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Dental trouble & apnea (lidocaine abstracts)

Rauni jenrun at newsguy.com
Tue Feb 2 16:56:13 EST 1999

I have has seizures after shots of lidocaine. I don't know if that is
common or not. Makes going to the dentist difficult. I need a melogram
and can't get one because of my reaction to lidocaine.  BTW I also
have a seizure disorder

On Tue, 02 Feb 1999 00:38:12 GMT, Brian Sandle
<bsandle at southern.co.nz> wrote:

>Apologies for a lengthy article. Perhaps more attention should be given 
>to disturbance of the breathing stimulus mechanism in the sinus area.
>I have ben asking about licdocaine neurological effects on 
>sci.med.dentistry and bionet.neuroscience.
>Now I wonder whether lidocaine may affect a person with a tendency to 
>multiple sclerosis in the breathing centre, perhaps, then sleep apnea 
>could set in and produce more nerological symptoms.
>Or the dental work might produce disturbance in the sinus which could 
>reduce breathing stimulus.
>My left nostril gets a bit more blocked with pressure since an upper big 
>molar root canal. Now it is 6 days since and I woke with a more blocked 
>nostril than before. It has cleared a bit.
>I have been having some of the neurological troubles mentioned by 
>stigmata1, but they have been clearing a bit since the root canal. The 
>dentist found a fair bit of pus under the root dressing which had been in 
>for a month.
>Brian Sandle
> ***********************   
>   Sleep Apnea
>   Author:   prepster <prepster at mindspring.com>
>   Date:   1999/01/14
>   Forum:   alt.support.sleep-disorder
>I have had Sleep Apnea for a while and only recently took action on it. My
>doctor says he wants to correct a deviated nasal septum, remove my tonsils
>and do an UPPP.
>I refuse to do the UPPP; it is painful with side effects and has a low
>success rate...comments? Would it also help to have my adenoids removed?
>   Re: Chronic Pain Down Right since April
>   Author:   Barry Kaplan <kaplanfamily at worldnet.att.net>
>   Date:   1998/12/22
>   Forums:   alt.support.chronic-pain, alt.med.fibromyalgia
>   more headers author posting history prev next
>   _________________________________________________________________
>What did they fill the root canal with?
>The most common root canal filling material is called "gutta percha" and it
>is fairly innocuous.
>In years past, two other materials were used.  One is called "silver
>points".  They are not good, but they shouldn't cause the pain you are
>reporting.  They just corrode over time.
>The other material that is out of favor is called "sargenti paste" This
>stuff can be real bad news.  I have heard of syptoms similar to yours, but
>not NEARLY as bad nor widespread in distribution.
>However, it is also possible that the thing causing the pain may not have
>been of dental origin.  The distribution of the nerves in the mouth has
>nothing to do with the nerves in your arm and leg. If you reported the pain
>and tic only in your face, I might suspect things like trigeminal neuralgia
>(tic Douluoroeux).
>I know you said you saw 23 doctors, but there are two things you need to be
>certain to do (if you haven't already). First of all, I would make sure I
>had a second opinion onthe root canal by a board certified endodontist (root
>canal specialist)
>Secondly, you might consider seeing a neurologist about your other
>It is possible that the tooth you had the root canal done on may not have
>been the problem. I have never seen mouth pain refer farther than the
>sinuses or neck.  You may have had a different problem to begin with.
>There are at least two physicians that often respond to posts an this
>newsgroup.  Hopefully Mike, Todd ,and anyone else with anything to add will
>pipe up
>Barry (DDS)
>stigmata1 at hotmail.com wrote in message <75p0a9$tug$1 at nnrp1.dejanews.com>...
>>I hope there's an answer! In April of 1998 I went to get some routine
>>work done, and found that I required a root canal, which I assented to.
>>Almost immediately after the procedure, I started experiencing excrutiating
>>pain in that tooth, which seemed to inflame the entire right side of my
>>It was so bad I wanted to be knocked out and have it removed on site.
>>However, since I'm 23 all doctors advised me against removal and assured me
>>that within a month the pain would subside. Well, the pain became so bad
>>twice that I went to the emergency room because I couldn't take it, and
>>gave me Percocet, Which I ended up being on for about two months. During
>>time period, I started feeling a burning pain sensation "creeping" down my
>>arm and my leg, as well as the already established pain in my face, eye,
>>saggital plan, which led to a facial tic that I have to this day. But as
>>pain started creeping down my extremities, I found it more and more
>>to move my hand and my foot, writing was very difficult, I had trouble
>>holding the pen. Gradually, the excruciating pain gave way to a lesser
>>and I was moved off of Percocet down to Hydrocodone, Then just OTC pain
>>relievers. I'm not lying prostrate in pain anymore, but I still have a
>>constant, low level pain that's down the right side of my body. When I sigh
>>or yawn or exhale deeply, I feel "bolts" of pain race down my right arm
>>it 'hits' at the tips of the fingers. I also experience a phenomenon 
>when I
>>hold my computer mouse, where my right hand will get 'cold shots' all over
>>the top of my hand when surrounding the mouse. There seem to be pain focal
>>points at the top of my spine and the bottom, and I feel the pain connected
>>and start to run down what feels like the center of my leg and arm where
>>limb is subumerged in a burning sensation. Anyone know what this is, how it
>>came about, and the cure?
>>Any answers appreciated,
>>Dave Canova,
>>stigmata1 at hotmail.com
>   Neurology 1992 Nov;42(11):2088-93
>Lidocaine unmasks silent demyelinative lesions in multiple sclerosis.
>    Sakurai M, Mannen T, Kanazawa I, Tanabe H
>   Department of Neurology, School of Medicine, University of Tokyo,
>   Japan.
>   Blockage of a small number of sodium channels may prevent impulse
>   conduction in some demyelinated segments of nerve fibers with low
>   safety factors, thereby unmasking subclinical demyelinative lesions.
>   On the basis of this hypothesis, lidocaine, a sodium channel blocker,
>   was administered intravenously to 28 MS patients and to 19 normal
>   subjects and seven patients with nondemyelinating diseases. As
>   predicted, lidocaine (mean plasma level, 2.7 micrograms/ml) elicited
>   reversible subclinical symptoms in 23 of the MS patients, but it had
>   not effect on the control subjects. We made a quantitative study of
>   the visual functions (visual acuity, color vision, visual evoked
>   potential [VEP]) that were impaired in 15 MS patients. Of the 23
>   affected eyes, nine showed normal VEPs, indicative of the test's
>   sensitivity to focal lesions. This test should be useful in the
>   diagnosis of MS and in the evaluation of the subclinical activity of
>   MS as well.
>   PMID: 1331868, UI: 93063903   
>   Masui 1998 May;47(5):570-5
>[Midazolam for anesthetic induction in neonates].
>   [Article in Japanese]
>    Kawakami K, Ohata J, Kadosaki M, Saito I, Iwasawa K, Mitono H
>   Department of Anesthesiology, Nagano Children's Hospital.
>   The purpose of this study is to evaluate the effects of midazolam on
>   circulation, respiration, sedation, and liver function of the
>   neonates. The study subjects are 27 neonates (body weight 2.1 to 3.8
>   kg, gestational age at birth 34 to 41 weeks) who underwent surgery in
>   neonatal period. Of 27, 13 patients received lidocaine (1.5 mg.kg-1)
>   immediately before tracheal intubation (group L), and 14 had
>   midazolam (0.1 mg.kg-1) with lidocaine (group ML). We compared the
>   effects of midazolam in the presence of lidocaine on the following
>   parameters: (1) the incidence of hypotension (systolic blood pressure
>   < 50 mmHg) and bradycardia (heart rate < 100 beats.min-1), (2) the
>   incidence of apnea and desaturation of oxygen (< 80%), (3) the degree
>   of sedation, and (4) the serum levels of bilirubin and unbound
>   bilirubin after surgery. In group L, there were hypotension (1/13)
>   and desaturation (1/13). In group ML, there were desaturation (1/14)
>   and post-operative apnea (1/14). None in both groups developed
>   bradycardia or intracranial hemorrhage. A single-dose of lidocaine
>   induced sedation only in 4 neonates, while combination of midazolam
>   and lidocaine in 11. None had elevation of either total or unbound
>   bilirubin after surgery. In conclusion, the titrated dose of
>   midazolam with lidocaine is useful for anesthetic induction of
>   neonates, although cares should be taken on its adverse effects such
>   as hypotension, desaturation, and post-operative apnea.
>   Publication Types:
>     * Clinical trial
>   PMID: 9621667, UI: 98284687
>     _________________
>   Anesthesiology 1998 Mar;88(3):761-7
>Hypoxia causes apnea during epidural anesthesia in rabbits.
>    Hogan QH, Amuzu J, Clifford PS, Bosnjak ZJ, Kampine JP
>   Department of Anesthesiology, Medical College of Wisconsin and the
>   Zablocki Veterans Administration Medical Center, Milwaukee 53226,
>   USA.
>   BACKGROUND: Although pulmonary function is minimally changed by
>   neuraxial blockade in most cases, ventilatory arrest may ensue in
>   rare cases. The authors examined the mechanism of apnea in a rabbit
>   model of sudden ventilatory arrest during the combination of epidural
>   anesthesia and hypoxia. METHODS: Rabbits were studied during
>   alpha-chloralose sedation and spontaneous ventilation through a
>   tracheostomy tube. Heart rate and mean arterial pressure were
>   monitored by intraarterial cannulation. Respiratory rate and tidal
>   volume were measured by pneumotachograph. Responses were recorded
>   during administration of oxygen at inspired oxygen concentrations of
>   11% for 2.5 min and 0% for 40 s, before and after either
>   thoracolumbar epidural blockade (0.4 ml/kg lidocaine, 1.5%) or
>   intramuscular lidocaine (15 mg/kg). In a third group of animals,
>   epinephrine was given intravenously during epidural blockade to
>   return mean arterial pressure to baseline values before hypoxia. In a
>   fourth group of animals, which did not get lidocaine, sympathetic
>   blockade and hypotension were produced with intravenously
>   administered trimethaphan rather than epidural blockade. RESULTS:
>   Thoracolumbar epidural anesthesia decreased mean arterial pressure
>   from 76 +/- 4 mmHg (mean +/- SE) to 42 +/- 2 mmHg. Apnea during
>   hypoxia occurred in 90% of these animals (nine of ten) but in only
>   11% of animals (one of nine) after intramuscularly administered
>   lidocaine (P < 0.01). Treatment of epidural hypotension with
>   epinephrine prevented apnea (zero of nine animals). Apnea during
>   hypoxia occurred in 50% (three of six) of animals given trimethaphan.
>   Apnea in all groups was sudden in onset, with no preceding decreases
>   in respiratory rate or tidal volume. CONCLUSIONS: Epidural anesthesia
>   results in a narrowed margin of safety for oxygen delivery to the
>   brain and predisposes subjects to ventilatory arrest during hypoxia.
>   This results from the combined effects of decreased blood oxygen
>   content, which is due to decreased inspired oxygen concentration
>   superimposed on circulatory depression due to neural blockade.
>   PMID: 9523821, UI: 98181995                            
>   Am J Respir Crit Care Med 1995 Jun;151(6):1857-61
>Effect of upper airway anesthesia on obstructive sleep apnea.
>    Berry RB, Kouchi KG, Bower JL, Light RW
>   Department of Medicine, Long Beach VA Medical Center, CA 90822, USA.
>   We hypothesized that upper airway mechanoreceptors contribute to the
>   arousal stimulus that occurs with upper airway occlusion in
>   obstructive sleep apnea (OSA). If so, upper airway anesthesia (UAA)
>   should reduce the arousal stimulus and impair the arousal response.
>   To test this hypothesis, we studied the effects of UAA on apnea
>   duration and the esophageal pressure deflection before arousal in a
>   group of patients with severe OSA. On two study nights separated by
>   one week, subjects were monitored for 2 h after lights out. They were
>   then awakened and either 5 cc of 4% lidocaine or saline (random
>   order) was dripped into the upper airway via the nose over 10 min.
>   Another 2 h of monitoring was then performed. Variables on the first
>   and second parts of the control (C1 and C2) and lidocaine nights (L1
>   and L2) were compared during non-rapid eye movement sleep using the
>   analysis of variance. With lidocaine, the mean (+/- SEM) apnea
>   duration increased from 24.2 +/- 2.6 (L1) to 30.7 +/- 2.3 (L2) s but
>   with saline the apnea length was unchanged from 23.3 +/- 1.5 (C1) to
>   23.4 +/- 1.6 (C2) (L2 > [L1, C1, C2], p < 0.01). In addition, the
>   maximum esophageal pressure deflection (cm H2O) before arousal
>   increased after lidocaine from 63.6 +/- 14.5 (L1) to 84.1 +/- 14.7
>   (L2) but after saline was unchanged from 62.1 +/- 15.4 (C1) to 60.0
>   +/- 15.2 (C2), (L2 > [L1, C1, C2], p < 0.05). We conclude that UAA
>   impairs the arousal response to airway occlusion. This suggests that
>   input from upper airway mechanoreceptors during obstructive events
>   contributes to the total arousal stimulus in patients with OSA.
>   Publication Types:
>     * Clinical trial
>     * Randomized controlled trial
>   PMID: 7767531, UI: 95285040
>     _____________________________________________________
>   Am J Respir Crit Care Med 1995 Apr;151(4):1108-12
>Topical oropharyngeal anesthesia in patients with obstructive sleep apnea.
>    Deegan PC, Mulloy E, McNicholas WT
>   Department of Respiratory Medicine, University College, Dublin,
>   Ireland.
>   Topical oropharyngeal anesthesia (TOPA) increases obstructive sleep
>   apnea (OSA) frequency in both normal subjects and loud snorers. The
>   effects of TOPA in established OSA were assessed in six male patients
>   with a mean age (+/- SEM) of 50 +/- 5.3 yr. Following an
>   acclimatization night, each subject underwent two overnight sleep
>   studies, randomly assigned to TOPA (10% lidocaine spray and 0.25%
>   bupivocaine gargle) and control (C) (saline placebo). Patients
>   demonstrated sleep efficiencies of 93 +/- 2.9% (mean +/- SEM) during
>   C and 88 +/- 2.9% during TOPA. Overall apnea-hypopnea (AH) frequency,
>   using inductance plethysmography, showed little change: 21.2 +/- 3.6
>   on C versus 25.1 +/- 3.5 events/h on TOPA nights (p = 0.12). There
>   was no significant increase in AH duration with TOPA, and oxygen
>   desaturation (> or = 4%) frequency was similar: 21.1 +/- 3.9 per hour
>   during TOPA versus 23.6 +/- 5.9 during C. However, obstructive AHs
>   showed a change in thoracoabdominal motion from C to TOPA nights,
>   with an increase in events with abdominal paradox from 3.1 +/- 1.1 to
>   10.3 +/- 3.1 per hour (p = 0.03), and a reduction in events with
>   ribcage paradox from 13.1 +/- 1.6 to 8.2 +/- 2.4 per hour (p = 0.08).
>   Central and mixed AHs demonstrated similar frequencies on both
>   nights. These data support an impairment of upper airway (UA)
>   protective reflexes among patients with OSA.
>   Publication Types:
>     * Clinical trial
>     * Randomized controlled trial
>   PMID: 7697239, UI: 95211324                            
>   Brain Res 1991 Sep 27;560(1-2):321-5
>Trigeminal mediation of the diving response in the muskrat.
>    Panneton WM
>   Department of Anatomy and Neurobiology, St. Louis School of Medicine,
>   MO 63104.
>   Stimulation of the nasal cavity elicits powerful cardiorespiratory
>   responses similar to the diving response. In the present study,
>   bradycardia and apnea were elicited in muskrats by stimulation of the
>   nasal cavity with ammonia vapors. These responses could be blocked by
>   injections of 2% lidocaine made bilaterally into the medullary dorsal
>   horns of the trigeminal sensory complex. However, the bradycardia due
>   to activation of the baroreceptor reflex with intravenous
>   phenylephrine was retained. These data implicate trigeminal neurons
>   in the medullary dorsal horn as modulators of autonomic activity,
>   especially in the cardiorespiratory adjustments after nasal
>   stimulation.
>   PMID: 1760738, UI: 92103521
>     ________________________________________________________________
>   Other Formats: [Citation Format] [MEDLINE Format]
>   Links: [114 medline neighbors]
>   Am Rev Respir Dis 1991 Apr;143(4 Pt 1):810-3
>Obstructive sleep apnea following topical oropharyngeal anesthesia in loud
>    Chadwick GA, Crowley P, Fitzgerald MX, O'Regan RG, McNicholas WT
>   Department of Respiratory Medicine, University College, Dublin,
>   Ireland.
>   Previous studies support the presence of an upper airway reflex
>   mechanism that contributes to the maintenance of upper airway patency
>   during sleep. We investigated the possibility that interference with
>   this reflex mechanism contributes to the development of obstructive
>   sleep apnea. Eight otherwise asymptomatic snorers (seven male and one
>   female), age 39 +/- 5.3 yr (mean +/- SEM), underwent overnight sleep
>   studies on three successive nights. An acclimatization night was
>   followed by two study nights randomly assigned to control (C) and
>   oropharyngeal anesthesia (OPA). On the OPA night topical anesthesia
>   was induced using 10% lidocaine spray and 0.25% bupivacaine gargle. A
>   saline placebo was used on night C. All subjects slept well on both
>   study nights (mean sleep duration was 6.2 h on both study nights),
>   and sleep stage distribution was similar on both nights. Obstructive
>   apneas and hypopneas (OAH) rose from 114 +/- 43 during C to 170 +/-
>   49 during OPA (p less than 0.02). Central apneas and hypopneas (CAH)
>   were unchanged between the two nights (8 +/- 4.9 versus 7 +/- 3). The
>   duration of OAH was similar on both study nights (20 +/- 1.9 s during
>   C versus 20 +/- 1.5 s during OPA). The frequency of movement arousals
>   terminating OAH tended to be higher during OPA (7 +/- 2.9/h) than
>   during C (3 +/- 0.7); P = NS. The frequency of oxyhemoglobin
>   desaturations was also higher during OPA (5 +/- 2.1/h) than during C
>   (3 +/- 1.4), p less than 0.07.
>   PMID: 2008992, UI: 91181783
>     ________________________________________________________________
>   Other Formats: [Citation Format] [MEDLINE Format]
>   Links: [109 medline neighbors]
>   Am Rev Respir Dis 1985 Nov;132(5):972-5
>The effects of nasal anesthesia on breathing during sleep.
>    White DP, Cadieux RJ, Lombard RM, Bixler EO, Kales A, Zwillich CW
>   Inability to breathe through the nose is an increasingly recognized
>   cause of disordered breathing during sleep. To test the hypothesis
>   that this respiratory dysrhythmia could result from loss of neuronal
>   input to respiration from receptors located in the nose, we
>   anesthetized the nasal passages of 10 normal men during sleep. Each
>   subject spent 4 consecutive nights in the sleep laboratory while
>   sleep stages, breathing patterns, respiratory effort, and arterial
>   oxygen saturation were monitored. Night 1 was for acclimatization
>   with Nights 3 and 4 being randomized to nasal spraying with either 4%
>   lidocaine or placebo. On the lidocaine and placebo nights (Nights 3
>   and 4) the nasal passages were also sprayed with a decongestant to
>   prevent increased nasal air-flow resistance resulting from mucosal
>   swelling. To control for the possible effects of this decongestant,
>   an additional night (Night 2) was included during which the nasal
>   passages were sprayed with room air. Parallel studies conducted
>   during wakefulness demonstrated low nasal resistance during the
>   lidocaine-decongestant regimen. Because of the short duration of
>   anesthesia with lidocaine, spraying was done at lights out and 2.5
>   and 5 h later. On the placebo night (decongestant plus saline) there
>   were 6.4 +/- 1.8 (SEM) disordered breathing events (apneas plus
>   hypopneas) per subject, whereas with lidocaine (plus decongestant)
>   this increased fourfold to 25.8 +/- 7.8 events per subject (p less
>   than 0.05). The majority of the disordered breathing events were
>   apneas and were fairly evenly distributed between central and
>   obstructive events. The magnitude of these changes is similar to that
>   previously reported with complete nasal obstruction. These results
>   suggest that nasal receptors sensitive to air flow may be important
>   in maintaining breathing rhythmicity during sleep.
>   Publication Types:
>     * Clinical trial
>     * Randomized controlled trial
>   PMID: 4062052, UI: 86048887                         this document
>   Am J Perinatol 1987 Apr;4(2):164-6
>Lidocaine toxicity after maternal pudendal anesthesia in a term infant with
>fetal distress.
>    Bozynski ME, Rubarth LB, Patel JA
>   There have been many reports of lidocaine toxicity especially after
>   maternal paracervical block anesthesia. We recently treated a term
>   infant with evidence of fetal distress who presented with symptoms of
>   lidocaine toxicity after maternal pudendal anesthesia. The infant
>   developed apnea and bradycardia soon after birth which responded to
>   mechanical ventilation and epinephrine. A prolonged Q-T interval was
>   noted on day 1 which normalized by day 3. Cord blood was assayed and
>   revealed an elevated lidocaine level. Lidocaine toxicity has been
>   associated with fetal distress secondary to fetal ion trapping in the
>   presence of acidosis. Although good response to supportive therapy
>   occurred in our patient, other methods of therapy such as exchange
>   transfusion and treatment of seizures may be required in some cases.
>   Awareness of this now uncommon syndrome will lead to prompt
>   diagnosis, appropriate work-up, and management.
>   PMID: 3566884, UI: 87184830
>     ________________________________________________________________
>   Other Formats: [Citation Format] [MEDLINE Format]
>   Links: [169 medline neighbors]
>   Am J Physiol 1977 Jul;233(1):R30-6
>Properties of the laryngeal chemoreflex in neonatal piglets.
>    Lee JC, Stoll BJ, Downing SE
>   Cardiorespiratory reflex responses to laryngeal chemoreceptor
>   stimulation were studied in 62 piglets of both sexes varying in age
>   from 1 to 79 days. The distal trachea was cannulated to provide a
>   free airway and the proximal end used to introduce fluids into the
>   laryngeal area. Introduction of either water or milk produced apnea,
>   bradycardia, and hypertension. Swab application of test fluids to the
>   laryngeal epithelium produced similar responses. The reflex could be
>   interrupted by flushing the laryngeal region with saline, by cutting
>   the superior laryngeal nerves (SLN) or by anesthetizing the laryngeal
>   epithelium with lidocaine. Electrical stimulation of SLN elicited
>   identical responses. Respiratory inhibition by the reflex was
>   enhanced following central depression with chloralose and overridden
>   by administration of the respiratory stimulant, aminophylline. The
>   relative potency of the laryngeal reflex was estimated to be
>   equivalent to about 40% of the dose of chloralose which produced
>   permanent respiratory arrest. It is concluded that in circumstances
>   where respiratory drive is reduced the laryngeal inhibitory reflex is
>   capable of caused persistent apnea and asphyxial death in the young
>   piglet.
>   PMID: 18025, UI: 77219523
>     ________________________________________________________________
>   Other Formats: [Citation Format] [MEDLINE Format]
>   Links: [102 medline neighbors]
>   Rev Bras Pesqui Med Biol 1976 Dec;9(5-6):229-37
>Lethal effect of the serotonin-xylocaineR association in ganglion-blocked
>    Valle LB, Oliveira-Filho RM, Armonia PL, Saraceni G Jr, Nassif M, De 
>Lucia R
>   In rats anestetized with urethane and under ganglionic blockade by
>   hexamethonium (20 mg/kg, i.v.), the i.v. injection of serotonin (60
>   mug/kg) determined apnea, ECG alterations and a brief hypotensive
>   response which is similar to that as elicited when 5-HT is given to
>   intact rats. During the hypertension which follows that initial
>   response, apnea is still present along with more severe ECG changes.
>   After that, blood pressure falls into a prolonged hypotension, which
>   is invariably accompanied by death. Neither norepinephrine, nor
>   respiratory analeptics (CoramineR, RemeflinF) were able to prevent
>   the fatal outcome. Only artificial respiration was found to be useful
>   in some instances. It was concluded that the association serotonin
>   plus lidocaine becomes lethal when given to ganglion-blocked rate,
>   and this toxic effect can be ascribed mainly to the respiratory
>   depressor activity of the drugs.
>   PMID: 1013401, UI: 77103742
>     ___________________________
>   Z Orthop Ihre Grenzgeb 1974 Oct;112(5):1053-62

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