Tension Pneumothorax Associated With Hyperbaric Oxygen Therapy DANIEL G. MURPHY, MD,* EDWARD P. SLOAN, MD,t RAYMOND G. HART, MD,+ KRIS NARASIMHAN, MD,5 RONALD S. BARRECA, MD5 The authors present three patients who developed a tension pneumothorax while receiving emergent hyperbaric oxygen therapy for acute carbon monoxide poisoning. Each patient was intubated and received closed chest compressions for cardiac arrest prior to hyperbaric oxygenation. Despite the apparent absence of pneumothorax prior to hyperbaric therapy, tension pneumothorax was detected soon after decompression. These cases illustrate the need for vigilance in detecting and addressing pneumothorax prior to hyperbaric decompression in obtunded patients. Serial physical examinations, arterial blood gas determinations, properly positioned chest radiographs, and a high index of suspicion for pneumothorax in the setting of emergent hyperbaric therapy are recommended. (Am J Emerg Med 1991;9:176-179. Copyright 0 1991 by W.B. Saunders Company)
Tension pneumothorax development during hyperbaric chamber decompression is a recognized yet rarely reported complication.‘,’ We encountered three tension pneumothoraces over a IO-year period (two cases within 6 weeks) among 297 patients who received emergent hyperbaric oxygen therapy (HBOT) for acute carbon monoxide poisoning.? Each episode occurred in a multiplace hyperbaric chamber (custom built by the York Division, Borg-Warner Industries, York, PA) located in a university-afftliated teaching hospital in suburban Chicago, IL. A respiratory therapist trained in HBOT externally controlled the hyperbaric dives, which were completed according to standard Navy dive tab1es.4 Each patient was ventilated during HBOT by a Mark 7 pressure-cycled ventilator (Bird Inc, Palm Springs, CA) and was accompanied by a critical care nurse and respiratory therapist, who were fully equipped to provide advanced life support and who were in communication with an emergency physician. The ventilator pressure settings were determined by the adequacy of chest expansions, breath sounds. and serial arterial blood gas analyses. During descent and ascent, the patient was manually ventilated with an ambu-bag for 5 minutes every half hour.
PRESENTATION
OF THREE CASES
Case Report 1 A 26year-old woman with a history of depression was found in cardiac arrest inside an enclosed garage near a running automobile (I l:OO). Cardiopulmonary resuscitation (CPR) was initiated and the
patient received epinephrine. bicarbonate. naloxone. oxygen, and ventilations by bag-valve-mask. The patient was intubated and dopamine and lidocaine drips were initiated at the closest emergency department (ED). where a blood pressure of 130/82 mm Hg was achieved (I I :37). The patient had fixed and dilated pupils, flaccid paralysis. and nonreactive oculocephalic, oculovestibular. and cornea1 reflexes. An arterial blood gas (ABG) showed pH. 7.34; Pco,. 31: PO,. 392: bicarbonate. 16; 0, saturation. 100%~.Clear breath sounds were auscultated bilaterally and a supine portable chest radiograph was unremarkable (12:OO). The carboxyhemoglobin level was 50%‘. interhospital transfer by ambulance to the ED of the hospital equipped with the hyperbaric oxygen chamber was performed without complication. On arrival. the patient was in sinus tachycardia with a blood pressure Il2/76 mm Hg and pulse rate of 124 beatsimin (1390). A second portable chest roentgenogram was normal. Hyperbaric compression was initiated. Fifteen minutes into the dive. the blood pressure was noted to be 188/138 mm Hg, whereupon the dopamine drip was discontinued (13:45). One hour later. at 3 atm pressure, “distant” breath sounds were noted on the left side by the critical care nurse. The blood pressure decreased to 90/76 mm Hg. The dopamine infusion was resumed and no other orders were given. At completion of the dive tlS:38). the blood pressure was 1261100 mm Hg, with no improvement in neurologic status. The patient was transferred to the intensive care unit (ICU), where decreased left-sided breath sounds were confirmed and an ABG read pH 7.53: PO,, 66: Pco,, 32. A portable anteroposterior CAP) chest roentgenogram showed a left tension pneumothorax (16:15). The endotracheal tube was in proper position. An ABG drawn after thoracostomy showed a PO? of 205. An electroencephalogram the next day was isoelectric and the patient was declared brain dead. The family consented to discontinue all life-support and the patient died. Case Report 2
From the *Department of Emergency Medicine and the tDivision of Trauma Suraerv. Cook Countv Hosoital, Chicaao. iL, the *Department of Emergency Medicine, Humana Hospsal Southwest, Louisville, KY, and the SDivision of Emergency Medicine, Lutheran General Hospital Hyperbaric Facility, Park Ridge, IL. Manuscript received July 11, 1990; revision accepted October 10, 1990. Address reprint requests to Dr Murphy, Department of Emergency Medicine, Cook County Hospital, 1900 W Polk St, 10th Floor, Chicago, IL 60612. Key Words: Hyperbaric oxygen therapy, tension pneumothorax. Copyright 0 1991 by W.B. Saunders Company 07356757/91/0902-0020$5.00/O 176
A 72-year-old woman was found in cardiac arrest on the floor of her smoke-filled living room during a tire. The patient was intubated, CPR was initiated. and atropine (2 mg), epinephrine (3 mg), bicarbonate (50 mEq), and oxygen were administered, yielding a pulse and blood pressure (0196). ED evaluation (01: I I) noted a comatose elderly woman in atriai fibrillation with a pulse rate of 100 beatsimin. blood pressure of 128/52 mm Hg, fixed and dilated pupils, and flaccid paralysis. The patient then sustained cardiac arrest funspecified rhythm) and was resuscitated to atriai fibrillation with a blood pressure of 140/80 mm Hg after receiving epinephrine (I mg). atropine (I mg). and bicarbonate (100 mEq). A dopamine drip was started and three attempts to insert a right internal jugular venous catheter were unsuccessful. The carboxyhemogiobin level was 51%. Transfer by ground transport to the HBOT facility required 35
MURPHY
ET AL n TENSION
PNEUMOTHORAX
177
AND HBOT
minutes and occurred without incident. Large amounts of black sooty aspirate were suctioned from the endotracheal tube. Lung sounds were equal, with coarse, bilateral wheezing. The neck was normal with a midline trachea. No bums were noted. An ABG read pH, 7.34; Pco,, 20; PO,, 316; bicarbonate. 11; 0, saturation, 100%. A portable supine chest roentgenogram was normal. After the initiation of HBOT, diminished left-sided breath sounds were noted and reported by the critical care nurse (02:30). No intervention was ordered. One hour into the dive, the right side of the patient’s neck was observed to be swollen with ecchymosis spreading anteriorly. The vital signs remained stable throughout the dive. With completion of the dive (0359) and decompression to the surface, the blood pressure immediately fell to 50 mm Hg systolic. The dopamine infusion rate was increased. On return to the ED, there was cyanosis of the head and neck, no blood pressure. no pulse, absent left-sided breath sounds, and subcutaneous emphysema of the neck. The abdomen was distended. CPR was initiated and a 16 gauge needle was inserted into the left second intercostal space at the anterior axillary line (04: 11). Air was noted to evacuate through the needle and the patient’s blood pressure subsequently stabilized at 130170 mm Hg. A chest tube was inserted and the patient was transferred to the KU. On the second hospital day the patient was diagnosed as brain dead and died after discontinuance of lifesupport.
Case Report 3 A 17-year-old girl with a history of asthma was found in cardiac arrest inside a running automobile in an enclosed garage (1516). After intubation and the initiation of CPR. course ventricular fibril-
lation was noted and the patient was defibrillated to sinus tachycardia after receiving epinephrine (5 mg) and atropine (2 mg). Bicarbonate (150 mEq) was administered and dopamine and dobutamine infusions were initiated in the ED (1550). The patient was comatose and areflexic, with fixed and dilated pupils, a lactate level of 12.3, and a carboxyhemoglobin of 51%. The patient was transferred and arrived at the HBOT facility with a blood pressure of 70 mm Hg systolic and a heart rate of 108 beats/min (16:59). The heart and lung examination results were normal. The pupils were fixed at 6 mm and the patient had no response to painful stimuli. A portable supine chest radiograph noted the tip of the endotracheal tube to be in the proximal portion of the right mainstem bronchus, which was corrected prior to HBOT. The patient sustained pulseless ventricular tachycardia 5 minutes into the dive and was immediately cardioverted by the critical care nurse to sinus tachycardia with a blood pressure of 98 mm Hg systolic (17:25). No change in pulmonary examination was noted. An ABG drawn when 3 atm was achieved was pH 7.44; Pcq, 18; PO,, 816; 0: saturation, 100% (1815). ‘Swelling and subcutaneous air” were noted around the site of an external jugular intravenous line. During the remainder of the dive, the dopamine and dobutamine infusions were periodically increased to maintain a systolic blood pressure that fluctuated between 60 and 90 mm Hg. There was no improvement in neurological status (19:30). The patient arrived in the KU with a blood pressure of 78 mm Hg systolic and heart rate of 130 beats/min. Physical examination noted decreased chest wall motion and decreased breath sounds on the right side (19:45). The abdomen was distended. The fullness had increased at the site of the right external jugular intravenous line. A portable chest roentgenogram (Fig. 1A) noted a tension pneumo-
FIGURE 1. Case 3. Supine AP chest radiographs showing (A) tension pneumothorax same patient after chest tube placement, with the “double diaphragm” sign.
discovered soon after hyperbaric oxygen therapy; (B)
AMERICANJOURNAL OF EMERGENCY MEDICINEn Volume 9, Number 2 n March 1991
178
thorax with a shift of the mediastinum to the left. Right-sided rib fractures were also noted on this chest roentgenogram. A chest tube was placed and the systolic blood pressure immediately improved to 140 mm Hg. The patient was pronounced brain dead on the next day and died after discontinuing life-support.
DISCUSSION Hyperbaric oxygen therapy (HBOT) is recommended for patients who sustain exposures to carbon monoxide associated with loss of consciousness, abnormal psychometric examinations, seizures, chest pain, high carboxyhemoglobin levels, electrocardiographic abnormalities, persistent acidosis, or persistent milder symptoms, such as headache, despite 100% 0, therapy.“’ HBOT reduces the half-life of carboxyhemoglobin to less than 30 minutes at 3 atm.5.x Patients who are severely poisoned with carbon monoxide frequently require intubation, positive pressure ventilation, chest compressions, or central venous catheterization during resuscitation,3 interventions that are all associated with the risk of iatrogenic pneumothorax.‘-‘* If air becomes trapped in the intrapleuraf space or alveoli distal to an outflow obstruction during hyperbaric compression (descent) or at depth, it will expand during decompression (ascent) accord-
‘Qu
3At mospheres
FIGURE 2. Mechanism for the development mothorax during hyperbaric decompression.
of a tension pneu-
ing to Boyle’s Law (Figure 2). The reslllting barotrauma can manifest itself as an arterial air embollJln, pneumomediastinum, pneumoperitoneum. subcutaneous emphysema, or a pneumothorax.‘3-’ Consequently. every attempt must be made to anticipate and detect intrapleural air before a course of hyperbaric oxygenation has been completed and the decision is made to ascend to normobaric conditions. In each of the three cases, important physical findings were overlooked or obscured by the grave clinical status of the patient. Each of the three patients had unilaterally decreased breath sounds or subcutaneous emphysema of the neck that was detected before decompression and that warranted a thoracostomy in the chamber. In one case, wheezing after smoke inhalation was not treated, predisposing the patient to alveolar air trapping. Rib fractures that were possibly caused by chest compressions went undetected in another case until after the tension pneumothorax developed. In light of the number of risk factors for pneumothorax present, a higher index of suspicion was warranted and might have lead to more timely thoracostomies. Diagnostic evaluation immediately before hyperbaric therapy in each case included a negative supine AP portable chest radiograph. While this suggests that there was no intrapleural air. one cannot exclude the possibility of undiagnosed pneumothorax due to poor radiographic technique or reader error. Even a moderate pneumothorax can be missed on a supine portable AP film, because intrapleural air can layer uniformly beneath the anterior thorax in the supine position. If the optimal upright end-expiratory film cannot be taken on an obtunded or intubated patient, alternative techniques can be used. A lateral decubitus chest radiograph, in which the side of the suspected pneumothorax is elevated, or a horizontal beam lateral chest radiograph seeking air beneath the sternum are two techniques which can be used.” Interestingly. one of the secondary signs of pneumothorax that can sometimes be identified on a routine supine AP film. the “double diaphragm. ‘+I’ is seen on a portable chest roentgenogram from case 3 (Figure IB), which shows residual intrapleural air over the right hemidiaphragm that persists despite chest tube placement. These tension pneumothoraces make up 1% of 297 consecutive cases of carbon monoxide toxicity that were treated with emergent HBOT over a IO-year period at our facility.’ Among the subgroup of patients who were comatose and intubated after having received chest compressions for cardiac arrest (n = 23), the incidence of tension pneumothorax was 12%. Consequently, we suggest the prophylactic placement of bilateral chest tubes in comatose, high-risk patients who are to receive HBOT in a monoplace chamber, where the patient cannot be instrumented during the dive. We feel that in this extremely toxic subgroup, chest tubes will not contribute significant morbidity but will eliminate another potential life-threat. In summary, the profoundly toxic clinical condition of a patient should not preclude a proper and deliberate patient assessment prior to the delivery of HBOT. These cases suggest the importance of serial physical examinations, arterial biood gas determinations, and sensitive to the presence of intraplural air chest radiographs when providing emergent HBOT to obtunded patients. Furthermore. needle and chest tube thoracostomies should be performed immediately if any
MURPHY
ET AL n TENSION
PNEUMOTHORAX
AND HBOT
evidence of pneumothorax exists and before hyperbaric compression is allowed to proceed.
179
de-
REFERENCES 1. Unsworth IP: Pulmonary barotrauma in a hyperbaric chamber. Anaesthesia 1973;28:675-678 2. James PB: The detection of pneumothorax by ultrasound. Proceedings of the 6th International Congress on Hyperbaric Medicine. Aberdeen, Scotland, Aberdeen University Press, 1977, 445-448 3. Sloan EP, Murphy DG, Hart R, et al: Complications and protocol considerations in carbon monoxide poisoned patients who require hyperbaric oxygen therapy: Report from a ten year experience. Ann Emerg Med 1989;18:629-634 4. U.S. Navy Standard Air Decompression Tables, in U.S. Navy Diving Manual, Volume 1; NAVSEA 0994-LP-001-9010: 1980, Carson, CA, Best Publishing Co 5. Davis JC: Hyperbaric oxygen therapy. A committee report. Bethesda, MD, Undersea Medical Society, Inc, 1983, pp 6-8 6. Ginsburg R, Roman0 J: Carbon monoxide encephalopathy: Need for appropriate treatment. Am J Psychiatr 1976;3:317320 7. Epstein FB, Eilers MA: Poisoning. In Rosen P, Baker FJ, Barkin RM, et al (eds): Emergency Medicine (ed 2). St Louis, MO, Mosby, 1988, pp 321-361
8. Kindwall EP: Carbon monoxide poisoning treated with hyperbaric oxygen. Respir Ther 1975;5:29-33 9. Haake R, Schlichtig R, Ulstad DR, Henschen RR: Barotrauma. Pathophysiology, risk factors, and prevention. Chest 1987;91:609-613 10. Zwillich CW, Pierson DJ, Creagh CE, et al: Complications of assisted ventilation. A prospective study of 354 consecutive episodes. Am J Med 1974;57:161-169 11. Powner DJ, Holcombe PA, Mello LA: Cardiopulmonary resuscitation-related injuries. Crit Care Med 1984;12:54-55 12. Bjork RJ, Snyder BD, Campion BC, et al: Medical complications of cardiopulmonary arrest. Arch Intern Med 1982; 142:500-504 13. Hamman L: Mediastinal emphysema. JAMA 1945;128:1-6 14. Macklin CC: Pneumothorax with massive collapse from experimental local over-inflation of the lung substance. Can Med Assoc J 1937;4:414-420 15. Macklin MT, Macklin CC: Malignant interstitial emphysema of the lungs and mediastinum as an important occult complication in many respiratory diseases and other conditions: An interpretation of the clinical literature in the light of laboratory experiment. Medicine 1944;23:281-358 16. Goodman LR, Putman CE: The Acute Care Unit: Radiographical Considerations, in Teplick JG, Haskin ME, (eds): Surgical Radiology (ed 2). Philadelphia, PA, Saunders, 1981, pp l-22 17. Cooke DA, Cooke JC: The supine pneumothorax. Ann R Coll Surg Engl 1987;69:130-134
Tension pneumothorax development during hyperbaric chamber decompression is a recognized yet rarely reported complication.‘,’ We encountered three tension pneumothoraces over a IO-year period (two cases within 6 weeks) among 297 patients who received emergent hyperbaric oxygen therapy (HBOT) for acute carbon monoxide poisoning.? Each episode occurred in a multiplace hyperbaric chamber (custom built by the York Division, Borg-Warner Industries, York, PA) located in a university-afftliated teaching hospital in suburban Chicago, IL. A respiratory therapist trained in HBOT externally controlled the hyperbaric dives, which were completed according to standard Navy dive tab1es.4 Each patient was ventilated during HBOT by a Mark 7 pressure-cycled ventilator (Bird Inc, Palm Springs, CA) and was accompanied by a critical care nurse and respiratory therapist, who were fully equipped to provide advanced life support and who were in communication with an emergency physician. The ventilator pressure settings were determined by the adequacy of chest expansions, breath sounds. and serial arterial blood gas analyses. During descent and ascent, the patient was manually ventilated with an ambu-bag for 5 minutes every half hour.
PRESENTATION
OF THREE CASES
Case Report 1 A 26year-old woman with a history of depression was found in cardiac arrest inside an enclosed garage near a running automobile (I l:OO). Cardiopulmonary resuscitation (CPR) was initiated and the
patient received epinephrine. bicarbonate. naloxone. oxygen, and ventilations by bag-valve-mask. The patient was intubated and dopamine and lidocaine drips were initiated at the closest emergency department (ED). where a blood pressure of 130/82 mm Hg was achieved (I I :37). The patient had fixed and dilated pupils, flaccid paralysis. and nonreactive oculocephalic, oculovestibular. and cornea1 reflexes. An arterial blood gas (ABG) showed pH. 7.34; Pco,. 31: PO,. 392: bicarbonate. 16; 0, saturation. 100%~.Clear breath sounds were auscultated bilaterally and a supine portable chest radiograph was unremarkable (12:OO). The carboxyhemoglobin level was 50%‘. interhospital transfer by ambulance to the ED of the hospital equipped with the hyperbaric oxygen chamber was performed without complication. On arrival. the patient was in sinus tachycardia with a blood pressure Il2/76 mm Hg and pulse rate of 124 beatsimin (1390). A second portable chest roentgenogram was normal. Hyperbaric compression was initiated. Fifteen minutes into the dive. the blood pressure was noted to be 188/138 mm Hg, whereupon the dopamine drip was discontinued (13:45). One hour later. at 3 atm pressure, “distant” breath sounds were noted on the left side by the critical care nurse. The blood pressure decreased to 90/76 mm Hg. The dopamine infusion was resumed and no other orders were given. At completion of the dive tlS:38). the blood pressure was 1261100 mm Hg, with no improvement in neurologic status. The patient was transferred to the intensive care unit (ICU), where decreased left-sided breath sounds were confirmed and an ABG read pH 7.53: PO,, 66: Pco,, 32. A portable anteroposterior CAP) chest roentgenogram showed a left tension pneumothorax (16:15). The endotracheal tube was in proper position. An ABG drawn after thoracostomy showed a PO? of 205. An electroencephalogram the next day was isoelectric and the patient was declared brain dead. The family consented to discontinue all life-support and the patient died. Case Report 2
From the *Department of Emergency Medicine and the tDivision of Trauma Suraerv. Cook Countv Hosoital, Chicaao. iL, the *Department of Emergency Medicine, Humana Hospsal Southwest, Louisville, KY, and the SDivision of Emergency Medicine, Lutheran General Hospital Hyperbaric Facility, Park Ridge, IL. Manuscript received July 11, 1990; revision accepted October 10, 1990. Address reprint requests to Dr Murphy, Department of Emergency Medicine, Cook County Hospital, 1900 W Polk St, 10th Floor, Chicago, IL 60612. Key Words: Hyperbaric oxygen therapy, tension pneumothorax. Copyright 0 1991 by W.B. Saunders Company 07356757/91/0902-0020$5.00/O 176
A 72-year-old woman was found in cardiac arrest on the floor of her smoke-filled living room during a tire. The patient was intubated, CPR was initiated. and atropine (2 mg), epinephrine (3 mg), bicarbonate (50 mEq), and oxygen were administered, yielding a pulse and blood pressure (0196). ED evaluation (01: I I) noted a comatose elderly woman in atriai fibrillation with a pulse rate of 100 beatsimin. blood pressure of 128/52 mm Hg, fixed and dilated pupils, and flaccid paralysis. The patient then sustained cardiac arrest funspecified rhythm) and was resuscitated to atriai fibrillation with a blood pressure of 140/80 mm Hg after receiving epinephrine (I mg). atropine (I mg). and bicarbonate (100 mEq). A dopamine drip was started and three attempts to insert a right internal jugular venous catheter were unsuccessful. The carboxyhemogiobin level was 51%. Transfer by ground transport to the HBOT facility required 35
MURPHY
ET AL n TENSION
PNEUMOTHORAX
177
AND HBOT
minutes and occurred without incident. Large amounts of black sooty aspirate were suctioned from the endotracheal tube. Lung sounds were equal, with coarse, bilateral wheezing. The neck was normal with a midline trachea. No bums were noted. An ABG read pH, 7.34; Pco,, 20; PO,, 316; bicarbonate. 11; 0, saturation, 100%. A portable supine chest roentgenogram was normal. After the initiation of HBOT, diminished left-sided breath sounds were noted and reported by the critical care nurse (02:30). No intervention was ordered. One hour into the dive, the right side of the patient’s neck was observed to be swollen with ecchymosis spreading anteriorly. The vital signs remained stable throughout the dive. With completion of the dive (0359) and decompression to the surface, the blood pressure immediately fell to 50 mm Hg systolic. The dopamine infusion rate was increased. On return to the ED, there was cyanosis of the head and neck, no blood pressure. no pulse, absent left-sided breath sounds, and subcutaneous emphysema of the neck. The abdomen was distended. CPR was initiated and a 16 gauge needle was inserted into the left second intercostal space at the anterior axillary line (04: 11). Air was noted to evacuate through the needle and the patient’s blood pressure subsequently stabilized at 130170 mm Hg. A chest tube was inserted and the patient was transferred to the KU. On the second hospital day the patient was diagnosed as brain dead and died after discontinuance of lifesupport.
Case Report 3 A 17-year-old girl with a history of asthma was found in cardiac arrest inside a running automobile in an enclosed garage (1516). After intubation and the initiation of CPR. course ventricular fibril-
lation was noted and the patient was defibrillated to sinus tachycardia after receiving epinephrine (5 mg) and atropine (2 mg). Bicarbonate (150 mEq) was administered and dopamine and dobutamine infusions were initiated in the ED (1550). The patient was comatose and areflexic, with fixed and dilated pupils, a lactate level of 12.3, and a carboxyhemoglobin of 51%. The patient was transferred and arrived at the HBOT facility with a blood pressure of 70 mm Hg systolic and a heart rate of 108 beats/min (16:59). The heart and lung examination results were normal. The pupils were fixed at 6 mm and the patient had no response to painful stimuli. A portable supine chest radiograph noted the tip of the endotracheal tube to be in the proximal portion of the right mainstem bronchus, which was corrected prior to HBOT. The patient sustained pulseless ventricular tachycardia 5 minutes into the dive and was immediately cardioverted by the critical care nurse to sinus tachycardia with a blood pressure of 98 mm Hg systolic (17:25). No change in pulmonary examination was noted. An ABG drawn when 3 atm was achieved was pH 7.44; Pcq, 18; PO,, 816; 0: saturation, 100% (1815). ‘Swelling and subcutaneous air” were noted around the site of an external jugular intravenous line. During the remainder of the dive, the dopamine and dobutamine infusions were periodically increased to maintain a systolic blood pressure that fluctuated between 60 and 90 mm Hg. There was no improvement in neurological status (19:30). The patient arrived in the KU with a blood pressure of 78 mm Hg systolic and heart rate of 130 beats/min. Physical examination noted decreased chest wall motion and decreased breath sounds on the right side (19:45). The abdomen was distended. The fullness had increased at the site of the right external jugular intravenous line. A portable chest roentgenogram (Fig. 1A) noted a tension pneumo-
FIGURE 1. Case 3. Supine AP chest radiographs showing (A) tension pneumothorax same patient after chest tube placement, with the “double diaphragm” sign.
discovered soon after hyperbaric oxygen therapy; (B)
AMERICANJOURNAL OF EMERGENCY MEDICINEn Volume 9, Number 2 n March 1991
178
thorax with a shift of the mediastinum to the left. Right-sided rib fractures were also noted on this chest roentgenogram. A chest tube was placed and the systolic blood pressure immediately improved to 140 mm Hg. The patient was pronounced brain dead on the next day and died after discontinuing life-support.
DISCUSSION Hyperbaric oxygen therapy (HBOT) is recommended for patients who sustain exposures to carbon monoxide associated with loss of consciousness, abnormal psychometric examinations, seizures, chest pain, high carboxyhemoglobin levels, electrocardiographic abnormalities, persistent acidosis, or persistent milder symptoms, such as headache, despite 100% 0, therapy.“’ HBOT reduces the half-life of carboxyhemoglobin to less than 30 minutes at 3 atm.5.x Patients who are severely poisoned with carbon monoxide frequently require intubation, positive pressure ventilation, chest compressions, or central venous catheterization during resuscitation,3 interventions that are all associated with the risk of iatrogenic pneumothorax.‘-‘* If air becomes trapped in the intrapleuraf space or alveoli distal to an outflow obstruction during hyperbaric compression (descent) or at depth, it will expand during decompression (ascent) accord-
‘Qu
3At mospheres
FIGURE 2. Mechanism for the development mothorax during hyperbaric decompression.
of a tension pneu-
ing to Boyle’s Law (Figure 2). The reslllting barotrauma can manifest itself as an arterial air embollJln, pneumomediastinum, pneumoperitoneum. subcutaneous emphysema, or a pneumothorax.‘3-’ Consequently. every attempt must be made to anticipate and detect intrapleural air before a course of hyperbaric oxygenation has been completed and the decision is made to ascend to normobaric conditions. In each of the three cases, important physical findings were overlooked or obscured by the grave clinical status of the patient. Each of the three patients had unilaterally decreased breath sounds or subcutaneous emphysema of the neck that was detected before decompression and that warranted a thoracostomy in the chamber. In one case, wheezing after smoke inhalation was not treated, predisposing the patient to alveolar air trapping. Rib fractures that were possibly caused by chest compressions went undetected in another case until after the tension pneumothorax developed. In light of the number of risk factors for pneumothorax present, a higher index of suspicion was warranted and might have lead to more timely thoracostomies. Diagnostic evaluation immediately before hyperbaric therapy in each case included a negative supine AP portable chest radiograph. While this suggests that there was no intrapleural air. one cannot exclude the possibility of undiagnosed pneumothorax due to poor radiographic technique or reader error. Even a moderate pneumothorax can be missed on a supine portable AP film, because intrapleural air can layer uniformly beneath the anterior thorax in the supine position. If the optimal upright end-expiratory film cannot be taken on an obtunded or intubated patient, alternative techniques can be used. A lateral decubitus chest radiograph, in which the side of the suspected pneumothorax is elevated, or a horizontal beam lateral chest radiograph seeking air beneath the sternum are two techniques which can be used.” Interestingly. one of the secondary signs of pneumothorax that can sometimes be identified on a routine supine AP film. the “double diaphragm. ‘+I’ is seen on a portable chest roentgenogram from case 3 (Figure IB), which shows residual intrapleural air over the right hemidiaphragm that persists despite chest tube placement. These tension pneumothoraces make up 1% of 297 consecutive cases of carbon monoxide toxicity that were treated with emergent HBOT over a IO-year period at our facility.’ Among the subgroup of patients who were comatose and intubated after having received chest compressions for cardiac arrest (n = 23), the incidence of tension pneumothorax was 12%. Consequently, we suggest the prophylactic placement of bilateral chest tubes in comatose, high-risk patients who are to receive HBOT in a monoplace chamber, where the patient cannot be instrumented during the dive. We feel that in this extremely toxic subgroup, chest tubes will not contribute significant morbidity but will eliminate another potential life-threat. In summary, the profoundly toxic clinical condition of a patient should not preclude a proper and deliberate patient assessment prior to the delivery of HBOT. These cases suggest the importance of serial physical examinations, arterial biood gas determinations, and sensitive to the presence of intraplural air chest radiographs when providing emergent HBOT to obtunded patients. Furthermore. needle and chest tube thoracostomies should be performed immediately if any
MURPHY
ET AL n TENSION
PNEUMOTHORAX
AND HBOT
evidence of pneumothorax exists and before hyperbaric compression is allowed to proceed.
179
de-
REFERENCES 1. Unsworth IP: Pulmonary barotrauma in a hyperbaric chamber. Anaesthesia 1973;28:675-678 2. James PB: The detection of pneumothorax by ultrasound. Proceedings of the 6th International Congress on Hyperbaric Medicine. Aberdeen, Scotland, Aberdeen University Press, 1977, 445-448 3. Sloan EP, Murphy DG, Hart R, et al: Complications and protocol considerations in carbon monoxide poisoned patients who require hyperbaric oxygen therapy: Report from a ten year experience. Ann Emerg Med 1989;18:629-634 4. U.S. Navy Standard Air Decompression Tables, in U.S. Navy Diving Manual, Volume 1; NAVSEA 0994-LP-001-9010: 1980, Carson, CA, Best Publishing Co 5. Davis JC: Hyperbaric oxygen therapy. A committee report. Bethesda, MD, Undersea Medical Society, Inc, 1983, pp 6-8 6. Ginsburg R, Roman0 J: Carbon monoxide encephalopathy: Need for appropriate treatment. Am J Psychiatr 1976;3:317320 7. Epstein FB, Eilers MA: Poisoning. In Rosen P, Baker FJ, Barkin RM, et al (eds): Emergency Medicine (ed 2). St Louis, MO, Mosby, 1988, pp 321-361
8. Kindwall EP: Carbon monoxide poisoning treated with hyperbaric oxygen. Respir Ther 1975;5:29-33 9. Haake R, Schlichtig R, Ulstad DR, Henschen RR: Barotrauma. Pathophysiology, risk factors, and prevention. Chest 1987;91:609-613 10. Zwillich CW, Pierson DJ, Creagh CE, et al: Complications of assisted ventilation. A prospective study of 354 consecutive episodes. Am J Med 1974;57:161-169 11. Powner DJ, Holcombe PA, Mello LA: Cardiopulmonary resuscitation-related injuries. Crit Care Med 1984;12:54-55 12. Bjork RJ, Snyder BD, Campion BC, et al: Medical complications of cardiopulmonary arrest. Arch Intern Med 1982; 142:500-504 13. Hamman L: Mediastinal emphysema. JAMA 1945;128:1-6 14. Macklin CC: Pneumothorax with massive collapse from experimental local over-inflation of the lung substance. Can Med Assoc J 1937;4:414-420 15. Macklin MT, Macklin CC: Malignant interstitial emphysema of the lungs and mediastinum as an important occult complication in many respiratory diseases and other conditions: An interpretation of the clinical literature in the light of laboratory experiment. Medicine 1944;23:281-358 16. Goodman LR, Putman CE: The Acute Care Unit: Radiographical Considerations, in Teplick JG, Haskin ME, (eds): Surgical Radiology (ed 2). Philadelphia, PA, Saunders, 1981, pp l-22 17. Cooke DA, Cooke JC: The supine pneumothorax. Ann R Coll Surg Engl 1987;69:130-134
