ASTHMA EXACERBATION Chronic inflammatory disease of the airways that is characterized by increased responsiveness of the tracheobronchial tree to multiple

e stimuli leading to episodic reversible airflow obstruction. Clinical manifestations include COUGH, WHEEZING, and CHEST TIGHTNESS. Asthma is an episodic disease. Acute exacerbations are interspersed with symptom free periods. Most attacks are short lived, lasting minutes to hours. Some attacks may persist and become severe despite passage of time and medical intervention this is called Status Asthmaticus EPIDEMIOLOGY Asthma affects 7% of the population of the US and all industrialized nations. Asthma is the most common disease of childhood. Half of all cases of asthma are diagnosed prior to the age of 10. One third of all cases of asthma are diagnosed prior to the age of 40. Before the age of 10, asthma affects more boys than girls at a ratio of 2:1. By the age of 30, the ratio is 1:1. Despite seemingly improving treatment modalities, asthma is one of the few diseases that consistently increases in frequency, morbidity and mortality. Over the past two decades, the self reported prevalence of asthma has increased 75% and death rates increased 55%.. Idiosyncratic asthma no personal or family history of asthma. develop after a respiratory illness and last for days to months. Early onset strong allergic component. *later in life non-allergic or idiosyncratic. Allergic asthma is often associated with a personal and/or family history of allergic diseases such as rhinitis, urticaria, and eczema. Allergic asthma is associated with increased serum levels of IgE. ***** ATOPY LARGEST RISK FACTOR Pathophysiology The hallmark of asthma is a reduction in airway diameter caused by: Smooth muscle contraction/bronchoconstriction Vascular congestion Bronchial wall edema Thick secretions Decreased mucociliary clearance of secretions combined with the previously noted pathological findings leads to airflow obstruction. Airway inflammation may be acute, subacute, or chronic. The acute response is characterized by early recruitment of cells to the airway. Antigens come into contact with mast cells in the submucosa. PATHOPHYSIOLOGY SEQUENCE Allergen/Antigen is inhaled into the lung tissues, specifically the respiratory epithelium. In the lung, allergens trigger immune cells (B cells) to produce abnormal amounts of allergen specific defense proteins called IgE antibodies. The antibodies attach to mast cells in the submucosa. On repeat exposure to the antigen, IgE molecules cross link and mast cells degranulate. Mast cells release inflammatory mediators such as histamine, heparin, prostaglandin, leukotrienes, cytokines. These inflammatory mediators produce an intense inflammatory reaction resulting in: BRONCHOCONSTRICTION VASCULAR CONGESTION EDEMA FORMATION INCREASED MUCOUS PRODUCTION IMPAIRED MUCOCILIARY TRANSPORT Eosinophils, IgE are the dominant findings in an early asthma eacerbation. Later on, platelets, and polymorphonuclear leukocytes (neutrophils) are recruited to the site, activated, and contribute further to the inflammatory cycle that has already been inititated. This process is thought to be responsible for the late asthmatic response. EOSINOPHILS AND BASOPHILS are predominant in Asthma. Neutrophils contribute to the late (prolonged) asthmatic response. The reaction previously described typically begins within 10-30 minutes of inhalation of the offending antigens, peaks in 30 minutes and resolves in 3-4 hours. In patients who develop a late asthmatic response, the airway narrowing persists and either does not return to baseline or recurs after 3-4 hours. Pathophysiological Manifestations COUGH WHEEZING CHEST TIGHTNESS ASTHMA TRIGGERS Viral Infections (#1) Dust mites Cockroach Pollen, Trees Animal Dander Cigarette smoke Air pollution NSAIDS, ASA Beta Blockers Exercise Cold Air GERD Endocrine changes Shell fish Chemicals Historical Red Flags Risk Factors for SUDDEN DEATH: Prior intubation Prior ICU admit Prolonged attack Current use of steroids or recent withdrawal from oral steroids Prior history of severe attack >=2 hospitalizations in past year Hospitalization or ED visit in past month Use of >= 2 albuterol cannisters per month Comorbid illness COPD/CAD Illicit drug use Psychiatric disease Low socioeconomic status Poor perception of airflow obstruction Inconsistent/Non-compliant medical follow up PE findings VITALS are key!!! Possible PE findings include: Increased AP diameter Hyperresonance on percussion Wheezing

PE Red Flags Risks for SUDDEN DEATH: Patient tripod position Tachycardia > 120 Inability to speak in > 1-2 words Sternocleidomastoid retractions Diaphoresis AMS SILENT CHEST on exam Cyanosis Pulsus Paradoxus > 20 mmhg PEFR < 30% expected Diagnostics Peak Flow Meter Best, and most objective way to assess patient stability and improvement PULSE OXIMETRY Goal is Room Air saturation > 92% (Although patient is considered hypoxic when O2 sat falls below 95%.) ONLY ORDER CHEST XRAY IF: Fever Foreign body First episode of wheezing Focal lung exam Failure to improve ABG ONLY NEEDED IF PULSE OX IS BELOW 92% or patient fails to improve/decompensates with standard treatment TREATMENT of the Asthma Exacerbation O2 2-4L NC - Keep O2 above 92% Peak Flow Meter Assessment if patient can tolerate ALBUTEROL NEB (Q 20 min x 3 then Q 1-4 hours) ATROVENT NEB (Combined with 1st Albuterol Neb) CORTICOSTEROIDS used in all moderate and severe exacerbations. (PO prednsione or Solumedrol IV) (A moderate exacerbation is one in which the patient needs a second albuterol neb.) FREQUENTLY REASSESS PATIENT. BETWEEN EACH TREATMENT/NEB, check peak flow if possible and reexamine patient. Continues to DECOMPENSATE but still ALERT: Non invasive positive airway pressure BiPAP CPAP ABG Magnesium sulfate 1-2gm IV Heliox (80% helium and 20% O2) Terbutaline sulfate (.25mg SC) Epinephrine (SC) (in patients with no present or history of arrhythmias.) DECOMPENSATE and altered mental status: Mechanical ventilation (Ketamine as induction agent has a secondary side effect of bronchodilation) ADMISSION CRITERIA: Failure to improve ED visit for same within 3 days Comorbidity, i.e. coexisting pneumonia on CXR Hypoxia (O2 < 92%) Desaturation with ambulation Symptomatic patient with PEF < 70% of predicted or personal best or no improvement of at least 15% from initial peak flow assessment Discharge criteria: Improved with treatment Speaking in full sentences Ambulates in ED and does NOT drop O2 sat (No desaturation with exertion) The patient may be discharged from the hospital if the PEF or the patients personal best expiratory flow rate is 70% or more of predicted rate and if symptoms are minimal or absent. Patients who have mild symptoms but have PEF of 50-69% of predicted or personal best could be considered for discharge if high-risk factors for relapse are not present. Discharge with Albuterol and Steroids (Steroids are a must unless the patient completely cleared after only one Albuterol neb.) Patient Peak Expiratory Flow Rate improved > 15% of initial value Patient has appropriate follow up. Discharge Plan: Patient education regarding Asthma Triggers Provide follow up instructions - follow up appointment with Primary Care Provider and instructions to return to ED immediately if symptoms return or worsen. Patient education regarding importance of routine Peak Flow Meter use/assessments. Provide prescriptions for Albuterol and Steroid MDIs as well as education regarding MDIs. (Steroid MDIs, like Flovent, while not used in treating the acute asthma exacerbation may prevent future exacerbations if used properly.) Provide prescription for short course of oral steroids in all but the mildest of exacerbations. (I.e., Prednisone 40-60mg qd x 5 days.)