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Acute Respiratory Distress Syndrome After Airway Anesthesia With Lidocaine

D'Elia, Tommaso MD; Ghio, Loredana MD

Journal of Bronchology & Interventional Pulmonology: July 2010 - Volume 17 - Issue 3 - pp 245-247
doi: 10.1097/LBR.0b013e3181e65320
Case Reports

Adequate anesthesia of the upper and proximal lower airways is a critical prerequisite for a smooth and successful bronchoscopic procedure. Lidocaine is the most commonly used local anesthetic agent for flexible bronchoscopy. Adverse reactions to this agent have rarely been reported. Nevertheless, we recently observed a life-threatening reaction to airway lidocaine anesthesia in a 33-year-old man who was to undergo flexible bronchoscopy for the evaluation of an intrathoracic lymphadenopathy. Before the procedure, the patient developed noncardiogenic pulmonary edema. Only 2 such cases after airway anesthesia with nontoxic doses of lidocaine for a bronchoscopic procedure have been reported in the literature. Unlike in these cases, the episode was brief and self-limiting, with adverse reaction confined to the respiratory tract without development of shock or systemic involvement.

Department of Pneumology, Service of Thoracic Endoscopy, General Hospital of Crema, Crema, Italy

Reprints: Tommaso D'Elia, MD, Department of Pneumology, General Hospital, Ugo Dossena Square no 2, Crema (Province of Cremona) 26013, Italy (e-mail:

Received for publication March 1, 2010; accepted April 2, 2010

There is no conflict of interest.

Adequate anesthesia of the upper and proximal lower airways is a critical prerequisite for a smooth and successful bronchoscopic procedure.1 At our bronchoscopy suite, after achieving conscious sedation with intravenous midazolam, we proceed with anesthesia of the vocal cords and tracheobronchial mucosa by transcricoid injection of 5 mL of 2% lidocaine.1,2 Anesthesia of the upper airways, from the nasal mucosa down to the larynx, is achieved by intranasal instillation of small aliquots of 2% lidocaine. Finally, lidocaine jelly is used to lubricate the flexible bronchoscope for its smooth transnasal insertion. In adults without liver or cardiac impairment we administer a total amount of lidocaine well below the recommended dose of 8.2 mg/kg lean body weight3: usually 300 mg or less.

In over 30 years of experience at our institution, no life-threatening reactions to local anesthesia with lidocaine have been encountered. Lidocaine is the most commonly used local anesthetic agent for flexible bronchoscopy, and has a relatively wide margin of safety.2,4 Nevertheless, we recently observed a serious adverse event to airway lidocaine anesthesia in a 33-year-old man.

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A 33-year-old man was to undergo flexible bronchoscopy for the evaluation of an intrathoracic lymphadenopathy, discovered by a chest radiograph after a motorcycle accident. He was a life-long nonsmoker and worked in the food industry as a storekeeper. The patient denied any history of cardiac, renal, or hepatic impairment or drug allergies. For the past 2 years, he had complained of migrant arthralgias, and in the past 1 month had developed dry cough. In addition to hilar and mediastinal lymphadenopathy, computed tomography of the chest revealed small nodular bilateral opacities. Routine laboratory tests, electrocardiogram, and pulmonary functional tests, including diffusion capacity, were within normal limits.

Immediately before the endoscopic procedure, the patient's arterial blood pressure was 115/76 and his arterial pulse oximetry reading (SpO2) was 97%. A few minutes after local anesthesia and before introduction of the bronchoscope, the patient began to feel restless and to complain of increasing cough and dyspnea. His breathing soon became noisy and gurgling, with expectoration of foamy sputum. Labial cyanosis appeared, while SpO2 dropped below 80%. No relevant change of arterial blood pressure was observed, while the electrocardiogram showed sinus tachycardia. There was no jugular venous distention. Diffuse inspiratory and expiratory rales, but no bronchospasm, were heard throughout all lung fields. Arterial blood gas levels on a fractional-inspired oxygen concentration of 1.0 were as follows: pH 7.43, pO2 58 mm Hg, pCO2 39 mm Hg. An echocardiogram performed during the episode was reported to be unremarkable, with a systolic pulmonary arterial pressure of 22 mm Hg, and biochemical markers of myocardial necrosis and B-type natriuretic peptide were normal. An anteroposterior portable chest radiograph, performed 20 minutes after the onset of symptoms, showed bilateral fluffy and patchy infiltrates (Fig. 1).

In addition to high-dose oxygen, flumazenil 0.3 mg, methylprednisolone 2 mg/kg (160 mg), and promethazine 50 mg were administered intravenously. The patient improved rapidly, and 48 hours later arterial blood gas levels on room air were as follows: pH 7.44, pO2 78 mm Hg, pCO2 38 mm Hg. During hospitalization, the patient was maintained on therapy with methylprednisolone 80 mg daily, and was discharged with tapering doses of oral prednisone and with a diagnosis of noncardiogenic pulmonary edema as adverse reaction to airway lidocaine anesthesia.

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Currently, lidocaine is the topical anesthetic of choice for bronchoscopic procedures and can be delivered to the airways through several techniques, including atomization, ultrasonic or jet nebulization, dropper instillation, transcricoid injection, and instillation, or through the bronchoscope channel (“spray as you go”).1–5

The incidence of complications occurring during the preparation phase for bronchoscopy (local anesthesia plus premedication) has been reported to be as low as 0.09% of all procedures.6 Compared with other local anesthetics, lidocaine has a better safety profile, and adverse reactions to this agent have rarely been reported. Side effects of airway anesthesia with lidocaine include drug toxicity, bronchospasm, and hypersensitivity reactions. Toxic, nonallergic reactions usually involve central nervous or cardiovascular systems, often resulting in seizure or cardiac depression, and are mostly associated with high serum concentrations arising from excessive delivered doses or impaired clearance, particularly in patients with liver, renal, or cardiac dysfunction.7,8 Another dose-dependent complication of topical anesthesia is methemoglobinemia, that is, the presence of elevated blood level of methemoglobin, an oxidized form of hemoglobin, unable to carry oxygen and carbon dioxide. Many oxidant substances, including anesthetic agents, can accelerate the formation and dangerously increase the circulating fraction of methemoglobin, which is normally less than 2% of total hemoglobin. Methemoglobinemia occurs more rarely with lidocaine than with other local anesthetics, but if it is unrecognized it can lead to death. The severity of symptoms and consequences depends on the methemoglobin level, ranging from central cyanosis (>15% of total hemoglobin) to neurologic and cardiac dysfunction (>45%) to death (>70%). Methemoglobinemia should be suspected if sudden development of cyanosis, refractory to oxygen administration, occurs after administration of a topical anesthetic agent. In addition, it is suggested by a distinctive chocolate-brown color of arterial blood and by a discrepancy between a low SpO2, despite oxygen administration, and a normal or even elevated pO2.9,10

Inhalation of nebulized lidocaine can cause bronchospasm in a significant portion of asthmatics.11 Airway anesthesia with lidocaine may be fatal in patients suffering from severe airway disease.12 Anaphylaxis rarely occurs after local administration of lidocaine, but can also be a fatal complication.4 To the best of our knowledge, only 2 cases of noncardiogenic pulmonary edema after airway anesthesia with nontoxic doses of lidocaine for bronchoscopic procedure have been reported in the literature.13,14 A similar case of lidocaine-induced adult respiratory distress syndrome (ARDS) was described after subcutaneous administration of lidocaine for suturing a wound.15 These cases were all associated with the development of shock and noncardiogenic pulmonary edema. One of the cases resulted in death, and autopsy confirmed the diagnosis of ARDS.

In our case, no neurologic or cardiovascular symptom attributable to drug toxicity was observed. The patient remained awake and cooperative throughout the adverse event.

Hemodynamic instability or arrhythmias did not develop. Methemoglobinemia was ruled out by clinical context, normal aspect of arterial blood, resolution of cyanosis after oxygen administration, and absence of discrepancy between SpO2 and pO2.9,10 There were no signs of anaphylactic or anaphylactoid reaction, such as hypotension, angioedema, or cutaneous wheals. Unlike cases reported earlier,13–15 the episode was brief and self-limiting, with adverse reaction confined to the respiratory tract without development of shock or systemic involvement. Clinical presentation was undoubtedly pathognomonic of pulmonary edema. A cardiac genesis was ruled out by a set of laboratory, clinical, radiographic, and echocardiographic findings. Acute onset of bilateral pulmonary infiltrates, severity of hypoxemia as defined by pO2/FiO2 ratio less than 200 (in our case, 58), and exclusion of a cardiac genesis have met all criteria of the American-European Consensus Conference for the diagnosis of ARDS.16

In conclusion, clinicians who administer the local anesthetic agent lidocaine should be aware that life-threatening reactions, though rare, may occur with its use. Before any procedure, provision for tools to quickly diagnose and manage such complications should be made.

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lidocaine; topical anesthesia; acute respiratory distress syndrome; bronchoscopy; noncardiogenic pulmonary edema

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