COMPLICATIONS OF LARYNGOSCOPY & INTUBATION
The complications of laryngoscopy and intuba-tion include hypoxia, hypercarbia, dental and air-way trauma, tube malpositioning, physiological responses to airway instrumentation, or tube mal-function. These complications can occur during laryngoscopy and intubation, while the tube is in place, or following extubation ( Table 19–6).
Instrumentation with a metal laryngoscope blade and insertion of a stiff TT often traumatizes delicate airway tissues. Tooth damage is a common cause of (relatively small) malpractice claims against anes-thesiologists. Laryngoscopy and intubation can lead to a range of complications from sore throat to tra-cheal stenosis. Most of these are due to prolonged external pressure on sensitive airway structures. When these pressures exceed the capillary–arteriolar blood pressure (approximately 30 mm Hg), tissue ischemia can lead to a sequence of inflammation, ulceration, granulation, and stenosis. Inflation of a TT cuff to the minimum pressure that creates a seal during routine positive-pressure ventilation (usually at least 20 mm Hg) reduces tracheal blood flow by 75% at the cuff site. Further cuff inflation or induced hypotension can totally eliminate mucosal blood flow.
Postintubation croup caused by glottic, laryn-geal, or tracheal edema is particularly serious in children. The efficacy of corticosteroids (eg, dexamethasone—0.2 mg/kg, up to a maximum of 12 mg) in preventing postextubation airway edema remains controversial; however, corticosteroids have been demonstrated to be efficacious in children with croup from other causes. Vocal cord paralysis from cuff compression or other trauma to the recurrent laryngeal nerve results in hoarseness and increases the risk of aspiration. The incidence of postopera-tive hoarseness seems to increase with obesity, dif-ficult intubations, and anesthetics of long duration. Curiously, applying a water-soluble lubricant or a local anesthetic-containing gel to the tip or cuff of the does not decrease the incidence of postoperative sore throat or hoarseness, and, in some studies, actu-ally increased the incidence of these complications. Smaller tubes (size 6.5 in women and size 7.0 in men) are associated with fewer complaints of postoperative sore throat. Repeated attempts at laryngoscopy during a difficult intubation may lead to periglottic edema and the inability to ventilate with a face mask, thus turning a bad situation into a life-threatening one.
Unrecognized esophageal intubation can pro-duce catastrophic results. Prevention of thiscomplication depends on direct visualization of the tip of the TT passing through the vocal cords, care-ful auscultation for the presence of bilateral breath sounds and the absence of gastric gurgling while ventilating through the TT, analysis of exhaled gas for the presence of CO2 (the most reliable automated method), chest radiography, or the use of an FOB.
Even though it is confirmed that the tube is in the trachea, it may not be correctly positioned. Overly “deep” insertion usually results in intubation of the right (rather than left) main-stem bronchus because of the right bronchus’ less acute angle with the trachea. Clues to the diagnosis of bronchial intubation include unilateral breath sounds,unexpected hypoxia with pulse oximetry (unreliable with high inspired oxygen concentrations), inability to palpate the TT cuff in the sternal notch during cuff inflation, and decreased breathing-bag compli-ance (high peak inspiratory pressures).
In contrast, inadequate insertion depth will position the cuff in the larynx, predisposing the patient to laryngeal trauma. Inadequate depth of insertion can be detected by palpating the cuff over the thyroid cartilage.
Because no one technique protects against all possibilities for misplacing a TT, minimal testing should include chest auscultation, routine capnog-raphy, and occasionally cuff palpation.
If the patient is repositioned, tube placement must be reconfirmed. Neck extension or lateral rota-tion most often moves a TT away from the carina, whereas neck flexion most often moves the tube toward the carina.
At no time should excessive force be employed during intubation. Esophageal intubations can result in esophageal rupture and mediastinitis. Mediastinitis presents as severe sore throat, fever, sepsis, and subcutaneous air often manifesting as crepitus. Early intervention is necessary to avoid mortality. If esophageal perforation is suspected, consultation with an otolaryngologist or thoracic surgeon is recommended.
Laryngoscopy and tracheal intubation violate the patient’s protective airway reflexes and predictably lead to hypertension and tachycardia when per-formed under “light” planes of general anesthesia. The insertion of an LMA is typically associated with less hemodynamic change. Hemodynamic changes can be attenuated by intravenous admin-istration of lidocaine, opioids, or β-blockers or deeper planes of inhalation anesthesia in the min-utes before laryngoscopy. Hypotensive agents, including sodium nitroprusside, nitroglycerin, esmolol and nicardipine, have also been shown to effectively attenuate the transient hypertensive response associated with laryngoscopy and intuba-tion. Cardiac arrhythmias—particularly ventricu-lar bigeminy—sometimes occur during intubation and may indicate light anesthesia.
Laryngospasm is a forceful involuntary spasmof the laryngeal musculature caused by sensory stimulation of the superior laryngeal nerve. Triggering stimuli include pharyngeal secretions or passing a TT through the larynx during extuba-tion. Laryngospasm is usually prevented by extu-bating patients either deeply asleep or fully awake, but it can occur—albeit rarely—in an awake patient. Treatment of laryngospasm includes pro-viding gentle positive-pressure ventilation with an anesthesia bag and mask using 100% oxygen or administering intravenous lidocaine (1–1.5 mg/kg). If laryngospasm persists and hypoxia develops, small doses of succinylcholine (0.25–0.5 mg/kg) may be required (perhaps in combination with small doses of propofol or another anesthetic) to relax the laryngeal muscles and to allow controlled ventilation. The large negative intrathoracic pressures generated by a struggling patientduring laryngospasm can result in the develop-ment of negative-pressure pulmonary edema, even in healthy patients.
Whereas laryngospasm may result from an abnormally sensitive reflex, aspiration can result from depression of laryngeal reflexes following pro-longed intubation and general anesthesia.
Bronchospasm is another reflex response to intubation and is most common in asthmatic patients. Bronchospasm can sometimes be a clue to bronchial intubation. Other pathophysiological effects of intubation include increased intracranial and intraocular pressures.
TTs do not always function as intended. Polyvinyl chloride tubes may be ignited by cautery or laser in an oxygen/nitrous oxide-enriched environment. Valve or cuff damage is not unusual and should be excluded prior to insertion. TT obstruction can result from kinking, from foreign body aspira-tion, or from thick or inspissated secretions in the lumen.