Status Asthmatic Us

STATUS ASTHMATICUS Introduction -Status asthmaticus is an acute exacerbation of asthma that remains unresponsive to initial treatment with bronchodilators. -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. Pathophysiology -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 crossbridging 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. -These mediators cause:  Bronchial smooth muscle constriction  Vascular leakage

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Inflammatory cell recruitment (with further mediator release)  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. -Physiologically, asthma has 2 components: an early acute bronchospastic aspect marked by smooth muscle bronchoconstriction and a later inflammatory component resulting in airway swelling and edema. Early bronchospastic response Mediators, including histamine, prostaglandin D2, and leukotriene C4. These substances cause airway smooth muscle contraction, increased capillary permeability, mucus secretion, and activation of neuronal reflexes. Early asthmatic response is characterized by bronchoconstriction that is generally responsive to bronchodilators, such as beta2-agonist agents

Clinical presentation History -The symptoms of asthma consist of a triad of  Dyspnea  Cough

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wheezing  Chest tightness -Wheezing regarded as the sine qua non for asthma. -Cough is non productive initially then thick sputum later - Personal or family history of allergic diseases such as eczema, rhinitis, or urticaria is valuable contributory evidence.

Late inflammatory response Release of inflammatory mediators prime adhesion molecules in the airway epithelium and capillary endothelium, which then allows inflammatory cells, such as eosinophils, neutrophils, and basophils, to attach to the epithelium and endothelium and subsequently migrate into the tissues of the airway. Eosinophils release eosinophilic cationic protein (ECP) and major basic protein (MBP). Both ECP and MBP induce desquamation of the airway epithelium and expose nerve endings. This interaction promotes further airway hyperresponsiveness in asthma. The 2 phases of asthma lead to:

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increased airway resistance and obstruction. Air trapping results in lung hyperinflation Ventilation/perfusion (V/Q) mismatch Increased dead space ventilation.

Decreased compliance and increased work of breathing. -The increased pleural and intra-alveolar pressures that result from obstruction and hyperinflation, together with the mechanical forces of the distended alveoli, eventually lead to a decrease in alveolar perfusion. -The combination of atelectasis and decreased perfusion leads to V/Q mismatch within lung units. The V/Q mismatch and resultant hypoxemia trigger an increase in minute ventilation. The early stages of acute asthma, hyperventilation may result in respiratory alkalosis but later respiratory acidosis occurs V/Q mismatch. Sex: In infants, males generally have more severe disease than females. In older children, males and females are equally affected. Asthma has a higher incidence among adult females. Age: Asthma is well distributed among people of all age groups. Children who have asthma in the first year of life and those aged 9-16 years tend to have much more severe disease. DDx -Pulmonary Hypertension, Primary -Congestive heart failure- Orthopnea, moist basilar rales, gallop rhythms, blood-tinged sputum -Croup -Stridor -Upper airway obstruction -Foreign-body aspiration -Neoplasm -Bronchial stenosis. -Recurrent episodes of bronchospasm can occur with carcinoid tumors -Recurrent pulmonary emboli - Chronic bronchitis - Eosinophilic pneumonias are often associated with asthmatic symptoms, as are various chemical pneumonias and exposures to insecticides and cholinergic drugs. -Bronchospasm occasionally is a manifestation of systemic vasculitis with pulmonary involvement.

INVESTIGATIONS 1-Spirometry -The diagnosis of asthma is established by demonstrating reversible airway obstruction. -The evaluation for asthma should include spirometry (FEV1, FVC, FEV1/FVC) before and after the administration of a short-acting bronchodilator. -Reversibility is traditionally defined as a 15% or greater increase in FEV1 after two puffs of a badrenergic agonist -In severe airflow obstruction with significant air