Authors: Sarah S. Long
Categories: Article
Source: Principles and Practice of Pediatric Infectious Disease
Authors: Sarah S. Long
Mucopurulent rhinorrhea, or purulent nasal discharge, denotes nasal discharge that is thick, opaque, and colored. It occurs at any age, usually as a manifestation of self-limited, uncomplicated viral upper respiratory tract infection (URI). Mucopurulent rhinorrhea is most problematic in children younger than 3 years because (1) protracted course and frequent recurrence, especially in those in out-of-home child care;^1^ (2) parental concern about and misperception of etiology; and (3) overprescription of antibiotics by healthcare providers.^2–5^ Occasionally, this symptom is a clue to diagnosis of a treatable bacterial infection or underlying condition.
Acute, sporadic mucopurulent rhinorrhea has an infectious cause and almost always is the manifestation of the uncomplicated “common cold” due to rhinovirus, coronavirus, or other circulating viruses.^6^ When the problem is chronic or recurrent, or persistent and unilateral, broader underlying anatomic, obstructive, immunologic, and allergic disorders are considered (Table 23-1
).^7–10^ Onset in an infant younger than 3 months heightens suspicion of anatomic anomaly, ciliary dyskinesia, or cystic fibrosis. Accompanying sinusitis, otitis media, or pneumonia raises consideration of an immunologic deficiency (especially immunoglobulin deficiency or dysfunction, as in hypogammaglobulinemia or human immunodeficiency virus (HIV) infection), neutrophil defect, cystic fibrosis, or ciliary dyskinesia. URIs are conspicuously severe in such instances, with recrudescence almost immediately after discontinuation of antibiotic therapy. Unilateral nasal discharge and obstruction should prompt investigation for a foreign body, mass lesion, or unilateral posterior choanal atresia.TABLE 23-1Causes of Mucopurulent RhinorrheaChronic or RecurrentAcuteUnderlying ConditionsObstructing LesionsViral nasopharyngitisBacterial sinusitisAcute otitis mediaStreptococcal nasopharyngitisAnaerobic bacterial nasopharyngitis (nasal foreign body)AdenoiditisSyphilisPertussisAllergya Medicationsa(antihypertensives, oral estrogens, aspirin and nonsteroidal anti-inflammatory drugs)Pregnancya Hypothyroidisma Rhinitis medicamentosaa(αs1-adrenergic agonists)Immunoglobulin deficiencyHuman immuno-deficiency virus infectionCystic fibrosisCiliary dyskinesiaPolypsCongenital nasal anomalies (choanal atresia or stenosis, Tornwaldt cyst, deviated septum)Neuroembryonal mass (dermoid, encephalocele, glioma, teratoma)Tumor (hemangioma, angiofibroma, neurofibroma, lipoma, craniopharyngioma)Neoplasm (lymphoma, rhabdomyosarcoma, nasopharyngeal carcinoma)aRhinorrhea is characteristically clear, but opaque white discharge is not unusual.
Table 23-2 shows differentiating features of important or common causes of acute mucopurulent rhinorrhea; allergic rhinitis is included because it is frequently part of the differential diagnosis in older children and adolescents.TABLE 23-2Differentiating Among Causes of Nasal DischargeaViral Nasopharyngitis^1,^^11–15^Acute Bacterial Sinusitis^16,^^17,^^24^Streptococcal Nasopharyngitis^25^Foreign Body-Related Rhinitis (Bacterial)^18^Allergic Rhinitis^10^HISTORYPeak agePeak in first 2 years after “new recruitment” into childcare or schoolAny< 3 years< 3 years> 2 years; peak in adolescenceOnsetDryness, burning in nose or nasopharynxInsidious, with cough day and night; occasionally, acute, febrile, toxicInsidious; occasional acute, febrile, toxicInsidiousSeasonal; precipitantsAssociated symptomsNasal congestion, sneezing malaiseMalodorous breath; head or facial pain, edemaMalodorous breath ± hyponasal voiceSneezing; nasal or palatal pruritus; tearing; snoringFeverYes/noNo/yesLow/highNoNoDuration of discharge3–8 days= 10 days> 5 daysChronicChronic, recurrentPHYSICAL EXAMINATIONAssociated findingsRed, excoriated nares; sometimes, acute otitis mediaPeriorbital swelling, facial tenderness; mucopurulent postnasal dischargeAnterior cervical lymphadenitis; impetiginous lesions below noseMouth-breathingTransverse nasal or lower eyelid crease; periorbital hyperpigmentation; cobblestone conjunctivae or posterior pharynxCharacter of dischargeClear or colored, watery or thickThick, coloredThick, coloredUnilateral, purulent, putrid blood-stainedWatery, clear, or whiteRhinoscopyHyperemic mucosa; dry or glazed early, edematous later; crusted dischargeNormal mucosa; discharge from middle meatusNormal, hyperemic, or excoriated mucosaIdentifiable object (button, pit, nut), boggy mass (vegetable), or rhinolithPale or blue, edematous turbinatesDIAGNOSTIC TESTSNone; nasal smear shows polynuclear and mononuclear cells ± inclusion bodies, pyknotic epithelial cellsNone; sinus radiograph (> 6 years of age)Nasopharyngeal culture for streptococcus onlyRhinoscopyNasal smear shows goblet cells and eosinophils; skin test or radioallergosorbent test (RAST)CAUSEMultiple agents, depending on age and seasonStreptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis**Streptococcus pyogenesNormal nasopharyngeal facultative and anaerobic bacteriaAllergens in predisposed individualTHERAPYSaline nasal drops, humidification; amoxicillin if acute otitis mediaAmoxicillin; β-lactamase stable agentPenicillin VRemoval of obstruction; amoxicillin-clavulanate or clindamycin if tissue or sinus complicationAvoidance; oral antihistamine/decongestant; or topical corticosteroid; cromolynaSuperscript numbers indicate references.
In uncomplicated viral nasopharyngitis or rhinitis, nasal discharge is initially clear but can become white, yellow, or green (related to mucous secretions, dryness, blood, exfoliation of damaged epithelial cells and cilia, and leukocytic inflammatory response). Presence of high fever and persistence of discharge depend on the specific viral cause but are more common in uncomplicated infection than generally perceived.
In a study of hospitalized children, more than 50% of those with uncomplicated adenovirus, influenza, parainfluenza, or respiratory syncytial virus infection had temperatures >39°C, and 12% had temperatures >40°C; height of fever in these children was not different from that in children with serious bacterial infection.^11^ Fever persisted for 5 days or longer in 37% of the children in the study; 20% to 30% of those with adenovirus or influenza A infection had fever for 7 days or longer. In another study, nasal discharge or congestion associated with uncomplicated URI persisted for 6.6 days in 1- to 2-year-old children who were in home care and for 8.9 days in children younger than 1 year in daycare centers.^1^ In this study, 13% of 2- to 3-year-old children in out-of-home childcare had symptoms for more than 15 days.
The bacteriology of nasopharyngeal flora in children with uncomplicated viral respiratory illnesses, mucopurulent rhinorrhea, acute otitis media, and sinusitis has been evaluated and compared with that in normal children.^6,^ ^12–23^ Viral infection is associated with acquisition of new serotypes of Streptococcus pneumoniae and with temporally increased risk of acute otitis media.^21^ Quantitative, and some qualitative, differences in nasopharyngeal flora have been found in children with purulent nasopharyngitis (and uncomplicated viral upper respiratory illnesses), with excessive isolation rates reported for S. pneumoniae and Haemophilus influenzae, ^13,^ ^18^ Peptostreptococcus spp., Fusobacterium spp., and Prevotella melaninogenica. ^18,^ ^19^ The significance of such findings is unclear; isolation of such organisms may reflect exuberant proliferation in virus-induced inflammatory mucus or acquisition of a more robust specimen than is collected in healthy subjects. Furthermore, “high” rates of isolation of S. pneumoniae in 25% to 46% of subjects do not exceed those in normal young children when fastidious technique is used.^22^
Only two systematically performed studies on the course of mucopurulent rhinorrhea have been published. In one study, prospective evaluation showed that there was no difference in duration of illness or complications in children with clear or purulent nasal discharge.^14^ In a placebo-controlled, blinded study of 142 children 3 months to 3 years old with mucopurulent rhinorrhea of any duration, antibiotic therapy (cephalexin), systemic use of an antihistamine-decongestant, or both had no effect on the course or complications of mucopurulent rhinorrhea.^12^ In a small pilot study of 13 children younger than 2 years whose purulent nasal discharge had persisted for at least 10 days without improvement, amoxicillin-clavulanate (40 mg/kg per day divided into 3 doses for 10 days) was significantly associated with resolution of symptoms in comparison with placebo.^15^
Response to antimicrobial therapy does not necessarily validate an entity of bacterial nasopharyngitis, however; it seems more likely that children with such responses have an incomplete symptom complex of ethmoid sinusitis. Acute bacterial adenoiditis is postulated to be another cause of purulent nasal discharge (1) tympanic membranes are normal; (2) S. pyogenes is not found in culture specimens; and (3) radiographs show an enlarged adenoid shadow but no sinus abnormality.^23,^ ^24^ Critical study has not been performed to validate this entity. A comparison of clinical and radiographic assessments of adenoidal enlargement may be an important first step.^25^
Mucopurulent rhinorrhea of 10 or more days' duration without improvement (or recrudescence after improvement) that is associated with daytime cough (which is frequently worse at night), or malodorous breath, facial pain, edema, headache, or fever is highly suggestive of paranasal sinusitis.^17,^ ^26^ Sinus radiographs show significant abnormalities in nearly 90% of children 2 to 6 years old with such findings (see Chapter 34, Sinusitis), and thus support the validity of clinical diagnosis without need for imaging.
In children younger than 3 years, S. pyogenes has been associated with high fever, toxicity, and clear rhinorrhea or indolent infection with irregular fever and purulent nasal discharge, sometimes with associated excoriation of nares or tender anterior cervical lymphadenitis.^13,^ ^18,^ ^25^ In a streptococcal outbreak studied in a childcare facility for school-aged and young children, 26% of children younger than 3 years were affected, but pharyngitis was predominant, with no case of nasal streptococcosis.^27^
Bacterial nasopharyngitis associated with nasal foreign body is typified by the young age of the patient and putrid, commonly blood-stained unilateral nasal discharge. Fever is unusual unless infection has spread to contiguous sinuses or distant sites. Prevotella, Fusobacterium, and Peptostreptococcus spp. as well as facultative flora are responsible. Nasal discharge can be the first manifestation of congenital syphilis and a later finding in nasal diphtheria, in which discharge is putrid and sanguineous and contains pieces of pseudomembrane.
Allergic rhinitis typically begins in the second decade of life, is uncommon before age 3 years, and may be rising in incidence in children between these ages. Diagnosis is suspected from the season, environmental precipitants, personal and family history of allergy, other associated symptoms and physical findings, and the response to specific interventions of avoidance or pharmacotherapy (see Table 23-2). Nasal secretions are usually clear or whitish. Diagnostic usefulness of nasal cytologic analysis is controversial.^10,^ ^28^ Relative eosinophilia (above 20%) is suggestive but not diagnostic of allergic rhinitis. The findings in vasomotor rhinorrhea, which is thought to be due to increased parasympathetic tone of the nasal mucosa, are similar to those in allergic rhinitis, except that symptoms of allergy and nasal eosinophils are absent. In severe allergic rhinitis, the inflammatory phase of response can cause accumulation of neutrophils and mononuclear cells.^10^
In the vast majority of children with purulent nasal discharge (even if thick and green) of up to 1 week in duration, history and setting of illness, associated symptoms, and physical findings suggest uncomplicated viral URI. Antimicrobial therapy is inappropriate unless acute otitis media or sinusitis is diagnosed from additional findings (see Chapter 34, Sinusitis). Symptomatic therapy with saline nose drops or lavage facilitates expulsion of secretions and provides humidification. Its effectiveness reduces parental pressure to prescribe an antibiotic.^29^
If mucopurulent rhinorrhea persists for more than 5 days, and especially if some findings (e.g., anterior cervical lymphadenitis, scarlatiniform rash, excoriation around nostrils) or the epidemiology heightens the likelihood of group A streptococcal disease, nasopharyngeal specimens should be obtained for culture of S. pyogenes only. If findings are positive, penicillin V is given for 10 days. Routine culture for, or recovery of, S. pneumoniae, H. influenzae, Moraxella catarrhalis, or Staphylococcus aureus has no meaning and is an opportunity for misinterpretation.
If mucopurulent rhinorrhea persists for more than 10 days without diminution, and especially if other symptoms are present, paranasal sinusitis is likely. Nasal mucosa is examined after use of single or second (5 minutes after the first) application of a topical vasoconstrictor such as oxymetazoline.^15^ If purulent secretions flow from the middle meatus, the diagnosis of acute sinusitis is confirmed. Signs of allergic rhinitis can also be confirmed. Radiographs may be helpful in patients older than 6 years to confirm sinusitis (or possibly to suggest adenoiditis). Pending definitive efficacy studies, many clinicians would treat children who have purulent nasal discharge of greater than 10 days' duration as for acute sinusitis, usually with amoxicillin initially. When antimicrobial therapy is effective, substantial improvement of symptoms is expected within 48 to 72 hours. Therapy is continued for 1 week beyond complete resolution of respiratory symptoms.
Stridor is a rough, crowing sound caused by passage of air through a narrowed upper airway, which includes the extrathoracic trachea, larynx, and hypopharynx. Because the extrathoracic airway normally narrows during the inspiratory phase of respiration, stridor due to upper-airway disease occurs during inspiration (or is more pronounced during inspiration if severe narrowing causes obstruction during inspiration and expiration). Because the intrathoracic trachea normally narrows during expiration, obstruction of the intrathoracic trachea, such as that due to extrinsic compression of vascular ring or intraluminal obstruction of foreign body, inflammation, or tracheomalacia, causes a loud noise, acoustically like stridor, heard during both phases of respiration but more pronounced on expiration. Extrathoracic obstruction (inspiratory stridor) is associated with prolonged inspiration and underaeration of the chest, whereas intrathoracic obstruction (expiratory stridor or wheezing) is associated with prolonged expiration and overinflated chest. Stridor can be associated with mild tachypnea, but a respiratory rate >50 breaths/minute should not be ascribed to upper-airway obstruction alone.
The timbre of the stridulous sound provides a clue to etiology; for example, (1) the high-pitched, fixed, dry sound of congenital subglottic stenosis; (2) the wet, rhonchal changing sound of inflammatory laryngotracheitis; and (3) the low-pitched, vibratory, somewhat positional sound of laryngomalacia. Associated voice changes are useful in specifying disease as well. Vocal cord paralysis causes a weak, dysphonic cry; supraglottic obstruction, a muffled voice; and laryngotracheitis, hoarseness or aphonia, frequently with a barking cough.
Categorization of the setting and duration of stridor as acute, persistent, or recurrent or episodic provides a framework for considering likely causes (Table 23-3 ).^30–34^ Infectious agents cause most acute upper-airway obstruction, from intraluminal, epithelial inflammation or by encroachment on the airway by reactive or infected lymphoid tissue in parapharyngeal or paratracheal spaces. Fungal or viral tracheobronchitis must be considered when stridor occurs in an immunocompromised child; odynophagia and dysphagia are also commonly present.^31^ Congenital anatomic abnormalities are considered, especially in infants whose persistent stridor began neonatally. Acquired obstruction can have abrupt onset and an obvious cause (such as foreign-body aspiration or necrotizing tracheobronchitis in ventilated neonates) or more insidious onset and inapparent cause (such as expanding laryngotracheal papillomas or hemangioma or an extrinsic compressing mass). The younger the infant, the more likely that sudden obstruction, apnea, or feeding difficulties overshadow a singular complaint of stridor.TABLE 23-3Causes of Upper-Airway Obstruction and Stridora30AcutePersistent^30^ INFECTIOUS Viral laryngotracheitis (croup)Bacterial tracheitisEpiglottitis, supraglottitisPeritonsillar, retropharyngeal, or parapharyngeal abscessTracheobronchitis associated with immunodeficiency^31^
CONGENITAL Laryngotracheal web, cleft, cyst, hemangiomaTracheal stenosisVascular ringLaryngotracheal malaciaNeuromuscular disorderCystic hygroma NONINFECTIOUS AngioedemaForeign bodyNecrotizing tracheobronchitis in neonates^32,^ ^33^ Recurrent/episodicSpasmodic croupGastroesophageal reflux^4^
ACQUIRED Posttraumatic tracheal stenosisForeign-body aspirationMediastinal mass (tumor, lymphatic, vascular)Papilloma (perinatally acquired)Posttraumatic spinal cord, vagal or glossopharyngeal nerve, or vocal cord damageBulbar neuropathy (infectious, postinfectious, malignant)aSuperscript numbers indicate references.
Recognition, care to avoid precipitating sudden airway occlusion, and urgent, expert intervention to establish an airway when indicated are paramount to avert disastrous outcomes of acute upper-airway obstruction. Table 23-4 shows characteristic features of infectious causes of stridor and acute airway obstruction.^35–45^ Viral laryngotracheitis (infectious croup) or laryngotracheobronchitis due to parainfluenza viruses is by far the most common.^35,^ ^36^ Influenza viruses, respiratory syncytial virus, adenoviruses, and other viruses typically cause symptomatic disease elsewhere in the respiratory tract, but during epidemic seasons, stridor is the predominant feature in a minority of infected children. Bacterial tracheitis is usually a complication of viral laryngotracheitis (with concordant peak age and season) but can occur at any age or as a complication of oropharyngeal surgery.^46^ Staphylococcus aureus is the most common cause, followed by Streptococcus pyogenes; the role of anaerobic bacteria is less clear.^43,^ ^46^ With the universal use of H. influenzae b vaccine, epiglottitis is a rare cause of stridor; current cases of supraglottitis are more likely to affect the aryepiglottic region and to be caused by streptococci. Parapharyngeal and retropharyngeal infections in young children must also be considered; their incidence is increasing^45,^ ^47,^ ^48^ (see Chapter 30, Infections Related to the Upper and Middle Airways).TABLE 23-4Differentiating Among Infectious Causes of Upper-Airway ObstructionaViral Laryngotracheitis^35–37^Supraglottitis^38,^^39^Bacterial Tracheitis^40–43^Retropharyngeal Abscess^38,^^40,^^44,^^45^HISTORYPeak age1–2 years3–6 years, any2–4 years, any< 3 yearsPeak seasonLate fall, late springAnyLate fall, late spring; anyAnyProdromeViral illnessUncommonViral illnessUncommonOnset of stridorGradualAbruptAbruptAbruptPHYSICAL EXAMINATIONPeak temperature (°C)38–39> 39> 39> 39Predominant findingsBrassy cough, stridorToxicity, stridorToxicity, stridorToxicity, stridorAssociated findingsBark, rhinorrheaSore throat, odynophagia, dysphagia, anxiety, droolingBrassy cough, anxietyLethargyVoiceHoarse, raspyNormal, muffled, muteHoarse, raspyMuffled, mutePositionAny; thrashing“Sniffing dog”; stillAny; thrashing“Sniffing dog”; stillAirway occlusionPredictable from degree of stridorSuddenSuddenSuddenResponse to racemic epinephrine?Yes, with reboundNoNo or partialNoLABORATORY TESTSPeripheral neutrophilsNormal or lowHighImmatureImmatureRADIOGRAPHHypopharynxDistendedDistendedDistendedAnteriorly displacedAirwaySubglottic narrowing; edema cordsSwollen epiglottitis, aryepiglottic foldsSubglottic narrowing; irregular trachea intraluminal massPrevertebral soft-tissue mass with (not valid sign if expiratory film, flexed neck)ChestUnderaerated ± cardiomegalyUnderaerated ± cardiomegalyPatchy parenchymal peribronchial infiltrateUnderaerated ± cardiomegalyENDOSCOPYRed, edematous subglottis; crusting pseudomembraneRed, edematous supraglottic structuresRed, edematous, eroded trachea and bronchi; purulence, pseudomembraneBulging mass in posterior pharyngeal wall; purulenceCAUSEParainfluenza viruses (epidemic); other viruses (sporadic)Streptococcus pyogenes, Streptococcus pneumoniae, Haemophilus influenzae bStaphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae**Streptococcus pyogenes; Staphylococcus aureus; rare Streptococcus pneumoniaeaSuperscript numbers indicate references.
The history surrounding the onset of stridor and the patient's age and demeanor are the most helpful clues to the likely site and cause of infection. The child with viral laryngotracheitis usually has had 2 to 3 days of typical upper respiratory tract illness when cough worsens and stridor begins. The child with bacterial tracheitis has usually had a similar background illness and then has sudden high fever, toxicity, and rapid progression of airway obstruction. The young child with retropharyngeal abscess or adolescent with peritonsillar abscess has less stridor but refuses to swallow, has a muffled voice, and a guarded posture to maximize the oropharyngeal airway. Trismus is an expected and useful finding in patients with peritonsillar abscess as well as in some with lateral pharyngeal space infections of odontogenic origin.^38^ Epiglottitis and supraglottitis cause the patient to guard anxiously in a sitting posture with arms back, jaw forward, and chin raised (“sniffing dog”) to maximize “lift” of the epiglottis away from the airway. In contrast, subglottic, tracheal obstruction cannot be lessened by position; patients with laryngotracheitis or bacterial tracheitis thrash about with the anxiety of suffocation.
The expected course and sequelae of acute infectious airway obstruction are shown in Table 23-5 .^49,^ ^50^ Children with viral laryngotracheitis are less prone to sudden complete obstruction; hourly course is predictable by degree of stridor and adequacy of aeration; response to racemic epinephrine and corticosteroid therapy usually averts intubation. Establishment of an artificial airway is urgently required for almost all patients with stridor due to acute supraglottic and bacterial tracheal infection, and for many with retropharyngeal infection. The course of disease in children with bacterial tracheitis can be further complicated, because infection (and obstructive consequences) commonly extends for the length of the trachea and below.TABLE 23-5Expected Course and Sequelae of Acute Infectious Upper-Airway ObstructionViral Laryngotracheitis^37,^^49,^^50^Supraglottitis, EpiglottitisBacterial Tracheitis^41,^^42^Retropharyngeal AbscessArtificial airway (% of cases)< 20> 90> 75= 75Median intubation period4 days2 days6 days2 daysAirway occlusion after intubationRareNoYesNoDeath during hospitalizationNoNoYesNoAirway sequelae (% of cases)< 3Rare<3No^a^ Superscript numbers indicate references.
Cough is a critical protective mechanism to expel particulate matter from the larynx and trachea as well as a cardinal sign of infectious and noninfectious respiratory tract and nonrespiratory tract disorders. Although the vast majority of coughs are related to self-limited infections, occasional life-threatening infectious and noninfectious causes may be overlooked unless the clinician adopts a disciplined approach. Careful assessment of a pathologic cough – its onset, duration, clinical context, and association with other findings as well as its specific timbre, pattern, and productivity – frequently predicts the site of pathophysiology and narrows the differential diagnosis to a limited number of entities. Table 23-6 provides a framework for assessment and lists the differentiating features of the various causes of cough.TABLE 23-6Differentiating Among Causes of CoughPeak AgeNature of CoughCough Dominant Feature?Anticipated/Associated FindingsINFECTIONS OF THE RESPIRATORY TRACTViral laryngotracheitis> 5 yearsBrassy, painfulYesHoarse, raspy voice; viral URI complexaViral laryngotracheitis/laryngotracheobronchitis4 months–3 yearsBarking, brassyCodominant with stridorStridor, hoarseness, viral URI complexaMycoplasmal tracheobronchitisAdolescentHacking, paroxysmal, painfulYesProdromal, fever, headache, myalgia; then gradual worsening coughPertussisInfancy, adolescenceSudden paroxysm of explosive machine-gun bursts (15–30 per breath)YesBulging, watering eyes during paroxysm, posttussive emesis; skin and conjunctival hemorrhages; afebrile, without lower respiratory tract symptoms or symptoms between paroxysmsChlamydia trachomatis pneumonia1–3 monthsStaccato, dry (single cough per breath)YesHistory can include conjunctivitis; afebrile, tachypnea, ralesBronchiolitis4 months–2 yearsHigh-pitched or gruntNoWheezing, rhinorrhea, respiratory distress;Pneumonia (bacterial or viral)AnyWet, productive or nonproductiveCodominant with respiratory distressTachypnea, rales, respiratory distress; feverPleurodyniaAnyInspiratory hitch; expiratory gruntCodominant with chest painChest pain; costochondral tendernessSinusitisAnyIrritative; occurs in day and worsens at nightSometimesMucopurulent rhinorrhea, postnasal discharge; facial pain, swelling, or tenderness; headache;Tracheoesophagitis (fungal or viral)AnyIrritativeNoOdynophagia or dysphagia; immune-compromised host; hoarseness; oropharyngeal lesionsCystic fibrosis< 2 years; anyWet, productive; paroxysmal, hackingSometimesPoor growth; persistent and recurrent sinusitis, pneumonia; digital clubbingCARDIAC CONDITIONSPurulent pericarditisAnyGruntSometimesFever, toxicity, respiratory distress/dyspnea; displaced point of maximum impulse; muffled heart soundsMyocarditisAnyGruntSometimesFatigue, dyspnea, tachypnea;Congestive heart failureAnyGrunt, wet, or brassySometimesFatigue, dyspnea, sweating, tachycardia, tachypnea; ± fever; distended neck veins, liverNONINFECTIOUS AIRWAY ABNORMALITIESGastroesophageal reflux6 weeks–6 monthsHigh-pitched, dryCodominant with other symptomsStridor, choking, gagging, irritability, arching (Sandifer syndrome)Reactive airway6 months–adolescenceIrritative dry, repetitive (not paroxysmal); night especiallySometimesAtopic, precipitants, seasonal; ± wheezing; response to β-agonistCongenital vascular rings, pulmonary slingInfancyBrassyNoStridor; onset of symptoms in first month of lifeCompression on airway or glossopharyngeal or phrenic nerveAnyIrritative, drySometimes initiallyCan be positional (tumors, other masses), associated with other neuropathies, stridor, changes in phonationPSYCHOGENICAdolescenceVibratory, low-pitched, honkingYesFamily dynamics and other somatizationaViral upper respiratory tract infection (URI) complex consists of fever, rhinorrhea, sore throat, conjunctivitis, exanthem, enanthem.
Cough should not be accepted as a sign of self-limited URI in infants younger than 3 months. The mnemonic CRADLE may be useful to call to mind important considerations for such ^51^ C, cystic fibrosis; R, respiratory tract infections (especially pneumonia and pertussis); A, aspiration (swallowing dysfunction, gastroesophageal reflux, tracheoesophageal fistula); D, dyskinesia of cilia; L, lung, vascular, or airway malformations; E, edema (heart failure, pulmonary lymphangiectasia).
There is considerable overlap in symptomatology of cough caused by certain infectious agents, such as Bordetella pertussis or Mycoplasma pneumoniae in adolescents,^52^ because of a common tracheobronchial site of pathophysiology and frequent dual infection by microbes and viruses.^53^ Chlamydophila pneumoniae also can cause similar symptoms.^54^ Although both B. pertussis and Chlamydia trachomatis infections are associated with prominent cough in the absence of fever in young infants, there should be little difficulty in distinguishing the two entities. B. pertussis causes a dramatic, debilitating paroxysmal cough without airway or lower tract abnormalities (unless secondary pneumonia occurs, leading to fever and toxicity), whereas C. trachomatis causes pneumonia with prominent the cough is only important because it brings the child to medical attention (see Chapter 162, Bordetella pertussis [Pertussis] and Other Species; Chapter 167, Chlamydia trachomatis).
Diagnosis of pneumonia is based on signs of lower respiratory tract involvement, such as tachypnea and retractions, in addition to cough, and the likely causative agent is determined from the constellation of clinical findings (Tables 23-7 and 23-8 ). Protracted cough is the major symptom of recurrent or persistent pneumonia (see Chapter 37, Persistent and Recurrent Pneumonia). Cystic fibrosis can masquerade as pertussis, asthma, or bronchitis because of prominence of cough. Diagnosis of purulent pericarditis is frequently delayed, symptoms being misinterpreted as those of respiratory tract infection. Stretch of the pericardium, ischemic compression of the myocardium, or compression of pericardial mass on the airway can cause “cough” that is a hitch at the end of inspiration or, more frequently, a grunting expiratory sound.TABLE 23-7Symptoms and Signs of PneumoniaSymptomsSignsPhysical ExaminationsFeverFeverRalesCoughCoughWheezesRapid breathingTachypneaDiminished breath soundsDifficulty breathingDyspneaTubular breath soundsVomitingRetractionsDullness to percussionPoor feedingNasal flaringDecreased tactile and vocal fremitusIrritabilityGruntingLethargySplintingMeningismusChest painCyanosisIleusAbdominal painPleural friction rubShoulder painTABLE 23-8Clinical Features of Pneumonia in Infants Younger Than 3 MonthsRespiratory Syncytial VirusOther Respiratory VirusesChlamydiaCytomegalovirusPertussisaHISTORYSeasonWinterUnique to eachAnyAnyAny; peak July–OctoberOnsetAcute, daysAcute, daysInsidiousInsidiousProgressive, daysIllness in othersURIURI, “flu,” croupNoNoCoughFeverHalf of casesMajority of casesNoUnusualNoCoughYesYesYes/staccatoYesYes/paroxysmalAssociated featuresApnea, URIURI, croup, conjunctivitisConjunctivitis (prior or current)Failure to thrive, hepatosplenomegalyApnea, cyanosis, posttussive vomitingPHYSICAL EXAMINATIONPredominant featureRespiratory distressRespiratory distressCoughFailure to thriveCoughGeneral appearanceIll, not toxicIll, not toxicWell, tachypneicChronically illWell between paroxysmsDegree of respiratory findingsDegree of illness = findingsDegree of illness = findingsFindings > degree of illnessIll general appearance > respiratory illnessIll only during coughAuscultationWheezes, coarse cracklesCrackles, wheezesDiffuse cracklesCrackles, ± wheezesClearLABORATORY STUDIESChest radiographHyperaeration, sub-segmental atelectasisHyperaeration, ± peribronchial thickening, ± diffuse interstitial infiltratesHyperaeration, diffuse alveolar and interstitial infiltratesDiffuse interstitial infiltratesNormal or perihilar infiltrateWhite blood cell countNormal or lymphocytosisNormal, lymphocytosis, neutropeniaEosinophiliaNormal, eosinophilia, lymphocytosis, neutropeniaLymphocytosis; eosinophilia unusualOther findingsHypoxemiaIncreases in IgG, IgA, IgMIncreases in IgG, IgA, IgM; thrombocytopeniaDiagnostic testsNasal wash EIA, DFA, cultureNasal wash EIA, DFA, culture; throat cultureConjunctival, NP DFA, EIAThroat, bronchoscopy, lung biopsy, or urine cultureNP DFA, culture, PCRDFA, direct fluorescent antibody (test); EIA, enzyme immunoassay; Ig, immunoglobulin; NP, nasopharyngeal specimen; PCR, polymerase chain reaction; URI, upper respiratory tract infection.aPertussis is included in this table because it should be considered in young infants with cough and respiratory distress, although pneumonia is characteristically absent.
Lack of context of an acute infection, prolonged duration of cough, presence of inciting factors, or specific physical findings suggest noninfectious causes. Infants with congenital anomalies of great vessels that compress and confine the trachea, esophagus, or both usually have respiratory symptoms (stridor, cough, or difficulty breathing during feeding) dated “from birth.” Secondary pneumonia or aspiration can complicate the disorder or confuse the diagnosis. Coughing as a manifestation of milk allergy in infants is not well established. Increased postprandial coughing has been documented when thickened feedings are used as therapy for suspected or proven gastroesophageal reflux; the mechanism is ill defined.^55^ Cough, stridor, or choking spells, without regurgitation, can be a manifestation of gastroesophageal reflux in infants.^34,^ ^56^ Clues to this diagnosis (1) typical age of onset at 6 weeks to 6 months; (2) postprandial occurrence of cough; and (3) history of pneumonia. Diagnosis is best confirmed by esophageal pH study.
Cough can be the result of irritation of normal airways by mucus or purulent secretions (e.g., postnasal discharge or sinusitis) or of hyperreactive airways by secretions, infection, environmental stimuli, or smoke. Dry cough and frequent throat-clearing are clues to irritation of postnasal secretions. Sinusitis and cough-variant asthma are the most common causes of chronic cough in children, even for those younger than 2 years (with a normal chest radiograph).^57^ Pertussis and tracheal anomalies are frequently missed diagnoses when protracted cough is incorrectly ascribed to sinusitis or cough-variant asthma. Sinusitis as a cause can usually be uncovered by noting its association with infectious prodrome, the occurrence of cough day and night, or associated symptomatology; radiographs or limited computed tomographic study frequently clarify a confusing situation (see Chapter 34, Sinusitis).
Cough of asthma is suspected when there is family or patient history of allergies and symptoms are recurrent, are not associated with acute illness, are exaggerated at nighttime, or are provoked by exercise, cold, smoke, specific allergens, or pollutants. A diagnostic trial of bronchodilator therapy can be used in young children if the clinical history is compelling and other diagnoses are excluded or highly unlikely. Respiratory function is tested in older children, with a diagnostic trial of bronchodilator therapy if the result is abnormal, or methacholine challenge if the result is normal.^58^
Additional considerations in children whose cough is not explained by acute infection or allergic process include compression of the trachea by tumor mass, lymph nodes, or enlarged vessels; irritation of the diaphragm by an abdominal disease process; and irritation of the pleura or phrenic nerve by tumor, inflammatory fluid, mass, or blood. Cough is usually irritative (dry, occurring at end of inspiration, diminished by voluntarily decreased inspiratory excursion). Neuropathy, myopathy, and bulbar involvement in infectious, metabolic, and immunologic disorders or malignancy (especially neuroblastoma and rhabdomyosarcoma) are considered when symptoms are otherwise unexplained. Cough is almost invariably associated with other signs, such as gurgling, weak cry, hoarse or quiet voice, and stridor.
Habit cough has a classic presentation, usually after an uncomplicated “starter” URI in an adolescent (commonly a girl). The cough is loud, rattling, resonant, and low-pitched, occasionally with canine or seal-like bark. It never awakens the patient from sleep. Others, but not the patient, are bothered by the cough. This diagnosis is not tenable in the presence of weight loss or systemic illness. Invasive diagnostic procedures and narcotic cough suppressants are inappropriate and ineffective, and further foster the family's misplaced focus. Reassurance, redirection of focus, and frequent visits to the primary care provider for examination and caring support are curative.
Tachypnea can be a voluntary or involuntary response to anxiety, fright, or pain; an abnormal breathing pattern related to central nervous system dysfunction; or the physiologic response to increased temperature or metabolic state. It is most usually the response to respiratory acidosis or hypoxemia of acute infection or the attempt to restore pH balance during metabolic acidosis (e.g., diabetes, salicylate poisoning, dehydration). Metabolic causes should not be forgotten, while the clinician pursues the much more likely primary pulmonary causes. Additionally, tachypnea can result from primary cardiac abnormalities (congestive heart failure, cyanotic congenital heart disease), pulmonary vascular abnormalities (cardiac shunts, capillary dilatation, hemorrhage, obstructed return to the heart, or infarction), impaired lymphatic flow (congenital lymphangiectasia, tumor) or pleural fluid collections (hemorrhagic, purulent, transudative, or lymphatic fluid or a misplaced infusion from a vascular catheter).
Tachypnea is thought to be the best clinical predictor of lower respiratory tract infection in children. Reference values for normal respiratory rates have been reconfirmed in healthy and febrile infants and young children.^59–62^ Roughly, respiratory rates >60 breaths/minute in infants younger than 6 months, >50 breaths/minute in infants 6 to 11 months old, and >40 breaths/minute in children 12 to 59 months old have a sensitivity of 50% to 85% for diagnosis of lower respiratory tract infection with specificity of 70% to 97%. A useful cutoff respiratory rate for febrile children 5 years of age and older might be 30 breaths/minute. For infants younger than 24 months, the younger the patient, the less likely that pneumonia is present if tachypnea is absent. Performance of a chest radiograph in febrile infants without an apparent focus of infection to exclude pneumonia “missed” by physical examination has extremely low yield in the absence of tachypnea.^63,^ ^64^ In one study, for infants younger than 2 months, respiratory rate of 60 breaths/minute, retractions, or nasal flaring had sensitivity for diagnosis of pneumonia of 91%.^62^
Other symptoms and signs associated with pneumonia, such as cough, are more sensitive but are nonspecific; nasal flaring, intercostal retractions, and cyanosis have less sensitivity (25%, 9%, and 9%, respectively) but high specificity (87%, 93%, and 94%, respectively).^61^
Grunting is an expiratory sound produced in the larynx when vocal cords are adducted to generate positive end-expiratory pressure (self-induced PEEP) and increased resting volume of the lung. Its causes are myriad but never trivial. Grunting can be a sign of surfactant deficiency in the neonate, or of pulmonary edema, foreign-body aspiration, severe pneumonia, mediastinal mass or severe mediastinal shift from any cause, pleuritic or musculoskeletal chest pain, or myopericarditis or other cardiac abnormalities at any age.^65^ Care must be taken with sedation, positioning, or intubation of such patients; the sudden removal of the self-induced PEEP can cause hypoxemia and respiratory arrest.
Adventitial respiratory sounds usually indicate lower respiratory tract disease, pulmonary edema, or hemorrhage. Wheezes are musical continuous sounds present predominantly on expiration and are a sign of airway obstruction. Widespread bronchiolar narrowing, as most commonly occurs with the inflammation of virus-associated lower respiratory tract infection, produces heterophonous high-pitched, sibilant wheezes of variable pitch and presence in different lung fields. Fixed obstruction in a larger airway, as from foreign body or anomaly, produces homophonous, monotonous wheeze. Rhonchi, sometimes also termed low-pitched wheezes, or coarse crackles, are nonrepetitive, nonmusical, low-pitched sounds frequently present on early inspiration and expiration; they are usually a sign of turbulent airflow through secretions in large airways. Fine crackles (the term preferred by pulmonologists for rales, which has a variety of meanings across languages)^66^ are high-pitched, low-amplitude, end-inspiratory, discontinuous popping sounds indicative of the opening of peripheral air–fluid interfaces. Fine crackle is the auscultatory finding suggestive of the diagnosis of pneumonia. Auscultatory abnormalities of crackles and wheezing have disparate diagnostic usefulness among various studies, depending on the categorization of bronchiolitis. Tachypnea is a more sensitive finding than crackles for bacterial pneumonia; wheezing is more sensitive than tachypnea for bronchiolitis.
Diminished or distant breath sounds, dullness to percussion, and decreased vocal fremitus indicate peripheral pulmonary consolidation, pleural mass, or fluid collection. Tubular breath sounds (low-pitched sound of similar intensity throughout inspiration and expiration, as normally heard in the intrascapular area), dullness to percussion, and increased vocal fremitus indicate parenchymal consolidation, atelectasis, or the presence of another continuous tissue or fluid density abutting both a bronchus and the chest wall.
Table 23-7 shows symptoms and signs of pneumonia in infants and children. Although fever, cough, and tachypnea are cardinal features, any or all of them can be overshadowed or overlooked in patients who come to medical attention for pneumonia-associated stiff neck, abdominal pain, or chest pain or for nonspecific symptoms of illness as well as in infants with feeding difficulty. Classic symptoms of pneumonia reported in adolescents and adults are fever, chills, pleuritic chest pain, and cough productive of purulent sputum, with less noticeable tachypnea.^67^
In young infants, acute infection with bacterial and nonbacterial respiratory tract pathogens frequently leads to lower respiratory tract infection. Except in the first few days of life, when pneumonia is due predominantly to bacteria acquired from the mother's genital tract or to organisms acquired transplacentally, nonbacterial pathogens are overwhelmingly predominant.^68^ As perinatally acquired agents persist, community exposures increase, and maternally derived antibody protection wanes, the infant between 3 weeks and 3 months old is vulnerable to a unique array of lower respiratory tract pathogens.^69^ Clinical setting, specific symptom complex, and severity of illness in proportion to findings on physical examination aid distinction of likely causes and guide the diagnostic and therapeutic approach (see Table 23-8). Although the pathogens listed in Table 23-8 are frequently referred to as causing “afebrile pneumonia,” this is a misnomer, because Bordetella pertussis infrequently causes lower respiratory tract abnormalities,^70,^ ^71^ and respiratory syncytial virus and especially other respiratory viruses frequently cause fever.^11,^ ^68,^ ^72,^ ^73^ A causal role for Ureaplasma urealyticum is not completely defined, because the situation is confounded by the asymptomatic presence of this organism in women and young infants. Pneumonia due to Pneumocystis carinii is probably confined to infants with severe debilitation or immune defects.
A number of studies using complex diagnostic methodologies have confirmed the specific cause of pneumonia in 45% to 85% of cases.^74–78^ Viral etiologies predominate, and, currently, most are amenable to diagnosis. Table 23-9 categorizes the features of acute pneumonia in older infants, children, and adolescents by etiology. No single fact in history or finding on examination is unique for any agent, but when they are taken together, a working diagnosis emerges and guides intervention or further diagnostic testing. Chest radiography and laboratory tests are reserved for patients who are ill or whose clinical picture is not compelling for a category of etiologic agents. The efficacy trial and postmarketing studies of heptavalent conjugate pneumococcal vaccine infers Streptococcus pneumoniae as a relatively common cause of pneumonia with patchy or consolidative infiltrates.^79,^ ^80^ Urine antigen detection test in children with lobar pneumonia also supports the important role of S. pneumoniae.^81^ Currently, ascribing a causal role to S. pneumoniae is confounded by the findings of prolonged asymptomatic carriage and inconsistent serologic results among studies.^82^ TABLE 23-9Clinical Features of Acute Pneumonia in Children and AdolescentsBacteriaVirusMycoplasmaTuberculosisHISTORYAgeAny; infants especiallyAnySchool ageAny; < 4 years and 15–19 years especiallyTemperature (°C) ≥ 39Most < 39Most < 39Most < 39 (unless empyema)OnsetAbruptGradualWorsening coughInsidious coughOthers in home illNoYes, concurrent; upper respiratory tract infection, rash, conjunctivitisYes, weeks apart; pharyngitis, “flu,” coughYes, persistent coughAssociated signs, symptomsToxicity, rigorsMyalgia, rash, mucous membrane involvementHeadache, sore throat, chills, myalgia, rash, pharyngitis, myringitisWeight loss, night sweats (late)CoughWet, productiveNonproductiveHacking, paroxysmal, usually nonproductiveIrritative or productivePHYSICAL EXAMINATIONPredominant featureToxicity, respiratory distressRespiratory distressCoughPersistent coughDegree of respiratory findingDegree of illness ≥ findingsDegree of illness = findingsDegree of illness < findingsWell → no findings (± cough); ill → findingsPleuritic chest painNo/yesNoNoNo/occasionalAuscultationUnilateral, anatomically confined or no crackles; dullness, diminished or tubular soundsDiffuse, bilateral crackles, wheezesUnilateral, anatomically confined crackles;Most normal; or unilateralLABORATORY STUDIESChest radiographHyperaeration, patchy alveolar infiltrate or consolidation in lobe, segment, subsegmentHyperaeration, interstitial infiltrate in diffuse or perihilar distribution; “wandering” atelectasisPatchy alveolar and/or interstitial infiltrate in single or contiguous, usually lower lobe(s), unilaterally; perihilar adenopathyPatchy alveolar infiltrate in single or contiguous lobes with disproportionate hilar adenopathy; or miliary or lobar consolidationPleural fluidNo/yes → largeNo/yes → smallNo/yes → smallNo/yes → small, largePeripheral white blood cell count (cells per mm^3^)Majority > 15,000; neutrophils ± bandsMajority < 15,000;Majority < 15,000; neutrophilsMajority < 15,000;Sedimentation rate > 40 mm/hourUsualInfrequentInfrequentFrequentSputumCopious, purulent; neutrophils, abundant bacteriaScant mucoid; epithelial, Mononuclear cellsScant mucoid; mixed mononuclear cells/neutrophilsScant → copious; neutrophils (if copious)Diagnostic testsSputum Gram stain, culture; blood cultureNasal wash, throat, bronchoscopy specimen for antigen detection, culture; acute and convalescent serologyCold agglutinin; acute and convalescent specific serology; throat culture, antigen detection, DNA techniquesGastric aspirate; sputum stain and culture
Hemoptysis, defined as coughing up of blood that originated below the larynx, is uncommon in children; most commonly, supposed episodes are due to a posteriorly draining nosebleed. Mechanisms of hemoptysis include bleeding (1) congenital or acquired abnormal bronchial or pulmonary blood flow, venous obstruction, or vascular abnormalities; (2) immune-mediated endothelial damage; or (3) infectious or traumatic erosion of tracheal, bronchial, or bronchiolar epithelium. Hemorrhage can be mild (tracheitis, tracheobronchitis) or massive (congenital malformations, foreign body, bronchiectasis, pulmonary hemosiderosis). Causes of hemoptysis in children are listed in Table 23-10 . Infection is the most common cause of mild hemoptysis. Panton–Valentine leukocidin-producing Staphylococcus aureus pneumonia is specifically associated with hemoptysis.^83^ Epstein–Barr virus was implicated in a single case.^84^ For more severe hemoptysis, bronchiectasis associated with cystic fibrosis accounts for as many cases as all other causes combined.^85^ TABLE 23-10Causes of Hemoptysis in ChildrenEpithelial DamageVascular Abnormality/DamageAcute infectionBronchiectasis (cystic fibrosis, immunodeficiency, retained foreign body)Trauma (airway or chest)Foreign bodyTumor (primary airway or pulmonary, metastatic)Congenital heart disease or pulmonary vascular anomalies (venous obstruction, arteriovenous fistulae)Congenital malformation (pulmonary sequestration)Autoimmune vasculitis (systemic lupus erythematosus, Wegener granulomatosis, inflammatory bowel disease, Goodpasture syndrome)Sickle-cell diseasePulmonary hemosiderosisNonspecific endothelial damage (chemical, drug)
Rigid bronchoscopy, computed tomography, and magnetic resonance imaging are useful diagnostic modalities in most cases of hemoptysis. Digital subtraction angiography and, occasionally, cardiac catheterization or arteriography are required.