Upper Respiratory Infection
Upper respiratory infection (URI) is common in children presenting for anesthesia and the most common infection overall in children. The average child will have 6 to 8 URIs per year. Thus, it is important to understand the pathogenesis, clinical features, risk stratification, and anesthetic management of children with a URI.
URIs are almost always viral. Rhinoviruses are the most common, but influenza, parainfluenza, respiratory syncytial virus (RSV), adenovirus, and coronavirus are also seen. Although the specific virus can be identified by laboratory testing, this is rarely performed.
Viral transmission most commonly occurs via mucosal contact from hands contaminated with infectious material, inhalation of airborne particles, or droplet contact with mucosa (e.g., sneezing). For this reason, patients with a URI will likely be on both contact and droplet type precautions when hospitalized, mainly to protect staff. Symptoms are caused by the child’s immune response to the virus. For example, the influx of polymorphonuclear (PMN) cells in response to cytokine signals results in increased nasal secretions.
The symptoms of a URI vary based on the age of the patient and the specific virus. Most commonly, patients will present with nasal congestion, rhinorrhea, cough, and sneezing. Fever is less common (reported in approximately 15% of cases) and, if persistent, may be the sign of a bacterial infection such as otitis media, Streptococcal tonsillitis, or pneumonia. The color of nasal secretions is not indicative of severity of infection; rather, color is dictated by the number and activity of the PMN cells in the immune response.
A current or recent URI increases the risk for a perioperative respiratory adverse event (PRAE). These events range from benign coughing to serious laryngospasm, bronchospasm, or hypoxia that results in the need for escalation of care. Some clues to the risks of URI can be gleaned by the results of a 2010 study in over 9000 patients. A positive respiratory history (nocturnal dry cough, wheezing during exercise, wheezing more than three times in the past 12 months, or a history of present or past eczema) in a child with a URI was associated with an increased risk for intraoperative bronchospasm, laryngospasm, and perioperative cough, desaturation, or airway obstruction. In addition, a history of at least two family members having asthma, atopy, or smoking increased the risk for PRAEs.
The risk for a PRAE decreases with time after initial infection, although controversy exists about the duration of time required for reduction of risk (ranging from 2 to 6 weeks). Because of this uncertainty, there is also no consensus when to schedule elective surgery after an acute URI. In a 1979 publication that described the development of lower respiratory symptoms during general anesthesia in children with a URI, McGill and colleagues from National Children’s Hospital wrote: “the optimal period of recovery from the URI that should be allowed before considering the patient a candidate for an elective surgical procedure has not been defined.” More than 40 years later, this is still true. Subclinical pathology, such as airway edema, atelectasis, and bronchial reactivity may remain for up to several weeks after the symptoms of the acute URI have resolved, depending on the specific type of viral agent. Three to 4 weeks seems to be a reasonable waiting time, but for many children this merely represents the period between successive infections.
With these possible complications in mind, when a child presents with a URI, it is intuitive that an elective procedure requiring general anesthesia should be canceled. But, because so many children have a concurrent URI at the time of their scheduled surgery and long-term negative outcomes have not been demonstrated, this decision process is complex. How should the anesthesia provider decide when to cancel an elective procedure in a child with a URI? First, one should assess the severity of the child’s illness. The child with a runny nose without additional findings may be suffering from vasomotor or allergic rhinitis, which is usually not associated with perioperative airway complications. If it is likely that the illness is viral, one must then identify the factors that increase perioperative complications. These include the following:
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Significant coexisting medical disease (especially cardiac, pulmonary, or neuromuscular disease)
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History of prematurity
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Lower respiratory tract signs (e.g., wheezing, rales)
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High fever (>102 °F)
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Productive cough
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Major airway, abdominal, or thoracic surgery
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Parent is worried about proceeding
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Surgeon is worried about proceeding (That’ll be the day!)
If any of these risk factors are present, it may be prudent to perform the procedure when the child is in better health.
On the other hand, there are a variety of additional factors that may influence your decision to proceed with surgery. The most common reason for proceeding with a case even though risk factors are present is the presence of a URI that will likely continue without surgical intervention. This occurs when children require adenoidectomy or myringotomy to relieve chronic middle ear fluid collections. Nonmedical factors that might sway you to proceed with the case are logistical family concerns, such as the parents taking a day off from work, difficulty obtaining day care, traveling a long distance at a great inconvenience, and so forth. Because outcomes are not proven to be worse after surgery in children with a URI, these factors may play a role in the decision of whether or not to proceed. Most children who present with a URI have neither extremely mild symptoms nor severe symptoms. For these in-between children we must use our judgment to determine the proper course of action based on what we believe is best for the child.
Racial identity may influence risk. In a 2018 publication from the University of Texas, African American children were shown to have significantly higher odds of PRAEs compared with a Caucasian group.
For urgent or emergent procedures, a discussion with the patient and family about the risk for PRAEs is prudent. In these situations, surgery will often need to proceed because of the risk for delaying. To optimize the patient preoperatively, additional treatments can be considered including:
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Inhaled beta agonist therapy (e.g., albuterol) is useful in patients with a history of asthma, although may also be of benefit to those with no prior diagnosis who present with wheezing secondary to a URI.
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Anticholinergics (e.g., glycopyrrolate) can be given to dry secretions but their use has not been proven effective.
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Steroids are rarely beneficial for a simple URI, except when the patient is presenting with a concomitant asthma exacerbation.
The risk for a PRAE can be approximately determined by clues from the preoperative evaluation. A history of fever, increased work of breathing, productive cough, wheeze, shortness of breath, copious secretions, or lethargy are important symptoms that may increase risk. Passive exposure to cigarette smoke and a history of atopy are additional risk factors. On physical exam, a toxic appearance or abnormal lung sounds, such as wheezing or rales, are also important predictors of increased risk. Additional evaluation with imaging or laboratory information is rarely needed.
Anesthetic management of the child with an active URI should be tailored to minimize airway irritability. Administration of a neuromuscular blocker to facilitate tracheal intubation will prevent laryngospasm. Humidification of airway gases may prevent the thickening of secretions that is commonly encountered in these children. Some authors suggest administration of an anticholinergic agent, such as atropine or glycopyrrolate, to attenuate vagally mediated airway complications; however, this remains untested.
The anesthesiologist should also carefully consider the appropriate type of airway management based on the patient’s history and the surgical procedure. When possible, airway instrumentation and placement of an endotracheal tube should be avoided as multiple studies have shown an increased risk for PRAEs (bronchospasm, desaturation, cough, and breath holding) in these patients. A natural airway or use of a laryngeal mask airway may decrease risk, but even LMA placement may be associated with complications in children with a URI. Ventilation should be carefully tailored with judicious positive end–expiratory pressure (PEEP) to avoid the development of atelectasis. Anesthesia providers should expect PRAEs such as bronchospasm or laryngospasm and be prepared to treat these immediately.
In infants and children with a URI, apneic oxygenation is less effective; thus, oxyhemoglobin desaturation may occur faster than usual during rapid sequence induction when the child may not be receiving positive-pressure ventilation.
Postoperatively, the majority of patients with a URI will have an uneventful recovery without need for additional respiratory management. Patients with underlying pulmonary or cardiac comorbidities, however, are at higher risk for PRAEs.
Transient postoperative hypoxemia, postintubation croup, and postoperative pneumonia are probably more likely to occur in children with a URI. Long-term complications and true outcomes are difficult to define and quantify and may not differ between normal children and those with a current or recent URI.
Asthma
Asthma, or reactive airway disease, is an acute-on-chronic inflammatory disease of both larger and smaller airways. With a prevalence of 8%, it is the most common chronic illness in children in the United States and in other resource-rich countries and is concentrated in urban geographic areas that have a predominantly African American or Hispanic population. There is a strong genetic component and a correlation to other allergic-type conditions such as seasonal allergies and eczema. The majority of children present early in life (80% by age 5), although the presentation is often earlier and more severe in children with underlying pulmonary conditions such as bronchopulmonary dysplasia or respiratory syncytial virus infection.
The pathophysiology of asthma consists of the classic triad of bronchial hyperreactivity, inflammation, and mucous secretion. Triggers such as inhaled allergens (e.g., dust, pet dander, pollen, etc.), viruses, smoke, exercise, or even administration of nonsteroidal antiinflammatory drugs (NSAIDs) result in activation of an immunoglobulin E-mediated and nonimmunologic response in the airway. Specifically, mast cells located in the airway mucosa release mediators such as histamine, tryptase, leukotrienes, and prostaglandins that result in contraction of airway smooth muscle (i.e., bronchoconstriction). These mediators also result in the hypersecretion of mucous, infiltration of inflammatory cells, and airway edema. Because of the continued immune response with the infiltration of more and more inflammatory cells, the airway remains hyperreactive. In addition to the immune response, the parasympathetic nervous system also plays a role in maintaining airway tone; when activated because of histamine release or other stimuli such as inhaled cold air or airway instrumentation, increased parasympathetic output via the vagus nerve results in an intracellular signaling cascade and ultimately, bronchoconstriction. Depending on the type and duration of exposure to the trigger, and the patient’s immune and parasympathetic responses, exacerbations of asthma can last for hours or days, some resolving spontaneously whereas others require aggressive medical therapy.
Clinically, patients with asthma classically present with wheeze because of the narrowing of their airways from dynamic bronchoconstriction. Children may also demonstrate a persistent cough (often worse at night) and dyspnea on exertion. During an acute exacerbation, marked respiratory distress occurs, which may include chest wall retractions and a prolonged expiratory phase secondary to lower airway obstruction. The degree of audible wheeze, which is directly related to the amount of airflow in the airways, can fluctuate during an acute exacerbation. As the severity of an asthma exacerbation worsens and bronchoconstriction increases, the degree of audible wheeze may first increase because of airway narrowing but ultimately can decrease as the severity of bronchospasm results in lack of air flow. Thus, lack of wheeze can actually be a sign of impending respiratory failure.
The treatment of children with asthma targets the underlying pathophysiology, specifically bronchoconstriction and the hyperactive airway immune response. For patients with known triggers such as allergens and irritants, avoidance is key. Further chronic treatments are stratified based of the frequency of symptoms ( Table 4.1 ) and the type of treatment used ( Table 4.2 ).
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