NMBAs can cause anaphylaxis via both IgE-mediated and non-immunologic direct mast cell activation. The most implicated agents include atracurium, pancuronium, rocuronium, succinylcholine, and vecuronium. The ammonium ion of NMBAs is the main allergenic determinant. Anaphylaxis is more common with rocuronium and succinylcholine than with others. Suggamadex, a reversal agent for steroidal NMBAs (such as rocuronium) also causes anaphylaxis; cross activity exists among NMBAs.

Antibiotics are often used to prevent wound infections during surgery, and were responsible for 12–15% of identifiable triggers in European studies. But, it accounts for 50% of IgE-mediated reactions and is the most common cause of perioperative anaphylaxis in the United States. β(beta)-lactam antibiotics (including penicillins and cepholosporins and vancomycin) are the most common triggers. Βeta-lactam antibiotics cause IgE-mediated anaphylaxis while vancomycin causes a reaction secondary to direct histamine release from mast cells.

Latex anaphylaxis in the United States is less common since the introduction of latex-free products in surgical suites. However, occult exposure to natural rubber latex still accounts for a significant number of perioperative anaphylaxis. The latex allergy is an IgE-mediated process resulting from formation of a specific IgE against the protein in the natural rubber latex. The common latex resources are gloves, drains, and catheters. Latex allergy is likely to occur more often in patients with repeated exposure to latex gloves, or catheters from prior surgery or from occupational use, in patients with spina bifida, and in healthcare workers. Reactions to latex usually occur later in the surgical procedure, generally 30 min or more after the start of intervention.

Risk factors for perioperative anaphylaxis include the female sex, past history of anaphylaxis, allergic drug reactions, allergic conditions such as eczema or hay fever, multiple past surgeries and procedures, and mast cell disorders. Patients with asthma are at a greater risk for perioperative anaphylaxis.

The overall incidence is under 1% in both adults and pediatric patients, but laryngospasm occurs twice as often in pediatric patients between birth and 9 years old, while 3 times as often during the newborn to 3-month-old age. However, much higher incidence of laryngospasm (9%) is reported in pediatric patients with history of respiratory problems.

Glottic closure is a protective airway reflex that exists to prevent aspiration. A laryngospasm is an abnormal reflex that persists for a longer period. It is normally triggered by peri-glottic stimuli, mediated via the vagus nerve. Sensory fibers from the laryngeal mechanical, chemical, and thermal receptors ascend via the vagus nerve and via the internal branch of the superior laryngeal nerve (SLN). The motor response is mediated by the recurrent laryngeal nerve via the 3 intrinsic laryngeal muscles consisting of the lateral cricoarytenoids, thyroarytenoids, and cricoarytenoids. Glottis closure occurs by ether true vocal cord adduction alone or in combination of the false vocal cords. The supraglottic soft tissues are thought to impact the glottis as they are pulled down by an increasing translaryngeal pressure gradient during obstructed inspiratory effort.

A laryngospasm must be considered if there is airway obstruction during anesthesia that was not relieved by basic airway maneuvers. Common signs of laryngospasm include inspiratory stridor, increased respiratory efforts, tracheal tug, desaturation with or without bradycardia, and airway obstruction that was not relieved by an upper airway device. Differential diagnoses are breath holding, bronchospasm, and pulmonary aspiration.

Prevention of laryngospasm:

Once a laryngospasm is recognized, prompt therapy should be initiated and help may be called.

Treatment of laryngospasm:

General anesthesia and anesthetics inhibit protective airway reflexes, including apnea with laryngospasm, coughing, expiration, and spasmodic panting that protects lungs from aspiration. Lower esophageal sphincter (LES) tone and barrier pressure are likely reduced under inhalational and propofol anesthesia. The upper esophageal sphincter (UES) of the cricopharyngeal muscle is reduced by most anesthetics, except ketamine. The depression of protective airway reflexes, in combination with reduction in LES and UES tone, make anesthetized patients prone to aspiration. Aspiration occurs once gastric contents (liquid or particulate matter, et al.) enter into the tracheobronchial tree as a consequence of passive regurgitation or active vomiting. Depending on the composite of aspirates, patients can experience different clinical consequences: (1) acid-associated aspiration pneumonitis, (2) bacterial infection, and (3) particle-associated aspiration.

Aspiration results in parenchymal damage in two phases. The first phase is marked by direct toxic damage to respiratory epithelium by acid. The second phase is marked by an acute inflammatory response. Aspiration of gastric acid induces a chemical burn, triggering the release of various inflammatory mediators such as cytokines, chemokines, and adhesion molecules. These mediators cause inflammatory response and attract neutrophils and alveolar macrophages to activate leukocytes.

Factors that increase the risk of perioperative pulmonary aspiration are as follows:

Visible gastric contents in the oropharynx always warrant suspicions of aspiration. Clinical manifestation of aspiration pneumonitis could be both asymptomatic and symptomatic. Aspiration of at least 0.4 ml/kg in volume and pH of contents of <2.5 is required to produce symptoms. Classic symptoms associated with pulmonary aspiration include sudden onset of wheezing, shortness of breath (in awake patients), bronchospasm, desaturation, cyanosis, and tachycardia. The severity of bronchitis may relate to the pH and volume of the aspirated content, however, the presence of particles is most important. A chest X-ray (CXR) may be useful in diagnosing aspiration pneumonitis. However, CXR can be normal in patients with uncomplicated clinical cases. In one-third of aspiration cases, the initial CXR does not represent the full extent of lung involvement. Both the right and left lung can be affected; however, occurrence in the lower lobes is more common. CXR can show infiltrates as small, irregular opacities, confluent opacities, acinar opacities, or mixed patterns [29].

Prevention is the key to reduce morbidity and mortality of aspiration pneumonitis.