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ASTHMA IN THE PICU

ASTHMA IN THE PICU. Epidemiology. 14-15 million Americans Nearly 5 million children 5,000 people (mostly adults) die each year Incidence, hospitalization rate, and death rate is increasing each year. 15-24 year-olds are at higher risk of dying from asthma than are 0-4 year olds.

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ASTHMA IN THE PICU

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  1. ASTHMA IN THE PICU

  2. Epidemiology • 14-15 million Americans • Nearly 5 million children • 5,000 people (mostly adults) die each year • Incidence, hospitalization rate, and death rate is increasing each year. • 15-24 year-olds are at higher risk of dying from asthma than are 0-4 year olds. • Prior asthma episode requiring mechanical ventilation is strong predictor of subsequent asthma death.

  3. Pathogenesis • Asthma is a chronic inflammatory disease of the airways. • Asthma is characterized by bronchospasm, airway edema, and mucus production • Asthma has several components: • Cellular • Cytokines • Neurologic

  4. Pathophysiology • Asthma is an obstructive pulmonary disease. • Air-trapping and over-expansion of alveoli is a hallmark of asthma. • Air-trapping may lead to air-leak, which can be fatal. • In addition, active expiration may be required to return the lung volume to FRC. • Muscles of expiration are not designed for active expiration and quickly become fatigued, leading to respiratory failure and death.

  5. Triggers • Numerous things can trigger asthma attacks: • Allergens • Exercise • Stress • Viruses • Medicines • Noxious stimuli

  6. Cellular component • Numerous cells involved: • Mast cells • Eosinophils • Lymphocytes (TH-2 cells) • Neutrophils • Epithelial cells

  7. Cytokines • Numerous soluble products of the cells exacerbate asthma: • Interleukins • Bradykinins • Histamine

  8. Neurologic • Parasympathetic • Stimulation via the vagus leads to airway constriction. • Sympathetic • Plays little role in humans since only pulmonary vasculature, not airway smooth muscle, is innervated • Non-adrenergic non-cholinergic (NANC) • Role in humans not determined. • Vasoactive intestinal polypeptide, Substance P, NO

  9. Receptors • Beta • 3 subtypes • 2 is common in airway smooth muscle • Activation leads to increase in cAMP • Alpha: little role • Cholinergic • Muscarinic receptors: • M2 receptor inhibits acetylcholine release, leading to bronchodilation. • M3 receptor cause bronchoconstriction

  10. Physical Exam • Respiratory Rate • Work-of-Breathing • Breath Sounds • Inspiratory:Expiratory Phase • Cyanosis • Mental status

  11. Respiratory rate • Normal • Infants: <40 • Toddlers: <30 • Preschoolers: <30 • Elementary School: low 20s • High school: upper teens

  12. Work-of-breathing • Nasal Flaring • Retractions • Supraclavicular • Intercostal • Substernal • Paradoxical Breathing

  13. Breath sounds • Lung Fields • Air flow • Good, fair, poor • Expiratory Wheeze • Polysyllabic vs. Monosyllabic • Inspiratory Wheeze • Common, even in non-diseased states

  14. Phases • Normally, expiratory phase is the same as, or shorter than the inspiratory phase. • In asthma, the expiratory phase is prolonged as airway collapse and air-trapping occur. • Intrathoracic pressure becomes higher than the large airway pressure, leading to collapse of the airways. • Airway edema, bronchospasm, and mucus impede air movement.

  15. Cyanosis • Need 5gm/dl of unoxygenated hemoglobin before cyanosis present • Cyanosis will be more pronounced in children with high hematocrits: dehydrated, cyanotic heart disease • Cyanosis can be a sign of impending respiratory failure….or not.

  16. Mental Status • Hypoxia and hypercarbia can lead to mental status changes. • Fatigue can, too. • Improvement can, too. • Watch for agitation, delirium, unresponsiveness, especially to pain.

  17. Laboratory tests • PEFR • PFTs • Asthma Scores • IgE • Allergy tests • Blood gas • CXR

  18. Treatments • Oxygen • Steroids • Inhaled • Systemic • Beta Agonists • Short-acting • Long-acting • Anticholinergics • Leukotriene Inhibitors • Methylxanthines • Magnesium

  19. Oxygen/Fluid • Ventilation/perfusion mismatch can be quite high • Oxygen lends to patient comfort • In absence of chronic pulmonary disease, i. e., CO2 retention, supplemental oxygen will not suppress the respiratory drive • Most patients with asthma are dehydrated (increased insensible losses, decreased intake) • Overhydration can exacerbate pulmonary edema. • Watch for SIADH.

  20. Steroids • Only drug that addresses the underlying pathophysiology • Solumedrol • 2mg/kg/day divided q6hr • Max is 60mg/day “kids,” 180mg/day “adults” • IV • Prednisone or Prednisolone • Oral

  21. Steroids • No difference between IV and po • Usually give IV in severe attack because of nausea and high respiratory rate increases risk of aspiration • 5 day course of therapy won’t suppress adrenal system • Start to work in 8-12 hours

  22. Steroids • Complications • Hypertension • Hyperglycemia • Hypokalemia • Gastritis

  23. Inhaled Steroids • For long term control • Fewer side effects than systemic steroids, but may be associated with long-term growth suppression. • Beclomethasone • Budenoside • Flunisolide • Fluticasone • Triamcinolone

  24. Beta-agonists • Work via the 2 receptor to bronchodilate • Albuterol • Terbutaline • Can cause hypokalemia, tremors, nausea, vomiting, tachycardia

  25. Beta-agonists • Give via MDI or nebs • Dose: • Depends upon size, severity of disease, and delivery device. Titrate to heart rate and response • Usual neb dose: • <10kg: 2.5mg/hr • 10-20kg: 5mg/hr • 20-30kg: 10mg/hr • >30kg: 15mh/hr

  26. Anti-cholinergics • Atropine and atrovent • Bronchodilate and decrease mucus production • Additive effect with beta-agonists. • Use for beta-blocker induced asthma • Complications include drying of the airways and rarely, increased wheezing • Atrovent dose: 250-500mcg/dose up to q 20min, usually q2-4hrs.

  27. Leukotriene inhibitors • Block the actions of leukotrienes • Zafirlukast and zileuton • Used for long-term control • Little use in acute attacks • May be as effective as inhaled steroids • Rare side effects (liver damage)

  28. Methylxanthines • Theophylline and aminophylline • Actions are several: • Phosphodiesterase inhibitor (increases cAMP) • Stimulates catecholamine release • Diueresis • Augments diaphragm contractility • Prostoglandin antagonist • May be of little benefit in routine use for acute asthma • High risk of side effects: N/V, tachycardia, agitation, cardiac arrythmias, hypotension, seizures, death

  29. Magnesium • Mechanism unclear, but may be a direct bronchodilator through blocking calcium • Raising the Mg levels up to 2-4 mg/dL significantly improved expiratory air flow in adults • One study in children showed that MgSO4 25mg/kg over 20 minutes significantly improved PFTs, but did not change hospitalization rate or length of stay in the ED. • Relatively safe. Levels >12 can cause weakness, areflexia, respiratory depression, and cardiac arrhythmias

  30. Weaning protocol • Patients selected by attending/resident • Physician writes order • Physician writes initial dose and frequency of bronchodilator • Respiratory therapist evaluates patient and changes therapy in accordance with protocol

  31. Treatment levels • Level 1: Continuous albuterol at > 0.6 mg/kg/hr • Level 2: Continuous albuterol at 0.3 mg/kg/hr • (Max 15 mg/hr) • Level 3: Continuous albuterol at 0.15mg/kg/hr • Level 4: Albuterol at about 0.3mg/kg q2hours • Infants <5kg use 1.0 mg • Infants 5 - 10 kg use 2.5 mg • Children 10 - 20 kg use 5.0 mg • Children > 20 kg round to closest multiple of 2.5 mg (2.5, 5.0, 7.5, etc)

  32. Treatment levels • Level 5 : Albuterol q3 hours at same dose as level 4 • When the patient has been stable on q3 hour treatments for 2 treatment intervals, therapist is to call the physician to evaluate for possible transfer out of the PICU (anytime of day or night). • If the patient is also receiving intermittent Atrovent nebulizations q2 or q4 hours, the therapist should make these q3 to coincide with the albuterol treatments. • Level 6 : Albuterol q4 hours, same dose as level 4 and 5 • Level 7 : Albuterol q4 hours at about 0.15mg/kg if dose for previous levels is above 2.5 mg • Level 8 : Albuterol q6 hours, same dose

  33. Acute Asthma ScoreModified from Woods, et al, AJDC, 1972

  34. Weaning criteria A. Respiratory therapist has evaluated patient and feels the patient is not acutely distressed, AND B. The asthma score is less than or equal to 3, AND C. If the patient is over 6 years and cooperative, the peak flows are > 70% of predicted, AND D. The patient must be stable at these criteria for 3 hours or for two treatment intervals, whichever is longer.

  35. Failure criteria • The therapist (or nurse) judges the patient to be in increased distress, but not severe distress. OR B. The asthma score increases to greater than 3 but less than 5. OR C. The PEFR drops to less than 70% predicted but greater than 50% of predicted.

  36. Deterioration criteria A. The respiratory therapist (or nurse) judges the patient has developed severe distress. OR B. The asthma score increases to more than or equal to 5. OR C. The PEFR drops to less than 50% of predicted.

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