Asthma, respiratory arrest: The bougie is in but I can’t pass the tube!

Asthmatic respiratory arrest, able to pass bougie but not the tube!

A scary case

We received and ambulance call informing us of a moderately unwell asthmatic in her 50s.

Next thing a paramedic pops his head in the ambulance door, points at resus and says “Chris, we’ll need you in there soon”

Intriguing (well, strange, but it was James).

I headed out to the ambulance.

It turns out the patient had been not to unwell when the paramedics got to the patient’s house: wheezy but talking easily.  They had given her a couple of nebulisers en route.  A few minutes before arrival at hospital the patient had suddenly become agitated.  The paramedics had given some IM adrenaline but she had continue to deteriorate.

So as I got to the ambulance I saw a large woman on the trolley in the back of the ambulance staring blankly into space and … not breathing.

We elected to dash to resus.

In resus I bag valve mask (BVM) ventilated her,  slowly and gently, with difficulty.

I briefly considered intubating but decide not to – the primary problem was with B not A.

I put in an oropharyngeal airway, little improvement.

I placed bilateral nasopharyngeal airways with good effect -> I could ventilate reasonably.  She had bilateral breath sounds with moderate wheeze.

Circulation check: No palpable pulse, sinus tachy on the monitor.  We started chest compressions for presumed PEA arrest.

After a minute of chest compressions we stopped and reassessed.  Good radial pulse.  I elected to give 100mcg adrenaline for immediate brondilatory effect (in retrospect 250mcg of salbutamol would have been a better idea but we had adrenaline in hand in a prefilled syringe for the PEA arrest)

Over a few minutes her oxygen sats climbed from 65 to 100%.

The senior nurse asks if I wanted any help.  “Yep, an anaesthetist might be good for this one”

An amazing nurse got in a good IV line in and baseline bloods were sent and 200mg of hydrocortisone was given.

We ventilated slowly and carefully for a few minutes.  Bedside ultrasound (at the depth limit of the linear probe) shows bilateral pleural sliding – no pneumothorax.

The anaesthetist (a good one, yay) arrives promptly. The patient is making weak respiratory effort but is unresponsive to pain.

We generally avoid intubation in asthma – patients with asthma don’t tend to do well on ventilators – so we usually try to mange them on BiPAP instead.   However it didn’t look like this patient was going to wake up anytime soon, so the anaesthetist and I decided we would intubate.

I decided to do an RSI even though the patient was unresponsive.  Intubation without drugs may have caused laryngospasm or worsened her bronchospasm.

We set up for an RSI with high flow O2 by nasal prongs and ramping (for obese patients we put lots of sheets and pillows behind their upper back and head to try to get their air way alignment optimised – this is called ramping).

Ketamine 150mg and rocuronium 100mg push.

Good view with a video laryngoscope, but she had an anterior larynx and I was unable to pass tube through cords even with a good hockey stick bend on the stylet and laryngeal manipulation.

I passed a bougie easily into the trachea but I was unable to advance a size 7.5 tube into the trachea.   The tip of the tube went through the cords but the balloon seemed to hang up at the cords.  I tried rotating the tube both ways but it wouldn’t go.

Sats had dropped to 85% by now.   I pulled out and we BVMd her until her sats were  back at 100% for a minute then started again.

Bougie, size 7.0 tube.  Same result.  I’m thinking : “Has she got a subglottic stenosis?  Are we going to have to cric (cricothyroidotomy) her?” I admit defeat for the first time in over 6 years since I’ve been a consultant, and handed over to the anaesthetist.  He has the same problem.  He then put another pillow behind the patient’s head and passed the tube easily.

He thought my initial ramping wasn’t adequate, the airway angles were wrong and the ETT tube was hitting against the anterior wall of the trachea.  Makes sense.

We generally believe that the key to ramping is  to have the tragus of the ear anterior to the sternal notch.  This is hard to see from the head of the bed and I should have got someone to have a look from the side of the bed.

ramp1

The blue line indicates the line from tragus to sternal notch

(image from http://crashingpatient.com/resuscitation/airway/airway.htm/)

Somewhere in the middle of all of this the internal medicine physician arrived and asked if we had done an ECG.  The senior nurse dryly replied “No doctor, we haven’t passed A yet.”

Then I had an all to frequent disagreement with the anaesthetist regarding ventilator settings.  This woman was’t tall.  I thought her ideal body weight (IBW) might be 60kg.  I wanted a tidal volume (TV) of 6ml/kg IBW = 360ml (lung portective strategy).  The anaesthetist wanted a TV of 500ml.  “You don’t need to worry about the airway pressures, the alveoli won’t see that.”

I reminded him that one of his colleagues had given my last patient life threatening asthma  bilateral pneumothoraces and set the TV at 350ml.  Later it was calculated that her IBW was 53kg.  We are often fulled thinking that obese people have big lungs.  Think of those CTs with tiny lungs surrounded by lots of padding.

In retrospect I am very glad I didn’t try a crash intubation on arrival in resus.  I think that would have been a disaster.  I think it was better to manage her airway with basic airways and adjuncts first, attempt to optimise her positioning, then to a controlled RSI.  Even if she had been a normal body weight patient I think I would still avoid intubation as patients with respiratory arrest from asthma will often respond to some BVM ventilation and wake up quite quickly and not need intubation.

Bottom line

Positioning, positioning, positioning for airways in obese patients.

 

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Bullous Impetigo

Bullous impetigo is not that common but it is worth knowing about.

This 3-year-old had had one spot on her R lateral chest about a week earlier.  She had developed more spots that were becoming more sore, and in the last day had been itchy.  A few days previously there had been one fluid filled blister.

She had no medical history and was systemically well.

She was using paracetamol and ibuprofen for pain.

IMG_2842

IMG_2852

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At about day 3 she had seen a GP who thought she might have shingles.  Now the lesions crossed the mid line and she had some on her legs so it didn’t look dermatomal now.

With the peeling skin around the edges I wondered if this was a mild case of stapylococcal scalded skin syndrome.  Looking at these photos the on-call paediatrician quickly put me right that this is actually bullous impetigo, a less serious condition.

The strain of staphylococcus aureus releases a toxin that lyses skin.

Staphylococcal scaled skin syndrome tends to be in neonates, the child is febrile and irritable, the rash is more widespread, has more widespread erythema, and surrounding intact appearing skin shears off easily with light touch (Nikolsky’s sign)

A swab was sent and she was admitted for a couple of days if IV antibiotics: flucloxacillin 50mg/kg 4 times daily.

Everyone was encouraged to be particularly careful with their handwashing.

References

UpToDate

Thanks to the child’s mother for permission to publish these photographs.

Pocast

Song on podcast Souffrance  by Orange Blossom

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