Status Asthmaticus Management

Amina Al-Qaysi

Status Asthmaticus• Acute exacerbation of asthma that is severe at

its onset or progresses rapidly despite standard therapy, and remains unresponsive to initial treatment with bronchodilators.

• Usually occur during sleep when airway inflammation & hyperresponsiveness

are at their peak.

Management1. Focused history2. Clinical assessment3. Risk factors for asthma morbidity & mortality4. Treatment

1. Focused History:

• Onset of current exacerbation• Frequency & severity of daytime & night time

symptoms, activity limitation• Frequency of rescue bronchodilator use• Current medications, allergies• Potential triggers• Hx of systemic steroid courses, ER visits,

hospitalization, intubation, or life-threatening episodes.

2. Clinical Assessment:

• Vital signs• Breathlessness, air movement, accessory

muscles use, retractions, anxiety, mental status alteration• Pulse oximetry• Lung function (defer if Pt with moderate-

severe distress)

Manifestation Mild Moderate Severe

Alertness Normal Agitated May be drowsy

Dyspnea Absent, speaks complete sentence

Speaks short phrases, soft short cry

Speaks short phrases, words

Pulsus paradoxus (mmHg)

Less than 10 10-25 25-40

Accessory muscle use None Retractions, sternocleidomastoid

Severe retractions, nasal flaring

Skin color Good Pale Cyanotic

Auscultation End-expiratory wheeze

Inspiratory, expiratory wheeze

Quiet breath sounds

O2 saturation (%)PCO2 (mm Hg)PEFR (% of predicted or best)

More than 95Less than 42More than 80

91-94Less than 4250-80

Less than 91More than or equal 42Less than 50

3. Risk Factors for Asthma Morbidity & Mortality:• Biologic:Previous severe asthma exacerbationSevere airflow obstructionHx of rapidly occurring attacksSevere airway hyper-responsivenessIncreasing & large diurnal variation in peak flowsDecreased chemosensitivity and perception of

dyspneaPoor response to systemic corticosteroid therapyLow birth weightMale gender, Non-white ethnicity

• Environmental:Allergen exposureEnvironmental tobacco smoke exposureAir pollution exposureUrban environment• Economic & Psychological:Poverty, Crowding, Mother younger than 20 yrMother with less than high school educationInadequate medical carePsychopathology in the parent or childFamily problemsAlcohol or substance abuse

4. Treatment

• Oxygen: Mask or nasal cannula

• Monitor pulse oximetry• Maintain oxygen saturation higher than 92%• Cardio-respiratory monitoring

Drug MOA & DosageInhaled short-acting B agonist Bronchodilation

Albuterol nebulizer solution (5 mg/ml concentrate; 2.5 mg/3ml, 1.25 mg/3ml, 0.63 mg/3ml)

Nebulizer: 0.15 mg/kg (minimum 2.5 mg)every 20 min for 3 doses as needed, then 0.15-0.3 mg/kg up to 10 mg every 1-4 hr as needed, or up to 0.5 mg/kg/hr by continuous nebulization

Albuterol MDI (90 Mg/puff)

Levalbuterol (Xopenex) nebulizer solution (1.25 mg/0.5 ml concentrate, 0.31 mg/3ml, 0.63 mg/3ml, 1.25 mg/3ml)

2-8 puffs up to every20 min for 3 doses as needed, then every 1-4 hr as needed

0.075 mg/kg (minimum 1.25 mg) every 20 min for 3 doses, then 0.075-0.15 mg/kg up to 5 mg every 1-4 hr as needed, or 0.25 mg/kg/hr by continuous nebulization

• Nebulizer: when given concentrated forms, dilute with saline to 3 ml total nebulized volume

• For MDI use spacer/holding chamber

• During exacerbations, frequent or continuous doses can cause pulmonary vasodilatation, V/Q mismatch, & hypoxia

• Levalbuterol 0.63 mg is equivalent to 1.25 mg of standard albuterol for both efficacy & AE

• AE: palpitations, tachycardia, arrhythmias, tremor, hypoxemia

Systemic Corticosteroids Anti-inflammatory

Prednisone1, 2.5, 5, 10, 20, 50 mg tablets

Methyl-Prednisolone (Medrol)2, 4, 8, 16, 24, 32 mg tablets

Prednisolone5 mg tablets; 5 mg/5 ml and 15 mg/5 ml solution

Depo-Medrol (IM), Solu-Medrol (IV)

0.5-1 mg/kg every 6-12 hr for 48 hr, then 1-2 mg/kg/day bid (maximum 60 mg/day)

Short course burst for exacerbation: 1-2 mg/kg/day qd or bid for 3-7 days

• Systemic Corticosteroids

• If exposed to chicken pox or measles, consider passive Ig prophylaxis. Also risk of complications with herpes simplex & TB

• For daily dosing, 8 AM administration minimizes adrenal suppression

• Children may benefit from tapering if course exceeds 7 days

Anticholinergics Mucolytic/Bronchodilator

IpratropiumAtrovent (nebulizer solution 0.5 mg/2.5 ml; MDI 18 Mg/inhalation)

Ipratropium with albuterolDuoNeb nebulizer solution (0.5 mg ipratropium + 2.5 mg albuterol/3 ml vial)

Nebulizer :0.5 mg q6-8 hr (tid-qid) as neededMDI 2 puffs qid

1 vial by nebulizer qid

• Anticholinergics:

• Shouldn’t be used as first line therapy; added to B2-agonists

• Nebulizer: may mix ipratropium with albuterol

Injectable Sympathomimitics Bronchodilator

EpinephrineAdrenalin 1 mg/ml (1:1000)EpiPen autoinjection device (0.3 mg; EpiPen Jr 0.15 mg)

TerutalineBerthine 1mg/ml

SC or IM: 0.01 mg/kg (maximum dose 0.5 mg); may repeat after 15-30 min

Continuous IV infusion (terbutaline only): 2-10 Mg/kg loading dose, followed by 0.1-0.4 Mg/kg/min. Titrate in 0.1-0.2 Mg/kg/min increment every 30 min, depending on clinical response

• Injectable Sympathomimitics

• For (extreme circumstances e.g. Impending respiratory failure despite high dose inhaled SABA, respiratory failure)

• Terbutaline is B-agonist selective relative to epinephrine

• Monitoring with continuous infusion: cardiorespiratory, pulse oximetry, BP, serum K

• AE: tremor, tachycardia, palpitations, arrhythmias, HTN, headache, nervousness, nausea, vomiting, hypoxemia

Risk assessment for discharge

• Medical stability: symptoms improvement, bronchodilator tt are at least 3 hr apart, normal physical findings, PEF 70% of predicted or personal best, O2 saturation 92% on room air

• Home supervision: capability to administer intervention, and observe and respond to clinical deterioration

• Asthma education

Respiratory DistressManagement

Respiratory Distress• Clinical condition of increased Respiratory Rate &

use of accessory muscles of respiration.• Can progress into respiratory failure (clinical

condition of inadequate oxygenation or ventilation).

• It’s the primary diagnosis of 50% of patients admitted to the paediatrics ICU

CausesLUNG:• Central airway obstruction

• Peripheral airway obstruction

• Diffuse alveolar damage

RESPIRATORY PUMP:• Chest wall deformity

• Brainstem

• Spinal cord

• neuromuscular

Management• Emergency management: ABCDE.• In patient is not in impending respiratory failure

then non-invasive methods of respiratory support should be tried before initiating mechanical ventilation

• Advantages of non-invasive ventilation:1. Decreased risk of pneumonia.2. No risk of developing ventilator-induced lung

injury.3. Need for less overall sedation.

Oxygen Only Nasal cannula

Simple face mask

Non-rebreather face mask

Deliver up to 4 L O2Deliver up to 10 L O2Deliver up to 15 L O2

Oxygen + non-invasive pressure support

Nasal CPAP; effective in neonates & patients less than 8 Kg

BiPAP; in older children or patients more than 8 Kg

Can provide continuous positive airway pressure with a backup rate

Can provide 2 levels of support with inspiratory positive airway pressure & expiratory positive airway pressure

Non-Invasive Modes of Respiratory Support

• Goal of treatment is the restoration of adequate gas exchange with a minimum of complications.

• Eliminate the initiating factors as quickly as possible.

• Unfortunately, in these acute illnesses the response to treatment is not immediate and frequently the respiratory function must be artificially supported.

• Hypoxemia is more dangerous than hypercarbia.• Administration of supplemental oxygen is a safe

and wise precaution in all patients even in the absence of initial evidence of hypoxemia.

• Mechanical ventilation is necessary in patients of pneumonia with severe hypoxemia and hypercarbia because even the most effective antibiotic therapy require time (at least 24 hrs)

• Ventilatory support must be initiated in the absence of alterations in arterial PCO2 when dysfunction of other systems places gas exchange at jeopardy (e.g. Cardiovascular shock).

References:

• Nelson Textbook of Pediatrics, 18th Edition, Page 421-424, 966-969.

• Ski’s Essential Pediatrics, 2nd edition, Page 654-659.