RothschillerMD.com rev 2024-02-02
Bronchospasm and Epinephrine
When dealing with bronchospasm I first try to determine the cause (hyperreactivity vs hypersensitivity) by how the patient responds to different treatments.
For intraoperative bronchospasm I will first determine if it is due to mechanical hyperreactivity (ETT stimulates the carina or right bronchi) by pulling back the tube and auscultation, which can be more pronounced in the presence of RAD. I would also squirt 20 mg (1mL of 2%) lidocaine down the tube to obtain a mucosal/recurrent laryngeal nerve (RLNN) block.
Epinephrine has always worked for immune-mediated bronchospasm. If the bronchospasm is due to a chemical/topical cause, gastric acid from reflux, epinephrine has not helped. With acid aspiration it found it takes longer to improve SpO2s. I speculate it is time needed to neutralize the acid and remove the irritant.
For immune-mediated hypersensitivity (mast cell release of histamine/etc.):
2) I will switch to a less pungent gas (Sevoflurane) and deepen the anesthetic.
3) If maintaining reasonable SpO2s (80s) I will try an in-line albuterol nebulizer
4) Low SpO2s-severe bronchospasm I go to epinephrine 1-2 mcg/kg
I have colleagues that have used endotracheal epi with success. I have always had an IV with bronchospasm. However, I would not hesitate to give a drug (epi, lido, atropine, naloxone) endotracheal. In the event of chemical/topical cause, gastric acid from reflux, I suspect it helps dilute the acid.
It is interesting that most drugs can be given via any route. It is the dose and bioavailability that matters. Drinking ondansetron is an example- can be given after the IV is removed. Another one that comes to mind is oral hydrocodone or midazolam. I rarely re-dose it after a child spits out the medicine or vomits. Especially if they hold it in their mouth (which goes under their tongue) which has a very high bioavailability.
Pulmonary Aspiration – Perioperative – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5806178/
Aspiration of gastric fluids may cause damage to airway epithelium, not only because acidity is toxic to bronchial epithelial cells but also due to the effect of digestive enzymes such as pepsin and bile salts. Experimental models have shown that direct instillation of these factors to airways epithelia cause damage with a consequential inflammatory response. The pathophysiology of these responses is gradually being dissected, with better understanding of acute gastric aspiration injury, a major cause of acute lung injury, providing opportunities for therapeutic intervention and potentially, ultimately, improved understanding of the chronic airway response to aspiration. Ultimately, clarification of the inflammatory pathways which are related to micro-aspiration via pepsin and bile acid salts.