Crashing Asthmatic POD

We treat asthma on a daily basis, especially in the peds ED. But what if duonebs x3, steroids, and mag isn’t doing the trick?

THE CRASHING ASTHMATIC

• Nebulized epinephrine may help.

• If no improvement, start dosing IM epi as if it were anaphylaxis: 0.5 mg (0.01 mg/kg) q 10 min, or start a drip at 5 mcg/min and titrate to effect.

• Keep going with continuous albuterol nebs.

• If pharmacy isn’t around to make an epi drip, consider a “dirty” epi drip: 1 mg epi (an entire vial of code cart epi) added to 1 L NS or LR, start at 2 drops per second and titrate up.

• Alternatively, terbutaline IV can be started: 10 mcg/kg bolus over 10 min and then drip starting at 0.4 mcg/kg/min and titrate up. Terbutaline is a systemic beta agonist. Perhaps they’re so tight that the albuterol you’re nebulizing is not getting where it needs to go due to profound bronchoconstriction. The main adverse effect is here is vasodilation-related hypotension.

By this point, your intubation stuff should be ready and the patient should be in resus.

They also will be having insensible losses so should get as 20 cc/kg IVF bolus.

Still getting worse.

Now this gets interesting.

We are really trying to avoid intubating any asthmatic because of historically poor outcomes with intubation, but sometimes it is unavoidable.

Next step is to try BiPAP. BiPAP could also be started simultaneously with epi. If they can’t tolerate BiPAP, consider ketamine to help them tolerate BiPAP. Ketamine can be dosed numerous ways. If sub-dissociative dosing is pursued, you risk them freaking out. If dissociative dosing, there’s a higher risk of laryngospasm. But consider this, they’re on the brink of getting intubated anyway. If your last-ditch-effort-ketamine gives them laryngospasm, that might be your cue to push a paralytic.

Ketamine and BiPAP has failed.

Time to intubate. Preoxygenate as much as possible. Use the largest ETT possible. First pass success is key. Induce with ketamine 2 mg/kg if they’re not already in the K-Hole. Roc or Sux.

Now they’re intubated

• They have OBSTRUCTIVE LUNG PHYSIOLOGY. It will take them way longer than usual to exhale. Thus:

• Low respiratory rate! 8 breaths/min

• Lung protective tidal volume: 7 cc/kg ideal body weight

• Minimal PEEP: 0 (ZEEP) - 2 cc H2O

• High inspiratory flow rate: 90 LPM or I:E 1:5

• FiO2 100%

• The ventilator will alarm due to high PEAK pressures. This is OK. Have the respiratory therapist fix it to raise the alarm threshold. The high peak pressures are a consequence of their tight bronchioles.

• If running into issues with ventilator dyssynchrony, consider paralyzing with cisatracuium

• Relative hypoxia (sat mid 80s, goal >90%) and hypercarbia (goal >7.15) is OK

• Aggressive airway suctioning

• If they begin crashing, disconnect from vent and push on chest to ensure breath stacking is not the issue; rule out pneumothorax; rule out displaced/clogged/kinked ETT

Still doing poorly

• Call the ECMO team for VV ECMO

• Anesthesia to set up inhaled anesthetics! e.g. desflurane, sevoflurane. Not tons of evidence, but in case series' and anecdotally, this works really well.

• Fun fact, CO2 can be dialyzed out of someone rather than ventilated out of someone. However, you need to be in a center where ECMO is also done, because it’s basically putting a piece of the ECMO circuit into a CVVHD circuit. Yes. Blew my mind too.

See Reuben’s algorithm on this at https://emupdates.com/when-the-patient-cant-breathe-and-you-cant-think-the-emergency-departement-life-threatening-asthma-flowsheet/

Hemoptysis Pearl

Let’s Talk Hemoptysis

So your patient thinks they’re coughing up blood...

Initial questions:

• Are they actually coughing up blood?

• Or are they having hematemesis?

• Or epistaxis?

Seems like they actually are. So what could they have? What should you ask in your history?

• Infectious/inflammatory causes are very common:

  • Acute bronchitis - if you cough enough, you will get some inflammation of your airways and BOOM, hemoptysis)

  • COPD can cause neoangiogenesis to enhance alveolar blood delivery, new fragile blood vessels can rupture

  • In immunosuppressed patients, consider aspergillus and of course TB causing necrotic badness, thus also ask travel history

  • Lung parasites! paragonimiasis, echinococcus, schistosomiasis - ask about travel

  • Neoplastic

    • Bronchogenic carcinoma, bronchial adenoma, squamous cell carcinoma — ask about weight loss and constitutional sx, but know that tumors can also cause massive hemoptysis

    • Structural

      • Aortobronchial fistula — good point, if their giant thoracic aortic aneurysm eroded into one of their bronchi, they would be in extremis to say the least and you wouldn’t be taking this detailed history…

      • Tracheo-innominate fistula — usually 3d-6w after tracheostomy placement, life-threatening and scary, we’ll save management of TIF for another POD

      • Other chronic lung diseases leading to bronchiectasis —> chronic inflammation —>destruction of cartellagenous support —> ruptured blood vessels

      • Vasculitides and collagen-vascular diseases

        • Goodpastures - remember this? Me neither. Autoimmune disease where antibodies attack the basement membrane of the kidneys and lungs — so if known renal failure or hematuria + hemoptysis, think about this

        • Granulomatosis with polyangiitis, SLE, and Behçet’s can all do similar things — h/o autoimmune disorders, family history…

        • Cardiovascular

          • PE can cause a pulmonary infarction —> ischemia/necrosis of lung tissue—> bleeding — ask about PE risk factors!

          • Pulmonary hypertension — ?CHF ?mitral stenosis

OK, enough of that. Let’s break down management.

Are they bleeding a lot? Coughing up large amounts of copious bright red frothy blood in front of you and in respiratory distress? 

Massive Hemoptysis

They need

airway management (often emergent intubation), STAT labs/portable CXR, bronchoscopy, CT surgery/IR/ICU consults, CT scan if stable enough

. Also,

position them on their side with the bleeding lung down

so that gravity doesn’t wash all the blood into their ventilated lung. I like this algorithm from Tinti’s below. The only confusing acronyms are MDCT (multidetector computed tomography) and BAE (bronchial artery embolization).

You may be able to intubate the healthy mainstream

as shown below in order to protect the side you’re able to ventilate. As another option pulmonology/IR may help with placement of a Fogarty catheter to tamponade the bleeding side.

If it’s

mild hemoptysis

, think about whether quarantine and TB workup is needed. If not, they most likely have bronchitis, and may only need a CXR, but refer to this simpler algorithm to tell you when you need a little more. It’s unlikely that they’ll have a diagnosis by the time they leave, but they will continue their workup with PCP or pulmonology for definitive diagnosis and management. 

Bipap Settings

BIPAP Principles:This one goes out to our rising Resus Residents: Bipap has settings that can ameliorate the two primary causes of respiratory failure: oxygenation (CHF, pneumonia) and ventilation (COPD, etc).

Improve hypoxemia two ways: 1. FiO2 2. PEEP (recruit more alveoli) Improve ventilation (hypercarbia) 1. Tidal Volume 2. Respiratory Rate

Settings on Bipap: IPAP – Inspiratory positive airway pressure (e.g. the high number) EPAP – Expiratory positive airway pressure (e.g. the low number) FiO2 – Fraction of inspired O2 (%) There are more, mentioned below, however lets touch on these first.

It is important to understand the cause of your respiratory failure to apply the proper settings. Physiology! Time to move on to practical application:

For HYPOXEMIA generally start with IPAP of 10cmH2O. EPAP can generally start at 5cmH2O

Example:

• CHF (hypoxemia): Start at IPAP of 10cmH2O with an EPAP of 5cmH20 (remember you want EPAP here to prevent atelectasis. o Pressure will improve oxygenation o May always increase FiO2 as well to improve oxygenation Conversely, for HYPERCARBIA (COPD) start with a similar IPAP of 5-10cmH20 however EPAP may not even be necessary. o Remember the difference in IPAP and EPAP is related to tidal volume, and this is one thing that effects hypercarbia!! Greater the difference = greater tidal volume. o You may also change the respiratory rate (described below)

Other settings/points: • Respiratory rate as well as I:E (inspiratory:expiratory) ratio can also be adjusted (however these settings may or may not be as helpful in a patient who is breathing on their own). I don’t want to get into this too much, but a couple points: • For HYPERCARBIA increased ventilation is desired with a HIGHER respiratory rate to blow off CO2. • For asthma keep EPAP lower (blow out more air in expiration) and setup a lower I:E ratio (e.g. 1:5) to prevent “breath stacking.” • Titrate by 2 – 3 cmH20 every 5 – 10 minutes. • Max IPAP is generally considered 20cmH2O (this is because lower esophageal sphincter tone is roughly 23 – 25cmH20, don’t over insufflate the stomach). • Remember to get a blood gas.

Sources: JB Life in the Fast Lane Rebel EM UpToDate