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Wheeze
View on Wikipedia| Wheezing | |
|---|---|
| Other names | Sibilant rhonchi |
| The sound of wheezing as heard with a stethoscope | |
| Specialty | Pulmonology |
| Causes | virus, bacteria, common cold, allergy, pneumonia, asthma, tuberculosis |
A wheeze is a clinical symptom of a continuous, coarse, whistling sound produced in the respiratory airways during breathing.[1] For wheezes to occur, part of the respiratory tree must be narrowed or obstructed (for example narrowing of the lower respiratory tract in an asthmatic attack), or airflow velocity within the respiratory tree must be heightened. Wheezing is commonly experienced by persons with a lung disease; the most common cause of recurrent wheezing is asthma, though it can also be a symptom of lung cancer, congestive heart failure, and certain types of heart diseases.
The differential diagnosis of wheezing is wide, and the reason for wheezing in a given patient is determined by considering the characteristics of the wheezes and the historical and clinical findings made by the examining physician.
The term "wheeze" is also used as a clinical condition describing wheezing in preschool children, termed as "preschool wheeze".[2]
Clinical symptom
[edit]Wheeze
[edit]Wheezes occupy different portions of the respiratory cycle depending on the site of airway obstruction and its nature. The fraction of the respiratory cycle during which a wheeze is produced roughly corresponds to the degree of airway obstruction.[3][4] Bronchiolar disease usually causes wheezing that occurs in the expiratory phase of respiration. As a rule, extrathoracic airway obstruction produce inspiratory sounds. Intrathoracic major airway obstruction produces inspiratory as well as expiratory sounds. Distal airway obstruction predominantly produces expiratory sounds.[5]
The presence of expiratory phase wheezing signifies that the patient's peak expiratory flow rate is less than 50% of normal.[6] Wheezing heard in the inspiratory phase, on the other hand, is often a sign of a stiff stenosis, usually caused by tumors, foreign bodies or scarring. This is especially true if the wheeze is monotonal, occurs throughout the inspiratory phase (i.e. is "holoinspiratory"), and is heard more proximally, in the trachea. Inspiratory wheezing also occurs in hypersensitivity pneumonitis.[7] Wheezes heard at the end of both expiratory and inspiratory phases usually signify the periodic opening of deflated alveoli, as occurs in some diseases that lead to collapse of parts of the lungs.
The location of the wheeze can also be an important clue to the diagnosis. Diffuse processes that affect most parts of the lungs are more likely to produce wheezing that may be heard throughout the chest via a stethoscope. Localized processes, such as the occlusion of a portion of the respiratory tree, are more likely to produce wheezing at that location, hence the sound will be loudest and radiate outwardly. The pitch of a wheeze does not reliably predict the degree of narrowing in the affected airway.[8]
Stridor
[edit]A special type of wheeze is stridor. Stridor — the word is from the Latin, strīdor[9] — is a harsh, high-pitched, vibrating sound that is heard in respiratory tract obstruction. Stridor heard solely in the inspiratory phase of respiration usually indicates an upper respiratory tract obstruction, "as with aspiration of a foreign body (such as the fabled pediatric peanut)."[10] Stridor in the inspiratory phase is usually heard with obstruction in the upper airways, such as the trachea, epiglottis, or larynx; because a block here means that no air may reach either lung, this condition is a medical emergency. Biphasic stridor (occurring during both the inspiratory and expiratory phases) indicates narrowing at the level of the glottis or subglottis, the point between the upper and lower airways.
Preschool wheeze
[edit]Preschool wheezing is a clinical condition that describes wheezing preschool children that do not fulfill the criteria of "asthma" fully as asthma would require a person to demonstrate a history of at least three episodes of exacerbations (worsening of symptoms) or chronic cough or wheeze for the past six months.[2] Besides, a number of wheezing preschool children would have their symptoms resolved after they had grown up, unlike asthma which persists into adulthood. Preschool wheezing can be divided into "viral-induced wheeze" and "multi-trigger wheeze". Viral-induced wheezing accounts for about two-thirds of all preschool wheezes. The wheezing symptom is episodic and the child is completely normal in between wheezing episodes. It has a good prognosis and only supportive treatment is required. Meanwhile, multi-trigger wheezing is associated with allergy and a family history of asthma. Symptoms occur in between wheezing episodes and are likely to persist beyond early childhood. Due to difficulty in differentiating both types of wheeze, the diagnosis of viral-induced versus multi-trigger wheeze may be delayed for a period of time until its clinical course has become clear.[2]
To wheeze (slang)
[edit]To wheeze implies an inability to speak clearly, so in politics it refers to an unorthodox or less than ethical maneuver that is not actually illegal, but relies on an element of deception or sleight of hand, being an intermediate between a workaround and a scam.[11]
In this context wheezing is notably linked with the slang expression Joe Blow meaning any external person or group beyond a secretive fraternity.[12] (See also insider trading.)
See also
[edit]- Crackles (also called "crepitations" or "rales")
- Rhonchi
- Squawk (sound)
References
[edit]- ^ Sengupta N, Sahidullah M, Saha G (August 2016). "Lung sound classification using cepstral-based statistical features". Computers in Biology and Medicine. 75 (1): 118–129. doi:10.1016/j.compbiomed.2016.05.013. PMID 27286184.
- ^ a b c Van Bever HP, Han E, Shek L, Yi Chng S, Goh D (November 2010). "An approach to preschool wheezing: to label as asthma?". The World Allergy Organization Journal. 3 (11): 253–257. doi:10.1097/WOX.0b013e3181fc7fa1. PMC 3651058. PMID 23282943.
- ^ Baughman RP, Loudon RG (November 1984). "Quantitation of wheezing in acute asthma". Chest. 86 (5): 718–722. doi:10.1378/chest.86.5.718. PMID 6488909.
- ^ Pasterkamp H, Tal A, Leahy F, Fenton R, Chernick V (July 1985). "The effect of anticholinergic treatment on postexertional wheezing in asthma studied by phonopneumography and spirometry". The American Review of Respiratory Disease. 132 (1): 16–21. doi:10.1164/arrd.1985.132.1.16 (inactive 12 July 2025). PMID 3160273.
{{cite journal}}: CS1 maint: DOI inactive as of July 2025 (link) - ^ Ghai, OP (2014). Essential Pediatrics. CBS Publishers & Distributors. p. 372. ISBN 978-81-239-2334-5.
- ^ Shim CS, Williams MH (May 1983). "Relationship of wheezing to the severity of obstruction in asthma". Archives of Internal Medicine. 143 (5): 890–892. doi:10.1001/archinte.143.5.890. PMID 6679232.
- ^ Earis JE, Marsh K, Pearson MG, Ogilvie CM (December 1982). "The inspiratory "squawk" in extrinsic allergic alveolitis and other pulmonary fibroses". Thorax. 37 (12): 923–926. doi:10.1136/thx.37.12.923. PMC 459459. PMID 7170682.
- ^ Meslier N, Charbonneau G, Racineux JL (November 1995). "Wheezes". The European Respiratory Journal. 8 (11): 1942–1948. doi:10.1183/09031936.95.08111942. PMID 8620967.
- ^ Simpson JA, Weiner ESC (eds). "stridor, n. 2." Oxford English Dictionary 2nd ed. Oxford: Clarendon Press, 1989. OED Online Oxford University Press. Accessed September 10, 2005. http://dictionary.oed.com Archived 2006-06-25 at the Wayback Machine.
- ^ Sapira JD, Orient JM (2000). Sapira's art & science of bedside diagnosis (2nd ed.). Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 978-0-683-30714-6.
- ^ Word Reference Wheeze Accessed 02 July 2024
- ^ Vocabulary.com: Joe Blow Accessed 02 July 2024
Further reading
[edit]External links
[edit]- Audio Breath Sounds Archived 2020-12-15 at the Wayback Machine - Multiple case studies with audio files of lung sounds.
- R.A.L.E. Repository - sound files of breath sounds
Wheeze
View on GrokipediaDefinition and Characteristics
Medical Definition
Wheeze is defined as a continuous, high-pitched, musical whistling sound produced by turbulent airflow through narrowed lower airways during expiration.[2] This adventitious lung sound arises from the vibration of airway walls or secretions within abnormally constricted passages, distinguishing it as a hallmark of respiratory obstruction.[6] The term "wheeze" originates from the Old Norse word hvæsa, meaning to hiss or whistle, derived from the Indo-European root kwes signifying to pant; it entered English in the mid-15th century and appeared in medical literature around that time to describe labored breathing.[7] Unlike normal breath sounds, which are generated by smooth airflow through unobstructed airways, wheeze signals pathology in the intrathoracic lower airways, particularly the small airways with internal diameters typically less than 2 mm.[8] These small airways normally contribute minimally to resistance but become significant sites of dysfunction when narrowed, leading to the characteristic sound.[9] It is often associated with obstructive conditions like asthma.[3]Auditory and Clinical Features
Wheeze is a high-pitched, musical adventitious lung sound, typically characterized by periodic waveforms with dominant frequencies >400 Hz.[10] It often presents as polyphonic, featuring multiple simultaneous pitches generated from turbulent airflow at various airway levels, which distinguishes it from monophonic wheezes limited to a single dominant frequency.[11] Predominantly expiratory in nature due to greater airway narrowing during exhalation, wheeze can also be biphasic, occurring during both inspiration and expiration in cases of more severe obstruction.[2] This sound arises continuously from turbulent airflow through narrowed or compressed airways.[2] In clinical presentation, wheeze is commonly associated with signs of respiratory distress, including dyspnea, tachypnea, and recruitment of accessory muscles such as the sternocleidomastoid and intercostals to aid breathing.[12] These features reflect the underlying airflow limitation and are particularly prominent in acute exacerbations of conditions like asthma or chronic obstructive pulmonary disease.[13] During examination, wheeze is typically louder over the lung fields than underlying breath sounds and may be audible without a stethoscope in severe cases, such as over the trachea or at the open mouth.[14] Auscultation for wheeze requires a stethoscope in a quiet environment, ideally with the patient in a sitting position to facilitate clear detection and comparison of breath sounds bilaterally.[14] If the patient is supine or unable to sit, the examiner can roll the patient side-to-side or use alternative positioning to access all lung fields.[14] Systematic auscultation proceeds from apex to base and laterally, allowing localization of wheeze to specific lung zones, such as upper versus lower lobes, to guide differential diagnosis.[15]Pathophysiology
Airflow Mechanisms
Wheeze arises from the vibration of airway walls induced by turbulent airflow through partially obstructed bronchi and bronchioles. In normal breathing, airflow in the respiratory tract is predominantly laminar, producing minimal sound. However, when airways are narrowed, the increased velocity of air passing through the constriction creates pressure differences according to Bernoulli's principle, leading to instability and flutter of the compliant airway walls. This flutter generates oscillatory vibrations that propagate as musical, high-pitched sounds audible during auscultation, typically during expiration when flow rates are higher.[16] The transition from laminar to turbulent flow, which is essential for wheeze production, is governed by the Reynolds number (Re), a dimensionless parameter that quantifies the ratio of inertial to viscous forces in fluid dynamics. In the context of respiratory airflow, Re is calculated as: where is the density of the gas (air or mixture), is the mean airflow velocity, is the airway diameter, and is the dynamic viscosity of the gas. Laminar flow predominates when Re < 2000, but turbulence emerges as Re exceeds this threshold, particularly in larger airways like the bronchi where velocities can reach critical levels during obstruction. This turbulent regime promotes the chaotic eddies and shear stresses that destabilize the airway walls, amplifying vibrations and sound intensity.[17][16] Several factors modulate the intensity and characteristics of wheeze. The degree of airway narrowing plays a pivotal role; moderate to severe obstructions optimize conditions for wall flutter and sound generation by balancing flow limitation with sufficient velocity to induce turbulence without complete occlusion. Higher airflow velocities, often seen in expiration, further elevate Re and enhance vibration amplitude. Additionally, gas density influences Re directly—increasing density (e.g., with humidified or denser gas mixtures) can promote turbulence at lower velocities, potentially intensifying wheeze. These physical principles underpin wheeze as a marker of dynamic airway instability.[16]Inflammatory and Structural Factors
The inflammatory cascade underlying wheeze involves the activation of mast cells in the airway mucosa, which release preformed and newly synthesized mediators upon exposure to allergens or irritants. These mediators include histamine, which promotes vascular permeability and smooth muscle contraction, and leukotrienes such as LTC4 and LTD4, which induce prolonged bronchoconstriction, mucosal edema, and excessive mucus production by goblet cells.[18][19] This cascade contributes to acute airway narrowing, exacerbating the turbulent airflow that produces the characteristic wheezing sound.[2] In chronic conditions associated with recurrent wheeze, structural changes known as airway remodeling occur, leading to persistent alterations in airway architecture. Key features include hypertrophy and hyperplasia of airway smooth muscle, which increases the capacity for contraction and reduces airway caliber, as well as subepithelial fibrosis resulting from deposition of extracellular matrix proteins like collagen beneath the basement membrane.[20][21] These changes, driven by ongoing inflammation, impair reversibility of obstruction and contribute to fixed airflow limitation over time.[22] Neural mechanisms also play a role in wheeze pathogenesis through hyperactivity of the vagal reflex, which amplifies bronchospasm via parasympathetic innervation of the airways. Stimulation of irritant receptors in the epithelium triggers afferent vagal fibers, leading to efferent cholinergic signaling that causes smooth muscle contraction and mucus secretion.[2][23] This reflex pathway can be sensitized in inflammatory states, resulting in exaggerated responses to otherwise innocuous stimuli.[24]Causes and Risk Factors
Common Etiologies in Adults
In adults, wheezing is most commonly associated with obstructive lung diseases, particularly asthma and chronic obstructive pulmonary disease (COPD). Asthma, a chronic inflammatory condition of the airways, leads to recurrent episodes of wheezing due to reversible airflow obstruction, often triggered by allergens, irritants, or infections; it can manifest as allergic (atopic) asthma, driven by immunoglobulin E-mediated responses to environmental allergens like pollen or dust mites, or non-allergic asthma, which involves non-immunologic triggers such as exercise or cold air.[25][26] COPD, encompassing emphysema and chronic bronchitis, causes persistent wheezing exacerbated during acute flares, resulting from irreversible airway damage and mucus hypersecretion, frequently precipitated by respiratory infections or pollutant exposure.[3][27] Infectious etiologies also frequently produce wheezing in adults through airway inflammation and mucus production. Acute bronchitis, typically viral in origin, induces transient wheezing alongside cough and sputum production, resolving within weeks without chronic sequelae.[28][29] Pneumonia, particularly community-acquired bacterial or atypical forms like those caused by Mycoplasma pneumoniae, can present with wheezing due to alveolar and bronchial involvement, often accompanied by fever and dyspnea.[30][26] Pertussis (whooping cough), caused by Bordetella pertussis, may trigger paroxysmal coughing and wheezing in adults, especially those with underlying respiratory conditions, leading to prolonged symptoms beyond the initial catarrhal phase.[31][32] Other notable causes include mechanical obstructions and systemic conditions mimicking primary pulmonary issues. Foreign body aspiration, though less common in adults than children, can cause unilateral wheezing and cough if an object lodges in the airways, often requiring bronchoscopic removal.[33] Heart failure, termed "cardiac asthma," produces wheezing from pulmonary edema and bronchial compression, typically in older adults with left ventricular dysfunction.[34] Anaphylaxis, a severe allergic reaction, leads to acute wheezing from bronchospasm and laryngeal edema, often following exposure to foods, medications, or insect stings.[35][36] Vocal cord dysfunction involves paradoxical vocal fold adduction during inspiration, producing wheezing that may be mistaken for asthma, commonly triggered by irritants or stress.[37][38] Key risk factors for wheezing in adults include modifiable exposures that exacerbate or initiate these conditions. Smoking, a primary driver of COPD and a trigger for asthma exacerbations, increases wheeze risk through chronic airway irritation and inflammation.[39][40] Occupational exposures to irritants like dust, chemicals, or fumes heighten susceptibility, particularly in non-atopic individuals developing occupational asthma.[40][41] Obesity contributes via mechanical effects on lung volumes and systemic inflammation, elevating the odds of adult-onset asthma and wheeze severity.[40][42]Etiologies in Children
In school-aged children (typically 6 years and older), wheezing often arises from reactive airway diseases, with asthma being the most prevalent etiology. Asthma typically manifests as recurrent episodes of reversible airflow obstruction triggered by inflammation and bronchial hyperresponsiveness, affecting approximately 5-10% of school-aged children globally, with regional variations.[43] Cystic fibrosis, a genetic disorder impairing mucociliary clearance, leads to chronic wheezing due to viscous secretions causing airway obstruction and recurrent infections, often presenting with failure to thrive and persistent cough in affected children.[44] Congenital anomalies can contribute to wheezing through structural compression or instability of the airways, though less commonly presenting for the first time in school age. Tracheomalacia, characterized by flaccidity of the tracheal cartilage, results in expiratory collapse and monophonic wheezing, particularly during respiratory infections or crying, and may persist into school age in children with a history of prolonged intubation or congenital defects.[45] Vascular rings, such as double aortic arch, encircle and compress the trachea and esophagus, producing biphasic wheezing, stridor, and recurrent respiratory distress that may mimic asthma but requires surgical intervention for resolution.[46] Recurrent viral infections play a role in school-aged wheezing, often exacerbating underlying conditions. Respiratory syncytial virus (RSV) and parainfluenza viruses can cause acute wheezing episodes in 20-40% of infected children, particularly those with prior early-life infections leading to airway remodeling and increased susceptibility.[47] Post-infectious hyperreactivity often follows these viral illnesses, where damaged epithelium and heightened immune responses provoke persistent bronchial sensitivity and recurrent wheeze, associated with approximately a 2-fold increased risk of asthma development in affected children.[48] Environmental exposures significantly exacerbate wheezing in school-aged children. Passive tobacco smoke exposure heightens the risk of recurrent wheezing by 20-30%, promoting airway inflammation and impairing lung function through oxidative stress and irritant effects.[49] Allergens such as dust mites, pet dander, and pollen trigger immunoglobulin E-mediated responses in sensitized children, leading to seasonal or perennial wheezing in those with underlying atopy, often compounding asthma severity in urban school environments.[50]Clinical Evaluation and Differential Diagnosis
History and Physical Examination
The clinical evaluation of wheeze begins with a detailed history to characterize the symptom and identify potential underlying causes. Key elements include assessing the onset, distinguishing between acute and chronic presentations, as acute onset may indicate an urgent condition while chronic patterns suggest ongoing respiratory disorders. Triggers such as exercise, allergens, irritants, or infections should be explored, along with associated symptoms like cough, dyspnea, chest tightness, or fever, which help narrow differential diagnoses. Family history of atopy, including asthma, allergic rhinitis, or eczema, is crucial for evaluating genetic predispositions.[2][51][52] The physical examination focuses on signs of respiratory compromise and structural abnormalities. Vital signs are evaluated first, with particular attention to oxygen saturation (typically aiming for >95% in stable patients) and respiratory rate (elevated rates, such as >30 breaths per minute, indicating severity). Inspection reveals accessory muscle use, retractions (intercostal or supraclavicular), or increased work of breathing. Percussion may yield hyperresonance due to air trapping, while palpation assesses for chest asymmetry or reduced tactile fremitus, suggesting uneven ventilation or focal pathology. Auscultation confirms the high-pitched, musical wheeze, often more prominent during expiration.[2][51][52] Certain findings warrant immediate concern as red flags. Sudden onset of wheeze, particularly in children, raises suspicion for foreign body aspiration requiring urgent intervention. Nocturnal worsening or persistent symptoms despite initial management may indicate poorly controlled asthma or alternative etiologies like gastroesophageal reflux. Absence of wheeze on exam despite distress signals severe airway obstruction.[2][51][52]Distinction from Stridor and Other Sounds
Wheeze is characterized as a continuous, high-pitched, musical sound predominantly occurring during expiration, resulting from turbulent airflow through narrowed intrathoracic lower airways, such as the bronchi.[15] In distinction, stridor is a harsh, high-pitched, monophonic sound typically heard during inspiration, arising from obstruction or narrowing in the extrathoracic upper airways, including the larynx or trachea, as seen in conditions like croup or epiglottitis.[53] 05071-7/fulltext) While wheezes are often polyphonic, involving multiple vibrating frequencies from widespread small airway involvement, stridor remains more uniform in pitch due to focal upper airway turbulence.[15] Both sounds stem from airflow turbulence caused by airway narrowing, but their localization—lower for wheeze and upper for stridor—guides diagnostic focus.[15] Wheeze must also be differentiated from other adventitious lung sounds like rhonchi and crackles. Rhonchi are low-pitched, continuous, snoring-like noises generated by air moving through mucus or secretions in larger airways, and they characteristically diminish or resolve after coughing, unlike the persistent nature of wheezes from fixed narrowing.[54] [15] Crackles, conversely, are discontinuous, short-duration popping or bubbling sounds produced by the explosive opening of collapsed alveoli or small airways during inspiration, reflecting interstitial or alveolar pathology rather than the sustained turbulent flow of wheezes.[15] [54] These auditory distinctions carry significant clinical implications for evaluation and initial management. Stridor often signals an acute upper airway obstruction that may progress to respiratory failure, necessitating urgent interventions such as airway securing or nebulized epinephrine to avert complications.[55] [53] Wheeze, indicating lower airway disease like bronchospasm, typically prompts a trial of bronchodilators, such as beta-agonists, to alleviate reversible obstruction in conditions including asthma exacerbations.[56] Accurate differentiation during auscultation thus directs timely, targeted therapy and prevents mismanagement.05071-7/fulltext)Management and Treatment
Management of wheezing primarily targets the underlying cause, as identified through clinical evaluation. For infectious causes like bacterial bronchitis or pneumonia, antibiotics such as amoxicillin or azithromycin may be prescribed if bacterial etiology is confirmed.[3] In cases of anaphylaxis, intramuscular epinephrine is the first-line treatment to reverse airway obstruction.[3] Foreign body aspiration requires urgent bronchoscopy for removal.[4] For cardiac causes like heart failure, diuretics and vasodilators address fluid overload.[3] Gastroesophageal reflux-related wheezing may benefit from proton pump inhibitors or lifestyle modifications.[3] When wheezing stems from reversible airway obstruction, such as in asthma exacerbations, specific interventions are employed as detailed below.Acute Interventions
Acute wheezing episodes, often resulting from asthma exacerbations or other reversible airway obstructions, necessitate immediate interventions to alleviate bronchospasm, reduce inflammation, and prevent respiratory failure.[57][58] The primary goal is rapid stabilization through bronchodilation and supportive measures, with escalation if response is inadequate.[59] Short-acting beta-agonists (SABAs), such as albuterol, form the cornerstone of acute therapy by relaxing bronchial smooth muscle and improving airflow. These are administered via metered-dose inhaler (MDI) with spacer or nebulizer, with typical dosing of 4-8 puffs (or equivalent nebulized dose) every 20 minutes for up to 1 hour, titrated based on clinical response.[58][59] In severe cases, continuous nebulization may be employed, and addition of ipratropium bromide can enhance bronchodilation when SABA alone is insufficient.[56] Guidelines recommend avoiding SABA monotherapy as a reliever; as-needed ICS-formoterol is preferred where available to reduce exacerbation risk.[60] For moderate to severe episodes, systemic corticosteroids are administered promptly to suppress airway inflammation and hasten recovery. Oral prednisone (40-60 mg daily for 5-7 days) is preferred when feasible, with intravenous methylprednisolone (60-125 mg) reserved for those unable to tolerate oral intake or with life-threatening features; no tapering is typically needed for short courses.[60][57] Supportive care includes supplemental oxygen to maintain saturation at 92-95% in hypoxic patients, delivered via nasal cannula or mask and monitored closely to avoid hyperoxia.[60][59] For refractory wheezing despite initial bronchodilators and steroids, intravenous magnesium sulfate (2 g over 20 minutes) provides additional smooth muscle relaxation and may reduce the need for hospitalization.[57][58] Escalation to advanced airway management, such as intubation and mechanical ventilation, is indicated for impending respiratory failure, evidenced by altered mental status, severe distress, hypercapnia (PaCO2 >60 mm Hg), or failure to respond to maximal medical therapy.[59][58] Noninvasive ventilation may be trialed first in select cases to avoid intubation risks.[57]Chronic Management and Prevention
Chronic management of wheezing, particularly in the context of persistent asthma, focuses on controller therapies to suppress underlying airway inflammation and prevent recurrent episodes. Inhaled corticosteroids (ICS) form the cornerstone of therapy, as they effectively reduce inflammation, symptoms, and the risk of exacerbations when used regularly at low doses.[60] The preferred approach (Track 1) uses low-dose ICS-formoterol as both maintenance and reliever therapy across all steps. Long-acting beta-agonists (LABA) are recommended in combination with ICS for patients whose symptoms remain uncontrolled on low-dose ICS alone, providing sustained bronchodilation and further reducing exacerbation frequency.[60] Leukotriene modifiers, such as montelukast, offer an oral alternative for mild persistent asthma but are generally less effective than ICS and carry risks of neuropsychiatric side effects.[60] Lifestyle modifications play a vital role in preventing wheeze exacerbations by minimizing triggers. Strategies to reduce exposure to indoor allergens, such as using allergen-proof bedding and controlling dust mites, can help decrease symptom frequency in sensitized individuals.[61] Smoking cessation is strongly advised at every clinical visit, as tobacco smoke exacerbates airway inflammation and impairs response to controller medications; counseling and resources should be provided to support quitting.[60] Annual influenza vaccination and pneumococcal immunization are recommended for all patients with chronic respiratory conditions like asthma to prevent infections that could trigger wheezing.[62] Ongoing monitoring ensures effective control and timely adjustments to therapy. Peak flow meters allow patients to track daily variability in expiratory flow, helping identify early signs of worsening obstruction.[60] Personalized asthma action plans, developed in collaboration with healthcare providers, guide self-management by outlining steps to adjust medications and seek emergency care based on symptoms or peak flow readings.[60] Early intervention with controller therapies, particularly ICS, improves long-term prognosis by mitigating airway remodeling and preserving lung function, as delayed treatment is associated with persistent structural changes.[60]Wheeze in Preschool Children
Epidemiology and Phenotypes
According to the 2024 European Respiratory Society (ERS) statement, preschool wheezing disorders are defined in children aged 0–<6 years with clinician-confirmed wheezing on at least one occasion and more than one episode.[63] Wheezing affects a substantial proportion of preschool children, with longitudinal studies estimating that 25% to 50% experience at least one episode by age 3 years, and nearly half of these cases involving recurrent episodes.[64][65] Most episodes in this age group are triggered by viral respiratory infections, which account for approximately 90% of wheezing illnesses during the first 3 years of life.[66] Prevalence tends to be higher among males, who face an elevated risk for early and persistent forms of wheeze compared to females.[67][68] Additionally, a family history of atopy significantly increases susceptibility, serving as one of the strongest predictors for the onset of wheezing in early childhood.[69][70] Phenotypes of preschool wheeze are heterogeneous, reflecting distinct clinical patterns and underlying mechanisms. Traditional temporal classifications include the transient early wheeze phenotype, which typically emerges in infancy, often linked to diminished lung function or viral triggers, and resolves spontaneously by age 3 years without progression to chronic respiratory disease. In contrast, the persistent wheeze phenotype begins before age 3 and continues beyond, frequently associated with atopy, impaired lung growth, and a higher likelihood of evolving into asthma; this group represents about 15-20% of early wheezers in cohort studies.[71][72] Earlier symptom-based classifications, such as episodic (viral) wheeze—characterized by symptoms confined to viral illnesses with symptom-free intervals—and multiple-trigger wheeze, where episodes are provoked by diverse factors like allergens, exercise, or irritants with possible ongoing symptoms, have been used to guide management but show overlap with temporal phenotypes and limited correlation with underlying pathology.[73][71] Recent guidelines, including the 2024 ERS statement and Global Initiative for Asthma (GINA) report, recommend moving beyond these traditional phenotypes due to their limited clinical utility, toward a "treatable traits" approach that identifies modifiable factors like type-2 inflammation (e.g., via elevated blood eosinophils or fractional exhaled nitric oxide [FeNO]) and aeroallergen sensitization to inform personalized diagnosis and therapy.[63][74] Among children with recurrent preschool wheeze, 30% to 50% progress to school-age asthma, with the risk amplified in persistent or multiple-trigger phenotypes due to factors like atopy and early lung function deficits.[75] This progression underscores the importance of early identification, as viral-induced episodes in atopic children carry a particularly elevated odds of persistent disease into later childhood.[76]Diagnosis and Prognosis
Diagnosing wheeze in preschool children primarily depends on a thorough clinical history, as young children under 5 years are typically unable to perform reliable spirometry due to poor cooperation and technical challenges in obtaining acceptable measurements.[77] Key elements of the history include the frequency and pattern of wheezing episodes, triggers such as viral infections or exercise, associated symptoms like cough or dyspnea, and response to previous treatments, which help confirm the presence of wheeze and rule out mimics like upper airway issues.[78] A trial of short-acting bronchodilators, such as inhaled salbutamol, is often used diagnostically; a positive response—defined as symptom improvement within minutes—supports reversible airway obstruction and guides further management.[79] Allergy testing, including skin prick tests or serum-specific IgE measurements, is recommended to assess for atopy, particularly in recurrent cases, as sensitization to common aeroallergens like house dust mite correlates with wheeze severity.[80] The 2024 ERS statement emphasizes incorporating biomarkers, such as blood eosinophils (>300 cells/μL indicating type-2 inflammation) or FeNO, and emerging tools like volatile organic compounds in exhaled breath, to identify treatable traits and improve diagnostic precision beyond clinical history alone.[63] Diagnostic challenges arise from the overlap between transient, virus-induced wheeze and early manifestations of persistent asthma, making it difficult to predict long-term outcomes without longitudinal observation.[81] Questionnaires such as the Asthma Predictive Index (API) address this by stratifying risk based on criteria like wheezing frequency (more than three episodes in the past year), at least one major risk factor (parental asthma or eczema), or two minor factors (physician-diagnosed eczema, wheezing apart from colds, or allergen sensitization); a positive API indicates a high likelihood (over 70%) of developing asthma by school age.[82] These tools are particularly valuable in preschoolers, where invasive or complex testing is impractical, though they require validation in diverse populations to account for phenotypic variations like viral versus multitrigger wheeze.[83] The prognosis for preschool wheeze is generally favorable, with approximately 60% of affected children outgrowing symptoms by age 6 and up to 80% by age 10, especially those with transient early-onset episodes linked to viral infections.[84] However, a subset persists into school-age asthma, with key predictors including atopy (sensitization to aeroallergens), personal history of eczema, and parental asthma, which increase the odds of persistence by twofold or more.[85] Early identification of these factors through history and testing allows for targeted interventions to potentially alter trajectories.[86]Non-Medical Uses
Slang Meanings
In contemporary slang, particularly in online and youth culture, "to wheeze" or "I'm wheezing" describes laughing uncontrollably to the point of breathlessness, producing raspy, audible exhalations that resemble wheezing sounds. This expression conveys intense amusement, often used in social media comments or reactions to humorous content, such as "That meme had me wheezing for minutes."[87][88] In British English, "wheeze" functions as a noun denoting a clever scheme, trick, or expedient plan, typically implying resourcefulness or mild deception, as in the idiomatic "a good wheeze" for a smart dodge around a problem. This usage emerged in the late 19th century from theater and music hall slang, where it specifically referred to improvised jokes, gags, or comic routines inserted by performers like clowns to engage audiences.[89][90][91] Culturally, the term's comedic ties persist in traditions like vaudeville and circus acts, where a "wheeze" signified a reliable humorous bit for eliciting laughs, evolving into modern internet memes that blend the laughter and scheme senses—such as exploitable comics satirizing over-the-top reactions or prank ideas. These applications highlight "wheeze" as a versatile slang evoking both physical comedy and witty ingenuity.[91]Etymological Origins
The word "wheeze" derives from the Middle English verb "whesen," meaning to breathe hard with a whistling sound, first recorded around the mid-15th century. It stems from a Scandinavian source, such as Old Norse "hvæsa" or "hvoesa," both meaning "to hiss," and is fundamentally onomatopoeic, imitating the raspy noise of strained respiration. This etymon traces back to the Proto-Indo-European root *ḱwes-, associated with panting or hissing actions.[92][93][88] The noun form, denoting the act or sound of wheezing, emerged in English by 1834, initially in medical literature to characterize a high-pitched respiratory noise. By the 1860s, it had branched into theater slang, referring to a repeated comedic catchphrase or gag, likely evoking the exaggerated, breathy delivery of performers. This slang sense further evolved in the late 19th and early 20th centuries to signify a clever scheme or plan, particularly in British usage, extending the idea of a predictable, rehearsed ploy.[94][92][91] Linguistically, "wheeze" connects to related onomatopoeic terms in Germanic languages, such as "whistle" from Old English "hwistlian," which shares roots in sounds of blowing or whistling, akin to Old English "hwǣst" (a blast of air) and Scandinavian cognates like Danish "hvæse." These terms highlight a broader Indo-European pattern of words mimicking airy, sibilant noises.[93]References
- https://en.wiktionary.org/wiki/wheeze
