Bronchopleural Fistula: Anesthetic Management

Angela Truong
Dam-Thuy Truong
Dilip Thakar
Bernhard Riedel

Clinical Vignette

Bronchopleural fistula is a direct communication between the central bronchial tree and the pleural cavity which results from disruption of a bronchial stump or tracheobronchial anastomosis, causing an air leak from the lung. This contrasts with a pneumothorax, in which the communication is peripheral, between a ruptured bleb or alveolar duct and the pleural cavity. When the fistula or sinus tract of a BPF extends to the skin of the chest wall it is termed a bronchopleural-cutaneous fistula. Although rare, BPF represents a challenging management problem; it is associated with high rates of morbidity and mortality and poses formidable challenges during anesthetic management because of the risks of life-threatening loss of ventilation, tension pneumothorax, and contamination of the remaining lung through the fistula.

Incidence

Bronchopleural fistula is relatively rare, with an overall reported incidence following pulmonary resection between 1.5% and 20%.^1,2 About two-thirds of cases occur as a postoperative complication of pulmonary resection, by far the most common cause of BPF. Other less common causes of BPF include necrotizing lung infections, persistent spontaneous pneumothorax, chemotherapy or radiotherapy (for lung cancer), and tuberculosis (Table 18–1). The incidence is higher with pneumonectomy than with lobectomy, since the lobes remaining after lobectomy may offer stabilization and protection to the bronchial stump. Left-sided pneumonectomy is less vulnerable than right-sided pneumonectomy because the bronchial stump is smaller and usually located just under the aortic arch, deriving some protection from it.

Table 18–1. Etiology of Bronchopleural Fistula

Etiology

The destruction of a bronchial wall that leads to BPF may result from a variety of etiologies; including surgical causes, anesthetic-related causes, and medical causes (Table 18–1).

BPF after Lung Resection: Pathophysiology, Risk Factors, and Types

An understanding of the pathophysiology and risk factors involved in BPF development is essential for its prevention and successful management. Not a distinct disease entity, BPF is rather a pathological process following lung resection. Necrosis of the wall between the bronchial system and the pleural cavity results from the complex interaction of three factors: trauma, infection, and poor wound healing. Each factor can potentiate the harmful effects of the other factors. For instance, infection not only contributes directly to the occurrence of BPF, but can also impede wound healing and render the affected area more vulnerable to trauma during subsequent airway manipulation.

Bronchopleural fistula is classified as acute or chronic, and each has a distinct presentation and treatment. Acute BPF classically occurs within the first week following lung resection, resulting from sudden dehiscence of the bronchial stump suture line. Acute BPF is essentially related to surgical technique, and infection and serious coexisting medical conditions play lesser roles. In contrast, chronic BPF, which may take weeks or months to develop, can occur after lung resection or be associated with nonsurgical conditions such as empyema or lung abscess. It usually occurs in patients with severe chronic debilitating comorbid conditions, and infection plays a primordial role.

The risk factors associated with development of BPF can be classified as preoperative, intraoperative, or postoperative. Preoperative factors include immunosuppression, prolonged corticosteroid therapy, preexisting infection such as active tuberculosis with pathogen-positive sputum, neoadjuvant radiotherapy/chemotherapy, chronic debility, malnutrition, and uncontrolled diabetes mellitus. Intraoperative or surgical risk factors include pneumonectomy, especially right-sided pneumonectomy, a long bronchial stump, and poor surgical technique that results in faulty stump closure and/or compromised blood supply to the bronchial stump. Postoperative factors include prolonged mechanical ventilation, atelectasis, pneumonia, empyema, re-intubation and frequent tracheobronchial suctioning, and residual tumor at the stump.^3,4 Importantly, these risk factors usually contribute to BPF formation through a combination of trauma, infection, and poor wound healing (Figure 18–1).

Figure 18–1. Graphical representation of factors that play central roles in BPF formation.

CLINICAL PRESENTATION

The clinical signs of BPF are determined by the size of the BPF and whether the BPF is acute or chronic in origin. When the fistula is small (of the order of a few millimeters, Figure 18–2), the predominant symptoms are cough, particularly when the patient is lying on the side of the fistula, and severe shortness of breath. A delay in cavity filling after pneumonectomy is also noted. When empyema is present, infectious symptoms dominate. When the fistula is large, formed by sudden massive dehiscence of the bronchial stump, copious expectoration of pleural fluid may be noted. This may result in sudden catastrophic flooding of the airway, and possibly even death by asphyxia due to the large communication between the fluid-filled pleural cavity and the tracheobronchial tree. If the patient is still intubated, positive pressure ventilation with a massive leak through a large BPF will cause severe loss of alveolar ventilation, resulting in acute hypoxia, hypercarbia, and respiratory acidosis. If the correct diagnosis of BPF is not made, desperate attempts to increase positive pressure ventilation will paradoxically worsen the hypoventilation by further increasing the air leak and enlarging the fistula. Furthermore, if a functioning chest tube is not in place, the air leak will quickly result in tension pneumothorax and cardiovascular collapse.

Figure 18–2. Bronchoscopy showing two small BPFs in the bronchial stump. Abbrev: RMSB, right main stem bronchus; LMSB, left main stem bronchus.

The onset is much more insidious in chronic BPF, with a relatively slow accumulation of purulent material in the pleural cavity and gradual erosion into the bronchial system. The clinical picture often consists of low-grade fever, fatigue, generalized malaise, and cough with purulent or blood-tinged sputum. Hemoptysis, fetid breath, and subcutaneous emphysema are less frequently observed. The clinical picture may be very difficult to differentiate from similar nonspecific symptoms associated with other complications observed during the postpneumonectomy period.

Diagnosis

The diagnosis of BPF is made by clinical examination, diagnostic imaging techniques, nuclear scintigraphy, and bronchoscopy, which is universally accepted as the “gold standard.”

Even though the clinical presentation of BPF is often nonspecific, a high index of suspicion based on the combination of suggestive signs and symptoms should alert clinicians to the potential diagnosis of BPF. In a simple bedside test that has been used to confirm the diagnosis of BPF, methylene blue is injected into the pleural space of a patient with a suspected BPF and the diagnosis confirmed through expectoration of blue-tinged sputum. Diagnostic imaging studies more often used for the detection of BPF include chest x-ray and CT. Bronchography and sinography may also be performed.

In the immediate period following lung resection, chest radiograph and CT scan normally show progressive accumulation of fluid in the postpneumonectomy space coupled with decreasing amounts of air. Because of the large empty space left behind after pneumonectomy, there is normally an accompanying gradual elevation of the ipsilateral hemidiaphragm and a slight shift of the mediastinum toward the side of surgery. In cases of BPF, these trends are reversed: air accumulation increases and fluid level decreases in the postpneumonectomy pleural space, air-fluid level drops by more than 2 cm, and mediastinal shift is absent or a previously shifted mediastinum returns to the unaffected side.^5–7 In severe cases, a tension pneumothorax may develop within the postpneumonectomy space, with accompanying mediastinal shift (Figure 18–3). In the immediate postoperative period, these radiographic findings are particularly valuable in making an early diagnosis of BPF in an otherwise asymptomatic patient.⁸

Figure 18–3. Chest x-ray showing postpneumonectomy pneumonitis and tension pneumothorax with mediastinal shift as a result of a BPF.

It is much more challenging to directly identify the fistula tract on CT scan (Figures 18–4 and 18–5), especially when the BPF is very small or has an extremely tortuous path. Visualization of the fistula tract on CT scan can be facilitated by special techniques such as spiral CT with thin sections and three-dimensional reconstruction.⁹ Bronchography or radiography of the bronchial system after intrabronchial instillation of a radio-opaque contrast medium allows visualization of the fistula. Similarly, if a bronchopleural cutaneous fistula is present, sinography or fistulography can be performed by injection of contrast dyes percutaneously into the fistula skin opening to outline the contour of the sinus tract.

Figure 18–4. CT scan identifying a BPF tract in the main stem bronchial stump following pneumonectomy for mesothelioma.

Figure 18-5. CT scan identifying a peripheral BPF in a patient 2 weeks after a left lower lobectomy, potentially related to cystic rupture of a subpleural metastasis.

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