Cours de DES du 6 Septembre 2005 Dr Chassery CCA anesthésie Asthme et Anesthésie Cours de DES du 6 Septembre 2005 Dr Chassery CCA anesthésie

Prévalence population générale 9 % des adultes 15% des enfants faible si stable mais > pop. Générale Incidence en progression Yunginger J.and coll.A community-based study of the epidemiology of asthma. Incidence rates, 1964-83. Am. Rev. Resp. Dis., 1992;146:888-894 International consensus report on diagnosis and treatment of asthma. Eur respir J 1992;5:601-41

Morbidité anesthésique Variable +++ Rétrospectives: 0.8% à >20% Warner DO. Anesthesiology 1996, 85:460-467 Olsson GL. Acta Anaesthesiol Scand 1987;31(3):244-52 Verner DF.Can J Anaesth 1994; 41:A55 Kumeta Y.Masui J 1995;44:396-401 Prospectives: 1.7% Forrest JB.Anesthesiology 1992;77(1):222 Essentiellement représenté par le bronchospasme et ces complications Olson 156 000 anesthésie Incidence de bronchospasme 0.16% sans asthme 0.8% avec asthme 4,1% si IVAS Kumeta 20% AG ou ALR Verner 206 enfants 23% Bronchospasme abstract Forrest 1,7% complications respiratoires 0,8% bronchospasme

Morbidité anesthésique 1.7% 706 patients sur 10 ans (10-36 ans) Asthme critère clairement définis + AG ou RA-APD 2 laryngospasmes pas lié à la maladie asthmatique 12 bronchospasmes (4 per op, 8 post op) dont 1 V post op. 2 laryngospasmes 40% des patients avaient un ttt de fond pour l’asthme dans l’ année qui précédait Warner DO. Anesthesiology 1996, 85:460-467

Morbidité anesthésique Incidence des complications respiratoires Asymptomatique à J-30: 0.8% Symptomatique à J-30: 4.5% Symptomatique à J0 = complication 50% des cas 2 complications sur 4 symptomatique le jour de la chirurgie Warner DO. Anesthesiology 1996, 85:460-467

Morbidité anesthésique Faible….mais….potentiellement grave 762 plaintes pour complication respiratoire 40 bronchospasmes (2% plaintes) 50% ATDC asthmatiques/BPCO/tabac 35 atteintes cérébrales Enquête sur les complications respiratoires effectuée à partir des plaintes déposées au EU évidemment biais de sélection Cheyney FW. Anesthesiology 1991;75(6):932-9

Morbidité anesthésique « persons with asthma but no symtoms are at low risk for severe morbidity from anesthesia » « persons with asthma are, however, at a low but increased risk for severe morbidity » Adverse outcomes from bronchospasm occur in patients with no previous history of asthma » Editorial par bishop The incidence of complications in the Mayo study for patients with symptoms within 30 days was actually 4.5%, as opposed to 0.8% in patients without symptoms in the previous 30 days. Other studies may not have considered that the patients had asthma if they had such a long symptom-free interval. Only 41% of the Mayo Clinic patients had received a prescription in the previous year, raising questions about the severity of the asthma. Of the four patients who had symptoms at the time of surgery, two had complications. Based on that 50% incidence, we could conclude that persons with symptoms of asthma are actually at very high risk. Bishop MJ, Cheney FW. Anesthesiology 1996,85:455-6

Physiologie Maladie inflammatoire chronique des voies respiratoires médiée LT, mastocyte,PNE. Contraction des muscles lisses de la paroi bronchique et œdème pariétal et production accrue de mucus. Obstruction bronchique diffuse variable réversible Toux, dyspnée sifflante et oppression thoracique Facteur déclanchant Pathophysiology of asthma. Current opinion in Anaesthesiology 1998. 11(1):61-66 Brichant JF, Hans P. JEPU 2005

A la consultation Recueillir l’historique de la maladie Hospitalisation, réanimation, facteur déclenchant… Évaluer la gravité de la maladie Noter le traitement Examen clinique Penser au diagnostic différentiel dans les formes atypiques Élaborer une stratégie péri opératoire

Gravité Brichant JF, Hans P. JEPU 2005

Diagnostic différentiel

Stratégie pré opératoire Asthme De novo Diag≠tiel Instable Stable Poursuite TTT Urgence Chir. Programmée B/D Corticoïdes Asthme de novo Dyspnée sifflante paroxystique Toux spasmodique sèche nocturne (enfant) Oppression thoracique Reversible au B2+ Durée limitée Facteurs déclenchants  Avis spécialisé «  obstructif variable réversible » Intensification TTT Cons. pneumologue Nébulisation B/D Corticoïdes IV +/- Antibiotiques TTT adapté Chirurgie à surseoir ALR si possible

Préparation Préopératoire

éta 2+ Inhalation ou nébulisation Courte ou longue durée d’action Effet préventif sur la B/C liée à l’IOT Wu RSC.BJA 2000,84:358-362

+17% - 6% Anesth Analg. 2001 Oct;93(4):898-902. 24 enfants asthmatiques mesure des Rvas avant et après iot sous sevo et N2O. 2 groupes un avec aérosol, l’autre avec This study shows that in children with mild to moderate asthma, a preanesthetic treatment with inhaled salbutamol can prevent the increase of respiratory system resistance. - 6%

METHODS: 120 (60+50 patients) 4 groupes induction propofol, mesure des R vas après iot en fct préparation et à 10 min sous isoflurane 1.5 mg/kg intravenous lidocaine or saline 3 min before tracheal intubation 4 puffs of inhaled albuterol or placebo 15-20 min before tracheal intubation

Anticholinergique Ipratropium bromide (Atrovent) Atropine IV Effet préventif sur la B/C liée à l’IOT Kil HK. Anesthesiology 1994;81:43-48 Effet < beta 2+ Wu RSC.BJA 2000,84:358-362 Utile si asthme instable Atropine IV Intérêt discuté 42 patients « types inhalation avt anesthésie albuterol (360 micrograms) inhaled ipratropium bromide (72 micrograms) a placebo inhalation (n = 15). IOT BAISSE RESISTANCE PULMONAIRE groupe albuterol et bromide / placebo après iot à 5 et 15 min 3 weezing dans groupe placebo

Corticoïdes CAT Crise d’asthme IOT IV = PO ↓ hospitalisation, prévient récidive Rowe B.Am J Emerg Med 1992, 10: 301-310 IOT ↓ incidence bronchospasme après 5 jours de ttt PO Silvanus MT. Anesthesiology 2004 ;100(5): 1052-57 CAT Continuer si prescrit pour asthme stable Débuter si asthme instable 10-15mg/kg/j HC IV 40 à 60mg / 6h solumédrol IV Délai action 6 heures min. Silvanus

31 patients induction Pento fenta vecuronium En noir les bronchospasme après iot 3 types de preparation 40 mg/j pdt 5 j 2b x 3/j pdt 5 j

Lidocaïne Efficacité et effets 2aires identiques 1,5mg/kg + 3mg/kg/h 5mg/kg lidoC 10% Chez des patients asthmatique que l’on expose à des C croissante d’histamine, on s’aperçoit que la lido quelle soi iv ou inhalée à un effet protecteur puisqu’il faut augmenter ces concentration pour obtenir une baisse du DEP. IV 2 microg/ml FEV forve expiratory volume Efficacité et effets 2aires identiques C(IV) x 2 >C(inh) mais << C toxique Groeben H. Am J Respir Crit Care Med 1999;159: 530-535

Lidocaïne IV >inhalée ↓ 27% DEP si Lidocaïne aérosol 2mg/kg+ 5mg/kg/h Malheureusement des études animales et clinique nous confirme que l’aérosol de lidoc entraine une BC initiale sauf si on ijecte de la lido iv, donc on ne peux recommander son utilisation. 5mg/kg lido4% Bulut Y. anesthesiology 1996, 85: 853-859

Anxiolytiques Hydroxizine Atarax® Midazolam hypnovel ®

AG ou ALR ?

Eviter les stimulations trachéales Bronchospasm during anaesthesia. A computer-aided incidence study of 136,929 patients. Acta Anaesthesiol Scand. 1987 Apr;31(3):244-52. Olsson GL. 156 064 anesthésies 246 bronchospasmes: 1.7 /1000 <9 ans: 4/1000 IVAS: 41/1000 BPCO/asthme: 22/1000 IOT: 9/1000 246 cases of bronchospasm in 156,064 anaesthetics were retrieved. This corresponds to one case in 634 anaesthetics or 1.7 per 1000 patients. High incidence figures were seen in the age group 0-9 years (4.0/1000) when the patients showed a respiratory infection (41.1/1000), a pathological preoperative ECG (24.3/1000), an obstructive lung disease (21.9/1000), were classified as belonging to ASA class III (23.8/1000), if a tracheal intubation was performed (9.1/1000) or a rectal anaesthesia (35.7/1000) was given. In the age group 50-69 years (1.8/1000), high incidence figures were seen when there was an airway obstruction (8.8/1000), an obstructive lung disease (7.7/1000), a previous myocardial infarction (5.4/1000), a bronchoscopy (7.6/1000) or a mediastinoscopy (7.8/1000) was performed. Most of the cases had no history of allergy or asthma recorded in the anaesthetic form. In this series the triggering factor more often seemed to be of mechanical origin. There were no intraoperative deaths. Eviter les stimulations trachéales

Anesthésie Locorégionale ↓ incidence des bronchospasmes ¼ des bronchospasmes surviennent sous ALR Chesney closed claims au USA Asthme instable = CI chirurgie réglée même si ALR possible Cheney FW. Anesthesiology 1991, 75:932-939

Anesthésie générale Profonde VS >IOT Shnider .Anesthesiology 1961; 22:886-892 B/C: 2% Vs 6,4% MLA > IOT ↓ réactions de B/C Management difficile Si bronchospasme Profonde The authors hypothesized that insertion of a laryngeal mask airway would be less likely to result in reversible bronchoconstriction than would insertion of an endotracheal tube. Methods: Fifty-two (45 men, 7 women) patients were randomized to receive a 7.5-mm (women) or 8-mm (men) endotracheal tube or a No. 4 (women) or No. 5 (men) laryngeal mask airway. Anesthesia was induced with 2 [micro sign]g/kg fentanyl and 5 mg/kg thiopental, and airway placement was facilitated with 1 mg/kg succinylcholine. When a seal to more than 20 cm water was verified, respiratory system resistance was measured immediately after airway placement. Inhalation anesthesia was begun with isoflurane to achieve an end-tidal concentration of 1% for 10 min. Respiratory system resistance was measured again during identical conditions. Results: Among patients receiving laryngeal mask airways, the initial respiratory system resistance was significantly less than among patients with endotracheal tubes (9.2 +/- 3.3 cm water [middle dot] 1-1 [middle dot] s (-1) [mean +/- SD] compared with 13.4 +/- 9.6 cm water [middle dot] 1-1 [middle dot] s-1; P < 0.05). After 10 min of isoflurane, the resistance decreased to 8.6 +/- 3.6 cm water [middle dot] 1-1 [middle dot] s-1 in the endotracheal tube group but remained unchanged at 9.1 +/- 3.3 cm water [middle dot] 1-1 [middle dot] s-1 in the laryngeal mask airway group. The decrease in respiratory system resistance in the endotracheal tube group of 4.7 +/- 7 cm water [middle dot] 1-1 [middle dot] s-1 was highly significant compared with the lack of change in the laryngeal mask airway group (P < 0.01). Conclusions: Resistance decreased rapidly only in patients with endotracheal tubes after they received isoflurane, a potent bronchodilator, suggesting that reversible bronchoconstriction was present in patients with endotracheal tubes but not in those with laryngeal mask airways. A laryngeal mask airway is a better choice of airway to minimize airway reaction. Kim ES. Anesthesiology 1999, 90:391-394

Quel produits anesthésiques ?

Propofol > thiopental Background: Methods: Fifty-nine asymptomatic asthmatic and 96 nonasthmatic patients of ASA physical status 1 and 2 were studied. All patients received 1.5 micro gram/kg fentanyl, oxygen, followed by either 5 mg/kg thiopental or thiamylal, 1.75 mg/kg methohexital or 2.5 mg/kg propofol, 1.5 mg/kg succinylcholine, tracheal intubation, and inhalational anesthesia. Wheezing was assessed by an independent blinded observer auscultating the lungs at 2 and 5 min postintubation. Data were analyzed by Pearson's chi-squared, Fisher's exact test, and multiple logistic regression with significance set at P < 0.05. Pizov R. Anesthesiology 1995, 82:1111-1116

Propofol>étomidate=thiopental Seventy-seven studies were conducted in 75 patients. Anesthesia was induced with either 2.5 mg/kg propofol, 0.4 mg/kg etomidate, or 5 mg/kg thiopental. Respiratory resistance was measured at 2 min after induction. RESULTS: Respiratory resistance at 2 min was 8.1 +/- 3.4 cmH2O.1(-1).s (mean +/- SD) for patients receiving propofol versus 11.3 +/- 5.3 for patients receiving etomidate and 12.3 +/- 7.9 for patients receiving thiopental (P < or = 0.05 for propofol vs. either etomidate or thiopental). CONCLUSIONS: Respiratory resistance after tracheal intubation is lower after induction with propofol than after induction with thiopental or after induction with high-dose etomidate. Succi +norcuron En noir B/C Eames WO.Anesthesiology. 1996 Jun;84(6):1307-11.

Kétamine Dose: 0.75 mg/kg/10min + 0.15mg/kg/h Réservé à l’asthme instable Atropine ≠ hypersécrétion Intérêt si instabilité hémodynamique pour l’induction Sarma VJ. Acta Anaesthesiol Scand 1992, 36: 106-107

Curares Succinylcholine Atracurium ≈ vécuronium Cisatracurium 2,1% bronchospasme Blobner M. Br J Anaesth 2000; 85: 724-31 Atracurium ≈ vécuronium 17%Vs 7% complications respiratoires (NS) Caldwell JE. Anesthesiology 95, 83: 986-991 Cisatracurium METHODS: Sixty patients aged 18-75 yr taking bronchodilators chronically for asthma were anesthetized with midazolam, fentanyl, nitrous oxide, and isoflurane; the trachea was intubated without paralysis. When anesthetic conditions and mechanical ventilation were stable, patients were randomly given 0.5 mg/kg atracurium or 0.1 mg/kg vecuronium over 5-10 s, and a blinded observer recorded cardiovascular, pulmonary, and cutaneous signs of adverse reactions for 6 min. RESULTS: Arterial pressures and heart rate decreased after atracurium, and systolic pressure and heart rate decreased with vecuronium; these changes were small in magnitude. Cardiovascular effects (decrease in blood pressure or change in heart rate) > 10% were common with both atracurium (60% of patients) and vecuronium (57%). Cardiovascular effects > 20% were more frequent with atracurium (37%) than with vecuronium (13%, P < 0.05). The incidence of noncardiovascular adverse events (increase in peak airway pressure > 5 cmH2O, tidal volume decrease > 10%, rashes, and wheezing) did not differ between atracurium (17%) and vecuronium (7%). The largest increase in peak airway pressure was 5.1 cmH2O in a patient whose tidal volume decreased 16% with vecuronium; in the remaining patients, tidal volume decreased < 10%. No patients experienced inspiratory wheezing, marked decreases in arterial oxygen saturation, or marked increases in end-tidal carbon dioxide tension. CONCLUSIONS: The authors conclude that, in patients with asthma, adverse cardiovascular events are more common with atracurium than with vecuronium. incidence of bronchospasm of 3.2% in 1,965 patients who received rapacuronium compared with 2.1% in 572 patients who received succinylcholine Abstract: Methods: Endotracheal intubation was accomplished without the use of neuromuscular blocking agents. Dynamic compliance, tidal volume, peak inspiratory flow rate, peak expiratory flow rate, and peak inflating pressure were measured after administration of either rapacuronium (1.5 mg/kg) or cis-atracurium (0.2 mg/kg) to 20 adult patients (10 received rapacuronium and 10 received cis-atracurium) anesthetized with propofol-remifentanil. Results: Statistically significant increases in peak inflating pressure (22 +/- 6 to 28 +/- 9 cm H2O, P = 0.0012) and decreases in dynamic compliance (108 +/- 43 to 77 +/- 41 ml/cm H2O, P = 0.0001), peak inspiratory flow rate (0.43 +/- 0.11 to 0.39 +/- 0.09 l/s, P = 0.0062), peak expiratory flow rate (0.67 +/- 0.10 to 0.59 +/- 0.09 l/s, P =0.0015), and tidal volume (744 +/- 152 to 647 +/- 135 ml, P = 0.0293) occurred after administration of rapacuronium. No changes were seen after administration of cis-atracurium. Tobias JD. Anesthesiology. 95(4):908-912, October 2001.

Agents Halogénés Rooke G. anesthesiology 1997; 86(6):1294-1299 Abstract TOP 66 patients pento, fenta, succy pouis norcuron ou pavulon puis 1.1 MAC agent. Background: After tracheal intubation, lung resistance and therefore respiratory system resistance (Rrs) routinely increase, sometimes to the point of clinical bronchospasm. Volatile anesthetics generally have been considered to be effective bronchodilators, although there are few human data comparing the efficacy of available agents. This study compared the bronchodilating efficacy of four anesthetic maintenance regimens: 1.1 minimum alveolar concentration (MAC) end-tidal sevoflurane, isoflurane or halothane, and thiopental/nitrous oxide. Methods: Sixty-six patients underwent tracheal intubation after administration of 2 micro gram/kg fentanyl, 5 mg/kg thiopental, and 1 mg/kg succinylcholine. Vecuronium or pancuronium (0.1 mg/kg) was then given to ensure paralysis during the rest of the study. Postintubation R sub rs was measured using the isovolume technique. Maintenance anesthesia was then randomized to thiopental 0.25 mg [center dot] kg sup -1 [center dot] min sup -1 plus 50% nitrous oxide, or 1.1 MAC end-tidal isoflurane, halothane, or sevoflurane. The Rrs was measured after 5 and 10 min of maintenance anesthesia. Data were expressed as means +/- SD. Results: Maintenance with thiopental/nitrous oxide failed to decrease Rrs, whereas all three volatile anesthetics significantly decreased Rrs at 5 min with little further improvement at 10 min. Sevoflurane decreased Rrs more than either halothane or isoflurane (P < 0.05; 58 +/- 14% of the postintubation Rrs vs. 69 +/- 20% and 75 +/- 13%, respectively). Conclusions: After tracheal intubation in persons without asthma, sevoflurane decreased Rrs as much or more than isoflurane or halothane did during a 10-min exposure at 1.1 MAC. Bronchospasm is a feared complication of anesthesia, [1] but fortunately it occurs only rarely. [2] Even audible wheezing occurs relatively infrequently, in approximately 0.17% of general anesthetics. [3] The low incidence of adverse outcomes may be partially attributed to good anesthetic management, care that often includes the use of potent inhalational anesthetics to prevent and manage bronchospasm. Although halothane is often recommended as the agent of choice in such situations, there is little evidence in humans that halothane is more effective than other volatile agents. [4,5] Sevoflurane compares favorably with halothane as less noxious to human airways than either isoflurane or enflurane. [6,7] In dog bronchospasm models, sevoflurane has not proved to be better than halothane or even isoflurane, [8,9] but the bronchodilatory properties of sevoflurane have not been examined in humans. It is difficult to study the relative efficacy of the volatile anesthetics during bronchospasm in humans because it occurs so rarely. One potential alternative is to examine the ability of volatile agents to block the effects of intubation. Besides being a common trigger for intraoperative bronchospasm, [1,10] tracheal intubation causes some degree of bronchoconstriction in most patients. In awake volunteers given topical anesthesia, tracheal intubation was associated with a 40% increase in airway resistance. [11] Additional indirect evidence for intubation-induced bronchoconstriction comes from measurements made exclusively after intubation. The respiratory resistance present after tracheal intubation decreases after bronchodilator therapy, [12] and different induction agents are associated with different degrees of postintubation resistance. [13] Tracheal intubation can therefore serve as a stimulus to increase lung resistance and permit comparison of the bronchodilating ability of various anesthetics. This study compared the degree of bronchodilation achieved with halothane, isoflurane, and sevoflurane maintenance anesthesia subsequent to the bronchoconstriction associated with standardized induction and intubation. A fourth group consisting of maintenance with a thiopental infusion plus nitrous oxide anesthesia served as a time control. Rooke G. anesthesiology 1997; 86(6):1294-1299

Agents Halogénés Sévoflurane = halothane > Desflurane pour B/D Habre X. Anest Analg 1999,89:1117-1181 Goff M.Anesthesiology 2000, 93: 404-408

Réveil En l’absence de bronchospasme En VS sous AG profonde ou parfaitement réveillé ? Question d’école Antagonisation à éviter de principe malgré Atropine

Bronchospasme  PI, wheezing Rare si asthme stable: 1,6 à 6/1000 50% patients sans ATCD respiratoire 70% induction, 25% entretient, 5% réveil Gravité potentielle élevée Allergie n’est pas un FDR de bronchospasme.

Diag≠tiel Bronchospasme Intubation sélective ou oesophagienne Hernie du ballonnet PNT CE, Bouchon muqueux Inhalation bronchique Pb de valve HTM IVG Blocage thoracique Anesthésie trop légère Morphiniques Remifentanil alfentanil RT, EtCO2 Ventilation manuelle, vérification respirateur. Aspiration +/-mobilisation sonde intubation.

Propofol®, Sévoflurane ® Stratégie O2 pur V manuelle* STOP stimuli Anaphylaxie ? Adré IV Propofol®, Sévoflurane ® ou Ketamine ®, atropine ® Approfondir AG Mg 2+? B/D (béta 2+ / Anticholinergique) Corticoïdes 2-20mg/kg solumédrol® OK Réanimation *silverman MS. Anesthesiology 1991, 71: A441

Effet antagoniste calcique  B/D Ttt adjuvant d’un Asthme résistant Can J Anaesth. 2003 Aug-Sep;50(7):732-46. Effet antagoniste calcique  B/D Ttt adjuvant d’un Asthme résistant Posologie: 2g sur 20 min + DEP, baisse durée hospitalisation Meta analyse