ASSESSMENT AND MANAGEMENT OF ACUTE SEVERE ASTHMA

TAREK SAFWAT PROFESSOR OF CHEST DISEASES AIN SHAMS FACULTY OF MEDICINE

Severe exacerbations of asthma are life-threatening medical emergencies. Care must be expeditious, and treatment is often most safely undertaken in a hospital or a hospital-based emergency department.

Exacerbations of asthma (asthma attacks) are episodes of rapidly progressive increase in shortness of breath, cough, wheezing, or chest tightness, or some combination of these symptoms and respiratory distress is common. Exacerbations are characterized by decreases in expiratory airflow that can be quantified by measurements of lung function (PEF or FEV1)

The severity of asthma exacerbations may range from mild to life threatening. Deterioration usually progresses over hours or days, but may occasionally occur precipitously over some minutes.

Patients at high risk of asthma- related death require prompt care, particularly close monitoring, and intensive patient education and include those patients with:
With a history of near- fatal asthma requiring intubations and mechanical ventilation, which puts patients at a 19-fold increased risk of needing intubations during subsequent exacerbations. who have hade a hospitalization or emergency care visit for asthma in the past year. Who are currently glucocorticosteroids. using or have recently stopped using oral

Who are not currently using inhaled glucocorticosteroids which appear to offer a protective effect against death or neat-fatal asthma. Who are over-dependent on rapid-acting inhaled B2-agonists especially those who use more than one canister of salbutamol (or equivalent) monthly. With a history of psychiatric disease or psychosocial problems, including the use of sedatives With a history of noncompliance with an asthma medication plan.

Severity of Asthma Exacerbations

Mild Moderate Severe Respiratory arrest imminent

Breathless

Walking

Talking

At rest
Intant stops feeding

Can lie down Talks in

Prefers sitting

Hunched forward Words

Sentences Phrases

Alertness

May be agitated

Usually agitated

Usually agitated

Drowsy or confused

Severity of Asthma Exacerbations. (cont.) Mild Moderate Severe

Respiratory rate Increased Increased Often >30/min

Accessory Muscles and suprasternal retraction

Usually not

Usually

Usually

Paradoxical thoracoabdominal movement

Wheeze

Moderate. Often only end expiratory

Loud

Usually loud

Absence of wheeze

Pulse/min.
Pulsus paradoxus

<100
Absent <10mm Hg

100-120
May be present 10-25 mm Hg

>120
Often present >25 mm Hg (adult) 20-40

Bradycardia
Absence suggests respiratory muscle

Severity of Asthma Exacerbations (cont.)

Mild moderate Severe
PEF after initial bronchodilator % Predicted or % Personal best Over 80% Approx 60-80% < 60% predicted or personal best (<100 L/min adults) or response lasts <2hrs <60 mm Hg Possible cyanosis. > 45 mm Hg; Possible respiratory failure . <90%

PaO2 (on air)

Normal Test not usually necessary. <45 mm Hg >95%

>60 mm Hg

and/or PaCO2

<45 mm Hg

SaO2% (on air)

91-95%

Assessment of severity
Physical signs in the patient with acute asthma that indicate a severe attack include severe dyspnea (e.g. inability to talk), marked tachypnea, obtundation or other disturbance of mental state, pulsus paradoxus exceeding 15 mm Hg, and obvious signs of exhaustion and dehydration. The most accurate assessment of the severity of an attack is to measure airflow: FEV1 and peak expiratory flow rate (PEFR) are equally useful and the latter is easier. A PEFR < 200 L/min indicates at least a moderate attack, and a value < 80 L/min means it is severe.

Assessment of severity (cont.)

Arterial blood gases typically show mild acute respiratory alkalosis (e.g. PCO2 30-35 mm Hg and pH 7.43-7.48). A normal or increased PCO2 or a decreased pH in a patient with an acute asthma attack implies a potentially life-threatening attack and mandates hospital admission. Severe hypoxemia (e.g. arterial PO2 <50 mm Hg while breathing air) also indicates the need for hospitalization, as does radiographic evidence of barotrauma, lobar atelectasis, or consolidation.

Hospital-Based Management of Asthma Exacerbations.

Initial Assessment
History, physical examination (auscultation, use of accessory muscles, heart rate, respiratory rate, PEF or FEV1,. Oxygen saturation, and arterial blood gases.

Inhaled rapid-acting 2 agonist, usually by nebulization, one dose every 20 minutes for 1 hour Oxygen to achieve O2 saturation 90% (95% in children) Systemic glucocorticosteroids if no immediate response, or if patient recently took oral glucocorticosteroid, or if episode is severe Sedation is contraindicated in the treatment of exacerbations.

Initial Treatment

Repeat Assessment PE, PEF, O2 saturation, other tests as needed

Hospital-Based Management of Asthma Exacerbations (cont.)

Moderate Episode

PEF 60-80% predicted/personal best Physical exam: moderate symptoms, accessory muscle use Inhaled 2 agonist, and inhaled anticholinergic every 60 minutes Consider glucocorticosteroids Continue treatment 1-3 hours, provided there is improvement

Hospital-Based Management of Asthma Exacerbations (cont.)

Severe Episode
PEF <60% predicted/personal best Physical exam: severe symptoms at rest, chest retraction Hx:high-risk patient No improvement after initial treatment Inhaled 2 agonist, and inhaled anticholinergic Oxygen Systemic glucocorticosteroid Consider subcutaneous, intramuscular, or intravenous 2 agonist Consider intravenous methylxanthines Consider intravenous magnesium

Hospital-Based Management of Asthma Exacerbations (cont.)

Good Response
Response sustained 60 minutes after last treatment Physical exam: normal PEF>70% No distress O2 saturation > 90% (95% children)

Discharge Home
Continue treatment with inhaled 2 agonist,

Consider, in most cases, oral glucocorticosteroids Patient education: Take medicine correctly Review action plan Close medical follow-up

Hospital-Based Management of Asthma Exacerbations (cont.)

Incomplete Response Within 1-2 Hours
Hx: high-risk patient Physical exam: mild to moderate symptoms PEF<70% O2 saturation not improving

Inhaled 2 agonist, inhaled anticholinergic Systemic glucocorticosteroid Oxygen Consider intravenous methylxanthines Monitor PEF, O2 saturation, pulse, theophylline

Admit to Hospital

Improve Discharge Home

If PEF>60% predicted/personal best and sustained on oral/inhaled medication

Not Improving Admit to Intensive Care

If no improvement within 6-12 hours

Hospital-Based Management of Asthma Exacerbations (cont.)

Poor Response Within 1 Hour
Hx: high-risk patient Physical exam: symptoms confusion PEF <30% PCO2 > 45 mm Hg PO2 < 60 mm Hg severe drowsiness,

Admit to Intensive Care

Inhaled 2 agonist, + anticholinergic Intravenous glucocorticosteroid Consider subcutaneous, intramuscular, or intravenous 2 agonist, Oxygen Consider intravenous methylxanthines Possible intubation and mechanical ventilation

Criteria for Admission to Intensive Care Unit

Severe asthma with a lack of response to initial therapy in the emergency department or worsening asthma despite adequate therapy.
Presence of confusion, drowsiness and other signs of impending respiratory arrest,or loss of consciousness Impending respiratory arrest: hypoxemia despite supplemental oxygen (PaO2 less than 60 mm Hg and / or PaCO2 greater than 45 mm Hg

Basic approach to therapy

The Keys to optimal management of acute asthma are correct assessment of severity, aggressive management of bronchospasm with beta agonists, treatment of inflamation with systemic corticosteroids, administration of supplemental oxygen, adequate hydration, and close monitoring, particularly during the early hours of hospitalization.

Basic approach to therapy (cont.)

Any patient admitted to the hospital for acute asthma should receive at the time of admission systemic corticosteroids (e.g. methylprednisolone 1 mg/Kg IV every 6 hours) . Beta agonist such as salbutamol should be given aggressively by aerosol; intravenous or subcutaneous administration is no more effective, and produces more tachycardia and other side effects, than high-dose inhaled salbutamol (e.g. the equivalent of 50-100 puffs via metered-dose inhaler [MDI] in the first 30-60 minutes in an adult patient). Ipratopium (e.g. 4-8 puffs every 4 hours) tends to be less helpful in asthma than in COPD. Aminophylline is now considered optional and if used, the target blood level should be 10-15 micrograms/mL.

Treatment

OXYGEN : To achieve arterial oxygen saturation of greater than or equal to 90 percent, oxygen should be administered by nasal cannulae or by mask,

Treatment (cont.)

INHALED B2 AGONISTS :, Although rapid-acting inhaled 2 agonist, are generally administered by nebulization, equivalent bronchodilatation with a more rapid onset, fewer side effects, and less time in the emergency department can be achieved using an MDI with a spacer.

Treatment (cont.)

Intravenous 2 agonist, may be added if there is no response to high-dose or continuous nebulized medication, although there are conflicting data about the utility of this treatment. Intravenous salbutamol or terbutaline should always be given in a monitored setting, as all studies show toxicity associated with the use of these medications.

Treatment (cont.)
EPINEPHRINE: subcutaneous or intramuscular injection of epinephrine (adrenaline) may be indicated for acute treatment of anaphylaxis and angioedema. Epinephrine can be used in the treatment of severe acute exacerbations of asthma if 2 agonist, (inhaled or parenteral) are not available. However, the possibility of adverse effects, particularly among hypoxic patients, is greater.

Treatment (cont.)

IPRATROPIUM BROMIDE: combination of nebulized 2 agonist with an anticholinergic ( ipratropium bromide) may produce better bronchodilatation than either drug alone, and should be administered before methylxanthines are considered.

Treatment (cont.)

METHYLXANTHINES: have equivalent bronchodilator effect to inhaled 2 agonist, but because of increased side effects, methylxanthines should only be considered as an alternate therapy.

Treatment (cont.)
MAGNESIUM: Present evidence suggests that intravenous magnesium should not be used routinely in asthma exacerbations, but can help reduce hospital admission rates in selected groups of patients: (adults with FEV1 25 to 30 % predicted at presentation); adults and children who fail to respond to initial treatment; and children whose FEV1 fails to improve 60 % predicted after 1 hour of care. Intravenous magnesium is usually given as a single 2-g infusion over 20 minutes. No additional monitoring is required and there are no reported side effects.

Treatment (cont.)

SYSTEMIC GLUCOCORTICOIDS:
speed resolution of exacerbations and should be considered integral to the management of all but the mildest exacerbations especially if:
The initial rapid-acting inhaled 2 agonist dose has failed to achieve lasting improvement The exacerbation developed even though the patient was already taking oral glucocorticosteroids Previous exacerbations required oral glucocorticosteroids.

Treatment (cont.)
Systemic glucocorticosteroids require at least 4 hours to produce clinical improvement. A meta-analysis has suggested that doses of systemic glucocorticosteroids equivalent to for 60 to 80 mg methylprednisolone or 300 to 400 mg hydrocortisone per day are adequate hospitalized patients, and even 40 methylprednisolone or 200 mg hydrocortisone is probably adequate. There are no convinicing data on the proper duration of oral prednisone treatment, although a 10-to 14-day course in adults and a 3-day to 5-day course in children is usually considered appropriate.

Treatment (cont.)

INHALED GLUCOCORTICOIDS; The optimum increase in maintenance inhaled glucocorticosteroids to prevent an

asthma exacebation is not well defined. Previous guidelines have recommended doubling the dose of inhaled glucocorticosteroids, but there is no evidence to support this recommendation. Higher dose may be appropriate,

Treatment (cont.)

HELIUM OXYGEN therapy: Studies that have evaluated the effect of a combination of helium and oxygen, compared to oxygen alone on airflow obstruction and dyspnea suggest that this treatment should not be used routinely for mild to moderate asthma, but should be reserved for patient with more severe disease.

Treatment (cont.)

ANTIBIOTICS are not routinely required unless there are signs of peneumonia or fever and purulent sputum suggesting bacteria infection, especially if bacterial sinusitis is suspected.

Treatment (cont.)

INHALED MUCOLYTICS : have not been shown to benefit treatment of exacerbations, and in severe cases they may worsen cough or airflow limitation.

Treatment (cont.)

SEDATION: should be strictly avoided during exacerbations of asthma because of the respiratory depressant effect of anxiolytic and hypnotic drugs.

Treatment (cont.)

ANTIHISTAMINICS and CHEST PHYSICAL THERAPY have no established role in the treatment of exacerbations.

INTUBATION may be needed if there is continued deterioration in clinical features despite optimal therapy, if the patient is exhausted, and/or if the PaCO2 is increasing.
If intravenous paralysis is used, thre is the risk of the development of myopathy. The duration of paralysis should be brief as possible.

Indication for intubation and ventilation

One clear indication for intubation in patients with acute asthma is obtundation or other alteration in mental status. The other main indication is failure of initial therapy, as evidenced by progressive respiratory acidosis over several hours. However, the decision to ventilate a given patient should be on the basis of te overall clinical picture rather than on a particular value of PCO2 or pH. Most patients who remain alert and cooperative will not require intubation, even if their initial PCO2 and pH values are over 50 mm Hg and/or under 7.30, respectively.

Practical guidelines
Patients with acute severe asthma who require ventilatory support should be intubated, in order to protect the airway during administration of appropriate sedation. The following are practical guidelines for initial ventilator management:
Mode: either assist-control or SIMV
Tidal volume 5-8 mL/Kg Initial rate 6-10 breaths/min Peak inspiratory flow rate 70-90 L/min End-inspiratory plateau pressure (static hold pressure) kept <35 cm H2O PEEP adjusted to 75-80 percent of measured autoPEEP level FIO2 sufficient to maintain arterial PCO2 60-80 mm Hg Sedation to prevent tachypnea and allow the patient to rest during 1st 24 hours

Overall ventilation strategy

Permissive hypercapnia is a ventilatory strategy that attempts to protect the lung from ventilator-induced lung injury by using smaller than usual tidal volumes and limiting alveolar distending pressure. Under these controlled circumstances, and with appropriate monitoring, PCO2 values of 60-80 mm Hg or more, along with pH values below 7.20, are remarkably free from adverse effects, and respiratory acidosis is relatively permitted and pose less clinical risk to the patient than the ventilator manipulations that would be required to achieve normal PCO2 and pH values.

Patients being managed with permissive hypercapnia generally require sedation. However, muscle relaxants should be avoided if possible.

Bronchodilator Therapy During Mechanical Ventilation

As mentioned earlier, beta agonists are more effective and produce fewer side effects when administered via aerosol. This is as true during mechanical ventilation as it is for spontaneously breathing patients, although higher doses are required because of deposition of the active agent on the walls of the endotracheal tube.

Complications
BAROTRAUMA Alveolar rupture, leading to pneumomediastinum, pneumothorax, subcutaneous emphysema, and other forms of extra-alveolar air is primarily due to alveolar over-distension. Although high peak (dynamic) airway pressures during mechanical ventilation indicate an increased risk for ventilatorinduced lung injury in conditions (such as ARDS). However this is not true in acute severe asthma. In the latter, the high airway resistance is caused by bronchospasm, airway edema, and inspissated secretions which lead to very high proximal airway pressures that are not transmitted to the alveoli. The most important monitors of the risk of barotrauma are the end-inspiratoy plateau pressure, and the frequent measurement of auto-PEEP

Complications (cont.)

Prolonged muscle weakness:

This reported phenomenon occurs in ventilated patients who have received both corticosteroids and neuromuscular blocking agents such as pancuronium, vecuronium, and atracurium. Patients with mild underlying renal insufficiency may accumulate the paralytic agent, and it may take 2-3 days or more to clear it and results in a condition of myopathy.

Discharge From Emergency Department

At discharge several actions are recommended:

At minimum a 7 to 10 day course of prednisone for adults and a shorter course (3 to 5 days) for children should be prescribed with continuation of bronchodilator therapy. The dose of bronchodilator can be gradually reduced, based on both symptomatic and objective improvement, until the patient returns to his or her pre-exacerbation use of rapid-acting inhaled 2 agonist. Ipratropium bromide is unlikely to give additive benefit beyond the acute phase and can be quickly discontinued.
Patients should continue or initiate inhaled

glucocorticosteroids