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238 Cards in this Set
- Front
- Back
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Airway differences btwn children and adults
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1. Small oral cavity and larger tongue
2. Larger lymphy tissues in smaller pharyngeal structures 3. Larynx and glottis higher in neck 4. Thyroid, cricoid adn tracheal cartilages immature and incomplete (easy collapse) 5. Large amount of soft tissue and loosely anchored mucous membranes lining airway 6. Fewer functional muscles in airway |
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Signs and symptoms of respiratory distress
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1. ^ RR (tachypnea)
2. ^HR (tachycardia) 3.^sweating (diaphoresis) 4.agitated/anxious/restless Also Hypoxia (keep O2 >92-93%) |
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Why are antitusssives avoided in pediatrics?
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b/c they may depress the cough reflex which ^ risk of aspiration. Decongestants also avoided - lead to agitation
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What organism most often causes epiglottitis?
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H. influenza - Hib vaccine prevents
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What are the Four D's of epiglottitis?
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Dysphonia (muffled voice)
Drooling Dysphasia ( difficult speech) Distress |
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Clinical manifestations of Epiglottitis
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Onset very rapid
High fever Appears toxic Irritable w/ marked drooling c/o sore throat Restless Absense of spontaneous cough Tripod position, tongue protrusion Stridor/retractions |
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Treatment of Epiglottitis
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*Protect the AIRWAY - high O2, elevate HOB
*Ampicillin and corticosteroids, IV then PO (decrease after 24 hours) *High humidity and hydration (IV) *Cardiac/Apnea monitor *Child closely monitored *Must have trach equipment at bedside at all times |
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What is considered an "ominous sign" with epiglottitis?
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The quieter the child, the greater the cause for concern.
Asking child to speak or trying to visualize the throat may lead to spasm - immediate obstruction - death |
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Clinical manifestations of Status Asthmaticus
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*May develop rapidly or gradually (strong trigger/med not working/non-compliant)
*SOB with air movement restricted to point of absent (can't hear breath sounds) accompanied by sudden rise in RR - ominous sign *orthopnic and diaphoresis - ominous sign *sudden restlessness/agitation or quiet - ominous sign |
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Four goals of therapy for status asthmaticus
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1. improvement of ventilation
2. correcting dehydration 3. correcting acidosis 4. treating any current infection |
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What is a caution with rehydrating a status asthmaticus patient?
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Must hydrate slowly to replace lost fluid or may ^insterstitial pulmonary fluid accumlation and exacerbate the problem
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Medications for Status Asthmaticus
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*Short-acting Beta-2 agonists (inhaled) - decrease bronchospasms
*Allupent/albuterol/xopenex (MDI or aerosol) - bronchodilation. May be placed on continous albuterol. *Racmic epinephrine - aerosol SHORT-ACTING relief of bronchospasm *Corticosteroids (IV) - reduces inflammation (Solumedrol.) May use oral prednisone. *Amminophyliine drips (IV) Many SE with these drips |
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Meds for Status Asthmaticus, Part 2
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*If not responding to Part1, MD may consider SQ epinephrine: 1:1000 at a dose of 0.01 mL/kg - MAX DOSE of 0.3 mL
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Meds for Status Asthmaticus, Part 3
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*Bicarb - to reduce acidosis from hyperventilation
*ATB - maybe be used, but not initially. Penicillins or Cephalosporins. |
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Status Asthmaticus, O2 issues
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*If O2 requirements increase (needs > 50% O2 to maintain Biox of >93%) then child admitted to ICU
*Humidified O2 Note: O2 is stimulus for respirations, high levels may DEPRESS respirations |
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Respiratory Failure: defined
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The inability of the respiratory system to:
1. Maintain adequate oxygenation of the blood with or without CO2 retention 2. Increased Work of Breathing Can be: *Sudden, with acute obstruction *Gradual progression (more easily recognized) |
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Intial S/S of respiratory distress/failure
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*Tachycardia
*Tachypnea *Diaphoresis *Restlessness |
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Decompensation s/s of respiratory distress/failure
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*Nasal flaring
*Retractions *Grunt *Wheeze |
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S/S of Imminent Respiratory Failure/Arrest
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*Dyspnea
*Bradycardia *Cyanosis *Stupor/coma *See-Saw breathing |
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Management of Respiratory Failure
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*Early identification
*Maintain Airway *May require intubation/trach or vent *Correct hypoxemia *Minimize complications *Correct underlying cause (e.g. choking) |
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Cystic Fibrosis - Etiology/Patho
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*Increased viscosity of mucous glands
*Excessive elevation of sweat electrolytes *Decreased pancreatic of bicarb and choloride *Increase in sodium and chloride in sweat *Abnormalities in autonomic nervous system |
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Cystic Fibrosis - defined
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Primarily a mechanical obstruction caused by thick mucous that is responsible for many of the clinical manfiestations. Abnormally thick mucous leads to obstruction of the secretory ducts of the pancreas (95% obstructed - malnutrition &diabetes), liver and reproductive organs.
*Sweat and salivary glands excrete excessive electrolytes |
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Cystic Fibrosis - diagnostic evidence
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*Family hx
*Absence of pancreatic enzymes *Sweat test for positive id. 2 to 5x the normal. Normal chlorides 40 mEq/L. C.F. is >60. Done TWICE. *frequent respiratory infections *Patchy atlectasis on CXR |
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Clinical Manifestations of C.F. - Meconium Ileus
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Meconium Ileus:
- no stool in 1st 24/36 hrs post birth - abd. distention at birth - vomiting, may be bile stained - rapid level of dehydration - chronic constipation |
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Clinical Manifestations of C.F. - Stools
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Large bulky stools
- Frequent - Foul - Frothy - Float Will also see this when they are non-complaint with their meds |
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Clinical Manifestations of C.F. - other GI
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*Biliary obstruction w/ rectal prolapse a KEY sign*
*voracious appetite early, anorexia later *Wt loss, tissue wasting *distended abd, thin extrem. *atrophy of buttocks/thighs *Defiency of fat-soluable vitamins A, D, E, F *FTT *Anemia *May develop reflux |
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Clinical Manfestations of C.F. - Pulmonary Initial signs
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*Wheezing
*Dry, non-productive cough *Chronic cough *Fatigue |
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*Clincial Manifestatios of C.F. Pulmonary (later)
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*Increased Dyspnea
*Paroxysmal cough *Patchy atelectasis *Obstructive emphysema |
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Clinical Manfestations of C.F. -Later Progression
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*Barrel chest
*Cyanosis *Frequent bronchitis and bronchopneumonia *Clubbing of fingers and toes |
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Goal of C.F. treatment
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Improve pulmonary function, eliminate bronchial secretions and PROMOTE NORMALCY
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Most common causative agents in C.F. respiratory infection
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*Pseudomonas
*H. flu *Burkholderia |
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What is a complication of repeated pulmonary infections and inflammation in C.F.
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May lead to bronchial cysts and emphysema may develop. Over time cysts may rupture - Pneumothorax
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Respiratory therapies in C.F.
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*Postural drainage and CPT - 2x daily and PRN (up to 6x da)
*Aerosol therapy: - bronchodilators - use of flutter clearance device - D-Nase (pulmozyme) for viscosity (mucolytic) *Breathing exercises - abdominal breathing - to improve ability to clear secretions *O2 therapy - used in acute episodes - can be issuse w/ chronic CO2 retention *Encourage physical activity - swimming is good |
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GI management of C.F.
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*PANCREATIC ENZYMES - thick mucous does not allow absorption of nutrients. Enzymes are enteric coated. Help to absorb fat and aid in digestion.
Will help reduce stools to 1-2s day. *VITAMINS - A, D, E, K (water soluable formulas) *GOLYTELY - constipation is an issue |
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Nutrition in C.F.
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*Low-fat diet
*Often require up to 150% of normal RDA *Salt replacement *special infant formulas - alimentum *May require supplemental tube feedings to promote G&D |
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Teaching in C.F.
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Genetic counseling
Children need all vaccines - flu yearly is mandatory. |
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Causes of superficial/first degree burns and appearance and tissue involved
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Flash, flame, U.V. (sunburn)
Dry, no blisters, edema Epidermal layers only. Pain is the predominant feature. Systemic effects rare. Heals in 5-10 days w/out scarring. |
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Causes of 2nd degree, partial thickness burns, appearance and tissues involved
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Contact with hot liquids or solids, flahs flame to clothing, direct flame, chemical.
Moist blebs, blisters. Mottled, with pink, red or waxy white areas w/ blisters. Epidermis, papillary, and reticular layers of dermis, may include fat domes of subq layer Sweat glands and hair follicles remain intact. Should heal in 14 days with variable amount of scarring. Sensitive to temp changes, air and light touch. |
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Causes of 3rd degree/full thickness burns, appearance, and tissues involved
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Contact with hot liquids or solids, flame, chemical, electricity.
Dry with leather eschar until debridement; charred blood vessels visible under eschar. Nerve endings, sweat glands, hair follicles destroyed. Down to and including subq tissue; may include faschia, muscle and bone. Systemic response w/ increase capillary permeability adn loss of plasma proteins, fluids, electrolytes. |
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Burn classifications
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Major - require special services and facilities such as Burn Unit >20% TBSA
Moderate - may be treated in hospital or Burn Unit >10%, up to 20% TBSA Minor burns - may be treated at home <10% TBSA |
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Capillary Seal
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Takes 36 hours. Stops fluid loss. Need 4 to 10x maintenance fluids until C.S. At risk for renal failure.
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Clinical Manifestations of Inhalation Injuries
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*Can take up to 24-48 hrs to appear
*Wheezing, increasing secretions, hoarseness, wet rales, and carbon like secretions *Erythema of tissues, followed by sloughing of respiratory mucusoa *Cobxyhemoglobin bonding effects *Deep burns on thorax may cause restriction of chest expanison |
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Carboxyhemoglobin Bonding Effects - 20%
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HA, SOB on exertion
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Carboxyhemoglobin Bonding Effects - 30%
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HA, CNS functions altered, disturbed judgement, irritability, decreased vision, dizziness
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Carboxyhemoglobin Bonding effects - 40-50%
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Marked CNS effects with confusion, collapse, and fainting with exertion
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Carboxyhemoglobin Bonding effects - 60-70%
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Seizures, apnea, unconciousness
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Carboxyhemoglobin Bonding effects - 80%
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Rapidly fatal
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Pathophysilogy - Superficial burns
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Minimal tissue damage
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Pathophysiology - Partial Thickness burns
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Considerable edema
More severe capillary damage Edema formation occurs in 8 -12 hrs after injury |
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Pathophysiology - Full thickness burns
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Burns >20% TBSA, there is systemic effect
Loss of plasma proteins, fluids and electrolytes Anemia r/t direct heat distruction of RBCs and hemolysis of injured RBCs Edema formation effect 18-24 hrs d/t hypovolemia 5-10x greater fluid turnover before capillary seal at 36hrs Metabolism is ^ to maintain body heat |
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Burn complications - Respiratory
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Airway compromise and shock
Pulmonary complications - r/t superheated air entering airways tissue destruction &inflammation w/ sloughing as aresult. Result is pulmonary edema, pneumonia, pulmonary emboli, & pulmonary insufficiency. A MAJOR cause of fatality in children. |
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Burn complications - respiratory - asphyxia
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Carbon monoxide w/ flame burn leads to carboxyhemoglobin - C02 binds with Hgb and directly affects heart and brain competing for cellular process. PATIENT REQUIRES 100% 02 to reverse effects.
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Burn complications - renal
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Unremitting shock (r/t fluid shift and loss) followed by renal shutdown
BUN and Cr elevated K+excess during the 1st week is a BIG problem |
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Burn complications - Infection
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Sign of wound sepsis - CONFUSION
Wound sepsis leading cause of death (esp staph and psuedomonas) Dead tissue ideal environment - begins day 3 and gets going by day 5 Early excision of eschar w/placement of autografts reduces incidents of sepsis |
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Burn complications - Anemia
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Caused by heat destruction of RBCs
heated RBC > hemoconcentration r/t fluid loss and decreased CO. Hemolysis of injured rbcs & trapping of rbcs in microvasculature>thrombi from damaged cells |
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Labs in Burns
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Decreased RBC, Hgb, Hct
Decreased electrolytes d/t ongoing losses from burn areas Decreased protein w/ protein breakdown Increased BUN/Cr w/tissue destruction and esp. in presence of oliguria Wound culture - identfies organisms if present |
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Metabolism in burns
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greatly excelerated w/ rapid protein and lipid breakdown (catabolism) leading to starvation
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Major GI complication of burns
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Curling Ulcer
Caused by superficial mucosal erosion when normal levels of stomach acid ^ 40 - 72 hrs post surgery MAJOR BURN PT - NPO |
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Cardiac response in burns
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Alteration in circulation immediate > may lead to burn shock and decreased cardiac output.
Restore fluids - Parkland formula. Decreasing CO leads to decreased perfusion, organ disfunction, death. |
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Burn complication - Growth and Development
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Severe delays up to 3 yrs after burn injury >30%TBSA
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How long does it take a burn area to mature
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up to one year.
Contractures and scarring major complication r/t effectiveness of rehab and infection |
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Ice or Cool water to treat burn
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Cool Water!
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Emergency care of burn
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Stop burn process
Remove burned clothes Do not open blisters Do not apply anything to wound Cover with clean cloth ABC - asses airway 1st Flush chemical burns throughly |
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TX of minor burns
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All emergency care steps
Debride any non-viable skin. Apply antimicrobials (sulfmylon, gentamycin, betadine) use of non-adherent fine mesh gauze Tetanus booster if no hx or >5yrs since last booster PAIN MGMNT very important May need ATB Educate - dressing change, s/s infection, ROM or splinting |
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Major Burns
3 steps of care |
Acute - 24 to 48 hours
Maintenance Rehab |
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Major Burns - tx
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Maintain patent airway & ventilation
- assess airway, keep pt calm, humidified o2 prn Fluid replacement - rapid fluid and electrolyte shift in 1st 24 hours - IV access a priority |
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Major Burns - fluid replacement concerns
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Fluid & electrolyte shift leads to hypovolemia, hypoproteinimia, hyperkalemia
Fluid loss 5 - 10x greater than normal Cap seal in 36 hrs Parkland Formula |
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Parkland Formula for fluid loss in burns
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Replace 1/2 of fluid loss in the 1st 8 hrs using lactated ringers or 0.9%NS. The remainder of calculated fluids given over the next 16 hrs
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Fluid replacment - burns
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Restores plasma volume
Reduces ongoing losses Replaces evaporative loss Corrects acidosis Maitains perfusion to organs & tissues - preserving renal function. CAUTION - MONITOR FOR FLUID OVERLOAD IN LUNGS |
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Monitor for renal failure in burns
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UO s/b 10-20mL/hr or 20-30 for older children
Foley catheter to monitor output and HOURLY specific gravity |
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Wound management in burns - signs of sepsis
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Infection is a major complication
confusion, ^ cap refill time may indicate wound sepsis BP may remain normotensive even in hypovolemia |
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Wound management
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Primary exicision asap w/ skin coverage (after shock phase and fluid restoration)
Sterile dressing change bid Hydrotherapy daily |
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Hydrotherapy in burn wound mgmnt
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Removes non-viable skin, old topical meds and exudate
Cleanses wound and allows for visual inspection Prepares wound for excision Allows for ROM while in water bath Protects wound from exposure to air - very painful Preps skin for grafting |
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Antimicrobials in burns
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Silvadene - applied 2x daily, alwasy sterile procedure
can also use bacitracin, sulfamylon |
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Autograft
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permanent "self" skin
from upper thigh, back or buttocks (if avail.) usually split thickness (top layers) 3 to 10 inches |
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Isograft
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Skin taken from identical twin
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Homografts (allograft)
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Cadaver skin, temporary graft
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Xenografts
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pigskin - replaced q2-3 days
can also be used to replace eschar |
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Synthetic
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Biobane - man-made similar to human skin
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Cultured epithelium
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Made from full thickness skin biopsy and is very small - postage stamp size
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Full Thickness Skin grafts (sheet graft)
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Full thickness of skin from nape of neck, groin or behind ears to cover facial burns for cosmetic purposes
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Split thickness skin grafts
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meshed grafts
the top layer of skin,very thin, used to cover as much open area as possible |
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Meshing of grafts
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Dermatome removes skin (graft)
mesher makes chevrons to allow for stretch May be meshed 2-1, 10-1, 20-1 |
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Donor sites
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Considered to be equivalent to treating a partial thickness burn but under sterile conditions
Pressure dressings x 24-48hrs to increase adherence and decrease blebs. Xeroform, scarlet red, opsite, silvadine and adaptc |
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Nursing considerations - burns
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Airway
I&O Wound care - sterile dressing chage bid Nutrition Splints - bedtime & naptime, nuetral position Prevent contractures - Jobst garment 23/24hrs a day, mask for facial burns, may need tissue expanders Support Relieve itching - atarax and benedryl Keep skin supple - nivea, eucerin to healed areas Protect skin |
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Cerebal Palsy - defined
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A non-specific term
Disorders characterized by early onset of impaired nueromuscular control. Non-progressive May be accomp. by perceptual problems, language defecits adn intellectual impairments (30%) The most common permanent disability of childhood. 1.5 to 3/1000 live births Primary disturbance is abnoraml muscle tone and abnormal coordination. |
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CP - Etiology
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Various prenatal, perinatal, postnatal factors -
*Prenatal brain abnormalities *Intrauterine exposure to maternal infections *ELBW and VLBW *Kernicterus *Cerbral anoxia *assoc w/ cerebral damage - esp prenatal and perinatal |
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CP Patho
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May be evidence of gross malformation in the brain or evidence of vascular occlusion, atrophy, loss of nuerons and degeneration.
*Anoxia plays most significant role in the patho of brain damage* Trauma, toxins, neonatal infections, prematurity and unknown factors |
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C.P. Classifcations
Hypotonia |
Floppy w/ diminished reflex response.
Positive parachute beyond 6 mos |
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C.P. Classifications
Hypertonia (spastic) |
One or both sides of body.
Tense, tight muscles, uncoordianted, awkward, affects balance and coordinated motion. Impaired fine and gross motor activity - rigid and spastic, scissoring Active attempts at motion increase abn postures and overflow to other body parts. Often causes affected limbs to be shorter and thinner. May develop scoliosis. |
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CP Classifications
Athetoid (dyskinetic)f |
Abnormal, involuntary movements.
Slow, uncontrollable writing movements of the hands, feet adn legs - more severe distally. Hyperactive facial muscles cause child to frown/drool. Constant worm-like writhing movements (usually all extremeties.) |
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CP - Ataxia
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Affects balance and depth perception.
Poor and irregular muscle coordination. Unsteady, wide-based gait. Child unable to make quick or precise movements such as writing or buttoning a shirt. |
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CP - Clinical manifestations
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Delayed gross motor development.
Abnormal motor performance. Alteration of muscle tone. Abnormal posturing. Abnormal reflexes - persistent infantile refexes Associated disabilities - *Mental retardation (30 - 50%) *Learning disabilities *Behavioral/interpersonal relationship impairment *Sensory impairment and seizures *Vision/hearing |
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CP - Diagnostic
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CT shows underdeveloped or cysts/tumors.
MRI or cranial ultrasound shows abnormal areas. Knowledge of normal motor development. Persistent infantile reflexes - beyond 4 mos is "suspect." Beyond 6 mos is "diagnostic." Neurologic exam. Clincial manifestations. EARLY RECOGNITION MAY BE DIFFICULT. |
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CP - Therapeutic Management
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Early recognition is key.
Early assessment is key - assess: General appearance Motor function Ability to swallow. Identify problems with speech, sensation, perception. Evaluate cog. devel. and abilities. Skin integrity - esp with assistive devices! |
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CP - Implementation of management
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*Establish locomotion and communication self-help
*May need help w/ feeding - manual jaw thrust, keeping head elevated *Gain optimum appearance & integration of motor function. *Correct assoc. defects (vision/hearing) *Provide educational opportunities that are adapted to ind. needs & capabilities *Promote socialization *Teach and support for chid/family *Care for child in hospital - chroncially ill child |
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CP - Advanced Management
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Treatment over time r/t contracture development and assoc dissabilities
*Anti-anxiety meds *Muscle relaxers - injected (Botox):Baclophen - can be placed in spine(implanted); PO - baclophen, valium; intrathecal (marcaine) *Anti-convulsants for seizures *Dorsal rhizotomy - split nerve fibers, will relax the muscle |
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Spina bifida occulta
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a defect in the bony spine invisibile to the eye w/ no clinical manifestations.
Sometimes a tuft of hair or a dimple over the spot. |
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Spina bifida cystica
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A defect in the bony spine visible at birth with a sac-like protrusion, with various clincial manfiestations. There are two types - menigocele and mylomeningocele.
S/B delivered C-section |
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Miningocele (spina bifida cystica)
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SBC witch consises of a sac-like cyst filled with MENINGES and CSF
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Mylomeningocele (SBC)
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SBC which consists of a sac-like cyst filled w MENINGES, CSF AND NERVES (SPINAL CORD) with a hernial protrusion.
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Encephalocele
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Herniation of the brain through a skull defect or fontanel
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Ancephaly
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Abscence of brain w/ exposed vascular mass, no bony coverings
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Etiology of SB/neural tube defects
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Mostly unknown, but assocated w/ low folic acid during fetal development.
May have genetic cause May be viral in origin. The degree of defect is r/t anatomic level and amount of nerve involvment |
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Folic acid requirments daily
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Normally, 400 - 600 mcg
If previous neural tube defect - 4000mcg |
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Hydrocelphalus in SB
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Frequently assoc. complication (90 to 95%)
OFC daily! |
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Dx of Spinal bifida
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Clinical manifestations present at birth.
Transillumination (light behind cyst.) Radiography. Skull tomography |
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Prenatal detection of SB
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Ultrasonic scan.
Elevated concentration of alpha-fetal protein, taken @ 16-20wks. Chorionic villus sampling. |
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Nursing considerations of SB
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The PRIMARY nursing goal prior to surgical closure is PREVENTION of INFECTION.
Surgical correction usually takes place w/ in 24 hrs post birth. -prevent rupture -no diapering -evaluate airway r/t feeding pre-op - fruequent assess, esp OFC - promote bonding -teaching -support muliti-disciplinary approach Note - in infancy, tx is either primary closure or wait and see option. |
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Problems assoc with SB
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Hydrocephalus
Continued cerebral hemmorhage Orthopedic GU/GI Infection Visual and hearing impairments Other defecits or assoc prob. |
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S/S of thoracic level lesion in spina bifida
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Respiratory compromise w/ high thoracic lesion.
Flaccid paralysis of LE. Variable weakness in the abd. trunk muscles. Absence of bowel and bladder function. |
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S/S. of high lumbar lesion in SB
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Voluntary hip flexion and adduction.
Flaccid paralysis of the knees, ankles and feet. Absence of bowel and bladder control |
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S/S of Midlumbar lesion in SB
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Strong hip flexion and adduction.
Fair knee extension flaccid paraysis of the ankles and feet. |
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S/S of low lumbar lesion in SB
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Strong hip flexion, extension and adduction and knee extension.
May have limited bowel and bladder function. |
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S/S of sacral lesion in SB
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Down to S2 injury bowel and bladder are affected.
Normal function of the LE S3-S5 normal bowel and bladder function. |
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Nursing considerations in SB
Infection (meningitis) |
Assess the sac for CSF leaks - use glucose stick. If + for glucose, then CSF leak.
All infection indicators. |
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Nursing considerations in SB
Trauma to sac |
Careful handeling.
Avoid stretching of other nerve roots. Tethered cord is acommon problem even with spina bifida oculta. Keep prone and in frog leg position. Avoid pressure to sac. Diapering may be contraindicated. |
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Nursing considerations in SB
Respiratory assessment |
Prone to aspiration w/ feeding.
- can only elevate 10 - 15 degrees. Only give 10 mL at a time. May have associated defects such as: - cardiac - tracheoesphageal fistula. -developmental dysplasia of the hip. - polydactly. |
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Nuero assessment SB
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Assess for spontaneous movement at birth and daily
- Measure OFC daily - Assess for s/s of ^ ICP |
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Other assessement SB
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Orthopedic
Skin - Latex allergy - irritation due to frequent stooling - sac leakage Also Cardiac, TEF, DDH, etc Coping of family |
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Urologic assessment SB
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Urologic - myelom. frequent cause of neurogenic bladder. Assess for dribbling of urine
Urologic problems can require: - reg. care and eval of urine patterns - bladder training and emptying (I&O, cath q4-6) - drugs to improve bladder storage and continence - may require surgical implant of artificial urinary sphincter. Long term intervention may include MONTI procedure or bladder pacemaker |
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Execretory function - SB
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Assess bowel function.
Bowel sphincter is frequently affected. There is a continual passage of stool often misinterpreted as diarrhea. Long term intervention - MACE procedure |
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Surgical repair of SB defect
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Early closure 18-24 hrs after birth.
Reduces infection risk |
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Tethered cord in SB
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Stretching the cord.
Surgery will help to avoid stretching of the cord. |
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Hydrocephalus in SB
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Shunt placement at birth
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Correct Arnold-Chiari malformation in SB
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A malformation that pulls the brain stem downward toward the spinal column. A-C is as congenital anamaly where the cerebellum & medulla oblongata extend down through the foramen magnum, a common occurence w/ SB.
Causes breathing and feeding difficulty in infant and lac of coordination and spasms in the older child. Assoc, w/ myelo. |
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Prevention of SB
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Folic acid
childbearing age group - 0.4mg daily Previous SB infant - 4mg daily and preg mom is closely supervised. |
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Hydrocephalus
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A serious condition caused by an imbalance in the production and absorption of CSF.
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Pathology of hydrocephalus
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An imbalance in the production of of CSF caused by:
- poor absorption - obstruction of CSF - Neoplasms - infections - trauma - considered to be a developmental defect - major problem that results from hydrocephalus is Arnold-Chiari malformation - With a dysfunction in the ventricular system of the brain there is an accumulation of CSF that leads to dilation adn compression of the brain against the cranium. If this occurs before closure of sutures - enlargement of the skull. |
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Dx of hydrocephalus
|
*Head enlargement b/4 closure of the sutures, based on head circumference.
*Measuring of OFC until 18-24mos helps to detect hydrocephalus *Other testing is needed to detect CSF flow and location of obstruction. *CAT scan primary tool *MRI and CAT scan can be done in utero. |
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Hydrocephalus in older children
|
associated with trauma or a space occupying lesion
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Clinical manifestations of hydrocephalus - early signs
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Lethargy, irritability
Bulging fontanels Cries when picked up or put down. Change in LOC Opisthotonos |
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Clinical manifestations of hydrocephalus - adavanced
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Difficulty feeding or sucking.
Shrill, high-pitched cry Widening of the cranial sutures Cardiopulmonary problems |
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CM of hydrocephalus - infant
|
Abnormal rapid head growth
Bulging fontanels - tense, non pulsable Dilated scalp veins Separated sutures Macwen sign |
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CM of hydrocephalus - later infancy
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Frontal enlargement (frontal bossing)
Depressed eyes Setting sun eyes - sclera is visible above iris Pupils sluggish w/ unequal response |
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CM of hydrocephalus - child
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H/A on awakening w/ improvement after vomiting
Papilledema Stabismus Ataxia Irritability Lethargy Confusion Apathy, bx changes Incoherent |
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Ventricular shunt for OFC
Nursing considerations Pre op |
*Measure OFC daily
*Assess fontanels, cranial sutures, LOC and bx Qshift and PRN *Support head and neck *May require sheep skin under head *Feed small, frequent to decrease risk of vomiting/aspiration *Encourage bonding |
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Ventricular shunt
post op |
*Assess for s/s of ^ ICP
- measure OFC daily - measure abd. girth daily *Assess bx *Position on side opposite shunt *Assess dressings *Strict I/0 |
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Medications for hydrocephalus
|
*Osmotic diuretics
*Acetazolamide to decrease CSF production *ATB as preventative |
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Shunt revisions:
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*Done immediately w
- infection a persistent infection may require use of EVD. Allows for drainage of CSF while infection clears. Child on EVD can only be off it 1 hr day. Position of pt.directed by physician. - malfunction - growth |
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Duchene Muscular Dystrophy Etiology
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X-linked inheritance - rare females get it due to gene mutation
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Duchene Muscular Dystrophy
Clinical Manifestations |
MD leads to delay in motor development, muscle weakness, and gait deformities* no CM apparent at birth*Meets milestones early in life*onset appears 3rd year- difficulty walking/climbing stairs- frequent falls/wide based gait -Waddling gait- Gower sign (uses hands to push up)
- lordosis- enlarged muscles,esp calf r/t fatty infiltration - contractures of ankles and knees- mild mental delay in 30% - wheelchair dependent by age 12-life expectancy early to mid 20's |
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DMD
Pathology |
Approx 1/3rd of all cases fresh mutations.
Results from mutation of gene that encodes dystrophin. Dystrophin is a protein produced in skeletal muscle - absent in DMD |
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DMD
Diagnosis |
*Suspected based on CM
*Elevated CPK & Andolase (extremely high). Andolase is a muscle protein that breaks down when dystrophin is absent. *Muscle biopsy shows degen. muscle fibers *EMG *Decrease in amplitude and duration of muscle potential *CXR & EKG - identify cardiac and pulm. problems CBC - to detect infections |
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Goals in DMD treatment
|
*Maintain functioning in unaffected muscles as long as possible - NO CURE
*Assess and support airway- may need CPAP - percussion, postural drainage, suction, trach & mechan. vent - treat respiratory infections aggressively *ROM *Surgical - release of contractures *Skin integrity - esp under assistive devices. Proper alignment. Daily exercise. *Genetic counseling *Teach |
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Characteristics of CP
Diplegia |
Involvment of LE usually spastic
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Characeristics of CP
Quadraplegia |
All extremeties involved w/arms in flexion and legs extended
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Diabetes Mellitus - type 1
|
Characterized by a destruction of pancreatic beta cells - absolute insulin deficiency. Immune mediated diabetes mellitus.
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Diabetes mellitus
Patho. |
Destruction of 80-90% or more of pancreatic beta cells results in a significant drop in insulin secretion. The loss of insulin, a major anabolic hormone, leads to a catabolic state characterized by high serum glucose levels, hyperglycemia, ketoacidosis
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Hyperglycemia - patho
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creates osmotic diuresis - fluid leaves ICF and enters ECF - secreted through kidneys. When serum glucose exceeds renal threshold (persistant >180) glucose excreted in urine and osmotic diversion of water.
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Hypoglycemia - s/s
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Rapid onset (min)*labile, irritable,nervous, weepy
diff. concentrating, speaking, focusing, coord.*nightmares* shaky feeling, hunger*HA, dizziness*pallor, sweating*shallow, normal RR*tachy HR, palpitations*no breath odor*late s/s: hyperreflexia, dilated pupils, seizure, shock,coma * Blood glucose <60mg/dl*negative ketones, normal hct,bicarb, ph* normal urine output, glucose, no ketones/trace*Diplopia |
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Hyperglycemia -s/s
|
gradual onset (days)*lethargic*dulled sensorium*confusion*
thirst*weakness**N/V/abdominal pain*flushed* signs of dehydration*dry, crusty mucous membranes* deep, rapid RR (Kusmal's)*HR less rapid, weak *breath frutiy/acetone*diminished reflexes*parasthesia Ominous sign: acidosis,coma BG >=250mg/dl*high,large ketones*ph low<=7.25* Hct high*bicarb >20mEq/L*Polyuria early to oliguria(late) enuresis*nocturia*ketones in urine*blurred vision |
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Glycogenesis
|
When protein is wated during insulin deficiency,liver metabolizes it and converts ito to glucose, which further contributes to hyperglycemia
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Ketoacidosis
|
Glucagon, growth hormone and cortisol levels ^ in response to hyperglyc. which stim. release of fatty acids and ketone bodies. Excreted in urine - ketonuria - & breath. Ketone in blood strong acids lower pH - ketoacidosis. In conjunction w/ osmotic diuresis leads to metabolic acidosis.
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Kussumal Respirations
|
The respiratory system will attempt to eliminate C02 (from metab. acidosis) by increasing rate and depth of breathing
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|
Hypoglycemia - treat
|
Use of simple sugars to ^BG
15/15 (15g carb, repeat BG in 15 min) Do not leave pt. alone Hypogly. at risk for during peak of insulin |
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Rapid acting insulin
|
Novolog (Aspart)
Lispro (Humalog) Onset - 5 to 15 min Peak - 30 to 90 min Duration 5 hours |
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Short Acting Insulin
|
Regular U100
Onset - 30 to 60 min Peak - 2 to 3 hours Duration - 5 to 8 hours |
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Intermediate acting insulin
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NPH
Onset 2 to 4 hours Peak 4 to 10 hours Duration - 10 to 16 hours |
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Long acting insulin
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Glargine (Lantus)
Onset 2 to 4 hours Peak - No peak Duration - 20 to 24 hours |
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A1C levels
|
4 to 6 % in non diabetic
7 to 7.5% diabetic |
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Insulin in illness
|
Must adjust by about 10 to 20% in times of illness
Decrease in food intake increases need for insulin Test urine for ketones Lispro (fast acting) is good choice |
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Hgb levels
|
12 to 18 years
Male 13.0 to 16.0 g/dl Female 12.0 to 16.0 g/dl ages 6 to 12 years 11.5 to 15.5 g/dl |
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Hct levels
|
Ages 12 to 18 yrs
Male 37 to 49% Female 36 to 46% Age 6 to 12 years 35 to 45% |
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RBC count
|
Ages 12 to 18 years
Male 4.5 to 5.3 mil/mm3 Female 4.1 to 5.1 mil/mm3 |
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WBC count
|
Ages 4 to 7 years
5.5 to 15.5 Ages 8 to 13 years 4.5 to 13.5 Adult 4.5 to 11.0 |
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Leukemia
|
Cancer of the blood forrming tissues.
peak onset 2 to 6 years Short hx and rapid declining course. Abnormal cells competing for nutrtion w RBCs. Leads to death in 3 to 6 mos if not treated. May act like a minor illness initially. |
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Acute lymphocytic leukemia
ALL |
Occurs 85 to 90% of the time.
Most leukemia is acute (95%) adn involves proliferation of very immature WBCs or blasts. Results from malignant changes in lymphocytes or their precursors. Highly vascular organs (liver, spleen) are severely affected. SURVIVAL 80% |
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Acute nonlymphocytic luekemia ANLL
|
less common in children
abnormal cells off myeloid -granulocyte or monocyte Survival 45 to 50% |
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Pathophys of leukemia
|
Abnormal malignant cells arise from precursor cells in the bone marrow.
A gene mutation is discovered in 40 to 50% of pts w/ leuk. The proliferating cells depress bone marrow of all of the formed elements, and rapidly proliferate adn accum. then crowd out normal bonemarrow elements, spilling into peripheral blood adn even. all body organs. REPLACEMENT OF NORMAL ELEMENTS -> bone marrow suppression |
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Blast cells
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Normal < 5% of circulation
Leukemia 60 to 100% od circulation |
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Bone marrow suppression
|
Marked by decreased normal RBC, WBC and platelet production.
Leads to Anemia (decreased RBC) Neutropenia (decreased WBC) Thrombocytopenia (decreased platelet production.) Increased risk for infection and hemorrahge. Tendency toward fractures. Bone weakness w/ invasion of the periosteum - bone pain. |
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Signs of infiltration by abnormal cells in leukemia
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Spleen, liver, lymph glands - marked enlargement & eventually fibrosis. Lymph node >1.5 cm is suspect
CNS infiltration - ^ ICP Other possible sites: kidney, testes, prostrate,GI and lungs |
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Metabolic starvation in leukemia
|
hypermetabolic leukemic cells eventually deprive all body cells of nutrients nec. for survival, their uncontrolled growth leads to metabolic starvation
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Clinical manifestations in leukemia
|
R/t infiltration
Most common is bone infiltration - cx of PAIN Anemia Bleeding Immunosuppression hepatosplenomegaly, bone pain, lymphadenopathy CNS sx (metastasis) - HA, ICP, unsteady gait General s/s - wt loss, anorexia, vomiting, achexia Bone pain w/ ^ blast cell production/relapse |
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How to calculate ANC
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Determine total % neutrophils (add together polys or segs and bands)
multiply WBC by % neutrophils Ex. WBC = 1000, Neutro. 7%, nonseg neutro. (bands) 7% Step 1: 7% +7% = 14% Step 2: 0.14 x 1000 = 140 ANC Desirable to have ANC >500mm ^ risk for infection <500mm |
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Remission induction phase of luekemia tx
|
Begun almost immediately
Goal is to reduce # of concer cells and achieve complete remission, blasts <5% *lasts 4 - 6 wks *chemo therapy *many of drugs lead to myelosupression |
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Chemotherapy in leukemia
ALL |
Corticosteroids
- Dexamethasone (IV) - given long term: monitor for GI irritation, infection, edema,wt gain, HTN, mood chngs, acne AT MOST RISK FOR OVERWHELMING SEPSIS *Vincristine (oncovin) neurotoxic - constipation, bone pain *L-asparginase (elspar) - nephrotoxic - pancreatitis, nephrotoxicity Cisplatin, cytarabine, 6-Mp - hepatotoxic |
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Chemotherapy - AML
|
Doxorubicin and daunorubicin
- cardiotoxic dysrhythmias, CHF, anaphalaxis |
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Platelets during chemotherapy
|
Must monitor
Normal - 150,000 to 400,000/mm3 <100,000 - ^ bleeding risk <50,000 - provide gentle care < 20,000 - risk for spontaneous bleed Packed RBCs are used to correct |
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Intensification therapy stage of chemotherapy
|
High dose/intenisfied tx after remission is achieved. Eradicate residual luekemic cells and greatly reduce blast cells.
6 month time period. L-asparaginase, methotrexate, cytarabine, vincristine |
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CNS prophalactic therapy of leukemia
|
To prevent cancer cells from invading CNS and gonads (protected by blood/brain barrier.)
Tx begun in 1st 6 to 8 weeks after dx. Use of radiation to brain, spinal cord, testes (2nd most common site of metastasis.) TX w/ intrathecal meds: Methotrexate Triple intrathecal chemotherapy |
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Maintenance therapy in leukemia
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To decrease risk of reoccurance - prevent relapse.
Use of combined drug therapy. Daily oral - Mercaptopurine Weekly - Methotrexate Periodic - Vincristine and Prednisone Given over remaining 2 to 3 year period CBC done periodically to evaluate bone marrow response. |
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Reinduction following relapse in leukemia
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Presence of leukemic cells in bone marrow, CNS or testes = relapse.
Prognosis becomes worse after each relapse. |
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Management of relapse in leukemia
|
Hematopoietic stem cell transplant (HSCT)
- successful in treating ALL & AML. Not rec. for 1st remission in ALL b/c excellent chemo results |
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Risks after HSCT in leukemia relapse
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Increased mortality and morbidity
Graft-vs-host- disease Overwhelming sepsis and severe organ damage |
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Prognosis w/ relapse in leukemia
|
Depends on:
Initial WBC count - low WBC is better initially Age at dx - younger child better prognosis. Age 2-9 best prognosis. Sex - females have better prognosis. Chromosomes - morphology (type of cells.) |
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Assessment and intervention of Infection during leukemia tx
|
Assess for infection at time of dx and relapse, and after HSCT.
Assess after prolonged use of ATB. REVERSE ISOLATION. Nursing must: maitain isolation use strict hand washing assess areas of potential infection - IV site,bone marrow asp. site, IT Know how to calculate ANC |
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Assessment and intervention of Hemorrhage during leukemia tx
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Infection causes tendency to bleed, and bleeding sites are more prone to infection.
Limit puncture sites. Perform central line/PICC line dressing changes, usually q72hrs Avoid rectal temps Monitor for decreased WBC Monitor for bleeds - petechiae, ecchymoses, hematemesis, bleeding gums, tarry stools. |
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Treatment of anemia
child w/ leukemia |
At the time of dx r/t bone marrow suppression.
Blood transfusions may be needed and is often life saving - know SE of blood transfusions. Need consent, type and cross match & check w/ other nurse, have NS hanging w/ blood |
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Manage drug toxicity issues w/ chemotherapy
|
N/V - give anti-emetics 1/2 hr b4 chemo drugs. Zofran may be combined w/ dextramethasone.
Anorexia - may need supplementation w/ TPN Ulcerations - mucosal, rectal Neuropathy - assess LOC daily Hemorrhagic cystitis - chemo rugs - liberal fluids, may need 1 to 1 1/2 x maintenance fluids to flush from body Renal function, I&O, daily wt mutogenicity,anaphalaxis |
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Mutogennicity - s/s
|
The ability to alter body cells in a chemical environment
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Signs & symptoms of impending death
|
Increase in sleep.
decrease in appetite. less responsive. slow, shallow breaths. sleeps w/ eyes slightly open. Pale, may feel cold or numb. |
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Late effects of chemotherapy
|
Delayed G&D
Cardiotoxicity/organ toxicity another malignancy - ie brain, bone |
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|
Brain tumors
|
2nd to leukemia/cancer in kids
Most <15yrs 2/3 below tentorium-infratntorial: brain stem, cerebellum, and 4th ventricle 1/3rd above |
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Etiology of brain tumors
|
heredity, environmental, congenital, neurfibromastosis, immunosuppression, hx of other cancers/tumors - eg. Wilms tumor (kidney) leads to brain tumor
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|
Patho of brain tumors
|
Tumors enlarge and obstruct CSF circulation
CM vary Surgery/radiation may be needed As tumors grow the exert pressure on the nervous system. Results in ^ ICP |
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|
Astrocytomas (23%)
|
Slow growing
Cerebellar most common infiltrates brain parenchyma w/out distal boundaries. CM: HA, Nausea, seizures. Sometimes bizarre bx - sttaring or autonomic movemnts.) visual disturbances, ^ICP Mgmnt - extensive surgery, followd by chemo & irradiation Prognosis: 5 yr - 75 - 85% |
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Medulloblastoma (20 - 25%)
|
Fast growing and highly malignant.
Arise from embryonic cerebellum. CM: HA, vomiting, ataxia Mgmnt: excision of all or most of tumor, followed by chemo w/ or w/out irradiation. Prognosis: Overall 5yr is >70% Period of risk of recurrance is age at dx + 9 mos |
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Brainstem Glioma (15%)
|
This tumor grows very large b4 causing problems.
Most difficult to resect b/c develops own blood supply. CM: Strabismus - lazy eye facial weakness, and difficulty walking HA & vomitting are uncommon! Mgmnt: surgical excision is diff.but attempted when possible, followd by irradiation. Prognosis: poor, since highly resistant to therapy. |
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Ependymona (4%)
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Usually benign, but can be fatal.
Usually encapsulated. Most invade the ventricles, obstructing flow of CSF CM: HA, vomiting, ataxia, hemiparesis, papilledeam, and hydrocephalus in infants Mgmnt - goal of surgery is total resection Prognosis: overall 5 year is about 45%. Improves to 80% if no post-op residual tumor. |
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|
Strabisimus (lazy eye)
|
A normal finding for the 1st 5 to 6 mos of life d/t immature musculature. Commonly seen w/ brain injury or brain tumor. If not corrected, may lead to blindness.
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|
|
CM of brain tumors
(depends on location of tumor) |
HA - most common s/s esp on awakening (any time pressure on pain sensitve areas from tumor) *Vomiting - not r/t feeding. Usually projectile and in am. Occurs from ICP, compress brain stem, stimulates vomit center in medulla *Neruomuscular changes - ataxia, hypotonia, decreased reflexes, clumsiness, weakness, spasticity or paralysis, poor fine motor coordination slurred speech, +babinski sign
*Behavior change *Cranial nerve neuropathy - head tilt - visual chaanges - nystagmus, diplopia, strabismus, graying out *Vital sign changes- decreased pulse and RR - ^ BP - hypo or hyperthermia *Other seizures, cranial enlargement, tense or bulging fontanel AT REST, nuchal rigidity, papilledema (edema of optic nerve) |
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|
DX of brain tumor
|
CT scan and MRI may detect lesion.
Angiography may detect source of blood supply. PET scan detect blood flow. |
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|
Management of brain tumors
|
Neurosurgery to remove
Chemo Radiation Management of ^ ICP Neurological dysfunc. mgmnt similar to that of child w/ brain injury. |
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|
Nursing implementation - brain tumor - post op
|
Frequent monitoring, VS, ICP
Position on non-op site Elevate HOB Eye care to prevent corneal irritation Fluid regulation - NPO, vomiting predisposes child to aspiration, ^ ICP may lead to incisional rupture. IV insertion at 1/2 to 2/3 maintenance (don't want to add to circulatory volume). Assess s/s of infection at suture site. support pt/fam - will affect G&D - delays Teach parent to be patinet w/ child. |
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|
Complications w brain tumor
|
may develop another lesion or regrowth of retained tumor.
May develop diabetes insipidus, esp if lesion midbrain that compresses hypothalamus or pituitary gland - polyuria, polydipsia (relieved by water feeding) |
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|
Osteogenic sarcoma
|
Most frequently encountered malignant bone cancer in children.
Peak incidence btwn 10 - 25 yrs, usually adol. boys. Primary sites metaphysis of long bones, esp. LE. Tumor arises from bone cells (prob osteoblast.) Femur (more than 50%),esp distal portion. Humerous, tibia, pelivis, jaw, phlanges |
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|
DX of Osteogenic sarcoma
|
Hx of localized pain in affected site.
CXR, MRI, CT scan, radioisotope bone scan, needle or bone biopsy. MRI shows sunburst appearance. |
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|
CM of Osteogenic sarcoma
|
Pain - severe or dull. Often relieved by position or flexion.
May have night sweats/fever. Regional lymphadanopathy. Brought in for eval when:limps, curtails physical activity, unable to hold heavy objects. |
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|
Management of Osteosarcoma
|
Limb salvage procedure - may attempt first. Annual surgical intervention.
Resection - amputation at least 3 inches above proximal tumor. Followed by agressive chemo. Still controvers. Van Ness Procedure - rare. 1 in 3 are successful. |
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|
Prognosis of osteosarcoma
|
65 to 85% of those w/ non metastasis can expect long term survival.
Metastasis - <50% |
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|
Normal RBCs in kids
|
NB 5.9
1 yr 4.6 5 yrs 4.7 8 to 12 yrs 5 |
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|
Hgb in children
|
NB 19
1 year 12 5 years 13.5 8 to 12 yrs 14 |
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|
WBC in children
|
NB
17,000 1 year 10,000 5 years 8,000 8 to 12 years 8,000 |
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|
Hct %
|
NB 54 +10
1 year 36 5 years 38 8 to 12 40 |
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|
Platelets
|
NB 350,000
8 to 12 years 260,000 |
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|
Heart rate NB
|
resting awake 100 - 180
sleep - 80 to 160 fever/exercise up to 220 |
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|
Heart Rate 1 wk to 3mos
|
resting/awake 100 to 220
sleep 80 to 220 exercise/fever up to 220 |
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|
HR 3mos to 2 year s
|
resting awake 80 to 150
sleeping 70 to 120 ex/fever up to 200 |
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|
HR 2 years to 10 years
|
resting awake 70 - 110
sleeping 60 to 90 ex/fever up to 200 |
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|
HR 10 yrs to adult
|
resting 55 - 90
sleep 50 - 90 ex/fever up to 200 |
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|
Acyanotic defects w/ increased pulmonary blood flow
|
ASD
VSD atrioventricular canal defect PDA |
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|
Acyanotic defects that restrict ventricular blood flow
|
Coarctation of the aorta
Aortic stenosis Pulmonic stenosis |
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|
Cyanotic defects with decreased pulmonary blood flow
|
Tetrallogy of Fallot
Tricuspid atresia |
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|
Cyanotic defects - mixed blood flow
|
Transposition of the great vessels.
Total anomalaous pulmonary venous connection (dont join to left ventricle) Truncus arteriosus Hypoplastic left heart syndrome |
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|
Tetralogy of Fallot
|
PROV
Pulmonary stenosis Right ventricular hypertrophy Overiding Aorta - blood goes up aorta instead of pulmonary artery Ventricular septal defect Give PGE to keep PDA open until repair |
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|
how to treat TET spells
|
Immediately place child in knee-chest postion
Remain calm and calm child Administer O2 100% blow by Call for help IV push morphine if ordered No procedures can be done at this time May need IV fluids for volume expansion Notify MD Palliative or corrective surgery scheduled asap |
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|
S/S of TET spells
|
jCaused by sudden infudibular spasms which increase Rt - Lt shunting
Increased rate and depth of respirations. Incrased cyanosis and tachycardia. Pallor and poor tissue perfusion. Agitation/irritable Progressively cyanotic and limp Loses consciousness Like to have seizure or CVA May suddenly die |
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|
Transpostion of the great arteries
|
Cyanotic
Emergency surgical repair is needed. Mixed blood flow. Severe cyanois shortly after birth, as PDA closes. |
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|
Tricuspid atresia
|
Cyanotic
PGE is used to increase bld flow - keeps PDA open. Severe cyanosis shortly after birth as PDa closes. CHF & FTT |
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|
Hypoplastic left heart
|
Cyanotic
Mixed blood flow. requires several surgeries or transplant. Severe cyanosis. Severe decrease in CO PGE to keep PDA open. |
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|
PDA
Acyanotic |
Closes naturally or w/ indocin (prostaglandin inhibitor)
Enlargement of lft ventricle (sign) |
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|
ASD
Acyanotic |
closes naturally, may need surgery.
Greater O2 sats in right atrium. mixing of blood w/ in heart |
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|
VSD
Acyanotic |
Most common cardiac defect
60% close naturally 02 sat higher in rt ventricle. May be asymptomatic |
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|
Pulmonary stenosis
acyanotic |
slows down blood flow
balloon angioplasty or surgery to open. leads to rt. ventric. enlargement. |
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|
Aortic stenosis
Acyanotic |
Opened w/ balloon angioplasty
left ventricular enlargemnt chest pain, lowered CO |
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|
Cooarctation of the Aorta
|
surgical correction is needed.
Absence of femoral pulses (or faint) nosebleeds, HA, vertigo Increase BP & O2 sats in UE when compared to LE CHF & low CO poorer perfusion of abd. organs and LE |
