الصفحة الرئيسية

من نحن

الأقسام

المجلة الطبية

موقع الوزارة

راسلنا

الأرشيف

 

In-Hospital Management of Acute Asthma.

All patients with asthma are at risk of developing exacerbations characterized by a progressive increase in shortness of breath, cough, wheezing or chest tightness, and by a decrease in expiratory airflow. The severity of exacerbations may range from mild to near-fatal, and deterioration usually progresses over hours, days, or weeks; however, a few patients develop sudden (over minutes) and unexpected increases in airway obstruction.

Progressive airway narrowing, due to airway inflammation and/or increased bronchiolar smooth-muscle tone, is the hallmark of an asthma attack and leads to (1) increased flow resistance; (2) pulmonary hyperinflation; and (3) ventilation/perfusion mismatching.

Without correction of the airway obstruction, respiratory failure is a consequence of increased work of breathing, gas exchange inefficiency, and respiratory muscle exhaustion. The combination of acute hypercapnia and high intrathoracic pressures can produce a significant rise in intracranial pressure and neurologic signs, such as unilateral or bilateral mydriasis, quadriparesis, and subarachnoid and subconjunctival hemorrhages during an acute episode (Fig 1).

 

 

 

 

Figure 1. A 35-year-old white man with severe exacerbation of asthma. After 2 days of progressive bronchospasm, he received medical treatment (high doses of inhaled β-agonists) at his home by an emergency medical service. After this treatment, his condition showed an improvement, and he was admitted to an ICU to continue treatment. A few hours after admission, he presented bipalpebral hematomas (left), along with subconjunctival hemorrhages (right).

When airway inflammation is predominant, patients show a progressive (over many hours, days, or even weeks) clinical and functional deterioration (type 1 or slow-onset acute asthma) (Table 1).

In the less common asthma progression scenario, bronchospasm is predominant and patients presented with a sudden-onset asthma attack (type 2 or asphyxic orhyperacuteasthma). Surprisingly, these patients show a more rapid and complete response to treatment.

Table 1 Main Characteristics of Patients With Acute Asthma and Sudden or Slow-Evolution*

Type 1. Slow-progression

Type 2. Sudden-progression

Slow-onset acute asthma

Sudden-onset, asphyxic, brittle or hyperacute asthma

Progressive deterioration: >6 h
(usually days or weeks)

Rapid deterioration: <6 h

80 to 90% of patients who presented to an ED

10 to 20% of patients who presented to an ED

Female predominance

Male predominance

More likely to be triggered by upper-respiratory infections

More likely to be triggered by respiratory allergens, exercise, and psychosocial stress

Less severe obstruction at presentation

More severe obstruction at presentation

Slow response to treatment and higher hospital admissions

Rapid response to treatment and lower hospital admissions

Airflow inflammation mechanism

Bronchospastic mechanism of deterioration

 

Fatal Asthma

Death occurs typically in patients with a poorly controlled disease, and the condition gradually deteriorates over a period of days, or even weeks, before the fatal attack.

Infrequently, death occurs in a sudden fashion. Previous ventilatory assistance, admission to an ICU, and a history of recurrent hospitalizations are the most specific markers associated with an increased risk of dying from asthma. Nevertheless, <40% of fatal cases have these risk factors. Data suggest that it is very uncommon to die without substantial luminal obstruction.

Therefore, the most probable cause of death is asphyxia, due to severe limitation of airflow and hypoxemia. Smooth muscle contraction and production of inflammatory mucus exudates are important mechanisms for fatal attacks in young and old individuals with asthma.

Assessment

The assessment of an episode of asthma exacerbation has two different dimensions: (1) a static assessment to determine the severity of attack; and (2) a dynamic assessment to evaluate the response to treatment (Table 2).

The severity of airflow obstruction cannot be accurately judged by means of symptoms and physical examination. Only 15% of patients with acute severe asthma have tachycardia (>120 beats/min), and <20% show tachypnea (respiratory rate >30 breaths/min).

The presence of wheeze and dyspnea correlated poorly with the degree of airflow limitation, and pulsus paradoxus has been abandoned as an indicator of severity, because it is frequently difficult to measure.

On the contrary, the presence of sternocleidomastoid or suprasternal retractions correlate with impairment in lung function and can be considered a useful sign of severe airflow obstruction.

Table 2 Main Dimensions of the Assessment of the Adult Patient With Acute Asthma in the ED*

Dimensions

Meaning
Static assessment:
  • Accessory muscle use

  • Spirometry (PEFR or FEV1)

  • Pulse oximetry (Spo2)

Severity of attack (determines intensity of treatment)
  • Sign of severe airflow obstruction

  • Objective assessment of airflow obstruction
    (<50% of predicted = severe attack)

Determination of hypoxemia level (goal of treatment ≥92%)

Dynamic assessment
  • Serial measurements of lung function (PEFR or FEV1), each 30 min

  • Continuous Spo2 monitoring

Response of treatment (treatment guide and outcome prediction)
  • Variation from baseline
    (PEFR >50 L/min and >40%, at 30 min, are predictors of good outcome)

Achieving and keeping target Spo2 ≥92%

 

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Dr: Shaban mourtaga

Msc. ENT

 

  وزارة الصحة - مركز المعلومات - قسم النشر الالكتروني - 2005