C T Deshmukh
Management of Acute Exacerbation of Asthma
Asthma exacerbations are acute episodes of progressive worsening of breathing, cough, wheeze and chest tightness. These exacerbations are characterized by decrease in PEFR whish in turn can be easily quantified by PEFR meter or spirometer. These objective measurements indicate severity more accurately than symptoms.

The aim in management of acute asthma is:
1.    Correct significant hypoxemia – (O2, mechanical ventilation rarely needed)
2.    Reverse airflow obstruction as rapidly as possible.
3.    Reduce inflammation and risk of recurrence by intensifying therapy.

Early treatment is important to prevent hospitalization and/or the attack from becoming severe. The following points are important for the same:
1)    Written instruction to patient for self treatment.
2)    Early diagnosis of worsening by PEFR meter or spirometer.
3)    Early contact with doctor regarding clinical or PEFR changes.
4)    Early increase in therapy (ß2 agonist, oral steroids).
5)    Remove precipitating factor if any.

Patients with high risk for asthma deaths need extra attention.
High risk factors for death in asthma:
1)    Past history of severe exacerbations.
2)    History of intubation mechanical ventilation for asthma.
3)    More than two hospitalizations for asthma in past one year.
4)    History admission to Pediatric intensive Care unit for asthma.
5)    Use of oral steroids for current attack.
6)    Excessive use of  b2 agonist.
7)    Frequent emergency visits for acute asthma.
8)    Associated cardio-respiratory diseases.

The diagnostic phase in a child with acute asthma should be short and comprise a brief history taking, inspection and auscultation of the thorax, transcutaneous oxygen measurement and, if possible, peak flow measurement (PEFR).
•     Patients should be treated immediately with oxygen, which should always be humidified.
•     Beta 2 agonists should be given immediately by inhalation if they are capable of effective inhalations or by injection if severely dyspneic. Frequent doses should be given and the duration and effect can be monitored  by clinical assessment and PEFR measurement.
•     High dose corticosteroids should be administered promptly by mouth if there is no concern regarding retention, and parenterally if the patient is obtunded or vomiting.
•     Monitor clinical parameters, pulse oximetry and PEFR. PEFR should be monitored every 30 minutes until patient is out of danger.
•     Blood gases should be done if :                                                                                                            
  1. O2 saturation < 94  % at room air and patient dyspneic  or
  2. O2 saturation < 90 % regardless of clinical findings.
After initial management one has to decide if patients needs hospitalization or needs to be sent home on medication.

Guidelines for admission:
Do not admit if:
1.    Comfortable at rest.
2.    No chest retractions.
3.    Not using accessory muscles of respiration.
4.    O2 saturation > 90 % at room air.

Admit if:
1.    Labored respirations continue.
2.    O2 saturation < 90 % at room air.
3.    Dehydration, which requires intravenous fluids.
4.    Past history of rapid deteriorations.
5.    PEFR < 50 % or diurnal variation > 25 %.
6.    Presence of complications such as subcutaneous emphysema and pneumothorax.

Do not keep patient for observation with simple measures for more than 3 – 4 hours, it is better to admit such patients for more intensive therapy and observation.

Treatment after admission:
•    Continue humidified oxygen monitoring pulse oximeter.
•    Continue inhaled ß2 agonist frequently depending on clinical and PEFR findings.
•    Intravenous fluids are needed in most with severe asthma as they are dehydrated due to - increased metabolism, increased insensible losses, decreased intake, vomiting. Dehydration can increase viscosity of secretions, thereby increasing bronchiolar plugging and atelectasis. Over hydration can cause pulmonary edema. Hence correct the dehydration, then provide maintenance fluids, monitor fluid and electrolytes and correct accordingly.
•    Medications:
1.   Inhaled ß 2 agonist by nebulization either ½ hr to 1 hourly or continuous (continuous nebulization 0.1 to 0.3 mg/kg/hr to max 10-15mg/hr).     
2.    Corticosteroids are the most important drugs in treating asthma
  • Can be given oral if patient can take PO steroid without emesis
  • Intravenous methyprednisolone 1-2mg/kg/dose q6hrs, then depending on clinical course should be continued orally.
  • Inhaled therapy may be as effective as IV in acute therapy.
3.    Anticholinergics: Ipratropium Bromide can be used and  has additive effect to beta-agonists. Can be given as 250mcg (1cc) nebulization every 3 – 4 hourly.
4.    Aminophylline drip may be useful by increasing diaphragm contractility, increasing mucociliary clearance, anti-inflammatory properties and bronchodilatation, so it may be of some added benefit in patients with poor response to B-agonist.
5.    Others routes of  ß 2 agonist
a)    Subcutaneous Epinephrine or Terbutaline may also be given as an alternative. This route is selected if no other route is available/acceptable.
b)    Salbutamol intravenous may be tried if minimal effect with inhalation therapy.
c)    Intravenous continuous infusion (terbutaline, isoproterenol, albuterol) can be used when no improvement with inhaled bronchodilators. Terbutaline - bolus 10mcg/kg over 30 min, infuse with 0.1mcg/kg/min. Needs close monitoring of heart rate, cardiogram and oximeter
6. Other drugs:
i.    Antibiotics - no role for routine use. May use if there is evidence of infection(sputum predominantly PMNs , sinus infection, pneumonia, suspicion of Mycoplasma or Chlamydia).
ii.    Magnesium SO4 – Used as bronchodilator. The mechanism is not clear, but may be due to inhibition of Ca++ mediated smooth muscle contraction or direct inhibition of smooth muscle contraction. There are no controlled studies in children and has been tried IV in the dose of 30-70 mg/kg over 20-30 min. (max=2g).
•    Blood gases: Hypoxemia in asthma is because of either V/P mismatch or respiratory failure and only pulse oximetry will not be able to differentiate the two, blood gases are important at this stage. Blood gases should be asked for when:
- O2 saturation is less than 94% on room air and patient is dyspneic.
- or if O2 saturation < 90% regardless of signs or symptoms.
•    Other investigations may be needed:  
a.    WBC - demarginated PMNs due to stress, steroids and infection.
b.    Electrolytes – i.  hypokalemia due to beta 2 agonist
                ii. bicarbonate low due to metabolic acidosis
c.    X-ray chest to look for complications.

Indications to transfer to PICU:
1.    Altered consciousness
2.    Exhaustion
3.    Sitting position accompanied by diaphoresis
4.    Severe decrease air entry
5.    Monosyllable speech
6.    PCO2 rising, near normal, elevated,
7.    Pneumothorax, subcutaneous emphysema.
8.    Drug toxicity
9.    No improvement with standard therapy as above.
10.    Cardiac/respiratory arrest
11.    Metabolic acidosis
12.    PFT’s deteriorating despite treatment.

Indicators of impending respiratory failure:
1.    Altered Level of Consciousness.  
2.    Monosyllable or not able to speak.
3.    Markedly decreased or absent breath sounds
4.    Cyanosis
5.    Severe chest retractions and use of accessory muscles.
6.    Pulsus paradoxus > 10mm Hg

Treatment in PICU:
•    Continue IV bronchodilators, continuous nebulizations, anticholinergics, steroids and O2.
•    Treatment of acidosis: Acidosis is caused by hypoxemia, hypoperfusion and respiratory failure. Acidosis leads to myocardial depression, decreased effectiveness of B-agonists and ineffective rapid shallow breathing. Correct metabolic by giving bicarbonate (keep pH > 7.20) 1 meq/kg.
•    Sedatives: May be given to prevent ineffective ventilation and interference with nebulization therapy. Preferably use those with bronchodilating effect  e.g. droperidol  or ketamine. Use only in PICU setting or when patient on ventilator.
•    Mechanical Ventilation: Indications-
1.    Cardiorespiratory arrest
2.    Severe altered mental status
3.    Progressive exhaustion
4.    Failure to respond to maximal medical treatment (acidotic, pCO2 > 50 and rising, minimal chest movements, cyanosis and hypoxemia).
5.     Pneumomediastinum
Goals of ventilation:
1.    Oxygenate and ventilate
2.    Let trapped air escape
3.    Prevent barotrauma
4.    Give rest to respiratory muscles
5.    Give time for anti-inflammatory medications to work
Non-conventional interventions
•    CPAP/ non-invasive positive pressure ventilation
•    Inhalation anesthetics
•    Bronchoscopy
•    Heliox
•    ECMO
•    NO
Patients may be discharged if they are comfortable at rest without retractions or use of accessory muscles of respiration, and if O2 saturation is greater than 90% on room air. Early follow-up is important.

Out patient management summary
•    Main areas: Treatment, education and follow-up
•    Treatment – Start or continue appropriate anti-inflammatory drugs (inhaled steroids). Use Bronchodilators when needed and also to prevent exercise induced asthma. Change to MDI in hospital before discharge. Treat exacerbating factors (GER, sinusitis, allergies).
•    Education – About signs and symptoms of asthma, what are the precipating factors and how to detect and remove them, what to do if an attack occurs, importance of follow-up regularly and use of PEFR meter.

Asthma Asthma 12/21/2000
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