Nr 602 Midterm Study Guide: Part 1

NR 602 MIDTERM STUDY GUIDE: PART- 1NR 602 MIDTERM STUDY GUIDE: PART- 1 TOPICS Covered o Chalazions o Blepharitis o Conjunctivitis o Hand-foot-mouth syndrome o Strep pharyngitis o Kawasaki disease o Rheumatic fever o Milia o Port-wine stain/Nevus flammeus o Salmon patch o Café-au lait spot o Impetigo o Molluscum Contagiosum o Verruca Vulgaris o Herpetic Whitlow o Hemanginoma o Otitis media o Otitis Externa CHALAZIONS – Benign, chronic lipogranulomatous inflammation of the eyelid Causes – blockage of the meibomian cyst Risk – hordeolum or any condition which may impede flow through the meibomian gland. Also mite species that reside in lash follicles Assessment – PAINLESS, NOT INVOLVING LASHES Lid edema, or palpable mass Red or grey mass on the inner aspect of lid margin Prevention – good eye hygiene Treatment – warm, moist compresses 3x per day Antibiotics not indicated because chalazion is granulomatous condition, if secondarily infected consider SULFACETAMIDE, ERYTHROMYCINFollow up – 2-4 weeks, if still present after 6 weeks follow up with ophthalmologist BLEPHARITIS – Inflamation/infection of the lid margins (chronic problem) 2 types – seborrheic (non ulcerative) : irritants (smoke, make up, chemicals) s&s – chronic inflammation of the eyelid, erythema, greasy scaling of anterior eyelid, loss of eyelashes, seborrhea dermatitis of eyebrows and scalp Ulcerative- infection with staphylococcus or streptococcus s&s – itching, tearing, recurrent styes, chalazia, photophobia, small ulceration at eyelid margin, broken or absent eyelashes ● the most frequent complaint is ongoing eye irritation and conjunctiva redness Treatment – clean with baby shampoo 2-4 times a day, warm compresses, lid massage (right after warm compress) For infected eyelids – antistaphyloccocal antibiotics BACITRACIN, ERYTHROMYCIN 0.05% for 1 week AND QUIONOLONE OINTMENTS For infection resistant to topical – TETRACYCLINE 250 MG PO X4 DOXYCYCLINE 100 MG PO X2 CONJUCTIVITIS – inflammation or irritation of conjuctiva Bacterial (PINK EYE) – in peds bacteria is the mosts common cause, contact lens, rubbing eyes, trauma, S&S – purulent exudate, initially unilateral, then bilateral Sensation of having foreign body in the eye is common Key findings – redness, yellow green, puru,ent discharge, crust and matted eyelids in am Self limiting 5-7 days. Eye drops – polytrim, erythromycin, tobramycin or cipro Improvement 2-4 days Most common organism H. influenza 7 Viral – adenovirus, coxsackie virus, herpes, molluscumS&S – profuse tearing, mucous discharge, burning, concurrent URI, enlarged or tender preauricular nose Antihistamines/decongestant Improvement, self limiting, 7-14 days Chlamydial – chlamydia trachomatis S&S – profuse exudate, associated with genitourinary symptoms, 1-2 weeks after birth Gonococcal – 2-4 days after birth, most concern can cause blidness PO azithromycin, doxycycline (tetracyclines increase photosensitivity, don’t use in pregnancy) Improvement 2-3 weeks Allergic – IgE mast cell reaction, environmental, cosmetics S&S – marked conjuctival edema, severe itching, tearing, sneezing Topical antihistamine or topical steroids Improvement 2-3 days Chemical –thimerosal, erythromycin, silver nitrate S&S conjuctival erythema, 30 minutes afer prophylactic antibiotics drops Avoid contact Can consider steroids Conjunctivitis never accompany vision changes Diagnostic studies: swap and scraping must be done, gram and Giemsa staining, ELISA, PCR testing, newborn 2 weeks needs to be tested for gonorrhea Non –pharm – clean towels, change pillows, warm compress, no contacts, no eye make up – mascara Gonococcal conjunctivitis: newborn – give Ceftriaaxone IM once (don’t give if hyperbilirubinemia, Non-gonococcal – erythromycin 0.5% ointment Consider fluorescein staining if abrasion suspected CDC recommends prophylactic administration of antibiotic eye ointment (ERYTHROMYCIN) 1 hour after delivery Refer to ophthalmologist if herpes, hemorrhagic conjunctivitis or ulcerations present May return to work/school 24 hours after topical HAND-FOOT-AND-MOUTH DISEASE – HIGHLY CONTAGIOUS, viral illnessclinical entity evidenced by fever, vesicular eruptions in the oropharynx that may ulcerate and a maculopapular rash involving hands and feet, the rash evolves to vesicles, especially on the dorsa of the hands and feet. Last 1 to 2 weeks. lesions appear on the buccal mucosa, palate, palms of hands, soles of feet and buttocs most common cause – COXSACKIE A 16 common in children 5 S&S – low grade fever, malaise, abdominal pain, enlarged anterior cervical nodes or submandibular Oral – small red papules on the tongue and buccal mucosa, which will progress to ulcerative vesicles EXANTHEM (papulovesicular) – occurs 1-2 days after oral lesions Differential – herpangina, Stevens- Johnson syndrome Treatment – maintain hydration, cool liquids, avoid spicy food, rest Topical aluminum hydroxide/ magnesium hydroxide gel with diphenhydramine applied to painful lesions Topical anesthetics – Kank A, Orabase Resolution with 7 days STREP PHARYNGITIS – An acute inflammation of pharynx/tonsils, associated with crowding (school) rare in children 3 Viral – rhinovirus, adenovirus, parainfluenza, Epstein-barr virus Bacterial- group A beta hemolytic streptococcus Risk – family hx of rheumatic fever, day care S&S – sore throat, tonsillar exidate, malaise Strep: cervical adenopathy, fever 102F, no cough or nasal congestion, petechiae on soft palate, ―Beefy Red‖ tonsils, ―sandpaper‖ rash (nose, neck and torso), abdominal pain, headache Suggestive of viral : conjunctivitis, nasal congestion, cough, diarrhea When cough - almost always exclude Streptococcus Tests – rapid strep test CBC: WBC shift to left Monospot if mono suspectedTreatment: gargling with salt water, change toothbrush, incubation period 2-5 days PCN – one IM or 10 days treatment PO First generation cephalosporins – 10 days treatment Azithromycin (if PCN allergy) Consult/referral – evidence of acute renal failure and reddish, tea collared urine (2-3 weeks post infection) No longer contagious after 24 hours on antibiotics, peak fever on days 2and 3, last 4-10 days KAWASAKI DISEASE (also known as mucocutaneous lymph nodesyndrome or infantile polyarteritis– an acute, febrile, immune-medicated, self-limited disease characterized by vasculitis. Leading cause of acquired heart disease in children 85% 5 years old most prevalent in Japan S&S Stage 1 -Acute (1-2 weeks) – high fever 103-105 for at least 5 days unresponsive to antibiotics, oral mucosa lesions may last 1-2 weeks, perineal rash, non-tender cervical adenopathy, painful rash and edema on feet Diagnosis requires fever for 5 days and 4 of these criteria: Edema or erythema of hands and feet, conjuctival injection (bilat), cervical adenopathy, rash (non-vesicular and polymorphous), exudative pharyngitis, diffuse oral arythema, STRAWBERRY TONGUE, crusting of lips and mouth Stage 2 - Subacute (2-8 weeks after onset) – without treatment: desquamation of palms, feet, periungual area, coronary artery aneurysm, joint aches and pains, acute MI may be seen, Pancardidis, diarrhea, jaundice, hepatosplenomagaly, platelet couns 10, 000 000 per mm Stage 3 – Convalescent – clinical signs have resolved, completed when all lab values are normal, however nail changes include Beau lines (deep transverse grooves across the nails)It is a fatal disease in small % of children who develop coronary artery problems despite treatment Differentials: Group A strep: scarlet fever Measles Epstein barr Toxic shock Rocky mountain spotted fever Steven-johnson syndrome Juvenile RA Tests: based on S&S and diff CBC, anemia, platelets 50% 450 000 ESR 100 C-reactive protein EKG – prolonged PR intervals, decrease QRS Chest Xray – dilated heart, pleural effusion Pyuria/mild proteinuria Pharmacology IVIG single dose of 2g/kg for over 12 hours in the first 10 days Aspirin 80-100 mg/kg/d in 4 doses (Reye’s syndrome) Complications MI Development and rupture of coronary artery aneurysm may lead to emboli, HF, heart valve problems, dysrhythmias, myocarditis RHEUMATIC FEVER – An inflammatory disease that develops in 1-3% of children who have untreated infection with group A strep (GAS). This can affect the heart, blood vessels, joints , skin, CNS, connective tissuesS&S – hx of pharyngitis 2-4 weeks prior onset of symptoms. Modified Jones criteria used to diagnose patient: 2 major, or 1 major and 2 minor criteria must be presented as evidence Major – carditis: 65% have with murmurs Polyarthritis:75% Chorea: 15% Erythema marginatum (macular rash with erythematous border Subcutaneous nodules Minor Fever 101-104F Artharlgias Elevated ESR, C-reactive protein Prolonged PR intervals on EKG Tests: throat cultures, negative antigen test ESR, C-reactive protein ASO tites EKG Chest xray CBC Treatment: first line PCN, if allergic Azithromycin Prednisone Aspirin AHA 2010 no longer recommends prophylaxis treatment for endocarditis in those with rheumatic fever PEDIATRIC BENIGN SKIN LESIONS MILIA (superficials cysts filled with keratin) – white papules found on the forehead, face, chin, and cheeks of infants, 1-2 mm in size, disappear few weeks after birth, may appear on palate – EPSTEIN’S PEARLS’SPORT-WINE STAIN (Nevus flammeus) – permanent defect that grows with child, if forehead and eyelids are involved, there is potential for multiple symptoms, includidng Sturge-Weber, Klippel-Trenaunay-Weber and Parkes Weber. Flat port wine stain- dark red to deep purple lesions present at birth, frequently found on face, do not fade with time SALMON PATCH – fade with time, usually by 5 or 6 years old, no treatment needed.Salmon patches (called a "stork bite" at the back of the neck or an "angel's kiss" between the eyes) are simple nests of blood vessels (probably caused by maternal hormones) that fade on their own after a few weeks or months. Occasionally stork bites never go away. CAFÉ AU LAIT SPOT – smooth, regular borders, Child 5, 6 or more , 1.5 cm - possible Von Recklinghausen’s disease (90 -100%) *LEOPARD syndrome (Lentigines, Electrographic abnormalities, Ocular hypertelorism, Pulmonary stenosis, Abnormalities of genitalia, Retardation of growth, Deafness In child 5 years, 5 or more , 0.5 cm suggests neurofibromatosis Smaller 1-4 cm in diameter I axillae ( axillary freckling or Crow’s sign) rare but diagnostic sign of neurofibromatosis HEMANGIOMA – (dilation of capillaries) – raised, cavernous: appear bluish, located deep beneath the skin, NOT present at birth, appear within a few month and then disappear before the end of first decade of life. Capillary- STRAWBERRY hemangiomas : bright red vascular overgrowth, elevated, vary in sizePossible steroids IMPETIGO – Superficial infection of the skin which begins as small superficial vesicles which rupture and form honey colored crust 2- 5 years Bullous – is caused by Staphyloccocus aureus or group A strep Non – Bullous – MRSA 1-2 mm vesicles which rupture and form honey colored crusts, weeping shallow red ulcer common on mouth, face, nose, or site of insect bites fluid filled vesicles 0.5 cm appear as red macules and papules or pustulesregional lymphadenopathy Treatment: good hygiene, hand washing Mupirocin (Bactroban) topical – 3x a day, don’t use 2 month Retapamulin (Altabax) - 9 months, apply thin film 2 x a day For large area- first generation cephalosporin, if unable to use PCN, consider macrolide Resolve within 7-10 days MOLLUSCUM CONTAGIOSUM Molluscum contagiosum is an infection caused by a poxvirus (molluscum contagiosum virus). The result of the infection is usually a benign, mild skin disease characterized by lesions (growths) that may appear anywhere on the body. Within 6-12 months, Molluscum contagiosum typically resolves without scarring but may take as long as 4 years. The lesions, known as Mollusca, are small, raised, and usually white, pink, or flesh-colored with a dimple or pit in the center. They often have a pearly appearance. They’re usually smooth and firm. In most people, the lesions range from about the size of a pinhead to as large as a pencil eraser (2 to 5 millimeters in diameter). They may become itchy, sore, red, and/or swollen. Mollusca may occur anywhere on the body including the face, neck, arms, legs, abdomen, and genital area, alone or in groups. The lesions are rarely found on the palms of the hands or the soles of the feet. The virus that causes molluscum spreads from direct person-to-person physical contact and through contaminated fomites. Fomites are inanimate objects that can become contaminated with virus; in the instance of molluscum contagiosum this can include linens such as clothing and towels, bathing sponges, pool equipment, and toys. Although the virus might be spread by sharing swimming pools, baths, saunas, or other wet and warm environments, this has not been proven. TREATMENT- Because molluscum contagiosum is self-limited in healthy individuals, treatment may be unnecessary. Nonetheless, issues such as lesion visibility, underlying atopic disease, and the desire to prevent transmission may prompt therapy. Other options for topical therapy include iodine and salicylic acid, potassium hydroxide, tretinoin, cantharidin VERRUCA VULGARIS - WARTpainless, benign skin tumors which are viral and can be transmitted by touch HPV 6 or 11 Common wart – rough surface, elevated, flesh-colored papules Avoid contact with wart exudate from self Treatment- paring and debridement of wart prior to any treatment Soak in warm water, occlude with waterproof tape for 1 week and leave open to air for 8-12 hours, then reocclude for 1 week Topical Duofil, Oclussal Hp must be applied up to 12 weeks CRYOTHERAPY with liquid nitrogen ( 5 second freeze until an ice ball forms Warts resistant to treatment - biopsy 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. ● Lesions occur in children of all ages, are contagious as long as they are present, and have an incubation period of 2 to 12 days.● Primary lesions usually occur before 5 years old, are more painful and extensive, and last longer. S&S - primary herpes, fever, malaise, sore throat, and decreased fluid intake - Deep-appearing vesicles on fingers Diagnostic Studies ● A Tzanck smear can be done on fluid from the lesions to identify epidermal giant cells, but does not distinguish HSV-1 from HSV-2. ● Viral cultures are the gold standard for definitive diagnosis. ● Direct fluorescent antibody (DFA) tests, enzyme-linked immunosorbent assay (ELISA) serology, and polymerase chain reaction (PCR) tests are usually only used with severe forms of HSV infection. Management ● Burrow solution compresses three times a day to alleviate discomfort ● Oral acyclovir 200 mg five times a day for 5 to 10 days may speed healing of herpetic whitlow ● Antibiotics for secondary bacterial (usually staphylococcal) infection: ● Offer supportive care, such as antipyretics, analgesics, hydration, and good oral hygiene ● Recurrent, frequent, and severe HSV infection may be treated with acyclovir prophylaxis for 6 month. Otitis media acute infection of the middle ear. RSV and influenza 2 viruses most responsible SX- rapid onsent of sx, ear pain, irritability, otorrhea, fever, bulging TM, decreased translucency of TM, erythema or amber is indicitve of effusion Risk factors- prematurity, unimmunized, breastfeeding less than 6 months, overweight, parental smoking, feeding in supine position TX- Tylenol or ibuprofen, topical analgesics (benzocaine/antipyrine otic drops), abx (amoxicillin or if amox in the last 30 days augmentin) watchful waiting for 48-72 hrs before prescribing OM w/ effusion- can occur after AOM, viral illness, barotrauma, allergies, or anatomic abnormalities. SX- fullness in the hear, hearing loss, dizziness, popping TX-3 month watchful waiting Otitis externa (swimmers ear)- inflammation of EAC that can involve pinna or TM. Result from damaged mechanical or chemical mechanisms, retained moisture acidic environment, chronic swimming pool, excessive cleaning of ears SX- pain with movement of tragus, swollen EAC making visualization of TM impossible, occasional regional lymphadenopathy, raised area of induration that can be deep and diffuse or superficial, red crusty or spreading lesions, thick otorrhea TX- ear drops with acetic acid or abx w/ or w/o corticosteroid, should improve in 7 days. Do not use neomycin, polymyxin or hydrocortisone drops if TM is not intact (can damage cochlea) Quinolones are effective against pseudomonas, aureus & pneumonia. Asthmachronic resp disease characterized by periods of coughing, wheezing, resp distress, and bronchospasm. Pathophysiology: result of immunohistopathology responses that produce shedding of airway epithelium and collagen deposits beneath the basement membrane. Factors that precipitate- viral/bacterial infections, exposure to known irritants, GERD, tobacco smoke, environmental changes, exercise, AR/sinusitis, drugs, food, allergies- dust, mites Sx- wheezing, continuous/persistent cough, long expiratory phase, diminished breath sounds, signs of resp distress- tachypnea, retractions, nasal flaring, accessory muscles, apprehension, drowsiness, tachycardia, cyanosis of lips Dx- o2 sat, PFT- spirometry FEV1- amount of air expelled in 1 sec FVC 75%- normal 80-120%- normal 60-75 mild obstruct 70-79%- mild 50-59% moderate obstruct 50-69%- moderate 49% severe obstruct 50%- severe Levels of Severity pg 567 Mild -Wheezing @ end of expiration or no wheezing -No or minimal intercostal retraction along posterior axillary line -slight prolongation of expiratory phase -normal aeration in al 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 -inspir and expir wheezing or no wheezing heard w/ poor air exchange -suprasternal retractions w/ abd breathing -decreased breath sounds throughout base Impending resp arrest -Diminished breath sounds over entire lung field -tiring, inability to maintain resp -severely prolonged expiration if breath sounds are heard -drowsy, confused See pg 572/573 for table and stepwise treatment. RSV Bronchiolitis RSVChildren less than 2Highly contagious, spread through resp droplets Sx- wheezing, URI sx, worsening cough, rhinorrhea, irritability Increase WOB, prolonged expiration, grunting intercostal retraction, nasal flaring Tx- supportaive, hydration nutrition Bronchiolitis-pg 817- disease that causes inflammation, necrosis, and edema of resp epithelial cells in lining of airways. Most commonly caused by respiratory syncytial virus (RSV). Common in children 2. Contagious, spread thru droplet. Sc- URI sx of cough coryza, rhinorrhea, progresses over 3-7 days, gradual resp distress noisy raspy breathing, audible exp wheeze, low grade to mod fever, decrease in appetite. Worsening fever with bacterial infection. Tachypnea, retractions, exp wheeze, fine/coarse crackeles Dx- CXR if needed. Tx- supportive care, supplemental O2 Growth and development Birth -1 month -may lose 5-8% of birth wt but should regain in 10-14 days. 10% requires close monitoring. Nutrition 110 kcal/kg/day -sleep 16/24 hrs day -Reflexes: sucking, rooting, asymmetric tonic neck, Moro, grasp- should be + and symmetric. -Head lag -Should orient to light and sound, self soothe -Vision 8-12in from face 1-3month -Growth spurt 6-8 wks. More defined sleep patterns 15-16 hrs day. -Fine motor skills: attempt to grasp, visible head control, lifting head off bed when prone. -More social, imitate parents expressions- social smile. Can self soothe @ 3 mo-Extension, nondirected hand swipes, rooting reflex 4-5 months 4-6 months, infant doubles birth weight. -Social smile -Begins babbling -More consistent sleep w/ 5 feedings and 1 @ night. Grasping and holding bottle. Roll, stronger head control with no head lag when pulled to sitting. -Hands to mouth, swing @ toys -Recognize parents meeting needs w/ breast or bottle.. Sleep thru night w/o feeding. 6-8 months -Teething around 6 mo-8 mo, 1st illness can erupt at this time. -Crawling. Growth may slow down with adding solids into diet. -Vocalization increases. “mama” “dada”-Use gestures (pointing, reaching). Stranger and separation anxiety may appear. Understands cause and effect relationship. -Introduce solid foods @ 6 mo. -Palmar grasp, pass things from hand to hand -Sits independently, rolls over, supports wt, bounces when held. 9-12 months -child proof house. -Separation anxiety/stranger -Understands simple commands, imitation, gives to on request, -Understands gestures like bye-bye/peek a boo -Feeds self/ Pincer grasp -Crawls and cruises around furniture, pull to stand, bears weight 12 mo: 15 mo -Can use sippy -Feeds self w/ spoon -Stands & walks independently -Drinks from cup -Points/clasps hands together -Follows commands -Knows @ least 3-4 words, knows name w/ gestures -Growth rate slows -knows 4-6 words *Health maintenance: check for anemia and lead 18 mo. 24 mo (2yr) -Turns page of book -Runs, throws, kicks -Walk up steps -uses spoon, scribble -Knows 10-20 words -2-3 word sentences -Point @ body parts -up stairs w/ same -Pushes & pulls toys foot -Walks well independently -Temper, “No” -Toilet training, transitional toy -Speech understood by family 36 mo (3yr) 42 mo (4 yr) -Full name, age, sex -Understand # -Speaks in complete sent. 3-5 words -Hops on foot -Knows 3 #’s and colors -Future & past tense -Copies a circle -Tells stories -Builds towers/rides tricycle -Copies a cross + -Imagination play -Little help w/ dress -“Oedipal stage”- interested in opposite sex -Group play, does not like to take turns or share-Speech understood by stranger 60 mo (5 yr) 6 yr (Kindergarten) -Counts 10 or more things -Rides bike -Speaks clearly -Copies triangle -Puts shoes on and ties laces -Ties shoes -Prints own name -Bathes self -Can draw person w/ 6 body parts 7-11( Middle Childhood) -Succeed in school and interact w/ peer group -Thinks of future PURPLE cryingPeak of crying Unexpected Resists soothing Pain-like face Long lasting Evening Fontanelles- 12 months- not palpapble. Anterior closes by 18-19 months Pediatric Physical Exam:  Gestational and birth history (including maternal gestational history, smoking, and illicit drug use)  Immunizations  Hospitalizations  Major illnesses or trauma (includes fractures, stitches, et cetera)  Family history of disease  Social: who the child lives with, members of the household in the home and ages, smoking in the home, electricity and clean water access, parents or guardians education and reading level, current school attending if appropriate, smoking,drug, or alcohol use in child, if appropriate, sexual activity in child, if appropriate, piercings or tattoos, if appropriate. -The American Academy of Pediatrics recommends well-child visits at 2 weeks and then at 2, 4, 6, 9, 12, 15, 18, and 24 months, annually up to age 6, and every 2 years from age 6 through adolescence2. Puberty (pg 121) -Biologic process that ultimately leads to fertility -Adolescence defintion: psychosocial & emotional transition from childhood to adulthood -onset of puberty until sexual maturity Females: earlier than males -ovaries increase in size, breast budding btw 9-10, breast buds 6 months before pubic hair, menstrual cycle 10-.5-14.5 yrs. Decrease in lean body mass and increase body fat. Males: initial sign is testicular enlargement avg age 11. Release sperm age 13.5-14.5, elong and widening of penis, rapid height growth, hair growth, increase muscle mass and lose body fat. 3. Tanner Stages[Leik Book pg 427] Stage Girls Boys Pubic Hair I Prepuberty Prepuberty None II Breast bud Testes enlarge Rugae on scrotum Sparse, few straight III Breast & areola- 1 mound Penis lengthens Tests continue to grow Darker, starts to curl IV Breast & areolasecondary mound Penis widens Thicker, curly, dark, coarse V Adult pattern Adult pattern Adult pattern, spreads to inner thigh and lower abd Adolescence 1. Early Adolescence (11-14yrs) 2. Middle Adolescence (15-17) 3. Late Adolescence (18-21) 4. Growth and Development (birth-17) -infant loses 5-8% of birth wt but should regain in 2 wks., double birth wt by 6 mo and triple birth wt by 12 mo. -Infant Weight: 0-6 mo- 6-8 oz/wk and 1 inch per month 6-12 mo- 3-4 oz/wk and ½ inch per month - Head circumference measured til 36 months , will increase by 12 cm first 12 months 5. Vaccinations Common side effects of vaccinations are as follows.  Localized erythema, swelling, and pain, particularly with DTaP and Varicella vaccines  Pain with injection  Low grade fever (Note that activation of the immune system will cause low grade fever, which is desired in vaccinations.) Currently, there is not enough evidence to establish that antipyretic use prior to vaccination has benefit and it may harm antibody response Vaccine contraindications in childhood:  Any secondary dose of a vaccine after severe allergic reaction to a prior vaccination.  If the patient has severe combined immunodeficiency (SCID), they should not have rotavirus, Varicella, measles mumps rubella (MMR), zoster, or live influenza virus vaccines. Live influenza virus should also not be used in children with asthma, diabetes, or cardiac or renal disease. Influenza inactivated injectable vaccine (IIV) can be used. -Live viruses not given until 12 months (not effective r/t immature immune system) EX: MMR and varicella (Vaccine Breakdown) Pneumonic 2 B DR HIP, 4 DR HIP, B DR HIP IN 6, 12 MAD HPV, VERRY DIM at 4-6, Tada human Men, Hep B: 1. Birth 2. 1-2 mo 3. 6-18 mo. Rotavirus: 1. 2 mo 2. 4 mo 3. 6 mo Dtap: 1. 2 mo 2. 4 mo 3. 6 mo 4. 16-18 mo 5. 4-6 yrs Hib: 1. 2 mo 2. 4 mo 3. 6 mo 4. 12 mo Pneumococcal (PC4): 1. 2 mo 2. 4 mo 3. 6 mo 4. 12-15 mo Inactivated polio (IPV) 1. 2 mo 2. 4 mo 3. 6-18 mo 4. 4-6 yrs MMR 1. 12 mo 2. 4-6 yr Varicella 1. 12 mo 2. 4-6 yr ----Flu vaccine can be given @ 6 mo.MIDTERM STUDY GUIDE PART TWO: - TOPICS COVERED o Diarrhea ▪ Acute ● Cryptosporidium- ▪ Chronic o C-difff o EColi o Rotavirus o Salmonella o Pyloric stenosis o Intussusception o Celiac disease o Juvenile idiopathic arthritis o Osteomyelitis o Juvenile rheumatoid arthritis o Dysplasia of the hip o Transient Synovitis of the hip o Legg-Calve’-Perthes Disease o Idopathic Scoliosis o Scoliosis o Osgood-Schlatter o Week-4, Lesson:2 o Contraceptives o Testicular torsion o Wilms tumor o Week-4, lesson:3 o Iron-deficicency anemia o Febrile seizureDiarrhea - Do not give hypotonic fluids to prevent hyponatremia - Diarrhea o Contains 10-90 sodium, 10-80 potassium, and 40 HCO3 o S& S of dehydration:- lack of external jugular venous filling when supine, sunken fontanelle, oliguria, AMS, decreased cap refill. ▪ Total body water makes 50-75% of total body mass ▪ Highest in infants and young children Acute Diarrhea ● is a disruption of the normal intestinal net absorptive versus secretory mechanisms of fluids and electrolytes, resulting in excessive loss of fluid into the intestinal lumen. ● This can lead to dehydration, electrolyte imbalance, and in severe cases, death ● In children younger than 2 years old, this translates to a daily stool volume of more than 10 mL/kg (this definition excludes the normal breastfeeding stooling of five or six stools per day). ● In children older than 2 years old, diarrheal stooling is described as occurring four or more times in 24 hours. The duration can last up to 14 days. Epidemiology ● Females have higher rates of Campylobacter species infections and hemolytic uremic syndrome; ● otherwise the incidence of cases shows no gender preference. Nontyphoidal Salmonella, Shigella, Campylobacter, E. coli organisms (bacteria); rotavirus, norovirus, ● In the United States, those most vulnerable include Native Americans and Native Alaskans, ● The most common viral pathogens are noroviruses and rotavirus, followed by adenoviruses and astroviruses. ● Food-borne bacterial or parasitic diarrheal diseases are most commonly due to Salmonella and Campylobacter species, followed by Shigella, Cryptosporidium, E. coli O157:H7, Yersinia, Listeria, Vibrio (Vibrio cholerae and other species), and Cyclospora species. potentially serious infection in the upper intestine indicators • Food-borne illness suspected • Bloody diarrhea, weight loss, dehydration, severe abdominal pain, and fever • Diarrhea lasting several days with more than three stools per day • Neurologic involvement on physical examination Diagnostic Studies Diagnostic studies are ordered if the symptoms of more serious infection are present. • Stool examination & Stool cultures • Electrolytes • CBC Management The foundation of all treatment of acute diarrhea is fourfold: • Restore and maintain hydration and correct/maintain electrolyte and acid-base balance. - Oral rehydration with an oral electrolyte solution should be attempted when dehydration is assessed between 3% and 9%. • Antibiotics are recommended for acute diarrhea caused by G. lamblia, V. cholerae, and Shigella species and can be considered for infections caused by E. coli(if infection prolonged), Yersinia for those with sickle cell disease, and Salmonella in young infants with fever or positive blood culture findings . - Children with HIV at risk for acute diarrhea may benefit from cotrimoxazole and vitamin A- Flagyl (1st line for c-diff) Amoxicillin (salmonella, shigella), azithromycin, vanco & Cipro (ecoli, c-diff), ceftriaxone. • loperamide in children older than 3 years old is safe and decreases the duration and frequency of diarrhea - Children younger than 3 years old and those who are malnourished, those with moderate or severe dehydration, those who are systemically ill, or those who have bloody diarrhea should not be treated with this drug - Some over-the-counter products intended for diarrhea contain salicylates (e.g., Pepto-Bismol), and there is concern for Reye syndrome. Cryptosporidium- microscopic parasite that causes the diarrheal disease S&S: watery Diarrhea, stomach cramps or pain, dehydration, Nausea, Vomiting, Fever, Weight loss Testing: stool sample TX: Nitazoxanide Chronic Diarrhea - Chronic diarrhea is defined as loose stools of less than 10 mL/kg/day in infants and less than 200 g/24 hours in older children. continuing diarrheal illness that started as acute diarrhea and is affecting growth. - TABLE 33-13 Common Causes of Chronic Diarrhea Seen in Children Age Conditions 0 to 6 months old • Carbohydrate malabsorption (acquired, congenital) (e.g., CMPI) • Protein hypersensitivity • Excessive intake of formula or other fluid (water, juice [especially those containing sorbitol/fructose], high-carbohydrate liquids) • Postenteritis • Infections • CF or other fat absorption conditions • Neuroblastoma (rare) • Immunodeficiency (e.g., HIV/AIDS and others) • Lymphangiectasia (rare) • Hirschsprung disease • Neonatal or infant enteropathies (rare) • Radiation treatments 7 to 24 months old First eight bulleted conditions listed above plus: • Chronic nonspecific diarrhea • Small-bowel overgrowth • Celiac disease • Graft-versus-host enteropathy • Autoimmune enteropathy • Radiation treatments24 months old • Excessive intake of fruit juice/high-carbohydrate drinks • Infections • Small-bowel bacterial overgrowth • Celiac disease • Munchausen syndrome by proxy • Grant-versus-host enteropathy • Carbohydrate malabsorption • IBS • Adult-type hypolactasia • Encopresis • IBD (e.g., Crohn disease) • Excessive use of laxatives • Radiation treatments • Acquired lactase deficiency in older children, primarily of African, Asian, or Middle Eastern descent • Perforated appendix History and Physical • Occurrence of three or more watery stools per day for more than 2 weeks; 10 watery/runny stools per day that often contain undigested food particles is more typical of ―toddler's diarrhea‖ • Presence of red flags: • Hematochezia or melena • Persistent fever • Weight loss or growth arrest • Anemia • Weight and height measurements; any weight loss • Growth retardation • Clubbing of fingers • Abdominal examination • Rectal examination (skin tags, impaction, tenderness) Diagnostic Studies • Stool: Culture, O&P (best done on three specimens collected on separate days), pH, reducing substances, occult blood, leukocytes, fat and fecal elastase (to evaluate for pancreatic insufficiency) (Normal stool pH greater than 5.5 indicates negative carbohydrate.) • CBC with differential, electrolytes, and albumin • UA and culture in young children The following are ordered as indicated by the history, physical examination, and consideration of differential diagnoses: • ESR, CRP • Hormonal studies to assess for secretory tumors (vasoactive intestinal peptide, gastrin, secretin, urine assay for 5- hydroxytryptamine [5-HT]) • Breath hydrogen test for lactose or sucrose intolerance (difficult to assess in infants) • Viral serologies, such as HIV or CMV • Sweat chloride test • Endoscopy, barium studies Management • Treat the underlying cause.• Chronic nonspecific diarrhea (toddler's diarrhea): Normalize the diet; remove offending foods and fluids; eliminate sorbitol and fructose-containing fluids; reduce fluid intake to no greater than 90 mL/kg/24 hours (give half of fluid as milk [whole or 2%]); increase fat to 35% to 40% of the diet; and increase fiber to bulk up stools. • Treat carbohydrate malabsorption by decreasing lactose or sucrose; add lactase or sacrosidase as indicated by particular carbohydrate intolerance. • Post-gastroenteritis malabsorption syndrome (evidenced in infants with weight loss and fat globules in the stool) can be given a predigested formula (e.g., Pregestimil or Alimentum), if tolerated, for 3 to 4 weeks (elemental formula can be used if those are not tolerated). Refer the following patients to a gastroenterologist: Newborns with diarrhea in first hours of life; patients with growth delay or failure or abnormal physical findings (anorexia, abdominal pain, chronic bloating, vomiting, or weakness); or those with severe illness. Pyloric stenosis Patho: - Pyloric stenosis is the narrowing of the lower portion of the stomach that leads into the small intestine. - The muscles of the stomach thicken, narrow the pylorus and prevent food from moving from the stomach to the intestine. - The environment and genetics play a role. sign and symptoms: - forceful projectile vomiting, olive shaped abdominal mass, visible peristalsis, weight loss, dehydration, fewer bowl movements, constipation, jaundice and lack of energy. diagnosis - included a firm olive mass in the mid abdomen - Blood tests, barium swallow and abdominal ultrasound Treatment - Pyloric stenosis is treated with IV fluids and then pyloromyotomy is performed. - This surgery uses an open or laparoscopic approach that opens up the tight muscle that caused the narrowing. - The outcome is great, there is only 1% chance for pyloric stenosis to occur Intussusception Pathophysiology ▪ Is a condition where the one section of the intestine folds into the another section of the intestine resulting in obstruction. The proximal bowel is trapped in the distal segment o The trapped bowel can exert pressure on the walls which squeezes the blood vessels and leads to ischemia and infarction Cause: ▪ Most cases are idiopathic, but many cases were associated with hyperplastic lymphoid tissue, suggesting an infectious cause, ▪ Predisposing factors include:- polyps, Meckel diverticulum, constipation, lymphomas, lipomas, parasites, rotavirus, adenovirus, and foreign bodies Risk factors: ▪ Infants between 6 and 12 months ▪ Male gender ▪ History of previous intussusception▪ History of intestinal malrotation ▪ Family history ▪ Prior viral illness Epidemiology - It is considered to be the most common cause of intestinal obstruction in children older than 3 months up to 6 years. ▪ In the US, intussusception occurs in 18 to 56 per 100,000 infants ▪ It most commonly occurs in infants between 5 and 10 months of age. ▪ 2/3 of the intussusception happens in infants under one year of age, but it even occur in adults Signs and symptoms ▪ Classical triad symptoms include intermittent/ colicky abdominal pain, vomiting, and bloody mucous stools characterized as ―currant jelly‖) ▪ Emesis is usually nonbilious. ▪ Other symptoms include lethargy, history of URI, fever, sausage like mass in the right upper quadrant or in right lower when abdomen is empty, tender and distended abdomen Diagnostic Studies ▪ The most accurate diagnostic tool recommended is an abdominal ultrasound. ▪ It shows ―bull’s eye‖ which is telescoped intestine on end. ▪ Other diagnostic tools such as x-ray , CT, and Air contrast enema can also be used Management ▪ Intussuception can develop suddenly putting the infant at a potential risk for developing ischemia and possible infection and even sepsis. Therefore, rapid treatment is necessary. ▪ MEDICAL EMERGENCY ▪ Rehydration and correction of electrolyte imbalance is very important. ▪ After correction of dehydration and electrolyte imbalance, the gold standard is radiologic reduction via air contrast enema under fluoroscopy ▪ The Outcome of air or contrast enema reduction is 100% cure, but 10% recurrence has been identified. ▪ Surgical reduction is also associated with a recurrence rate of 2 to 5%. Celiac disease ● Malabsorption syndromes can be caused by many different genetic, congenital, and acquired conditions and usually lead to an initial decrease in weight followed by a deceleration in height velocity. ● Celiac disease is an immune-mediated systemic disorder triggered by dietary exposure to wheat gluten and related proteins in barley and rye. ● It is characterized by the presence of a variable combination of gluten-dependent clinical manifestations, celiac disease–specific antibodies, HLA-DQ2.5 or HLA-DQ8 haplotypes, and enteropathy. ● Celiac disease has a worldwide distribution with overall prevalence of 1% Risk factors - Demographic changes - Increased gluten exposure - infants born by cesarean section; - The most typical presentation occurs between 6 months and 2 years old.Parent reported gastroenteritis occurring at the time gluten was introduced into the child's diet does not appear to be associated with celiac disease. Clinical Findings • Chronic or intermittent diarrhea, persistent or unexplained GI symptoms (e.g., nausea and vomiting), sudden or unexpected weight loss, and prolonged fatigue. • Delayed puberty can coexist with malabsorption, Impaired growth, FTT, unexplained iron deficiency anemia, abdominal distention, bloating or cramping pain • May have no symptoms at all despite evidence of small bowel changes; ● maintain a high suspicion for celiac disease in children with metabolic bone disease (such as rickets or osteomalacia), low-trauma fractures, or those with dental enamel defects. ● An estimated 85% to 90% of individuals with celiac disease are undiagnosed • Pallor, fatigue, hair and dermatologic abnormalities, digital clubbing, dizziness, cheilosis, glossitis, peripheral neuropathy (symptoms of vitamin deficiency seen with malabsorption), Skinfold thickness and lean body mass Diagnostic Studies • See chronic diarrhea tests 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 ● EMA is more expensive and less accurate in children younger than 2 years old • Home blood testing is not recommended ● 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 • Careful follow-up of growth parameters, tTGA testing after 6 months of gluten-free diet (GFD), and then yearly • 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 ● Adding pure oats to a GFD can improve palatability and increase fiber and vitamin B intake without causing a systemic or autoantibody response Complications and Prognosis ● Growth failure is the primary complication of celiac disease. ● 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 ● 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.Diarrheal Illnesses Due to Common Bacterial or Vial Pathogens 1. Rotavirus Incubation Period: 1 to 3 days; prevalent during cooler months in temperate climates Signs and Symptoms: 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 Duration of illness: 3 to 8 days Route of Transmission: Fecal-oral; viable on inanimate objects; rarely contaminated water or food Laboratory Testing: Enzyme immunoassay and latex agglutination assays for group A rotavirus antigen; virus can be found by electron microscopy and specific nucleic acid amplification methods. Treatment and Complications: Supportive care: May need to correct dehydration and electrolyte imbalances. Oral IG has been used in those immunocompromised. Preventive care: Rotavirus vaccine; hygiene and diapering precautions in day care facilities. 2. Salmonella Incubation Period: 1 to 3 days Signs and Symptoms: Diarrhea, fever, abdominal cramps, rebound tenderness, vomiting. S. typhi and S. paratyphi produce typhoid with insidious onset characterized by fever, headache, constipation, malaise, chills, and myalgia; diarrhea is uncommon, and vomiting is not usually severe Duration of illness: 4 to 7 days Route of Transmission: Contaminated eggs, poultry, unpasteurized milk or juice, cheese, contaminated raw fruits and vegetables (alfalfa sprouts, melons) S. typhi epidemics are often related to fecal contamination of water supplies or street-vended foods Laboratory Testing: Routine stool cultures; positive leukocytes and gross blood. CBC: WBC can be slightly ↑ with left shift, ↓, or normal. Treatment and Complications: Supportive care: Only consider antibiotics (other than for S. typhi or S. paratyphi) for infants 3 months old, those with chronic GI disease, malignant neoplasm, hemoglobinopathies, HIV, other immunosuppressive illnesses or therapies.If indicated, consider ampicillin or amoxicillin, azithromycin, or TMP-SMX; if resistance shown to any of those, use IM ceftriaxone, cefotaxime; or azithromycin or quinolones. A vaccine exists for S. typhi in certain cases. 3. Clostridium difficile Incubation Period: Unknown Signs and Symptoms: Variety of symptoms and severity are seen: mild to explosive diarrhea, bloody stools, abdominal pain, fever, nausea, vomiting Mild to moderate illness is characterized by watery diarrhea, low-grade fever, and mild abdominal pain Duration of illness: During or after several weeks of antibiotic use; can occur without being associated with such treatment Route pf Transmission: Acquired from the environment or from stool of other colonized or infected people by the fecal-oral route Laboratory Testing: Stool cultures; enzyme immunoassay for toxin A, or A and B; positive gross blood, leukocytes; CBC: ↑ WBCs; ESR normal Treatment and Cmoplications: Discontinue current 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 (drug of choice in children) or vancomycin for 7 to 10 days. Supplement with probiotics. Lactobacillus GG, Saccharomyces boulardii are recommended (Jones, 2010; Shane, 2010). Complications include pseudomembranous colitis, toxic megacolon, colonic perforation, relapse, intractable proctitis, death in debilitated children 4. Enterotoxigenic E. coli(ETEC) and enteroadherent E. coli (frequent cause of traveler's diarrhea) Incubation Period: 1 to 3 days Signs and Symptoms: Watery diarrhea, abdominal cramps, some vomiting; often cause of mild traveler's diarrhea Duration of illness: 3 to 7 days Route of Transmission: Water or food contaminated with human feces Laboratory Testing: Stool culture. ETEC requires special laboratory techniques for identification. If suspected, must request specific testing.Treatment and Cmoplications: Supportive care: Antibiotics are rarely needed except in severe cases. Recommended antibiotics include TMP-SMX and quinolones. See 5. Enterohemorrhagic Escherichia coli(EHEC) including E. coli O157:H7 and other Shiga toxin– producing E. coli(STEC) Incubation Period: 1 to 8 days Signs and Symptoms: Severe diarrhea that is often bloody, abdominal pain and vomiting Usually little or no fever, More common in children 4 years old Duration of illness: 5 to 10 days Route of Transmission: Undercooked beef, especially hamburger, unpasteurized milk and juice, raw fruits, vegetables (e.g., sprouts, spinach, lettuce), salami (rarely) Contaminated water; petting zoos Laboratory Testing: Stool culture; E. coli O157:H7 requires special media to grow. If E. coliO157:H7 is suspected, specific testing must be requested. Shiga toxin testing may be done using commercial kits; positive isolates should be forwarded to public health laboratories for confirmation and serotyping. Stool grossly positive for blood. Treatment and Cmoplications: Supportive care: Monitor CBC, platelets, and kidney function closely. E. coli O157:H7 infection is also associated with HUS, which can cause lifelong complications. Studies indicate that antibiotics may promote the development of HUS.Juvenile idiopathic arthritis and osteomyelitis Condition Age pain Historical Findings Clinical Findings Causative Factors Management Juvenile arthritis (JA) Child to 16 yearo f age + Fever, rashes, ↑ WBCs; some iritis; joint stiffness and swelling; S&S 3 months Mono- /polyarticular arthropathy; + ANA (25% to 88%); ↑ ESR in moderate/sev ere JA Unknown; genetic (HLA) or environmen tal Treat with NSAIDs initially; may need sulfasalazine , methotrexate ; corticosteroi ds; joint replacements when older Acute Hematogenou s osteomyelitis Toddler, child, adolescen t + Varied: malaise, low-grade to high fever; may have severe constitution al symptoms; toxicity Refusal to walk or move limb; point tenderness; limp; 7 to 10 days to see radiographic bony changes; 25% ↑ WBCs; ↑ CRP S.aureus Organism (Likely) Appropriate antibiotic coverage (generally 7 days, IV; 4 to 6 weeks total or until ESR normal) Juvenile Idiopathic Arthritis ● Also as juvenile rheumatoid arthritis (JRA), now encompasses several disorders that have a common feature of arthritis. ● 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 Juvenile Idiopathic Arthritis Subtypes and Clinical Joint Characteristics Juvenile Idiopathic Arthritis Subtype Clinical Joint CharacteristicsOligoarticular 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 Most forms of JIA have unclear ● environmentally induced in genetically predisposed individual. ● Human leukocytic antigen (HLA) class I and II alleles have been associated with JIA ● An environmental trigger, such as infection or trauma, is also important in the pathogenetic process in JIA. Systemic juvenile idiopathic arthritis (SJIA) ● does not have HLA gene association, ● may be the result of an autoinflammatory response from the innate immune system. ● The female to male ratio in systemic onset is equal Oligoarticular and rheumatoid factor (RF)-positive polyarticular JIA ● there is autoimmunity with involvement of the adaptive immune system ● The presence of positive ANAs and RF is associated with HLA genes. ● Approximately 1 in 1000 children are affected with oligoarticular JIA, the most common arthritic subtype. ● The rate of JIA is significantly higher in girls than in boys, typically in oligoarticular and pauciarticular JIA.● The approximate percentage of occurrence and age breakdown for each of the subtypes follows: systemic (10%) occurs at any age; polyarticular (40%) has a late (6 to 12 years old) or early childhood (1 to 4 years old) onset; and oligoarticular (50%) has a late or early onset. ● Adolescents tend to have more RF-positive disease Clinical Findings • Pain—generally a mild to moderate aching • Joint stiffness—worse in the morning and after rest; arthralgia may occur during the day • Joint effusion and warmth, tenderness • Non-migratory monoarticular or polyarticular involvement of large or proximal interphalangeal joints for more than 3 months • Systemic manifestations—anorexia, fatigue fever, salmon-colored rashes, leukocytosis, serositis, lymphadenopathy, and rheumatoid nodules, uveitis - growth failure, or leg-length discrepancy if unilateral. • Loss of joint range of motion and function; child typically holds the affected joints in slight flexion and may walk with limp Diagnostic Studies - JIA is a diagnosis of exclusion. - physical findings and history of arthritis lasting for 6 weeks or longer. o polyarticular and systemic-onset typically have elevated acute-phase reactants and anemia of chronic disease. o positive RF occurs in less than 10% of children with JIA and rarely in those with SJIA. o ANA may be present in up to 50% of children with oligoarticular disease o The anti-CCP antibody test is highly specific in polyarticular JIA o 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. o Imaging studies (MRI) can help in managing joint pathologic conditions. o Analysis of synovial fluid is not helpful in the diagnosis of JIA. Management o Ophthalmology referral and evaluation is critical in a child with a positive ANA (Uveitis) o The main treatment goals are to suppress inflammation, preserve and maximize joint function, prevent joint deformities, and prevent blindness. o there is no curative treatment o Aggressive early treatment to induce a remission is a key consideration in JIA management in order to prevent deformity and improve o Aspirin therapy has largely been replaced with the use of nonsteroidal anti-inflammatory drugs (NSAIDs). o NSAIDs: Children with oligoarthritis generally respond well to NSAIDs o Ibuprofen: 30 to 40 mg/kg/day three to four divided doses (maximum single dose is 800 mg; maximum daily dose 2400 mg/day) o Naproxen, Indomethacin, Celecoxib (Older than 2 years old and adolescents) o Oral, parenteral, intraarticular corticosteroids: o Disease-modifying antirheumatic drugs (DMARDso Nonbiologic DMARD treatment: methotrexate, sulfasalazine, leflunomide (managed by pediatric rheumatologist) o Physical therapy—range of motion muscle-strengthening exercises and heat. Rest and splinting are used if indicated. passive, active, and resistive exercises o Ophthalmologic follow-up every 3 months for 4 years (even if it has resolved) for all ANApositive JIA children. The disease process of JIA wanes with age and completely subsides in 85% of children; however, systemic onset, a positive RF, poor response to therapy, and the radiologic evidence of erosion are associated with a poor prognosis. Onset of disease in the teenage years is related to progression to adult rheumatoid disease. Dysplasia of the hip ● The femoral head and the acetabulum are in improper alignment and/or grow abnormally. ● Includes:- dysplastic, subluxated, dislocatable, and dislocated hips. ● Dysplasia is characterized by a shallow more vertical acetabular socket with an immature hip/acetabulum. ● Dysplasia may be diagnosed many years after the newborn period. Risk factors o hormonal effect of maternal estrogen and relaxin that are released near delivery and produce a temporary laxity of the hip joint. o Mechanical factors in utero o This is seen with first pregnancy, oligohydramnios, and breech presentation, 4x more in girls, positive family history (genetic risk factors) increases o Increased in cultures swaddle infants in extended position or cradleboard placement o In the newborn, the left hip is most often involved because this hip typically is the one in a forced adduction position against the mother's sacrum. o 60 to 80% of abnormal hips of newborns resolves by 2 to 8 weeks (self-limiting, but close observation) Clinical Findings. In the older infant, 6 to 18 months old: • Limited abduction of the affected hip and shortening of the thigh is a reliable sign ● Normal abduction with comfort is 70 to 80 degrees bilaterally. ● Limited abduction less than 60 degrees of abduction or unequal abduction ● Positive Galeazzi sign ● Asymmetry of inguinal or gluteal folds- NOT thigh-fold ● 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 • 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 ● A waddling gait may also be noted.Diagnostic Studies ● Screening tests are serial physical examinations of the hip and lower extremities. ● Barlow and Ortolani tests are used to screen for DDH in neonates. o Less reliable after 2-3 months ● Klisic and Galeazzi tests are used to screen older infants. ● Routine ultrasonography is not recommended; however, an ultrasound should be obtained if there is a high index of suspicion of dysplasia based on a positive clinical examination. ● Ultrasound recommended for infants after 4 weeks of age. (before 4 weeks false-positive results) ● Radiologic evaluation of the newborn to detect and evaluate DDH is recommended once the proximal epiphysis ossifies, usually by 4 to 6 months o AP and lateral Lauenstein (frog-leg) position radiographs of the pelvis are indicated. 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. ● Early phase is a Pavlik harness. - The harness is worn 24 hours a day, except for bathing. - seen weekly to ensure it fits properly - 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. ● The 6- to 18-month-old infant with a dislocated hip is likely to require either closed manipulation or open reduction. o Preoperative traction, adductor tenotomy, and gentle reduction are especially helpful in preventing osteonecrosis of the femoral head. o After the closed or open reduction, a hip spica cast is applied o Annual or biennial follow-up including radiographs o 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. o The Ortolani test should only be used in the first 2 to 3 months of age. Transient Synovitis of the hip pg 1079 Self-limited inflamm disorder of the hip, common in boys, r/o septic arthritis Cause-inflammatory rx, URI, unknown Sx-mild to mod fever, irritability, limited hip motion, ESR 25 mm/h3-8 year olds Tx- rest Legg-Calve’-Perthes Disease self-limiting disease of femoral head comprising of necrosis, collapse, repair and remodeling -Cause-familial, breech birth, prior trauma Sx- acute or chronic onset, pain in hip, groin, knee stiffness (male). + trendelenburg, shortening, decreased abduction, internal rotation, hip extension, + radiographs but not early Tx- BR, traction, PT, brace surgery may be needed Idopathic Scoliosis pg 1057 Occurs in adolescence, mild curve, sexes -lateral curve of the spine in the frontal plan Dx- Cobb method that measures angle btw superior and inferior end vertebrae Cause-usually unknown that’s why termed idiopathic, may have familial or genetic---most common type Infantile 0-3 Juvenile 3-10 Adolescent 11 and up Generally painless and insidious onset. Adam’s forward bend test---unequal shoulder height, scapula prominences, waist angles, rib heights. Dx-AP and lateral spine, cobb angle, MRI for underlying cause Tx-goal is to delay spinal fusion, observation for less than 20 degree, bracing or surgery for larger curve Scoliosis Osgood-Schlatter pg 1068 -caused by micotrauma in deep fibers of patellar tendor @ insertion to tibial tuberosity Dx- clinical h & p Hx- recent physical activity, pain increase during and immed after, running/jumping/kneeling/squatting, and up and down stairs exacerbates Physical exam- pain reproduced by extending need against resistance, stressing quad, squatting with knee full flexed, focal swelling, heat and point tenderness, full ROM of knee Tx-self-limiting, modifying activity, ice/cold, stretching, NSAIDs, neoprene sleeveWEEK-4: LESSON-2 Endocrine malfunction can lead to delays in growth, short stature, significant illness, developmental or cognitive impairment or delays, and even death ● At birth: Routine state newborn screenings should test for endocrine diseases like congenital hypothyroidism and congenital adrenal hyperplasia (CAH). ● At each well child exam: At each well-child exam, the child should be monitored appropriately for height and weight, HC, growth velocity, and rapid changes in weight loss or gain. These are important screenings for endocrine disorders. ● well-child assessment should include tanner staging of breasts and genitals, along with pubic and axillary hair development. o Height measured standing after age 2 if possible o Infants should only be measured with a dry diaper on and supine length must be accurate and possibly measured more than once. ● Endocrine system to function properly not only must the endocrine organs themselves be working, but also the neurologic and central nervous systems. ● There are seven classic endocrine glands; the pituitary, thyroid, parathyroid, testes, ovaries, adrenal (cortex and medulla), and endocrine pancreas. ● Hormones released from an endocrine gland either work directly on the gland itself, or travel through circulation to target tissue and cells where they exert action on the cell or cell nucleus directly. ● The hypothalamus and pituitary gland of the brain are critical to this process because the hypothalamus stimulates the pituitary gland action. Delayed Puberty: Males • No secondary sexual characteristics by 14 years • 5 years since first signs of puberty to Tanner V • Causes: constitutional growth delay, primary or secondary gonadal failure, malnutrition or disordered eating, Klinefelter’s syndrome Delayed Puberty: Females • Evaluated if no pubertal signs by 13, or no menarche by 16 • Failure to complete development Tanner V within 4 years of onset of secondary sex characteristics • Most common cause: constitutional growth delay (delayed skeletal muscle growth) • Other causes: Turner’s Syndrome, extreme athleticism, disordered eating, primary or secondary gonadal failure. Precocious Puberty - Pubertal development prior to normal age of onset GIRLS: • Before 8 years old in Caucasian, 7 years old African-American and Latino • Pubertal onset advanced in obesity • Central: Breast development, followed by pubic hair growth, menarche *Note that girls who are obese can have breast bud development without other signs of puberty. BOYS:• Secondary sexual characteristics prior to age 9 BOTH Bone age on X-ray will be older than chronological age. • Treatment in both is medications to stop stimulation of their hypothalamus-pituitary-adrenal axis. Contraceptives Epidemiology ● Unintended pregnancy rates are highest among poor and low-income women, women aged 18–24, cohabiting women and minority women • Rates tend to be lowest among higher-income women, white women, college graduates and married women. • highest rate of unintended pregnancy was seen among women 20 to 24 years of age, followed by women 18 to 19 and women 25 to 29 years of age. • IUCs, implants, and sterilization are considered a ―top-tier‖ method because less than 1 pregnancy per 100 women occurs in a year with the use of these methods. • These methods are more effective in preventing pregnancy than the second tier methods, not due to their mechanisms of action, but because they are easier to use properly. Once the top tier methods are initiated, they require little additional action to provide highly effective contraception. Sterilization • Vasectomy is an outpatient surgical procedure for male sterilization. - The failure rate of vasectomy is very low—0.10 % with perfect use and 0.15 % with typical use. - Vasectomy is cheaper, safer, and more effective than female sterilization• Traditional tubal occlusion o A surgical procedure (either by minilaparotomy or laparoscopy). o Requires a small abdominal incision and general or regional anesthesia. o Occlusion techniques include tying (ligating) and blocking with mechanical devices, such as clips or rings and cauterizing. o Typical failure rates are less than 1%. • Newer tubal occlusion: transcervical sterilization (nonsurgical methods)Essure: o Employ micro-inserts that expand and occlude the fallopian tubes as tissue grows in and around the insert. o Involve a half-hour procedure, using a hyster