asthma attack treatment
Treatment of acute asthma attacks
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| asthma attack |
The cause of acute attack
The cause of acute onset is frequent viral upper / lower respiratory tract infections and intense allergen exposure. In addition, long-term treatment and follow-up of the cases may cause partial partial disruption of treatment. In addition, exposure to intense air pollution, cigarette smoke, rapid atmospheric, or environmental air changes can also trigger an episode. Children with moderate and severe persisting asthma, those who have had severe and life-threatening episodes of previous episodes, those with more than 2 episodes of emergency room and hospital admission in the last year, children who need frequent short-term use, high-dose inhaled steroids, systemic steroids, patients with treatment and follow-up problems are at high risk for acute attack.
Determination of severity of acute attack
The most effective factor on mortality and morbidity in acute attack is to accurately determine the severity of the attack and to draw an appropriate and effective treatment plan accordingly. In the determination of the severity of the attack, arterial oxygenation parameters are used, if possible, with the symptoms of the animal, physical examination findings, respiratory function tests. Attacks should be classified as mild, moderate, severe (severe) and life-threatening. In Table 1, a modified classification is given.Symptoms; "General condition" is normal in mild attack, it is seen as restless-agitated in moderate and severe attack, irrit and confi in case of life-threatening attack. "Speech" is normal in mild attacks, while in middle attacks speaks a few words and in severe attacks speaks intermittently. "Dyspnea" is the most important symptom and is seen only in exacerbation in mild agitation, in middle agility, and in severe agility, it is even followed. Disclosure of dyspnea for young children may be short crying, feeding refusal, vomiting and intermittent speech in a mild attack, or orthopnea position in a severe attack.
Physical examination findings; are basically indirect lesions associated with respiratory distress and are characterized by the weight of the lung.
I. The respiratory rate has increased (tachypnea). Because the resulting bronchospasm has caused hypoxia, the initial physiological response to it is tachycardia and tachypnea. There is also a slight attack, but obvious tachypnea may not be observed. However, in the middle attack there is a pronounced, severe attack and very severe tachypnea is observed. If a life-threatening collision is taking place, if a very severe tachypnea lasts for a long time, a surface that is tied to fatigue and decline in central sensitivity may become sickened. However, when evaluating astigmatism, it is absolutely necessary to consider the values of normal respiration according to the ages in children. The Tashipne border should be taken between 40 and 60 minutes between the ages of 1-5 and 30 / min over the age of 6 years.
ii. Heart rate, mild exacerbation heart rate is normal. However, there is marked tachycardia in the severe attack, with fewer in the middle attack. In severe attacks, myocardium is prolonged due to prolonged and severe hypoxia, and malnutrition and bracardia are observed at His level. For children, the limit of tachycardia should be 120 / min at 1-2 years and 110 / min over 2 years.
iii. Use of assisted respiratory muscles and withdrawals are more pronounced and more frequent in early age groups. Although it is not seen in mild attacks, it is frequently observed in the middle attack, and in severe attacks it is present in the whole. First, nasal airway breathing and suprasternal withdrawal, then lower intercostal, then upper intercostal, and most recent subcostal withdrawal weight gain. In life-threatening episodes, thoracoabdominal paradoxical respiration is observed.
iv. The wheezing sensation in the aquaculture is equal to the inspiration in the exhilaration expiration in the mild exacerbation. There is a pronounced severe exacerbation of the central ataxia, and very intense inspiration and expiration of the extreme atrophy and wheezing. This is also apparent from the outside in the case of a moderate attack and a severe attack. In a life-threatening attack, a silent lung is followed. However, complications of acute ataxia should also be considered when auscultation is performed. In a severe life-threatening episode, you may develop atelectasis somewhere else in the right middle lobe, where breathing sounds may be reduced. Yada mediastinum can develop epiphytic infections, subcutaneous emphysema.
vi. Pulsus paradoxus is not observed in mild agitation (<10 mmHg). 20-20 mmHg in the middle attack, 10-20 mmHg in the severe attack, and not in the life threatening attack (Figure 1).
Functional evaluations; It is used to show the obstruction of expiration and to determine the state of oxygenation.
I. PEF is a simple instrument that can be used very easily in the emergency room, office and clinical monitoring of the expiratory peak flow rate. At the end of the measurement, the expiratory peak flow rate is determined as l / min and correlated with the medium and small air flow rate. If done properly and the child's compliance is as valuable as FEV1. The values below 80%, 50-80% and 50% in the case of mild attack are observed. However, in order to obtain these results it is necessary to use the normal values according to age, height and weight, but much more ideally the child's previous stable PEF value.
ii. SatO2 is quite easy to do with a percutaneous pulse oximeter. It is over 95% in light attack. It is 91-95% in the middle attack and <91% in the severe attack.
iii. PaO2 is not routinely used except for severe and life-threatening attacks. Mild attack is normal, 60-80% in middle attack, <60% in severe attack.
iv. PaCO2 is also routinely unavailable. In mild and moderate attacks <42 mmHg, but in severe attacks> 42 mmHg. Above this value is a very important stimulant for the initiation of respiratory failure in a child with asthma.Acute Attack Treatment
Since the cause of acute attack is acute bronchospasm and / or varying degrees of hypoxia caused by an inflammatory response, the most basic in acute attack treatment is the premature termination of this bronchospasm and suppression of inflammation. Because bronchospasm leads to hypoxia, which triggers bronchospasm, bronchodilatation must first be achieved and hypoxia should be relieved. For this reason, epileptic treatment starts at home.
Attack treatment at home; where the child's findings are felt by the family and if PEF can be measured, 2-4 doses of PED salbutamol are taken first, followed by 0.15 mg / kg of nebulized doses. If complete recovery and PEF is 80%, the doctor will tell you about 24-48 hours inhale salbutamole. However, if the PEF is 60-80% and there is a partial reduction in the findings, continue to salbutamole and take oral steroids (0.5 -1 mg / kg) to the emergency department. If PEF is <60% and severe findings, take salbutamol and steroids and apply immediately.
The treatment plan should be planned according to this severity after the severity of the attack is determined in the emergency department or hospital. However, it should be remembered that when this plan is made, it is observed that the end of the anatomy is terminated with frequent evaluations, but it should be remembered that the implant may become more severe and it may be necessary to go to the upper treatment line. For this reason, a milk step can be passed in the instant assessment of the patient.
In light attacks; the most important first step in a child is to achieve a rapid bronchodilatation. If the patient does not have an increase in exacerbation, the three-nebulisation salbutamol 0.15 mg / kg / dose (maximum 2.5 mg / dose), which is often given at 20-minute intervals, is sufficient. This can be repeated after 2 hours. If there is no nebuliser, the attack can be terminated with 2-4 puffs of PAID at the same intervals. If the attack is terminated, ie PEF> 80%, loss of tangible and listening findings occurs, chronic treatment is continued by passing to a higher step. However, if the attack does not end, the upper step (moderate attack) is continued from the end of the first hour.
In a moderate attack; it is appropriate to start with oxygen inhalation (with a preferred maximum of 40% FiO2 to keep SatO2 above 95%). The patient can be seen in the emergency department. Because hypoxia provokes bronchospasm, bronchospasm enters a vicious circle that causes hypoxia. At the same time, salbutamol is started to nebulize. This is the first hour, again 20 minutes call 3 times. The patient is evaluated after the last nebulization. Then, according to the next one is repeated in only 2-4 hours. Salbutamol can also be used with 2-4 puffs of PEP as a dose of salbutamol to nebulize in the same way. Salbutamol is administered intravenously in the oral cavity as a systemic steroid prednisolone of 0.5-1 mg / kg / dose (maximum 60 mg). At the end of the attack, 1-2 mg / kg / day of 2 doses are divided and salbutamol is continued for 3-5 days at 4-6 hours. If the attack is not on, it will go to a higher step. Partial response (PEF 60-80%, decreased physical signs) is hospitalized and the same treatment is continued.
Heavy attack; oxygen inhalation is started as if it were immediately in the middle attack. This patient is strictly monitored by hospitalization and intensive care conditions are kept ready. Simultaneously, salbutamol is administered at the rate of 0.15 mg / kg / dose for the first hour and again for 20 minutes for 3 times, followed by continuous nebulization at the dose of 0.15 mg / kg. At the same time, additif effective ipratropium bromide 125-250 mcgr / dose is added to the potential of bronchodilatation, if necessary, again with sabutamol 3 times in the first hour and then 4-6 hours treatment is added. Salbutamol nebulization is repeated every 1-2 hours. If necessary, ipratropium bromide may be potentially infused with theophylline with an infusion of 0.5-1 mg / kg / h followed by bronchodilatation first (preferably before ipratropium). 1-2 mg / kg / dose prednisolone (max 60 mg) is started intravenously. At the end of the challenge, 1-2 mg / kg / day divided into two equal doses and continued for 3-10 days. Other alternative treatments that can be used in acute attacks can also be used if the attack is not over. These will be mentioned below. However, in the cases where the part of the heavy horse is responded, the treatment such as the middle attack should be continued but if no response is obtained, intensive care is required.
Vital threat (respiratory arrest imminent); It starts immediately like a severe attack and if possible intensive care. Frequent continuous salbutamol inhalation and 4-hour prednisolone are preferred. Additif bronchodilatation is attempted by the addition of ipratropium bromide and theophylline. Even subcutaneous / intravenous salbutamol can be used to reduce the patient's ventilator indications. If you have magnesium sulfate, heliox and other alternative acute bronchodilator treatments can be tried. If there is progression in the table and the table does not retract after 12 hours, the ventilator is evaluated for indications in the intensive care setting.
Although not strictly indications for ventilator, PaCO2 'There is an indication of ventilator in cases of an increase of more than 45 mmHg, generalized disability, and increased weight. Anesthesia is recommended for entubation with succinylcholine and ketamine. In childhood, however, ventilator indications are very rare.
The initial assessment of the patient with an acute attack and the return of the physical examination findings, including complete response to PEF, or over 80% of predicted values for FEV1-like values, if possible, and loss of sibilance during treatment. In partial response, a partial reduction in PEF value (such as 60-80%) and a partial improvement in physical examination findings. Yada attack can get worse. In this case, according to the treatment provided, the treatment of the stage may be continued or it may be passed to an upper step. The assessment of the patient's initial response to initial treatment and the response to treatment may lead to some differences for each patient. For this reason, each patient should be evaluated according to their own characteristics and risk factors should be considered.
The characteristics of asthmatic children at high risk for mortality and morbidity for acute asthma are:
1. Recently, patients using systemic steroids
2. Patients who have defined a recent episode and have an emergency department visit within the past year
3. Inadequate responses in the first 2 hours of treatment
4. PEF value of less than 50%
5. Patients who have previously been treated for intensive care and intensive care
6. Those with long-term exacerbation clinic before enrollment7. Life-threatening attacks
8. PaO2 <60 mmHg, PaCO2> 45 mmHg, Sat O2> 90%.
9. People with general disorientation and unconsciousness.
In the follow-up of exacerbations, if the attack is terminated, the patient is placed on long-term asthma treatment and follow-up program to prevent recurrence after radical rescue treatment and radical biotherapy. If it is being treated, one step is taken up, if not, the treatment is planned according to the severity score.
Alternative and New Methods for Acute Attack
Although acute attack has not yet been introduced into the standard applications of standard applications and consensus reports, alternative treatment methods are used besides the algorithm that we are talking about. These treatment methods are sometimes inexpensive, sometimes with fewer side effects, often preferred for effective and strong bronchodilatation. The basics of these are mentioned below.
1. Inhaled glucocorticosteroids: High dose inhalation, the use of preferred nebulized steroids with salbutamol in acute exacerbations alone may provide more effective bronchodilation than salbutamol. At the same time, less anxiety can lead to relapse in these patients. Systemic and high dose nebulized steroids have less relapse than those using systemic steroid alone. Even high-dose nebulized steroids have rheumatoid arthritis equivalent to 40 mg / day prednisone. However, the cost of inhaled steroids is a rather high treatment and there is a need for longer doses in this area.
2. Magnesium: Provides additive bronchodilatation when given intravenously. It can be used in situations where additive bronchodilatation is not required in routine practice. Particularly useful in children with a PEF or FEV 1 of less than 40% to reduce indications for admission to the hospital and also to reduce intensive care and ventilator indications in children with severe attacks.
3. Helium-Oxygen mixture: Not recommended for mild and moderate atmospheres. The aim of this treatment is to provide better oxygen diffusion, overcome airway resistance and contribute to bronchodilatation. For this reason, it is recommended to use it in severe attacks and life threatening attacks.
4. Levalbuterol: The results are especially limited in children with acute asthma. The drug is the R-isomer of albuterol. It has been reported that in children, salbutamole results in a significant reduction in indications for admission to the hospital. But the price has the disadvantage.
5. Leukotriene modifying drugs: They can help bronchodilatation in acute attacks. These may be 5-LO inhibitors, leukotriene receptor antagonists. Intravenous montelukast has been shown to contribute 10% or more in bronchodilatation. However, this data is rather limited in children. However, the use of salbutamol and similar short acting beta-2 agonist in children with poor response may be considered in the future.
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