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(Chest. 2002;121:284-286.)
© 2002 American College of Chest Physicians

Management of Tension Pneumatocele With High- Frequency Oscillatory Ventilation*

Hsiu-Nien Shen, MD; Frank Leigh Lu, MD; Huey-Dong Wu, MD; Chong-Jen Yu, MD, PhD, FCCP and Pan-Chyr Yang, MD, PhD, FCCP

* From the Departments of Internal Medicine and Pediatrics, National Taiwan University Hospital, Taipei, Taiwan.

Correspondence to: Chong-Jen Yu, MD, PhD, FCCP, Department of Internal Medicine, National Taiwan University Hospital, No. 7 Chung-Shan South Rd, Taipei, Taiwan 100; e-mail: jeffery{at}ha.mc.ntu.edu.tw


    Abstract
 TOP
 Abstract
 Introduction
 Case Report
 Discussion
 References
 
We report the successful application of high-frequency oscillatory ventilation in a patient with tension pneumatocele (TP). The proposed check-valve mechanism for the development of pneumatoceles predicts that positive-pressure ventilation could lead to distension of these airspaces and formation of TPs. Therefore, high-frequency ventilation could be more applicable in conditions, such as massive air leak due to bronchopleural fistula, that are difficult to manage by conventional ventilator modes.

Key Words: bronchopleural fistula • high-frequency oscillatory ventilation • pneumatocele • Streptococcus pneumoniae


    Introduction
 TOP
 Abstract
 Introduction
 Case Report
 Discussion
 References
 
We present a case of severe pneumonia, enlarging pneumatoceles, and pneumothorax in a patient receiving conventional mechanical ventilation (CMV). Pneumatoceles decreased after the application of high-frequency oscillatory ventilation (HFOV).


    Case Report
 TOP
 Abstract
 Introduction
 Case Report
 Discussion
 References
 
A 3-year-old girl had a temperature of up to 40°C, cough, and rhinorrhea. She had had no history of specific medical illnesses. Four days after initial symptoms appeared, poor appetite, hyperpnea, and dyspnea developed. She was then admitted to a hospital. A chest radiograph (CXR) on the first day disclosed right upper lobe (RUL) pneumonia and pleural effusion (Fig 1 , top left). A normal WBC count (5,900/µL) with severe left shift (39% band form) was noted. Empirical antibiotics were administered, but the symptoms still progressed. Disseminated intravascular coagulation was suspected by thrombocytopenia and coagulopathy. Hypotension and hypoxemia developed soon after.



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Figure 1.. Top left: CXR on day 1 showed RUL pneumonia and pleural effusion. Top right: CXR on day 5 disclosed multiple pneumatoceles bilaterally, especially on the right side. Bottom, left: CXR on day 11 (day 2 of HFOV) showed the overinflated lungs and a large pneumatocele on the RUL; pneumothorax was present on the right side. Bottom right: CXR on day 24 (day 15 of HFOV) showed the resolution of pneumonia and pneumatoceles.

 
She was intubated, and treatment with inotropic medications was initiated, along with ventilatory support with time-cycled pressure control. A throat swab culture, blood culture, and pleural fluid studies were performed. Results of these microbiological studies showed positive pneumococcal antigen in the pleural effusion. Culture findings from all other sites were negative. A chest tube was inserted due to the clinical diagnosis of complicated parapneumonic effusion; pleural effusion data included WBC, 1,512/µL; and lactate dehydrogenase, 1,779 U/L. Antibiotics were switched to ceftriaxone, erythromycin, and vancomycin on the next day.

In the days that followed, hemodynamics and oxygenation became stabilized, yet fever and leukocytosis persisted. Serial CXRs revealed RUL consolidation with multiple, progressively enlarging pneumatoceles. One week later, the chest tube was removed, but pneumothorax on the same side developed thereafter (Fig 1 , top right). After reinsertion of a new chest tube, massive air leak was noted. Low-pressure suction (10 cm H2O) through the chest tube was applied. On the next day (day 9 of hospitalization), she was transferred to our hospital. On hospital admission, she appeared lethargic and confused. Her body weight was 12 kg. Vital signs were as follows: body temperature, 38°C; heart rate, 160 beats/min; BP, 94/76 mm Hg; and respiratory rate (RR), 30 breaths/min. The patient received time-cycled pressure control ventilation, with settings of peak inspiratory pressure at 30 cm H2O; flow rate, 25 L/min; peak end-expiratory pressure, 4 cm H2O; RR, 30 breaths/min, and fraction of inspired oxygen (FIO2), 100%. Oxygen saturation, as measured by pulse oximetry, was 88.6%. Chest examinations revealed persistent air leak from the chest tube on the right side. Rales and rhonchi were audible. The edge of the liver was 3 cm below the right costal margin. All other data were unremarkable. Laboratory studies revealed marked leukocytosis (WBC, 43,730/µL) and a slightly elevated aminotransferase level. The rest of the laboratory study results were within normal limits. Arterial blood gas levels are shown in Table 1 .


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Table 1.. Arterial Blood Gas Levels Before and After the Use of HFOV*

 
On day 10, because of massive air leak and persistence of poor oxygenation with CMV, HFOV (model 3100A; SensorMedics; Yorba Linda, CA) was applied. Initial settings were as follows: amplitude, 47 cm H2O, with visible vibrations of the chest wall; frequency, 10 Hz; flow rate, 28 L/min, inspiratory/expiratory ratio, 0.33; and FIO2, 80%. Mean airway pressure (MAP) was raised up to 25.5 cm H2O where the hemodynamics remained stable and the improvement in oxygenation reached a plateau (Fig 2 ). Improvement of the air leak was noted. After the clinical condition and oxygenation became stable, MAP was reduced gradually to the lowest acceptable level where a sudden drop of oxygenation occurred with further reduction in MAP. While MAP was lowered from 25 cm H2O on day 11 (day 2 of HFOV) to 14 cm H2O on day 14 (day 5 of HFOV), the size of RUL pneumatocele decreased on serial CXRs (Fig 1 , bottom left and bottom right). However, fever, leukocytosis, and mild air leak persisted. Nevertheless, weaning of HFOV proceeded without difficulty. After the patient was withdrawn from sedation and paralysis, spontaneous breathing during HFOV was allowed, since the airway pressure, vital signs, and blood gas data were relatively stable. During the course, treatment with antibiotics was partially modified, with a switch from ceftriaxone to cefotaxime on day 12 because of jaundice and gallbladder sludge on abdominal ultrasonography. Erythromycin was administered for 2 weeks. Cefotaxime was replaced by piperacillin sodium/tazobactam sodium on day 21 for suspected drug fever. On day 24 (day 15 of HFOV), ventilatory support was shifted from HFOV to a T piece, and after 2 h of an external T-piece trial, she was extubated uneventfully. Meanwhile, treatment with piperacillin sodium/tazobactam sodium was discontinued on day 25, and fluconazole was added on day 28 for superimposed candidal infection of the thoracostomy wound. Vancomycin was administered for a course of 30 days. General conditions improved gradually with good oxygenation with room air breathing, though mild tachydyspnea still persisted. An air leak remained until day 34 when the chest tube was removed after temporary clamping. A follow-up CXR showed marked improvement without evidence of pneumatoceles. The patient was discharged on day 39.



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Figure 2.. Clinical course. The oxygenation deteriorated on day 8 and improved gradually after using HFOV.

 

    Discussion
 TOP
 Abstract
 Introduction
 Case Report
 Discussion
 References
 
Pulmonary pneumatoceles are thin-walled, air-containing spaces that have been recognized as a possible complication of pneumonia with various infectious etiologies.1 2 Among the bacterial agents, Staphylococcus aureus is the most commonly implicated.1 On the other hand, Streptococcus pneumoniae is rarely reported as a cause of pneumatoceles.3 Postinfectious pneumatoceles usually appear within the first week of pneumonia and disappear in an average of 6 weeks.1 3

Complications of pneumatoceles included secondary infection and enlargement with tension formation.4 The latter could cause cardiopulmonary instability by itself. In some instances, it could subsequently rupture with pneumothorax or lead to the formation of bronchopleural fistula (BPF), especially during positive-pressure ventilation.2 4 5 As in the case presented, the initial use of CMV might have predisposed a patient to the enlargement of pneumatoceles, with subsequent rupture and prolonged air leak.

The proposed check-valve mechanism suggests that mechanical ventilation with positive airway pressure could lead to distension of these spaces.6 Once tension occurs, the principle of management is similar to that for pneumothorax. Emergent decompression is thus indicated. There have been several case reports of percutaneous decompression of tension pneumatocele (TP) by needle aspiration,5 catheter drainage,2 4 or chest tube drainage5 under CT or fluoroscopic guidance. Surgical pneumonostomy with subsequent pulmonary resection has also been reported.7

In the present case report, surgery was initially considered in managing the complicated pulmonary conditions during the early course of treatment. However, it was not recommended, since extensive debridement might compromise residual lung function. On the other hand, initial unstable conditions prohibited the transportation to facilities for further radiologic-guided procedures.

Persistent air leak during mechanical ventilation is a serious complication of ventilator therapy. In critically ill patients, the loss of a substantial portion of inspired tidal volume through BPF may significantly alter the intrapulmonary distribution of ventilation, ventilation-perfusion matching, and arterial blood gases. Several techniques have been used to decrease air loss through BPF, promote closure, and maintain good gas exchange.8 High-frequency ventilation is one of these procedures.8 9 The rationales for its use are to decrease airway pressure, reduce risk of barotrauma, and improve ventilation/perfusion matching and gas exchange.8 As noted in this case, we switched ventilator mode from CMV to HFOV. Not only did TP not enlarge, it further decreased in size with the reduction of MAP and amplitude. This observation supported the proposed mechanism of HFOV in patients with TP.


    Footnotes
 
Abbreviations: BPF = bronchopleural fistula; CMV = conventional mechanical ventilation; CXR = chest radiograph; FIO2 = fraction of inspired oxygen; HFOV = high-frequency oscillatory ventilation; MAP = mean airway pressure; RR = respiratory rate; RUL = right upper lobe; TP = tension pneumatocele

Received for publication November 6, 2000. Accepted for publication June 1, 2001.


    References
 TOP
 Abstract
 Introduction
 Case Report
 Discussion
 References
 

  1. Dines, DE (1968) Diagnostic significance of pneumatocele of the lung. JAMA 204,79-82[CrossRef][Medline]
  2. Sewall, LE, Franco, AI, Wojtowycz, MM, et al (1993) Pneumatoceles causing respiratory compromise: treatment by percutaneous decompression. Chest 103,1266-1267[Abstract/Free Full Text]
  3. Donnelly, LF, Klosterman, LA (1998) Cavitary necrosis complicating pneumonia in children: sequential findings on chest radiography. AJR Am J Roentgenol 171,253-256[Abstract/Free Full Text]
  4. Zuhdi, MK, Spear, RM, Worthen, HM, et al (1996) Percutaneous catheter drainage of tension pneumatocele, secondarily infected pneumatocele, and lung abscess in children. Crit Care Med 24,330-333[CrossRef][ISI][Medline]
  5. McGarry, T, Giosa, R, Rohman, M, et al (1987) Pneumatocele formation in adult pneumonia. Chest 92,717-720[Abstract/Free Full Text]
  6. Caffey, D (1940) Regional obstructive pulmonary emphysema in infants and children. Am J Dis Child 60,586-605
  7. Wu, MH, Tseng, YL, Lin, MY, et al (1997) Surgical treatment of pediatric lung abscess. Pediatr Surg Int 12,293-295[ISI][Medline]
  8. Baumann, MH, Sahn, SA (1990) Medical management and therapy of bronchopleural fistulas in the mechanically ventilated patient. Chest 97,721-728[Abstract/Free Full Text]
  9. Coghill, CH, Haywood, JL, Chatburn, RL, et al (1991) Neonatal and pediatric high-frequency ventilation: principles and practice. Respir Care 36,596-612



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This Article
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