PEDIATRICS NOTES
Professionalism
 Various definitions for professionalism:
o (1) Lifelong developmental process that informs the effective, ethical, & safe practice of healing skills.
 Importance of professionalism:
o Types of professionalism lapses:
 Minor: degrading of professional colleague/patients/family, expressed hostility of the system, expressing oneself or acting in a negative way
(what about toxic positivity?)
 Major: institutional/public attention
 boundary issues – sexual misconduct w/ patients or parents
 conflict of interest – collaboration w/ industry goes against primacy of patient care, overutilization of services, acceptance of gifts
 confidentiality – failure to keep medical data private
 impairment, - drug/etoh abuse or mental illness detract from professional behaviors
 misrepresentation – board certification or other achievements are falsely claimed
 greed – see conflict of interest
 Key elements of professionalism
o Professionalization
o Professional conduct: way a professional acts in daily interactions w/ patients, colleagues, institutions, community, society.
o Cultural sensitivity
 Teaching professionalism: Good role models are most important source.
 Assessing professionalism
o There are many methods of assessing professionalism, including
 monthly rotational formative and summative evaluations
 mini-evaluation exercises
 multisource feedback
 peer assessments
 professionalism scorecards
 parent/patient assessments
 portfolios of positive and negative reports
 Self-assessments
 OSCEs (objective structured clinical examinations)
 Professionalism vs humanism
o Humanism = spirit by which we achieve professionalism. Caring, empathetic, humble
o The article doesn’t distinguish when humanism might come in conflict with professionalism.
 Burnout  Lapses in Professionalism
o Burnout = emotional/physical fatigue, depersonalization, ↓ self-worth or self-efficacy; caused by XS work, lack of flexibility perfectionism/fear of
error, imbalanced effort: reward ratios, goal misalignment.
o Interventions to avoid burnout:
 Individual: mindfulness, stress management,
 Systemic/organizational: small-group discussions, duty-hour limitation, locally-developed modifications to clinical work processes
Infant Formulas
 Objectives:
o 1. Describe macronutrients in infant formulas used as substitutes for hman milk for term vs preterm infants
o 2. ID appropriate clinical applications of infant formulas that have altered nutrient contents based on physiologic significance of specific
changes in formula composition
o 3. Discuss the physiologic role & potential health benefits a/w 4 components added to infant formulas in the past decade.
o 4. Delineate current regulatory guidelines defining standars for composition, performance, & safety criteria for commercial infant formulas
 Historical background:
o Late 1800s: infant formulas start to be developed – cow milk + added products with understanding that alterations were needed to improve
acceptability for human consumption
o 1941: Government regulation of infant formulas in US begins
o 1980: Barter-like syndrome episdemic (hypochloremic, hypokalemic metabolic alkalosis) occurs 2/2 chloride-deficient soy formula  Infant
Formula Act of 1980 & 1986 amendments define minimum concentrations of 29 nutrients, quality control standards.
o 2004: IOM (Institute of Medicine) establishes regulatory + research procedures to assess safety of potential new ingredients in infant formulas
as manufacturers compete a/g one another in creating formula mimicking breast milk
o Cronobacter sakazakii – (formerly Enterobacter sakazakii)
 Infants: causes sepsis or severe meningitis  seizures c/ bbrain abscesses, infarcts, hydrocephalus, etc  long-term neurologic problems
w/ mortality rate as high as 40%. Linked to babies who consume powdered formula.
 Abbott laboratories recently closed 2/2 infection w/ this organism (May 2022) – FYI Abbott Labs produces Similac
 No comprehensive mechanism for detecting or investigating Cronobacter infections; only 1 state Minnesota req docts to
report cases to CDC.
 Formulas for Term Infants
o Cow-Milk Based
 Standard infant formulas = 20 kcal/oz = 67 kcal/dL
 Exist as powder or liquid concentrates to be mixed w/ water to yield caloric densities b/w 20-30 kcal/oz.
 Protein:
o Human breast milk = higher whey-to-casein ratio (70:30)
o Bovine milk whey-to-casein ratio = 18:82
 Casein forms large curds on exposure to gastric acid
 Whey is resistant to precipitation & has more rapid passage thru GI tract
o Infant formulas have been designed to modify why:casein ratios; they contain 50% higher total protein content (2.1 – 2.2 g/100
kcal) than human milk + supplemental taurine (why?)
 Different formulas – whey-predominant (60:40), casein predominant (20:80), 100% whey
o
o
o
o
 All have been show to support normal growth patterns in both term & preterm infants
o ***Note whey in cows vs humans have different compositions & functions (source?)
o Amino acid serum profile differences in infants – significance is unclear.
 Carbs
o Lactose = primary carb in cow milk-based formulas and human milk.
o A/t
 Fats:
o Based on strong research evidence, formulas supplemented with LCPUFAs = long-chain polyunsaturated fatty acids s.a. DHA
(Docohexaenoic acid) (between 0.3% and 0.5% of total fatty acids) and at least equal amounts of ARA (arachidonic acid) are
beneficial for visual and neurological development.
o More studies are needed to define better the benefits and the correct dose needed for supplementation.
 Vitamins/Minerals
o TLDR = use iron-fortified formulas as iron in bovine milk is less bioavailable than in human milk (20-50% in human milk vs 47% in bovine milk)
o Fortified formulas contain 1.8 mg/100kcal Fe vs 0.45 – 0.9/100kcal in human milk
 Nucleotides:
o Conditionally essential during periods of rapid growth given immunomodulating capabilities  enhances growth for SGA infants,
promotes IgA & IgM concentrations in pretrerm infants, ↓ incidence of diarrheal disease, &enhances Ab response to certain
vaccines
 Prebiotics, probiotics, & Synbiotics:
o Bacteria differences in breastfed vs formula-fed infants:
 Human milk: Bifidobacterium + Lactobacillus
 Promote nutrient absorption, protect a/g pathogen colonization, development of intestinal & systemic immune systems,
acquisition of mucosal tolerance.
 Formula-fed infants = Bifidobacterium, Lactobacilus, Bacteroides, Enterobacteriacea, Clostridium, Streptococcus
o Prebiotics = nondigestible schort-chain carbs (galacto-oligosaccharides, fructo-oligosaccharides, or lactulose) that promote
growth & fxn of specific spp of bacteria.  concentrations of Bifidobacteria & Lactobacilli in stools of preterm & term infants.
 Clinical note: Fermentation of prebiotics in the colon  acidic, more frequent, & looser stools but are safe at prescribed
doses.
o Probiotics = live cultures that survive digestion & colonize the colon  colonic microbiotia
o Synbiotics = combos of prebiotics & probiotics. Allow for notrmal growth in infancy.
o Evidence that prebiotics + probiotics may be used for prevention & treatment of allergy (eczema, cow-milk protein
allergy) esp in high-risk infants (parent or sibling w/ atopY)
o Probiotics important in the prevention of NEC in VLBW infants association of infant formula with NEC is huge (currently
ongoing suits in the US); use of probiotics  ↓ NEC incidence by 30% but no Δs in mortality or sepsis.
 Concerns about probiotic safety: risks for transmission of antibiotic resistance, negative effect on neurodevelopment (?) –
while effective to reduce NEC, further research needed to discover effective type of probiotics, dose, & duration of probiotic
therapy.
 Efficacy in ELBW infants: inconclusive
Preterm infant formulas:
 24 kcal/oz = 80kcal/dL + supplemental taurine, 3-3.3 g/100kcal of whey-predominant protein
 Fat & carb composition designed to overcome nutrient loss from ↓↓concentrations of lipase, bile salts, & intestinal lactase;
 Fats: MCT (medium chain triglyceride) oil provides 40-50% of total fat; MCT is absorbed directly into portal vascular system & doesn’t
depend on availability of bile acids for micelle solubilization.
 Carbs: Lactase concentrations do not reach maximal values until 8-12 weeks post-term, carbs given in a 60:40 or 50:50 mix of
glucose polymers lactose to promote calcium absorption & as a prebiotic (note that calcium intake is done during the third trimester,
and preterm babies will be physiologically hypocalcemic)
 Minterals + vitamins: Higher concentrations esp of Ca, PO43--, Vit A, Vit D. These may be XSive if consumed > 12 oz/day (3560 mL) &
risk  as infant’s weight approaches 2 kg.
 Discontinue preterm formulas prior to hospital discharge.
Preterm Transitional Formulas:
 Marketed to bridge gap b/w preterm & term formulas  22kcal/oz or 73 kcal/dL to be switched at 1800-2000 g or 34 weeks GA.
 Babies are continued until 6-9 mo of age.
 Achieve Vit/min goals w/o additional supplementation but data on neurodevelopment has been disappointing – no evidence t hat fedding
enriched vs standard formulas to premies a/f discharge  improvements in growth or neurodevelopment by 18 mo.
Human Milk Fortifiers:
 Esp in VLBW infants (<1500 g) human milk inadequate for nutritional needs of premies
 Fortifieres contain protein, carbs, fat, & up to 23 vit/minerals matching growth & metabolic effects of preterm infant formulas
 Adverse effect – XS intake of certain nutrients known potential for toxicity
 Clinical practice: use fortifiers + standard infant formulas to fortify milk in premies who have progressed beyond specific age, weight, and
intake volumes.
Soy formulas:
 NOT RECOMMENDED FOR PRETERM INFANTS
 Soy phytates have high binding affinity for Ca, P, Zn, & Fe & interfere w/ intestinal absorption  ↓ bioavailability  osteopenia
 Soy formulas have  [Al] which competes w/ Ca for absorption  osteopenia
 Adverse effects/questions:
 Concerns about  [isovlavones/phytoestrogens]  bind to estrogen receptors & reported to have negative effects on estrogenrelated functions in animal studies but results are conflicting and may be species-speciic; retrospective follow-up study showed no
reproductive or estrogen -related adverse effects in adults fed soy formula exclusively as infants.
 When to use:
o
o
 Limit use of soy formulas > 6 mo of age w/ signs c/w IgE-mediated allergy a/f successful clinical challenge (soy formulas do not have
lactose & are indicated when strict lactose avoidance is required) as is the case of congenital lactase deficiency or in the
management of galactosemia.
 Any lactose-free formula may be used in transient lactase deficiencies s.a. postviral enteropathies
 Strict vegetarian families may prefer soy formula for their infants.
 Not indicated for:
 Infantile colic, cow-milk protein allergy (CMPA; 30-64% cross-reaction to soy)
Hydrolyzed & AA-based formulas
 Protein content:
 Babies w/ CMPA (2-3% all infants) unable to digest or tolerate formulas containing intact cow milk protein; casein is heat-treated,
enzymatically hydrolyzed = protein source for these formulas.
 Hydrolysis  free AA & short-chain peptidesw/ supplementation of certain AA to improve biologic value of nitrogenous content.
 Carb content: All products are lactose free. Glucose polymers from various combos of ingredients are the primary carb source in
extensively hydrolyzed formulas (EHFs)
 Fat content
 Carb & fat content impt in EHF b/c these EHF formulas have expanded to not just address CMPA but also short bowel syndrome,
hepatobiliary disease, pancreatic insufficiency autoimmune dz, immunodeficiency syndromes.
 Atopy:
 2008: AAP updated guidelines – infants @ high-risk for atopy who are not exclusively breastfed for 4-6 mo or are formula fed  atopic
dermatitis is delayed or prevented by use of EHF or partially hydrolyzed formula compared w/ standard cow-milk formula.
 Breast milk > EHF > standard cow milk
Thickened formula:
 Thickened infant formulas are commonly used to help manage gastroesophageal reflux disease (GERD).
Intimate Partner Violence in the Adolescent
 Aims:
o To provide universal education & anticipatory guidance re: healthy relationships, including sexual ones
o Understand the profound impact of trauma + violence on adolescent health/families and how to prevent and intervene in abusive relationships
o Improve sills in eliciting sexual hx that empowers adolescents to recognize healthy & abusive relationships
o Advocate for healthy + safety by connecting youth w/ local/online resources for relationship abuse.
 Overview:
o CDC Definition for IPV: physical, emotional, or sexual violence b/w 2 people in an intimate relationship. May include repeated physical
abuse/injury, progressive isolation, intimidation, demanding sex, and other controlling behaviors (e.g. financial).
 Reproductive coercion = distinct form of IPV involves pressuring a partner to become pregnant or sabotaging contraceptive attempts.
o Complications of IPV & reproductive coercion: unintended pregnancy, STIs, depression, anxiety, PTSD, antecedent of child maltreatment
(physical/emotional abuse of children)
 Epidemiology:
o Occurs in 1/3 women globally including US; lifetime prevalence is 30%
o Occurs among heterosexual, same-sex, bisexual, and transgender relationships
o Adolescents:
 High school students of any physical or sexual IPV in F 21%; M 10%
 College females: 50% experienced IPV
o Risk factors:
 Sex inequality, alcohol use, childhood abuse, witnessing parental domestic violence, depression, EtOH/drug use, previous violence
victimization (bullying/homophobic teasing), having a disability, marginalization & discrimination 2/2 sexual orientation or sex identity, social
norms condoning sexual violence, laws & policies that perpetuate sex inequality. Adolescent boys who endorse traditional sex roles have a
greater likelihood of IPV perpetration in adolescence compared with adolescents with more equitable attitudes regardless of race/ethnicity.
o Mortality: 1544 deaths in 2004; ¾ victims are female (underestimate as deaths may not be reported resulting from of IPV)
 IPV & effect on children (Clinical Manifestations):
 Given relationship of IPV  child maltreatment, parents who disclose IPV should be offered support & resources to ensure own and
children’s safety.
o In utero:
 3-19% of pregnant women are IPV victims w/ potential harm to the fetus.
 In utero exposure  risk of preterm labor, low birthweight, intracranial hemorrhage, and neonatal death.
 IPV = costly  offspring of women who have been victims of IPV use healthcare more frequently, even if the abuse ceased before
delivery.
o Children & adolescents:
 Adults raised in homes where a parent experienced IPV:
 Risk of physical abuse  4.8x, emotional abuse  6x, sexual abuse  2.6x
 Behavioral:
 Internalizing behaviors: Depression, suicidal ideation, anxiety, withdrawal, somatic complaints (chronic abdominal pain, headaches,
etc), poor sleep, school avoidance, disordered eating (overeating & food restriction)
 Externalizing behaviors: attention problems, academic underachievement, aggressive behavior at school, at home, or in the
community, rule-breaking behaviors, difficulty forming and maintaining stable relationships with peers, bullying behaviors, substance
abuse, sexual health behaviors s.a. early-onset sexual activity, multiple partners, difficulty negotiating partner condom use.
o Failure to keep medical appointments, frequent medical visits with somatic complaints that don’t fit w/ medical hx, reluctance to
answer questions about discipline strategies at home.
 Organic: STIs
 Failure to recognize particular behaviors as abuse: being pressured to have sex, partner threatening to hit pt, condom manipulation,
birth control sabotage, pressure for pregnancy against her wishes  failure to recognize reproductive autonomy.
 Management:
o Screening:
 Patients may not disclose being in an unhealthy or abusive relationship for many reasons including (1) fear of perpetrator worsening IPV (2)
fear of breaches of confidentiality (3) lack of trust in adults including healthcare professionals & clinicians (4) desire to protet the abusive
partner or parent (5) self-blame & inappropriately placed guilt (6) lack of recognition of what constiutues abusive behaviors (7) inability to
access care (lack of transportation, uncertainty about insurance coverage), (8) lack of knowledge of services or scope of services
(uncertainty abt where to seek care).
 Routine questioning:
 First always establish confidentiality and consent of adolescents to keep ea adolescent victim of IPV safer. Reporting to CPS or
law enforcement w/o consultation with social work & other multidisciplinary teammates (including victim service advocates) may result
in compromising a young person’s safety. When filing a child abuse report on behalf of an adolescent, ewheneve3r possible, the
adolescent should be including in the filing process.
o Confidentiality and consent: “Everything we talk about without a parent in the room is confidential, meaning I am not going to
share with your parent what you tell me unless it is life-threatening or dangerous. With all young people I take care of, if I learn
that they are in danger, I work hard to partner with them to keep them safe, and sometimes we need outside support to make that
happen. My job is to keep all young people safe and healthy, so you can be an active manager of your own health. What
questions do you have for me about that?”
 Caution in the era of electronic health records: If pt portal allows access to parents re: existence of sexual relationships, consider
using the following phrase: “A detailed psychosocial assessment was conducted and documented confidentially & appropriate
resources & educational materials were reviewed with the patient.” Work with your your HER to ensure that there is a way to protect
the confidentiality of adolescent records.
 Frame in a routine manner: “I ask all my pts about the relationships they are in, and how everyone deserves to be treated with
respect and trust. Some of my patients tell me about how a friend or partner constantly checks up on them or puts them down; has
anything like that ever happened to you?”
 Types of questions:
o “Has anyone done anything sexually that made you uncomfortable?”
o “Does the person you’re seeing get mad at you if you do not respond to his/her calls right away?”
o “Has someone you were going out with ever monitored your phone or texts in a controlling way?”
o “I am glad tto hear that’s not happening to you. If you know a friend who could use this information, please take along this link for
them. Feel free to take several to share with others who could use them.”
 Provide universal education to pts about healthy & unhealthy relationships of disclosure to experiencing IPV – providing brochures allows
them to be an active “upstander” vs passive bystander for friends/family going through IPV.
 Do NOT force patients or parents to disclose – the goal is to ensure parents and pts receive info about IPV and the effect on their child’s
health and their own health.
 National Domestic Violence Hotline [www.thehotline.org]
 Educational safety cards for parents available from IPV Health Partners [www.ipvhealth.org]
 That’s Not Cool [www.thatsnotcool.com]
 Loveisrespect.org
o Prevention:
 Primary prevention: educating & supporting teens/tweens to recognize healthy & unhealthy relationships and to be advocates for their and
their peers’ healthy/safety. Middle schoolers start dating, so anticipatory guidance re: unhealthy relationship behaviors include:
 Monitoring a partner’s cell phone use, controlling where/with whom a partner can talk or hang out; telling a partner what he/she cannot
wear, manipulating contraceptive use, including refusing to use condoms or putting holes in them, throwing away contraceptive pill
packs,, possessive behaviors including isolating an adolescent from friends/family; inappropriate anger at the victim if calls are not
answered or responded to immediately, pressure to participate in sexting or textual harassment.
 Promote sharing materials with friends and family.
 Digital media: ask about media use and help teens become aware of digital footprint, create boundaries for themselves, and support
those boundaries for friends.
 Secondary prevention: Recognizing and addressing a problem in its early stages.
 Diagnosis of recurrent STIs, adolescent pregnancy, depression, academic underachievement, or other problems should trigger the
clinician to consider possibility of IPV & overlapping concerns of sexual assault/exploitation in differential.
o “When I see a pattern of STIs or infections or when I detect a teen pregnancy, I worry about people making you do things sexual
when you didn’t want to. Could that be part of your story?”…”Tell me more”
 HEADDSS assessment: Home, Education/Employment, Activities, Drugs, Depression, Sexuality, Safety, Suicide
 Tertiary prevention: treat a problem once recognized & take step to reduce likelihood of it happening again.
 Although disclosure is not the goal, disclosures do occur, especially if the adolescent trusts the clinician. The clinician should know
how to make a “warm referral,”  connect a patient with an advocate in person, by phone, or virtual visit rather than only handing out
a hotline number. Helps to reduce barriers to seeking help
 Barriers include: self-blame, not recognizing what is happening as abuse, limited knowledge of services, and thinking that victim
services are limited just to crises.
 If a young woman is experiencing reproductive coercion, be prepared to offer & discuss forms of contraception that a partner cannot
interfere with (IUD, implant, or injection).
o Treatment see tertiary prevention
Sexually Transmitted Infections Part I: Genital Bumps & Ulcers
 Objectives:
o 1. ID the STIs that commonly present w/ bumps & ulcers
o 2. Understand the evaluation, DDx, & diagnostic techniques for common STIs caused by HPV & HSV.
o 3. Plan management of these STIs using most recent CDC treatment guidelines.
o 4. Prevent the incidence of STIs in adolescents using educational resources, preventative counseling, and appropriate vaccination.
 Epidemiology:
o Most common in 15-25 yo.
o Most common STIs: (1) Chlamydia, (2)
 Prevention:
o Primary prevention: prevent acquisition of disease. Multipronged approach addressing education, ensuring confidentiality, and providing easy
access to services for adolescents.
 Address confidentiality & its limits w/ parents & pts in the pre-teen/teenage WC visits so that teens are aware they can have private
conversations – obtain patient’s cell phone # at the initial visit so that confidential communication can occur.
 Have conversations about sexuality, condom use, reproductive health issues, & STIs at the annual physical. Make teens aware of what sx
and signs may indicate the presence of an STI and that in many cases a person with an STI may be completely asx.
 Emphasize early STI diagnosis & tx prevents complications and sequelae
 Providing educational handouts in waiting rooms or if possible have separate waiting areas for adolescents that have teen-friendly
informational brochures.
 Provide free condoms & resources to obtain reproductive health counseling
 Observe for s/s of sexual trafficking, sexual/emotional/physical abuse, ask questions that may allow disclosure. Provide posteres/handouts
in waiting room, bathroom, and and practicing trauma informed care may help adolescents disclose especially if they feel privacy and
safety are ensured.
 Offer HPV & HepB vaccination
 Consider using EHR allowing privacy to be maintained for teens by blocking confidential information (s.a. contraception) in physical forms.
o Secondary prevention: In STIs, involves early diagnosis & tx to prevent further transmission of an acquired infection.
 Accessible & confidential healthcare services for infected person & others affected by his/her infection.
 Easy access to clinical providers who can dx/tx infection via private practice pediatricians, public hospitals w/ designated STI sclinics, &
nonprofit organizations providing free confidential testing, counseling, and tx.
 Expedited partner tx allowing for tx of the partner by provider treating the target case.
 Discussing the possible presence of “sexual networks” = teenagers need to be counseled that while they may have only one partner, their
partner may have had or currently has several active partners who are high risk allowing for the acquisition or transmission of STIs.
 Recommend counseling services that provide support and education for the affected adolescent, thereby helping the adolescent
understand the implications of the infection, the importance of partner treatment, and necessity for a “test of cure” if appropriate and
reinforcing the use of condoms.
Genital Warts
 Genital warts 2/2 condyloma acuminatum:
o Pathophysiology: Caused by HPV-6 & HPV-11 (dsDNA, nonenveloped DNA viruses) transmitted from direct physical contact w/ skin/mucosa
of infected person usually during sex.
 Incubation period: 3 weeks to 8 months.
 Transmission: Presence of a wart is not essential for transmission b/c the virus is shed even after the warts disappear.
 Fomites can carry the virus, but do not usually cause the virus to be transmitted.
 Vertical transmission during delivery which may rarely cause the fetus to have recurrent respiratory papillomatosis
o Natural disease course: 30% of untreated warts regress spontaneously if not treated in 1-3 months. Other untreated warts may persist and in
some pts spread or proliferate.
o Epidemiology:
 Most common viral STI in US w/ highest prevalence in 20-24 yo; 1 per 1000 person-years in the age group of 15-19 & 3 per 1000 person
years in 20-25 yo.
 Most are non-oncogenic HPV 6 & 11; oncogenic strains are 16 & 18, plus 31,33,45,52,58.
 Risk factors: Multiple sexual partners, sexual activity w/ an infected person, MSM (men having sex with men), and receptive anal
intercourse (both men and women). Immunosuppressed individuals are more likely to contract HPV.
o Presentation:
 Flesh-colored, pink, or gray papules that can appear cauliflowerlike, smooth, or hyperkeratotic papules & occasionally as flat macules in the
genital or anal area. Present on perineum, vulva, penis, or scrotum or internally in the urethral meatus, anus, vaginal introitus, or vagina or
over the cervix.
 Usually painless but may p/w itching or bleeding.
 Depending on location may cause dysuria, hematuria (urethral warts), pain, or bleeding on defecation.
o Diagnosis: Clinical.
 Indications to perform a biopsy rare; would include immunocompromised host (unusual appearance of the wart), failure to respond to
standard treatments, and presence of danger signs (erosion, XS bleeding, or ulceration.
 Anogenital warts do not usually predict changes in Papanicolaou test results & pts ≥21 yo should have Pap tests regularly according to
ACOG guidelines.
o DDx:
 Infectious:
 Molluscum contagiosum: poxvirus appearing as small papules a few mm in size w/ characteristic umbilication or appearance of a
small dimple in the center of the papule. Does not usually occur on mucosal surfaces.
 Condyloma lata: manifestation of secondary syphilis & consists of a graying smooth, moist, & highly infectious papule present on on
external genitalia. These lesions are teeming w/ Treponema pallidum & a/w (+) dark-field microscopy & serological tests for syphilis.
 Noninfectous:
 Physiologic variants:
o Fordyce spots: white/yellow papules few mm in size that represent enlarged ectopically placed sebaceous glands that may be
present on labia minora or majora, usually symmetrically, also seen in oral mucosa/vermillion border
o Acrochordon/skin tags: benign overgrowths of normal skin that are pedunculated & seen at sites of friction.
o Pearly pink papules over the penis: tiny benign papules arranged circumferentially on the sulcus or corona of the glans penis.
 Skin conditions:
o Benign papillary growths over the vulva
o Seborrheic keratosis: immature keratinocytes single cauliflowerlike benign tumor “stuck on” on the genitalia or other parts of the
body.
o Papulosquamous lichen planus: raised or flat papules, itchy, and violet in color
 Neoplasms:
o Giant condyloma acuminatum: low-grade squamous cell carcinoma occurs over penis or perianal area & cauliflowerlike in
appearance & may have fistulae or abscesses.
o Bowenoid papulosis: This papule is linked to HPV-16 & considered a benign condition yet may progress to a low-grade arcinoma
in situ. P/w reddish-brown papules located usually over the penis in young men.
o Treatment:
 Choice of treatment is guided by the location of the warts, resources available, cost/convenience to the patient, and how experienced the
provider is in administering treatment. Number, size, & shape of warts may influence choice of tx. Pts may prefer self-administered therapy
b/c of privacy & convenience.
 Patient administered:
o Podophyllin: podofilox gel (0.5%) or lotion applied qhs w/ a cotton-tipped swab or gloved finger for 3 consecutive nights followed
by a 4 day hiatus. Up to 4 cycles may be needed to eliminate the warts. Patients should use a maximum of 0.5 mL of the solution
per day & the total area treated should not be more than 10 cm 2 or 1.5 square inches.
o Imiquimod cream: 3.75% cream daily or a 5% cream applied 3x per week for a duration not exceeding 4 months. Patients are
advised to apply it at night & wash off the area w/ soap and water a/f 6-10 hours.
o Sinecatechin ointment: OTC as a 15% ointment. Derived from green tea leaves and was approved in 2006by the FDA for tx of
genital warts. Apply a small strip of cream (p.5 cm) over the wart 3x/d & do not wash off the cream. Apply sinecatechin until the
wart clears but not for more than 16 weeks/4 months.
o ***Sinecatechin & imiquimod REDUCES THE EFFICACY OF CONDOMS & FEMALE DIAPHRAGMS.
o ***CONTRAINDICATION: Pregnant women.
 Provider-administered:
o Cryotherapy: performed with liquid nitrogen using a cotton-tipped swab or a cryoprobe make sure to avoid touching unaffected
skin. Local anesthetic cream s.a. mixture of lidocaine and prilocaine can be applied 20 min b/f application 91 g sufficient to
provide analgesia for 0.5 inches of skin to be treated).
o Trichloroacetic acid or bichloroacetic acid (80-90%) – effective in tx of warts & have the advantage that they can be used in
pregnant women. Application is best performed using a cotton-tipped swab & allowing wart to dry a/f tx. The wart will turn “white”
w/ effective tx. This tx may need to be repeated weekly for up to 8 weeks to allow for all the warts to be treated. Do NOT touch
unaffected skin b/c this can be painful. If pain is intense a/f tx, the area may be washed with liquid soapo or covered with sodium
bicarbonate or talc to neutralize XS acid.
 Surgical removal:
o Warts in the urethral meatus or those that are intra-anal, intravaginal, or cervical will require a referral to a gynecologist or
surgeon for surgical removal. Removal is done a/f anesthetizing the area & using scalpel, scissors, CO2 laser,or electrocautery.
 Follow-up:
 Resolution w/ tx usually occurs in approximately 3 mo.
 Changes in tx modality may be considered if pt is having severe adverse effects or there is no response to tx.
 Continue to follow the pt to check for adverse effects, resolution, or recurrence of warts. Serious adverse effects rarely occur, but
ablative therapies & tx w/ immune modulators may cause scarring or pigmentary changes esp if lesions are not allowed to heal
adequately b/w applications.
o Prevention & counselling:
 Advise pts to avoid sexual contact w/ partners who have active lesions & inform partneres w/ resolved warts that they may still continue to
shed the virus.
 Reinforcing condom use w/ the caveat that the HPV may spread from sites that are not covered by the condom.
 Explain having genital warts does not indicate any increased risk of cancer b/c genital warts are caused by HPV strains that are not a/w
cervical cancer.
 Pap test screening for cervical cancer should occur as per ACOG schedule.
 Offer pts testing for other STIs & HIV.
 Promote HPV vaccination. 9-valent vax provides immunity against some oncogenic strains that cause approximately 2/3 of all cancers
attributed to HPV 7 protect against 90% of HPV types that cause genital warts (6 & 11).
Genital Ulcers
 Overview
 Pathophysiology:
o Caused by HSV-1 and HSV-2 transmitted infected persons shedding the virus directly or via infected secretions from oral and genital areas.
 dsDNA virus w/ 74 genes. Penetrates thru mucosal surface & finds its way along peripheral axons to the local ganglion  latent chronic
infection.
 Resurfaces 2/2 emotional stress, environmental factors, sun exposure, other infections  fever/immunosuppression, & traumer.
 Viral shedding can occur from the genital areas whether the ptis symptomatic or not.
o Transmission occurs at a 6x higher rate from M to F than F to males.
o Maternal active genital herpes is an indication for a lower-segment cesarean delivery. Viral transmission from pregnant women to their
fetus during vaginal delivery through direct contact w/ the skin or mucosa.
o Fomites do not usually transmit herpes but can be transmitted from the genitalia to other sites including the eyes by finger contact.
o Incubation period: 2-12 days w/ mean of 4 days.
 Epidemiology:
o 776,000 per year 45% occurring in young people aged 15-24 yo.
o HSV-2 is the more common etiologic factor in recurrent genital herpes although HSV-1 also causes the disease.
 HSV-2 disease is found to be higher in women with women having double the seroprevalence of men.
 Race affects seroprevalence; AA M & F have higher rate of infection than white individuals
 HSV-2 Seroprevalence  with age, # of sex partners.
o HSV-1 genital herpes more likely to be seen in F adolescents, young adults, college students, and MSM. This may be due to a greater
incidence of oral genital sex in this age groupo but could also be to initial exposure to HSV-1 ocuring with onset of sexual activity.
 Presentation:
o
First clinical episode:
 Primary genital infection: Occurs in pts w/o HSV-1 or HSV-2 immunity. Multiple grouped, clustered, often bilateral vesicles that soon
progress to painful ulcers & then dry crusts. Lesions a/w pain & itching, w/ occasional vaginal discharge in F & urethral discharge in M. Pt
may have tender inguinal lymphadenopathy & systemic sx s.a. fever, myalgias for 5-7 days. Occasionally a/w aseptic meningitis.
 If left untreated, lesions will continue to shed the virus for 12 days usually until the crusts are formed & then resolve spontaneously in
approximately 3 weeks.
 Herpes cervicitis: Virus can infect the cervix in women w/ or w/o sx, although in most pts the cervix appears inflamed, may have
ulcers, & bleeds on touch.
 Herpes proctitis: Fever, anal discharge, painful defecation, ulcers in anal area.
 HIV+ pts: mass or pseudotumor found to be colorectal mucosa w/ cytopathic changes in rectal/anal area & may have difficulty
urinating.
 Herpes urethritis: dysuria, clear urethral discharge
 Nonprimary infection: Term used for pt who’s p/w sx of genital herpes due to HSV and as been exposed in the past to the other herpes
virus type. Non-primary infection may occur in pts who have an asx infection w/ one of the viruses, have antibodies to that same type, and
are reexposed to the same type. Usually these inds have milder sx.
o Recurrent symptomatic infection: s/s are similar but milder to first episode. Process of vesicles to crusting is shortened, & systemic sx are
usually not present. Often lesions are unilateral. Neuropathic sx s.a. tingling/burning may precede th appearance of the vesicles. Frequency of
reactivation of HSV-2 reduces a/f the first year of infection from 5 episodes per year to 3-4 & that of HSV-1 decreases from 1 episode per year
in the first year to non afterward.
o Asymptomatic infections: 80% of individuals who have HSV-2 antibodies have never been diagnosed as having hsv infection b/c they have
been asx. most of these may have subtle signs that are noticed & inds may be shedding the virus & inadvertently infecting their partners.
Education about these sx may help prevent transmission
 Diagnosis:
o Clinical features alone are not enough to dx HSV b/c presentation is often atypical & pt may not have s/s.
o Furthermore, the type of HSV cannot be determined by clinical evaluation alone. Impt to type the kind of SHV b/c it indicates clinical course of
dz & possibility of recurrence. CDC recommends viral Cx or PCR-based test.
o PCR is currently gold standard, but other tests include:
 Viral cx (prior to PCR)
 Antigen tests (direct fluorescent antibody testing can be used to detect HSV antigen but is less sensitive than viral cx or pcr)
 Cytologic analysis – Tzanck smear not considered reliable & should not be used
 Serological tests: type-specific IgG Ab develop 2 wk – 3 mo a/f initial infection. Order type-specific assays when there is a hx of clinical
herpes not confirmed by viral Cx or PCR, the sex partner has a Hx of genital herpes, pt has atypical or recurrent lesions w/ (-) viral cx, or pt
is a high-risk individual (HIV + or at risk for HIV acquisition).
 Work-up:
o Direct swab of vesicular lesions (w/I 72 hours of onset) idea – avoid lesions that have evidence of crusting or healing. Do not clean area w/
topical EtOH b/f acquiring material. Swab skin via unroofing vesicles w/ sterile needle, urethra sterile swab, cervix thru vaginal speculum, urine,
swabbing conjunctiva, and rectal swabs through protoscopes
o HSV serotyping, PCR (if direct swab not possible)
o US/urinalysis as sx can mimic acute UTI
o Given STI, consider further STI work-up GC/CT, HIV, (known interaction b/w HSV-2 & HIV in which concurrent infection may occur faster than if
HSV-2 was not present), RPR
 Based on strong recommendation (level A evidence), as per CDC and USPSTF guidelines, all males and females aged 13 - 64 yo should
be screened for HIV, including all patients who seek evaluation or treatment for STIs.
 Treatment:
ACYCLOVIR
VALACYCLOVIR
400 mg orally 3 times per day for 7–10
days OR 200 mg 5 times per day for 7–
First clinical episodea 10 da
FAMCICLOVIR
250 mg orally 3 times per day for 7–10
1 g orally twice per day for 7–10 da
da
125 mg orally twice per day for 5 d OR 1
400 mg orally 3 times per day for 3 d OR
g orally twice per day for 1 d OR 500 mg
Episodic (for recurrent 800 mg orally twice per day for 2 d OR 500 mg orally twice per day for 3 d OR 1 once orally followed by 250 mg orally
genital herpes)
800 mg orally 3 times per day for 2 d
g daily for 5 d
twice per day for 2 d
Suppressive therapy
500 mg orally once a dayb OR 1 g orally
(for recurrent genital
herpes)
400 mg orally once a day
once a day
250 mg orally twice per day
a. Tx may be extended if healing is not complete after 10d of therapy
b. Valacyclovir 500 mg daily may not be adequate suppressive tx for those who have ≥ 10 episodes/yr.
 Prevention & Counseling
o HSV is a chronic treatable disease, but recurrences can occur, although less often with HSV-1. Studies have shown that genital herpes caused
by HSV-1 has fewer or no recurrences after the first year.
o HSV recurrences can be triggered by physical and emotional stress, fatigue, trauma, exposure to sunlight, sexual intercourse, and other
unknown factors.
o Treatment for HSV is available and can shorten the course of the illness and reduce viral shedding if started early, both with the primary
infection and recurrences. The patient should be counseled about both episodic and suppressive therapy.
o Patients should know about the signs and symptoms of recurrent infection and the imminent signs and symptoms of recurrence (prodromal
symptoms).
o Patients should be aware of the modes of transmission, including perinatal transmission, especially in the case of pregnant teens. Adolescents
and young adults who are pregnant or are planning a pregnancy should be aware of the risks of HSV transmission.
o Patients should be aware that asymptomatic shedding of HSV (more with HSV-2 than with HSV-1) occurs from the genital areas of both males
and females and that suppressive therapy with an appropriate antiviral agent can reduce this shedding by 70% to 80%.
o
Patients should know that transmission to an HSV-2–negative partner can be reduced by being abstinent when a patient has active lesions and
that although condoms reduce HSV transmission, condoms do not completely prevent transmission. Patients should also know that taking daily
valacyclovir may reduce the chances that their partner becomes positive for HSV-2.
 Complications:
o Aseptic meningitis, oral ulcers, neuropathic sx, occasionally radiculopathy, herpetic whitlow, congenital HSV infection (herpes neonatorum)
o Herpes neonatorum:
 Pregnant women who are seropositive for HSV-2 or have a partner who has HSV-2W should be counseled about risk of transmission; most
transmission occurs at the time of delivery &  should be counseled if they have lesions at the time of labor a lower-segment cesarean is
indicated.
 If no active lesions, they can deliver vaginally.
 If a pregnant woman is (-) and partner is (+) for HSV-2 both partners should avoid intercourse in last trimester b/c transmission chances to
fetus highest when mother acquires HSV closer to delivery.
 Safety of oral antiviral drugs in pregnancy has not been established.
o HSV & HIV:
 HIV+ inds are often co-infected w/ HSV-2. HSV inection in HIV+ inds tends to be more severe w/ recalcitrant lesions & persistent viral
shedding esp in those who are severely immunosuppressed. Antiretroviral therapy can reduce occurrence of sign and sx but does not
affect the shedding. Often the ulcers get worse w/ the commencement of antiretroviral therapy 2/2 immun ereconstitution inflammatory
syndrome.
 Genital infection w/ HSV-2 also  chances of acquiring and transmitting HIV & HSV; suppressive therapy does not affect transmission.
 HIV-infected HSV pts can have HIV present in the herpetic ulcers and serve as a source of infection to their partners esp during a
reactivation episode of HSV-2.
 HSV vaccine: No current vaccine exists but there are vaccines in development that could prevent HSV2 seronegative inds from acquiring the
infection from an HSV-2 positive individual & other vaccines that could prevent recurrences & slow transmission in those who are already infected.
 DDx:
o Infectious:
 Painful ulcers:
 HSV-1 & HSV-2
 Chancroid: low prevalence rate in US – painful ulcers & suppurative inguinal lymph nodes called buboes 2/2 infection with
Hemophilus ducreyi. Transmission is via sexual contact, or nonsexual transmission can occur through contact w/ pus. Incubation
period 4-10 days. Ulcers can cause dysuria, dyspareunia, & sometimes painful defecation depending on location. Diagnosis via
culture b/c no FDA-approved PCR is available in the US. Clinical diagnosis if syphilis is excluded by testing and HSV is not detected in
the exudate. Tx w/ azithromycin, erythromycin, ceftriaxone, or ciprofloxacin.
 Painless ulcers:
 Syphilitic chancre: Primary syphilis p/w papule macule  develops into painless ulcer called a chancre. Punched out appearsnce w/
smooth firm, raised border & not usually a/w lymphadenopathy. Chancre is highly infectious & resolves spontaneously in
approximately 5 weeks. Causative organism = T pallidum. Transmission is via sexual contact. Clinical diagnosis; dark-field microscopy
will reveal T pallidum. Confirmation of diagnosis is by treponemal antibody tests & nontreponemal tests (not as specific for syphilis but
useful in monitoring treatment). Treat w/ penicillin G benzathine 2.4 million units IM once or doxycycline 100 mg PO BID for 14d.
 Granuloma inguinale (donovanosis): painless beefy red ulcers w/ no regional lymphadenopathy. A/w subcutaneous granulomas.
Incubation period 1-12 weeks, more common in India, Papua New Guina, Caribbean, & southern Africa. Caused by Klebsiella
granulomatis. Diagnosis is by identifying dark-staining Donovan bodies (on biopsy or tissue crush preparation). Tx = doxycycline 100
mg BID for 3 weeks.
 Lymphogranuloma venerum: presents as small papule and/or painless ulcer in the primary stage. Subsequently there is painful,
usually unilateral femoral or inguinal lymphadenopathy or painful buboes. The tertiary stage is characterized by scarring and
destruction of genitalia.
o Incubation period: 3-30d
o Receptive anal intercourse: presentation is usually w/ proctocolitis & if untreated can progress to colonic rectal fistulae or rectal
strictures. Causative organism is chlamydia trachomatis serovars L1, L2, or L3.
o Diagnosis: Clinical + Bacterial Cx & NAAT via PCR for genital/lymph node aspirates. Only culture can be used from rectal
specimens.
o Tx: doxycyclinel/erythromycin in early stages; later stages require antibiotic drugs + surgical intervention w/ drainage or
reconstruction.
 Non-sexually transmitted infections: rarely non-STIs may cause genital ulcerations s.a. tuberculosis, amebiasis, & leishmaniasis.
 Lipshutz ulcer (non-sexually acquired acute genital ulceration = NAGU), = rare vulvar skin condition = immune response to a recent
infection (EBV, CMV, mycoplasma, & Lyme disease)
o Noninfectious: fixed drug reactions, Behcet syndrome, neoplasms, Crohn disease, trauma.
Constipation
 No matter what is causing the constipation, the most important thing is to relieve the patient of their symptoms!
 Red flags for constipation (see table) – important to r/o red flags b/f resorting to dx of functional constipation
Passage of meconium >48 h
Constipation in the first month after birth
Family history of Hirschsprung disease
Hirschsprung disease
Family history of autoimmune disease such as celiac
disease, type 1 diabetes
Celiac disease
Pancreatic insufficiency
Family history of cystic fibrosis
Meconium ileus equivalent
Chronic pancreatitis
1
Hirschsprung disease (∼2.6% of patients with Down syndrome [ ])
Intestinal malformation (atresia)
Chromosomal abnormality (ie, Down syndrome)
Intestinal web
Physical asymmetry
Intestinal malformation
Ribbon stools
Rectal narrowing or atresia with fistula
Blood in the stool in the absence of anal fissures
Inflammation (NEC), milk allergy, polyp, intussusception
Hirschsprung disease
Weight loss or inadequate weight gain
Numerous medical conditions
Hirschsprung disease
Lagging growth
Chronic illness
Bilious vomiting
Intestinal obstruction
Intestinal obstruction; ileus; severe obstipation
Severe abdominal distention
Hirschsprung disease
Intussusception
Episodes of inconsolable crampy abdominal pain
(especially if followed by sense of exhaustion)
Volvulus or torsion
Urinary tract symptoms
Urinary tract disorder including obstruction or infection
Abnormal thyroid gland/function
Hypothyroidism
Imperforate anus with fistula
Abnormal position of the anus
Anterior displacement with malpositioning of colon
Absent anal or cremasteric reflex
Decreased lower extremity strength/tone/reflex
Sacral dimple
Tuft of hair on spine
Gluteal cleft deviation
Spinal cord lesions (including sacrococcygeal teratoma)
Dilated colon +/– ureters
Pseudo-obstruction disorders including neuropathies
Medication consumption
Iron intake, diuretics (dehydration), antispasmodics, calciumcontaining medications, aluminum antacids, opioids, SSRIs and TCAs,
unknown drugs, and herbals
Low fiber
Restricted diet
Unbalanced intake
Physical activity
Too sedentary, any chronic illness
 Functional Constipation: Based on Rome Criteria
o EBM:
 Based on some randomized controlled trials (evidence quality “B”), (26)(28) observational studies, and expert opinion (evidence quality “C”
and “D”), (6)(25)(27) clinicians almost universally accept that for many patients with FGIDs, co-management with a pediatric psychologist is
a great asset, if not a necessity. We look forward to the greater acceptance by medical leadership and insurers of the key role that mental
health providers play.
 The work performed by the Rome Foundation has been modified, and their previous insistence that to diagnose an FGID there needed to
be no evidence of organic disease has appropriately been updated to allow the diagnosis if “after appropriate medical evaluation the
symptoms cannot be attributed to another medical condition.” This is important progress because it allows the clinician flexibility regarding
the amount (if any) of testing deemed appropriate. It becomes easier for us to understand and to accept that FGIDs can coexist with other
organic disorders, such as inflammatory bowel disease.
 Based on expert opinion, case reports, and reasoning from first principles (evidence quality “D”) and on some observational studies
(evidence quality “C”), the American Psychiatric Association definition of encopresis has been partially aligned with the Rome criteria
diagnosis of nonretentive fecal incontinence, (2)(6) and we can look forward to greater harmony in these definitions in the future.
 ased on expert opinion, case reports, and observational studies (evidence quality “D” and “C”), (6)(7)(13)(25)(27) the importance of the
biobehavioral model continues to expand. Furthermore, the biobehavioral model will be further advanced as the field of
neurogastroenterology matures and future basic science and clinical research begins to clarify how the brain-gut interactions affect the
o
o
o
o
FGIDs. The role of the gut microbiome and its effect on gut signaling and its consequences will no doubt yield many new questions and, we
hope, a few answers.
Infant dyschezia:
 Prevalence: Infant <1%
 Physiology: apparent cause of infant dyschezia = newborn’s inability to coordinate the voluntary and involuntary body movements to expel
stool (successful expulsion of stool requires coordination of pelvic floor movement, abdominal muscle contractions, and relaxation of anal
sphincters)
 Clinical presentation:
 Infants w/ dx restricted < 9 mo, no other health problems; babies appear well in office w/ parents reporting isolated episodes of
distressing straining + crying w/ baby face transiently turning deep red in apparent effort to defecate.
o Rome criteria: 9 mo, > 10 min straining & crying b/f while trying to stool, no other health problems
 Sx last for 10 min but usually resolved on their own by 20 min
 Stools sometimes soft but other times failure to pass stool during the pisode – failure to pass stool leads parents to believe that baby
is experiencing constipation.
 Babies are totally fine a/f these acute episodes, but can be distressing for parents to witness.
 Episodes do not last for more than 1 month.
 Tx: Reassurance & comfort baby during crying episodes (gentle massage of abdomen, cuddling, holding)
 . Parents SHOULD NOT resort to rectal stimulation or use of glycerin suppositories; rectal stim has risk of conditioning the infant to
wait for stimulation to defecate, risk of injuring infant; laxatives have no role in tx.
 Time eventually will resolve the problem.
 Changing infant formula or stopping breastfeeding will not speed the process of resolving infant dyschezia.
Functional constipation
 Infant: 12.1%, toddler 18.5%, child/adolescent > 4 14.1%
 Epidemiology: May begin at any time in childhood but highest incidence a/w toilet training.
 M > F (greater incidence of soiling)
 Factors predisposing to FC include 1) dietary inadequacy (too much or too little of fcmpnts in feed s.a. low fiber, too much milk, autism
kids w/ unusual or restricted diets) (2) cognitive decisions on part of pt that may be self-limiting requiring no intervention; (3) cognitive
decisions on part of pt requiring some intervention to tx FC s.a. providing a note that a school age child be allowed to use the nurse’s
bathroom using the students’ toilet
 Clinical presentation:
 Hard, painful bowel movements, but sometimes may report loose stools = overflow of waterstool past a bolus of hard stool
(paradoxical diarrhea).
 Voluntary withholding has a significant role at the time of toilet training (vicious cycle b/c when stool is held water absorption increases
making stool harder and drier  more difficult to passs w/ or w/o pain).
 Pathophys: Accumulation of stool in the rectum  reflex ↓↓ in gastric emptying which may be a/w abdominal distension, pain, anorexia,
nausea.
 Tx:
 1) Adequate disilmpaction: clean out the retained stool.
o Disimpassion at home:
 Oral:
 PEG 17g/8 oz water/juice or other liquid
 Mg citrate: 4 mL/kg/d given on 2 consecutive evenings
 Lactulose: 1 mL/kg 2x/d for up to 12 weeks then tapered over 4 wks
 Rectal:
 Normal saline enema
 Sodium phosphaste enema
 Mineral oil enema
 Biscodyl suppositories
o Some pts may need hospitalization for clean out
 PEG 3350 (Mix 255 g in 64 oz of balanced multi-electrolyte solution – or 32 g in 8 oz)
 Bowel cleanout (oral) – give 8 oz/hr until stool is clear
 Bowel cleanout (NG tube) – administer 10 mL/kg/hr & increase as tolerated by 10020 mL q1-2h to a max of ~40
mL/kg/hr
 2) Maintence therapy for chronic constipation
o Osmotic laxatives (PEG 3350, lactulose, MgOH)
o Stool softeners/lubricants (docusate, mineral oil)
o Stimulant laxatives (senna, bisocdyl)
o Chloride channel activators (lubprostone, linaclotide) = new prescription meds approved only for adults w/ very limited pediatric
(off-label) experience
Nonretentive fecal incontinence
 Child/adolescent: 0.2%
Any functional GI disorder
 Infant 37.9%, toddler (1-<4) 21.4%, child > 4 = 25%
Vaccine schedules
Factors Influencing the Vaccination Schedule
Vaccination immunology: • Immune maturity, maternal antibodies, magnitude of immune response, and immune memory are important
considerations in determining vaccination schedules
Local epidemiology:
• Ideally, the dose of vaccine should precede the earliest, most susceptible age at acquisition of disease
• High incidence and prevalence generally favors earlier immunization
• Eradication of disease/infection could lead to elimination of use of certain vaccines, eg, small pox vaccine
Programmatic
considerations:
• Organization of vaccination drives, educating local practitioners
• Availability of combined vaccines
• Cost (eg, acellular pertussis is more expensive than whole cell pertussis), maintaining cold storage, and heat
stability are some important factors influencing the inclusion and timing of vaccines in the schedules
 Age at First Dose and the 2-, 4-, 6-month Schedule
o Priming doses are required to generate immune memory. These are the initial doses that generate a germinal center reaction and result in
production of memory B cells and plasma cells that produce antibodies.
o Priming doses of DTaP, Hib, rotavirus, PCV13, and inactivated polio vaccine (IPV) are all given at 2, 4, and 6 mo, a/t some formulations of Hib
& rotavirus are given at 2 + 4 months. Infants ≤ 1 year have the greatest risk of mortality from pertussis, and mortality from diphtheria is highest
in those younger than 10 years.
o A minimum of 3 weeks between primary doses prevents interference of primary waves of immune response. This is because a primary
response self-terminates in 3 to 6 weeks. Vaccines are spaced out at 4- to 8-week intervals to avoid competing immune responses between
primary waves of germinal center reaction.
 Prime-Boost Schedule:
o Affinity maturation = process by which memory B cells complete process of developing antigen specificity, which takes 4-6 months.
 Ab generated in initial wave of primary response during priming doses eventually wane over a period of months.
 Allowing at least a 6-month gap b/w last primary dose & first booster dose allows completion of affinity maturation & development of highly
specific memory B cells. The longer the gap b/w the primary & booster dose, the better the immune persistence.
o Booster doses  immune memory & triggers memory B cells to transform into plasma cells & generate ab. Abs persist in blood for several
months – years & neutralize antigens produced by microbes b/f have an opportunity to cause disease.
o Spreading out vaccine doses for better immune memory needs to be balanced w/ providing effective protection b/f an exposed child develops
dz.  local epidemiology must be taken into consideration when determining vaccine timing.
Headaches in Children
 Hx:
1. When did you first begin having headache(s)?
2. What is the temporal pattern of your headaches?
 sudden onset of first lifetime headache
 episodic headaches, normal in between
 frequent nonprogressive headaches
 gradually worsening headaches
 a mixture of daily headache with episodic worsening
3. Where does your head hurt with your headaches?
4.
What do your headaches feel like (throbbing, pounding, stabbing, squeezing, etc)?
5.
What do you do when you get a headache?
6.
How long do your headaches typically last?
7. With your headaches do you have:
 nausea
 - dizziness
 vomiting
 - numbness
 - photophobia
 - weakness
 - phonophobia
 - double vision
8. Do you get a warning sign or can you tell a headache is coming on?
9. Has a headache ever awoken you at night or is present first thing on awakening?
10. Have you ever had a seizure?
11. Do any activities, foods, or medications make your headaches worse?
 Distinguish b/w primary & secondary headaches:
Historical feature
Primary HA
Secondary HA
Length of illness
Chronic, >6 mo
Acute, subacute
Temporal pattern
Recurrent or daily
Progressive
Location
Frontal/temporal
Posterior
Quality
Throbbing, squeezing
Pressure
Time of day
Anytime
Early morning, awakening
Frequency/duration
Varied/hours to days
Constant
Nausea/vomiting
Nausea > vomiting
Vomiting > nausea
Visual aura/diplopia
Aura
Diplopia
Photophobia/phonophobia
+++
-- In addition to migraine, tension headaches, and medication overuse headache/rebound headache, there are childhood periodic syndromes to be
aware of: (in all these syndromes pt is sx-free w/ normal neurologic exams b/w attacks). These kids are at higher risk of developing migraines in the
future.
1. Abdominal migraine: paroxysmal abdominal pain w/ or w/o vomiting lasting hours to days
 A. At least 5 attacks of abdominal pain fulfilling criteria B through D
 B. Pain has at least 2 of the following 3 characteristics: midline location, periumbilical or poorly localized; dull or “just sore” quality; and
moderate or severe intensity
 C. At least 2 of the following 4 associated symptoms or signs: anorexia, nausea, vomiting, and pallor
 D. Attacks last 2 to 72 hours when untreated or unsuccessfully treated
 E. Complete freedom from symptoms between attacks
2.
3.
4.
 TX:
o
 F. Not attributed to another disorder
Cyclical vomiting syndrome: hours to days of vomiting occurring at regular predictable intervals = self-limiting episodic condition in childhood
w/ periods of complete normality b/w episodes
 A. At least 5 attacks of intense nausea and vomiting, fulfilling criteria B and C
 B. Stereotypical in the individual patient and recurring with predictable periodicity
 C. All of criteria D through H
 D. Nausea and vomiting occur at least 4 times per hour
 E. Attacks last at least 1 hour, up to 10 days
 F. Attacks occur at least 1 week apart
 G. Complete freedom from symptoms between attacks
 H. Not attributed to another disorder
Benign paroxysmal vertigo – can be seen in younger children
Benign paroxysmal torticollis in very young children – torticollis recurrent episodes + associated sx lasting minutes to days.
Lifestyle modification
 Hydration status  aim for a certain # of urinations per day vs a set amt of water as this better accounts for physical activity or exertion
variations – suggest drinking enough water to have 6 or more urinations per day)
 Dietary & exercise habits  healthy eating, weight, do not skip meals – some dietary items mayi trigger the headaches
 Dietary triggers for headaches: caffeine (soda/coffee/tea), MSG/soy products, chocolate, nitrite foods (hot dogs, lunch meats,
sausage), artificial sweeteners (saccharin, aspartame), cheeses/dairy (aged cheese, sour cream, yogurt, whole milk, buttermilk, ice
cream), nuts, vinegar & vingegar containing condiments (ketchup, mustard, mayo), fruits (citrus, plums, passion fruit, dates,
avocados), veggies (lima beans, fava beans, navy beans, sauerkraut, pea pods, lentils), snack foods, beer/wine
 Safe alternative foods: American or cottage chees, low fat milk, pasta, potatoes, rice cereal, lamb, chicken, broccoli, cauliflower,
cabbage, apples, jelly/jam/hard candy/honey, gelatin, sherbet, cookies
 Screen for depression, anxiety, stress
 Screen for medication overuse – if r/o, counsel pt about how to prevent medication overuse
o
Meds:
 Abortives:
 Tylenol
 NSAIDs: ibuprofen, naproxen, ketorolac
 Antihistamines: diphenhydramine
 Dopamine antagonists: metoclopramide, prochloperazine
 AEDs: valproic acid
 Anti-serotonin: triptans(sumatriptan, zolmitriptan
 Preventives:
 Antihistamines
 Antiepileptics
 Antidepressants/anxiolytics
 Antihypertensives
Pediatric Chest Pain
CAUSE
FEATURES
MANAGEMENT
Musculoskeletal system
Often >1 costochondral junction, typically involving
second to fifth rib junctions
Costochondritis
Reproducible pain on palpation
Largely supportive management with NSAIDs and avoidance of painprovoking activity
Often only 1 costochondral junction affected at the level
of the second or third rib junction
Tietze syndrome
Visible swelling with reproducible pain on palpation
Largely supportive management with NSAIDs and avoidance of painprovoking activity
Often involving costal cartilages of the eighth, ninth, or
tenth ribs
Slipping rib
syndrome
Perceived slipping sensation of the rib
Initially trigger avoidance; if necessary, strapping the affected ribs or
local nerve blocks
Well-localized and sharp pain occurs at rest
Precordial catch
syndrome
Pain abruptly subsides
Muscle strain
Due to trauma or overuse, especially in athletes or those
with chronic cough
Rest, stretching as tolerated, NSAIDs
Reassurance with explanation of benign nature of the condition
Assess for associated injuries, with rib fracture in young children
raising abuse concern
Trauma
May have chest wall bruising but less likely to have
fractures compared with adults
Assess for intrathoracic trauma, especially if pneumothorax or
hemothorax at presentation
CAUSE
FEATURES
MANAGEMENT
Pulmonology system
Bronchodilator treatment
Asthma
Respiratory
infections
Pain most often with exercise-induced variants or
perception of “tightness” as pain
Encourage gradual warm-up to lessen severity
Suspect with focal findings on auscultation
Consider chest radiography if presenting with febrile illness and
associated symptoms
Often present with cough in the context of a febrile
illness
Treatment with antibiotic drugs when bacterial cause likely, often with
pleural irritation
Sharp and spasmodic chest pain
Pleurodynia
Presents with fever due to infectious etiology; coxsackie Self-resolving over weeks; analgesics to minimize pain when
B most common
necessary
Gastrointestinal system
Commonly presents epigastric pain and regurgitation
Gastroesophageal
reflux
May have associated burning sensation
Acid suppression using either histamine receptor blockade or proton
pump inhibitors
Diagnosis based on endoscopy and biopsy findings
Treatment of underlying condition; controlling reflux as above,
treating infectious causes and changing medications if found to be
causative
Esophagitis
Foreign body
ingestion
Due to reflux, allergic, infectious, or iatrogenic causes
due to medications
Eosinophilic esophagitis treated with elimination diet and topical
corticosteroids
Common in children <5 y old presenting with suddenonset symptoms
Chest radiography including posterior-anterior and lateral imaging
May have drooling or reluctance to swallow
Endoscopy may ultimately be needed both for diagnosis and
treatment in removal of foreign body
Often presents with fever and is typically retrosternal
Obtain an ECG to assess for described findings
Patients often sit upright and lean forward to alleviate
pain
NSAIDs or aspirin in older children as analgesia and to control
inflammation
Cardiac system
Friction rub on auscultation and widespread ST-segment
elevation and PR depression on ECG
Corticosteroids or colchicine also used occasionally
Pericarditis
Myocarditis
Often viral or idiopathic cause
May present with nonspecific symptoms mimicking
respiratory disease or sepsis
Low threshold to obtain ECG, especially when respiratory diagnosis
is uncertain
Often viral causes, including group B coxsackie as well
as parvovirus B19 and human herpesvirus 6
Treatment relies on supportive therapy for left ventricular function,
including pharmacologic therapies for circulatory support or
occasionally mechanical support
No specific treatment
Antibiotic prophylaxis not required
Occasional symptomatic treatment with β-blockers
Associated with a mid-to-late systolic click with a highMitral valve prolapse pitched late systolic murmur
Arrhythmia
Severe regurgitation may require surgical intervention
Supraventricular tachycardia
Hemodynamically stable supraventricular tachycardia
• Most common dysrhythmia, tracing with narrowcomplex QRS
• Initial treatment with vagal maneuvers, rapid push adenosine if
ineffective
Ventricular tachycardia
Hemodynamically stable ventricular tachycardia
CAUSE
FEATURES
MANAGEMENT
• Many potential causes all requiring prompt treatment to
avoid ensuing hypotension and degeneration into
ventricular fibrillation
• Identify and treat underlying abnormalities
Hemodynamically unstable supraventricular or ventricular
tachycardia
• Direct current cardioversion
Increased myocardial demand
Various causes all requiring thorough history and physical
examination
• Left ventricular hypertrophy
• ECG to be obtained on abnormal findings
• Right ventricular hypertrophy
• Echocardiography likely indicated (see Table 2)
Decreased myocardial supply
Cardiology consult and follow-up likely required
• Acquired (Kawasaki disease, cocaine/stimulant use,
thrombotic event)
Ischemia
• Congenital (aberrant coronary course, stenotic coronary
orifice, coronary arising from pulmonary artery)
Most prevalent in older children
• Often with recent stressor
• May have specific fears regarding heart attack or heart Attempt to limit unnecessary testing with thorough history; provide
Psychogenic causes disease
reassurance if psychogenic cause most likely
Seizures in Children
 Objectives.
o
Broadly classify various seizure types based on the current seizure classification schema.
o
Recognize seizure mimics and be able to triage patients to the correct specialty.
o
Obtain a seizure history and determine appropriate next diagnostic steps.
o
Counsel families regarding common antiseizure medications and potential adverse effects.
o
Identify commonly encountered comorbidities of epilepsy.
 Epidemiology:
o
Epilepsy = one of most common of neurologic disorders seen in children, with incidence rates ranging from 33.3 to 82 cases per 100,000 per
year; Incidence highest in 1st yr of life and ↓↓ in teen years.
o
Etiology unknown in 50% of pts.
 Approach to diagnosis:
o
Is this a seizure? Exclude other seizure mimics
o
If a seizure, is this provoked? Exclude acute provoked seizures s.a. febrile seizures
o
If unprovoked, what type of seizure is this?
o
Is this epilepsy?
o
What is the epilepsy type?
o
Is there an epilepsy syndrome?
o
What is the etiology?
o
What other comorbidities are present?
EPILEPSY MIMIC
AFFECTED AGE
Benign sleep myoclonus
Neonate and early infantile
Jitteriness
Neonates
Benign myoclonus of infancy
Infancy
Shuddering attacks
Late infancy
Breath-holding spells—
cyanotic or pallid
Infancy, early childhood
Sandifer syndrome
Infancy, early childhood
CLINICAL CLUES
• Myoclonus of ≥1 limbs or the face, occurs in brief flurries lasting <3–5 s with pauses of variable duration
• Occurs in sleep only and abolished on waking
• Otherwise healthy infant
• Affects ≥1 limbs, often switching sides from event to event
• Often spreads in nonanatomical pattern (ie, left leg to right arm)
• Increased when the infant is unwrapped, stimulated, startled, or crying, but suppresses when the infant is
wrapped or the affected limb is held gently
• Brief jerking of ≥1 limbs, lasting <5 s each, without altered awareness
• Occurs in both wakefulness and sleep
• Otherwise healthy infant
• Brief stiffening with shoulder shaking like shivering, without altered awareness
• Often provoked by excitement or frustration
• Otherwise normal infant
• Triggered by pain, crying, fright
• Child usually cries (crying may be absent with pallid breath-holding), holds breath at the end of
expiration, then becomes briefly tonic
• Associated color change—cyanotic or pallid
• Back arching, dystonic posturing of the limbs, and turning/tilting of the head
• May be provoked by feeding and lying flat
• May be alleviated with sitting up
• Often seen in neurologically abnormal children
EPILEPSY MIMIC
Stereotypies
Hyperekplexia
Self-stimulatory behavior
Benign paroxysmal vertigo
Cyclic vomiting
Daydreaming
Parasomnias
Tantrums/rage attacks
Tics
Periodic leg movements in
sleep
Vasovagal syncope
Postural orthostatic
tachycardia syndrome
Panic attacks
Narcolepsy/cataplexy
Hemiplegic migraine
Psychogenic nonepileptic
spells
Cardiac syncope—long QT
AFFECTED AGE
CLINICAL CLUES
• Due to gastroesophageal reflux
• Mannerisms that may be simple (such as body rocking, head banging) or complex (such as finger
movements or wrist flexion/extension)
Infancy–childhood
• These are interruptable by tactile and, at times, verbal stimulation
• May occur in healthy individuals but are seen more commonly in those with autism or intellectual
disability
• Infancy: babies are hypertonic but not spastic; excessive startle is seen with noise or touch, with flexion
of limbs, and with neck retraction; this at times can be associated with apnea and cyanosis
Infancy to adolescence but
becomes less severe with age • A gentle tap using the tip of the examiner's finger on the glabella should trigger an excessive startle that
does not habituate with repeated taps
• Rhythmic hip flexion and adduction with leg crossing, often accompanied by a distant expression
Early childhood
• Interruptable, although the child may be irritable if interrupted
• Abrupt onset of anxiety, feeling off balance; child often grasps onto parent
Early childhood
• May have associated nystagmus
• Paroxysmal events of recurrent emesis that may last hours and be interspersed and symptom-free
Childhood
periods of weeks to months
• Staring off, more likely to occur when engaged in quiet activity such as schoolwork
Childhood
• Can be interrupted with tactile stimulation
• Night terrors, sleepwalking, and confusional arousals are behaviors that arise out of deep non-REM
sleep most commonly in the first few hours after falling asleep; they typically last longer than 3–5 min and
Childhood and, rarely,
occur intermittently
adolescence
• These must be distinguished from nocturnal frontal lobe seizures, which are brief (typically <2 min), very
frequent (multiple per night), and occur throughout the night
• Tantrums are primarily seen in young children and involve relatively brief periods of behavioral
dyscontrol in response to a stimulus; consciousness in not impaired
Childhood to adolescence
• Rage reactions occur predominantly in older children and teens and, while triggered by minor stimuli, are
characteristically out of proportion; patients are often aggressive during these periods, which can last for
half an hour or longer
• Involuntary, sudden, rapid, repetitive, nonrhythmic, simple, or complex movements or vocalizations,
which often occur multiple times per day
Childhood and adolescence
• These are interruptable and can be suppressed, albeit often for only a matter of seconds
• Tics abate during sleep
• Repetitive stereotyped flexion of toes, ankles, knees, and hips
Childhood and adolescence
• Resolve with waking
• Typically triggered by prolonged standing, dehydration, change in posture, warm environment, or
emotional upset (eg, blood draw)
• Preceded by lightheadedness, blurred vision, ringing in the ears, pallor, diaphoresis, abdominal
Childhood and adolescence
discomfort
• Loss of tone that may be followed by brief myoclonic jerks or tonic posturing
• Rapid return to awareness but may remain lightheaded for a brief period thereafter
• Episodic periods of lightheadedness, chest pain, blurred vision, abdominal pain
Adolescence
• Comes on with standing and resolves with sitting/lying down
• Brief episodes, lasting minutes only, with sudden feeling of impending doom, accompanied by shortness
of breath, choking sensation, palpitations, chest pain, paresthesia, dizziness, sweating, trembling, and
feeling faint
Adolescence
• Patient is very frightened but aware
• No postictal sleepiness/confusion
Adolescence, occasionally
• Excessive daytime sleepiness, cataplexy (loss of tone in response to strong emotion), hypnagogic
childhood
hallucinations, and sleep paralysis
• Aura of focal weakness +/- speech disturbance, visual symptoms, and paresthesia onsets before typical
Adolescence, occasionally older
migraine-like headache
childhood
• Often family history is positive
• 2 main semiologies: 1) unresponsive periods without motor phenomena or 2) motor phenomena with
bizarre, irregular jerking and thrashing
Adolescence, occasionally
• Often prolonged >15–30 min
childhood
• Often minimal postictal phase
• Frequent and refractory from onset
• Sudden loss of consciousness, with pallor, atonia, or tonic posturing
Any age
• Often triggered by fright, exercise, surprise, and immersion in water
• Family history of syncope may be present
 Provoked vs unprovoked seizures
o
Febrile seizures affect 3-5% of all children & most do not evolve into epilepsy.
o
Febrile seizure: occurs in children 6 mo – 5 yo w/o hx of epilepsy a/w fever (T >100.9) w/o evidence of an intracranial infection.
o
Other provoking factors: intracranial infection, electrolyte disturbance,s hypoglycemia, TBI.
o
Most cases of provoked seizures are not considered epilepsy (2+ unprovoked seizures occurring > 24 hrs apart or 1 unprovoked or reflex
seizures w/ high probability of recurrence).
o
However, in some types of epilepsy specific triggers may induced certain seizure types (s.a. photosensitive seizures in juvenile myoclonic
epilepsy).
 Seizure types
Surgical Emergencies in the Pediatric Office
 Pediatric pts often p/w chief complaints that may (or may not) be manifestations of surgical emergencies. The pediatrician must consider surgical
etiologies for any chief complaint.
 Complicating factors in surgical consultation: (1) Is this an acute surgical process (2) Non-familiarity/ambiguity of consultation process, (3)
disorganized communication b/w pediatrician, patient, and surgeon, all which can lead to inappropriate referral.
o
o
Inappropriate referrals > wrong specialty/service vs insufficient info to assess urgency or relevance.  unnecessary travel, increased
healthcare costs, patient frustration, inefficient utilization of resources
Solution: Direct communication b/w providers – pick up the phone and have a conversation about triage & referral to address any
concerns/recommendations – e.g. fluid resuscitation initiation
Central Nervous System Tumors in Children
 Presentation:
o
Duration:
Sign/Symptom
Bilious Emesis
 Acute: Signs of  ICP (HA, N/V, gait/coordination abnormalities,
papilledema, Cushing’s triad [HTN, bradycardia, respiratory s esp
bradypnea] = late sign of acute  in ICP). Cushing’s triad may be
o
absent in chronic
hydrocephalus
 Chronic:
Location:
Abdominal
distension
ICP; Macrocephaly in pts w/ open fontanelle 
Acholic stools
Bloody stools
Scrotal Mass
SUMMARY TABLE
Differential Diagnosis

SBO

Malrotation +/- volvulus

Incarcerated inguinal hernia

Internal hernia

Intussusception

Postoperative

Posttraumatic
All

Intestinal obstruction

Malrotation

Internal hernia

Intussusception

Postoperative

Posttraumatic
Infants + children

Hirschsprung-associated enterocolitis

Incarcerated inguinal hernia
Infants

Cholestasis

Biliary atresia
Infants

Intestinal obstruction c/b bowel ischemia

Intussusception

Hirschprung-associated enterocolitis

Postoperative anastomotic ulcers
Children

Intussusception

Polyps

Meckel’s diverticulum

Henoch-Schonlein purpura (IgA vasculitis)

Infectious colitis

Postoperative anastomotic ulcers
Adolescents

Meckel diverticulum

Infectious colitis

IBD

Postoperative anastomotic ulcers
Child

Varicocele

Inguinal hernia
Child & adolescents

Testicular torsion

Torsion of testicular appendage

Testicular tumor

Inguinal hernia
Age Group
All