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Sent: Friday, June 21, 2002 10:59
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Subject: URG-L: cas clinique + QUESTION
à la liste
Surtout question, et question surtout aux français de
france, diplomés de souche.
jeune femme japonaise résidant à Parisse.
Diarrhée abondante > 10 par jour, ni sang ni mucus, depuis un
jour
Vomissements = 10, crampes abdo.
Arthralgies
Asthénie tendance lipothymique au lever
Température 36 °8 sub lingual (no comment !) soit une fièvre
(pour une japonaise; je n'ai rien trouvé sur la température
des japonais dans pubmed mais de fait ils ont le sang froid, ou des
thermos mal étalonnés).Sa température usuelle: 35°5...
Examen ressemble à une gastroentérite, douleur du cadre
colique rien de péritonéal. Rien d'autre.
Pas de voyage exotique.
Perfusion de 500 de salé et 500 de polyionique potassé
sucré, métoclopramide IVD 10 mg , paracétamol 1g per
os, lopéramide une capsule.
Au bout de 10 minutes de traitement, la patient a un air bizarre, commence
à vouloir se lever de son brancard confortable, essaie de se retirer
la perfusion.
Diagnostic ?
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Acathisie iatrogène: neuroleptique.
Après explication du syndrome de son origine de sa bénignité,
5 mg de valium per os (mouais, pas futé, j'ai hésité
avec le lepticur) et encouragement à se promener dans le service
(elle avait eu un bon bolus de salé) , elle se calme.
MA QUESTION
Je ne sais pas ce qui traite le mieux cela. La tropatépine (Lepticur
) marche-t-elle comme dans les dyskinésies ?
QUELLE EST VOTRE EXPEriENCE ?
Je suis surpris de la fréquence de 30% d'acathisie environ
après neuroleptiques dans les vomissements/migraines (larga manu
en Amérique du Nord) , pour utiliser le prompéran larga manu
ego quoque, je trouve ça rare (ou je ne veux pas le voir, le patient
demandant à partir considéré comme guéri)
Encephale 1976;2(2):115-21 Related Articles, Books, LinkOut
[A new synthetic antiparkinsonian drug, tropatepine hydrochloride in
extrapyramidal syndromes induced by neuroleptics]
[Article in French]
Lambert A, dachary JM, Marie C, Oules J, Pagot R, Sales M, Vauterin
C.
Tropatepine hydrochloride was given per oral route to 184 patients
and per injections to 34 patients. Average prescribed doses were about
20 mg (2 tablets). This clinical study has shown that tropatepine hydrochloride
has an antiparkinson activity against neuroleptic-induced extra-pyramidal
syndrome. In comparison to the activity of the other synthetic antiparkinson
drugs, the activity of tropatepine hydrochloride is: -- similar on akineto-hypertonia
and on tremor; -- better on akathisia and, though less frequently, on anormal
dyskinetic movements due to long term neuroleptic treatment. Tolerance
is good ; furthermore clinical and biological performed examinations have
shown that the drug seems free of toxic effects In more than 200 treated
patients no severe mental aberration and no habituation have been reported.
========
Akathisia (Rosen 2001)
Akathisia is a state of motor restlessness characterized by a physical
need to be moving constantly. It occurs most often in middle-age patients
during the first few months after the initiation of therapy.[49] Patients
are usually observed pacing the room and expressing a sense of inner tension
that is not relieved by activity. If asked, they will state that they do
not want to be constantly moving but feel physically compelled to do so.
This reaction can easily be mistaken for a decompensating psychosis, leading
to a vicious cycle in which more medication is given to treat a side effect
caused by the same drug. This misdiagnosis can be avoided by carefully
evaluating the patient for the exacerbation of positive psychotic symptoms,
which are not increased by akathisia. Akathisia is treated with ?-blockers
(e.g., propranolol, 30 to 60 mg/day) or anticholinergic drugs (e.g., benztropine,
1 mg twice to four times daily). A new potential agent for the treatment
of akathisia is glycine, a nonessential amino acid that stimulates glutamatergic
neurotransmission.[50] In addition, if possible, the dosage of the antipsychotic
agent should be lowered.
======
Diphenhydramine for the prevention of akathisia induced by prochlorperazine:
a randomized, controlled trial.
Vinson DR - Ann Emerg Med - 01-Feb-2001; 37(2): 125-31
Abstract:
STUDY OBJECTIVES: The utility of intravenous prochlorperazine as an
antiemetic agent and abortive therapy for headache may be limited by the
frequent occurrence of akathisia, the distressing effects of which have
been shown to disrupt patient care. We tested the hypothesis that adjuvant
diphenhydramine reduces the incidence of akathisia induced by prochlorperazine.
METHODS: This randomized, double-blind, placebo-controlled trial was conducted
in the emergency department of an academic tertiary care medical center
with an annual census of 95,000 emergency patient visits. We enrolled a
convenience sample of 100 adult patients who received 10 mg of intravenous
prochlorperazine for the treatment of nausea/vomiting or headache. Subjects
were randomly assigned to receive a 2-minute infusion of prochlorperazine
with either 50 mg of diphenhydramine or placebo. The incidence of akathisia
at 1 hour was measured by using explicit diagnostic criteria. To measure
the influence of treatment on sedation, the subjects noted, on a 100-mm
visual analog scale, their degree of sedation before and after treatment.
RESULTS: Akathisia developed in 18 (36%) of 50 subjects in the control
group and in 7 (14%) of 50 subjects in the diphenhydramine group, a 61%
relative reduction. The addition of adjunct diphenhydramine resulted in
an absolute reduction of 22% in the incidence of akathisia (95% confidence
interval [CI] 6% to 38%; P = .01). The odds ratio for akathisia with the
use of adjuvant diphenhydramine was 0.39 (95% CI 0.18 to 0.85). Mean sedation
scores increased 12 mm after infusion of prochlorperazine alone (95% CI
3 to 21 mm) compared with a 33-mm increase after infusion of prochlorperazine
with adjuvant diphenhydramine (95% CI 24 to 42 mm). The 12-mm difference
between the groups was statistically significant (95% CI 9 to 34 mm, P
< .001). CONCLUSION: Adjuvant diphenhydramine reduces the incidence
of akathisia induced by prochlorperazine and is associated with an increase
in sedation.
Am J Psychiatry 1992 May;149(5):647-50 Related Articles, Books, LinkOut
======
Randomized, double-blind, crossover, placebo-controlled comparison of
propranolol and betaxolol in the treatment of neuroleptic-induced akathisia.
Dumon JP, Catteau J, Lanvin F, Dupuis BA.
Department of Pharmacology, School of Medicine, University of Lille,
France.
OBJECTIVE: Beta-blocking agents, particularly propranolol, are considered
effective in the treatment of neuroleptic-induced akathisia, but considerable
controversy exists about the involved receptor subtype(s). The authors
conducted a randomized, controlled trial comparing the effects of propranolol
and betaxolol to determine whether central beta 1-adrenoceptor blockade
is sufficient to correct neuroleptic-induced akathisia. METHOD: The subjects
were 19 patients whose neuroleptic-induced akathisia responded to 20 mg/day
of propranolol and subsequently reemerged during a placebo washout period.
They were randomly assigned to propranolol (20 or 40 mg/day) or betaxolol
(10 or 20 mg/day) and, after another placebo period, were switched to the
second beta blocker. RESULTS: There was no significant difference in the
antiakathisia effects of propranolol and betaxolol. CONCLUSIONS: The lack
of difference between propranolol and betaxolol suggests that beta 1-adrenoceptor
blockade is sufficient to improve neuroleptic-induced akathisia. The results
of this explanatory study need therapeutic confirmation.
======
http://www.vh.org/Providers/Conferences/CPS/07.html
AKATHISIA
Presentation
Akathisia refers to the subjective experience of motor restlessness
(Tarsy 1983, Van Putten et al 1984). Patients may complain of an inability
to sit or stand still, or a compulsion to pace or cross and uncross their
legs. They may also complain of being restless and having to be in constant
motion. While standing they may rock to and fro or shift their weight from
one leg to another. Patients may also suffer from initial insomnia because
they cannot lie motionless in bed long enough to fall asleep. Ninety percent
of cases develop within the first 73 days of treatment and 50% within the
first month of initiation of the antipsychotic (Ayd 1961).
Estimates of the incidence of akathisia range from 21 to 75% (Ayd 1961,
Van Putten 1984). Females are approximately twice as likely to develop
akathisia compared to males; it demonstrates equal prevalence across all
age groups (Ayd 1961, Ganzini et al 1991, Casey 1994). An accurate diagnosis
is important since misdiagnosis may lead to an unnecessary increase in
antipsychotic dose with potential worsening of akathisia.
Anticholinergics
Although numerous anticholinergics are available for management of
antipsychotic-induced EPS, comparative studies between agents comparing
efficacy and side effects have not been performed. If a patient does not
respond to one anticholinergic at maximal doses, a trial with another may
be done empirically. There is no support for combining anticholinergics.
Doses of anticholinergics should be initiated with benztropine 1-2 mg/d
or its equivalent (i.e., trihexyphenidyl 2-4 mg/d). Smaller initial doses
should be used with geriatric patients. Benztropine can usually be administered
effectively and safely in doses up to 6 mg/d, though some patients may
require and tolerate doses to 8 mg/d. The dose is administered preferably
at bedtime because of possible sedation. No information is available on
single-daily dosing of other anticholinergics; these are usually administered
two to three times per day.
Acute Treatment. When akathisia develops, it is appropriate in some
clinical situations to change to an antipsychotic less likely to produce
EPS (i.e., thioridazine, chlorpromazine) or to lower the dose of the antipsychotic
causing the reaction. These drugs should be considered for patients at
a high risk of developing specific types of acute-onset EPS. Upon discontinuation
of the antipsychotic, akathisia symptoms generally resolve in seven to
ten days, but may take several weeks depending upon the drug, the dose,
and the patient.
The use of anticholinergics in the treatment of akathisia has been reviewed
(Fleischhacker et al 1990). Of nine studies, four were double-blind in
design. Five reports indicated anticholinergics were effective in akathisia,
two had negative findings, and two had equivocal results. In studies that
reported their results in percent response, the range was 30 to 100 percent
(average 62%). However, not all patients in the positive studies had complete
resolution of their akathisia. The time for akathisia to respond to anticholinergics
is usually three to seven days. Most studies reported that anticholinergics
were effective for akathisia in patients that had concomitant parkinsonism.
Therefore, anticholinergics might be considered first-line treatment for
patients with akathisia and concurrent parkinsonism.
--
Axel Ellrodt
Essonne, France
http://zzorglub.ifrance.com/
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