LOWER AIRWAYS CONDITIONS

Condition Viral Induced Asthma Bronchitis BronchiolitisDescription Exaggerated response

of Bronchi to infection

Bronchospasm, Exudation, Edema of Bronchi

Associated with URI

Seldom an Isolated Entity (ex. Penumonia 2ndary to Bronchitis)

More common infectious disease of Lower Airways

Acute Viral Infection with Maximum effect at bronchiolar level

Age Group Affected and

Occurence

Late Infancy and Early Childhood

First 4 years of life Children 2 – 12 monthsRare after 2y/oPeak at 6months

Occurs primarily at winter and spring (Phil: Oct – Feb)

Etiologic Agent Usually Viruses but may be any variety of URI Pathogens

Secondary are Allergens

Usually Viruses

Bacteria, fungi, allergic disorders, airborne irritants can trigger symptoms

VirusesPredominantly RESPI SYNCYTIAL VIRUSESproduced from multinucleated cell & able to produce cytoplasm to adjacent cells* Adenovirus* Parainfluenza Viruses* Mycoplasma Pneumoniae

These are viruses that can cause PNEUMOCYSTIS CARINIA PNEUMONIA

Predominant Characteristics

Wheezing (musical, ↑ pitch)

Productive Cough

Persistent, dry hacking cough (worse @ night) that becomes productive in 2 – 3 days

DyspneaParoxysmal non prod cough Tachypnea w/ retractionsNasal FlaringEmphysemaWheezing

Treatment Bronchodilators (to ease breathing)

Corticosteroids

Cough Suppressants if needed (ex. Antitussives)

Humidify Secretions

Oxygen Mist

Ribavirin or Palivizumab (anti – viral) for high risk populations

Bronchiolitis

o Easily spread to eye, nose, or other mucous membrane

o Pathophysiology: Bronchial Walls are infiltrate (penetrated) with cells edema and swelling (inflammatory response) manifestations emphysema (air trapping)

VIRAL INDUCED ASTHMA

DIAGNOSTIC EVALUATION

1. Clinical Manifestations, History, and Physical Examinationa. Cough: hacking, paroxysmal, irritative, and non productive, becomes rattling and

productive of clear, frothy sputumb. Respiratory: SOB, prolonged expiration, audible wheeze, malar flush (reddened ear &

face), deep lips dark red in color, restlessness, and apprehensionc. Client: Hyperresonance (booming; emphysematous lung), loud breath sounds, wheezes

throughout lung fields, general inspiratory and exiratory wheezing, crackles, prolonged expiration.

2. Skin Test for Allergens3. Provocative Testing – direct exposure to suspected antigens in ↑ concentrations; identify

inhaled allergens4. Radioallergosorbent Assay Test (RAST) – identify antigen against various foods;

determine appropriate therapy

MANAGEMENT

1. Allergen Control: Prevent and Reduce exposure to airborne allergens and irritants2. Drug Therapy: Prevent and Control exacerbations and reverse airflow obstruction

CATEGORIES OF ASTHMA MEDICATIONS

1. LONG TERM Control Medications (Preventive Medicines) – control of inflammation2. QUICK RELIEF Medications (Rescue Medicines) – treat symptoms and exacerbations a. MDI (Metered Dose Inhaler) – during attacks onlyb. Nebulization

amt of chemical = amt of h20 (ex. 1 nebule = 1 cc of NSS; 1 nebule and 1 1/2 = 2cc NSS) close first to soften secretions then open to prevent overhydration

c. Corticosteroids Anti – Inflammatory drugs to treat reversible airflow obstruction Reduce bronchial hyperactivity in chronic asthma

d. Cromolyn Sodium Stabilizes mast cell membranes; Inhibits increase of cytoplasm Inhibits activation and release of mediators from Eosinophil and Epithelial Cells

Inhibits acute airway narrowing after exposure to exercise, cold dry air, & sulphur dioxide

e. Nedocromil Sodium Maintenance Therapy; Anti-allergenic and Anti- Inflammatory (ex. Budecort Ventolin) Not given if patient started in cromolyn sodium

f. Beta Adrogernic Agonists (Tertabutile, Albuterol, Metaproternol) Bronchodilator (can increase HR; always check for Cardiac Rate); For acute

exacerbations Prevention of exercise induced bronchospasm via inhalation/ oral / parenteral

a. Inhaled – not be taken > 3 – 4 x daily for acute symptomsb. Salmeterol (Serevent) – long acting bronchodilator used 2x/day

g. Methylxanthineso Principally Theophylline (stock of 250ml/10ml); Now considered 3rd line agent and

unnecessary to treat exacerbationso Bronchodilator, Respiratory Stimulant, ↑ Respiratory Muscle Contractilityo Dosage: 5 – 15 mcg / mlo Side Effects: Nausea and Vomiting, Headache, Irritability, Insomniao Theophylline Toxicity: serum levels > 20 mcg / mlo Early signs of toxicity: nausea, tachycardia, and irritabilityo Seizure and dysrhythmias: > 30 mcg /ml level

h. Leukotriene Modifierso Mediators of Inflammation that can increase Airway Hyperresonsiveness o Zafirlukast, Zileuton, & Montelukast Soidum that blocks inflammation and

bronchospasmo Given Orally with Beta Agonists and Corticosteroids to provide long term control and

prevent Symptoms

3. Exercise – ROM exercises, turn patient side to side every 2 hrs for adult and every 1 hour for babies to prevent hypostatic pneumonia

4. Chest Physiotherapy – not recommended during exacerbations; wrapping to increase secretions

5. Hyposensitization – injections given only with EMERGENCY equipment and meds readily available during anpaylactic reaction

Prognosis: Varies; Poor prognosis if s/s are more long standing & prolonged

Complication: STATUS ASTHMATICUS

o Continuous to display respiratory distress despite therapeutic measures, especially use of sympathomimetics are considered to this condition.

o Therapy directed toward improvement of ventilation, correction of dehydration and acidosis, and treatment of any concurrent infection

o Intubation and mechanical ventilation with 100% oxygen for impending or actual respiratory distress, decreased mental alertness, increased fatigue or partial pressure of arterial carbon dioxide (PaCO2) > or = to 42 mmHg

o Nebulized Beta 2 Agonisto Anti-cholinergic such as Ipratropiumo IV Corticosteroids

Nursing Considerations:

1. Avoid Allergens / Airborne Irritants / Triggers (ex. pollen, food)2. Relieve Bronchospasm3. Provide acute asthma care

a. Orthopneic Positionb. Hydratec. Back kept dry to prevent pneumonia

4. Support child and family

RESPIRATORY DISTRESS SYNDROME (HYALINE MEMBRANE DISEASE)

Syndrome of Premature Neonates that is characterized by progressive and usually fatal respiratory failure resulting from Atelectasis (lung collapse) and Immaturity of the lungs

Incidence:

1. Common in Premature Neonates weighing between 1,000 – 1,500g and between 28 – 37 AOG.

2. In Neonate’s 28 – 30 weeks AOG, incidence is 50% - 70% and increases degree of prematurity.

Diagnosis: Fatal; those who survived are at risk for chronic respiratory and neurologic complications

Etiology and Pathophysiology

1. Adequate Pulmonary Function at birth depends on:a. Adequate Amount of Surfactant lining the Aveolar Cells that allows alveolar stability and

prevents alveolar collapse at the end of expiration.b. Adequate surface area in air spaces to allow gas exchange

2. ↓ Surfactant, Incomplete Structural development of lung, and highly compliant chest wall

3. Factors that ↓ Surfactanta. Prematurity and Immaturity of Alveoli Lung b. Acidosisc. Hypothermiad. Hypoxia (decreased o2 in tissues)e. Hypovolemia (decreased blood volume)f. Diabetesg. Elective CS

h. Fetal or Intrapartum Stress that compromises blood supply to fetal lungs: vaginal bleding, maternal hypertension, difficult resuscitation associated with birth.

i. Non Pulmonary Factors* cardiac defects* airway obstruction and acute blood loss* sepsis* hypoglycaemia* intraventricular hemmorhage

4. Surfactant Production is deficient by TYPE II Alveolar Cells. Surfactant ↓ d/t:a. Extreme Immaturity of alveolar lining cellsb. Diminished or Impaired Production Rate d/t fetal or early neonatal stressc. Impaired release of PHOSPHOLIPIDS from Type II Alveolar Cellsd. Death of many Type II Alveolar Cells

PHOSPHOLIPIDS – enzyme produced inside the lungs that maintain the stability of:

a. Surfactantb. Lining of Alveolic. Tension d/t stretching of alveolar

5. More oxygen and energy is required to expand alveoli with each breath, causing FATIGUE. 6. Decreased no. of alveoli that expands which results from atelectasis and aveoli instability7. RDS is usually self – limiting disease and symptoms peak in about 3 – 4 days

a. Moderately Ill Infant that don’t require ventilation - slow improvement by 48 hours and rapid recovery over 3 – 4 days with few complication

b. Severly Ill and Very Immature Infants who require some ventilation - demonstrate rapid deterioration (decreased cardiac flow and arterial pressure, apneic episodes, cyanosis, pallor, flaccid, “UNRESPONSIVE SHOCK LIKE STATE”

Clinical Manifestations

1. Primary Signs and Symptoms ****a. Expiratory grunting or whining (when infant isn’t crying)b. Retractions (Sternal, Suprasternal, and Intercostal) progressing to seesaw respirationsc. Nasal Flaringd. Tachypnea < 60 bpme. Hypothermiaf. Cyanosis when child is in room air (infants with severe disease may be cyanotic even

when oxygen is given), increasing need of oxygeng. Decreased breath sounds and dry “SANDPAPER” breath sounds (@ right bronchus)h. Pulmonary Edema

As the disease progresses:

a. Seesaw Retractions with abdominal protrusions on expiration

b. Peripheral Edema increases (clubbing)

c. Cyanosis increased. Muscle tone decreased

e. Body Temp dropsf. Short Periods of Apneag. Bradycardia may occur (decreased

HR)h. Pale Gray Skin Color

2. Secondary S/S:a. Hypotensionb. Edema of face and handsc. Absent bowel sounds early in illnessd. Decreased Urine Output

Diagnostic Evaluation

a. LECITHINSPHINGOMYELIN RATIO – tests surfactant phospholipids in Amniotic Fluid (Normal is 2:1)

b. PHOSPHATIDYLCHOLINE AND PHOSPHATIDYLGYCEROL (PG) – phospholipids that stabilize surfactant