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Pneumothorax complicating continuous ventilatory support
Pneumothorax complicating continuous ventilatory support Pneumothorax is more likely to occur during continuous respiratory support in the patient with chronic emphysema who is using a volume-controlled respirator that delivers a high tidal volume and incorporates positive end-expiratory pressure (PEEP). Pneumothorax which occurs during pressure breathing is highly dangerous. It is characterized by a dramatic onset which is readily recognized and demands immediate management.
Michael Steier, M.D. (by invitation), Nathaniel Ching, M.D. (by invitation), Enrique Bonfils Roberts, M.D. (by invitation), and Thomas F. Nealon, Jr., M.D., New York, N. Y.
DUring the past four years the yearly incidence of pneumothorax has increased forty-five per cent at our institution. Analysis of our cases reveals that the increased incidence is primarily due to the use of techniques developed to improve the resuscitation and care of critically ill patients. These include external cardiac massage, subclavian venotomy for monitoring central venous pressure or intravenous feeding, and continuous ventilatory support. It is the purpose of this report to examine those factors which may contribute to its occurrence during continuous ventilatory support and to emphasize the importance of early recognition and prompt treatment of pneumothorax occurring during continuous ventilatory support. Materials and methods
All diagnosed cases of pneumothorax in St. Vincent's Hospital and Medical Center of New York City in the period from Jan. 1, 1965, to Dec. 31, 1972, were reviewed. From the Departments of Surgery, SI. Vincent's Hospital and Medical Center of New York, 153 West 11th Street, New York, N. Y. 10011, and New York University School of Medicine, New York, N. Y. Read at the Fifty-third Annual Meeting of The American Association for Thoracic Surgery, Dallas, Texas, April 16, 17, and 18, 1973.
The institution is a 900 bed general hospital located in the heart of Greenwich Village and serves a varied general population in lower Manhattan. The occurrences include a hospital-wide survey primarily from the separate medical and surgical intensive care units. The surgical service is responsible for closed-chest tube thoracostomies. In the period from Jan. 1, 1965, to Dec. 31, 1972, 544 patients sustained a pneumothorax. The etiology was identified as follows: (l) iatrogenic, 209 cases; (2) traumatic, 179 cases; (3) spontaneous, 150 cases; and (4) infectious, 6 cases. The yearly incidence of traumatic and spontaneous pneumothorax has remained fairly constant; however, iatrogenic pneumothorax has increased precipitously during the last 5 years from 12 cases in 1968 to 54 cases in 1972 (Fig. 1). The iatrogenic category included ( I ) external cardiac massage, 62 cases; (2) the percutaneous subclavian route for canal cannulation, 60 cases; (3) continuous ventilatory support, 74 cases; and (4) miscellaneous, 13 cases. Of the patients who developed pneumothorax during continuous ventilatory support there were 44 males and 30 females. The mean age of the group was 68 years, ranging from 1 day to 82 years. The primary 1 7
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SPONTANEOUS TRAUMATIC
1965 1966 1967 1968 1969 1970 1971 1972
YEAR Fig. 1. The incidence of pneumothorax, 1965 to 1972, is classified as to etiology (544 cases). There has been a precipitous increase in iatrogenic pneumothorax from 12 cases in 1968 to 54 cases in 1972. The incidence of spontaneous and traumatic pneumothorax has remained constant.
Table I. Patients developing pneumothorax during continuous ventilation Primary diagnosis
Surgical Nonthoracic Thoracic Medical Sepsis Cardiovascular Chronic respiratory insufficiency Aspiration Idiopathic Total
No. of patients
31 3 16 9 7 6 2 74
illnesses of these patients are listed in Table I. Thirty-four surgical patients developed acute respiratory insufficiency in the postoperative period. The incidence of nonthoracic surgical cases reflects the large number of seriously ill patients undergoing general surgical procedures at our hospital. Of the 40 medical patients, there were only 7 in whom chronic respiratory insufficiency was the primary diagnosis. In the remaining 33, acute respiratory failure was secondary to sepsis (16 cases), cardiovascular shock (9 cases), and aspiration (6 cases). The cause in 2 cases was not identified. In the majority of those with sepsis, the condition was caused by infection with gram-negative organisms. Acute respiratory failure was defined as inability of the patient to maintain normal
blood gas values without overworking. Access to the upper airway was obtained by endotracheal intubation in 49 cases and by tracheostomy in 25 cases. Pneumothorax occurred on the right side in 36 instances, on the left in 33, and bilaterally in 5 cases. The percentage pneumothorax varied from 10 to 100, with a mean of 80 per cent in those who had a chest x-ray before tube thoracostomy. A tension component, as evidenced by a shift of the mediastinum, was detected by chest roentgenogram or by clinical examination in 71 of the 74 cases. Pneumothorax occurred between the first and twelfth days of continuous ventilatory support, with 75 per cent developing between the second and fourth days. The diagnosis of pneumothorax was made on a clinical basis in 45 cases. The clinical presentation was sudden and dramatic in onset. Subcutaneous emphysema was recognized in all 74 cases. It presented initially in the supraclavicular fossa and cervical regions and often rapidly extended to the face, thorax, and even to the scrotum. Tachycardia as high as 150 beats per minute (70 cases), diminished breath sounds (65 cases), hyperresonance (63 cases) , and pressure below 90 mm. Hg (60 cases) occurred in most instances (Fig. 2). Arterial blood gas results were available on 51 patients after the onset of pneumothorax and prior to closed-chest tube thoracostomy. The mean Pao~ of this group was 47 mm. Hg, and the mean Paco~ was 62 mm.Hg. Results
Twelve of the 74 patients died as a result of this problem, for an over-all mortality rate of 16 per cent. Treatment was delayed between 30 minutes and 8 hours in 29 patients during which the diagnosis of pneumothorax awaited confirmation by chest roentgenogram. Nine of these died of pneumothorax, for an incidence of 31 per cent as compared to a mortality rate of 7 per cent in the group of 45 patients who had immediate treatment based on clinical diagnosis.
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Pneumothorax
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25 Subcutaneous Emphysema
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Tachycardia Diminished B.S. Hyperresonance Hypotension Cyanosis Diaphoresis Tracheal Deviation Asynchronous Motion Pulse Irregularity
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Fig. 2. Clinical presentation of pneumothorax complicating ventilatory support (74 cases). Subcutaneous emphysema was recognized in all 74 cases (100 per cent). B.s., Breath sounds.
Contributing factors The following factors seem to influence the incidence of pneumothorax during continuous ventilatory support. Volume-cycled ventilator. A volumecycled ventilator was employed in 70 cases and a pressure-cycled ventilator in 4. Approximately 600 patients a year receive ventilatory assistance for longer than 24 hours at our hospital. One third of these require volume-controlled ventilators. Approximately 7 per cent of patients receiving volume-regulated ventilatory support develop pneumothorax, whereas only 0.25 per cent of those receiving pressure-regulated ventilatory support develop the condition. Chronic obstructive lung disease. Sixtytwo patients had clinical, roentgenographic, or pulmonary function studies indicative of pre-existing chronic lung disease. Symptoms of chronic cough, purulent and copious expectoration, exertional dyspnea, and cor pulmonale were present to some degree in all 62 patients. Roentgenographic studies demonstrated local or generalized increased depth of the retrosternal air spaces, oligemia, localized or diffuse bullae, and in more severe cases prominent hilar pulmonary arteries and cardiac enlargement. Twenty-five of the 62 patients had recent pulmonary function tests available for analysis. These demonstrated decreased forced expiratory volume 1.0, increased total lung capacity and functional residual capacity, decreased vital capacity, and increased
residual volume-total lung capacity in ranges compatible with emphysematous disease. Excessive tidal volumes. When initiating continuous ventilatory support, we usually begin with a tidal volume in the range of 10 c.c. per kilogram of body weight. This is then adjusted to effect normal blood Pco, levels. At the time that pneumothorax occurred, the mean tidal volume was available in 62 cases and was 18 c.c. per kilogram, with a range of between 14 and 21 c.c. per kilogram. Increased end-inspiratory pressure. The pressure reached at the peak of inspiration is a reflection of lung compliance. In 48 instances the end-inspiratory pressure was known prior to the development of pneumothorax. In this group of patients the mean end-inspiratory pressure was 46 em. of water with a range between 38 and 55 em. of water. Positive end-expiratory pressure (PEEP). Approximately 10 per cent of our patients with acute respiratory failure failed to respond to standard methods of continuous ventilatory support. Specifically, these patients were unable to maintain a Paoz above 60 mm. Hg while being ventilated with a gaseous mixture containing 60 per cent oxygen. Rather than risk the danger of oxygen toxicity by increasing the concentration of oxygen above 60 per cent, we have preferred to utilize PEEP.! This modality was used in 14 of the 74 cases. Ten per cent of our patients receiving volume-
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regulated ventilatory support (20 patients per year) require PEEP, and, each year, 3.5 or 17 per cent of these patients develop pneumothorax. We customarily initiate PEEP with low pressures in the range of 2 to 3 em. of water and gradually increase the pressure as required to maintain a Pao2 between 70 and 80 mm. Hg with relatively low concentrations of inspired oxygen. In the 14 patients who were receiving PEEP at the time of pneumothorax occurrence, the mean endexpiratory pressure was 12 cm. of water with a range between 8 and 17 em. of water. Percutaneous subclavian venipuncture during pressure breathing. In addition to these 74 patients, 9 others developed pneumothorax as a percutaneous subclavian catheter was being inserted while ventilatory assistance continued. The heightened intrathoracic pressure substantially increases the likelihood of puncturing the lung, and assistance should be stopped during venotomy. Discussion As is often the case, new techniques developed to improve medical care contribute their own series of complications. Fleming and Bowen- reported that 15 per cent of their ventilated patients developed pneumothorax, primarily as a result of infection. Pontoppidan and associates" have stressed that tension pneumothorax occurs with greater frequency in patients with chronic obstructive lung disease who require mechanical ventilation because of acute respiratory failure. Mediastinal emphysema and/or pneumothorax has been reported to occur with the use of continuous positivepressure ventilation.v" The purpose of this report is not to discourage the use of ventilatory support but to alert physicians who use the technique to the occurrence of pneumothorax, the importance of early diagnosis, and means of preventing the complication. The presence of the associated factors should increase the awareness of the possibility of pneumothorax. The development of pneumothorax in a patient ventilated with positive-pressure
techniques is an acute surgical emergency which demands immediate decompression. The diagnosis should be made on a clinical basis. The patient on ventilatory support who develops a sudden extreme change in his pulmonary or cardiovascular status is a prime suspect. All 74 patients with pneumothorax developed subcutaneous emphysema. Our results are a clear demonstration that any delay in diagnosis contributes substantially to the possibility of death. It is our practice to use volume-controlled respirators on more seriously ill patients. This may account for some increase in deaths, but the main factor seems to be related to the delay in providing proper treatment.
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REFERENCES Ashbaugh, D. G., Petty, T. L., Bigelow, D. B., and Harris, T. M.: Continuous Positive-Pressure Breathing (CPPB) in Adult Respiratory Distress Syndrome, I. THORAC. CARDIOVASC. SURG. 57: 31, 1969. Fleming, W. H., and Bowen, I. c.: Early Complications of Long-Term Respiratory Support, 1. THORAC. CARDIOVASC. SURG. 64: 729, 1972. Pontoppidan, H., Geffin, B., and Lowenstein, E.: Acute Respiratory Failure in the Adult (Second of Three Parts), N. EngI. I. Med. 287: 743, 1972. Kumar, A., Falke, K. J., and Geffin, B.: Continuous Positive Ventilation in Acute Respiratory Failure, N. EngI. I. Med. 283: 1430, 1970. Ashbaugh, D. G., and Petty, T. L.: Positive End-Expiratory Pressure: Physiology, Indications, and Contraindications, I. THORAC. CARDIOVASC. SURG. 65: 165, 1973. Kolff, I., Webb, 1. A., Jr., and Loop, F. D.: Electrical Analogues of Methods for Continuous Positive-Pressure Ventilation. I. THORAC. CARDIOVASC. SURG. 64: 586, 1972. Pontoppidan, H., Geffin, B., and Lowenstein, E.: Acute Respiratory Failure in the Adult (Third of Three Parts), N. EngI. J. Med. 287: 799, 1972. Sugurman, H. I., Rogers, R. M., and Miller, L. D.: Positive End-Expiratory Pressure (PEEP): Indications and Physiologic Considerations, Chest 62: 865, 1972.
Discussion DR. WILLIAM H. FLEMING Atlanta, Ga.
I would like to compliment Dr. Steier on an excellent study. I find it interesting to see the same problems appearing in civilian practice that we first encountered in Vietnam. Part of that work
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was presented before this Association last year. There are several significant differences between this civilian work and our Vietnam work. It will be important for all of us as we translate military experience to civilian practice to look for these differences. The greatest difference I notice here is in the average age. Whereas our patients averaged 20 years, Dr. Steier's averaged 68 years of age. The military personnel, of course, were free of chronic lung disease as an antecedent problem, whereas it was very common in Dr. Steier's patients. [Slide] In the whole spectrum of complications of pulmonary ventilatory support, incidence of secondary pneumothorax was 19 of 128 respirator patients followed prospectively. [Slide] In contrast to Dr. Steier's patients, 17 of our 19 patients seemed to have pulmonary sepsis as an etiologic factor, usually with necrotizing organisms. [Slide] Only 2 of our 19 patients had peak airway pressures over 40 em. of water. We did not find that pneumothorax correlated with volume rather than pressure respirators, since our incidence was the same as the incidence of patient days on each type of respirator. DR. HANSON Syracuse, N. Y.
This subject is of genuine concern and merits discussion. At the Upstate Medical Center, we have been as aggressive as the authors with our therapy, but our experience is different. Using positive end-expiratory pressure (PEEP) and continuous positive-pressure breathing (CPPB) in over 200 cases postoperatively and in more than 50 patients with aspiration, we have observed only three instances of pneumothorax and five of pneumomediastinum. In none of the latter did we see subcutaneous emphysema. We think that there are several things that account for this. First, the expiratory port must be large, 2 to 3 cm. in size, or the usual size of expiratory tubing on a ventilator. Second, the measurements of airway pressure must be accurate. Adequate gauges properly placed in the system must be used in order to gain an accurate measurement of tracheal pressure. Certain volume-cycled respirators have gauges much to distal on the expiratory line to give accurate airway pressure measurements. Finally, the likelihood of a rupture when alveolar pressure is greater than 50 em. must be emphasized. Coughing is particularly dangerous in this regard, as is breathing out of phase with the ventilator. It is very important to keep the patient sedated and paralyzed or to maintain hypocapnia to remove the respiratory drive. We feel that if these guidelines are followed, the incidence of pneumothorax will be infrequent.
DR. ROBERT F. WILSON Detroit, Mich.
I would like to emphasize a few points concerning the use of respirators in patients with sepsis, trauma, or shock. Ventilator assistance with a respirator for such patients must be done prophylactically. If ventilator assistance is not begun until there is clinical evidence of respiratory failure, the mortality rate may be increased tenfold. Respirators should probably be used if the clinical situation even suggests only that the patient might need respirator therapy. When in doubt we have followed the patient's blood gases; if the shunting in the lung is rising or exceeds 40 per cent, or if the A-ADO, on room air exceeds 55 mm. Hg, the patient should be put on a respirator. Respiratory failure must be treated by maintaining maximal alveolar inflation and by dehydrating the patient vigorously. Although we try to use the highest tidal volumes possible, preferable 12 to 15 ml. per kilogram, we try to keep the inflation pressures below 40 to 45 ern. of water. If the inflation pressures are higher, the risk of pneumothorax is greatly increased. This tidal volume can be reduced somewhat if adequate alveolar ventilation is maintained with a PEEP of 5 to 8 em. of water. It is important to check the inflation pressures as the tidal volume is being increased. When the inflation pressures begin to rise disproportionate to the tidal volume, or exceed 40 em. of water, you may be starting to exceed the elastic limit of the lungs and the tidal volume should be reduced. If high inflation pressure is needed to overcome an increased airway resistance, bronchodilators should be given; unfortunately, clinical signs of increased airway resistance are usually not apparent until it is two to four times normal. It is also important to use the lowest concentration of inspired oxygen possible. We try to keep the inhaled oxygen concentration at 40 per cent or lower and try to keep the arterial Po, at 80 to 90 mm, Hg, If we have to use 70 per cent or more oxygen, we are satisfied with an arterial Po, of 60 mm. Hg or higher. It is extremely important to dehydrate these patients as much as possible, keeping the hemoglobin level above 12.5 Grn. per cent and the albumin levels above 3.5 Gm. per cent by using digitalis and diuretics aggressively. Secretions in the smaller bronchi must be removed frequently, preferably with a fiberoptic scope. Secretions beget secretions. If the lungs are kept clear, it will be less likely that the high inflation pressures which can cause pneumothoraces will be needed. Moving the patient up and down and from sideto-side in bed is extremely important. This in itself can reduce inflation pressures by 5 to 10 ern, water or more.
The Journal of
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Steier et aI.
Thoracic and Cardiovascular Surgery
By using all these techniques, we can correct virtually all respiratory failure unless there is concomitant sepsis; accordingly, pus must be drained and antibiotics used aggressively. With penetrating lung injuries, we have found that even if the patient does not have a pneumothorax, the surgeon should probably insert a chest tube prior to any general anesthetic, especially if there is any subcutaneous air. If we have to put in a subclavian catheter, we prefer to have the patient off the respirator or using low inflation pressures at the time of insertion. A pneumothorax is usually a serious problem only if the diagnosis is delayed. Shift of the trachea and subcutaneous emphysema are both late signs. If someone is watching the inflation pressures and the central venous pressures closely, the diagnosis can generally be made much earlier. DR. ARTHUR N. THOMAS San Francisco, Calif.
Of trauma patients at San Francisco General Hospital who require prolonged ventilation and PEEP, 20 to 30 per cent develop pneumothorax. After pneumothorax has been controlled by tube thoracostomy, we have noted that pulmonary function does not immediately return to the level that pre-existed this complication. In some of these cases, cardiovascular or cerebral deterioration may also occur. The possibility that arterial air embolism may playa role in clinical deterioration after expansion rupture of the lung was investigated in some dog experiments. Dogs with an open chest and closed, controlled ventilation were subjected to expansion rupture of the lungs. Often, intravascular air was recovered from the left side of the heart. Perhaps Dr. Steier would comment on the possible role of air embolism as a cause for the high morbidity and mortality rates in patients with expansion rupture of the lungs. DR. C. FREDERICK KITTLE Evanston, Ill.
I wish to point out an additional factor of importance in causing pneumothorax in patients on ventilatory support. This occurs when we set the machine for the sigh maneuver. In one way or another this adds 400 or 500 c.c, of air when the sigh takes place. Thus, at this particular moment, the inspiratory pressure will be higher than usual. I would like to ask the authors whether in selected cases they think there is an indication for prophylactic tube thoracostomy. We have had such an experience in 2 patients. One patient had heroin-induced pulmonary edema and required an inspiratory pressure between 50 and 55 cm. of
water. After discussion, we electively placed bilateral intrapleural tubes so that we would not be concerned at one time or another with the problem of a pneumothorax. The second patient had been on ventilatory support for several days. He was middle aged and had chronic obstructive lung disease. After he developed a pneumothorax on one side, we electively placed an intrapleural tube in the other side. Since the incidence of pneumothorax is high in patients on ventilatory support, should we not consider prophylactic tube thoracostomies in selected instances? DR. NEALON (Closing) I would like to thank the discussers. Certainly, the type of patient we are dealing with is substantially different from those whom Dr. Fleming has seen and possibly those whom the other groups have treated. We are the community hospital for Greenwich Village. Bordering this area is the Bowery. Some of these people, because of long-standing habits and ultimate neglect of themselves, are in very poor general condition before they ever come into the hospital. A large percentage of them have chronic pulmonary disease. They then develop a serious illness and, accordingly, ignore it. When they do present themselves, they are in desperate condition. However, some of these problems are the same. I certainly agree with Dr. Fleming that many of the basic problems that can occur will occur in either group but certainly are more likely to occur in (1) older patients and (2) those with chronic pulmonary disease. . Dr. Hanson, I guess, we don't pay as much attention to our pressure measurements as we might. However, we don't feel this is the important point insofar as these patients are concerned. We pay a great deal of attention to their general condition, their vital signs, and particularly their blood gas measurements. We attempt to adjust their vetilation so as to obtain normal values. If we are unable to maintain normal blood gas oxygen measurements with a ventilating gas containing up to 60 per cent oxygen, we then depend upon PEEP or some other means to elevate the level. We will even accept a lower Po, in the blod, provided there is no evidence of clinical deterioration, rather than raise the concentration of oxygen in the ventilating gas beyond that point. In terms of the care of the patients, we agree with much of what Dr. Wilson recommended. We do make every effort to keep the tracheobronchial tree clear. In instances in which the patient has a problem which involves removing particulate matter from the tracheobronchial tree, we do not think an endotracheal tube is adequate. We think that an endotracheal tube is
Volume 67 Number 1
Pneumothorax
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January, 1974
an adequate means for a limited period of time of moving gas in and out of the tracheobronchial tree, However, if there are pulmonary secretions, we feel the patient then requires a tracheostomy in order to remove the secretions. When we do have a tracheostomy, we do not depend upon endoscopy to handle it further. Dr. Kittle, we have not done tube thoracotomies prophylacti-
cally on such patients but it sounds worthwhile. Finally, we have not seen air embolism as a complication. We want to emphasize that the majority of pneumothoraces that arise during continuous ventilation are tension pneumothoraces which require immediate decompression.
Michael Steier, M.D. (by invitation), Nathaniel Ching, M.D. (by invitation), Enrique Bonfils Roberts, M.D. (by invitation), and Thomas F. Nealon, Jr., M.D., New York, N. Y.
DUring the past four years the yearly incidence of pneumothorax has increased forty-five per cent at our institution. Analysis of our cases reveals that the increased incidence is primarily due to the use of techniques developed to improve the resuscitation and care of critically ill patients. These include external cardiac massage, subclavian venotomy for monitoring central venous pressure or intravenous feeding, and continuous ventilatory support. It is the purpose of this report to examine those factors which may contribute to its occurrence during continuous ventilatory support and to emphasize the importance of early recognition and prompt treatment of pneumothorax occurring during continuous ventilatory support. Materials and methods
All diagnosed cases of pneumothorax in St. Vincent's Hospital and Medical Center of New York City in the period from Jan. 1, 1965, to Dec. 31, 1972, were reviewed. From the Departments of Surgery, SI. Vincent's Hospital and Medical Center of New York, 153 West 11th Street, New York, N. Y. 10011, and New York University School of Medicine, New York, N. Y. Read at the Fifty-third Annual Meeting of The American Association for Thoracic Surgery, Dallas, Texas, April 16, 17, and 18, 1973.
The institution is a 900 bed general hospital located in the heart of Greenwich Village and serves a varied general population in lower Manhattan. The occurrences include a hospital-wide survey primarily from the separate medical and surgical intensive care units. The surgical service is responsible for closed-chest tube thoracostomies. In the period from Jan. 1, 1965, to Dec. 31, 1972, 544 patients sustained a pneumothorax. The etiology was identified as follows: (l) iatrogenic, 209 cases; (2) traumatic, 179 cases; (3) spontaneous, 150 cases; and (4) infectious, 6 cases. The yearly incidence of traumatic and spontaneous pneumothorax has remained fairly constant; however, iatrogenic pneumothorax has increased precipitously during the last 5 years from 12 cases in 1968 to 54 cases in 1972 (Fig. 1). The iatrogenic category included ( I ) external cardiac massage, 62 cases; (2) the percutaneous subclavian route for canal cannulation, 60 cases; (3) continuous ventilatory support, 74 cases; and (4) miscellaneous, 13 cases. Of the patients who developed pneumothorax during continuous ventilatory support there were 44 males and 30 females. The mean age of the group was 68 years, ranging from 1 day to 82 years. The primary 1 7
18
The Journol of Thorocic ond Cordiovosculor Surgery
Steier et al.
.-.
60
IATROGENIC
./
C/)
w
./
40
C/)
o 20 0
0/°
f
..-.~-.-.-~-~/ .
__e--
0-°"
SPONTANEOUS TRAUMATIC
1965 1966 1967 1968 1969 1970 1971 1972
YEAR Fig. 1. The incidence of pneumothorax, 1965 to 1972, is classified as to etiology (544 cases). There has been a precipitous increase in iatrogenic pneumothorax from 12 cases in 1968 to 54 cases in 1972. The incidence of spontaneous and traumatic pneumothorax has remained constant.
Table I. Patients developing pneumothorax during continuous ventilation Primary diagnosis
Surgical Nonthoracic Thoracic Medical Sepsis Cardiovascular Chronic respiratory insufficiency Aspiration Idiopathic Total
No. of patients
31 3 16 9 7 6 2 74
illnesses of these patients are listed in Table I. Thirty-four surgical patients developed acute respiratory insufficiency in the postoperative period. The incidence of nonthoracic surgical cases reflects the large number of seriously ill patients undergoing general surgical procedures at our hospital. Of the 40 medical patients, there were only 7 in whom chronic respiratory insufficiency was the primary diagnosis. In the remaining 33, acute respiratory failure was secondary to sepsis (16 cases), cardiovascular shock (9 cases), and aspiration (6 cases). The cause in 2 cases was not identified. In the majority of those with sepsis, the condition was caused by infection with gram-negative organisms. Acute respiratory failure was defined as inability of the patient to maintain normal
blood gas values without overworking. Access to the upper airway was obtained by endotracheal intubation in 49 cases and by tracheostomy in 25 cases. Pneumothorax occurred on the right side in 36 instances, on the left in 33, and bilaterally in 5 cases. The percentage pneumothorax varied from 10 to 100, with a mean of 80 per cent in those who had a chest x-ray before tube thoracostomy. A tension component, as evidenced by a shift of the mediastinum, was detected by chest roentgenogram or by clinical examination in 71 of the 74 cases. Pneumothorax occurred between the first and twelfth days of continuous ventilatory support, with 75 per cent developing between the second and fourth days. The diagnosis of pneumothorax was made on a clinical basis in 45 cases. The clinical presentation was sudden and dramatic in onset. Subcutaneous emphysema was recognized in all 74 cases. It presented initially in the supraclavicular fossa and cervical regions and often rapidly extended to the face, thorax, and even to the scrotum. Tachycardia as high as 150 beats per minute (70 cases), diminished breath sounds (65 cases), hyperresonance (63 cases) , and pressure below 90 mm. Hg (60 cases) occurred in most instances (Fig. 2). Arterial blood gas results were available on 51 patients after the onset of pneumothorax and prior to closed-chest tube thoracostomy. The mean Pao~ of this group was 47 mm. Hg, and the mean Paco~ was 62 mm.Hg. Results
Twelve of the 74 patients died as a result of this problem, for an over-all mortality rate of 16 per cent. Treatment was delayed between 30 minutes and 8 hours in 29 patients during which the diagnosis of pneumothorax awaited confirmation by chest roentgenogram. Nine of these died of pneumothorax, for an incidence of 31 per cent as compared to a mortality rate of 7 per cent in the group of 45 patients who had immediate treatment based on clinical diagnosis.
Volume 67
Pneumothorax
Number 1
19
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Tachycardia Diminished B.S. Hyperresonance Hypotension Cyanosis Diaphoresis Tracheal Deviation Asynchronous Motion Pulse Irregularity
I
I
I
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I
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Fig. 2. Clinical presentation of pneumothorax complicating ventilatory support (74 cases). Subcutaneous emphysema was recognized in all 74 cases (100 per cent). B.s., Breath sounds.
Contributing factors The following factors seem to influence the incidence of pneumothorax during continuous ventilatory support. Volume-cycled ventilator. A volumecycled ventilator was employed in 70 cases and a pressure-cycled ventilator in 4. Approximately 600 patients a year receive ventilatory assistance for longer than 24 hours at our hospital. One third of these require volume-controlled ventilators. Approximately 7 per cent of patients receiving volume-regulated ventilatory support develop pneumothorax, whereas only 0.25 per cent of those receiving pressure-regulated ventilatory support develop the condition. Chronic obstructive lung disease. Sixtytwo patients had clinical, roentgenographic, or pulmonary function studies indicative of pre-existing chronic lung disease. Symptoms of chronic cough, purulent and copious expectoration, exertional dyspnea, and cor pulmonale were present to some degree in all 62 patients. Roentgenographic studies demonstrated local or generalized increased depth of the retrosternal air spaces, oligemia, localized or diffuse bullae, and in more severe cases prominent hilar pulmonary arteries and cardiac enlargement. Twenty-five of the 62 patients had recent pulmonary function tests available for analysis. These demonstrated decreased forced expiratory volume 1.0, increased total lung capacity and functional residual capacity, decreased vital capacity, and increased
residual volume-total lung capacity in ranges compatible with emphysematous disease. Excessive tidal volumes. When initiating continuous ventilatory support, we usually begin with a tidal volume in the range of 10 c.c. per kilogram of body weight. This is then adjusted to effect normal blood Pco, levels. At the time that pneumothorax occurred, the mean tidal volume was available in 62 cases and was 18 c.c. per kilogram, with a range of between 14 and 21 c.c. per kilogram. Increased end-inspiratory pressure. The pressure reached at the peak of inspiration is a reflection of lung compliance. In 48 instances the end-inspiratory pressure was known prior to the development of pneumothorax. In this group of patients the mean end-inspiratory pressure was 46 em. of water with a range between 38 and 55 em. of water. Positive end-expiratory pressure (PEEP). Approximately 10 per cent of our patients with acute respiratory failure failed to respond to standard methods of continuous ventilatory support. Specifically, these patients were unable to maintain a Paoz above 60 mm. Hg while being ventilated with a gaseous mixture containing 60 per cent oxygen. Rather than risk the danger of oxygen toxicity by increasing the concentration of oxygen above 60 per cent, we have preferred to utilize PEEP.! This modality was used in 14 of the 74 cases. Ten per cent of our patients receiving volume-
20
Steier et
The Journal af Thoracic and Cardiavascular
at.
Surgery
regulated ventilatory support (20 patients per year) require PEEP, and, each year, 3.5 or 17 per cent of these patients develop pneumothorax. We customarily initiate PEEP with low pressures in the range of 2 to 3 em. of water and gradually increase the pressure as required to maintain a Pao2 between 70 and 80 mm. Hg with relatively low concentrations of inspired oxygen. In the 14 patients who were receiving PEEP at the time of pneumothorax occurrence, the mean endexpiratory pressure was 12 cm. of water with a range between 8 and 17 em. of water. Percutaneous subclavian venipuncture during pressure breathing. In addition to these 74 patients, 9 others developed pneumothorax as a percutaneous subclavian catheter was being inserted while ventilatory assistance continued. The heightened intrathoracic pressure substantially increases the likelihood of puncturing the lung, and assistance should be stopped during venotomy. Discussion As is often the case, new techniques developed to improve medical care contribute their own series of complications. Fleming and Bowen- reported that 15 per cent of their ventilated patients developed pneumothorax, primarily as a result of infection. Pontoppidan and associates" have stressed that tension pneumothorax occurs with greater frequency in patients with chronic obstructive lung disease who require mechanical ventilation because of acute respiratory failure. Mediastinal emphysema and/or pneumothorax has been reported to occur with the use of continuous positivepressure ventilation.v" The purpose of this report is not to discourage the use of ventilatory support but to alert physicians who use the technique to the occurrence of pneumothorax, the importance of early diagnosis, and means of preventing the complication. The presence of the associated factors should increase the awareness of the possibility of pneumothorax. The development of pneumothorax in a patient ventilated with positive-pressure
techniques is an acute surgical emergency which demands immediate decompression. The diagnosis should be made on a clinical basis. The patient on ventilatory support who develops a sudden extreme change in his pulmonary or cardiovascular status is a prime suspect. All 74 patients with pneumothorax developed subcutaneous emphysema. Our results are a clear demonstration that any delay in diagnosis contributes substantially to the possibility of death. It is our practice to use volume-controlled respirators on more seriously ill patients. This may account for some increase in deaths, but the main factor seems to be related to the delay in providing proper treatment.
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REFERENCES Ashbaugh, D. G., Petty, T. L., Bigelow, D. B., and Harris, T. M.: Continuous Positive-Pressure Breathing (CPPB) in Adult Respiratory Distress Syndrome, I. THORAC. CARDIOVASC. SURG. 57: 31, 1969. Fleming, W. H., and Bowen, I. c.: Early Complications of Long-Term Respiratory Support, 1. THORAC. CARDIOVASC. SURG. 64: 729, 1972. Pontoppidan, H., Geffin, B., and Lowenstein, E.: Acute Respiratory Failure in the Adult (Second of Three Parts), N. EngI. I. Med. 287: 743, 1972. Kumar, A., Falke, K. J., and Geffin, B.: Continuous Positive Ventilation in Acute Respiratory Failure, N. EngI. I. Med. 283: 1430, 1970. Ashbaugh, D. G., and Petty, T. L.: Positive End-Expiratory Pressure: Physiology, Indications, and Contraindications, I. THORAC. CARDIOVASC. SURG. 65: 165, 1973. Kolff, I., Webb, 1. A., Jr., and Loop, F. D.: Electrical Analogues of Methods for Continuous Positive-Pressure Ventilation. I. THORAC. CARDIOVASC. SURG. 64: 586, 1972. Pontoppidan, H., Geffin, B., and Lowenstein, E.: Acute Respiratory Failure in the Adult (Third of Three Parts), N. EngI. J. Med. 287: 799, 1972. Sugurman, H. I., Rogers, R. M., and Miller, L. D.: Positive End-Expiratory Pressure (PEEP): Indications and Physiologic Considerations, Chest 62: 865, 1972.
Discussion DR. WILLIAM H. FLEMING Atlanta, Ga.
I would like to compliment Dr. Steier on an excellent study. I find it interesting to see the same problems appearing in civilian practice that we first encountered in Vietnam. Part of that work
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was presented before this Association last year. There are several significant differences between this civilian work and our Vietnam work. It will be important for all of us as we translate military experience to civilian practice to look for these differences. The greatest difference I notice here is in the average age. Whereas our patients averaged 20 years, Dr. Steier's averaged 68 years of age. The military personnel, of course, were free of chronic lung disease as an antecedent problem, whereas it was very common in Dr. Steier's patients. [Slide] In the whole spectrum of complications of pulmonary ventilatory support, incidence of secondary pneumothorax was 19 of 128 respirator patients followed prospectively. [Slide] In contrast to Dr. Steier's patients, 17 of our 19 patients seemed to have pulmonary sepsis as an etiologic factor, usually with necrotizing organisms. [Slide] Only 2 of our 19 patients had peak airway pressures over 40 em. of water. We did not find that pneumothorax correlated with volume rather than pressure respirators, since our incidence was the same as the incidence of patient days on each type of respirator. DR. HANSON Syracuse, N. Y.
This subject is of genuine concern and merits discussion. At the Upstate Medical Center, we have been as aggressive as the authors with our therapy, but our experience is different. Using positive end-expiratory pressure (PEEP) and continuous positive-pressure breathing (CPPB) in over 200 cases postoperatively and in more than 50 patients with aspiration, we have observed only three instances of pneumothorax and five of pneumomediastinum. In none of the latter did we see subcutaneous emphysema. We think that there are several things that account for this. First, the expiratory port must be large, 2 to 3 cm. in size, or the usual size of expiratory tubing on a ventilator. Second, the measurements of airway pressure must be accurate. Adequate gauges properly placed in the system must be used in order to gain an accurate measurement of tracheal pressure. Certain volume-cycled respirators have gauges much to distal on the expiratory line to give accurate airway pressure measurements. Finally, the likelihood of a rupture when alveolar pressure is greater than 50 em. must be emphasized. Coughing is particularly dangerous in this regard, as is breathing out of phase with the ventilator. It is very important to keep the patient sedated and paralyzed or to maintain hypocapnia to remove the respiratory drive. We feel that if these guidelines are followed, the incidence of pneumothorax will be infrequent.
DR. ROBERT F. WILSON Detroit, Mich.
I would like to emphasize a few points concerning the use of respirators in patients with sepsis, trauma, or shock. Ventilator assistance with a respirator for such patients must be done prophylactically. If ventilator assistance is not begun until there is clinical evidence of respiratory failure, the mortality rate may be increased tenfold. Respirators should probably be used if the clinical situation even suggests only that the patient might need respirator therapy. When in doubt we have followed the patient's blood gases; if the shunting in the lung is rising or exceeds 40 per cent, or if the A-ADO, on room air exceeds 55 mm. Hg, the patient should be put on a respirator. Respiratory failure must be treated by maintaining maximal alveolar inflation and by dehydrating the patient vigorously. Although we try to use the highest tidal volumes possible, preferable 12 to 15 ml. per kilogram, we try to keep the inflation pressures below 40 to 45 ern. of water. If the inflation pressures are higher, the risk of pneumothorax is greatly increased. This tidal volume can be reduced somewhat if adequate alveolar ventilation is maintained with a PEEP of 5 to 8 em. of water. It is important to check the inflation pressures as the tidal volume is being increased. When the inflation pressures begin to rise disproportionate to the tidal volume, or exceed 40 em. of water, you may be starting to exceed the elastic limit of the lungs and the tidal volume should be reduced. If high inflation pressure is needed to overcome an increased airway resistance, bronchodilators should be given; unfortunately, clinical signs of increased airway resistance are usually not apparent until it is two to four times normal. It is also important to use the lowest concentration of inspired oxygen possible. We try to keep the inhaled oxygen concentration at 40 per cent or lower and try to keep the arterial Po, at 80 to 90 mm, Hg, If we have to use 70 per cent or more oxygen, we are satisfied with an arterial Po, of 60 mm. Hg or higher. It is extremely important to dehydrate these patients as much as possible, keeping the hemoglobin level above 12.5 Grn. per cent and the albumin levels above 3.5 Gm. per cent by using digitalis and diuretics aggressively. Secretions in the smaller bronchi must be removed frequently, preferably with a fiberoptic scope. Secretions beget secretions. If the lungs are kept clear, it will be less likely that the high inflation pressures which can cause pneumothoraces will be needed. Moving the patient up and down and from sideto-side in bed is extremely important. This in itself can reduce inflation pressures by 5 to 10 ern, water or more.
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Thoracic and Cardiovascular Surgery
By using all these techniques, we can correct virtually all respiratory failure unless there is concomitant sepsis; accordingly, pus must be drained and antibiotics used aggressively. With penetrating lung injuries, we have found that even if the patient does not have a pneumothorax, the surgeon should probably insert a chest tube prior to any general anesthetic, especially if there is any subcutaneous air. If we have to put in a subclavian catheter, we prefer to have the patient off the respirator or using low inflation pressures at the time of insertion. A pneumothorax is usually a serious problem only if the diagnosis is delayed. Shift of the trachea and subcutaneous emphysema are both late signs. If someone is watching the inflation pressures and the central venous pressures closely, the diagnosis can generally be made much earlier. DR. ARTHUR N. THOMAS San Francisco, Calif.
Of trauma patients at San Francisco General Hospital who require prolonged ventilation and PEEP, 20 to 30 per cent develop pneumothorax. After pneumothorax has been controlled by tube thoracostomy, we have noted that pulmonary function does not immediately return to the level that pre-existed this complication. In some of these cases, cardiovascular or cerebral deterioration may also occur. The possibility that arterial air embolism may playa role in clinical deterioration after expansion rupture of the lung was investigated in some dog experiments. Dogs with an open chest and closed, controlled ventilation were subjected to expansion rupture of the lungs. Often, intravascular air was recovered from the left side of the heart. Perhaps Dr. Steier would comment on the possible role of air embolism as a cause for the high morbidity and mortality rates in patients with expansion rupture of the lungs. DR. C. FREDERICK KITTLE Evanston, Ill.
I wish to point out an additional factor of importance in causing pneumothorax in patients on ventilatory support. This occurs when we set the machine for the sigh maneuver. In one way or another this adds 400 or 500 c.c, of air when the sigh takes place. Thus, at this particular moment, the inspiratory pressure will be higher than usual. I would like to ask the authors whether in selected cases they think there is an indication for prophylactic tube thoracostomy. We have had such an experience in 2 patients. One patient had heroin-induced pulmonary edema and required an inspiratory pressure between 50 and 55 cm. of
water. After discussion, we electively placed bilateral intrapleural tubes so that we would not be concerned at one time or another with the problem of a pneumothorax. The second patient had been on ventilatory support for several days. He was middle aged and had chronic obstructive lung disease. After he developed a pneumothorax on one side, we electively placed an intrapleural tube in the other side. Since the incidence of pneumothorax is high in patients on ventilatory support, should we not consider prophylactic tube thoracostomies in selected instances? DR. NEALON (Closing) I would like to thank the discussers. Certainly, the type of patient we are dealing with is substantially different from those whom Dr. Fleming has seen and possibly those whom the other groups have treated. We are the community hospital for Greenwich Village. Bordering this area is the Bowery. Some of these people, because of long-standing habits and ultimate neglect of themselves, are in very poor general condition before they ever come into the hospital. A large percentage of them have chronic pulmonary disease. They then develop a serious illness and, accordingly, ignore it. When they do present themselves, they are in desperate condition. However, some of these problems are the same. I certainly agree with Dr. Fleming that many of the basic problems that can occur will occur in either group but certainly are more likely to occur in (1) older patients and (2) those with chronic pulmonary disease. . Dr. Hanson, I guess, we don't pay as much attention to our pressure measurements as we might. However, we don't feel this is the important point insofar as these patients are concerned. We pay a great deal of attention to their general condition, their vital signs, and particularly their blood gas measurements. We attempt to adjust their vetilation so as to obtain normal values. If we are unable to maintain normal blood gas oxygen measurements with a ventilating gas containing up to 60 per cent oxygen, we then depend upon PEEP or some other means to elevate the level. We will even accept a lower Po, in the blod, provided there is no evidence of clinical deterioration, rather than raise the concentration of oxygen in the ventilating gas beyond that point. In terms of the care of the patients, we agree with much of what Dr. Wilson recommended. We do make every effort to keep the tracheobronchial tree clear. In instances in which the patient has a problem which involves removing particulate matter from the tracheobronchial tree, we do not think an endotracheal tube is adequate. We think that an endotracheal tube is
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an adequate means for a limited period of time of moving gas in and out of the tracheobronchial tree, However, if there are pulmonary secretions, we feel the patient then requires a tracheostomy in order to remove the secretions. When we do have a tracheostomy, we do not depend upon endoscopy to handle it further. Dr. Kittle, we have not done tube thoracotomies prophylacti-
cally on such patients but it sounds worthwhile. Finally, we have not seen air embolism as a complication. We want to emphasize that the majority of pneumothoraces that arise during continuous ventilation are tension pneumothoraces which require immediate decompression.