Secondary Logo

Journal Logo

Is Bronchoscopy Indicated in the Management of Atelectasis?: Pro: Bronchoscopy

Mehrishi, Sandeep M.D., F.C.C.P.

Controversy
Free

Nassau University Medical Center, East Meadow, New York, U.S.A.

Address reprint requests to Sandeep Mehrishi M.D., Director, Interventional Pulmonology Unit, Nassau University Medical Center, 2201 Hempstead Turnpike, East Meadow, NY 11554-1153 U.S.A.; e-mail: mehrishis@aol.com

Atelectasis is a common problem in critically ill patients. Major factors leading to persistent atelectasis are retained airway secretions, increased production of mucus, decreased cough efficiency, altered compliance of lung tissue, and impaired regional ventilation. 1 Atelectasis is especially common during the postoperative period (particularly in patients undergoing abdominal, thoracic, or cranial surgery), in neuromuscular diseases, or after sedation and/or neuromuscular blockade. Specific risk factors that have been shown to increase the incidence of atelectasis are smoking, obesity, duration of anesthesia, upper abdominal surgery, obstructive lung disease, and the presence of upper respiratory infection. 2

Mechanically ventilated patients are especially at high risk for the development of atelectasis, and consequently infectious complications result from impaired mucus transport 3 and ineffective cough because of the lack of adequate glottic closure.

Atelectasis is usually segmental and generally is not life-threatening. However, life-threatening, acute, massive, whole-lung collapse may occur, necessitating emergent treatment. If not treated quickly, it may predispose to impaired gas exchange, infectious complications, or, more rarely, may evolve into fibrosis, 1 leading to increased morbidity and mortality.

Soon after the availability of flexible bronchoscopy (FFB), physicians began using it frequently for the treatment and assessment of atelectasis. Conventional FFB became a useful adjunct with chest physiotherapy in the clearance of tracheobronchial secretions, and today many physicians use FFB frequently to treat atelectasis. At times, emergent FFB is attempted for the management of respiratory crisis secondary to atelectasis and airway mucus retention. Hasegawa et al. 4 reported atelectasis/airway mucus retention as the most common indication of 191 emergency bronchoscopies performed in critically ill patients. However, because of a lack of well-controlled clinical trials, it is still debated whether FFB is superior to chest physiotherapy in the treatment of atelectasis.

FFB has been used in atelectasis for the reasons presented in Table 1.

TABLE 1

TABLE 1

Studies assessing the usefulness of physiotherapy (e.g., chest physiotherapy, percussion therapy [P], kinetic bed therapy [KT]) have shown that these therapies are effective in the treatment and prevention of atelectasis in critically ill patients. Although there is no doubt that FFB is effective in removing mucus plugs and excessive secretions, there is still a lack of consensus on whether FFB is a better, safe, and effective therapy in treatment of atelectasis compared with standard chest physiotherapy.

Back to Top | Article Outline

EFFECT OF CHEST PHYSIOTHERAPY IN CRITICALLY ILL PATIENTS

Chest physiotherapy is considered a traditional and safe method for the treatment of atelectasis in the majority of critically ill patients. The most common techniques used by physiotherapists in the intensive care unit (ICU) are positioning, mobilization, limb exercises, manual hyperinflation, percussion, vibrations, suction, cough, and various breathing exercises. 5 However, despite their effectiveness and safety, these physical therapy techniques may not be so useful and, in fact, may impact negatively on the already-compromised clinical state of the critically ill patient.

Gormezano and Branthwaite 6 assessed changes in gas exchange as long as 30 minutes after chest physiotherapy in 42 mechanically ventilated patients. The reasons for ventilatory support were major general surgery, respiratory failure, and cardiac disease. They found a significant decrease in the partial pressure of oxygen (P < 0.05) and an increase in the partial pressure of carbon dioxide (P < 0.001) after chest physiotherapy, which was worse in patients with low cardiac output. They postulated that the increase in intrathoracic pressure exerted by chest physiotherapy could lower the cardiac output so that for a given shunt effect, mixed venous oxygen will fall, leading to a decrease in arterial oxygenation. Connors et al. 7 studied the effect of postural drainage and chest percussion (PDP) on oxygenation in 22 patients with a variety of acute nonsurgical pulmonary disorders. They observed a decline in the partial pressure of oxygen of approximately 17 mmHg immediately after PDP, which deteriorated further after return of the patient to the pretreatment position, especially in patients with either no sputum or with a small amount of mucoid sputum. They concluded that the fall in the partial pressure of oxygen was the result of ventilation–perfusion mismatch and suggested that PDP could be potentially dangerous, especially in patients without sputum production. Tracheobronchial suctioning, an essential component of chest physiotherapy, is also associated with hypoxemia, hemodynamic instability, and tracheobronchial erosion and hemorrhage.

Notable effects on the cardiovascular system during chest physiotherapy have been reported. Many authors demonstrated marked alteration in various cardiovascular responses including cardiac output, heart rate, blood pressure, and pulmonary arterial pressure during PDP. 8,9 Hammon et al. 10 studied the prevalence and type of arrhythmias that occurred during PDP treatment in critically ill patients. They found that 36% of the 72 patients developed arrhythmias, of whom 11% experienced major arrhythmias including more than six premature ventricular contractions per minute, multifocal and coupled premature ventricular contractions, and paroxysmal atrial tachycardia, whereas 25% experienced minor arrhythmias (less than six premature ventricular contractions per minute, premature atrial contractions, and supraventricular tachycardia). They observed that increased age and presence of acute cardiac condition were associated with a higher prevalence of cardiac arrhythmias. An increase in sympathetic nervous activity and elevated plasma catecholamine levels may play a role in cardiac arrhythmias during PDP. 11

Weissman and Kemper 12 found, in postoperative mechanically ventilated patients, that during chest physiotherapy, oxygen consumption, oxygen extraction, and oxygen delivery increased by a mean of 52%, 35%, and 17% respectively. In addition to an increase in the partial pressure of carbon dioxide, an increase in heart rate, cardiac output, blood pressure, and pulmonary arterial pressure was also noted. They concluded that the increase in oxygen demand caused by chest physiotherapy triggered an integrated physiologic response that resulted in increased respiratory and cardiac performance. In a different study 13 they demonstrated that chest physiotherapy was associated with maximum metabolic increases (>35% above lowest values) compared with other routine daily care activities like bathing, performance of physical examination, etc. They also demonstrated increases in heart rate and blood pressure, and concluded that even routine daily care activities in the ICU can alter metabolic rate significantly.

Although physical therapy may be useful in improving the respiratory status of the critically ill patient, it may require a substantial number of personnel and their time to achieve this goal. Recently, Wong 14 described the successful use of intensive physical therapy in a 66-year-old man with a history of chronic obstructive pulmonary disease who was admitted to the ICU with respiratory failure. Intensive physical therapy was administered every 2 hours for the first 12 hours, with a total of six sessions on day 1 and five sessions on day 2. He demonstrated improvement in oxygenation, radiographic resolution of infiltrates, and was able to avoid endotracheal intubation and mechanical ventilation. He highlighted the potential beneficial use of 24-hour availability of intensive physical therapy in ICUs. However, in routine practice, physical therapy by trained physical therapists is not available for 24 hours in most ICUs in these days of cost restraint. A recently conducted “postal questionnaire” profile of European ICU physiotherapists 15 demonstrated that the availability of nighttime physiotherapists is variable across many European countries. Only 34% of the respondents said they have physiotherapists available during the night. The profile also indicated that the involvement of physiotherapists in more specialized techniques is also a function of the number of physiotherapists working exclusively in an ICU. An argument can be made that the nurses are capable of providing physiotherapy to their patients and can fill in for the physical therapists in their absence. Although this is true, it is practically impossible for a nurse to provide adequate physical therapy in ICUs with a high turnover rate of patients, a low nurse-to-patient ratio, and a lack of adequate training in principles of physiotherapy. This is especially true in respiratory care units, particularly in city hospitals, where most of the patients are chronically vented and the nurse-to-patient ratio is less. 16

One of the newer modalities that has become available in past few years is KT+P. Raoof et al. 16 conducted a prospective randomized study comparing the effect of conventional chest physiotherapy (group 1, control) with KT+P (group 2, test) on the resolution of atelectasis in critically ill patients. Bronchoscopy was allowed in both groups in patients who were failing the therapy. They demonstrated that more than 80% of patients receiving KT+P, in contrast to less than 20% of patients who received conventional therapy, showed marked improvement in atelectasis. Three of seven patients in the control group and 0 of 17 patients in the test group underwent FFB. This study, however, was small, and may have been biased because performance of FFB depended on the pulmonary physician from the same group who was aware of the study being conducted. Raoof et al. 16 demonstrated that only three of seven patients in group 1and 0 of 17 patients in group 2 underwent bronchoscopy. However, FFB was offered to 3 of 17 patients (18%) in group 2 who failed KT+P, and was offered to the remaining three of four patients in group 1 who failed conventional chest physiotherapy. This means an additional 6 of 21 patients (28%) would have undergone bronchoscopy because of either failed conventional chest physiotherapy or failed KT+P. Even continuous lateral rotation therapy has not been shown to increase mucus removal from the lungs in critically ill patients, 17 not to mention the potential of losing airway or venous access in continuously moving critically ill patients, with disastrous consequences.

Back to Top | Article Outline

ROLE OF BRONCHOSCOPY IN THE TREATMENT OF ATELECTASIS

The study most often cited to claim that FFB is not useful in the treatment of atelectasis is the prospective study by Marini et al. 1 that compares, in a randomized fashion, the clinical outcome of patients treated for atelectasis with either respiratory therapy maneuvers only or by FFB combined with conventional chest physiotherapy. The study included two groups, respectively, of 14 patients (group 1) and 17 patients (group 2). Group 1 patients underwent immediate FFB followed by intensive respiratory therapy for 2 days whereas the patients in group 2 underwent respiratory therapy without FFB. They found that the rate of resolution of atelectasis in group 1 and group 2 was similar and did not recur or advance in any of the patients who received chest physiotherapy at frequent intervals. They also found that the presence of an air bronchogram predicted delayed resolution of atelectasis. This study, however, was small and fraught with many drawbacks. Myers 18 questioned the validity of the study because various factors like hemodynamic stability, arterial blood gas results, and respiratory status of the patient were not clearly stated. In addition, whether the two groups were comparable in age, neuromuscular function, or ability to cooperate with respiratory therapy treatments was not clear.

Moreover, the two groups differed in one major way in that 64% of patients in group 1 were intubated at the time of FFB compared with only 35% of patients in group 2. Furthermore, 47% of patients who received respiratory therapy for the first 24 hours had 50% or less improvement in atelectasis and required delayed FFB. True, FFB was not very effective when an air bronchogram was present, but chest physiotherapy was also relatively ineffective in a similar scenario. Friedman 19 believed that the data of Marini et al. 1 demonstrated a slightly better result in those intubated patients who were treated with FFB compared with those patients who were treated with chest physiotherapy. However, he found FFB to be of definite superiority over chest physiotherapy in nonintubated patients with atelectasis. This indicates that directional suctioning plays an important role in clearing out tracheobronchial secretions. Because FFB is nothing more than suctioning under direct vision, which may only be slightly better than routinely applied undirected suctioning in intubated patients, it is obvious that FFB would be more effective in nonintubated patients in whom nonbronchoscopic-directed suctioning is not possible. Also, frequent tracheobronchial suctioning is easy in intubated patients; in nonintubated patients it is not feasible and may not be tolerated by the patient. Therefore, in this subgroup of patients, early use of FFB may be desirable to prevent progression to respiratory failure. 18 Lastly, not only did they exclude the patients with rib fractures or spinal injury, a subgroup of patients that may be more prone to develop atelectasis, the study by Marini et al. 1 also relied on radiologic resolution to compare the outcome of the two groups despite the fact that clinical improvement often precedes radiologic changes.

Atelectasis currently is the most common indication for therapeutic bronchoscopy in the critical care unit. 20 Prompt removal of thick mucus secretions and plugs, especially in patients with underlying pulmonary disease, is life saving in marked hypoxemia. Indeed, the presence of profound hypoxemia on the presumptive basis of retained secretions is by itself an indication for therapeutic bronchoscopy. Not only is FFB effective in removing the mucus plugs rapidly, it also helps in identifying the etiology of atelectasis by visualizing the tracheobronchial tree (e.g., recognition of an unanticipated blood clot as a cause for atelectasis) because as many as 30% of endobronchial blood clots occur without evidence of hemoptysis. 21

Wanner et al. 22 described the successful use of bronchoscopy in 27 patients with atelectasis, of whom 25 demonstrated lobar collapse and two had segmental collapse. Of the total 34 procedures, 79% resulted in clinical improvement and 85% resulted in roentgenologic improvement. In 62% of patients, improvement in chest roentgenogram was noted within 3 hours after FFB whereas 23% had roentgenographic improvement within 24 hours. All patients with impacted mucus plugs responded favorably to bronchial toilet. They concluded that FFB is effective in aspirating inspissated secretions in atelectasis and is well tolerated in acutely ill patients. Mahajan et al. 23 also demonstrated convincingly that FFB is efficient and safe for removing major bronchial mucus plugs in acutely ill surgical and nonsurgical patients with notable pulmonary collapse.

FFB seems to be of great benefit in patients with neuromuscular disease and atelectasis. Patients with Guillain–Barré syndrome requiring mechanical ventilation frequently sustain proximal atelectasis secondary to ineffective clearance and mucus plugging. FFB has been shown to improve atelectasis and oxygenation rapidly. 24 Severe postlobectomy atelectasis is a common complication after lobectomy or bilobectomy (Fig. 1A). It is associated with an increase in hospital and ICU stay, and with a marked increase in the cost of care. In addition to anatomical rearrangement of bronchi, poor ciliary clearance of bloody secretions after intraoperative surgical manipulation may result in the pooling of mucus and blood in the proximal large airways, leading to lung collapse. FFB can be extremely useful in this situation 25 (Fig. 1B). Acute, life-threatening intraoperative atelectasis may at times require emergent use of FFB to relieve severe hypoxemia and to determine the underlying pathophysiology of atelectasis. 26 Of course, chest physiotherapy, and KT+P are not feasible at the time of surgery. Snow and Lucas 27 found that in critically ill surgical patients, FFB is most useful in patients with lobar collapse, and the procedure is relatively safe. It has been found to be especially useful in performing bronchial toilet in lung transplant recipients and in patients with bronchiectasis and cystic fibrosis. 28

FIG. 1.

FIG. 1.

At times when the atelectasis is not resolved even after thorough removal of mucopurulent secretions, FFB with positive pressure ventilation has been shown to reexpand the refractory atelectasis. Harada et al. 29 demonstrated successful expansion of the atelectatic lung using an inflator device consisting of a flexible bronchoscope with a small balloon cuff at the distal end. Using insufflation of air, they demonstrated successful reexpansion of the atelectatic lung in 93% of patients (14 of 15). Since then, there have been many reports of the successful use of FFB in the reexpansion of refractory atelectasis.

Severe mucus plugging at times may be the main reason for progressive airflow obstruction in patients with severe asthma. This mucus plugging may lead to worsening gas exchange, increasing inspiratory pressure, and progressive dynamic hyperinflation. FFB with mucolytic therapy 30 in patients who fail to respond to conventional therapy has been shown to improve gas exchange and airway dynamics by removing the extensive mucus plugs from the airways. In addition, other therapeutic modalities like the instillation of 1:10,000 epinephrine solution to reduce mucosal edema can be attempted during FFB to alleviate the predisposing factor for atelectasis.

The other notable advantage of performing FFB in atelectasis, in addition to therapeutic drainage, is diagnostic. Because atelectasis predisposes to infection, protected specimen brushing and bronchoalveolar lavage can be performed easily at the same time as therapeutic suctioning. This may enhance the chances of precise treatment of atelectasis associated with pneumonia. Unsuspected tumor can also be identified at the time of therapeutic suctioning, leading to a dramatic change in the patient's management plan. Direct visualization of the tracheobronchial tree increases the chances of identifying foreign bodies as a cause for atelectasis.

One of the other important issues is the cost of a particular method used in the management of a disease. The cost of performing FFB and the cost of procuring a kinetic bed per day varies from hospital to hospital. The actual cost of performing FFB in our hospital varies from $290 to $320 (US) 16 and the cost for the procurement of a kinetic bed is $175 (US) per day. The actual number of days these beds are used is variable. Although FFB is used only once, KT+P are usually used for many days. In one study, 16 the average length of time KT+P was used was 7.3 ± 5.2 days. As is obvious, even a 2-day use of KT+P is more expensive than FFB, and the cost will be enormous if the therapy is used frequently and for prolonged periods of time. In addition, the cost may increase further if FFB is required subsequently for KT+P-refractory atelectasis, not to mention the increased length of stay in the ICU and the increased risk of developing complications secondary to hypoxemia and retained secretions.

FFB has been proven safe in nonmechanically ventilated patients and has a low complication rate (<10%) in mechanically ventilated patients. The overall incidence rate of major complications ranges from 0.08 to 0.15%, and the mortality rate ranges from 0.01 to 0.04%. 31 Minor complications occur in 6.5% of patients. If adequate precautions are taken, FFB is safe in high-risk critically ill patients on mechanical ventilation. Based on the safety and usefulness of FFB, it has been suggested that every physician in the critical care unit be able to use a flexible bronchoscope in the therapeutic suctioning of the tracheobronchial tree.

In summary, FFB is a safe and effective method of treating atelectasis in critically ill patients. The situations in which there is some consensus among physicians to use FFB in the treatment of atelectasis include (1) lobar atelectasis from retained secretions with an air bronchogram pattern that is visible only to the level of the segmental bronchi; (2) when standard chest physiotherapy has been administered properly for retained secretions without positive results; (3) life-threatening near-or whole-lung atelectasis; (4) when a symptomatic patient is unable to undergo vigorous respiratory therapy treatments from chest trauma, unstable vertebral fractures, extensive burns, smoke inhalation, neuromuscular diseases, etc.; and (5) when an important diagnostic question exists.

Back to Top | Article Outline

REFERENCES

1. Marini JJ, Pierson DJ, Hudson LD. Acute lobar atelectasis: a prospective comparison of fiberoptic bronchoscopy and respiratory therapy. Am Rev Respir Dis 1979; 119:971–8.
2. Lewis FR. Management of atelectasis and pneumonia. Surg Clin North Am 1980; 60:1391–401.
3. Konrad F, Schreiber T, Brecht–Kraus D, et al. Mucociliary transport in ICU patients. Chest 1994; 105:237–41.
4. Hasegawa S, Terada Y, Murakawa M, et al. Emergency bronchoscopy. J Bronchol 1998; 5:284–7.
5. Stiller K. Physiotherapy in intensive care: towards an evidence-based practice. Chest 2000; 118:1801–13.
6. Gormezano J, Branthwaite MA. Effects of physiotherapy during intermittent positive pressure ventilation: changes in arterial blood gas tensions. Anesthesia 1972; 27:258–64.
7. Connors Jr, AF Hammon WE, Martin RJ, et al. Chest physical therapy: the immediate effect on oxygenation in acutely ill patients. Chest 1980; 78:559–64.
8. Laws AK, McIntyre RW. Chest physiotherapy: a physiological assessment during intermittent positive pressure ventilation in respiratory failure. Can Anaesth Soc J 1969; 16:487–93.
9. Cohen D, Horiuchi K, Kemper M, et al. Modulating effects of propofol on metabolic and cardiopulmonary responses to stressful intensive care unit procedures. Crit Care Med 1996; 24:612–7.
10. Hammon WE, Connors Jr, AF McCaffree DR. Cardiac arrhythmias during postural drainage and chest percussion of critically ill patients. Chest 1992; 102:1836–41.
11. Aitkenhead AR, Taylor S, Hunt CW, et al. Effect of respiratory therapy on plasma catecholamine [abstract]. Anesthesiology 1984; 61:A44.
12. Weissman C, Kemper M. Stressing the critically ill patient: the cardiopulmonary and metabolic responses to an acute increase in oxygen consumption. J Crit Care 1993; 8:100–8.
13. Weissman C, Kemper M, Damask MC, et al. Effect of routine intensive care interactions on metabolic rate. Chest 1984; 86:815–8.
14. Wong WP. Physical therapy for a patient in acute respiratory failure. Phys Ther 2000; 80:662–70.
15. Norrenberg M, Vincent JL. A profile of European intensive care unit physiotherapists. European Society of Intensive Care Medicine. Intensive Care Med 2000; 26:988–94.
16. Raoof S, Chowdhrey N, Raoof S, et al. Effect of combined kinetic therapy and percussion therapy on the resolution of atelectasis in critically ill patients. Chest 1999; 115:1658–66.
17. Dolovich M, Rushbrook J, Churchill E, et al. Effect of continuous lateral rotational therapy on lung mucus transport in mechanically ventilated patients. J Crit Care 1998; 13:119–25.
18. Myers DJ. Can fiberoptic bronchoscopy reverse acute lobar atelectasis? Indiana Med 1986; 79:593–5.
19. Friedman SA. Comparison of fiberoptic bronchoscopy and respiratory therapy. Am Rev Respir Dis 1982; 126:367–8.
20. Prakash UBS. Bronchoscopy in the critical care unit. Semin Respir Med 1997; 18:583–91.
21. Arney KL, Judson MA, Sahn SA. Airway obstruction arising from blood clot: three reports and a review of the literature. Chest 1999; 115:293–300.
22. Wanner A, Landa JF, Nieman Jr, RE et al. Bedside bronchofibroscopy for atelectasis and lung abscess. JAMA 1973; 224:1281–3.
23. Mahajan VK, Catron PW, Huber GL. The value of fiberoptic bronchoscopy in the management of pulmonary collapse. Chest 1978; 73:817–20.
24. Jolliet P, Chevrolet JC. Bronchoscopy in the intensive care unit. Intensive Care Med 1992; 18:160–9.
25. Korst RJ, Humphrey CB. Complete lobar collapse following pulmonary lobectomy: its incidence, predisposing factors, and clinical ramifications. Chest 1997; 111:1285–9.
26. Pivalizza EG, Tonnesen AS. Acute life-threatening intraoperative atelectasis. Can J Anaesth 1994; 41:857–60.
27. Snow N, Lucas AE. Bronchoscopy in the critically ill surgical patient. Am Surg 1984; 50:441–5.
28. Shennib H, Baslaim G. Bronchoscopy in the intensive care unit. Chest Surg Clin Am 1996; 6:349–61.
29. Harada K, Mutsuda T, Saoyama N, et al. Re-expansion of refractory atelectasis using a bronchofiberscope with a balloon cuff. Chest 1983; 84:725–8.
30. Henke CA, Hertz M, Gustafson P. Combined bronchoscopy and mucolytic therapy for patients with severe refractory status asthmaticus on mechanical ventilation: a case report and review of the literature. Crit Care Med 1994; 22:1880–3.
31. Raoof S, Mehrishi S, Prakash U. Role of bronchoscopy in modern medical intensive care unit. Clin Chest Med 2001; 22:241–261.
© 2002 Lippincott Williams & Wilkins, Inc.