Pediatrics_Nelson

Pediatrics_Nelson. The major difficulty is differentiation of acute OM from OM with effusion, which also is referred to as chronic OM. Acute OM is accompanied by signs of acute illness, such as fever, pain, and upper respiratory tract inflammation. OM with effusion is the presence of effusion without any of the other signs and symptoms.


Pediatrics_Nelson

Pediatrics_Nelson. Recommendations for treatment are based on certainty of diagnosis and severity of illness. A certain diagnosis can be made if there is rapid onset, signs of middle ear effusion, and signs and symptoms of middle ear inflammation. The recommended first-line therapy for most children with a certain diagnosis of acute OM or those with an uncertain diagnosis but who are younger than 2 years of age or have fever greater than 39° C or otalgia is amoxicillin (80 to 90 mg/kg/day in two divided doses). Children with an uncertain diagnosis who are older than 2 years of age may be observed if appropriate follow-up can be arranged. Failure of initial therapy with amoxicillin at 3 days suggests infection with β-lactamase-producing H. influenza, M. catarrhalis or resistant S. pneumoniae. Recommended next-step treatments include high-dose amoxicillin-clavulanate (amoxicillin 80 to 90 mg/kg/day), cefuroxime axetil, cefdinir, or ceftriaxone (50 mg/kg intramuscularly in daily doses for 1 to 3 days).


Pediatrics_Nelson

Pediatrics_Nelson. next-step treatments include high-dose amoxicillin-clavulanate (amoxicillin 80 to 90 mg/kg/day), cefuroxime axetil, cefdinir, or ceftriaxone (50 mg/kg intramuscularly in daily doses for 1 to 3 days). Intramuscular ceftriaxone is especially appropriate for children younger than 3 years of age with vomiting that precludes oral treatment. Tympanocentesis may be required for patients who are difficult to treat or who do not respond to therapy. Acetaminophen and ibuprofen are recommended for fever. Decongestants or antihistamines are not effective.


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Pediatrics_Nelson. Available @ StudentConsult.com The complications of OM are chronic effusion, hearing loss, cholesteatoma (mass-like keratinized epithelial growth), petrositis, intracranial extension (brain abscess, subdural empyema, or venous thrombosis), and mastoiditis. Acute mastoiditis is a suppurative complication of OM with inflammation and potential destruction of the mastoid air spaces. The disease progresses from a periostitis to an osteitis with mastoid abscess formation. Posterior auricular tenderness, swelling, and erythema, in addition to the signs of OM, are present. The pinna is displaced downward and outward. Radiographs or computed tomography scan of the mastoid reveals clouding of the air cells, demineralization, or bone destruction. Treatment includes systemic antibiotics and drainage if the disease has progressed to abscess formation.


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Pediatrics_Nelson. OM with effusion is the most frequent sequela of acute OM and occurs most frequently in the first 2 years of life. Persistent middle ear effusion may last for many weeks or months in some children but usually resolves by 3 months following infection. Evaluating young children for this condition is part of all well-child examinations. Conductive hearing loss should be assumed to be present with persistent middle ear effusion; the loss is mild to moderate and often is transient or fluctuating. Normal tympanograms after 1 month of treatment obviate the need for further follow-up. In children at developmental risk or with frequent episodes of recurrent acute OM, 3 months of persistent effusion with significant bilateral hearing loss is a reasonable indicator of need for intervention with insertion of pressure equalization tubes.


Pediatrics_Nelson

Pediatrics_Nelson. Parents should be encouraged to continue exclusive breastfeeding as long as possible and should be cautioned about the risks of bottle-propping and of children taking a bottle to bed. The home should be a smoke-free environment. Children identified at high-risk for recurrent acute OM are candidates for prolonged courses of antimicrobial prophylaxis, which can reduce recurrences significantly. Amoxicillin (20 to 30 mg/kg/day) or sulfisoxazole (50 mg/kg/day) given once daily at bedtime for 3 to 6 months or longer is used for prophylaxis. The conjugate S. pneumoniae vaccine reduces pneumococcal OM caused by vaccine serotypes by 50%, all pneumococcal OM by 33%, and all OM by 6%. Annual immunization against influenza virus may be helpful in high-risk children.


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Pediatrics_Nelson. Otitis externa, also known as swimmer’s ear, is defined byinflammation and exudation in the external auditory canal inthe absence of other disorders, such as otitis media or mastoiditis. The most common bacterial pathogens are Pseudomonas aeruginosa, especially in association with swimming in pools or lakes, and Staphylococcus aureus. Otitis externa develops in approximately 20% of children with tympanostomy tubes, associated with S. aureus, Streptococcus pneumoniae, Moraxellacatarrhalis, Proteus, Klebsiella, and occasionally anaerobes.Coagulase-negative staphylococci and Corynebacterium are isolated frequently from cultures of the external canal but representnormal flora. Malignant otitis externa is caused by P. aeruginosa in immunocompromised persons and adults with diabetes.


Pediatrics_Nelson

Pediatrics_Nelson. Otitis externa cases peak in summer, in contrast to otitis media, which occurs primarily in colder seasons in association with viral upper respiratory tract infections. Cleaning of the auditory canal, swimming, and, in particular, diving disrupt the integrity of the cutaneous lining of the ear canal and local defenses such as cerumen, predisposing to otitis externa. Available @ StudentConsult.com


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Pediatrics_Nelson. Available @ StudentConsult.com Pain, tenderness, and aural discharge are the characteristic clinical findings of otitis externa. Fever is notably absent, and hearing is unaffected. Tenderness with movement of the pinna, especially the tragus, and with chewing is particularly characteristic, symptoms notably absent in otitis media. Inspection usually reveals that the lining of the auditory canal is inflamed with mild to severe erythema and edema. Scant to copious discharge from the auditory canal may obscure the tympanic membrane. The most common symptoms of malignant otitis externa are similar, but facial nerve palsy occasionally occurs. The most common physical findings are swelling and granulation tissue in the canal, usually with a discharge from the external auditory canal.


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Pediatrics_Nelson. The diagnosis of uncomplicated otitis externa usually is established solely on the basis of the clinical symptoms and physical examination findings without the need for additional laboratory or microbiologic evaluation. In malignant otitis externa, an elevated erythrocyte sedimentation rate is a constant finding. Cultures are required to identify the etiologic agent, which is usually P. aeruginosa, and the antimicrobial susceptibility. Otitis media with tympanic perforation and discharge into the auditory canal may be confused with otitis externa. Pain on movement of the pinnae or tragus, typical of otitis externa, is not present. Local and systemic signs of mastoiditis indicate a process more extensive than otitis externa. Malignancies or cholesteatoma presenting in the auditory canal are rare in children but may present with discharge, unusual pain, or hearing loss.


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Pediatrics_Nelson. Topical antimicrobial/corticosteroid otic preparations (such as ofloxacin, ciprofloxacin with hydrocortisone or dexamethasone, and polymyxin B-neosporin-hydrocortisone) are sufficient in most cases of otitis externa. These preparations are equally effective and are active against S. aureus and most gram-negative bacteria, including P. aeruginosa. None of these antibiotics has any antifungal activity. Use of aminoglycosides such as neomycin should be avoided in cases of tympanic membrane rupture due to their ototoxicity. Tympanostomy tube otorrhea is best treated with quinolone otic drugs, which is considered less likely to be ototoxic.


Pediatrics_Nelson

Pediatrics_Nelson. Treatment with topical otic analgesics and cerumenolytics is usually unnecessary. It is important with any topical therapy to remove purulent discharge from the external auditory canal with a swab or with suction to permit instillation of the solution. Excess water should be removed after bathing and the ear canal dried using a hairdryer. The predisposing activity, such as swimming or diving, should be avoided until the inflammation has resolved. Fungi such as Aspergillus, Candida, and dermatophytes occasionally are isolated from the external ear. It may be difficult to determine whether they represent normal flora or are the cause of inflammation. In most cases, local therapy and restoration of normal pH as recommended for bacterial otitis externa are sufficient.


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Pediatrics_Nelson. Malignant otitis externa is treated by parenteral antimicrobials with activity against P. aeruginosa, such as an expand-ed-spectrum penicillin (mezlocillin, piperacillin-tazobactam) or a cephalosporin with activity against P. aeruginosa (ceftazidime, cefepime) plus an aminoglycoside. Acute otitis externa usually resolves promptly without complications within 1 to 2 days of initiating treatment. Persistent pain, especially if severe or if accompanied by other symptoms such as fever, should prompt re-evaluation for other conditions. Complications of malignant otitis externa include invasion of the bones of the base of the skull, which may cause cranial nerve palsies. A mortality of 15% to 20% occurs in adults with malignant otitis media. Relapses within the first year after treatment are common.


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Pediatrics_Nelson. Overvigorous cleaning of an asymptomatic auditory canal should be avoided. Drying the auditory canals with acetic acid (2%), Burow solution, or diluted isopropyl alcohol (rubbing alcohol) after swimming may be used prophylactically to help prevent the maceration that facilitates bacterial invasion. Often underwater gear, such as earplugs or diving equipment, must be avoided to prevent recurrent disease. There is no role for prophylactic otic antibiotics.


Pediatrics_Nelson

Pediatrics_Nelson. Croup, or laryngotracheobronchitis, is the most common infection of the middle respiratory tract (Table 107-1). The most common causes of croup are parainfluenza viruses (types 1, 2, 3, and 4) and respiratory syncytial virus. Laryngotracheal airway inflammation disproportionately affects children because a small decrease in diameter secondary to mucosal edema and inflammation exponentially increases airway resistance and the work of breathing. During inspiration, the walls of the subglottic space are drawn together, aggravating the obstruction and producing the stridor characteristic of croup. Croup is most common in children 6 months to 3 years of age, with a peak in fall and early winter. It typically follows a common cold. Symptomatic reinfection is common, yet reinfections are usually mild. In adolescents, it manifests as laryngitis. Available @ StudentConsult.com


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Pediatrics_Nelson. Available @ StudentConsult.com The manifestations of croup are a harsh cough described as barking or brassy, hoarseness, inspiratory stridor, low-grade fever, and respiratory distress that may develop slowly or quickly. Stridor is a harsh, high-pitched respiratory sound produced by turbulent airflow. It is usually inspiratory, but it may be biphasic and is a sign of upper airway obstruction. Signs of upper airway obstruction, such as labored breathing and marked suprasternal, intercostal, and subcostal retractions, may be evident on examination (see Chapter 135). Wheezing may be present if there is associated lower airway involvement.


Pediatrics_Nelson

Pediatrics_Nelson. Anteroposterior radiographs of the neck often show the diagnostic subglottic narrowing of croup known as the steeple sign (Fig. 107-1). Routine laboratory studies are not useful in establishing the diagnosis. Leukocytosis is uncommon and suggests epiglottitis or bacterial tracheitis. Many rapid tests (using polymerase chain reaction or fluorescent antibodies) are available for parainfluenza viruses, respiratory syncytial virus, and other less common viral causes of croup, such as influenza and adenoviruses.


Pediatrics_Nelson

Pediatrics_Nelson. The diagnosis of croup usually is established by clinical manifestations. The infectious differential diagnosis includes epiglottitis, bacterial tracheitis, and parapharyngeal abscess. Noninfectious causes of stridor include mechanical and anatomic causes (foreign body aspiration, laryngomalacia, subglottic stenosis, hemangioma, vascular ring, vocal cord paralysis). Stridor in infants younger than 4 months of age or persistence of symptoms for longer than 1 week indicates an increased probability of another lesion and the need for imaging and direct laryngoscopy (see Chapter 135).


Pediatrics_Nelson

Pediatrics_Nelson. Epiglottitis is a medical emergency because of the risk of sudden airway obstruction. This illness is now rare and usually caused by group A streptococcus or Staphylococcus aureus or Haemophilus influenza type b in unimmunized patients. Patients typically prefer sitting, often with the head held forward, the mouth open, and the jaw thrust forward (sniffing position). Lateral radiograph reveals thickened and bulging epiglottis (thumb sign) and swelling of the aryepiglottic folds. The diagnosis is confirmed by direct observation of the inflamed and swollen supraglottic structures and swollen, cherry-red epiglottitis, which should be performed only in the operating room with an anesthesiologist and a competent surgeon prepared to place an endotracheal tube or perform a tracheostomy if needed. Epiglottitis requires antibiotic therapy and endotracheal intubation to maintain the airway. Clinical recovery is rapid, and most children can be extubated safely within 48 to 72 hours.


Pediatrics_Nelson

Pediatrics_Nelson. Bacterial tracheitis is a rare but serious superinfection of the trachea that may follow viral croup and is most commonly caused by S. aureus. Spasmodic croup describes sudden onset of croup symptoms, usually at night, but without a significant upper respiratory tract prodrome. These episodes may be recurrent and severe but usually are of short duration. Spasmodic croup has a milder course than viral croup and responds to relatively simple therapies, such as exposure to cool or humidified air. The etiology is not well understood and may be allergic. Oral or intramuscular dexamethasone for children with mild, moderate, or severe croup reduces symptoms, the need for hospitalization, and shortens hospital stays. Dexamethasone Onset of illness Gradual Acute Acute Sudden (at night) Quality of stridor Harsh Mild Harsh Harsh Drooling, neck – ++ + – hyperextension


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Pediatrics_Nelson. Onset of illness Gradual Acute Acute Sudden (at night) Quality of stridor Harsh Mild Harsh Harsh Drooling, neck – ++ + – hyperextension From Bell LM: Middle respiratory tract infections. In Jenson HB, Baltimore RS: Pediatric Infectious Diseases: Principles and Practice, ed 2, Philadelphia, 2002, Saunders, p 772. +, frequently present; –, absent; ±, may or may not be present; ++, present and usually pronounced.


Pediatrics_Nelson

Pediatrics_Nelson. Figure 107-1 Croup (laryngotracheobronchitis). A, Posteroanterior view of the upper airway shows the so-called steeple sign, the tapered narrowing of the immediate subglottic airway (arrows). B, Lateral view of the upper airway shows good delineation of the supraglottic anatomy. The subglottic trachea is hazy and poorly defined (arrow) because of the inflammatory edema that has obliterated the sharp undersurface of the vocal cords and extends down the trachea in a diminishing manner. (From Bell LM: Middle respiratory tract infections. In Jenson HB, Baltimore RS: Pediatric Infectious Diseases: Principles and Practice, ed 2, Philadelphia, 2002, Saunders, p 774.) phosphate (0.6 to 1 mg/kg) may be given once intramuscularly or dexamethasone (0.6 to 1 mg/kg) once orally. Alternatively prednisolone (2 mg/kg per day) may be given orally in two to three divided doses. For significant airway compromise, administration of aerosolized racemic (Dand L-) epinephrine reduces subglottic edema by


Pediatrics_Nelson

Pediatrics_Nelson. (2 mg/kg per day) may be given orally in two to three divided doses. For significant airway compromise, administration of aerosolized racemic (Dand L-) epinephrine reduces subglottic edema by adrenergic vasoconstriction, temporarily producing marked clinical improvement. The peak effect is within 10 to 30 minutes and fades within 60 to 90 minutes. A rebound effect may occur, with worsening of symptoms as the effect of the drug dissipates. Aerosol treatment may need to be repeated every 20 minutes (for no more than 1 to 2 hours) in severe cases.


Pediatrics_Nelson

Pediatrics_Nelson. Children should be kept as calm as possible to minimize forceful inspiration. One useful calming method is for a child with croup to sit on the parent’s lap. Sedatives should be used cautiously and in the intensive care unit only. Cool mist administered by face mask may help prevent drying of the secretions around the larynx. Hospitalization is often required for children with stridor at rest. Children receiving aerosol treatment should be hospitalized or observed for at least 2 to 3 hours because of the risk of rebound airway obstruction. Decreased symptoms may indicate improvement or fatigue and impending respiratory failure. The most common complication of croup is viral pneumonia, which occurs in 1% to 2% of children. Parainfluenza virus pneumonia and secondary bacterial pneumonia are more common in immunocompromised persons. Bacterial tracheitis may also be a complication of croup.


Pediatrics_Nelson

Pediatrics_Nelson. The prognosis for croup is excellent. Illness usually lasts approximately 5 days. As children grow, they become less susceptible to the airway effects of viral infections of the middle respiratory tract. There is no vaccine for parainfluenza. Classic pertussis (whooping cough) is caused by B. pertussis,a gram-negative pleomorphic bacillus with fastidious growth requirements. B. pertussis infects only humans and is transmitted person to person by coughing.


Pediatrics_Nelson

Pediatrics_Nelson. The incubation period is 7 to 10 days. Patients are most contagious during the first 2 weeks of cough. The peak incidence of pertussis in the United States is among those less than 4 months of age—infants too young to be completely immunized and most likely to have severe complications. The annual rate of pertussis was approximately 100 to 200 cases per 100,000 population in the prevaccination era; worldwide there are an estimated 30 to 50 million cases of pertussis and 300,000 deaths annually. In the United States, the incidence of pertussis decreased after the introduction of vaccine but has increased steadily since the 1980s with more than 27,000 cases reported in 2010. Infections in adolescents have also been rising, likely due to waning immunity from previous vaccines. Likewise when vaccination rates are low, pertussis rates increase: there was a steady decline in the incidence of pertussis until the late 1970s in the United Kingdom, when the incidence increased dramatically as


Pediatrics_Nelson

Pediatrics_Nelson. vaccination rates are low, pertussis rates increase: there was a steady decline in the incidence of pertussis until the late 1970s in the United Kingdom, when the incidence increased dramatically as the vaccination rate declined. Epidemics also occur in fully immunized patients, as vaccine-induced immunity wanes.


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Available @ StudentConsult.com

Pediatrics_Nelson. Available @ StudentConsult.com


Pediatrics_Nelson

Pediatrics_Nelson. Classic pertussis is seen in children between 1 and 10 years old. The progression of the disease is divided into catarrhal, paroxysmal, and convalescent stages. The catarrhal stage is marked by nonspecific signs (increased nasal secretions andlow-grade fever) lasting 1 to 2 weeks. The paroxysmal stage is the most distinctive stage of pertussis and lasts 2 to 4 weeks.Coughing occurs in paroxysms during expiration, causingyoung children to lose their breath. This pattern of coughingis needed to dislodge plugs of necrotic bronchial epithelialtissues and thick mucus. The forceful inhalation against a narrowed glottis that follows this paroxysm of cough producesthe characteristic whoop. Posttussive emesis is common. The convalescent stage is marked by gradual resolution of symptoms over 1 to 2 weeks. Coughing becomes less severe, andthe paroxysms and whoops slowly disappear. Although thedisease typically lasts 6 to 8 weeks, residual cough may persist for months, especially with physical


Pediatrics_Nelson

Pediatrics_Nelson. 2 weeks. Coughing becomes less severe, andthe paroxysms and whoops slowly disappear. Although thedisease typically lasts 6 to 8 weeks, residual cough may persist for months, especially with physical stress or respiratoryirritants.


Pediatrics_Nelson

Pediatrics_Nelson. Infants may not display the classic findings, and the first sign in the neonate may be apnea. Young infants are unlikely to have the classic whoop, more likely to have central nervous system damage as a result of hypoxia, and more likely to have secondary bacterial pneumonia. Adolescents and adults with pertussis usually present with a prolonged bronchitic illness with persistent, nonproductive cough that often begins as a nonspecific upper respiratory tract infection. Generally adolescents and adults do not have a whoop with the cough, although they may have severe paroxysms. The cough may persist many weeks to months.


Pediatrics_Nelson

Pediatrics_Nelson. The diagnosis depends on isolation of B. pertussis or detection of its nucleic acids. Culture on specialized media is usually accomplished during the early phases of illness on specimens from nasopharyngeal swabs or aspirates but can be difficult to accomplish given the organism’s fastidious nature. Polymerase chain reaction, although potentially lacking sensitivity in previously immunized individuals, is likely as sensitive as culture and is available in many clinical laboratories. False positive results can occur. Direct fluorescent antibody staining is not recommended. Serologic tests are not useful for diagnosing acute infection but can be confirmatory in the convalescent phase of illness, though there are no commercial kits approved by the U.S. Food and Drug Administration.


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Pediatrics_Nelson. Lymphocytosis is present in 75% to 85% of infants and young children but is not diagnostic. The white blood cell count may increase from 20,000 cells/mm3 to more than 50,000 cells/mm3, consisting primarily of mature lymphocytes. Physical examination and radiographic signs of segmental lung atelectasis may develop during pertussis, especially during the paroxysmal stage. Perihilar infiltrates are common and are similar to those seen in viral pneumonia. For a young child with classic pertussis, the diagnosis based on the pattern of illness is quite accurate. The paroxysmal stage is the most distinctive part of the syndrome. Other causes of per-tussis-like prolonged cough illnesses include Bordetella parapertussis, which causes a similar but milder illness and is not prevented by B. pertussis vaccination, Mycoplasma pneumoniae, Chlamydia pneumoniae and Chlamydophila pneumoniae, adenoviruses, and respiratory syncytial virus.


Pediatrics_Nelson

Pediatrics_Nelson. Azithromycin, clarithromycin, or erythromycin are recommended for children under 1 month of age. Azithromycin should be used in neonates due to the association between erythromycin treatment and the development of pyloric stenosis. Treatment during the catarrhal phase eradicates nasopharyngeal carriage of organisms within 3 to 4 days and may lessen symptom severity. Treatment in the paroxysmal stage does not alter the course of illness but decreases the potential for spread to others. Trimethoprim-sulfamethoxazole is an alternative therapy among children older than 2 months, though studies of its use for this indication are limited.


Pediatrics_Nelson

Pediatrics_Nelson. Major complications are most common among infants andyoung children and include hypoxia, apnea, pneumonia, seizures, encephalopathy, malnutrition, and death. The mostfrequent complication is pneumonia caused by B. pertussis itself or resulting from secondary bacterial infection with Streptococcus pneumoniae, Haemophilus influenzae, and Staphylococcus aureus. Atelectasis may develop secondaryto mucous plugs. The force of the paroxysm may producepneumomediastinum, pneumothorax, or interstitial or subcutaneous emphysema; epistaxis; hernias; and retinal andsubconjunctival hemorrhages. Otitis media and sinusitis may occur. Most children recover normal pulmonary function with complete healing of the respiratory epithelium. Most permanent disability is a result of encephalopathy.


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Pediatrics_Nelson. Most children recover normal pulmonary function with complete healing of the respiratory epithelium. Most permanent disability is a result of encephalopathy. Active immunity is induced with acellular pertussis components given as a vaccine in combination with the tetanus and diphtheria toxoids (DTaP). The acellular pertussis vaccines contain two to five antigens of B. pertussis, including pertussis toxin, pertactin, filamentous hemagglutinin, and fimbrial agglutinogens, FIM-2 and FIM-3. DTaP vaccine is recommended at 2, 4, 6, and 15 to 18 months, with a booster at 4 to 6 years, and has an efficacy of 70% to 90%. A single booster dose of Tdap vaccine is recommended at 11 to 12 years or once for all adults.


Pediatrics_Nelson

Pediatrics_Nelson. Macrolides are effective in preventing secondary cases in contacts exposed to pertussis. Underimmunized close contacts under 7 years of age should receive a booster dose of DTaP (unless a booster dose has been given within the preceding 3 years), whereas those 7 to 10 years of age should receive Tdap. All close contacts should receive prophylactic antibiotics for 5 days (azithromycin) or 7 to 14 days (clarithromycin or erythromycin, duration based on age). Bronchiolitis is a disease of small bronchioles with increased mucus production and occasional bronchospasm, sometimes leading to airway obstruction. It is most commonly caused by a viral lower respiratory tract infection. Bronchiolitis is most commonly seen in infants and young children, with most severe cases occurring among infants. Bronchiolitis is potentially life-threatening.


Pediatrics_Nelson

Pediatrics_Nelson. Respiratory syncytial virus (RSV) is a primary cause ofbronchiolitis, followed in frequency by human metapneumovirus, parainfluenza viruses, influenza viruses, adenoviruses,rhinoviruses, coronaviruses, and, infrequently, Mycoplasma pneumoniae. Viral bronchiolitis is extremely contagiousand is spread by contact with infected respiratory secretions. Although coughing produces aerosols, hand carriageof contaminated secretions is the most frequent mode oftransmission.


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Pediatrics_Nelson. Bronchiolitis is a leading cause of hospitalization of infants. Bronchiolitis occurs almost exclusively during the first 2 years of life, with a peak age at 2 to 6 months. Many healthy children with bronchiolitis can be managed as outpatients; however, premature infants and children with chronic lung disease of prematurity, hemodynamically significant congenital heart disease, neuromuscular weakness, or immunodeficiency are at increased risk of severe, potentially fatal disease. Children acquire infection after exposure to infected family members, who typically have symptoms of an upper respiratory tract infection, or from infected children in day care. In the United States, annual peaks are usually in the late winter months from December through March. Available @ StudentConsult.com


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Pediatrics_Nelson. Available @ StudentConsult.com Bronchiolitis caused by RSV has an incubation period of 4 to6 days. Bronchiolitis classically presents as a progressive respiratory illness similar to the common cold in its early phasewith cough and rhinorrhea. It progresses over 3 to 7 days tonoisy, raspy breathing and audible wheezing. There is usually a low-grade fever accompanied by irritability, which mayreflect the increased work of breathing. In contrast to the classic progression of disease, young infants infected with RSV may not have a prodrome and may have apnea as the first signof infection.


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Pediatrics_Nelson. Physical signs of bronchiolar obstruction include prolongation of the expiratory phase of breathing, nasal flaring, intercostal retractions, suprasternal retractions, and air trapping with hyperexpansion of the lungs. During the wheezing phase, percussion of the chest usually reveals only hyperresonance, but auscultation usually reveals diffuse wheezes and crackles throughout the breathing cycle. With more severe disease, grunting and cyanosis may be present. Routine laboratory tests are not required to confirm the diagnosis. It is important to assess oxygenation in severe cases of bronchiolitis. Pulse oximetry is adequate for monitoring oxygen saturation. Frequent, regular assessments and cardiorespiratory monitoring of infants are necessary because respiratory failure may develop precipitously in very tired infants even though blood gas values taken before rapid decompensation are reassuring.


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Pediatrics_Nelson. Antigen tests (usually by immunofluorescence or enzyme-linked immunosorbent assay [also referred to as ELISA]) of nasopharyngeal secretions for RSV, parainfluenza viruses, influenza viruses, and adenoviruses are sensitive tests to confirm the infection. Rapid viral diagnosis also is performed by polymerase chain reaction. Identifying the viral agent is helpful for cohorting children with the same infection but is not necessary to make the diagnosis of bronchiolitis. Chest radiographs frequently show signs of lung hyperinflation, including increased lung lucency and flattened or depressed diaphragms. Areas of increased density may represent either viral pneumonia or localized atelectasis.


Pediatrics_Nelson

Pediatrics_Nelson. The major difficulty in the diagnosis of bronchiolitis is to differentiate other diseases associated with wheezing. It may be difficult to differentiate asthma from bronchiolitis by physical examination, but age of presentation, presence of fever, and absence of personal or family history of asthma are the major differential factors. Bronchiolitis occurs primarily in the first year of life and is accompanied by fever, whereas asthma usually presents in older children with previous wheezing episodes typically unaccompanied by fever unless a respiratory tract infection is the trigger for the asthma exacerbation.


Pediatrics_Nelson

Pediatrics_Nelson. Wheezing also may be due to an airway foreign body, congenital airway obstructive lesion, cystic fibrosis, exacerbation of chronic lung disease, viral or bacterial pneumonia, and other lower respiratory tract diseases (see Chapter 78). Cardiogenic asthma, which can be confused with bronchiolitis in infants, is wheezing associated with pulmonary congestion secondary to left-sided heart failure. Wheezing associated with gastroesophageal reflux is likely to be chronic or recurrent, and the patient may have a history of frequent emesis. Cystic fibrosis is associated with poor growth, chronic diarrhea, and a positive family history. A focal area on radiography that does not inflate or deflate suggests foreign body aspiration.


Pediatrics_Nelson

Pediatrics_Nelson. Bronchiolitis treatment consists of supportive therapy, including respiratory monitoring, control of fever, hydration, upper airway suctioning, and, if needed, oxygen administration. Indications for hospitalization include moderate to marked respiratory distress, hypoxemia, apnea, inability to tolerate oral feeding, and lack of appropriate care available at home. Hospitalization of high-risk children with bronchiolitis should be considered. Among hospitalized infants, supplemental oxygen by nasal cannula is often necessary, but intubation and ventilatory assistance for respiratory failure or apnea are required in fewer than 10% of these infants. Bronchodilators and corticosteroids are seldom effective and are not generally recommended.


Pediatrics_Nelson

Pediatrics_Nelson. Most hospitalized children show marked improvement in 2 to 5 days with supportive treatment alone. The course of the wheezing phase varies, however. Tachypnea and hypoxia may progress to respiratory failure requiring assisted ventilation. Apnea is a major concern for very young infants with bronchiolitis. Most cases of bronchiolitis resolve completely, although minor abnormalities of pulmonary function and bronchial hyperreactivity may persist for several years. Recurrence is common but tends to be mild and should be assessed and treated similarly to the first episode. The incidence of asthma seems to be higher for children hospitalized for bronchiolitis as infants, but it is unclear whether this is causal or whether children prone to asthma are more likely to be hospitalized with bronchiolitis. There is a 1% to 2% mortality rate, highest among infants with preexisting cardiopulmonary or immunologic impairment.


Pediatrics_Nelson

Pediatrics_Nelson. Monthly injections of palivizumab, an RSV-specific monoclonal antibody, initiated just before the onset of the RSV season confers some protection from severe RSV disease. Palivizumab is indicated for some infants under 2 years old with chronic lung disease, very low birth weight, and those with hemodynamically significant cyanotic and acyanotic congenital heart disease. Immunization with influenza vaccine is recommended for all children older than 6 months and may prevent influenza-associated disease.


Pediatrics_Nelson

Pediatrics_Nelson. Pneumonia is an infection of the lower respiratory tract that involves the airways and parenchyma with consolidation of the alveolar spaces. The term lower respiratory tract infection is often used to encompass bronchitis, bronchiolitis (see Chapter 109), pneumonia, or any combination of the three. Pneumonitis is a general term for lung inflammation that may or may not be associated with consolidation. Lobar pneumonia describes pneumonia localized to one or more lobes of the lung. Atypical pneumonia describes patterns typically more diffuse or interstitial than lobar pneumonia. Bronchopneumonia refers to inflammation of the lung that is centered in the bronchioles and leads to the production of a mucopurulent exudate that obstructs some of these small airways and causes patchy consolidation of the adjacent lobules. Interstitial pneumonitis refers to inflammation of the interstitium, which is composed of the walls of the alveoli, the alveolar sacs and ducts, and the bronchioles.


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Pediatrics_Nelson. of the adjacent lobules. Interstitial pneumonitis refers to inflammation of the interstitium, which is composed of the walls of the alveoli, the alveolar sacs and ducts, and the bronchioles. Interstitial pneumonitis is characteristic of acute viral infections but also may be a chronic inflammatory or fibrosing process.


Pediatrics_Nelson

Pediatrics_Nelson. Defects in host defenses increase the risk of pneumonia. Lower airways and secretions are sterile as a result of a multifactorial system. Airway contaminants are caught in the mucus secreted by the goblet cells. Cilia on epithelial surfaces, composing the ciliary elevator system, beat synchronously to move particles upward toward central airways and into the throat, where they are swallowed or expectorated. Polymorphonuclear neutrophils from the blood and tissue macrophages ingest and kill microorganisms. IgA secreted into the upper airway fluid protects against invasive infections and facilitates viral neutralization.


Pediatrics_Nelson

Pediatrics_Nelson. Infectious agents that commonly cause community-acquired pneumonia vary by age (Table 110-1). Most common causes are respiratory syncytial virus (RSV) in infants (see Chapter 109), other respiratory viruses (parainfluenza viruses, influenza viruses, human metapneumovirus, adenoviruses) in children younger than 5 years old, and Mycoplasma pneumoniae in children older than age 5 years. Streptococcus pneumoniae is the most common bacterial cause of lobar pneumonia, and occurs in children of any age outside the neonatal period. M. pneumoniae and Chlamydophila pneumoniae are principal causes of atypical pneumonia.


Pediatrics_Nelson

Pediatrics_Nelson. M. pneumoniae and Chlamydophila pneumoniae are principal causes of atypical pneumonia. Chlamydia trachomatis and less commonly Mycoplasma hominis, Ureaplasma urealyticum, and cytomegalovirus (CMV) cause a similar respiratory syndrome in infants 1 to 3 months of age with subacute onset of an afebrile pneumonia; cough and hyperinflation are the predominant signs. These infections are difficult to diagnose and to distinguish from each other. In adults these organisms are carried primarily as part of the genital mucosal flora. Women who harbor these agents may transmit them perinatally to newborns.


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Pediatrics_Nelson. Additional agents occasionally cause pneumonia. Severe acute respiratory syndrome (SARS) is due to SARS-associated coronavirus (SARS-CoV). Avian influenza (bird flu) is a highly contagious viral disease of poultry and other birds caused by influenza A (H5N1). There were outbreaks among humans in South East Asia in 1997 and 2003 to 2004 with high mortality rates. A novel influenza A (H1N1) of swine origin began circulating in 2009. Other etiologic agents to consider, based on specific exposure history, include Mycobacterium tuberculosis, Francisella tularensis, Brucella spp., Coxiella burnetii, Chlamydophila psittaci, Legionella pneumophila, hantavirus, Histoplasma capsulatum, Coccidioides immitis, and Blastomyces dermatitidis.


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Pediatrics_Nelson. Causes of pneumonia in immunocompromised persons include gram-negative enteric bacteria, mycobacteria (M. avium complex), fungi (aspergillosis), viruses (CMV), and Pneumocystis jiroveci (carinii). Pneumonia in patients with cystic fibrosis usually is caused by Staphylococcus aureus in infancy and Pseudomonas aeruginosa or Burkholderia cepacia in older patients.


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Pediatrics_Nelson. Immunizations have had a great impact on the incidence of pneumonia caused by pertussis, diphtheria, measles, Haemophilus influenza type b, and S. pneumoniae. Where used, bacille Calmette-Guerin (BCG) for tuberculosis also has had an impact. An estimated 2 million deaths in developing countries are due to acute respiratory tract infections annually. Risk factors for lower respiratory tract infections include gastroesophageal reflux, neurologic impairment (aspiration), immunocompromised states, anatomic abnormalities of the respiratory tract, residence in residential care facilities, and hospitalization, especially in an intensive care unit. Available @ StudentConsult.com Cough Wheezing Hemoptysis Chest Pain Abdominal Pain Failure to Thrive Acidemia


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Pediatrics_Nelson. Available @ StudentConsult.com Cough Wheezing Hemoptysis Chest Pain Abdominal Pain Failure to Thrive Acidemia Age is a determinant in the clinical manifestations of pneumonia. Neonates may have fever or hypoxia only, with subtle or absent physical examination findings (see Chapter 65). With a young infant, apnea may be the first sign of pneumonia. Fever, chills, tachypnea, cough, malaise, pleuritic chest pain, retractions, and apprehension, because of difficulty breathing or shortness of breath, are common in older infants and children. Physical examination findings cannot reliably distinguish viral and bacterial pneumonias, but complete physical examination may help identify other foci of disease or associated findings to suggest an etiology.


Pediatrics_Nelson

Pediatrics_Nelson. In general viral pneumonias are associated more often with cough, wheezing, or stridor; fever is less prominent than with bacterial pneumonia. Mucosal congestion and upper airway inflammation suggest a viral infection. Bacterial pneumonias typically are associated with higher fever, chills, cough, dyspnea, and auscultatory findings of lung consolidation. Atypical pneumonia in young infants is characterized by tachypnea, cough, crackles on auscultation, and concomitant (chlamydial) conjunctivitis (infants) may be present. Other signs of respiratory distress include nasal flaring, intercostal and subcostal retractions, and grunting.


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Pediatrics_Nelson. Asymmetry or shallow breathing may be due to splinting from pain. Hyperexpansion, common in asthma but also frequently accompanying viral lower respiratory infections, may cause a low diaphragm or liver. Poor diaphragmatic excursion may indicate hyperexpanded lungs or an inability for expansion due to a large consolidation or effusion. Dullness to percussion may be due to lobar or segmental infiltrates or pleural fluid. Auscultation may be normal in early or very focal pneumonia, but the presence of localized crackles, rhonchi, and wheezes may help one detect and locate pneumonia. Distant breath sounds may indicate a large, poorly ventilated area of consolidation or pleural fluid.


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Pediatrics_Nelson. Table 110-1 Etiologic Agents and Empirical Antimicrobial Therapy for Pneumonia in Patients without History of Recent Antibiotic Therapy AGE GROUP COMMON PATHOGENS* (IN APPROXIMATE ORDER OF FREQUENCY) LESS COMMON PATHOGENS OUTPATIENTS† (7–10 DAYS TOTAL DURATION OF TREATMENT) PATIENTS REQUIRING HOSPITALIZATION‡ (10–14 DAYS TOTAL DURATION OF TREATMENT) PATIENTS REQUIRING INTENSIVE CARE*,‡ (10–14 DAYS TOTAL DURATION OF TREATMENT) 1 to 3 months Amoxicillin or ampicillin if fully immunized for age for S. pneumoniae and H. influenzae type b. Alternatives: cefotaxime or ceftriaxone if not fully immunized or local S. pneumoniae penicillin resistance is significant, with clindamycin if MRSA suspected Cefotaxime or ceftriaxone plus nafcillin, oxacillin, clindamycin, or vancomycin 3 months to 5 Respiratory syncytial years virus, other respiratory viruses (parainfluenza viruses, influenza viruses, human metapneumovirus adenoviruses), S. pneumoniae,


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Pediatrics_Nelson. H. influenzae (type b,§ nontypable) C. trachomatis, Mycoplasma Amoxicillin plus pneumoniae, Chlamydophila erythromycin, azithromycin, pneumoniae, group A or clarithromycin if atypical streptococcus, Staphylococcus pneumonia suspected aureus, Mycobacterium tuberculosis Ampicillin Alternatives: Cefuroxime or ceftriaxone plus cefotaxime or ceftriaxone if azithromycin, erythromycin or not fully immunized or local clarithromycin with or without S. pneumoniae penicillin clindamycin or vancomycin resistance is significant, with clindamycin if MRSA suspected; Add erythromycin, azithromycin, or clarithromycin if atypical pneumonia suspected MRSA, Methicillin-resistant Staphylococcus aureus. *Severe pneumonia, from S. pneumoniae, S. aureus, group A streptococcus, H. influenzae, or M. pneumoniae requiring admission to an intensive care unit. Antipseudomonal agents should be added if Pseudomonas is suspected. †Oral administration.


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Pediatrics_Nelson. †Oral administration. ‡Intravenous administration for inpatients except for the macrolides (erythromycin, azithromycin, and clarithromycin), which are given orally. §H. influenzae type b infection is uncommon with universal H. influenzae type b immunization. ǁFluoroquinolones are contraindicated for children younger than 18 years of age and pregnant or lactating women. Tetracyclines are not recommended for children younger than 9 years. Bacterial flora of the upper respiratory tract do not accurately reflect flora present in lower respiratory tract infections, and high-quality sputum is rarely obtainable from children. In otherwise healthy children without life-threatening disease, invasive procedures to obtain lower respiratory tissue or secretions usually are not indicated. Serologic tests are not useful for the most common causes of bacterial pneumonia.


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Pediatrics_Nelson. The white blood cell (WBC) count with viral pneumonias is often normal or mildly elevated, with a predominance of lymphocytes, whereas with bacterial pneumonias the WBC count is elevated (>20,000/mm3) with a predominance of neutrophils. Mild eosinophilia is characteristic of infant C. trachomatis pneumonia. Blood cultures should be performed on hospitalized children to attempt to diagnose a bacterial cause of pneumonia. Blood cultures are positive in 10% to 20% of bacterial pneumonia and are considered to be confirmatory of the cause of pneumonia if positive for a recognized respiratory pathogen. Urinary antigen tests are especially useful for L. pneumophila (legionnaires’ disease).


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Pediatrics_Nelson. Viral respiratory pathogens can be diagnosed using polymerase chain reaction (PCR) or rapid viral antigen detection, but neither rules out concomitant bacterial pneumonia. M. pneumoniae should be suspected if cold agglutinins are present in peripheral blood samples and can be confirmed by Mycoplasma PCR. CMV and enterovirus can be cultured from the nasopharynx, urine, or bronchoalveolar lavage fluid. The diagnosis of M. tuberculosis is established by tuberculin skin test, serum interferon-gamma release assay, or analysis of sputum or gastric aspirates by culture, antigen detection, or PCR.


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Pediatrics_Nelson. The need to establish an etiologic diagnosis of pneumonia is greater for patients who are ill enough to require hospitalization, immunocompromised patients, patients with recurrent pneumonia, or patients with pneumonia unresponsive to empirical therapy. For these patients, bronchoscopy with bronchoalveolar lavage and brush mucosal biopsy, needle aspiration of the lung, and open lung biopsy are methods of obtaining material for microbiologic diagnosis.


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Pediatrics_Nelson. When there is a pleural effusion or empyema, a thoracentesis to obtain pleural fluid can be diagnostic and therapeutic. Evaluation differentiates between empyema and a sterile parapneumonic effusion caused by irritation of the pleura contiguous with the pneumonia. Gram stain, culture, or broad-range bacterial PCR may lead to microbiologic diagnosis. The pleural fluid should be cultured for bacteria, mycobacteria, fungi, and viruses. If the fluid is grossly purulent, removal reduces the patient’s toxicity and associated discomfort and may facilitate more rapid recovery. If the accumulation is large and impairs the ability of the lung to expand, removal of the fluid improves pulmonary mechanics and gas exchange.


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Pediatrics_Nelson. Frontal and lateral radiographs are required to localize disease and adequately visualize retrocardiac infiltrates and are recommended for diagnosis among hospitalized children, but they are not necessary to confirm the diagnosis in well-appearing outpatients. Although there are characteristic radiographic findings of pneumonia, radiography alone cannot provide a definitive microbiologic diagnosis. Bacterial pneumonia characteristically shows lobar consolidation, or a round pneumonia, with pleural effusion in 10% to 30% of cases (Fig. 110-1).Viral pneumonia characteristically shows diffuse, streaky infiltrates of bronchopneumonia (Fig. 110-2) and hyperinflation. Atypical pneumonia, such as with M. pneumoniae and


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Pediatrics_Nelson. Figure 110-1 Acute lobar pneumonia of the lingula in a 6-year-old child with high fever, cough, and chest pain. Frontal chest radiograph shows airspace consolidation, which obliterates the silhouette of the heart border on the left. The left hemidiaphragm is mildly elevated as a result of splinting. (From Markowitz RI: Diagnostic imaging. In Jen-son HB, Baltimore RS, editors: Pediatric Infectious Diseases: Principles and Practice, ed 2, Philadelphia, Saunders, 2002, p 133.)


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Pediatrics_Nelson. Figure 110-2 Diffuse viral bronchopneumonia in a 12-year-old boy with cough, fever, and wheezing. Frontal chest radiograph shows bilateral, perihilar, peribronchial thickening, and shaggy infiltrate. Focal airspace disease representing consolidation or atelectasis is present in the medial portion of the right upper lobe. The findings are typical of bronchopneumonia. (From Markowitz RI: Diagnostic imaging. In Jenson HB, Baltimore RS, editors: Pediatric Infectious Diseases: Principles and Practice, ed 2, Philadelphia, Saunders, 2002, p 132.)


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Pediatrics_Nelson. C. pneumoniae, shows increased interstitial markings or bronchopneumonia (Fig. 110-3). Chest radiographs may be normal in early pneumonia, with infiltrates appearing during treatment as hydration is restored. Hilar lymphadenopathy is uncommon with bacterial pneumonia but may be a sign of tuberculosis, histoplasmosis, or an underlying malignant neoplasm. Decubitus views or ultrasound should be used to assess size of pleural effusions and whether they are freely mobile.


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Pediatrics_Nelson. Figure 110-3 Mycoplasma pneumoniae infection (atypical pneumonia) in a 14-year-old boy with malaise, dry cough, and mild shortness of breath for 1 week. Frontal chest radiograph shows a diffuse pattern of increased interstitial markings, including Kerley lines. The heart is normal, and there are no focal infiltrates. Cold agglutinins were markedly elevated, and the patient responded to erythromycin. This radiographic pattern of reticulonodular interstitial disease is observed in 25% to 30% of patients with pneumonia caused by Mycoplasma pneumoniae. (From Baltimore RS: Pneumonia. In Jenson HB, Baltimore RS, editors: Pediatric Infectious Diseases: Principles and Practice, ed 2, Philadelphia, Saunders, 2002, p 808.)


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Pediatrics_Nelson. Computed tomography (CT) is used to evaluate serious disease, pleural abscesses, bronchiectasis, and effusion characteristics. Unusual etiologies or recurrent pneumonias require special considerations (Table 110-2). Lung abscesses, pneumatoceles, and empyema all require special management. Pneumonia must be differentiated from other acute pulmonary diseases, including allergic pneumonitis, asthma, and cystic fibrosis; cardiac diseases, such as pulmonary edema caused by heart failure; and autoimmune diseases, such as certain vasculitides and systemic lupus erythematosus. Radiographically pneumonia must be differentiated from lung trauma and contusion, hemorrhage, foreign body aspiration, and sympathetic effusion due to subdiaphragmatic inflammation. Available @ StudentConsult.com


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Pediatrics_Nelson. Available @ StudentConsult.com Therapy for pneumonia includes supportive and specific treatment and depends on the degree of illness, complications, and knowledge of the infectious agent likely causing the pneumonia. Most cases of pneumonia in healthy children can be managed on an outpatient basis. However children with hypoxemia, inability to maintain adequate hydration, or moderate to severe respiratory distress should be hospitalized. Hospitalization should be considered in infants under 6 months with suspected bacterial pneumonia, those in whom there is a concern for a pathogen with increased virulence (e.g., methicillin-resistant Staphylococcus aureus), or when concern exists about a family’s ability to care for the child and to assess symptom progression.


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Pediatrics_Nelson. Because viruses cause most community-acquired pneumonias in young children, not all children require empirical antibiotic treatment for pneumonia. Recommended therapies in those without recent antibiotic exposure are listed in Table 110-1. Exceptional situations include lack of response to empirical therapy, unusually severe presentations, nosocomial pneumonia, and immunocompromised children susceptible to infections with opportunistic pathogens (Table 110-3). In contrast to pneumococcal meningitis, presumed pneumococcal pneumonia can be treated with high-dose cephalosporin therapy even with high-level penicillin resistance. Vancomycin can be used if the isolate shows high-level resistance and the patient is severely ill. For infants 4 to 18 weeks old with afebrile pneumonia most likely caused by C. trachomatis, a macrolide is the recommended treatment. Oseltamivir or zanamivir should be used if influenza is identified or suspected, ideally within 48 hours of symptom onset.


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Pediatrics_Nelson. Table 110-3 Antimicrobial Therapy for Pneumonia Caused by Specific Pathogens* PATHOGEN RECOMMENDED TREATMENT ALTERNATIVE TREATMENT Streptococcus pneumoniae with MIC for penicillin ≤2.0 μg/mL Ampicillin or penicillin IV; amoxicillin PO Ceftriaxone, cefotaxime, clindamycin or vancomycin IV; Cefuroxime, cefpodoxime, levofloxacin†, or linezolid PO Streptococcus pneumoniae with MIC for Ceftriaxone IV; levofloxacin† or linezolid PO Ampicillin, levofloxacin†, clindamycin or penicillin ≥4.0 μg/mL Group A streptococcus Penicillin or ampicillin IV; amoxicillin or Ceftriaxone, cefotaxime, clindamycin or penicillin PO vancomycin IV; clindamycin PO Group B streptococcus Penicillin or ampicillin IV; amoxicillin or Ceftriaxone, cefotaxime, clindamycin or penicillin PO vancomycin IV; clindamycin PO Staphylococcus aureus, methicillin Cefazolin, oxacillin, or nafcillin IV; cephalexin Clindamycin or vancomycin IV; clindamycin susceptible (MSSA) PO PO


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Pediatrics_Nelson. Staphylococcus aureus, methicillin Cefazolin, oxacillin, or nafcillin IV; cephalexin Clindamycin or vancomycin IV; clindamycin susceptible (MSSA) PO PO Staphylococcus aureus, methicillin resistant Clindamycin or vancomycin IV; clindamycin Linezolid IV or PO (MRSA) PO IV, Intravenous; MIC, minimum inhibitory concentration; PO, per os (orally); TMP-SMX, trimethoprim-sulfamethoxazole. *Oral outpatient therapy may be used for mild illness. Intravenous inpatient therapy should be used for moderate to severe illness. †Appropriate fluoroquinolones include moxifloxacin, gatifloxacin, levofloxacin, and gemifloxacin. Fluoroquinolones are contraindicated for children younger than 18 years of age and pregnant or lactating women. Tetracyclines are not recommended for children younger than 9 years. ‡Aminoglycoside dosing should be guided by serum antibiotic concentrations after a steady state has been reached.


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Pediatrics_Nelson. ‡Aminoglycoside dosing should be guided by serum antibiotic concentrations after a steady state has been reached. Bacterial pneumonias frequently cause inflammatory fluid to collect in the adjacent pleural space, causing a parapneumonic effusion or, if grossly purulent, an empyema. Small effusions may not require any special therapy. Large effusions may restrict breathing and require drainage. Air dissection within lung tissue results in a pneumatocele. Scarring of the airways and lung tissue may leave dilated bronchi, resulting in bronchiectasis and increased risk for recurrent infection.


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Pediatrics_Nelson. Pneumonia that causes necrosis of lung tissue may evolve into a lung abscess. Lung abscess is an uncommon problem in children and usually is caused by aspiration, infection behind an obstructed bronchus, or certain virulent organisms. Anaerobic bacteria usually predominate, along with various streptococci, Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, and Staphylococcus aureus. Chest radiograph or CT scan reveals a cavitary lesion, often with an air-fluid level, surrounded by parenchymal inflammation. If the cavity communicates with the bronchi, organisms may be isolated from sputum. Diagnostic bronchoscopy may be indicated to exclude a foreign body and obtain microbiologic specimens. Lung abscesses usually respond to appropriate antimicrobial therapy with clindamycin, penicillin G, or ampicillin-sulbactam.


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Pediatrics_Nelson. Most children recover from pneumonia rapidly and completely, although radiographic abnormalities may take 6 to 8 weeks to return to normal. In a few children, pneumonia may persist longer than 1 month or may be recurrent. In such cases, the possibility of underlying disease must be investigated further, such as with tuberculin skin test, sweat chloride determination for cystic fibrosis, serum immunoglobulin and IgG subclass determinations, bronchoscopy to identify anatomic abnormalities or foreign body, and barium swallow for gastroesophageal reflux. Severe adenovirus pneumonia may result in bronchiolitis obliterans, a subacute inflammatory process in which the small airways are replaced by scar tissue, resulting in a reduction in lung volume and lung compliance. Unilateral hyper-lucent lung, or Swyer-James syndrome, is a focal sequela of severe necrotizing pneumonia in which all or part of a lung has increased translucency radiographically; it has been linked to adenovirus type 21.


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Pediatrics_Nelson. Annual influenza vaccine is recommended for all children over 6 months of age (see Chapter 94). Trivalent, inactivated influenza vaccine is licensed for use beginning at 6 months of age; live, attenuated vaccine can be used for persons 2 to 49 years of age. Universal childhood vaccination with conjugate vaccines for H. influenzae type b and S. pneumoniae has greatly diminished the incidence of these pneumonias. The severity of RSV infections can be reduced by use of palivizumab in high-risk patients (see Chapter 109).


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Pediatrics_Nelson. Reducing the duration of mechanical ventilation and administering antibiotics judiciously reduces the incidence of ventilator-associated pneumonias. The head of the bed should be raised to 30 to 45 degrees for intubated patients to minimize risk of aspiration, and all suctioning equipment and saline should be sterile. Hand washing before and after every patient contact and use of gloves for invasive procedures are important measures to prevent nosocomial transmission of infections. Hospital staff with respiratory illnesses or who are carriers of certain organisms, such as methicillin-resistant S. aureus, should comply with infection control policies to prevent transfer of organisms to patients. Treating sources of aerosols, such as air coolers, can prevent Legionella pneumonia.


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Pediatrics_Nelson. S. aureus, should comply with infection control policies to prevent transfer of organisms to patients. Treating sources of aerosols, such as air coolers, can prevent Legionella pneumonia. Infective endocarditis is an infection on the endothelial surface of the heart, including the heart valves. The management of infections on the endothelial surfaces of blood vessels is very similar. Infectious endothelial lesions, called vegetations, usually occur on the valve leaflets and are composed of microorganisms trapped in a fibrin mesh that extends into the bloodstream.


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Pediatrics_Nelson. Many microorganisms have been reported to cause endocarditis, although there are only a few principal causes in children (Table 111-1). Viridans streptococci are the principal causes in children with congenital heart diseases without previous surgery. Staphylococcus aureus and coagulase-negative staphylococci are important causes of endocarditis, especially following cardiac surgery and in the presence of prosthetic cardiac and endovascular materials.


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Pediatrics_Nelson. Infective endocarditis among children is primarily a complication of congenital heart disease and cardiac surgery, although it can occur in a previously normal native valve. Patients at high risk for infective endocarditis include those with prosthetic cardiac valves or prior infective endocarditis; children who have unrepaired cyanotic congenital heart disease, are within 6 months of repair using prosthetic material, or have residual defects at or near a site of prosthetic material; or transplant patients who develop valvular lesions. The risk is increased after dental and oral procedures or instrumentation or surgical procedures of the respiratory tract, genitourinary tract, or gastrointestinal tract. Rheumatic heart disease is a risk factor but is uncommon. Neonatal endocarditis is associated with the use of central vascular catheters and surgery Viridans streptococci (the most common causative organism at all ages)*


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Pediatrics_Nelson. Viridans streptococci (the most common causative organism at all ages)* Hemolytic streptococci: groups A, B (in neonates and elderly), C, G, D HACEK organisms (i.e., Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae) Coxiella burnetii (Q fever) Chlamydia Agents of culture-negative endocarditis *Most common causes of infective endocarditis in children. in neonates. Endocarditis is a sporadic disease with no geographic predisposition and little gender or socioeconomic predisposition in children. Available @ StudentConsult.com


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Pediatrics_Nelson. in neonates. Endocarditis is a sporadic disease with no geographic predisposition and little gender or socioeconomic predisposition in children. Available @ StudentConsult.com The most common early symptoms of infective endocarditis are nonspecific and include fever, malaise, and weight loss. Tachycardia and a new or changed heart murmur are common findings. The subtle and nonspecific findings underscore the need to obtain blood cultures if endocarditis is suspected, especially for children with congenital heart disease and for unexplained illness after dental or surgical procedures. Endocarditis is usually a subacute, slowly progressive process, but acute endocarditis is often due to S. aureus and may resemble sepsis. Heart failure, splenomegaly, petechiae, and embolic phenomena (Osler nodes, Roth spots, Janeway lesions, and splinter hemorrhages) may be present.


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Pediatrics_Nelson. The key to diagnosis is confirming continuous bacteremia or fungemia by culturing the blood. Multiple blood cultures are performed before initiating antibiotic therapy. Three separate venipunctures for blood culture achieve near-maximal sensitivity (about 95%) among patients who have not been treated recently with antibiotics. Patients who have been treated with antibiotics recently or who are currently receiving antibiotics should have additional serial cultures performed. Despite adequate blood culture techniques, the microbiologic diagnosis is not confirmed in 10% to 15% of cases, known as culture-negative endocarditis. Erythrocyte sedimentation rate and C-reactive protein are often elevated. Leukocytosis, anemia, and hematuria are common laboratory findings. A positive rheumatoid factor or antinuclear antibody may also be seen.


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Pediatrics_Nelson. Echocardiography visualizes endocardial and valvular vegetations measuring 2 mm or greater. Transesophageal echocardiography is more sensitive than transthoracic echocardiography for adolescents and adults and for patients with prosthetic valves but is often unnecessary in children. Infective endocarditis must be differentiated from other causes of bacteremia or other cardiac conditions using the Modified Duke Criteria for categorizing the strength of the endocarditis diagnosis (Table 111-2). Noninfectious causes of endocardial vegetations must be excluded, such as sterile clots and vegetations associated with rheumatoid disease and lupus erythematosus. Prolonged bacteremia can be caused by infectious endothelial foci outside of the heart, often associated with congenital malformations, vascular trauma, an infected venous thrombosis, and previous vascular surgery.


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Pediatrics_Nelson. Severely ill patients must be stabilized with supportive therapies for cardiac failure, pulmonary edema, and low cardiac output (see Chapter 145). Empirical antibiotic therapy may be started for acutely ill persons after blood cultures are obtained. With subacute disease, awaiting results of blood cultures to confirm the diagnosis is recommended to direct therapy according to the susceptibility of the isolate. Because antibiotics must reach the organisms by passive diffusion through the fibrin mesh, high doses of bactericidal antibiotics are required for an extended period of treatment (4 to 8 weeks). Infective carditis from susceptible viridans streptococci can be treated with monotherapy penicillin G for 4 weeks. A 2-week regimen of penicillin G plus an aminoglycoside is effective in adults. Surgery is indicated if medical treatment is unsuccessful, with persistent bacteremia, an unusual or difficult to treat pathogen (fungal endocarditis), valve annulus or myocardial abscess,


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Pediatrics_Nelson. in adults. Surgery is indicated if medical treatment is unsuccessful, with persistent bacteremia, an unusual or difficult to treat pathogen (fungal endocarditis), valve annulus or myocardial abscess, rupture of a valve leaflet, valvular insufficiency with acute or refractory heart failure, recurrent serious embolic complications, or refractory prosthetic valve disease.


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Pediatrics_Nelson. The major complications of infective endocarditis are direct damage to the heart and heart valves and distant complications secondary to sterile and septic emboli from vegetations. Damage to the heart and heart valves may include regurgitation with vegetations or actual defects in the leaflets resulting from embolization of the leaflet tissue, abscess of the valve


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Pediatrics_Nelson. Histopathologic Criteria Microorganisms shown by culture or histopathologic examination in a vegetation, emboli, intracardiac abscess or Active endocardial lesions on pathologic examination Clinical Criteria Two major criteria or one major and three minor criteria or five minor criteria) Major Criteria Positive blood cultures Two or more separate cultures positive with typical organisms for infective endocarditis Two or more positive cultures of blood drawn more than 12 hours apart or 4 positive blood cultures irrespective of timing of obtaining specimen A positive blood culture for Coxiella burnetii or positive IgG titer >1:800 Evidence of endocardial involvement Positive findings on echocardiogram (vegetation on valve or supporting structure, abscess, new valvular regurgitation) Minor Criteria Predisposition—predisposing heart condition or injection drug use Fever—temperature >38° C (>100.4° F) Vascular phenomena (major arterial emboli, septic pulmonary infarcts, mycotic aneurysm,


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Pediatrics_Nelson. Criteria Predisposition—predisposing heart condition or injection drug use Fever—temperature >38° C (>100.4° F) Vascular phenomena (major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions) Immunologic phenomena (glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor)


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Pediatrics_Nelson. Microbiologic evidence (positive blood culture result, but not meeting major criteria, or serologic evidence of active infection with organism consistent with infective endocarditis) Firm alternative diagnosis for manifestations of endocarditis or Resolution of manifestations of endocarditis with antibiotic therapy for <4 days or No pathologic evidence of endocarditis at surgery or autopsy after antibiotic therapy of >4 days or does not meet criteria for possible endocarditis Adapted from Tissieres P, Gervaix A, Beghetti M, et al: Value and limitations of the van Reyn, Duke, and modified Duke criteria for the diagnosis of infective endocarditis in children, Pediatrics 112: e467−e471, 2003. ring, or myocardial abscess. These complications should be monitored by physical examination and echocardiography. Cerebral abscesses or aneurysms can cause a stroke-like picture. Splenic abscesses can cause fatal bleeding.


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Pediatrics_Nelson. The outcome of infective endocarditis caused by the most common organisms is often good. The cure rate is greater than 90% in uncomplicated endocarditis caused by viridans streptococci on a natural valve, 75% to 90% for Enterococcus endocarditis treated by a synergistic combination of antibiotics, and 60% to 75% for S. aureus endocarditis with an acute, severe presentation. The prognosis for endocarditis caused by gram-negative bacilli and rarer organisms is poor. Fungal endocarditis has the poorest prognosis, with a cure rate of about 50% even with valve replacement.


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Pediatrics_Nelson. In high-risk patients, prophylactic antibiotics are required before and during all dental procedures that involve manipulation of gingival tissue or the periapical region as well as invasive procedures of the respiratory tract, infected skin, or muscle. In most cases, oral amoxicillin 50 mg/kg (maximum dose, 2 g) taken 30 to 60 minutes before the procedure is the recommended regimen. Clindamycin or azithromycin are alternative regimens indicated for most patients allergic to β-lactams. Prolonged or continuous antibiotic prophylaxis is not recommended.


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Pediatrics_Nelson. Acute enteritis or acute gastroenteritis refers to diarrhea, which is abnormally frequent, and liquidity of fecal discharges. Diarrhea is caused by different infectious or inflammatory processes in the intestine that directly affect enterocyte secretory and absorptive functions. Enteritis has many viral, bacterial, and parasitic causes (Table 112-1). Some of these processes act by increasing cyclic adenosine monophosphate levels (Vibrio cholerae, Escherichia coli heat-labile toxin). Other processes (Shigella toxin) cause secretory diarrhea by affecting ion channels or by unknown mechanisms (Table 112-2).


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Pediatrics_Nelson. Diarrhea is a leading cause of morbidity and a common disease in children in the United States. In the developing world, it is a major cause of childhood fatality. The epidemiology of gastroenteritis depends on the specific organisms. Some organisms are spread person to person, others are spread via contaminated food or water, and some are spread from animal to human. Many organisms spread by multiple routes. The ability of an organism to infect relates to the mode of spread, ability to colonize the gastrointestinal tract, and minimum number of organisms required to cause disease.


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Pediatrics_Nelson. Viral causes of gastroenteritis in children include rotaviruses, caliciviruses (including the noroviruses), astroviruses,and enteric adenoviruses (serotypes 40 and 41). Rotavirus is the most frequent cause of diarrhea during the wintermonths. Vomiting may last 3 to 4 days, and diarrhea maylast 7 to 10 days. Dehydration is common in younger children. Primary infection with rotavirus may cause moderate to severe disease in infancy but is less severe later in life. Thisillness is much less common in areas where infants receive the rotavirus vaccine. Rotaviruses Damage to microvilli Caliciviruses (noroviruses) Mucosal lesion Astroviruses Mucosal lesion Enteric adenoviruses Mucosal lesion Campylobacter jejuni Invasion, enterotoxin Clostridium difficile Cytotoxin, enterotoxin Enteropathogenic (EPEC) Adherence, effacement


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Pediatrics_Nelson. Campylobacter jejuni Invasion, enterotoxin Clostridium difficile Cytotoxin, enterotoxin Enteropathogenic (EPEC) Adherence, effacement Enterotoxigenic (ETEC) Enterotoxins (heat-stable or heat(traveler’s diarrhea) labile) Enteroinvasive (EIEC) Invasion of mucosa Enterohemorrhagic (EHEC) Adherence, effacement, cytotoxin (includes O157: H7 causing HUS) Enteroaggregative (EAEC) Adherence, mucosal damage Salmonella Invasion, enterotoxin Shigella Invasion, enterotoxin, cytotoxin Vibrio cholerae Enterotoxin Vibrio parahaemolyticus Invasion, cytotoxin Yersinia enterocolitica Invasion, enterotoxin Entamoeba histolytica Invasion, enzyme and cytotoxin production; cyst resistant to physical destruction Giardia lamblia Adheres to mucosa; cyst resistant to physical destruction Spore-forming intestinal Adherence, inflammation protozoa (Enterocytozoon bieneusi, Encephalitozoon intestinalis) HUS, Hemolytic uremic syndrome.


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Pediatrics_Nelson. Spore-forming intestinal Adherence, inflammation protozoa (Enterocytozoon bieneusi, Encephalitozoon intestinalis) HUS, Hemolytic uremic syndrome. Typhoid fever is caused by Salmonella typhi and, occasionally, Salmonella paratyphi. Worldwide, there are an estimated 16 million cases of typhoid fever annually, resulting in 600,000 deaths. The typhoid bacillus infects humans only. These infections are distinguished by prolonged fever and extraintestinal manifestations, despite inconsistent presence of diarrhea. In the United States, approximately 400 cases of typhoid fever occur each year. Most occur in travelers returning from other countries. The incubation period of typhoid fever is usually 7 to 14 days (range 3 to 60 days). Infected persons without symptoms, or chronic carriers, serve as reservoirs and sources of continuous spread. Carriers often have cholelithiasis. Nontyphoidal Salmonella produces diarrhea by invading the intestinal mucosa. The organisms are transmitted through


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Pediatrics_Nelson. Nontyphoidal Salmonella produces diarrhea by invading the intestinal mucosa. The organisms are transmitted through Table 112-2 Mechanisms of Infectious Diarrhea PRIMARY MECHANISM DEFECT STOOL EXAMINATION EXAMPLES COMMENTS Secretory Decreased absorption, increased secretion: electrolyte transport Watery, normal osmolality; osmoles = 2 × (Na+ + K+) Cholera, toxigenic Escherichia coli (EPEC, ETEC); carcinoid, Clostridium difficile, Persists during fasting; bile salt malabsorption also may increase intestinal water secretion; From Wyllie R: Major symptoms and signs of digestive tract disorders. In Kliegman RM, Behrman RE, Jenson HB, editors: Nelson Textbook of Pediatrics, ed 18, Philadelphia, 2007, Saunders, Table 303-7, p 152. WBCs, White blood cells; infection may also contribute to increased motility.


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Pediatrics_Nelson. Philadelphia, 2007, Saunders, Table 303-7, p 152. WBCs, White blood cells; infection may also contribute to increased motility. contact with infected animals (chickens, pet iguanas, other reptiles, turtles) or from contaminated food products, such as dairy products, eggs, and poultry. A large inoculum, of 1000 to 10 billion organisms, is required because Salmonella is killed by gastric acidity. The incubation period for gastroenteritis ranges from 6 to 72 hours but usually is less than 24 hours. Shigella dysenteriae may cause disease by producing Shiga toxin, either alone or combined with tissue invasion. The incubation period is 1 to 7 days. Infected adults may shed organisms for 1 month. Infection is spread by person-to-person contact or by the ingestion of contaminated food with 10 to 100 organisms. The colon is selectively affected. High fever and febrile seizures may occur in addition to diarrhea.


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Pediatrics_Nelson. Only certain strains of E. coli produce diarrhea. E. coli strains associated with enteritis are classified by the mechanism of diarrhea: enterotoxigenic (ETEC), enterohemorrhagic (EHEC), enteroinvasive (EIEC), enteropathogenic (EPEC), or enteroaggregative (EAEC). ETEC strains produce heat-labile (cholera-like) enterotoxin, heat-stable enterotoxin, or both. ETEC causes 40% to 60% of cases of traveler’s diarrhea. ETEC adhere to the epithelial cells in the upper small intestine and produce disease by liberating toxins that induce intestinal secretion and limit absorption. EHEC, especially the E. coli O157:H7 strain, produce a Shiga-like toxin that is responsible for a hemorrhagic colitis and most cases of diarrhea associated with hemolytic uremic syndrome (HUS), which is a syndrome of microangiopathic hemolytic anemia, thrombocytopenia, and renal failure (see Chapter 164). EHEC is associated with contaminated food, including unpasteurized fruit juices and, especially, undercooked beef.


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Pediatrics_Nelson. hemolytic anemia, thrombocytopenia, and renal failure (see Chapter 164). EHEC is associated with contaminated food, including unpasteurized fruit juices and, especially, undercooked beef. EHEC is associated with a self-limited form of gastroenteritis, usually with bloody diarrhea, but production of this toxin blocks host cell protein synthesis and affects vascular endothelial cells and glomeruli, resulting in the clinical manifestations of HUS. EIEC invades the colonic mucosa, producing widespread mucosal damage with acute inflammation, similar to Shigella. EPEC is responsible for many of the epidemics of diarrhea in newborn nurseries and in day care centers.


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Pediatrics_Nelson. Campylobacter jejuni is spread by person-to-person contact and by contaminated water and food, especially poultry, raw milk, and cheese. The organism invades the mucosa of the jejunum, ileum, and colon. Yersinia enterocolitica is transmitted by pets and contaminated food, especially chitterlings. Infants and young children characteristically have a diarrheal disease, whereas older children usually have acute lesions of the terminal ileum or acute mesenteric lymphadenitis mimicking appendicitis or Crohnʼs disease. Postinfectious arthritis, rash, and spondylopathy may develop. Clostridium difficile causes C. difficile-associated diarrhea or antibiotic-associated diarrhea, secondary to its toxin. The organism produces spores that spread from person to person. C. difficile-associated diarrhea may follow exposure to any antibiotic.


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Pediatrics_Nelson. Important enteric parasites found in North America includeEntamoeba histolytica (amebiasis), Giardia lamblia, and Cryptosporidium parvum. Amebiasis occurs in warmer climates, whereas giardiasis is endemic throughout the United Statesand is common among infants in day care centers. E. histolytica infects the colon; amebae may pass through the bowel walland invade the liver, lung, and brain. Diarrhea is of acute onset,is bloody, and contains leukocytes. G. lamblia is transmitted through ingestion of cysts, either from contact with an infectedindividual or from food or freshwater or well water contaminated with infected feces. The organism adheres to the micro-villi of the duodenal and jejunal epithelium. Insidious onset ofprogressive anorexia, nausea, gaseousness, abdominal distention, watery diarrhea, secondary lactose intolerance, and weightloss is characteristic of giardiasis. Cryptosporidium causes mild, watery diarrhea in immunocompetent persons that resolveswithout treatment. It


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Pediatrics_Nelson. diarrhea, secondary lactose intolerance, and weightloss is characteristic of giardiasis. Cryptosporidium causes mild, watery diarrhea in immunocompetent persons that resolveswithout treatment. It produces severe, prolonged diarrhea inpersons with acquired immunodeficiency syndrome (AIDS)(see Chapter 125).


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Pediatrics_Nelson. Available @ StudentConsult.com Gastroenteritis may be accompanied by systemic findings, suchas fever, lethargy, and abdominal pain. Patients often presentwith clinical syndromes. Viral diarrhea is characterized bywatery stools, with no blood or mucus. Vomiting may be present, and dehydration may be prominent, especially in infantsand younger children. Fever, when present, is low grade. Typhoid fever is characterized by bacteremia and fever that usually precede the final enteric phase. Fever, headache, and abdominal pain worsen over 48 to 72 hours with nausea, decreased appetite, and constipation over the first week. If untreated, the disease persists for 2 to 3 weeks marked by significant weight loss and, occasionally, hematochezia or melena. Bowel perforation is a common complication in adults but is rare in children. Infected persons without symptoms, or chronic carriers, serve as reservoirs and sources of continuous spread.


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Pediatrics_Nelson. Dysentery is enteritis involving the colon and rectum, with blood and mucus, possibly foul smelling stools, and fever. Shigella is the prototype cause of dysentery, which must be differentiated from infection with EIEC, EHEC, E. histolytica (amebic dysentery), C. jejuni, Y. enterocolitica, and nontyphoidal Salmonella. Gastrointestinal bleeding and blood loss may be significant. Enterotoxigenic disease is caused by agents that produce enterotoxins, such as V. cholerae and ETEC. Fever is absent or low grade. Diarrhea usually involves the ileum with watery stools without blood or mucus and usually lasts 3 to 4 days with four to five loose stools per day.


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Pediatrics_Nelson. A chief consideration in management of a child with diarrhea is to assess the degree of dehydration as evident from clinical signs and symptoms, ongoing losses, and daily requirements(see Chapter 33). The degree of dehydration dictates the urgencyof the situation and the volume of fluid needed for rehydration.Mild to moderate dehydration usually can be treated with oralrehydration; severe dehydration usually requires intravenous (IV) rehydration and may require ICU admission. Initial laboratory evaluation of moderate to severe diarrhea includes electrolytes, blood urea nitrogen, creatinine, and urinalysis for specific gravity as an indicator of hydration. Stool specimens should be examined for mucus, blood, and leukocytes, which indicate colitis in response to bacteria that diffusely invade the colonic mucosa, such as Shigella, Salmonella,


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Pediatrics_Nelson. C. jejuni, and invasive E. coli. Patients infected with Shiga toxin-producing E. coli and E. histolytica generally have minimal fecal leukocytes.


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Pediatrics_Nelson. A rapid diagnostic test for rotavirus in stool should be performed, especially during the winter. Bacterial stool culturesare recommended for patients with fever, profuse diarrhea, anddehydration or if HUS or pseudomembranous colitis is suspected. If the stool test result is negative for blood and leukocytes,and there is no history to suggest contaminated food ingestion, aviral etiology is most likely. Stool evaluation for parasitic agentsshould be considered for acute dysenteric illness, especially inreturning travelers, and in protracted cases of diarrhea in whichno bacterial agent is identified. The diagnosis of E. histolytica is based on identification of the organism in the stool. Serologictests are useful for diagnosis of extraintestinal amebiasis, including amebic hepatic abscess. Giardiasis can be diagnosed by identifying trophozoites or cysts in stool but require three specimens.More specific and sensitive fecal immunoassays are the diagnostic tests of choice.


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Pediatrics_Nelson. Positive blood cultures are uncommon with bacterial enteritis except for S. typhi (typhoid fever), nontyphoidal Salmonella, and E. coli enteritis in very young infants. Intyphoid fever, blood cultures are positive early in the disease, whereas stool cultures become positive only after the secondary bacteremia. Available @ StudentConsult.com Abdominal Pain Vomiting Diarrhea Failure to Thrive


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Pediatrics_Nelson. Available @ StudentConsult.com Abdominal Pain Vomiting Diarrhea Failure to Thrive Diarrhea can be caused by infection, toxins, gastrointestinal allergy (including allergy to milk or soy proteins), malabsorption defects, inflammatory bowel disease, celiac disease, or any injury to enterocytes. Specific infections are differentiated from each other by the use of stool cultures and enzyme-linked immunosorbent assay or polymerase chain reaction tests, when necessary. Acute enteritis may mimic other acute diseases, such as intussusception and acute appendicitis, which are best identified by diagnostic imaging. Many noninfectious causes of diarrhea produce chronic diarrhea, with persistence for more than 14 days. Persistent or chronic diarrhea may require tests for malabsorption or invasive studies, including endoscopy and small bowel biopsy (see Chapter 129).


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Pediatrics_Nelson. Common-source diarrhea usually is associated with ingestion of contaminated food. In the United States, the most common bacterial food-borne causes (in order of frequency) are nontyphoidal Salmonella, Campylobacter, Shigella, E. coli O157:H7, Yersinia, Listeria monocytogenes, and V. cholerae. The most common parasitic food-borne causes are Cryptosporidium parvum and Cyclospora cayetanensis. Common-source diarrhea also includes ingestion of preformed enterotoxins produced by bacteria, such as S. aureus and Bacillus cereus, which multiply in contaminated foods, and nonbacterial toxins such as from fish, shellfish, and mushrooms. After a short incubation period, vomiting and cramps are prominent symptoms, and diarrhea may or may not be present. Heavy metals that leach into canned food or drinks causing gastric irritation and emetic syndromes may mimic symptoms of acute infectious enteritis.


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Pediatrics_Nelson. Most infectious causes of diarrhea in children are self-limited. Management of viral and most bacterial causes of diarrhea is primarily supportive and consists of correcting dehydration and ongoing fluid and electrolyte deficits and managing secondary complications resulting from mucosal injury. Hyponatremia is common; hypernatremia is less common. Metabolic acidosis results from losses of bicarbonate in stool, lactic acidosis results from shock, and phosphate retention results from transient prerenal-renal insufficiency. Traditionally therapy for 24 hours with oral rehydration solutions alone is effective for viral diarrhea. Therapy for severe fluid and electrolyte losses involves IV hydration. Less severe degrees of dehydration (<10%) in the absence of excessive vomiting or shock may be managed with oral rehydration solutions containing glucose and electrolytes. Ondansetron may be administered to reduce emesis when persistent.


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Pediatrics_Nelson. Antibiotic therapy is necessary only for patients with S. typhi(typhoid fever) and sepsis or bacteremia with signs of systemic toxicity, those with metastatic foci, or infants younger than 3 months with nontyphoidal salmonella. Antibiotic treatment of Shigella produces a bacteriologic cure in 80% of patients after 48 hours, reducing the spread of the disease. Many Shigella sonnei isolates, the predominant strain affecting children, are resistant to amoxicillin and trimethoprim-sulfamethoxazole. Recommended treatment for children is an oral third-generation cephalosporin or a fluoroquinolone for patients 18 years and older.


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Pediatrics_Nelson. Treatment of C. difficile (pseudomembranous colitis) includesdiscontinuation of the antibiotic and, if diarrhea is severe, oral metronidazole or vancomycin. E. histolytica dysentery is treatedwith metronidazole followed by a luminal agent, such as iodoquinol. The treatment of G. lamblia is with albendazole, metronidazole, furazolidone, or quinacrine. Nitazoxanide can be usedin children younger than 12 months of age for the treatment ofCryptosporidium. The major complication of gastroenteritis is dehydration and hypovolemic shock. Seizures may occur with high fever, especially with Shigella. Intestinal abscesses can form with Shigella and Salmonella infections, especially typhoid fever, leading to intestinal perforation, a life-threatening complication. Severe vomiting associated with gastroenteritis can cause esophageal tears or aspiration pneumonia.


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Pediatrics_Nelson. Deaths resulting from diarrhea reflect the principal problem of disruption of fluid and electrolyte homeostasis, which leads to dehydration, electrolyte imbalance, vascular instability, and shock. In the United States, approximately 75 to 150 deaths occur annually from diarrheal disease, primarily in children under 1 year of age. These deaths occur in a seasonal pattern between October and February, concurrent with the rotavirus season. At least 10% of patients who have typhoid fever shed S. typhifor about 3 months, and 4% become chronic carriers. The risk of becoming a chronic carrier is low in children. Ciprofloxacin is recommended for adult carriers with persistent Salmonella excretion.


Pediatrics_Nelson

Pediatrics_Nelson. The most important means of preventing childhood diarrhea is the provision of clean, uncontaminated water and proper hygiene in growing, collecting, and preparing foods. Good hygienic measures, especially good hand washing with soap and water, are the best means of controlling person-to-person spread of most organisms causing gastroenteritis. Similarly poultry products should be considered potentially contaminated with Salmonella and should be handled and cooked appropriately.


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Pediatrics_Nelson. Immunization against rotavirus infection is recommended for all children beginning at 6 weeks of age, with the first dose by 14 weeks 6 days and the last dose by 8 months (see Chapter 94). Two typhoid vaccines are licensed in the United States: an oral live attenuated vaccine (Ty21a) for children 6 years and older, and a capsular polysaccharide vaccine (ViCPS) for intramuscular administration for persons 2 years and older. These are recommended for travelers to endemic areas of developing countries or for household contacts of S. typhi chronic carriers. Families should be aware of the risk of acquiring salmonellosis from household reptile pets. Transmission of Salmonella from reptiles can be prevented by thorough hand washing with soap and water after handling reptiles or reptile cages. Children under 5 years of age and immunocompromised persons should avoid contact with reptiles.


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Pediatrics_Nelson. The risk for traveler’s diarrhea, caused primarily by ETEC, may be minimized by avoiding uncooked food and untreated drinking water. Prophylaxis with bismuth subsalicylate (Pepto-Bismol) for adults (2 oz or two tablets orally four times a day) may be effective for prevention but is not recommended for children. Symptomatic self-treatment for mild diarrhea with loperamide (Imodium) and WHO oral rehydration solution is recommended for children at least 6 years of age and adults. Self-treatment of moderate diarrhea and fever with a fluoroquinolone is recommended in adults of at least 18 years old. Prompt medical evaluation is indicated for disease persisting more than 3 days, bloody stools, fever above 102° F (38.9° C) or chills, persistent vomiting, or moderate to severe dehydration, especially in children.


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Pediatrics_Nelson. Lactobacillus acidophilus is a probiotic and reduces the incidence of community-acquired and antibiotic-associated diarrhea in children treated with oral antibiotics for other infectious diseases. There are six primary hepatotropic viruses:Hepatitis A virus (HAV)Hepatitis B virus (HBV)Hepatitis C virus (HCV)Hepatitis D virus (HDV)Hepatitis E virus (HEV)Hepatitis G virus (HGV) They differ in their virologic characteristics, transmission, severity, likelihood of persistence, and subsequent risk of hepatocellular carcinoma (Table 113-1). HDV, also known as the delta agent, is a defective virus that requires HBV for spread and causes either coinfection with HBV or superinfection in chronic HBsAg (hepatitis B surface antigen) carriers. HBV, HCV, and HDV infections can result in chronic hepatitis, or a chronic carrier state, which facilitates spread. The cause of 10% to 15% of cases of acute hepatitis is unknown.


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Pediatrics_Nelson. HAV causes approximately half of all cases of viral hepatitis in the United States. Among U.S. children, approximately 70% to 80% of all new cases of viral hepatitis are caused by HAV, 5% to 30% by HBV, and 5% to 15% by HCV. The major risk factors for HBV and HCV are injectable drug use, frequent exposure Table 113-1 Characteristics of Agents Causing Acute Viral Hepatitis HEPATITIS VIRUSES FEATURE HAV* HBV HCV† HDV HEV‡ HGV TTV, SEN-V Viral structure 27-nm ssRNA virus 42-nm dsDNA virus 30to 60-nm ssRNA virus 36-nm circular ssRNA hybrid 27–34 nm ssRNA virus 50to 100-nm ssRNA virus 30to 50nm ssDNA virus particle with HBsAg coat


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Pediatrics_Nelson. Increased No Yes Yes No No Unknown risk of hepatocellular carcinoma dsDNA, Double-stranded DNA; HAV, hepatitis A virus; HBV, hepatitis B virus; HCV, hepatitis C virus; HDV, hepatitis D virus; HEV, hepatitis E virus; HGV, hepatitis G virus; PCR, polymerase chain reaction; RIBA, recombinant immunoblot assay; RT-PCR, reverse transcriptase-polymerase chain reaction; ssDNA/ssRNA, single- stranded DNA/RNA; TTV, transfusion-transmitted virus. *I.e., enterovirus 72. †Formerly posttransfusion non-A, non-B virus. ‡Formerly enteral non-A, non-B virus. to blood products, and prenatal transmission from maternal infection. HEV occurs following travel to endemic areas outside of the United States. HGV is prevalent in HIV-infected persons. HBV and HCV cause chronic infection, which may lead to cirrhosis and is a significant risk factor for hepatocellular carcinoma and represents a persistent risk of transmission. Available @ StudentConsult.com


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Pediatrics_Nelson. Available @ StudentConsult.com There is considerable overlap in the characteristic clinical courses of HAV, HBV, and HCV (Fig. 113-1). The preicteric phase, which lasts approximately 1 week, is characterized by headache, anorexia, malaise, abdominal discomfort, nausea, and vomiting and usually precedes the onset of clinically detectable disease. Infants with perinatal acquired HBV may have immune complexes accompanied by urticaria and arthritis before the onset of icterus. Jaundice and tender hepatomegaly are the most common physical findings and are characteristic of the icteric phase. Prodromal symptoms, particularly in children, may abate during the icteric phase. Asymptomatic or mild, nonspecific illness without icterus is common with HAV, HBV, and HCV, especially in young children. Hepatic enzymes may increase 15to 20-fold. Resolution of the hyperbilirubinemia and normalization of the transaminases may take 6 to 8 weeks.


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Pediatrics_Nelson. Alanine aminotransferase and aspartate aminotransferase levels are elevated and generally reflect the degree of parenchymal inflammation. Alkaline phosphatase, 5α-nucleotidase, and total and direct (conjugated) bilirubin levels indicate the degree of cholestasis, which results from hepatocellular and bile duct damage. The prothrombin time is a good predictor Figure 113-1 Clinical course and laboratory findings associated with hepatitis A, hepatitis B, and hepatitis C. ALT, Alanine aminotransferase; HAV, hepatitis A virus; anti-HBc, antibody to hepatitis B core antigen; HBeAg, hepatitis B early antigen; anti-HBe, antibody to hepatitis B early antigen; HBsAg, hepatitis B surface antigen; anti-HBs, antibody to hepatitis B surface antigen; HCV, hepatitis C virus; PCR, polymerase chain reaction. of severe hepatocellular injury and progression to fulminant hepatic failure (see Chapter 130).


Pediatrics_Nelson

Pediatrics_Nelson. The diagnosis of viral hepatitis is confirmed by serologic testing (see Table 113-1 and Fig. 113-1). The presence of IgM-specific antibody to HAV with low or absent IgG antibody to HAV is presumptive evidence of HAV. There is no chronic carrier state of HAV. The presence of HBsAg signifies acute or chronic infection with HBV. Antigenemia appears early in the illness and is usually transient but is characteristic of chronic infection. Maternal HBsAg status should always be determined when HBV infection is diagnosed in children younger than 1 year of age because of the likelihood of vertical transmission. Hepatitis B early antigen (HBeAg) appears in the serum with acute HBV. The continued presence of HBsAg and HBeAg in the absence of antibody to e antigen (anti-HBe) indicates high risk of transmissibility that is associated with ongoing viral replication. Clearance of HBsAg from the serum precedes a variable window period followed by the emergence of the antibody to surface antigen


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Pediatrics_Nelson. of transmissibility that is associated with ongoing viral replication. Clearance of HBsAg from the serum precedes a variable window period followed by the emergence of the antibody to surface antigen (anti-HBs), which indicates development of lifelong immunity and is also a marker of immunization. Antibody to core antigen (anti-HBc) is a useful marker for recognizing HBV infection during the window phase (when HBsAg has disappeared but before the appearance of anti-HBs). Anti-HBe is useful in predicting a low degree of infectivity during the carrier state. Seroconversion after HCV infection may occur 6 months after infection. A positive result of HCV enzyme-linked immunosorbent assay should be confirmed with the more specific recombinant immunoblot assay, which detects antibodies to multiple HCV antigens. Detection of HCV RNA by polymerase chain reaction (PCR) is a sensitive marker for active infection, and results of this test may be positive 3 days after inoculation.


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Pediatrics_Nelson. Many other viruses may cause hepatitis as part of systemic infection, including Epstein-Barr virus, cytomegalovirus, varicella zoster virus (chickenpox), herpes simplex virus, and adenoviruses. Bacterial infections that may cause hepatitis include Escherichia coli sepsis and leptospirosis. Patients with cholecystitis, cholangitis, and choledocholithiasis may present with acute symptoms and jaundice. Other causes of acute liver disease in childhood include drugs (isoniazid, phenytoin, valproic acid, carbamazepine, oral contraceptives, acetaminophen), toxins (ethanol, poisonous mushroom), Wilson disease, metabolic disease (galactosemia, tyrosinemia), α1-antitrypsin deficiency, tumor, shock, anoxia, and graft-versus-host disease (see Chapter 130).


Pediatrics_Nelson

Pediatrics_Nelson. The treatment of acute hepatitis is largely supportive andinvolves rest, hydration, and adequate nutrition. Hospitalizationis indicated for persons with severe vomiting and dehydration,a prolonged prothrombin time, or signs of hepatic encephalopathy. When the diagnosis of viral hepatitis is established, attention should be directed toward preventing its spread to closecontacts. For HAV, hygienic measures include hand washingand careful disposal of excreta, contaminated diapers or clothing, needles, and other blood-contaminated items.