Due to immaturity of system.

Have to build up immunity.

eustachian tube starts out straight (prone to a lot of ear infections)

Tonsils grow rapidly then atrophy.

They're belly breathers and nose breathers are first.

Hyaline Membrane Syndrome. Usually in premature babies.

Result of inadequate production of surfactant. Normally release in lung tissue. Keeps alveoli expanded.

Alveoli collapse and eventually hyaline membrane forms.

Decreased O2 levels. 

May develop acutely over time.

Increased respirations (norm 30-60)

Flaring, retractions, grunting

Apneic periods and cyanosis.

Breath sounds diminished.

Ideally prior to delivery by amniocentesis.

Surfactant is produced 7-8th month.

Measure levels of lecithin, which is a major component of surfactant.

If levels are low give glucocorticosteroids if delivery is inevitable. This triggers babies lungs to make surfactant.

Once delivered will be based on symptoms and chest xray. Xray will show dark streaks and ground glass appearance.

Delays lung maturity.

They'll still do the amniocentesis.

Administer sufactant (synthetic/natural) by endotracheal tube right after birth.

Oxygen, IVS, ABGs, pulse ox.

By 1st week of life they'll produce on their own and gradually improve.

 Intrauterine stress/asphyxia usual cause.

Inhalation of meconium in utero or with first breath.

Meconium stained fluid.

Meconium stained baby-green tinge. Stress before labor for long period of time. They have meconium in lungs.

May have green stain to skin.

Tachypnea, dyspnea at birth.

Grunting, flaring, retractions

Hypothermia, hypoglycemia, hypocalcemia

Cyanosis, pallor, hypotonia (very limp)

DX: the fluid breaks. take laryngscope and look into respiratory tract ot see if baby inhaled meconium.

xray-patches/streaks in lungs and atelectasis. Based on symptoms.

TX: suctioning prior to delivery of chest when head is out. Oxygen therapy. Possibly ventilator. IVs. Antibiotics. Corticosteriods.

Sudden Infant Death Syndrome (SIDS)

"Crib Death"
 

Sudden death of basically healthy infant.

Cannot explain why the child died even after autopsy.

Risk factors: 2-4 months, winter months, males, ethnic descent, prematurity, low birth weight, recent mild illness

Brainstem abnormality in regulation of cardiorespiratory control.

Maternal Risk Factors: smoking during pregnancy, poor prenatal care, substance abuse, and exposure to tobacco smoke after birth.

Sudden Infant Death Syndrome (SIDS)

Autopsy

Will show pulmonary edema and evidence of intrathoracic hemorrhages, but there's no conclusive cause of death.

Once one child dies from SIDS it increases any subsequent children dying from SIDS by 4-5 times.

Child not breathing

But unusual sounds/cries prior to episode.

Frothy, blood tinged fluid.

Skin white ashen color, cool.

Autopsy is the only conclusive way to determine.

Preventions: back to sleep.

Apnea monitoring for subsequent children.

Parents deal with guilt, blame self, caregivers.

Extensive support for parents adn siblings.

Infection/inflammation of smaller airways/bronchioles.

Cause: usually RSV (respiratory syncytial virus) or other virus.

Secretions block airways.

Happens to children under age 3. Usually 2-5 months.

They're membranes swell. RSV transmitted by droplet.

Starts with rhinorrhea and low grade fever.

Progresses to deep cough, wheezing, tachypnea, retractions, flaring, cyanosis (alll signs of respiratory distress)

Also have listlessness, anorexia, irritability, dehydration becomes a concern.

DX: ELISA test (enzyme linked immunosorbent assay)-looks for antibodies. CXR may also confirm.

TX: Treat the symptoms b/c it's viral.

Cool humidified O2.

Meds PRN to maintain patent airways, decrease inflamm, and thin secretions.

Adequate fluid intake.

Possible administration of Ribavirin. (antiviral agent for higher risk pts who have other resp issues/cardiac issues. It's expensive and aersol admin. Has toxic effects. Used as last resort)

Contact precautions/isolation

Close respiratory monitoring

Monitor hydration/nutrition status

Term represents group of respiratory illnesses.

Result of inflammation of larynx, trachea, and large bronchi.

Characteristic barking cough (not seen with all types)

Can be a viral/bacterial cause.

Croup Syndrome

Epiglottitis (acute)

Inflammation of the epiglottis

Caused by bacterial infeciton.

Potentially life threatening.

Hib vaccine to decrease incidence.

2-6yrs old get it.

Croup Syndrome

Epiglottitis

S/SX

Symptoms develop rapidly

Sudden high fever, sore throat, dysphagia.

Drooling, tripod position (leaning forward)

Epiglottis is red and edematous.

**Do not use tongue blade/initiate gag reflex!!!**

No cough/struggling to breathe/anxious

Croup Syndrome

Epiglottitis

DX & TX

DX: based on symptoms

TX: have intubation equipment on hand.

Humidified O2.

IV antibiotics.

24-48hrs starts clearing up.

Close repiratory observation.

Croup Syndrome

Acute Laryngotracheaobronchitis LTB

Most common type.

Usually viral cause, follows upper respiratory infection.

Inflammation of mucosa lining, larynx, and trachea.

Children 5 and under.

Croup Syndrome

Acute Laryngotracheaobronchitis LTB

S/SX

Gradual onset of low fever, barking seal like cough usually worse at night.

Inspiratory stridor, retractions, nasal flaring, tachypnea, tachycardia, restlessness, irritability. (signs of resp distress)

Croup Syndrome

Acute Laryngotracheaobronchitis LTB

DX & TX

DX: Clinical findings. CXR to rule out certain things.

TX: maintain patent airway.

Mild cases managed at home.

High humidity & cool air.

Nebulized epinephrine if needed.

Possible corticosteroids.

Antibiotics if bacterial.

Close monitoring of respiratory status.

Bedrest, fluids as tolerated.

Croup Syndrome

Acute Spasmodic Layrngitis

Attacks of laryngeal obstruction

Occur mainly at night. "Midnight Croup"

Mild to no signs of inflammation

Child usually between ages of 1-3 yrs.

Cause: Unknown, possible infectious or allergen origin.

Acute Spasmodic Layrngitis

S/SX

Child awakens with barking cough, hoarseness, respiratory difficulty, restlessness increases

S/SX subside in a few hours.

Acute Spasmodic Layrngitis

TX

Managed at home with cool air or warm mist.

Disease is self limiting. Parents should be instructed to seek help if S/SX worsen or persist.

Croup Syndrome

Tracheitis

Bacterial infection of upper trachea.

Most often kids under 3 yrs.

It's serious. Can cause respiratory arrest.

It's a possible complication of LTB (acute laryngotracheaobroncitis).

Causes: Staph aureus or H influenza

Tracheitits

S/SX & TX

S/SX: Similiar to LTB, but doesn't respond to TX (cool air).

They have HX of upper respiratory infections, cough, stridor, high fever.

Major sign: thick purulent secretions. 

This can lead to respiratory arrest by obstructing airways.

TX: Aggressive and may include intubation, antibiotics, antipyretics, O2.

Tonsils are lymphoid tissue that filters and protects respiratory and GI tracts and have a role in antibody formation.

3 sets

pharyngeal: adenoids

palatine: faucial (visible and enlarge, come out with tonsillectomy) Inflamm of the palatine tonsils can be viral/bacterial.

lingual

Tonsillitis & Adenoiditis

S/SX

Difficulty swallowing and breathing. 

Sore throat, mouth breathing (adenoids inflammed)

Halitosis, cough.

Occasionally otitis media.

Tonsillitis and Adenoiditis

DX & TX

DX: Culture

TX: Antibiotics if bacterial

Analgesics and antipyretics. Encourage fluids.

Surgical intervention only if causing difficulty breathing or eating or repeated episodes. Don't usually do before age 3-4 because they can grow back. Tonsils also can shrink when they get older and that may solve they problem.

Tonsillitis and Adenoiditis

Post OP Care

Bleeding is a BIG concern. Especially when they're older.

Provide comfort, minimize activity.

Side lying/prone until fully awake to prevent aspiration.

Discourage coughing, clearning throat, or blowing nose b/c it causes irritation.

Watch for hemmorhage. They'll have frequent swallowing, be restless and tachycardiac, vomit bright red blood. Can happen 5-7 days after surgery.

Need liquids and soft food. Avoid red liquid, milk and spicy foods up to 2 weeks after surgery.

Inherited disorder of the exocrine/mucous producing glands.

Effects primarily caucasians.

Defective chloride ion and water transport across cell membranes.

Thick mucous produced obstructs organs: pancreas, liver, reproductive system, lungs.

They'll have an increase in sodium and chloride levels in both saliva and sweat sometimes 2-5 times higher than normal.

Cystic Fibrosis

S/SX

Meconium ileus because of the thickness and stickiness. Distention and possible vomitting.

Salty taste on skin. Steatorrhea (fatty stools with mucuos)

Respiratory system biggest problem:

Increase thick mucous & resistance to ciliary action

Frequent upper respiratory infections

Altered gas exchange

Cystic Fibrosis 

Long Term Effects

Clubbing of Fingers & barrel chest

Atelectasis

Emphysema

Pulmonary fibrosis

Eventually pneumothorax

Right ventricular hypertrophy

Cystic Fibrosis

DX

Based on family HX

Symptoms of failure to thrice

Stool analysis for fat and enzymes

Sweat test analyze and CXR

Cystic Fibrosis

TX

Primary Goal: Improve quality of life and provide long term survival.

Pancreatic enzymes help improve digestion of fats and proteins.

Diet changes: increased carbs & proteins and low fat.

Salt and vitamin supplements: ADEK (fat soluble)

Meds as needed: bronchodilators to thin secretions

Chest physiotherapy & exercise program as tolerated.

Chronic inflammation disorder of airways.

Edema of bronchial mucosa.

Increased mucus production

Bronchial muscle spasms

Often triggered by allergic reaction, stress, cold, and exercise. The cells release histamine.

Periods of exacerbations and remission.

Asthma

S/SX & DX

S/SX: Suddenly or over several days dry, hacking cough

Tightness in chest

Wheezing, dyspnea

DX: Based on hx, symptoms, sometimes CXR

Asthma

TX

Focus on preventing symptoms and reoccurence and attacks.

Avoid triggers.

Keep diary, clean carpets, get rid of pets, stop smoking.

Regulation of meds: bronchodilators, antinflmmatories, and other as ordered.

Can be anywhere from moderate to severe.

3-4th week of gestation is the development of the heart and circulatory system.

By the 8th week it's completely formed.

By the 28th day around the heart starts beating.

Heart starts as a simple tube that just recieves blood from placenta and pumps out to body. Transforms into 4 chambers.

Maternal drug/alcohol use

Advanced maternal age (35+)

Maternal condition (lupus/diabetes)

Familial history

Some defects are life threatening, taken immediately to surgery. Some you can wait.

Allow blood flow from high pressure left side of heart to lower pressure right side of heart.

Causes increased pulmonary blood flow usually causes CHF.

3 major defects:

VSD, ASD PDA

Results from abnormal opening in septum b/w left and right ventricle. Can be tiny/large. 

Tiny-asymptomatic. 

Large-loud, audible murmur, hear the blood. S/SX: of dyspnea, of CHF, more prone to resp infections

DX: by listening, EKG, CXR TX: some close on own, srugery before child is 2, suture/patch

Opening in the septum between the left and right atria.

The formen ovalie stays open (usually the cause).

Blood flows from L atria to R atria and back to lungs. can lead to ventricularhypertrophy.

Sometimes asymptomatic or very soft heart murmur. As child gets older they get fatigued, delayed growth, and prone to CHF.

DX: EKG TX: suture/patch

Closes within 15hours of birth normally.

When ductus arteriosus remains patent, blood continues to shunt from aorta to the pulmonary artery.

S/SX: machine like murmur. Loud and audible, wide pulse pressure, bounding pulses, tired and fatigue, not growing, risk for CHF.

DX: hear murmur, EKC, cardiac cath

TX:meds, indomethacin prostaglandin inhibitor helps close a patent ductus. Surgery.

blood exiting heart meets an anatomic narrowing causing obstruction to blood flow.

2 major defects:

coarctation of the aorta

aortic stenosis (narrowing)

narrowing of the aorta specifically at the arch.

heart is working harder to pus hblood through.

Leads to CHF over time.

Causes increased pressure in upper extremities and decreased pressure in lower extremities.

Depends on the degree of defect.

Dyspnea, tachycardia, CHF,

BP and pulse increased in upper extremities, diminished in lower extremities

C/O cramping legs, H/A because of circulation

If not treated can result in HTN, aortic aneurysm

Stroke, cardiac failure

Surgery done by age 2.

Try to widen it or remove it and graft.

Decreased Pulmonary Blood Flow

(Cyanotic Defect)

Obstruction of pulmonary blood flow and anatomic defect b/w right and left side of heart. Septel defect.

Blood has difficulty leaving heart through pulmonary artery so right sided pressure increases.

Destaurated blood is shunted right to left resulting in hypoexemia.

Most common defect: Tetralogy of Fallot.

Most Common Defect of decreased pulmonary blood flow.

4 Seperate combined defects.

Pulmonary Stenosis-narrowing of pulmonary valve

VSD-ventricular septal defect. (hole)

Overriding aorta-aorta comes off both ventricles

Right ventricular hypertrophy.

The blood has a hard time getting to the lungs.

S/SX of Decreased Pulmonary Blood Flow

(Tetralogy of Fallot)

Some will be acutely cyanotic at birth.

Does vary in degree. Can slowly progress over first year.

Murmur is often audible.

Feeding difficulties, poor wt gain. Slowed growth and development

Prone to tet spells/blue spells. Dyspnea, gasping respir, increased cyanosis that can lead to loss of consciousness and possible convulsions. They seem to be stresssed induced. 

Some older kids will drop into squatting postion (knees to chest) in attempt to get O2 into body.

They develop polycythemia (Increase in RBCs) in attempt to get more O2 to bind.

DX decreased pulmonary blood flow

(tetralogy of fallot)

Confirm with echocardiogram

EKG

TX decreased pulmonary blood flow

(tetralogy of fallot)

Usually repaired by the time the child is two.

Surgery.

The more the severe it is the earlier they'll do it.

They widen the valve to fix the stenosis or possibly replace the vave.

They close VSD, which also resolves the overriding aorta.

Overtime the hypertrophy will gradually disappear.

Mixed Blood Flow Defect

Cyanotic

Saturated Systemic blood and desaturated pulmonary blood mix in heart, aorta, and pulmonary vessels.

results in desaturation of systemic blood.

Most common defect: transposition of the great arteries

Most common defect of mixed blood flow.

Aorta comes off right ventricle and pulmonary artery leaves left ventricle. They've switched places.

Problem: there's no O2!!!

TX Mixed Blood Flow Defect

(Transposition of the Great Arteries)

Only thing that can save baby is a defect in the septum to let blood mix or a patent ductus. Otherwise they need immediate surgery!!!

If you give O2 to child it doesn't help. Usually this can be picked up on ultrasound.

Prostaglandin EI given IV maintains pantency of ductus arteriosis so blood can still mix.

Septostomy (balloon) inserted to make defect larger to allow more blood to mix.

By 1 week they NEED to have surgery to switch vessels and close septal defect as well.

S/SX: Mixed Blood Flow Defect

(Transposition of the Great Arteries)

Cyanosis doesn't improve with O2

Hypoxemia, CHF, Increased respiratory rate

Tachypnea, they need very freq rest periods

Acquired Heart Diseases

CHF

manifestations similiar to adults, but symptoms may be different in children.

S/SX: *tachycardia, crackles, edema, fatigue with feeding, tachypnea, flaring retractions, grunting, poor wt gain.

TX: diuretics, Digoxin (strengthen heart), promote oxygenation

Acquired Heart Disease

Kawasaki Disease

Acute systemic inflammatory illness

Also termed mucocutaneous lymph node syndrome.

S/SX present in 3 phases acute, subacute, convalescent.

Cause: unknown. Often seen later winter, early spring.

Can lead to cardiac complications affecting heart muscles and cardiac blood vessels.

Lasts 6-8weeks.

Acute: High fever, irritable, inflamm of conjuctiva, red throat, strawberry colored tongue, rash, edema in hands & feet, enlarged cervical lymph nodes. (lasts several weeks)

Subacute: Skin on lips, hands, and feet all slough off. C/O joint pain, serious cardiac complications can occur during this phase such as thrombosis, aneurysms of coronary arteries, and MI.

Convalescent: Symptoms gradually diminish. Energy & appetite returns.

Based on fever and 4 of these symptoms

-elevation of WBC and ESR (erthrocyte sed rate)

-conjuctivitis

-cervical lymphadenopathy

-rash

-changes in extremities & lymphadenopathy

EKG

TX of Kawasaki Disease

(acquired heart disease)

IV immunoglobin to reduce fever and imflammatory response.

ASA to reduce fever and it's an antiplatlet.

Close observation & comfort measures

Nutritional support clear liquid diet

ROM, minimize strain on heart.

Acquired Heart Diseases

Rheumatic Fever

Inflammatory Disease

Usually follows group A beta Strep trigged by autoiummune response.

Potential damage to heart, joints, CNS, and skin.

Most significant complication: cardiac valve damage

S/SX of Rheumatic Fever

acquired heart disease

Can be anywhere from few days to 6 weeks

Painful, inflammed joints, rash, lethargy, anorexia

Chorea- uncontrollable muscle tremors and emotional instability. Lasts a few weeks to 2 years. Primarily affects face and extremities. Can be mild-severe.

Cardiac effects-tachycardia & murmurs. Cardititis, major cause of permanent mitral and aortic valve damage.

DX & TX Rheumatic Fever

(acquired heart disease)

DX: Jones criteria along with lab tests

TX: aimed at preventing heart disease.

Bedrest to decrease cardiac workload

Steroids

Antibiotics to treat strep.

Bleeding disorder with hereditary link. Result is delayed coagulation of blood.

2 main forms: Factor VIII and Factor IX

X linked recessive disorder. Mom carries gene. Men usually get the disease.

Factor VIII: Hemophilia A. More common.

Factor IX: Hemophilia B/Christmas disease. Rare.

Bleeding into soft tissue or during invasive procedure.

Not seen initiatially.

Bleeding into joints (hemathrosis). Will be painful and edemitis. If not treated can cause severe deformitites.

Bruising easily. Epistaxis. Hematuria.

Bleeds into brain/tissue around airway.

PTT (partial thromboplastin time)

HX, assessment

Reveals low factor VIII or IX

Factor VIII or IX needed to form thromboplastin.

Classified as mild, moderate or severe. It's based on levels.

Factor VIII/IX replacement. Given IV.

Teach parent how to do it once child is past 2 years old. They need it throughout life.

Synthetic vasopressin (DDAVP) helps to stimulate factor VIII/IX. Used only for mild cases. 

Corticosterioids for hemoarthrosis.

NSAIDs rarely b/c they inhibit platlets.

NO ASA b/c of bleeding.

Narcotics occasionally for joint pain.

Ice packs, immobilization. NO HEAT!

Regular exercise to build muscle tone around joints.

Teach safety measures.

Hereditary Disorder where normal Hgb is replaced by Hgb S.

Causes the RBCs to take on sickle shape. You have trait or anemia.

If they get gene from 1 parent they have the trait. They'll have normal Hgb and no symptoms, but can pass it onto their children.

If both parents have trait there's a 25% chance with each pregnancy that child will develop anemia.

It primarily affects african americans, indians, mediterrean countries.

Asymptomatic for 4-6 months because of prescence of Hgb F. Prevents cells from getting into abnormal shape.

When symptoms do occur: Result of obstruction of vessels by sickled cells and increase RBC destruction/anemia.

Often triggered by periods of stress. Such as rapid growth spurt, illness, dehydration, increased exercise.

More sickle celled shapes get released into blood stream. Hypoxia, ischemia, and anemia occurs.

Abd pain, muscle spasms (b/c bloods not flowing there), joint pain and swelling, fever and nausea, pallor, coolness of skin.

Will impact the organs.

Heart-cardiomegaly, murmurs.

Lungs-pulmonary insufficiency, infection.

Kidneys-hematuria, inability to concentrate urine.

Liver- hepatomegaly, cirrhosis

Spleen-enlargement, fibrosis, infection

Extremities-Infection, degeneration of bones, leg ulcers, osteomyelitis

CNS-stroke, seizures, h/a, visual disturbances, aphasia, hemiparesis

Sickledex screen for Hgb S.

Fingerstick/heelstick.

If positive will do hemoglobin electrophoresis to confirm if trait or disease. It's done on newborns.

Prevent Crisis:

Promote hydration, minimize tissue hypoxia, freq rest periods, avoid highly strenous activities, avoid high altitudes, avoid infection, vaccinations, prophlatics antibiotics sometimes.

If have crisis:

Bedrest, hydration and electrolytes, analgesics, oxygen, blood transfusions. 

It's a chronic, life threatening disease. No cure, but can be managed!

Acute Lymphoblastic Leukemia (ALL): lymphoblastic can be replaced with lymphocytic, lymphoid, or lymphoblastoid. They're all the same.

Acute Myeloid Leukemia (AML): Also known as myelogenous leukemia

Acute Leukemia

Acute Lymphoblastic Leukemia ALL

Lymphocytes divide rapidly but do not mature so they have no function. They release from the bone marrow.

Numbers increase and impact normal WBCs, RBCs, and platlets. They are still prone to infection.

It's the more common type. Has the best cure rate.

Acute Leukemia

Acute Myeloid Leukemia AML

Also known as acute myelogenous leukemia.

Rapid growth of abnormal WBCs that accumulate in bone marrow.

Interferes with production of normal WBCs, RBCs, and platlets.

Lower cure rate.

Diagnosed at age 2-6. Males have slightly higher incidence.

Based on hx, labwork.

Confirmed with bone marrow aspiration.

Symptoms are a result of anemia, infection, bleeding.

Fever, pallor, fatigue, anorexia, hemmorhage, bone and joint pain, *enlarged lymph nodes and spleen and liver, petichiae, bleeding gums, bruising, abd pain, distention, N/V.

Chemo therapy done in phases.

Induction: to achieve resmission. Give steroids.

Sanctuary: Keep abnormal cells from invading CNS. Intrathecal chemo. Do a lumbar puncture and put chemo right into cerebrospinal fluid.

Maintence: To maintain state of remission. Steriods. Phase lasts 2-3 years.

If relapse occurs additional therapy is needed. With each relapse it makes the prognosis worse.

Infection Prevention

Monitor for bruising and bleeding

Monitor kidney function

Watch fluid and nutritional status

Pain relief & emotional support.

ALL: try to hold off on bone marrow if relapse. AML: might choose to do bone marrow transplant if relapse.

if lip fails to close. can be unilater or bilateral. the extent varies.

Dental animolies are common. Missing/deformed teeth common on the side of the cleft.

Cleft can be complete both through bone and tissue.

Bone structure but not overlying mucous membranes.

It looks normal

have to do newborn exam to tell.

Normally palate closes by 10th week gestation. Unknown causes.

Combo of genetic and environmental influences. Linked to folic acid levels, maternal alcohol ingestion, and smoking.

DX: lip-visual and ultrasound

palate-inspection/exam to palpate

S/SX:newborn has trouble sucking. no adequate suction. at risk for choking.

Surgical. Do Lip closure first usually.

Some surgeons do surgery within a couple days of birth. Usually do surgery within 3 months at the latest.

Closure of palate is done in stages. It's multiple surgeries with multiple specialists (plastic surgeon, dentists, orthodontists)

They're prone to ear infections.

Goal is to prevent trauma and infection of suture line whether it's lip/palate.

Have feeding adaptions

Careful positioning.

NEVER on abdomen. May use elbow restraints.

Logan barre-device to reduce tension on suture line for lip.

Might need scar revisions as they grow.

Abscence of normal body opening

Or abnormal closure of body passage.

Esphogaus ends in blind pouch (normally ends in stomach)

Connecting trachea and espohagus. (so air and fluids are mixing)

And in some cases there's both a fistula and atresia.

Constant secretions, lots of respiratory distress, cyanosis, choking, distention, bloated (air gets into stomach)

DX: NG tube stops (normally it'd go into stomach)

TX: prevent resp complications until surgery can be performed. Suctioning and no oral feeds.

If no other anamolies surgery will be performed within first few days of life.

Gastronomy feed if have to wait for surgery.

Once fixed normal growth and development should occur.

Obstruction of pyloric canal as a result of thickening of plyoric sphincter and narrowing of passage between stomach and duodenum.

The pylorus also elongates.

Can cause total obstruction and dilation of stomach.

Rarely seen until 2-4th week of life.

As child continues to take fluids they will start to vomit after feeds to point of projectile.

They'll become irritable, hungry, wt loss, dehydration. They're born with it, but symptoms don't present at birth.

In RUQ they will feel round mass, you can see peristaltic waves.

What's their hx? Are they throwing up? 

Palpate for mass.

Do xray to confirm or ultrasound.

Pyloromyotomy-aka Fredet Ramstedt procedure circular muscle fibers or pylorus is cut to widen the canal.

NPO, IVS, surgery then 4-6hrs after normal liquids then progress, surgical incision care, analgesics, I&O

Relaxation of cardiac sphincter.

Allows gastric contents to "reflux" up into esophagus.

More common in premies or child with neurological impairment, but can affect full term babies as well.

S/SX: Spitting up with feeds, irritation of esophagus, infant (irritable) older (heartburn), indigestion, abdominal pain, chest pain, with infants if bad will develop failure to thrive. Usually resolves in about 18 months b/c sphincter matures.

HX, feeding patterns, growth patterns

Endoscopy, barium swallow

Changing formula, adding rice to thicken formula

Small freq feeds, don't lay flat after feeds

Surgery (rare)

Kid usually grows out of it

Baby can sleep on stomach (exception!)

Teach parents about respiratory distress

Aka Congenital Aganglionic megacolon (without)

Autonomic paraympathetic ganglia in muscular wall of intestine are absent.

Leads to persistent constipation/obstruction. 

Usually shows early in life, but may not until teens.

In this case internal sphincter does not relax so constipation occurs. Everything's backed up. Area distended with feces and gas.

Common with down syndrome.

Newborn: failure to pass meconium, refusing to suck, abdominal distention, bile stained or meconium emesis

Older child: HX of abdominal distention, chronic constipation with passage of ribbon like foul smelling stools or pellet stools.

Barium studies

Rectal biopsy, which confirms absence of nerve cells.

Surgery to remove aganglionic portion of bowel to relieve obstruction. May be done in stages.

May need temporary colostomy to let the other parts of intestine rest. (depends on how bad megacolon gets)

Prior to surgery: IVs, TPN

Post OP: I&O, wound care, fluids

Toxic levels of lead in the blood

Lead based paint is primary source.

Children absorb and retain more lead in proportion to body wt.

Lead interferes with normal cell function particulary nervous system.

Can affect also brain, blood cells, kidneys, vitamin D, calcium, metabolium.

Once in body (through GI tract) it gets deposited in bones and teeth and is slowly released.

Will take awhile for toxic levels to be normal, because still in body.

Early: Irritability, hyperactive, poor concentration, aggression, impulsiveness

May also develop learning disabilities, hearing impairment, and growth delays.

Can lead to encephalopathy or degenerative disease of brain.

VERY SERIOUS PERMANENT CONSEQUENCES IF NOT RESOLVED.

DX: Blood test to measure lead levels.

TX: Chelation therapy give meds to bind/pull lead out. Helps increase rate of excretion.

Doctor prescribes based on individuals blood test.

Early prognosis is encouraging but not certain. Follow ups for long period of time. Find and remove source!

Viral or bacterial inflammation of intestinal tract.

Diarrhea or vomitting can lead to dehydration

TX: to stop diarrhea including antibiotics if bacterical.

REHYDRATE!

Disorder affecting body's ability to use protein

Child lacks liver enzyme, Phenlalanine hyadroxlyaze needed to convert phenylalanine into tyrosine.

Can lead to mental retardation.

Test done on newborns, must be treated.

Have to have had milk before test b/c they need protein in system.

When uretheral opening is along surface of penis isntead of the tip.

Commonly seen with chordee-ventral curvature of penis.

DX: at birth, sometimes ultrasound

Surgical: extend urethra in some cases.

6-18 months most common time. Often several stages.

When infant presents will not circumsize at birth because will use skin as part of repairing process.

Urerethral stints often placed.

Urethral opening on dorsal or upper surface of penis.

Often seen with extrophy of bladder (when bladder is on external surface of abdomen)

Surgery done immediately within 48hours if extrophy!

Cryptorchidism

Congenital Disorder

Undescended Testicle(s)

If not corrected can result in sterility.

S/SX: newborn exam palpate scrotum can be unilateral/bilateral.

TX: wait and see sometimes they descend on their own. Administer HCG to facilitate descent. 

Will do orichiopexy by age 2 (surgery)

Can carry increased risk of testicular cancer.

Wilm's Tumor/Nephroblastoma

Noncongenital Disorder

Highly metastatic cancerous tumor in kidney region.

Usually detected in children 2-5 yrs old.

Thought to be genetic link. Thought to come from bits of leftover embryonic tissue.

May be none. Mass detected on routine exam.

Hematuria and HTN. Swelling and mass within abdomen.

Abdomen MUST NOT be palpated once mass is discovered b/c it can rupture.

Mass will be one sided, firm, non tender initially.

Ultrasound, CT, MRI

Will evaluate for metastasis to liver, lungs, and bone.

Surgery followed by chemo within 48hrs of diagnosis.

Removed kidney and any affected lymph nodes.

Also radiation if larage tumor or extensive metastasizes.

Watch I&O, fluid and electrolyte balance

Offer plenty of emotional support.

Clinical state characterized by edema, proteinuria, hypoalbuminemia, hyperlipidemia, altered immunity.

Two kinds:

Primary & Secondary

AKA minimal change nephrotic syndrome (MCNS)

Affects ONLY the kidneys

And frequently follows infection such as pyleonephritis.

Result/tied in with a systemic illness.

More involved often with lupus/diabetes/sickle cell anemia.

Is altered in both primary & secondary nephrotic syndrome.

As a result of alteration albumin moves from blood to urine (not good!) and results in hypoalbuminemia and proteinurea.

This changes osmotic pressure of blood and as a result kidneys start absorbing sodium and water and causes edema.

The low osmotic pressure stimulates the liver to make lipoproteins leading to the hyperlipidemia.

Edema-periorbital, lower extrem, scrotum, abdomen (can lead to ascites) all happens gradually

HTN & anorexia, irritability

Possible respiratory distress

Increased suceptibility to infection.

Urine anaysis (U/A) 

Albumin levels will be high and protein in urine

Possible renal biopsy

Chronic disorder that can last from 12-18months.

Tend to have periods of remissions and exacerbations.

Prone to getting it again if it's secondary.

Corticosterioids to reduce edema.

Cytoxan (chemo drug) helps to promote long term remission, but compromises immunity even more.

Diuretics reduce edema. Good skin care.

Frequent urine testing. I&O. Low sodium diet.

Inflammation of glomeruli and nephrons of the kidneys.

Thought to be an allergic reaction to certain infection most commonly group A beta strep.

Antigen antibody reaction that blocks to glomeruli allowing RBCs and protein to get into urine (oh no!)

1-3 weeks after strep infection

Hematuria, tea colored urine

Oliguria, proteinuria

Periorbital edema, anorexia, h/a

malaise, fever, irritability

sometimes a slightly elevated BP

DX: Based on U/A and look to see if they had a strep infection.

TX: bedrest, antibiotics, diuretics, I&O, wts, urine testing, low sodium diets

Usually resolves completely. There's potential for this to be a chronic form if s/sx persist for more than a year.

Spina bifida

Spina Bifida oculta

Spina bidia cystica (meningocele, myelogmeningocele)

Failure of posterior lamina of the vertebrae to close.

Meninges and spinal cord can protrude.

Cause: genetic predisposition, folic acid deficiency

hidden defect. Nothing external.

L5S1, slight dimple in skin or tuft of hair.

Doesn't present any problems.

protrusion.

(meningocele, myelomeningocele)

Meninges protrude, sac protrudes.

Herniation of the meninges, but no nerves roots of the tissue.

No paralysis/sensory loss.

Sac could rupture/perforate and can get meningitis.

spinal nerves and sometimes part of the spinal cord protruding out of the defect.

no innervation, no sensation. paralysis below site.

*more severe form

nerve roots embedded in sac.

impacts bowel and bladder spchinter.

In utero 13-16weeks. Alpha fetoprotein blood test. Look for elevated levels which can indicated possible neural tube defects. Not 100%

Ultrasound, CT/MRI (after born, to see extent of involvement of nerves)

Have to do C section if cyst is protruding (spina bifida cystica), surgical correction usually within 12-18 hours ideally.

Protect integrity of sac

Cover with sterile dressing

monitor for infection

have them lie in prone position

if paralysis do ROM and skin care

Emotional support

Post op care and teaching

*does not affect their intelligence!

excesssss of cerebrospinal fluid within ventricles of brain "water in the brain"

Noncommunicating & communicatingg

Can result from head injury/meningitis

Obstruction present so CSF cannot pass b/w ventricles and spinal cord.

Most cases.

enlarged head at birth, anterior fontanel buldges, shiny scalp, veins prounounced and dilated, setting sun eyes

Increased intracranial pressure, lethary, vommitting, irritability, high pitched cry*

ultrasound in utero

Catscan, MRI

ventriculography (watch flow of fluid to see if it's communicating or noncommunicating)

relive ventricular pressure

Shunt placement. Divert fluid from ventriculars to different part of body.

Most common: VP- ventriculoperitoneal (ventricles to peritoneum where it's absorbed)

VA-ventriculoatria (ventricles to R atrium)

Both will need revised when child grows.

Possible for infection or obstruction especially in first month

Keep them flat, take head circumferences, postion on non operative side, do neuro checks

Observe for abdominal distention, check incision sites, monitor for infection, check bowel sounds & abd girth

Do parent teaching

Inflamm of meninges caused by 

bacterial-meningococci, pneumococci, haemophilus influenza (most severe form)

virus

TB

Bacterial: vaccines avaliable meningococcal most severe form.

Viral meningitis can't do anything about. Have to just let it run it's course.

high pitched cry, fever, diarrhea, muchal rigidity (stiff neck), vomitting, h/a, irritability

convlusions, coma in less than 24 hours (especially older child)

hemorrhagic rash(meningococcal)

DX: early dx is essential for complete recovery. LP, possibly nose & throat cultures.

TX: isolation, possibly ICU, IV antibiotics for bacterial, hydration, NSAIDs for fever and pain, steriods will help decrease risk for neurological complications (deafness)

Anticonvulsants (if convulsions), needle aspiration of fluid in subdural space (this fluid can cause symptoms)

Close observations of vital signs & LOC, side lying postion, I&O and electrolyte check, emphasize need for immunizations

Periods of sudden discharge of electrical activity in brain that causes involuntary muscle activity, changes in LOC or altered beavior and sensory manifestation.

May be a result of genetic favots, pathologic condition or rapid temp elevation.

peidatrics usually

rise in temperature at any temp can happen.

Recurrent/chronic seizures

Primary-no known cause

Secondary-head trauma/disease

febrile seizures occur suddenly, child is irritable, restless

may have tonic clonic movements-sustained contractions of skeletal muscles that occur involuntary followed by clonic phase-quick jerking movement of arms, legs, and facial muscles.

epileptic seizures may be partial seizures which are limited to particular area of the brain or generalized which involve both hemispheres.

DX: EEG, CT scans, MRI

TX: anticonvulsants, surgery if cause is tumor, ketogenic diet (high in fat, low in carbs)

Safety of child is imporant, note time when seizure starts and stops as well as factors occuring before onset.

Evaluate after for LOC, pupil response, general behavior.

Teach parents to avoid triggers like blinking lights, excess activity/exercise.

Group of disorders that is a result of malfunction of motor centers and neural pathways in brain affecting motor function and posture.

Most common permanent physical disability in childhood.

Prenatal, perinatal, and postnatal factors may contribute to development.

Prenatal: maternal infection, nutritional deficiences, RH incapability, any O2 problems

Perinatal: anoxia (without O2) before, during, or after birth, birth trauma, prematurity, interference with respiratory function

Postnatal:head trauma, infection, CVA

Prenatal-keep track of nurtion

Perinatal-babies response to contraction. Possible with c sections to reduce trauma.

Postnatal-teach parents how to keep child safe and prevent injuries.

Primarily characterized by abnormal muscle tone and lack of coordination.

Seizures, mental impairment, sensory defects, behvarior disorders, difficulty meeting milestones.

Signs right after birth: weak/absent sucking, jitterness, and slow/absent reflexes.

Involves one or both sides

Impairment of fine and gross motor skills.

Hyperactive stretch reflex in affected muscle groups.

Increased activity of deep tendon reflexes.

Clonus (rapid, involuntary muscle movement)

Scissor like gait. Contractures affecting extensor muscle of legs especially heels (walk on toes)

Abnormal involuntary movement. Can't sit still.

Constant slow, wormlike writhing movement. Usually of extremities, trunk, neck, facial muscles, and tongue.

Involvement of pharyngeal, laryngeal, and oral muscles cause drooling and poor speech.

May not be diagnosed until child starts to walk.

Wide based gait, lack of coordination particullarly of upper extremities.

Sometimes have combinations of CP, which are more severe.

May not occur until child tries to walk

Neuro exam

HX are primary focus

MRI and nerve conduction studies to show abnormal motor function

Focus on improving motor functions and communication skills to help child read highest potential.

Child needs to maintain muscle tone as much as possible.

Wear braces, do exercises, prevent further contractures.

eye muscles are uncoordinated so they can't direct their focus at an object at the same time.

Child gets diplopia (double vision)

They squint/close one eye often or frown.

They reach for object and grab next to it.

If one eye they path the unaffected eye. Forces the bad eye to develop muscles to focus.

Eyedrops, orthoptics, lenses

Last resort: surgery

DX & early TX to prevent vision loss.

Very common b/c of structure of eustacian tube. It's shorter & wider so bacteria sits in there.

Increased incidence in babies that are bottle fed, 2nd hand smoke, and upper respiratory infections.

Similiar to upper respiratory infection.

Congestion & fever

Ear discomfort & pain

Crying & pulling on ear

Waking up during night

Vomitting & diarrhea

Bleeding (d/t rupture)

DX:  Visual look at internal ear. Normally looks pearly gray and has light reflex.

If otitis media it will be red, inflammed, buldging, and have no light reflex.

If eardrum ruptures purulent discharge and bleeding will occur. They'll not be as irritable b/c pressure will be released.

TX:  for eardrops for children pull down & back.

Antibiotics & decongestants.

Use prophalatic antibiotics or do myringotomy (tubes in ears so drainage can leak out)

Tubes are in for 6-12 months. Can cause hearing loss for as long as 6 months.

Any hearing loss can affect child's speech.

Prevention: Don't prop bottle, hold them properly.

thyroid disorder. absent/deficient in thyroid hormone.

S/SX: few months after birth symptoms occur.

Thickening of tongue and lips, puffy eyes

dull expression, often develop jaundice

feeding problems, lethargic

poor muscle tone affects mobility so they have chronic constipation and abdominal bloating

All newborns are required to have mandatory T4 and TSH levels drawn.

If TX is not started early enough it can lead to mental impairment and cannot be undone.

TX: Synthroid/thryoid drug for rest of life.

Usually dysfunction of the ceells that are supposed to be secreting insulin.

S/SX: polyuria, polydypsia, polyphagia

Have ABRUPT onset. Adults tend to have gradual onset.

Kids may also have wt loss, H/A, fatigue

DX: checking glucose levels.

TX: insulin, diet, exercise, going to need insulin almost all cases. many children are on insulin pump. 

It's a lifelong experience.

***watch for S/SX of hypo & hyperglycemia

1 Trust vs mistrust - 1 yr (need to be held fed)

2 Autonomy vs Shame & Doubt - 1-3yrs (indepedent)

3 Initiative vs guilt - 3-6yrs preschool (trying to please)

4 Industry vs inferiority - 6-12yrs (desire to learn, can act out)

5 identity vs role confusion - 12-18yrs adolescence (develop own identity, trying to fit in, thinks their infallible)

Directed towards parents.

Hold child to interact.

Encourage parent to be with child as much as possible to help with care.

Keep it simple & brief. No medical terminology.

Talk to them right before procedure.

They have no sense of time. Relate it to meal times.

Be honest.

They use cause and effect, but not correct associations.

Use therapeutic play to get their feelings out.

They can begin to take an active role in their care.

They understand instructions.

They'll ask questions.

They can be responsible for certain aspects for their care.

Their responsive to 1:1 care.

Want to know, but may be embarrassed.

They're modest.

1:1 is helpful.

Build trust and ask open ended questions.

Might be bitter/frustrated/angry/noncooperative.

Do not judge them.

Separation anxiety.

They want their mom.

longer separation goes they find another caregiver to attach to. It can become an issue.

Regression typically happens. (bedwetting)

Also nightmares/neg behavior.

Mutilation and bodily harm.

They have an active imagination.

Tend to misinterpret words. Keep it simple.

They'll see illness as a punishment.

Regression sometimes occurs.

Therapeutic play very helpful.

Pain and bodily injury.

Fear of loss of control.

Fears related to what they're missing in school and peers.

Ask questions.

Separation isn't a big issue.

Start first when doing vitals.

Infants and young children (2-3) are abdominal breathers so watch bellies.

Watch for flaring and retractions. Chest looks like it's caving in. Ribcage almost sucking in. Distressed.

Infants and young children count for a full minute b/c they're irregular and almost like cheynes stokes.

Route depends on age.

4 and under axillary/temporal.

Never leave a child while taking a temp.

Usually do apical.

Radial is too hard to find.

5 & under apical for full minute.

**kids change very quickly!

Don't routinely do on little ones unless surgery/illness.

Cover 2/3 of upper arm.

Most younger kids done electronically.

Always explain that it's going to squeeze.

careful monitoring

Sites checked every 30-60min

 Overload can be fatal

Children IV in foot/scalp b/c IVS can be dislodged.

Scalp veins close to surface.

Apply to children

Explain to child what they're taking

And if it's going to hurt and that it's okay to cry

Watch them take med

P.O  liquid for smaller child/infant

Don't mix med unless you absolutely have to.

If you have to mix use very little liquid. Don't put it in bottle.

IM if baby is 1yr/younger. Gluteal muscles are not developed. Give in vastus lateralis.

Link to physical cause such as cleft palate/cardiac problems/malabsorption.

Kids tend to be irritable, can starve to death, even if caught early can have developmental issues.

Often from abuse. No physical cause

No bond between parent & child. No interaction.

Kids tend to be irritable, can starve to death. Even if caught early can have developmental issues.

Complex developmental disability.

result of a neurological disorder that affects normla funcitioning of brain.

Mild-severe effects.

Impaired/difficult social interactions

Diff in verbal and nonverbal communication

Restricted and repetitive behavior (headbanging/twirling)

Stereotyped interests/activites (focused)

Some have intellectual disabilities, motor defects, ADHD

Some are intellectually gifted and excel in certain areas.

Effects males more.

NOT caused by thimerosal in vaccines

NOT caused by MMR vaccine

Research bio-chemical problem involving neurotransmitters or

Due to abnormalities in CNS and brain metabolism

Increased occurances in paternal age over 50 and under 25

S/SX begin before age 3. Sometimes within the first month.

Infant-shows little or no response to human interaction

Avoids eye contact

Difficulty feeding and sleeping

Shows lack of response to sounds.

Some babies are perfectly fine in infancy than regress.

no babbling or responding to name by 12 months

Not speaking by 16 months

Toddler may suddenly be unable to communicate verbally

May exhibit echolalia (repeating words over and over again)

Possible self destructive acts

May have some sx but have obsessive interest in single subject

have high level of vocab and formal speech patterns

Might be clumsy

high end intellectually (single subject)

Rule out other conditions

3 categories of characteristics

-inability to relate to others

-inability to communicate well with others

-obviously limited activities and intersts

No cure

Behavior modification/highly structured environment

Increasing social awareness

Teach verbal communication skills

Decrease unacceptable behavior

Meds-SSRI, antipsychotic, Ritalin

Superficial skin infection caused by staph/strep.

Usually seen on face, hands, neck.

It oftens follows insect bite/scratch.

Highly contagious until lesions heal

Occurs often in toddlers in preschoolers.

Lesions progress from macule (not elevated) to pustule and rupture to honey colored crusts.

Pururitus is very common.

DX: sometimes do bacterial cultures

TX: antibiotics, soaks, handwashing, separate linens, contact precautions.

Very rare.

can develop into glomerulinephritis or rheumatic fever.

Unknown cause but thought to be allergic response.

1. hereditary

2. hypersensitivity of deeper skin layers to protein or protein like allergens

3.specific allergens to which child is sensitive may be:

a.ingested-milk, eggs, citrus, peanuts

b. inhaled-dust, pollen, animal dander, perfumes, smoke

c. direct contact- wool, plastic, soaps

Infantile Eczema/Atopic Dermatitis

S/SX

Cheeks are where it's usually first seen, but may spread to forehead, scalp, neck, trunk, arms, legs.

Starts as reddened areas followed by papule and vesicle formation.

Vesicles ooze, seep fluid then form crusts.

Itching, irritability.

Open areas prone to staph/strep infection (impetigo)

Infantile Eczema/Atopic Dermatitis

DX/TX

DX: seldom determined during initial episode, usually starts with elimination of foods, etc that are thought to be causing reaction.

TX: major goals:

1. hydrate skin (lotions)

2. relieve puritus (oral steriods, benadryl)

3.reduce inflammation

4.prevent/control infection

1. thermal - flames/hot liquid

2. chemicals - bleaches/cleansers

3. electrical

4. radiation - sunburn

TX: relates to amount of tissue destroyed.

Rule of nines not used

% of body surface area burned as well as the depth of the burn. 

Prognosis depends on age, general health and location of wound.

1st degree-superficial epidermis blister heals in about 7 days

2nd degree or partial thickness dermis epidermis. most painful b/c of nerve endings exposed. serous fluid leaking out.

3rd degree or full thickness most severe, no pain b/c nerve endings destroyed. SubQtissue. blackish leathery skin. prolonged healing. usually get grafts

degrees do not vary from child-adult.

Decrease cardiac output.

Lost fluids

Vasodilation

Increase capillary permeability

renal vasoconstriction b/c of loss of fluids leads to depressed glomeruli filtration.

Decreased output

Shunts blood away from liver and GI tract.

Distention occurs and vomitting.

Peristalsis slowed way down

In childrem gets accelerated.

Energy needs are almost twice than normal.

Nutritional supplments are common.

Stop burning process

Observe ABC (airway, breathing circulation)-especially electrical

If small area-apply cool (suppress edema)

Remove clothing near burn to prevent further irritation

Focus on maintaing patient airway and manging for hypovolemic shock.

IVS fluids, TPN, high protein for healing

1st degree burns usually treated as outpatient if determined to involved 15% or more of body surface will require hospilization.

careful monitoring of urinary status. make sure they don't go into renal failure.

infection control, strict sterile technique. sometimes reverse isolation.

pain control, wound care can be painful. theraputic play impt.

Sometimes PT depending on where they were burned. Scar tissue limits mobility.

24-96hrs after injury the child will revert and go into diuretic phase.

Have to cut back on IVS otherwise they'll go into hypervolemic.

Output will increase dramatically.

Affects newborns.

Deformity can affect one or sometimes both feet.

Foot is inverted, heel is drawn up, front of foot is adducted (turning inward).

Can be associated with other defects.

Cause unknown. Increased incidence in males.

May be d/t positioning in utero or maybe fixed deformity

Ultrasound

Xray catscan

Also can be readily seen.

Affected foot is usually smaller.

Limb is often shorter. There may be atrophy in calf muscle.

Nonsurgical: cast application up to mid thigh. Changed frequently. Possibly orthopedic shoes or denis browne splint (following casting).

Surgery to release tendons. Possible pin fixation.

Proper cast care, circulation checks, cap refill, keep cast dry.

Congenital hip dysplasia (DDP)

Developmental Dysplasia of hip

shortening of femus, uneven thigh and gluteal folds, limited abduction of hip along with clicking sound.

Increased risk in utero in breach position and can be hereditary.

Can develop lordosis if not fixed and lead to hip, back, and posture problems when child begins to walk. Also potential for possible limp.

Hip maintained in abducted position through use of diapers or harness.

Good skin care with harness.

If cast necessary observe closely for breathing difficulty or vomitting after feeds as well as good skin care.

Harness can't go on bare skin. Check skin periodically.

inherited that causes muscular degeneration and wasting.

Due to an abscence of dystrophin protein involved in maintaining muscle integrity. Progressess over the years.

Most common form: duschenne dystrophy

Carried by women and passed onto men.

difficulty standing and walking, trunk muscle weakness

tire very easily, tripping & falling

waddling gait, have lordosis by schoolage

gowers manuever (use upper extremities to sit upright)

mild-mod mental impairment, age 10-12 wheelchair bound

death from respiratory paralysis.

Observation, serum creatinine phosphokinase (CPK levels)

muscle biopsy

TX: no cure, child kept as active for as long as possible. PT, braces, wheelchair as needed, respiratory and cardiac problems become focus near end.

lateral curvature of the spine with rotation of spine and hips.

Functional-d/t posture, muscle spasms or unequal length.

Structural-more common, unknown cause. Congential deformitis of spine as it grows.

develop slowly, shoulders and hips different heights

may be one sided hump and prominent scapular from rotation of vertebra and ribs

spinal column curved when child bends over.

DX: screenings followed by xray to confirm

TX: depends on degree of curvature

Limit/stop progression of deformity

mild: tx with exercise, improves muscle tone and posture

Moderate: brace 23hours/day

Severe: sometimes traction, involved surgery, fusing spine with rods and screws...very painful (ouch!)