Pediatric Anesthesia 2005

15: 446–454

doi:10.1111/j.1460-9592.2005.01602.x

Review article

Anesthesia and the child with asthma G A R Y M . D O H E R T Y M B B C h * †, A N T H O N Y C H I S A K U T A M B B C h †, P E T ER C R E A N M B B C h † A N D M I C H A E L D . S H I E L D S M D *† *Department of Child Health, Queen’s University Belfast and †Royal Belfast Hospital for Sick Children, Belfast, UK

Keywords: Anesthesia; asthma; pathophysiology; treatment

Introduction Aim The rising prevalence of asthma in childhood means that anesthetists are encountering children with this disorder scheduled for surgery with increasing frequency (1–3). The increase in the volume of daycase surgery has limited the time available for the assessment of both the child’s medical condition and possible anesthetic risk (4). However, adverse events during anesthesia of children with asthma are fortunately rare (5). Nonetheless, the potential remains for routine anesthesia to become complicated or even dangerous. In this article, the literature relevant to the child with asthma and progress through preoperative, operative, and postoperative care is reviewed.

Pathophysiology of childhood wheeze Although there is an increased understanding of the pathology associated with asthma, this condition remains difficult to define as the fundamental factors determining the development of asthma remain unknown. The increasing prevalence of asthma symptoms throughout the second-half of the last century has possibly slowed or peaked (3,6). However, up to 30% of young teenagers in the UK still report asthmatic symptoms in the past year (6,7). Correspondence to: Dr G. M. Doherty, Department of Child Health, Institute of Clinical Science, Queen’s University Belfast, Grosvenor Road, Belfast BT12 6BJ, UK (email: [email protected] or [email protected]).

446

Genetic predisposition, atopy, prenatal, and earlylife environment and the influence of chronic airway inflammation on a susceptible airway all appear to influence the development of asthma. The association between atopy and asthma is particularly strong. Atopy is the tendency towards immunoglobin-E (IgE) mediated-hypersensitivity and is implicated in several disease processes including allergy, allergic rhinitis, and atopic dermatitis. It has been recognized for a long time, however, that many children who wheeze, especially young children, do not have atopic asthma. Several large cohort studies have helped to define the different characteristics of these groups of children, and have suggested differing pathologies (8,9). In particular, the Tucson Children’s Respiratory Study has clarified the distinction between ‘wheezy bronchitis’ and asthma with the suggestion that children who wheeze can be classified as transient wheezers, nonatopic wheezers, and atopic wheezers (10–12). Transient wheezers are characterized by reduced lung function in infancy. They wheeze in response to viral infections, possibly reflecting reduced airway caliber. Their symptoms resolve after the first few years of life. Nonatopic wheezers are children who wheeze beyond the first few years of life, often in response to viral infections, but persistence of wheeze is less likely than in atopic wheeze. Atopic wheezers are the classical asthmatics. Early atopic wheezers are most at risk from severe, persistent symptoms. The relevance of this distinction to the anesthetist is unclear. It is probably wise to assume  2005 Blackwell Publishing Ltd

A N E S T H ES I A A N D A S T H M A

that any child with a history of reactive airways disease is at increased risk of perioperative bronchospasm. In addition, children with atopy have increased risk of severe allergic reactions. Inflammation of the airways is the hallmark of asthma. This inflammation is typically eosinophilic (13), although neutrophilic inflammation may be seen in severe asthma or acute exacerbations (14,15). The inflamed airway is hyperresponsive to irritant stimuli with subsequent bronchospasm and mucus secretion. The general anti-inflammatory effect of inhaled or systemic corticosteroids has proven the most effective maintenance therapy for asthma to date. Other characteristic changes occur in the airways of asthmatic children. These changes are grouped together as remodeling and include goblet cell hyperplasia, thickening of the basement membrane underlying the epithelium, and thickening of the smooth muscle layer. Remodeling was previously thought to be a consequence of long-standing unresolved airway inflammation. However, recent evidence shows these changes early in the course of the disease (16,17). Remodeling may proceed concomitantly with inflammation. Remodeling influences the anatomy and function of the airway. It has been linked to both irreversible airway obstruction and increased bronchial hyperreactivity (18,19).

Preoperative assessment Diagnosis. Asthma in childhood is a notoriously difficult condition to diagnose with confidence – ‘there is no confirmatory diagnostic blood test, radiographic or histopathological investigation’ (20). It is characterized by variable and intermittent airflow obstruction. In children this is manifest most frequently as wheeze and cough. Older children may complain of shortness of breath, or chest tightness or discomfort. Is the child with a history of airway symptoms likely to have asthma or some other pathology? Some features are uncharacteristic of asthma. Unremitting wheeze or stridor is suggestive of a fixed obstruction. A dry nonproductive cough is often seen in asthma, but a persistent wet, productive cough is suggestive of suppurative lung disease (cystic fibrosis, primary ciliary dyskinesia, immuno 2005 Blackwell Publishing Ltd, Pediatric Anesthesia, 15, 446–454

4 47

deficiency, following infection, etc.). Asthma may present as cough without wheeze. However, this is often a postviral bronchitis. There is evidence that asthma may be overdiagnosed in these circumstances (21,22). Tracheo- or bronchomalacia often produce intermittent wheeze that can be difficult to distinguish from asthma. However, symptoms are often present from birth, which is rarely the case with asthma. Assessment. In children with asthma, it is important to establish both how severe their disease is and how well controlled it is currently. The two aspects are closely linked. Mild asthma, which is poorly controlled, may appear severe in terms of frequent and persistent symptoms. In contrast, a child with severe asthma may currently have well-controlled symptoms but require high doses of inhaled corticosteroids to maintain control. Poorly controlled asthma is defined by various features such as the frequency of symptoms and use of reliever medication. Frequent emergency attendances, hospital admissions or use of oral steroids also indicate inadequate control. Both the British Thoracic Society (BTS) and the National Heart, Lung and Blood Institute define the severity of asthma in a step-wise fashion depending on the amount of treatment required to control symptoms (20,23). The five steps of the BTS guidelines equate to the number and sequence of treatments required for symptom control (Table 1) (20). The first step requires occasional use of short-acting b2-agonists, with the second step being the addition of inhaled steroids at up to 400 lg of beclomethasone diproprionate (BDP) or equivalent per day. The third step is the addition of a third therapy such as a long acting b2-agonist (LABA) or leukotriene-receptor antagonist (LTRA). The addition of another drug may obviate the need for an increase in inhaled steroids. The fourth step of the BTS guidelines suggests a cautious increase of inhaled steroids to a maximum of 800 lg BDP per day, with addition of a fourth drug if required. The final step may be the introduction of oral steroids, high-dose inhaled steroids (>1000 lg BDP per day) or other systemic steroid-sparing agents. Most children will be on the first two steps of this treatment protocol. Anesthetists will naturally be very cautious when anesthetizing children on steps four or five.

4 48

G .M . D O H E R T Y ET AL .

Table 1 Medications for the treatment of chronic asthma in children aged 5–12 years (following the BTS Guidelines) (20) Step

Steroids

1 2 3

None Up to 400 lgÆday)1 BDP Up to 400 lgÆday)1 BDP

4 5

Up to 800 lgÆday)1 BDP High dose BDP (‡800 lgÆday)1) plus oral steroids

Add-on therapy Inhaled b2-agonists (e.g. salbutamol 100–200 lg PRN) LABA [e.g. salmeterol 50 lg bd (‡ 4 years), formoterol 12 lg bd (‡6 years)] LTRA [e.g. Montelukast 4 mg nocte (2–5 years), 5 mg nocte (6–14 years)] LABA/LTRA/aminophylline Additional therapy as required to reduce steroid dose. Lowest oral steroid dose to control symptoms.

BTS, British Thoracic Society; BDP, beclomethasone diproprionate; LABA, long-acting b2-agonist; LTRA, leukotriene-receptor antagonist;

Difficult asthma is defined as asthma which is poorly controlled in spite of apparently taking highdose inhaled steroids (‡800 lg BDP equivalent per day, or steps four or five) (24). Although some children do have asthma which is poorly responsive to steroids, the most common reasons for ‘difficult asthma’ are poor compliance with treatment, inadequate inhaler technique or an incorrect diagnosis of asthma (25). In addition, a small group of children have life-threatening asthma. These children may have poorly controlled asthma, or ‘brittle’ asthma with sudden onset of asphyxiating or anaphylactictype asthmatic attacks. A previous history of severe or life-threatening exacerbations, especially if requiring intensive care, is indicative of a particularly vulnerable group of children. Sudden asphyxiating asthma may also be precipitated by nonsteroidal analgesics or irritant gases (both used in anesthesia) (26). Investigations. Objective testing is not diagnostic but can support a clinical diagnosis. Most tests have a reasonable positive predictive value but a poor negative predictive value. Some tests may also help in assessing current control or severity of airways inflammation. 1. Imaging. A chest radiograph is rarely useful unless a condition other than asthma is felt to be present or if a pneumothorax is suspected in an acute exacerbation. Similarly, computed tomography (CT) scanning may demonstrate bronchomalacia or bronchial wall thickening in chronic asthma (27,28), and areas of atelectasis in acute asthma (29). However, it is useful only in research or if excluding other pathology in difficult asthma (30). 2. Pulmonary function tests. Pulmonary function testing may detect airway obstruction or hyperreactivity. Diurnal variation in peak expiratory flow

(PEF) may indicate poor control of asthma. PEF is also useful in assessing the severity of an acute exacerbation. However, it is likely to be of limited use in assessing asthma prior to surgery. Reductions in PEF are likely to be accompanied by reported symptoms or clinical signs. Artificially high values may be obtained in children with asthma who have learned to produce a ‘blasting’ maneuver using the cheek muscles. Peak expiratory flow measures large airway function. Forced expiratory volume in 1 s (FEV1) is a better measure of obstruction and may be reduced at baseline in poorly controlled asthma; or in response to irritant stimuli such as exercise or methacholine. A methacholine challenge is usually impractical to perform in young children. Reversible airways obstruction may be demonstrated by increases in PEF or FEV1 following inhaled bronchodilator. 3. Inflammatory markers. Evidence of inflammation to help diagnose or monitor asthma has been sought in blood, urine, and exhaled air. These remain largely research tools. Peripheral blood eosinophilia is a simple measure which is approximately related to the severity of asthma (31). Other serum markers such as eosinophilic cationic protein bear some relation (32–34). Urinary leukotrienes and eosinophil-derived protein X (EPX) have been used in a research setting as a surrogate for airway inflammation (35,36). Currently, the only direct noninvasive measurements of airway inflammation detect byproducts of inflammation in exhaled air such as exhaled nitric oxide (ENO) or hydrogen peroxide. ENO is a sensitive marker of airway inflammation in children even in the absence of symptoms, but requires expertise for its measurement and interpretation (37–40). It can also be rapidly affected by steroid therapy and possibly by other drugs (41,42).  2005 Blackwell Publishing Ltd, Pediatric Anesthesia, 15, 446–454

A N E S T H ES I A A N D A S T H M A

Measures of atopy include total serum IgE levels, antigen-specific IgE levels (RAST) and skin prick testing (SPT). None are likely to be useful in determining the likelihood of bronchospasm, but RAST and SPT may be useful in investigating potential allergies (such as latex). However, SPT carries a small risk of anaphylaxis and should be carried out in the proper environment. Preoperative arrangements. In addition to the concerns about lung function and bronchospasm in children with asthma undergoing anesthesia, the anesthetist must be aware of other associated problems. In particular, atopic asthmatics are prone to allergic reactions and may develop anaphylaxis precipitated by allergens such as drugs, drug excipients or latex (43). Potential allergies to drugs such as antibiotics or previous anesthetic agents should be sought. Premedication. Asthmatic children can safely receive certain premedications, such as midazolam, (44). In addition they should be encouraged to take their inhalers as normal on the day of surgery, and should take inhaled b2-agonists prior to the theater. This may help abolish the increase in respiratory resistance seen with some anesthetic agents (45,46). It is possible that LABA or LTRA which provide additional or more prolonged protection from exerciseinduced symptoms may also prove useful before anesthesia (although there is no trial evidence for this indication at present). Corticosteroids may help to prevent perioperative bronchospasm, although evidence appears limited to one uncontrolled trial which measured changes in cytokine concentrations (47). Intravenous hydrocortisone is recommended to avoid adrenal crisis in those on systemic corticosteroids (23,48) and possibly high-dose inhaled corticosteroids (49). Rarely, severe asthmatics previously exposed to intravenous corticosteroids may have an anaphylactic response to these agents (50). Various inhaled topical anesthetic agents such as lidocaine have been used to attenuate the bronchoconstrictive effect of intubation, and have been investigated extensively by Groeben et al. (51–53). Paradoxically, these agents can induce irritation and bronchospasm, although this effect may be negated by the concurrent administration of b2-agonists.  2005 Blackwell Publishing Ltd, Pediatric Anesthesia, 15, 446–454

4 49

Induction of anesthesia Intravenous induction. Both gaseous and intravenous inductions are common in pediatric anesthesia practice, and the choice of route or agent may be influenced by a history of asthma. Amethocaine or EMLA cream should be used for local anesthesia prior to venous cannulation. Severe allergic reactions to either of these agents when applied topically have not been reported, although systemic absorption via broken or inflamed skin (such as in atopic dermatitis) may lead to toxicity (54,55). Ketamine has been advocated as the intravenous agent of choice for induction of anesthesia in patients with severe asthma (56). It has a bronchodilator effect possibly mediated by direct relaxation of airway smooth muscle, in addition to inhibition of vagal pathways and augmentation of catecholamine release. However, it may increase airway secretions unless administered with an anticholinergic. Its effectiveness has not been demonstrated in a controlled trial (57,58). Propofol has the advantage of producing less bronchoconstriction than other agents such as barbiturates in asthmatics (59–61). However, as with any drug there may be idiosyncratic reactions and there are case reports of severe bronchospasm with the use of propofol (62). The choice of other agents may be dictated by in vitro rather than in vivo evidence. For example, drugs which precipitate the release of histamine from mast cells might contribute to bronchospasm. Morphine appears to induce histamine release more easily than fentanyl, and atracurium more so than suxamethonium (56). Gaseous induction. Volatile anesthetic agents used for gaseous inductions are well-known as bronchodilating drugs, occasionally being used as a last resort in unresponsive status asthmaticus (63). However, during induction of anesthesia even these drugs appear to increase airway resistance as they are unable to completely abrogate the bronchoconstrictive response to intubation (64). The effects of these drugs differ slightly. Halothane was previously advocated when anesthetizing children with asthma, but its use has now declined in popularity. Sevoflurane is less pungent and therefore less irritant than isoflurane (65). The small increase in airways resistance seen even with sevoflurane appears to be

4 50

G .M . D O H E R T Y ET AL .

abolished by premedication with an inhaled b2agonist (46). Moreover, sevoflurane appears to predispose to fewer cardiac arrhythmias than halothane (66). Intubation. Tracheal intubation is felt more likely to produce adverse respiratory events in an asthmatic patient than the use of a laryngeal mask airway (LMA) with asthma. This has not been investigated directly in children. It is known that in children with upper respiratory tract infections, who also have reactive airways, the incidence of complications with the LMA was significantly less than with tracheal intubation (67–69). For very short procedures in children with reactive airways it would seem reasonable to avoid instrumentation of the oropharynx altogether by use of a facemask only. Recognizing and treating complications. Children with asthma are more likely to develop several complications during anesthesia, the most significant of which are bronchospasm, anaphylaxis, and possibly adrenal crisis. 1. Bronchospasm. Asthmatics may develop bronchospasm because of their increased airway reactivity, or secondary to an anaphylactic reaction. Bronchospasm is recognized by polyphonic, bilateral expiratory wheeze, prolonged expiration, active expiration with increased respiratory effort, increased airway pressures, rising endtidal CO2, and possibly hypoxemia. Hypoxemia may become manifest more quickly in the child where the respiratory drive has been blunted by anesthesia. Bronchospasm may usually be treated simply and effectively by inhaled b2-agonists, either nebulized or via a metered-dose inhaler (MDI) and spacer via the tracheal tube. Intravenous salbutamol or aminophylline may be used to treat severe bronchospasm. The evidence to favor one over the other in children is scanty. In acute exacerbations of asthma, aminophylline may be marginally more effective at the cost of increased side-effects (70,71). Aminophylline may present an increased risk of cardiac arrhythmia especially in conjunction with some volatile anesthetics (72,73). Hypokalemia is a side-effect of almost all anti-asthmatic medications and also carries a theoretical risk of arrhythmia which is fortunately rare in practice (74). Other options include intravenous magnesium, or increasing concentrations of

volatile anesthetics (see Table 2). Children who have anything other than minor bronchospasm should also receive corticosteroids if they have not already done so. Any evidence of systemic involvement should suggest that this reaction is anaphylactic rather than asthmatic. It is safer to over-treat bronchospasm as anaphylaxis than to delay treatment of true anaphylaxis. 2. Anaphylaxis. Anaphylaxis is a rare but potentially catastrophic complication of anesthesia. Neuromuscular-blocking drugs (NMD), antibiotics or latex are the most common precipitants (75). Although reactions to NMD are more common, reactions to latex appear to be more closely associated with atopy. Latex allergy is most common in children who have encountered this antigen before. For example, children who have had previous surgery or have required intermittent bladder catheterization may have been sensitized (76,77). In addition, crossreactivity may exist between latex and various fruit antigens (such as avocado, kiwi, and banana) (48). Patients with a proven or suspected allergy to latex or rubber should be managed in a latex-free environment, possibly with premedication, although some centers omit premedication (76). Premedication regimes include intravenous steroids, and H1 and H2-receptor antagonists (see Table 3). Premedication does not obviate the need for a latex-free environment (78). Providing this environment requires careful thought and preparation (79). Signs of anaphylaxis include angioedema, flushing or urticaria; and tachycardia, reduced perfusion, and hypotension secondary to hypovolemia. Angioedema may be present on the face or lips. Angioedema of the upper airway may manifest itself as stridor. Unfortunately, in the anesthetized patient, prodromal symptoms such as perioral tingling, urticaria or angioedema may be absent. The most common presentation is cardiovascular collapse (with an absent pulse noted) or bronchospasm (with difficulty in ventilating the patient). Anaphylaxis should be treated quickly and aggressively according to established protocols with the administration of intramuscular adrenaline, nebulized salbutamol, and fluid resuscitation (80). Corticosteroids and antihistamines should also be considered. Intramuscular adrenaline is first-line  2005 Blackwell Publishing Ltd, Pediatric Anesthesia, 15, 446–454

A N E S T H ES I A A N D A S T H M A

Table 2 Emergency treatment of bronchospasma

Drug

Route Nebulized

b2-agonists

MDI + spacer Intravenous Ipratropium bromide Corticosteroids Aminophylline

Nebulized Intravenous Oral Intravenous

Magnesium Anesthetic agents

Intravenous Ketamine Halothane Isoflurane

4 51

Dose Bolus (2.5–5 mg) every 20–30 min, or continuous nebulizationb Up to 10 puffs (1 mg) every 20–30 min Bolus (15 lgÆkg)1) over 20 min Infusion (1–5 lgÆkg)1Æmin)1)c Bolus ()125–250 lg) every 20–30 min 4 mgÆkg)1 hydrocortisone 1–2 mgÆkg)1 prednisolone Bolus (5 mgÆkg)1) over 10 min Infusion (1 mgÆkg)1Æh)1) Caution if already on theophyllines 40 mgÆkg)1 over 20 min 1–2 mgÆkg)1 bolus then 12.5–45 lgÆkg)1Æmin)1 infusion (58,99,100) 0.5–1.5% of inhaled air (63,101) 0.5–2% of inhaled air (63,101)

a

Where possible the doses suggested follow the BTS guidelines. Note that the dose, efficacy, and safety of some treatments have not been tested in controlled trials in pediatric asthma. This applies particularly to anesthetic agents. b Continuous nebulization is not the same as continuously nebulizing bolus doses, and requires an appropriate nebulizer. The total dose has not been standardized. 10 mgÆh)1 is often quoted although higher doses have been used. c Note different units for salbutamol and aminophylline bolus doses and infusions.

Table 3 Pretreatment of children with latex allergy (48) Drug

Dose

Methylprednisolone Ranitidine (100)

1 mgÆkg)1 1 mgÆkg)1

Chlorpheniramine (100)

250 lgÆkg)1 (1 month to 1 year) 5 mg (1–5 years) 10 mg (5–12 years)

Schedule 6 h i.v. 6 h i.v. over 20 min 6 h i.v. 6 h i.v. 6 h i.v.

Doses to be given for 12 h (i.e. two doses) preoperatively and 24 h postoperatively (48).

therapy although in patient with intravenous access, careful administration of intravenous adrenaline may be considered (1 : 10 000 solution of epinephrine titrated to effect). The Association of Anesthetists recommends that protocols for the management of anaphylaxis in the anesthetized patient should be available in operating theaters and regularly rehearsed (81). Any suspected anaphylactic reaction should be investigated and referred for follow-up. 3. Adrenal crisis. Suppression of the hypothalamic–pituitary–adrenal (HPA) axis may occur with steroid therapy. Adrenal crisis is then precipitated by a stress such as surgery. The presentation may be dramatic with hypotension, hypoglycemia or seizures. The patient will usually respond to intra 2005 Blackwell Publishing Ltd, Pediatric Anesthesia, 15, 446–454

venous hydrocortisone and fluid resuscitation with saline or colloid to increase intravascular volume, and dextrose as required to correct any hypoglycemia. Hypothalamic–pituitary–adrenal suppression must be assumed in any child who has received significant doses of steroids for a prolonged period. Short courses of prednisolone used to treat asthma exacerbations can affect HPA function for up to 10 days but dysfunction is unlikely to be prolonged (82,83). High doses, prolonged therapy (>3 weeks), evening dosing and continuous (as opposed to alternate day) dosing will all increase suppression of the HPA axis and therefore delay recovery of function, which may take up to a year (84,85). High-dose inhaled steroid therapy has also been associated with HPA suppression with several cases of adrenal crisis reported including one postoperatively (86). HPA suppression may occur without obvious growth retardation (87). The Committee on the Safety of Medicines advises that inhaled steroids may be associated with adrenal insufficiency (88). Perioperative steroid cover is indicated for those recently requiring systemic steroids and should be considered for those on high-dose inhaled steroids (48,89).

4 52

G .M . D O H E R T Y ET AL .

Postoperative care Nonsteroidal analgesics are commonly used in pediatric surgery, often administered immediately after induction of anesthesia. The association of nonsteroidals with a sudden deterioration of asthma is often a cause for concern. Although aspirin (NSAID) hypersensitivity appears much less common in children than in adults, it does occur (90–92). Cross-reactivity between NSAID is also common, although cross-reactivity with paracetamol is rare and reactions to paracetamol are usually mild (90). Aspirin is rarely used in childhood beyond certain very specific indications. Ibuprofen is commonly used even in asthmatic children, and is usually safe, although occasional reactions do occur (92,93). Even more potent NSAID such as diclofenac have been used safely in cohorts of asthmatic children (94). These studies on drug safety are, however, severely limited by the small numbers of children involved, as shown by secondary surveillance (95). Older children, especially those with severe symptoms and rhinitis are at increased risk, but the link with atopy is not clear (96,97). A recent metaanalysis suggested avoiding NSAID in severe asthmatics who have not previously received a nonsteroidal, and in anyone with a history of a previous adverse reaction to a nonsteroidal (90). Postoperative lung function is reduced in children undergoing anesthesia and this reduction may prove more important in the child with preexisting pulmonary disease such as asthma (98).

Conclusions Children with asthma frequently undergo anesthesia safely and without incident. The evidence-base for the safety of many medications used in anesthetizing the child with asthma remains poor. However, an awareness of the potential problems together with careful preoperative assessment and preparation will hopefully make already rare complications even less common.

References 1 Burr ML, Butland BK, King S et al. Changes in asthma prevalence: two surveys 15 years apart. Arch Dis Child 1989; 64: 1452–1456.

2 Kuehni CE, Davis A, Brooke AM et al. Are all wheezing disorders in very young (preschool) children increasing in prevalence? Lancet 2001; 357: 1821–1825. 3 Toelle BG, Ng K, Belousova E et al. Prevalence of asthma and allergy in schoolchildren in Belmont, Australia: three cross sectional surveys over 20 years. BMJ 2004; 328: 386–387. 4 Brennan LJ. Modern day-case anaesthesia for children. Br J Anaesth 1999; 83: 91–103. 5 Warner DO, Warner MA, Barnes RD et al. Perioperative respiratory complications in patients with asthma. Anesthesiology 1996; 85: 460–467. 6 Anderson HR, Ruggles R, Strachan DP et al. Trends in prevalence of symptoms of asthma, hay fever, and eczema in 12– 14 year olds in the British Isles, 1995–2002: questionnaire survey. BMJ 2004; 328: 1052–1053. 7 The International Study of Asthma and Allergies in Childhood (ISAAC) Steering Committee. Worldwide variation in prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and atopic eczema: ISAAC. Lancet 1998; 351: 1225–1232. 8 Sears MR, Greene JM, Willan AR et al. A longitudinal, population-based, cohort study of childhood asthma followed to adulthood. N Engl J Med 2003; 349: 1414–1422. 9 Strachan DP, Butland BK, Anderson HR. Incidence and prognosis of asthma and wheezing illness from early childhood to age 33 in a national British cohort. BMJ 1996; 312: 1195–1199. 10 Martinez FD. Development of wheezing disorders and asthma in preschool children. Pediatrics 2002; 109: 362–367. 11 Stein RT, Holberg CJ, Morgan WJ et al. Peak flow variability, methacholine responsiveness and atopy as markers for detecting different wheezing phenotypes in childhood. Thorax 1997; 52: 946–952. 12 Taussig LM, Wright AL, Holberg CJ et al. Tucson Children’s Respiratory Study: 1980 to present. J Allergy Clin Immunol 2003; 111: 661–675. 13 Bousquet J, Chanez P, Lacoste JY et al. Eosinophilic inflammation in asthma. N Engl J Med 1990; 323: 1033–1039. 14 Ennis M. Neutrophils in asthma pathophysiology. Curr Allergy Asthma Rep 2003; 3: 159–165. 15 Gibson PG, Simpson JL, Saltos N. Heterogeneity of airway inflammation in persistent asthma: evidence of neutrophilic inflammation and increased sputum interleukin-8. Chest 2001; 119: 1329–1336. 16 Cokugras H, Akcakaya N, Seckin I et al. Ultrastructural examination of bronchial biopsy specimens from children with moderate asthma. Thorax 2001; 56: 25–29. 17 Pohunek P, Roche WR, Tarzikova J et al. Eosinophilic inflammation in the bronchial mucosa in children with bronchial asthma. Eur Respir J 2000; 11(Suppl. 25): 160. 18 Davies DE, Wicks J, Powell RM et al. Airway remodeling in asthma: new insights. J Allergy Clin Immunol 2003; 111: 215–225. 19 Bousquet J, Jeffery PK, Busse WW et al. Asthma. From bronchoconstriction to airways inflammation and remodeling. Am J Respir Crit Care Med 2000; 161: 1720–1745. 20 British Thoracic Society and Scottish Intercollegiate Guidelines Network. British guideline on the management of asthma. (Revised edition, April 2004) http://www.sign.ac.uk 21 de Jongste JC, Shields MD. Cough 2: chronic cough in children. Thorax 2003; 58: 998–1003. 22 Thomson F, Masters IB, Chang AB. Persistent cough in children and the overuse of medications. J Paediatr Child Health 2002; 38: 578–581.

 2005 Blackwell Publishing Ltd, Pediatric Anesthesia, 15, 446–454

A N E S T H ES I A A N D A S T H M A

23 National Asthma Education and Prevention Program. Expert Panel Report: Guidelines for the Diagnosis and Management of Asthma (update on selected topics 2002), 02-5074, 1-6-2003. Bethesda, MD, National Institute of Health. 24 McKenzie SA, Bush A. Difficult asthma in children. Thorax 2002; 57: 915–916. 25 Balfour-Lynn I. Difficult asthma: beyond the guidelines. Arch Dis Child 1999; 80: 201–206. 26 Plaza V, Serrano J, Picado C et al. Frequency and clinical characteristics of rapid-onset fatal and near-fatal asthma. Eur Respir J 2002; 19: 846–852. 27 James A, King G. The computed tomographic scan: a new tool to monitor asthma treatment? Am J Med 2004; 116: 775–777. 28 Takemura M, Niimi A, Minakuchi M et al. Bronchial dilatation in asthma: relation to clinical and sputum indices. Chest 2004; 125: 1352–1358. 29 De Boeck K, Willems T, Van Gysel D et al. Outcome after right middle lobe syndrome. Chest 1995; 108: 150–152. 30 Eastham KM, Fall AJ, Mitchell L et al. The need to redefine non-cystic fibrosis bronchiectasis in childhood. Thorax 2004; 59: 324–327. 31 Hughes JM, Rimmer SJ, Salome CM et al. Eosinophilia, interleukin-5, and tumour necrosis factor-alpha in asthmatic children. Allergy 2001; 56: 412–418. 32 Fitch PS, Brown V, Schock BC et al. Serum eosinophil cationic protein (ECP): reference values in healthy nonatopic children. Allergy 1999; 54: 1199–1203. 33 Kips JC, Pauwels RA. Serum eosinophil cationic protein in asthma: what does it mean? Clin Exp Allergy 1998; 28: 1–3. 34 Shields MD, Brown V, Stevenson EC et al. Serum eosinophilic cationic protein and blood eosinophil counts for the prediction of the presence of airways inflammation in children with wheezing. Clin Exp Allergy 1999; 29: 1382–1389. 35 Severien C, Artlich A, Jonas S et al. Urinary excretion of leukotriene E4 and eosinophil protein X in children with atopic asthma. Eur Respir J 2000; 16: 588–592. 36 Strunk RC, Szefler SJ, Phillips BR et al. Relationship of exhaled nitric oxide to clinical and inflammatory markers of persistent asthma in children. J Allergy Clin Immunol 2003; 112: 883–892. 37 Lim S, Jatakanon A, Meah S et al. Relationship between exhaled nitric oxide and mucosal eosinophilic inflammation in mild to moderately severe asthma. Thorax 2000; 55: 184–188. 38 van den Toorn LM, Prins JB, Overbeek SE et al. Adolescents in clinical remission of atopic asthma have elevated exhaled nitric oxide levels and bronchial hyperresponsiveness. Am J Respir Crit Care Med 2000; 162: 953–957. 39 Warke TJ, Fitch PS, Brown V et al. Exhaled nitric oxide correlates with airway eosinophils in childhood asthma. Thorax 2002; 57: 383–387. 40 Warke TJ, Fitch PS, Brown V et al. Outgrown asthma does not mean no airways inflammation. Eur Respir J 2002; 19: 284–287. 41 Bruce C, Yates DH, Thomas PS. Caffeine decreases exhaled nitric oxide. Thorax 2002; 57: 361–363. 42 Warke TJ, Shields MD, Finnegan J et al. Caffeine and exhaled nitric oxide. Thorax 2003; 58: 281. 43 Hepner DL. Sudden bronchospasm on intubation: latex anaphylaxis? J Clin Anesth 2000; 12: 162–166. 44 Kil N, Zhu JF, VanWagnen C et al. The effects of midazolam on pediatric patients with asthma. Pediatr Dent 2003; 25: 137–142. 45 Wu RS, Wu KC, Wong TK et al. Effects of fenoterol and ipratropium on respiratory resistance of asthmatics after tracheal intubation. Br J Anaesth 2000; 84: 358–362.

 2005 Blackwell Publishing Ltd, Pediatric Anesthesia, 15, 446–454

4 53

46 Scalfaro P, Sly PD, Sims C et al. Salbutamol prevents the increase of respiratory resistance caused by tracheal intubation during sevoflurane anesthesia in asthmatic children. Anesth Analg 2001; 93: 898–902. 47 Mitsuta K, Shimoda T, Fukushima C et al. Preoperative steroid therapy inhibits cytokine production in the lung parenchyma in asthmatic patients. Chest 2001; 120: 1175–1183. 48 Black AE. Medical assessment of the paediatric patient. Br J Anaesth 1999; 83: 3–15. 49 Dunlop KA, Carson DJ, Shields MD. Hypoglycemia due to adrenal suppression secondary to high-dose nebulized corticosteroid. Pediatr Pulmonol 2002; 34: 85–86. 50 Nakamura H, Matsuse H, Obase Y et al. Clinical evaluation of anaphylactic reactions to intravenous corticosteroids in adult asthmatics. Respiration 2002; 69: 309–313. 51 Groeben H, Schlicht M, Stieglitz S et al. Both local anesthetics and salbutamol pretreatment affect reflex bronchoconstriction in volunteers with asthma undergoing awake fiberoptic intubation. Anesthesiology 2002; 97: 1445–1450. 52 Groeben H, Grosswendt T, Silvanus M et al. Lidocaine inhalation for local anaesthesia and attenuation of bronchial hyper-reactivity with least airway irritation. Effect of three different dose regimens. Eur J Anaesthesiol 2000; 17: 672–679. 53 Groeben H, Silvanus MT, Beste M et al. Combined lidocaine and salbutamol inhalation for airway anesthesia markedly protects against reflex bronchoconstriction. Chest 2000; 118: 509–515. 54 Parker JF, Vats A, Bauer G. EMLA toxicity after application for allergy skin testing. Pediatrics 2004; 113: 410–411. 55 Mancini AJ. Skin. Pediatrics 2004; 113: 1114–1119. 56 Pradal M, Vialet R, Soula F et al. The risk of anesthesia in the asthmatic child. Pediatr Pulmonol Suppl 1995; 11: 51–52. 57 Howton JC, Rose J, Duffy S et al. Randomized, double-blind, placebo-controlled trial of intravenous ketamine in acute asthma. Ann Emerg Med 1996; 27: 170–175. 58 Youssef-Ahmed MZ, Silver P, Nimkoff L et al. Continuous infusion of ketamine in mechanically ventilated children with refractory bronchospasm. Intensive Care Med 1996; 22: 972–976. 59 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: 1111–1116. 60 Wu RSC, Wu KC, Sum DCW et al. Comparative effects of thiopentone and propofol on respiratory resistance after tracheal intubation. Br J Anaesth 1996; 77: 735–738. 61 Hirota K, Sato T, Hashimoto Y et al. Relaxant effect of propofol on the airway in dogs. Br J Anaesth 1999; 83: 292–295. 62 Nishiyama T, Hanaoka K. Propofol-induced bronchoconstriction: two case reports. Anesth Analg 2001; 93: 645–646. 63 Werner HA. Status asthmaticus in children: a review. Chest 2001; 119: 1913–1929. 64 Bishop MJ, Rooke GA. Sevoflurane for patients with asthma. Anesth Analg 2000; 91: 245–246. 65 Pappas AL, Sukhani R, Lurie J et al. Severity of airway hyperreactivity associated with laryngeal mask airway removal: correlation with volatile anesthetic choice and depth of anesthesia. J Clin Anesth 2001; 13: 498–503. 66 Blayney MR, Malins AF, Cooper GM. Cardiac arrhythmias in children during outpatient general anaesthesia for dentistry: a prospective randomised trial. Lancet 1999; 354: 1864–1866. 67 Tait AR, Pandit UA, Voepel-Lewis T et al. Use of the laryngeal mask airway in children with upper respiratory tract

4 54

68

69

70

71 72 73

74

75

76 77

78

79 80 81

82

83

84

G .M . D O H E R T Y ET AL .

infections: a comparison with endotracheal intubation. Anesth Analg 1998; 86: 706–711. Cohen MM, Cameron CB. Should you cancel the operation when a child has an upper respiratory tract infection? Anesth Analg 1991; 72: 282–288. Parnis SJ, Barker DS, van der Walt JH. Clinical predictors of anaesthetic complications in children with respiratory tract infections. Paediatr Anaesth 2001; 11: 29–40. Roberts G, Newsom D, Gomez K et al. Intravenous salbutamol bolus compared with an aminophylline infusion in children with severe asthma: a randomised controlled trial. Thorax 2003; 58: 306–310. South M. Second line treatment for severe acute childhood asthma. Thorax 2003; 58: 284–285. Redden RJ. Possible theophylline toxicity during anesthesia. Anesth Prog 1996; 43: 67–72. Richards W, Thompson J, Lewis G et al. Cardiac arrest associated with halothane anesthesia in a patient receiving theophylline. Ann Allergy 1988; 61: 83–84. Molfino NA, Nannini LJ, Martelli AN et al. Respiratory arrest in near-fatal asthma [see Comments]. N Engl J Med 1991; 324: 285–288. Laxenaire MC, Mertes PM. Anaphylaxis during anaesthesia. Results of a two-year survey in France. Br J Anaesth 2001; 87: 549–558. Holzman RS. Clinical management of latex-allergic children. Anesth Analg 1997; 85: 529–533. Kelly KJ, Pearson ML, Kurup VP et al. A cluster of anaphylactic reactions in children with spina bifida during general anesthesia: epidemiologic features, risk factors, and latex hypersensitivity. J Allergy Clin Immunol 1994; 94: 53–61. Kwittken PL, Sweinberg SK, Campbell DE et al. Latex hypersensitivity in children: clinical presentation and detection of latex-specific immunoglobulin E. Pediatrics 1995; 95: 693–699. Dakin MJ, Yentis SM. Latex allergy: a strategy for management. Anaesthesia 1998; 53: 774–781. Advanced Life Support Group. Advanced Paediatric Life Support: The Practical Approach, 3rd edn. London: BMJ Books. Association of Anaesthetists of Great Britain and Ireland and British Society of Allergy and Clinical Immunology. Suspected Anaphylactic Reactions Associated with Anaesthesia. Zora JA, Zimmerman D, Carey TL et al. Hypothalamic–pituitary–adrenal axis suppression after short-term, high-dose glucocorticoid therapy in children with asthma. J Allergy Clin Immunol 1986; 77: 9–13. Ducharme FM, Chabot G, Polychronakos C et al. Safety profile of frequent short courses of oral glucocorticoids in acute pediatric asthma: impact on bone metabolism, bone density, and adrenal function. Pediatrics 2003; 111: 376–383. Dolan LM, Kesarwala HH, Holroyde JC et al. Short-term, high-dose, systemic steroids in children with asthma: the effect on the hypothalamic–pituitary–adrenal axis. J Allergy Clin Immunol 1987; 80: 81–87.

85 Axelrod L. Perioperative management of patients treated with glucocorticoids. Endocrinol Metab Clin North Am 2003; 32: 367– 383. 86 Todd GRG, Acerini CL, Ross-Russell R et al. Survey of adrenal crisis associated with inhaled corticosteroids in the United Kingdom. Arch Dis Child 2002; 87: 457–461. 87 Dunlop KA, Carson DJ, Steen HJ et al. Monitoring growth in asthmatic children treated with high dose inhaled glucocorticoids does not predict adrenal suppression. Arch Dis Child 2004; 89: 713–716. 88 Committee on Safety of Medicines. Inhaled corticosteroids and adrenal suppression in children. Curr Probl Pharmacovigil 2002; 28: 7. 89 Committee on Safety of Medicines. Withdrawal of systemic corticosteroids. Curr Prob Pharmacovigil 1998; 24: 5–6. 90 Jenkins C, Costello J, Hodge L. Systematic review of prevalence of aspirin induced asthma and its implications for clinical practice. BMJ 2004; 328: 434–440. 91 Lesko SM. The safety of ibuprofen suspension in children. Int J Clin Pract Suppl 2003; 50–53. 92 Lesko SM, Louik C, Vezina RM et al. Asthma morbidity after the short-term use of ibuprofen in children. Pediatrics 2002; 109: E20. 93 Goraya JS, Virdi VS. To the editor: exacerbation of asthma by ibuprofen in a very young child. Pediatr Pulmonol 2001; 32: 262. 94 Short JA, Barr CA, Palmer CD et al. Use of diclofenac in children with asthma. Anaesthesia 2000; 55: 334–337. 95 Gupta D, Aggarwal AN, Aggarwal PN et al. Near fatal asthma following ingestion of diclofenac sodium tablet. J Assoc Physicians India 2000; 48: 258–259. 96 Szczeklik A, Nizankowska E, Duplaga M. Natural history of aspirin-induced asthma. AIANE investigators. European network on aspirin-induced asthma. Eur Respir J 2000; 16: 432–436. 97 Vally H, Taylor ML, Thompson PJ. The prevalence of aspirin intolerant asthma (AIA) in Australian asthmatic patients. Thorax 2002; 57: 569–574. 98 May HA, Smyth RL, Romer HC et al. Effect of anaesthesia on lung function in children with asthma. Br J Anaesth 1996; 77: 200–202. 99 Petrillo TM, Fortenberry JD, Linzer JF et al. Emergency department use of ketamine in pediatric status asthmaticus. J Asthma 2001; 38: 657–664. 100 Royal College of Paediatrics and Child Health, Neonatal and Paediatric Pharmacists Group. Medicines for Children, 2nd edn. London: RCPCH Publications Ltd., 2003. 101 Joint Formulary Committee. British National Formulary, 48 edn. London: British Medical Association and Royal Pharmaceutical Society of Great Britain, 2004.

Accepted 3 December 2004

 2005 Blackwell Publishing Ltd, Pediatric Anesthesia, 15, 446–454

Anesthesia and the child with asthma - Wiley Online Library

The rising prevalence of asthma in childhood means that anesthetists are encountering children with this disorder scheduled for surgery with increasing frequency (1–3). The increase in the volume of day- case surgery has limited the time available for the assessment of both the child's medical condition and possible ...

101KB Sizes 2 Downloads 144 Views

Recommend Documents

The retreat from overgeneralization in child ... - Wiley Online Library
Page 1. Advanced Review. The retreat from overgeneralization in child language acquisition: word learning, morphology, and verb argument structure. Ben Ambridge,. ∗ ... Advanced Review wires.wiley.com/cogsci when speakers combine words to produce e

XIIntention and the Self - Wiley Online Library
May 9, 2011 - The former result is a potential basis for a Butlerian circularity objection to. Lockean theories of personal identity. The latter result undercuts a prom- inent Lockean reply to 'the thinking animal' objection which has recently suppla

Micturition and the soul - Wiley Online Library
Page 1 ... turition to signal important messages as territorial demarcation and sexual attraction. For ... important messages such as the demarcation of territory.

ELTGOL - Wiley Online Library
ABSTRACT. Background and objective: Exacerbations of COPD are often characterized by increased mucus production that is difficult to treat and worsens patients' outcome. This study evaluated the efficacy of a chest physio- therapy technique (expirati

The geography of divergence with gene flow ... - Wiley Online Library
Oct 18, 2015 - 1Institute of Ecology and Evolution, University of Oregon, Eugene, Oregon, 97401. 2E-mail: [email protected]. 3Department of Biological ...

Rockets and feathers: Understanding ... - Wiley Online Library
been much progress in terms of theoretical explanations for this widespread ... explains how an asymmetric response of prices to costs can arise in highly ...

Openness and Inflation - Wiley Online Library
Keywords: inflation bias, terms of trade, monopoly markups. DOES INFLATION RISE OR FALL as an economy becomes more open? One way to approach this ...

competition and disclosure - Wiley Online Library
There are many laws that require sellers to disclose private information ... nutrition label. Similar legislation exists in the European Union1 and elsewhere. Prior to the introduction of these laws, labeling was voluntary. There are many other ... Ð

Openness and Inflation - Wiley Online Library
related to monopoly markups, a greater degree of openness may lead the policymaker to exploit the short-run Phillips curve more aggressively, even.

Climate change and - Wiley Online Library
Climate change has rarely been out of the public spotlight in the first decade of this century. The high-profile international meetings and controversies such as 'climategate' have highlighted the fact that it is as much a political issue as it is a

Phenotypic abnormalities: Terminology and ... - Wiley Online Library
Oxford: Oxford University Press. 1 p]. The major approach to reach this has been ... Amsterdam, The Netherlands. E-mail: [email protected]. Received 15 ...

Wealth, Population, and Inequality - Wiley Online Library
Simon Szreter. This journal is devoted to addressing the central issues of population and development, the subject ... *Review of Thomas Piketty, Capital in the Twenty-First Century. Translated by Arthur Goldhammer. .... As Piketty is well aware, wit

Inconstancy and Content - Wiley Online Library
disagreement – tell against their accounts of inconstancy and in favor of another .... and that the truth values of de re modal predications really can change as our.

Scholarship and disciplinary practices - Wiley Online Library
Introduction. Research on disciplinary practice has been growing and maturing in the social sciences in recent decades. At the same time, disciplinary and.

Anaphylaxis and cardiovascular disease - Wiley Online Library
38138, USA. E-mail: [email protected]. Cite this as: P. Lieberman, F. E. R.. Simons. Clinical & Experimental. Allergy, 2015 (45) 1288–1295. Summary.

Enlightenment, Revolution and Democracy - Wiley Online Library
Within a century such typological or static evaluation had given way to diachronic analysis in Greek thought. However, in the twentieth century this development was reversed. This reversal has affected the way we understand democracy, which tends to

poly(styrene - Wiley Online Library
Dec 27, 2007 - (4VP) but immiscible with PS4VP-30 (where the number following the hyphen refers to the percentage 4VP in the polymer) and PSMA-20 (where the number following the hyphen refers to the percentage methacrylic acid in the polymer) over th

Recurvirostra avosetta - Wiley Online Library
broodrearing capacity. Proceedings of the Royal Society B: Biological. Sciences, 263, 1719–1724. Hills, S. (1983) Incubation capacity as a limiting factor of shorebird clutch size. MS thesis, University of Washington, Seattle, Washington. Hötker,

Kitaev Transformation - Wiley Online Library
Jul 1, 2015 - Quantum chemistry is an important area of application for quantum computation. In particular, quantum algorithms applied to the electronic ...

The knowledge economy: emerging ... - Wiley Online Library
explain the microfoundations and market mechanisms that underpin organizational disaggregation and the communal gover- nance forms observed in the knowledge economy. Because of the increasingly cen- tral role of HR professionals in knowledge manageme