Severe Asthma Attack

Severe Asthma Attack - Uncontrolled asthma, with its inherent variability, can progress to an acute state where inflammation, airways edema, excessive accumulation of mucus, and severe bronchospasm result in a profound airways narrowing that is poorly responsive to usual bronchodilator therapy (see Clinical Presentation: Severe Acute Asthma). Although this progression is the most common scenario, some patients experience rapid onset or hyperacute attacks.

Hyperacute attacks are associated with neutrophilic as opposed to eosinophilic infiltration and resolve rapidly with bronchodilator therapy, suggesting that smooth muscle spasm is the major pathogenic mechanism. In most cases, emergency department visits for severe acute asthma represent the failure of an adequate therapeutic regimen for persistent asthma. Underuse of antiinflammatory drugs and excessive reliance on short-acting inhaled β2-agonists are the major risk factors for severe exacerbations. A blunted perception of airway obstruction may predispose certain individuals to fatal asthma attacks.

Clinical Presentation

General

■ An episode can progress over several days or hours (usual scenario) or can progress rapidly over 1 to 2 hours.

Symptoms

■ The patient is anxious in acute distress and complains of severe dyspnea, shortness of breath, chest tightness, or burning. The patient is only able to say a few words with each breath. Symptoms are unresponsive to usual measures (inhaled shortacting β2-agonist administration).

Signs

■ Signs include expiratory and inspiratory wheezing on auscultation (breath sounds may be diminished with very severe obstruction), dry hacking cough, tachypnea, tachycardia, pale or cyanotic skin, hyperinflated chest with intercostal and supraclavicular retractions, and hypoxic seizures if very severe.

Laboratory

■ PEF and/or FEV1 less than 50% of normal predicted values. Decreased arterial oxygen (PaO2), and O2 saturations by pulse oximetry (SaO2 less than 90% on room air is severe). Decreased arterial or capillary CO2 if mild, but in the normal range or increased in moderate to severe obstruction.

Other Diagnostic Tests

■ Blood gases to assess metabolic acidosis (lactic acidosis) in severe obstruction. Complete blood count if there are signs of infection (fever and purulent sputum). Serum electrolytes as therapy with β2-agonist and corticosteroids can lower serum potassium and magnesium and increase glucose.Chest radiograph if signs of consolidation on auscultation.

Factors Contributing to Asthma Severity

Viral Respiratory Infections

Viral respiratory infections are primarily responsible for exacerbations of asthma, particularly in children younger than age 10 years. Infants are particularly susceptible to airways obstruction and wheezing with viral infections because of their small airways. The most common cause of exacerbations in both children and adults is the common rhinovirus. Other viruses isolated include respiratory syncytial virus, parainfluenza virus, coronavirus, and influenza viruses. The inflammatory response to viral infection is thought to be associated directly with the increasing BHR. Certain viruses (respiratory syncytial virus and parainfluenza virus) are capable of inducing specific IgE antibodies, and rhinovirus can activate eosinophils directly in asthmatics.

The increase in asthma symptoms and BHR that occurs may last for days or weeks following resolution of the symptoms of the viral infection. Recent evidence does not support a beneficial effect of influenza vaccine for preventing asthma exacerbations from subsequent influenza infections.

Envirenmental And Occupational

Table below lists the agents, events, and mechanisms that are known to trigger asthma. The general mechanisms are unknown but presumably are the result of epithelial damage and inflammation in the airway mucosa. Ozone and sulfur dioxide, common components of air pollution, have been used to induce BHR in animals. Exposure to 0.2 parts per million ozone for 2 to 3 hours can induce bronchoconstriction and increase BHR in asthmatics. Sulfur dioxide in the ambient atmosphere is highly irritating. It presumably induces bronchoconstriction through mast cell or irritantreceptor involvement. 

Asthma produced by repeated prolonged exposure to industrial inhalants is a significant health problem. It has been estimated that occupational asthma accounts for 2% of all asthmatic persons. Persons with occupational asthma have the typical symptoms of asthma with cough, dyspnea, and wheeze. Typically, the symptoms are related to work and improve on weekends and during vacations. In some instances, symptoms may persist even after termination of exposure.

Stress, Depression, And Psychosocial

Observational studies demonstrate an association between increased stress and worsening asthma, but the role is not clearly defined. Bronchoconstriction from psychological factors appears to be mediated primarily through excess parasympathetic input. Atropine has been shown to block experimental psychogenic bronchoconstriction. It is most important to emphasize to both patients and parents that asthma is not an emotional disease; however, coping skills may benefit the patient who becomes emotionally distraught during an asthma attack.

Rhinitis And Sinusitis

Disorders of the upper respiratory tract, particularly rhinitis and sinusitis, have been linked with asthma for many years. As many as 40% to 50% of asthmatics have abnormal sinus radiographs. However, chronic sinusitis may just represent a nonbacterial coexisting condition with allergic asthmatics because the histologic changes in the paranasal sinuses are similar to those seen in the lung and nose. Treatment of upper airway disease may optimize overall asthma control. The mechanism by which sinusitis aggravates asthma is unknown. The treatment of allergic rhinitis with inhaled corticosteroids and cromolyn but not antihistamines will reduce BHR in asthmatic patients. It has been postulated that transport of mucus chemotactic factors and inflammatory mediators from nasal passages during allergic rhinitis into the lung may accentuate BHR.

Gastroesophageal Reflux Disease

Symptoms of gastroesophageal reflux disease are common in both children and adults who have asthma. Nocturnal asthma may be associated with nighttime reflux. Reflux of acidic gastric contents into the esophagus is thought to initiate a vagally mediated reflex bronchoconstriction. Also of concern is that most medications that decrease airways smooth muscle tone also have a relaxant effect on gastroesophageal sphincter tone. Although a systematic review concluded there was no significant improvement in asthma symptoms from medical management of gastroesophageal reflux disease, the standard approach is to initiate standard antireflux therapy in those patients who are exhibiting symptoms of reflux (particularly with nocturnal asthma) and observe the asthma symptoms.

Female Hormones And Asthma

Premenstrual worsening of asthma has been reported in as many as 30% to 40% of women in some studies, whereas worsening of pulmonary functions has been reported even in women who are unaware of worsening symptoms. The pathophysiology is uncertain because estrogen replacement in postmenopausal women worsens asthma, whereas estradiol and progesterone administration have been variably reported to improve or have no effect on asthma in women with premenstrual asthma. The clinical significance of menstruation-related asthma is still unclear because some studies report that up to 50% of emergency department visits by women were premenstrual, whereas others report no association with menstrual phase. Studies indicate that, in general, BHR and symptoms improve in asthmatics during pregnancy.

Treatment

The primary goal is prevention of life-threatening asthma by early recognition of signs of deterioration and early intervention. As such, the principal goals of treatment include

• Correction of significant hypoxemia.

• Rapid reversal of airflow obstruction

• Reduction of the likelihood of relapse of the exacerbation or future recurrence of severe airflow obstruction

• Development of a written asthma action plan in case of a further exacerbation

These goals are best achieved by early initiation or intensification of treatment and close monitoring of objective measures of oxygen-ation and lung function. Early response to treatment as measured by the improvement in FEV1 at 30 minutes following inhaled β2-agonists is the best predictor of outcome. Providing adequate oxygen supplementation to maintain oxygen (O2) saturations above 90% (or above 95% in pregnant women and those who have coexistent heart disease) is essential. In children younger than 6 years of age, in whom lung function measures are difficult to obtain, a combination of objective (e.g., oxygen saturation, capillary CO2, respiratory rate, and heart rate) and subjective measures may be used to assess severity.

Salam

by Umaee

Severe Asthma Attack

Source: Pharmacotherapy 7th

Image: babble.com

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