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Injuries of the Spinal Cord
Injuries of the Spinal Cord L. W. FREEMAN, M.D., PH.D.*
ADVANCES in various phases of medicine have made it possible to maintain patients with spinal cord injuries in good health for many years. Indeed, the initial mortality (even under combat conditions) has been reduced so drastically that the major problem at present is the provision of adequate facilities for rehabilitation. For those qualified patients to whom all progressive therapy is provided, social and economic rehabilitation has been a regular phenomenon. To reach this circumstance has required diligent attention and care by groups of physicians oriented to integrated approaches. Thus, the patient is not successively a neurosurgical, urological, plastic, psychiatric and orthopedic "problem," but is continually treated by all at the most propitious moments. However well the integrative activities of various specialities might be resolved, there is no substitute for functional return. The neurological surgeon devotes himself to the preservation of functioning neural tissue or the protection from further damage of tissue which might regain function. In the past, a majority have been concerned by the appalling mortality of operative approaches and by the infrequency with which assistance to functional return could be demonstrated. This experience brought about two avenues of approach, that of waiting for some days before operating or operating only when observation showed a progression of neurological symptoms. At the onset of our participation in hostilities on the African and European continents, enthusiastic surgeons operated upon spinal cord injuries with fury and enthusiasm. Since the procedures were being done under far less than ideal circumstances and with careful postoperative attention being quite impossible, it was inevitable that additional reasons for nonoperative treatment would accumulate. Since combat wounds are usually open and compounded, they differ from the usual spinal cord injury in civil life where closed injuries are most common. However, that combat-injured patients could be treated expeditiously by operation, with low mortality, low morbidity, and a high de-
* Professor of Surgery and Director, Surgical Experimental Laboratories, Attending Neurological Surgeon to the Indiana University Medical Center and the Veterans Administration Hospital, Indiana University School of Medicine, Indianapolis, Indiana. 1131
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gree of functional return was demonstrated in the Korean conflict.2 Also, there have been those who have advocated early surgical intervention for civil injuries. 4 , 9, 10, 12 It is proposed that consideration of pertinent data will weigh heavily in favor of emergency operative intervention in most cases of spinal cord injury. REASONS GIVEN FOR NONOPERATIVE TREATMENT
1. The maximal injury has occurred at the instant of the insult and cannot be assessed. 2. Complete loss of motion and sensation indicate anatomical transection of the spinal cord. 3. The injury to the spinal cord is not confined to the point of maximal impact but spreads up and down. 4. When there is a flow of spinal fluid, adequate decompression is present. 5. Traction will accomplish as much decompression as can be expected from laminectomy. 6. Shock is present and the patients do not tolerate major surgery. 7. Surgical wounds do not heal well in paralyzed tissues. 8. Surgery is an unnecessary additional insult to a severely injured patient. 9. There is nothing to be gained by early surgical intervention which later operation cannot equal and with a greater margin of safety to the patient. These reasons will be touched upon or considered at some length in the sections which follow. ACUTE PATHOPHYSIOLOGY OF SPINAL CORD INJURY
There is some confusion about injuries of the spine which is traceable to the fact that the neurosurgeon tends to minimize the bony injury whereas the orthopedist tends to concentrate upon it. Very few injuries to the spinal cord occur without bony damage (ice picks, pen knives, concussive forces), so it is not at all difficult to see how this situation might arise. Although standard nomenclature is in use, the records of these patients are usually classified according to the admitting service (orthopedic-fracture of spine; neurosurgery-traumatic myelitis; urology-cord bladder). Even when consulting services are readily available and are used to maximum extent, the tendency is to categorize the cases as those of fracture of the spine. These remarks are entered for it becomes obvious that not all patients with spinal cord damage will be seen by a given consulting service in any but exceptional locales. As a result, many transient spinal cord injuries are not seen by neurosurgeons, and other patients with no initial spinal cord injury are seen only after manipulation has brought about the change in status. Until spinal fractures, like skull fractures, are considered to be
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the full responsibility of the neurological surgeon, not much progress can be expected in unraveling the complete picture of the range of minimal to maximal injury. Perhaps the greatest single deterrent to a complete knowledge of spinal cord injury has been the roentgenogram. This is true because all too often the course of action is dictated by the roentgenographic findings-or the counter assumption is made that the findings are not representative of the circumstances at the time of insult. Further, the films may be of such poor quality (which is understandable, for good spine films are not easily obtained without perfect positioning) that small pieces of bone impinging on the spinal cord may be overlooked. Finally, soft tissue encroachment into the spinal canal is not visualized. The usual concentration on the bony injury is therefore decried. With this orientation, the spinal cord injury is emphasized, and the bony injury is relegated to secondary consideration. Classification
There are many proposed classifications of spinal injuries but most of them are too complicated. The separation of closed and open injuries is not necessarily a good one except in regard to probability of contamination, and antibiotic therapy is quite reliable. Many thoracic spinal injuries, for example, include dural, pleural and pulmonary tears with direct communication to the spinal canal of potentially infected material. Missile injuries may produce minimal damage to the structural supporting tissues while inducing maximal spinal cord injuries. It is suggested that the spinal cord injury be classified primarily, and that mode of production and possible contamination be secondarily entered. For the total picture, especially in regard to morbidity, the status of the supporting structure can be described. Several differences are important when attempts are made to compare the brain with the spinal cord. The gray matter lies inside of the white in the cord. The vascular supply and drainage is peculiar and does not lend itself to description with the clarity found in the literature. Observations on laboratory animals and clinical subjects lend some credence to the consideration that the white matter is supplied to the mid-dorsal region by the arterial supply from above down and from the lumbar area upwards, and that the gray matter is supplied segmentally. There are numerous anastomoses between these elements as well as arteriovenous communications. Because of these circumstances, level of injury assumes some importance in regard to the sequence of events. Experimental data has shown clearly that gray matter is more susceptible than white to injury .. The high concentration of function in the cord contrasts markedly to the situation in most of the cerebrum, and the number of fibers is surprisingly small. The gross appearance of thE; spinal cord is extremely misleading, for the profile that is viewed consists of the pial mantle with
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the blood vessels. Beneath this may lie a completely normal cord or an almost completely destroyed cord, making it difficult to categori~e the injury from gross appearance. This can lead to prognostications which are not in keeping with the true state of affairs. Since most injured spinal cords come to microscopic examination with many complicating factors preceding death of the patient, or with only crude neurological evaluations just prior to death, the only reasonable classification is a functional one, with gross and microscopic findings being of secondary importance. Certainly this is true from a clinical point of view, and it is hardly possible to translate any but the crudest of observations from animal experiments to potentially similar circumstances in man. It is obvious, therefore, that some of the categories are conjectural, or hypothetical at best. 1. Concussion. Under this category would fall all of those injuries which fail to give permanently detectable neurological signs. "Commotio spinalis" might be an acceptable term. Grossly, there would be no changes observable except perhaps some engorgement of the blood vessels. Microscopically, there are vaguely defined cellular changes in the gray matter similar to the changes seen in the cerebral cortex. In the white matter, there are no findings. Clinically, there is a momentary disturbance of function which disappears rapidly and leaves no signs, early or late. 2. Contusion. Here are included those injuries which exceed concussion to the point where small vessels are ruptured within the substance of the cord (not the vessels of the pia mater). Grossly, there may be no early external evidences of the lesion, for the vascular net of the gray matter is more often affected. Subpial hemorrhage is not considered to have much functional significance, although it is the most obvious finding in injury. Microscopically, extravasations of blood and cellular destruction are evident. In more severe instances, there may be disruption of fibers in the white matter. These alterations can extend widely from the point of maximal impact (see Fig. 292) and would include the serpentine dissecting hematomyelias. The end result would depend upon the disposition of the blood and necrotic material. Later, there may be syrinxes which occupy the zones of destruction and dissection. Functionally, there is always a residual of this type of injury, ranging from scarcely detectable motor signs to complete loss of all cortical connections. It is in this category that surgical intervention has most to offer. 3. Laceration. In this category, elements other than those within the cord itself are implicated. There is actual incision of cord material well beyond the pia. (Pial incision alone need give no appreciable sequelae.) Grossly, the damage is obvious and ranges from scarcely discernible incisions such as imparted by the scalpel, to wide bands of blunt tearing by dislocated bone, and includes anatomical transection. As long as the pia mater is intact, laceration is excluded. Microscopically, the disrup-
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tion of pathways in the white, destruction of cells in the gray, and hemorrhage are observed. Functionally, the gamut from scarcely detectable changes to partial lesions (such as the infrequent Brown-Sequard), on to complete loss of function are observed. There are always permanent
Fig. 292. Diagrammatic illustration of the radiation of forces from the point of maximal impact (A) with the recoil of the bony structures into relatively normal locations (B) and the residual damage that such a blow may have upon the spinal cord.
changes from such injuries, but they are not necessarily completely disabling. Mode of Production of These Three Types of Pathological Change
There is no concise demarcation between concussion, contusion and laceration. Missiles may produce concussion or contusion without entering the spinal canal, or on entering the canal, will lacerate the cord locally, contuse the adjacent tissue, and concuss the tissue beyond. Thus,
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there may be a changing neurological status. Forces sufficient to produce simple compression of vertebral bodies generally produce concussion but not often contusion. Those forces which comminute the laminae or bodies lead most frequently to contusion, infrequently to concussion or laceration. In fracture-dislocation, the limiting factor is the anterior longitudinalligament, for those forces sufficient to disrupt this powerful tissue cause the bony structure to shear the cord. Those dislocations which do not tear the anterior longitudinal ligament do not lacerate the cord but produce concussion or contusion. Such injuries may involve separation of bony spicules which will penetrate the cord. Flexion injuries are more common than extension ones, probably indicating the resistance of the anterior longitudinal ligament as contrasted to that of the posterior structures. Most of the considerations have been based upon static circumstances, which are never the case except for concussion. Here the recovery of the cells and tracts is rapid, for little or no cellular destruction occurs, and the cessation of impulse conduction is temporary. When actual damage to cellular and fibrillar structure occurs, the vasomotor balance is disturbed. Exchange of both gaseous and flllid elements is retarded, producing anoxia and transudation of fluid (edema). These changes may continue to the point where further cellular damage results, or the accumulated carbon dioxide and other tissue elements (histamine) may induce local vascular responses which restore the supply of oxygen and remove the edema fluid, leaving only intrinsic cellular destruction or repair evidences of the injury. When vessels are torn and blood enters the intracellular spaces, it continues to progress until tissue resistance exceeds the pressure of the involved vessels. For torn capillaries, this does not involve much more than a few cells. As the caliber of the vessel increases, the amount of blood becomes greater, never being great quantities (for the pressure in the largest spinal vessels is quite low) unless wide spaces are created by pial and tract disruption, and this is limited because the arteries close off very rapidly. However, the high specific gravity fluid is also extremely active osmotically, drawing fluid to it and holding it, constituting a foreign body. In time, this fluid may be absorbed, or it may be retained to occupy a space in which destruction has occurred. These are the cavities seen in contusion, varying in size from very minute to large ones occupying most of the cord in the transverse plane. These accumulations also induce anoxia and may lead to further tissue destruction, adding the necrotic tissue elements to the osmotic activity of the foreign body. The importance of such fluid accumulations has been demonstrated spectacularly in a number of patients who had an ipsilateral Horner's syndrome when they were lying in either lateral position; in 2 of these patients these symptoms disappeared when the syrinx was evacuated. The foreign elements (blood and necrotic debris) induce cellular reaction patterns with glial and collagen elements, which in subsequent maturation may further embarrass the vascular supply to tracts.
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There is a common circumstance wherein pial tears come in contact with torn ligament, muscle, bone, cartilage 01' other foreign elements. Coupled with the contusion that coexists, these areas which go on to collagen scars, form constricting bands which may deform the cord and prevent the return of function (Fig. 293). Quite often, in fracture-dislocation, there is a herniation of the intervertebral material which remains
Fig. 293. Diagrammatic representation of the manner in which posterior bands of scar deform the spinal cord, preventing the return of function and contributing to further damage as the scar contracts.
Fig. 294. Diagram of a frequent occurrence in spinal injury demonstrating one manner in which radiolucent materials-in this instance the partially extruded intervertebral disk material-may compress the spinal cord.
protruding in the Hpinal canal when the vertebrae rehound into plaee (to give a "normal" roentgenogram), giving a continued source of compression unless removed (Fig. 294). Finally, there is the completely divided spinal cord, most frequently following upon a tremendous insult such as a complete fracture-dislocation or a missile of large caliber penetrating the spinal canal. In these circumstances, there has been actual complete anatomical destruction of the continuity of the cord. This is a rather rare occurrence, for there is usually some tissue between the ends. Small missiles may pass through
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the canal to give only minor' anatomical wounds, and they may have spent their energy by the time they reach the canal. Or, the fracturedislocation force may be completely expended before actual tearing of the cord occurs. The case is called to mind of a soldier who complained of hyperesthesia of one thigh-on roentgen examination, there was seen to be a Japanese 25 caliber bullet lying in the cauda equina! When the completely severed cord is seen soon after injury, to the classic histologic findings so nicely presented by CajaP one can add a much greater element of mesenchymal participation to the pattern, which ultimately leads to considerable retrograde degeneration of fibers, vacuolization, gliosis, and the formation of considerable connective tissue. These changes may reach' for more than a segment away from the point of maximal insult. When seen very late, these cords appear like tendons at the site of injury, and are just as hard, being little more than almost avascular connective tissue, with scattered astrocytes and microglia. However, the belief that division of the spinal cord leads to isolation atrophy of the distal segment is entirely erroneous. The major factors which lead to this idea are that all too often the severely infected and ulcerated patient may show only transient reflex action which disappears as he approaches death. In such a patient, the normally innervated segments show a similar diminution of reflex activity. Secondly, poorly positioned patients can easily get pressure atrophy of peripheral nerves; with the extensor reflexes being last to make their appearance, the assumption is made that no reflex action is present and thus the distal cord must have atrophied. The conus medullaris has the best blood supply of any segment of the spinal cord, save perhaps the cervical enlargement, and it is indeed rare that the so-called conus medullaris lesion is actually present. In more than a thousand patients, there have been but two who might have had such lesions. Usually, there are other factors which have led to the conditions found, and rarely has the blood supply to the distal Eegment been so jeopardized that atrophy of all of it takes place. SPINAL CORD AND REFLEX ACTION
It is indeed unfortunate that a term which was introduced to describe a set of circumstances surrounding the relative activity of the central nervous system should have be~n so enthusiastically misunderstood and taken from its original meaning to represent the phenomenon of surgical shock. The similarities between these two circumstances are almost too superficial to discuss, for the differences are very great. Certainly, any wound that will produce surgical shock will do so even if it also happens to involve the spinal cord. However, low blood pressure and partial areflexia are the nearest that one could come to comparing spinal cord injured patients with patients in surgical shock. Surgical shock is a condition in which compensatory cardiorespiratory mechanisms are incapable of coping with the altered circumstances.
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There is every evidence to present spinal shock as one of the most remarkable examples of complete and controlled compensations that the total organism is ever called upon to conduct. Even in quadriplegia, if mechanical difficulties are overcome, respirations are conducted at an even and slow pace. Blood pressure is lowered, but urine is still formed at a normal rate. The pulse remains within normal limits, and the temperature-regulating mechanisms act extremely well, unless the centers become involved in edema, or cystitis develops. Indeed, if the blood pressure cuff were never devised, not even a novice would make the mistake of saying that a ratient with simple paraplegia was in shock. If the signs of shock are present, one can rest assured that there are concomitant injuries, for ~ hich a diligent search should be made so that therapy can be started. Tr.ere are indications that the time schedule generally thought of in regard to the time of suspension of spinal cord reflexes in man is incorrect. Certainly there is a transient phase of disordered reflex action in incomplete lesions and this grades to a total abolition of all reflexes below the point of insult. Between these h 0 extremes, it is only natural to assume that, like in virtually all biological phenomena, there would be intermediate grades-or the reflex actions would conform totally to the allor-none response. If the reflex arcs under consideration were to use all of the same central pathways, then it would be reasonable to assume that all of the reflexes would be abolished. However, just as is true under many other circumstances, the more primitive types of reflex action tend to go last and return first. Also,. those reflexes which commonly utilize pathways lying chiefly distal in the cord would be more remote from the point of cervical and dorsal spinal cord injuries. The bladder would qualify as the most primitive distal organ that might show reflex action early. Indeed it does just that, for if the bladder has been protected against injurious distention (which could occur at any capacity whatever, depending upon the intrinsic and reflex tone at the time of injury; one need only reflect to a time of personal anxiety to recall the terrific amount of pain that accompanies the urgency to empty an almost empty bladder to gain some realization of this statement), reflex action can be observed by cystometric examination within hours after complete lesions. Once distended injuriously, the bladder responds with no evidence of reflex action or tone, thus the "atonic" bladder, which under the continuous insult of overdistention becomes the "conus" bladder, implying by the term tLat the reflex connections of the bladder have been completely destroyed. However, there is ample evidence that the bladder has an intrinsic reflex activity which continues in spite of total denervation,l1 lending credence to the statement that' it should be possible to detect the presence at least of local reflex action very soon after injury. Other reflexes begin to appear after injury more or less in direct pro-
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portion to the relative state of general health that the patient can maintain. If all factors of nutrition are kept perfectly in balance, withdrawal reflexes are seen within the first few weeks and may be followed soon thereafter by extensor reflexes, even when the spinal cord is anatomically transected. This is in sharp contrast to the general teaching that there must be cerebral connections for this type of reflex action to be exhibited. It is possible in many such patients to demonstrate the presence of a dominant pattern of withdrawal reflexes but with the weaker extensor responses being brought out by eliciting the action from a favorable position for the response to occur. It is frequent also that crossed-extension can be demonstrated. In contrast to the foregoing statements, it must be emphasized that any reflex that is ordinarily elicited soon after injury is good evidence of the incompleteness of the spinal cord lesion-but this is absolutely not to be extended to reflex action seen later, as Bastian and Bruhns led so many to believe. METABOLIC ALTERATIONS
Perhaps the most poorly understood part of the complex which ensues after injury of the spinal cord is in the realm of metabolism. In some measure, this might be part of the pattern which the lowered blood pressure fits into. The most remarkable change that is seen with the highest frequency is a rapid catabolism of protein, marked by an increase in the output of nitrogen in the urine and by a fall in the serum protein, followed by a drop in the protein stores of the body, and by a fall in the total circulating hemoglobin. This change is sometimes so intense that frequent transfusions must be resorted to in order that extreme degrees of emaciation are not reached. At about one week, these influences reach a point where the hemoglobin begins to fall. lt is relatively useless to concern oneself with much more than the hemoglobin for this is one of the last proteins to be involved and one can be assured that the other changes have taken place, if serial determinations are available for reference. Thus, at about this time in the sequence of events, decubitus ulcers begin to form. Probably pressure exerted with great enough force for long enough periods of time could produce decubitus ulcers in normal people. But the pain induced by prolonged pressure induces reflex turning or moving, thus avoiding this dire consequence. What the safe time for given pressures applied to tissues overlying resistant bony prominences might be is not exactly known but it is doubtful that denervation alone makes the difference. 8 Since the patient with a spinal cord injury gives every indication of having a functional partial sympathectomy, it would be assumed that the peripheral vessels are in a state of dilatation, which would be compatible with the lowered blood pressure. This should insure an adequate blood supply, and the capillaries are always under greater control from local metabolites than they are from any central neural influences. So-called trophic
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changes are not seen in adequately nourished patients whose denervated parts receive proper attention. The only remaining possibility for the explanation of why so many decubiti form when they do is that actual cellular nutrition is deficient in its most vital element-protein. This is, as was pointed out, the case. Not that prolonged pressure can ever be tolerated, even to enervated areas, but this period is much more critical. Once a mass of tissue has necrosed--and it should be emphasized that the skin loss is the least of the damage for the destruction is a wide inverted cone which often includes the bony cortex-infection ensues and further protein- destruction goes apace. 6 Some measure of the stark reality of the situation can be reached when one realizes that it may take up to 400 grams of protein intake daily to put such a patient in positive nitrogen balance. It is at this same time that edema of the legs occurs, probably as a result of a combination of decreased arterial pressure, decreased venous flow (lack of muscle action), and decreased serum protein. Soon after recumbency is assumed-even in normal persons-there begins a rapid excretion of calcium in the urine. This has nothing to do with the absorptive or reabsorptive mechanisms, and it is unlikely that either vitamin D or the parathyroid glands participate in this response except in a reactive way. Rather, it is a simple phenomenon of removing stress and strain from the long bones, which is the mechanism for holding the calcium within the protein matrix. Great concentrations of calcium appear in the urine unless the urinary output is kept very high, and stones become an almost invariable consequence, especially if infection is added. 7 A corollary of this situation exists in the areas around decubiti and the fascial tracts reaching from them, wherein abnormal soft tissue calcification occurs (neurogenic ossifying fibromyositis). There -is some question as to whether certain changes do not occur in the adrenal glands after spinal cord injury, with depletion of the hormones that act to regulate electrolytes, influence accessory genital tissue (gynecomastia and testicular regression),3 and participate in carbohydrate metabolism. ADDITIONAL DISCUSSION OF NONOPERATIVE TREATMENT
The idea that surgical wounds do not heal well in paralyzed tissues is pure fiction. No wounds heal well in debilitated patients, and the problem is not one of lack of normal impulses-indeed, surgical wounds heal better in paralyzed extremities because they are at complete resto-but one of nutrition. It should be clear that the mere demonstration of a flow of spinal fluid has little or no meaning in injury, whereas it does have value in gradually occluding disorders. Since surgical shock is not often present in these patients, this does not constitute a contraindication to operation. Laminectomy can be done as a relatively nontraumatic operation. If the operator cannot do it in this fashion, obviously he should avoid it. That surgical intervention
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is an added insult can hardly be denied, but as to whether it is unnecessary is an opinion that can only be answered when and if sufficient early and well conducted operations are done to provide adequate data for comparison. Certainly, the data now available indicate that nothing is lost by operation conducted by skilled and careful operators who realize that the spinal cord is unable to resist rongeurR or the pressure of the "palpating" finger. One cannot abuse the spinal cord like one does the brain for the reasons previously referred to. Later operations may be of benefit, but they can hardly equal emergency operation in theoretic value. The ideal time for surgery would be in the first 20 minutes but failing that, every minute lost could mean further circulatory embarrassment and one would think that if decompression were to be of any value at all, it would relieve pressure so that circulation could be restored. Late operation would then have as its design only the prevention of the sequelae of scarring. The dynamics of wounding are such that there would almost have to be changes away from, the point of maximal impact, and surgical drainage would provide the best means of egress of this material. The central nervous system is almost remarkable for its "Rip van Winkle" method of dealing with injury and there is no substitute for surgical drainage of damaging collections of extravasated blood, provided that the surgical drainage itself is not injurious. These statements are a result of careful study in experimental animals." It is obvious that there is no way to predict just what cases might benefit from surgery, but it is often difficult to do the same for those who would not. The statement has sometimes been made that one can expect explosive eruption of spinal cord if one is brash enough to violate the integrity of the spinal dura in a case of spinal cord injury. When the pia mater is torn, a certain amount of cord tissue will have been severely contused. This will extrude, and better so. If the tears are small, additional undamaged cord may be pushed out as edema begins, for where else would the pressure go? Thus, this is only a further indication for obtaining a wide decompression of the spinal cord itself, without too much regard for decompression of the spinal canal. Finally, a word about traction and manipulation may be appropriate. Manipulation should have absolutely no place in the treatment of spinal cord injury, and neither should any other design which purports to reduce fractures without considering the major injury-that of the neural tissue. Many of the orthopedic surgeons who advocated such approaches are today reducing openly even simple long bone fractures because they have come to realize the hazards inherent in moving sharp bone edges near vItal structures like blood vessels and nerves. In the cervical region, the hazards are even greater. Traction has a place, but only to provide support. Perhaps the clearest evidence for the need for surgery is in these patients, for mortality becomes insignificant by comparison. The clas-
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sical progressive difficulty with respiration, high temperature and so on are seldom seen in surgically treated patients. One could pose the question immediately about the desirability of being heroic in his efforts to intervene in such cases where the ultimate prognosis for rehabilitation may not he good and it would be difficult to defend the approach apart from compassion alone. However, when traction is used, there is little point in using anything but skeletal application. It should be used before laminectomy to provide a margin of safety as far as motion is concerned. OPERATIVE TREATMENT
Lumbar Spine. The tip of the conus medullaris reaches to anywhere from the first to the second lumbar vertebra. Thus, the lower lumbar spinal injuries are not injuries of the spinal cord but of the spinal nerve roots. For closed injuries, operation and debridement are generally accepted as the best course of management, for in reality these injuries are similar to those of peripheral nerves. The dura mater should be opened and thoroughly cleansed of all foreign material. Severed spinal nerve roots should be resutured by the plasma clot technique, * using grafts (intercostal nerves are good) if necessary. Exact identification of the roots would be best, but there are experimental evidences that errors need not be disastrous (Freeman). The dura should be closed, unless there is absolutely no assurance that perfect hemostasis has been obtained. Dorsal and Dorsolumbar Spines. In these regions, great care should be exercised in avoiding movement of the fracture site, most especially in placing the patient in position for operation. The operator must not cause movement of the fracture site, and thus the safest technique is to do the muscle stripping by sharp dissection in contrast to the usual rough subperiosteal stripping. The laminae must be removed without inserting the lower jaw of the rongeur beneath the edge but rather by gradual chewing away. Fractured laminae should be secured with a large clamp before being rongeured-the dorsal process serves as the best holding device. With the spinal canal open short of the facets, it is possible to assess the status of the bodies in relation to each other. Relocation can usually be accomplished without disturbing the contents of the dura. The status of the interspaces is best determined after the dura mater is opened. The dentitions should be used for rotation, and should all be cut for a thorough examination. Extruded disk material that has not torn the dura can be removed extradurally-intradurally if the dura is torn. The spinal cord should be examined for pulsations, since normally there is a perceptible throb to it, unlike that which is imparted by the
* Draw 10 cc. of the patient's blood in a syringe containing 1 mg. of heparin solution. Place in sterile tube and centrifuge. Draw off plasma, place several drops in trough containing closely approximated root ends and add dry bovine thrombin. Dissect clot from trough. Test strength of suture and add clot if necessary.
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respiratory fluctuations transmitted through the spinal fluid. The spinal cord will float up to fill a dural opening unless the arachnoid is tom laterally to allow the escape of spinal fluid. The presence of pial tears should be determined. When these are small they can be disregarded, provided that the pia mater is opened for a distance of more than 3 cm. in the mid-dorsal aspect of the cord. A blunt probe should then be passed most of the way through the cord and drawn longitudinally for the distance of the pial incision. This will usually traverse any areas of hematomyelia or necrosis, and will serve as lateral relief for edema. One of the best tip-offs that the spinal cord is not normal, if there are no gross tears and no obvious contusions, comes from noting the distentions of the vessels in the subpial zone. Normally, the vessels on the posterior surface of the cord are not very impressive in size or course,. but when the intenor of the cord is being SUbjected to raised pressures, regardless of the cause (blood, edema, etc.), the surface vessels become engorged and tortuous. Indeed, the veins may seem to be carrying arterial blood. It may be difficult to reach a decision to cut the pia mater in the face of vessels of such large size. However, once the internal pressure in the cord is relieved, most of these vessels resume their normal small sizefurther evidence that the pial incision and myelotomy have been beneficial. Necrotic material and blood should be irrigated from the interior of the incision with a gentle stream of Ringer's solution. Hemostasis of the surface vessels is easily achieved by the gentle application of one of the hemostatic agents. Absolute hemostasis must be secured before closing, and it is not necessary to leave the dura mater open if the normal contour of the spinal canal has been attained. It is wise to pass a small (No.8 F.) soft rubber catheter in all four quadrants both upward and downward to explore for damage distal and proximal to the area under vision. Bone grafting procedures are rarely necessary and should be done as a separate operation at a later time. The turning bed devices are so far superior to other methods of handling that other means can be disregarded. Cervical Spine. Without delay, even as a bedside procedure, the skull traction should be applied. Again the turning frame device stands alone as the best bed to which the patient should be transferred immediately upon admission to the hospital. The tongs can be placed easily on this bed, and the frame can be used on supports as the operating table while traction is being maintained. For laminectomy, no effort at all should be made to position the patient for ease of operation. If local anesthesia is not the surgeon's preference, intubation should be done blindly without moving the head or neck. It is likely that the greatest contributor to surgical mortality in cervical laminectomy is movement of the spine during induction and intubation or in positioning of the patient. If the abdomen is not compressed, an adequate airway can be maintained.
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If the fracture has distorted the pharynx, tracheotomy may be the best means of handling the situation. However, local anesthesia without airway can be used in most patients. As in the dorsal and dorsolumbar laminectomies, ordinary muscle stripping should not be used. Instead, this should be done by sharp dissection. Laminar fractures are almost a constant finding in cervical spine injuries and great caution must be exercised that the loose bone is not pushed into the co~. Relocation of vertebrae is easily accomplished once the dura has been exposed by careful biting away of the laminae, often by no more than prying facets out of their locked positions. The extruded disk material can be removed intra- or extra-durally. The dentate attachments should be severed, and all handling of the cord should be done by grasping the dentate ligaments. It is more important here to incise the pia mater and do a median myelotomy, for the proportion of gray to white is greater, and it takes far less trauma to induce changes internally. Here the problem of vessels is even more perplexing, for the vessels are more numerous. Suspicious areas should be explored with a 27 gauge needle, and if the maximum injury appears to lie laterally, the myelotomy should be done laterally rather than medially. Gentle irrigation with Ringer's solution should be used to wash out debris and blood. The exit of the roots nearest the injury should be explored, with deroofing of the canal being done when necessary. The quadrants should be explored with a fine soft catheter. Extreme gentleness must be observed at all times, and the spinal cord should not be touched, even by a palpating finger. Again, the dura mater can be tightly closed if the contour of t.he spinal canal has been restored. Traction should be maintained for at. least. six weeks, and then some method of support in ext.ension should be maintained for at least six months or unt.il definite evidences of bony healing are seen. Bone grafting is again a secondary procedure and should be reserved for a later date. ESSENTIALS OF EARLY CARE
1. The spine must be supported to prevent rotation or flexion which may sever the spinal cord. 2. Emergency laminectomy by an experienced operator should be done; if one is not available the deformity of the spine should be prompt.ly reduced by traction or hyperext.ension or both. 3. The patient. must be turned at least every two hours. 4. The bladder must be emptied at once by small catheter; tidal drainage should be instituted early and watched carefully; urinary tract infections are the most frequent causes of fever and should be treated vigorously. 5. Maintain a high protein diet, using supplemental feedings of protein-rich liquid if necessary, and whole blood as indicated.
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6. A void intestinal distention, or treat it by rectal tube and pituitrin or neostigmine; give enemas every other day. 7. Be on the alert for complicating emotional reactions and help the patient accept the reality of his difficulty. SUMMARY Injury of the spinal cord is discussed in its various aspects, with the contention that emergency operative treatment is superior to other types of management. Functional restoration is more desirable than rehabilitation, and surgery offers the best method of reaching this goal consistently. REFERENCES 1. Cajal, S. Ramon y.: Degeneration and Regeneration of the Nervous System. Trans!. R. M. May. London, Oxford Univ. Press, 1928. 2. Campbell, E. and Meirowsky, A.: Penetrating Wounds of the Spinal Cord. Chapter 7 in Surgery of Trauma, edited by W. F. Bowers, Philadelphia, J. B. Lippincott Co., 1953. 3. Cooper, I. S. and Hoen, T. I.: Metabolic Disorders in Paraplegics. Neurology 2: 332--340, 1952. 4. Freeman, L. W.: Treatment of Paraplegia Resulting from Trauma to the Spinal Cord. J.A.M.A. 140: 949-958 and 1015-1022, 1949. 5. Freeman, L. W.: Experimental Observations on Concussion and Contusion of the Spinal Cord. Ann. Surg. 137: 433-443, 1953. 6. Freeman, L. W.: Decubitus Ulcers-Cause, Prevention, and Cure. Quart. Bull. Indiana Univ. M. Center 11: 43-46, 1949. 7. Freeman, L. W.: The Metabolism of Calcium in Patients with Spinal Cord Injuries. Ann. Surg. 129: 177-184, 1949. 8. Gibbon, J. H., Jr. and Freeman, L. W.: The Primary Closure of Decubitus Ulcers. Ann. Surg. 124: 1148-1164, 1946. 9. Kennedy, F., Denker, P. G. and Osborne, R. L.: Early Laminectomy for Spinal Cord Injury Not Due to Subluxation. Am. J. Surg. 60: 13-21, 1943. 10. McCravey, A.: Personal communication. 11. Meirowsky, A. M., Scheibert, C. D. and Hinchey, T. R.: Studies on the Sacral Reflex Are in Paraplegia. I. Response of the Bladder to Surgical Elimination of Sacral Nerve Impulses by Rhizotomy. J. Neurosurg. 7: 33-38, 1950. 12. Semmes, H. E.: Spinal Cord Surgery. Memphis M. J., Aug. 16,1929. Indiana University Medical Center 1040-1232 West Michigan Street Indianapolis 7, Indiana
ADVANCES in various phases of medicine have made it possible to maintain patients with spinal cord injuries in good health for many years. Indeed, the initial mortality (even under combat conditions) has been reduced so drastically that the major problem at present is the provision of adequate facilities for rehabilitation. For those qualified patients to whom all progressive therapy is provided, social and economic rehabilitation has been a regular phenomenon. To reach this circumstance has required diligent attention and care by groups of physicians oriented to integrated approaches. Thus, the patient is not successively a neurosurgical, urological, plastic, psychiatric and orthopedic "problem," but is continually treated by all at the most propitious moments. However well the integrative activities of various specialities might be resolved, there is no substitute for functional return. The neurological surgeon devotes himself to the preservation of functioning neural tissue or the protection from further damage of tissue which might regain function. In the past, a majority have been concerned by the appalling mortality of operative approaches and by the infrequency with which assistance to functional return could be demonstrated. This experience brought about two avenues of approach, that of waiting for some days before operating or operating only when observation showed a progression of neurological symptoms. At the onset of our participation in hostilities on the African and European continents, enthusiastic surgeons operated upon spinal cord injuries with fury and enthusiasm. Since the procedures were being done under far less than ideal circumstances and with careful postoperative attention being quite impossible, it was inevitable that additional reasons for nonoperative treatment would accumulate. Since combat wounds are usually open and compounded, they differ from the usual spinal cord injury in civil life where closed injuries are most common. However, that combat-injured patients could be treated expeditiously by operation, with low mortality, low morbidity, and a high de-
* Professor of Surgery and Director, Surgical Experimental Laboratories, Attending Neurological Surgeon to the Indiana University Medical Center and the Veterans Administration Hospital, Indiana University School of Medicine, Indianapolis, Indiana. 1131
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gree of functional return was demonstrated in the Korean conflict.2 Also, there have been those who have advocated early surgical intervention for civil injuries. 4 , 9, 10, 12 It is proposed that consideration of pertinent data will weigh heavily in favor of emergency operative intervention in most cases of spinal cord injury. REASONS GIVEN FOR NONOPERATIVE TREATMENT
1. The maximal injury has occurred at the instant of the insult and cannot be assessed. 2. Complete loss of motion and sensation indicate anatomical transection of the spinal cord. 3. The injury to the spinal cord is not confined to the point of maximal impact but spreads up and down. 4. When there is a flow of spinal fluid, adequate decompression is present. 5. Traction will accomplish as much decompression as can be expected from laminectomy. 6. Shock is present and the patients do not tolerate major surgery. 7. Surgical wounds do not heal well in paralyzed tissues. 8. Surgery is an unnecessary additional insult to a severely injured patient. 9. There is nothing to be gained by early surgical intervention which later operation cannot equal and with a greater margin of safety to the patient. These reasons will be touched upon or considered at some length in the sections which follow. ACUTE PATHOPHYSIOLOGY OF SPINAL CORD INJURY
There is some confusion about injuries of the spine which is traceable to the fact that the neurosurgeon tends to minimize the bony injury whereas the orthopedist tends to concentrate upon it. Very few injuries to the spinal cord occur without bony damage (ice picks, pen knives, concussive forces), so it is not at all difficult to see how this situation might arise. Although standard nomenclature is in use, the records of these patients are usually classified according to the admitting service (orthopedic-fracture of spine; neurosurgery-traumatic myelitis; urology-cord bladder). Even when consulting services are readily available and are used to maximum extent, the tendency is to categorize the cases as those of fracture of the spine. These remarks are entered for it becomes obvious that not all patients with spinal cord damage will be seen by a given consulting service in any but exceptional locales. As a result, many transient spinal cord injuries are not seen by neurosurgeons, and other patients with no initial spinal cord injury are seen only after manipulation has brought about the change in status. Until spinal fractures, like skull fractures, are considered to be
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the full responsibility of the neurological surgeon, not much progress can be expected in unraveling the complete picture of the range of minimal to maximal injury. Perhaps the greatest single deterrent to a complete knowledge of spinal cord injury has been the roentgenogram. This is true because all too often the course of action is dictated by the roentgenographic findings-or the counter assumption is made that the findings are not representative of the circumstances at the time of insult. Further, the films may be of such poor quality (which is understandable, for good spine films are not easily obtained without perfect positioning) that small pieces of bone impinging on the spinal cord may be overlooked. Finally, soft tissue encroachment into the spinal canal is not visualized. The usual concentration on the bony injury is therefore decried. With this orientation, the spinal cord injury is emphasized, and the bony injury is relegated to secondary consideration. Classification
There are many proposed classifications of spinal injuries but most of them are too complicated. The separation of closed and open injuries is not necessarily a good one except in regard to probability of contamination, and antibiotic therapy is quite reliable. Many thoracic spinal injuries, for example, include dural, pleural and pulmonary tears with direct communication to the spinal canal of potentially infected material. Missile injuries may produce minimal damage to the structural supporting tissues while inducing maximal spinal cord injuries. It is suggested that the spinal cord injury be classified primarily, and that mode of production and possible contamination be secondarily entered. For the total picture, especially in regard to morbidity, the status of the supporting structure can be described. Several differences are important when attempts are made to compare the brain with the spinal cord. The gray matter lies inside of the white in the cord. The vascular supply and drainage is peculiar and does not lend itself to description with the clarity found in the literature. Observations on laboratory animals and clinical subjects lend some credence to the consideration that the white matter is supplied to the mid-dorsal region by the arterial supply from above down and from the lumbar area upwards, and that the gray matter is supplied segmentally. There are numerous anastomoses between these elements as well as arteriovenous communications. Because of these circumstances, level of injury assumes some importance in regard to the sequence of events. Experimental data has shown clearly that gray matter is more susceptible than white to injury .. The high concentration of function in the cord contrasts markedly to the situation in most of the cerebrum, and the number of fibers is surprisingly small. The gross appearance of thE; spinal cord is extremely misleading, for the profile that is viewed consists of the pial mantle with
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the blood vessels. Beneath this may lie a completely normal cord or an almost completely destroyed cord, making it difficult to categori~e the injury from gross appearance. This can lead to prognostications which are not in keeping with the true state of affairs. Since most injured spinal cords come to microscopic examination with many complicating factors preceding death of the patient, or with only crude neurological evaluations just prior to death, the only reasonable classification is a functional one, with gross and microscopic findings being of secondary importance. Certainly this is true from a clinical point of view, and it is hardly possible to translate any but the crudest of observations from animal experiments to potentially similar circumstances in man. It is obvious, therefore, that some of the categories are conjectural, or hypothetical at best. 1. Concussion. Under this category would fall all of those injuries which fail to give permanently detectable neurological signs. "Commotio spinalis" might be an acceptable term. Grossly, there would be no changes observable except perhaps some engorgement of the blood vessels. Microscopically, there are vaguely defined cellular changes in the gray matter similar to the changes seen in the cerebral cortex. In the white matter, there are no findings. Clinically, there is a momentary disturbance of function which disappears rapidly and leaves no signs, early or late. 2. Contusion. Here are included those injuries which exceed concussion to the point where small vessels are ruptured within the substance of the cord (not the vessels of the pia mater). Grossly, there may be no early external evidences of the lesion, for the vascular net of the gray matter is more often affected. Subpial hemorrhage is not considered to have much functional significance, although it is the most obvious finding in injury. Microscopically, extravasations of blood and cellular destruction are evident. In more severe instances, there may be disruption of fibers in the white matter. These alterations can extend widely from the point of maximal impact (see Fig. 292) and would include the serpentine dissecting hematomyelias. The end result would depend upon the disposition of the blood and necrotic material. Later, there may be syrinxes which occupy the zones of destruction and dissection. Functionally, there is always a residual of this type of injury, ranging from scarcely detectable motor signs to complete loss of all cortical connections. It is in this category that surgical intervention has most to offer. 3. Laceration. In this category, elements other than those within the cord itself are implicated. There is actual incision of cord material well beyond the pia. (Pial incision alone need give no appreciable sequelae.) Grossly, the damage is obvious and ranges from scarcely discernible incisions such as imparted by the scalpel, to wide bands of blunt tearing by dislocated bone, and includes anatomical transection. As long as the pia mater is intact, laceration is excluded. Microscopically, the disrup-
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tion of pathways in the white, destruction of cells in the gray, and hemorrhage are observed. Functionally, the gamut from scarcely detectable changes to partial lesions (such as the infrequent Brown-Sequard), on to complete loss of function are observed. There are always permanent
Fig. 292. Diagrammatic illustration of the radiation of forces from the point of maximal impact (A) with the recoil of the bony structures into relatively normal locations (B) and the residual damage that such a blow may have upon the spinal cord.
changes from such injuries, but they are not necessarily completely disabling. Mode of Production of These Three Types of Pathological Change
There is no concise demarcation between concussion, contusion and laceration. Missiles may produce concussion or contusion without entering the spinal canal, or on entering the canal, will lacerate the cord locally, contuse the adjacent tissue, and concuss the tissue beyond. Thus,
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there may be a changing neurological status. Forces sufficient to produce simple compression of vertebral bodies generally produce concussion but not often contusion. Those forces which comminute the laminae or bodies lead most frequently to contusion, infrequently to concussion or laceration. In fracture-dislocation, the limiting factor is the anterior longitudinalligament, for those forces sufficient to disrupt this powerful tissue cause the bony structure to shear the cord. Those dislocations which do not tear the anterior longitudinal ligament do not lacerate the cord but produce concussion or contusion. Such injuries may involve separation of bony spicules which will penetrate the cord. Flexion injuries are more common than extension ones, probably indicating the resistance of the anterior longitudinal ligament as contrasted to that of the posterior structures. Most of the considerations have been based upon static circumstances, which are never the case except for concussion. Here the recovery of the cells and tracts is rapid, for little or no cellular destruction occurs, and the cessation of impulse conduction is temporary. When actual damage to cellular and fibrillar structure occurs, the vasomotor balance is disturbed. Exchange of both gaseous and flllid elements is retarded, producing anoxia and transudation of fluid (edema). These changes may continue to the point where further cellular damage results, or the accumulated carbon dioxide and other tissue elements (histamine) may induce local vascular responses which restore the supply of oxygen and remove the edema fluid, leaving only intrinsic cellular destruction or repair evidences of the injury. When vessels are torn and blood enters the intracellular spaces, it continues to progress until tissue resistance exceeds the pressure of the involved vessels. For torn capillaries, this does not involve much more than a few cells. As the caliber of the vessel increases, the amount of blood becomes greater, never being great quantities (for the pressure in the largest spinal vessels is quite low) unless wide spaces are created by pial and tract disruption, and this is limited because the arteries close off very rapidly. However, the high specific gravity fluid is also extremely active osmotically, drawing fluid to it and holding it, constituting a foreign body. In time, this fluid may be absorbed, or it may be retained to occupy a space in which destruction has occurred. These are the cavities seen in contusion, varying in size from very minute to large ones occupying most of the cord in the transverse plane. These accumulations also induce anoxia and may lead to further tissue destruction, adding the necrotic tissue elements to the osmotic activity of the foreign body. The importance of such fluid accumulations has been demonstrated spectacularly in a number of patients who had an ipsilateral Horner's syndrome when they were lying in either lateral position; in 2 of these patients these symptoms disappeared when the syrinx was evacuated. The foreign elements (blood and necrotic debris) induce cellular reaction patterns with glial and collagen elements, which in subsequent maturation may further embarrass the vascular supply to tracts.
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There is a common circumstance wherein pial tears come in contact with torn ligament, muscle, bone, cartilage 01' other foreign elements. Coupled with the contusion that coexists, these areas which go on to collagen scars, form constricting bands which may deform the cord and prevent the return of function (Fig. 293). Quite often, in fracture-dislocation, there is a herniation of the intervertebral material which remains
Fig. 293. Diagrammatic representation of the manner in which posterior bands of scar deform the spinal cord, preventing the return of function and contributing to further damage as the scar contracts.
Fig. 294. Diagram of a frequent occurrence in spinal injury demonstrating one manner in which radiolucent materials-in this instance the partially extruded intervertebral disk material-may compress the spinal cord.
protruding in the Hpinal canal when the vertebrae rehound into plaee (to give a "normal" roentgenogram), giving a continued source of compression unless removed (Fig. 294). Finally, there is the completely divided spinal cord, most frequently following upon a tremendous insult such as a complete fracture-dislocation or a missile of large caliber penetrating the spinal canal. In these circumstances, there has been actual complete anatomical destruction of the continuity of the cord. This is a rather rare occurrence, for there is usually some tissue between the ends. Small missiles may pass through
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the canal to give only minor' anatomical wounds, and they may have spent their energy by the time they reach the canal. Or, the fracturedislocation force may be completely expended before actual tearing of the cord occurs. The case is called to mind of a soldier who complained of hyperesthesia of one thigh-on roentgen examination, there was seen to be a Japanese 25 caliber bullet lying in the cauda equina! When the completely severed cord is seen soon after injury, to the classic histologic findings so nicely presented by CajaP one can add a much greater element of mesenchymal participation to the pattern, which ultimately leads to considerable retrograde degeneration of fibers, vacuolization, gliosis, and the formation of considerable connective tissue. These changes may reach' for more than a segment away from the point of maximal insult. When seen very late, these cords appear like tendons at the site of injury, and are just as hard, being little more than almost avascular connective tissue, with scattered astrocytes and microglia. However, the belief that division of the spinal cord leads to isolation atrophy of the distal segment is entirely erroneous. The major factors which lead to this idea are that all too often the severely infected and ulcerated patient may show only transient reflex action which disappears as he approaches death. In such a patient, the normally innervated segments show a similar diminution of reflex activity. Secondly, poorly positioned patients can easily get pressure atrophy of peripheral nerves; with the extensor reflexes being last to make their appearance, the assumption is made that no reflex action is present and thus the distal cord must have atrophied. The conus medullaris has the best blood supply of any segment of the spinal cord, save perhaps the cervical enlargement, and it is indeed rare that the so-called conus medullaris lesion is actually present. In more than a thousand patients, there have been but two who might have had such lesions. Usually, there are other factors which have led to the conditions found, and rarely has the blood supply to the distal Eegment been so jeopardized that atrophy of all of it takes place. SPINAL CORD AND REFLEX ACTION
It is indeed unfortunate that a term which was introduced to describe a set of circumstances surrounding the relative activity of the central nervous system should have be~n so enthusiastically misunderstood and taken from its original meaning to represent the phenomenon of surgical shock. The similarities between these two circumstances are almost too superficial to discuss, for the differences are very great. Certainly, any wound that will produce surgical shock will do so even if it also happens to involve the spinal cord. However, low blood pressure and partial areflexia are the nearest that one could come to comparing spinal cord injured patients with patients in surgical shock. Surgical shock is a condition in which compensatory cardiorespiratory mechanisms are incapable of coping with the altered circumstances.
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There is every evidence to present spinal shock as one of the most remarkable examples of complete and controlled compensations that the total organism is ever called upon to conduct. Even in quadriplegia, if mechanical difficulties are overcome, respirations are conducted at an even and slow pace. Blood pressure is lowered, but urine is still formed at a normal rate. The pulse remains within normal limits, and the temperature-regulating mechanisms act extremely well, unless the centers become involved in edema, or cystitis develops. Indeed, if the blood pressure cuff were never devised, not even a novice would make the mistake of saying that a ratient with simple paraplegia was in shock. If the signs of shock are present, one can rest assured that there are concomitant injuries, for ~ hich a diligent search should be made so that therapy can be started. Tr.ere are indications that the time schedule generally thought of in regard to the time of suspension of spinal cord reflexes in man is incorrect. Certainly there is a transient phase of disordered reflex action in incomplete lesions and this grades to a total abolition of all reflexes below the point of insult. Between these h 0 extremes, it is only natural to assume that, like in virtually all biological phenomena, there would be intermediate grades-or the reflex actions would conform totally to the allor-none response. If the reflex arcs under consideration were to use all of the same central pathways, then it would be reasonable to assume that all of the reflexes would be abolished. However, just as is true under many other circumstances, the more primitive types of reflex action tend to go last and return first. Also,. those reflexes which commonly utilize pathways lying chiefly distal in the cord would be more remote from the point of cervical and dorsal spinal cord injuries. The bladder would qualify as the most primitive distal organ that might show reflex action early. Indeed it does just that, for if the bladder has been protected against injurious distention (which could occur at any capacity whatever, depending upon the intrinsic and reflex tone at the time of injury; one need only reflect to a time of personal anxiety to recall the terrific amount of pain that accompanies the urgency to empty an almost empty bladder to gain some realization of this statement), reflex action can be observed by cystometric examination within hours after complete lesions. Once distended injuriously, the bladder responds with no evidence of reflex action or tone, thus the "atonic" bladder, which under the continuous insult of overdistention becomes the "conus" bladder, implying by the term tLat the reflex connections of the bladder have been completely destroyed. However, there is ample evidence that the bladder has an intrinsic reflex activity which continues in spite of total denervation,l1 lending credence to the statement that' it should be possible to detect the presence at least of local reflex action very soon after injury. Other reflexes begin to appear after injury more or less in direct pro-
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portion to the relative state of general health that the patient can maintain. If all factors of nutrition are kept perfectly in balance, withdrawal reflexes are seen within the first few weeks and may be followed soon thereafter by extensor reflexes, even when the spinal cord is anatomically transected. This is in sharp contrast to the general teaching that there must be cerebral connections for this type of reflex action to be exhibited. It is possible in many such patients to demonstrate the presence of a dominant pattern of withdrawal reflexes but with the weaker extensor responses being brought out by eliciting the action from a favorable position for the response to occur. It is frequent also that crossed-extension can be demonstrated. In contrast to the foregoing statements, it must be emphasized that any reflex that is ordinarily elicited soon after injury is good evidence of the incompleteness of the spinal cord lesion-but this is absolutely not to be extended to reflex action seen later, as Bastian and Bruhns led so many to believe. METABOLIC ALTERATIONS
Perhaps the most poorly understood part of the complex which ensues after injury of the spinal cord is in the realm of metabolism. In some measure, this might be part of the pattern which the lowered blood pressure fits into. The most remarkable change that is seen with the highest frequency is a rapid catabolism of protein, marked by an increase in the output of nitrogen in the urine and by a fall in the serum protein, followed by a drop in the protein stores of the body, and by a fall in the total circulating hemoglobin. This change is sometimes so intense that frequent transfusions must be resorted to in order that extreme degrees of emaciation are not reached. At about one week, these influences reach a point where the hemoglobin begins to fall. lt is relatively useless to concern oneself with much more than the hemoglobin for this is one of the last proteins to be involved and one can be assured that the other changes have taken place, if serial determinations are available for reference. Thus, at about this time in the sequence of events, decubitus ulcers begin to form. Probably pressure exerted with great enough force for long enough periods of time could produce decubitus ulcers in normal people. But the pain induced by prolonged pressure induces reflex turning or moving, thus avoiding this dire consequence. What the safe time for given pressures applied to tissues overlying resistant bony prominences might be is not exactly known but it is doubtful that denervation alone makes the difference. 8 Since the patient with a spinal cord injury gives every indication of having a functional partial sympathectomy, it would be assumed that the peripheral vessels are in a state of dilatation, which would be compatible with the lowered blood pressure. This should insure an adequate blood supply, and the capillaries are always under greater control from local metabolites than they are from any central neural influences. So-called trophic
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changes are not seen in adequately nourished patients whose denervated parts receive proper attention. The only remaining possibility for the explanation of why so many decubiti form when they do is that actual cellular nutrition is deficient in its most vital element-protein. This is, as was pointed out, the case. Not that prolonged pressure can ever be tolerated, even to enervated areas, but this period is much more critical. Once a mass of tissue has necrosed--and it should be emphasized that the skin loss is the least of the damage for the destruction is a wide inverted cone which often includes the bony cortex-infection ensues and further protein- destruction goes apace. 6 Some measure of the stark reality of the situation can be reached when one realizes that it may take up to 400 grams of protein intake daily to put such a patient in positive nitrogen balance. It is at this same time that edema of the legs occurs, probably as a result of a combination of decreased arterial pressure, decreased venous flow (lack of muscle action), and decreased serum protein. Soon after recumbency is assumed-even in normal persons-there begins a rapid excretion of calcium in the urine. This has nothing to do with the absorptive or reabsorptive mechanisms, and it is unlikely that either vitamin D or the parathyroid glands participate in this response except in a reactive way. Rather, it is a simple phenomenon of removing stress and strain from the long bones, which is the mechanism for holding the calcium within the protein matrix. Great concentrations of calcium appear in the urine unless the urinary output is kept very high, and stones become an almost invariable consequence, especially if infection is added. 7 A corollary of this situation exists in the areas around decubiti and the fascial tracts reaching from them, wherein abnormal soft tissue calcification occurs (neurogenic ossifying fibromyositis). There -is some question as to whether certain changes do not occur in the adrenal glands after spinal cord injury, with depletion of the hormones that act to regulate electrolytes, influence accessory genital tissue (gynecomastia and testicular regression),3 and participate in carbohydrate metabolism. ADDITIONAL DISCUSSION OF NONOPERATIVE TREATMENT
The idea that surgical wounds do not heal well in paralyzed tissues is pure fiction. No wounds heal well in debilitated patients, and the problem is not one of lack of normal impulses-indeed, surgical wounds heal better in paralyzed extremities because they are at complete resto-but one of nutrition. It should be clear that the mere demonstration of a flow of spinal fluid has little or no meaning in injury, whereas it does have value in gradually occluding disorders. Since surgical shock is not often present in these patients, this does not constitute a contraindication to operation. Laminectomy can be done as a relatively nontraumatic operation. If the operator cannot do it in this fashion, obviously he should avoid it. That surgical intervention
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is an added insult can hardly be denied, but as to whether it is unnecessary is an opinion that can only be answered when and if sufficient early and well conducted operations are done to provide adequate data for comparison. Certainly, the data now available indicate that nothing is lost by operation conducted by skilled and careful operators who realize that the spinal cord is unable to resist rongeurR or the pressure of the "palpating" finger. One cannot abuse the spinal cord like one does the brain for the reasons previously referred to. Later operations may be of benefit, but they can hardly equal emergency operation in theoretic value. The ideal time for surgery would be in the first 20 minutes but failing that, every minute lost could mean further circulatory embarrassment and one would think that if decompression were to be of any value at all, it would relieve pressure so that circulation could be restored. Late operation would then have as its design only the prevention of the sequelae of scarring. The dynamics of wounding are such that there would almost have to be changes away from, the point of maximal impact, and surgical drainage would provide the best means of egress of this material. The central nervous system is almost remarkable for its "Rip van Winkle" method of dealing with injury and there is no substitute for surgical drainage of damaging collections of extravasated blood, provided that the surgical drainage itself is not injurious. These statements are a result of careful study in experimental animals." It is obvious that there is no way to predict just what cases might benefit from surgery, but it is often difficult to do the same for those who would not. The statement has sometimes been made that one can expect explosive eruption of spinal cord if one is brash enough to violate the integrity of the spinal dura in a case of spinal cord injury. When the pia mater is torn, a certain amount of cord tissue will have been severely contused. This will extrude, and better so. If the tears are small, additional undamaged cord may be pushed out as edema begins, for where else would the pressure go? Thus, this is only a further indication for obtaining a wide decompression of the spinal cord itself, without too much regard for decompression of the spinal canal. Finally, a word about traction and manipulation may be appropriate. Manipulation should have absolutely no place in the treatment of spinal cord injury, and neither should any other design which purports to reduce fractures without considering the major injury-that of the neural tissue. Many of the orthopedic surgeons who advocated such approaches are today reducing openly even simple long bone fractures because they have come to realize the hazards inherent in moving sharp bone edges near vItal structures like blood vessels and nerves. In the cervical region, the hazards are even greater. Traction has a place, but only to provide support. Perhaps the clearest evidence for the need for surgery is in these patients, for mortality becomes insignificant by comparison. The clas-
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sical progressive difficulty with respiration, high temperature and so on are seldom seen in surgically treated patients. One could pose the question immediately about the desirability of being heroic in his efforts to intervene in such cases where the ultimate prognosis for rehabilitation may not he good and it would be difficult to defend the approach apart from compassion alone. However, when traction is used, there is little point in using anything but skeletal application. It should be used before laminectomy to provide a margin of safety as far as motion is concerned. OPERATIVE TREATMENT
Lumbar Spine. The tip of the conus medullaris reaches to anywhere from the first to the second lumbar vertebra. Thus, the lower lumbar spinal injuries are not injuries of the spinal cord but of the spinal nerve roots. For closed injuries, operation and debridement are generally accepted as the best course of management, for in reality these injuries are similar to those of peripheral nerves. The dura mater should be opened and thoroughly cleansed of all foreign material. Severed spinal nerve roots should be resutured by the plasma clot technique, * using grafts (intercostal nerves are good) if necessary. Exact identification of the roots would be best, but there are experimental evidences that errors need not be disastrous (Freeman). The dura should be closed, unless there is absolutely no assurance that perfect hemostasis has been obtained. Dorsal and Dorsolumbar Spines. In these regions, great care should be exercised in avoiding movement of the fracture site, most especially in placing the patient in position for operation. The operator must not cause movement of the fracture site, and thus the safest technique is to do the muscle stripping by sharp dissection in contrast to the usual rough subperiosteal stripping. The laminae must be removed without inserting the lower jaw of the rongeur beneath the edge but rather by gradual chewing away. Fractured laminae should be secured with a large clamp before being rongeured-the dorsal process serves as the best holding device. With the spinal canal open short of the facets, it is possible to assess the status of the bodies in relation to each other. Relocation can usually be accomplished without disturbing the contents of the dura. The status of the interspaces is best determined after the dura mater is opened. The dentitions should be used for rotation, and should all be cut for a thorough examination. Extruded disk material that has not torn the dura can be removed extradurally-intradurally if the dura is torn. The spinal cord should be examined for pulsations, since normally there is a perceptible throb to it, unlike that which is imparted by the
* Draw 10 cc. of the patient's blood in a syringe containing 1 mg. of heparin solution. Place in sterile tube and centrifuge. Draw off plasma, place several drops in trough containing closely approximated root ends and add dry bovine thrombin. Dissect clot from trough. Test strength of suture and add clot if necessary.
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respiratory fluctuations transmitted through the spinal fluid. The spinal cord will float up to fill a dural opening unless the arachnoid is tom laterally to allow the escape of spinal fluid. The presence of pial tears should be determined. When these are small they can be disregarded, provided that the pia mater is opened for a distance of more than 3 cm. in the mid-dorsal aspect of the cord. A blunt probe should then be passed most of the way through the cord and drawn longitudinally for the distance of the pial incision. This will usually traverse any areas of hematomyelia or necrosis, and will serve as lateral relief for edema. One of the best tip-offs that the spinal cord is not normal, if there are no gross tears and no obvious contusions, comes from noting the distentions of the vessels in the subpial zone. Normally, the vessels on the posterior surface of the cord are not very impressive in size or course,. but when the intenor of the cord is being SUbjected to raised pressures, regardless of the cause (blood, edema, etc.), the surface vessels become engorged and tortuous. Indeed, the veins may seem to be carrying arterial blood. It may be difficult to reach a decision to cut the pia mater in the face of vessels of such large size. However, once the internal pressure in the cord is relieved, most of these vessels resume their normal small sizefurther evidence that the pial incision and myelotomy have been beneficial. Necrotic material and blood should be irrigated from the interior of the incision with a gentle stream of Ringer's solution. Hemostasis of the surface vessels is easily achieved by the gentle application of one of the hemostatic agents. Absolute hemostasis must be secured before closing, and it is not necessary to leave the dura mater open if the normal contour of the spinal canal has been attained. It is wise to pass a small (No.8 F.) soft rubber catheter in all four quadrants both upward and downward to explore for damage distal and proximal to the area under vision. Bone grafting procedures are rarely necessary and should be done as a separate operation at a later time. The turning bed devices are so far superior to other methods of handling that other means can be disregarded. Cervical Spine. Without delay, even as a bedside procedure, the skull traction should be applied. Again the turning frame device stands alone as the best bed to which the patient should be transferred immediately upon admission to the hospital. The tongs can be placed easily on this bed, and the frame can be used on supports as the operating table while traction is being maintained. For laminectomy, no effort at all should be made to position the patient for ease of operation. If local anesthesia is not the surgeon's preference, intubation should be done blindly without moving the head or neck. It is likely that the greatest contributor to surgical mortality in cervical laminectomy is movement of the spine during induction and intubation or in positioning of the patient. If the abdomen is not compressed, an adequate airway can be maintained.
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If the fracture has distorted the pharynx, tracheotomy may be the best means of handling the situation. However, local anesthesia without airway can be used in most patients. As in the dorsal and dorsolumbar laminectomies, ordinary muscle stripping should not be used. Instead, this should be done by sharp dissection. Laminar fractures are almost a constant finding in cervical spine injuries and great caution must be exercised that the loose bone is not pushed into the co~. Relocation of vertebrae is easily accomplished once the dura has been exposed by careful biting away of the laminae, often by no more than prying facets out of their locked positions. The extruded disk material can be removed intra- or extra-durally. The dentate attachments should be severed, and all handling of the cord should be done by grasping the dentate ligaments. It is more important here to incise the pia mater and do a median myelotomy, for the proportion of gray to white is greater, and it takes far less trauma to induce changes internally. Here the problem of vessels is even more perplexing, for the vessels are more numerous. Suspicious areas should be explored with a 27 gauge needle, and if the maximum injury appears to lie laterally, the myelotomy should be done laterally rather than medially. Gentle irrigation with Ringer's solution should be used to wash out debris and blood. The exit of the roots nearest the injury should be explored, with deroofing of the canal being done when necessary. The quadrants should be explored with a fine soft catheter. Extreme gentleness must be observed at all times, and the spinal cord should not be touched, even by a palpating finger. Again, the dura mater can be tightly closed if the contour of t.he spinal canal has been restored. Traction should be maintained for at. least. six weeks, and then some method of support in ext.ension should be maintained for at least six months or unt.il definite evidences of bony healing are seen. Bone grafting is again a secondary procedure and should be reserved for a later date. ESSENTIALS OF EARLY CARE
1. The spine must be supported to prevent rotation or flexion which may sever the spinal cord. 2. Emergency laminectomy by an experienced operator should be done; if one is not available the deformity of the spine should be prompt.ly reduced by traction or hyperext.ension or both. 3. The patient. must be turned at least every two hours. 4. The bladder must be emptied at once by small catheter; tidal drainage should be instituted early and watched carefully; urinary tract infections are the most frequent causes of fever and should be treated vigorously. 5. Maintain a high protein diet, using supplemental feedings of protein-rich liquid if necessary, and whole blood as indicated.
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6. A void intestinal distention, or treat it by rectal tube and pituitrin or neostigmine; give enemas every other day. 7. Be on the alert for complicating emotional reactions and help the patient accept the reality of his difficulty. SUMMARY Injury of the spinal cord is discussed in its various aspects, with the contention that emergency operative treatment is superior to other types of management. Functional restoration is more desirable than rehabilitation, and surgery offers the best method of reaching this goal consistently. REFERENCES 1. Cajal, S. Ramon y.: Degeneration and Regeneration of the Nervous System. Trans!. R. M. May. London, Oxford Univ. Press, 1928. 2. Campbell, E. and Meirowsky, A.: Penetrating Wounds of the Spinal Cord. Chapter 7 in Surgery of Trauma, edited by W. F. Bowers, Philadelphia, J. B. Lippincott Co., 1953. 3. Cooper, I. S. and Hoen, T. I.: Metabolic Disorders in Paraplegics. Neurology 2: 332--340, 1952. 4. Freeman, L. W.: Treatment of Paraplegia Resulting from Trauma to the Spinal Cord. J.A.M.A. 140: 949-958 and 1015-1022, 1949. 5. Freeman, L. W.: Experimental Observations on Concussion and Contusion of the Spinal Cord. Ann. Surg. 137: 433-443, 1953. 6. Freeman, L. W.: Decubitus Ulcers-Cause, Prevention, and Cure. Quart. Bull. Indiana Univ. M. Center 11: 43-46, 1949. 7. Freeman, L. W.: The Metabolism of Calcium in Patients with Spinal Cord Injuries. Ann. Surg. 129: 177-184, 1949. 8. Gibbon, J. H., Jr. and Freeman, L. W.: The Primary Closure of Decubitus Ulcers. Ann. Surg. 124: 1148-1164, 1946. 9. Kennedy, F., Denker, P. G. and Osborne, R. L.: Early Laminectomy for Spinal Cord Injury Not Due to Subluxation. Am. J. Surg. 60: 13-21, 1943. 10. McCravey, A.: Personal communication. 11. Meirowsky, A. M., Scheibert, C. D. and Hinchey, T. R.: Studies on the Sacral Reflex Are in Paraplegia. I. Response of the Bladder to Surgical Elimination of Sacral Nerve Impulses by Rhizotomy. J. Neurosurg. 7: 33-38, 1950. 12. Semmes, H. E.: Spinal Cord Surgery. Memphis M. J., Aug. 16,1929. Indiana University Medical Center 1040-1232 West Michigan Street Indianapolis 7, Indiana