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Penetrating Craniocerebral Trauma
Contemporary Problems in Trauma Surgery
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Penetrating Craniocerebral Trauma
Robert H. Rosenwasser, MD, FACS, * David W. Andrews, MD,t and D. Fernando Jimenez, MD:j:
In the United States, trauma is the primary cause of death in people aged 1 to 45 years. 48 In men aged 45 to 64 years, trauma exceeds even stroke and cancer as a cause of death. In more than 50% of trauma-related deaths, head injury contributes significantly to the morbidity and directly to the outcome. In patients with multiple injuries, the head is the most commonly involved part. In nearly 75% of the victims of fatal road accidents, injury to the central nervous system (CNS) is found at autopsy. In 1974, the first survey was performed on head and spinal cord injury.28 The report, written by the National Institute of Neurological and Communicative Disorders and Stroke, estimated 422,000 cases of head injury during 1974, or 200 cases per 100,000 population. lO As hospital admission was a criterion for inclusion in the study, one can surmise that the true incidence is much higher. In 1976, the National Safety Council reported approximately 100,000 deaths from accidental injury in a population of 211,000,000. 35 There have been few studies regarding the epidemiologic nature of head injury in the United States. Difficulties with the studies have often been methodological, therefore confusing the conclusions that can be drawn. However, the data do indicate an incidence of head injury of approximately 200 to 300 per 100,000 persons. Applied to the population in this country, this means that approximately 500,000 new cases of head injury occur yearly, of which 30% to 40% are moderate to severe, with mortality and serious morbidity rates of perhaps 10% each. One can deduce that as many as 50,000 US citizens are killed, and another 50,000 disabled, by head injuries each year. 4. 5.15.27 One can see from the above statistics that the combined medical and *Associate Professor, Neurosurgery and Physiology, and Director, Neurosurgical Intensive Care Unit, Temple University Hospital, Philadelphia, Pennsylvania tAssistant Professor, Neurosurgery, Temple University School of Medicine, Philadelphia, Pennsylvania tChief Resident, Neurosurgery, Temple University Hospital and St. Christopher's Hospital for Children, Philadelphia, Pennsylvania
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social costs for caring for a head injury are extensive. On the basis of 1977 figures, such costs have been approximately $6 billion a year and lost income from head injury deaths approximately $22 billion. PATHOPHYSIOLOGY AND SECONDARY CENTRAL NERVOUS SYSTEM INJURY Primary brain injury is defined as that event at the time the missile or other instrument penetrates the skull, causing the injury. It also occurs at the time the head goes through the windshield or experiences severe acceleration-deceleration. The rate of primary injury will be reduced only through public awareness and education, as well as through improvement of the safety of our vehicles. Secondary injury, which occurs as a direct consequence of loss of autoregulation, hypoxia, or infection, is a significant contributor to morbidity after CNS injury. As alluded to previously, serious head injury is often associated with severe systemic abnormalities of hypotension and hypoxia. Without a doubt, these are the most commonly associated causes of secondary brain injury with CNS injuries. Numerous studies have confirmed that de saturation of arterial blood gases, as well as hypotension, markedly increase the probability of a poor outcome. These patients often have abnormal vascular autoregulation, elevated intracranial pressure, and abnormal metabolic response from the primary injury, which may exacerbate the secondary phenomenon. PERFORATING AND PENETRATING WOUNDS Wounds that result from a stab to the cranium may lacerate eloquent areas of the brain and result in a deficit or provoke massive intracranial hemorrhage, leading to neurologic deterioration or death. 17 However, most patients with this type of injury are conscious when first seen and may have a marked deficit or no deficit at all. Thus, the absence of a deficit should not give a false sense of security to the initial examiner. If unnoted, these injuries may result in severe infection such as meningitis or brain abscess, which increase the morbidity of head injury markedly. Small punctate wounds of the face and skull should be looked for, as is routinely performed on the ventral and surface aspect of all extremities and the trunk of trauma victims. Particularly silent are wounds of the anterior cranial fossa and middle fossa, as anterior temporal regions as well as anterior frontal regions are not neurologically eloquent. 9 • 18 Vascular lesions are often associated with perforating wounds and may present as a carotid-cavernous or arteriovenous fistula, arterial occlusion, arterial transection, or traumatic aneurysm. 2 Most of the injury that occurs after a penetrating missile wound is imparted by the velocity of the missile, because the kinetic energy varies with the square of velocity. There have been reports from the military literature that indicate a 23% mortality rate in high-velocity injuries, as
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opposed to a 7.5% mortality rate in injuries by lower-velocity fragments. 25 With low-velocity missiles, however, the skull may be fractured on the inner table, and a portion of this bone may enter the cerebral parenchyma as a missile in its own right without actual penetration of the cranial cavity. According to Hopkinson and Marshall,26 injury to the CNS parenchyma results from three mechanisms, dependent on missile velocity. At less than 320 mIs, injury results from direct disruption and laceration of tissue. At greater than 320 mIs, shock waves and tissue cavitation resulting from passage of the missile become increasing important. Shock waves at 15 to 20 milliseconds, traveling at the speed of sound, emanate from the missile, and, with high-velocity injuries, wounds can attain amplitudes of 80 kg! cm 2. Summation of the reflected shock waves may produce significant pressure gradients, although this is less common with low-velocity injuries. It is the pressure gradients that disrupt neural structure and function remote from the path of the missile. Lastly, a missile imparts a centrifugaJ movement to the parenchyma, resulting in cavitation. The temporary cavity may have a diameter of more than 30 times that of the missile, generating significant strains in surrounding tissue and causing severe axonal tear and vascular disruption. The cavity collapses within 10 to 20 milliseconds but may reverberate, with five or six cycles of expansion and relaxation. In experimental studies, it has been demonstrated that the intracranial pressure may rise to 100 mm Hg, with a concomitant fall in cerebrovascular resistance and blood volume. 30 Initial Evaluation The emergency room management of patients with perforating and penetrating head injuries is identical to that of the polytrauma patient with other systemic injuries. Restitution and maintenance of respiratory and cardiovascular functions is paramount. Performance and documentation of appropriate clinical neurologic and general physical examinations are essential. Finally, it is important to plan and execute all appropriate diagnostic procedures in a timely fashion. Neurologic assessment is often made by the trauma surgeon prior to the arrival of the neurologic surgeon but should include basics such as pupillary function, spontaneous breathing, the presence or absence of decerebrate or decorticate posturing, and the presence or absence of gross focal neurologic deficits such as hemiparesis or paraparesis. Radiologic Evaluation Computed tomography (CT) has virtually eliminated the need for standard skull radiographs, although if they can be obtained in a timely fashion in the emergency area, they may be helpful in assessing the presence of the injury. As in all polytrauma patients, cervical spine films should be obtained prior to manipulation of the head and neck. Computed tomography of the frontobasal region also assesses the extent and severity of injuries to the osseous extracranial soft tissue and intracranial components. The scan outlines the trajectory of the missile, associated parenchymal hematomas, and the amount of foreign debris along the missile tract. The presence or absence of basal cisterns correlates directly with outcome.
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Severe cerebral swelling with loss of cisterns indicates an 80% to 90% mortality rate secondary to intractable high intracranial pressure. 8 When perforating or penetrating injuries involve portions of the sphenoid bone, temporal bone, and posterior fossa, vascular structures such as the carotid and vertebral arteries may be involved. Prior to craniotomy, cerebral arteriography should be performed to rule out a vascular occlusion, traumatic dissection, or false aneurysm. Follow-up CT scans should be performed 12, 24, and 36 hours after the initial surgical procedure to rule out delayed hematoma formation in areas of damaged parenchymal tissue, which occurs in as many as 30% of cases. 46 Operative Management of Penetrating and Perforating Wounds Penetrating and perforating wounds of the skull and brain are compound: the dura has been torn, and in most cases, the underlying brain has been lacerated and penetrated. Perforating wounds created by sharp objects are often treated in an exact fashion as an open depressed fracture. The scalp flap should be outlined according to general neurosurgical principles of vascular supply of the scalp. In general terms, burr holes usually are created in normal bone, and craniectomy is performed around the protruding fragment or knife blade. No attempt to remove the wounding instrument in the emergency room or the operating theater should be made until the cranial opening is completed and the surgeon is ready to open the dura widely to manage underlying hemorrhage once the object is removed. This should always be done under direct vision. As indicated earlier, if a vascular injury is confirmed by arteriography, obViously, proximal and distal control of vessels within the intracranial compartment, as well as extracranially, should be gained before removing the instrument of penetration. Operative Management of Missile Injuries As with perforating wounds, missile injuries are considered compound and dirty and require surgical debridement and closure. One would be reluctant to take a patient to the operating room for debridement if pupillary reflexes are absent, oculocephalic responses are absent, and there are virtually no somatic reflexes of any kind, because this patient is clinically brain dead, and the mortality rate will be virtually 100%. Even if the patient does survive, he or she will be vegetative. All other patients should be prepared for surgery for debridement of the missile tract, to remove fragments, and to prevent delayed infection. Antibiotics should be administered in meningitic doses prior to the surgical incision. During the Vietnam conflict, penicillin and chloramphenicol were the most commonly used antibiotics for this type of injury.24 In recent times, third-generation cephalosporins, in conjunction with either nafcillin or vancomycin in meningitic doses, have been efficacious in preventing delayed meningitis and brain abscess. Antibiotics are usually continued for 10 days to 2 weeks after the injury.l, 3 Also, epilepsy occurs in 30% or more of patients with penetrating brain wounds, and therefore, anticonvulsant therapy is strongly recommended. 45, 49 Phenytoin, carbam-
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azepine, and phenobarbital are all acceptable, and blood levels should be monitored. The therapeutic levels of those drugs are 10 to 20 mg/dl, 4 to 12 mg/dl, and 20 to 40 mg/dl, respectively. The scalp incision may be performed in one of several manners. An Sshaped or curvilinear incision may be used to expand the missile tract to gain adequate exposure for craniectomy. In the case of a frontal and temporal wound, a large question-mark incision may be useful in debriding the tract, as well as in performing temporal lobectomy and frontal lobectomy to aid in the management of elevated intracranial pressure. Grossly contaminated bone fragments should not be replaced; cranioplasty may be performed later if the patient survives the initial insult and the cosmetic deformity is severe. As a general rule, two to four burr holes are placed 2 to 3 cm from the entry site, and the craniectomy is made in a circumferential fashion around the missile tract. The dura is then opened in a cruciate fashion, gaining adequate exposure to the entry site. All devitalized br<\in tissue, as well as bone fragments, should be removed with gentle suction and irrigation, and hemostasis should be meticulous. It is recommended that dural closure be watertight; pericranial grafts or cadaveric dural substitutes lJsually are adequate. At the time of dural closure, either ventriculostomy or subdural catheters are placed for postoperative pressure monitoring. If the brain is extremely swollen, the dura may be left open and the bone flap left out to aid in cerebral decompression. Vascular injuries should be handled according to the specific type of injury. An injury to the intracranial carotid or anterior or middle cerebral artery may be treated with direct repair and suture, using 10-0 Prolene and the operating microscope. Often, ligation of the vessel with an extraanatomic bypass is necessary. False aneurysms noted on the arteriogram require ligation proximally and distally. If a major vessel is involved with the traumatic aneurysm, then an extracranial-to-intracranial bypass may be created using a saphenous vein graft or superficial temporal artery. Damage to the superior sagittal sinus in the posterior two thirds requires repair, as ligation of this structure beyond this point will cause significant venous infarction and death. The anterior one third may be ligated safely if it is disrupted. As with the brain, all devitalized scalp tissue should be debrided. Generally, with undermining, a tension-free closure can be obtained. In cases of large tissue loss, free vascularized flaps may be used to cover the defect.
NEUROSURGICAL INTENSIVE CARE IN THE PERIOPERATIVE PERIOD The discussion of the perioperative management of perforating and penetrating wounds will address six areas: respiratory problems, cardiovascular system, infection, intracranial pressure, fluids and electrolytes, and nutritional support.
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Respiratory Problems Hypoxia, pulmonary edema, aspiration, and insufficient breathing occur in approximately 25% of patients with head injuries. 5 In our unit, we routinely use pulse oximetry to monitor saturation levels of oxygen. Control of the airway is performed routinely in patients with a Glasgow coma score of less than 7 or 8, primarily to control the airway even if oxygenation is satisfactory. Orally placed endotracheal tubes are preferred to nasotracheal tubes to avoid infectious sinusitis. 16 On the basis of the report of Dunham and Lamonica, we have left endotracheal tubes in place for 2 weeks and then performed tracheostomy, as those authors have shown no difference in the frequency of laryngeal damage in patients who receive early or delayed tracheostomy.19 Although it is not within the scope of this article to discuss control of ventilation, a few recommendations concerning the head-injured patient will be discussed. With elevated intracranial pressure, hyperventilation is an excellent acute countermeasure. Generally, its effects are negated within 72 to 96 hours because of buffering of the pH in the cerebrospinal fluid. 32, 33,38 If the elevated intracranial pressure can be controlled with osmotherapy or barbiturates, attempts at achieving normocapnia should be made. One of the mechanisms by which hyperventilation lowers the intracranial pressure is vasoconstriction. One of the secondary injuries that occurs in traumatic brain injury is an ischemic insult, and therefore, theoretically, this could increase border zone ischemia. 34 Suctioning and airway toilet should be performed with the patient sedated, using 25 to 100 mg of lidocaine either intravenously or through the endotracheal tube prior to any suctioning maneuver. In addition, if paralysis is to be used to control the intracranial pressure, appropriate doses should be supplemented with either morphine sulfate or fentanyl to enhance the sedative effects. One should never paralyze a patient without adding sedation. Narcotic sedatives are recommended over benzodiazepines and barbiturates, as the former can be reversed readily to assess neurologic function. Cardiovascular System It is imperative to maintain, at minimum, a normal circulating blood volume. The idea of volume depletion and keeping the patients "dry" is an outmoded form of therapy that often is injurious to an already ischemic brain. Intracranial pressure can often be controlled with the normal circulating blood volume while maintaining osmolality in the range of 300 to 310 mOsm. Most of these patients have suffered multiple trauma and often have a Swan-Ganz catheter to assess and maintain adequate rightsided cardiac filling pressures, to monitor systemic vascular resistance, and to help to manage their fluid balance in the face of adult respiratory distress syndrome. If barbiturate therapy is instituted, Swan-Ganz catheterization is essential, as one of the early signs of barbiturate toxicity is a reduction in the cardiac index, as well as a relative hypervolemia secondary to low systemic vascular resistance. This can be managed safely only with a pulmonary arterial catheter.
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Intracranial Pressure The management of elevated intracranial pressure begins in the operating room with debridement of devitalized brain tissue. In addition, in our unit, we are often extremely radical in leaving the bone plate out and the dura open to permit adequate cerebral decompression if it appears that this will be necessary from the severity of the initial injury on the CT scan. These patients are mandatorily intubated, paralyzed, and mechanically ventilated to avoid any spontaneous posturing, which elevates intracranial pressure, or "bucking" of the ventilator when airway toilet is being performed. As previously mentioned, during the acute phase of elevated intracranial pressure, or if spikes become a problem, hyperventilation to a Pco 2 of 25 mm Hg is recommended. Maintenance of normal circulating blood volume is essential, but osmotherapy is carried out using a dose of 0.25 gm of mannitol per kilogram every 6 hours either by bolus or by constant infusion. It is essential to maintain a high serum osmolality and to avoid hyponatremia and hypo-osmolality, as this condition causes a shift of water osmoles into the CNS, aggravating the elevated intracranial pressure. If osmotherapy and hyperventilation are ineffective in controlling the intracranial pressure below 15 mm Hg, we begin aggressive prophylactic barbiturate therapy. This technique is controversial, but preliminary evidence suggests that prophylactic barbiturate therapy is of benefit. As previously stated, these patients already have indwelling Swan-Ganz catheters, and the barbiturate, specifically pentobarbital, is given at a loading dose of 5 gmlkg, and a constant infusion is then maintained to achieve burst suppression on the electroencephalogram at the rate of 6 to 8 bursts per minute. Blood levels are often not measured, as the maximum benefit in lowering the intracranial pressure does not correlate with absolute blood levels but rather with maintaining electrocerebral silence interspersed with burst activity. The use of barbiturate therapy requires the utmost in intensive management in a neurosurgical intensive care unit and must be managed by one-on-one nursing by experienced personnel. Barbiturate therapy clearly predisposes to infection, presumably by affecting chemotaxis,39 as will be addressed in another section. Fluids and Electrolytes In patients with either open or closed head injury, there is increased autonomic activity with constriction of renal arterioles, causing decreased urine output and salt retention. Stress hormone production is increased: adrenocorticotropic hormone glucocorticoids, and aldosterone, which further increase water retention that exceeds sodium retention. 44 Water intoxication may develop, with resultant dilutional hyponatremia, reduced serum osmolality, and exacerbation of cerebral edema. Many neurosurgeons continue to treat patients with head injury with fluid restriction; however, dilutional hyponatremia with a normal circulating blood volume can be avoided by the administration of hypertonic salt solution (3% to 5% saline) with concomitant administration of low doses of furosemide, which will cause excretion of water in excess of salt. In the neurosurgical setting, hyponatremia has a different definition: serum sodium concentrations of 130 mEq/L are a serious concern, whereas in the general medical patient
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or trauma patient, sodium concentrations of 120 to 125 mEq/L are easily tolerated. In eNS dysfunction, control of intracranial pressure and seizures becomes a significant issue and is much more difficult at relatively lower reductions of serum sodium. In addition, hypomagnesemia will potentiate eNS irritability, with resultant seizure activity, possibly exacerbating the secondary eNS trauma, as previously discussed. Fluid and electrolyte disturbances, particularly the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and diabetes insipidus, will be discussed briefly. Water balance is controlled primarily by the posterior pituitary hormone known as vasopressin or antidiuretic hormone (ADH). This hormone is produced in the anterior hypothalamus and transported to the posterior pituitary gland, where it is secreted and carried to the renal system. There, it acts on the distal tubules to allow retention of free water. In head injury, this balance is often disturbed as a result of increased secretion of ADH, causing retention of water with hyponatremia, defined as a serum sodium concentration below 134 mEq/L. Hyponatremia often presents as deterioration in the level of consciousness and, as mentioned previously, can precipitate seizure activity. Diagnostic criteria for SIADH include normal renal function and adrenal function, serum osmolality of less than 280 mOsm/L, high urine osmolality, and urinary sodium secretion of greater than 25 mEq/L. This definition assumes that the patient is not receiving constant diuretic medications. Therapy of SIADH consists of mild fluid restriction, if indicated, although we prefer administration of hypertonic sodium 3% plus furosemide. Diabetes insipidus is different in its mechanism, in that it is usually attributable to trauma to the pituitary-hypothalamic axis, with resultant loss of vasopressin production. The presenting symptoms are polyuria and polydipsia, particularly in the awake patient. Urine output may exceed 15 Lid, with an associated low concentration, the specific gravity generally being below 1.003. Hypernatremia often develops and is defined as a serum sodium greater than 145 mEq/L. Severe hypernatremia with a severe free water deficit often results. Aqueous vasopressin may be administered in doses of 2.5 to 5 units every 4 to 6 hours if the urine output remains at 200 to 300 mllh and the serum sodium continues to be elevated. The replacement solution generally is 5% glucose in water, and hyperglycemia may be treated with insulin administration if indicated. Nutritional Support In the past, little attention was given to the nutritional requirements of patients with head injuries. Although these patients often have an intact gastrointestinal tract, they frequently develop an ileus from impaired hypothalamic function. 4O Enteral feeding therefore often is delayed for several days, and this, combined with fluid restriction, as has been practiced in the past, complicated the use of intravenous hyperalimentation. With trends concerning fluid management in head injury changing, early parenteral hyperalimentation is being used more in many intensive care units. In comparison with patients with polytrauma, bums, and sepsis, the increase in the resting metabolic expenditure in patients with open and closed head injuries is not overtly high, usually being equivalent to the
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values reported in patients with 30% burns, multiple trauma, or severe sepsis. n , 13,22 In some studies of patients with head injury, higher values (1. 7 to 1.8 times those expected) were found for long periods of time, reflecting that some head-injury patients have resting metabolic expenditure equivalent to that of patients with 40% to 50% burns, 20, 36 The extent of nitrogen excretion in relation to the increase in resting metabolic expenditure was higher than were the values reported for any group of injured patients, resulting in a per cent of calories consumed of approximately 24%, A value of greater than 20% has been reported in very critical patients, particularly victims of burns, sepsis, and trauma, In the past, steroids, particularly dexamethasone, were administered to patients with open or closed head injuries, and it is possible that the extreme nitrogen loss found in these earlier studies was related to the medication,23 New data are being evaluated by many investigators to determine whether nitrogen loss is markedly decreased in the absence of steroid administration, , Several studies have indicated that severe nitrogen excretion may occur, as much as 25 gm/d or 338 mg/kg per day,31, 47 Increases in caloric expenditure from 120% to 270% of the basal metabolic rate have been observed,14 Prospectively studying patients with head injuries for as long as 10 days after the insult, Long and coworkers observed a mean peak 24hour caloric expenditure of 160% of the basal metabolic rate that occurred between day 5 and day 8 in all patients studied, 21 Currently, we are aggressive in beginning early total parenteral nutrition in patients with head injuries, Immediately postoperatively, a solution of 25% glucose and 4,25% amino acids is begun as a constant infusion, The rate of infusion is increased over a 3- to 4-day period, up to 3000 ml per day, providing 20.4 gm of nitrogen and 2650 kilocalories, In addition, we have increased the caloric input by the administration of 500 ml of Intralipid (Kabivitrum, Alameda, CA), providing an additional intake of 510 kilocalories per day, Problems with parenteral nutrition are primarily hyperglycemia, which is associated with increased carbon dioxide production and oxygen consumption, In addition, there are preliminary experimental data indicating that hyperglycemia may potentiate cerebral ischemic injury by increasing lactic acid production,37, 42, 43 We maintain tight control of the serum glucose at levels of no more than 200 mg/dl. Insulin may be added to the infusions as indicated, Once the ileus has passed, we institute enteral feedings, generally through a small nasogastric or nasoduodenal tube, To minimize the risk of aspiration, the rate and concentration of the feeding solution are increased slowly, the gastric content is aspirated every 6 hours, and the patient's head is kept elevated at greater than or equal to 30 degrees, Many products are available, such as Ensure (Ross Laboratories, Columbus, OH) and Osmolyte (Ross Laboratories), which provide 1 calorie per milliliter and 38 gm of protein per liter, The concentration and rate are increased progressively over a l-week period, to provide a maximum intake of 1.5 to 2 gm of proteinikg per day and 2500 to 3000 kilocalories, Lomotil may be administered if diarrhea becomes a problem, Water and electrolytes, including potassium, can be given parenterally to maintain the electrolyte balance,
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Disorders of Coagulation Approximately 40% to 70% of patients with either open or closed head injury have abnormal clotting factors and either clinical or subclinical coagulopathy.12,29 This abnormality has been related to the release of large quantities of brain thromboplastin into the circulation and activation of the coagulation factors. The incidence of coagulation disorder secondary to head injuries is directly proportional to the severity of the injury, according to numerous authors, In the study of Sande and Van der Velkamp, the incidence of abnormalities in coagulation was directly related to the level of consciousness and brainstem function. 41 Almost all of their patients with Glasgow coma scores of less than 8 had abnormal coagulation tests, If disseminated intravascular coagulation does develop in the neurosurgical patient, treatment generally is similar to that used when the problem accompanies damage to other organ systems; however, one is extremely reluctant to treat with heparin in the perioperative period after neurosurgical injury. Replacement therapy is given as fresh frozen plasma and platelet concentrates, although the argument has been made that blood component administration may potentiate the coagulation cascade. 12
REFERENCES 1. Aarobi B: Comparative study of bacteriological contamination between primary and secondary exploration of missile head injuries. Neurosurgery 20:610-616, 1987 2. Aarobi B: Traumatic aneurysms of the brain due to high velocity missile head wounds. Neurosurgery 24:1056-1063, 1988 3. Aarobi B: Causes of infections in penetrating head wounds in the Iran-Iraq War. Neurosurgery 25:923-926, 1989 4. Annegus JF, Grabow JD, Kurland LT, et al: The incidence, causes, and secular trends in head injury in Olmstead County, Minnesota, 1935-1974. Neurology 30:912-919, 1980 5. Baigelman W, O'Brien JC: Pulmonary effects of head trauma. Neurosurgery 9:729-740, 1981 6. Barrett-Connor E, Marshall LF, et al: The epidemiology of head injury: A prospective of an entire community: San Diego County, California. Epidemiology 113:500-509, 1981 7. Bucci MN, Hoff JT: Barbiturate therapy in neurosurgery: A reappraisal. Contemp Neurosurg 8:18, 1986 8. Bullock R, Golek J, Blake G: Traumatic intracerebral hematoma-which patients should undergo surgical evaluation? CT scan features and ICP monitoring as a basis for decision making. Surg NeuroI32:181-187, 1989 9. Bursick DM, Selker RG: Intracranial pencil injuries. Surg NeuroI16:427-431, 1981 10. Caveness WF: Incidence of craniocerebral trauma in the United States in 1976 with trend from 1970-1975. Acta Neurol 22:1-3, 1979 11. Chioles R, Hutz Y, Lemarchand T, et al: Hormonal and metabolic changes following severe head injury or non-cranial injury. JPEN 13:5-12, 1989 12. Clark JA, Tinelli RE, Metsky MG: Disseminated intravascular coagulation following cranial trauma. J Neurosurg 52:266-269, 1980 13. Clifton GL, Robertson CS, Grossman RG: Management of the cardio-vascular and metabolic response to severe head injury. In Becker DP, Povlishock JD (eds): Central Nervous System Trauma: Status Report. Bethesda, National Institute of Communicative Disorders and Stroke, 1985, pp 135-159 14. Clifton GL, Robertson CS, Grossman RG, et al: The metabolic response to severe head injury. J Neurosurg 60:687-696, 1984 15. Cooper JD, Tobaddor K, Hauser WA: The epidemiology of head injury in the Bronx. Neuroepidemiology 2:70-88, 1983
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16. Deutschman CW, Wilton PB, Sinow J, et al: Paranasal sinusitis: A common complication of nasotracheal intubation in neurosurgical patients. Neurosurgery 17:196-200, 1985 17. DeVilliers JC: Stab wounds of the brain and skull. In Vinken pJ, Breym GW (eds): Handbook of Clinical Neurology, vol 23. Amsterdam, Elsevier-North Holland, 1975, pp 477-503 18. DuJoung M, Osgood CP, Maroon JC, et al: Penetrating intracranial foreign bodies in children. J Trauma 15:981-986, 1975 19. Dunham CM, Lemonica D: Prolonged tracheal intubation in the trauma patient. J Trauma 24:120-124, 1984 20. Fell D, Benner B, Billings A, et al: Metabolic profiles in patients with acute neurosurgical seizures. Crit Care Med 12:649-652, 1984 21. Foy C, Schaffel N, Geiger JW, et al: Metabolic response to injury and illness: Estimation of energy and protein needs from indirect calorimetry and nitrogen balance. JPEN 3:452-456, 1979 22. Gadisseaux D, Ward JP, Young HF, et al: Nutrition and the neurosurgical patient. J Neurosurg 60:219-232, 1984 23. Greenblatt SH, Foy CL, Blakemore WS, et al: Catabolic effect of dexamethasone in patients with major head injury. JPEN 13:373-376, 1989 24. Hagan RE: Early complications following penetrating wounds of the brain. J Neurosutg 34:132-141, 1971 25. Hammon WM: Analysis of 2,187 consecutive penetrating wounds of the brain from Viet Nam. J Neurosurg 34:127-131, 1971 26. Hopkinson DAW, Marshall TK: Firearm injuries. Br J Surg 54:344-353, 1967 27. Jagger J, Levine J, Jane J, et al: Epidemiologic features of head injury in a predominantly rural population. J Trauma 24:40-44, 1984 28. Kalsbeek WD, McLaurin RL, Hanes BSH, et al: The national head and spinal cord injury survey: Major findings. J Neurosurg 53:519-531, 1980 29. Kaufman HH: Delayed and recurrent intracranial hematomas related to disseminated intravascular clotting and fibrinolysis in head injury. Neurosurgery 7:445-449, 1980 30. Kirkpatrick JB, DiMaio V: Civilian gunshot wounds of the brain. J Neurosurg 49:185198, 1978 31. Kolpek JH, Ott LG, Record KE, et al: Comparison of urinary urea nitrogen excretion and measured energy expenditure in spinal cord injury and nonsteroid-treated severe head trauma patients. JPEN 13:277-280, 1989 32. Marshall LF, Marshall SB: Medical management of intracranial pressure. In Cooper PR (ed): Head Injury, ed 2. Baltimore, Williams & Wilkins, 1987, pp 177-196 33. Miller JD: Intracranial pressure monitoring. Arch Neurol 41:1191-1193, 1985 34. Muizelaar JP, Obrist WD: Cerebral blood flow and brain metabolism with brain injury. In Becker DP, Povlishock JT (eds): Central Nervous System Trauma: Status Report. Bethesda, National Institute of Communicative Disorders and Stroke, 1985, pp 123138 35. National Safety Council: Accident Facts. Chicago, National Safety Council, 1976 36. Piek J, Luminta CB, Beck WJ: Protein and amino acid metabolism after cerebral trauma. Intens Care Med 11:192-198, 1985 37. Plum F: What causes infarction in ischemic brain? The Robert Wartenberg Lecture. Neurology 33:222-233, 1983 38. Raichle ME, Posner JR, Plum F: Cerebral blood flow during and after hyperventilation. Arch Neurol 23:294-303, 1970 39. Rosenwasser RH, Winer J: Acute barbiturate therapy in head injury: A systematic approach. Presented to the American Association of Neurological Surgeons. Nashville, April 1990 40. Rowlands BJ, Litofsky NS, Kaufman H: Metabolic physiology, pathophysiology and management. In Mirth FP, Ratcheson RA (eds): Neurosurgical Critical Care. Baltimore, Williams & Wilkins, 1987, pp 81-108 41. Sande JJ, Van der Velkamp JJ: Head injury and coagulation disorders. J Neurosurg 94:357, 1978 42. Seisjo BK: Cell damage in the brain: A speculative synthesis. J Cereb Blood Flow Metab 1:155-185, 1981 43. Seisjo BK, Wieloch T: Brain injury: Neurochemical agents. In Becker DP, Povlishock JT
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(eds): Central Nervous System Trauma: Status Report. Bethesda, National Institute of Neurological and Communicative Disorders and Stroke, 1985, pp 513-532 Shoemaker WC: Fluids and electrolytes in the acutely ill adult. In Textbook of Critical Care. Philadelphia, WB Saunders-Society of Critical Care Medicine, 1984, pp 614640 Soroker N, Groswasser Z, Coste/f H: Practice of prophylactic anticonvulsant treatment in head injury. Brain Injury 3:137-140, 1989 Tanaka T, Sakai T, Uemura K, et al: MR imaging as predictor of delayed post-traumatic cerebral hemorrhage. J Neurosurg 69:203-209, 1988 Tuyman D, Young AB, Norton JA, et al: High protein enteral feedings: A means of achieving positive nitrogen balance in head injured patients. JPEN 9:679-684, 1985 US Department of Health, Education and Welfare: Facts of Life and Death. Publication No. (HRS) 74-1222. Rockville, MD, National Center for Health Statistics, 1974 Weiss GH, Salazan AM, Vance SC, et al: Predicting post-traumatic epilepsy in penetrating head injury. Arch Neurol 43:771-773, 1986
Address reprint requests to Robert H. Rosenwasser, MD, FACS Neurosurgical Intensive Care Unit Temple University Hospital 3401 North Broad Street Philadelphia, Pennsylvania 19140
0039-6109/91 $0.00
+ .20
Penetrating Craniocerebral Trauma
Robert H. Rosenwasser, MD, FACS, * David W. Andrews, MD,t and D. Fernando Jimenez, MD:j:
In the United States, trauma is the primary cause of death in people aged 1 to 45 years. 48 In men aged 45 to 64 years, trauma exceeds even stroke and cancer as a cause of death. In more than 50% of trauma-related deaths, head injury contributes significantly to the morbidity and directly to the outcome. In patients with multiple injuries, the head is the most commonly involved part. In nearly 75% of the victims of fatal road accidents, injury to the central nervous system (CNS) is found at autopsy. In 1974, the first survey was performed on head and spinal cord injury.28 The report, written by the National Institute of Neurological and Communicative Disorders and Stroke, estimated 422,000 cases of head injury during 1974, or 200 cases per 100,000 population. lO As hospital admission was a criterion for inclusion in the study, one can surmise that the true incidence is much higher. In 1976, the National Safety Council reported approximately 100,000 deaths from accidental injury in a population of 211,000,000. 35 There have been few studies regarding the epidemiologic nature of head injury in the United States. Difficulties with the studies have often been methodological, therefore confusing the conclusions that can be drawn. However, the data do indicate an incidence of head injury of approximately 200 to 300 per 100,000 persons. Applied to the population in this country, this means that approximately 500,000 new cases of head injury occur yearly, of which 30% to 40% are moderate to severe, with mortality and serious morbidity rates of perhaps 10% each. One can deduce that as many as 50,000 US citizens are killed, and another 50,000 disabled, by head injuries each year. 4. 5.15.27 One can see from the above statistics that the combined medical and *Associate Professor, Neurosurgery and Physiology, and Director, Neurosurgical Intensive Care Unit, Temple University Hospital, Philadelphia, Pennsylvania tAssistant Professor, Neurosurgery, Temple University School of Medicine, Philadelphia, Pennsylvania tChief Resident, Neurosurgery, Temple University Hospital and St. Christopher's Hospital for Children, Philadelphia, Pennsylvania
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social costs for caring for a head injury are extensive. On the basis of 1977 figures, such costs have been approximately $6 billion a year and lost income from head injury deaths approximately $22 billion. PATHOPHYSIOLOGY AND SECONDARY CENTRAL NERVOUS SYSTEM INJURY Primary brain injury is defined as that event at the time the missile or other instrument penetrates the skull, causing the injury. It also occurs at the time the head goes through the windshield or experiences severe acceleration-deceleration. The rate of primary injury will be reduced only through public awareness and education, as well as through improvement of the safety of our vehicles. Secondary injury, which occurs as a direct consequence of loss of autoregulation, hypoxia, or infection, is a significant contributor to morbidity after CNS injury. As alluded to previously, serious head injury is often associated with severe systemic abnormalities of hypotension and hypoxia. Without a doubt, these are the most commonly associated causes of secondary brain injury with CNS injuries. Numerous studies have confirmed that de saturation of arterial blood gases, as well as hypotension, markedly increase the probability of a poor outcome. These patients often have abnormal vascular autoregulation, elevated intracranial pressure, and abnormal metabolic response from the primary injury, which may exacerbate the secondary phenomenon. PERFORATING AND PENETRATING WOUNDS Wounds that result from a stab to the cranium may lacerate eloquent areas of the brain and result in a deficit or provoke massive intracranial hemorrhage, leading to neurologic deterioration or death. 17 However, most patients with this type of injury are conscious when first seen and may have a marked deficit or no deficit at all. Thus, the absence of a deficit should not give a false sense of security to the initial examiner. If unnoted, these injuries may result in severe infection such as meningitis or brain abscess, which increase the morbidity of head injury markedly. Small punctate wounds of the face and skull should be looked for, as is routinely performed on the ventral and surface aspect of all extremities and the trunk of trauma victims. Particularly silent are wounds of the anterior cranial fossa and middle fossa, as anterior temporal regions as well as anterior frontal regions are not neurologically eloquent. 9 • 18 Vascular lesions are often associated with perforating wounds and may present as a carotid-cavernous or arteriovenous fistula, arterial occlusion, arterial transection, or traumatic aneurysm. 2 Most of the injury that occurs after a penetrating missile wound is imparted by the velocity of the missile, because the kinetic energy varies with the square of velocity. There have been reports from the military literature that indicate a 23% mortality rate in high-velocity injuries, as
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opposed to a 7.5% mortality rate in injuries by lower-velocity fragments. 25 With low-velocity missiles, however, the skull may be fractured on the inner table, and a portion of this bone may enter the cerebral parenchyma as a missile in its own right without actual penetration of the cranial cavity. According to Hopkinson and Marshall,26 injury to the CNS parenchyma results from three mechanisms, dependent on missile velocity. At less than 320 mIs, injury results from direct disruption and laceration of tissue. At greater than 320 mIs, shock waves and tissue cavitation resulting from passage of the missile become increasing important. Shock waves at 15 to 20 milliseconds, traveling at the speed of sound, emanate from the missile, and, with high-velocity injuries, wounds can attain amplitudes of 80 kg! cm 2. Summation of the reflected shock waves may produce significant pressure gradients, although this is less common with low-velocity injuries. It is the pressure gradients that disrupt neural structure and function remote from the path of the missile. Lastly, a missile imparts a centrifugaJ movement to the parenchyma, resulting in cavitation. The temporary cavity may have a diameter of more than 30 times that of the missile, generating significant strains in surrounding tissue and causing severe axonal tear and vascular disruption. The cavity collapses within 10 to 20 milliseconds but may reverberate, with five or six cycles of expansion and relaxation. In experimental studies, it has been demonstrated that the intracranial pressure may rise to 100 mm Hg, with a concomitant fall in cerebrovascular resistance and blood volume. 30 Initial Evaluation The emergency room management of patients with perforating and penetrating head injuries is identical to that of the polytrauma patient with other systemic injuries. Restitution and maintenance of respiratory and cardiovascular functions is paramount. Performance and documentation of appropriate clinical neurologic and general physical examinations are essential. Finally, it is important to plan and execute all appropriate diagnostic procedures in a timely fashion. Neurologic assessment is often made by the trauma surgeon prior to the arrival of the neurologic surgeon but should include basics such as pupillary function, spontaneous breathing, the presence or absence of decerebrate or decorticate posturing, and the presence or absence of gross focal neurologic deficits such as hemiparesis or paraparesis. Radiologic Evaluation Computed tomography (CT) has virtually eliminated the need for standard skull radiographs, although if they can be obtained in a timely fashion in the emergency area, they may be helpful in assessing the presence of the injury. As in all polytrauma patients, cervical spine films should be obtained prior to manipulation of the head and neck. Computed tomography of the frontobasal region also assesses the extent and severity of injuries to the osseous extracranial soft tissue and intracranial components. The scan outlines the trajectory of the missile, associated parenchymal hematomas, and the amount of foreign debris along the missile tract. The presence or absence of basal cisterns correlates directly with outcome.
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Severe cerebral swelling with loss of cisterns indicates an 80% to 90% mortality rate secondary to intractable high intracranial pressure. 8 When perforating or penetrating injuries involve portions of the sphenoid bone, temporal bone, and posterior fossa, vascular structures such as the carotid and vertebral arteries may be involved. Prior to craniotomy, cerebral arteriography should be performed to rule out a vascular occlusion, traumatic dissection, or false aneurysm. Follow-up CT scans should be performed 12, 24, and 36 hours after the initial surgical procedure to rule out delayed hematoma formation in areas of damaged parenchymal tissue, which occurs in as many as 30% of cases. 46 Operative Management of Penetrating and Perforating Wounds Penetrating and perforating wounds of the skull and brain are compound: the dura has been torn, and in most cases, the underlying brain has been lacerated and penetrated. Perforating wounds created by sharp objects are often treated in an exact fashion as an open depressed fracture. The scalp flap should be outlined according to general neurosurgical principles of vascular supply of the scalp. In general terms, burr holes usually are created in normal bone, and craniectomy is performed around the protruding fragment or knife blade. No attempt to remove the wounding instrument in the emergency room or the operating theater should be made until the cranial opening is completed and the surgeon is ready to open the dura widely to manage underlying hemorrhage once the object is removed. This should always be done under direct vision. As indicated earlier, if a vascular injury is confirmed by arteriography, obViously, proximal and distal control of vessels within the intracranial compartment, as well as extracranially, should be gained before removing the instrument of penetration. Operative Management of Missile Injuries As with perforating wounds, missile injuries are considered compound and dirty and require surgical debridement and closure. One would be reluctant to take a patient to the operating room for debridement if pupillary reflexes are absent, oculocephalic responses are absent, and there are virtually no somatic reflexes of any kind, because this patient is clinically brain dead, and the mortality rate will be virtually 100%. Even if the patient does survive, he or she will be vegetative. All other patients should be prepared for surgery for debridement of the missile tract, to remove fragments, and to prevent delayed infection. Antibiotics should be administered in meningitic doses prior to the surgical incision. During the Vietnam conflict, penicillin and chloramphenicol were the most commonly used antibiotics for this type of injury.24 In recent times, third-generation cephalosporins, in conjunction with either nafcillin or vancomycin in meningitic doses, have been efficacious in preventing delayed meningitis and brain abscess. Antibiotics are usually continued for 10 days to 2 weeks after the injury.l, 3 Also, epilepsy occurs in 30% or more of patients with penetrating brain wounds, and therefore, anticonvulsant therapy is strongly recommended. 45, 49 Phenytoin, carbam-
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azepine, and phenobarbital are all acceptable, and blood levels should be monitored. The therapeutic levels of those drugs are 10 to 20 mg/dl, 4 to 12 mg/dl, and 20 to 40 mg/dl, respectively. The scalp incision may be performed in one of several manners. An Sshaped or curvilinear incision may be used to expand the missile tract to gain adequate exposure for craniectomy. In the case of a frontal and temporal wound, a large question-mark incision may be useful in debriding the tract, as well as in performing temporal lobectomy and frontal lobectomy to aid in the management of elevated intracranial pressure. Grossly contaminated bone fragments should not be replaced; cranioplasty may be performed later if the patient survives the initial insult and the cosmetic deformity is severe. As a general rule, two to four burr holes are placed 2 to 3 cm from the entry site, and the craniectomy is made in a circumferential fashion around the missile tract. The dura is then opened in a cruciate fashion, gaining adequate exposure to the entry site. All devitalized br<\in tissue, as well as bone fragments, should be removed with gentle suction and irrigation, and hemostasis should be meticulous. It is recommended that dural closure be watertight; pericranial grafts or cadaveric dural substitutes lJsually are adequate. At the time of dural closure, either ventriculostomy or subdural catheters are placed for postoperative pressure monitoring. If the brain is extremely swollen, the dura may be left open and the bone flap left out to aid in cerebral decompression. Vascular injuries should be handled according to the specific type of injury. An injury to the intracranial carotid or anterior or middle cerebral artery may be treated with direct repair and suture, using 10-0 Prolene and the operating microscope. Often, ligation of the vessel with an extraanatomic bypass is necessary. False aneurysms noted on the arteriogram require ligation proximally and distally. If a major vessel is involved with the traumatic aneurysm, then an extracranial-to-intracranial bypass may be created using a saphenous vein graft or superficial temporal artery. Damage to the superior sagittal sinus in the posterior two thirds requires repair, as ligation of this structure beyond this point will cause significant venous infarction and death. The anterior one third may be ligated safely if it is disrupted. As with the brain, all devitalized scalp tissue should be debrided. Generally, with undermining, a tension-free closure can be obtained. In cases of large tissue loss, free vascularized flaps may be used to cover the defect.
NEUROSURGICAL INTENSIVE CARE IN THE PERIOPERATIVE PERIOD The discussion of the perioperative management of perforating and penetrating wounds will address six areas: respiratory problems, cardiovascular system, infection, intracranial pressure, fluids and electrolytes, and nutritional support.
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Respiratory Problems Hypoxia, pulmonary edema, aspiration, and insufficient breathing occur in approximately 25% of patients with head injuries. 5 In our unit, we routinely use pulse oximetry to monitor saturation levels of oxygen. Control of the airway is performed routinely in patients with a Glasgow coma score of less than 7 or 8, primarily to control the airway even if oxygenation is satisfactory. Orally placed endotracheal tubes are preferred to nasotracheal tubes to avoid infectious sinusitis. 16 On the basis of the report of Dunham and Lamonica, we have left endotracheal tubes in place for 2 weeks and then performed tracheostomy, as those authors have shown no difference in the frequency of laryngeal damage in patients who receive early or delayed tracheostomy.19 Although it is not within the scope of this article to discuss control of ventilation, a few recommendations concerning the head-injured patient will be discussed. With elevated intracranial pressure, hyperventilation is an excellent acute countermeasure. Generally, its effects are negated within 72 to 96 hours because of buffering of the pH in the cerebrospinal fluid. 32, 33,38 If the elevated intracranial pressure can be controlled with osmotherapy or barbiturates, attempts at achieving normocapnia should be made. One of the mechanisms by which hyperventilation lowers the intracranial pressure is vasoconstriction. One of the secondary injuries that occurs in traumatic brain injury is an ischemic insult, and therefore, theoretically, this could increase border zone ischemia. 34 Suctioning and airway toilet should be performed with the patient sedated, using 25 to 100 mg of lidocaine either intravenously or through the endotracheal tube prior to any suctioning maneuver. In addition, if paralysis is to be used to control the intracranial pressure, appropriate doses should be supplemented with either morphine sulfate or fentanyl to enhance the sedative effects. One should never paralyze a patient without adding sedation. Narcotic sedatives are recommended over benzodiazepines and barbiturates, as the former can be reversed readily to assess neurologic function. Cardiovascular System It is imperative to maintain, at minimum, a normal circulating blood volume. The idea of volume depletion and keeping the patients "dry" is an outmoded form of therapy that often is injurious to an already ischemic brain. Intracranial pressure can often be controlled with the normal circulating blood volume while maintaining osmolality in the range of 300 to 310 mOsm. Most of these patients have suffered multiple trauma and often have a Swan-Ganz catheter to assess and maintain adequate rightsided cardiac filling pressures, to monitor systemic vascular resistance, and to help to manage their fluid balance in the face of adult respiratory distress syndrome. If barbiturate therapy is instituted, Swan-Ganz catheterization is essential, as one of the early signs of barbiturate toxicity is a reduction in the cardiac index, as well as a relative hypervolemia secondary to low systemic vascular resistance. This can be managed safely only with a pulmonary arterial catheter.
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Intracranial Pressure The management of elevated intracranial pressure begins in the operating room with debridement of devitalized brain tissue. In addition, in our unit, we are often extremely radical in leaving the bone plate out and the dura open to permit adequate cerebral decompression if it appears that this will be necessary from the severity of the initial injury on the CT scan. These patients are mandatorily intubated, paralyzed, and mechanically ventilated to avoid any spontaneous posturing, which elevates intracranial pressure, or "bucking" of the ventilator when airway toilet is being performed. As previously mentioned, during the acute phase of elevated intracranial pressure, or if spikes become a problem, hyperventilation to a Pco 2 of 25 mm Hg is recommended. Maintenance of normal circulating blood volume is essential, but osmotherapy is carried out using a dose of 0.25 gm of mannitol per kilogram every 6 hours either by bolus or by constant infusion. It is essential to maintain a high serum osmolality and to avoid hyponatremia and hypo-osmolality, as this condition causes a shift of water osmoles into the CNS, aggravating the elevated intracranial pressure. If osmotherapy and hyperventilation are ineffective in controlling the intracranial pressure below 15 mm Hg, we begin aggressive prophylactic barbiturate therapy. This technique is controversial, but preliminary evidence suggests that prophylactic barbiturate therapy is of benefit. As previously stated, these patients already have indwelling Swan-Ganz catheters, and the barbiturate, specifically pentobarbital, is given at a loading dose of 5 gmlkg, and a constant infusion is then maintained to achieve burst suppression on the electroencephalogram at the rate of 6 to 8 bursts per minute. Blood levels are often not measured, as the maximum benefit in lowering the intracranial pressure does not correlate with absolute blood levels but rather with maintaining electrocerebral silence interspersed with burst activity. The use of barbiturate therapy requires the utmost in intensive management in a neurosurgical intensive care unit and must be managed by one-on-one nursing by experienced personnel. Barbiturate therapy clearly predisposes to infection, presumably by affecting chemotaxis,39 as will be addressed in another section. Fluids and Electrolytes In patients with either open or closed head injury, there is increased autonomic activity with constriction of renal arterioles, causing decreased urine output and salt retention. Stress hormone production is increased: adrenocorticotropic hormone glucocorticoids, and aldosterone, which further increase water retention that exceeds sodium retention. 44 Water intoxication may develop, with resultant dilutional hyponatremia, reduced serum osmolality, and exacerbation of cerebral edema. Many neurosurgeons continue to treat patients with head injury with fluid restriction; however, dilutional hyponatremia with a normal circulating blood volume can be avoided by the administration of hypertonic salt solution (3% to 5% saline) with concomitant administration of low doses of furosemide, which will cause excretion of water in excess of salt. In the neurosurgical setting, hyponatremia has a different definition: serum sodium concentrations of 130 mEq/L are a serious concern, whereas in the general medical patient
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or trauma patient, sodium concentrations of 120 to 125 mEq/L are easily tolerated. In eNS dysfunction, control of intracranial pressure and seizures becomes a significant issue and is much more difficult at relatively lower reductions of serum sodium. In addition, hypomagnesemia will potentiate eNS irritability, with resultant seizure activity, possibly exacerbating the secondary eNS trauma, as previously discussed. Fluid and electrolyte disturbances, particularly the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and diabetes insipidus, will be discussed briefly. Water balance is controlled primarily by the posterior pituitary hormone known as vasopressin or antidiuretic hormone (ADH). This hormone is produced in the anterior hypothalamus and transported to the posterior pituitary gland, where it is secreted and carried to the renal system. There, it acts on the distal tubules to allow retention of free water. In head injury, this balance is often disturbed as a result of increased secretion of ADH, causing retention of water with hyponatremia, defined as a serum sodium concentration below 134 mEq/L. Hyponatremia often presents as deterioration in the level of consciousness and, as mentioned previously, can precipitate seizure activity. Diagnostic criteria for SIADH include normal renal function and adrenal function, serum osmolality of less than 280 mOsm/L, high urine osmolality, and urinary sodium secretion of greater than 25 mEq/L. This definition assumes that the patient is not receiving constant diuretic medications. Therapy of SIADH consists of mild fluid restriction, if indicated, although we prefer administration of hypertonic sodium 3% plus furosemide. Diabetes insipidus is different in its mechanism, in that it is usually attributable to trauma to the pituitary-hypothalamic axis, with resultant loss of vasopressin production. The presenting symptoms are polyuria and polydipsia, particularly in the awake patient. Urine output may exceed 15 Lid, with an associated low concentration, the specific gravity generally being below 1.003. Hypernatremia often develops and is defined as a serum sodium greater than 145 mEq/L. Severe hypernatremia with a severe free water deficit often results. Aqueous vasopressin may be administered in doses of 2.5 to 5 units every 4 to 6 hours if the urine output remains at 200 to 300 mllh and the serum sodium continues to be elevated. The replacement solution generally is 5% glucose in water, and hyperglycemia may be treated with insulin administration if indicated. Nutritional Support In the past, little attention was given to the nutritional requirements of patients with head injuries. Although these patients often have an intact gastrointestinal tract, they frequently develop an ileus from impaired hypothalamic function. 4O Enteral feeding therefore often is delayed for several days, and this, combined with fluid restriction, as has been practiced in the past, complicated the use of intravenous hyperalimentation. With trends concerning fluid management in head injury changing, early parenteral hyperalimentation is being used more in many intensive care units. In comparison with patients with polytrauma, bums, and sepsis, the increase in the resting metabolic expenditure in patients with open and closed head injuries is not overtly high, usually being equivalent to the
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values reported in patients with 30% burns, multiple trauma, or severe sepsis. n , 13,22 In some studies of patients with head injury, higher values (1. 7 to 1.8 times those expected) were found for long periods of time, reflecting that some head-injury patients have resting metabolic expenditure equivalent to that of patients with 40% to 50% burns, 20, 36 The extent of nitrogen excretion in relation to the increase in resting metabolic expenditure was higher than were the values reported for any group of injured patients, resulting in a per cent of calories consumed of approximately 24%, A value of greater than 20% has been reported in very critical patients, particularly victims of burns, sepsis, and trauma, In the past, steroids, particularly dexamethasone, were administered to patients with open or closed head injuries, and it is possible that the extreme nitrogen loss found in these earlier studies was related to the medication,23 New data are being evaluated by many investigators to determine whether nitrogen loss is markedly decreased in the absence of steroid administration, , Several studies have indicated that severe nitrogen excretion may occur, as much as 25 gm/d or 338 mg/kg per day,31, 47 Increases in caloric expenditure from 120% to 270% of the basal metabolic rate have been observed,14 Prospectively studying patients with head injuries for as long as 10 days after the insult, Long and coworkers observed a mean peak 24hour caloric expenditure of 160% of the basal metabolic rate that occurred between day 5 and day 8 in all patients studied, 21 Currently, we are aggressive in beginning early total parenteral nutrition in patients with head injuries, Immediately postoperatively, a solution of 25% glucose and 4,25% amino acids is begun as a constant infusion, The rate of infusion is increased over a 3- to 4-day period, up to 3000 ml per day, providing 20.4 gm of nitrogen and 2650 kilocalories, In addition, we have increased the caloric input by the administration of 500 ml of Intralipid (Kabivitrum, Alameda, CA), providing an additional intake of 510 kilocalories per day, Problems with parenteral nutrition are primarily hyperglycemia, which is associated with increased carbon dioxide production and oxygen consumption, In addition, there are preliminary experimental data indicating that hyperglycemia may potentiate cerebral ischemic injury by increasing lactic acid production,37, 42, 43 We maintain tight control of the serum glucose at levels of no more than 200 mg/dl. Insulin may be added to the infusions as indicated, Once the ileus has passed, we institute enteral feedings, generally through a small nasogastric or nasoduodenal tube, To minimize the risk of aspiration, the rate and concentration of the feeding solution are increased slowly, the gastric content is aspirated every 6 hours, and the patient's head is kept elevated at greater than or equal to 30 degrees, Many products are available, such as Ensure (Ross Laboratories, Columbus, OH) and Osmolyte (Ross Laboratories), which provide 1 calorie per milliliter and 38 gm of protein per liter, The concentration and rate are increased progressively over a l-week period, to provide a maximum intake of 1.5 to 2 gm of proteinikg per day and 2500 to 3000 kilocalories, Lomotil may be administered if diarrhea becomes a problem, Water and electrolytes, including potassium, can be given parenterally to maintain the electrolyte balance,
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Disorders of Coagulation Approximately 40% to 70% of patients with either open or closed head injury have abnormal clotting factors and either clinical or subclinical coagulopathy.12,29 This abnormality has been related to the release of large quantities of brain thromboplastin into the circulation and activation of the coagulation factors. The incidence of coagulation disorder secondary to head injuries is directly proportional to the severity of the injury, according to numerous authors, In the study of Sande and Van der Velkamp, the incidence of abnormalities in coagulation was directly related to the level of consciousness and brainstem function. 41 Almost all of their patients with Glasgow coma scores of less than 8 had abnormal coagulation tests, If disseminated intravascular coagulation does develop in the neurosurgical patient, treatment generally is similar to that used when the problem accompanies damage to other organ systems; however, one is extremely reluctant to treat with heparin in the perioperative period after neurosurgical injury. Replacement therapy is given as fresh frozen plasma and platelet concentrates, although the argument has been made that blood component administration may potentiate the coagulation cascade. 12
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Address reprint requests to Robert H. Rosenwasser, MD, FACS Neurosurgical Intensive Care Unit Temple University Hospital 3401 North Broad Street Philadelphia, Pennsylvania 19140