PEDIATRICS Flashcards
IMPETIGO
- common, contagious, superficial skin infection
- highly contagious, superficial vesiculopustular skin infection
Typically occurs at sites of superficial skin trauma (ex: insect bite)
- primarily occurs on exposed surfaces (ex: ** FACE ** or extremities)
RISK FACTORS
⦁ warm / humid conditions
⦁ poor personal hygiene
CAUSE
⦁ strep pyogenes (GABHS)
⦁ staph aureus - produces exfoliative toxin A
⦁ combo
- high incidence in children
- self limiting (will eventually go away), but if not treated = may last weeks to months
** POST - STREP GLOMERULONEPHRITIS **
⦁ Occurring most commonly in children age 5-12 years
⦁ Patients develop symptoms 3- 6 weeks after streptococcal impetigo
⦁ Symptoms of PSGN include gross hematuria, facial edema, renal insufficiency, brown colored urine, and hypertension
PE
⦁ nonbullous and/or bullous
⦁ have vesicles and bullae containing clear yellow or slightly turbid fluid without surrounding erythema
⦁ superficial small vesicle or pustules 1-3 cm lesions
⦁ ** GOLDEN - YELLOW, HONEY CRUSTED LESION **
TYPES OF IMPETIGO
⦁ NONBULLOUS = impetigo contagiosa = vesicles, pustules = characteristic “honey colored crust” = MC type. Is associated with regional lymphadenopathy. MC etiology = ** STAPH AUREUS ** (2nd MC = GABHS)
⦁ BULLOUS = vesicles rapidly form large bullae –> lead to think “varnish-like crusts”. Have fever, diarrhea
- MC = ** STAPH AUREUS**
- this form of impetigo is rare - usually seen in newborns / young children if at all
⦁ ECTHYMA = ulcerative pyoderma caused by
** GABHS ** - heals with scarring. Not common
TREATMENT
⦁ BACTROBAN (MUPIROCIN) OINTMENT - mild = MC treatment - apply TID x 10 days
⦁ Bacitracin
⦁ Wash area gently with soap / water. good skin hygiene
If extensive disease or having systemic symptoms (fever) = systemic abx
⦁ oral abx - ** Cephalexin (Keflex**), dicloxacillin (especially effective against Staph), clindamycin, erythromycin, azithromycin, clarithromycin
⦁ In severe cases = oral antibiotics to cover for MRSA = Bactrim, doxycycline, clindamycin
VARICELLA (CHICKENPOX)
Caused by HHV-3 - Varicella Zoster Virus
Chicken Pox = Primary varicella infection
Transmission = respiratory droplets, direct contact
The virus spreads mainly by touching or breathing in the virus particles that come from chickenpox blisters, and possibly through tiny droplets from infected people that get into the air after they breathe or talk
10-20 day incubation period
It takes about 2 weeks (from 10 to 21 days) after exposure to a person with chickenpox or shingles for someone to develop chickenpox
Usually lasts 5-7 days
- highly contagious!
⦁ is highly contagious from 2 days before onset of rash until all lesions have crusted
A person with chickenpox can spread the disease from 1 to 2 days before they get the rash until all their chickenpox blisters have formed scabs (usually 5-7 days).
RASH
- appears on face + trunk (chest / back), then spreads to extremities
- CENTRIPETAL RASH = lesions mostly distributed on face / trunk, less so on extremities
(smallpox = centrifugal - mostly face + extremities)
⦁ vesicles - “dew drops on a rose petal” = clusters of vesicles on erythematous base
⦁ pruritic
⦁ become pustules + crust over
vesicles are in ** DIFFERENT STAGES **
- have macules, papules, vesicles, pustules, and crusted lesions
SYMPTOMS - may begin to show 1-2 days prior to rash ⦁ fever ⦁ malaise ⦁ headache ⦁ decreased appetite
- more severe presentation may occur in adults
Some people who have been vaccinated against chickenpox can still get the disease. However, the symptoms are usually milder with fewer red spots or blisters and mild or no fever. Though uncommon, some vaccinated people who get chickenpox will develop illness as serious as chickenpox in unvaccinated persons.
Chickenpox can be spread from people with shingles to others who have never had chickenpox or received the chickenpox vaccine. This can happen if a person touches or breathes in virus from shingles blisters
If a person vaccinated for chickenpox gets the disease, they can still spread it to others.
For most people, getting chickenpox once provides immunity for life. However, for a few people, they can get chickenpox more than once, although this is not common.
Chickenpox vaccine is very safe and effective at preventing the disease. Most people who get the vaccine will not get chickenpox. If a vaccinated person does get chickenpox, it is usually mild—with fewer red spots or blisters and mild or no fever. The chickenpox vaccine prevents almost all cases of severe disease.
TREATMENT
- usually self-limiting
- Calamine lotion and colloidal oatmeal baths may help relieve some of the itching
- Keeping fingernails trimmed short may help prevent skin infections caused by scratching blisters
- if symptomatic
⦁ benadryl for pruritus
⦁ tylenol for fever
Do not use aspirin or aspirin-containing products to relieve fever from chickenpox. The use of aspirin in children with chickenpox has been associated with Reye’s syndrome, a severe disease that affects the liver and brain and can cause death
- Systemic
⦁ Acyclovir (Zovirax)
Acyclovir, an antiviral medication, is licensed for treatment of chickenpox. The medication works best if it is given within the first 24 hours after the rash starts. Other antiviral medications that may also work against chickenpox include valacyclovir and famciclovir
The best way to prevent chickenpox is to get the chickenpox vaccine. Children, adolescents, and adults should get two doses of chickenpox vaccine. CDC recommends two doses of chickenpox vaccine for children, adolescents, and adults. Children should receive two doses of the vaccine—the 1st dose at 12-15 months and 2nd dose at 4-6 years old
CYSTIC FIBROSIS
- “smaller than other children their age”
- “hacking” cough
- bronchodilators
- cough so forceful it occasionally causes him to vomit
- “bulky + frothy stools” - due to formula intolerance - due to lack of pancreatic enzymes - so food just goes right through –> “frothy”
- nasal polyps**
MC cause of Bronchiectasis is CF
- Bronchiectasis = bronchial dilation due to transmural inflammation –> destruction of muscular / elastic tissues of bronchial wall
WHAT IS CF? - Autosomal recessive disease of the Exocrine gland system. Defective chloride channels result in highly viscous secretions - decrease in chloride secretion leads to relative dehydration + abnormal mucociliary clearance
- autosomal recessive - so both parents must at least be a carrier = 1/32 adults - Caucasian
- CF = obstructive disease (like asthma and COPD)
- genetic condition that affects the lungs…but the name cystic fibrosis refers to the effects on the pancreas (cysts + excess CT that replaces normal tissue in an organ)
CF = autosomal recessive; CFTR gene codes for CFTR protein
- need to inherit 2 mutated CFTR genes (so both parents need to have been carriers)
- CF = more common in European descent
CFTR protein is a channel protein = pumps chloride ions into various secretions; the chloride ions help draw water into the secretions to thin the secretion
⦁ phenylalanine is deleted from 508th amino acid –> becomes misfolded
- this causes lack of CFTR channel protein on epithelial surface = can’t pump chloride ions out into secretions –> SECRETIONS ARE LEFT OVERLY THICK
EFFECT ON MECONIUM
- in Newborns, the thickened secretion can apply to meconium (first stool) in which the stool becomes THICK + STICKY and gets stuck in the intestines and not come out = MECONIUM ILEUS (surgical emergency)
PANCREATIC INSUFFICIENCY
- Most prominent effect of CF in childhood
- thick secretions block the pancreatic duct, and therefore prevent pancreatic digestive enzymes from making it to the small intestines –> proteins + fat NOT absorbed
⦁ over time –> leads to poor weight gain and FTT (failure to thrive)
⦁ Steatorrhea (fat containing stools - float)
⦁ Pancreas gets damaged - backed up digestive enzymes degrade the cells that line the pancreatic duct –> local inflammation –> can lead to acute pancreatitis and with repeated episodes, chronic pancreatitis. Development of CYSTS and FIBROSIS of pancreas
- *Protein + Fat Malabsorption
- failure to thrive, hypoalbuminemia, vitamin ADEK deficiency, steatorrhea
Liver disease
- cholestatic jaundice, steatohepatitis, portal hypertension —-» CIRRHOSIS
ENDOCRINE DYSFUNCTION
- pancreas destruction can damage the endocrine function of the pancreas –> lead to insulin-dependent diabetes
CLINICAL MANIFESTATIONS
- lung problems usually don’t develop until later in childhood; the cilia typically do a good job of keeping lungs clean by moving mucus (catches debris / bacteria) and moves it back up to the pharynx
- in CF, becomes difficult for the cilia to clear THICK MUCUS –> mucociliary action becomes defective –> Bacteria chronically colonizes the lungs
- With a sudden increased bacterial load --> CF Exacerbation ⦁ Cough ⦁ Fever ⦁ Changes on CXR - Requires antibiotics
MC Bacteria
⦁ In 1st decade of life: Staph Aureus (gram +) and H. flu (gram -) = MC
⦁ In 2nd + 3rd decade of life: Pseudomonas (gram -) = MC
⦁ Staph Aureus & Pseudomonas = big players
⦁ kids = staph; adults = pseudomonas
chronic infection –> destruction of bronchi –> bronchiectasis –> creates obstructive lung disease
FLOW CHART
1) abnormal CFTR –>
2) impaired mucociliary clearance –>
3) infection & inflammation –>
4) bronchiectasis & lung damage –>
5) functional airway impairment
- Chronic bacterial infections and therefore inflammation –> BRONCHIECTASIS (airway wall damage which leads to permanent dilation of the bronchi)
- Occasionally if the inflammation erodes into a blood vessel –> can even have HEMOPTYSIS
Repeated CF exacerbations can lead to RESPIRATORY FAILURE = leading cause of death in CF
OTHER CF RELATED ISSUES
⦁ Infertility in Men = male CF patients commonly lack vas deferens
⦁ Digital clubbing
⦁ Nasal polyps
⦁ Allergic Bronchopulmonary Aspergillosis - hypersensitivity rxn to Aspergillus Fumigatus
CLINICAL FEATURES OF CF - Respiratory Insufficiency ⦁ pulmonary fibrosis ⦁ obstruction ⦁ frequent infections ⦁ chronic sinusitis ⦁ nasal polyps
- Pancreatic Insufficiency
⦁ malabsorption of fats + proteins (steatorrhea = fat in stool) (meconium ileus = bowel obstruction - not pooping - dehydrated)
⦁ failure to thrive
DIAGNOSIS
- CXR
- pulse ox
- CBC with diff
- sputum studies of possible
- sweat chloride testing - measures amount of chloride in the sweat after small electrical stimulation
- PPD if worried about TB
- consult with pediatric pulmonologist
o newborn screening
⦁ IRT = detects Pancreatic Enzyme IRT (immunoreactive trypsinogen) = released into the blood when the pancreas is damaged
⦁ DNA testing
⦁ pilocarpine sweat chloride test (not done in babies < 48hrs - difficult to perform at this age)
- CF can be detected through sweat chloride test = standard for diagnosis of CF
- Elevated sweat chloride > 60 = positive result
- parents often first notice that baby tastes salty when they kiss their baby
The lack of normal CFTR functions alters chloride conductance in the sweat gland –> excessively high sweat sodium & chloride levels in sweat (no CFTR channel to transport chloride out of sweat glands). In lungs and pancreas = no CFTR channel to transport chloride in to thin secretions
Hyponatremia, hypochloremic metabolic alkalosis
DIAGNOSIS OF CF
⦁ Sweat Chloride test = screening test in all babies, but not if < 48 hours old
⦁ IRT Assay - final say of CF
⦁ DNA Assay - final say of CF
⦁ typical pulmonary + GI symptoms as well as positive Fam hx
TREATMENT
PANCREATIC TREATMENT
⦁ pancreatic enzyme supplements
⦁ fat soluble vitamin supplements (ADEK)
⦁ high calorie/high protein diet
- Pulmonary Treatment
⦁ Chest physiotherapy - loosens mucus by banging on the chest
⦁ inhalers - Other Mediations
⦁ N-Acetylcysteine - cleaves disulfide bonds in mucus glycoproteins (loosens)
⦁ Dornase Alfa Nuclease - cuts up nucleic acid in mucus (loosens) - PFTs often done to monitor the disease
- Lung transplant may be needed; due to chronic infections and loss of pulmonary function over time
- test for CF at birth, but 2% are missed - so even if test is negative - check for other clues
TREATMENT
- Tobramycin + Piperacillin or Ticarcillin (Aminoglycoside + antipseudomonal penicillin)
- nebulized bronchodilators
- oxygen therapy as needed
- chest physiotherapy
- mucolytics
- steroids (prn)
⦁ common SE of aminoglycoside (tobramycin/gentamycin) = nephro/ototoxicity
⦁ sinusitis = very prevalent in CF population
⦁ problem with using Cipro for pseudomonal coverage = risk of tendon rupture
- primary morbidity with CF = from progressive obstructive lung disease
- advances in pulmonary medicine/development of pancreatic enzyme replacement meds have increased survival in CF patients (median survival = 31 years)
- often diagnosed at birth in hospital (17%) because of meconium ileus** - CF is suspected if meconium is not passed in 24 hours (obstruction) - signs also include abdominal distention + thick/sticky meconium with enema exam
- failure to thrive, respiratory compromise, both
- some patients are not diagnosed until adulthood
PITYRIASIS ROSEA
- ETIOLOGY = unclear, but likely a viral source (HHV7)
- is self-limiting
- primarily occurs in older children / young adults
- increased prevalence in the spring/fall
- can mimic syphilis (order RPR if patient is sexually active)
CLINICAL MANIFESTATIONS
**First sign = “HERALD PATCH” (solitary salmon-colored macule on trunk 2-6cm in diameter)
–> then multiple new lesions appear 1-2 weeks later = smaller, pruritic, 1cm round/oval salmon-colored papules with white circular scaling in a ***“CHRISTMAS TREE DISTRIBUTION” on the back
- lesions are often oval with long-axis paralleling the lines of skin stress; oval, erythematous papules and small plaques
- mostly on the trunk, but may have some satellite lesions on the arm (usually proximal) - the face is usually spared
- lesions resolve in 6-12 weeks
- may be pruritic
- not contagious
ESSENTIAL CLINICAL FEATURES
⦁ discrete circular lesions
⦁ scaling on most lesions
⦁ peripheral collarette scaling with central clearance on at least two lesions.
OPTIONCAL CLINICAL FEATURES
⦁ truncal and proximal limb distribution
⦁ most lesions appearing along cleavage lines
⦁ herald patch for at least 2 days before the rash or other lesions begin.
Pityriasis rosea may have an accompanying upper respiratory infection.
- In many individuals with pityriasis rosea, the characteristic rash develops after vague, nonspecific symptoms that resemble those associated with an upper respiratory infection
Pityriasis rosea can be mistaken for secondary syphilis - very similar looking rash, except syphilis also will appear on palms/soles of hands/feet
- secondary syphilis must be excluded to diagnose pityriasis rosea
- VDRL testing (venereal disease research lab test)
- FTA-Abs test (fluorescent treponemal antibody absorption = blood test - checks for antibodies to Treponema pallidum bacteria - cause syphilis
DIAGNOSIS
⦁ A biopsy of pityriasis rosea will have extravasated erythrocytes within dermal papillae.
TREATMENT
- none needed!
⦁ if needed for pruritus = give medium potency topical steroids, PO antihistamines, oatmeal baths
⦁ Acyclovir or Phototherapy for severe cases
TOURETTE’S SYNDROME
ONSET
- usually in childhood (2-5 y/o)
- MC in boys
*** Associated with OCD + ADHD
CLINICAL MANIFESTATIONS = TICS
TIC = quick, non-rhythmic movements or vocalizations that happen over and over again. Are not caused by another disorder such as Huntington’s or substance abuse
1) MOTOR TICS*** of the face, head and neck
⦁ blinking
⦁ shrugging
⦁ head thrusting
⦁ sniffling
⦁ obscene gestures (copropraxia)
⦁ repeating motions of others (echopraxia)
2) VERBAL or PHONETIC TICS*** ⦁ grunts ⦁ throat clearing ⦁ obscene words (coprolalia) ⦁ repetitive phrases ⦁ repeating the words/phrases of others (echolalia)
3) SELF-MUTILATING TICS
⦁ hair pulling
⦁ nail biting
⦁ lip biting
- Abnormal because they occur in inappropriate situations
- May engage in repetitive behaviors such as clapping, grimacing or grunting, or even hidden behaviors such as moving the tongue
⦁ Simple Tics = usually shorter (milliseconds) such as blinking / clearing throat
⦁ Complex Tics = a bit longer (seconds / minute) and are a combination of tics such as shaking head + shrugging shoulders
DIAGNOSIS - Need a Tic + additional criteria ⦁ A) number of tics ⦁ B) duration of tics ⦁ C) age on onset
- For diagnosis of Tourette’s
⦁ A) need 2+ motor tics AND 1+ vocal tic (don’t have to happen at same time)
⦁ B) tics must persist for 1+ year
⦁ C) onset must be before 18
If < 1 year = diagnosed with Provisional Tic Disorder
TREATMENT
⦁ Habit reversal therapy / CBT = 1st line tx
- 50% have symptom resolution by 18 y/o
- Medications = usually only if severe
⦁ dopamine blocking agents (antipsychotics) = haloperidol, risperidone, fluphenazine, pimozide
Pimozide = only FDA approved drug for Tourette’s
⦁ alpha-adrenergics = clonidine, guanfacine (usually if in addition to ADHD) or strattera
In a patient with Tourette syndrome, it is important to avoid CNS stimulants that can further increase dopaminergic signaling
⦁ benzos = clonazepam (klonopin)
⦁ can also use botox
Tics tend to lessen when person is calm, so treating anxiety / depression can also help
LICE
Ectoparasites that live on the body and feed on human blood after piercing the skin.
⦁ Pediculosis capitus: head lice
⦁ Pediculosis corporis: body lice
⦁ Pediculosis pubis: pubic lice
Very common
Body and scalp lice are about 1-3 mm long
Unable to jump or fly
Gray-brown to red-brown.
Host specific- cannot live off host more than 24-48 hrs - need blood
Life Cycle: unhatched egg (nit), three molt stages(growing), adult reproductive stage, death.
⦁ nits hatch after 1 week
⦁ take 1 week to become mature louse
⦁ mature louse lay eggs x 1 month
Females lay their eggs along the hair shafts –150-300 eggs per life span. They live 30-50 days.
Feed on human host blood. Spit has anticoagulant in it to help promote feeding –> increased histamine release –> pruritus
TRANSMISSION = person to person usually; can also spread through fomites (hats, headsets, clothing, bedding) but not as common
Body lice: Act a little different. Can live up to 14 days off of host. Transferred mostly through infested clothes, blankets.
Pubic Lice: Spread through intimate contact.
Head Lice: Incidence is higher among girls. Being spread from combs and hats is not the usual mode. It is mostly hair to hair contact.
CLINICAL PRESENTATION OF LICE
⦁ intense pruritus* (make take 2-6 weeks to develop after exposure) - especially occipital area
⦁ papular urticaria near lice bites**
⦁ nits = white oval-shaped egg capsules at base of hair shafts - must be removed with a comb
⦁ itching + scratching can lead to secondary cellulitis - secondary skin infection commonly staph
⦁ pubic lice = should prompt eval for other STIs
⦁ typical lesion of body lice = macule at bite site that may develop vesicles/wheals
⦁ nocturnal pruritus** = common
DIAGNOSIS = Observation of:
⦁ Eggs (nits)
⦁ Nymphs
⦁ Mature lice
Commonly found behind ears and on back of the neck
Wood lamp of area
⦁ Yellow-green fluorescence of lice/nits
TREATMENT
- 2 mechanisms
o Neurotoxicity
⦁ Permethrin (Nix) = 1st line
- sodium channel blocker –> paralysis
- capitus = permethrin shampoo - leave on x 10 min
- pubis / corporis = permethrin lotion x 8-10 hrs
- permethrin = safe in children 2+ y/o
⦁ Lindane = 2nd line
- SE = Neurotoxic*** - headaches / seizures - do not use after showering
⦁ Malathion
⦁ Ivermectin - lotion or oral; must be repeated in 1 week, as it does not kill unhatched lice. Oral ivermectin can be used in refractory cases
o Suffocation via “coating”
⦁ benzyl alcohol lotion (Ulesfia)
- MOA = louse asphyxiation. It does not destroy their eggs; a 2nd treatment is needed again after 7 days
- Spinosaid (Natroba) = promotes hyperexcitation + death by paralysis
Environmental control = treat all ppl in contact with infested patient (especially sexual partners), then use nit combs to get rid of unhatched eggs
Bedding/clothing = laundry in hot water + dryer
Toys that can’t be washed = place in air-tight plastic bags x 14 days
CLUB FOOT
- also called congenital talipes equinovarus,
- Club foot is a congenital deformity where the affected foot appears to have been rotated internally at the ankle
⦁ 1/1000 births
⦁ 50% of babies with clubfoot = bilateral
⦁ Boys = 2x MC
Anatomic changes of talus plantar flexed, heel cord tight, and forefoot adducted/supinated
- In clubfoot, the tendons that connect the leg muscles to the foot bones are short and tight, causing the foot to twist inward
- have underdevelopment of soft tissues of medial foot with concomitant displacement of talo-calcaneo-navicular joint.
Although clubfoot is diagnosed at birth, many cases are first detected during a prenatal ultrasound
In limbs affected by clubfoot, the foot and leg are slightly shorter than normal, and the calf is thinner due to underdeveloped muscles. These differences are more obvious in children with unilateral clubfoot
- Without treatment, people with club feet often appear to walk on their ankles or on the sides of their feet. Clubfoot will not improve without treatment. A child with an untreated clubfoot will walk on the outer edge of the foot instead of the sole, develop painful calluses, be unable to wear shoes, and have lifelong painful feet that often severely limit activity.
With treatment, the vast majority of patients recover completely during early childhood and are able to walk and participate in athletics just as well as patients born without club foot
The initial treatment of clubfoot is nonsurgical, regardless of how severe the deformity is.
- most can be treated conservatively
** PONSETI METHOD ** (MC conservative tx) = Casting + percutaneous heel cord lengthening
⦁ Each week this process of stretching, re-positioning, and casting is repeated until the foot is largely improved. For most infants, this improvement takes about 6-8 weeks.
⦁ Achilles tenotomy- after manipulation / casting period, most babies require a minor procedure to release continued tightness in the Achilles tendon (heel cord). New cast then placed to protect tendon as it heals - usually takes about 3 weeks. When cast is removed, the Achilles tendon has regrown to a proper, longer length, and clubfoot has been fully corrected.
⦁ Bracing - even after successful correction with casting, clubfeet have a natural tendency to recur. To ensure that the foot will permanently stay in the correct position, your baby will need to wear a brace for a few years. First 3 months = wear brace full time. Over time, slowly decreased to just overnight. Bracing done usually for 3-4 years
Another conservative tx option = FRENCH METHOD = physical therapy / splinting focused
Treatment should ideally begin shortly after birth, but older babies have also been treated successfully with the Ponseti method
Severe, long-standing deformity may require several surgeries
LEGG-CALVE-PERTHES DISEASE
- childhood hip disorder in which the blood supply to the femoral head gets disrupted, leading to death and necrosis of the tissue
= idiopathic osteonecrosis of femoral head
- MC in children 4-10 y/o
- 4-5x MC in boys
There is an increased incidence in patients with a positive family history, exposure to cigarette smoke, and low birth weight
Hip joint = ball + socket joint in which the femoral head sits in the acetabulum, allowing the leg to move in almost all directions
The head of the femur is supplied by branches of 3 arteries
⦁ medial femoral circumflex artery
⦁ lateral femoral circumflex artery
⦁ ligamentum teres artery
These arteries that branch from the neck to the head of the femur provide nutritional needs for growth and to maintain spherical shape
In Legg-calve-perthes disease, the blood supply to femoral head gets interrupted, not entirely known why
- Result = AVASCULAR NECROSIS (tissue begins to die off due to lack of blood supply)
When this occurs, new blood vessel formation to necrotized bone allows dead tissue to be removed by immune cells called macrophages. This process causes the head of femur to lose mass, becoming weak and prone to fractures. The head is then misshapen, and can no longer smoothly rotate within the acetabulum –» reduced range of motion**
Over time, LCP disease typically self-resolves, and bone is able to heal (not known why/how this happens)
- when bone remodeling occurs, new bone replaces necrosed bone, and spherical shape is restored. With time, normal functioning of the joint is restored as well
Symptoms typically last < 18 months; over this time, necrosed bone is remodeled with healthy bone, and blood supply is restored
SYMPTOMS
⦁ painless limping*
⦁ may have hip pain or stiffness
⦁ pain sometimes referred to knee / groin / thigh
⦁ pain worsens with activity - especially @ end of day
⦁ limited ROM**
⦁ loss of abduction + internal rotation***** (just like with SCFE)
⦁ muscles of affected leg may atrophy due to lack of use –> affected leg may look smaller than other leg
typically presents with painless limp - insidious onset, which causes intermittent knee or thigh pain
Long-term concerns with Legg–Calvé–Perthes disease include
⦁ permanent femoral head deformity
⦁ increased risk of osteoarthritis in adulthood
DIAGNOSIS
⦁ X-RAY - reveals flattened and misshapen femoral head, widening of cartilage space, crescent sign*
⦁ MRI - can see shape of bone as well as see formation of new blood vessels
TREATMENT
- since LCP disease can sometimes resolve by itself over time, so tx = conservative
⦁ rest
⦁ pain management - NSAIDS
⦁ physical therapy
⦁ brace or cast
⦁ surgery = if child > 8, if > 50% of femoral head is damaged, or if conservative therapy fails. Surgery = Osteotomy - helps realign femoral head within acetabulum
Treatment goals are to decrease pain and prevent femoral head deformity. Mechanical pressure on the joint should be reduced, which can be aided by bedrest, limitation of running and contact sports, overnight traction devices, physical therapy, and braces.
One of the methods of treatment of Legg–Calvé–Perthes disease is traction, which involves moving the femur away from the pelvis to decrease the wear on the bone.
Recommended exercise = swimming, due to its effect on mobility with minimal impact on the joints
PES PLANUS (FLAT FEET)
- immature foot
- initially common for infants / toddlers to have flat feet
- arch starts to form around age 4-6**
if toddler has flat feet = reassure parent that this is a normal finding until around age 4-6; feet are much more flexible, as the arch has not developed yet
- in adults = a postural deformity in which the arches of the foot collapse, with the entire sole of the foot coming into complete or near-complete contact with the ground.
Some individuals (an estimated 20–30% of the general population) have an arch that simply never develops in one foot (unilaterally) or both feet (bilaterally).
**too many toes sign - if patient standing to the back, should only be able to see one pinky toe - the rest should be covered by calf. With Pes Planus = see multiple toes lateral to calf
TREATMENT
⦁ A painless deformity that can be accommodated by normal footwear and allows for normal gait does not require treatment.
⦁ If painful = can seek out arch supports, wedges, stretching, supportive shoes, Podiatrist / Ortho, surgery
GENU VARUS (BOW-LEGGED)
- physiologic bowing (normal)
⦁ usually corrects by age 2
⦁ symmetrical and painless bowing
⦁ usually associated with in-toeing and often with a propensity for tripping
⦁ This problem will resolve spontaneously without treatment, as a result of normal growth - All that is required is parental education and periodic follow-up to verify resolution. During the wait for the predicted spontaneous correction, reversing the shoes may reduce the frequency of tripping.
- Pathological etiologies
o Blount’s disease = growth disturbance of proximal medial tibia; causes damage to tibial epiphysis. Can present any time from infancy to adolescence. May need bracing or surgery
o Rickets (Vitamin D deficiency) = lack vitamin D metabolites –> hypophosphatemia
o Achondroplasia - dwarfism
DIAGNOSIS = XRAY - measure lateral distal femoral angle and proximal medial tibial angle at joint
TREATMENT = reassurance if physiological bowing (resolves by age 2). If does not resolve = braces, surgery (osteotomy)
Bowing may be unilateral or bilateral
GENU VALGUS (KNOCK-KNEES)
- most occur spontaneously
- braces & modified shoes are not effective
toddlers aged 2-6 years may have physiologic genu valgum. For this age group, typical features include ligamentous laxity, symmetry, and lack of pain or functional limitations.
- no treatment is warranted for this self-limiting condition. Bracing is meddlesome and expensive, and shoe modifications are unwarranted. Annual follow-up until resolution may help to assuage their fears.
- after age 11-13 - may need surgery for marked deformity, as adolescent idiopathic genu valgum is not self-limiting.Teenagers may present with a circumduction gait, anterior knee pain, and, occasionally, patellofemoral instability. May indicate premature degenerative changes in the patellofemoral joint and in the lateral compartment of the knee.
Various other conditions, including postaxial limb deficiencies, genetic disorders such as Down syndrome, hereditary multiple exostoses, neurofibromatosis, and vitamin D–resistant rickets may cause persistent and symptomatic genu valgum.
surgical intervention is still likely to be necessary to correct the malalignment of the knees.
BOXER’S FRACTURE
- fracture at the neck of the 5th metacarpal bone (± 4th metacarpal fracture)
PHYSICAL EXAM
⦁ ± rotational deformity = when flexing at MCP joint, the pinky finger goes under or over the ring finger
⦁ ± loss of knuckle on exam
MOA = punching with a clenched fist
DIAGNOSIS = XRAY
- if fracture is at the base of the metacarpal bone, need to also look for any carpal bone injuries
TREATMENT = ** Ulnar Gutter Splint **
- with joints in at least 60 degree flexion
- any fracture > 25 - 30 degrees angulation should be reduced
- any fracture > 40 degrees angulation = ORIF (open reduction, internal fixation)
- ** ALWAYS check for bite wounds ** - if present = treat with appropriate antibiotics (Augmentin)
FEVER OF UNKNOWN ORIGIN
a condition in which the patient has an elevated temperature (fever) but despite investigations by a physician no explanation has been found
- Fever of unknown origin is a specific diagnosis and is thought to be due to
⦁ *** INFECTION in 30-40% of cases ***
⦁ neoplasms in 20-30% of cases
⦁ collagen vascular disease in 10-20% of cases
⦁ other diseases in 15-20% of cases
FUO is a specific diagnosis requiring
⦁ fever higher than 38.3ºC (101ºF) on several occasions
⦁ duration of fever for at least 3 weeks
⦁ uncertain diagnosis after one week in hospital
This differs from its common use describing the undifferentiated patient with a fever, which is inaccurate.
Common infections causing FUO include abscesses, TB, UTIs, endocarditis, osteomyelitis, and hepatobiliary infections
ROSEOLA INFANTUM
SIXTH’S DISEASE
MC caused by HHV-6** (can be caused by HHV6 or 7)
- also known as exanthem subitum.
- infection is very common
- MC occurs < 5 y/o (MC in 6 months - 3 years)
- seroprevalence in most countries approaches 100% in children over 2 years old
- Complications are uncommon (seizures can occur during febrile period)
TRANSMISSION = respiratory droplets (saliva!)
- Virus is acquired from close contact with saliva from parents or sibling
- 10 day incubation period
** major cause of infantile FEBRILE SEIZURES **
CLINICAL MANIFESTATIONS
⦁ **Abrupt onset of high fever (101 - 106) that lasts 3-5 days, then fever resolves, then erythematous maculopapular rash appears several hours later
⦁ fever resolves before onset of a ROSE, PINK nonpruritic maculopapular, blanchable rash on trunk / back that spreads to face
⦁ rash lasts up to 1-2 days
⦁ only childhood viral exanthem that STARTS ON TRUNK*** and THEN SPREADS TO FACE **
- child appears “well + alert” during febrile phase; may be irritable
- rash spontaneously resolves - may not appear for 1-2 days until after fever breaks
- fever gets so high, can lead to seizures
- usually kids are brought in for the rash, not the fever
kid often given amoxicillin for fever, then rash breaks out - ppl think their kid is allergic to amoxicillin
- lights up bright red in warm environment (bath)
TREATMENT
- supportive = anti-inflammatories, antipyretics (to prevent febrile seizures) [ ibuprofen for both! ] or acetaminophen / Tylenol for antipyretic properties
- tepid baths (do not put child in cool or cold water)
- may apply cool packs to groin/underarms in older kids
SCABIES
also known as the seven-year itch
- a contagious skin infestation by the mite Sarcoptes scabiei
- mites are transmitted through prolonged, close skin-skin contact or fomites (clothing / bedding)
- mites cannot survive off of human body for > 4 days (head lice = 24-48 hrs, but body lice = 2 weeks)
Female mites BURROW INTO SKIN to lay eggs, feed and defecate
- scybala = fecal particles that precipitate a hypersensitivity reaction in the skin
SYMPTOMS
⦁ ** SEVERE ITCHINESS **
⦁ pimple-like rash
⦁ may see tiny burrows in the skin
⦁ symptoms can be present across most of the body, but MC areas = wrists, between fingers, and along waistline
⦁ itch = worst at night and after hot shower
- Intensely pruritic lesions = papules, vesicles and LINEAR BURROWS*** commonly found in intertriginous zones (web spaces between fingers/toes)
- usually spares the neck and face
- linear burrows at wrist, ankles, finger webs, axillary folds, genitalia
- intense pruritus with minimal skin findings and increased intensity at night**
Red itchy pruritic papules or nodules on the scrotum, glans or penile shaft, and body folds = pathognomonic for scabies
Infected patients may remain without symptoms for up to 4-6 weeks**
Common locations for infestation = crowded living conditions - dorms, prisons, army barracks
DIAGNOSIS
- often a clinical diagnosis
- skin scraping (15 blade) of unscratched papule / burrow region to identify mites / eggs
- CBC will show eosinophilia…
TREATMENT
⦁ Permethrin topical (Elimite, Nix) = drug of choice** - apply topically from neck down x 8-14 hrs, then shower
- repeat in 1 week
- permethrin = safe in pregnancy
⦁ Lindane (neurotoxin) = cheaper than permethrin…but
- do NOT use after bath/shower - can cause SEIZURES d/t increased absorption through open pores
- teratogenic - so don’t use in pregnant or breastfeeding women, or in children < 2
⦁ 6-10% sulfur in petroleum jelly for pregnant women and infants
⦁ oral ivermectin if extensive
⦁ place all clothing / bedding in plastic bag for at least 72 hrs, then wash / dry in heat
**also need to treat household members and intimate partners **
OTITIS EXTERNA
= ** SWIMMER’S EAR **
- inflammation of the outer ear + ear canal
- seen more in elderly + kids
Cause = EXCESS WATER or LOCAL TRAUMA that changes the normal acidic pH of the ear, causing bacterial overgrowth
frequent water exposure can slightly raise the pH, making the canal more favorable for bacterial or fungal overgrowth
Causes
⦁ Infectious - MC Pseudomonas (swimming)
⦁ Allergic
⦁ Dermal disease (eczema / psoriasis)
MC BACTERIAL ETIOLOGY = ** PSEUDOMONAS ** (gram negative rod / bacilli)
- other causes = Proteus, staph aureus, staph epidermidis, GABHS, anaerobes (peptostreptococcus), aspergillus if fungal
Risk Factors
- swimming (pseudomonas)
- warm / wet environment
- overcleaning / cottonswabs
- seb derm / psoriasis
- otomycosis = fungal ear infection
- diabetes
- too much ear wax
- any manipulation / damage to the ear
CLINICAL MANIFESTATIONS ⦁ 1-2 days of INTENSE EAR PAIN ⦁ PRURITUS in the ear canal ⦁ may have recently swam ⦁ AURICULAR DISCHARGE ⦁ feeling of pressure / fullness in ear ⦁ hearing usually preserved, may be decreased
generally presents with canal itching and pain with movement of the ear
PHYSICAL EXAM
⦁ intense pain simply with traction of ear canal / tragus
⦁ external auditory canal erythema, edema + debris
- should see an edematous + erythematous ear canal
- may see yellow / brown / white / or grey debris
- should be no middle ear fluid (fluid behind TM - if you can see it through the debris/edema)
- the TM should be mobile (if you can see it)
If the canal is closed, Weber is expected to lateralize to the side of the blocked canal.
If the TM is not visible, only use drops that are not ototoxic in case of perforated eardrum - Ofloxacin is safe; do NOT use drops with aminoglycosides
Extremely painful - start with drops to clean/relieve some debris = very scabbed. Do not try to remove scabs
DIAGNOSIS: cultures are not routinely required for diagnosis of otitis externa; usually a clinical diagnosis with otoscopy
In contrast to acute otitis media, the tympanic membrane moves normally with pneumatic otoscopy in a patient with otitis externa.
TREATMENT
- protect ear from moisture
- drying agents can help - isopropyl alcohol or acetic acid (vinegar)**
- can use hydrogen peroxide to try to clean debris
- topical antibiotics
1) Fluoroquinolone ± steroid
⦁ ciprofloxacin or ofloxacin ± dexamethasone or hydrocortisone
⦁ cipro HC = ciprofloxacin + hydrocortisone
⦁ ciprodex = ciprofloxacin + dexamethasone
The initial treatment of otitis externa is ciprofloxacin.
2) Aminoglycoside combination
⦁ cortisporin = neomycin + polytrim -B + hydrocortisone
⦁ tobradex = tobramycin + dexamethasone
- do NOT use aminoglycoside combo unless can verify that TM is not perforated
3) If fungal = amphotericin B, clotrimazole, itraconazole
MALIGNANT OTITIS EXTERNA
- A severe form of otitis externa that presents in diabetic and immunocompromised patients
- An invasive infection of the external auditory canal and skull base
- **typically occurs in the elderly + patients with DM (most likely uncontrolled) + immunocompromised / HIV
- MC bacterial agent = ** PSEUDOMONAS ** (gram negative rod / bacilli)
- 2nd MC cause = staph aureus
Malignant otitis externa, or necrotizing external otitis, is an uncommon form of otitis that occurs primarily in immunocompromised patients and early diabetic patients, particularly when DM is being poorly managed. It typically begins as a case of acute otitis externa, which is characterized by ear pain, swelling of the ear canal, and occasionally decreased hearing.
CLINICAL MANIFESTATIONS
⦁ otalgia - pain more severe than with otitis externa
⦁ otorrhea
Unlike acute otitis externa, malignant otitis externa is potentially fatal and commonly presents with severe, deep pain, greenish foul smelling discharge and hearing loss.
COMPLICATIONS ⦁ Osteomyelitis of the base of the skull ⦁ Mastoiditis ⦁ TMJ osteomyelitis ⦁ Cranial nerve palsies
MOE is caused by extension of the outer ear infection into the bony ear canal and soft tissues deep to the bony canal and can result in skull base osteomyelitis and multiple cranial nerve palsies.
DIAGNOSIS ⦁ otoscopy = see granulation in the inferior portion of the EAC ⦁ Elevated ESR ⦁ Positive culture ⦁ Imaging
TREATMENT = - no role for topical abx!!
The offending pathogen is almost always Pseudomonas aeruginosa and, unlike acute otitis externa, malignant otitis externa requires oral or intravenous antibiotics.
The initial treatment of malignant otitis externa is CIPROFLOXACIN***
⦁ CIPRO bid po x 6-8 weeks
⦁ pip/tazo (as pseudomonas is growing more resistant)
⦁ steroids to reduce itching / inflammation
NURSEMAID’S ELBOW
Nursemaid’s elbow is a partial dislocation of the elbow joint caused by a sudden pull on the extended pronated forearm, such as by an adult tugging on an uncooperative child or by swinging the child by the arms during play.
The technical term is radial head subluxation
The etiology of nursemaid’s elbow involves the radial head slipping under the annular ligament.
Common upper extremity injury in infants and young children
Generally, occurs with a pulling upward type of motion while the child has an outstretched arm
MECHANISM: lifting / swinging / pulling a child while the forearm is pronated + extended
==> the radial head wedges into the stretched annular ligament***
MC in 2-5 y/o
CLINICAL MANIFESTATIONS
⦁ children present with arm extended
⦁ refuse to move or use arm
⦁ Often has arm across abdomen, as if broken
⦁ usually no swelling
⦁ tenderness to palpation of radial head
On physical exam, the forearm of a child with nursemaid elbow will be in incomplete extension with the forearm partially pronated (opposite of tx = supination + flexion)
- May have referred pain to wrist
- xrays typically normal
- dislocation is often reduced by radiology tech while they are trying to get xrays
TREATMENT: Manual reduction
- The supination-flexion technique is the classic method of reducing a subluxated radial head. It has a success rate of 80-92%
- another method of hyperpronation
- child often experiences immediate pain relief after manual reduction, and can resume normal activities shortly after
Always ensure the child spontaneously uses the arm after reduction before discharging to confirm success
- if child uses arm after 15 minutes = no xrays needed
- if child does not use arm after 15 minutes = may want to do xrays to rule out fracture, or reattempt reduction
GENERALIZED ANXIETY DISORDER (GAD)
GAD = EXCESSIVE ANXIETY OR WORRY FOR
6+ MONTHS ABOUT VARIOUS ASPECTS OF LIFE
Excessive, persistent, and unreasonable anxiety about everyday things
Can range from mild (able to function socially and hold down a job) to severe (completely debilitated)
- feelings of anxiety may worsen or improve over time
GAD is not episodic (like panic disorder)
GAD is not situational (like phobias)
GAD is not focal
Associated with >/= 3 of the following symptoms ⦁ fatigue ⦁ restlessness ⦁ difficulty concentrating ⦁ muscle tension ⦁ sleep disturbance** (common - can have significant impact on physical well-being) ⦁ irritability ⦁ shakiness ⦁ headaches
= NOT due to medical illness
GAD = more common in FEMALES
onset of symptoms = usually in early 20’s
SIGNS/SYMPTOMS ⦁ can't relax ⦁ startle easily ⦁ have difficulty concentrating ⦁ trembling ⦁ irritability ⦁ sweating
- may have stomach pain from eating too much or not eating enough (due to anxiety)
Generalized anxiety disorder (GAD) involves persistent and excessive worry pertaining to multiple events or domains that continues for > 6 months
Anxiety is not related to a specific focus, but rather is generalized to most issues
GAD is the most common psychiatric illness seen by primary care providers.**
DSM-5 DIAGNOSTIC CRITERIA FOR GAD
o Excessive anxiety and worry (apprehensive expectation), occurring more days than not for at least 6 months, about a number of events or activities (such as work or school performance).
o The individual finds it difficult to control the worry.
o The anxiety and worry are associated with three (or more) of the following six symptoms (with at least some symptoms having been present for more days than not for the past 6 months): Note: Only one item is required in children.
- present for 90+ days out of 180 days
- adults = 3+ symptoms
- children = 1+ symptom
⦁ Restlessness or feeling keyed up or on edge.
⦁ Being easily fatigued.
⦁ Difficulty concentrating or mind going blank.
⦁ Irritability.
⦁ Muscle tension
⦁ Sleep disturbance (difficulty falling or staying asleep, or restless, unsatisfying sleep).
The anxiety, worry, or physical symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of
The disturbance is not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication) or another medical condition (e.g., hyperthyroidism).
EVERYDAY ANXIETY VS ANXIETY DISORDER
- Everyday Anxiety
⦁ worry about paying bills, landing a job, a romantic breakup, other important life events
⦁ embarrassment or self-consciousness in an uncomfortable or awkward social situation
⦁ nerves/sweating before a big test, business presentation, stage performance, etc.
⦁ realistic fear of a dangerous object, place or situation
⦁ anxiety, sadness or difficulty sleeping immediately after a traumatic event
- Anxiety Disorder
⦁ constant worry that causes significant distress + interferes with daily life
⦁ avoiding social situations for fear of being judged / embarrassed / humiliated
⦁ out of the blue panic attacks, preoccupation with the fear of having another panic attack
⦁ irrational fear or avoidance of an object / place / situation that poses little or not threat of danger
⦁ recurring nightmares / flashbacks / emotional numbing related to a traumatic event that occurred several months or years before
Anxiety is not related to a specific person, situation, or event in generalized anxiety disorder.
At least 80% of patients with GAD have had at least one other anxiety disorder in their lifetime.
Patients with GAD are at increased risk of developing other conditions such as depression and bipolar disorder.
CAUSE = uncertain, but thought to be a combination of genetic + environmental factors
GABA and serotonin levels are DECREASED in patients with generalized anxiety disorder.
⦁ MOST IMPORTANT = decreased GABA levels*****
do have decreased serotonin as well
Norepinephrine levels are INCREASED in patients with generalized anxiety disorder
GAD-7 scale = out of 21 points = 0 / 1 / 2 / 3 on 7 questions regarding feelings of anxiety in past 2 weeks
TREATMENT FOR GAD
- 1st line = Combo or Monotherapy of
⦁ Psychotherapy (CBT) - alone or with SSRI
⦁ SSRI: Paroxetine (Paxil), Sertraline (Zoloft), Escitalopram (Lexapro)
*****SSRI of choice = Paxil; sertraline is more activating - has more stimulation, which is not good for GAD…unless patient also has significant depression
⦁ SNRI = alternative to 1st line - Effexor (venlafaxine) or Duloxetine (Cymbalta)
SNRI of choice = Effexor
- 2nd line =
⦁ Buspirone (Buspar) - can be used solo or with SSRI
= stimulates serotonin receptors, and blocks dopamine receptors. May take several weeks to see clinical improvement - ** Buspirone does NOT cause sedation**
- SE = nausea, RLS, EPS, dizziness
⦁ Benzo’s (low dose)
- short half life = alprazolam (Xanax) (11.2 hrs) or lorazepam (Ativan) (12 hrs) - longer half life = diazepam (valium) (45-100 hrs) or flurazepam (dalmane) (74-90hrs)
Benzos = short term use only) - used in interim until SSRI takes effect or for acute exacerbations / anxiety attacks / panic attacks (not used long-term due to abuse potential)
⦁ TCAs
⦁ Beta-Blockers
⦁ Pregabalin (Lyrica)
OSGOOD SCHLATTER DISEASE
TIBIAL TUBERCLE APOPHYSITIS
INFLAMMATION OF THE PATELLAR TENDON- right where it inserts at the tibial tuberosity
Results in PAINFUL SWELLING just below the knee
Osteochondritis of the patellar tendon at the tibial tuberosity from OVERUSE (repetitive stress) or from small avulsions due to quadriceps contraction on the patellar tendon insertion into the tibia
Tibial tuberosity = Apophysis - bony prominence that serves as a site for tendon attachment
Ligament connects bone to bone
Tendon connects muscle to bone
When patellar ligament contracts (shortens), it extends the knee out
The proximal epiphysis of tibia is mostly cartilage at birth with an ossification center. Ossification center starts to ossify (turn to bone) around age 9-15. By age 18, becomes a bony tuberosity
Osgood Schlatter typically occurs between ages 9-15, when the tuberosity has not yet ossified, and is therefore is not strong enough to resist traction of the patellar ligament
This is why Osgood-Schlatter is COMMON in YOUNG ADOLESCENTS who PLAY SPORTS
** MC CAUSE OF CHRONIC KNEE PAIN IN YOUNG, ACTIVE ADOLESCENTS **
*** MC IN MALES, age 10-15, in ATHLETES DURING GROWTH SPURTS - bone growth is faster than soft tissue growth, so as femur and tibia grow, this puts excess strain / stretches the patellar tendon insertion; also the quadriceps contraction is transmitted through patellar tendon to the tuberosity insertion
Repetitive contraction of the quadriceps muscle exerts excess traction on the tibial tuberosity via the patellar tendon, which then gets strained and inflamed
The ossification center can actually crack, and then result in a callus - this resolves itself as ossification process continues
Repetitive traction of the apophysis of the tibial tuberosity results in microtrauma and micro-avulsion
CLINICAL MANIFESTATIONS ⦁ Activity-related knee pain / swelling - with running / jumping / kneeling *** ⦁ Painful + palpable lump below the knee ⦁ Tenderness to the anterior tibial tubercle ⦁ Pain with resisted knee extension * hurts to go up/down stairs
DIAGNOSIS
⦁ clinical diagnosis based on hx + pe
⦁ Lateral Xray of the knee - may be normal, or may show prominence or heterotopic ossification at the tibial tuberosity - see irregularity + fragmentation of tibial tubercle
⦁ Ultrasound can show soft tissue swelling
- usually resolves with time*
- majority of the time, Osgood Schlatter is outgrown with the closure of the physis
**Complications:
Osgood Schlatter can result in AVASCULAR NECROSIS at the tibial tuberosity, or an AVULSION FRACTURE, with the tibial tuberosity separating from the tibia.
TREATMENT
⦁ RICE (rest, ice) - reduce aggravating activities - but not bed rest - should still remain physically active to strengthen surrounding muscles
⦁ NSAIDS (ibuprofen)
⦁ Quadriceps stretching
⦁ Physical Therapy
⦁ surgery only in refractory cases, and if done, is usually performed after growth plate has closed
FIFTH DISEASE = ERYTHEMA INFECTIOSUM
SLAPPED CHEEK DISEASE
Caused by Parvovirus B19* - single stranded DNA virus
- transmission = respiratory droplets (or blood)
- 4-14 day incubation period
a mild febrile illness with rash. It often occurs in outbreaks among school-aged children, although it can occur in adults as well
⦁ MC in children < 10 y/o
CLINICAL PRESENTATION
1) coryza (non-allergic rhinitis) + fever, runny nose, headache, sore throat
==> “slapped cheek” on face with circumoral pallor (central clearing) x 2-4 days ==> about 24hrs later- LACY RETICULAR RASH on extremities (especially upper extremities) - rash spares palms + soles
- the rash resolves by 2-3 weeks; rash may last few days to several weeks
- rash = frequently pruritic
2) Arthropathy / Arthralgias in older children + adults (usually occurs in adult women)*** (Also seen with RUBELLA - german measles)
3) Associated with fetal loss in pregnancy - fetal hydrops, CHF, and spontaneous abortion
- mild febrile exanthematous disease, little or no prodrome
- low grade fever, varying degrees of conjunctivitis, upper respiratory complaints - runny nose, cough, coryza, myalgia in older children / adults, itching, nausea, diarrhea
- SLAPPED FACE - fiery red erythema of cheeks
- bilaterally symmetrical appearance. 24 hours later, rash appears on arms/legs/trunk
a child with fever that later develops red rash on their cheeks that fades as a reticular rash spreads across the body
** Reappearance of rash - after it clears, this may occur if skin is irritated/traumatized by sunlight, heat, cold or friction
- illness usually mild - may include ⦁ low grade fever ⦁ URI symptoms (cough / coryza) ⦁ mild malaise (but may not have any of these symptoms)
Rash = flat, LACY, reticular, often pruritic - located on cheeks, trunk and extremities
Children are NOT contagious once the rash appears
** Parvovirus B19 may cause APLASTIC CRISIS (Reticulocytopenia - decreased # of immature RBCs) - in children with weakened immune systems - Sickle Cell Disease***, G6PD deficiency, HIV, Leukemia, thalassemia etc (NOT megaloblastic anemia - only in patients with chronic hemolytic anemia)
aplastic crisis is an infection caused by parvovirus B19. It causes production of RBCs in the marrow to be shut down for up to 10 days.
The aplastic crisis is temporary cessation of red cell production. Because of the markedly shortened red cell survival time in patients with sickle cell disease, a precipitous drop in hemoglobin occurs in the absence of adequate reticulocytosis
DIAGNOSIS
- Diagnosis is based primarily on clinical observations, history, and physical exam.
- Elevated titer of IgM anti-parvovirus antibodies
- PCR in serum
- Serology: associated with enlarged nuclei** with peripherally displaced chromatin
TREATMENT
- symptomatic treatment = NSAIDS, antipyretic
NEVUS SIMPLEX (STORK BITE) or NEVUS FLAMMEUS NUCHAE
- Areas of surface capillary dilation
- MC seen on nape of neck, forehead, or eyelids
- may also be called crow’s nest if on forehead, above eyes
TREATMENT
1) Observation - most will resolve spontaneously by age 2. Don’t usually darken over time
- sometimes will remain there for life, just get lighter over time
2) Laser Therapy when older can reduce appearance of lesions if doesn’t resolve spontaneously
RICKETS
Rickets is a bone mineralization disorder which can lead to a varus deformity, short stature, and other bone abnormalities. The most common cause is Vitamin D deficiency, which can develop due to poor diet, prolonged breastfeeding, or reduced exposure to sunlight.
One of the most common conditions to consider when approaching a patient with a varus deformity is rickets. Rickets is caused by decreased mineralization of bone, leading to an increase in osteoid and cartilage, which allow bones to be more flexible. This leads to the characteristic bow-leggedness and short stature, and can also affect other areas with rapidly growing bones such as the wrist and chest.
The most common cause of rickets is Vitamin D deficiency. Vitamin D plays a key role in bone mineralization by ensuring adequate amounts of calcium and phosphate are present in the body. Vitamin D deficiency is usually secondary to inadequate intake or a lack of exposure to sunlight. Interestingly, children who are breastfed are at risk of developing Vitamin D deficiency unless they take daily supplements. To treat and prevent this condition from worsening, children should be given daily Vitamin D supplements.
Other causes of rickets include anti-convulsants, X-linked dominant hypophosphatemic rickets, and renal or hepatic disease.
Rickets can present with a genu valgum or a genu varum (bow legs).
HIRSCHSPRUNG’S DISEASE
= CONGENITAL AGANGLIONIC MEGACOLON
- missing cluster of nerves (aganglionic) in the colon that is present since birth (congenital) that is causing the colon to get blocked up and enlarge (megacolon)
- lack of enteric nervous system ganglia
- 1/5000 births
- The intestines move waste via peristalsis (automatic) that occurs via SMOOTH MUSCLE
- lumen –> mucosa –> submucosa –> Muscularis propria –> serosa / adventitia
⦁ mucosa (epithelium, lamina propria, muscularis mucosa)
⦁ submucosa (Meissner’s (submucosal) plexus)
⦁ muscularis propria (circular + longitudinal muscle. Auerbach’s (myenteric) plexus in both muscle layers)
⦁ serosa / adventitia
Circular muscle of smooth muscle layer is responsible for contracting and constricting the muscle behind the waste, preventing it from moving backward
Longitudinal muscle of smooth muscle layer relaxes and lengthens in front of the waste, and therefore pulls waste forward
⦁ Plexus = network of nerves
⦁ Within Plexus = Ganglia, which are clusters of individual nerves that help coordinate muscle contraction and relaxation
o Auerbach’s Plexus (Myenteric Plexus) - primarily causes smooth muscle relaxation
o Meissner’s Plexus (Submucosal Plexus) - helps control blood flow as well as epithelial cell absorption and secretion
In Hirschsprung disease = both Auerbach’s Plexus + Meissner’s Plexus are GONE - completely absent in some parts of the colon
CAUSE
- during fetal development, neural crest cells migrate away and differentiate into different cell types
- some become neuroblasts, which eventually become nerve fibers, some of which are present in the plexus’ of the gut
- neuroblasts travel down from the mouth to the anus. Around week 8 = get to the proximal colon (cecum, ascending and transverse colon)
- then goes to the distal colon (descending + sigmoid)
Around week 12 = gets to the rectum (left side)
**deficiency of neural crest cells* - failure of neural crest cells to fully migrate to the distal most aspect of the colon to form the enteric nervous system.
Hirschsprung’s disease is a result of failed neural crest cell migration during fetal development.
** A disruption in this neuroblast development means that nerve fibers don’t develop in the rectum and parts of the colon
** RECTUM + DISTAL SIGMOID COLON = locations most commonly affected by Hirschsprung disease **
- the Rectum is ALWAYS affected…may or may not involve parts of the colon. Usually will involve the distal sigmoid colon. Severe cases = entirety of colon
Mutations in either RET (MC**) or EDNRB genes can cause disruption of migration and development of these nerve fibers –> absence of these plexus’
RET gene mutations have also been linked to Down Syndrome, which may explain association between HIRSCHSPRUNG DISEASE + DOWN SYNDROME***
** 10% of all Hirschsprung disease cases occur in children with down syndrome **
No nerves –> peristalsis is seriously impaired. Smooth muscle can’t relax anymore, and stays in contracted position, which blocks the movement of feces
Babies born with Hirschsprung disease fail to pass their first stool (meconium) within first 48hrs - usually occurs within first 24 hours after birth (95% of infants pass meconium within first 24hrs)
Usually constriction occurs in rectum and distal sigmoid colon, so feces gets blocked there and starts backing up
⦁ constipation
⦁ colon dilation - “Megacolon” = at risk for rupture
CLINICAL MANIFESTATIONS / PHYSICAL EXAM
Hirschsprung disease commonly presents with
⦁ bilious emesis (vomiting)
⦁ abdominal distention
⦁ failure to pass meconium in the first 48 hours
⦁ chronic constipation
⦁ may have absent bowel sounds on exam
⦁ small rectal / distal colon diameter
⦁ DRE leads to explosive passage of stool
⦁ Gas accumulation in abdomen
DIAGNOSIS
⦁ Anorectal Manometry = often used as initial screening test - lack of relaxation of internal sphincter with balloon rectal distention
⦁ xray with contrast (barium enema) - may show dilated colon (megacolon) filled with lots of stool that is blocked, and small rectal/distal colon diameter; see transition zone at area between normal + affected bowel
⦁ * DEFINITIVE DIAGNOSIS = VIA RECTAL SUCTION BIOPSY of the narrowed area of the colon = a biopsy of both the mucosa and submucosa (whereas a normal biopsy = just of mucosa) - can therefore see if Meissner’s Plexus is present or not
- Upon biopsy, will see Lack of ganglion cells and hypertrophied nerve fibers***
- Best place to obtain biopsy = distal to expanded segment
- Proximal to expanded segment would most likely be normal
A rectal biopsy is the gold standard for diagnosis of Hirschsprung disease but barium enema and anorectal manometry are also used to assist in the diagnosis
TREATMENT
⦁ surgical resection of area that is lacking nerve fibers
⦁ healthy end of colon is then connected to the anus
Treatment for Hirschsprung’s disease entails stabilizing the bowel through rectal washouts, decompression via nasogastric tube and antibiotic therapy if indicated. This is followed by surgical resection of the aganglionic portions of the colon and anastomosis of the functioning bowel to the anus.
PYLORIC STENOSIS
INFANTILE HYPERTROPHIC PYLORIC STENOSIS
- congenital condition in which the pylorus (region between stomach and doudenum) grows in size (hypertrophy), and therefore narrows the opening between stomach and duodenum
MC cause of gastric outlet obstruction in infants
Pylorus =
⦁ pyloric antrum - connects to the body of the stomach
⦁ pyloric canal - connects to the duodenum
⦁ pyloric sphincter - at the end of the pyloric canal = ring of smooth muscle that contracts and acts like a valve, letting food pass down into the duodenum. Prevents food from moving back into the stomach
- *** pyloric stenosis occurs a FEW WEEKS AFTER BIRTH. The pylorus is normal at birth **
- After a few weeks, the smooth muscle of the pyloric antrum undergoes hypertrophy + hyperplasia (increase in size of cells as well as increase in overall # of cells)
This causes the pyloric antrum to nearly double in size, which stenoses the lumen itself –> blocks the pathway of food - makes it harder for stomach contents to leave and enter the small intestine
- The enlarged pylorus feels like an “olive” in the RUQ or epigastric region - “moves left to right when feeding”
- Stenosis of pyloric lumen causes stomach to have to contract even harder (peristalsis) to push contents through to small intestine —> can end up causing hypertrophy of the stomach as well
⦁ can end up feeling or seeing peristalsis of the stomach at that point
CLINICAL MANIFESTATIONS
⦁ VOMITING* - food builds up in stomach, and has nowhere to go
- this usually occurs around 2-6 weeks of age
- increases in intensity over time, until it ultimately starts causing PROJECTILE VOMITING* after feeding
- Vomit is NON-BILIOUS** (as it does not reach the duodenum where the bile duct comes in, unlike with Hirschsprung disease, which is bilious vomiting)
- vomiting –> loss of stomach acid –> hypochloremia (loss of hydrochloric acid)
- vomiting –> dehydration –> low blood volume –> kidneys retain sodium to try and retain water, and excrete potassium in exchange –> hypokalemia
⦁ HYPOCHLOREMIA** (normal = 98 - 106)
⦁ HYPOKALEMIA** (normal = 3.5 - 5.0)
⦁ METABOLIC ALKALOSIS** (HCO3= 22-30)
Hypokalemia causes potassium to start moving out of cells in exchange for Hydrogen ions. Also causes H+ ions to be secreted and HCO3- to be reabsorbed
- all of these cause a decrease in acidity (increase in pH) —> METABOLIC ALKALOSIS** (normal = 22-30)
- child remains hungry
- see signs of dehydration + malnutrition
CAUSE OF PYLORIC STENOSIS
- unknown - likely involves genetic + environmental factors
⦁ MC in infant boys
⦁ MC in first-borns
⦁ MC in caucasians
⦁ Also associated with exposure to MACROLIDE Antibiotics (Erythromycin) - both macrolide treatment in infants as well as macrolide treatment in late pregnancy for mother
95% of cases present in first 3-12 weeks of life; rare in babies > 6 months
- if occurs in adults = associated with chronic ulcer disease
DIAGNOSIS
⦁ serious vomiting in infant that is a few weeks old
⦁ “olive” mass upon abdominal palpation = nontender, is mobile, hard. Can be palpated especially after the infant has vomited
⦁ seeing or feeling peristalsis of stomach
- IMAGING =
⦁ Ultrasound = 1st line test** - see elongation / thickening of the pylorus. No radiation risk, and is more sensitive = best initial test
⦁ Xray - Upper GI Contrast = see “STRING SIGN” - as the dye goes through the narrowed channel. See delayed gastric emptying = most accurate test
LABS
⦁ will show hypochloremic, hypokalemic, metabolic alkalosis
TREATMENT
⦁ initially = hydration with IV fluids + correction of electrolytes
- definitive = PYLOROMYOTOMY***** (RAMSTEDT’S PROCEDURE) = muscles of pylorus are cut, allowing food to pass through more easily
- start breastfeeding or formula feeding within 24 hrs after pyloromyotomy - small and frequent feedings. May resume full feeding within 2 days, every 4-6 hrs
IMMUNIZATION SCHEDULE
0 = HEP B
2 MONTHS ⦁ Pediarix (DTaP + IPV + Hep B) ⦁ Rotateq ⦁ HIB ⦁ PCV 13 (Prevnar) - pneumococcal
4 MONTHS ⦁ Pediarix (DTaP + IPV + Hep B) ⦁ Rotateq ⦁ HIB ⦁ PCV13
6 MONTHS ⦁ Pediarix (DTaP + IPV + Hep B) ⦁ Rotateq ⦁ HIB ⦁ PCV13 ⦁ Influenza
For patients 6 months - 8 yrs = require 2 doses of influenza vaccine. If first time getting vaccine = will need 2nd dose at least 1 month later. If have had flu vaccine before, but never had 2 doses = will need 2nd dose this time - at least 1 month later
12-15 MONTHS ⦁ DTaP ⦁ HIB booster ⦁ PCV13 booster ⦁ Proquad (MMR + Varicella) ⦁ Hep A
- 2nd Hep A dose = > 6 months later (2 years)
4-6 YEARS ⦁ Proquad (MMR + Varicella) ⦁ DTaP ⦁ IPV booster (Kinrix = DTaP + IPV)
TDap = every 10 years afterwards
HPV = 9y/o +
- need it at 0, 2 months, 6 months apart
11-12 YEARS
⦁ MCV4 - Meningococcal
16 YEARS
⦁ MCV4 - Meningococcal
SLIPPED CAPITAL FEMORAL EPIPHYSIS
SCFE
- common hip disorder in adolescents** in which the growth plate (physis) of the femur fractures = *SALTER HARRIS TYPE 1
- leads to a “slippage” between the neck of the femur and the overlying head of the femur (epiphysis)
MC hip disorder in adolescents
epiphysis - physis - metaphysis - diaphysis (shaft) - metaphysis - physis - epiphysis
The physis (growth plate) contains cartilaginous cells that grow and divide, particularly during growth spurts, to allow the bone to grow in length - eventually the growth plate ossifies and fuses with the epiphysis around age 16 in females, 19 in males
During growth spurt, the growth plate is weak
Perichondrial ring = dense connective tissue ring around the growth plate that connects the metaphysis to the epiphysis
- The perichondrial ring helps resist shearing forces so that the femoral head and femoral neck done slip away from each other
Femoral head sits in the ACETABULUM and is supported by the joint capsule as well as the LIGAMENTUM TERES
- PATHOPHYSIOLOGY*
- during SCFE, the perichondrial ring becomes too weak to resist the shearing forces between femoral head and femoral neck, causing them to gradually slip away from each other
despite what the name suggests, it is NOT the epiphysis that gets slipped away, as it is being held tight in the acetabulum by joint capsule and ligamentum teres femoris
The neck gets displaced anterolaterally and superiorly (diagonally up and out) - whereas the epiphysis has slipped down and backwards (diagonally down)
If the displacement is severe = can tear the epiphyseal blood vessels = interrupting the blood supply to the femoral head
- the epiphyseal cells can starve and start dying off = AVASCULAR NECROSIS OF FEMORAL HEAD
CAUSE
- not entirely well known
RISK FACTORS
⦁ Obesity - increased pressure on epiphysis / physis junction –> slippage
⦁ African American
⦁ MC in males
⦁ Family hx of SCFE
⦁ Growth hormone or Sex hormone imbalances
⦁ Hypothyroidism**, Hypopituitarism - if seen in children before puberty - suspect hormonal / systemic disorders
Due to weakness of growth plate + hormonal changes at puberty**
CLINICAL MANIFESTATIONS o MILD CASES ⦁ can cause intermittent pain in groin ⦁ pain may also be referred to thigh or knee - along the distribution of the obturator nerve ⦁ pain worsens with activity ⦁ pain may cause a limp
o SEVERE CASES
⦁ unable to walk
⦁ affected leg appears LONGER and EXTERNALLY ROTATED and FLEXED compared to unaffected leg
⦁ over time, can become difficult to perform internal rotation or abduction with affected leg (just like with Legg-Calve-Perthes Disease - also avascular necrosis)
DIAGNOSIS
⦁ pelvix XRAY - frog leg lateral view - to help visualize the joint
- caution; frog leg lateral view may further exacerbate an unstable case of SCFE
- see widening of joint space
- also femoral head looks displaced (posteroinferiorly)
TREATMENT
⦁ surgery - to stabilize femoral head and prevent further slipping, as well as avascular necrosis
- place screws through growth plate to femoral head
- requires period of rest / limited weight bearing until hip heals and becomes more stable
ORIF = open reduction internal fixation
⦁ may have prophylactic fixing of the contralateral hip
often develop SCFE on contralateral side shortly after due to compensating for pain with other side, putting more weight/pressure on unaffected hip
TARSAL BONES
Tiger Cub Needs MILC ⦁ Talus ⦁ Calcaneus ⦁ Navicular (on big toe side) ⦁ medial cuneiform ⦁ intermediate cuneiform ⦁ lateral cuneiform ⦁ cuboid (on pinky toe side)
CARPAL BONES
Straight Line To Pinky, Here Comes The Thumb
⦁ scaphoid ⦁ lunate ⦁ triquetrum ⦁ pisiform ⦁ hamate ⦁ capitate ⦁ trapezoid ⦁ trapezium (directly underneath thumb bone)
ACUTE OTITIS MEDIA
Inflammatory condition of the middle ear, with or without effusion
Otitis media = Infection of the middle ear caused by a virus or bacteria
Infection of the middle ear, temporal bone + mastoid air cells
** MC PRECEDED BY A VIRAL URI **
Is characterized by the presence of fluid in the middle ear, along with symptoms of inflammation
MC occurs in children due to straighter / shorter / narrower eustachian tube in childhood
Often time frame = 6 months - 3 years
6-18 months = peak age
- **Most commonly preceded by a viral URI –> causes eustachian tube edema –> negative pressure –> transudation of fluid + mucus in the middle ear from sinuses –> secondary colonization of bacteria + flora
Acute otitis media = rapid onset + signs / symptoms of inflammation
Otitis Media with Effusion = asymptomatic - no inflammation, but has drainage/discharge
Common bacterial causes include
⦁ Streptococcus pneumoniae** (MC) - 50%
⦁ Haemophilus influenzae - 30%
⦁ Moraxella catarrhalis - 10-15%
⦁ Strep pyogenes (same organism as with acute sinusitis)
usually viral, but if bacterial, most likely strep pneumo.
RISK FACTORS
- Eustachian Tube (ET) Dysfunction
- young age (shorter / narrower / more horizontal ET)
- caretaker smoking
- bottle propping - bottle feeding while supine
- pacifier use
- day care attendance
- formula feeding / not being breastfeed
- family hx
- male gender (MC in boys)
** Children with an upper respiratory infection or those regularly exposed to smoke = at increased risk of developing ear infections
- breastfeeding = protective against OM
COMPLICATIONS = ** Conductive Hearing Loss **
- hearing loss may occur due to chronic inflammation, perforation of TM, or damage to anatomy of inner ear
CLINICAL MANIFESTATIONS
⦁ ear pain (otalgia)
⦁ fever (more often afebrile though)
⦁ accompanying URI symptoms
- may present with abrupt onset ear pain in young children along with
⦁ pulling/tugging at the ear
⦁ increased crying
⦁ poor sleep
⦁ conductive hearing loss / stuffiness
⦁ decreased appetite (sucking / chewing can aggravate inner ear pain)
PHYSICAL EXAM
⦁ red, bulging TM with effusion
⦁ decreased TM mobility with pneumatic otoscopy
** if bullae seen on TM = suspect MYCOPLASMA pneumoniae
- multiple ear infections can cause scarring of middle ear structures
- If TM perforation occurs = Rapid relief of pain + otorrhea (usually heals in 1-2 days)
TREATMENT
- 1st line = Amoxicillin (90mg/kg BID) x 10-14 days
- 2nd line = Augmentin (if resistant to amoxicillin) - SE = diarrhea
- If allergic to PCN = Azithromycin or
- Cephalosporin (ceftriaxone/Rocephin) if mild allergy to PCN (SE / reactions)
- if received Amoxicillin in last month = give Augmentin
- if not seeing any clinical improvement = switch to Augmentin
- can give ibuprofen / Tylenol for pain + fever
H. flu + M. cat = produce beta lactamases = PCNs won’t work
- if under 2 = just give abx
- educate parents with kids over the age of 2 about waiting prior to using antibiotics
symptoms usually spontaneously resolve in 2/3 of children by 24 hours, and` 80% in 2-10 days
- irrigation, then lay on affected side
for chronic / recurrent cases
- myringotomy (incision in eardrum) to help relieve pressure / fluid buildup
- tympanostomy tubes
