Abstract

A 22-year-old woman with no history of asthma developed an acute recurrent attack of severe bronchoconstriction and right upper lobe atelectasis immediately after laryngoscopy and endotracheal intubation. The first attack had taken place 2 months earlier under identical circumstances. Induction of anesthesia for tracheal intubation was achieved using propofol, fentanyl, and rocuronium. Bronchial obstruction and bronchial intubation were excluded by bronchoscopy. The atelectasis was quickly resolved with mechanical ventilation and spasmolytic treatment on both occasions. The surgical procedure could proceed soon after resolution of the atelectasis.

Keywords

anesthesia, general; propofol; pulmonary atelectasis;

1. Introduction

Major lung collapse secondary to inadvertent bron-chial  intubation1 or  intrabronchial  obstruction²⁻⁴ has  been  sporadically  reported.  Case  reports  on  lung  collapse  associated  with  acute  reflex  bron-choconstriction  in  the  absence  of  intrabronchial  obstruction during induction of anesthesia are very rare.⁵⁻⁷  We  report  herein  a  case  of  a  seeming  healthy young female who twice developed severe bronchoconstriction, with resultant acute collapse of  the  right  upper  lobe  (RUL)  immediately  after  induction of anesthesia in the operating room. The first  attack  had  taken  place  2  months  earlier  in  identical circumstances.

2. Case Report

A 22-year-old, 77-kg, 168-cm woman with a history of hypertension for 8 years and cigarette smoking (< 1 pack/day) for 6 years was scheduled for extracranial-intracranial arterial bypass for moyamoya disease. Four months before this admission the patient had undergone laparoscopic cholecystectomy smoothly under general anesthesia with sevoflurane-50% ni-trous  oxide  (N₂O)  in  oxygen.  Current  medication  included  irbesartan  (300  mg  daily)  and  triflusal  (300  mg  3  times  daily).  There  was  no  history  of  asthma, drug allergies, or pulmonary diseases. The patient denied any bronchitic or upper respiratory symptoms  (e.g.,  coughing  or  phlegm  production). 

Laboratory  data  (including  complete  blood  count  and urinalysis) were within normal limits. Physical examination,  including  heart  and  lung  ausculta-tion, revealed no evident acute or chronic disease. Preoperative  blood  pressure  was  132/82  mmHg,  heart rate was 76 beats/min, respiratory rate was 13 breaths/min, and oral temperature was 36.8ºC. The  patient  was  premedicated  with  midazolam  7.5   mg   orally   60   minutes   before   induction   of   anesthesia.

After  insertion  of  an  intravenous  cannula  and  placement  of  routine  intraoperative  monitoring  devices  (including  an  electrocardiogram,  invasive  blood  pressure  monitor,  and  pulse  oximeter),  an-esthesia was induced with target-controlled infusion of propofol with a target of 4 μg/mL (Astra-Zeneca, Macclesfield, UK), fentanyl 1.5 μg/kg and rocuronium 1.5 mg/kg. Three minutes after induction, the tra-chea was easily intubated with a 7.0-mm endotra-cheal tube, which was secured between the lips at the  22-cm  mark,  and  the  patient  was  ventilated  with 50% N₂O in oxygen. Immediately following in-tubation, auscultation of the chest revealed bilateral expiratory wheezing, louder on the left than on the right, suggestive of bronchospasm. The peak inspir-atory pressure then increased up to 35−45 cmH₂O, and the tidal volume decreased to less than 200 mL within 10 minutes of initiation of mechanical ven-tilation. N₂O was discontinued, but her percutane-ous  hemoglobin  oxygen  saturation  decreased  to  92% while breathing 100% oxygen. Chest radiogra-phy taken at this juncture revealed RUL atelectasis (Figure 1A). The tip of the tracheal tube was 2.5 cm above  the  carina.  The  bronchospasm  was  treated  successfully  with  aerosolized  albuterol,  methyl-prednisolone 125 mg intravenously, and an amino-phylline  infusion  at  20  μg/kg/min,  and  flexible  fiberoptic  bronchoscopy  showed  that  the  trachea and the right and left endobronchial system were free of obstruction by mucous or foreign bodies.

The  surgery  was  cancelled,  and  the  residual  neuromuscular block was reversed with pyridostig-mine  15  mg  and  glycopyrrolate  0.4  mg  intrave-nously. Satisfactory percutaneous hemoglobin oxygen saturation  (96−98%)  could  be  maintained  while  spontaneously breathing 100% oxygen without any sign of respiratory distress. The endotracheal tube was then removed and the patient was transported to the recovery room where she stayed for 2 hours before  being  returned  to  the  ward.  Subsequent  chest X-ray, taken immediately after arrival at the recovery  room,  revealed  full  re-expansion  of  the  collapsed  RUL.  Chest  auscultation  revealed  ab-sence of wheezing, and the breathing sounds were equal  bilaterally.  The  patient  had  no  respiratory  problems afterwards and was discharged from hos-pital 5 days later.

Two  months  later,  the  surgery  for  moyamoya  disease  was  rescheduled,  because  her  symptoms  were  aggravated  with  right  arm  monoparesis  and  intermittent dysarthria setting in. Following insti-tution of standard monitoring and preoxygenation, anesthetic induction and tracheal intubation were achieved using propofol, fentanyl, and rocuronium followed by continuous infusion of propofol with a target of 4 μg/mL, as in the previous anesthesia. As before,  the  patient  developed  generalized  bron-chospasm with wheezing rales over the entire lung fields  shortly  after  endotracheal  intubation.  The  peak inspiratory pressure increased up to 40 cmH2O and tidal volume progressively decreased to 200 mL. Chest radiography revealed RUL collapse with the tip  of  the  tracheal  tube  3.0  cm  above  the  carina  (Figure  1B).  The  bronchospasm  was  treated  suc-cessfully  with  aerosolized  albuterol,  intravenous  methylprednisolone,  aminophylline  infusion,  and mechanical  ventilation.  Fiberoptic  bronchoscopy  showed that the trachea and bronchial tree were free from obstruction. The surgery was called off, and the residual neuromuscular block was reversed. The patient was transported to the recovery room, and  a  follow-up  chest  X-ray  revealed  nothing  of  note.  Chest  computed  tomography  taken  2  days  afterwards  showed  no  anatomic  anomalies  of  the  tracheobronchial tree (e.g., tracheal bronchus)⁸ or extraluminal mass. Neither the methacholine and histamine bronchial provocation test, nor the skin test  for  propofol,  fentanyl  and  rocuronium  per-formed  3  days  after  the  second  episode  of  atel-ectasis showed positive findings.

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Figure 1 Chest radiograph immediately after endotracheal intubation showing collapse of the right upper lobe at first (A) and second (B) attempts of anesthesia for surgery of moyamoya disease.

3. Discussion

It is generally agreed that atelectasis is caused by obstruction of a bronchus (either because of mas-sive secretion, aspiration, encroachment of a for-eign body or intrabronchial intubation) followed by rapid absorption of the trapped alveolar gas. In our case, however, right main and upper lobe bronchi were free from obstruction on fiberoptic bronchos-copy. A stimulus that increases vagal tone is known to  play  an  important  role  in  triggering  bronchial  obstruction, resulting in “reflex atelectasis”, which is  characterized  by  fast  onset,  absence  of  intra-bronchial obstruction, and signs of parasympathetic stimulation.⁵⁻⁷ Mechanical stimulation of the laryn-geal mucosa has been demonstrated to reflexively enhance  vagal  activity,  irritating  the  trachea  and  bronchi and increasing total lung resistance.⁹ Acute RUL atelectasis was likely to have been associated with the vagally-induced airway reflex in our case, as manifested by acute onset of bronchospasm in the absence of intrabronchial obstruction.

Interestingly, the patient did not show any signs of acute bronchoconstriction during anesthetic in-duction  for  laparoscopic  cholecystectomy  in  the  previous  surgery,  performed  4  months  before.  At  that time, anesthesia was induced with thiopental sodium  375  mg  and  succinylcholine  80  mg,  and  maintained with sevoflurane 2−3% and 50% N₂O in oxygen  and  vecuronium,  while  the  two  consecu-tive anesthesias were induced with propofol, fen-tanyl and rocuronium.

Unlike  thiopental,  propofol  may  decrease  res-piratory resistance and hence could prevent bron-chospasm resulting from airway instrumentation.10 Moreover,  propofol  has  been  demonstrated  to  significantly  inhibit  vagally-induced  bronchocon-striction.¹¹  Nevertheless,  propofol  is  responsible  for  perioperative  anaphylactic  shock  in  France  in  1.2% of cases.¹² Previous investigators have docu-mented that propofol could cause bronchospam.¹³⁻¹⁵ Although  exceedingly  rare,  allergic  reactions  to  fentanyl,  IntralipidTM  and  rocuronium  have  also  been described.^12,16 Thus, drug (propofol, fentanyl, or  rocuronium)-induced  bronchospasm  may  have  played a role in inducing intraoperative respiratory difficulties.  However,  the  absence  of  a  severe  hypotensive episode and generalized erythema at the  onset  of  the  wheezing  would  argue  against  drug-induced histamine release as a priming event in our case. In addition, the patient did not show any signs of adverse reactions immediately after the intravenous  administration  of  those  drugs  before  the intubation. Moreover, neither the methacholine and histamine bronchial provocation test, nor the skin  test  for  propofol,  fentanyl  and  rocuronium  performed a few days thereafter were positive.

A bronchospasm without anaphylactoid reaction after propofol administration has been reported in a patient with sick house syndrome.¹⁷ In this case, the drug lymphocyte stimulation test showed a pos-itive reaction against propofol although a skin test was  negative,  suggesting  that  propofol  could  be  responsible  for  the  bronchospasm  during  the  in-duction of anesthesia. It is suggested that bronchial hypersensitivity may trigger bronchospasm in res-ponse  to  a  sensitizing  drug.  Angiotensin-converting  enzyme inhibitors have also been demonstrated to enhance  bronchial  responsiveness  especially  in  smokers.¹⁸⁻²⁰  As  our  patient  was  a  smoker  taking  irbesartan, we could not rule out the possibility that irbesartan could be responsible for enhancing the bronchospasm induced by propofol.

Although  the  underlying  mechanisms  are  un-clear,  most  acute  lobar  collapses  associated  with  bronchospasm  after  anesthesia  induction  devel-oped selectively in RUL.^3,5,7 It has been postulated that  the  relatively  straight,  right  mainstem  bron-chus and an almost 90° take-off of the RUL bronchus may create a favorable condition for the Bernoulli effect  around  the  opening  of  RUL  bronchus.²¹ Sprung et al⁷ suggested that this effect should be con-spicuous when the lungs are vigorously ventilated, because  of  increased  resistance  (bronchospasm),  causing rapid laminar air flow to be preferentially directed toward the right lower and middle lobes, bypassing  the  RUL  bronchus,  quickly  drawing  gas  out of the RUL and causing acute lobar collapse.

It may be difficult to decide whether the sched-uled  surgery  should  be  carried  out  or  not  if  the  patient develops “reflex atelectasis”. The operation for moyamoya disease may be of long duration, and it requires tight control of arterial carbon dioxide tension during surgery. Therefore, under such cir-cumstances, we postponed the surgery for our pa-tient. In most reported cases, however, the scheduled surgeries  proceeded  uneventfully  without  recur-rence or aggravation, since the atelectasis resolved within an hour.^6,7 Therefore, it may be reasonable to proceed with the operation soon after the atel-ectasis has resolved.

In  conclusion,  it  is  suggested  that  acute  lobar  atelectasis with bronchospasm during induction of anesthesia may recur in a patient who had devel-oped it previously. However, this reflex atelectasis could  be  readily  treated  with  mechanical  venti-lation  and  bronchodilators.  It  appears  logical  to  proceed  with  the  planned  procedure  soon  after  resolution of the atelectasis.