An asthmatic attack refractory to two treatments with inhaled or parenteral sympathomimetics is defined as status asthmaticus.
PHYSIOLOGY OF AN ASTHMATIC ATTACK
In an appropriate host, a variety of insults (viral infections, exercise, cold air, immunologie reactions, and psychological stress) result in edema, mucous plugging, and smooth muscle spasm of the airway. Physiologically, this results in an obstructive defect consisting of an elevated functional residual capacity (FRC), residual volume (RV), and total lung capacity (TLC) as demonstrated in Figure 1. Presumably this is a result of the patient's attempt to tether open the airways and thus overcome the obstruction (Figure 2). To do this the patient creates unusually negative pleural pressures1 as well as possibly closing the vocal cords in an attempt at self peeping.2 If the elevated lung volume cannot be maintained (administration of sedatives, for example), airway narrowing occurs with a concomitant elevation in airway resistance and work of breathing. This obstructive defect leads to a ventilation/profusion mismatch resulting in hypoxemia and eventual carbon dioxide retention as illustrated in Figure 3.3 In childhood these changes are usually reversible.
Acute asthmatic attacks are so prevalent and Have such a characteristic appearance that the physician often forgets to consider other diagnoses which may be confused with it. The conditions cited in Table 1 may all superficially resemble them. Asking the question "Is this child's history, physical examination, and response to therapy typical of an acute asthmatic attack?" will allow the physician to decide if further diagnostic workup is warranted.
The following information should be obtained:
1. Historical Data
Is a child known to have asthma? Is this typical oí this patients attack? If not, why not?
What medication(s) is the patient taking? How much? By what route? When? Has the child vomited the medication?
Has the child been on steroids during the past year?
Does the child have any other significant medical condition (s)?
2. Physical Examination
A brief physical examination is directed toward physiologic assessment as well as ruling out other medical conditions. One should note: 1) mental status, 2) color, 3) use of accessory muscles, 4) quality of inspiratory breath sounds, and 5) vital signs including the measurement pulses paradoxus. Pulsus paradoxiis is the difference between systolic pressure on inspiration and expiration. Levels of >20 mmHg correlate with carbon dioxide retention.4
3. Measurement of Air Flow
An objective measurement of obstruction to air flow and response to treatment should be performed in patients who are able to cooperate. Peak flow rates are simple and sensitive enough for this purpose. Generally a self-contained meter measuring air flow in liters per minute is used. The patient's flow is compared to the expected values based on height. These measurements are significantly more accurate than physical assessment.
FIgure 1. Status asthmaticus results in patients breathing at high lung volumes with decreased expiratory flow rates.
FIgure 2. Forces hoiding open the airways during an asthmatic attack.
FIgure 3. Gas exchange abnormalities associated with status asthmaticus.3
4. Arterial Blood Gas
The arterial blood gas taken in room air is the "bottom line" indicating how the patient is doing. These are particularly helpful if he or she is unable to perform a peak flow measurement. The sequence of changes are discussed above.
5. Radiographie Evaluation
Radiographie evaluation is rarely helpful unless one is led to suspect another condition.
Treatment is based on the severity of the episode, previous therapy, and response to therapy.
Oxygen. Infants and children in status asthmaticus should be given oxygen since they are hypoxemic in room air. Treatment with sympathomimetics and theophylline transiently increases the ventilation to profusion mismatch and thus causes a further decrease in oxygenation.
Fluids. These children are often dehydrated due to decreased fluid intake and increased metabolism. Although generous rehydration was widely practiced in the past, the awareness of a tendency toward pulmonary edema secondary to unusually negative intrathoracic pressures5 has resulted in a somewhat more cautious rehydration program. In fact, if not clinically dehydrated, we generally recommend that fluids be given at a maintenance level.
Sympathomimetics (Table 2). These are the most rapid acting and effective agents currently available for the treatment of an acute attack. By and large the inhaled route is as effective and is better tolerated than parenteral administration.6 Furthermore, compared with theophylline, these agents work more rapidly and effectively. Several studies have compared the efficacy of epinephrine injections vs. inhalation of isoproterenol or metaproterenol and concluded that inhaled medications work more effectively and are longer lasting than the epinephrine shots.7'8 They are clearly better tolerated by children and are probably safer.
Theophylline (Table 2). Theophylline is a bronchodilator and has recently been recognized as an agent which enhances diaphragmmatic contractility.9 It does not work quite as rapidly as do the sympathomimetics. Although there has been evidence that a therapeutic level of theophylline coupled with sympathomitnetic treatment is more effective than sympathomimetics alone, this widely accepted belief has recently been questioned. ~,I1 Until more data are available, the author continues to use both.
Steroids (Table 2). The role of steroids in acute asthma is debated. Literature can be found to support or refute their use during an acute attack. 1213 They may play a role in shortening the period of morbidity during an attack. There is general agreement that patients who are currently on steroids (either orally or by inhalation), have been taking these medications in the past 6 months, or who are seriously ill (carbon dioxide retention) should receive them. The current economic pressure to shorten hospitalization is undoubtedly increasing their use.
Antibiotics. Viral and Mycoplasnia infections have been convincingly demonstrated to precipitate asthmatic attacks. Standard bacterial infections do not. Therefore, antibiotic therapy offers no real advantage unless one has reason to suspect a Mycoplasma infection. If so, erythromycin is the drug of choice. Theophylline levels should be monitored when using erythromycin since it may slow the metabolism of methylxanthines.
TREATMENT OF SEVERE OR PROGRESS WE RESPIRATORY INSUFFICIENCY
The hallmarks of respiratory insufficiency are change in mental status, sweating, increasing pulsus paradoxus, and decreasing inspiratory breath sounds. Confirmation is demonstrated by carbon dioxide retention. Treatment includes continuous administration of sympathomimetics by intravenous route or by continuous inhalation. Progressive respiratory failure is treated by mechanical ventilation. Under extreme circumstances inhalational anesthetic agents have been used.14
DRUGS FOR THE TREATMENT OF STATUS ASTHIMATICUS
Complications in well-treated status asthmaticus are rare. Younger children often are found to have patchy areas of atelectasis which resolves with time. Older children commonly develop a pneumomediastinum which is generally self-limited. On rare occasions one will see a pneumothorax.
The vast majority of pediatrie patients arriving at the hospital in status asthmaticus do well. Under 5% need intravenous sympathomimetics and/or mechanical ventilation. Death from childhood asthma is rare. It is usually found in the setting of lack of recognition of the severity of the obstruction by the patient (and family) and/or the physician. Withholding steroids may also contribute to some of these deaths.15,16
PREVENTION OF STATUS ASTHMATICUS
Skillful medical care will prevent status asthmaticus in the vast majority of children. In the 1980s, one should rarely need to admit children with this condition. However, the shocking fact is that almost 100,000 children a year are still discharged from hospitals with this diagnosis.
1. Permount Physiologic changes in (ht acute asthmatic attack, in Annen KF. Lkhlemttin LM (ed): Asuana: Physiologic immunaplianiucalofl and Treatment. AcaJemk Press. New Yotk, |97). pp 15-27.
2. Collen PW. Branca! isano T. Enge) LA: Changes in the glottic aperture during bronchial asihma. Am Rn Reifto Du 1983; 128:719-723.
3. McFadden ERJr, Lyons HA: Arterial blood gas tension in asthma. N Engt} Mtd 1968; 278:1027-1032.
4. Calant SP. GroncyCE. Shaw KC: THe valúe of pu bus paradoxus m aucuin« the child with status asthmaticus. Romanics 1978:61:46-51.
5. Sralcup SA. Melìins RB: Mechanical forces producing pulmonary edema in acute asthma. N En¿i Med 1977; 297:592-595.
6. Becker AB, et al; Inhaled salbutantol (aibuteiol) vs. injected epmephrine in the treatment of acute asthma in children. } fítdiaa 1983; 102:465-469.
7. Ben -Z v i Z. Lam C. Spohn WA. et al: An evaluation of repealed injections without epinephnne for the initial treatment of asthma. Am Rev Reipir Dis 1983; 127:101-105.
8. Ben-Zvi Z. Lam C, Hoffman ], et al: An evaluation of the initial treatment of acute asthma. Efeduirici 1982; 70:348-353.
9. Aubier M. DeTroyer A, Sampson M. et al: Ammophvlline improves diaphragmatic contractility. N EflíU Med 1981; 305:249-252.
10. Rossing TH. Fants CH, McFadden ERJr. et al: A con t toi ted trial oí the use of single versus, combined dtug therapy in the treatment of acute episodes oí asthma. Am Rev RespírDií I981; 123:190-194.
11. Siegel D. Sheppard D. Gelb A. et al: Ammophylline increases the toxiciry hut not eftcacy of an inhaled beta-athenergic agonist in the treannem of acute exacerbations of asthma. Am Rt* Resprr Du 1985; 132:233-286.
12. Pierson WE. Bierman CW, Kelley VC: A double-blind trial of air r icos te roid therapy in status asthmaticus. ftdiarrici 1974: 54:282-288.
13. Kattan M, Gurwitf D, Levison H: Corticosteroidi m status asthmaticm. ] ItJiarr 1980; 96:596-599.
14. O'Rourke PP, Crone RK: Habthane in status asthmalicus. Cm Cure Moi 1982; 10:)41-343.
15. Kravits LP1 KcMi GB: Unexpected deatb m childhood asthma. Am J Do CbId 1985; 139:558-563.
16. Strunk RC. Mraiek DA, Fuhrmann GS, et al: Physiologie and psychological characteristics associated with deaths due tc asihma in childhood: A case -con trolled study. JAMA 1985; 254:1193-1198.
DRUGS FOR THE TREATMENT OF STATUS ASTHIMATICUS