EXAM II STUDY GUIDE
MODULE 7: GI CONDITIONS
Refeeding
● Monosaccharides (i.e., glucose, fructose) require no digestion, used for refeeding after gastroenteritis
● Disaccharides (i.e., sucrose and lactose) in order to be broken down requires disaccharidases (the enzyme
that is temporarily lost after gastroenteritis) - avoid during refeeding
○ If not absorbed, will increase water in the gut and cause diarrhea
● Polysaccharides (i.e., starch and glycogen) will not irritate the gut as much as disaccharides
Obesity
● Contributing factors
○ Genetics contributes greatly; definite hereditary factors (twin studies)
○ Type of food consumed (HFCS contributes to weight gain; incorporate antioxidants, fish oil,
probiotics; vitamin D, calcium, and protein influence satiety)
■ Higher calcium and vitamin D at breakfast made them burn more fat, more calories, and
decreased intake for the next two meals - encourage low-fat milk or almond milk at
breakfast
○ Microbiota flora of gut (lean individuals have a different microbiome than obese)
■ If an obese individual gets a fecal transplant from a lean individual - they will lose weight
○ SES
○ Females more affected
● What manageable interventions for an obese child - change one thing (be realistic i.e., diet change, increase
outdoor activity)
● In an obese child, it is important to check CMP - higher incidence of nonalcoholic fatty liver
Recurrent Abdominal Pain
● 3 patterns
○ Primary periumbilical paroxysmal pain - classic, functional, non-organic
○ Primary peptic - non-ulcer dyspepsia (recurrent epigastric pain, postprandial fullness, nausea, early
satiety, belching) GERD
○ Lower abdominal pain - IBS or Crohn’s; altered bowel pattern, pain relieved by defecation,
feelings of incomplete evacuation; with Crohn’s will have joint pain, FTT (abnormal growth
curves), anal tags
● Functional, non-organic accounts for 90% of RAP in children - NO structural, infectious, or inflammatory
cause identified
○ Clinical features
■ Crampy pain that lasts minutes to hours
■ Pain is central or poorly localized (periumbilical)
■ Pain is often present on awakening and rarely occurs while sleeping
■ No relationship to meals or BM
■ Pain episodes occur daily or many days or weeks apart
■ During an attack - the child may exhibit a variety of motor behaviors, including doubling
over, grimacing, crying, rolling around in bed or on the floor, clenching and pushing on
the abdomen *makes it appear like something is actually wrong but it is functional
○ Increased incidence of anxiety disorders (80%), depressive disorders, internalizing behaviors,
normal distribution of intelligence
○ Evaluation
■ Ask about red flags - fever, vomiting, diarrhea, weight loss, rash, joint symptoms,
headache, dysuria, bloody stools, pain awakening child at night
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● A red flag is a pain that is not periumbilical or generalized
■ Concurrent somatic symptoms - headache, fatigue, muscle soreness
■ Get detailed social history including family stressors
○ Physical Exam
■ Tenderness to deep palpation on lower abdomen without rebound (over colon in IBS)
■ A rectal exam may reveal hard stool from constipation
■ Careful evaluation of G&D to ensure normal - check growth charts
■ May see autonomic instability (sweaty palms, cold extremities, mild HTN)
Red flags for organic disease
○ Pain not central in location.
○ Pain awakens the child - wakes the individual up at night
○ Pain is related to meals
○ School attendance is normal
○ Vomiting, especially hematemesis
○ Diarrhea, with or without blood
○ Absence of obvious stressful life events
○ Weight loss, or failure to gain appropriately
○ H&P suggestive (anal tags, perianal disease, anemia, fever, age < 5)
Most common organic etiology - fecal retention/constipation
Most common serious pathology - UTI
Recommended initial screening tests - CBC, ESR/CRP, UA with culture, stool for GSA and occult blood,
celiac disease, milk and wheat IgG levels
Always consider CD
○ Anti-gliadin antibody (IgA and IgG) and anti-endomysial IgA antibody serum testing may be
helpful, and TTG IgA antibodies
■ Screen with TTG before putting the patient on GF diet
Encopresis
● Chronic stool leaking in children > 4 years (stool holding, retained stool, dilation of the rectum, decreased
neural sensation and muscle tone)
● Diagnosis - H&P
○ History of constipation or painful BM, leading to holding back stool; patient states they do not feel
the urge to defecate; parents unaware of the loss of sensation; patient oblivious to fecal odor; may
have anxiety and depression from the loss of control;
■ As infant/toddler may have had constipation; during toilet training may have had
increased family stress, over aggressive or “lax” training, toilet fears, painful defecation;
school-age may have fear of public bathroom, ADHD, stress
○ Physical exam - rectal exam *required for diagnosis
■ May palpate stool/megacolon abdominally; will find rectal ampulla full of stool
● Management
○ Educate patient and family on patho
○ Discuss treatments in terms of regaining muscle strength and sensation
○ Discuss long-term (6-12 months) treatment phase *can take up to 1 year to fix
● Treatment
○ Initial - may need both hypophosphate enema QD x 2-3 (to ensure large stool is out) and PO
laxative
○ Day 3 onward continue long-term oral softener or laxative QD - will need to titrate to have formed
not loose stools
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■ Miralax is recommended (daily laxative) and fiber supplements
■ Natural - milk of magnesia, magnesium citrate, senna
Begin twice daily toilet sitting for 10 minutes - emphasis not on producing BM but taking time to
sit; after meals is best
■ Continue BID until regular BM at one of these times, then QD at the time of usual BM
■ Continue for 4-6 months
Regular FU is essential - recommended PE at end of week 1
Long-term management includes nutritional counseling (high fiber, probiotics, fish oil, avoid
simple carbs, increase water), behavioral counseling (self-esteem)
■ Regular visits at first every 1-2 weeks x 2, then monthly, or at least phone contact
Simple Constipation
● Easier to treat because not behavioral; nutritional changes can correct
● May need to soften BM for initial BM with enema or glycerin suppository once
● May need to temporarily increase motility with bisacodyl, MOM, senna
● Add dietary fiber long-term to prevent
● Limit dairy and simple carbs (refined foods, white bread) - exacerbate constipation
GERD
● In infancy - very common and not severe enough for medication; cardiac sphincter involved
○ Symptoms - frequent spitting up, chronic mild upper respiratory mucus; if severe will have
chronic cough and have signs of pain (including arching back)
○ Treatment■ If mild - reflux precautions (r side lying, thickened feeds ie enfamil AR); nasal saline;
most outgrow by age 1
■ If severe - H2RA, Famotidine 1 mg/kg/day divided into two doses in ages 1+
● PPIs if failed H2RA therapy: 1-11 yrs= 15 mg QD <30kg; 30 mg QD >30 kg
● If more severe… also need peristalsis-enhancing meds: erythromycin preferred
dt less AE
● Older children - consider in chronic cough or wheezing; may have heartburn, epigastric pain, sensation of
reflux; halitosis may be present
○ Treatment is usually symptomatic - smaller meals, wait 1h to lie down after meals, elevate HOB,
avoid excess high calcium foods (stimulates acid production)
○ Meds used if painful symptoms or respiratory symptoms
Parasitic Infections - Giardia and Pinworm are most common in developed countries
● Giardiasis - transmitted direct fecal-oral route, from infected feces, contaminated food and water
○ Symptoms - chronic abdominal pain, flatulence, diarrhea
○ Diagnosis - examination of fresh stool for Giardia specific antigen
■ O&P can miss it because the trophoblasts and cysts are still attached to gut wall
○ Treatment - Furazolidone or Metronidazole
● Pinworm
○ Symptoms - rectal itching that is worse at night
○ Diagnosis - complaints of rectal itching, scotch tape test reveals eggs, direct visualization of
mature females around the anus at night
○ Treatment - oral, OTC medication such as Pin-X (one dose, repeat in 2 weeks)
Hepatitis
● HAV - common illness; seen less commonly as more immunized
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Transmitted fecal-oral route
High risk - low SES, endemic areas worldwide, attack rate highest among preschool and
elementary
○ Infection spread during pre-icteric phase; in children, frequently anicteric and clinically inapparent
○ Symptoms - nonspecific; fever, headache, anorexia, nausea, RUQ pain, HSM
○ 99% - full recovery
○ Treatment
■ Give IgG within 2 weeks of exposure = complete prevention of infection 75% of time
■ Give IgG to post-exposure household contacts
■ Limit activity while hepatomegaly
■ Best to prevent - immunize all > 12 months
● Given at either 12&18 mo or @ 12&24mo
HBV - immunization given at birth, 2, 4, and 6-9 months
○ Transmission - can transmit many ways including oral-oral
■ Can transmit when sick or healthy chronic carriers *HAV only spreads when sick
○ Course of infection
■ HBsAg detectable 2-8 weeks before symptoms, insidious onset 50-180 days after
exposure
■ Prodrome of arthritis, arthralgias, body rash - important if patient presents with joint
pain
■ Jaundice (not common), N/V
■ Alterations of LFTs apparent 4-16 weeks post-exposure
○ Lab markers of infection
■ HBsAg 1-10 weeks post exposure
■ Anti-HBc - may be only serological marker of HBV infection after clearance of HBsAg
and prior to rise in HBsAb
■ HBsAb - seen in recovery phase and includes immunity to HBV
○ HBsAg positive mother can transmit to infant, needs immediate HBV immunization and HBV Igimmune globulin
○ Prevention - Vaccine schedule says at 0, 2, and 4-6 months
■ if HbsAg is negative, don’t have to give the birth dose, can give that dose at the 2-month
visit
■ If more than 2 months between 2nd and 3rd immunization, get a much better
immunogenic response
■ Look at the population that you are serving - if it is difficult to make it to FU, then give it
to them at 0, 2, 4 months, or 2, 4, 6 months. But if more likely to be able to come to FU,
give at 0, 2 months and think about giving 3rd 4 to 6 months after the second one, better
booster response
Gastroenteritis
● Most can be managed with PO rehydration and feeding
● Causes of GE in children-- majority are d/t rotavirus infection
● Management
○ Prevention - hygiene, BF, vaccine part of routine infant schedule
○ Must give food and fluids - do not starve patient
○ Dehydration secondary to net losses of ECF (sodium, chloride, water, bicarbonate)
■ Replacement should resemble ECF - water needs sodium in order to be absorbed, sodium
is being excreted
■ Even without dehydration - give fluids to prevent dehydration
Fluid therapy
■ Deficit replacement - estimate % dehydration and electrolyte deficit
● Rapidly restore water, sodium, and chloride
● Slowly restore potassium and bicarbonate
■ Replacement of ongoing losses *just because you rehydrate does not mean they will not
continue to have diarrhea or vomiting
■ Maintenance therapy - maintain homeostasis
● Replace total body water and electrolytes
● Give calories - ensure after 4h rehydration period that you are giving food
○ Assessment of dehydration
■ Mild (common) - will have normal BP and HR; 3-5% of body weight lost
● BP and HR normal
● Skin turgor, fontanelle, mental status normal
● Mucous membranes slightly dry
● UO slightly decreased
● Thirst slightly increased
■ Moderate - 6-9% weight loss
● BP normal but HR increased
● Skin turgor decreased
● Fontanelle sunken
● Mucous membranes dry
● Eyes slightly sunken
● Delayed capillary refill
● Mental status normal to listless
● UO < 1 mL/kg/hr
● Thirst moderately increased
■ Severe - 10% or more weight loss
● BP reduced and HR increased
● Skin turgor decreased
● Fontanelle sunken
● Mucous membranes dry
● Eyes deeply sunken
● Delayed capillary refill and cool, mottled skin
● Mental status normal to lethargic
● UO much less than 1 mL/kg/hr
● Thirst very high or too lethargic to indicate
Treatment - rehydrate, feed, continue rehydration
○ Mild - rehydration with ORS 60 mL/kg over 4 hours, maintenance with BM, formula, food, ORS
■ Give fluid every 3-5 minutes
○ Moderate - rehydration with ORS 110 mL/kg over 4 hours, maintenance with BM, formula, food,
ORS
■ Give fluid every 3-5 minutes
○ Severe - IVF (Ringer’s Lactate) at 20 mL/kg boluses every 30 minutes until pulse and
consciousness normal
■ After VSS - may use ORT above
What to feed after a 4-hour period
○ BM or lactose-free formula (brush border destroyed, avoid disaccharides)
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Soy, almond, rice, or lactose-free cow’s milk for older child
Potatoes, wheat products, rice, cereals
Apples, bananas, pears, melon, beans, peas, carrots, squash
Protein such as turkey, chicken, beef, tofu, eggs, yogurt, nut butters
Small frequent feeds are best, even in older children
Remember to avoid hyperosmotic foods/liquids - avoid very salty or very sweet food or drinks
MODULE 8: OBESITY AND NUTRITION
Vitamins & obesity
● Vitamin D - found in milk, juices, grains, egg yolk, fish and fish oils; exposure to sunlight increases
endogenous vitamin D production
○ Helps control cravings
■ Deficiency is associated with insulin deficiency, insulin resistance, obesity, heart disease,
and autoimmune disorders along with cancers
■ Low levels may contribute to fatigue, depression, and cognitive impairments
○ Children with severe asthma have lower vitamin D
○ Screen 25-OH D levels and treat if < 60
■ Normal is 60-80; 30 is risk for Rickets
○ Supplement with 1000 IU/day vitamin D3 if normal
○ Supplement with 2000-4000IU/day if deficient; supplement should be liquid or gel tablet (more
bioavailable in oil)
■ Can also give weekly doses since it is fat-soluble (one dose a week of 28000 IU)
○ DEFICIENCY DISEASE: RICKETS
● B12 - found in fish, meat, eggs, dairy; relies on intrinsic factor
○ Injected or sublingual supplements
○ Deficiencies - mental changes from confusion and irritability to severe dementia; can also produce
macrocytic anemia
○ ​It remains to be established if prolonged treatment with B vitamins can reduce the risk of dementia
in later life
○ DEFICIENCY DISEASE: PERNICIOUS ANEMIA
● Vitamin C - foods and supplements, bioflavonoids (free radical scavengers and antioxidants)
○ Blueberries contain polyphenolic compounds, predominantly anthocyanins, which have
antioxidant and anti-inflammatory effects; anthocyanins have been associated with increased
neuronal signaling in brain centers, mediating memory function, and improved glucose disposal
■ Anthocyanins responsible for the colors, red, purple, and blue, are in fruits and
vegetables. Berries, currants, grapes, and some tropical fruits have high anthocyanins
content. Red to purplish blue-colored leafy vegetables, grains, roots, and tubers are the
edible vegetables that contain a high level of anthocyanins
○ Results show strong DNA protective effects of the substances tested in accordance with
epidemiological studies linking a diet rich in antioxidative micronutrients with a lowered risk for
cancer development
○ DEFICIENCY DISEASE: SCURVY
● Vitamin E - food and supplements, α-tocopherol (free radical scavengers and antioxidants)
○ Study from class notes - investigated the relations between adiposity and serum concentrations of
carotenoids, retinol, and vitamin E among Mexican-American children 8 to 15 years
○ Significant inverse associations were found between serum concentrations of carotenoids and
vitamin E and adiposity among Mexican–American children, but serum retinol concentrations
were positively associated with adiposity
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DEFICIENCY DISEASE: almost always linked to certain diseases in which fat is not properly
digested or absorbed. Examples include Crohn's disease, cystic fibrosis, and certain rare genetic
diseases such as abetalipoproteinemia and ataxia with vitamin E deficiency (AVED)
The antioxidant supplementation through vitamin E and C and the mineral zinc apparently enhanced
antioxidant protection against oxidative stress and allowed less time for wound healing
○ AND also decrease risk of autism
○ Antioxidant strategies can be used as add-on neuroprotective therapy after perinatal oxidative
stress
○ Antioxidant cocktail (S-adenosylmethionine, vitamin E, and vitamin C) to protect against the
effect of the sucrose on meal-induced insulin sensitization
○ Probable mechanism for the benefits of supplemented formula for decreasing the severity of NEC
by preserving the antioxidant systems
HFCS & obesity
● HFCS causes obesity in rats (increased body weight, body fat, and TG levels)
● Rats with 12-h access to HFCS gained significantly more body weight than animals given equal access to
10% sucrose, even though they consumed the same number of total calories from chow and sugar each day
and fewer calories from HFCS than sucrose.
● Over the course of 6months, both male and female rats with access to HFCS gained significantly more
body weight than control groups. This increase in body weight with HFCS was accompanied by an increase
in adipose fat, notably in the abdominal region, and elevated circulating triglyceride levels
Vegan diet - most at risk for poor nutritional status
● Common deficiencies include calories, iron, calcium, vitamin D, omega-3, zinc, B12, folate
○ Check for IDA and B12/folate deficiency if vegan
○ Monitor 25 OH-D if vegan
● Use of fortified foods very helpful
● Use of calorie-dense foods is helpful (avocado, nuts, healthy oils, dried fruits)
MODULE 9: RESPIRATORY CONDITIONS
Common Mechanisms of Antibiotic Resistance
● Changes in outer membrane proteins which prevent antibiotics from penetrating bacterial cell walls
○ Pneumococcus (i.e., Streptococcus pneumoniae)
○ Treat with high-dose Amoxicillin
● Production of enzymes that inactivate antibiotics
○ Haemophilus influenzae and Moraxella catarrhalis
○ Production of β-lactamase, an enzyme that hydrolyzes the β-lactam rings of penicillin and some
cephalosporins
○ Certain chemicals (K clavulanate or clavulanic acid) can protect antibiotics from enzymatic
breakdown by β-lactamase. These β-lactamase inhibitors lack antibacterial activity - they simply
grant β-lactamase stability to antibiotics which lack this characteristic.
○ Treat with Augmentin
● Changes in affinity for bacterial enzymes - develops ability to hinder binding of the antibiotic to the
appropriate site of antibacterial action
○ Streptococcus pneumoniae develops a resistance to penicillin by altering penicillin binding sites
● Efflux pump development - removes antibiotics from the bacteria
○ Streptococcus pneumoniae infections
○ Seen most recently with use of macrolide antibiotics (i.e., Erythromycin, Clarithromycin,
Azithromycin)
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Biofilm development - play a central role in chronic infections and infections associated with implantable
devices. Importantly, recent research has detected the presence of biofilms in infected tissue involved in
otorhinolaryngological pathology
○ Biofilms are microbial communities which attach to biological or non-biological surfaces and
produce their own matrix. Within biofilm communities, there are cell towers with pores and water
channels for nutrient and waste exchange. The shape of the colony is dictated by the shear forces it
experiences, with colonies varying from mushroom shaped to tadpole shaped. Colony cells have
different roles; their cell specialization is achieved by differential gene expression which alters the
phenotype of individual microbes. Phenotypic changes occur in response to intercellular signaling
or physicochemical gradients within the biofilm. The microbes secrete a matrix of
polysaccharides, nucleic acids and extracellular polymeric substances, termed a glycocalyx; this
has a slimy consistency and is predominantly water.
○ The organisms have varying growth rates, and a proportion will be in a dormant phase at any
particular time. (i.e., Staphylococcus aureus, Pseudomonas, Candida, Streptococcus pneumoniae)
Drugs not effective against β-lactamase producing organisms
○ Amoxicillin, Ampicillin, TMP/SMX, 1st generation cephalosporins and some 3rd generations
Drugs effective against β-lactamase producing organisms
○ Augmentin, Cefpodoxime, Cefprozil, Cefuroxime, Cefdinir, Clarithromycin, Rocephin
(Ceftriaxone), Azithromycin
Penicillin-resistant S. pneumococcus (PRSP)
○ If truly fully resistant to pen/oxacillin, usually the only choice available for peds is Vancomycin
○ If intermed resistance, consider high-dose Amoxicillin, Cefuroxime, or Rocephin (Ceftriaxone)
UPPER
​Inhaled Foreign Bodies
● History may be unreliable
● Reported symptoms can be vague and resemble common respiratory or GI illnesses
● FB inhalation respiratory tract is the most common cause of accidental death in the home in children < 6
years old in the U.S., 85% are children < 3 years old
● Common inhaled FBs - coins, nuts, hot dogs, grapes, candy, vegetables, metal or plastic objects, bones
● Aspirated FB
○ Accurate history and high level of clinical suspicion
○ Up to 64% have negative initial history; 25% asymptomatic at presentation; 40% can have normal
PE
○ If symptoms are not abrupt and acute - can mimic chronic asthma, pneumonia, croup, or
bronchiolitis
○ PE can include wheezing, stridor, crackles, dyspnea, retractions, decreased or asymmetric air
entry, tachypnea, rhonchi, hoarseness, cyanosis, apnea and fever
○ CXR will be helpful, even if the object is not radio-opaque
■ Lung abnormalities caused by the FB are detectable
○ CT if aspiration was not recent, or if CXR negative and you still suspect aspirated FB
Allergic Rhinitis - most commonly inhalants in toddlers
● Symptoms
○ Clear rhinorrhea
○ Nasal mucosa white-gray or pale pink *NOT beefy red - if red consider cold
■ Sometimes edematous nasal mucosa; externally trans-nasal crease (allergic salute)
○ Sometimes allergic shiners and/or Dennie’s lines
■ Itchy, watery eyes, injection of conjunctiva
■ Atopic dermatitis - especially in infants
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■ Frequent wheezing
■ Frequent bacterial and viral URIs
Diagnosis made based on PE
Diagnosis of allergy
○ RAST or immunocap testing of venous blood for specific allergens - be sure test is for specific IgE
allergens
■ Can order specific items to be tested
■ Is common to a particular age group or geographical area (i.e., trees in area)
■ Not as reliable as intradermal skin testing or elimination but easier
○ Elimination trials - useful for food or certain environmental allergens
■ If suspect food allergy, put child on limited hypoallergenic diet, then gradually
reintroduce one food at a time; symptoms of true food allergy usually are present within
1-2 days of beginning the offending food (skin or GI symptoms)
○ Skin testing - most reliable for determining inhalant allergies but it is painful, anxiety-provoking,
and expensive *not recommended for young child
○ Symptomatic treatment - if symptoms improve with empirical treatment of PO antihistamine, you
have confirmed diagnosis of an allergy
Treatment - in addition to avoidance, medications used (begin with antihistamines, if not controlled + nasal
steroid spray, if not controlled + leukotriene modifier)
○ Non-sedating antihistamines
■ Claritin (Loratadine) 10 mg tablet, 5 & 10 mg chewables, 5 mg/5cc liquid for children >
6 months
● First-line; OTC and easy to use (one-dose)
■ Clarinex (Desloratadine) 5 mg tablet, 2.5 & 5 mg chewables, 2.5 mg/5cc liquid for
children > 6 months
● No generic; prescription and $$
■ Allegra (Fexofenadine) 30, 60, 180 mg tablet, 30 mg chewable, 30 mg/5cc liquid for
children > 6 months
● OTC
○ Benadryl is sedating and has too many adverse effects - avoid
○ Leukotriene modifier usually not used as monotherapy; BBW risk for depression, educate parent
Sinusitis - most commonly affected in children is maxillary and ethmoid
● Symptoms
○ Most common history is prior URI which persists without improvement > 7-10 days
○ Purulent rhinorrhea and/or PND > 7-10 days without improvement = standard for diagnosis
○ Malodorous breath
○ Older child may have HA, toothache, fullness, facial pain, and pain to direct palpation of sinuses
● Diagnosis
○ + if history of worsening PRN > 7-10 days with or without other symptoms OR onset is sudden
and acute, with fever
○ PE - purulent muco-pus, very erythematous nasal mucosa, PND may be present
● Etiology - same bug as AOM - Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis
○ others: Streptococcus viridans, Streptococcus pyogenes, Staphylococcus aureus
● Treatment - usually not treated with antibiotics, nasal saline is first line
○ If no periorbital symptoms, fever, or signs of serious illness - symptom treatment first
■ Copious nasal saline every 30-60 minutes and topical corticosteroid spray BID for 3-7
days then QD for 2 weeks
● And/or topical decongestant drops or spray BID for 3 days
ALWAYS use saline first
● If using decongestant drops, use them second; if using corticosteroid spray, use
after saline and decongestant drops
If no improvement after 2-3 days, or if child appears ill/febrile, systemic antibiotics used
■ Augmentin 90 mg/kg/day divided into twice a day doses max 4 gram/day for pediatric
sinusitis
● If allergic to penicillin - cephalosporin used (if anaphylaxis to penicillin, cannot
use cephalo, use macrolide- SMX/TMP & clarithromycin
■ Probiotics - Lactobacillus and Bifidus (10-20 billion IU/day) BID while on antibiotics
and for at least 1 month afterward
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AOM
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Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis
○ Over 50% can be B-lactamase producing, and S. pneumo is penicillin resistant - use high-dose
Amoxicillin that is resistant to B-lactamase - AUGMENTIN
Symptoms - can range from no pain to acute ear pain
○ Younger child - pull at ear, shake head, cry at night
○ Older child - ear pain, fullness, decreased hearing
○ Usually following URI or pharyngitis/tonsillitis
Diagnosis - can only be made using an otoscope with pneumatic insufflator; a red tympanic membrane does
not indicate AOM
○ Can only be diagnosed by one of the following
■ TM immobile with pneumatic otoscopy
■ Frank pus visualized in the MES
■ TM visibly bulging
■ Obvious bullous lesion on TM
Treatment - 50-80% will resolve without antibiotics
○ If watchful waiting - pain control (Ibuprofen, Acetaminophen, topical anesthetic drops), FU 2-3
days, consider giving antibiotic if worsening, FU 2-4 weeks to ensure resolved
○ Antibiotics needed for most children < 2 years, especially if fever and severe pain; older child with
fever and severe pain; any child with concurrent bacterial process
■ First line is Amoxicillin 90 mg/kg/day divided into two doses for 10 days - AAP
Guidelines
■ Augmentin 45 mg/kg/day divided BID for 10 days
● Use 90 mg/kg/day if using first line - Recent Lit, use lower dose if you have
already been treated with 90 mg/kg/d of Amoxicillin without improvement
(should have eradicated pen-susceptible pneumococcus)
LOWER
Influenza
● Vaccination - if 6 months to 9 years old will need a booster one month if first flu shot; if > 9 years, no
booster
COVID-19 - can only immunize 12+
● Symptoms - fever, fatigue, headache, myalgia, cough, rhinorrhea, new loss of taste or smell, sore throat,
dyspnea, abdominal pain, diarrhea, N/V, poor appetite especially in babies under 1 yo
○ Most common in children - cough and fever
● Diagnosis
○ Nasopharyngeal - rapid antigen, PCR
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○ Spit PCR - results in 24 hours
Treatment
MIS-C
○ Diagnosis
■ An individual < 21 years with fever, lab evidence of inflammation, and evidence of
clinically severe illness requiring hospitalization with > 2 organ involvement (cardiac,
renal, respiratory, hematologic, GI, dermatologic, or neurological)
● Inflammatory markers - elevated CRP, sedimentation rate, fibrinogen,
procalcitonin, D-dimer, ferritin, LDH, IL6, or increased neutrophils OR low
albumin
■ AND no alternative plausible diagnosis
■ AND positive for current or recent COVID-19 by PCR, serology, or antigen test OR
exposure to a suspected or confirmed COVID-19 case within the 4 weeks prior to
symptom onset
○ Symptoms - usually present with persistent fever, abdominal pain, vomiting, diarrhea, skin rash,
mucocutaneous lesions and, in severe cases, with hypotension and shock
■ Elevated laboratory markers of inflammation (i.e., CRP, ferritin), and in a majority of
patients laboratory markers of damage to the heart (i.e., troponin; BNP or proBNP)
■ May develop myocarditis, cardiac dysfunction, and acute kidney injury
■ *Kawasaki disease is a differential diagnosis
Strep Throat
● Most common - GABHS (Streptococcus pyogenes)
○ Must swab ALL inflamed throats unless you are treating with an anti-strep antibiotic (augmentin
or amoxicillin)
■ GABHS is most common cause of any anterior cervical lymphadenopathy even in
absence of other symptoms - must swab child
○ Best GABHS detection - antigen detection testing with throat culture if negative antigen test
■ Can only rule out strep when negative rapid test AND negative throat culture
■ Can also detect GABHS via serum testing: ASO titer, AntiDNaseB, Anti-streptozyme
● After acute infection has resolved
● Symptoms - sore throat, dysphagia, fever, headache, stomach ache, vomiting, tender anterior cervical,
tonsillar, submandibular lymph nodes
○ PE - red pharynx and tonsil, possible exudate, possible petechiae of post palate (strawberry
tongue), malodorous breath, anterior cervical, tonsillar, and submandibular lymphadenopathy
○ Scarlatiniform rash (scarlet fever) - fine, red, rough papular rash, usually begins in the groin and
ends with the peeling of the fingers and/or toes
● Treatment - Penicillin first line if no allergy
○ Bicillin 50,000 U/kg/dose IM single dose
○ If allergic to penicillin - PO Cephalosporin or Macrolide
○ Amoxicillin 750 mg QD for 10 days OR 45 mg/kg/day divided BID for 10 days
○ If resistant
■ Augmentin 45 mg/kg/day divided BID for 2 weeks
■ Clindamycin 20-30 mg/kg/day divided TID for 2 weeks
■ If still resistant after either of these, refer to ENT
Asthma - true asthma symptoms are REVERSIBLE
● Features of asthma
○
●
●
1. Peri-bronchial smooth muscle contraction in response to irritant - typically first phase of airway
narrowing and easiest to reverse with bronchodilator
○ 2. Inflammatory response of airways due to presence of histamine causes edema of airways,
further narrowing them - second phase of airway narrowing and requires antiinflammatories like
corticosteroids to reverse
○ 3. Increased mucus production *not always r/t asthma, can occur with CF
■ If asthma NO structural changes
○ Structural abnormalities are NOT asthma
Symptoms
○ Asthma in early childhood
■ Transient early wheezing (will outgrow, uses bronchodilator PRN)
● At risk - siblings with it, daycare, mom smoking, premature, RSV 1st 2-3mo,
exclusive formula feeding
● Usually resolves by school age
● Onset by 1 year, associated with viral URI, cockroaches and house dust, males
■ Non-atopic wheezing
● Dec by 10 yo
● Associated with viral URI (RSV) in 1st 2 to 3 years of life, premature, formula
feeding
■ Allergic/IgE associated/atopic wheezing – don’t outgrow
● Allergic rhinitis, eczema
○ Can range from slight cough to severe respiratory distress
○ Some patients may only have a prolonged expiratory phase to signal airway compromise
■ Wheezing does not have to present to diagnose asthma
■ Some may only present with a chronic or recurrent cough
Diagnosis
○ Intermittent (symptoms only present when sick) - have flare ups but completely fine in between
episodes of wheezing
■ Normal spirometry, normal peak flow, no coughing at night, normal exercise tolerance
■ Only medications during flare up - treated with bronchodilator PRN
○ Mild persistent (inhaled corticosteroid daily and possibly PO leukotriene modifier)
○ Moderate persistent
○ Severe persistent
■
■
■
■
●
●
Largely a clinical diagnosis, child with FH of asthma presents with episodic and recurring
chest tightness, cough, difficulty breathing, or wheezing in response to common triggers
who also demonstrates improvement with a SABA
< 5 years - unable to reliably obtain PFTs
● Asthma Predictive Index - clinical tool applied to children < 3 with wheezing to
treat and diagnosis of asthma or to measure for airway inflammation using
fractional excretion of nitric oxide (FeNO)
Older - demonstration of reversible bronchospasm on PFT is diagnostic
PFT
● FEV1 - forced expiratory volume in 1 sec; FEV1% - ratio of FEV1 to forced
vital capacity
○ FEV1% < 0.8 is diagnostic for airflow obstruction, and reversibility
with bronchodilator is diagnostic of asthma
○ FEV1% > 0.8 is NORMAL
■
Management
○ Long-term control (used to prevent/control symptoms in persistent asthma)
■ Inhaled corticosteroid (i.e., Fluticasone) *want one with high binding affinity
● Mainstay of long-term therapy
● Can be used 2-4 times a day in acute exacerbation
■ Leukotriene modifier (i.e., Montelukast)
● Approved for children as young as 1 years old
● Once daily dosing
● May be helpful in allergic rhinitis
○ Quick-relief medication (for ALL exacerbations - intermittent or persistent asthma)
■ SABA (i.e., Albuterol)
■ Anticholinergic (i.e., Ipratropium bromide) - may + with beta-blocker, not first line
■ Systemic corticosteroids (i.e., Prednisone) do not need to taper if < 10 days
■ Inhaled corticosteroids off-label can use BID-QID in acute exacerbations
Management of acute exacerbation in outpatient
○
○
●
Immediate SABA in nebulizer or with spacer
If no improvement within a few minutes - 2nd dose of SABA, consider adding 0.25-0.5 mg of
Ipratropium (optional in this step), start chest PT
○ If no improvement after 2nd dose - systemic corticosteroid (PO, IM, IV), 3rd dose of SABA plus
Ipratropium, chest PT
■ Patient should have improvement after 2 hours of systemic corticosteroid
○ Inhaled SABA and Ipratropium hourly for 2 hours
○ If it improves and has response sustained for 60 minutes after last treatment - home
○ If no improvement - hospitalize
Management of severe exacerbation - immediate O2, systemic corticosteroid, and add Ipratropium to 1st
nebulizer if pulse ox < 91%, tachypnea, or increased work of breathing
Bronchiolitis - usually in children < 2 years
● Symptoms - respiratory illness of acute onset
○ Tachypnea - prolonged expiratory phase
○ Wheezing
○ Young infant - respiratory distress (retractions, nasal flaring)
○ A lot of clear nasal secretions, cough impressive, clear rhinorrhea
○ Rarely cyanotic, rarely need CXR, no decreased breath sounds
○ Usually parent describes mildly ill infant
○ Low grade fever may be present
● Mild - normal pulse ox, moderate tachypnea, minimal respiratory distress, infant alert/awake/feeding well
● Moderate-severe - abnormal pulse ox, increased WOB, tired/lethargic/poor feeds/irritable
● Complications - respiratory fatigue leading to abrupt respiratory failure; having bronchiolitis as infant
associated with developing asthma
● Treatment
○ Mild - supportive
■ Keep the nose clear - aggressive nasal saline (every 30-60 minutes to clear airway)
■ Humidified, clean air
■ Chest PT and postural drainage (butt higher than head to drain)
■ Inhaled bronchodilator if positive clinical response to point-of-care neb - will send home
with beta 2 albuterol
■ Consider PO steroid for 3 to 5 days - not common
■ Careful observation at home with daily FU
○ Moderate-severe - hospitalize
● Immunization available (monoclonal antibody) - Synagis is given IM monthly during the RSV season to
susceptible infants.. NP’s job to see if their patients qualify…
Pneumonia - infection of alveoli (viral, bacterial, or mixed)
● Symptoms
○ History of cough
○ May be associated with URI
○ Fever present or absent depending on etiology
● PE
○ Fine rales (crackles) audible over lower airway
○ May or may not have decreased BS
○ May or may not have changes in percussive sounds
○
●
●
●
Percuss lung fields - areas of well-aerated lung will be resonant, or tympanic, to percussion.
Dullness to percussion indicates denser tissue, such as zones of effusion or consolidation
○ Egophony - while listening to the chest with a stethoscope, ask the patient to say the vowel “e”.
Over normal lung tissues, the same “e” (as in "beet") will be heard. If the lung tissue is
consolidated, the “e” sound will change to a nasal “a” (as in "say").
○ Bacterial - usually produces tachypnea independent of fever - this means if you treat fever and 30
minutes later, they still have tachypnea it is likely bacterial pneumonia (Strep pneumo)
■ Tachypnea independent of fever typically represents bacterial pneumonia
● Caused by Strep pneumo
■ < 5 years most commonly viral - RSV, influenza, parainfluenza, adenoviruses
● 20% bacterial - S. pneumo, H. flu, M. cat
■ > 5 years most commonly - Mycoplasma and CAP
○ Only CXR if toxic appearing child, respiratory distress, absent breath sounds in lobe or section of
lung
■ Consider FB if acute onset and slow resolution
Typical (classic pneumococcal)
○ Acute lobar or segmental pneumonia
○ Ill-appearing
○ Fever 102+, cough
○ Leukocytosis (WBC > 15,000)
○ Tachypnea or difficulty breathing
○ Inspiratory crackles
○ Coarse rhonchi
○ Dullness to percussion
○ May describe abdominal pain
○ Good clinical response to B-lactam antibiotics (penicillin and cephalosporins)
○ PCV immunization continues to decrease pneumococcal pneumonia incidence
■ Other causes - GABHS, Staph, H. Flu
Atypical (mycoplasmic)
○ Sub-acute (gradual) onset
○ Little or no fever
○ Not ill-appearing
○ Cough for days to weeks before seeking medical attention
○ No significant leukocytosis
○ Normal RR
○ Can have prominent extra-pulm symptoms - headache, sore throat, URI symptoms
○ Crackles localized or diffuse
○ CXR not helpful
○ No clinical response to B-lactam antibiotics – will not improve with penicillin or cephalosporin
○ Slower improvement - FU IN ONE WEEK
○ Other causes - C. pneumoniae, influenza, adenovirus, RSV, hMPV
○ *Mycoplasma pneumonia or chlamydia pneumonia is cause of this - will treat with macrolide
(Arithomyin, Azithromycin, Clarithromycin)
FU appointment for both typical and atypical in office apt in one week
MODULE 10: RHEUMATOLOGY AND IMMUNOLOGY
● Most common humoral (immune) antibody deficiency is selective IgA deficiency
○ Chronic infections of sinuses and middle ear are common
○
Tend to outgrow this
Primary Immunodeficiency
● Signs
○ Family history (unexplained death, sepsis, recurrent infection)
○ Frequency of infection (> 8 in one year OM or > 1 in one year pneumonia)
○ Chronicity of infection - persistent OM, sinusitis, recurrent abscesses, bronchiectasis, sepsis,
meningitis
○ Severity of infection
○ Infectious complications (mastoiditis from OM)
○ Multiple infection sites
○ Infecting organisms are recurrent or opportunistic
○ Poor response to therapy (treatment for 2 months without effect)
○ FTT, diarrhea, dermatitis
● Testing
○ Quantitative immunoglobulins with IgG subclasses (IgA, IgE, IgM, IgG and 4 subclasses)
○ CBC (focusing on total lymphocyte count and total neutrophil count)
○ CH50
JIA
●
●
●
●
Arthritis in at least 1 joint for 6 weeks or more in a child under 16 years
○ Arthritis defined as swelling OR 2 of the following - decreased ROM, tenderness to palpation,
pain with motion, joint warmth
Symptoms - arthritis, morning stiffness, night pain, limp, refusal to walk
○ Can be systemic - fever (think ALL), fatigue, anorexia, weight loss, irritability
Oligoarthritis - no hips or SI joints
○ Persistent - never more than 4 joints, young age at onset, leg length discrepancy seen
■ Usually not severe
○ Extended - > 4 joints after first 6 months
■ Destructive
Differentials
○ Infection
■ Lyme if monoarthritis (one joint) Alachua county actually has a lot of lyme ticks…
○ Reactive arthritis
■ Rheumatic fever (missed strep!!)
● ASO, anti dnaseB
■ Post-vaccine
■ Serum sickness
■ Viral: HBV, toxic synovitis
■ Bacterial: septic arthritis
● Sed rate, CRP- these will be abnormal if bacterial!
○ Connective tissue disease
■ SLE
● Incidence in childhood generally after age 5, and more common in adolescence
● Fever, malaise, weight loss, malar erythematous photosensitive rash
● Arthritis, commonly small joints of hands, wrists, elbows, shoulders, knees and
ankles, arthritis commonly transient and migratory
● Arthritis pain more severe than objective findings
●
●
●
○
HSM, nephritis, pericarditis
Anemia, leukopenia, thrombocytopenia
SLE Diagnosis: 4 of the following 11 criteria
○ Malar rash, discoid-lupus rash, photosensitivity, oral/nasal
mucocutaneous ulcerations, non-erosive arthritis, nephritis (proteinuria,
casts), encephalopathy (seizures, psychosis), pleuritis or pericarditis,
cytopenia, ANA+, Immunoserology + (nDNA, Sm nuclear antigen,
false + syphilis)
■ Inflam bowel disease
■ Scleroderma
● Skin: Reynaud's, calcifications, ulcerations, telangiectasias, pigmentation
● Musculoskeletal: contractures, weakness, atrophy
● GI tract: abnl esoph motility
● Pulmonary: abnl diffusion and vital capacity
● CV: CHF, cardiomegaly, EKG abnormalities
● Labs: abnormal ANA
■ Vasculitis (HSP) Henoch-Schonlein purpura (IgA vasculitis)
■ Dermatomyositis
● An acute transient myositis occurs in some children following viral illness.
● Symptoms: muscle weakness, muscle contractures and atrophy, muscle pain and
tenderness, rash, arthritis and arthralgia, Reynaud's, Elevated serum muscle
enzymes (creatinine kinase, aspartate transaminase, alanine transaminase and
aldolase)
Neoplasias
■ ALL
● Any time they say their arm or leg hurts you gotta think ALL, especially with
FEVER
● COMMON SYMPTOMS: Fever, malaise, bone/joint pain, bruising/petechiae,
H/SM, lymphadenopathy, normal WBC, anemia, thrombocytopenia
MODULE 11: MSK CONDITIONS
Genu Varus (Bowlegs) - normal positional variant
● 2 positional anomalies - femoral anteversion (femur pointed outward) and internal tibial torsion (femur and
knee straight but tibia is internally rotated)
● If not too severe, will outgrow - ensure hips have good ROM
○ Refer if, when medial malleoli compressed the distance between the knees exceeds 5 cm in 2 year
old, or 8 to 10 cm in 5 year old
Genu Valgus (Knock knees) - also a normal positional variant
● Refer if, when knees compressed the distance between the medial malleoli exceeds 5 cm in 2 year old, or 8
to 10 cm in 5 year old
DDH
●
●
Early detection and treatment - complete correction; missed diagnosis can lead to permanent hip dysplasia
○ Assess every infant and toddler
○ Treatment, if instituted early in infancy (by 4-8 weeks of age) - complete growth of a normal
acetabulum
If a suspicious hip is detected, simple U/S can establish diagnose
○ NB will have a + Ortolani’s and + Barlow’s sign
■
○
*Ortolani and Barlow will become normal by 4-6 months of age, even with DDH (normal
ligamentous tightening) - will have to look at other abnormalities (thigh fold creases,
etc.)
Older children will have asymmetrical thigh fold creases, one thigh appearing shorter than the
other, abnormal abduction, abnormalities of gait, and + Galeazzi sign (unequal knee heights)
Torticollis
● Results from congenitally shortened sternocleidomastoid muscle on affected side - causes head tilt to
affected side
○ Apparent as early as 2 to 3 weeks of age but more noticeable 2 to 4 months old (more apparent
when child can hold head up)
● Must assess SCM muscle for masses - if none found, ensure infant’s head can be passively manipulated to a
neutral position
○ If barely noticeable torticollis and infant is neurologically normal - daily home PT (overstretching
to other side for at least 30-60 seconds several times per day, this is not pleasant; also try placing
objects of interest to the side that is not affected so child is forced to move head into neutral
position) *usually resolves by 9 to 12 months of age with intervention
Scoliosis
● Lateral curvature of vertebral column, may have rotational component
● Signs
○ Sometimes evident by palpation of each spinous process with child standing
○ Asymmetry of iliac crest height or scapular height
■ One shoulder higher or one shoulder blade higher and more prominent
○ Head not centered over body
○ Unequal gaps between arms and trunk
○ One hip more prominent
● Examine child standing and Adam’s forward bending test (bent over with arms dangling and head down)
○ Examine spinous process for alignment - ensure you assess entire spine
○ Examine both sides of ribcage for symmetry - one rib may be higher than other (usually of T spine
indicating rotational deformity)
● Diagnosis
○ Scoliometer - normal is zero degrees
■ > 7 degrees - XR
○ May require XR to include Cobb’s angle measurement of curvature
■ Refer to ortho if Cobb’s angle is > 20 degrees, especially in early puberty during growth
● Management
○ Must have regular FU during growth, even if no treatment (every 3 months until epiphyses fuses)
○ Recommended PT
Legg-Calve-Perthes Disease (LCPD) *limp in school-age
● Affects more males than females; average age of onset is school-age around 7
● Avascular necrosis of head of femur - requires early diagnosis and treatment to prevent hip replacement
○ Prognosis is excellent if discovered before extensive damage
● Symptoms - limp (sometimes with pain localized to affected hip), commonly complain of thigh or knee
pain *will not say hip hurts
● PE - internal rotation is limited and painful; + Trendelenberg sign (failure to maintain a leveled pelvis
while standing on affected leg)
●
●
Diagnosis
○ Labs - normal CBC, elevated ESR
○ H&P and U/S
Treatment - requires referral to ortho always
○ Non-weight bearing on affected hip for 9-18 months if severe
■ Sometimes decreased activity and NSAIDs are enough
Slipped Capital Femoral Epiphysis *limp in adolescent
● Males more affected; onset early adolescence - more common in overweight adolescents
● Unilateral most of the time and L more affected
● Symptoms
○ Pre-slipping phase - mild hip pain (perhaps referred to knee or thigh), usually after a minor strain
or injury
■ Pain persists and eventually will have limp and decreased mobility
○ Acute slip phase - acute pain and obvious limp with very limited mobility
● PE - very limited internal rotation and flexion of hip
○ Position of comfort - external rotation
● Diagnosis - XR
● Treatment - surgical reduction and pinning; refer to ortho
Wrist Fracture
● History - child falls, breaks fall with hand or arm outstretched (FOOSH - fall on out-stretched hands)
○ History compatible with injury - important for abuse
● Most commonly the radius, or both radius and ulna, are fractured, usually distally
● Fracture PE reveals point tenderness over the site of the fracture
○ May or may not be edema or ecchymosis present
● If neurovascular status is normal and XR reveals a non-displaced fracture, can treat with simple
immobilization with cast or splint and FU in 4 to 6 weeks *in scope of practice
Radial head dislocation (nurse maid’s elbow)
● History is of sudden pull or tug on lower half of arm, with immediate pain and refusal to use affected arm at
all
○ As long as the arm is immobile and slightly pronated, pain is absent or minimal
● Complete exam without moving elbow
● No XR
● Treatment - easily reducible especially if diagnosis is made within a few hours before edema forms
○ Ensure no fractures present before reduction - check bones from neck to fingertips before
performing
○ Stabilize elbow with one hand and grasp child’s hand as though shaking hands
○ Reduce by simultaneously supinating the hand while applying pressure toward the elbow, then flex
the arm at the elbow
○ If reduction is successful - will immediately be able to use the arm without pain but may be
hesitant to do so at first
Ankle Sprain
● History - important
○ MOI
○ Pain - if heard/felt a pop may indicate more serious ligament damage
○
●
Previous injury to site
PE
○
●
●
Observe child walk if able to; if cannot bear weight > 4 steps and pain to palpation of malleus will
need XR (Ottawa)
○ Observe active ROM
Palpation
○ Bony structures - should be non-tender with sprain
■ Tenderness - XR to rule out fracture
○ Ligaments - lateral ligaments first (anterior talofibular - most common; calcaneofibular and
posterior talofibula - second most common sites) then medially (deltoid ligament complex)
■ Lateral more common than medial
Treatment
○ First begin with ROM - stretching - strengthening - proprioception
○ Anterior Drawer
■ The test is performed with the patient's foot in a neutral position. The lower leg is
stabilized by the examiner with one hand. With the other hand, the examiner grasps the
heel while the patient's foot rests on the anterior aspect of the examiner's arm. An anterior
force (direction of the arrow) is applied to the heel while holding the distal anterior leg
fixed. Excessive anterior displacement suggests ligamentous injury.
○ Inversion Test
■ The knee is flexed at 90 degrees while hanging over the edge of the table, and the
gastrocnemius is relaxed. Patient is short sitting.
■ The heel is held by one hand and the tibia and fibula are held with the other hand. The
hand on the heel is placed somewhat inferiorly lateral to push the calcaneus and talus into
inversion. The other hand is on the medial side of the lower leg.
■ Provide an inversion stress by pushing the calcaneus and talus inward while pushing the
lower leg laterally. Repeat with the ankle plantar flexed.
■ + = When the talus tilts excessively on the injured side more than the uninjured side. Pain
can also be associated on the injured side.
Grades of Sprain
● Grade 1 - common, can manage in office
○ Stretching or very minor tear of the ligament
○ Mild edema and tenderness over the injured ligament
○ Pain to palpation of the injured ligament
○ No instability (negative drawer and tilt tests) and minimal loss of function
● Grade 2 - XR and refer
○ Incomplete but more significant tear of the ligament
○ Moderate swelling at the site, with further edema surrounding the site; mild to moderate
ecchymosis
○ Pain with palpation of the ligament
○ Moderate functional loss and decreased ROM
○ Mild instability (positive drawer or tilt test)
● Grade 3 - refer to ortho
○ Complete tear of the ligament
○ Severe edema and ecchymosis
○ Loss of function and ROM
○ Significantly positive drawer or tilt test
Knee Injuries
● Meniscus - cushion in knee
● Most common - ACL injuries, MOI typically planting the foot then turning, patient usually hears or feels a
“pop” and experiences immediate pain
● Tests to diagnose ACL tear
○ Anterior drawer test - knee at 90 degrees, stabilize foot, grasp lower leg below knee, pull towards
you
■ If any movement - abnormal and must refer
○ Lachman test - knee at 30 degrees, grasp thigh and push posteriorly while grasping lower leg
below knee and pulling anteriorly
■ If any movement - abnormal and must refer
○ Confirmation of torn ACL diagnosis - MRI
● Treatment - rest, ice, PT, surgery if no improvement
Knee Pain & Meniscal Tear
● Differentials
○ Baker’s cyst - popliteal cysts (RA, OA, internal derangements of knee) can rupture causing
posterior pain, erythema, swelling
○ Patellar tendonitis - not present unless rupture has occurred large effusion and limited ROM
extension
○ ACL tear - history of injury with popping, swelling, and giving way of knee
○ MCL tear - history of injury with pain, joint instability, force against lateral knee
● History - age, OLD CARTS, history of swelling, any trauma, medications/surgeries
● PE - inspection, palpation, ROM (start on unaffected side), strength, neurovascular, special maneuvers
● Diagnostics
○ Location of pain
■ Anterior - patella, patellar tendon patellofemoral pain syndrome, patellar tendinopathy,
osgood-schlatter, prepatellar bursitis
■ Medial or Lateral - meniscal injury, sprain or rupture of collateral ligament MCL/LCL
sprain/rupture, IT band syndrome
■ Posterior - PCL, posterior meniscus PCL tear, hamstring tendinopathy
■ Diffuse - chronic, infectious malignancy OA, RA, gouty arthritis
○ Special Maneuvers
■ ACL pivot shift test, Lachman test, Anterior Drawer Test
■ Effusion ballottement test, noticeable swelling
■ Meniscal tear
● Thessaly test - patient stands on one foot, knee at 20 degree flexion, then
internally and externally rotates knee 3 times
○ Positive if pain on medial or lateral joint line
● McMurray test - bend the knee, then straighten and rotate it; this puts tension on
a torn meniscus. If pt has a meniscus tear, this movement may cause pain,
clicking, or a clunking sensation within the joint
○ The knee is then fully bent and pulled toward outwards in a
"knock-kneed" position
■ Start rotating the foot internally while extending the knee
■ Any pain or "clicks" - lateral tear
○ The knee is fully bent and pulled toward outwards in a "bow-legged"
position
■ Start rotating the foot externally while extending the knee
■
●
Any pain or "clicks" - medial tear
Imaging
○ XR
■
●
●
Ottawa knee rule - >55yr, inability to bear weight for 4 steps immediately after injury or
in ED, inability to flex knee @ 90 degrees, tenderness over head of fibula or isolated to
patella w/o other bony tenderness
■ Pittsburgh Knee Rule - 12-50 yr, fall or blunt trauma 55yr, inability to bear weight for 4
steps immediately after injury or in ED
○ US - effusions
○ MRI - ACL/PCL or meniscal tears
Treatment - RICE, NSAIDs/APAP, PT, OT
Referral & FU
○ URGENT REFERRAL IF - severe pain, immediate swelling, instability or inability to bear weight
due to acute trauma or signs of infection (fever, swelling, erythema with limited ROM)
■ Could be rupture of knee, consider infectious arthritis
○ To ortho if - trauma with effusion, fever erythema and edema, pain with infection, bleeding
disorders, anticoag, symptoms that limit activity, locked knee, severe pain
Osgood-Schlatter’s Disease
● Overuse of thigh muscle (i.e., squatting, biking), quadriceps tendon is avulsed away from tibial tuberosity
producing tibial apophysitis
○ More common in adolescents and resolves when growth plate fuses
● History - no injury
● Diagnosis
○ Knee pain
○ Exam reveals swollen, tender area over the anterior tibial tubercle, painful to direct palpation
○ All other aspects of knee are normal
● Treatment - ice, NSAIDs, avoidance of activities requiring repetitive knee bending
○ Usually self-limiting, may take years to resolve (when growth complete)
Sever’s Disease
● Calcaneal apophysitis - common in adolescents (during active bone growth ages 10-14)
○ An inflammatory condition of the growth plate of the calcaneus
● Presents with heel pain, worse with walking/running/direct palpation of heel
○ On exam - pain on distal calcaneus
● Treatment - ice, rest, soft heel inserts in shoes
○ Self-limiting; symptoms resolve once bone growth is finalized (age 16-22)
Toxic Synovitis of Hip *limp in preschooler
● Common viral infection of the hip following any viral illness
● Acute onset of limp and obvious hip pain on exam; PE reveals no erythema, edema, or systemic symptoms
○ Child is recovering from a cold, goes to bed fine, wakes up and unable to bear weight on legs
● Decreased ROM of hip and obvious limp with antalgic gait (very little time on affected leg).
● Labs - CBC and ESR/CRP
○ If these are normal - unlikely something serious
● Treatment - Ibuprofen and should see improvement in 3 to 5 days
Must always consider Septic Arthritis when a child presents with limp
●
●
●
●
●
●
●
Usually hematogenous spread
○ Usually S. aureus
○ Can be H. influenza in 1 to 5 year old
An acute bacterial process of the hip which presents as a limp
Most commonly hips and knees affected; older child may have joint pain; may be fever but can be afebrile
Child can appear more ill
PE - joint pain with ROM
CBC - indicated bacterial; ESR/CRP - markedly elevated
Requires immediate ortho consult for aspiration
PCL -
JIA TYPE
JRA TYPE
INC
IDE
NC
E
CHARACTERISTICS
M/F
RF/
ANA
EY
E
SX
SEVERE
ARTHRI
TIS
Systemic
Systemic
10%
Arthritis + systemic sx
50% remit in 1st year
Large and small joints
With or preceded by daily F x
2 weeks plus 1:
-rash: evanescent, transient,
erythematous
-generalized lymphadenopathy
-HSM
-pericarditis/serositis
M=F
-/-
No
25%
F>M
-/
+25
%
15
%
10-15%
Peak onset 1-6 yrs
Can have generalized growth
abnormalities
Polyarthritis
RF -
Polyarticular
RF -
20%
5+ joints involved
Large and small joints
10% devel destr joint dz
Polyarthritis
RF +
Polyarticular
RF +
5%
5+ joints involved
Large and small joints
Rheumatoid nodules
Severe destr joint dz
Like adult RA
Seen more in older children
RF+ x 2 tests 2 mos apart
F>M
Oligoarthriti
s:
Pauciarticula
r
Early onset
40%
< 5 joints
No hips or SI joints
F>M
Never > 4 joints
Young age at onset
Leg length discrepancy seen
-Persistent
+/+5
0 to
75%
No
Majority
-/+6
0%
Yes
if
AN
A+
Usually
not
severe
> 4 joints after 1st 6 mos
-Extended
-/Occ
as
Enthesitis-R
elated
Arthritis
Pauciarticula
r
Late onset
15%
< 5 joints
SI and hips involved
HLA B27+
M>F
-/-
Psoriatic
Arthritis
Excluded
<5
%
Arthr AND Psoriasis
OR
Arth and at least 2:
-Dactylitis, nail abnormalities,
FH psoriasis 1º relative
-/-
Other
Excluded
5-10
%
Unknown cause
Persists at least 6 weeks
Doesn’t fulfill criteria for any
category or fulfills criteria for
more than 1 category
-/-
Occ
as
Occ
as
Destruct
ive
Ankylos
ing
spondyli
tis
Sometim
es
present