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        Asthma is a disorder of variable intensity, typified by sentinel symptoms, airway obstruction, inflammation, and hyperresponsiveness. The asthmatic patient undergoing surgery is at risk for perioperative morbidity and mortality.

       A history of asthma has several implications in the perioperative setting. The patient may present for an anesthetic poorly optimized, particularly in the setting of urgent or emergent surgery. Because of airway hyperreactivity, bronchospasm may readily be precipitated by instrumentation, a variety of drugs, and perioperative complications such as aspiration, infection, or trauma. Emergence from anesthesia presents a constant risk of laryngospasm and bronchospasm. Pain, fluid shifts, and delayed mobilization can contribute to an increased risk of postoperative pulmonary complications in these patients. These risks are exacerbated by the coexistence of chronic obstructive pulmonary disease (COPD) or active smoking. Advances in understanding the pathogenesis and management of bronchospasm have made anesthesia and the perioperative period much safer for patients with asthma.



       Bronchial asthma is a chronic inflammatory disorder of the airways associated with airway hyperresponsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness and coughing particularly at night or in the early morning. These episodes are usually associated with widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment.



      Asthma is a heterogeneous disease with interplay between genetic and environmental factors. Several risk

factors have been implicated (Table 3.1). The strongest identifiable predisposing factor for the development of asthma is atopy, but obesity is increasingly recognized as a risk factor. Exposure of sensitive patients to inhaled allergens increases airway inflammation, airway hyper- responsiveness, and symptoms. Symptoms may develop immediately (immediate asthmatic response) or 4-6 hours after allergen exposure (late asthmatic response). Common allergens include house dust mites (often found in pillows, mattresses, upholstered furniture, carpets, and drapes), cockroaches, cat dander, and seasonal pollens. Substantially reducing exposure reduces pathologic findings and clinical symptoms.

     Nonspecific precipitants of asthma include exercise, upper respiratory tract infections, rhinitis, sinusitis, postnasal drip, aspiration, gastroesophageal reflux, changes in the weather, and stress. Exposure to environmental tobacco smoke increases asthma symptoms and the need for medications and reduces lung function. Increased air levels of respirable particles, ozone, SO2, and NO2 precipitate asthma symptoms and increase emergency department visits and hospitalizations. Selected individuals may experience asthma symptoms after exposure to aspirin, nonsteroidal anti-inflammatory drugs, or tartrazine dyes. Certain other medications may also precipitate asthma symptoms. Occupational asthma is triggered by various agents in the workplace and may occur weeks to years after initial exposure and sensitization. Women may experience catamenial asthma at predictable times during the menstrual cycle. Exercise-induced bronchoconstriction begins during exercise or within 3 minutes after its end, peaks within 10–15 minutes, and then resolves by 60 minutes. This phenomenon is thought to be a consequence of the airways’ attempt to warm and humidify an increased volume of expired air during exercise. “Cardiac asthma” is wheezing precipitated by uncompensated congestive heart failure.

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      The severity of the disease process is related to the severity of airway inflammation, which governs hyperresponsiveness, the degree of obstruction, and symptomatology (Fig. 3.1). Broncho-constriction results from contraction of bronchial smooth muscle induced by a myriad possible stimuli, including intrinsic factors, allergens, exercise, stress, or cold air (Table 3.1). Vagal and sympathetic factors directly modulate airway tone. Inflammatory edema and mucous plugging exacerbate airflow limitation and progressively impair the response to bronchodilator therapy. Airway remodelling, thickening, and abnormal communications between the injured airway epithelium and the pulmonary mesenchyme confer resistance to corticosteroid therapy as well. Airway smooth muscle changes have been implicated in chronic, poorly responsive bronchospastic disease—both as a mechanical and as an inflammatory mediator.

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       The immunologic-inflammatory pathways involved in the pathogenesis of asthma are complex and include lymphocytes (both TH1 and TH2), immunoglobulin E, eosinophils, neutrophils, mast cells, leukotrienes, and cytokines. These pathways are triggered and modified by extrinsic and environmental factors such as allergens, respiratory infections, smoke, and occupation-related exposure. Thus, asthma ultimately represents a dynamic interaction between host and environmental factors.

     Airway narrowing is the final common pathway leading to symptoms and physiological changes in asthma. Several factors contribute to the development of airway narrowing in asthma (Table 3.2).

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        Airway hyperresponsiveness, the characteristic func- tional abnormality of asthma, results in airway narrowing in a patient with asthma in response to stimulus that would be innocuous in a normal person. In turn, this airway narrowing leads to variable airflow limitation and intermittent symptoms. Airway hyperresponsiveness is linked to both inflammation and repair of the airways and is partially reversible with therapy. Its mechanisms (Table 3.3) are incompletely understood.

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Structural changes in the airways

      In addition to the inflammatory response, there are characteristic structural changes, often described as airway remodeling, in the airways of asthmatic patients. Some of these changes are related to the severity of the disease and may result in relatively irreversible narrowing of the airways. These changes may represent repair in response to chronic inflammation (Table 3.4).

Table 3.4: Structural changes in the airways in bronchial asthma

  • Subepithelial fibrosis results from the deposition of collagen fibers and proteoglycans under the basement membrane and is seen in all asthmatic patients, including children, even before the onset of symptoms but may be influenced by treatment. Fibrosis occurs in other layers of the airway wall, with deposition of collagen and proteoglycans.

  • Airway smooth muscle increases, due both to hypertrophy (increased size of individual cells) and hyperplasia (increased cell division), and contributes to the increased thickness of the airway wall. This process may relate to disease severity and is caused by inflammatory mediators, such as growth factors.

  • Blood vessels in airway walls proliferate due to the influence of growth factors such as vascular endothelial growth factor and may contribute to increased airway wall thickness.

  • Mucus hypersecretion results from increased size of submucosal glands

Assessment and monitoring of asthma


      Consider a diagnosis of asthma and performing spirometry if any of the following indicators is present. These indicators are not diagnostic by themselves, but the presence of multiple key indicators increases the probability of a diagnosis of asthma.6 (Note: Eczema, hay fever, or a family history of asthma or atopic diseases are often associated with asthma, but they are not key indicators). Spirometry is needed to establish a diagnosis of asthma.

  • Wheezing—High-pitched whistling sounds when breathing out—especially in children. (Lack of wheezing and a normal chest examination do not exclude asthma).

  • History of any of the following:

    • Cough, worse particularly at night

    • Recurrent wheeze

    • Recurrent difficulty in breathing

    • Recurrent chest tightness.

  • Symptoms occur or worsen in the presence of:

    • Exercise

    • Viral infection

    • Animals with fur or hair

    • House-dust mites (in mattresses, pillows, uphol-stered furniture, carpets)

    • Mold

    • Smoke (tobacco, wood)

    • Pollen

    • Changes in weather

    • Strong emotional expression (laughing or crying hard) Airborne chemicals or dusts

    • Menstrual cycles.

  • Symptoms occur or worsen at night, awakening the patient

  • The functions of assessment and monitoring are closely linked to the concepts of severity, control, and responsiveness to treatment:

  • Severity: The intrinsic intensity of the disease process. Severity is most easily and directly measured in a patient who is not currently receiving long-term control treatment.

  • Control: The degree to which the manifestations of asthma (symptoms, functional impairments, and risks of untoward events) are minimized and the goals of therapy are met.

  • Responsiveness: The ease with which control is achieved by therapy.

      Spirometry typically measures the maximal volume of air forcibly exhaled from the point of maximal inhalation (FVC) and the volume of air exhaled during the first second of this maneuver (FEV1). For diagnostic purposes, spirometry is generally recommended over measurements by a peak flow meter in the clinician’s office because there is wide variability even in the published predicted peak expiratory flow (PEF) reference values. Peak flow meters are designed as monitoring, not as diagnostic, tools.

     Significant reversibility is indicated by American Thoracic Society (ATS) standards as an increase in FEV1 of >200 mL and ≥12 percent from the baseline measure after inhalation of a short-acting bronchodilator (e.g. albuterol, 2–4 puffs of 90 μg/puff).

Drug therapy for asthma

Drug therapy

     Historically, medications for asthma have been classified according to mechanism and target. More recently, a short- vs long-term relief schema has become popular, particularly as newer drugs defy the old classification. This paradigm is considered to be more amenable to patient compliance and simplifies the perioperative approach to therapy.

Quick-acting drugs

       Short-acting β -selective adrenergic agonists (SABA) provided by metered-dose inhalers (MDIs) are the mainstay

for fast relief of bronchoconstriction. Examples of this class of drugs are albuterol (salbutamol), levalbuterol

(levosalbutamol), and pirbuterol. Their onset of action occurs within 5 min, peak effect is within 1 h, and their

duration of action is 4–6 h. Patients with poor inhalation technique should use a valved holding chamber (spacer).

These drugs are recommended only for short-term relief of symptoms or before known triggers such as exercise;

β2 -agonists are not contraindicated in patients taking β-blockers for cardiac disease. Side-effects such as tremor, anxiety, palpitations, and tachycardia occur but are not common at standard doses. Levalbuterol, the R-enantiomer of albuterol, has been touted to have fewer side-effects than its parent, but differences in tachycardia have not been observed in critical care patients. Hypokalemia and hypomagnesemia occasionally result from stimulation of the Na+/K+ ATPase cellular pump (and can be an effective therapeutic modality in acute renal failure). Paradoxical bronchospasm has been reported with excessive use of both albuterol and levalbuterol. Parenteral administration of short-acting β2-agonists is discouraged because of slow onset time, diminished potency, and considerably greater systemic adverse effects.

Anticholinergic bronchodilators such as ipratropium are not recommended (or approved by the Food and Drug Administration [FDA]) for quick relief of asthmatic symptoms. They take longer to start working (20 to 30 minutes) and cause less bronchodilation than inhaled β-agonist bronchodilators. Anticholinergic bronchodilators should be used only in the rare case of a patient with intolerance to all β-agonist bronchodilators or for the treatment of severe asthmatic attacks or asthmatic attacks induced by beta-blockers.

     Although not short acting, oral systemic corticosteroids are used for moderate and severe exacerbations as adjunct to SABAs to speed recovery and prevent recurrence of exacerbations.

     A summary of the quick-relief medications for bronchial asthma is compiled in Table 3.5.

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Long-acting drugs

          Anti-inflammatory agents, long-acting bronchodilators, and leukotriene modifiers comprise the important long-term control medications (Table 3.6).

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       Individual drugs are described below:

Long-acting β2-selective agonists

      Long-acting β2 -selective agonists, such as formoterol, and salmeterol, provide bronchodilation for >12 h and

are largely free of side-effects. Unfortunately, some of the bronchoprotective effect of the long-acting β2 -selective agonists decreases with time; short-acting β2 -selective agonist effect is not blunted by this phenomenon. The long- acting agents do not suppress inflammation and should not be used without antiinflammatory treatment for the control of asthma.


      Inhaled corticosteroids, for example, beclomethasone, budesonide, fluticasone, and triamcinolone, are the

cornerstone of therapy to stabilize and improve persistent asthma. Their consistent use has probably contributed

to the decreased morbidity and mortality observed in asthma, at the same time that the disease has become

more widespread. Some formulations combine a steroid and a long-acting β2 -selective agonist, for example, budesonide–formoterol and fluticasone–salmeterol. None- theless, inhaled corticosteroids are suppressive rather than curative. No clinically important adrenal suppression has been found with their administration in low to moderate doses.

      No significant therapeutic differences appear to exist between different formulations.

      Parenteral steroids remain a mainstay of the treatment of acute asthma. However, their beneficial effect on airway mechanics can take 4–6 h in acute bronchospasm, a noteworthy point in the poorly controlled asthmatic requiring urgent or emergent surgery. Adrenal suppression, infection, delayed healing, hyperglycemia, and fluid retention are common complications of prolonged therapy. However, delayed wound healing and increased infection have not been observed in asthmatic patients treated with perioperative systemic steroids. Patients who have been taking systemic corticosteroids equivalent to more than 10 mg prednisolone daily (or who have received such a dose within the last 3 months) should be considered at risk for adrenal suppression in the setting of severe acute disease, trauma, or major surgery, and receive a physiological replacement regimen (discussed later).

Leukotriene modifiers

       Include leukotriene receptor antagonists (LTRAs) such as montelukast, zafirlukast, pranlukast, and a 5-lipoxygenase pathway inhibitor such as zileuton. Evidence of their beneficial effect on inflammation is conflicting. They are not useful for acute treatment of bronchospasm. Zileuton use has been associated with hepatic injury, and  Leukotrienereceptor antagonist use with Churg–Strauss vasculitis, especially when steroids dosage is decreased. In short, LTRAs are alternative, but not preferred, therapy for the treatment of mild persistent asthma.

Anticholinergic agents

       Anticholinergic bronchodilators such as ipratropium have a more limited role in the therapy of acute asthmatic

bronchospasm than β2 -selective agonists. They act by inhibiting cyclic guanosine monophosphate formation and

block vagus nerve-mediated bronchoconstriction, which is an important component of bronchospasm in patients with COPD. Indications for their use include, as implied, patients with COPD, but also patients who are intolerant 

of β2 -selective agonists, or who are severely asthmatic, or have β-blocker-induced bronchospasm.

     Anticholinergic agents dry airway secretions. Although controversy exists as to whether this improves inflammation or worsens inspissation, it certainly decreases airway hyperresponsiveness, an important consideration for the anesthetist.

Other Therapies

      Mucolytic agents such as N-acetylcysteine are not recom- mended. Not only do they increase secretions, which worsen airway hyperreactivity, but they are irritating to the airway and can themselves provoke bronchospasm.

Theophylline has a narrow therapeutic dose range and a wide array of side-effects and has been replaced by inhaled

corticosteroids and long-acting β2-agonists.

      Mast cell stabilizers such as cromolyn are of limited benefit, require several weeks for action, and have been replaced by inhaled steroids and Leukotriene modifiers.

      Anti-IgE therapy, specifically omalizumab, is reserved for patients with moderate to severe persistent asthma who do not respond to standard treatment. It is costly and has no role in the acute management of bronchospasm.


Preop evaluation

       Well-controlled asthma does not seem to be a risk factor for either intraoperative or postoperative complications. However, patients who are poorly controlled, as shown by wheezing at the time of anesthesia induction, have a higher risk of perioperative complications. The medical history also provides clues that indicate higher risk.

      Before elective surgery, clinicians should treat patients with asthma according to a stepwise approach as outlined in

a report by the National Asthma Education and Prevention Program (NAEPP) Expert Panel Report. This approach stratifies patients based on severity and provides guidance regarding the selection of specific agents and treatment intensity based on severity.


      Preoperative evaluation begins with a clinical history to elicit the severity and characteristics of the patient’s asthma. Patients can be asymptomatic at the time of evaluation. Preoperative evaluation of patients with asthma requires an assessment of disease severity and the effectiveness of current pharmacologic management and the potential need for additional therapy prior to surgery. However, key clues to severe disease include a history of frequent exacerbations, hospital visits, and, most importantly, prior tracheal intubation and mechanical ventilation to deal with a severe attack. Prior perioperative exacerbation of respiratory disease is also significant. The patient should be interrogated regarding their most common triggering agents—They will usually be acutely aware of them. Type, dose, frequency, and degree of benefit of therapy provide important clues to the severity and control of the disease. This applies especially to steroid therapy: inhaled vs systemic use, duration of exposure, and side-effects should be elicited. Respiratory infections, including sinus infections, can trigger an asthmatic attack; thus, any recent fever, change in cough or sputum, and other evidence of respiratory infection should raise concern. Airway hyperreactivity can remain for several weeks after resolution of infectious symptoms. Patients with moderate or severe asthma can be provided with a peak expiratory flow rate (PEFR) meter for home assessment. The normal range (200–600 liter/min) varies widely depending on age, gender, height, and weight; what is relevant is how the PEFR varies from the patient’s own baseline.

Physical Examination

      The preoperative physical examination should focus on detecting signs of acute bronchospasm or active lung infection (which should defer elective surgery), chronic lung disease, and right heart failure. When expiratory airflow is markedly decreased, breath sounds are diminished or inaudible. A simple screening test for prolonged exhalation is the forced expiratory time (FET), which can be assessed by listening over the trachea while the patient exhales forcibly and fully. An FET >6 s correlates with a substantially lowered FEV1/FVC ratio and should initiate further investigation.


       Laboratory studies are guided by the history and physical examination. Formal pulmonary function tests (PFTs) help detect chronic residua of acute asthma and help stratify the severity of the disease. However, in many patients, PFTs normalize between attacks, so normal values do not guarantee an uncomplicated perioperative course. Measurement of arterial blood gases is indicated if there is any question about the adequacy of ventilation or oxygenation, but can be normal at baseline. The ECG can show right atrial or ventricular hypertrophy, acute strain, right axis deviation, and right bundle branch block. ECG may also show tachycardia due to the use of β2- agonists. Chest radiographs reveal flattened diaphragms if the lungs are hyperinflated, and are useful to evaluate for pulmonary congestion, edema, or infiltrate. Blood eosinophil counts often parallel the degree of airway inflammation, and airway hyperreactivity provides an indirect assessment of the current status of the disease.

      Before elective surgery, patients should be free of wheezes, cough, or dyspnea and have peak expiratory flows greater than 80% of predicted, or their personal best. Well- controlled asthma is characterized by daytime symptoms no more than twice per week and nighttime symptoms no more than twice per month.


Preop preparation

      The patient should be advised to stop smoking at least 2 months before elective surgery. This will allow the greatest recovery of endobronchial cilial mucus clearance. Anti-inflammatory and bronchodilator therapy should be continued until the time of anesthesia induction. Supplementation with “stress dose” corticosteroids may be indicated before major surgery if hypothalamic-pituitary- adrenal suppression by drugs used to treat asthma is a possibility. However, hypothalamic-pituitary-adrenal suppression is very unlikely with inhaled corticosteroids. In selected patients, a preoperative course of oral corti- costeroids may be useful. Oral methylprednisolone 40 mg for 5 days before surgery has been shown to decrease post-intubation wheezing in newly diagnosed or poorly compliant patients with reversible airway obstruction.

     If the patient is first evaluated immediately before operation and steroids are indicated, then IV corticosteroids 

may be useful. Steroid-induced suppression of perioperative adrenal function is unlikely to occur unless the patient has been on systemic steroids for >2 weeks within the prior 6 months and is undergoing major stress or surgery. These patients should be prescribed a short-acting steroid such as hydrocortisone (e.g. 100 mg i.v. every 8 h) during the perioperative period. Short-acting bronchodilator therapy given prophylactically has likely benefit; MDI or nebulizer delivery is equivalent if proper technique is used.

     Elective surgery should not be performed in the pre- sence of active bronchospasm, and the cause (e.g. a new respiratory infection) and symptoms should be actively treated until the patient is back to baseline status.

     An optimal premedication allays anxiety, improves work of breathing, and possibly averts the induction of bronchospasm, while avoiding oversedation and respir- atory depression. No ideal drug or drug combination exists for this. The patient’s own MDIs should be brought to the operating theatre.


Intraop management

      Bronchospasm can be provoked by laryngoscopy, tracheal intubation, airway suctioning, cold inspired gases, and tracheal extubation. Airway tone is increased by vagal stimulation caused by endoscopy, peritoneal, or visceral stretch. Application of excessive levels of PEEP can worsen incipient or increasing air trapping.

     During induction and maintenance of anesthesia in asthmatic patients, it is necessary to suppress airway reflexes to avoid bronchoconstriction in response to mechanical stimulation of these hyperreactive airways. Stimuli that do not ordinarily evoke airway responses can precipitate life-threatening bronchoconstriction in patients with asthma.

When general anesthesia is selected, induction of anesthesia is most often accomplished with an intravenous induction drug. The incidence of wheezing is higher in asthmatic patients receiving thiopental for induction than in those given propofol. Thiopental itself does not cause bronchospasm, but it may inadequately suppress upper airway reflexes so airway instrumentation may trigger bronchospasm. The mechanism of propofol’s relative bronchodilating effect is unknown. Ketamine has excellent induction characteristics and induces bronchodilation, possibly by interfering with the endothelin pathway. Ketamine may produce smooth muscle relaxation and contribute to decreased airway resistance, especially in patients who are actively wheezing.

     The decision whether to intubate the trachea, provide anesthesia by mask, or use a laryngeal mask airway (LMA) is a clinical one. However, there is evidence that tracheal intubation causes reversible increases in airway resistance not observed with placement of an LMA. Inadequate depth of anesthesia at any point can allow bronchospasm to be precipitated.

     After unconsciousness is produced, the lungs are often ventilated for a time with a gas mixture containing a volatile anesthetic. The goal is to establish a depth of anesthesia that depresses hyperreactive airway reflexes sufficiently to permit tracheal intubation without precipitating bronchospasm. The lesser pungency of halothane and sevoflurane (compared with isoflurane and desflurane) may make coughing, which can trigger bronchospasm, less likely. Sevoflurane is well tolerated as an inhalational induction agent and has good bronchodilatory effect. Halothane has been favored in the past, but is more blood-soluble leading to longer induction times, and in the setting of hypoxemia or acidemia could potentiate arrhythmias. An alternative method to suppress airway reflexes prior to intubation is the intravenous or intratracheal injection of lidocaine 1 to 3 minutes before tracheal intubation.12 However, inhalation of lidocaine is itself irritating and can precipitate or worsen bronchospasm. Intravenous injection of lidocaine quickly achieves adequate airway anesthesia, but even when administered by this route bronchial tone can be increased.

     Opioids are one of the main components of general anesthesia. When alfentanil or sufentanil are used on induction of anesthesia, thorax rigidity can be observed and easily misinterpreted as bronchospasm. This effect increases with increasing speed of injection and with the age of the patient. With slow injection, it is hardly observed at all. Otherwise, despite histamine release on injection of very high doses of morphine, opioids are unproblematic drugs in patients with increased bronchial reactivity. Sometimes the suppression of cough and the deepening of anesthesia can be used beneficially in patients with asthma.

    Skeletal muscle relaxation is usually provided with nondepolarizing muscle relaxants. In general, muscle relaxants interfere with acetylcholine receptor binding, ie, with muscarinic receptors also. Muscle relaxants like vecuronium, rocuronium and pancuronium do not cause bronchoconstriction. But gallamine and pipecuronium can cause and enhance bronchoconstriction. Benzylchinolones like atracurium and mivacurium dose-dependently release histamine and can lead to increased bronchial tone. This effect has not been observed with cisatracurium. Although histamine release has been attributed to succinylcholine, there is no evidence that this drug is associated with the appearance of increased airway resistance in asthmatic patients. Rapid sequence or standard induction should be performed as indicated as long as adequate anesthesia is assured.

     Theoretically, antagonism of neuromuscular blockade with anticholinesterase drugs could precipitate bronchospasm secondary to stimulation of postganglionic cholinergic receptors in airway smooth muscle.14 Parasympathomimetic agents like neostigmine or physostigmine cause bradycardia and increased secretion, and can increase bronchial tone and reactivity. This effect is partially antagonized by co-administration of atropine or glycopyrrolate. There are no data available for optimal mixtures of these substances for asthmatic patients. Therefore, the dose of the parasympatholytic drug should be adjusted to the cardiovascular tolerance of the patient. Overall, it has to be decided from case to case whether muscle relaxation and its reversal are required at all. Drugs are currently under development which directly bind and eliminate muscle relaxants; these agents might change this whole question.

     Intraoperatively, the desirable level of arterial oxygenation and ventilation are best provided by mechanical ventilation. Sufficient time for exhalation is necessary to prevent air trapping. This can be facilitated by using higher inspiratory flow rates or smaller tidal volumes than usual. Humidification and warming of inspired gases may be especially useful in patients with exercise-induced asthma, in whom bronchospasm is presumably due to transmucosal loss of heat. Liberal administration of fluids during the perioperative period is important for maintaining adequate hydration and ensuring the presence of less viscous airway secretions that can be removed more easily. It may be noted that fluid overload, pulmonary congestion, and oedema can precipitate bronchospasm (‘cardiac asthma’).

     ‘Deep extubation’ (tracheal extubation while anesthesia is still sufficient to suppress hyperreactive airway reflexes) has been practised for many years, especially in children, but it has its own inherent hazards. It mandates full reversal of neuromuscular block. Even if tracheal extubation is smooth, emergence through the arousal stage can initiate severe bronchospasm with an unprotected airway. The risk of regurgitation and aspiration is ever-present. When it is deemed unwise to extubate the trachea before the patient is fully awake, suppressing airway reflexes and/or the risk of bronchospasm by administration of intravenous lidocaine or pretreatment with inhaled bronchodilators should be considered.


Regional anesthesia

      Instrumentation of the airways can elicit bronchospasm and life-threatening complications. Undoubtedly the use of regional anesthesia helps to avoid airway irritation. It is therefore not surprising that surgical procedures performed under spinal or epidural anesthesia are associated with fewer respiratory complications as compared to the same procedures under general anesthesia. The same can be expected for single nerve or plexus blockades. Because the phrenic nerve is part of the upper part of the brachial plexus, while performing brachial plexus blockade a decrease of at least 30% of vital capacity has to be expected.

     The use of high thoracic epidural anesthesia in patients with compromised respiratory function has raised two major concerns. First, the motor blockade associated with epidural anesthesia would not be tolerated by patients with an already compromised respiratory function. Second, the accompanying sympathetic blockade would lead to increased bronchial tone and reactivity. Even in patients with severe obstructive airway disease, high thoracic epidural anesthesia was used safely as the only anesthetic technique for partial or total mastectomies with axillary lymph node dissections, as shown by Groeben, et al. Vital capacity was reduced by not more than 10% and the procedure was well tolerated with no postoperative respiratory complications. Concerning bronchial reactivity, pulmonary sympathetic blockade with high thoracic epidural anesthesia does not increase reactivity, but the systemic effects of the local anesthetics even attenuates bronchial reactivity. Moreover, these beneficial effects are also effective in combined general and epidural anesthesia. The reasons cited for the above effect are earlier extubation of the patients, better analgesia during mobilization and coughing, and improved diaphragmatic function.

     Overall, the use of regional anesthesia as the main anesthetic technique or in combination with general anesthesia can be recommended in patients with respiratory compromise.


Intraop bronchospasm


  • Increase in airway pressure or “tight bag”

  • Up-slopping of capnogram tracing (ET CO2)

  • Drop in oxygen saturation (SPO2)

  • Wheeze/silent chest on auscultation

Differential diagnosis of intraoperative bronchospasm/“tight bag”:

  • Endobronchial intubation

  • Kinking of the tracheal tube

  • Prolapse of the endotracheal tube (ETT) cuff to obstruct tube

  • Eccentric cuff inflation, pushing the tube against the tracheal wall

  • Mucus plugging

  • Foreign body aspiration

  • High intraabdominal pressure 3⁄4 Pulmonary edema

  • Pneumothorax

  • Air-trapping (auto-PEEP).

Immediate action:

  • Increase FiO2 (fraction of inspired oxygen).

  • Increase concentration of volatile anesthetic agent. Sevoflurane is least irritant and is less likely to precipitate dysrhythmias in presence of hypercapnia (halothane is most likely to do so).

  • Light plane of anesthesia may be a trigger for bronchospasm. Hence ensure adequate neuro- muscular blockade/analgesia.

  • Short-acting β2-agonists may be administered as nebulisation.

  • Consider aminophylline infusion.(According to a metaanalysis of the Cochrane institute aminophylline and theophylline do not play a role in treatment of acute bronchospasm when compared to β2-adrenergic agonists).

Subsequent management:

  • Consider nebulization with anticholinergics (ipratropium bromide); injection ketamine (1-2 mg/kg);

  • Magnesium– 2 Gm IV over 20 minutes;

  • Subcutaneous injection of terbutaline 0.25 mg every 30 minutes.

  • IV Hydrocortisone bolus dose.

  • Check the drug chart and notes for possible drug allergies to agents already administered.

  • Chest X-ray–To rule out pneumothorax and to check ETT tip position (withdraw, if carinal position).

  • Arterial blood gas analysis.

  • Check serum electrolytes – Prolonged nebulization with β2- agonists can lead to hypokalemia. 

  • If the bronchospasm is refractory, refer to ICU for further management.


Postop management

The keys to minimizing postoperative pulmonary complications are:

  • Vigilance for bronchospasm and its causes

  • Bronchodilator therapy

  • Good pain control, be it by the neuraxial route or patient- controlled analgesia (PCA)

  • Incentive spirometry, deep breathing exercises, and early mobilization

  • Control of gastroesophageal reflux is beneficial in asthma

  • Noninvasive positive pressure ventilation is an option in some asthmatics who have persistent bronchospasm after

tracheal extubation.

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