Anesth Analg 1999;89:252
© 1999 International Anesthesia Research Society
CASE REPORT
Mainstem Bronchial Obstruction During Laparoscopic Fundoplication
Govind R. C. Rajan, MD, and
Vafa Foroughi, MD
Department of Anesthesiology, St. Louis University Health Sciences Center, St. Louis, Missouri
Address correspondence and reprint requests to Govind R. C. Rajan, MD, Department of Anesthesiology, Washington University School of Medicine, at Washington University Medical Center, Campus Box 8054, 660 S. Euclid Ave., St. Louis, MO 63110-1093. Address e-mail to govind-r{at}hotmail.com
 |
Introduction
|
|---|
Laparoscopic surgeries are associated with lower morbidity and motality (1,2) compared with open abdominal procedures. Subcutaneous emphysema (SE) and pneumothorax (PTX) often develop during laparoscopic fundoplication (LF) (3).1 Increasing peak airway pressure (Paw) and ETCO2 and decreasing SaO2 may indicate development of PTX (3–10).1 We report the case of a patient who developed massive increases in ETCO2 and Paw caused by obstruction to the mainstem bronchus secondary to pneumomediastinum.
|
Case Report
|
|---|
A 48-yr-old woman weighing 68 kg presented for LF for repair of paraesophageal hiatus hernia. She had 30-pack per year history of smoking. Before the surgery, the surgeons indicated that they might resort to open thoracotomy. Accordingly, after the induction of anesthesia, the trachea was intubated with a size 7 Univent endotracheal tube. The position of the tube was confirmed with fiberoptic bronchoscopy (FOB). The tube was secured 3–4 cm above the carina with the bronchial blocker completely retracted. Anesthesia was maintained with isoflurane in oxygen, and paralysis was induced with rocuronium. In addition to routine monitoring, a radial arterial line was placed in anticipation of the possibility of one-lung ventilation.
Carbon dioxide (CO2) pneumoperitoneum was created by using a pressure-controlled high-flow insufflator to an intraabdominal pressure of 16–18 mm Hg. The first 90 min of the case proceeded uneventfully. We increased the minute ventilation slightly to compensate for the anticipated hypercarbia (Table 1). In the ensuing 20–30 min, a persistent increase in ETCO2 with tachycardia and hypertension was noticed. Examination of the patient revealed SE over the left neck and chest wall. On auscultation, normal bilateral breath sounds were heard. Minute ventilation was further increased, with no change in the Paw. Surgeons were working around the esophageal foramen at the level of the diaphragm. Within the next few minutes, tense SE rapidly spread to involve the neck and chest wall bilaterally. At this stage, Paw started to increase. Manual ventilation revealed very poor static compliance. No breath sounds were heard over the left lung fields. The possibility of left-sided PTX was discussed with the surgeons, who indicated that they could directly visualize the left lung, which appeared hyperinflated. The right chest was clear to auscultation. The anesthetic circuit and endotracheal tube were examined for kinks or occlusions. FOB ruled out endobronchial intubation, but at the carina, the posterior membranous portion of the trachea appeared to protrude into the tracheal lumen. We were not aware of the significance of this finding. The patient remained hemodynamically stable. We decided to discontinue surgery and to deflate the abdomen, with no immediate improvement in the ease of ventilation. Arterial blood gas analysis revealed a pH of 7.11, PaCO2 of 74 mm Hg, and PaO2 of 413 mm Hg. We continued to manually hyperventilate the lungs. An albuteral nebulizer was tried without benefit. Gradually, in the next several minutes, definite improvement in lung compliance was noticed. SE completely disappeared, and, surprisingly, compliance returned to normal. Because the patient seemed stable, surgery was restarted with lowered insufflation pressure at 12 mm Hg. Within 20 min, massive SE reappeared and Paw increased to 70 cm H2O. Clinical examination revealed no air entry on the left side, and repeat FOB revealed herniation of the posterior membranous portion of trachea into the lumen with complete obliteration of the left mainstem bronchus. In the next few minutes, surgery was completed, and the abdomen was deflated. A chest radiograph revealed minimal PTX on the left side with no evidence of lung collapse or shift of the mediastinum. Manual hyperventilation was continued, with rapid improvement in lung compliance and disappearance of SE. Repeat bronchoscopy revealed normal tracheobronchial anatomy. In the next few minutes, the trachea was extubated with the patient awake, and the patient was transferred to the recovery unit. The patient reported no further complications. Table 1 shows how the respiratory variables changed during the course of this case.
|
Discussion
|
|---|
PTX, pneumomediastinum, and SE developing during upper abdominal laparoscopic procedures are well described (3–10).1 SE is frequently noted during surgical dissection around the esophagus (5,10). The most consistent finding is a sudden and brisk increase in ETCO2 and a marked increase in PaCO2 coincident with the appearance of subcutaneous emphysema in the upper body (5,6,8–10). This is attributed to the greater absorption of CO2 from SE.1 A trend toward increasing Paw or decreasing lung compliance with decreasing SaO2 indicates the presence of PTX (10). Interestingly, asymptomatic PTX often develops during LF associated with minimal changes in the Paw (3). In our case, a completely inflated left lung and normal breath sounds on the right side ruled out high-pressure PTX on either side. Our patient developed a sustained but completely reversible increase in the Paw (>70 cm H2O) with marked decrease in pulmonary compliance (<10 mL/cm H2O) on two different occasions in the absence of PTX or endobronchial intubation. The finding on direct visual (laparoscopic) examination of a fully expanded left lung with absent breath sounds on auscultation suggests the possibility of one-way valvular obstruction to ventilation at the level of major airways. The collapse of the left mainstem bronchus seems to have been secondary to herniation of the membranous portion of the trachea at the carina. During positive pressure ventilation, partial obstruction of the mainstem bronchus may cause hyperinflation of the affected lung because the obstruction tends to get worse during the expiratory phase. Surprisingly, in our patient, these events were associated with impaired CO2 removal but excellent oxygenation. This can be explained by the insufflation of the left lung with 100% oxygen. The impairment in CO2 removal reflects not only our inability to augment minute ventilation (high Paw) to adequately compensate for the increased CO2 absorption, but also an increase in alveolar dead space secondary to compression of pulmonary vasculature with alveolar overdistension. It seems that high pressure in the pneumomediastinum resulted in herniation of membranous portion of the trachea at the carina. Rapid reabsorption of the CO2 (highly soluble) from the tissue planes, along with pulmonary washout, may explain the patient's complete and quick recovery with continued manual hyperventilation. Airway pressure is usually higher during CO2 insufflation because of increased intraabdominal pressure. A further modest increase in the airway pressure is an invariable consequence of increasing minute ventilation to maintain normocarbia (10–12). The ratio of the tidal volume and plateau inspiratory pressure has been suggested to evaluate the changing compliance under such circumstances (11). The gradual but persistent increase in Paw in our patient seems to have been initially caused by partial obstruction of the main stem bronchus with resultant overdistension of the left lung. Eventually, with the completion of the mainstem bronchial obstruction with time, we were essentially ventilating one lung (right) in the presence of an overdistended left lung.
Rapid and massive increases in ETCO2 occur in the presence of SE, which significantly increases the CO2 absorption.1 Chiche et al.1 suggest that CO2 absorption is limited as long as CO2 remains in the abdominal cavity, probably due to collapse of peritoneal vessels secondary to increased intraabdominal pressure. The etiology of SE in the neck and over the thorax during pneumoperitoneum is unclear. During dissection around the esophagus at the diaphragmatic hiatus or due to a breach in the retroperitoneum (13), CO2 tracks along the tissue planes, creating first pneumomediastinum, then SE in the neck and thorax. Therefore, there must be a significant gradient for the gas to move from the abdomen to the neck, and at equilibrium, the pressure in the pneumomediastinum can be as high as the insufflating pressure in the abdomen. This level of pressure in the mediastinum may cause the collapse of the intrathoracic airways, leading to difficulty in ventilation with high airway pressures. This obstruction is expected to worsen during expiration, predisposing the lungs to air trapping. Up to 60% of patients undergoing LF may develop SE in the region of the neck and thorax.1 Because both PTX and pneumomediastinum are caused by passive movement of intraabdominal CO2 into the pleural cavity and mediastinum along the pressure gradient, the application of prophylactic positive end-expiratory pressure during LF may decrease the incidence and extent of pulmonary complications by decreasing the drive pressure between intrathoracic and intraabdominal compartments. Joris et al. (3) report the benefit of positive end-expiratory pressure in the treatment of clinically significant PTX during LF.
The most frequently encountered pulmonary complications during LF are PTX, SE, and pneumomediastinum. Tension PTX and the major intrathoracic airway collapse can be life-threatening. The anesthesiologist should remain vigilant to these possibilities. The earliest manifestations include increases in Paw and ETCO2 and the development of SE over the chest and upper thorax. Chest radiography and FOB are helpful in making the diagnosis. The first step in the management involves discontinuing abdominal insufflation and pulmonary hyperventilation. Prompt absorption of CO2 from various tissue planes and body cavities leads to a quick and complete recovery. Surgical decompression of the PTX is rarely instituted if the above-mentioned measure fails.
In summary, this is the first reported case of severe, reversible ventilatory difficulty caused by the collapse of the mainstem bronchus, presumably secondary to pneumomediastinum (invariably the route of development of SE in the neck and thorax), developing in a patient during LF. Both tension PTX and mainstem bronchial obstruction may have similar clinical presentations. Collapse of the mainstem bronchus was visualized by FOB. Hyperventilation with CO2 washout resulted in uncomplicated, complete recovery. This should always be considered in the differential diagnosis whenever a significant increase in Paw and ETCO2 develops in the presence of SE in the neck and thorax during upper abdominal laparoscopic procedures.
|
Footnotes
|
|---|
1 Chiche JD, Joris J, Lamy M. Respiratory changes induced by subcutaneous emphysema during laparoscopic fundoplication [abstract]. Br J Anaesth 1994;72:37. 
|
References
|
|---|
-
Grace PA, Quereshi A, Coleman J, et al. Reduced postoperative hospitalization after laparoscopic cholecystectomy. Br J Surg 1991;78:160–2.[ISI][Medline]
-
Joris J, Cigarini I, Legrand M, et al. Metabolic and respiratory changes after cholecystectomy performed via laparotomy or laparoscopy. Br J Anaesth 1992;69:341–5.[Abstract/Free Full Text]
-
Joris JL, Chiche JD, Lamy M. Pneumothorax during laparoscopic fundoplication : diagnosis and treatment with positive end-expiratory pressure. Anesth Analg 1995;81:993–1000.[Abstract]
-
Pearce DJ. Respiratory acidosis and subcutaneous emphysema during laparoscopic cholecystectomy. Can J Anaesth 1994;114:988–92.
-
Chui PT, Gin T, Chung SCS. Subcutaneous emphysema, pneumomediastinum and pneumothorax complicating laparoscopic vagotomy. Anaesthesia 1993;48:978–81.[ISI][Medline]
-
Whiston RJ, Eggars KA, Morris RW, Stamatakis JD. Tension pneumothorax during laparoscopic cholecystectomy. Br J Surg 1991;78:1325–6.[ISI][Medline]
-
Hasel R, Arora SK, Hickey DR. Intraoperative complications of laparoscopic cholecystectomy. Can J Anaesth 1993;40:459–64.
-
Gabbott DA, Dunkley AB, Roberts FL. Carbon dioxide pneumothorax during laparoscopic cholecystectomy. Anaesthesia 1992;78:587–8.
-
Woolner DF, Johnson DM. Bilateral pneumothorax and surgical emphysema associated with laparoscopic cholecystectomy. Anaesth Intensive Care 1993;21:108–10.[ISI][Medline]
-
Wahba RWM, Tessler MJ, Kleinman SJ. Acute ventilatory complication during laparoscopic upper abdominal surgery. Can J Anaesth 1996;43:177–83.
-
Wabha RWM, Beique F, Kleinman SJ. Cardiopulmonary function and laparoscopic cholecystectomy. Can J Anaesth 1995;42:51–63.[Abstract/Free Full Text]
-
Wahba RWM, Mamazza J. Ventilatory requirement during laparoscopic cholecystectomy. Anaesth 1993;40:206–10.
-
Webb T. Pneumothorax and pneumomediastinum during colonoscopy. Intensive Care 1998;26:302–4.
Accepted for publication March 16, 1999.
This article has been cited by other articles:
|
|
|
|
 
F. W Dupont
Anesthesia for Esophageal Surgery
Seminars in Cardiothoracic and Vascular Anesthesia,
March 1, 2000;
4(1):
2 - 17.
[Abstract]
[PDF]
|
|
|
Top
Introduction
Case Report
