ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Anesthesia for adult patients with asthma

Anesthesia for adult patients with asthma
Literature review current through: Jan 2024.
This topic last updated: Aug 11, 2023.

INTRODUCTION — Asthma is a chronic lung disease characterized by inflammation and narrowing of the airways, resulting in reversible airflow obstruction. Asthma has increased in prevalence over the past three decades and currently impacts an estimated 300 million people worldwide. [1]. Asthmatic patients presenting for surgery can pose challenges for the anesthesia provider. Wheezing due to bronchospasm can happen at any time during anesthesia, most commonly during induction of general anesthesia and endotracheal intubation. Although bronchospasm is usually transient and treated without sequelae, it can be severe and may cause significant morbidity or even mortality.

This topic will discuss preoperative assessment and preparation of adult patients with asthma and intraoperative management. Evaluation and management of asthma is discussed in more depth separately:

(See "An overview of asthma management".)

(See "Asthma in adolescents and adults: Evaluation and diagnosis".)

(See "Ongoing monitoring and titration of asthma therapies in adolescents and adults".)

(See "Initiating asthma therapy and monitoring in adolescents and adults".)

(See "Treatment of severe asthma in adolescents and adults".)

(See "Acute exacerbations of asthma in adults: Home and office management".)

(See "Acute exacerbations of asthma in adults: Emergency department and inpatient management".)

PREOPERATIVE EVALUATION

Timing and goals — We assess patients with asthma at least one week prior to elective surgery to allow time for modification of treatment, if necessary. This is especially important for patients scheduled for procedures with a high risk of postoperative pulmonary complications such as thoracic or upper abdominal surgery, open aortic aneurysm repair, head and neck surgery, or neurosurgery [2,3]. (See "Strategies to reduce postoperative pulmonary complications in adults".)

The goal of preoperative preparation is optimization of therapy to reduce the risk of perioperative pulmonary complications. Risk of such complications in well-controlled asthmatic patients is low, whereas poorly controlled asthma increases risk [4,5]. National and international organizations have developed guidelines that suggest a stepwise approach to the treatment of asthma (table 1). Preferred and alternative medications are prescribed based on severity and control of symptoms. (See "An overview of asthma management".)

Medical management typically starts with intermittent use of short-acting beta2 agonists, progressing as necessary through the addition of inhaled glucocorticoids in increasing doses, long-acting beta2 agonists, possible leukotriene receptor antagonists, methylxanthines, omalizumab (an antiasthma antibody medication), and oral glucocorticoids. The asthmatic patient should not be wheezing at the time of surgery.

Clinical assessment

Asthma severity and control — Details regarding the assessment of asthma control are presented separately. (See "An overview of asthma management", section on 'Symptom and risk assessment'.)

The history given by the patient at the time of preoperative evaluation is useful to determine the severity of asthma, level of control (table 2), and likelihood of perioperative bronchospasm. Important historical data include:

Severity of asthma as assessed by patient

Allergies and atopy

Asthma medication use

Triggering factors

Frequency of use of inhaled short-acting beta-agonist therapy

History of hospitalizations and/or emergency department visits

History of intubation with severe attack

Frequency and most recent use of oral glucocorticoids

Recent upper respiratory infection (URI), sinus infection, cough, or fever

Baseline and current peak expiratory flow or forced expiratory volume in one second (FEV1)

There are limited data regarding the impact of each of these factors on the likelihood of perioperative bronchospasm. However, retrospective analysis suggests that perioperative bronchospasm and laryngospasm are more likely in patients who used asthma medications, noted asthma symptoms, or visited a medical facility for asthma treatment within the past year, particularly if within 30 days [6-8]. Overall, the level of control of asthma is classified as well controlled, partly controlled, or uncontrolled (table 2). Patients with asthma that is not well controlled should be referred to their primary care clinician or asthma specialist for treatment optimization prior to elective surgery.

Recent upper respiratory infection — Timing of anesthesia and elective surgery for the asthmatic patient with a URI is a difficult issue that depends on the severity of the patient's asthma, the degree of asthma control, and the implications for delay of surgery. Airway hyperreactivity may last from two to six weeks after a URI [9]. However, a retrospective study from 1996 found no increase in the incidence of intraoperative bronchospasm in patients with well controlled asthma and recent URI [6]. (See "Anesthesia for adults with upper respiratory infection".)

Physical examination — Preoperative physical examination for asthmatics should focus on respiratory rate, wheezing, signs of lung infection, and air movement. During acute severe bronchospasm, breath sounds may be diminished or absent. (See "Asthma in adolescents and adults: Evaluation and diagnosis", section on 'Physical findings'.)

Preoperative testing — Patients who have well controlled asthma that is not steroid-dependent generally do not need additional testing beyond that performed for patients without asthma. The baseline pulse oximetry value should be noted. Preoperative pulmonary function testing is usually reserved for patients with moderate to severe asthma undergoing particularly high-risk procedures. In addition, use of asthma medications impacts preoperative laboratory testing.

Pulmonary function testing – Peak expiratory flow rate (PEFR) and spirometry are two methods commonly used to evaluate lung function in asthmatics. PEFR can be measured with a handheld peak flow meter at home or in the preadmission test clinic, and many moderate or severe asthmatics use it to monitor their disease. A peak flow >80 percent of predicted suggests that asthma is well controlled. However, there is wide variability in PEFR; a one-time measurement may not be useful for evaluating airway obstruction. In general, a PEFR ≤80 percent of predicted should be evaluated further with spirometry, unless the value is known to be consistent with good control in that individual. (See "Overview of pulmonary function testing in adults", section on 'Preoperative testing' and "Peak expiratory flow monitoring in asthma".)

Spirometry, specifically FEV1 and the FEV1 to forced vital capacity (FVC) ratio (FEV1/FVC), is used to monitor asthma in the office setting. Such testing may be indicated preoperatively when the degree of asthma control is in question or when a patient with asthma is to undergo a particularly high-risk procedure (eg, upper abdominal, cardiothoracic surgery). When asthma is well controlled, the FEV1 is >80 percent predicted.

Laboratory testing – Indications for preoperative blood tests are similar to those for patients without asthma. However, use of high-dose beta2-adrenergic agonists can result in hypokalemia, hyperglycemia, and hypomagnesemia; thus, preoperative tests of these parameters should be obtained in patients taking these medications at high doses.

Arterial blood gas testing – Preoperative arterial blood gas testing is not routinely indicated, though it may be useful during an acute asthma attack [5].

Electrocardiogram (ECG) – ECG should be obtained in accordance with the American College of Cardiology/American Heart Association (ACC/AHA) 2014 Guidelines for Perioperative Cardiovascular Evaluation and Care for Noncardiac Surgery [10,11]. Older studies evaluating ECG changes during acute asthma exacerbations did not note changes specific for asthma; any changes normalized with resolution of the attack [12].

Chest radiograph – A chest radiograph may show signs of hyperinflated lungs, such as flattened diaphragm, but is not routinely indicated unless the patient reports dyspnea, cough, or fever, or has wheezing or crackles on chest examination.

PREOPERATIVE MEDICATION MANAGEMENT — While formal guidelines are lacking, our approach to preoperative management is based on our assessment of asthma severity and degree of control. Asthma specialists optimize medications prior to surgery as an important component of management of patients with poorly controlled symptoms. (See "An overview of asthma management" and "Ongoing monitoring and titration of asthma therapies in adolescents and adults" and "Initiating asthma therapy and monitoring in adolescents and adults" and "Treatment of severe asthma in adolescents and adults".)

Maintenance medications — Asthmatic patients should continue their usual medication up to and including the day of surgery, with the exception of theophylline, which should be discontinued the evening prior to surgery. Continuation of inhaled medications, including inhaled glucocorticoids, has been shown to reduce the incidence of postoperative pulmonary complications [13,14]. (See "Perioperative medication management".)

Treatment of poorly controlled asthma — For patients with poorly controlled asthma who will require endotracheal intubation for high-risk surgery, we suggest a course of supplemental glucocorticoids administered preoperatively. We usually administer prednisone 40 mg once daily for five days. Intravenous (IV) hydrocortisone (100 mg every eight hours) can be used as an alternative for patients unable to tolerate oral medications. For these purposes, high-risk surgery includes thoracic surgery, upper abdominal surgery, open aortic aneurysm repair, neurosurgery, and head and neck procedures.

In a prospective study of inpatients with untreated, severe bronchospasm, five days of oral steroid therapy in combination with five days of inhaled short-acting beta2 agonist significantly decreased postintubation bronchospasm compared with either medication alone [15]. Other studies have looked at the incidence of perioperative complications in asthmatic patients who received preoperative systemic glucocorticoids and have not found evidence of increased postoperative infections, wound infection, delayed wound healing, or asthma exacerbation [16-18].

Stress dose steroids — Patients taking oral or high-dose inhaled (table 3) glucocorticoids may be at risk for hypothalamic pituitary axis (HPA) suppression and adrenal insufficiency during anesthesia and surgery. The likelihood of HPA suppression is estimated based on the dose and duration of glucocorticoid therapy, as discussed separately. (See "The management of the surgical patient taking glucocorticoids" and "Major adverse effects of systemic glucocorticoids", section on 'Metabolic and endocrine effects'.)

For patients with a high likelihood of adrenal suppression, supplemental glucocorticoids are given in accordance with the magnitude of the anticipated stress of the procedure (table 4). (See "The management of the surgical patient taking glucocorticoids".)

For patients taking high doses of inhaled glucocorticoids, the risk of symptomatic adrenal suppression or acute crisis appears to be very small. However, patients who have taken inhaled fluticasone >750 mcg/day or other inhaled glucocorticoids >1500 mcg/day should receive stress-dose steroids prior to induction of anesthesia. (See "Major side effects of inhaled glucocorticoids", section on 'Adrenal suppression'.)

PREMEDICATION — Premedication for patients with asthma generally includes administration of a short-acting beta2 agonist by either multidose inhaler (eg, albuterol two to four puffs) or nebulizer (albuterol 2.5 mg) 20 to 30 minutes prior to airway manipulation. In patients with concomitant bronchorrhea, pretreatment with combination moderate-acting beta2 agonist with an anticholinergic may be considered (eg, ipratropium bromide-salbutamol, 3 mL vial via nebulization). Although not available in the United States, penehyclidine hydrochloride (PHC) appears to exert favorable effects including bronchodilation as well as attenuation of its effects on Toll-like receptors and downstream effects on inflammation [19,20].

A sedative and/or opioid, carefully titrated to avoid oversedation and respiratory depression may be appropriate in some patients. Reassurance and explanation of expected procedures are often sufficient to allay preprocedural anxiety. If needed, midazolam in small, incremental doses (eg, 0.5 mg) will be effective for many patients. For those patients who require potentially painful procedures prior to anesthetic induction (eg, placement of an intra-arterial or epidural catheter), small doses of an opioid such as fentanyl may be used.

The use of premedications to dry secretions is variable and depends on the procedure. Anticholinergic administration (eg, intravenous [IV] glycopyrrolate 0.2 mg or atropine 0.4 mg) dries secretions and decreases airway vagal responses. These agents are considered for patients who will tolerate the tachycardia that may result.

CHOICE OF ANESTHETIC TECHNIQUE — Endotracheal intubation is a very potent stimulus for bronchoconstriction. When possible, avoidance of endotracheal intubation should decrease the chance of intraoperative bronchospasm. However, bronchospasm can occur with any type of anesthesia.

Regional anesthesia — When possible, regional anesthesia is a good anesthetic choice since manipulation of the airway is avoided. Regional anesthesia should be considered for peripheral procedures that can be done with relatively low-level neuraxial anesthesia, either epidural or spinal, or with peripheral nerve blocks. The following two types of regional anesthesia require special consideration:

Neuraxial anesthesia – Midthoracic or higher levels of neuraxial anesthesia can result in paralysis of accessory muscles of breathing. Asthmatic patients may depend on active exhalation for adequate gas exchange, and high levels of sensory or motor block may provoke anxiety and precipitate bronchospasm. (See "Overview of neuraxial anesthesia".)

Brachial plexus blocks – Some brachial plexus blocks for upper extremity surgery paralyze the diaphragm by blocking the phrenic nerve, potentially for many hours, which may not be tolerated by patients with respiratory compromise. The likelihood of this occurrence is decreased with ultrasound guidance. (See "Upper extremity nerve blocks: Techniques".)

General anesthesia — General anesthesia may be associated with increased risk of bronchospasm due to mechanical stimulation of the airway during laryngoscopy, endotracheal intubation, or extubation (as the depth of anesthesia necessarily lightens). In addition, bronchospasm can result from airway suctioning, inhalation of cold anesthetic gases, pulmonary aspiration of stomach contents, or as a side effect of some medications administered in the perioperative period. Also, airway tone may increase because of vagally stimulating events such as peritoneal insufflation during laparoscopy, manipulation of viscera, or endoscopy.

INDUCTION OF ANESTHESIA

Airway management — A goal of induction of anesthesia in the asthmatic patient is to minimize the risk of a bronchoconstrictive response to airway management. While the risk of bronchospasm is lower with a laryngeal mask airway (LMA) or mask ventilation compared with endotracheal intubation, decisions regarding placement of an LMA or an endotracheal tube (ETT) should be similar to patients without asthma. (See "Airway management for induction of general anesthesia".)

A randomized trial compared LMA with endotracheal intubation in 52 adults undergoing elective surgery [21]. Patients taking bronchodilators were excluded. The initial increase in airway resistance that occurs with endotracheal intubation did not occur with LMA placement, although there was no difference in airway resistance after 10 minutes of inhalation anesthesia with isoflurane.

Importantly, airway suctioning should be done only as necessary and only under a deep level of anesthesia. Tracheal suction is a potent airway irritant.

Anesthetic agents — A goal of induction of anesthesia is achievement of sufficient depth of anesthesia prior to intubation. This is particularly important in the patient with asthma.

Intravenous induction agents – If endotracheal intubation is planned, a primary induction agent and adjuvant medications, usually an opioid and/or lidocaine, as well as a neuromuscular blocking agent (NMBA) are typically administered. (See "General anesthesia: Intravenous induction agents".)

Primary induction agent – While propofol is the most commonly selected intravenous (IV) induction agent, certain clinical scenarios may warrant use of other agents:

-PropofolPropofol is typically selected for hemodynamically stable asthmatic patients. It has been shown to attenuate the bronchospastic response to intubation in both asthmatic and nonasthmatic patients [21-23]. However, rare allergic reactions with significant bronchospasm have occurred with propofol administration, possibly due to the sodium metabisulfite used as a preservative in some preparations [22,24-26]. (See "General anesthesia: Intravenous induction agents", section on 'Propofol'.)

-KetamineKetamine has sympathomimetic bronchodilatory properties that make it useful for induction, particularly in the hemodynamically unstable patient, though ketamine-induced bronchodilation may not be as pronounced as that of propofol [27,28]. (See "General anesthesia: Intravenous induction agents", section on 'Ketamine'.)

-EtomidateEtomidate is particularly useful for induction of hemodynamically unstable patients. Although it lacks the bronchodilatory effects of propofol, etomidate can be used safely for induction in asthmatic patients [22]. Notably, etomidate administration results in transient acute adrenal insufficiency. (See "General anesthesia: Intravenous induction agents", section on 'Etomidate'.)

-BarbituratesMethohexital does not release histamine and can be used as an alternative to the induction agents discussed. However, induction with methohexital is associated with more bronchoconstriction than propofol when endotracheal intubation is performed [28]. (See "General anesthesia: Intravenous induction agents", section on 'Methohexital'.)

Adjuvant induction agents

-Opioids – An opioid (eg, fentanyl 50 to 100 mcg) is typically administered during induction to supplement sedation and suppress airway reflexes that may result in coughing and/or bronchospasm during laryngoscopy and intubation. Most opioids release some amount of histamine, which can theoretically cause bronchospasm. The synthetic opioids fentanyl, remifentanil, sufentanil, and hydromorphone release little histamine, have been used safely in asthmatic patients, and are generally preferred during induction and maintenance, as well as in the post-anesthesia care unit (PACU) [29,30]. By contrast, meperidine releases relatively high levels of histamine [31], as does morphine if administered rapidly and/or in large doses [32,33]. (See "General anesthesia: Intravenous induction agents", section on 'Opioids' and "Perioperative uses of intravenous opioids in adults: General considerations".)

-Lidocaine – IV lidocaine 1 to 1.5 mg/kg is typically administered during induction to suppress the cough reflex during laryngoscopy and intubation [34-43]. Although lidocaine may mildly increase airway tone, it reduces airway responsiveness to noxious stimuli and to drugs that cause bronchospasm, thereby potentially preventing bronchospasm [44-46]. We avoid inhaled nebulized lidocaine since it is an airway irritant and may cause bronchospasm [47]. (See "General anesthesia: Intravenous induction agents", section on 'Lidocaine'.)

-Dexmedetomidine – The alpha2 agonist dexmedetomidine may be used as an adjuvant agent during IV induction in selected patients, particularly if spontaneous ventilation via an LMA or mask is planned [48]. Dexmedetomidine has analgesic, sedative, anxiolytic, and sympatholytic properties, causes drying of secretions without respiratory depression, and protects against histamine-induced bronchoconstriction in dogs [49]. (See "Maintenance of general anesthesia: Overview", section on 'Dexmedetomidine'.)

Inhalation induction agents – If an inhalation induction technique is preferred, sevoflurane is typically selected since it has the most pronounced bronchodilatory properties of the available potent volatile inhalation agents [50,51]. Isoflurane is a good bronchodilator, but it is not ideal for induction of anesthesia since it is more pungent than sevoflurane and halothane and has a slower onset than sevoflurane. Halothane also has excellent bronchodilatory properties and remains an acceptable alternative for induction, although it is no longer available in the United States. We avoid desflurane during induction of anesthesia in patients with chronic obstructive pulmonary disease (COPD). Because of its extreme pungency, desflurane may increase secretions and cause coughing, laryngospasm, and/or bronchospasm during induction, particularly in current smokers, and it may increase airway resistance [51-53]. (See "Inhalation anesthetic agents: Clinical effects and uses", section on 'Induction of general anesthesia'.)

Neuromuscular blocking agents – NMBAs are the most common cause of intraoperative allergic reactions, which may cause bronchospasm [54-58]. NMBAs that do not release appreciable amounts of histamine (eg, rocuronium, cisatracurium, and vecuronium) are preferred over those that do (eg, succinylcholine and atracurium). While succinylcholine releases low levels of histamine, it has been safely used in asthmatic patients [59]. Atracurium releases histamine in a dose-related manner; bronchospasm is rare in the clinical dose range. (See "Perioperative anaphylaxis: Clinical manifestations, etiology, and management", section on 'Neuromuscular-blocking agents' and "Clinical use of neuromuscular blocking agents in anesthesia".)

MAINTENANCE OF ANESTHESIA

Inhalation agents – For most asthmatic patients, sevoflurane or isoflurane is used for maintenance of anesthesia. Desflurane may be an airway irritant and should be used cautiously in asthmatics. (See "Inhalation anesthetic agents: Clinical effects and uses".)

Most potent inhalation anesthetic agents (eg, isoflurane, sevoflurane, and halothane) are bronchodilators, decrease airway responsiveness, and attenuate bronchospasm. Their bronchodilatory properties may result from beta2 receptor stimulation, which results in an increase in intracellular cyclic adenosine monophosphate, causing relaxation of bronchial smooth muscle [51]. These volatile agents have been used for treatment of status asthmaticus. (See "Inhalation anesthetic agents: Clinical effects and uses", section on 'Respiratory effects'.)

Choice among these agents depends upon availability. Sevoflurane, isoflurane, and halothane are safe and effective for maintenance of anesthesia [60-62]. Sevoflurane is generally preferred because it has the most pronounced bronchodilatory properties of the available potent inhalation agents. Halothane is no longer available in the United States but remains an acceptable alternative to sevoflurane in some countries.

Desflurane, another potent inhalation anesthetic, can produce an increase in secretions, coughing, laryngospasm, and bronchospasm because of its extreme pungency. Desflurane causes increased airway resistance when compared with sevoflurane and isoflurane, particularly in current smokers [52]. When desflurane is used in a patient with asthma, we start with a low dose and titrate slowly, as tolerated.

Nitrous oxide (N2O) is a relatively weak inhaled anesthetic that is often used in conjunction with a potent inhalational agent or with intravenous (IV) anesthetics to maintain general anesthesia. N2O is administered in much higher concentration than other agents discussed above. It is not an airway irritant, but it is also not a bronchodilator [51]. It can be used safely in most asthmatics who have no other contraindication to its use and who do not require 100 percent oxygen.

Intravenous agents – Total intravenous anesthesia (TIVA) may be preferred for some patients or procedures. (See "Maintenance of general anesthesia: Overview", section on 'Total intravenous anesthesia'.)

IV anesthetic medications may be used by either bolus or infusion along with inhalation agents, or as part of TIVA. Combinations of propofol, ketamine, lidocaine, and dexmedetomidine, as well as a variety of opioids, are used in this way. (See 'Anesthetic agents' above and "Maintenance of general anesthesia: Overview", section on 'Total intravenous anesthesia'.)

Each of these IV agents in isolation has been shown to be safe; however, there are no studies that establish beneficial effects of combinations of these agents in asthmatic patients.

Caution in use of beta blockers – Beta blockers, commonly administered during anesthesia to control heart rate (HR) and blood pressure (BP), should be used cautiously in patients with asthma. When required, the lowest possible dose of a beta1 selective agent should be administered.

Beta blockade with nonselective drugs, which are those that block both beta1 and beta2 receptors, can cause bronchospasm because of their beta2-blocking effects and may reduce the efficacy of beta2 agonist medication.

Esmolol and metoprolol, two beta1 selective drugs that are commonly administered IV during anesthesia, are much less likely to cause bronchospasm. However, at high doses, their selectivity may diminish [63]. Labetalol, a combined beta and alpha blocker, is even less likely to cause bronchospasm [64]. (See "Major side effects of beta blockers", section on 'Increased airways resistance'.)

The use of beta blockers in patients with asthma is discussed in more detail separately. (See "Treatment of hypertension in asthma and COPD", section on 'Beta blockers'.)

CONTROLLED VENTILATION DURING ANESTHESIA — Ventilatory strategy during controlled ventilation should be designed to reduce air trapping [65-67]. Patients with airflow obstruction need prolonged expiration. Stacked breaths occur when mechanical breaths are delivered without complete exhalation. These may result in a falsely low end-tidal carbon dioxide (ETCO2) (figure 1) and can result in air trapping, dynamic hyperinflation, and, in the extreme, barotrauma [68]. Reduction of the inspiratory/expiratory ratio is an important strategy to reduce air trapping, but the most effective maneuver is to reduce minute ventilation by reducing both rate and tidal volume [65]. (See "Diagnosis, management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults".)

Lung-protective ventilation is now considered best clinical practice for patients with acute respiratory distress syndrome (ARDS). However, risks and benefits may differ for patients with other conditions.

For those with severe asthma, our preferred approach for ventilation during anesthesia includes:

Controlled hypoventilation with reduced tidal volumes (eg, 6 mL/kg)

Reduced respiratory rate with longer expiratory time

Reduced inspiratory time

Cautious use of titrated positive end-expiratory pressure (PEEP)

If indicated, recruitment maneuvers used gently and sparingly (eg, approximately 30 minutes), ensuring adequate time for exhalation before reinstituting mechanical ventilation

Administration of inhaled bronchodilator to reduce resistance to expiratory flow

Caution is necessary when titrating PEEP in asthmatic patients. Use of PEEP may prevent airway collapse by stenting airways open, thereby decreasing air trapping. However, excess PEEP may lead to nondynamic hyperinflation, elevated driving pressures, and possible barotrauma. For this reason, we tend to avoid higher PEEP levels [69]. (See "Invasive mechanical ventilation in adults with acute exacerbations of asthma", section on 'Dynamic hyperinflation'.)

INTRAOPERATIVE BRONCHOSPASM

Identification — Signs of bronchospasm under anesthesia include:

Wheezing on chest auscultation

Change in end-tidal carbon dioxide (ETCO2)

Upsloping ETCO2 waveform

Severely decreased or absent ETCO2 waveform

Decreased tidal volume

High inspiratory pressure

Decreasing oxygen saturation

Non-bronchospastic causes of the above findings should be ruled out while setting the fraction of inspired oxygen (FiO2) to 100 percent and changing to hand ventilation to assess compliance and exhalation. During bronchospasm, compliance is decreased and exhalation is prolonged. The following complications may mimic bronchospasm:

Endobronchial intubation – Decreased breath sounds on one side (usually left) and a deep endotracheal tube (ETT).

Pneumothorax – Decreased breath sounds on one side; asymmetric chest rise, particularly if high peak inspiratory pressures have been used or in a clinical scenario where pneumothorax is likely (eg, trauma, diaphragm injury).

Pulmonary edema – Frothy secretions in the ETT; crackles on pulmonary examination.

Kinked or obstructed ETT – Difficulty passing a suction catheter and/or removal of secretions upon suctioning.

Bronchospasm may be part of an anaphylactic reaction. Signs that suggest anaphylaxis include hypotension, tachycardia, and rash. The management of anaphylaxis is presented separately (table 5). (See "Perioperative anaphylaxis: Clinical manifestations, etiology, and management".)

Management — When bronchospasm is suspected, initial management includes administration of 100 percent oxygen and hand ventilation. Mild bronchospasm is commonly treated by deepening the anesthetic. This can be accomplished by administering a bolus of intravenous (IV) propofol or ketamine, or by deepening the level of inhaled anesthetic.

Patients with bronchospasm that persists after deepening anesthesia should receive short-acting beta2 agonist therapy. A rapidly acting beta2 agonist such as albuterol should be administered by nebulizer connected to the breathing circuit or by metered dose inhaler (MDI) via the ETT with an adapter. Eight to 10 puffs of short-acting beta2 agonist therapy should be used since much of the medication will condense in the ETT.

More severe bronchospasm requires further intervention with one or more of the following:

AnticholinergicsGlycopyrrolate (3.2 mcg/kg or approximately 0.2 mg in the adult patient administered IV), atropine (6 to 10 mcg/kg or approximately 0.4 mg in the adult patient administered IV), and ipratropium (500 mcg by nebulizer or four to eight puffs via MDI) have bronchodilatory properties. When compared with atropine, glycopyrrolate produces bronchodilation of longer duration (>4 versus 3 to 4 hours) [70]. Onset of effect takes 20 to 30 minutes, so anticholinergic use should be combined with more rapidly acting treatment such as albuterol. IV anticholinergics often cause significant tachycardia.

Epinephrine – For refractory bronchospasm, epinephrine in the operating room (OR) is given IV in a bolus of 10 to 50 mcg, and/or by continuous infusion via an infusion pump at 2 to 10 mcg/minute.

Magnesium sulfateMagnesium sulfate (up to 2 g IV over 20 minutes) may be helpful with refractory cases of bronchospasm. A meta-analysis supports its use in acute exacerbations of asthma [71]. High doses and blood levels of magnesium produce skeletal muscle weakness and central nervous system depression. Magnesium may cause hypotension due to reduction in systemic vascular resistance.

Glucocorticoids – High-dose glucocorticoids (hydrocortisone 100 mg IV or methylprednisolone 60 to 80 mg IV) will not be effective for four to six hours and should be combined with rapidly acting medication. Perioperative steroids have not been shown to increase surgical complications. (See 'Treatment of poorly controlled asthma' above.)

Some interventions have been described in case reports but are not commonly employed. The following agents and interventions are rarely used:

Nitroglycerin – While rarely used for the treatment of asthma, IV nitroglycerin has been shown to be effective in the treatment of acute bronchospasm by direct smooth-muscle relaxation [72,73]. Nitroglycerin may cause hypotension.

Heliox – Helium and oxygen (heliox) mixtures have occasionally been used in cases of acute, severe bronchospasm. However, heliox can only provide a fraction of inspired oxygen (FiO2) of 21 to 30 percent and does not reverse bronchospasm, so it is used as a temporizing measure while bronchospasm is treated [74]. In addition, technical constraints limit the ability to use heliox during anesthesia. (See "Physiology and clinical use of heliox".)

Extracorporeal membrane oxygenation – Extracorporeal membrane oxygenation (ECMO) is reserved for the most severe bronchospasm that is refractory to maximal medical and mechanical ventilatory therapy. (See "Extracorporeal life support in adults in the intensive care unit: Overview".)

EMERGENCE FROM ANESTHESIA — Bronchospasm can occur with reversal of neuromuscular block and emergence from anesthesia when the endotracheal tube (ETT) is in place and the level of anesthesia is reduced. Airway obstruction, laryngospasm, inadequate ventilation, and hypoxia can all occur. The goal should be to achieve a smooth, controlled emergence. (See "Maintenance of general anesthesia: Overview", section on 'Transition to the emergence phase' and "Extubation following anesthesia", section on 'Minimizing physiologic response to extubation'.)

Reversal of neuromuscular blocking agents (NMBAs) with anticholinesterase agents such as neostigmine can cause an increase in bronchial secretions and airway reactivity and trigger bronchospasm [75], although this is rare. Neostigmine is administered with anticholinergic medication, either glycopyrrolate or atropine, to block the muscarinic receptors responsible for this effect. Sugammadex is another reversal agent for rocuronium or vecuronium that works by encapsulation of these steroidal NMBAs. It is devoid of muscarinic and bronchial smooth muscle effects, and has generally been well-tolerated [76]. However, a study of sugammadex administered in doses of 2 to 4 mg/kg to patients with pulmonary disease noted a 2.6 percent incidence of bronchospasm [77], and there are several case reports describing bronchospasm with anaphylaxis after sugammadex administration [78]. Postmarketing analysis has confirmed an association between sugammadex usage and bronchospasm and coronary arteriospasm adverse events [79]. Thus, this agent is used cautiously in patients with asthma. (See "Clinical use of neuromuscular blocking agents in anesthesia", section on 'Reversal of neuromuscular block'.)

A short-acting beta2 agonist (eg, albuterol 8 to 10 puffs through the ETT) should be administered during emergence and postoperatively, as needed. Intravenous (IV) lidocaine (1 mg/kg) may help attenuate airway reactivity as well, especially for patients who have had an episode of bronchospasm during anesthesia. Positioning the patient in a head-up position can help prevent atelectasis and maintain oxygenation.

Deep extubation, or removal of the ETT prior to emergence from anesthesia, can be considered, although it is not without risk. Though deep extubation allows the patient to awaken without the irritant of the ETT, they will emerge with an airway unprotected from stomach contents and secretions, and bronchospasm may still occur. Importantly, aspiration of stomach contents can induce bronchospasm. (See "Extubation following anesthesia", section on 'Deep extubation'.)

POSTOPERATIVE MANAGEMENT — The intraoperative course for the asthmatic patient dictates the postoperative course. If the intraoperative course is uneventful and pain, nausea, and pulmonary status are well controlled, postoperative management of the asthmatic patient is similar to that of the nonasthmatic [80].

If severe bronchospasm has occurred during anesthesia, postoperative ventilation may be considered to allow time for maximal medical treatment, return of airway function, and perhaps recovery from neuromuscular blocking agents (NMBAs) without the need for reversal. Noninvasive ventilation may be beneficial for asthmatics with bronchospasm after extubation. (See "Noninvasive ventilation in adults with acute respiratory failure: Benefits and contraindications", section on 'Asthma exacerbation' and "Respiratory problems in the post-anesthesia care unit (PACU)".)

Adequate pain control, bronchodilator therapy, incentive spirometry, deep breathing maneuvers, and early mobilization are important in avoiding postoperative pulmonary complications [66] (see "Strategies to reduce postoperative pulmonary complications in adults"). Postoperative epidural analgesia may be beneficial, especially for patients having upper abdominal and thoracic surgery. Effective epidural analgesia may reduce splinting, reduce atelectasis, maintain respiratory muscle function, and provide superior pain control [81]. Nerve blocks (eg, intercostal or paravertebral blocks) may achieve similar goals in patients who cannot have epidural placement. (See "Approach to the management of acute pain in adults", section on 'Regional anesthesia techniques'.)

Ketorolac is a nonsteroidal antiinflammatory agent (NSAID; inhibits cyclooxygenase-1 and -2) used parenterally to relieve moderate to severe acute pain. We avoid this agent in patients with aspirin-exacerbated respiratory disease, as it can precipitate acute bronchoconstriction [82]. (See "Aspirin-exacerbated respiratory disease: NSAID challenge and desensitization", section on 'Ketorolac nasal provocation'.)

SPECIAL POPULATIONS

Emergency surgery — Induction of general anesthesia for an emergency procedure in an asthmatic patient requires a balance between the need for rapid control of the airway and avoidance of bronchospasm with intubation. (See "Rapid sequence induction and intubation (RSII) for anesthesia" and "Rapid sequence intubation in adults for emergency medicine and critical care".)

Except in truly life-threatening emergencies, there is usually time to conduct a basic evaluation and to administer an inhaled bronchodilator. A rapid preoperative assessment of the asthmatic patient presenting for emergency surgery should at least include a brief history that identifies precipitating factors, current medical management, degree of pulmonary disability, and previous episodes of bronchospasm under anesthesia.

Patients who have sustained trauma may be hemodynamically unstable, making it difficult to achieve the depth of anesthesia that is necessary for endotracheal intubation. We typically employ a rapid sequence induction and intubation (RSII) to secure the airway in this setting. The bronchodilatory properties of ketamine and propofol make either drug useful in this situation, depending upon patient hemodynamic stability. (See "Rapid sequence induction and intubation (RSII) for anesthesia".)

Injuries of the chest and airway can mimic the onset of bronchospasm. Conditions such as tension pneumothorax, tracheobronchial disruption, pulmonary hemorrhage, and ball-valve obstruction of the endotracheal tube (ETT) by foreign bodies or blood clots should be quickly ruled out by an Advanced Trauma Life Support survey. (See "Initial evaluation and management of blunt thoracic trauma in adults", section on 'Primary survey' and "Initial evaluation and management of penetrating thoracic trauma in adults", section on 'Initial evaluation and management'.)

Asthmatic patients with increased intracranial pressure — Ventilation for the asthmatic patient with increased intracranial pressure (ICP) can be especially challenging. Hyperventilation to decrease ICP may be difficult and may result in hyperinflation and barotrauma. Volatile anesthetics, especially in higher concentrations and without hyperventilation, can decrease cerebral perfusion pressure (CPP) and increase ICP. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Hyperventilation'.)

Propofol can be used for induction of anesthesia in the hemodynamically stable patient if measures are taken to maintain blood pressure (BP) and, therefore, CPP. Etomidate reduces ICP, cerebral blood flow (CBF), and cerebral metabolic rate for oxygen (CMRO2), and maintains CPP and BP [83]. Ketamine may also be used, as a number of studies have shown that it does not increase ICP [84-86]. (See 'Anesthetic agents' above.)

Asthmatic obstetric patients — For most asthmatic patients, we suggest epidural analgesia for labor. Low-dose epidural local anesthetics and opioids can provide analgesia while maintaining normal motor function and ventilation, and reduce the stress, anxiety, and ventilatory requirements of labor. In addition, establishment of a working labor epidural reduces the chance that general anesthesia and endotracheal intubation would be required should an emergent cesarean section become necessary since the level of epidural anesthesia can be increased quickly.

Spinal or epidural regional anesthesia is typically used for cesarean section. A midthoracic level of motor and sensory anesthesia is necessary, and accessory muscles of respiration may be paralyzed. As discussed above, asthmatic patients may not tolerate high levels of regional anesthesia. (See 'Regional anesthesia' above.)

General anesthesia may be required for emergent cesarean section. In such situations, a short-acting bronchodilator should be administered, if possible. These patients are at high risk of bronchospasm since a rapid sequence induction and a relatively light depth of anesthesia are employed.

15-methyl prostaglandin F2 alpha is used as a uterotonic agent for treatment of uterine atony. It is a bronchoconstrictor and should not be used in asthmatic patients [87]. Although rare, there are case reports of bronchospasm following administration of an ergot alkaloid, such as methylergonovine, to increase uterine tone [88].

Other issues surrounding pregnancy in asthmatic patients are presented separately. (See "Management of asthma during pregnancy".)

Ambulatory surgery — Uncontrolled asthma is generally a contraindication for ambulatory surgery.

Bronchial thermoplasty procedures — Bronchial thermoplasty (BT) involves targeted application of heat (via radiofrequency waves) to the airways, and is approved for use in selected adults with severe asthma that is poorly controlled with inhaled glucocorticoids and long-acting beta agonists. Data from ongoing clinical trials and registries have noted modest improvements in symptoms and quality of life. (See "Treatment of severe asthma in adolescents and adults", section on 'Bronchial thermoplasty'.)

BT consists of three separate outpatient bronchoscopic procedures that can be performed with monitored anesthesia care (MAC) with airway topical anesthesia and moderate sedation, or with general anesthesia. Glycopyrrolate (3.2 mcg/kg IV) should be administered before each procedure to minimize secretions.

If MAC is selected, dexmedetomidine or propofol infusions or fentanyl and midazolam boluses can be used. The patient must remain still during the 10-second radiofrequency ablation, and cough should be avoided. General anesthesia may be required for patients who cannot cooperate or have a high risk for pulmonary aspiration, or may be selected because of surgeon or patient preference. In such cases, a total intravenous anesthesia (TIVA) technique is a good choice since this avoids contamination of the operating room with anesthetic gases. Either a larger ETT (eg, ≥8.0 mm internal diameter) or a laryngeal mask airway is inserted for airway management [89,90]. (See "Anesthesia for adult bronchoscopy", section on 'Total intravenous anesthesia' and "Anesthesia for adult bronchoscopy", section on 'Airway control'.)

SUMMARY AND RECOMMENDATIONS

Preoperative evaluation – Asthma control should be optimized prior to anesthesia. We assess patients at least one week before elective surgery to allow time for treatment modification, if necessary. Patients should continue usual asthma treatment throughout the perioperative period. (See 'Timing and goals' above and 'Preoperative medication management' above.)

Treatment of poorly controlled asthma – For patients with poorly controlled asthma who require endotracheal intubation for major surgery such as thoracic or upper abdominal surgery, open aortic aneurysm repair, neurosurgery, or head and neck procedures, we suggest a course of supplemental glucocorticoids administered preoperatively (Grade 2C). We administer either five days of oral prednisone (eg, 40 mg daily) or five days of intravenous (IV) hydrocortisone (eg, 100 mg every eight hours). For patients with a high likelihood of adrenal suppression, supplemental glucocorticoids are administered as noted in the table (table 4). (See 'Treatment of poorly controlled asthma' above.)

Choice of anesthetic technique – Since endotracheal intubation is a potent stimulus for bronchospasm, we avoid endotracheal intubation when possible by using regional anesthesia, mask ventilation, or a laryngeal mask airway (LMA) during general anesthesia. In particular, for parturients with asthma, epidural labor analgesia is beneficial. (See 'Choice of anesthetic technique' above and 'Asthmatic obstetric patients' above.)

General anesthesia: Induction agents

For most hemodynamically stable patients undergoing general anesthesia, we suggest induction with propofol rather than other agents (Grade 2C). Agents such as ketamine (which has bronchodilatory properties) or etomidate may be preferred for hemodynamically unstable patients. (See 'Induction of anesthesia' above and 'Anesthetic agents' above.)

Adjuvant IV medications, typically an opioid and/or lidocaine, are often employed to suppress airway reflexes and supplement sedative effects of the primary anesthetic induction agent if endotracheal intubation is planned. (See 'Induction of anesthesia' above and 'Anesthetic agents' above.)

General anesthesia: Maintenance agents

Sevoflurane, isoflurane, or halothane should be used for maintenance of anesthesia. Desflurane may be an airway irritant and is avoided or used with caution. Total IV anesthesia (TIVA) may be preferred for selected patients or procedures. (See 'Maintenance of anesthesia' above.)

Neuromuscular blocking agents (NMBAs) that do not release appreciable amounts of histamine (eg, rocuronium, cisatracurium, and vecuronium) are preferred rather than agents such as succinylcholine and atracurium that do release histamine. Rarely, neostigmine (used for reversal of NMBAs) may cause bronchospasm. (See 'Anesthetic agents' above and 'Emergence from anesthesia' above.)

Morphine and meperidine can release histamine when given in high doses or very rapidly. Thus, synthetic opioids that do not release histamine are preferred. (See 'Anesthetic agents' above.)

Ventilation – During general anesthesia, controlled hypoventilation includes use of low tidal volumes, reduced inspiratory time, increased expiratory time, and cautious use of positive end-expiratory pressure (PEEP). Hyperinflation, stacked breaths, air trapping, and barotrauma are carefully avoided. (See 'Controlled ventilation during anesthesia' above.)

Treatment of intraoperative bronchospasm – Initial treatment of intraoperative bronchospasm includes (see 'Intraoperative bronchospasm' above):

Increasing fraction of inspired oxygen (FiO2) to 100 percent

Hand ventilation

Deepening anesthesia

Patients with persistent bronchospasm should receive short-acting beta2 agonist therapy: 8 to 10 puffs via metered dose inhaler or 2.5 mg via nebulizer. More severe bronchospasm may require intervention with glycopyrrolate or atropine, epinephrine, magnesium, and/or steroids. In rare cases, extracorporeal membrane oxygenation (ECMO) is used to treat severe bronchospasm.

Emergence from general anesthesia – Aim for smooth emergence from anesthesia. Patients with a complicated intraoperative course may benefit from postoperative sedation and controlled ventilation. (See 'Emergence from anesthesia' above.)

Postoperative pain management – Excellent postoperative pain control, continuation of asthma medications (including short-acting beta2 agonists), incentive spirometry, and early mobilization are beneficial. (See 'Postoperative management' above.)

Emergency procedures – For emergency procedures, induction of anesthesia balances rapidly controlling the airway, maintaining hemodynamic stability, and establishing adequate depth of anesthesia to avoid bronchospasm during endotracheal intubation. (See 'Emergency surgery' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Jeffrey B Dobyns, DO, who contributed to earlier versions of this topic review.

  1. Stern J, Pier J, Litonjua AA. Asthma epidemiology and risk factors. Semin Immunopathol 2020; 42:5.
  2. Smetana GW, Lawrence VA, Cornell JE, American College of Physicians. Preoperative pulmonary risk stratification for noncardiothoracic surgery: systematic review for the American College of Physicians. Ann Intern Med 2006; 144:581.
  3. Kanat F, Golcuk A, Teke T, Golcuk M. Risk factors for postoperative pulmonary complications in upper abdominal surgery. ANZ J Surg 2007; 77:135.
  4. Woods BD, Sladen RN. Perioperative considerations for the patient with asthma and bronchospasm. Br J Anaesth 2009; 103 Suppl 1:i57.
  5. Smetana GW, Conde MV. Preoperative pulmonary update. Clin Geriatr Med 2008; 24:607.
  6. Warner DO, Warner MA, Barnes RD, et al. Perioperative respiratory complications in patients with asthma. Anesthesiology 1996; 85:460.
  7. McCarren M, McDermott MF, Zalenski RJ, et al. Prediction of relapse within eight weeks after an acute asthma exacerbation in adults. J Clin Epidemiol 1998; 51:107.
  8. Emerman CL, Cydulka RK. Factors associated with relapse after emergency department treatment for acute asthma. Ann Emerg Med 1995; 26:6.
  9. Aquilina AT, Hall WJ, Douglas RG Jr, Utell MJ. Airway reactivity in subjects with viral upper respiratory tract infections: the effects of exercise and cold air. Am Rev Respir Dis 1980; 122:3.
  10. Fleisher LA, Fleischmann KE, Auerbach AD, et al. 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2014; 130:2215.
  11. Fleisher LA, Fleischmann KE, Auerbach AD, et al. 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines. J Am Coll Cardiol 2014; 64:e77.
  12. Siegler D. Reversible electrocardiographic changes in severe acute asthma. Thorax 1977; 32:328.
  13. Mercado DL, Petty BG. Perioperative medication management. Med Clin North Am 2003; 87:41.
  14. Hollevoet I, Herregods S, Vereecke H, et al. Medication in the perioperative period: stop or continue? A review. Acta Anaesthesiol Belg 2011; 62:193.
  15. Silvanus MT, Groeben H, Peters J. Corticosteroids and inhaled salbutamol in patients with reversible airway obstruction markedly decrease the incidence of bronchospasm after tracheal intubation. Anesthesiology 2004; 100:1052.
  16. Kabalin CS, Yarnold PR, Grammer LC. Low complication rate of corticosteroid-treated asthmatics undergoing surgical procedures. Arch Intern Med 1995; 155:1379.
  17. Pien LC, Grammer LC, Patterson R. Minimal complications in a surgical population with severe asthma receiving prophylactic corticosteroids. J Allergy Clin Immunol 1988; 82:696.
  18. Su FW, Beckman DB, Yarnold PA, Grammer LC. Low incidence of complications in asthmatic patients treated with preoperative corticosteroids. Allergy Asthma Proc 2004; 25:327.
  19. Xiao HT, Liao Z, Tong RS. Penehyclidine hydrochloride: a potential drug for treating COPD by attenuating Toll-like receptors. Drug Des Devel Ther 2012; 6:317.
  20. Yan T, Liang XQ, Wang GJ, et al. Prophylactic Penehyclidine Inhalation for Prevention of Postoperative Pulmonary Complications in High-risk Patients: A Double-blind Randomized Trial. Anesthesiology 2022; 136:551.
  21. Kim ES, Bishop MJ. Endotracheal intubation, but not laryngeal mask airway insertion, produces reversible bronchoconstriction. Anesthesiology 1999; 90:391.
  22. Eames WO, Rooke GA, Wu RS, Bishop MJ. Comparison of the effects of etomidate, propofol, and thiopental on respiratory resistance after tracheal intubation. Anesthesiology 1996; 84:1307.
  23. Wu RS, Wu KC, Sum DC, Bishop MJ. Comparative effects of thiopentone and propofol on respiratory resistance after tracheal intubation. Br J Anaesth 1996; 77:735.
  24. Forget P, Pirson E, Scholtès JL. Anaphylactic bronchospasm due to propofol. Anaesth Intensive Care 2009; 37:865.
  25. You BC, Jang AS, Han JS, et al. A case of propofol-induced oropharyngeal angioedema and bronchospasm. Allergy Asthma Immunol Res 2012; 4:46.
  26. Asserhøj LL, Mosbech H, Krøigaard M, Garvey LH. No evidence for contraindications to the use of propofol in adults allergic to egg, soy or peanut†. Br J Anaesth 2016; 116:77.
  27. Pedersen CM, Thirstrup S, Nielsen-Kudsk JE. Smooth muscle relaxant effects of propofol and ketamine in isolated guinea-pig trachea. Eur J Pharmacol 1993; 238:75.
  28. Pizov R, Brown RH, Weiss YS, et al. Wheezing during induction of general anesthesia in patients with and without asthma. A randomized, blinded trial. Anesthesiology 1995; 82:1111.
  29. Rosow CE, Moss J, Philbin DM, Savarese JJ. Histamine release during morphine and fentanyl anesthesia. Anesthesiology 1982; 56:93.
  30. Guedes AG, Papich MG, Rude EP, Rider MA. Comparison of plasma histamine levels after intravenous administration of hydromorphone and morphine in dogs. J Vet Pharmacol Ther 2007; 30:516.
  31. Flacke JW, Flacke WE, Bloor BC, et al. Histamine release by four narcotics: a double-blind study in humans. Anesth Analg 1987; 66:723.
  32. Philbin DM, Moss J, Akins CW, et al. The use of H1 and H2 histamine antagonists with morphine anesthesia: a double-blind study. Anesthesiology 1981; 55:292.
  33. Prieto-Lastra L, Iglesias-Cadarso A, Reaño-Martos MM, et al. Pharmacological stimuli in asthma/urticaria. Allergol Immunopathol (Madr) 2006; 34:224.
  34. STEINHAUS JE, GASKIN L. A study of intravenous lidocaine as a suppressant of cough reflex. Anesthesiology 1963; 24:285.
  35. Aouad MT, Sayyid SS, Zalaket MI, Baraka AS. Intravenous lidocaine as adjuvant to sevoflurane anesthesia for endotracheal intubation in children. Anesth Analg 2003; 96:1325.
  36. Davidson JA, Gillespie JA. Tracheal intubation after induction of anaesthesia with propofol, alfentanil and i.v. lignocaine. Br J Anaesth 1993; 70:163.
  37. Jakobsen CJ, Ahlburg P, Holdgård HO, et al. Comparison of intravenous and topical lidocaine as a suppressant of coughing after bronchoscopy during general anesthesia. Acta Anaesthesiol Scand 1991; 35:238.
  38. Lin CS, Sun WZ, Chan WH, et al. Intravenous lidocaine and ephedrine, but not propofol, suppress fentanyl-induced cough. Can J Anaesth 2004; 51:654.
  39. Nishino T, Hiraga K, Sugimori K. Effects of i.v. lignocaine on airway reflexes elicited by irritation of the tracheal mucosa in humans anaesthetized with enflurane. Br J Anaesth 1990; 64:682.
  40. Pandey CK, Raza M, Ranjan R, et al. Intravenous lidocaine suppresses fentanyl-induced coughing: a double-blind, prospective, randomized placebo-controlled study. Anesth Analg 2004; 99:1696.
  41. Pandey CK, Raza M, Ranjan R, et al. Intravenous lidocaine 0.5 mg.kg-1 effectively suppresses fentanyl-induced cough. Can J Anaesth 2005; 52:172.
  42. Warner LO, Balch DR, Davidson PJ. Is intravenous lidocaine an effective adjuvant for endotracheal intubation in children undergoing induction of anesthesia with halothane-nitrous oxide? J Clin Anesth 1997; 9:270.
  43. Yukioka H, Hayashi M, Terai T, Fujimori M. Intravenous lidocaine as a suppressant of coughing during tracheal intubation in elderly patients. Anesth Analg 1993; 77:309.
  44. Adamzik M, Groeben H, Farahani R, et al. Intravenous lidocaine after tracheal intubation mitigates bronchoconstriction in patients with asthma. Anesth Analg 2007; 104:168.
  45. Chang HY, Togias A, Brown RH. The effects of systemic lidocaine on airway tone and pulmonary function in asthmatic subjects. Anesth Analg 2007; 104:1109.
  46. Maslow AD, Regan MM, Israel E, et al. Inhaled albuterol, but not intravenous lidocaine, protects against intubation-induced bronchoconstriction in asthma. Anesthesiology 2000; 93:1198.
  47. Slaton RM, Thomas RH, Mbathi JW. Evidence for therapeutic uses of nebulized lidocaine in the treatment of intractable cough and asthma. Ann Pharmacother 2013; 47:578.
  48. Naaz S, Ozair E. Dexmedetomidine in current anaesthesia practice- a review. J Clin Diagn Res 2014; 8:GE01.
  49. Groeben H, Mitzner W, Brown RH. Effects of the alpha2-adrenoceptor agonist dexmedetomidine on bronchoconstriction in dogs. Anesthesiology 2004; 100:359.
  50. Yamakage M, Iwasaki S, Namiki A. Guideline-oriented perioperative management of patients with bronchial asthma and chronic obstructive pulmonary disease. J Anesth 2008; 22:412.
  51. Rooke GA, Choi JH, Bishop MJ. The effect of isoflurane, halothane, sevoflurane, and thiopental/nitrous oxide on respiratory system resistance after tracheal intubation. Anesthesiology 1997; 86:1294.
  52. Goff MJ, Arain SR, Ficke DJ, et al. Absence of bronchodilation during desflurane anesthesia: a comparison to sevoflurane and thiopental. Anesthesiology 2000; 93:404.
  53. Dikmen Y, Eminoglu E, Salihoglu Z, Demiroluk S. Pulmonary mechanics during isoflurane, sevoflurane and desflurane anaesthesia. Anaesthesia 2003; 58:745.
  54. Laxenaire MC, Mertes PM, Groupe d'Etudes des Réactions Anaphylactoïdes Peranesthésiques. Anaphylaxis during anaesthesia. Results of a two-year survey in France. Br J Anaesth 2001; 87:549.
  55. Laake JH, Røttingen JA. Rocuronium and anaphylaxis--a statistical challenge. Acta Anaesthesiol Scand 2001; 45:1196.
  56. Sadleir PH, Clarke RC, Bunning DL, Platt PR. Anaphylaxis to neuromuscular blocking drugs: incidence and cross-reactivity in Western Australia from 2002 to 2011. Br J Anaesth 2013; 110:981.
  57. Reddy JI, Cooke PJ, van Schalkwyk JM, et al. Anaphylaxis is more common with rocuronium and succinylcholine than with atracurium. Anesthesiology 2015; 122:39.
  58. Crilly H, Rose M. Anaphylaxis and anaesthesia - can treating a cough kill? Aust Prescr 2014; 37:74.
  59. Basta SJ. Modulation of histamine release by neuromuscular-blocking drugs. Curr Opin Anesthesiol 1992; 5:572.
  60. Bayable SD, Melesse DY, Lema GF, Ahmed SA. Perioperative management of patients with asthma during elective surgery: A systematic review. Ann Med Surg (Lond) 2021; 70:102874.
  61. Pasch T, Kamp HD, Petermann H. [The effect of halothane, enflurane and isoflurane on resistance and compliance in patients with asthma or chronic obstructive lung diseases]. Anaesthesist 1991; 40:65.
  62. Turner DA, Heitz D, Cooper MK, et al. Isoflurane for life-threatening bronchospasm: a 15-year single-center experience. Respir Care 2012; 57:1857.
  63. Khosla S, Kunjummen B, Khaleel R, et al. Safety of therapeutic beta-blockade in patients with coexisting bronchospastic airway disease and coronary artery disease. Am J Ther 2003; 10:48.
  64. Morales DR, Jackson C, Lipworth BJ, et al. Adverse respiratory effect of acute β-blocker exposure in asthma: a systematic review and meta-analysis of randomized controlled trials. Chest 2014; 145:779.
  65. Stather DR, Stewart TE. Clinical review: Mechanical ventilation in severe asthma. Crit Care 2005; 9:581.
  66. Qaseem A, Snow V, Fitterman N, et al. Risk assessment for and strategies to reduce perioperative pulmonary complications for patients undergoing noncardiothoracic surgery: a guideline from the American College of Physicians. Ann Intern Med 2006; 144:575.
  67. Futier E, Constantin JM, Paugam-Burtz C, et al. A trial of intraoperative low-tidal-volume ventilation in abdominal surgery. N Engl J Med 2013; 369:428.
  68. van der Meer AN, de Jong K, Hoekstra-Kuik A, et al. Targeting dynamic hyperinflation in moderate-to-severe asthma: a randomised controlled trial. ERJ Open Res 2021; 7.
  69. Marini JJ. Dynamic hyperinflation and auto-positive end-expiratory pressure: lessons learned over 30 years. Am J Respir Crit Care Med 2011; 184:756.
  70. Gal TJ, Suratt PM. Atropine and glycopyrrolate effects on lung mechanics in normal man. Anesth Analg 1981; 60:85.
  71. Shan Z, Rong Y, Yang W, et al. Intravenous and nebulized magnesium sulfate for treating acute asthma in adults and children: a systematic review and meta-analysis. Respir Med 2013; 107:321.
  72. Baraka A, Nawfal M, Haroun-Bizri S, Yaniut I. Nitroglycerin for intra-operative bronchospasm. Anaesthesia 1999; 54:395.
  73. Mikulandra S, Hirs I, Deutsch J. Unusual use of nitroglycerin for severe bronchospasm during coiling embolization of ruptured intracranial aneurysm. J Neurosurg Anesthesiol 2008; 20:207.
  74. Rodrigo GJ, Rodrigo C, Pollack CV, Rowe B. Use of helium-oxygen mixtures in the treatment of acute asthma: a systematic review. Chest 2003; 123:891.
  75. Hazizaj A, Hatija A. Bronchospasm caused by neostigmine. Eur J Anaesthesiol 2006; 23:85.
  76. Yoshioka N, Hanazaki M, Fujita Y, et al. Effect of sugammadex on bronchial smooth muscle function in rats. J Smooth Muscle Res 2012; 48:59.
  77. Amao R, Zornow MH, Cowan RM, et al. Use of sugammadex in patients with a history of pulmonary disease. J Clin Anesth 2012; 24:289.
  78. Tsur A, Kalansky A. Hypersensitivity associated with sugammadex administration: a systematic review. Anaesthesia 2014; 69:1251.
  79. Aggarwal P. Risk of bronchospasm and coronary arteriospasm with sugammadex use: a post marketing analysis. Ther Adv Drug Saf 2019; 10:2042098619869077.
  80. Lenart J, Applegate R, Lauer R, et al. The perioperative management of asthma. J Aller Ther 2013; S11:1.
  81. Manion SC, Brennan TJ. Thoracic epidural analgesia and acute pain management. Anesthesiology 2011; 115:181.
  82. Dias MA, Biedlingmaier JF. Ketorlac-induced status asthmaticus after endoscopic sinus surgery in a patient with Samter's triad. Otolaryngol Head Neck Surg 1997; 117:S176.
  83. Milde LN, Milde JH, Michenfelder JD. Cerebral functional, metabolic, and hemodynamic effects of etomidate in dogs. Anesthesiology 1985; 63:371.
  84. Mayberg TS, Lam AM, Matta BF, et al. Ketamine does not increase cerebral blood flow velocity or intracranial pressure during isoflurane/nitrous oxide anesthesia in patients undergoing craniotomy. Anesth Analg 1995; 81:84.
  85. Himmelseher S, Durieux ME. Revising a dogma: ketamine for patients with neurological injury? Anesth Analg 2005; 101:524.
  86. Chang LC, Raty SR, Ortiz J, et al. The emerging use of ketamine for anesthesia and sedation in traumatic brain injuries. CNS Neurosci Ther 2013; 19:390.
  87. Andersen LH, Secher NJ. Pattern of total and regional lung function in subjects with bronchoconstriction induced by 15-me PGF2 alpha. Thorax 1976; 31:685.
  88. Liccardi G, Salzillo A, Sofia M, et al. Bronchial asthma. Curr Opin Anaesthesiol 2012; 25:30.
  89. Lee JA, Rowen DW, Rose DD. Bronchial thermoplasty: a novel treatment for severe asthma requiring monitored anesthesia care. AANA J 2011; 79:480.
  90. Duhamel DR, Hales JB. Bronchial thermoplasty: a novel therapeutic approach to severe asthma. J Vis Exp 2010.
Topic 94358 Version 24.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟