Acute Asthma in Adults

Acute Asthma in Adults

Krit Kuruchaiyapanich, MD

DefinitionAsthma is a chronic inflammatory

disorder of the airways in which many cells and cellular elements play a role.◦This inflammation causes recurrent

episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning.

◦Associated with widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment.

National Asthma Education and Prevention Program, EPR3: Guidelines for the Diagnosis and Management of Asthma. Publication No. 08-4051,2007

DefinitionStatus asthmaticus

◦severe bronchospasm that does not respond to aggressive therapies within 30 to 60 minutes.

Near-fatal ◦respiratory arrest or evidence of

respiratory failure (Paco2 > 50 mm Hg).

Definition

National Asthma Education and Prevention Program, EPR3: Guidelines for the Diagnosis and Management of Asthma. Publication No. 08-4051. 2007

Severe/Refractory asthma

American Thoracic Society workshop consensus for definition of severe/refractory asthma (requires one or both major and two minor criteria and that other conditions have been excluded, exacerbating factors have been treated, and patient is generally compliant).

Pathophysiology

Hallmark reduction in airway diameter caused by◦smooth muscle contraction ◦vascular congestion ◦bronchial wall edema ◦thick secretions

Bronchoconstriction occurs due to◦1. allergic mediators and metabolic

products from inflammatory cells◦2. nonallergic exercise, aspirin-induced,

and menstrual-related asthma

Pathophysiology

PathophysiologyEarly asthmatic response

◦Release of preformed histamine from mast cell granules bronchial smooth muscle and airway edema wheezing and airflow obstruction (resolves within an hour )

Late asthmatic response◦cytokines generated and released by

mast cells and other local and recruited inflammatory cells prolonged airflow obstruction and bronchospasm

PathophysiologyEosinophils are major effector cells in

asthma Airway epithelial cells : produced Nitric

oxide (NO) potent vasodilator and may reflect the presence of inflammation in asthma

Airway remodeling : Inflammation, mucus hypersecretion , subepithelial fibrosis airway smooth muscle hypertrophy, angiogenesischronic irreversible airflow limitation

Aspirin-exacerbated respiratory disease (AERD) Triad

◦aspirin sensitivity, asthma, and nasal polyps NSAIDs also precipitate AERD (but not reported

after administration of COX-2 inhibitors )common precipitant of life-threatening

asthmaSymptoms

◦ occur within 3 hoursprofuse rhinorrhea, conjunctival injection, periorbital edema, and occasionally a scarlet flushing of the head and neck

Definitive diagnosis : provocation challenges

Aspirin-exacerbated respiratory disease (AERD)

Exercise-induced asthma (EIA) Etiology is unclear Atopy is strongly associated with

EIA, and up to 40% of patients with allergic rhinitis have EIA

Symptom◦occur 3-8 min of exercise, peak 8-15

min after exercise, spontaneous recovery occurs within 60 min

Prophylaxis : warm-up and a short-acting inhaled beta2-agonist

Menstruation-associated asthma Perimenstrual reductions in PEFR of

35 to 80% Estradiol inhibits eosinophil

degranulation and suppresses LT activity.

Progesterone have bronchodilator and anti-inflammatory activity.

Tx : LT antagonists, LABA , estradiol, progesterone, and gonadotropin-releasing hormone analogues

CLINICAL FEATURES Classification

◦1. Type 1 (Slow onset> 6 hr) 80-90% Female>male Etiology: URI Inflammation less severity than type 2 slower response to therapy

◦2. Type 2 (Sudden onset< 6 hr) 10-20% Male>female Etiology: respiratory allergen, exercise, stress Bronchoconstriction more severe faster response to therapy

Picado C. Classification of severe asthma exacerbations: a proposal. Eur Respir J 1996; 9: 1775-8.

CLINICAL FEATURES Symptom : Triad

◦dyspnea, wheezing, and coughEarly chest constriction and coughExacerbation progresses wheezing,

prolonged expiration and accessory muscle used(indicates diaphragmatic fatigue)

Tachypnea and tachycardia >120 beats/min are associated with severe obstruction, but a lower rate does not R/O severe asthma.

The "silent chest" reflects very severe airflow obstruction

CLINICAL FEATURES bronchiolar smooth muscle tone

airway resistance, pulponary infiltration, V/Q missmatch

Dynamic hyperinflation auto-PEEP pulsus paradoxus, diastolic LV dysfn

Acute hypercapnia+ intrathoracic pressure ICP

Signs of impending respiratory failure (1)

◦ inability to speak, altered mental status, intercostal retraction, worsening fatigue, and a PCO2 of ≥42 mmHg

(1) National Asthma Education and Prevention Program, EPR3: Guidelines for the Diagnosis and Management of Asthma. Publication No. 08-4051. 2007

SEVERITY OF ASTHMAEXACERBATIONS


Risk factors for death from asthma

DIAGNOSTIC STRATEGIESPulmonary Function Studies

◦FEV1 or PEFR◦the best of 3 consecutive values should

be recorded Arterial Blood Gas (mild to moderate

hypoxemia with resp. alkalosis)◦1. predicted PFTs of < 30%◦2. clinical course is perplexing ◦3. capnography is not available. ◦acute ventilatory failure hypoventilation

with CO2 retention and resp. acidosis

Indication

DIAGNOSTIC STRATEGIESCXR suspected…

◦pneumonia, pneumothorax, ateltctasis, pneumomediastinum, or CHF

ECG should not be routinely obtained, except ◦patients >40 yr, a separate complaint

(e.g., chest pain), Hx of significant CVD◦severe asthma: a RV strain pattern

Others◦LTE4 in the urine ◦exhaled nitric oxide

Assessment Summary The severity of airflow

obstruction cannot be accurately judged by patients’ symptoms, PE , and laboratory tests. Serial measurements of airflow obstruction (FEV1 or PEFR) are key components of disease assessment and response to therapy .

Peak Flow Meter

Management

Emergency Treatment of Asthma, N ENGL J MED 363;8 nejm.org august 19, 2010

MedicationThe goal of treatment of acute asthma in the ED is to reverse airflow obstruction rapidly by repetitive or continuous administration of inhaled B 2-agonists, ensure adequate oxygenation, and relieve inflammation

Medication1. Relievers

- B2-adrenergic , Anticholinergics, Theophyline

2. Controller- Glucocorticoids, Leukotriene modifiers, Cromones, Anti-IgE

β2-Adrenergic AgonistsRelaxation of bronchial smooth

muscle, inhibit mediator release and promote mucociliary clearance.

Most common side effect: skeletal muscle tremor.◦others: nervousness, anxiety,

insomnia, headache, hyperglycemia, palpitations, tachycardia, and hypertension.

β2-Adrenergic AgonistsSABA (Solution=MDI)

◦ First line drug◦ Nebulization = MDI + spacer (prefer

nebulization)◦ Salbutamol 2.5 – 5 * 3 time/hr◦MDI with spacer 4– 8 puffs q 20 min

up to 4 h, then q 1–4 h as needed.

β2-Adrenergic AgonistsIV form (not recommened in USA)

◦severe nonresponsive acute asthma. ◦albuterol loading dose 4 μg/kg for 2-5 min

then infusion of 0.1 to 0.2 μg/kg/min ◦Epinephrine IV titrated to effect (average 1.5

μg/min with a range of 0.5–13.3 μg/min) SC form

◦may be used in pt who cannot adequately inhale albuterol or who experience severe bronchospasm.

◦Epinephrine (1:1000 ) 0.2-0.5 mL q 20 -30 min◦Terbutaline 0.25 mg SC q 20 min * 3 dose

Corticosteroids Action in the airways

◦ inhibition of recruitment of inflammatory cells and inhibition of release of proinflammatory mediators and cytokines from activated inflammatory and epithelial cells, activate cytoplasmic glucocorticoid receptors to regulate directly or indirectly the transcription of certain target genes resulting in the synthesis of new proteins.

Two forms◦1. Systemic ◦2. Inhaled

Corticosteroids1. Systemic (IV and oral)

◦speeds the resolution of airflow obstruction, reduces the rate of relapse and may decrease admissions in severe, but not in mild to moderate attacks.

◦Prednisone 40-60 mg oral loading◦Methylprednisolone 40–80 mg/day in one

dose or two divided doses◦Demethasone 5 mg ◦given q 6 hr until PEFR reaches 70% of

predicted value or a personal best value

CorticosteroidsIV = oralSide effects

◦short-term (hours or days) reversible increases in glucose (important in diabetics) and decreases in potassium, fluid retention with wt gain, mood alterations including rare psychosis, hypertension, peptic ulcers, aseptic necrosis of the femur

Corticosteroids2. Inhaled

ICS + SABA NB: reducing airway reactivity and edema more effectively

reduce rates of hospitalization Side effect : Dysphonia, Reflex cough and

bronchospasm, Oral candidiasisDischarged

Prednisone 40-60 mg oral for 7 day ICS high-dose budesonide (400 μg, two puffs

twice per day)

Anticholinergic Agents

Atropa Belladonna Leave

Anticholinergic AgentsBlock smooth muscle constrictor and

secretory consequences of the PNS, blocking reflex bronchoconstriction and reversing acute airway obstruction.

affect large, central airways, but adrenergic drugs dilate smaller airways.

Side effect◦dry mouth, thirst, and difficulty swallowing.

Less commonly, tachycardia, restlessness, irritability, confusion, difficulty in micturition, ileus, blurring of vision, or an increase in IOP

Anticholinergic AgentsInhaled-ipratropium bromide

◦Nebulizer solution (0.25 mg/ml) 0.5 mg q 20 min for 1 hr (three doses), then as needed;

◦MDI (18 μg/puff) 8 puffs q 20 min as needed, for up to 3 hr

◦not recommended as monotherapy in ED slow onset of action

◦added to SABA for a greater and longer-lasting bronchodilator effect, reduce rates of hospitalization by approximately 25% in severe asthma


Magnesium Sulfaterelaxes bronchial smooth muscle and dilates

asthmatic airways.I/C (recommended IV > NB)

◦ severe asthma attacks (FEV1 < 25% predicted) improves airflow obstruction and decreases the need for hospital admission

◦MgSO4 2 -3 g IV over 20 min or at rates of up to 1 g/min to patients with severe refractory asthma

Side effect◦warmth, flushing, sweating, N/V, muscle

weakness and loss of DTR, hypotension, and respiratory depression.

Treatments That Are Not Recommended

1. Methylxanthines ◦lack of demonstrated efficacy and increases in

adverse events2. Antibiotics

◦should be reserved for pt with bacterial infection (e.g., pneumonia or sinusitis) seems likely.

3. Aggressive hydration4. Mucolytic agents

◦worsen cough or airflow obstruction5. Sedation


Leukotriene Modifiersnon-beta-mediated bronchodilating effectsZafirlukast (20 mg twice a day)

Montelukast (10 mg daily)

Currently, there is no indication for the use of any of the leukotriene modifiers in the ED.

PregnancyThe principles of managing acute asthma in

pregnancy and during lactation are similar to those for the nonpregnant state.

Early intervention during acute exacerbation is key to the prevention of impaired maternal and fetal oxygenation.

PaO2 <70 mm Hg severe hypoxemiaPaCO2 >35 mm Hg respiratory failureB2-agonist and ICS : safe during pregnancy

and are recommended as a routine part of asthma management

NPPVBiPAP

◦ well tolerated by children , decrease the need for intubation and mechanical ventilation.

◦Consider for pt. who decline intubation and pt. who cooperate with mask therapy

◦but more data are needed to recommend this approach

Patient must be alert mental status and intact airway reflexesEmergency Treatment of Asthma, N ENGL J MED 363;8 nejm.org august 19, 2010

Ketaminepotent bronchodilator effectsno randomized trials have been

conducted.not recommended for therapy of

acute asthma in the nonintubated patient

Ketamine 1–2 mg/kg IVSide effect

◦increased airway secretions and emergence reactions

Intubation and Ventilator Strategy

Avoid nasotracheal routeIntubate before the crisis of respiratory arrestSelected largest ET-tube as soon as possible.Pretreatment

◦Lidocaine 1.5 mg/kg IVInduction

◦Midazolam 1 mg IV q 2-3 min◦Ketamine 1–2 mg/kg IV

Neuromuscular blocking agent◦Preferred Rocuronium (1 mg/kg) > Succinylcholine

(1.5 mg/kg) less associated with myopathy

Rodrigo GJ, Rodrigo C, Hall JB. Acute asthma in adult: a review. Chest 2004; 125: 1081-102

Ventilator strategy◦adequate oxygenation and ventilation,

minimizing high airway pressure, barotrauma, and systemic hypotension

Permissive hypercapnia technique◦TV 6–8 mL/kg, MV 6-8 LPM◦I:E > 1:3, RR 11-14 /min◦End-inspiratory pressure < 35 cmH2O◦pH maintained at 7.15–7.2 ◦Paco2 <100 mm Hg


Complications of mechanical ventilation◦Hypotension and barotrauma ◦Pneumothorax !!!

sudden clinical deterioration hypotension significant rise in peak inspiratory ventilator

pressures and falling oxygen saturation. External lateral chest compression :

patients cannot exhale esp; children


Cardiopulmonary arrestMay result from unrecognized

barotrauma.◦Empirical bilateral tube thoracostomy

should be performed if unexplained cardiac arrest occurs, especially in the context of dramatic increases in peak inspiratory pressure.

◦ IV epinephrine has both cardiostimulatory and bronchodilatory properties.

DISPOSITIONWhen should be discharged

◦FEV11or PEF after treatment is >= of the personal best or predicted value

◦Improvements in lung function and symptoms > 60 min


DISPOSITION


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Acute Asthma in Adults

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