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Airway obstruction caused by an oleothorax
Airway Obstruction Caused by an Oleothorax A n d r e w J. Patterson, MD, Michael S. Leong, MD, Jay B. Brodsky, MD, and James B.D. Mark, MD HE AUTHORS recently anesthetized a patient who experienced dyspnea caused by tracheal compression 50 years after surgical creation of an oleothorax. A Clagett procedure was performed to facilitate continuous drainage from the cavity. Because of the unique etiology of her problem, the management differed from that usually recommended for a variable intrathoracic airway obstruction, and the case is presented.
T
CASE REPORT A 73-year-old, American Society of Anesthesiologists (ASA) II female patient presented for open drainage of an oleothorax. Fifty years earlier, mineral oil had been injected into a surgically created extrapleural space to achieve collapse therapy for pulmonary tuberculosis. Several years later, she underwent 5 years of therapy with isoniazid (INH) and streptomycin. Seventeen years before this admission, the mineral oil had been removed from the oleothorax cavity after the patient developed dyspnea. She experienced no additional problems until 2 years before this admission, when symptoms of dyspnea reappeared. A radiograph at that time showed a large intrathoracic cavity compressing her airway. Percutaneous needle aspiration of fluid from the oleothorax cavity temporarily relieved the dyspnea. However, over the subsequent 2 years, she required increasingly more frequent aspirations of the cavity, and at the time of admission she was undergoing fluid drainage approximately once every 3 months. The reason the fluid began accumulating in the cavity after so many years is unclear. The patient's past medical history was significant for pulmonary tuberculosis, mild asthma that was treated with albuterol inhalers, and hypertension. She was admitted to Stanford University Medical Center, Stanford, CA, for creation of a permanent thoracostomy (Clagett procedure) under general anesthesia. Fluid (800 mL) had last been aspirated from the cavity 3 months earlier. At the time of the Clagett procedure, the patient was clinically asymptomatic. In the operating room, routine monitors were applied. After breathing 100% oxygen by mask for 3 minutes, general anesthesia was induced with thiopental, 300 mg intravenous (IV), and fentanyl, 100 gg IV. At the time of induction, the thoracic surgery team was present and a rigid bronchoscope was immediately available as were several sizes of anode endotracheal tubes. Once it was shown that the patient could be ventilated safely by mask, succinylcholine, 80 mg IV, was administered and direct laryngoscopy was performed. A 7.0-mm ID endotracheal tube was placed into her trachea and advanced to the 22-cm mark. Tube placement in the trachea was confirmed by auscultation and by the presence of end-tidal carbon dioxide on the capnograph. General anesthesia was maintained with isoflurane 1.5% and oxygen. Muscle relaxation was obtained with pancuronium, 5 mg IV. The patient's lungs were mechanically ventilated with a tidal volume of 700 mL at a peak inspiratory pressure of 30 cm H20. The 45-minute surgery was uneventful. Approximately 300 mL of fibrino-calcific material and 900 mL of clear yellow fluid Journal o f Cardiothoracic and Vascular Anesthesia,
were removed from the oleothorax cavity. Peak airway pressures did not change throughout the procedure. At the completion of surgery, muscle relaxation was reversed and the patient immediately began breathing spontaneously. Once awake, her trachea was extubated without difficulty. The thoracic surgery team was present during extubation and a rigid bronchoscope was immediately available in the event that a malacic segment of trachea impaired the patient's ventilation when the endotracheal tube was removed. DISCUSSION Before 1955, treatment of cavitary pulmonary tuberculosis often consisted of intentional collapse of the involved lung by thoracoplasty or plombage. Plombage refers to the surgical creation of a plane of dissection deep to the ribs over the upper chest to establish an intrathoracic, but extrapleural, space. The space was filled with foreign material that prevented the diseased lung from expanding and thereby allowed the atelectatic lung tissue to heal. Various substances were injected to maintain the integrity of the plombage space.l-5 These included air, olive and mineral oil, gauze, paraffin wax, rubber sheeting or bags, and methyl methacrylate (Lucite; Nichols Products Co, Moorestown, NJ) balls. Oleothorax refers to the use of oil to distend the plombage space. Oil, injected 2 or 3 months after the cavity was created, was used for long-term therapy because its absorption is very slow. 2 With the introduction of streptomycin in 1945, paraaminosalicylic acid in 1946, and INH in 1951, pharmacologic therapy became the mainstay of tuberculosis treatment and plombage was discontinued. Most plombs were surgically removed within 5 years of placement because of complications. 1 However, patients remain with plombs intact and have occasionally presented with complications as long as 50 years after initial treatment. 6 The usual problems associated with plombage have been infection or migration of the foreign material, and complications are treated by surgical removal of the packing material. This patient's problem, airway obstruction secondary to a fluid-filled oleothorax, is unique. Her symptom of dyspnea was immediately relieved by periodic needle aspiration of fluid from the oleothorax cavity. Figures 1 and 2 illustrate the extent of the airway obstruction by the distended oleothorax that impinged on her trachea. It is postulated that the partially calcified wall of the cavity behaved like a semipermeable membrane, allowing fluid to enter the space while preventing the fluid from escaping. The gradually
From the Departments of Anesthesiology and Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, CA. Address reprint requests to Andrew J. Patterson, MD, Department of Anesthesiology, H-3580, Stanford University Medical Center, Stanford, CA, 94305. Copyright © 1998 by W.B. Saunders Company 1053-0770/98/1202-001458.00/0 Key words: tuberculosis, plombage, oleothorax, dyspnea, variable intrathoracic airway obstruction
Vo[ 12, No 2 (April), 1998:pp 189-191
189
190
Fig 1. Computed tomographic scan of the upper thorax shows a large fluid-filled cavity occupying the entire right hemithorax, The trachea is markedly compressed by the oleothorax,
expanding cavity periodically compressed the airway, causing this patient's symptoms. The patient's preoperative pulmonary function test results (Fig 3 and 4) were consistent with the diagnosis of variable intrathoracic obstruction with a plateau of the maximal expiratory flow-volume curve as well as decreased peak expiratory flow rate. Flow-volume curves were obtained only in the upright position. Maximum voluntary ventilation (MVV) and forced expiratory volume in 1 second (FEVI) were markedly reduced. As predicted for a variable intrathoracic airway obstruction, airflow improved during inspiration, whereas during expiration the fluid-filled oleothorax cavity compressed the
Fig 2. Radiograph of the chest shows a large oleothorax cavity compressing the trachea and distorting the upper airway.
PATTERSON ET AL
Pre-Drug Spirometry
Actual
% Predicted
Predicted
FVC (L) FEV1 (L) FEV3 (L) FEF 25%-75% (L/S) FEFmax (L/S) FEV1/FVC (%) FEV3/FVC (%) MVV (L/MIN) Test Length (SEC)
1.02 0.79 1.01 0.65 0.94 77 98 22 12.00
36 39 36 29 16 109 101 26
Post-Drug Spirometry FVC (L) FEV1 (L) FEV3 (L) FEF 25%-75% (L/S) FEFmax (L/S) FEV1/FVC (%) FEV3/FVC (%) MVV (L/MIN) Test Length (SEC)
Actual 0.98 0.70 0,92 0.49 0.82 71 94 26 12.00
% Post 34 35 33 22 14 101 96 31
% Change -4 11 -8 -23 -12 -7 -4 17
Lung Volumes TLC (L) FRC (L) RV (L) VC (L) IC (L) ERV (L) RV/TLC (%)
Actual 2.58 1.78 1.44 1.14 0.80 0.34 56
% Predicted 53 61 70 40 40 40 134
Predicted 4.92 2.89 2.04 2.88 2.02 0.85 42
2.88 2.02 2.79 2.26 5.77 70 97 84
Fig 3. Results of pulmonary function studies show markedly reduced maximum voluntary ventilation (MVV) and forced expiratory volume in 1 second (FEV1).
airway causing obstruction.7 Figure 5 shows the dramatic resolution achieved by aspiration of the cavity. The anesthetic management of a variable intrathoracic airway obstruction depends on the size and composition of the mass as well as the extent of the tracheal compression. Solid tumors in the anterior mediastinum (lymphoma, thymoma, metastatic malignancy) are the usual etiology of this type of obstruction. 8 For a patient with an anterior mediastinal tumor, general anesthesia is usually induced after fiberoptic-assisted intubation of the airway in an awake patient. There is a risk that the solid tumor will prevent adequate positive-pressure ventilation by mask or successful placement of an endotracheal tube. If airway distal to the endotracheal tube is involved, muscle relaxants are usually avoided and the patient may have to breathe spontaneously, even during thoracotomy. It is not suggested that all patients with intrathoracic airway obstructions be managed during induction of anesthesia as this patient was managed. A case-by-case assessment of the pathophysiology is imperative. Criteria that might indicate that the authors' technique is appropriate include the malleable character of the mass, the immediate availability of a rigid bronchoscope, and a physician with proficiency using this instrument. This patient's fluid-filled oleothorax was malleable. Positivepressure ventilation by mask was easily achieved during induction of anesthesia because the obstructing mass could be displaced. Similarly, endotracheal tube placement past the obstruction was uneventful. The authors were prepared to perform percutaneous needle aspiration to decompress the
AIRWAY OBSTRUCTION CAUSED BY AN OLEOTHORAX
191
4- I . / S e o 3. 2.
!:Fj
2 (L)
Fig 5. Radiograph of the chest shows dramatic opening of the previously compressed airway after the fluid has been aspirated from the oleothorax cavity. The wall of the oleothorax is partially calcified, preventing complete collapse of the cavity.
FUC PRE3/PST5 Fig 4. This patient's flow-volume loop shows plateauing of the maximal expiratory curve.
cavity at any time during the induction of general anesthesia to relieve airway obstruction had it occurred. The Clagett procedure created a permanent pleuro-cutaneous fistula, which effectively drained the fluid and eliminated the cause of airway obstruction. For this reason, extubation and resumption of spontaneous breathing were uneventful.
REFERENCES
1. Thomas GE, Chandrasekhar B, Grannis FW Jr: Surgical treatment of complications 45 years after extraperiosteal pneumolysis and plombage using acrylic resin balls for cavitary pulmonary tuberculosis. Chest 108:1163-1164, 1995 2. Proctor OS: Four years' experience with extrapleural pneumothorax and oleothorax. J Thorac Surg 9:392-412, 1940 3. Wilson DA: Extrapleural pneumolysis with lucite plombage. J Thorac Surg 17:111-122, 1948 4. Trent JC, Moody JD, Hiatt JS: An evaluation of extrapleural pneumonolysis with lucite plombage. J Thorac Surg 18:173-180, 1949
5. Walkup HE, Murphy JD: Extrapleural pneumolysis with ptombage versus thoracoplasty. Dis Chest 16:18-20, 1949 6. Horowitz MD, Olero M, Thurer RJ, Bolooki H: Late complication of plombage. Ann Thorac Surg 53:803-806, 1992 7. Acres JC, Kryger MH: Clinical significance of pulmonary function tests: Upper airway obstruction. Chest 80:207-211,1981 8. Heffner JE, Sahn SA: Diseases of the mediastinum and chest wall, in Kelley WN (ed): Internal Medicine (ed 2). Philadelphia, PA, Lippincott, 1992, pp 1786-1788
T
CASE REPORT A 73-year-old, American Society of Anesthesiologists (ASA) II female patient presented for open drainage of an oleothorax. Fifty years earlier, mineral oil had been injected into a surgically created extrapleural space to achieve collapse therapy for pulmonary tuberculosis. Several years later, she underwent 5 years of therapy with isoniazid (INH) and streptomycin. Seventeen years before this admission, the mineral oil had been removed from the oleothorax cavity after the patient developed dyspnea. She experienced no additional problems until 2 years before this admission, when symptoms of dyspnea reappeared. A radiograph at that time showed a large intrathoracic cavity compressing her airway. Percutaneous needle aspiration of fluid from the oleothorax cavity temporarily relieved the dyspnea. However, over the subsequent 2 years, she required increasingly more frequent aspirations of the cavity, and at the time of admission she was undergoing fluid drainage approximately once every 3 months. The reason the fluid began accumulating in the cavity after so many years is unclear. The patient's past medical history was significant for pulmonary tuberculosis, mild asthma that was treated with albuterol inhalers, and hypertension. She was admitted to Stanford University Medical Center, Stanford, CA, for creation of a permanent thoracostomy (Clagett procedure) under general anesthesia. Fluid (800 mL) had last been aspirated from the cavity 3 months earlier. At the time of the Clagett procedure, the patient was clinically asymptomatic. In the operating room, routine monitors were applied. After breathing 100% oxygen by mask for 3 minutes, general anesthesia was induced with thiopental, 300 mg intravenous (IV), and fentanyl, 100 gg IV. At the time of induction, the thoracic surgery team was present and a rigid bronchoscope was immediately available as were several sizes of anode endotracheal tubes. Once it was shown that the patient could be ventilated safely by mask, succinylcholine, 80 mg IV, was administered and direct laryngoscopy was performed. A 7.0-mm ID endotracheal tube was placed into her trachea and advanced to the 22-cm mark. Tube placement in the trachea was confirmed by auscultation and by the presence of end-tidal carbon dioxide on the capnograph. General anesthesia was maintained with isoflurane 1.5% and oxygen. Muscle relaxation was obtained with pancuronium, 5 mg IV. The patient's lungs were mechanically ventilated with a tidal volume of 700 mL at a peak inspiratory pressure of 30 cm H20. The 45-minute surgery was uneventful. Approximately 300 mL of fibrino-calcific material and 900 mL of clear yellow fluid Journal o f Cardiothoracic and Vascular Anesthesia,
were removed from the oleothorax cavity. Peak airway pressures did not change throughout the procedure. At the completion of surgery, muscle relaxation was reversed and the patient immediately began breathing spontaneously. Once awake, her trachea was extubated without difficulty. The thoracic surgery team was present during extubation and a rigid bronchoscope was immediately available in the event that a malacic segment of trachea impaired the patient's ventilation when the endotracheal tube was removed. DISCUSSION Before 1955, treatment of cavitary pulmonary tuberculosis often consisted of intentional collapse of the involved lung by thoracoplasty or plombage. Plombage refers to the surgical creation of a plane of dissection deep to the ribs over the upper chest to establish an intrathoracic, but extrapleural, space. The space was filled with foreign material that prevented the diseased lung from expanding and thereby allowed the atelectatic lung tissue to heal. Various substances were injected to maintain the integrity of the plombage space.l-5 These included air, olive and mineral oil, gauze, paraffin wax, rubber sheeting or bags, and methyl methacrylate (Lucite; Nichols Products Co, Moorestown, NJ) balls. Oleothorax refers to the use of oil to distend the plombage space. Oil, injected 2 or 3 months after the cavity was created, was used for long-term therapy because its absorption is very slow. 2 With the introduction of streptomycin in 1945, paraaminosalicylic acid in 1946, and INH in 1951, pharmacologic therapy became the mainstay of tuberculosis treatment and plombage was discontinued. Most plombs were surgically removed within 5 years of placement because of complications. 1 However, patients remain with plombs intact and have occasionally presented with complications as long as 50 years after initial treatment. 6 The usual problems associated with plombage have been infection or migration of the foreign material, and complications are treated by surgical removal of the packing material. This patient's problem, airway obstruction secondary to a fluid-filled oleothorax, is unique. Her symptom of dyspnea was immediately relieved by periodic needle aspiration of fluid from the oleothorax cavity. Figures 1 and 2 illustrate the extent of the airway obstruction by the distended oleothorax that impinged on her trachea. It is postulated that the partially calcified wall of the cavity behaved like a semipermeable membrane, allowing fluid to enter the space while preventing the fluid from escaping. The gradually
From the Departments of Anesthesiology and Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, CA. Address reprint requests to Andrew J. Patterson, MD, Department of Anesthesiology, H-3580, Stanford University Medical Center, Stanford, CA, 94305. Copyright © 1998 by W.B. Saunders Company 1053-0770/98/1202-001458.00/0 Key words: tuberculosis, plombage, oleothorax, dyspnea, variable intrathoracic airway obstruction
Vo[ 12, No 2 (April), 1998:pp 189-191
189
190
Fig 1. Computed tomographic scan of the upper thorax shows a large fluid-filled cavity occupying the entire right hemithorax, The trachea is markedly compressed by the oleothorax,
expanding cavity periodically compressed the airway, causing this patient's symptoms. The patient's preoperative pulmonary function test results (Fig 3 and 4) were consistent with the diagnosis of variable intrathoracic obstruction with a plateau of the maximal expiratory flow-volume curve as well as decreased peak expiratory flow rate. Flow-volume curves were obtained only in the upright position. Maximum voluntary ventilation (MVV) and forced expiratory volume in 1 second (FEVI) were markedly reduced. As predicted for a variable intrathoracic airway obstruction, airflow improved during inspiration, whereas during expiration the fluid-filled oleothorax cavity compressed the
Fig 2. Radiograph of the chest shows a large oleothorax cavity compressing the trachea and distorting the upper airway.
PATTERSON ET AL
Pre-Drug Spirometry
Actual
% Predicted
Predicted
FVC (L) FEV1 (L) FEV3 (L) FEF 25%-75% (L/S) FEFmax (L/S) FEV1/FVC (%) FEV3/FVC (%) MVV (L/MIN) Test Length (SEC)
1.02 0.79 1.01 0.65 0.94 77 98 22 12.00
36 39 36 29 16 109 101 26
Post-Drug Spirometry FVC (L) FEV1 (L) FEV3 (L) FEF 25%-75% (L/S) FEFmax (L/S) FEV1/FVC (%) FEV3/FVC (%) MVV (L/MIN) Test Length (SEC)
Actual 0.98 0.70 0,92 0.49 0.82 71 94 26 12.00
% Post 34 35 33 22 14 101 96 31
% Change -4 11 -8 -23 -12 -7 -4 17
Lung Volumes TLC (L) FRC (L) RV (L) VC (L) IC (L) ERV (L) RV/TLC (%)
Actual 2.58 1.78 1.44 1.14 0.80 0.34 56
% Predicted 53 61 70 40 40 40 134
Predicted 4.92 2.89 2.04 2.88 2.02 0.85 42
2.88 2.02 2.79 2.26 5.77 70 97 84
Fig 3. Results of pulmonary function studies show markedly reduced maximum voluntary ventilation (MVV) and forced expiratory volume in 1 second (FEV1).
airway causing obstruction.7 Figure 5 shows the dramatic resolution achieved by aspiration of the cavity. The anesthetic management of a variable intrathoracic airway obstruction depends on the size and composition of the mass as well as the extent of the tracheal compression. Solid tumors in the anterior mediastinum (lymphoma, thymoma, metastatic malignancy) are the usual etiology of this type of obstruction. 8 For a patient with an anterior mediastinal tumor, general anesthesia is usually induced after fiberoptic-assisted intubation of the airway in an awake patient. There is a risk that the solid tumor will prevent adequate positive-pressure ventilation by mask or successful placement of an endotracheal tube. If airway distal to the endotracheal tube is involved, muscle relaxants are usually avoided and the patient may have to breathe spontaneously, even during thoracotomy. It is not suggested that all patients with intrathoracic airway obstructions be managed during induction of anesthesia as this patient was managed. A case-by-case assessment of the pathophysiology is imperative. Criteria that might indicate that the authors' technique is appropriate include the malleable character of the mass, the immediate availability of a rigid bronchoscope, and a physician with proficiency using this instrument. This patient's fluid-filled oleothorax was malleable. Positivepressure ventilation by mask was easily achieved during induction of anesthesia because the obstructing mass could be displaced. Similarly, endotracheal tube placement past the obstruction was uneventful. The authors were prepared to perform percutaneous needle aspiration to decompress the
AIRWAY OBSTRUCTION CAUSED BY AN OLEOTHORAX
191
4- I . / S e o 3. 2.
!:Fj
2 (L)
Fig 5. Radiograph of the chest shows dramatic opening of the previously compressed airway after the fluid has been aspirated from the oleothorax cavity. The wall of the oleothorax is partially calcified, preventing complete collapse of the cavity.
FUC PRE3/PST5 Fig 4. This patient's flow-volume loop shows plateauing of the maximal expiratory curve.
cavity at any time during the induction of general anesthesia to relieve airway obstruction had it occurred. The Clagett procedure created a permanent pleuro-cutaneous fistula, which effectively drained the fluid and eliminated the cause of airway obstruction. For this reason, extubation and resumption of spontaneous breathing were uneventful.
REFERENCES
1. Thomas GE, Chandrasekhar B, Grannis FW Jr: Surgical treatment of complications 45 years after extraperiosteal pneumolysis and plombage using acrylic resin balls for cavitary pulmonary tuberculosis. Chest 108:1163-1164, 1995 2. Proctor OS: Four years' experience with extrapleural pneumothorax and oleothorax. J Thorac Surg 9:392-412, 1940 3. Wilson DA: Extrapleural pneumolysis with lucite plombage. J Thorac Surg 17:111-122, 1948 4. Trent JC, Moody JD, Hiatt JS: An evaluation of extrapleural pneumonolysis with lucite plombage. J Thorac Surg 18:173-180, 1949
5. Walkup HE, Murphy JD: Extrapleural pneumolysis with ptombage versus thoracoplasty. Dis Chest 16:18-20, 1949 6. Horowitz MD, Olero M, Thurer RJ, Bolooki H: Late complication of plombage. Ann Thorac Surg 53:803-806, 1992 7. Acres JC, Kryger MH: Clinical significance of pulmonary function tests: Upper airway obstruction. Chest 80:207-211,1981 8. Heffner JE, Sahn SA: Diseases of the mediastinum and chest wall, in Kelley WN (ed): Internal Medicine (ed 2). Philadelphia, PA, Lippincott, 1992, pp 1786-1788