LOWER AIRWAYS CONDITIONS

Condition Description Viral Induced Asthma Exaggerated response of Bronchi to infection Bronchospasm, Exudation, Edema of Bronchi Late Infancy and Early Childhood Bronchitis Associated with URI Seldom an Isolated Entity (ex. Penumonia 2ndary to Bronchitis) First 4 years of life Bronchiolitis More common infectious disease of Lower Airways Acute Viral Infection with Maximum effect at bronchiolar level Children 2 12 months Rare after 2y/o Peak at 6months Occurs primarily at winter and spring (Phil: Oct Feb) Viruses Predominantly RESPI SYNCYTIAL VIRUSES produced from multinucleated cell & able to produce cytoplasm to adjacent cells * Adenovirus * Parainfluenza Viruses * Mycoplasma Pneumoniae These are viruses that can cause PNEUMOCYSTIS CARINIA PNEUMONIA Dyspnea Paroxysmal non prod cough Tachypnea w/ retractions Nasal Flaring Emphysema Wheezing Oxygen Mist Ribavirin or Palivizumab (anti viral) for high risk populations

Age Group Affected and Occurence

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

Predominant Wheezing Characteristics (musical, pitch) Productive Cough

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

Treatment

Bronchodilators (to ease breathing) Corticosteroids

Cough Suppressants if needed (ex. Antitussives) Humidify Secretions

Bronchiolitis
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Easily spread to eye, nose, or other mucous membrane 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 Examination a. Cough: hacking, paroxysmal, irritative, and non productive, becomes rattling and productive of clear, frothy sputum b. Respiratory: SOB, prolonged expiration, audible wheeze, malar flush (reddened ear & face), deep lips dark red in color, restlessness, and apprehension c. Client: Hyperresonance (booming; emphysematous lung), loud breath sounds, wheezes throughout lung fields, general inspiratory and exiratory wheezing, crackles, prolonged expiration. 2. Skin Test for Allergens 3. Provocative Testing direct exposure to suspected antigens in concentrations; identify inhaled allergens 4. Radioallergosorbent Assay Test (RAST) identify antigen against various foods; determine appropriate therapy MANAGEMENT 1. Allergen Control: Prevent and Reduce exposure to airborne allergens and irritants 2. Drug Therapy: Prevent and Control exacerbations and reverse airflow obstruction CATEGORIES OF ASTHMA MEDICATIONS LONG TERM Control Medications (Preventive Medicines) control of inflammation QUICK RELIEF Medications (Rescue Medicines) treat symptoms and exacerbations MDI (Metered Dose Inhaler) during attacks only 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 1. 2. a. b.

 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 symptoms b. Salmeterol (Serevent) long acting bronchodilator used 2x/day

g. Methylxanthines o Principally Theophylline (stock of 250ml/10ml); Now considered 3rd line agent and unnecessary to treat exacerbations o Bronchodilator, Respiratory Stimulant, Respiratory Muscle Contractility o Dosage: 5 15 mcg / ml o Side Effects: Nausea and Vomiting, Headache, Irritability, Insomnia o Theophylline Toxicity: serum levels > 20 mcg / ml o Early signs of toxicity: nausea, tachycardia, and irritability o Seizure and dysrhythmias: > 30 mcg /ml level h. Leukotriene Modifiers o Mediators of Inflammation that can increase Airway Hyperresonsiveness o Zafirlukast, Zileuton, & Montelukast Soidum that blocks inflammation and bronchospasm o 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 o Continuous to display respiratory distress despite therapeutic measures, especially use of sympathomimetics are considered to this condition. Therapy directed toward improvement of ventilation, correction of dehydration and acidosis, and treatment of any concurrent infection

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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 Nebulized Beta 2 Agonist Anti-cholinergic such as Ipratropium IV Corticosteroids

Nursing Considerations: 1. Avoid Allergens / Airborne Irritants / Triggers (ex. pollen, food) 2. Relieve Bronchospasm 3. Provide acute asthma care a. Orthopneic Position b. Hydrate c. 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 Neonates 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 Surfactant a. Prematurity and Immaturity of Alveoli Lung b. Acidosis c. Hypothermia d. Hypoxia (decreased o2 in tissues) e. Hypovolemia (decreased blood volume) f. Diabetes g. 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 cells b. Diminished or Impaired Production Rate d/t fetal or early neonatal stress c. Impaired release of PHOSPHOLIPIDS from Type II Alveolar Cells d. Death of many Type II Alveolar Cells PHOSPHOLIPIDS enzyme produced inside the lungs that maintain the stability of: a. Surfactant b. Lining of Alveoli c. 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 instability 7. RDS is usually self limiting disease and symptoms peak in about 3 4 days a. Moderately Ill Infant that dont 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 isnt crying) b. Retractions (Sternal, Suprasternal, and Intercostal) progressing to seesaw respirations c. Nasal Flaring d. Tachypnea < 60 bpm e. Hypothermia f. Cyanosis when child is in room air (infants with severe disease may be cyanotic even when oxygen is given), increasing need of oxygen g. 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 increase d. Muscle tone decreased e. Body Temp drops f. Short Periods of Apnea g. Bradycardia may occur (decreased HR) h. Pale Gray Skin Color

2. Secondary S/S: a. Hypotension b. Edema of face and hands c. Absent bowel sounds early in illness d. 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