Intraoperative wheezing: Etiology and treatment

Published on 07/02/2015 by admin

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Last modified 22/04/2025

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Intraoperative wheezing: Etiology and treatment

Mary M. Rajala, MS, MD

Wheezing or rhonchi, lung sounds detected by auscultation, are produced when gas flows through a narrowed or obstructed upper or lower airway. The lung sounds are caused by turbulence or resistance to flow. The obstruction can be extrinsic to the airway, intrinsic (within the airway wall), or within the lumen (Box 154-1). For a patient who is intubated and ventilated, an increase in peak airway pressure, a decrease in tidal volume, or a decrease in the slope of the expiratory CO₂ curve may indicate airway narrowing or increased airway resistance. Persistent and severe airway obstruction may be followed by O₂ desaturation, hypercapnia, and hypotension secondary to increased intrathoracic pressure. Most (80%) of the resistance to flow in airways occurs in the large central airways, leaving 20% of airway resistance from the peripheral bronchioles. Thus, large changes in the caliber of small airways may result in small changes in resistance, making the small airways a clinically silent area. In the American Society of Anesthesiologists closed claims analysis, respiratory events that lead to death or permanent brain damage, 56 (11%) were associated with bronchospasm.

Reversible and irreversible airway disease

Wheezing may indicate the presence of obstructive lung disease—asthma, chronic obstructive pulmonary disease, chronic bronchitis, or cystic fibrosis. Asthma, a reactive airway disease, is manifest by reversible airway obstruction. Resting bronchial tone is regulated primarily by the parasympathetic nervous system via vagal nerve fibers and muscarinic acetylcholine receptors, of which 3 types exist, M₁ and M₃, which enhance the parasympathetic effects, and M₂, which is inhibitory. Numerous factors—including exercise, cold air, allergens, respiratory infections, emotional factors, β-adrenergic blockade, and the use of a prostaglandin inhibitor, such as aspirin—may override the baseline bronchial tone, provoking an attack in patients with bronchospastic disease. Cross-sensitivity between aspirin and other nonsteroidal antiinflammatory drugs is common and needs to be considered as a cause for bronchospasm, especially in patients with the triad of asthma, nasal polyps, and aspirin-induced asthma. The immunologic component to asthma is well recognized and includes immunoglobulin-E antibody fixed to mast cells and basophils, which release immune mediators in response to challenge with specific antigens. In adults, irritant reflexes are a more important cause, whereas, in children, allergy is an important component in reactive airway disease. The immune mediators include serotonin, eicosanoids, prostaglandins (PGD₂, PGF₂), thromboxane A₂ and leukotrienes (LTC₄, LTD₄, LTE₄), kinin, and perhaps histamine (H₁). Prostaglandins are produced from arachidonic acid by the cyclooxygenase pathway and are potent mast-cell mediators that cause bronchospasm. Leukotrienes are synthesized after mast-cell activation from the metabolism of arachidonic acid via the lipooxygenase pathway. Kinin, produced by mast cells and basophils, can cause bronchoconstriction. In addition, thromboxane A₂, and its metabolite B₂, produced in polymorphonuclear leukocytes and mast cells by the action of cyclooxygenase on arachidonic acid, also constrict pulmonary blood vessels and can lead to pulmonary hypertension.

Perioperative bronchospasm

Airway manipulation

Manipulation of the airway can cause reflex bronchoconstriction. Wheezing can be a sign of airway irritation from stimulation of the cholinergic system and subsequent bronchiolar constriction, which occurs when intubation is undertaken in a hyperreflexic airway or if the depth of anesthesia is inadequate at the time of intubation.

Anesthesia and associated drugs

The use of either propofol or ketamine offers advantages in patients with a history of bronchospasm. Propofol reduces airway resistance in patients with asthma and chronic obstructive disease. Ketamine helps protect against irritant reflexes, although it increases secretions from salivary and tracheobronchial mucus glands (which can be prevented pharmacologically). Ketamine also stimulates the sympathetic system and attenuates vagal reflexes, leading to smooth muscle relaxation. The newer S-stereoisomer form of ketamine has fewer psychomimetic effects but is also less effective in relaxing smooth muscles. The use of methohexital is associated with wheezing if other drugs are not used to blunt the effect or if adequate depth of anesthesia is not achieved before airway manipulation.

Inhalation anesthetic agents can be used to deepen the level of anesthesia prior to airway manipulation or surgical stimulation or when bronchospasm is mild. In true bronchospasm, the administration of inhalation anesthetic agents will depress airway reactivity and bronchoconstriction by blunting parasympathetic constrictive reflexes and directly relaxing bronchiolar smooth muscle.

Histamine release may occur with administration of anesthetic drugs, including atracurium, cis-atracurium meperidine, and morphine. When administered rapidly or in large doses (as occurs during induction and subsequent airway manipulation), these drugs are more likely to increase the risk of bronchoconstriction. The muscarinic action of cholinesterase inhibitors used for reversal of an anesthetic agent may precipitate bronchospasm. In these situations, prudence suggests using larger than usual doses of atropine (>1.0 mg), or glycopyrrolate (>0.5 mg) to minimize potential bronchospasm in patients who are actively wheezing.

The use of β₂-adrenergic receptor antagonists (labetolol, esmolol) may increase the risk of bronchoconstriction. Although they have been used without untoward effect in the treatment of hypertension in patients with stable chronic obstructive pulmonary disease, the American College of Chest Physicians recommends that these agents be used with extreme caution if at all in patients with reactive airways diseases.

Anaphylactic reactions

Bronchospasm may result from an anaphylactic or anaphylactoid reaction. Antibiotic drugs, blood products, or intravenously administered contrast agents may be the trigger, with an initial manifestation of wheezing accompanied by hypotension, periorbital and airway edema, urticaria, tachycardia, and arrhythmias.

Carcinoid syndrome

Rarely, carcinoid tumors may cause bronchospasm. Serotonin (5-hydroxytryptamine [5-HT]) secreted by carcinoid tumors causes bronchoconstriction, which can accompany the hypotension, diarrhea, flushing, and valvular heart disease of carcinoid syndrome. Conventional treatment for bronchospasm is not helpful and may actually provoke bronchospasm in these patients. Therefore, most recommendations are targeted toward preventing release of tumor substances. Anesthetic care involves avoiding histamine-releasing agents (morphine, atracurium), succinylcholine, indirect-acting or direct-acting catecholamines, and extremes of blood pressure to decrease the release of 5-HT from carcinoid tumors. Succinylcholine is thought to provoke release by increasing abdominal pressure and compressing the tumor, and not by intrinsic releasing properties. In addition to avoiding or treating bronchospasm, the anesthesia provider must be ready to intraoperatively deal with decreased peripheral resistance, hypotension, and hypertension in patients with carcinoid tumors. Somatostatin analog (Sandostatin) (100 μg – 600 μg, intravenously) should be administered prophylactically and, if a crisis occurs, rebolused. In addition to blocking the release of pituitary growth hormone and thyrotropin, somatostatin analog, which reduces hormone and exocrine secretions from the gut, has become the therapy of choice for preoperative, intraoperative, and postoperative management of carcinoid crises.

Miscellaneous pulmonary diseases

Aspiration pneumonitis, pulmonary edema, or pneumothorax may also trigger bronchospasm.

Treating perioperative bronchospasm

Preoperative/prevention

Patients with reversible airway obstruction or bronchial reactivity are at increased risk of developing bronchospasm. A history of recent upper respiratory infection (within 3 weeks, especially in patients with obstructive airway disease), recent smoking, cough, dyspnea, fever, chronic bronchitis, asthma, or intolerance to cold air, dust, or smoke and prior tolerance of general anesthesia with tracheal intubation are all pertinent in predicting intra operative wheezing. Management should be aimed at identifying these patients through preoperative evaluation and treating them with β₂-adrenergic receptor agonists or inhaled or orally administered corticosteroids. Consideration should be given to using a regional anesthetic technique. Because bronchospasm in children is more frequently due to allergens, the use of mediator inhibitors and anti inflammatory medications is important in prevention. In adults, reducing or reversing irritant reflexes should be the goal. Adequate anxiolysis plays a role in prevention. Treatment should be directed toward the cause of bronchospasm. Antimuscarinic drugs—such as atropine, ipratropium, and glycopyrrolate—have been used to treat bronchoconstriction. However, they are nonselective and, at low doses, may block the beneficial effects of M₂ more than M₁ and M₃, thereby worsening bronchoconstriction. At higher doses, antimuscarinic drugs block all three receptors, resulting in bronchodilation. Anesthetic depth should be adequate prior to intubation or airway manipulation. Lidocaine (1-2 mg/kg), administered topically through a tracheal tube or intravenously (1-3 min prior to intubation), is effective in preventing bronchoconstriction during airway manipulation or in treating acute intraoperative bronchoconstriction.

Intraoperative bronchospasm—crisis management

When intraoperative bronchospasm occurs and causes O₂ desaturation or inadequate ventilation, the following must occur almost simultaneously: administer 100% O₂, deepen anesthesia, cease stimulation or surgery, and immediately call for help. Next, remove the patient’s breathing system from the ventilator, hand ventilate, and listen for breath sounds over the chest and central epigastrium. These actions will exclude anesthesia machine and ventilator malfunction as potential causes and help exclude esophageal or bronchial intubation as the cause of desaturation or inadequate ventilation and will allow for assessment of airway resistance. If, while passing a suction catheter down the tracheal tube, the anesthesia provider encounters an obstruction or is able to aspirate secretions (analyzing pH to assess for gastric contents), the tracheal tube may be misplaced, kinked, or blocked. A β₂-adrenergic receptor agonist (e.g., 4-8 puffs of albuterol initially followed by 2 puffs every 10 min) should be administered via the tracheal tube, timed with patient inhalation, through a connector into the tracheal tube. Ipratropium (6 puffs, followed by 2 puffs every 10 min) can also be given in this manner. Once the initial assessment has been completed, corticosteroids (e.g., methylprednisolone 1-2 mg/kg) can be given.

For bronchospasm that does not resolve, an intravenously administered bronchodilator may need to be added to the regimen (e.g., magnesium, 2-4 mg; lidocaine, 1.5-2 mg/kg; or epinephrine, 0.1μg/kg bolus followed by 10-25 μg·kg⁻¹·min⁻¹ titrated to vital signs and response). Changing from an anesthesia machine ventilator to a higher performance intensive care unit ventilator and stopping the operation as quickly as possible may be necessary. The administration of inhalation anesthetic agents increases anesthetic depth, but doing so may be difficult in patients with acute bronchospasm because of ventilation/perfusion mismatch. Aminophylline and theophylline have less of a role in treating acute bronchospasm, as compared with β₂-adrenergic receptor agonists.

Postoperative management of a patient with intraoperative bronchospasm

Extubating a wheezing patient who is under deep anesthesia is not typically safe. Although deep extubation will likely reduce bronchospasm, it exposes the patient to residual anesthetic effects, including ventilation/perfusion mismatch, hypercapnia, narcosis, and aspiration of gastric contents.

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