In: Home » Cases

Can't Ventilate

(Thanks to Dr “N” for this contribution)

This case occured at a small hospital. The patient was a 65 year old female for elective revision of laparoscopic gastric banding. She had been told by the surgeon that the band had slipped, resulting in her experiencing dramatic weight gain and severe acid reflux. She had regained weight to 130kg (BMI 48). She also had a past history of asthma which she described as mild. She had had no hospital admissions for this, however she was using daily ventolin though she was not on preventative medications. About a month earlier she had had an upper respiratory tract infection. Her symptoms had settled down within a couple of weeks .  But she had required increased use of her salbutamol inhaler. She had not seen a respiratory physician previously, nor had any formal investigations such as spirometry.

Chest auscultation revealed no wheeze though her obesity made this assessment difficult. Once in the operating theatre prior to induction, I gained intravenous access and gave her a small dose of midazalam and some oxygen via a Hudson mask and I also put an arterial line for blood pressure monitoring prior to induction .

For the induction I gave 3 minutes of pre oxygenation with her head up 30 degrees. This was followed by a rapid sequence induction with cricoid pressure. I gave propofol  then suxamethonium. She was a grade two laryngoscopy, the arytenoid cartilages being just visible with the BURP manoeuvre.  The endotracheal tube felt to pass easily and I connected her up to the breathing circuit and started ventilating her with 100 % oxygen with the bag. She was very difficult to ventilate. After about six breathes there was no end-tidal CO2 on the monitor and there was no chest movement, though this was not easy to assess because of her obesity.

How did the bag feel at this time?

I  tightened the valve so it felt firm. I didn’t feel ventilation was a “brick wall” at this time. There was some compliance in the tubing. After more attempted ventilation there was still no capnograph trace. Her O2 saturation at this stage was about 95%. I did say to the anaesthetic nurse that I felt it essential to change the tube. This time I used a bougie which seemed to pass into the larynx and I could feel the “clicks” as it passed over the tracheal rings. A new endotracheal tube rail-roaded over the bougie without difficulty.

At that stage the blood pressure was still about 150/90 but the saturation had dropped to 93 and at that point I noted the high inspired ventilatory pressures around 50 mmHg.

Could you see any CO2 trace at this stage?

Absolutely no CO2 trace at this stage. I then disconnected the cartography line and blew into it and there was CO2 so there wasn’t a problem with the sampling of the CO2.  At this stage I wasn’t certain of the diagnosis. Was this a patient pathology, was the tube in the right spot or was there a problem with the equipment or the breathing circuit and so forth.  The saturations stayed in the 90s so I continued ventilating with oxygen and sevoflurane and oscultated the chest. As before there were no breath sounds, though that may have been her obesity.

At that point I really didn’t really know what was going on. It was quite frightening though the O2 saturation remained in the low 90’s, so even though there was no CO2 trace, I felt  the tube was in the correct place and she must have been getting some oxygenation as several minutes had elapsed after induction. There was the dilemma of what to do next.  I thought I would go to a completely different  set of equipment so I asked the nurse to get me an Air Viva self inflating bag to bypass the circle system. However there were still very high pressures even with the self inflating bag. It really did at that stage feel like trying to ventilate a brick wall. I didn’t think the patient was getting any ventilation at all. I switched her on to the ventilator to see if that improved the situation at all. The ventilator that pressure limited very quickly with very minimal tidal volume going in.

What is your differential diagnosis at this point?

At this stage my number one differential diagnosis was acute severe bronchi spasm. I remember thinking I hope this is not anaphylaxis. There were no other features of anaphylaxis in that hemodynamatically she was still stable, with a systolic blood pressure remaining over 120 and heart rate more or less unchanged at 100. There was no rash evident, nor swelling of mucous membranes.  At this point  the patient began spontaneously ventilation so I then, thinking I was not in any position to be exubating her, gave her a small of non-depolarising muscle relaxant. As I thought that the acute severe bronchospasm was likely so I started a trial of treatment for that. There was some salbutamol in the emergency drugs box, so I drew up 500 micrograms (which comes in a 1ml ampoule) up to 20mls and gave approximately 1 ml (approximately 25 micrograms intravenously.  I repeated that twice over probably the following five minutes while I got someone else to squeeze the bag. I drew up some adrenalin but at no time did I give that as she remained hemodynamatically stable . Within about two minutes a  low CO2 trace appeared and a wheeze became audible. I thought that I had probably confirmed the diagnosis at that stage and  gave some IV hydrocortisone 100mg.

Over the next ten minutes (although I don’t think you can estimate the time it felt like forever!) she improved such that I could then use the ventilator. This ventilator was volume cycled only.  I was getting reasonable tidal volumes of about 300 mls and a peak inspired pressure of 35 to 40 mm Hg.

Was the CO2 trace looking more normal by this stage?

Yes, it wasn’t until after the second dose of salbutamol that the CO2 appeared. The ET CO2 was initially 10 to 15 mmHg, and then after that it slowly came back to more normal levels. Once above 35  it actually went up to about 50. Over about five minutes the bronchospasm disappeared and the CO2 came back to about 40.

Can you tell us, just remind us how much salbutamol she had had by this time?

She had received three doses of 25 mcg of  salbutamol  which I think is a relatively small dose but that did seem to be sufficient. I had given her two further doses of 25 mcg in 10 mls of normal saline down the end- tracheal tube as I thought that was a more safe route of delivery at that stage.

 

Did you have a volatile agent running at this stage?

Yes I had sevoflurane running the whole time set at 4%. This was partly to guard against awareness and partly for its bronchodilator properties. Once an end-tidal sevoflurane level was obtained, I titrated I the level to 1 MAC.

We then did an arterial blood gas and the pO2 at this time was greater than 300 mm Hg.  I was still giving 100% oxygen. The pCO2 was down to 45 by this time. Over the next ten minutes the wheeze cleared and there was good air entry bilaterally.

My dilemma then was should we proceed with the surgery. One thing in the back of my mind was the patient was then paralysed and I wasn’t going to be able to exubate her in the near future.

The wheeze continued to settle, she was haemodynamically stable, and her blood gases were close to normal. I discussed this with the surgeon and we agreed that if she tolerates patient positioning and then she tolerates pneumoperitoneum, then we could proceed. And she did tolerate these so we proceeded. There were no further problems with bronchospasm during the case and she exubated well at the end of surgery. There were no problems following exubation or with her O2 saturations in recovery. She had a chest x-ray which was clear and I  referred her to a physician in the hospital to look after her post operatively and to follow up her up long term.

So in summary this was a case of acute severe bronchospasm following intubation which was challenging to definitively diagnose and treat appropriately.

 

What are the take home messages for this case?

Firstly, I think to beware of the poorly controlled asthmatic who has been using a lot of salbutamol and is possibly under-treated prior to surgery. Had I realised the severity of her asthma I may have given some salbutamol pre-op  or even postponed her surgery..

Also I think changing the ETT was a good move while trying to establish the correct diagnosis. Once I had done that I was certain that the tube was in the right place. I have heard of a number of cases where inability to ventilate with no CO2 trace was presumed to be severe bronchospasm, when in fact the ETT was in the oesophagus. And there have been other cases where the ETT has had its cuff obstructing its tip, or there has been a foreign body in the tube, in which case replacing the tube restored airway control.

Next I think it is important to rule out any circuit problems by introducing a self inflating bag. Equipment problems can frequently be the cause of inability to ventilate a patient.

And also optimising the patient position 30 degrees head up prior to pre-oxygenation, induction and attempting intubation. Effective pre-oxygenation will buy you more time to establish the airway if you encounter difficulties.

I think considering the diagnosis of anaphylaxis is important in situations like this. In this case there was no circulatory collapse or rash accompanying the inability to ventilate, so I felt anaphylaxis was unlikely. My understanding is that anaphylaxis very rarely presents as just bronchospasm .

 Nonetheless I had  drawn up some adrenaline immediately after having given the salbutamol just in case she did not improve.

 

Did you ensure that the filter was outside of the circuit?  What did you attach the self inflating bag to?

 

I must say I didn’t. I attached it to the filter, which also had a connector on it as well. In retrospect I probably should have put the self inflating bag directly on to the ET tube.

 

I only bring that up as there is a well known case in New Zealand some years ago, where the filter was obstructed and that was not removed from the circuit when the endotracheal tube was changed, nor when the self inflating bag was applied. 

 

And I have heard of other cases where there was obstruction of the curved connector to the ETT. This highlights the importance of removing all elements of the breathing circuit when faced with an inability to ventilate of uncertain cause.

 Any other take up messages from this case?

I guess we should always mention the importance of getting help when we are not getting on top of a situation. In an emergency we want all the help we can get. There were no other anaesthetists in this hospital at the time. However I did ask for some extra nursing staff from recovery to assist when these difficulties first presented.

 

Thanks to Dr “N” for discussing this thought provoking case.

Refresh