This lecture was conducted during the Nephrology Unit Grand Ground by Medical Student rotated under Nephrology Division under the supervision and administration of Prof. Jamal Al Wakeel, Head of Nephrology Unit, Department of Medicine and Dr. Abdulkareem Al Suwaida, Chairman of the Department of Medicine. Nephrology Unit is not responsible for the content of the presentation for it is intended for learning and /or education purpose only.

Presented by: Wael Albalawy Medical Student May 2008

*introduction. *the basic principles of the care. *severity assessments. *treatment. *indications of admission. *summery.

*B.A. is an inflammatory disorder of the airways characterized by variable airflow obstruction and airway hyper responsiveness to a variety of stimulus.

* The best strategy for management of acute exacerbation of B.A. is early recognition and intervention, before attacks become more severe and potentially life threatening.

*Assess the severity of attack. *used inhaled short-acting beta agonist early and frequent and consider concomitant use of ipratropium for severe exacerbation. *start systemic glucocorticoid if there is no an immediate and marked response.

 Make frequent (every 1-2 h) objective assessment of the response to treatment until definite,sustained improvement is documented.  admit pt who do not respond well after 4-6 h to a setting of high surveillance and care.  educate pt about principles of self management for early recognition of recurrent attack.

1- Initial response Instructions to pt regarding self administration of medication and self monitoring differ depends on : pt Hx, understand and follow directions. (Asthma action plan ).....individualized written, based on peak flow used peak flow meters to assess severity and response.

2- Detecting the onset of exacerbation Some people sensitive to increase symptoms of B.A.. Some,perceive decrease airflow only when it becomes marked. Decrease peak flow >20% of baseline consider deterioration. Fall <50% of baseline consider to be severe attack.

When detect deterioration, they should self administer short acting beta agonist 1/2-6 puffs, repeated in 20 min. 2/2 nebulized treatment,separated by 20 min. Then, repeat peak flow and base upon the initial response either: #cont. self management. #seek medical attention.

*PEFR > 80%..... Cont. the same self Rx Remove offending stimulus. Cont. inhaled short acting beta agonist Short course of oral glucocorticoids if not fully correct PEFR.

*** Quadrupling the dose of inhaled glucocorticoids in mild asthma,rather than oral May be of some benefit. But doubling the dose of inhaled.....Ineffective and not recommended.

If repeated PEFR (50-79%) Start oral glucocorticoids and contact clinician urgently Remove the stimulus Cont. short acting beta agonist Intermittent peak expiratory flowmetry

*** Timely administration of oral glucocorticoids for significant asthmatic exacerbation is the single most effective strategy for reducing E.R. visit and hospitalization for acute attack.

Seek immediate medical attention if: *PEF <50%. *severe exacerbation symptoms. *high risk for fatal asthmatic attack.

Risk factors for fatal attack *previous severe exacerbation. 2or more admission for asthma in the past year. *3 or more E.R. visit in the past year. *admission or E.R.visit in the past month. *Use of >2 canister of short acting beta agonist/ month. *low socioeconomic state. *comorbidities.

1-clinical finding. 2-peak flow rate. 3-gas exchange. 4-hypercapnia. 5-CXR.

Clinical Finding -pulsus paradoxus. -use accessory ms during inspiration. -diaphoresis. -inability to lie supine d.t. S.O.B. ****NOT sensitive indicator % of pt with severe airflow obstruction will not manifest any of these abnormalities.

Peak Flow PEFM is the best method for assessment of the severity of asthma attack. -Take less than one minute to perform -safe -inexpensive -repeated over times.

***Normal values differ with gender,HT, age. But peak flow rate < 200L/min indicate severe obstruction for all.

Gas Exchange Significant hypoxia (arterial Po2< 60 mmHg or SaO2< 90%) is infrequent but cause severe complication and death. *** Current guidelines recommended its use particularly among pt who are in -severe distress -PEFM<40% -Unable to perform lung function measurements.

Assessing Hypercapnia * respiratory drive is almost invariably increased in acute asthma.....hyperventilation decreased PaCO2. *elevated or normal PaCO2.....airway narrowing (respiratory system cannot respond to the output of respiratory center) *peak flow measurement is useful screening.

Hypercapnia occurs only when the peak expiratory flow falls <25%. *ABG indicated in: -pt with persisting dyspnea and expiratory flow remains below 25%.

CXR The most common abnormality is pulmonary hyperinflation. The abnormal findings are infrequent (pneumothorax, pneumomediastinum, pneumonia or atelactasis). *2% only.

Indication of CXR: *suspected complications (unexplained chest pain,fever>38.3, leukocytosis and hypoxia ) *high risk of comorbidities (drug abuse, immunosuppression, cancer, chest surgery and congestive heart failure)

The primary goal of therapy for acute severe asthma is rapid reversal of airway obstruction and correction of hypercapnia or hypoxemia. The most effective ways: *repeated inhaled bronchodilators *early systemic glucocorticoids *serial measurements of lung function.

Inhaled beta agonists Using short acting beta 2 selective adrenergic agonists( albuterol, levalbuterol and bitolterol). Standared regimen for initial care is albuterol *2.5-5 mg nebulization every 20 min for 3 doses, then mg every 1-4 h as needed.

*administration by Inhalation with spacer 4-8 puffs every 20 min for up to 4h, then every 1-4h *in ill pt, administering mg over one hour.

Nebulizer vs Inhaler Comparisons with Inhaled Rx with spacer systems, using the same beta agonist but in much reduced doses, have demonestered comparable improvements in lung function to those achieved by nebulized medication. *one prospective study shows: Inhalers treatment was associated with shorter E.R.stays,greater improvement in peak flow and lower cumulative dose.

Inhaled anticholinergics Recommend the addition of ipratropium for pt with severe exacerbation who are in E.R. but not during hospitalization. Dose: 500 mcg every 20 min for 3 doses then as needed. Inhalers 8 inhalations every 20 min then as needed for up to 3h.

There is controversy about advantages to combined albuterol and ipratropium over albuterol alone. Usually we use ipratropium for pt with severe obstruction failing to improve despite repeated administration of inhaled beta agonists.

Systemic Glucocorticoids Pt with continued wheezing and SOB despite intensive bronchodilator therapy have persistent airflow obstruction on the basis of airway inflammation and intraluminal mucus plugging. The rate of improvement typically slows after the first hour of Rx,since edema, cellular infiltiration and mucous hypersecretion. We use oral glucocorticoids speed the rate of improvement.

It is recommended to use early oral glucocorticoids: *moderate or severe exacerbation B.A. *not fully corrected the decrement in peak flow despite beta agonist. *any pt develop asthma exacerbation despite daily or alternate day oral glucocorticoid.

The onset of action: 6h after administration. The dose: mg/day in a single or divided dose. In the absence of vomitting,oral administration can be used instead of I.V. (highly absorbed and high bioavailability)

I.V. should be given in: *impending or actual respiratory arrest. *who respond poorly to oral administration.

Duration: Most severe attacks that require hospitalization will resolve in days. Pt can stop oral glucocorticoids based on resolution of symptoms and PEFM(>70%)

Magnesium sulfate *I.V. (2gm infused over 20 min.) has bronchodilator activity d.t. inhibition of Ca influx into airway smooth ms cells. *it is suggested for pt who have -life threating exacerbation. -exacerbation remaines severe (PEFR<40%) after 1h of intensive therapy. *it is safe but contraindicated in renal insufficiency

Non Standard Therapies *helium oxygen: decrease the work of breathing and improve ventilation. -it allows smaller particles to better penetrate to lung periphery. *leukotriene receptor antagonists: Used in chronic B.A. but its role unclear regarding acute attack.

Ineffective Therapies *I.V. methylxanthines (theophylline or aminophylline) *inhaled glucocorticoids *empiric antibiotic

Endotrcheal Intubation and Ventilation: Decision to intubate during the first few min of severe asthma attack is clinical. -slowing RR -depressed mental status -Inability to maintain respiratory effort -hypoxia during severe attack.

The Goal Of Mechanical Ventilation Maintain adequate oxygenation and ventilation while minimizing elevated airway pressure which accomplished by: -inspiratory flow rate ( L/min) -low tidal volume (6-8 ml/kg) _low RR(10-14 /min)

For close observation and availability of aggressive intervention To remove the pt from stimulus. Ensure medication compliance *peak expiratory flow less than 40% *peak expiratory flow(40-70%) : new onset of asthma, multiple prior hospitalization, used oral glucocorticoids)

*Early recognition and intervention are critical for successful management of asthma exacerbation. *In the urgent setting, the severity of B.A. assessed based on clinical finding, PEFM and oximetry. * Management based on frequent bronchodilator,systemic glucocoricoids and reassessment.

1-national asthma education and prevention program:expert panel reportIII:guidelinesfor the diagnosis and management of asthma S mohammed,S Goodacre.I.V.and nebulized Mg sulphate for acute asthma Fiel, stawly,walter. Journal of asthma, systemic corticosteroid therapy for acute asthma. June-July 2006