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Allergol Immunopathol (Madr) · Mar 1999
Review[Round Table: Severe asthma in pediatrics: treatment of acute crises].
- J M García Martínez.
- Sección de Alergia e Inmunología, Departamento de Pediatría, Hospital de Cruces, Baracaldo, Vizcaya, España.
- Allergol Immunopathol (Madr). 1999 Mar 1;27(2):53-62.
AbstractMorbidity and mortality derived from asthma continue to be a main public health problem in many countries, in spite of the advances in the knowledge on the disease and its treatment. There are several risk factors for asthma attack which have to be considered in the management of patients in order to prevent exacerbations and mortality. Smooth bronchial muscle constriction and inflammation with oedema of the bronchial wall are the facts that cause airway flow and resistance disturbances, with hyperinflation, leading to a bigger respiratory work. On the other hand, the bronchial obstruction leads to a ventilation-perfusion disequilibrium and hypoxia. At the beginning of the process there is hypocarbia, but when the attack progresses muscle fatigue happens, and retention of CO2, being a sing of alarm (predictive of respiratory failure) a normal and rising PaCO2. The evaluation of an acute asthmatic patient should accomplish a clinical and objective assessment (peak flow rate and saturation of O2), in order to classify the crisis in: mild, moderate or severe. Managing acute asthmatic patient includes: oxygen, bronchodilator ss2 agonists at high and even continuous doses and systemic corticosteroids to prevent the progression and to control inflammation. These procedures should be promptly instituted. Although there is less evidence on their beneficial effects other measures as intravenous aminophylline, nebulized anticholynergics, magnesium sulphate and intravenous ss2 agonists may be used when the conventional therapy is not quickly successful and the patient is in a critical situation, at a real risk of respiratory failure, and in order to avoid mechanical ventilation. If this is finally instituted, controlled hypoventilation with permissive hypercarbia is now recommended, to avoid barotrauma, which used to be a frequent complication when more aggressive attitude was the rule. Interaction between paralytic agents and corticosteroids may produce a miopathy, so the recommendation now is to try not to use paralytic agents, even with profound sedation of needed. Sixty four patients were treated on 77 occasions in the Pediatric Intensive Care Unit of our hospital. They were 0,5 to 13,9 years old, being 50% less than 5 years old. It was the first attack in 9 (14%) patients. The standard management consisted of oxygen, frequently or continuously nebulized salbutamol and intravenous methylprednisolone (1 to 6 mg/kg/day). Furthermore nebulized ipratropium bromide was administered 58 times (75%), as well as intravenous aminophylline 69 (89%), intravenous salbutamol 23 (30%), magnesium sulphate 16 (21%) and ketamine 10 (13%). Antibiotics were given 22 times (29%). Two 15 month old infants received mechanical ventilation in three occasions, and relevant complications happened (pneumothorax and myopathy, and pneumomediastinum and bronchiolitis obliterans respectively). Fifty six patients have been followed for a period of 3 to 110 months (median 48 months), and 16 (29%) have needed high doses (equal to or move than 800 mcg of budesonide or equivalent). There are data on lung function in 36 of them, FEV1 is normal (> 85% of predicted, between 86 and 127) in 26 (78%) and < 85% (65 to 84%) of predicted in 8 (22%) FEV1 rises more than 15% (16 to 23%) in four patients after the inhalation of a ss2 agonist. Inhaled anesthetic agents and heliox have been used in some pediatric cases. After a severe asthma attack the strategy of management should be reviewed, as well as the possible risk factors.
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