Elizabeth Burgamy, MD

A 4-week-old boy with tactile fever for the past 24 hours and fussiness of 2 weeks' duration is referred to the emergency department (ED). His parents report that he cries ceaselessly until he eventually falls asleep. His formula intake and urine and stool output have been normal. However, on further questioning, the mother is inconsistent in her explanation of how she mixes the formula.

The infant was born at 38 weeks' gestation to a 25-year-old gravida 1, para 0 after a normal spontaneous vaginal delivery. Apgar scores were 9 at both 1 and 5 minutes. The pregnancy and prenatal history were normal. Birth weight was 3500 g, length was 48 cm, and head circumference was 35 cm (all at the 50th percentile). At 1 week of life, his weight was 3400 g; examination findings were otherwise unremarkable.

The infant is extremely fussy but consolable. His temperature is 38.8°C (102°F) and blood pressure is 55/30 mm Hg; other vital signs are normal. There are no focal signs of infection. A review of systems yields normal findings.

A chemistry panel, obtained because of the possibility of incorrect formula concentration, is normal with the exception of a total calcium level of 5 mg/dL.

Which additional laboratory value(s) would you obtain before administration of calcium?

Answer: All of the laboratory values should be obtained.

To determine the cause of hypocalcemia, it is necessary to recall the mechanism of calcium homeostasis in the body. A calcium sensor on the parathyroid gland senses changes in the levels of ionized calcium. Low levels of ionized calcium trigger the release of PTH from the chief cells of the parathyroid gland. PTH has multiple sites of action. It acts directly on the distal renal tubule to increase calcium reabsorption (and phosphorus secretion) and mobilizes calcium and phosphorus from bone. It also stimulates the enzymatic activity of a1-hydroxylase in the kidney, which increases conversion of 25-hydroxyvitamin D to 1,25 dihydroxyvitamin D. The latter promotes calcium and phosphorus absorption from the GI tract and reabsorption from the renal tubules.

Thus, measurement of ionized calcium is a vital next step in the management of hypocalcemia. However, levels of PTH, magnesium, and 1,25 dihydroxyvitamin D should also be obtained because once calcium therapy is administered, these levels may become altered.

 In a stable hypocalcemic patient, it is important to obtain levels of ionized calcium, magnesium, PTH, and vitamin D before exogenous calcium 


 Neonatal hypocalcemia usually presents within 72 hours after birth and is often transient. Low calcium levels can be secondary to maternal factors (vitamin D deficiency, gestational diabetes, hyperparathyroidism) or neonatal factors (prematurity, low birth weight, intrauterine growth restriction, birth asphyxia). Neonatal factors theoretically cause hypocalcemia through blunting of PTH secretion and elevation of calcitonin levels; however, delayed maturation of vitamin D pathways is another mechanism. Transient neonatal hypocalcemia may also be caused by sepsis, respiratory distress syndrome, hypomagnesemia, hyperbilirubinemia, renal failure, and alkalosis.

 Transient hypocalcemia in a neonate may be secondary to a number of factors, including infection.

Other, less common causes of hypocalcemia

Hypocalcemia from ingestion of cow’s milk.

 Infants fed cow’s milk instead of formula may also present with hypocalcemia. High phosphate loads in certain milks, such as cow’s milk, can have 7 times the phosphate load of breast milk. Hyperphosphatemia causes calcium precipitation and hypercalciuria, which lead to hypocalcemia. In addition, the infant kidney is less effective at hydroxylation of 25-hydroxyvitamin D to 1,25 dihydroxyvitamin D, which results in less calcium resorption from bone.

 

 Hypocalcemia may also be secondary to Albright hereditary osteodystrophy, which is characterized by pseudohypoparathyroidism, or end-organ unresponsiveness to PTH in children with normal glandular secretion. Such children are usually obese and have round facies, short stature, short fourth metacarpals, developmental delay, and fibrous bony changes.



 Vitamin D deficiency or pseudodeficiency.

 In a child with chronically low calcium levels, vitamin D intake and metabolism must be assessed. Chronic hypocalcemia may be the result of vitamin D–deficient rickets, caused by reduced vitamin D intake or low UV light exposure, or vitamin D–dependent rickets (type I), in which 25-hydroxyvitamin D cannot be converted to 1,25 dihydroxyvitamin D. Type II vitamin D–dependent rickets is characterized by end-organ unresponsiveness to vitamin D. Patients with familial hypophosphatemic rickets, which is caused by a defect in proximal tubular reabsorption of phosphorus from the kidney, usually have normal calcium levels.

 Hypoparathyroidism in a hypocalcemic child may signal DiGeorge syndrome (absence or malformation of the parathyroid glands). This syndrome encompasses a constellation of symptoms, including cardiac anomalies (ventricular septal defect, right aortic arch, tetralogy of Fallot), abnormal facies (micrognathia, prominent nose, narrow palpebral fissures, cleft palate), thymic hypoplasia, and hypocalcemia. 

 Hypoparathyroidism in a hypocalcemic neonate warrants further workup for consideration of DiGeorge syndrome.

The infant's ionized calcium level was 2.3 mg/dL. PTH and 1,25 dihydroxyvitamin D levels were normal. Magnesium levels were also normal, as were his phosphorus levels on regular formula-which was less suggestive of vitamin D deficiency. He was given calcium gluconate 100 mg/kg IV in the ED and low doses of oral calcium (approximately 20 mg/kg/d) during his hospitalization. His calcium levels quickly normalized, his irritability resolved, and he defervesced. The finding of situs inversus totalis on a chest radiograph prompted fluorescence in situ hybridization testing for 22q11 deletion; results were negative. Results of an upper GI series were normal. Blood, urine, and cerebrospinal fluid cultures showed no growth of bacteria. At discharge, the parents were instructed to continue oral calcium therapy and to follow up with the infant's pediatrician. The hypocalcemia was thought to be secondary to possible infection.

Articles

A 4-week-old boy with tactile fever for the past 24 hours and fussiness of 2 weeks' duration is referred to the emergency department (ED).

Infant With Persistent Fever and Fussiness


  	Figure 1 – This patient's chest CT scan showed a left-sided pleural effusion with consolidation. The cause of the pneumonia was invasive group A streptococcal infection. 

A 9-year-old previously healthy boy presents to his pediatrician with acute onset of a nonproductive cough, left eye swelling without loss of visual acuity, persistent fever of 3 days' duration, chills, headache, chest pain, vomiting, and left knee pain with inability to bear weight. The child is admitted for further management; infectious disease and ophthalmology specialists are contacted for consultation.

There were multiple ill contacts at the patient's school; these children had a febrile illness whose symptoms-which included rhinorrhea and cough-appeared to be viral in origin. The patient does not have a history of allergies, and there is no travel history. The family history is noncontributory.

The patient is in moderate distress, has a flushed face, and is febrile (temperature 39.3°C [102.7°F]). He has significant tachycardia (heart rate, 109 beats per minute) but stable blood pressure (82/56 mm Hg). Examination of the head, ears, eyes, nose, and throat reveals significant periorbital swelling of the left eyelid with injected nonpurulent conjunctiva but no discharge; intact extraocular movement; dry oropharynx with tacky mucous membranes; and 2+ pink, nonpurulent tonsils. There are no other palatal findings. He does not demonstrate meningism. Cardiopulmonary examination reveals a nonradiating 2/6 systolic murmur at the left upper sternal border, with no rubs or gallops; absent breath sounds throughout the left lung field; and no rales or rhonchi on percussion. A musculoskeletal examination demonstrates significant swelling of the left knee with inability to bear weight. There is no point tenderness. Range of motion in the swollen knee is limited: he can flex it to only 45 degrees, and he can extend it only about 20 degrees from neutral.

A complete blood cell count reveals a white blood cell count of 21,500/μL, with a left shift (41% neutrophils, 17% band forms, 25% lymphocytes, 3% basophils, and 4% eosinophils). Liver transaminase levels are elevated (aspartate aminotransferase, 217 U/L; alanine aminotransferase, 398 U/L). Titers of anti-DNAse B and anti-streptolysin O (ASO) are markedly positive (ASO level, 1298 UI/mL). Culture of joint fluid obtained via arthrocentesis of the left knee grows group A β-hemolytic streptococci (

). Chest CT scan reveals a leftsided pleural effusion with consolidation (

Invasive, disseminated group A streptococcal (GAS) infection is diagnosed. Manifestations of the infection include left periorbital cellulitis with associated sinusitis, left-sided pneumonia with a parapneumonic effusion, and septic arthritis of the left knee.


 		From Hollm-Delgado MG, Allard R, Pilon PA. Invasive group A streptococcal infections, clinical manifestations and their predictors, Montreal, 1995-2001. 

http://www.cdc.gov/ncidod/EID/vol11no01/03-0651.htm

. Accessed July 13, 2010.  	Figure 2 – This graph shows both the annual incidence of and death rate for invasive group A streptococcal infection (IGASI) by age in Montreal between 1995 and 2001. Note that although the incidence of IGASI is lowest in children between the ages of 10 and 14 years, the death rate from IGASI is highest in that age-group. 

The most common manifestations of GAS infection are pharyngitis and simple skin infections. Between 15% and 30% of cases of acute pharyngitis are caused by GAS; the highest incidence is in children aged 5 to 11 years. The incubation period for streptococcal pharyngitis is short (2 to 5 days), and transmission occurs via inhalation of organisms in large droplets or by contact with respiratory secretions. Because GAS pharyngitis is self-limited (typically resolving in 3 to 5 days without therapy), this diagnosis is unlikely in patients in whom symptoms last longer than 4 or 5 days. Scarlet fever, characterized by an erythematous, diffuse, sandpapertextured exanthema, can accompany GAS pharyngitis (as well as other streptococcal illnesses). The rash is concentrated at skin creases (Pastia lines), blanches with pressure, and spares the circumoral region.

However, group A streptococci also cause a wide range of more serious clinical syndromes, including severe suppurative infections; direct complications,a such as retropharyngeal abscesses and streptococcal toxic shock syndrome (TSS); and immune-mediated complications, a such as acute rheumatic fever and acute glomerulonephritis. In invasive GAS infections (IGASI), 

may be spread via bodily secretions as well as via respiratory droplets.

 Practice Pearl 1: Group A streptococci can cause a wide variety of clinical symptoms; these range from simple skin infections and pharyngitis to suppurative infections and even toxic shock syndrome. Poll Results 	 	

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 A range of clinical identifiers are associated with IGASI, including pneumonia, bacteremia, soft tissue infections, streptococcal TSS, and death. Examples of typical soft tissue infections include fasciitis, myositis, cellulitis (as in this boy), and erysipelas. Bacteremia caused by IGASI is characterized by positive results on hemoculture in the absence of any identifiable source of infection. In pneumonia attributable to IGASI, a typical clinical picture might include streptococcal TSS without respiratory distress.

 Since the mid-1980s, concern has grown that IGASI has been increasing in severity and incidence. In particular, the emergence of streptococcal TSS has demonstrated the increasing severity of GAS infections. Infection with the M serotypes of S 

 (in particular, M1, M3, and M18) is more likely to result in severe disease. Other risk factors for IGASI include very young or very old age (

) and underlying medical conditions (including exposure to varicella).

 According to the CDC, the mortality from IGASI is close to 15%; mortality is highest among patients aged 10 to 14 years and those older than 70 years (see 

). The highest mortality rates, based on clinical manifestation, are seen in patients with pneumonia (almost 40%), followed by those with streptococcal TSS (35%), patients with bacteremia (20%), and those with soft tissue infections (10%). Of all the soft tissue IGASIs, necrotizing fasciitis is associated with the highest risk of death in all age groups.

 Practice Pearl 2: Invasive group A streptococcal infections have been increasing in incidence and severity, as evidenced by the emergence of streptococcal shock.

 Throat culture has long been the gold standard for the diagnosis of GAS pharyngitis. It has a 90% to 95% sensitivity for identifying GAS in the nasopharynx. Diagnosis has improved with the development of rapid antigen detection systems that can identify GAS. Standard rapid antigen tests have very high specificity (95% to 98%); however, their sensitivity varies from 70% to 90%. Serological testing for GAS pharyngitis generally is not useful in the diagnosis of acute infection because antistreptococcal antibodies increase only weeks after infection. Antibodies against streptolysin O, DNAse B, hyaluronidase, and streptokinase are used to confirm a recent-but not a current-GAS infection.

Keep in mind that accurate detection and treatment of GAS pharyngitis is needed to prevent acute rheumatic fever. All the same, unnecessary testing can result in misdiagnosis in chronic GAS carriers who are presenting with an intercurrent viral illness.

 Practice Pearl 3: When diagnosing group A streptococcal infection, standard rapid antigen tests have very high specificity but variable sensitivity; throat culture remains the gold standard. Serological testing is not useful in detecting current infection but can help confirm recent infection. 

 GAS remains universally sensitive to penicillin, and this agent is the first-line therapy once the causative organism has been identified and susceptibilities have been isolated. In patients who are allergic to penicillin, the drug of choice is erythromycin (or another macrolide). In patients with deep oropharyngeal abscesses, consider using ampicillin/sulbactam instead of penicillin to cover anaerobes and deep oropharyngeal flora. Antibiotic therapy for streptococcal TSS includes penicillin and clindamycin, along with intravenous immunoglobulin to neutralize toxins and ameliorate disease severity.

 Practice Pearl 4: Group A streptococcal infections remain universally sensitive to penicillin, which is the first-line therapy. 

 The patient's GAS pharyngitis resulted in sinusitis, which led, in turn, to the development of orbital cellulitis. His pneumonia was also a complication of the pharyngitis. Hematogenous spread was responsible for the septic arthritis in his left knee.

The patient's orbital cellulitis resolved with antibiotic therapy. However, serial chest radiographs confirmed a worsening pneumonia and parapneumonic effusion, which eventually required surgical intervention and chest tube drainage. He initially received supplemental oxygen but was weaned to room air quickly.

Imaging studies of his left knee showed soft tissue swelling and an effusion but no evidence of bony deterioration. Intraoperative arthrocentesis with washout and synovial biopsy was performed, with good recovery. Unfortunately, at a follow-up visit in the infectious disease clinic shortly after discharge, it was noted that the patient's left knee was still warm and swollen. He was readmitted and orthopedics was consulted. An intraoperative arthrocentesis revealed a communicating anterior thigh abscess, which was drained. Because neutropenia had developed, his antibiotic regimen was switched from penicillin G to clindamycin. His white blood cell and neutrophil counts returned to normal, and he was discharged on a regimen of oral clindamycin, with a recommendation for close monitoring.

 Complications of Group A Streptococcal Infection 	

 	Table – Criteria for streptococcal toxic shock syndrome 		

Hypotension or shock plus 2 of the following:

A definite case manifests hypotension, at least 2 of the above criteria, and isolation of group A streptococci from a sterile site. 		A probable case manifests hypotension, at least 2 of the above criteria, and isolation of group A streptococci from a nonsterile body site. 		

ARDS, acute respiratory distress syndrome. 		

Direct complications of streptococcal infections include retropharyngeal abscesses (abscess formation between the posterior pharyngeal wall and prevertebral fascia) and toxic shock syndrome (TSS). TSS can be caused by both streptococcal and staphylococcal bacteria. Criteria for establishing the diagnosis of TSS are shown in the 

The pathophysiology of streptococcal TSS involves massive cytokine release triggered by toxins that are produced by group A streptococci and that act as superantigens. Streptococcal TSS is often accompanied by a local infection, such as cellulitis or necrotizing fasciitis.

Indirect complications of group A streptococcal (GAS) infection include acute rheumatic fever and poststreptococcal glomerulonephritis, both of which follow acute untreated GAS infection after an asymptomatic latency period of about 7 to 10 days. These indirect complications can follow either a skin or a pharyngeal infection.

Acute rheumatic fever is a systemic illness characterized by carditis, polyarthritis, chorea, subcutaneous nodules, and erythema marginatum. Minor diagnostic criteria include fever, arthralgia, a prolonged PR interval, and elevated erythrocyte sedimentation rate and C-reactive protein level.

Acute poststreptococcal glomerulonephritis is characterized by edema, hematuria, proteinuria, and hypertension. It is an acute nephritis in which inflammation of the glomerulus is caused by cellular elements produced by an immunological mechanism.

 Jaggi P, Shulman ST. Group A streptococcal infections. 

 Stevens DL, Tanner MH, Winship J, et al. Severe group A streptococcal infections associated with a toxic shock-like syndrome and scarlet fever toxin A. 

 Weiss K, LaverdiÃ¨re M, Lovgren M, et al. Group A streptococcus carriage among close contacts of patients with invasive infections. 

 For a discussion of the direct and immune-mediated complications of group A streptococcal infections, visit our Web site at 

A 9-year-old previously healthy boy presents to his pediatrician with acute onset of a nonproductive cough, left eye swelling without loss of visual acuity, persistent fever of 3 days’ duration, chills, headache, chest pain, vomiting, and left knee pain with inability to bear weight.

Boy With Multifaceted Acute Illness

A 2-month-old boy is brought to the emergency department (ED) because of “noisy breathing” that has been present since birth. The parents report that they occasionally see the child’s ribs during inspiration when he is lying down.


 At a well-care visit 1 month earlier, the primary care pediatrician told the parents that findings from the infant’s examination were normal and that he would eventually outgrow these symptoms. One week before presentation, the infant’s breathing had worsened, and his parents brought him to an urgent care clinic with concerns that he was “breathing with his belly.” A chest radiograph was normal. The parents were told the infant had tracheomalacia and that the symptoms would abate as he grew older. Four days before presentation, the parents brought the infant to another ED, where he was given a dose of corticosteroids, after which a modest reduction in symptoms was noted.


 The infant is afebrile. Other vital signs and growth parameters are normal. Although the infant displays no signs of respiratory distress at rest, he is found to have inspiratory stridor that worsens with crying or when placed supine. He also has mild expiratory stridor heard on auscultation. Physical findings are otherwise unremarkable.

Which of the following would be the appropriate next step?

 Otorhinolaryngology (ENT) evaluation for possible laryngoscopy/bronchoscopy.


 Treatment with inhaled racemic epinephrine. 

(Answer and discussion begin on next page.)

Because this patient presented with no overt respiratory distress but with chronic worsening of symptoms after multiple visits to the pediatrician and ED, simple reassurance (choice A) is no longer appropriate. A single dose of an oral corticosteroid (choice B) would be a correct course of action in a case of laryngotracheobronchitis; however, the chronic nature of his stridor and his lack of fever and cough make this diagnosis unlikely. The finding of biphasic stridor that was more prominent with agitation and positioning suggest a fixed obstruction, which points to a probable anatomic cause. The next most appropriate step in this setting is an ENT evaluation (choice C). In this infant, laryngoscopy revealed a 

. Inhaled racemic epinephrine (choice D) is appropriate in the setting of acute inflammatory edema of the airway, often seen with infectious causes.

Stridor is a commonly encountered symptom in infants and children that can provoke anxiety in parents and providers alike. As airflow is forced through a narrowed airway, a local area of low pressure creates a vacuum effect distal to the narrowing. This causes the airway walls to collapse and vibrate, generating the highpitched noise of stridor.

When evaluating a child with stridor, regardless of age, attention must be paid to the duration of symptoms, phase of stridor, exacerbating or ameliorating factors, presence of fever, and signs of respiratory distress- such as use of accessory muscles of respiration, strength of cry, and ability to manage oral secretions.

Especially in neonates and infants, it is important to obtain a maternal history to rule out transmission of human papillomavirus infection. It is also critical in this population to determine a patient’s immunization status, because stridor can result from epiglottitis caused by Haemophilus influenzae type b infection.

 The history taking in the evaluation of stridor must include the patient’s immunization status and history of maternal human papillomavirus infection. 

Isolating the phase in the respiratory cycle during which stridor is heard can elucidate the cause. Inspiratory stridor usually signals airway obstruction at or above the level of the vocal cords and results from collapse of the soft tissues with the negative pressure generated by inspiration. Expiratory stridor most commonly indicates obstruction within the larger portions of the intrathoracic tracheobronchial tree that causes a decrease in airway diameter with expiration. Biphasic stridor usually signifies a fixed obstruction; one phase may be audible only with the aid of a stethoscope. In this patient, stridor was heard in both phases of respiration, with expiratory stridor heard on auscultation only.

 Careful examination of the phase of stridor-including what is audible both on initial survey and via auscultation-is a crucial step in identifying its cause. 

When considering the cause of stridor, it is helpful to divide suspected diagnoses into anatomic and infectious categories. Bear in mind that infectious causes predispose patients to stridor by changing the anatomy of the airway through edema or inflammation.



 
 Infectious causes of stridor are more common than anatomic causes. Fever, acute onset, and accompanying symptoms (such as cough and rhinorrhea) are clues that a patient’s stridor has an infectious, rather than a purely anatomic, cause.



 
 A purely anatomic cause of stridor often has a chronic or recurring course and may progressively worsen. Overt respiratory distress is not always present but may be elicited with agitation or with the patient supine. The most common anatomic causes of stridor in infants are laryngomalacia and tracheomalacia. These conditions present by age 6 weeks and usually remit by age 1 to 2 years; symptoms are more prominent with upper respiratory tract infections.

Another category of anatomic causes in infants includes laryngeal malformations, such as laryngeal webs, clefts, and cysts or mucoceles. Resulting from aberrant formation and canalization of the larynx during the embryological period, these conditions may present with not only stridor but also feeding difficulty or weak cry.

Extratracheal vascular malformations, commonly known as “rings and slings,” can externally compress the airway and cause stridor. Examples of these extratracheal abnormalities include double aortic arch, anomalous innominate artery, aberrant right subclavian artery, and vascular tracheal ring. On laryngoscopy, a pulsating airway indentation may be seen. Further imaging studies are necessary, and cardiothoracic surgical intervention is often required. Intratracheal vascular anomalies, such as airway hemangiomas, can also lead to recurrent stridor. Airway hemangiomas can present anywhere along the tracheobronchial tree. The usual presentation is stridor within a few weeks to a few months of birth. A postnatal proliferative phase-characterized by increased growth of the lesion and worsening obstruction-is followed by a plateau phase and later by spontaneous regression, usually by age 5 years. A tracheostomy may be necessary to bypass the airway obstruction until regression occurs. Newer therapies include laser vaporization and corticosteroid injections. A facial hemangioma may be a clue to an underlying airway hemangioma. Although not present in this patient, any child with a hemangioma in the beard distribution should be evaluated for airway hemangiomas.



 
 The possibility of a foreign body must always be considered, especially in a toddler or in an infant with young siblings. Radiographic findings may include air trapping and hyperinflation on the side of the obstruction. Angioedema in infants and young children with congenital C1-esterase deficiency, anaphylaxis in children with an allergic history, and severe recurrent gastroesophageal reflux disease can also cause laryngeal irritation and resultant inflammation.



 
 The infant was treated by otolaryngology with KTP laser therapy and intralesional triamcinolone injection. After discharge, the patient received oral corticosteroid therapy, which was tapered over the course of several weeks.

Infectious Causes of Stridor in Infants and Young Children

Common causes of viral croup include parainfluenza virus (types 1 and 3), metapneumovirus, adenovirus, influenza virus, and respiratory syncytial virus (making up the pneumonic "PM AIR"). These viruses cause subglottic inflammatory edema, resulting in inspiratory or biphasic stridor, barking cough, and fever. Treatments for croup are aimed at decreasing the airway edema. Thus, aerosolized racemic epinephrine and oral corticosteroids are effective therapies.



 Now less common in the era of routine vaccination against 

 type b, this acute, rapidly progressive infection of the epiglottis and aryepiglottic folds often follows a viral prodrome. Patients have fever of acute onset, sore throat, and a toxic appearance. They will often hyperextend the neck and drool because of the inability to swallow secretions. Securing the airway is essential. Thus, emergent consultation with an otorhinolaryngologist or anesthesiologist for endotracheal intubation is paramount.



 Retropharyngeal and peritonsillar abscesses.

 In children, infectious causes of stridor must also include retropharyngeal abscesses. An infection of the posterior pharynx is caused most commonly by 

 or anaerobic bacteria. In addition to stridor, patients may have arching of the neck, drooling, and fever as well as a thickened retropharyngeal space apparent on a lateral neck radiograph. In contrast, a peritonsillar abscess tends to occur in children older than 10 years and is caused most commonly by group A streptococci and anaerobic bacteria. Both conditions may present with biphasic stridor.


 Bacterial superinfection of a previous viral laryngotracheobronchitis can occur, usually in children older than 2 years. This severe illness is the result of secondary infection, most commonly with S aureus and less commonly with 

 Patients are toxic-appearing, with high fever, barking cough, stridor, and retractions, but usually maintain a normal position and exhibit no drooling or inability to manage secretions. Therapy includes ceftriaxone, and in severe cases, patients may require endotracheal intubation.



 These airway papillomas have a tendency toward spontaneous regression; however, they often necessitate laser therapy for years. Tracheostomy is avoided because this may predispose the patient to pulmonary parenchymal involvement. Human papillomavirus types 6 and 11, which can be acquired by passage through a birth canal affected with condyloma latum, can cause papillomatosis in an infant. Thus, obtaining a maternal history, especially in neonates and infants, is critical in the evaluation of stridor.

Holinger LD. Congenital anomalies of the larynx, trachea, and bronchi. In: Kliegman RM, Behrman RE, Jenson HB, Stanton B, eds. 

 18th ed. Philadelphia: Saunders; 2007:1767-1769.

Kliegman RM, Arnold JE. Airway obstruction in children. In: Kliegman RM, Lye PS, Greenbaum LA, eds. 

Practical Strategies in Pediatric Diagnosis and Therapy.

 2nd ed. New York: Elsevier Health Sciences; 2004:82-94.

Elizabeth Burgamy, MD

Articles

Infant With Persistent Fever and Fussiness

Boy With Multifaceted Acute Illness

Infant With Persistent Noisy Breathing