Asthma in the emergency department

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Asthma in the Emergency Department BY DR.MAHMOUD ALFEKY Pulmonary Diseases specialist MSc. Chest Diseases and tuberculosis, Faculty of Medicine, Cairo University

Transcript of Asthma in the emergency department

Page 1: Asthma in the emergency department

Asthma in the Emergency Department

BY DR.MAHMOUD ALFEKY

Pulmonary Diseases specialist

MSc. Chest Diseases and tuberculosis, Faculty

of Medicine, Cairo University

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What is Asthma?• Chronic inflammatory disorder of

airways

• Inflammation causes airway hyper - responsiveness often associated with symptoms (wheezes, cough, SOB).

• Obstruction is reversible

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Pathophysiology of Asthma (3Ss)

• 1. Spasm of smooth muscle hypertrophy which

contracts during an attack

• 2. Swelling or oedema of bronchial mucosa

• 3. Secretions from hypertrophy of mucus glands

leading to thick & tenacious mucus

• All the above cause bronchial narrowing

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Asthma: Pathological changes

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Asthma Exacerbation

• Episodes of progressive increase in shortness of

breath, cough, wheezing, or chest tightness, or

some combination of these symptoms.

• Respiratory viral infection, the main trigger of

severe exacerbations of asthma.

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Which aspects of asthmatics history are important to current

exacerbation?

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Others

• Prior hospitalizations

• ICU admissions

• Recent ED visits

• Current meds

• Co-morbid conditions

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How to assess Asthma severity?

Due to be updated 2007

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Indicators of Severe Asthma Clinically

• Anxious & diaphoretic appearance

• Breathlessness at rest; inability to speak in full

sentences

• PaCO2 normal or increased

• PEFR < 150 L/min or <50% predicted

• Pulse oximetry < 91% on room air

• Tachycardia (HR>120) and tachypnea (RR>30)

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Risk Factors for death From Asthma

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Risk Factors for Death From Asthma (continued)(continued)

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Management of severe asthma

Aim:

1 -Correction of significant hypoxemia.

Oxygen

2- To relieve airflow obstruction

Repetitive administration of rapidly acting

bronchodilators.

Early systemic corticosteroids

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Oxygen Assessment

• Pulse oximetry - in all severe asthmatic patients.

• Arterial desaturation and hypercarbia only

develop in life-threatening asthma.

• As result, pulse oximetry is a suitable means for

routine assessment of ventilatory status.

• Measure PEFR: patients with severe distress

if PEFR <50% predicted

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In interpretation of arterial blood gases

• in patients with suspected hypoventilation,

severe distress, or with or PEFR <30%

predicted after initial treatment

• primarily on PaCO2 with normal value in

breathless asthmatic being a warning sign of

impending hypoventilation.

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OXYGENTo achieve arterial oxygen saturation

of greater than or equal to 90

percent, oxygen should be

administered by nasal cannulae or

by mask

• values above (45 mm Hg) indicating a life

threatening attack and probable need for transfer

to a high dependency unit or intensive care unit

(ICU).

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CXR, Bloods and other investigations

• Chest radiograph is not routinely needed, for:

1. those who do not respond to initial

treatment

2. other diagnosis as pneumothorax or

pneumonia.

• Microbiological investigations are seldom

required, although purulent sputum should be

cultured if present.

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Inhaled bronchodilators

• Inhaled b2-agonists are the mainstay of

bronchodilator therapy

• Metered dose inhalers with a spacer produce

outcomes that are at least equivalent to

nebulizer therapy in severe asthma

• The addition of ipratropium bromide to inhaled

b2-agonist therapy provides an increase in the

bronchodilator response in severe asthma.

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• If PEFR <50%: Inhaled high-dose beta2-agonist and anticholinergic (ipratropium bromide) by nebulization every 20 minutes or continuously for 1 hour.

• Repeat assessment (symptoms, physical exam, PEF, O2 saturation, other tests as needed)

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Systemic corticosteroids

• There is no benefit in using very high intravenous doses in severe asthmatics needing hospital admission.

• intravenous hydrocortisone 50 mg four times a day for two days, followed by prednisone 20 mg daily, is as effective in resolving acute severe asthma as either hydrocortisone 200 mg or 500 mg four times daily followed by prednisone 40 or 60 mg daily, respectively.

• Prednisone is commonly given P.O in doses of 40-60mg

• Side effects of short term steroid use include rise in glucose, fluid retention, decrease in potassium, peptic ulcers.

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Route of administration• Oral cortisones are usually as effective as intravenous

and are preferred because this route of delivery is less invasive and less expensive.

• If vomiting has occurred shortly after administration of oral cortisones, then an equivalent dose should be re-administered intravenously.

• In patients discharged from the emergency department, intramuscular administration may be helpful.

• Oral cortisones require at least 4 hours to produce clinical improvement.

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Is there a role for IV aminophylline

• Has been used for hundred’s of years

• Narrow therapeutic window, should only be

considered as an alternate therapy

• Increase in adverse effects (palpitations,

vomiting)

• Used in severe life threatening asthma

• Serum theophylline concentration must be

done first.

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Magnesium Sulphate• Intravenous magnesium now recommended in

patients with life-threatening attacks. Not recommended for routine use in asthma exacerbations

• Its use leads to an improvement in lung function and a reduction in hospital admissions.

• Currently, a single dose (2 g MgSO4 diluted in 50 ml 0.9% normal saline administered over 30 min) .

• If an intravenous bronchodilator is to be administered, current evidence favours the use of intravenous magnesium rather than intravenous b2-agonist or aminophylline.

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Should IV β2-agonist therapy be used?

• No significant differences were found in IV

β2-agonists in addition to, or instead of,

inhaled β2-agonists

• If the patient can tolerate inhaled β-2

agonists, there is no evidence to support

the use of IV β2-agonists

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Does Pregnancy change the management of acute asthma?

NO! • Treat Aggressively

• Prevent Maternal Hypoxia

• Fetal Morbidity/Mortality

• “Risks from respiratory failure and severe acute asthma are greater than from therapy with standard medications”

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How can I tell if my patient is improving?

• Ask them how they feel

• Re-examine

• Obtain objective measurements

(PEFR)

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Who should be intubated?

• Endotracheal intubation is not curative, only a very small percentage of patients presenting to the ED with acute severe asthma will require endotracheal intubation and assisted ventilation.

• Exhaustion, hypoxaemia, deterioration in clinical features despite optimal therapy, PaCO2 is increasing, and depression of mental status strongly indications for intubation

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How should I decide if my patient can be discharged?

Hospitalize Patients with a pre-

treatment FEV1 or PEF < 25% percent predicted or personal best, or those with a post-treatment FEV1 or PEF < 40% percent predicted or personal best, usually require hospitalization.

Discharge• Patients with post-

treatment lung function of 40-60% predicted may be discharged, provided that adequate follow-up is available.

• Patients with post-treatment lung function ≥ 60 % predicted can be discharged.

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Antibiotics in severe asthma

• Purulent sputum may not indicate infection, and is usually a result of eosinophils in respiratory secretions

• Antibiotics should not be routinely prescribed as bacterial infections seldom provoke exacerbations (in contrast to viral respiratory tract infections), and their routine prescription does not influence outcome in exacerbations of asthma.

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SEDATION

should be strictly avoided during exacerbations of

asthma because of the respiratory depressant effect

of hypnotic drugs.

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ANTIHISTAMINICS and CHEST PHYSICAL THERAPY

No established role in the treatment of acute

asthma exacerbations.

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