{"id":5316,"date":"2011-07-14T20:25:25","date_gmt":"2011-07-15T00:25:25","guid":{"rendered":"http:\/\/crashtext.org\/misc\/awake-intubation-and-fiberoptic-intubation%c2%a0.htm\/"},"modified":"2014-08-11T07:30:19","modified_gmt":"2014-08-11T11:30:19","slug":"awake-intubation-and-fiberoptic-intubation","status":"publish","type":"post","link":"https:\/\/crashingpatient.com\/resuscitation\/airway\/awake-intubation-and-fiberoptic-intubation.htm\/","title":{"rendered":"Awake Intubation and Fiberoptic Intubation\u00a0"},"content":{"rendered":"

Best Article on Topicalization<\/a> Best Site for Fiberoptic Awake<\/a> See PODCAST 4 at emcrit.org<\/a> altering the gag reflex with pressure on the palm (Altering the Gag Reflex Via a Palm Pressure Point (JADA October 1, 2008 139(10): 1365) <\/p>\n

Antisalagogue (Choose 1)<\/h4>\n

\u00b7 Glycopyrolate 0.2 mg IV (actual dose 0.01 mg\/kg, may need doses of 0.4-0.8 mg in larger patients) Glycopyrrolate, like other anticholinergic (antimuscarinic) agents, inhibits the action of acetylcholine on structures innervated by postganglionic cholinergic nerves and on smooth muscles that respond to acetylcholine but lack cholinergic innervation. These peripheral cholinergic receptors are present in the autonomic effector cells of smooth muscle, cardiac muscle, the sinoatrial node, the atrioventricular node, exocrine glands and, to a limited degree, in the autonomic ganglia. Thus, it diminishes the volume and free acidity of gastric secretions and controls excessive pharyngeal, tracheal, and bronchial secretions. Glycopyrrolate antagonizes muscarinic symptoms (e.g., bronchorrhea, bronchospasm, bradycardia, and intestinal hypermotility) induced by cholinergic drugs such as the anticholinesterases. The highly polar quaternary ammonium group of Glycopyrrolate limits its passage across lipid membranes, such as the blood-brain barrier, in contrast to atropine sulfate and scopolamine hydrobromide, which are highly non-polar tertiary amines which penetrate lipid barriers easily. With intravenous injection, the onset of action is generally evident within one minute. Following intramuscular administration, the onset of action is noted in 15 to 30 minutes, with peak effects occurring within approximately 30 to 45 minutes. The vagal blocking effects persist for 2 to 3 hours and the antisialagogue effects persist up to 7 hours, periods longer than for atropine. or Atropine .01 mg\/kg IV <\/p>\n

Topicalization<\/h4>\n

(Choose 1 of the 4)<\/h4>\n

\u00b7 5 cc 2% lidocaine and 5cc 2% Lidocaine with 1:100,000 Epi nebulized \u00b7 Lidocaine 4% 5cc nebulized (minimal systemic absorption when using nebulizers [Chest 1977;71(3):346]) \u00b7 4cc of 4% Lidocaine and 1 cc of 0.5-1% Neosynephrine nebulized (alternative 3 cc of 4% and 3 cc of NS) \u00b7 Lidocaine\/Hurricaine spray (if no time for nebs) or use mucosal atomization device to spray 4% Lidocaine in oropharynx <\/p>\n

Anesthetize Lower Airways<\/h4>\n

\u00b7 Translaryngeal injection of 2-4 cc 4% lidocaine <\/p>\n

Nasal Vasoconstriction\/Anesthesia<\/h4>\n

\u00b7 Soak pledgets in 4% lidocaine and leave in nose for 5 minutes and\/or spray c 2% neo-synephrine. Or use 4% cocaine (max 1-3 mg\/kg) or Lidocaine with 1:25,000 epinephrine <\/p>\n

Sedate (Choose 1)<\/h4>\n

\u00b7 Versed 2-4 mg (takes 3-5 minutes for effect) \u00b7 50% Ketamine and 50% Propofol in a syringe (5 cc of each) Give in small aliquots. Ketamine alone, give 1\/5 dose intubating dose, wait and repeat if necessary (Volume 92(6) June 2001 pp 1465-1469 The Effects of Small-Dose Ketamine on Propofol Sedation: Respiration, Postoperative Mood, Perception, Cognition, and Pain) <\/p>\n