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Status asthmaticus


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Status asthmaticus

  1. 1. Status asthmaticus is a medical emergency in which asthma symptoms are resistant to initial bronchodilator therapy in the emergency department. Patients report chest tightness, rapidly progressive shortness of breath, dry cough, and wheezing. Typically, patients present a few days after the onset of a viral respiratory illness, following exposure to a potent allergen or irritant, or after exercise in a cold environment. It is a life-threatening episode of airway obstruction considered a medical emergency. Complications include cardiac and/or respiratory arrest. Pathophysiology Inflammation in asthma is characterized by an influx of eosinophils during the early-phase reaction and a mixed cellular infiltrate composed of eosinophils, mast cells, lymphocytes, and neutrophils during the late-phase (or chronic) reaction. The simple explanation for allergic inflammation in asthma begins with the development of a predominantly helper T2 lymphocyte–driven, as opposed to helper T1 lymphocyte–driven, immune milieu, perhaps caused by certain types of immune stimulation early in life. This is followed by allergen exposure in a genetically susceptible individual. Specific allergen exposure (eg, dust mites) under the influence of helper T2 lymphocytes leads to B-lymphocyte elaboration of immunoglobulin E (IgE) antibodies specific to that allergen. The IgE antibody attaches to surface receptors on airway mucosal mast cells. Subsequent specific allergen exposure leads to cross-bridging of IgE molecules and activation of mast cells, with elaboration and release of a vast array of mediators. These mediators include histamine; leukotrienes C4, D4, and E4; and a host of cytokines. Together, these mediators cause bronchial smooth muscle constriction, vascular leakage, inflammatory cell recruitment (with further mediator
  2. 2. release), and mucous gland secretion. These processes lead to airway obstruction by constriction of the smooth muscles, edema of the airways, influx of inflammatory cells, and formation of intraluminal mucus. In addition, ongoing airway inflammation is thought to cause the airway hyperreactivity characteristic of asthma. The more severe the airway obstruction, the more likely ventilation-perfusion mismatching will result in impaired gas exchange and hypoxemia. Clinical History - Patients with status asthmaticus have severe dyspnea that has developed over hours to days. - Frequently, patients have a prior history of endotracheal intubation and mechanical ventilation, frequent emergency department visits, and previous use of systemic corticosteroids. - Patients usually present with audible wheezing. Physical - Patients are usually tachypneic upon examination and, in early stages of status asthmaticus, may have significant wheezing. Initially, wheezing is heard only during expiration, but, later, wheezing occurs during both expiration and inspiration. - The chest is hyperexpanded, and accessory muscles, particularly the sternocleidomastoid, scalene, and intercostal muscles, are used. Later, as bronchoconstriction worsens, patients' wheezing may disappear, which may indicate severe airflow obstruction.
  3. 3. - Normally, the pulsus paradoxus (ie, the difference in systolic blood pressure between inspiration and expiration) does not exceed 15 mm Hg. In patients with severe asthma, a pulsus paradoxus of greater than 25 mm Hg usually indicates severe airway obstruction. Causes - In persons with acute asthma, bronchospasms occur as a result of one or more inciting factors that may include, but are not limited to, a viral upper or lower respiratory tract infection, significant allergic response to an allergen (eg, pollen, mold, animal dander, house dust mites), exposure to an irritant, or vigorous exercise in a cold environment. - Precipitating factors can include infection, allergen or irritant exposure, poor adherence to the medical regimen, strenuous exercise, and a rapid decrease in long-term oral steroid therapy. - Inflammation can be the result of infection; lymphocyte, mast cell, eosinophilic, and neutrophilic responses; and airway epithelial damage. In addition, elevated plasma lactate levels were noted in patients with this condition in the first hours of inhaled beta-agonist treatment. Differential diagnosis- Primary Pulmonary Hypertension - Congestive heart failure - Croup - Stridor
  4. 4. - Upper airway obstruction - Orthopnea Diagnosis- Obtain a CBC count and differential to evaluate for infectious causes (eg, pneumonia, viral infections such as croup), allergic bronchopulmonary aspergillosis, and Churg-Strauss vasculitis. As noted earlier, when elevated, serum lactate levels (when obtained early at the onset of status asthmaticus) can correlate with improved lung function. - Obtain an arterial blood gas (ABG) value to assess the severity of the asthma attack and to substantiate the need for more intensive care. ABG determinations are indicated when the peak expiratory flow (PEF) rate or forced expiratory volume in one second (FEV1) is less than or equal to 30% of the predicted value or when the patient shows evidence of fatigue or progressive airway obstruction despite treatment. - Obtain a chest radiograph to evaluate for pneumonia, pneumothorax, congestive heart failure, and signs of chronic obstructive pulmonary disease, which would complicate the patient's response to treatment or reduce the patient's baseline spirometry values. - The most important and readily available test to evaluate the severity of an asthma attack is the measurement of PEF (peak expiratory flow) - Hospitalization is generally indicated when the PEF or FEV1 after treatment is greater than 50% of the predicted value but less than 70% of the predicted value. Hospitalization in the
  5. 5. ICU is indicated when the PEF value or FEV1 is less than 50% of predicted. Staging- The 4 stages of status asthmaticus are based on ABG progressions in status asthma. Patients in stage 1 or 2 may be admitted to the hospital, depending on the severity of their dyspnea, their ability to use accessory muscles, and their PEF values or FEV1 after treatment (>50% but <70% of predicted values). Patients with ABG determinations characteristic of stages 3 and 4 require admission to the ICU. The PEF value or FEV1 is less than 50% of the predicted value after treatment. Stage 1- Patients are not hypoxemic, but they are hyperventilating and have a normal PO2. - Data suggest that to possibly facilitate hospital discharge, these patients may benefit from ipratropium treatment via a handheld nebulizer in the emergency setting as an adjunct to beta-agonists. Stage 2- This stage is similar to stage 1, but patients are hyperventilating and hypoxemic. - Such patients may still be discharged from the emergency department, depending on their response to bronchodilator treatment, but will require systemic corticosteroids. Stage 3- These patients are generally ill and have a normal PCO2 due to respiratory muscle fatigue. Their PCO2 is considered a falsenormal value and is a very serious sign of fatigue that signals a need for expanded care. This is generally an indication for elective
  6. 6. intubation and mechanical ventilation, and these patients require admission to the ICU. - Parenteral corticosteroids are indicated, as is continued aggressive use of an inhaled beta2-adrenergic bronchodilator. - These patients may benefit from theophylline. Stage 4- This is a very serious stage in which the PO2 is low and the PCO2 is high, signifying respiratory failure. - These patients have less than 20% lung function or FEV1 and require intubation and mechanical ventilation. - Patients in stage 4 should be admitted to the ICU. Switching from inhaled beta-2 agonists and anticholinergics to metereddose inhalers (MDIs) via mechanical ventilator tubing is indicated. - Parenteral steroids are essential, and theophylline may be added, as with patients in stage 3. TreatmentBronchodilator treatment with beta-2 agonists - The first line of therapy is bronchodilator treatment with a beta-2 agonist, typically albuterol. - Handheld nebulizer treatments may be administered either continuously (10-15 mg/h) or by frequent timing (eg, q520min), depending on the severity of the bronchospasm. Nonselective beta-2 agonists - Patients whose bronchoconstriction is resistant to continuous handheld nebulizer treatments with traditional beta-2 agonists
  7. 7. may be candidates for nonselective beta-2 agonists (eg, epinephrine [0.3-0.5 mg] or terbutaline [0.25 mg]) administered subcutaneously Ipratropium treatment (anticholinergic, m-cholino blockers) - Ipratropium, which comes in premixed vials at 0.2%, can be synergistic with albuterol or other beta-2 agonists. - Ipratropium is administered every 4-6 hours. - Because children appear to have more cholinergic receptors, they are more responsive to parasympathetic stimulation than adults Oxygen monitoring - Monitoring the patient's oxygen saturation is essential during the initial treatment. - ABG values are usually used to assess hypercapnia during the patient's initial assessment. Oxygen therapy - Oxygen therapy is essential. It can be administered via a nasal canula or mask, although patients with dyspnea often do not like masks. - With the advent of pulse oximetry, oxygen therapy can be easily titrated to maintain the patient's oxygen saturation above 92% (>95% in pregnant patients or those with cardiac disease). Glucocorticosteroids
  8. 8. - Steroids are the most important treatment for status asthmaticus. - The usual dose is oral prednisone at 1-2 mg/kg/d. Aminophylline - Starting intravenous aminophylline may be reasonable in patients who do not respond to medical treatment with bronchodilators, oxygen, corticosteroids, and intravenous fluids within 24 hours. - The loading dose is usually 5-6 mg/kg, followed by a continuous infusion of 0.5-0.9 mg/kg/h. MedicationsBeta-adrenergic agonists- Relieve reversible bronchospasm by relaxing smooth muscles of the bronchi. Albuterol (Ventolin, Proventil)- Use for bronchospasms refractory to epinephrine. Relaxes bronchial smooth muscles by action on beta-2 receptors, with little effect on cardiac muscle contractility. PO: 2-4 mg PO tid/qid; not to exceed 32 mg/d Inhaler: 1-2 puffs q4-6h; not to exceed 12 puffs/d Nebulizer: Dilute 0.5 mL (2.5 mg) of 0.5% inhalation solution in 1-2.5 mL of NS; administer 2.5-5 mg q4-6h, diluted in 2-5 mL sterile saline or water. Levalbuterol (Xopenex)- Moderately selective beta2-receptor agonist. Active enantiomer of racemic albuterol and more potent than racemic mixture. Decreased occurrence of adverse effects may allow use of more frequent nebulizer therapy in patients with acute
  9. 9. asthma with less concern over adverse effects of other bronchodilators (eg, albuterol, metaproterenol). Adult- 0.63-1.25 mg nebulized q6-8h; may be given more frequently during emergent situations. Mast cell stabilizers- These agents prevent histamine release from mast cells following stimuli by specific antigens. Cromolyn (Intal)- Inhibits degranulation of sensitized mast cells following their exposure to specific antigens. Adult dose-Powder in caps for use with Spinhaler: 20 mg inhaled qid at regular intervals - MDI: 2 puffs (800 mcg/puff) qid at regular intervals - Nebulizer: 20 mg inhaled qid at regular intervals - Once patient is stabilized, use lowest effective dose Corticosteroids- Maintenance medications that decrease inflammatory mediators to limit airway remodeling. Must be taken regularly to be beneficial. Glucocorticoids do not relieve acute bronchospasm, and short-acting bronchodilators must be available. Multiple formulations are available that are not equivalent on a perdose or per-mcg basis. Inhaled corticosteroids are one of the most important developments in asthma management because they decrease inflammation. Methylprednisolone (Solu-Medrol)- Loading dose: 125-250 mg IV Maintenance dose: 4 mg/kg/d IV divided q4-6h. Bronchodilators- Act to decrease muscle tone in both small and large airways in lungs, thereby increasing ventilation. Theophylline (Aminophyllin)- Potentiates exogenous catecholamines and stimulates endogenous catecholamine release and
  10. 10. diaphragmatic muscular relaxation, which, in turn, stimulates bronchodilation. For bronchodilation, near toxic (>20 mg/dL) levels are usually required. 5.6 mg/kg loading dose (based on aminophylline) IV over 20 min, followed by maintenance infusion of 0.1-1.1 mg/kg/h Anticholinergics- Regarding magnesium sulfate, more studies have not confirmed the effectiveness of intravenous administration of this agent. Its use is still controversial. However, inhaled magnesium sulfate has generated some interest in status asthmaticus when combined with beta-agonist use. Ipratropium bromide (Atrovent)- Synthetic ammonium compound very structurally similar to atropine. May provide additive benefit to inhaled beta-2 agonists when treating severe acute asthma exacerbations. Also may be alternative bronchodilator for patients unable to tolerate inhaled beta-2 agonists. Children may be more responsive to parasympathetic inhibition than adults because children appear to have more cholinergic receptors. MDI: 2 puffs (18 mcg/puff) qid 500 mcg tid/qi Nebulizer: Magnesium sulphate- Magnesium sulfate intravenously has been advocated in the past for the treatment of acute asthma. Usually 1 g or a maximum of 2.5 g during the initiation of therapy may be considered. Adult- 1-2 g IV