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Ann Thorac Surg 1998;65:563
© 1998 The Society of Thoracic Surgeons


How to Do It

Autoblood Plus OK432 Pleurodesis With Open Drainage for Persistent Air Leak After Lobectomy

Hiroyasu Yokomise, MD, Kiyoshi Satoh, MD, Nobuhiro Ohno, MD, Koiti Tamura, MD

Department of Thoracic Surgery, Japanese Red Cross Society Wakayama Medical Center, Wakayama City, Japan

Accepted for publication September 2, 1997.

Dr Yokomise, Department of Thoracic Surgery, Japanese Red Cross Society Wakayama Medical Center, Komatsubaradori, Wakayama City, 640, Japan.


    Abstract
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
Prolonged air leak with dead space after lobectomy was successfully treated with autoblood plus OK432 pleurodesis in 10 patients. We tried this method for the purpose of (1) reduction of dead space and (2) effective chemical sclerosis. This easy method was associated with acceptable side effects and should be considered as an option for the treatment of prolonged air leak after lobectomy, especially with dead space.


    Introduction
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
Adequate pleural drainage with reexpansion of the remaining lung is essential for the treatment of persistent air leak after pulmonary resection. Pleurodesis with sclerosing agents such as tetracycline, talc, or OK432 may sometimes be of use [1] [2] [3]. However, chemical pleurodesis often fails unless the lung is fully expanded.

Autologous blood pleurodesis has been reported to be a useful procedure for prolonged air leak [4]. Blood itself does not have a potent sclerosing effect. The mechanism of blood pleurodesis may be direct obliteration of bronchopleural fistula and reduction of dead space by clot. We tried pleurodesis with autologous blood plus OK432 (autoblood OK432 pleurodesis) for the purpose of (1) reduction of dead space and (2) effective chemical sclerosis. Using this method in 10 patients with persistent air leak and dead space after lobectomy, we achieved effective pleurodesis.


    Patients and Methods
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
From January 1996 to February 1997, 10 consecutive patients who underwent lobectomy for lung cancer were treated by blood OK432 pleurodesis because of persistent air leakage (Table 1). In all cases, we tried several procedures (decreasing, increasing, or stopping chest suction) before pleurodesis. In principle, patients with persistent air leak longer than 1 week (8.7 ± 4.7 days) were treated. In 4 patients, prior therapies (tetracycline, OK432, and another pleurodesis) were tried but failed. In 3 patients, pleurodesis was performed earlier than 1 week to stop massive air leak (almost continuous air leakage). In all 10 patients, moderate dead spaces were observed at the time of pleurodesis.


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Results of Blood OK432 Pleurodesis

 
Fifty milliliters of autologous blood was drawn from the patient and 5.0 KE of OK432 was mixed into it. The chest tube responsible for the air leak was disconnected from the suction device and the blood was injected into the thoracic space through this tube. With a 50-mL syringe, the blood was pumped to and fro to make a clot. After the patency of the chest tube was confirmed, it was connected to the suction device. The chest tube was then raised 60 cm above the patient. The chest tube was never clamped. Chest tube suction was set at -15 cm H2O. The position of the patient was changed for 2 hours.


    Results
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
Blood OK432 pleurodesis was done once in 6 patients and twice in 4 patients (see Table 1). In all patients, successful treatment of the air leak was achieved within few days (mean, 3.8 ± 2.0 days). The air leak actually stopped 1 to 2 days after pleurodesis in most patients. The chest tube was removed 1 to 2 days after the confirmation of no air leak. No major side effects were observed. In 5 patients, fever of less than 38°C was observed.

In patient 1, presented as an example, obliteration of the bronchopleural fistula and reduction of the dead space seemed to be achieved gradually by a natural coagulation process. Afterward, the dead space was eventually absorbed (Fig 1).



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(A) Before pleurodesis: a dead space was observed (arrow). (B) Just after pleurodesis: The dead space was filled with effusion and fibrin (arrow). (C) After extubation of the chest tube: effusion was absorbed. Reexpansion of the lung was achieved (arrow).

 
So far, no late empyemas have been observed. The longest observation period is 1 year. There was no failure of this procedure in our limited experience.


    Comment
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
Air leak after lobectomy usually ceases spontaneously if adequate reexpansion of the remaining lung is established. Even if a prolonged air leak occurs, pleurodesis with sclerosing agents such as tetracycline, talc, or OK432 may work [1] [2] [3]. However, chemical pleurodesis often fails to work if persistent air leak with dead space remains. Furthermore, without adequate reexpansion, the sclerosing agent itself may prevent reexpansion of the remaining lung because of thickening of the visceral pleura.

Autologous blood pleurodesis has been reported as a procedure for prolonged air leak of pneumothorax and pulmonary resection [4]. Blood itself does not have as potent a sclerosing effect as other sclerosing agents. Reduction of dead space by autologous blood contributes to reasonable reexpansion of the remaining lung. OK432 is a heat- and penicillin-treated lyophilized powder of the Su strain of Streptococcus pyogenes A3. This drug has been reported to have antitumor activity in cancer patients [5]. Furthermore, OK432 is one of the standard agents for pleurodesis in Japan [3]. The advantages over other sclerosing agents, such as tetracycline and talc [1] [2], are less pain and lack of carcinogenic property. The mechanism of OK432 responsible for pleurodesis is reported to be a nonspecific inflammatory effect. Considering the effects of these two procedures, we tried pleurodesis with autologous blood plus OK432.

After injection of the blood into the thorax, chest suction was kept at -15 cm H2O and the chest tube was raised 60 cm above the patient. By these procedures, reduction of dead space (by retention of blood in the thorax) and reexpansion of the remaining lung were obtained simultaneously. Occlusion of the chest tube was not observed in any patient. Obliteration of the bronchopulmonary fistula and reduction of the dead space were achieved by blood. Afterward, the air space was eventually absorbed (Fig 1Fig 2). In 4 patients, before blood OK432 pleurodesis we tried another pleurodesis (eg, tetracycline, OK432 alone), which failed, probably because of dead spaces. Even in these cases, blood OK432 pleurodesis was successful. In our limited experience, occlusion of the chest tube sometimes occurred after injection of fibrin glue into the thorax. Blood OK432 pleurodesis was successfully achieved with acceptable side effects, especially for patients with dead spaces.



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Schema of blood OK432 pleurodesis.

 

    References
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
  1. Alfageme I, Moreno L, Huertas C, Vargas A, Hernandez J, Beiztegui A Spontaneous pneumothorax: long-term results with tetracycline pleurodesis. Chest 1994;106:347-350.[Abstract/Free Full Text]
  2. Kennedy L, Rusch VW, Strange C, Ginsberg RJ, Sahn SA Pleurodesis using talc slurry. Chest 1994;106:342-346.[Abstract/Free Full Text]
  3. Ishihara K, Hasegawa T, Okazaki M, et al. OK432 chemical pleurodesis as a standard therapy of spontaneous pneumothorax. Nippon Kyobu Shikkan Gakkai Zasshi 1988;26:10-15.
  4. Dumire R, Crabbe MM, Mappin FG, Fontenelle LJ Autologous "blood patch" pleurodesis for persistent pulmonary air leak. Chest 1992;101:64-66.[Abstract/Free Full Text]
  5. Uchida A, Micksche M Intrapleural administration of OK432 in cancer patients: activation of NK cells and reduction of suppressor cells. Int J Cancer 1983;31:1-5.[Medline]



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