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.

      Prior asthma episode requiring mechanical ventilation is strong predictor of subsequent asthma death.

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

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.

Triggers

      Numerous things can trigger asthma attacks:

    Allergens

    Exercise

    Stress

    Viruses

    Medicines

    Noxious stimuli

Cellular component

      Numerous cells involved:

    Mast cells

    Eosinophils

    Lymphocytes (TH-2 cells)

    Neutrophils

    Epithelial cells

Cytokines

      Numerous soluble products of the cells exacerbate asthma:

    Interleukins

    Bradykinins

    Histamine

 

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

Receptors

      Beta

    3 subtypes

    b2 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

 

Physical Exam

      Respiratory Rate

      Work-of-Breathing

      Breath Sounds

      Inspiratory:Expiratory Phase

      Cyanosis

      Mental status

Respiratory rate

      Normal

    Infants: <40

    Toddlers: <30

    Preschoolers: <30

    Elementary School: low 20s

    High school: upper teens

Work-of-breathing

      Nasal Flaring

      Retractions

    Supraclavicular

    Intercostal

    Substernal

      Paradoxical Breathing

Breath sounds

 

      Lung Fields

      Air flow

    Good, fair, poor

      Expiratory Wheeze

    Polysyllabic vs. Monosyllabic

      Inspiratory Wheeze

    Common, even in non-diseased states

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.

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.

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.

Laboratory tests

      PEFR

      PFTs

      Asthma Scores

      IgE

      Allergy tests

      Blood gas

      CXR

Treatments

      Oxygen

      Steroids

    Inhaled

    Systemic

      Beta Agonists

    Short-acting

    Long-acting

      Anticholinergics

      Leukotriene Inhibitors

      Methylxanthines

      Magnesium

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.

 

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

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

Steroids

      Complications

    Hypertension

    Hyperglycemia

    Hypokalemia

    Gastritis

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

Beta-agonists

      Work via the b2 receptor to bronchodilate

      Albuterol

      Terbutaline

      Can cause hypokalemia, tremors, nausea, vomiting, tachycardia

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

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.

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)

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

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

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

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)

 

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

 

Acute Asthma Score
Modified from Woods, et al, AJDC, 1972

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.

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.

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.