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Dental trouble & apnea (lidocaine abstracts)

Joel M. Eichen joele at earthlink.net
Mon Feb 8 07:36:59 EST 1999


"K. Bennett" <klmwb at cybergal.com> wrote:

>I have also had SEVERE seizures from Lidocaine injections in Dental Offices. I
>found that I don't have that reaction from it if it is the type WITHOUT
>EPINEPHRINE!!! NO EPI...The injections usually are given with this included to
>help keep the med localized for longer...without it, it takes about 30 minutes
>before you have to have another shot! Tell the folks you deal with "NO EPI" and
>your shakes can be "normal" terror from sounds of drilling and smells of YOUR
>teeth being drilled!

>Also, I recently had a root canal redone, and they told me that they weren't
>gonna use Lidocaine at all because they preferred (?not sure heard exactly
>rightly?) DARVOCAINE? for that?

Carbocaine.

Cheers,

Joel

-----------


>Ask...

>K. Bennett

>"The more I know, the more I know I need to know more."
>(By:  A Smart Person...?)

>Rauni wrote:

>> 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
>> >   _________________________________________________________________
>> >
>> >Dave,
>> >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
>> >complaints.
>> >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
>> >dental
>> >>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
>> >face.
>> >>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
>> >they
>> >>gave me Percocet, Which I ended up being on for about two months. During
>> >this
>> >>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
>> >this
>> >>pain started creeping down my extremities, I found it more and more
>> >difficult
>> >>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
>> >pain,
>> >>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
>> >until
>> >>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
>> >the
>> >>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
>> >snorers.
>> >
>> >    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
>> >rats.
>> >
>> >    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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