exposure of the artery. Either diodrast 35 per cent or thorotrast 25 per cent is injected into the artery, and at the exact moment an x-ray film of the skull is taken. The vascular pattern of the anterior two thirds of the cerebral hemisphere on the side of injection is visualized and any defect in connection with this pattern such as aneurysm or arteriovenous anomalies. Tumors are identified by either a staining of their blood supply or displacement of the normal vascular pattern, which applies to intracerebral hemorrhage or abscess as well . . There· are two complications to the procedure. One is the production of a hemiplegia on the side opposite the injection, caused by either vascu~ lar_spasm or thrombosis. The other is an increase in bleeding. The former
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Robert A. Groff
is more likely to occur in the patient with arteriosclerosis or in one beyond the age of fifty years. Fortunately, both are rather uncommon, but the risk entailed with the test and the risk of the subarachnoid hemorrhage must be carefully weighed in order to evaluate the justification of the test. I~ When possible, arteriography should be performed when bleeding has subsided for two or three days. The condition of the patient, however, is the guide, for critical patients must be subjected to the procedure irrespective of possible complications if definitive treatment is to be successful. The important fact to determine is the presence of an aneurysm, where it is located and whether it is possible to treat it surgically. If the arteriogram reveals an aneurysm, the next step is ligation of the common carotid artery on the same side. For those aneurysms arising from the carotid syphon, the anterior cerebral artery near its origin and possibly the posterior communicating artery, this procedure is lifesaving. For those on other vessels, it is doubtful whether carotid ligation has any effect. In spite of this, the procedure should be done. The ligation of the common carotid artery is done under local anesthesia. The reason for this is to determine before ligation whether the artery can be occluded without causing a hemiplegia. Thus, after the vessel is exposed, it is occluded by a piece of rubber tissue or soft rubber catheter wound around the vessel and placing a clamp on the tissue or catheter to prevent slipping. The opposite arm and leg are tested every two or three minutes for fifteen minutes by the clock. At the end of this time, if no signs of weakness have developed, it is considered safe to ligate. In our Clinic, hernia silk is used and double ligations are performed about an inch apart. The upper ligature, or that one nearest the bifurcation of the common carotid into its internal and external branches, is placed no more than an inch below the "crotch" (Fig. 500). It is felt that little "dead space" in the carotid artery should be permitted, so that the reflex circulation from the external to the internal carotid artery will not eddy or stagnate. For this reason, clotting with subsequent emboli and/or propagating thrombus will be less likely to occur with the resulting sequelae of hemiplegia. If the patient, during the trial occlusion, exhibits weakness, it will be necessary to occlude the artery in stages. A broad (74: inch) metal clip cut from tantalum or other thin sheet metal is best suited for this purpose. Successive pinchings of the clip at three day intervals until the artery is occluded are satisfactory. An apparatus designed by Silverstone of Boston makes this procedure very simple. Should a delayed hemiplegia occur-that is, within the first twentyfour hours-the ligatures should be removed immediately. If this is accomplished within an hour of the complication, experience has shown: that the paralysis will usually disappear. At the same time the ligature is removed, a stellate ganglion block with 0.5 per cent procaine should be performed and repeated three 'or four times at four to six hour intervals. A better procedure is that suggested by Poppen. A thin polyethylene tube is placed underneath the fascia in close proximity to the stellate ganglion at the time of removing sutures from the artery and closing the wound. A slow drip of 0.5 per-cerit procaine is allowed to rilnthrough
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the tube. This is continued for two to three days, when the catheter is withdrawn. The example just presented is that of a patient without neurologic signs. If the patient was found to have a third nerve palsy-ptosis, complete internal ophthalmoplegia and paralysis of the superior, internal and inferior recti and inferior oblique eye muscles-the cause is probably an aneurysm arising from the syphon of the internal carotid or the posterior communicating artery. This sign localizes the lesion, and blood in the cerebrospinal fluid makes it a potential aneurysm. The patient should be taken to the operating room and the common carotid artery ligated on the side of the third nerve palsy.
Fig. 500. Schematic drawing showing position of ligatures for ligation of common carotid artery.
The procedure should be done under local anesthesia. By so doing, the possibility of further bleeding has been lessened, and some surgeons hold that the only additional therapy should be ligation of the internal carotid artery in a week or ten days following ligation of the common carotid artery. It is our opinion that the lesion should be verified by arteriography. If it can be approached surgically, an attack should be made upon it directly, either clipping the vessel on either side of the aneurysm or placing a clip upon the stalk. By this method, one can be certain that the lesion is under control. conclusion, it can be readily seen that when subarachnoid hemorrhage occurs in head injury, the cause is known and active treatment is instituted accordingly. On the other hand, when it occurs spontaneously, the etiology is not known. Because aneurysm and arteriovenous anomalies are responsible for a large percentage of the spontaneous variety, and because within recent years these lesions have been treated successfully by surgery, it is most important that active investigation be gotten underway as soon as possible.
In