36 Pulmonary Complications in Neurosurgery THOMAS B. DUCKER, M.D., F.A.C.S., AND JOSEPH S. REDDING, M.D., F.A.C.P.
DISEASE STATES
Neural Regulatory Dysfunction With any significant intracranial pathology, there are areas of the brain where metabolic derangement occurs with inadequate oxygen utilization and acidosis. While this can be demonstrated most commonly in both experimental and clinical brain injury, it does occur with any major pathological process that affects the central nervous system. The resultant low tissue oxygen partial pressure and the accumulation of acid by-products are reflected in the cerebrospinal fluid (9, 25, 26). The major fraction of the cerebral spinal fluid acid is lactic; at the same time, there is a concomitant marked reduction in the bicarbonate ion (13). With the flow of cerebrospinal fluid through the 4th ventricle by the respiratory centers in the medulla, there is commonly a change in the neural regulatory drive of respiration. The acid milieu acting on these respiratory centers results in an increased respiratory minute volume. This is reflected initially in a more rapid rate of respiration, but not in an increased tidal volume. In fact, the tidal volume is commonly diminished. Decreased tidal volumes, absence of sighing and coughing, and immobility of the patient so the same areas of lung remain dependent for protracted periods, lead to small airway closure. The result is reduction of residual lung volume and shunting of pulmonary blood flow through extensive areas of unventilated or collapsed lung. Since carbon dioxide is far more diffusible than oxygen, the increased minute volume of ventilation lowers arterial CO 2 tension below normal by hyperventilation of the aereated portions of the lung. Oxygen being less diffusible, the resultant hypoxemia can not be compensated by hyperventilation. Consequently, cerebral acidosis that causes a change in cerebrospinal fluid can result in a respiratory alkalosis and low arterial oxygen levels (2, 7, 8, 24). While the partial pressure of carbon dioxide is consistently low, the arterial oxygen may be only moderately depressed (12, 23, 25); but if the 483
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cerebral damage is associated with intracranial hypertension, then the arterial oxygen tension is likely to be more decreased (1). The systemic hypoxemia is due to pulmonary arteriovenous shunting, either by direct action of the effect of mass sympathetic discharge on the pulmonary vascular bed, or passively, as a consequence of changes in pulmonary blood flow resulting from small airway closure and uneven distribution of pulmonary gas. While the clinical neurosurgeon most commonly notes these events in the dramatic setting of an acute head injury, the same pulmonary problems readily occur in other central nervous system disorders, such as subarachnoid hemorrhage, brain tumor, and cerebrovascular accident (8, 14, 26). Mechanical Insufficiency Mechanical insufficiency is by far the most common problem in central nervous system disease, and obtunded airway reflexes are the most common type of mechanical problem (19). While complete airway obstruction can be corrected immediately, the hazards of partial airway obstruction-that is, heavy snoring-are often overlooked. Partial airway obstruction is usually accompanied by copious saliva production. When these secretions stimulate the vocal cords of an obtunded patient, severe laryngospasm may result. Moderately severe partial obstruction may lead to air swallowing, gastric distension, and explosive vomiting. If the obstruction is so severe that the patient must labor forcefully during inspiration to pull in air, he may generate enough negative airway pressure to pull capillary and interstitial fluid into his alveoli and thus precipitate pulmonary edema. Another type of mechanical insufficiency is that seen with muscle paralysis from trauma to the spinal cord or the phrenic nerve. Although the patient is usually left with adequate strength to breathe and maintain normal blood gases initially, he may not have enough reserve muscle strength to sigh, take deep breaths, and cough effectively. A monotonous respiratory pattern, unbroken by an occasional sigh or deep breath, will lead to diffuse microatelectasis of the lungs. The chest roentgenogram is normal in such instances, and the only manifestation is hypoxemia. If the patient cannot cough effectively, secretions will accumulate and obstruct small bronchioles. The unventilated areas of lung will subsequently develop macroatelectasis, and later pneumonia. These conditions may be predicted and prevented by measuring the patient's vital capacity upon admission. The vital capacity is an index of the ability to sigh and cough effectively. Awake patients can take their deepest breath and blow into a spirometer; obtunded patients should be
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intubated and the volume of a forceful cough determined. If the patient's vital capacity is less than 25% of his predicted normal, a mechanical ventilator should be utilized. Percussion of the chest, or pulmonary physiotherapy, is also needed. Even if there is neurological improvement, the vital capacity and respiratory function will improve in a week to 10 days. Initially, the intercostal spaces sink inward as the diaphragm descends during inspiration. As reflex intercostal muscle tone increases, this effect decreases and the patient is able to take deeper breaths and cough more effectively. A very similar type of problem is seen in patients who have the muscular ability to sigh and cough effectively but who simply fail to do so. Commonly, this is seen in patients during protracted recovery from frontal lobe injuries and cerebrovascular accidents (19). Occasionally, this abnormal pattern is seen in trauma patients with very subtle changes in intracranial pressure (18). While these patients may be responsive to command, they are frequently totally disinterested in their surroundings and well being. The respiratory pattern is marked by a monotonously constant rate and depth of respiration, uninterrupted by sighing, deep breathing, or coughing. The result is diffuse microatelectasis and hypoxemia. Reduction of the intracranial pressure will reverse the abnormal respiratory pattern in some trauma patients. Hourly hyperinflation of the lungs using a self-inflating bag may help others. In the more severe cases, mechanical ventilation for 24 hours, followed by intermittent mandatory ventilation at a rate of two breaths per minute, is effective in preventing microatelectasis.
Acute Pulmonary Edema In the last 10 years, the occurrence of pulmonary edema in association with central nervous system and multisystem trauma has received much attention. At least one variant of this syndrome appears to be neurogenic in origin: the acute fulminating type of pulmonary edema which may follow within minutes after a sudden rise of intracranial pressure (4). While there are cases where it has occurred in patients who did have a patent airway (endotracheal tube), it now appears that the combination of partial airway obstruction and increased intracranial pressure expedites the pathophysiological process (10). The partial airway obstruction causes labored breathing which, in turn, causes tremendous negative intrathoracic pressure. This pulls fluid out of the vascular bed into lung interstitial tissue and alveoli. At the same time, the increased intracranial pressure causes an increase in cardiac output and a rise in peripheral resistance (vasoconstriction) and engorgement of the pulmonary vascular bed (3, 5, 6). Elevation of pulmonary capillary pressure contributes to
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the occurrence of pulmonary edema (22): The two events, congested lung and the labored breathing, will cause an overwhelming pulmonary edema which, in many cases is fatal (4). Now that airway problems are quickly corrected, and many neurosurgical patients are treated with positive pressure hyperventilation, the incidence of acute "neurogenic" pulmonary edema has markedly diminished.
(Subacute) Respiratory Distress Syndrome In addition to the acute form of pulmonary edema just mentioned, there is a less acute variation which is generally referred to as the respiratory distress syndrome of the adult or "shock lung" syndrome. This appears to follow a variety of multisystem traumatic injuries, particularly after hemorrhagic or septic shock has occurred. The etiology remains uncertain, but it has generally been considered a result of various direct influences on the pulmonary capillary endothelium. Certainly, an underventilated and contaminated pulmonary bed contributes to the presence of this pathological state. More recently, an attractive unifying theory has been proposed which blames central nervous system hypoxemia as the initial event (17). Once the central nervous system has been injured, the sympathetic nervous system reacts with constriction of small pulmonary venules as well as increased pulmonary vascular resistance. When the pulmonary venular constriction persists, interstitial pulmonary edema is created. Subsequently, there is increased permeability of the pulmonary capillaries with loss of albumin into the interstitial space, closure of small airways, loss of pulmonary compliance, and hypoxemia. A vicious cycle is set in motion which leads to progressive pulmonary edema and respiratory failure. Oxygen toxicity added to the current problem only further complicates the condition. The edematous lung is more susceptible to infection, and a superimposed pneumonia may obscure the diagnosis, as well as adding further pulmonary damage.
Pulmonary Toxic Reactions Chemical and bacteria contamination commonly occur in the patient with significant central nervous system disease. It has been common knowledge since the work of Denney-Brown and Russel, in 1941, that in cerebral disorders gag and swallowing reflexes are impaired, and fluid runs freely into the unprotected trachea. Vomiting readily occurs, and the gastric contents may cause a severe inflammatory response in the lung, referred to as Mendelson's syndrome (15). With the acid gastric contents, a severe chemical pneumonitis occurs. In addition, focal atelectasis compounds the problem and accentuates the pulmonary
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inflammatory response. The damaged pulmonary bed interrupts gas exchange in the lung and can accentuate the existing pathology within the brain or spinal cord. Bacterial pneumonia can also further complicate the course of a patient with significant neurological disease. In a patient with a depressed state of consciousness carefully treated in a hospital, the respiratory bacterial flora changes to an enteric bacillus, coagulase positive staphylococci, Candida species, etc. These pathogens have ready access to the pulmonary bed (21). If the patient's defenses are further lowered, and if the pulmonary bed becomes further congested, a severe infection readily occurs. While it is possible to keep a patient in an unconscious state with either an endotracheal tube or a tracheostomy in supportive ventilation for a prolonged period of time without infection, the slightest break in technique, or change in the patient's internal milieu will allow bacterial contamination which requires therapy. PATIENT EVALUATION
In a patient with significant central nervous system disease, there are four essential questions to ask concerning that person's pulmonary function: 1. Are the neural mechanisms which insure respiratory drive and protective airway reflexes adequate? 2. Are there limitations in ventilatory function from others causes? 3. Are the patient's oxygen-carrying capacity, arterial oxygen tension, and cardiac output adequate for tissue oxygenation? 4. Are there superimposed chemical and bacterial toxins?
Neural Drive and Reflexes First, count the respiratory rate and carefully observe the patient's chest and abdominal excursions, noting the pattern of respiration. It is important to realize that the normal person in a basal state has a respiratory rate as low as 12 to 14 breaths per minute. A rate above 20 is distinctly abnormal. Commonly, such patients have a high rate with a low volume exchange, resulting in alveolar hypoventilation. Even when the brain stem reflex drive to respiration maintains a normal rate and volume, it may have a distinctly abnormal pattern. Intermittent sighs, or deep breaths, may be completely absent. Without sighing, there is not intermittent full expansion of all the alveolar spaces, and ventilation/ perfusion inequality readily occurs. A very slight change in intracranial pressure may be associated with the presence or absence of normal sighs in the respiratory pattern. Sufficient neural reflexes to open and close the glottis and control the swallowing mechanism can be readily tested by the clinician. A simple,
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modified corneal reflex using the eyelash can give important information. This is referred to by anesthesiologists as the lash reflex, and involves the V and VII cranial nerves. If there is involuntary winking when the lash is brushed gently, the gag and swallowing reflexes commonly are also present. Patients with intact medullary reflexes are unlikely to accumulate secretions and gastric material in their pulmonary beds.
Pulmonary Function The pulmonary function of the patient must be assessed. Pre-existing obstructive or restrictive problems are often present in the elderly patient prior to the onset of significant intracranial disease. In those patients who can cooperate, the measurement of vital capacity is the simplest and quickest way to ascertain ventilatory ability. An accurate and portable ventilometer (Wright respirometer) can be used for an approximation of this determination in intubated or tracheotomized patients. A timed vital capacity (TVC) is a recording of vital capacity as a function of time and can be measured with a portable McKesson Vitalor. The first second forced expiratory volume (FEV 1.0) is that volume which is recorded during the first second of the total forced expiratory volume measured from the maximal inspiratory position. By reference to standard nomograms calibrated for height and sex of the patient, the total vital capacity can be expressed as a percentage of predicted normal. Reduction of the observed vital capacity below 80% of the predicted normal indicates a restrictive defect of the lungs and/or thorax. Reduction of the FEV 1.0 below 750/0 of the observed vital capacity indicates existence of obstructive airway disease. Many patients exhibit a mixture of both components (20). Reduction of vital capacity below 250/0 of predicted normal, or reduction of FEV 1.0 below 40% of observed vital capacity, will result in ventilatory failure with hypercapnia usually compounded by hypoxemia (20). The success of the lungs in oxygenation. of blood is appreciated by serial measurements of the amount of intrapulmonary shunting. The standard formula which utilizes the relationship between pulmonary alveolar and systemic arterial oxygen tensions can be easily used for such determinations. An expanding gradient between alveolar and arterial oxygen tensions implies deteriorating pulmonary function,
Systemic Condition The patient's hemoglobin value is just as important as the blood gas determination. While- it is not advisable to have an excessively high hemoglobin in a patient with brain disease, it certainly is desirable to
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have a hemoglobin in the range of 12 gm. % in order to insure adequate oxygenation of the tissues (16). The delivery of oxygen is, of course, influenced by the arterial blood gas tensions. But high inspired oxygen tensions can be dangerous and are not necessary if the hemoglobin level is normal, if the cerebral blood flow is adequate, and if alveolar ventilation is maintained. The common occurrence of cerebral metabolic acidosis with resultant systemic respiratory alkalosis and hypoxemia can often be corrected by giving the patient respiratory support utilizing tidal volumes of 12 to 15 ml./kg. body weight and frequent sigh volumes of 20 ml./kg., combined with frequent changes in the patient's position. These measures minimize small airway closure with reduced residual lung volume and the resultant hypoxemia. Thus, the respirator rate and volume need to be adjusted first to correct abnormal blood gases. Finally, the inhaled oxygen concentration should be adjusted to correct any hypoxemia which exists in spite of the foregoing measures. The success of long term ventilation (longer than 24 hours) in part depends on the type of ventilator selected and the diligence of the nursing personnel. A pressure guaranteed, volume variable ventilator such as the Bird is often inadequate for patients on long term support and those with abnormal lungs since atelectasis will occur even with large volumes. The gases are not distributed uniformly leading to progressive ventilation perfusion mismatching and hypoxemia. Volume guaranteed, pressure variable ventilators such as Engstrom or Emerson as a class have superior flow characteristics permitting more physiological gas distribution within the lungs. However, regardless of volume or class of ventilator used, long term ventilatory support will lead to progressive hypoxia unless chest physiotherapy is vigorous and unless aseptic technique is strictly adhered to. Finally, the systemic condition is markedly altered by fat embolization. This can be concomitant with certain traumatic central nervous system disorders. The persistent hypoxemia that may occur even with ventilatory support needs to be corrected by increased inhaled oxygen concentrations. Use of glucocorticosteroids will reduce the inflammatory response associated with this phenomenon.
Chemical and Bacterial Toxins Chemical and bacterial toxins need immediate and direct treatment. If these conditions are superimposed, the patient has two distinct diagnoses, not just one. The presence of chemical and bacterial toxic pneumonitis can be determined by physical findings, chest x-ray, and pulmonary cultures. These disease states alter the ventilation/perfusion ratio in the lung beds and result in arterial hypoxemia. On occasion, the
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pneumonitis may cause transient bacteremias and set up infections in devitalized brain to further complicate the course of the patient. TREATMENT
Treatment of patients with pulmonary disorders secondary to nervous system disease cannot be meaningfully simplified. Initially, however, it is important to answer the five logical questions in the patient's evaluation in order to determine treatment. For example: 1. Must airway obstruction be corrected? 2. Does the patient require ventilatory support and protection against absent protective reflexes? 3. What measures are indicated to improve ventilatory function? 4. What measures will improve the systemic condition? 5. Is treatment of a chemical or bacterial pneumonitis indicated? An adequate airway and respiratory drive are vital to survival. If airway insufficiency is allowed to continue without active support, respiratory and circulatory exhaustion occur. Severe airway obstruction is most reliably recognized by placing the hand over the nose and mouth and recognizing absent or diminished air flow. Partial airway obstruction is recognized by hearing a "snore" on inspiration or palpating it immediately above the larynx. If a patient is too obtunded to respond to command, he may aspirate if he regurgitates. Not infrequently, a patient will respond to command when stimulated but lapse into a deeper state of unconsciousness when he is left alone. If the patient has an active lash reflex, a gag reflex, and responds purposeful to pain, he does not require intubation or tracheostomy. If these are not present, then the brain stem reflex centers are depressed, and the patient may readily aspirate and get a chemical pneumonitis. In such cases, either an endotracheal tube or a tracheostomy is required. Oral airways are basically worthless; instead, with transient sedation, a properly placed endotracheal tube will achieve good ventilatory support. Since irritation of the posterior pharynx may precipitate gagging and vomiting, an oral or nasal pharyngeal airway should be used only until a cuffed endotracheal tube is placed. The use of pharyngeal airways should be avoided in slightly unconscious patients because of the risk of vomiting. In these patients proper head and jaw position should be used to maintain airway patency until intubation. The anticipated duration of airway protection will influence the decision regarding use of a tracheostomy or prolonged intubation. Nasogastric intubation should be deferred until after the endotracheal tube is placed. The endotracheal tube cuff should be inflated until there is only a slight leak when the patient is sighed with an Ambu bag. This minimal leak technique should be used
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continuously until airway reflexes are intact. Humidification and warming of inspired gases, frequent aseptic suctioning of the trachea, and frequent change of the patient's position, and chest percussion, chest vibration, etc. will decrease the incidence of atelectasis followed by superimposed infection. If aspiration has occurred prior to intubation, methylprednisolone is administered in a dose of 250 mg. immediately and repeated every 6 hours for at least 2 days to reduce the inflammatory response. When wheezing is a problem, a bronchodilator such as an intravenous aminophylline drip can be considered. Bronchoscopy is necessary if the chest roentgenogram shows segmental or lobar atelectasis. Once the patient has a protected airway, the respiratory pattern should be carefully observed. If there is the typical fast rate and low volume exchange. then the patient should be placed on a ventilator utilizing large tidal volumes and frequent sighs. In patients with constant unvarying tidal volumes, a respirator may be required to induce sighing and prevent microatelectasis. Improvement in the patient's clinical condition can be monitored by repeated pulmonary function measurements, such as TVC. If there are problems in obstructive disease or restrictive disease, they require appropriate care. To improve the patient's systemic condition, the most important determination is the hemoglobin concentration. The patient needs sufficient oxygen-carrying capacity to maintain adequate oxygenation of the tissues. Finally, any chemical or bacterial toxin needs direct treatment consisting of the use of steroids and/or specific antibiotics. As recently pointed out, the syndrome of acute neurogenic pulmonary edema rarely occurs (10). The presence or absence of an adequate airway strongly influences its occurrence (11). When there is partial airway obstruction, tremendous intrathoracic negative pressure occurs. When there is increased intracranial pressure, the pulmonary bed is flooded (3, 6). The combination of events is probably necessary to cause the clinical syndrome. When it does occur, the patient should be intubated, ventilated with 100% O 2 , and, if necessary, gradual increments of positive end expiratory pressure (PEEP). Such patients may require sedation so that they do not struggle on the respiratory, even when they are suctioned. If intracranial pressure is elevated, further treatment of the pulmonary edema should be continued during an immediate decompressive procedure. If pulmonary edema persists postoperatively, positive end expiratory pressure must be applied sparingly to minimize its effect on increasing intracranial pressure. When the subacute respiratory distress syndrome of "shock lung" syndrome occurs, the patient most commonly has been in the hospital for
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2 to 3 days. In many cases, the syndtome can be prevented by early, active pulmonary support. The diagnosis is made primarily on the basis of history, a latent period is followed by onset of respiratory alkalosis and a progressively more severe hypoxemia. Usually the presence of interstitial edema on the chest film is noted. Treatment is primarily supportive at this time. Mechanical ventilation with PEEP helps to prevent small airway closure and permits adequate oxygenation with nontoxic oxygen concentrations. An adequate level of PEEP prevents further deterioration and appears to reduce the amount of edema present. Fluid restriction, mild diuresis, and the osmotic activity of albumin help prevent the accumulation of interstitial pulmonary edema. It must be stressed that maintenance of a hemoglobin concentration greater than 12 gm. per cent is essential and helps assure adequate oxygen delivery to the brain and other vital tissues. CONCLUSION
Hopefully, each neurosurgeon reading this chaper will remember all of it. In reality, that will not occur. Possibly it could be summed up in two ways. First, we are responsible for complete airway assessment. Secondly, aggressive pulmonary support is important for the patient with a serious neurosurgical disease. Complete airway assessment includes appreciation of the lash reflex, the gag reflex, and purposeful motor response. A patient without these reflexes will develop airway and pulmonary difficulties. Aggressive pulmonary support is best achieved by a cooperative effort by both anesthesia and neurosurgery. Early intubation is to be encouraged. Regulation of ventilation and maintenance of oxygen-carrying capacity and prevention of pulmonary toxic condition-all are important for the healing of diseased cerebral tissue in any postinjury or postoperative patient. REFERENCES 1. Berman, I. R., Ducker, T. B., and Simmons, R. L. The effects of increased intracranial pressure upon the oxygenation of blood in dogs. J. Neurosurg., 30: 532-536, 1969. 2. Brackett, C. E. In Head Injuries: Proceedings of an International Symposium on Respiratory Complications of Head Injury, p. 255-265. Williams & Wilkins Co., Baltimore, 1971. 3. Brashear, R. E., and Ross, J. C. Hemodynamic effects of elevated cerebrospinal fluid pressure: Alterations with adrenergic blockade. J. Clin. Invest., 49: 1324-1333,1970. 4. Ducker, T. B. Increased intracranial pressure and pulmonary edema, Part I, Clinical study of 11 patients. J. Neurosurg., 78: 112-117, 1968. 5. Ducker, T. B., Simmons, R. L., and Anderson, R. W. Increased intracranial pressure and pulmonary edema. Part 3: The effects of increased intracranial pressure of cardiovascular hemodynamics of chimpanzees. J. Neurosurg., 29: 475-483, 1968. 6. Ducker, T. B., Simmons, R. L., Anderson, R. W., and Kempe, L. G. Hemodynamic
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cardiovascular response to raised intracranial pressure. Med. Ann. D.C., 37: 523-525, 1968. Froman, C. Alterations of respiratory function in patients with severe head injuries. Br. J. Anaesth., 40: 354-360, 1968. Froman, C., and Smith, A. C. Hyperventilation associated with low pH of the cerebrospinal fluid after intracranial hemorrhage. Lancet 1: 780, 1966. Gordon, E. Some correlations between the clinical outcome of the acid-base status of blood and cerebrospinal fluid in patients with traumatic brain injury. Act. Anaesthesiol. Scand., 15: 209-228, 1971. Graf, C. J. Pulmonary edema and the central nervous system: A clinico-pathological study. Surg. Neurol., 4: 319-325, 1975. Graf, C. J. and Rossi, N. P. Cardiovascular and pulmonary effect of increased intracranial pressure. Presented at American Association of Neurological Surgeons Annual Meeting, 1975. Kaste, M., and Troupp, H. Effect of experimental brain injury on blood pressure, cerebral sinus pressure, cerebral venous oxygen tension, respiration, and acid-base balance. J. Neurosurg., 36: 625-633, 1972. Katsurada, K., Sugimoto, T., and Onju, Y. Significance of cerebrospinal fluid bicarbonate ions in the management of patients with cerebral injury. J. Trauma, 9: 799-805, 1969. Lassen, N. A. The luxury-perfusion syndrome and its possible relation to acute metabolic acidosis localized within the brain. Lancet, 2: 1113-1115, 1966. Mendolson, C. L. The aspiration of stomach contents into the lungs during obstetric anaesthesia. Am. J. Obstet. Gynecol., 52: 191, 1946. Mithoefer, J. 0., Keighley, J. F., et al. Response of the arterial P0 2 to oxygen administration in chronic pulmonary dissease: Interpretation of findings in a study of 46 patients with 14 normal subjects. Ann. Intern. Med., 74: 328-335, 1971. Moss, G., Staunton, C., and Stein, A. A. Cerebral etiology of the "Shock Lung Syndrome". J. Trauma, 12: 885-890, 1972. North, J. B. and Jannett, S. Abnormal breathing patterns associated with acute brain damage. Arch. Neurol., 31: 338-344, 1974. Parham, A. M., Ducker, T. B., and Redding, J. S. Lung dysfunction in the presence of central nervous system disease, performed in the procedure of NIH conference on Neurotrauma, March 1975. Redding, J. S., Yakaitis, R. W. Predicting need for ventilatory assistance. Md. State Med. J., 19: 53-57, 1970. Romig, D. A., Voth, D. W., Liu, Ch., and Brackett, C. E. Bacterial flora and infection in patients with brain injury. J. Neurosurg., 38: 710-716, 1973. Rudolph, A. M. Cardiac failure in children; a hemodynamic overview. Hosp. Prac., 5: 44-47, 53-55, 1970. Simmons, R. L., Martin, A. M., Heisterkamp. C. A., and Ducker, T. B. Respiratory insufficiency in combat casualties: II. Pulmonary edema following head injury. Ann. Surg., 170:(1): 34-44, 1969. Sinha, R. P., Ducker, T. B., Perot, P. L. Arterial oxygenation findings and its significance in central nervous system trauma patients. J. A. M. A., 224: 1258-1269, 1973. Zupping, R. Cerebral acid-base and gas metabolism in brain injury. J. Neurosurg., 33: 448-505, 1970. Zupping, R. Cerebral metabolism in patients with intracranial tumors. J. Neurosurg., 36: 451-462, 1972.
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DISEASE STATES
Neural Regulatory Dysfunction With any significant intracranial pathology, there are areas of the brain where metabolic derangement occurs with inadequate oxygen utilization and acidosis. While this can be demonstrated most commonly in both experimental and clinical brain injury, it does occur with any major pathological process that affects the central nervous system. The resultant low tissue oxygen partial pressure and the accumulation of acid by-products are reflected in the cerebrospinal fluid (9, 25, 26). The major fraction of the cerebral spinal fluid acid is lactic; at the same time, there is a concomitant marked reduction in the bicarbonate ion (13). With the flow of cerebrospinal fluid through the 4th ventricle by the respiratory centers in the medulla, there is commonly a change in the neural regulatory drive of respiration. The acid milieu acting on these respiratory centers results in an increased respiratory minute volume. This is reflected initially in a more rapid rate of respiration, but not in an increased tidal volume. In fact, the tidal volume is commonly diminished. Decreased tidal volumes, absence of sighing and coughing, and immobility of the patient so the same areas of lung remain dependent for protracted periods, lead to small airway closure. The result is reduction of residual lung volume and shunting of pulmonary blood flow through extensive areas of unventilated or collapsed lung. Since carbon dioxide is far more diffusible than oxygen, the increased minute volume of ventilation lowers arterial CO 2 tension below normal by hyperventilation of the aereated portions of the lung. Oxygen being less diffusible, the resultant hypoxemia can not be compensated by hyperventilation. Consequently, cerebral acidosis that causes a change in cerebrospinal fluid can result in a respiratory alkalosis and low arterial oxygen levels (2, 7, 8, 24). While the partial pressure of carbon dioxide is consistently low, the arterial oxygen may be only moderately depressed (12, 23, 25); but if the 483
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cerebral damage is associated with intracranial hypertension, then the arterial oxygen tension is likely to be more decreased (1). The systemic hypoxemia is due to pulmonary arteriovenous shunting, either by direct action of the effect of mass sympathetic discharge on the pulmonary vascular bed, or passively, as a consequence of changes in pulmonary blood flow resulting from small airway closure and uneven distribution of pulmonary gas. While the clinical neurosurgeon most commonly notes these events in the dramatic setting of an acute head injury, the same pulmonary problems readily occur in other central nervous system disorders, such as subarachnoid hemorrhage, brain tumor, and cerebrovascular accident (8, 14, 26). Mechanical Insufficiency Mechanical insufficiency is by far the most common problem in central nervous system disease, and obtunded airway reflexes are the most common type of mechanical problem (19). While complete airway obstruction can be corrected immediately, the hazards of partial airway obstruction-that is, heavy snoring-are often overlooked. Partial airway obstruction is usually accompanied by copious saliva production. When these secretions stimulate the vocal cords of an obtunded patient, severe laryngospasm may result. Moderately severe partial obstruction may lead to air swallowing, gastric distension, and explosive vomiting. If the obstruction is so severe that the patient must labor forcefully during inspiration to pull in air, he may generate enough negative airway pressure to pull capillary and interstitial fluid into his alveoli and thus precipitate pulmonary edema. Another type of mechanical insufficiency is that seen with muscle paralysis from trauma to the spinal cord or the phrenic nerve. Although the patient is usually left with adequate strength to breathe and maintain normal blood gases initially, he may not have enough reserve muscle strength to sigh, take deep breaths, and cough effectively. A monotonous respiratory pattern, unbroken by an occasional sigh or deep breath, will lead to diffuse microatelectasis of the lungs. The chest roentgenogram is normal in such instances, and the only manifestation is hypoxemia. If the patient cannot cough effectively, secretions will accumulate and obstruct small bronchioles. The unventilated areas of lung will subsequently develop macroatelectasis, and later pneumonia. These conditions may be predicted and prevented by measuring the patient's vital capacity upon admission. The vital capacity is an index of the ability to sigh and cough effectively. Awake patients can take their deepest breath and blow into a spirometer; obtunded patients should be
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intubated and the volume of a forceful cough determined. If the patient's vital capacity is less than 25% of his predicted normal, a mechanical ventilator should be utilized. Percussion of the chest, or pulmonary physiotherapy, is also needed. Even if there is neurological improvement, the vital capacity and respiratory function will improve in a week to 10 days. Initially, the intercostal spaces sink inward as the diaphragm descends during inspiration. As reflex intercostal muscle tone increases, this effect decreases and the patient is able to take deeper breaths and cough more effectively. A very similar type of problem is seen in patients who have the muscular ability to sigh and cough effectively but who simply fail to do so. Commonly, this is seen in patients during protracted recovery from frontal lobe injuries and cerebrovascular accidents (19). Occasionally, this abnormal pattern is seen in trauma patients with very subtle changes in intracranial pressure (18). While these patients may be responsive to command, they are frequently totally disinterested in their surroundings and well being. The respiratory pattern is marked by a monotonously constant rate and depth of respiration, uninterrupted by sighing, deep breathing, or coughing. The result is diffuse microatelectasis and hypoxemia. Reduction of the intracranial pressure will reverse the abnormal respiratory pattern in some trauma patients. Hourly hyperinflation of the lungs using a self-inflating bag may help others. In the more severe cases, mechanical ventilation for 24 hours, followed by intermittent mandatory ventilation at a rate of two breaths per minute, is effective in preventing microatelectasis.
Acute Pulmonary Edema In the last 10 years, the occurrence of pulmonary edema in association with central nervous system and multisystem trauma has received much attention. At least one variant of this syndrome appears to be neurogenic in origin: the acute fulminating type of pulmonary edema which may follow within minutes after a sudden rise of intracranial pressure (4). While there are cases where it has occurred in patients who did have a patent airway (endotracheal tube), it now appears that the combination of partial airway obstruction and increased intracranial pressure expedites the pathophysiological process (10). The partial airway obstruction causes labored breathing which, in turn, causes tremendous negative intrathoracic pressure. This pulls fluid out of the vascular bed into lung interstitial tissue and alveoli. At the same time, the increased intracranial pressure causes an increase in cardiac output and a rise in peripheral resistance (vasoconstriction) and engorgement of the pulmonary vascular bed (3, 5, 6). Elevation of pulmonary capillary pressure contributes to
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the occurrence of pulmonary edema (22): The two events, congested lung and the labored breathing, will cause an overwhelming pulmonary edema which, in many cases is fatal (4). Now that airway problems are quickly corrected, and many neurosurgical patients are treated with positive pressure hyperventilation, the incidence of acute "neurogenic" pulmonary edema has markedly diminished.
(Subacute) Respiratory Distress Syndrome In addition to the acute form of pulmonary edema just mentioned, there is a less acute variation which is generally referred to as the respiratory distress syndrome of the adult or "shock lung" syndrome. This appears to follow a variety of multisystem traumatic injuries, particularly after hemorrhagic or septic shock has occurred. The etiology remains uncertain, but it has generally been considered a result of various direct influences on the pulmonary capillary endothelium. Certainly, an underventilated and contaminated pulmonary bed contributes to the presence of this pathological state. More recently, an attractive unifying theory has been proposed which blames central nervous system hypoxemia as the initial event (17). Once the central nervous system has been injured, the sympathetic nervous system reacts with constriction of small pulmonary venules as well as increased pulmonary vascular resistance. When the pulmonary venular constriction persists, interstitial pulmonary edema is created. Subsequently, there is increased permeability of the pulmonary capillaries with loss of albumin into the interstitial space, closure of small airways, loss of pulmonary compliance, and hypoxemia. A vicious cycle is set in motion which leads to progressive pulmonary edema and respiratory failure. Oxygen toxicity added to the current problem only further complicates the condition. The edematous lung is more susceptible to infection, and a superimposed pneumonia may obscure the diagnosis, as well as adding further pulmonary damage.
Pulmonary Toxic Reactions Chemical and bacteria contamination commonly occur in the patient with significant central nervous system disease. It has been common knowledge since the work of Denney-Brown and Russel, in 1941, that in cerebral disorders gag and swallowing reflexes are impaired, and fluid runs freely into the unprotected trachea. Vomiting readily occurs, and the gastric contents may cause a severe inflammatory response in the lung, referred to as Mendelson's syndrome (15). With the acid gastric contents, a severe chemical pneumonitis occurs. In addition, focal atelectasis compounds the problem and accentuates the pulmonary
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inflammatory response. The damaged pulmonary bed interrupts gas exchange in the lung and can accentuate the existing pathology within the brain or spinal cord. Bacterial pneumonia can also further complicate the course of a patient with significant neurological disease. In a patient with a depressed state of consciousness carefully treated in a hospital, the respiratory bacterial flora changes to an enteric bacillus, coagulase positive staphylococci, Candida species, etc. These pathogens have ready access to the pulmonary bed (21). If the patient's defenses are further lowered, and if the pulmonary bed becomes further congested, a severe infection readily occurs. While it is possible to keep a patient in an unconscious state with either an endotracheal tube or a tracheostomy in supportive ventilation for a prolonged period of time without infection, the slightest break in technique, or change in the patient's internal milieu will allow bacterial contamination which requires therapy. PATIENT EVALUATION
In a patient with significant central nervous system disease, there are four essential questions to ask concerning that person's pulmonary function: 1. Are the neural mechanisms which insure respiratory drive and protective airway reflexes adequate? 2. Are there limitations in ventilatory function from others causes? 3. Are the patient's oxygen-carrying capacity, arterial oxygen tension, and cardiac output adequate for tissue oxygenation? 4. Are there superimposed chemical and bacterial toxins?
Neural Drive and Reflexes First, count the respiratory rate and carefully observe the patient's chest and abdominal excursions, noting the pattern of respiration. It is important to realize that the normal person in a basal state has a respiratory rate as low as 12 to 14 breaths per minute. A rate above 20 is distinctly abnormal. Commonly, such patients have a high rate with a low volume exchange, resulting in alveolar hypoventilation. Even when the brain stem reflex drive to respiration maintains a normal rate and volume, it may have a distinctly abnormal pattern. Intermittent sighs, or deep breaths, may be completely absent. Without sighing, there is not intermittent full expansion of all the alveolar spaces, and ventilation/ perfusion inequality readily occurs. A very slight change in intracranial pressure may be associated with the presence or absence of normal sighs in the respiratory pattern. Sufficient neural reflexes to open and close the glottis and control the swallowing mechanism can be readily tested by the clinician. A simple,
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modified corneal reflex using the eyelash can give important information. This is referred to by anesthesiologists as the lash reflex, and involves the V and VII cranial nerves. If there is involuntary winking when the lash is brushed gently, the gag and swallowing reflexes commonly are also present. Patients with intact medullary reflexes are unlikely to accumulate secretions and gastric material in their pulmonary beds.
Pulmonary Function The pulmonary function of the patient must be assessed. Pre-existing obstructive or restrictive problems are often present in the elderly patient prior to the onset of significant intracranial disease. In those patients who can cooperate, the measurement of vital capacity is the simplest and quickest way to ascertain ventilatory ability. An accurate and portable ventilometer (Wright respirometer) can be used for an approximation of this determination in intubated or tracheotomized patients. A timed vital capacity (TVC) is a recording of vital capacity as a function of time and can be measured with a portable McKesson Vitalor. The first second forced expiratory volume (FEV 1.0) is that volume which is recorded during the first second of the total forced expiratory volume measured from the maximal inspiratory position. By reference to standard nomograms calibrated for height and sex of the patient, the total vital capacity can be expressed as a percentage of predicted normal. Reduction of the observed vital capacity below 80% of the predicted normal indicates a restrictive defect of the lungs and/or thorax. Reduction of the FEV 1.0 below 750/0 of the observed vital capacity indicates existence of obstructive airway disease. Many patients exhibit a mixture of both components (20). Reduction of vital capacity below 250/0 of predicted normal, or reduction of FEV 1.0 below 40% of observed vital capacity, will result in ventilatory failure with hypercapnia usually compounded by hypoxemia (20). The success of the lungs in oxygenation. of blood is appreciated by serial measurements of the amount of intrapulmonary shunting. The standard formula which utilizes the relationship between pulmonary alveolar and systemic arterial oxygen tensions can be easily used for such determinations. An expanding gradient between alveolar and arterial oxygen tensions implies deteriorating pulmonary function,
Systemic Condition The patient's hemoglobin value is just as important as the blood gas determination. While- it is not advisable to have an excessively high hemoglobin in a patient with brain disease, it certainly is desirable to
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have a hemoglobin in the range of 12 gm. % in order to insure adequate oxygenation of the tissues (16). The delivery of oxygen is, of course, influenced by the arterial blood gas tensions. But high inspired oxygen tensions can be dangerous and are not necessary if the hemoglobin level is normal, if the cerebral blood flow is adequate, and if alveolar ventilation is maintained. The common occurrence of cerebral metabolic acidosis with resultant systemic respiratory alkalosis and hypoxemia can often be corrected by giving the patient respiratory support utilizing tidal volumes of 12 to 15 ml./kg. body weight and frequent sigh volumes of 20 ml./kg., combined with frequent changes in the patient's position. These measures minimize small airway closure with reduced residual lung volume and the resultant hypoxemia. Thus, the respirator rate and volume need to be adjusted first to correct abnormal blood gases. Finally, the inhaled oxygen concentration should be adjusted to correct any hypoxemia which exists in spite of the foregoing measures. The success of long term ventilation (longer than 24 hours) in part depends on the type of ventilator selected and the diligence of the nursing personnel. A pressure guaranteed, volume variable ventilator such as the Bird is often inadequate for patients on long term support and those with abnormal lungs since atelectasis will occur even with large volumes. The gases are not distributed uniformly leading to progressive ventilation perfusion mismatching and hypoxemia. Volume guaranteed, pressure variable ventilators such as Engstrom or Emerson as a class have superior flow characteristics permitting more physiological gas distribution within the lungs. However, regardless of volume or class of ventilator used, long term ventilatory support will lead to progressive hypoxia unless chest physiotherapy is vigorous and unless aseptic technique is strictly adhered to. Finally, the systemic condition is markedly altered by fat embolization. This can be concomitant with certain traumatic central nervous system disorders. The persistent hypoxemia that may occur even with ventilatory support needs to be corrected by increased inhaled oxygen concentrations. Use of glucocorticosteroids will reduce the inflammatory response associated with this phenomenon.
Chemical and Bacterial Toxins Chemical and bacterial toxins need immediate and direct treatment. If these conditions are superimposed, the patient has two distinct diagnoses, not just one. The presence of chemical and bacterial toxic pneumonitis can be determined by physical findings, chest x-ray, and pulmonary cultures. These disease states alter the ventilation/perfusion ratio in the lung beds and result in arterial hypoxemia. On occasion, the
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pneumonitis may cause transient bacteremias and set up infections in devitalized brain to further complicate the course of the patient. TREATMENT
Treatment of patients with pulmonary disorders secondary to nervous system disease cannot be meaningfully simplified. Initially, however, it is important to answer the five logical questions in the patient's evaluation in order to determine treatment. For example: 1. Must airway obstruction be corrected? 2. Does the patient require ventilatory support and protection against absent protective reflexes? 3. What measures are indicated to improve ventilatory function? 4. What measures will improve the systemic condition? 5. Is treatment of a chemical or bacterial pneumonitis indicated? An adequate airway and respiratory drive are vital to survival. If airway insufficiency is allowed to continue without active support, respiratory and circulatory exhaustion occur. Severe airway obstruction is most reliably recognized by placing the hand over the nose and mouth and recognizing absent or diminished air flow. Partial airway obstruction is recognized by hearing a "snore" on inspiration or palpating it immediately above the larynx. If a patient is too obtunded to respond to command, he may aspirate if he regurgitates. Not infrequently, a patient will respond to command when stimulated but lapse into a deeper state of unconsciousness when he is left alone. If the patient has an active lash reflex, a gag reflex, and responds purposeful to pain, he does not require intubation or tracheostomy. If these are not present, then the brain stem reflex centers are depressed, and the patient may readily aspirate and get a chemical pneumonitis. In such cases, either an endotracheal tube or a tracheostomy is required. Oral airways are basically worthless; instead, with transient sedation, a properly placed endotracheal tube will achieve good ventilatory support. Since irritation of the posterior pharynx may precipitate gagging and vomiting, an oral or nasal pharyngeal airway should be used only until a cuffed endotracheal tube is placed. The use of pharyngeal airways should be avoided in slightly unconscious patients because of the risk of vomiting. In these patients proper head and jaw position should be used to maintain airway patency until intubation. The anticipated duration of airway protection will influence the decision regarding use of a tracheostomy or prolonged intubation. Nasogastric intubation should be deferred until after the endotracheal tube is placed. The endotracheal tube cuff should be inflated until there is only a slight leak when the patient is sighed with an Ambu bag. This minimal leak technique should be used
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continuously until airway reflexes are intact. Humidification and warming of inspired gases, frequent aseptic suctioning of the trachea, and frequent change of the patient's position, and chest percussion, chest vibration, etc. will decrease the incidence of atelectasis followed by superimposed infection. If aspiration has occurred prior to intubation, methylprednisolone is administered in a dose of 250 mg. immediately and repeated every 6 hours for at least 2 days to reduce the inflammatory response. When wheezing is a problem, a bronchodilator such as an intravenous aminophylline drip can be considered. Bronchoscopy is necessary if the chest roentgenogram shows segmental or lobar atelectasis. Once the patient has a protected airway, the respiratory pattern should be carefully observed. If there is the typical fast rate and low volume exchange. then the patient should be placed on a ventilator utilizing large tidal volumes and frequent sighs. In patients with constant unvarying tidal volumes, a respirator may be required to induce sighing and prevent microatelectasis. Improvement in the patient's clinical condition can be monitored by repeated pulmonary function measurements, such as TVC. If there are problems in obstructive disease or restrictive disease, they require appropriate care. To improve the patient's systemic condition, the most important determination is the hemoglobin concentration. The patient needs sufficient oxygen-carrying capacity to maintain adequate oxygenation of the tissues. Finally, any chemical or bacterial toxin needs direct treatment consisting of the use of steroids and/or specific antibiotics. As recently pointed out, the syndrome of acute neurogenic pulmonary edema rarely occurs (10). The presence or absence of an adequate airway strongly influences its occurrence (11). When there is partial airway obstruction, tremendous intrathoracic negative pressure occurs. When there is increased intracranial pressure, the pulmonary bed is flooded (3, 6). The combination of events is probably necessary to cause the clinical syndrome. When it does occur, the patient should be intubated, ventilated with 100% O 2 , and, if necessary, gradual increments of positive end expiratory pressure (PEEP). Such patients may require sedation so that they do not struggle on the respiratory, even when they are suctioned. If intracranial pressure is elevated, further treatment of the pulmonary edema should be continued during an immediate decompressive procedure. If pulmonary edema persists postoperatively, positive end expiratory pressure must be applied sparingly to minimize its effect on increasing intracranial pressure. When the subacute respiratory distress syndrome of "shock lung" syndrome occurs, the patient most commonly has been in the hospital for
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2 to 3 days. In many cases, the syndtome can be prevented by early, active pulmonary support. The diagnosis is made primarily on the basis of history, a latent period is followed by onset of respiratory alkalosis and a progressively more severe hypoxemia. Usually the presence of interstitial edema on the chest film is noted. Treatment is primarily supportive at this time. Mechanical ventilation with PEEP helps to prevent small airway closure and permits adequate oxygenation with nontoxic oxygen concentrations. An adequate level of PEEP prevents further deterioration and appears to reduce the amount of edema present. Fluid restriction, mild diuresis, and the osmotic activity of albumin help prevent the accumulation of interstitial pulmonary edema. It must be stressed that maintenance of a hemoglobin concentration greater than 12 gm. per cent is essential and helps assure adequate oxygen delivery to the brain and other vital tissues. CONCLUSION
Hopefully, each neurosurgeon reading this chaper will remember all of it. In reality, that will not occur. Possibly it could be summed up in two ways. First, we are responsible for complete airway assessment. Secondly, aggressive pulmonary support is important for the patient with a serious neurosurgical disease. Complete airway assessment includes appreciation of the lash reflex, the gag reflex, and purposeful motor response. A patient without these reflexes will develop airway and pulmonary difficulties. Aggressive pulmonary support is best achieved by a cooperative effort by both anesthesia and neurosurgery. Early intubation is to be encouraged. Regulation of ventilation and maintenance of oxygen-carrying capacity and prevention of pulmonary toxic condition-all are important for the healing of diseased cerebral tissue in any postinjury or postoperative patient. REFERENCES 1. Berman, I. R., Ducker, T. B., and Simmons, R. L. The effects of increased intracranial pressure upon the oxygenation of blood in dogs. J. Neurosurg., 30: 532-536, 1969. 2. Brackett, C. E. In Head Injuries: Proceedings of an International Symposium on Respiratory Complications of Head Injury, p. 255-265. Williams & Wilkins Co., Baltimore, 1971. 3. Brashear, R. E., and Ross, J. C. Hemodynamic effects of elevated cerebrospinal fluid pressure: Alterations with adrenergic blockade. J. Clin. Invest., 49: 1324-1333,1970. 4. Ducker, T. B. Increased intracranial pressure and pulmonary edema, Part I, Clinical study of 11 patients. J. Neurosurg., 78: 112-117, 1968. 5. Ducker, T. B., Simmons, R. L., and Anderson, R. W. Increased intracranial pressure and pulmonary edema. Part 3: The effects of increased intracranial pressure of cardiovascular hemodynamics of chimpanzees. J. Neurosurg., 29: 475-483, 1968. 6. Ducker, T. B., Simmons, R. L., Anderson, R. W., and Kempe, L. G. Hemodynamic
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cardiovascular response to raised intracranial pressure. Med. Ann. D.C., 37: 523-525, 1968. Froman, C. Alterations of respiratory function in patients with severe head injuries. Br. J. Anaesth., 40: 354-360, 1968. Froman, C., and Smith, A. C. Hyperventilation associated with low pH of the cerebrospinal fluid after intracranial hemorrhage. Lancet 1: 780, 1966. Gordon, E. Some correlations between the clinical outcome of the acid-base status of blood and cerebrospinal fluid in patients with traumatic brain injury. Act. Anaesthesiol. Scand., 15: 209-228, 1971. Graf, C. J. Pulmonary edema and the central nervous system: A clinico-pathological study. Surg. Neurol., 4: 319-325, 1975. Graf, C. J. and Rossi, N. P. Cardiovascular and pulmonary effect of increased intracranial pressure. Presented at American Association of Neurological Surgeons Annual Meeting, 1975. Kaste, M., and Troupp, H. Effect of experimental brain injury on blood pressure, cerebral sinus pressure, cerebral venous oxygen tension, respiration, and acid-base balance. J. Neurosurg., 36: 625-633, 1972. Katsurada, K., Sugimoto, T., and Onju, Y. Significance of cerebrospinal fluid bicarbonate ions in the management of patients with cerebral injury. J. Trauma, 9: 799-805, 1969. Lassen, N. A. The luxury-perfusion syndrome and its possible relation to acute metabolic acidosis localized within the brain. Lancet, 2: 1113-1115, 1966. Mendolson, C. L. The aspiration of stomach contents into the lungs during obstetric anaesthesia. Am. J. Obstet. Gynecol., 52: 191, 1946. Mithoefer, J. 0., Keighley, J. F., et al. Response of the arterial P0 2 to oxygen administration in chronic pulmonary dissease: Interpretation of findings in a study of 46 patients with 14 normal subjects. Ann. Intern. Med., 74: 328-335, 1971. Moss, G., Staunton, C., and Stein, A. A. Cerebral etiology of the "Shock Lung Syndrome". J. Trauma, 12: 885-890, 1972. North, J. B. and Jannett, S. Abnormal breathing patterns associated with acute brain damage. Arch. Neurol., 31: 338-344, 1974. Parham, A. M., Ducker, T. B., and Redding, J. S. Lung dysfunction in the presence of central nervous system disease, performed in the procedure of NIH conference on Neurotrauma, March 1975. Redding, J. S., Yakaitis, R. W. Predicting need for ventilatory assistance. Md. State Med. J., 19: 53-57, 1970. Romig, D. A., Voth, D. W., Liu, Ch., and Brackett, C. E. Bacterial flora and infection in patients with brain injury. J. Neurosurg., 38: 710-716, 1973. Rudolph, A. M. Cardiac failure in children; a hemodynamic overview. Hosp. Prac., 5: 44-47, 53-55, 1970. Simmons, R. L., Martin, A. M., Heisterkamp. C. A., and Ducker, T. B. Respiratory insufficiency in combat casualties: II. Pulmonary edema following head injury. Ann. Surg., 170:(1): 34-44, 1969. Sinha, R. P., Ducker, T. B., Perot, P. L. Arterial oxygenation findings and its significance in central nervous system trauma patients. J. A. M. A., 224: 1258-1269, 1973. Zupping, R. Cerebral acid-base and gas metabolism in brain injury. J. Neurosurg., 33: 448-505, 1970. Zupping, R. Cerebral metabolism in patients with intracranial tumors. J. Neurosurg., 36: 451-462, 1972.
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