Lidocaine chemical structure
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Lidocaine

Lidocaine (INN) or lignocaine (former BAN) is a popular local anesthetic that is often used in dentistry or topically. The most commonly encountered lidocaine preparations are marketed by AstraZeneca under the brand names Xylocaine and Xylocard, though lidocaine is also found in many other proprietary preparations. more...

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Its name was coined after the local anesthetic procaine, which in turn replaced cocaine as an anesthetic in dental practice.

History

Lidocaine, the first amide-type local anesthetic, was developed by Nils Löfgren and Bengt Lundqvist in 1943 and first marketed in 1948.

Also used in pet medications.

Pharmacology

Lidocaine is metabolized in the liver to pharmacologically active breakdown products which are excreted by the kidneys. It is faster acting and longer lasting than procaine (Novocain).

When given intravenously, lidocaine is a class Ib antiarrhythmic agent and will block the sodium channel of the cardiac action potential, which decreases automaticity by reducing the slope of phase 4 depolarization with little effect on the PR interval, QRS complex or QT interval.

This drug is used in the treatment of ventricular cardiac arrhythmias and cardiac arrest with ventricular fibrillation, especially with acute ischemia, though it is not useful in the treatment of atrial arrhythmias.

The elimination half life of intravenous lidocaine is about 109 minutes, but because it is metabolized in the liver (which depends on liver blood flow), dosage should be reduced in patients with low cardiac output or who are in shock. In patients with cardiogenic shock, the half life may exceed ten hours.

Toxicity

Toxicity is most often seen when there has been an inadvertent intravascular injection of lidocaine when being used as a local anesthetic. Central nervous system toxicity manifests as tinnitus, dizziness, paresthesia (pins and needles), confusion and – in more severe cases – seizures or coma. Severe toxicity may also result in cardiovascular system collapse or ventricular fibrillation.

Related Information

  • Benzocaine
  • Bupivacaine
  • Procaine
  • Cocaine


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Lidocaine for the relief of incapacitating tinnitus
From Ear, Nose & Throat Journal, 4/1/04 by Sam Marzo

Abstract

Tinnitus is tolerated by most patients, but in others it is enough of a problem that they seek medical attention. Results of treatment have been mixed. On occasion, a patient is so distressed by tinnitus that he or she is incapacitated and seeks help in an emergency department. We describe what we believe is the first reported case of recurrent incapacitating tinnitus secondary to inner ear tertiary syphilis in which a patient successfully responded to emergency treatment with intravenous lidocaine.

Introduction

Tinnitus has many etiologies (table), and it is usually accompanied by sensorineural hearing loss. Countless numbers of people around the world live in a certain degree of harmony with their tinnitus. At some point, many of them have been examined by an otolaryngologist who provided treatment and advice to no avail. Most patients eventually realize that they simply must accept their tinnitus. However, on occasion, tinnitus is severe enough to warrant a visit to an emergency department and subsequent hospitalization.

In this article, we describe the case of a patient with a history of chronic tinnitus secondary to tertiary otosyphilis who developed an incapacitating exacerbation of her condition and who was treated successfully on an emergency basis with intravenous lidocaine.

Case report

A 48-year-old black woman underwent evaluation for an 8-year history of episodic vertigo, tinnitus, and progressive bilateral hearing loss. The results of a fluorescent treponcmal antibody absorption (FTA-ABS) test were positive, and she was diagnosed with tertiary otosyphilis. On the recommendation of an infectious disease consultant, she was treated with IV penicillin and a steroid for 6 weeks. However, numerous modes of medical therapy had not completely relieved her otologic symptoms. Although her vertigo and tinnitus had diminished somewhat, her hearing loss continued to worsen.

Several months later, the patient presented to the emergency department with a 3-week history of progressively louder tinnitus, which had reached the point that it caused her a great deal of discomfort and incapacitation. In fact, she was unable to function. She requested emergency admission to the hospital because she said her tinnitus was "driving me crazy." She described her tinnitus as "roaring" and not pulsatile. She had no vertigo at the time, but she noted that her hearing was worsening. She had earlier tried multiple doses of diazepam and prednisone without success.

Findings on her ENT examination were normal, as were her vital signs. No bruits were noted on auscultation. An audiogram showed that her sensorineural hearing loss was now 120 dB higher than her usual baseline 40-dB right sensorineural loss, primarily because of the tinnitus. In light of her high degree of morbidity and a favorable psychological evaluation, the patient was placed on a electrocardiographic (ECG) monitor while the administration of IV lidocaine was contemplated. In the meantime, a placebo bolus of 50 ml of normal saline was injected over 30 minutes, but the patient did not experience any relief. The decision was then made to try lidocaine.

The patient was given 1.5 mg/kg of IV lidocaine in saline over 30 minutes. Within 10 minutes of the completion of therapy, she reported that her tinnitus had decreased to its baseline level, which she found very tolerable. She was observed in the hospital for 24 hours, and she did not experience any recurrence of her incapacitating tinnitus. Her audiometric values returned to baseline.

During the next 2 years, she received three more injections of lidocaine under ECG monitoring in the emergency department for severe recurrences, and she achieved relief each time. Of interest, each of these injections was preceded by a placebo injection that failed to provide relief. At follow-up, her sensorineural hearing loss remained progressive, but her tinnitus was much better controlled.

Discussion

Approximately 35% of adults in industrialized nations have experienced tinnitus during their lifetimes. (1) In 8%, the tinnitus has a significant effect on their well-being, primarily by interfering with their sleep. (1) In approximately 0.5 % of the United States population, tinnitus is so severe that it is incapacitating. (1)

Epidemiologic studies have shown that tinnitus is positively correlated with increasing age, noise exposure, and lower socioeconomic status. (1) One interesting finding is that tinnitus, including severe tinnitus, is more common among women than men. This finding is more noteworthy when one realizes that noise-induced tinnitus is much more common in men.

Because tinnitus can be related to a lesion anywhere in the auditory pathway from the external ear canal to the cortex, the work-up must be thorough. It should include a complete history, physical examination, neurologic examination, and audiometry, including an assessment of speech discrimination. Laboratory studies should include SMA-12 tests and measurements of fasting blood glucose, triglyceride level, FTA-ABS (for syphilis), complete blood count with differential, and thyroid function. Further work-up as indicated may include electronystagmography and auditory brainstem-evoked response testing. Computed tomography and/or magnetic resonance imaging can be obtained to rule out cerebellopontine angle tumors and brainstem lesions, especially in patients with unilateral tinnitus.

The treatment of tinnitus is as varied as its causes. The pathophysiology is poorly understood, although we do know that there is a similarity between some types of tinnitus and neurologic disorders that may be caused by spontaneous neuronal hyperactivity, such as facial neuralgia and epilepsy. (1,2) Medications that have been used for treatment with varying degrees of success include anticonvulsants (e.g., carbamazepine), benzodiazepines, various local anesthetics (especially oral lidocaine), and vitamins. Authors of several reports of IV lidocaine for the treatment of marked tinnitus have described varied degrees of success, but none discussed its use in patients with incapacitating tinnitus. (2-5)

Tinnitus maskers include household items such as radios, televisions, and electric fans. For patients with more severe tinnitus, hearing aids and hearing aid-like maskers have been used with mixed results.

Without considering specific surgical treatments for the relief of an underlying problem (e.g., stapedectomy for otosclerosis or placement of an endolymphatic subarachnoid shunt for Meniere's disease), the surgical treatmerit of subjective tinnitus primarily involves labyrinthectomy or translabyrinthine section of the VIIIth cranial nerve. (6) However, even in cases when the cochlear nerve was sacrificed during tumor surgery, anecdotal reports suggest that only 50% of patients with preoperative tinnitus experience relief.

In our patient, IV lidocaine was given in a dose equivalent to the loading dose used in patients with cardiac arrhythmias--that is, 1.5 mg/kg injected over 30 minutes. Vital signs and cardiac rhythm were monitored during injection and for 30 minutes afterward. Our patient responded quickly, relaxed, and appeared to be less distressed.

Lidocaine may reduce abnormal spontaneous hyperactivity in the central nervous system, and it has been used to treat epileptic seizures. (2) Several reports, including one published as early as 1935 by Barany, (7) have indicated that lidocaine may have a beneficial effect on tinnitus. (2) Its major adverse effects are attributable to its actions on the central nervous system: drowsiness, paresthesia, convulsions, respiratory depression, and coma. Myocardial contractility may also be affected. Untoward effects are most common in patients who have hepatic insufficiency or congestive heart failure. (8) The risk that a single dose injected slowly during close monitoring will cause any problems is minimal, but in the extraordinary patient clinical discretion is advised.

Although tertiary or congenital syphilis can affect the inner ear and cause hearing loss, vertigo, and tinnitus, it rarely causes incapacitating tinnitus. (9-12) Treatment of otosyphilis requires high-dose IV penicillin and a steroid to reverse or control hearing loss and alleviate tinnitus and vertigo. Exacerbations of tinnitus require further treatment, and IV lidocaine may help in this limited group of patients. The use of psychological evaluation and counseling prior to any attempt at treatment is important to ascertain whether or not the tinnitus is real. Administration of a placebo can also help determine if the tinnitus is real.

To our knowledge, ours is the first report of a case in which a patient who presented to the emergency room with an incapacitating exacerbation of syphilitic inner ear tinnitus responded successfully to medical therapy. In most cases, otolaryngologists would be puzzled by a patient in as much distress as was our patient, and their immediate question would be, How do I treat this patient? We have shown that IV lidocaine can be easily and successfully administered in the emergency department or hospital setting to relieve such a patient's distress once all obvious causes have been ruled out.

References

(1.) Moller AR. Pathology of tinnitus. Ann Otol Rhinol Laryngol 1984:93:39-44.

(2.) Duckert LG, Rees TS. Treatment of tinnitus with intravenous lidocaine: A double blind randomized trial. Otolaryngol Head Neck Surg 1983;91:550-5.

(3.) Lyttkens L, Larsson B, Wasterstrom SA. Local anaesthetics and tinnitus. Proposed peripheral mechanism of action of lidocaine. ORL J Otorhinolaryngol Relat Spec 1984;46:17-23.

(4.) Israel JM, Connelly JS, McTigue ST, et al. Lidocaine in the treatment of tinnitus aurium. A double-blind study. Arch Otolaryngol 1982;108:471-3.

(5.) Otsuka K, Pulee JL, Suzuki M. Assessment of intravenous lidocaine for the treatment of subjective tinnitus. Ear Nose Throat J 2003: 82:781-4.

(6.) Pulec JL, Hodell SF, Anthony PF. Tinnitus: Diagnosis and treatment. Ann Otol Rhinol Laryngol 1978;87:821-33.

(7.) Barany R. Die Beeinflussung des Ohrensausens dutch iv Injizierte Lokalanaesthetica. Acta Otolaryngol 1935;23:201-3.

(8.) AMA Drug Evaluations. 4th ed. Chicago: American Medical Association, 1980:522.

(9.) Ahmad I, Lee WC. Otoncurosyphilis masquerading as neurofibromatosis type II. ORL J Otorhinolaryngol Relat Spec 1999; 61:37-40.

(10.) Linstrom CJ, Gleich LL. Otosyphilis: Diagnostic and therapeutic update. J Otolaryngol 1993;22:401-8.

(11.) Amenta CA III. Dayal VS. Flaherty J, Weil RJ. Luetic endolymphatic hydrops: Diagnosis and treatment. Am J Otol 1992;13: 516-24.

(12.) Steckelberg JM, McDonald TJ. Otologic involvement in late syphilis. Laryngoscope 1984;94:753-7.

From the Department of Otolaryngology--Head and Neck Surgery, Loyola University Medical Center, Maywood, Ill.

Reprint requests: James A. Stankiewicz, MD, Department of Otolaryngology--Head and Neck Surgery, Loyola University Medical Center, 2160 S. First Ave., Maywood, IL 60153. Phone: (708) 216-9637; fax: (708) 216-4834; e-mail: jstank@lumc.edu

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