Abstract
Lidocaine is commonly used for topical anesthesia of the upper airway in patient with anticipated difficult tracheal intubation undergoing awake fiberoptic intubation. Lidocaine toxicity is dose related and proportional to its plasma level. Although neurologic toxicity has been frequently observed with intravenous use, it has also been reported for topical use.
We report on a case of a patient with base tongue abscess who developed sudden seizures and coma during application of topical anesthesia with lidocaine for awake fiberoptic intubation. The presence of a deep neck infection that causes hyperemia and edema of the pharyngolaryngeal mucosa may enhance transmucosal systemic absorption of local anesthetic. Moreover, conditions such as hypercarbia, dysphagia, or hepatic diseases are known to facilitate onset of lidocaine neurologic toxicity with serum concentration lower than normal. These findings should be kept in mind before administering topical anesthesia of the upper airway. In the presence of any of these conditions above, either the total dose of local anesthetic or its concentration should be reduced as much as possible.
1
Introduction
Awake fiberoptic intubation has been recommended for airway management of patients with anticipated difficult tracheal intubation caused by infections or tumors . In such cases, a common cause of death may be due to the acute loss of the airway during an attempt to control it . Adequate preparation with local anesthesia of the upper airway in combination with a safe sedation scheme is essential to reducing airway irritation, cough, and laryngeal spasm, thereby preventing sudden airway loss .
Lidocaine is commonly used for topical anesthesia of the upper airway. It has a narrow therapeutic index, with only a small difference between therapeutic and potentially toxic concentrations. Lidocaine toxicity is dose related and proportional to its plasma level . Although neurologic toxicity has been frequently observed with intravenous use, it has also been reported for topical use .
We report on a case of a patient with base tongue abscess who developed sudden seizures and coma during application of topical anesthesia with lidocaine for awake fiberoptic intubation. Relationships between the sudden onset of neurologic symptoms and possible lidocaine toxicity are discussed.
2
Case report
A 55-year-old man came to our attention complaining of fever, dysphagia, sialorrhea, and inspiratory dyspnea with stridor starting 2 days earlier. Symptoms were preceded by 5 days of throat pain that the patient had treated with acetaminophen 3 g daily. Fiberoptic laryngoscopy showed a marked swelling of the tongue base pushing down an edematous epiglottis over the vocal cords. Blood cell count showed a mild leukocytosis (13,7100 per cubic millimeter with a neutrophylic granulocyte amount of 88.70%), and contrast-enhanced computed tomography of the head and neck showed a round-shaped collection of hypodense material within the tongue base, delimited by a contrast-enhanced wall markedly reducing patency of the hypopharynx ( Fig. 1 ). Blood gas analysis showed moderate hypoxemia and hypercarbia (pO 2 : 70 mm Hg; pCO 2 : 55 mm Hg; pH: 7.22 with a FiO 2 : 1). Clinical, laboratory, and radiological findings were consistent with the diagnosis of base tongue abscess. Urgent drainage of the abscess by median transcervical approach under general anesthesia was thus scheduled. Because of anticipated difficult tracheal intubation, awake fiberoptic intubation was planned. The patient received an anesthetic premedication with midazolam 4 mg IM immediately before surgery. Then, local anesthesia of the nasal fossae, hypopharynx, and larynx was achieved with lidocaine 10 mg/ml, 1% solution (three gargles with about 5–6 ml in total). The estimated total dose of lidocaine was about 200 mg. Twenty minutes after starting this procedure, the patient had psychomotor agitation, rapidly progressing to generalized tonic–clonic seizures and loss of consciousness. Repeated IV bolus doses of midazolam (4 mg total) were administered in order to control seizures and ventilation was assisted by bag–valve–mask ventilation. The patient underwent nasotracheal fiberoptic intubation. Then, midazolam 5 mg IV and cisatracurium 10 mg IV were administered and a contrast-enhanced computed tomography (CT) of the brain was promptly performed. The latter showed no evidence of intracranial ischemic or hemorrhagic lesions. Serum lidocaine concentration 20 minutes after the onset of seizures was 5.1 μg/ml. After having controlled vital signs, secured upper airways, and excluded cerebrovascular accidents, the patient underwent surgical drainage of the abscess by median anterior transcervical approach. Two suction drainages were placed into the surgical cavity. After surgery, the patient was transferred to the intensive care unit. Control contrast-enhanced CT scan of the brain was repeated 6 hours after the first, confirming the absence of intracranial ischemic or hemorrhagic lesions. Sedation was progressively tapered over postoperative days 1 and 2. Neurological examinations over these 2 days were unremarkable and an EEG showed no signs of epilepsy. Transnasal flexible fiberoptic laryngoscopy documented a marked reduction of the base tongue edema with regained upper airway patency and therefore the patient was extubated on day 2 after surgery, once fully awakened. He was transferred to the Otolaryngology Unit, where suction drainages were removed 3 days after surgery. Four days after surgery, as transnasal flexible fiberoptic laryngoscopy was unremarkable, the patient was discharged with oral amoxicillin and clavulanic acid 1 g three times daily and clindamycin 300 mg three times daily for 10 days.
2
Case report
A 55-year-old man came to our attention complaining of fever, dysphagia, sialorrhea, and inspiratory dyspnea with stridor starting 2 days earlier. Symptoms were preceded by 5 days of throat pain that the patient had treated with acetaminophen 3 g daily. Fiberoptic laryngoscopy showed a marked swelling of the tongue base pushing down an edematous epiglottis over the vocal cords. Blood cell count showed a mild leukocytosis (13,7100 per cubic millimeter with a neutrophylic granulocyte amount of 88.70%), and contrast-enhanced computed tomography of the head and neck showed a round-shaped collection of hypodense material within the tongue base, delimited by a contrast-enhanced wall markedly reducing patency of the hypopharynx ( Fig. 1 ). Blood gas analysis showed moderate hypoxemia and hypercarbia (pO 2 : 70 mm Hg; pCO 2 : 55 mm Hg; pH: 7.22 with a FiO 2 : 1). Clinical, laboratory, and radiological findings were consistent with the diagnosis of base tongue abscess. Urgent drainage of the abscess by median transcervical approach under general anesthesia was thus scheduled. Because of anticipated difficult tracheal intubation, awake fiberoptic intubation was planned. The patient received an anesthetic premedication with midazolam 4 mg IM immediately before surgery. Then, local anesthesia of the nasal fossae, hypopharynx, and larynx was achieved with lidocaine 10 mg/ml, 1% solution (three gargles with about 5–6 ml in total). The estimated total dose of lidocaine was about 200 mg. Twenty minutes after starting this procedure, the patient had psychomotor agitation, rapidly progressing to generalized tonic–clonic seizures and loss of consciousness. Repeated IV bolus doses of midazolam (4 mg total) were administered in order to control seizures and ventilation was assisted by bag–valve–mask ventilation. The patient underwent nasotracheal fiberoptic intubation. Then, midazolam 5 mg IV and cisatracurium 10 mg IV were administered and a contrast-enhanced computed tomography (CT) of the brain was promptly performed. The latter showed no evidence of intracranial ischemic or hemorrhagic lesions. Serum lidocaine concentration 20 minutes after the onset of seizures was 5.1 μg/ml. After having controlled vital signs, secured upper airways, and excluded cerebrovascular accidents, the patient underwent surgical drainage of the abscess by median anterior transcervical approach. Two suction drainages were placed into the surgical cavity. After surgery, the patient was transferred to the intensive care unit. Control contrast-enhanced CT scan of the brain was repeated 6 hours after the first, confirming the absence of intracranial ischemic or hemorrhagic lesions. Sedation was progressively tapered over postoperative days 1 and 2. Neurological examinations over these 2 days were unremarkable and an EEG showed no signs of epilepsy. Transnasal flexible fiberoptic laryngoscopy documented a marked reduction of the base tongue edema with regained upper airway patency and therefore the patient was extubated on day 2 after surgery, once fully awakened. He was transferred to the Otolaryngology Unit, where suction drainages were removed 3 days after surgery. Four days after surgery, as transnasal flexible fiberoptic laryngoscopy was unremarkable, the patient was discharged with oral amoxicillin and clavulanic acid 1 g three times daily and clindamycin 300 mg three times daily for 10 days.
