NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+, Exams of Nursing

Download NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ and more Exams Nursing in PDF only on Docsity! NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Chalazion Chalazion is a chronic sterile inflammation of the eyelid resulting from a lipogranuloma of the meibomian glands that line the posterior margins of the eyelids (see Fig. 29-7). It is deeper in the eyelid tissue than a hordeolum and may result from an internal hordeolum or retained lipid granular secretions. Clinical Findings Initially, mild erythema and slight swelling of the involved eyelid are seen. After a few days the inflammation resolves, and a slow growing, round, nonpigmented, painless (key finding) mass remains. It may persist for a long time and is a commonly acquired lid lesion seen in children (see Fig. 29-7 ). 727 Management • Acute lesions are treated with hot compresses. • Refer to an ophthalmologist for surgical incision or topical intralesional corticosteroid injections if the condition is unresolved or if the lesion causes cosmetic concerns. A chalazion can distort vision by causing astigmatism as a result of pressure on the orbit. Complications Recurrence is common. Fragile, vascular granulation tissue called pyogenic granuloma that enlarges and bleeds rapidly can occur if a chalazion breaks through the conjunctival surface. Blepharitis Blepharitis is an acute or chronic inflammation of the eyelash follicles or meibomian sebaceous glands of the eyelids (or both). It is usually bilateral. There may be a history of contact lens wear or physical contact with another symptomatic person. It is commonly caused by contaminated makeup or contact lens solution. Poor hygiene, tear deficiency, rosacea, and seborrheic dermatitis of the scalp and face are also possible etiologic factors. The ulcerative form of blepharitis is usually caused by S. aureus. Nonulcerative blepharitis is occasionally seen in children with psoriasis, seborrhea, eczema, allergies, lice infestation, or in children with trisomy 21. Clinical Findings • Swelling and erythema of the eyelid margins and palpebral conjunctiva 726 • Flaky, scaly debris over eyelid margins on awakening; presence of lice • Gritty, burning feeling in eyes • Mild bulbar conjunctival injection • Ulcerative form: Hard scales at the base of the lashes (if the crust is removed, ulceration is seen at the hair follicles, the lashes fall out, and an associated conjunctivitis is present) Differential Diagnosis Pediculosis of the eyelashes. Management Explain to the patient that this may be chronic or relapsing. Instructions for the patient include: • Scrub the eyelashes and eyelids with a cotton-tipped applicator containing a weak (50%) solution of no-tears shampoo to maintain proper hygiene and debride the scales. • Use warm compresses for 5 to 10 minutes at a time two to four times a day and wipe away lid debris. • At times antistaphylococcal antibiotic (e.g., erythromycin 0.5% ophthalmic ointment) is used until symptoms subside and for at least 1 NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ week thereafter. Ointment is preferable to eye drops because of increased duration of contact with the ocular tissue. Azithromycin 1% ophthalmic solution for 4 weeks may also be used (Shtein, 2014). • Treat associated seborrhea, psoriasis, eczema, or allergies as indicated. • Remove contact lenses and wear eyeglasses for the duration of the treatment period. Sterilize or clean lenses before reinserting. • Purchase new eye makeup; minimize use of mascara and eyeliner. • Use artificial tears for patients with inadequate tear pools. Chronic staphylococcal blepharitis and meibomian keratoconjunctivitis respond to oral erythromycin. Doxycycline, tetracycline, or minocycline can be used chronically in children older than 8 years old. NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ • Absent or decreased mobility of the TM • Air-fluid level behind the TM • Otorrhea 747 • Signs and symptoms of middle ear inflammation indicated by either: • Erythema of the TM (Amber is usually seen in otitis media with effusion [OME]; white or yellow may be seen in either AOM or OME [Shaikh et al, 2010 ].) or • Distinct otalgia that interferes with normal activity or sleep • In addition, the following TM findings may be present: • Increased vascularity with obscured or absent landmarks (see Fig. 30-4 ). • Red, yellow, or purple TM (Redness alone should not be used to diagnose AOM, especially in a crying child.) • Thin-walled, sagging bullae filled with straw-colored fluid seen with bullous myringitis Diagnostic Studies Pneumatic otoscopy is the simplest and most efficient way to diagnose AOM. Tympanometry reflects effusion (type B pattern). Tympanocentesis to identify the infecting organism is helpful in the treatment of infants younger than 2 months old. In older infants and children, tympanocentesis is rarely done and is useful only if the patient is toxic or immunocompromised or in the presence of resistant infection or acute pain from bullous myringitis. If a tympanocentesis is warranted, refer the patient to an otolaryngologist for this procedure. Differential Diagnosis OME, mastoiditis, dental abscess, sinusitis, lymphadenitis, parotitis, peritonsillar abscess, trauma, ETD, impacted teeth, temporomandibular joint dysfunction, and immune deficiency are differential diagnoses. Any infant 2 months old or younger with AOM should be evaluated for fever without focus and not just treated for an ear infection. Management Many changes have been made in the treatment of AOM because of the increasing rate of antibiotic-resistant bacteria related to the injudicious use of antibiotics. Ample evidence has been presented that symptom management may be all that is required in children with MEE without other symptoms of AOM (Lieberthal et al, 2013). Treatment guidelines are decided based on the child's age, illness severity, and the certainty of diagnosis. Table 30-5 shows the recommendation for the diagnosis and subsequent treatment of AOM. 1. Pain management is the first principle of treatment. • Weight-appropriate doses of ibuprofen or acetaminophen should be encouraged to decrease discomfort and fever. • Topical analgesics, such as benzocaine or antipyrine/benzocaine otic preparations, can be added to systemic pain management if the TM is known to be intact. Topical analgesics should not be used alone. • Distraction, oil application, or external use of heat or cold may be of some use. 2. Antibiotics are also effective. (Table 30-6 lists dosage recommendations.) • Amoxicillin remains the first-line antibiotic for AOM if there has not been a previous treated AOM in the previous 30 days, there is no conjunctivitis, and no penicillin allergy (Lieberthal et al, 2013). Beta-lactam coverage (amoxicillin/clavulanate, third- generation cephalosporin) is recommended when the child has been treated with amoxicillin in the previous 30 days, there is an allergy to penicillin, and the child has concurrent conjunctivitis or has recurrent otitis that has not responded to amoxicillin. If there is a documented hypersensitivity reaction to amoxicillin, the following antibiotics are acceptable, follow the non-type 1 hypersensitivity and type 1 hypersensitivity recommendations in Table 30-6: • Ceftriaxone may be effective for the vomiting child, the child unable to tolerate oral medications, or the child who has failed amoxicillin/clavulanate. 748 • Clindamycin may be considered for ceftriaxone failure but should only be used if susceptibilities are known. • Prophylactic antibiotics for chronic or recurrent AOM are not recommended. 3. Observation or “watchful waiting” for 48 to 72 hours (see Table 30-5 ) allows the patient to improve without antibiotic treatment. Pain relief should be provided, and a means of follow-up must be in place. Options for follow-up include: • Parent-initiated visit or phone call for worsening or no improvement • Scheduled follow-up appointment • Routine follow-up phone call NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ • Given a prescription to be started if the child's symptoms do not improve or if they worsen in 48 to 72 hours (Table 30-7 ) • Communication with the parent, reevaluation, and the ability to obtain medication must be in place. 4. Recommendations for follow-up include: • After 48 to 72 hours if a child has not showed improvement in ear symptomatology, the child should be seen to confirm or exclude the presence of AOM. If the initial management option was an antibacterial agent, the agent should be changed. Prevention and Education The following interventions, shown to be helpful in preventing AOM, should be encouraged: • Exclusive breastfeeding until at least 6 months of age seems to be protective against AOM NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ • Avoid bottle propping, feeding infants lying down, and passive smoke exposure •Avoid the use of pacifiers: Although the relationship cannot be fully explained, multiple studies have shown that pacifier use increases the incidence of AOM (Lieberthal et al, 2013). • Pneumococcal vaccine; specifically PCV13, which contains subtype 19A • Annual influenza vaccine may help prevent otitis media 750 • Xylitol liquid or chewing gum as tolerated • Choose licensed day care facilities with fewer children •Educate regarding the problem of drug-resistant bacteria and the need to avoid the use of antibiotics unless absolutely necessary; if antibiotics are used, the child needs to complete the entire course of the prescription and follow up if symptoms do not resolve Conjunctivitis An estimated 6 million cases of bacterial conjunctivitis occur in the United States annually, at an estimated cost of $377 million to $857 million (Azari and Barney, 2013). Conjunctivitis is an inflammation of the palpebral and occasionally the bulbar conjunctiva (Fig. 29-5). It is the most frequently seen ocular disorder in pediatric practice. In pediatric patients, bacteria are the most common cause of infection (50% to 75%) most commonly from December to April. Pathogens include H. influenzae, Streptococcus pneumoniae, and Moraxella species with both gram-negative and gram-positive organisms implicated (Azari and Barney, 2013 ). Conjunctivitis also occurs as a viral or fungal infection or as a response to allergens or chemical irritants. Bacterial conjunctivitis is often unilateral, whereas viral conjunctivitis is most often bilateral. Unilateral disease can also suggest a toxic, chemical, mechanical, or lacrimal cause. Blockage of the tear drainage system (e.g., from meibomianitis or blepharitis), injury, foreign body, abrasion or ulcers, keratitis, iritis, herpes simplex virus (HSV), and infantile glaucoma are other known causes. Patient age is a major indicator of etiology ( Table 29-6). Types of Conjunctivitis Type Incidence/Etiology Clinical Findings Diagnosis Management* Ophthalmia neonatorum Neonates: Chlamydia trachomatis, Staphylococcus aureus, Neisseria gonorrhoeae, HSV (silver nitrate reaction occurs in 10% of neonates) Erythema, chemosis, purulent exudate with N. gonorrhoeae; clear to mucoid exudate with chlamydia Culture (ELISA, PCR), Gram stain, R/O N. gonorrhoeae,chlamydia Saline irrigation to eyes until exudate gone; follow with erythromycin ointment For N. gonorrhoeae:ceftriaxone or IM or IV For chlamydia: erythromycin or possibly azithromycin PO For HSV: antivirals IV or PO NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ discharge, and erythema; (2) furuncles or small abscesses that form in hair follicles; or (3) impetigo or infection of the superficial layers of the epidermis. OE can also be classified as mycotic otitis externa, caused by fungus, or as chronic external otitis, a diffuse low-grade infection of the EAC. Severe infection or systemic infection can be seen in children who have diabetes mellitus, are immunocompromised, or have received head and neck irradiation. OE results when the protective barriers in the EAC are damaged by mechanical or chemical mechanisms. OE is most frequently caused by retained moisture in the EAC, which changes the usually acidic environment to a neutral or basic environment, thereby promoting bacterial or fungal growth. Chlorine in swimming pools adds to the 743problem because it kills the normal ear flora, allowing the growth of pathogens. Regular cleaning of the EAC removes cerumen, which is an important barrier to water and infection. Soapy deposits, NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ alkaline drops, debris from skin conditions, local trauma, sweating, allergy, stress, and hearing aids can also be responsible for causing OE (Rosenfeld et al, 2014 ). OE is most often caused by Pseudomonas aeruginosa and Staphylococcus aureus, but it is not uncommon for the infection to be polymicrobial. Furunculosis of the external canal is generally caused by S. aureus and Streptococcus pyogenes. Otomycosis is caused by Aspergillus or Candida and can be the result of systemic or topical antibiotics or steroids. Otomycosis is also more common in children with diabetes mellitus or immune dysfunction and in these cases is most commonly caused by Aspergillus niger, Escherichia coli, or Klebsiella pneumonia. Group B streptococci are a more common cause in neonates. Long-standing ear drainage may suggest a foreign body, chronic middle ear pathology (such as, a cholesteatoma), or granulomatous tissue. Bloody drainage may indicate trauma, severe otitis media, or granulation tissue. Chronic or recurrent OE may result from eczema, seborrhea, or psoriasis. Eczematous dermatitis, moist vesicles, and pustules are seen in acute infection, whereas crusting is more consistent with chronic infection. Clinical Findings History The following can be found: • Itching and irritation • Pain that seems disproportionate to what is seen on examination • Pressure and fullness in ear and occasionally hearing loss that can be conductive or sensorineural • Rare hearing loss and otorrhea or systemic complaints and symptoms • Sagging of the superior canal, periauricular edema, and preauricular and postauricular lymphadenopathy with more severe disease Extension to the surrounding soft tissue results in the obstruction of the canal with or without cellulitis. Physical Examination Findings on physical examination can include the following: • Pain, often quite severe, with movement of the tragus (when pushed) or pinna (when pulled) or on attempts to examine the ear with an otoscope • Swollen EAC with debris, making visualization of the TM difficult or impossible • Rare otorrhea • Occasional regional lymphadenopathy • Tragal tenderness with a red, raised area of induration that can be deep and diffuse or superficial and pointing, which is characteristic of furunculosis • Red, crusty, or pustular spreading lesions • Pruritus associated with thick otorrhea that can be black, gray, blue-green, yellow, or white, and black spots over the TM are indicative of mycotic infection • Dry-appearing canal with some atrophy or thinning of the canal and virtually no cerumen visible with chronic OE • Presence of pressure-equalizing tube or perforation of TM Diagnostic Studies Culturing the discharge from the ear is not customary but may be indicated if clinical improvement is not seen during or after treatment, severe pain persists, the child is a neonate, the child is immunocompromised, or chronic or recurrent OE is suspected. Culturing requires a swab premoistened with sterile nonbacteriostatic saline or water. Differential Diagnosis AOM with perforation, TTO, chronic suppurative otitis media (CSOM), necrotizing OE, cholesteatoma, mastoiditis, posterior auricular NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ lymphadenopathy, dental infection, and eczema are all possible differential diagnoses. Management The following steps outline the management of OE: • Eardrops are the mainstay of therapy for OE (see Table 30-3 ). Eardrops containing acetic acid or antibiotic with and without corticosteroid drops are the treatment of choice for OE. Symptoms should be markedly improved within 7 days, but resolution of the infection may take up to 2 weeks. Drops should be used until all symptoms have resolved. Ototoxic drugs should not be used if there is a risk of TM perforation. NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Acetaminophen or ibuprofen Antibiotics if GABHS Saltwater gargles Anesthetic lozenges for older childPharyngiti s NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Streptococcal Disease Streptococci are gram-positive spherical cocci that are broadly classified based on their ability to hemolyze RBCs. Complete hemolysis is known as beta-hemolytic. Partial hemolysis is alpha-hemolytic; non-hemolysis is gamma-hemolytic. Cell wall carbohydrate differences further subdivide the streptococci. These differences are identified as Lancefield antigen subgroups A-H and K-V. Subgroups A-H and K-O are associated with human disease. Group A beta-hemolytic streptococcus is the most virulent, although group B beta-hemolytic streptococcus can cause bacteremia and meningitis in infants younger than 3 months old (rarely older). Group A streptococcus (GAS) are also subdivided into more than 100 subtypes based upon their M protein antigen located on the cell surface and fimbriae on the cell's 535outer edge. The virulence of GAS is greatly dependent upon their M protein. If the M protein is present, GAS strains are able to resist phagocytosis; if the M protein is weak or absent, the strains are basically avirulent (e.g., chronic GAS pharyngeal carriers). GAS also produces many varieties of enzymes and toxins that may stimulate specific antitoxin antibodies for immunity or serve as evidence of past infection but not confer immunity. There may also not be cross-immunity between antibodies for different GAS strains (e.g., scarlet fever is caused by three different pyrogenic exotoxins, so the illness can recur). Some general remarks about specific illnesses due to GAS and non- group A and B streptococcus infection are discussed in this chapter; cross-references to specific chapters are noted for other GAS caused infections. Group A Streptococcus Streptococcus microbes most commonly invade the respiratory tract, skin, soft tissues, and blood. Transmission is primarily through infected upper respiratory tract secretions or, secondarily, through skin invasion. Fomites and household pets are not vectors. Food-borne outbreaks from contamination by food handlers have been reported. Both streptococcus pharyngitis and impetigo are associated with crowding, whether at home, school, or other institution. Streptococcal pharyngitis is rare in infants and children younger than 3 years old, but the incidence rises with age and is most common in the winter and early spring in temperate climates when respiratory viruses circulate. Carrier rates in asymptomatic children are up to 20% (Arnold and Nizet, 2012). By contrast, streptococcus skin infection (impetigo, pyoderma) is more common in toddlers and preschool-age children. Those at increased risk for invasive GAS are individuals with varicella infection, IV drug use, HIV, diabetes, chronic heart or lung disease, infants, and older adults. The incubation period is 2 to 5 days for pharyngitis and 7 to 10 days from skin acquisition to development of impetiginous lesions. In untreated individuals, the period of communicability is from the onset of symptoms up to a few months. Children are generally considered non-infectious 24 hours after the start of appropriate antibiotic therapy. Clinical Findings and Diagnostic Studies The following may be seen in GAS: • Respiratory tract infection: Streptococcal tonsillopharyngitis (GABHS) and pneumonia are described in Chapter 32. Peritonsillar abscess, cervical lymphadenitis, retropharyngeal abscess, otitis media, mastoiditis, and sinusitis symptoms may be clinical features. • Scarlet fever: This is caused by erythrogenic toxin. It is uncommon in children younger than 3 years old. The incubation period is approximately 3 days (the range is 1 to 7 days). There is abrupt illness with sore throat, vomiting, headache, chills, and malaise. Fever can reach 104° F (40° C). Tonsils are erythematous, swollen, and usually covered in exudate. The pharynx also is inflamed and can be covered with a gray-white exudate. The palate and uvula are erythematous and reddened, and petechiae are present. The tongue is usually coated and red. Desquamation of the coating leaves prominent papillae (strawberry tongue). The typical scarlatina rash appears 1 to 5 days following onset of symptoms but may be the presenting symptom. The exanthema is red, blanches to pressure, and is finely papular, making the skin feel coarse, with a sandpaper feel. The rash generally begins on the neck and spreads to the trunk and extremities becoming generalized within 24 hours. The face may be spared (cheeks may be reddened with circumoral pallor), but the rash becomes denser on the neck, axilla, and groin. Pastia lines, transverse linear hyperpigmented areas with tiny petechiae, are seen in the folds of the joints (see Fig. 24-3). In severe disease, small vesicles (miliary sudamina) can be found on the hands, feet, and abdomen. There is circumoral pallor and the cheeks are erythematous. The rash begins to fade and desquamate after 3 to 4 days starting on the face and slowly moving to the trunk and extremities and may include fingernail margins, palms, and soles; this process can take up to 6 weeks. Sore throat and constitutional NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ symptoms resolve in approximately 5 to 7 days (average 3 to 4 days). • Bacteremia: This can occur after respiratory (pharyngitis, tonsillitis, AOM) and localized skin infections. Some children have no obvious source of infection. Meningitis, osteomyelitis, septic arthritis, pyelonephritis, pneumonia, peritonitis, and bacterial endocarditis are rare but are associated with GAS bacteremia. (Neonatal sepsis due to group B streptococcus is discussed in Chapter 39 .) • Vaginitis and streptococcal toxic shock syndrome (see discussions in Chapter 36 ). • Perianal streptococcal cellulitis: Symptoms include local itching, pain, blood-streaked stools, erythema, and proctitis. Fever and systemic infections are uncommon. Although infection is usually the result of autoinoculation, sexual molestation is in the differential. • Skin infections (see Chapter 37); rheumatic heart disease (see Chapter 25); and necrotizing fasciitis (see Chapter 37). Refer to disease-specific chapters for diagnostic studies of disease-specific conditions. NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Differential Diagnosis, Management, and Complications Many viral pathogens are on the differential for acute pharyngitis, including influenza, parainfluenza, rhinovirus, coronavirus, adenovirus, and respiratory syncytial virus. EBV is common and is usually accompanied by other clinical findings (e.g., splenomegaly, generalized lymphadenopathy). Other causes of bacterial upper respiratory disease include (though rare) diphtheria, tularemia, toxoplasmosis, mycoplasma, tonsillar TB, salmonellosis, and brucellosis (Gerber, 2011). Staphylococcal impetigo must be differentiated from GABHS pyoderma. Septicemia, meningitis, osteomyelitis, septic arthritis, pyelonephritis, and bacterial endocarditis can result from other bacteria causing similar infections. 536 Antimicrobial therapy is recommended for GABHS-caused pharyngitis to decrease the risk of acute rheumatic fever, decrease the length of the illness, prevent complications, and reduce transmission to others. See appropriate aforementioned site-specific chapters for recommendations for managing specific infections. Complications are usually caused by the spread of the disease from the localized infection. Upper respiratory complications include cervical lymphadenitis, retropharyngeal abscess, otitis media, mastoiditis, and sinusitis if the primary infection is unrecognized or treatment is inadequate. Acute poststreptococcal glomerulonephritis can occur following skin or upper respiratory GAS infection, whereas acute rheumatic fever only occurs following GAS URIs. Poststreptococcal reactive arthritis can occur following GAS pharyngitis. Skin infection with GAS may progress to cellulitis, myositis, or necrotizing fasciitis. Other complications may be associated with invasive infections including pneumonia, pleural empyema, meningitis, osteomyelitis, and bacterial endocarditis. Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) is a group of neuropsychiatric disorders thought to result from the production of autoimmune antibodies; these include obsessive-compulsive disorders, tic disorders, and Tourette syndrome. See Chapter 19 for further discussion. Non–Group A or B Streptococci These streptococci or Lancefield groups (principally groups C and G) are associated with invasive disease in all age groups. They may cause septicemia, UTIs, endocarditis, respiratory disease (upper and lower), skin soft tissue infection, pharyngitis, brain abscesses, and meningitis in newborns, children, adolescents, and adults. The incubation period and communicability times are unknown. Positive culture from normally sterile body fluids is adequate for diagnosis. Penicillin G is the drug of choice with modification based on culture sensitivities. Pneumonia with empyema or abscess may respond slowly despite effective antimicrobial therapy with fevers lasting more than 7 days (Haslam and St. Geme, 2012 ). Kawasaki Disease KD (also known as mucocutaneous lymph node syndrome or infantile polyarteritis) is the second most common 563childhood vasculitis with a varying incidence from country to country, with Japan having the highest incidence of 239.6 per 100,000. The incidence is increasing in Japan, the United Kingdom, and India (Saundankar et al, 2014). The disease is characterized by an acute generalized systemic medium vessel vasculitis occurring throughout the body. Although its cause is unknown, it is believed that an infectious agent activates the immune system in a genetically susceptible host. Genetics may explain the higher incidence in Asia as well as a higher incidence in children of parents or siblings with a history of the disease. Recent data suggest T-cell activation plays a role in disease severity and susceptibility (Scuccimarri, 2012). KD exhibits geographic and seasonal outbreaks, in the late winter and early spring. Person-to- person spread is low. Referral of these children to a pediatrician is necessary. It is self-limited and the most common cause of acquired heart disease in children in Japan and the United States (Saundankar et al, 2014). The EULAR/PReS classification for KD includes a persistent fever for at least 5 days plus four of the following (Ozen et al, 2010): • Bilateral conjunctival injection • Changes of the lips and oral cavity • Cervical lymphadenopathy • Polymorphous exanthema • Changes in the peripheral extremities (swelling of the hands or feet) or perineal area NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ • Early diagnosis is essential to prevent aneurysms in the coronary and extraparenchymal muscular arteries. Treatment goals include: (1) evoking a rapid anti-inflammatory response, (2) preventing coronary thrombosis by inhibiting platelet aggregation, and (3) minimizing long-term coronary risk factors by exercise, a heart healthy diet, and smoking prevention. The child should be referred for initial treatment that includes the following medications and agents (Scuccimarri, 2012): • Intravenous immunoglobulin (IVIG) therapy (a single dose of 2 g/kg over 12 hours, ideally in the first 10 days of the illness) to reduce the incidence of coronary artery abnormalities. The use of immunoglobulin after the tenth day must be individualized. If a child is found to have an abnormal echocardiogram, fever, tachycardia, or other signs of inflammation beyond the tenth day, then immunoglobulin is still indicated. Retreatment with immunoglobulin may be useful for persistent or recurrent fevers. • High-dose aspirin is given for its anti-inflammatory properties (80 to 100 mg/kg/day in four divided doses—every 6 hours initially) until afebrile for at least 48 to 72 hours, then lowering the aspirin dose to 3 to 5 mg/kg/day until 6 to 8 weeks and then can NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ discontinue if the echocardiogram is normal. If significant coronary artery abnormalities develop and do not resolve, aspirin or other antiplatelet therapy is used indefinitely. • For patients with IVIG-resistant disease as indicated by a persistent fever 48 hours after treatment with IVIG and aspirin, a second treatment of IVIG at 2 mg/kg over 12 hours is initiated. If this is not successful, then methylprednisone IV at 30 mg/kg over 3 hours once a day for 1 to 3 days may be initiated. Infliximab 5 mg/kg may also be used. If the patient is still febrile, then the opposite anti- inflammatory can be used. (Methylprednisone in the infliximab groups, or infliximab in the methylprednisone group.) Other options include cyclosporine A, methotrexate or cyclophosphamide (Saneeymehri et al, 2015). • An echocardiogram should be obtained as soon as the diagnosis is established as a baseline study, with subsequent studies at 2 weeks and 6 to 8 weeks after onset of illness. If a child is found to have abnormalities, more frequent evaluations may be indicated. • All children on chronic aspirin therapy should receive inactivated influenza vaccination. If varicella or influenza develops, aspirin treatment should be stopped for 6 weeks and another antiplatelet drug substituted to minimize the risk of Reye syndrome. • Live virus vaccines should be delayed until 11 months after administration of IVIG (AAP Red Book, 2015). • Children without coronary or cardiac changes should be followed by a cardiologist during the first year after the onset of KD. If there are no cardiac changes during that first year, then the PCP may follow the patient with no activity restrictions imposed at that point. • Patients with any range of transient coronary artery dilation (including giant aneurysms) should be followed by a cardiologist for years; physical activity limitations may be imposed. • Follow and counsel all KD patients about a heart-healthy diet. Complications and Prognosis The acute disease is self-limited; however, during the initial stage (acute phase), inflammation of the arterioles, venules, and capillaries of the heart occurs and can later progress to coronary artery aneurysm in 15% to 25% of untreated children (less than 5% when treated appropriately). The process of aneurysm formation and subsequent thrombosis or scarring of the coronary artery may occur as late as 6 months after the initial illness. Other possible complications include recurrence of KD (less than 2%); CHF or massive myocardial infarction; myocarditis or pericarditis, or both (30%); pericardial effusion; and mitral valve insufficiency. Mortality (1.25%) from KD occurs from cardiac sequelae 15 to 45 days after onset of fever. Children with coronary dilation or aneurysms (especially those greater than 4 mm) may have long-term coronary endothelial changes that place the child at risk for early ischemic disease; 565they may also develop dyslipidemias (Wood and Tulloh, 2009). Studies from Japan raise concern about risk of early atherosclerosis (due to arterial damage, ongoing inflammatory process, and alteration in lipid profile and other atherosclerosis risk factors) even in children without coronary changes during acute febrile illness (Fukazawa and Ogawa, 2009). The risk of coronary aneurysm is reduced in patients older than 1 year old if IVIG is given within 10 days of the illness. Aneurysm regression occurs in half of all patients who develop them, commonly by 1 year after the illness (80% resolve within 5 years), but vessels do not dilate normally in response to increased oxygen demand by the myocardium. Prompt treatment of chest pain, dyspnea, extreme lethargy, or syncope is always warranted. Surgical revascularization and transcatheter revascularization are used for some coronary sequelae of KD (Wood and Tulloh, 2009). Acute Rheumatic Fever ARF is a nonsuppurative complication following a Lancefield GAS pharyngeal infection that results in an autoimmune inflammatory process involving the joints (polyarthritis), heart (rheumatic heart disease), CNS (Sydenham chorea), and subcutaneous tissue (subcutaneous nodules and erythema marginatum). Recurrent ARF with its multisystem responses can follow with subsequent GAS pharyngeal infections. Long- term effects on tissues are generally minimal except for the damage done to cardiac valves that leaves fibrosis and scarring and results in rheumatic heart disease. ARF is diagnosed based on a set of criteria called the revised Jones criteria (1992). These criteria are used for the initial attack of ARF. Further modifications of the Jones criteria are used for recurrent ARF. Clinical Findings and History The diagnosis of an initial attack of ARF is based on the following revised Jones criteria: • Evidence of documented (culture, rapid streptococcal antigen test, or ASO titer) GAS pharyngeal infection • Findings of two major manifestations or one major and two minor manifestations of ARF (Berard, 2012 ; Burke and Chang, 2014 ) Major Manifestations NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Children with fewer manifestations can also have ARF. Arthritis of large joints occurs in 65% of cases, carditis in 50%, chorea in 15% to 30%, cutaneous nodules in 5%, and subcutaneous nodules in less than 7%. There is some controversy regarding the use of the Jones criteria in developing countries where the ability for diagnostic testing may be limited; therefore, the World Health Organization (WHO) criteria (Box 25-2) may be used (Ferrieri, 2002 ; Seckel and Hoke, 2011 ). •Carditis is common (pancarditis, valves, pericardium, myocardium) and can cause chronic, life- threatening disease (i.e., congestive heart failure [CHF]) with estimates of 30% to 80% of patients with ARF experiencing carditis; it is more common in younger children than adolescents. The symptoms of carditis may be vague and insidious with decreased appetite, fatigue, and pains. A high-pitched holosystolic murmur is heard at the apex with radiation to the infrascapular area, as well as tachycardia and often a gallop rhythm. Mitral and possibly NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Chronic CHF can occur after an initial episode of ARF or follow recurrent episodes of ARF. Residual valvular damage is responsible for CHF. The risk of significant cardiac disease increases dramatically with each subsequent episode of ARF; thus prevention of subsequent GAS infections is critical. Engagement in the follow-up is essential to prevent the need for cardiac valvular repair. Bronchiolitis Bronchiolitis is also called infectious asthma, asthmatic bronchitis, wheezy bronchitis, or virus- induced asthma. Bronchiolitis is a disease that causes inflammation, necrosis, and edema of the respiratory epithelial cells in the lining of small airways, as well as copious mucus production (Ralston et al, 2014). Bronchiolitis is characterized by the insidious onset of URI symptoms over 2 to 3 days that progresses to lower respiratory symptoms that last as long as 10 days (Da Dalt et al, 2013 ). It is a communicable disease found primarily in infancy to 2 years old (Teshome et al, 2013 ) that accounts for 10% of visits to a primary provider the first 2 years of life (Schroeder and Mansbach, 2014). Bronchiolitis is a common diagnosis used for an infant seen with wheezing for the very first time and is the leading cause of hospitalizations for infants. The most common age for severe disease occurs in infants between 2 to 3 months due to the natural postnatal nadir in maternal immunoglobulins received via the placenta during the last trimester (Da Dalt et al, 2013). More than 80% of the cases of bronchiolitis occur in infants younger than 1 year of age with a male-to-female ratio of 1.5 : 1 (Welliver, 2009). In mild cases, symptoms can last for 1 to 3 days. In severe cases, cyanosis, air hunger, retractions, and nasal flaring with symptoms of severe respiratory distress within a few hours may be seen. Apnea can occur with a wide range of prevalence reported (Ralston et al, 2014) and may require mechanical ventilation. Newer understanding of the pathophysiology in bronchiolitis points to airway obstruction as a result of epithelial and inflammatory cellular debris due to infiltration of the virus into the small bronchiole epithelium and alveolar epithelial cells (AEC), types I and II. Membranous pneumatoceles, or AEC type I, are dominant and cover 96% of the respiratory tree. Their role is in gas exchange, whereas AEC type II are important to surfactant production (Chuquimia et al, 2013). It is a disease of the small bronchioles that are 2 mm in size. There is a sparing of basal cells in the bronchiole. The main lesion is epithelial necrosis, which leads to a dense plugging of the bronchial lining. This results in increased airway resistance, atelectasis, hyperinflation, and increased mucus production (Teshome et al, 2013 ). Bronchiolitis is a viral illness predominantly caused by RSV, especially in outbreaks (Da Dalt et al, 2013; Welliver, 2009). Recent data suggest that up to 30% of infants with severe bronchiolitis are co-infected with two or more viruses (Mansbach et al, 2012). In descending order after RSV, rhinovirus, parainfluenza, adenovirus, and mycoplasma are causes (Teshome et al, 2013 ). Metapneumovirus was discovered in 2001 and is a cause of bronchiolitis 7% of the time. Human bocavirus is a common co-infecting virus with RSV and is found up to 80% of the time (Teshome et al, 2013 ). RSV-specific immunoglobulin E (IgE), eosinophils, and chemokines may play a role in the pathogenesis of bronchiolitis (Welliver, 2009). Adenovirus and RSV can cause long-term complications. The incubation period for RSV is 2 to 8 days and typically occurs from November through March with virtually no outbreaks in the summer (Teshome et al, 2013; Welliver, 2009). Fever tends to be higher with adenovirus versus RSV (Teshome et al, 2013 ). Respiratory viruses are spread by close contact with infected respiratory secretions or fomites and can live on 818surfaces for up to 30 minutes (Teshome et al, 2013 ). The most frequent mode of transmission is hand carriage of contaminated secretion. The source of infection is an older child or adult family member with a “mild” URI. Older children and adults have larger airways and tolerate the swelling associated with this infection better than infants do. Most cases of bronchiolitis resolve completely, but recurrence of infection is common, and symptoms tend to be mild. Infants who are at higher risk of severe RSV include children with major chronic pulmonary disease, such as CF, neuromuscular disorders, or bronchopulmonary dysplasia; premature birth NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ before 35 weeks of gestational age; and infants with significant hemodynamically difficulties due to congenital heart disease (Teshome et al, 2013). Other risk factors for severe RSV disease are male gender, crowded household, lack of breastfeeding, smoke exposure, day care attendance, having siblings, birth during the winter months, and immunodeficiency (Da Dalt et al, 2013 ). Clinical Findings History The following are reported: • Initial presentation: Typically the illness begins with URI symptoms of cough, coryza, and rhinorrhea and progresses over 3 to 7 days (Smith, 2011 ). • Gradual development of respiratory distress marked by noisy, raspy breathing with audible expiratory wheezing. • Low-grade to moderate fever up to 102° F (38.9° C). • Decrease in appetite. • No prodrome in some infants; rather they have apnea as the initial symptom. NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ • Usually the patient's course is the worst by 48 to 72 hours after the wheezing starts and then the patient starts to improve. If the child has a bacterial illness, the child will continue to worsen with a high fever. Physical Examination Findings include the following: • Upper respiratory findings • Coryza • Mild conjunctivitis in 33% (Welliver, 2009 ) • Pharyngitis • Otitis media in up to 15% (Welliver, 2009 ) • Lower respiratory findings (Teshome et al, 2013 ) • Tachypnea (approximately 40 to 80 breaths per minute) • Substernal and/or intercostal retractions • Heterophonous expiratory wheezing • Fine or coarse crackles may be heard throughout the breathing cycle • Varying signs of respiratory distress and pulmonary involvement (e.g., nasal flaring, grunting, retractions, cyanosis, prolonged expiration) • Abdominal distention • Palpable liver and spleen, pushed down by hyperinflated lungs and a flattened diaphragm Diagnostic Studies A diagnosis of bronchiolitis should be based on the history and physical examination (Ralston et al, 2014). Overuse of diagnostic testing persists in clinical practice despite available guidelines on the diagnosis and management of bronchiolitis (Librizzi et al, 2014; Ralston et al, 2014; Turner et al, 2014). The routine use of chest radiographs in previously healthy infants with mild RSV bronchiolitis is not indicated. Evidence-based guidelines from the AAP and the Scottish Intercollegiate Guidelines Network (SIGN) are strongly against routine chest radiography, including those in previously healthy infants with mild RSV bronchiolitis ( Ralston et al, 2014 ; SIGN, 2006). In severe illness, a chest x-ray may be ordered to rule out pneumonia or pneumothorax, but its use must be weighed against the dangers of radiation exposure. The findings of chest radiography can vary, and even with severe illness the x-ray can be clear with a flattened diaphragm and an increase in anteroposterior diameter. Areas of atelectasis can appear like a pneumonitis, but true pneumonia is uncommon (early bacterial pneumonia can be difficult to detect and cannot be ruled out by radiographs). Routine virologic testing is not recommended. In selected situations (hospitalization or if an infant has received monthly palivizumab [Synagis]), enzyme-linked immunosorbent assays or fluorescent antibody techniques to look for RSV are the diagnostic procedures of choice in most laboratories. Viral culture of nasal washings can be done in severe cases to confirm RSV, parainfluenza viruses, influenza viruses, and adenoviruses. PCR is helpful in deciding about isolation of cohorts with the same infection in the hospital setting. The cost of the diagnostic viral testing may outweigh the clinical usefulness of knowing which virus is infecting the patient. Hematologic testing is not recommended in the latest guidelines. If a CBC is done for another reason, a mild leukocytosis may be seen with 12,000 to 16,000/mm3. Routine laboratory tests are usually not required to confirm the diagnosis, because they lack specificity. However, young infants pose a diagnostic dilemma, because they are at greater risk of a serious bacterial infection (SBI) and, therefore, blood cultures and CBC with differential are done with a higher rate of antibiotic use in infants who had these blood tests ( Librizzi et al, 2014 ). Urine cultures actually have a higher rate of positive results in the young febrile infant (up to 2.3% in a bronchiolitis study conducted by Librizzi and colleagues). Differential Diagnosis The diagnosis of bronchiolitis can be confused with asthma, but there are some differences that may be helpful. Asthma is an acute process due to airway hyperreactivity and inflammation, whereas the onset of bronchiolitis is insidious. The response to the usual asthma therapies of beta agonist and 819steroids is poor in infants with bronchiolitis. In contrast, certain viral illnesses in young children can induce wheezing that will respond to a β-agonist with good results. FB aspiration is discussed in greater detail later in this chapter, but this is usually a toddler with a history of choking who then develops focal areas of wheezing. Although children with congestive heart failure can wheeze, they also show symptoms of sweating and the signs of failure to thrive with a murmur and an S4 gallop rhythm. Other differentials include airway irritants, gastroesophageal reflux, pneumonia, allergic pneumonitis, vascular rings, lung cysts, and lobar emphysema (Teshome et al, 2013 ; Welliver, 2009 ). NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Complications The first 48 to 72 hours after the onset of cough are the most critical. Apneic spells are common in infants. The child is ill-appearing and toxic but gradually improves. The fatality rate associated with bronchiolitis is about 1% to 2%. Infants younger than 12 weeks old and those with underlying cardiorespiratory or immunodeficiency are at risk for severe disease. Prolonged apnea, uncompensated respiratory acidosis, and profound dehydration secondary to loss of water from tachypnea and an inability to drink are the factors leading to death in young infants with bronchiolitis. In some children, bronchiolitis can cause minor pulmonary function problems and a tendency for bronchial hyperreactivity that lasts for years. RSV bronchiolitis has been associated with the development of asthma, but its role in the causality of asthma is still debated. Recurrent episodes of wheezing can be seen during childhood NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ in patients with a history of bronchiolitis. This persists into adolescence with 10% of the children still wheezing. However, this figure may not be different from the general population (Welliver, 2009). Prevention Palivizumab (Synagis) is an RSV-specific monoclonal antibody used to provide some protection from severe RSV infection for high-risk infants (see Chapter 24 for guidelines). Educate caregivers about decreasing exposure to and transmission of RSV, especially those with high- risk infants. Advice should include limiting exposure to child care centers whenever possible; use of alcohol-based hand sanitizers if available or hand washing if the alcohol-based hand sanitizer is not available (Ralston et al, 2014); avoiding tobacco smoke exposure; and scheduling RSV prophylaxis vaccination, when indicated. Asthma Asthma is a chronic respiratory disease characterized by periods of coughing, wheezing, respiratory distress, and bronchospasm. Asthma can occur with a persistent cough without significant wheezing. It is the most common chronic respiratory disease of children, with an incidence as high as 30% of children in the Western world, and it is the leading cause of emergency department visits ( Jackson et al, 2011; Liu et al, 2011). The pathophysiology is the result of immunohistopathologic responses that produce shedding of airway epithelium and collagen deposition beneath the basement membrane, edema, mast cell activation and inflammatory infiltration by eosinophils, lymphocytes (Th2-like cells), and neutrophils (especially in fatal asthma). The persistent inflammation can result in irreversible changes, such as airway wall remodeling. Inflammation causes acute bronchoconstriction, airway edema, and mucous plug formation. In addition, airway inflammation can trigger a hyperresponsiveness to a variety of stimuli, including allergens, exercise, cold air, and physical, chemical, or pharmacologic agents. This results in bronchospasm, which presents as wheezing, breathlessness, chest tightness, and cough that can be worse at night or with exercise. The airflow obstruction is often reversible, either spontaneously or with treatment. Remodeling of the airway can occur secondary to persistent fibrotic changes in the airway lining. The fibrosis alters the airway caliber, leading to decreased airflow with permanent changes starting in childhood, but become recognizable in adults. Recent advances have shown that there are different “phenotypes” of this disease with different clinical manifestations, and data suggest that children who have symptoms before 3 years old are more likely to have changes in lung functioning at 6 years old (Szefler et al, 2014 ). Asthma in children is classified as intermittent, mild persistent, moderate persistent, or severe persistent depending on symptoms, recurrences, need for specific medications, and pulmonary function measurements (Table 25-2 ). Children classified at any level of asthma can have episodes involving mild, moderate, or severe exacerbations. Exacerbations involve progressive worsening of shortness of breath, cough, wheezing, chest tightness, or any combination of these symptoms. The degree of airway hyperresponsiveness is usually related to the severity of asthma that can change over time. A well-controlled child with asthma has only one exacerbation in 3 years on average ( Jackson et al, 2011). TABLE 25-2 Classification of Asthma Severity in Children: Clinical Features Before Treatment Classification and Step Symptoms* Nighttime Symptoms Lung Function Step 1: Intermittent Symptoms two times or less per week Asymptomatic and normal PEF between exacerbations Requires SABA 2 days/week Exacerbations brief (few hours or days); varying intensity No interference with normal activity Two times or less per month FEV1 >80% predicted Normal FEV1 between exacerbations Step 2: Mild persistent Symptoms more than two times per week but less than one time per day Requires SABA more than two days/week but not more than one per day Exacerbations may affect activity (minor) Three to four times per month FEV1 >80% predicted NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Step 3: Moderate persistent Daily symptoms Daily use of inhaled SABA Some limitations Exacerbations affect activity, two times or more per week; may last days More than one time per week but not nightly FEV1 >60% but <80% predicted Step 4: Severe persistent Continual symptoms Requires SABA several times/day Extremely limited physical activity Frequent exacerbations Often seven times per week FEV1 <60% predicted *Having at least one symptom in a particular step places the child in that particular classification. NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ • Family history of asthma or other related allergic disorders (e.g., eczema or AR) • Conditions associated with asthma (e.g., chronic sinusitis, nasal polyposis, gastroesophageal reflux, and chronic otitis media) • Complaints of chest tightness or dyspnea • Cough and wheezing particularly at night and in the early morning or shortness of breath with exercise or exertion (characteristic of asthma) • Seasonal, continuous, or episodic pattern of symptoms that may be associated with certain allergens or triggering agents • Episodes of recurrent “bronchitis” or pneumonia • Precipitation of symptoms by known aggravating factors (upper respiratory infections, acetaminophen, aspirin) • Level of alertness Physical Examination Table 25-3 outlines the physical assessment findings correlated with asthma severity. Broadly speaking, the following may be seen on physical examination: • Heterophonous wheezing (different pitches but may be absent if severe obstruction) • Continuous and persistent coughing • Prolonged expiratory phase, high-pitched rhonchi especially at the bases • Diminished breath sounds •Signs of respiratory distress, including tachypnea, retractions, nasal flaring, use of accessory muscles, increasing restlessness, apprehension, agitation, drowsiness to coma • Tachycardia, hypertension or hypotension, pulsus paradoxus • Cyanosis of lips and nail beds if hypoxic • Possible associated findings include sinusitis, AD, and AR. Physical Assessment of Asthma and Asthma Severity Severity of Asthma Physical Assessment Findings Mild Wheezing at the end of expiration or no wheezing No or minimal intercostal retractions along posterior axillary line Slight prolongation of expiratory phase Normal aeration in all lung fields Can talk in sentences Moderate Wheezing throughout expiration Intercostal retractions Prolonged expiratory phase Decreased breath sounds at the base Severe Use of accessory muscles plus lower rib and suprasternal retractions; nasal flaring Inspiratory and expiratory wheezing or no wheezing heard with poor air exchange Suprasternal retractions with abdominal breathing Decreased breath sounds throughout base Impending respiratory arrest Diminished breath sounds over entire lung filed Tiring, inability to maintain respirations Severely prolonged expiration if breath sounds are heard Drowsy, confused Diagnostic Studies Laboratory and radiographic tests should be individualized and based on symptoms, severity or chronology of the disease, response to NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ therapy, and age. Tests to consider include the following: •Oxygen saturation by pulse oximetry to assess severity of acute exacerbation. This should be a routine part of every assessment of a child with asthma. Pulse oximetry measures the oxygen saturation (SaO2) of hemoglobin—the percentage of total hemoglobin that is oxygenated. • A CBC if secondary infection or anemia is suspected (also check for elevated numbers of eosinophils). •Routine chest radiographs are not indicated in most children with asthma. Results are typically normal or only show hyperinflation. Again imaging should be ordered judiciously with consideration of the long-term risk. However, chest radiographs can be useful in the following situations: selected cases of asthma or suspected asthma or if the child has persistent wheezing without a clinical explanation. Children with hypoxia, fever, suspected pneumonia, and/or localized rales requiring admission are candidates for imaging. NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Infants with wheezing during the winter who have clinical bronchiolitis do not need imaging (Nelson and Zorc, 2013 ). • If sinusitis is suspected as the trigger, no diagnostic radiographic testing is needed. •Allergy evaluation should be considered, keeping in mind that history and physical examination are key in this consideration. (Refer child to pediatric allergist.) • Sweat test should be considered based on history in every patient with asthma. • Pulmonary function tests: • Spirometry testing is the gold standard for diagnosing asthma and should be used on a regular basis to monitor, evaluate, and manage asthma. Exercise challenges using spirometry can also be done to evaluate the child with exercised-induced asthma. Children older than 5 years can typically perform spirometry. 568 • To evaluate the accuracy of the spirometry, look for an initial sharp peak with an extension down to the baseline at the end of expiration that is reproducible at least two times. Compare the child's values with the predicted value for the child's age, height, sex, and race. • Look at the forced expiratory volume in 1 second (FEV1), which represents the amount of air exhaled in 1 second. The interpretation of percentage predicted is: • >75%: Normal • 60% to 75%: Mild obstruction • 50% to 59%: Moderate obstruction • <49%: Severe obstruction • The forced vital capacity (FVC) represents the amount of air expelled: • 80% to 120%: Normal • 70% to 79%: Mild reduction • 50% to 69%: Moderate reduction • <50%: Severe reduction • The FEV1/FVC represents the amount of air expelled in the first second over the total amount of air expelled and should be greater than 90% of the predicted value. Spirometry testing is done prior to a breathing treatment and 10 minutes after the treatment. If the child's FEV1 improves by 12%, the child likely has asthma because this illustrates hyperresponsiveness. • The forced expiratory flow (FEF) (FEF25 to FEF75) reflects the middle portion of the downward limb of the curve and is a good measure of smaller airway function. The interpretation of percentage predicted is: • >60%: Normal • 40% to 60%: Mild obstruction • 20% to 40%: Moderate obstruction • <10%: Severe obstruction • Doing spirometry during well-child checks and for sick visits gives the practitioner an excellent indication of the amount of inflammation and bronchospasm present in the airway (Kamakshya, 2012 ). Table 25- 4 represents abnormal spirometry patterns. TABLE 25-4 Abnormal Spirometry Findings Obstructive Restrictive NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ IgG monoclonal antibody that binds to human IgE on the 570surface of mast cells and basophils. This anti-IgE monoclonal antibody is used as a second-line treatment for children older than 12 who have moderate to severe allergy-related asthma and react to perennial allergens. It is used when symptoms are not controlled by inhaled corticosteroids. •Follow up with PCP after an exacerbation requiring emergency department care, and obtain a clear written asthma action plan. •Education regarding asthma basics, including triggers and prevention with environmental modification, as well as the different treatment modalities includes the techniques of administration and dispelling any myths regarding asthma medication. In terms of coping, the child and family need to be able to understand their emotions, worries, and uncertainty, as well as when to contact their PCP. Developing and understanding the asthma action plan is very important during a well-child visit (Archibald and Scott, 2014 ). The pharmacologic management of asthma in children is based on the severity of asthma and the child's age. The stepwise approach to treatment (Figs. 25-1 and 25-2) is based on severity of symptoms and the use of pharmacotherapy to control chronic symptoms, maintain normal activity, prevent recurrent exacerbations, and minimize adverse side effects and nearly “normal” pulmonary function. Within any classification, a child may experience mild, moderate, or severe exacerbations. NHLBI guidelines for assessing asthma control and NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ initiating and adjusting asthma therapy for the various pediatric age groups are found in Figures 25-3 and 25- 4. Important considerations to note in the pharmacologic treatment of asthma include the following: •Control of asthma should be gained as quickly as possible by starting at the classification step most appropriate to the initial severity of the child's symptoms or at a higher level (e.g., a course of systemic corticosteroids or higher dose of inhaled corticosteroid). After control of symptoms, decrease treatment to the least amount of medication needed to maintain control. •Systemic corticosteroids may be needed at any time and stepped up if there is a major flare-up of symptoms. 573Control of inflammation is a key principle in the management of asthma. • The combination of inhaled corticosteroids with a long-acting beta2-agonist (LABA) can further control asthma (Szefler, 2013 ). •Children with intermittent asthma may have long periods in which they are symptom-free; they can also have life-threatening exacerbations, often provoked by respiratory infection. In these situations, a short course of systemic corticosteroids should be used. • Variations in asthma necessitate individualized treatment plans. • β2 agonists can be administered with metered dose inhaler (MDI) therapy via spacer for children with mild and moderate exacerbations of asthma, but for children with severe airway obstruction who may have decreased deposition of drug in the base of the lung, a nebulizer may be better (Nelson and Zorc, 2013 ). There is need for more research on the use of MDI therapy and nebulizer therapy in the pediatric population (Szefler et al, 2014 ). A spacer or holding chamber with an attached mask enhances the delivery of MDI medications to the lower airways of a child. Spacers eliminate the need to synchronize inhalation with activation of MDI. Older children can use a spacer without the mask. •Dry powder inhalers (DPIs) do not need spacers or shaking before use. Instruct children to rinse their mouth with water and spit after inhalation. DPIs should not be used in children younger than 4 years old. •Different inhaled corticosteroids are not equal in potency to each other on a per puff or microgram basis. Tables 25-6 and 25-7 compare daily low, medium, and high doses of various inhaled corticosteroids used for children. Combination inhaled corticosteroid and LABA can be used in children from 4 years old (Taketomo et al, 2014 ). For treatment of exercise-induced bronchospasm: • Warm up before exercise for 5 to 10 minutes. • Use either an inhaled SABA or a mast cell stabilizer (cromolyn) or both prior to exercise. Combination of both types of drugs is the more effective therapy. A LABA can be used in older children. • Use two puffs of a β2 agonist and/or cromolyn MDI 15 to 30 minutes before exercise. Tolerance may develop if a β2 agonist is used more than a few times 574a week; it should not be used as a controller monotherapy. Those who exercise regularly and develop symptoms of asthma should use controller medication, preferably an inhaled corticosteroid. • Using a scarf or mask around the mouth may decrease exercise-induced asthma (EIA) induced by cold. Table 25-8 identifies the usual dosages for long-term control medications (exclusive of inhaled corticosteroids) used to treat asthma in children. Quick-relief medications are listed in Table 25- 9. Practice parameters are guides and should not replace individualized treatment based on clinical judgment and unique differences among children. Acute Exacerbations of Asthma NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ The treatment of acute episodes of asthma is also based on classification of the severity of the episode. Acute episodes 579are classified as mild, moderate, and severe. Signs and symptoms are summarized in Table 25-10. Early recognition of warning signs and treatment should be stressed in both patient or parent education, or both. The initial pharmacologic treatment for acute asthma exacerbations is shown in Figure 25-5. It consists of inhaled SABAs (albuterol), two to six puffs every 20 minutes for three treatments by way of MDI with a spacer, or a single nebulizer treatment (0.15 mg/kg; minimum 1.25 to 2.5 mg of 0.5% solution of albuterol in 2 to 3 mL of normal saline). If the initial treatment results in a good response (PEF/FEV1 > 70% of the patient's best), the inhaled SABAs can be continued every 3 to 4 hours for 24 to 48 hours with a 3-day course of oral steroids at 1 to 2 mg/kg/day to a maximum of 60 mg per day. Reassessment is important to ensure an adequate response and to further assess asthma severity. An incomplete response (PEF or FEV1 between 40% and 69% of personal best or symptoms recur within 4 hours of therapy) is treated by continuing β2 agonists and adding an oral corticosteroid. The β2 agonist can be given by nebulizer or MDI with spacer. Parents should be taught to call their PCP for additional instructions. If there is marked distress (severe acute symptoms) or a poor response (PEF or FEV1 <40%) to treatment, the child should have the β2 agonist repeated immediately and should be taken to the emergency department. Emergency medical rescue (911) transportation should be used if the distress is severe and the child is agitated and unable to talk. If children experience acute asthma exacerbations more than once every 4 to 6 weeks, their treatment plan should be reevaluated. 581 NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ History • Presence from birth, or age first noted • Progression of lesion • Familial tendencies for similar nevi, especially for history of melanoma 1031 Physical Examination Findings include the following (Box 37-8 ): • Vascular malformations or flat vascular nevi are present at birth and grow commensurate with the child's growth. • Hemangiomas are classified as superficial, deep (cavernous), or mixed. They may or may not be present at birth, but they usually emerge by 2 to 3 weeks of life. They may manifest initially as a pale macule, a telangiectatic lesion, or a bright red nodular papule. After appearing, hemangiomas go through a proliferative phase during which they grow rapidly and form nodular compressible masses, ranging in size from a few millimeters to several centimeters. Occasionally they may cover an entire limb, resulting in asymmetric limb growth. Rapidly growing lesions may ulcerate. The final phase of involution occurs slowly (10% per year) but spontaneously (30% by 3 years old, 50% by 5 years old, 70% by 7 years old, and 90% by 9 to 10 years old). Average involution begins between 12 and 24 months old, heralded by gray areas in the lesion followed by flattening from the center outward. Most hemangiomas appear as normal skin after involution, but others may have residual changes, such as telangiectasias, atrophy, fibrofatty residue, and scarring (Paller and Mancini, 2011 ). • Pigmented nevi may be present at birth or acquired during childhood. • Atypical nevi are larger than acquired nevi; have irregular, poorly defined borders; and have variable pigmentation. Box 37-8 C omm on Vas cu l ar an d Pigm en t ed Les i on s I. Vascular malformations or flat vascular nevi A. Salmon patch or nevus flammeus: Light pink macule of varying size and configuration. Commonly seen on the glabella, back of neck, forehead, or upper eyelids. B. Port-wine stain: Purple-red macules that occur unilaterally and tend to be large. Usually occur on face, occiput, or neck, although they may be on extremities. II. Hemangiomas A. Superficial (strawberry) hemangiomas are found in the upper dermis of the skin and account for the majority of hemangiomas. B. Deep cavernous hemangiomas are found in the subcutaneous and hypodermal layers of the skin; although similar to superficial hemangiomas, there is a blue tinge to their appearance. With pressure, there is blanching and a feeling of a soft, compressible tumor. Variable in size, they can occur in places other than skin. C. Mixed hemangiomas have attributes of both superficial and deep hemangiomas. III. Pigmented nevi A. Mongolian spots: Blue or slate-gray, irregular, variably sized macules. Common in the presacral or lumbosacral area of dark- skinned infants; also on the upper back, shoulders, and extremities. The majority of the pigment fades as the child gets older and the skin darkens. Solitary or multiple, often covering a large area. B. Café au lait spots: Tan to light brown macules found anywhere on the skin; oval or irregular shape; increase in number with age. C. Acquired melanocytic nevi are benign, light brown to dark brown to black, flat, or slightly raised, occurring anywhere on the body, especially on sun-exposed areas above the waist. 1. Junctional nevi represent the initial stage, with tiny, hairless, light brown to black macules. 2. Compound nevi—a few junctional nevi progress to more elevated, warty, or smooth lesions with hair. 3. Dermal nevi are the adult form, dome shaped with coarse hair. 4. Atypical nevi usually appear at puberty, have irregular borders, variegated pigmentation, are larger than normal nevi (6 to 15 mm); usually found on trunk, feet, scalp, and buttocks. 5. Halo nevi appear in late childhood with an area of depigmentation around a pigmented nevus, usually on trunk (see Fig. 37- 34). D. Acanthosis nigricans is velvety brown rows of hyperpigmentation in irregular folds of skin, usually the neck and axilla; tags may also be present. NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ E. Lentigines are small brown to black macules 1 to 2 mm in size appearing anywhere on the body in school-age children. F. Freckles: 1 to 5 mm light brown, pigmented macules in sun-exposed areas. Differential Diagnosis Hematomas or ecchymoses of child abuse are occasionally confused with some nevi. Non–insulin-dependent diabetes mellitus (NIDDM) often causes acanthosis nigricans. Management 1. Flat vascular nevi • Salmon patches: Fade with time, usually by 5 or 6 years old; no treatment is needed. NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ • Port-wine stains: A permanent defect that grows with the child, so cosmetic covering is often used. If forehead and eyelids are involved, there is potential for multiple syndromes, including Sturge-Weber, Klippel-Trenaunay-Weber, and Parkes Weber. Neurodevelopmental and ophthalmologic follow-up is needed. Referral to a dermatologist for possible laser treatment or cosmesis is required. 2. Hemangiomas • Reassure and educate the family about the nature and course of these nevi and that they are not related to anything the mother did during pregnancy. • Follow-up frequently, especially during the proliferation phase. Sequential photographs are helpful. • If the lesions are strategically placed (eye, lip, oral cavity, ear, airway, diaper area), ulcerating, multiple, very large, or grow very quickly, prompt referral to a dermatologist is indicated because early treatment is most effective. Steroids (intralesional and oral) are prescribed during the proliferation phase until growth is stabilized, then gradually tapered. Indications for steroid treatment are interference with physiologic functions (e.g., breathing, hearing, eating, and vision), recurrent bleeding or ulceration, high-output 1032congestive heart failure, Kasabach-Merritt syndrome, rapid growth that distorts facial features, or presence in the diaper area. Interferon-alpha may also be used. Treatment by surgery, cryotherapy, radiation, or injecting sclerosing agents often leads to scarring. Large, deep lesions can cause cardiovascular complications, disseminated intravascular coagulation, or compression of internal organs. • Involution (without treatment) occurs at a rate of 10% per year. Scarring may be present if ulceration occurs; fibrofatty masses, atrophy, and telangiectasis can occur following involution. Laser therapy is effective management for residual telangiectasias (Paller and Mancini, 2011 ). 3. Pigmented nevi: Educate family about the nature of these lesions. • Mongolian spots: Document to distinguish from bruise; fade with time, usually no traces by adulthood. • Blue nevus: Heavily pigmented melanocytes in papule or nodule that can develop melanoma. • Café au lait spots: If six or more lesions larger than 5 mm in diameter are present in children younger than 15 years old and more than 1.5 cm in diameter for older individuals, or if axillary freckling (Crowe's sign), neurofibromas, or iris hamartomas is also present, refer child to rule out neurofibromatosis, McCune-Albright syndrome, tuberous sclerosis, LEOPARD* syndrome, epidermal nevus syndrome, Bloom syndrome, ataxia-telangiectasia, and Silver-Russell syndrome (Cohen, 2013 ). Complications Ulceration, infection, platelet trapping, airway or visual obstruction, or cardiac decompensation can occur with large vascular nevi. Kasabach-Merritt syndrome occurs when thrombocytopenic hemorrhage occurs in a large, deep hemangioma. Melanoma in congenital nevi is possible. An autosomal dominant, familial, atypical mole and melanoma syndrome has been identified genetically. Children with multiple atypical nevi and family members with melanoma are at risk for childhood melanoma. Patient and Family Education Monitoring nevi that are at risk for developing melanoma is important as is teaching the family to watch nevi for any changes. Changes of particular concern are development of an off-center nodule or papule, color change, bleeding, persistent irritation, erosion, ulceration, and rapid growth. See Chapter 39 for more information. 1033 Impetigo Impetigo is a common contagious bacterial infection of the superficial layers of the skin. It has two forms: nonbullous, with honey-colored crusts on the lesions, and bullous (Fig. 37-4). Impetigo is usually caused by group A streptococcus (Streptococcus pyogenes), Staphylococcus aureus,or MRSA. Often streptococcus and staphylococcus can be 992cultured from an impetigo lesion. Nonbullous impetigo accounts for more than 70% of cases, with S. aureus as the most common pathogen. Nonbullous impetigo usually follows some type of skin trauma (e.g., bites, abrasions, or varicella) or another skin disease, such as atopic dermatitis. Bullous impetigo occurs sporadically, develops on intact skin, and is more common in infants and young children. Certain epidermal types of S. aureus produce a toxin that causes bullous skin lesions. NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ aureus. SSSS is most common in neonates (Ritter disease), infants, and children younger than 5 years old. It manifests abruptly with fever, malaise, and tender erythroderma, especially in the neck folds and axillae, rapidly becoming crusty around the eyes, nose, and mouth. Nikolsky sign (peeling of skin with a light rub to reveal a moist red surface) is a key finding. Treatment may include hospitalization and parenteral antibiotics, especially for young children (Berk and Bayliss, 2010 ). Antibiotics of choice are intravenous (IV) or oral dicloxacillin, a penicillinase-resistant penicillin, first- or second-generation cephalosporins, or clindamycin. Quicker healing without scarring results if steroids are avoided, there is minimal handling of the skin, and ointments and topical mupirocin are used at the infection site (Berk and Bayliss, 2010 ; Patel and Patel, 2010 ). Severe cases may need treatment similar to extensive burn care. Patient and Family Education • Thorough cleansing of any breaks in the skin helps prevent impetigo. NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ • Postinflammatory pigment changes can last weeks to months. • The patient should not return to school or day care until 24 hours of antibiotic treatment is completed. Molluscum Contagiosum A benign common childhood viral skin infection with little health risk, molluscum contagiosum often disappears on its own in a few weeks to months and is not easily treated ( Fig. 37-18 ). This poxvirus replicates in host epithelial cells. It attacks skin and mucous membranes and is spread by direct contact, by fomites, or by autoinoculation (typically scratching). It is commonly found in children and adolescents. The incubation period is about 2 to 7 weeks but may be as long as 6 months (Weston and Morelli, 2013 ). Infectivity is low but the child is contagious as long as lesions are present. Clinical Findings History • Itching at the site • Possible exposure to molluscum contagiosum Physical Examination • Very small, firm, pink to flesh-colored discrete papules 1 to 6 mm in size (occasionally up to 15 mm) • Papules progressing to become umbilicated (may not be evident) with a cheesy core; keratinous contents may extrude from the umbilication • Surrounding dermatitis is common • Face, axillae, antecubital area, trunk, popliteal fossae, crural area, and extremities are the most commonly involved areas; palms, soles, and scalp are spared • Single papule to numerous papules; most often numerous clustered papules and linear configurations • Sexually active or abused children can have genitally grouped lesions • Children with eczema or immunosuppression can have severe cases; those with human immunodeficiency virus (HIV) infection or AIDS can have hundreds of lesions Differential Diagnosis Warts, closed comedones, small epidermal cysts, blisters, folliculitis, and condyloma acuminatum are included in the differential diagnosis. Management • Untreated lesions usually disappear within 6 months to 2 years but may take up to 4 years to completely go away. There is no consensus on the management of molluscum contagiosum and no evidence-based literature to show that any treatment is superior to placebo. Therapy may be necessary to alleviate discomfort, reduce itching, minimize autoinoculation, limit transmission, and for cosmetic reasons. Genital lesions may need to be treated to prevent spread to sexual partners. • Mechanical removal of the central core is to prevent spread and autoinoculation. Using eutectic mixture of local anesthetics (EMLA) cream (lidocaine/prilocaine) 30 to 45 minutes before the procedure reduces discomfort. Curettage is done with a sharp blade to remove the papule. Piercing the papule and expressing the plug is an option but is painful. • There are reports that irritants (such as, surgical tape, adhesive tape, or duct tape) applied each night can result in lesion resolution. • Topical medications may prove beneficial. Recheck the patient in 1 to 2 weeks to determine need for retreatment. • Liquid nitrogen applied for 2 to 3 seconds (easiest but also painful). • Trichloroacetic acid 25% to 50% applied by dropper to the center of the lesion, followed by alcohol (use with caution). Surround the lesion first with petroleum jelly. • Cantharidin 0.7% in collodion applied by dropper to the center of the lesion, followed by alcohol. Salicylic or lactic acid or KOH or podophyllin can also be used. • Podofilox 0.5% topical solution or gel, or imiquimod 5% applied daily with a toothpick or cotton-tipped swab. NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ • Tretinoin or tazarotene cream or gel applied to lesion each night. • Silver nitrate, iodine 7% to 9%, or phenol 1% applied for 2 to 3 seconds. 1008 • Cimetidine 30 to 40 mg/kg/day in two divided doses orally for 6 weeks if topical treatment fails. • Sexual abuse of children with genitally grouped lesions should be suspected and evaluated. • Evaluate for HIV infection if hundreds of lesions are found. • Wait and see approach—spontaneous clearing occurs over years. Complications NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Herpetic whitlow, occurring on a finger or thumb, is a swollen, painful lesion with an erythematous base and ulceration resembling a paronychia. It occurs on fingers of thumb- sucking children with gingivostomatitis or adolescents with genital HSV infection. Management Management can be guided by considering the host (e.g., age, area and extent of involvement, and immune status) and the drug needed (Table 37-5 ). Treatment includes: 1. Burow solution compresses three times a day to alleviate discomfort 2. Acyclovir 20 to 40 mg/kg/dose orally five times a day for 5 days, or 200 mg five times a day for 7 to 10 days (maximum pediatric dose 1000 mg/day) may be indicated to help shorten the course and alleviate symptoms for children older than 2 years old with the following conditions: • Any underlying skin disorder (e.g., eczema) • A severe case • An immunocompromised disease • Systemic symptoms with primary genital infection • Occasionally for initial severe gingivostomatitis Acyclovir is most effective if started within 3 days of disease onset. Famciclovir or valacyclovir are additional antiviral agents approved for use in adults. 3. Topical acyclovir ointment may help for initial genital herpes infections but is often not beneficial for recurrent infections. 4. Oral acyclovir 200 mg five times a day for 5 to 10 days may speed healing of herpetic whitlow (see Fig. 37- 16). 5. Antibiotics for secondary bacterial (usually staphylococcal) infection: • Mupirocin: Topically three times a day for 5 days • Erythromycin: 40 mg/kg/day for 10 days • Dicloxacillin: 12.5 to 50 mg/kg/day for 10 days 6. Oral anesthetics for comfort; use with caution in children (the child needs to be able to rinse and spit): • Viscous lidocaine 2% topical • Liquid diphenhydramine alone or combined with aluminum hydroxide or magnesium hydroxide as a 1 : 1 rinse (maximum of 5 mg/kg/day diphenhydra-mine in case it is swallowed); it can also be applied to the lesions with cotton-tipped swabs 7. Newborn infant, immunosuppressed child, child with infected atopic dermatitis, or child with a lesion in the eye or on the eyelid margin; consult with or refer to an appropriate provider 8. Offer supportive care, such as antipyretics, analgesics, hydration, and good oral hygiene 1006 9. Exclude from day care only during the initial course (gingivostomatitis) and if the child cannot control secretions 10. Recurrent, frequent, and severe HSV infection may be treated with acyclovir prophylaxis for 6 months Patient and Family Education Recurrence of infection, possible triggering factors, and avoidance measures should be discussed. Triggers can include physical and psychological stress, trauma, fever, exposure to UV light, illness, menses, and extreme weather. Contagiousness of lesions and oral secretions must be understood. Explanation of the course of primary disease, with fever lasting up to 4 days and lesions taking at least 2 weeks to heal, is important. Variety of symptoms Discontinue current NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Clostridiu m difficil e Unknown and severity are seen: mild to explosive diarrhea, bloody stools, abdominal pain, fever, nausea, vomiting Mild to moderate illness is characteriz ed by watery diarrhea, low- grade fever, During or after severa l weeks of antibio t ic use; can occur withou t being associ at ed with such treatm e nt Acquired from the environme n t or from stool of other colonized or infected people by the fecal- oral route Stool cultures; enzyme immunoa s say for toxin A, or A and B; positive gross blood, leukocyt es ; CBC: ↑ WBCs; ESR normal antibiotic (any antibiotic, but notably ampicillin, clindamycin, second- and third- generation cephalosporins ). Fluids and electrolyte replacement are usually sufficient. If antibiotic is still needed or illness is severe, treat with oral metronidazole NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ and mild abdomin al pain (drug of choice in children) or vancomycin for 7 to 10 days. Supplement with probiotics. Lactobacillus GG, Saccharomyc es boulardii are recommended (Jones, 2010; Shane, 2010). Complications include pseudomembra no us colitis, toxic megacolon, colonic perforation, relapse, intractable proctitis, death in debilitated children. Rotavirus 1 to 3 days; preval e nt durin g cooler month s in tempe r ate climat e s Acute-onset fever, vomiting, and watery diarrhea occur 2 to 4 days later in children <5 years old, especially those between 3 to 24 months old 3 to 8 days Fecal-oral; viable on inanimate objects; rarely contamin at ed water or food Enzyme immunoa s say and latex agglutina ti on assays for group A rotavirus antigen; virus can be found by electron microsco p y and specific nucleic acid amplifica ti on methods. Supportive care: May need to correct dehydration and electrolyte imbalances. Oral IG has been used in those immunocompro mi sed. Preventive care: Rotavirus vaccine; hygiene and diapering precautions in day care facilities. Salmonell a spp. 1 to 3 days Diarrhea, fever, abdominal 4 to 7 days Contaminate d eggs, Routine stool cultures; Supportive care: Only consid er NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ reptiles, young animals Pyloric Stenosis Pyloric stenosis is characterized by hypertrophied pyloric muscle, causing a narrowing of the pyloric sphincter. Pyloric stenosis occurs in 3 per 1000 live births, with a fourfold increase in males compared with females ( Hunter and Liacourus, 2011b). It tends to be familial and is seen more commonly in Caucasian first-born males. Clinical Findings History. • Regurgitation and non-projectile vomiting during the first few weeks of life NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ • Projectile vomiting beginning at 2 to 3 weeks old • Insatiable appetite with weight loss, dehydration, and constipation • An association of pyloric stenosis with the administration of erythromycin in the first 2 weeks of life has been demonstrated Physical Examination. • Weight loss • Nonbilious vomitus that can contain blood • A distinct “olive” mass that is often palpated in the epigastrium to the right of midline • Reverse peristalsis visualized across the abdomen Diagnostic Studies. Ultrasound, with measurement of the pyloric muscle thickness, is used in most centers. An upper gastrointestinal series demonstrates a “string sign,” indicating a fine, elongated pyloric canal may be required if ultrasound is unavailable or inconclusive. Management and Prognosis Surgical intervention (pyloromyotomy) is indicated after correction of fluid and electrolyte imbalance. Vomiting can continue for a few days after surgery, although it is not as significant as it was preoperatively; feedings should be introduced gradually. The prognosis is excellent. Intussusception Intussusception involves a section of intestine being pulled antegrade into adjacent intestine with the proximal bowel trapped in the distal segment. The invagination of bowel begins proximal to the ileocecal valve and is usually ileocolic, but it can be ileoileal or colocolic. Intussusception is 859thought to be the most frequent reason for intestinal obstruction in children. Intussusception most commonly occurs between 5 and 10 months of age and is also the most common cause of intestinal obstruction in children 3 months to 6 years old; 80% of the cases occur before 2 years of age. In younger infants, intussusception is generally idiopathic and responds to nonoperative approaches. In some children, there is a known medical predisposing factor, such as polyps, Meckel diverticulum, Henoch-Schönlein purpura, constipation, lymphomas, lipomas, parasites, rotavirus, adenovirus, and foreign bodies. Intussusception may also be a complication of CF. Children older than 3 years are more likely to have a lead point caused by polyps, lymphoma, Meckel diverticulum, or Henoch-Schönlein purpura; therefore, a cause must be investigated. The currently approved rotavirus vaccines have not been associated with an increased risk of intussusception (Kennedy and Liacouras, 2011). Clinical Findings History • The classic triad for intussusception, intermittent colicky (crampy) abdominal pain, vomiting, and bloody mucous stools, are present in fewer than 15% of cases (Kennedy and Liacouras, 2011 ): • Paroxysmal, episodic abdominal pain with vomiting every 5 to 30 minutes. Vomiting is nonbilious initially. Some children do not have any pain. • Screaming with drawing up of the legs with periods of calm, sleeping, or lethargy between episodes. • Stool, possibly diarrhea in nature, with blood (“currant jelly”). • A history of a URI is common. • Lethargy is a common presenting symptom. • Fever may or may not be present; can be a late sign of transmural gangrene and infarction. NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ • Severe prostration is possible. Physical Examination • Observe the baby's appearance and behavior over a period of time; often the child appears glassy-eyed and groggy between episodes, almost as if sedated. • A sausage-like mass may be felt in the RUQ of the abdomen with emptiness in the RLQ (Dance sign); observe the infant when quiet between spasms. • The abdomen is often distended and tender to palpation. • Grossly bloody or guaiac-positive stools. NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Celiac Disease. • Chronic or intermittent diarrhea, persistent or unexplained GI symptoms (e.g., nausea and vomiting), sudden or unexpected weight loss, and prolonged fatigue Diagnostic Studies • Stool assessment for occult blood, WBCs, and culture; liquid stool for pH and reducing substances; 72-hour fecal fat collection or Sudan stain for stool fat • Spot stool testing for alpha 1-antitrypsin level to establish the diagnosis of protein-losing enteropathy • Sweat chloride test (in the presence of steatorrhea to evaluate for CF) • Stool for O&P: Giardiasis is a common intestinal infection causing malabsorption. See later discussion for symptoms suggestive of infestation. • CBC with differential, mean corpuscular hemoglobin concentration (MCHC), iron, folic acid, and ferritin • Serum calcium, phosphorus, magnesium, alkaline phosphatase, serum protein, liver function tests, vitamin D and its metabolites, vitamins A, B12, E, and K • Human immunodeficiency virus (HIV) testing (for symptoms of FTT and chronic diarrhea) • Small bowel biopsy helps identify diseases of the small bowel mucosa and obtain material for culture and sensitivity • Plain abdominal radiographs and barium contrast studies as indicated • Abdominal ultrasound can detect masses and stones in the hepatobiliary system • Retrograde studies of the pancreas and biliary tree if indicated • Bone age Specific Tests for Celiac Disease • Serologic testing should be done if there is clinical suspicion of celiac disease, the child has an associated disorder, or there is a first- degree relative with celiac disease. Gluten should be eaten in more than one meal every day for 6 weeks prior to testing. Recommended serologic tests include IgA tissue transglutaminase antibody (tTGA) and IgA endomysial antibody (EMA) because of their high sensitivity and specificity (Guandalini et al, 2014; Tran, 2014). EMA is more expensive and less accurate in children younger than 2 years old (Gelfand, 2013). • Home blood testing is not recommended (NICE, 2010). • If serologic testing is positive, refer for endoscopy with biopsy for a definitive diagnosis, although colonoscopy may not be necessary if the tTGA level is greater than 100 units/mL (Mubarak et al, 2011 ). • Careful follow-up of growth parameters, tTGA testing after 6 months of gluten-free diet (GFD), and then yearly (Hill et al, 2005 ). • Bone density testing (bone problems may be first symptom of celiac disease). Management Celiac Disease •A strict GFD for life is currently the only effective treatment for celiac disease. The standard for being gluten- free is a limit of 20 ppm of gluten (Hill et al, 2005 ). Adding pure oats to a GFD can improve palatability and increase fiber and vitamin B intake without causing a systemic or autoantibody response (Mubarak et al, 2012; Scanlon and Murray, 2011 ). •Alternative treatments are being explored, including enzyme therapy, developing genetically engineered grains, inhibiting tTGA in the intestine, and correcting intestinal barrier defects (particularly increased permeability). •A lactose-free diet for young children may be helpful. This is generally not the case in adolescents and adults unless they are lactose intolerant (Hill et al, 2005 ). Complications and Prognosis NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Celiac Disease Growth failure is the primary complication of celiac disease. With delayed diagnosis or inadequate treatment, there is risk for fractures and osteoporosis (due to reduced bone mineral density), lymphoma, autoimmune diseases (e.g., type 1 diabetes, thyroid disorders), primary biliary cirrhosis, and primary sclerosing cholangitis. Sensory peripheral neuropathy may be related to gluten sensitivity (Hadjivassiliou et al, 2010). Celiac crisis consisting of abdominal distention, explosive watery diarrhea, dehydration with hypoproteinemia, electrolyte imbalance, hypotensive shock, and lethargy, although rare, can be the first indication of celiac disease. Prognosis is improved with lifelong GFD. NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Juvenile Idiopathic Arthritis JIA, formerly known as juvenile rheumatoid arthritis (JRA), now encompasses several disorders that have a common feature of arthritis (e.g., enthesitis-related arthritis and psoriatic arthritis) and had not been identified under the nomenclature of JRA (Wu et al, 2011 ). The diagnosis of JIA requires a persistent arthritis for more than 6 weeks in a pediatric patient younger than 16 years old. Table 25-1 shows the most current classification system. TABLE 25-1 Juvenile Idiopathic Arthritis Subtypes and Clinical Joint Characteristics Juvenile Idiopathic Arthritis Clinical Joint Characteristics Subtype Oligoarticular Four or less joints with persistent disease never having more than four-joint involvement and extended disease progressing to more than four joints within the first 6 months Polyarticular (RF negative) Five or more joints with symmetrical involvement Polyarticular (RF positive) Symmetric involvement of both small and large joints with erosive joint disease Systemic Either polyarticular or oligoarticular disease Enthesitis-related arthritis Weight-bearing joints involved especially hip and intertarsal joints and a history of back pain, which is inflammatory in nature or sacroiliac joint involvement Psoriatic arthritis Asymmetric or symmetric small or large joints Undifferentiated RF, Rheumatoid factor. The underlying cause of most forms of JIA is unclear; however, it is a heterogenous disorder. It is likely environmentally induced in genetically predisposed individual. Human leukocytic NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ diagnosis. The diagnosis is classified as persistent or extended disease, depending on the number of joints involved. About 50% progress to extended disease where there is involvement of four or more joints after the first 6 months of disease. This involvement primarily is in larger or medium joints, such as the knee, ankle, wrists, and elbow; however, systemic symptoms are rare. The synovitis may be mild and painless with asymmetric joint involvement and unremarkable laboratory values. Uveitis occurs in 30% especially if the child has a positive ANA (Gowdie and Tse, 2012 ). 2. Polyarticular pattern: This involves five or more joints and is divided into RF-negative and RF-positive disease. Involved joints can be large or small with an acute or insidious onset. RF-negative ANA positive polyarticular JIA is difficult to distinguish from extended oligoarticular pattern disease. Using the number of joints involved and the timing of onset of the arthritis can be helpful. In contrast, RF- positive disease can have chronic pain and symmetric joint swelling, low-grade fever, fatigue, nodules, and anemia of chronic disease. An acute form of uveitis occurs in this subtype. Polyarticular JIA typically involves small joints of the hands, feet, ankles, wrists, knees, and can also involve the cervical spine. Adolescents with this type differ from those with early onset in that they exhibit a positive RF. Adolescents who develop late-onset polyarticular JIA have a course similar to the adult entity. Both forms of the disease are more common in females. NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ 3. SJIA: This is characterized by arthritis in one or more joints for 6 weeks' duration in a child younger than 16 years old with a fever of at least 2 weeks' duration with 553at least 3 days of daily fever. In addition, there is also a fleeting erythematous rash, lymphadenopathy, hepatomegaly, splenomegaly, and serositis (Ringold et al, 2013 ). Myocarditis with pericardial effusion occurs in approximately 10%. RF is rarely positive and the ANA is only positive in 5% to 10%; however, there may be anemia, thrombocytosis, increased acute phase reactants, and elevated transaminase levels. About 10% of children with SJIA develop a life-threatening macrophage activation syndrome (MAS) with fever, organomegaly, cytopenia, hyperferritinemia (acute phase reactant), hypertriglyceridemia, coagulopathy, and hypofibrinogenemia. 4. Enthesitis-related JIA: This typically entails arthritis of the lower limbs especially the hip and intertarsal joints with the sacroiliac joints involved later in the disease. Enthesitis involves inflammation at the insertion of tendons, ligaments, or joint capsules and is characterized by swelling, tenderness, and warmth. Enthesitis may present with joint or foot pain. There is a risk of anklyosing spondylitis 10 to 15 years later. It tends to occur in late childhood and adolescence and acute symptomatic uveitis occurs in about 7%. 5. Psoriatic arthritis: This is more common between the ages of 2 and 4 and again between 9 to 11 years old. There is usually a family history of psoriasis, or the child has psoriasis; however, the arthritis can precede the psoriasis by years. There can be dactylitis or a sausage-like swelling of the digits; involvement in the small digits is not uncommon. Diagnostic Studies JIA is a diagnosis of exclusion. The diagnosis is based on physical findings and history of arthritis lasting for 6 weeks or longer. There is no diagnostic laboratory test for JIA. Most children with oligoarticular arthritis have negative laboratory markers. Those with polyarticular and systemic-onset typically have elevated acute-phase reactants and anemia of chronic disease. A positive result for RF by latex fixation may be present, but a positive RF occurs in less than 10% of children with JIA and rarely in those with SJIA. ANA may be present in up to 50% of children with oligoarticular disease. A positive ANA helps identify children at higher risk for uveitis. The anti-CCP antibody test can be added to the initial workup of JIA, because citrullinated residues are part of the essential antigenic components that are recognized by autoantibodies in rheumatoid arthritis (Mehta, 2012). The anti-CCP antibodies are associated with more aggressive disease and may be present before the onset of symptoms. The anti-CCP antibody is highly specific, but its precise role has not been established because it is found primarily in children with polyarticular JIA (Mehta, 2012). Useful laboratory tests include a complete blood count (CBC) (to exclude leukemia); ESR, CRP, Lyme titers, and liver function tests. The results may reveal lymphopenia, anemia, elevated transaminases, and hypoalbuminemia; however, laboratory studies may be normal in these children. Imaging studies (MRI) can help in managing joint pathologic conditions. Analysis of synovial fluid is not helpful in the diagnosis of JIA. Differential Diagnosis The various causes of monoarticular arthritis are part of the differential diagnosis. However, Lyme disease must be excluded and other differentials, including tumors, leukemia, cancer, bacterial infections, toxic synovitis, rheumatic fever, SLE, spondyloarthropathies, inflammatory bowel disease, septic arthritis, and chondromalacia patellae, need to be carefully considered. Management A specialist in pediatric rheumatology should follow children with severe involvement. Ophthalmology referral and evaluation is critical in a child with a positive ANA. Uveitis needs immediate ophthalmologic management. It is most common in oligoarticular JIA and is highly associated with a positive ANA. Other pediatric subspecialists, such as orthopedists, pain management specialists, and cardiologists, may be consulted as needed. Therapy depends on the degree of local or systemic involvement. The main treatment goals are to suppress inflammation, preserve and maximize joint function, prevent joint deformities, and prevent blindness. Drug therapy is used to control the inflammation responsible for tissue injury with the goal of preventing permanent tissue changes, which is not always possible. Aggressive early treatment to induce a remission is a key consideration in JIA management in order to prevent deformity and improve outcomes and is now the goal of the practice guidelines for both polyarticular JIA and SJIA ( Ringold et al, 2013, 2014). Aspirin therapy has largely been replaced with the use of nonsteroidal anti-inflammatory drugs (NSAIDs). Pharmacologic agents commonly used in the management of JIA include the following (Gowdie and Tse, 2012 ): • NSAIDs: Children with oligoarthritis generally respond well to NSAIDs (Taketomo et al, 2014 ). • Ibuprofen: 30 to 40 mg/kg/day three to four divided doses (maximum single dose is 800 mg; maximum daily dose 2400 mg/day) • Tolmetin: 20 to 30 mg/kg/day divided in three to four doses (maximum dose is 1800 mg/day) • Naproxen: 10 mg/kg/day in two divided doses (maximum dose is 1000 mg/day) • Indomethacin: Older than 2 years old, 1 to 2 mg/kg/day divided in two to four doses (maximum dose is 4 mg/kg/day); adults, 25 to 50 mg/dose two or three times/day (maximum dose is 200 mg/day) • Celecoxib: Older than 2 years old and adolescents (≥10 kg to ≤25 kg), 50 mg twice daily; >25 kg, 100 mg twice daily NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ • Oral, parenteral, intraarticular corticosteroids: • Systemic arthritis: Can be used for 2 weeks as initial therapy for SJIA with involvement of more than four joints and a physician global assessment (using the Provider global assessment tool of disease activity) of 554less than 5 or a Provider global score of more than 5 without care about active joint involvement. Corticosteroids can be used as bridging therapy until other medications take effect (Ringold et al, 2013 ) • All the other types of arthritis: Prednisone in the lowest possible dose with optional intraarticular steroid injection (Ringold et al, 2014 ) • Disease-modifying antirheumatic drugs (DMARDs): Recent published guidelines vary related to the initiation of these agents depending on type of arthritis, joint involvement, and MD global assessment of functioning • Nonbiologic DMARD treatment: methotrexate, sulfasalazine, leflunomide (managed by pediatric rheumatologist) • Biologic DMARD treatment (managed by pediatric rheumatologist) NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ penetrates a bone or joint and is most commonly caused by P. aeruginosa in nondiabetic patients and is most commonly caused by S. aureus in diabetic patients (Baddour, 2013 ). Cat and dog bites can cause wound infection from Pasteurella multocida. When considering risk for infection, the location and depth of the wound and the presence of a foreign object are important components. For example, deep penetrating injuries to the forefoot with a dirty object, especially if they involve the plantar fascia, have a higher risk of infection than wounds to the arch or heel area. The forefoot has less overlying soft tissue than other plantar surfaces and is the major weight- bearing area of the foot; therefore, cartilage and bone can be involved. The metatarsophalangeal joint region is also at high risk for infection for the same reasons. Puncture wounds through the soles of tennis shoes can transfer bacteria into the tissue while simultaneously impairing wound drainage, placing the child at higher risk for a secondary infection. Assessment The assessment of a child with a minor wound begins by excluding more serious and sometimes occult injuries. History. Important information to elicit after a report or suspicion of a puncture wound includes the following: • Date and time of injury and history of wound care provided at time of injury and thereafter. • Identification of the penetrating object and the type and estimated depth of penetration. If it is not known what object penetrated the skin, the likelihood of an imbedded foreign body is high. • Location and condition of the penetrating object. Was the object clean or rusty, jagged or smooth? • Whether all or part of the foreign object was removed. • Type and condition of footwear that was being worn (pertinent to injuries to the foot) or if the child was barefoot. • Immunization status for tetanus coverage (see Chapter 24 ). • Presence of any medical condition that increases the risk for infectious complications. Physical Examination. A good light source is necessary to assess and treat a puncture wound. Note circulation, movement, and sensation of the area next to the injury. Determine the amount of involvement of underlying tissue or bone structures. For plantar puncture wounds, have the patient lie prone with the feet positioned at the head of the examining table and the knees slightly flexed ( Buttaravoli and Leffler, 2012 ). Assess the wound for length and depth, presence of debris or penetrating object, and signs of infection. Examination findings consistent with cellulitis include: • Localized pain or tenderness, swelling, and erythema at the puncture site (may be more obvious at dorsum of the foot for plantar puncture wounds) 1127 • Possible fever • Pain with flexion or extension of the extremity involved • Decreased ability to bear weight • For plantar puncture wounds, pain along the plantar aspect of the foot during extension or flexion of the toes may indicate deep tissue injury, thus a higher risk of infection Examination findings consistent with osteomyelitis-osteochondritis include: • Extension of pain and swelling around the puncture wound and to the adjacent bony structures • Exquisite point tenderness over the bone • Fever • Increasing erythema • Decreased use of the affected extremity Examination findings consistent with pyarthrosis (septic arthritis) include: • Pain, swelling, warmth, and erythema over the affected joint • Decreased range of motion and weight bearing of the affected joint • Fever NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Diagnostic Studies. Plain film radiograph should be ordered if any of the following occur: • A suspicion of a retained foreign object. • There is a tremendous amount of pain at the site of the wound, localized tenderness is noted over the wound, there is discoloration underneath the skin surface, or there is a palpable mass noted at or near the wound entry site (Baddour, 2013 ). • There was penetration of a joint space, bone or growth cartilage, or the plantar fascia of the foot. • The puncture site has signs of infection and is from a nail injury. NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ • Most metal and glass foreign bodies can be seen on a plain radiograph. However, if the foreign object is not radiopaque or if the x- ray is negative despite suspicion of foreign object in the wound, computed tomography (CT), ultrasound, and magnetic resonance imaging (MRI) are useful diagnostic tools (Buttaravoli and Leffler, 2012 ). • Bone scans are sensitive but not specific for osteomyelitis. Radiographs are specific, but findings for osteomyelitis are noted late. Clinical examination and laboratory studies and imaging should be considered early in the diagnosis of osteomyelitis (Erickson and Caprio, 2014 ). • A complete blood count (CBC) and blood culture may be needed. An elevation in the white blood cell count might indicate infection. • An erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are nonspecific inflammatory markers and are helpful in the diagnosis and management of bony inflammation and infection. • A wound culture is indicated prior to starting antibiotics if the wound appears infected. Differential Diagnosis The history and physical examination provide the diagnosis. Management The circumstance surrounding the penetrating injury and the presenting symptoms are the best indicators of whether the injury is superficial and will heal uneventfully or if it will result in infectious complications. Buttaravoli and Leffler (2012) suggest the following practical and straightforward approach to the management of puncture wounds: • For the majority of superficial or simple puncture wounds, débridement with an antiseptic solution after scrubbing the wound surface is sufficient. Consider the use of wound irrigation. Ensure that there are no foreign bodies present. • A No. 10 scalpel may be used to gently shave off the cornified epithelium surrounding the puncture wound to aid in the removal of debris that collected around the point of entry. • For wounds where debris is noted, gently slide the plastic sheath of an over-the-needle catheter down the wound track and move the catheter sheath in and out while irrigating with copious amounts of normal saline until debris no longer flows from the wound. A local anesthetic agent may be necessary for débridement and irrigation procedures. • Obtain imaging studies as indicated. If imaging studies demonstrate that the foreign object has invaded bone, growth cartilage, or a joint space, refer the child immediately to an orthopedic surgeon. Always suspect a retained foreign object if the puncture wound is infected, the infection is not responding to antibiotic therapy, or if pain or aching of the injured site is still present weeks after the injury. In order to prevent a catastrophic outcome, wounds that are deep or highly contaminated should be referred to an orthopedic surgeon so that débridement can take place in an operating room (Buttaravoli and Leffler, 2012 ). • Following careful wound cleansing, the wound can be covered with a simple bandage. Deeper wounds that require more extensive exploration should have a small sterile wick of iodoform gauze placed in the wound track in order to keep the edges open, thus aiding in granulation tissue growth and wound healing. Remove the gauze 2 to 3 days after placement (Selbst and Attia, 2010 ). • Children with simple, uncomplicated puncture wounds do not need antibiotics; however, if there are signs of infection, the puncture is the result of a cat bite, or if the wound is deep or contained debris, antibiotics should be part of the treatment plan. Appropriate antibiotics for puncture wounds include amoxicillin clavulanate or cephalexin. Clindamycin should be used when children are allergic to penicillins. Plantar puncture wounds require ciprofloxacin. If methicillin-resistant Staphylococcus aureus (MRSA) is cultured from the wound or pus is present at the puncture site, then trimethoprim-sulfamethoxazole (TMP-SMX) 1128or clindamycin is recommended until sensitivities are known. All antibiotics should be prescribed for 7 to 14 days depending on severity of infection (Baddour, 2013). A recheck appointment should be scheduled 48 hours from the start of antibiotics for the patient receiving outpatient therapy. • Surgical débridement for removal of a foreign body and/or abscess drainage should be considered with an infected puncture wound (Baddour, 2013 ). • Treatment for severe infections secondary to puncture wounds, such as septic arthritis and osteomyelitis, includes surgical débridement and parenteral antibiotics (Hosalkar et al, 2011 ). • Tetanus prophylaxis is indicated if it has been more than 5 years since the last tetanus vaccine or if the date of the last tetanus vaccine is unknown. Consider passive immunization with tetanus immune globulin (TIG) or initiation/continuation of a primary tetanus series (DTaP, Tdap, or Td as appropriate) for children who have never been immunized or are behind in their vaccinations (see Chapter 24 ). Patient and Parent Education Home care management for a puncture wound includes: NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ • Other findings include asymmetry of inguinal or gluteal folds (thigh-fold asymmetry is not related to the disorder [see Fig. 38-3, D ]) and unequal leg lengths, shorter on the affected side. In the ambulatory child who was not diagnosed earlier or was not corrected, the following might also be noted: • Short leg with toe walking on the affected side • Positive Trendelenburg sign (see Fig. 38-3, C ) • Marked lordosis or toe walking • Painless limping or waddling gait with child leaning to the affected side If the hips are dislocated bilaterally, asymmetries are not observed. Limited abduction is the primary indicator in this situation (see Fig. 38-5). Also in subluxation of the hip (not frankly dislocated), limited abduction again is the primary indicator. A waddling gait may also be noted. NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Diagnostic Studies. Ultrasound is superior to radiographs for evaluating cartilaginous structures and is recommended for infants after 4 weeks of age. Use of ultrasonography prior to 4 weeks old has a high incidence of producing false-positive results. Ultrasound is used to assess the relationship of the femur to the acetabulum and provides dynamic information about acetabular development and stability of the hip. Radiologic evaluation of the newborn to detect and evaluate DDH is recommended once the proximal epiphysis ossifies, usually by 4 to 6 months (Sankar et al, 2011). Radiography prior to this is unreliable, because so much of the hip joint is cartilaginous in the young infant. AP and lateral Lauenstein (frog-leg) position radiographs of the pelvis are indicated. Differential Diagnosis The condition is relatively unique. Management The goal of management is to restore the articulation of the femur within the acetabulum. Many newborns with positive screening tests and abnormal hips resolve without intervention; however, prompt referral to an orthopedist is important. The orthopedist needs to reexamine the newborn to determine whether early treatment is necessary. • The majority of neonatal hip instability cases resolve spontaneously by 6 to 8 weeks old. Close observation of these children is recommended. • The treatment of choice for subluxation and reducible dislocations identified in the early phase is a Pavlik harness. The harness is applied with hips having greater than 90 degrees of flexion and with adduction of the hip limited to a neutral position. The success rate of Pavlik harness treatment is reported to be between 80% and 97%. Radiographic or ultrasound documentation can be used during treatment to verify the position of the hip. If the infant does not respond to treatment with the harness, surgical treatment may be needed. 1062 • The earlier that treatment is started with the Pavlik harness, the better the prognosis for a successful outcome. The harness is worn 24 hours a day, except for bathing. The infant with a Pavlik harness should be seen weekly to ensure it fits properly, to identify complications associated with the use of the harness (e.g., avascular necrosis and femoral nerve palsy), and to ensure the femur is properly seated in the socket. Ultrasonography can be performed while the Pavlik harness is worn to assess hip reduction and acetabular development. The length of time the harness is worn depends on the age of the child, when it was applied, and whether or not reduction is successful. Generally the harness is worn full time for 3 to 6 weeks and then may be required only during waking hours for decreasing periods of time. • For a child in a Pavlik harness or spica cast, cast care, skin care, and car safety when the child cannot easily be placed in a car seat are issues to be addressed. Furthermore, the child needs special attention to maintain developmental stimulation while immobilized. An orthopedist should be immediately consulted for any infant seen in a primary care setting who is in a Pavlik harness and exhibits excessive hip flexion (beyond 100 degrees) or abduction (beyond 60 degrees). • The 6- to 18-month-old infant with a dislocated hip is likely to require either closed manipulation or open reduction. Preoperative traction, adductor tenotomy, and gentle reduction are especially helpful in preventing osteonecrosis of the femoral head. After the closed or open reduction, a hip spica cast is applied in order to maintain the hip in more than 90 degrees of flexion and avoid excessive internal or external rotation (Herring, 2014a). Triple diapering is not helpful, because the musculoskeletal forces far outweigh the force that can be exerted by the diaper material. • Annual or biennial follow-up including radiographs to the point of skeletal maturity is recommended to evaluate for the possibility of late asymmetric epiphyseal closure (Herring, 2014a). Support the child and family through the treatment phases. Explain management goals clearly. Complications The Pavlik harness and other positional devices may cause skin irritation, and a difference in leg length may remain. There may be delay in walking if the child is put in a body cast. The long-term outcomes depend on the age at diagnosis, the severity of the joint deformity, and the effectiveness of therapy. Untreated cases may result in a permanent dislocation of the femoral head so that it lies just under the iliac crest posteriorly. Clinically, the child has limited mobility of this pseudo joint and related short leg. Forceful reduction can result in avascular necrosis of the femoral head with permanent hip deformity. Redislocation or persistent dysplasia can occur. Adult degenerative arthritis is associated with acetabular dysplasia. NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Prevention The condition cannot be prevented, but early identification resulting in early treatment significantly reduces the long-term consequences of the problem. Screening of all neonates and infants should include full hip abduction; examination for unequal inguinal and gluteal folds and unequal leg lengths; and Barlow, Ortolani, and Galeazzi maneuvers at every examination. The hip can dislocate at any point in early development, even up to the point of first ambulation. In older children, limited abduction, gait, and standing position, including the Trendelenburg position, add important information. Charting should always include notation about hip findings, because these can change at subsequent visits. The Ortolani test should only be used in the first 2 to 3 months of age. Legg-Calvé-Perthes Disease LCPD is a childhood hip disorder that results in infarction of the bony epiphysis of the femoral head. It presents as avascular necrosis of the femoral head. The basic underlying cause of LCPD is insufficient blood supply to the femoral head. There is an initial ischemic episode of NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Complications Osteoarthritis related to femoral head deformity and decreased use of the hip joint may occur, depending on the femoral head remodeling status. Older children have a poorer prognosis owing to the decreased opportunity for femoral head remodeling in the remaining growth period. Females with LCPD also have a poorer prognosis. Prevention The condition is not preventable, but early identification and treatment reduce the long-term complications of the disorder, such as premature degenerative arthritis in early adult life. Idiopathic Scoliosis Adolescent scoliosis can resolve, remain static, or increase. As a result treatment options vary considerably. Treatment decisions are based on the natural history of each curvature. Infantile scoliosis can resolve spontaneously; however, progressive curves require bracing and surgery in an attempt to slow the curve progression and prevent complications (e.g., thoracic insufficiency syndrome). Juvenile scoliosis is found more frequently in girls, and the curves are at high risk for progression and often require surgical intervention. The goal in treatment is to delay spinal fusion, allowing time for the pulmonary system and thoracic cage to have matured and maximum trunk height to be achieved. (See the various surgical procedures described in the following section.) The natural history includes the degree of skeletal maturity or growth remaining, the magnitude of the curve, and any associated diagnoses or medical conditions. Observation is always indicated for curves less than 20 degrees. Bracing or surgery may be indicated for larger curves. Brace treatment may reduce the need for surgery, restore the sagittal profile, and change vertebral rotation. Indications for bracing are a curve more than 30 degrees. Additional indications for brace therapy include skeletally immature patients with curves of 20 to 25 degrees that have shown more than 5 degrees of progression. The efficacy of bracing for adolescent idiopathic scoliosis remains controversial. Some studies show brace treatment to be effective in preventing curvature progression; however, it has been found that the success of the treatment is proportional to the amount of time that the patient wears the brace. Various brace treatment protocols suggest wearing a brace as much as 23 hours per day; therefore, compliance is a significant factor for this treatment modality (Spiegel and Dormans, 2011 ). Surgical treatment is indicated for children and adolescents who have progressive spinal deformity that do not respond to bracing and for those with curvature exceeding 45 to 50 degrees (Richards et al, 2014). There are various surgical procedures; all aim to control progressive curvatures. In the past, surgery was limited to arthrodesis (surgical fusion) of the spine. In recent years, several procedures have been developed that are designed to postpone and, in some cases, eliminate the need for early spinal fusion and allow for growth. These include the vertical expandable prosthetic titanium rib (VEPTR). This procedure is indicated for children with restricted pulmonary function due to the curvature of their thoracic spine. The surgery involves implanting a prosthesis that serves to enlarge the constricted thorax. The prosthesis can be adjusted approximately every 4 to 6 months, thereby allowing for growth. The “growing rod” surgical procedure has shown success in patients with adolescent idiopathic scoliosis and involves inserting spinal rods that are used to exert distraction forces that are adjusted approximately every 6 months. The rods serve as an internal brace to control the curvature of the spine while allowing skeletal growth. A more recent procedure involves intervertebral spinal stapling or tethering. Unlike the VEPTR and growing rod procedures, intervertebral spinal stapling does not require repeat adjustments and, therefore, eliminates the need for repeat surgical procedures. Research on this technique is limited, and clinical indications have not been universally agreed upon. Further research is necessary and long-term results are yet to be determined. Referral to an orthopedist or a center that specializes in working with infants and children NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ with scoliosis is essential. Support must be given to the child and family 1060through the diagnostic and treatment phases, considering school and peer factors. The primary care provider needs to assist the child with psychological adjustment issues that arise if bracing or surgery is recommended and instituted. Some specific concerns of the child can include self-esteem problems, managing hostility and anger, learning about the disease and its care, wondering about the long-term prognosis, and concerns about clothing and participation in sports and other activities. Complications Progressive scoliosis can result in a severe deformity of the spinal column. Severe deformities can result in impairment of respiratory and cardiovascular function and limitation of physical activities and decreased comfort. The psychological consequences of an untreated scoliosis deformity can be severe. Prevention Prevention is not possible; however, screening and early identification of children with scoliosis may help avoid more expensive, invasive care and prevent the long-term consequences of the disorder. Screening is effective, however, only if identified children are referred for care. Parents must be notified, a referral arranged, and follow-up ensured. NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Scoliosis Scoliosis is a three-dimensional deformity most commonly described as a lateral curvature of the spine in the frontal plane. There are two types of scoliosis: nonstructural and structural. Nonstructural, also known as functional scoliosis, involves a curve in the spine without rotation of the vertebrae. The curve is reversible, considering it is caused by conditions such as poor posture, muscle spasms, pain, or leg length discrepancy. Structural scoliosis involves a rotational element of the spine and has various classifications depending on the cause. The remaining discussion pertains to structural scoliosis. The diagnosis is based on a curvature of more than 10 degrees using the Cobb method in which the angle between the superior and inferior end vertebrae (tilted into the curve) is measured by a radiologist (see Diagnostic Studies in the following text). In most pediatric cases, the etiology is unknown and is therefore termed and classified as idiopathic. Other classifications include congenital, in which vertebrae fail to form (e.g., hemivertebrae), and neuromuscular (e.g., cerebral palsy, neurofibromatosis, Marfan syndrome). Kyphosis, which results from disorders of sagittal alignment (such as, postural kyphosis and Scheuermann disease), is another classification of structural scoliosis. Kyphosis, commonly termed round back, is discussed following scoliosis. • Idiopathic: Etiology is unknown and is likely multifactorial. It is the most common type of scoliosis. There are three types classified by age at onset: • Infantile (0 to 3 years old) • Juvenile (3 to 10 years old) • Adolescent (11 years old and older) •Congenital: A structural anomaly present at birth (e.g., hemivertebrae) often associated with other congenital abnormalities, such as renal and cardiac anomalies; progression of curvature can worsen rapidly, particularly during periods of rapid growth (e.g., first 2 to 3 years of life and adolescence). •Neuromuscular: Most common in non-ambulatory patients. Secondary to weakness/imbalance/spasticity of the muscles of the trunk caused by primary neuromuscular problems (e.g., cerebral palsy or muscular dystrophy). In contrast to idiopathic and congenital scoliosis, curves caused by neuromuscular disorders can continue to progress after skeletal maturity. Idiopathic is the most common type of scoliosis. Its etiology is unknown, but it often has a familial or genetic pattern. The overall incidence of idiopathic scoliosis is approximately 2% to 3% with between 0.3% and 0.5% of children with scoliosis having curves greater than 20 degrees on radiography and less than 0.1% demonstrating curves greater than 40 degrees Cobb's angle. Hormonal changes play a role in the disease process, and a rapid growth period is believed to be a significant factor in the progression of curvature associated with idiopathic scoliosis. In addition, the risk of curve progression depends on the amount of growth remaining, the magnitude of the curve, and gender. Although the incidence of idiopathic scoliosis is nearly equal in girls and boys, females have a much higher risk of developing curves more than 30 degrees (Spiegel and Dormans, 2011). The most common type of idiopathic scoliosis is found in adolescents and is the major focus of the remaining discussion. Small to moderate scoliotic curves (10% to 30%) usually do not increase significantly after skeletal growth is complete but bear watching, particularly during periods of rapid growth velocity. Double S-curves and more severe curves are more likely to progress during the growth years. For a given child, however, the ability to predict progression is difficult, because even small curves (10% to 25%) can progress to severe deformity. Thus regular monitoring of any curve in a skeletally immature child is important (Table 38-2 ). The female-to-male ratio increases with increasing curve magnitude. For curves less than 20 degrees, the risk for progression of the curve is low; these curves generally just need to be observed. However, for curves between 20 and 45 degrees, the risk for progression is high during growth, and early intervention is of paramount importance. In children with curves greater than 50 degrees, the spine loses its ability NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Osgood-Schlatter Disease Osgood-Schlatter disease is caused by microtrauma in the deep fibers of the patellar tendon at its insertion on the tibial tuberosity. The diagnosis is usually based on history and physical examination. The quadriceps femoris muscle inserts on a relatively small area of the tibial tuberosity. Naturally high tension exists at the insertion site. In children, additional stress is placed on the cartilaginous site as a result of vigorous physical activity, leading to traumatic changes at insertion. Osgood-Schlatter disease is often seen in the adolescent years after undergoing a rapid growth spurt the previous year. It occurs more frequently in boys than girls, with a male-to-female ratio of 3 : 1. This difference is probably related to a greater participation in specific risk activities by boys than by girls (Sullivani, 2015). NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Clinical Findings History. • Recent physical activity (such as, running track, playing soccer or football, or surfboarding) commonly produces the condition. • Pain increases during and immediately after the activity and decreases when the activity is stopped for a while. • Running, jumping, kneeling, squatting, and ascending/descending stairs exacerbate the pain. • The pain is bilateral in 20% to 50% of cases. • Approximately 25% of patients give a history of precipitating trauma. Physical Examination. Characteristic findings include the following (Sullivan, 2015 ): • Pain may be reproduced by extending the knee against resistance, stressing the quadriceps, or squatting with the knee in full flexion • Focal swelling, heat, and point tenderness at the tibial tuberosity • Full range of motion of knee Diagnostic Studies. The diagnosis is based on history and physical examination. Radiographs are not needed unless another pathologic condition is suspected. Differential Diagnosis Other knee derangements, tumors (osteosarcoma), and hip problems with referred pain should be considered. The referred pain of hip problems is diffuse across the distal femur without point tenderness at the tibial tubercle. Management Osgood-Schlatter disease is a self-limiting condition, with symptom management the key consideration. The following steps are taken: • Avoid or modify activities that cause pain until the inflammation subsides. • Ice or cold therapy to reduce pain and inflammation. • Once the acute symptoms have subsided, quadriceps-stretching exercises, including hip extension for complete stretch of the extensor mechanism, may be performed to reduce tension on the tibial tubercle. Stretching of the hamstrings may also be useful. • Use of NSAIDs is recommended by some but thought ineffective by others. Because this condition may last up to 2 years, their chronic use may be problematic. • A neoprene sleeve over the knee may help stabilize the patella. • A patella tendon strap that wraps around the joint just below the knee reduces the strain on the tibial tuberosity. • Cylinder casting or bracing with limited weight bearing for 2 to 3 weeks may be used in severe cases. Complications In the postpubertal child, a residual ossicle in the tendon next to the bone may cause persistent pain. Surgical removal is indicated and will relieve the pain. Prevention The condition cannot be prevented, but earlier management may decrease the length of disability and the discomfort 1069associated with it. Avoid overuse and encourage balanced training and adequate warm-up before exercise or sports participation. The use of kneepads may help protect the tibial tuberosity from direct injury for those who engage in sports that result in knee contact. Febrile Seizures Febrile seizures are the most common type of seizures in children. They are brief, generalized, clonic or tonic-clonic in nature, and can be either simple or complex. A concurrent illness is present with rapid fever rise to at least more than 102.2° F (39° C), but the fever is not NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ necessarily that high at the time of the seizure. It is conjectured that these seizures may be related to peak temperature reached during the febrile episode. Minimal postictal confusion is associated with febrile seizures. Simple febrile seizures last less than 15 minutes and may recur during the same febrile illness period. Complex febrile seizures last longer than 15 minutes, can recur on the same day, and can have focal attributes (even during the postictal phase). Febrile SE is uncommon, rarely stops spontaneously, is fairly resistant to medications, and can persist for a long period of time. Most children in febrile SE require one or more medications to end the seizure. A report found that reducing the time from seizure onset to anticonvulsant medication administration was key to reducing the seizure duration during an episode (Seinfeld et al, 2014 ). The etiology of febrile seizures is unclear and by definition excludes seizures that are caused by intracranial illness or are related to an underlying CNS problem. The risk is higher in children with a family medical history for febrile seizures or in those with predisposing factors (e.g., neonatal intensive care unit [NICU] stay more than 30 days, developmental delay, day care attendance). NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Education The family should receive information about febrile seizures, their risks, and their management. Education should include information explaining the febrile seizure, reassurance that no long-term consequences are associated with febrile seizures, information that febrile seizures recur in some children and that nothing can be done to prevent the seizures, and first-aid information in case another seizure occurs at some time. The decision to use prophylaxis is up to the parents and the PCP on a case-by-case basis. A follow-up phone call after the event is useful. Complications Death or persisting motor deficits do not occur in patients with febrile seizures. No indication has been found that intellect or learning is impaired. An affected child has an increased risk for the development of epilepsy (less than 5%) if the seizure is prolonged and focal; if the child has repeated seizures with the same febrile episode; or if the child has had a prior neurologic deficit, a family history of epilepsy, or both. Two thirds of children who have had one simple febrile seizure will have no more. The younger the age at onset (younger than 18 months old) of the first febrile seizure, the lower the temperature threshold that is needed to cause the child to seize and the more likely the child is to have a recurrence. Testicular Torsion Testicular torsion is the result of twisting of the spermatic cord, which subsequently compromises the blood supply to the testicle. Generally, there is a 6-hour window following a testicular torsion before significant ischemic damage and alteration in spermatic morphology and formation occurs (Elder, 2011b). Normal fixation of the testis is absent, so the testis can rotate and block lymphatic and then blood flow. Torsion can occur after physical exertion, trauma, or on arising. Torsion can occur at any age but is most common in adolescence and is uncommon before 10 years old. The left side 946is twice as likely to be involved because of the longer spermatic cord. Clinical Findings History • Sudden onset of unilateral scrotal pain, often associated with nausea and vomiting. The pain is unrelenting. • History of bouts of intermittent testicular pain. Prior episodes of transient pain are reported in about half of patients. • Minor trauma, physical exertion, or onset of acute pain on arising is possible. • May be described as abdominal or inguinal pain by the embarrassed child. • Fever is minimal or absent. Physical Examination • Ill-appearing and anxious male, resisting movement • Gradual, progressive swelling of involved scrotum with redness, warmth, and tenderness • The ipsilateral scrotum can be edematous, erythematous, and warm • Testis swollen larger than opposite side, elevated, lying transversely, exquisitely painful • Spermatic cord thickened, twisted, and tender • Slight elevation of the testis increases pain (in epididymitis it relieves pain) • Transillumination can reveal a solid mass • The cremasteric reflex is absent on the side with torsion • Neonate—hard, painless, non-transilluminating mass with edema or discolored scrotal skin Diagnostic Studies • UA is usually normal and pyuria and bacteriuria indicate UTI, epididymitis, or orchitis. • Doppler ultrasound: Testicular flow scan considered if Doppler ultrasound within normal and time allows. NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Differential Diagnosis Torsion of the testicular or epididymal appendage, acute epididymitis (mild to moderate pain of gradual onset), orchitis, trauma (pain is better within an hour), hernia, hydrocele, and varicocele are included in the differential diagnosis. Management Testicular torsion is a surgical emergency, and identification with prompt surgical referral must occur immediately. Occasionally manual reduction can be performed, but surgery should follow within 6 to 12 hours to prevent retorsion, preserve fertility, and prevent abscess and atrophy. Contralateral orchiopexy may be done because of a 50% occurrence of torsion in nonfixed testes. Rest and scrotal support do not provide relief. NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+ Patient and Family Education, Prevention, and Prognosis Testicular atrophy, abscess, or decreased fertility and loss of the testis as a result of necrosis can occur if the torsion persists more than 24 hours. Clinical Presentation Disease History Physical Findings Laboratory Diagnosis Treatment Iron deficien c y Fatigue Irritability Excess milk intake Pallor or none RBC hypochromic , microcytic MCV ↓ Serum iron ↓ TIBC ↑ Percentage of saturation ↓ Ferritin ↓ Blood in stool or urine Ratio of MCV/RBC >13 Correct diet Eliminate source of bleeding Ferrous SO4 up to 6 mg/kg/day of elemental iron Iron Deficiency Anemia IDA is the most common nutritional disorder and hematologic condition in the world. Approximately 3% to 7% of children at age 1 year suffer from iron deficiency (Powers and Buchanan, 2014 ). Nine percent of adolescent girls develop iron deficiency and 2% to 3% between the ages of 12 and 19 years old develop anemia primarily due to rapid growth, heavy menses, and nutritionally inadequate diets 641(Abrams, 2014). The incidence of IDA among children in the United States has been declining slightly during the past four decades, although the prevalence remains high among children living at or below poverty level and in black and Hispanic children. Other risk factors include childhood obesity and a history of prematurity or low birth weight ( Mahoney, 2015). Iron deficiency correlates with rapid increases in body size and blood volume during the first 2 years, along with diets low in iron, such as occurs with an overuse of goat's or cow's milk. The deficient iron intake is also associated with prolonged bottle-feeding. Dietary iron is absorbed throughout the intestine but especially in the duodenum. Malabsorption of iron occurs in diseases that affect this segment of the intestine, such as celiac disease, Crohn disease, giardiasis, or resection of the proximal small intestine. Disorders causing GI blood loss such as inflammatory bowel disease, cow's milk–induced colitis, or chronic use of aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) also deplete iron stores and contribute to iron deficiency (Mahoney, 2015 ). Anemia (Hgb level <11 g/dL) is neither a sensitive nor a specific screen for iron deficiency because about two thirds of iron-deficient children are not anemic. Conversely, the detection of anemia is not specific to iron deficiency, because two thirds of anemic children have another cause for their anemia. The minimum laboratory screening for iron deficiency is the Hgb level. Often, the simplest and most cost-effective measurement is a CBC, which includes the Hgb, Hct, NR 602NR 602 Midterm STUDY GUIDE EXAM LATEST UPDATE 2021/2022 BEST EXAM SOLUTION RATEDA+