Status Asthmaticus

Risk factors
• Genetic
• GERD
• Viral infections
• Air pollutants
• Medications
• Cold exposure
• Exercise
Risk factors for developing status asthmaticus
• Increased use of home bronchodilators without improvement or
effect
• Previous intensive care unit (ICU) admissions, with or without
intubation
• Asthma exacerbation despite recent or current use of corticosteroids
• Frequent emergency department visits and/or hospitalization
• Less than 10% improvement in peak expiratory flow rate (PEFR)
• History of syncope or seizures during acuteexacerbation
• Oxygen saturation below 92% despite supplemental oxygen
Etiology
Etiology
• Acute Bronchospastic component marked by smooth muscle
bronchoconstriction.
• Later inflammatory airway swelling and edema
Early bronchospastic response
• Exposure to allergen
• Mast cell degranulation
• Release of histamine, PGD2, LT-C4
• airway smooth muscle contraction, increased capillary permeability,
mucus secretion, and activation of neuronal reflexes
• Bronchoconstriction typically responds to bronchodilator therapy like beta 2
agonist
Later inflammatory response
• Inflammatory mediators prime endothelium and epithelium of
bronchial mucosa.
• Inflammatory cells like eosinophils, neutrophils and basophils attach
to primed endothelium and epithelium and later enter into the
tissues
• Eosinophils release ECPand MBP which induce desquamation of
airway epithelium and expose nerve endings
• It leads to furtherhyper responsiveness.
Later inflammatory response
• Airway resistance and obstruction
• caused by Bronchospasm, mucus plugging, and edema in the
peripheral
• Air trapping
• results in lung hyperinflation, ventilation/perfusion (V/Q)
mismatch, and increased dead space ventilation.
Later inflammatory response
• Increase in pleural and intra alveolar pressure and distended alveoli
leads to VQ mismatch, hypoxemia and increase in minute ventilation.
History
• Severe dyspnea or hours or days.
• Previous intubation and ventilation
Physical Examination
• Tachypnea
• Wheezing in early stages
• Initially expiratory
• Later in both phases, may have absent breath sound in advancestage
• Use of accessory muscles
• Inability to speak more than 1 to 2 words
• Decreased oxygen saturation
• Tachycardia and Hypertension
• Signs of complication, tension pneumothorax, pneumomediastinum
• Peak expiratory flow meter measurement
Assessment of severity of asthma
exacerbation
• Moderate asthma exacerbation:
• Increasing symptoms.
• PEFR >50-75% best or predicted.
• No features of acute severeasthma.
• Acute severe asthma - any one of:
• PEFR 33-50% best or predicted.
• Respiratory rate ≥25 breaths/minute.
• Heart rate ≥110 beats/minute.
• Inability to complete sentences inone breath.
• Life-threatening asthma - any one of the following in a patient with severe
asthma:
• Clinical signs: altered conscious level, exhaustion, arrhythmia, hypotension, cyanosis, silent
chest, poor respiratory effort.
• Measurements: PEFR <33% best or predicted, SpO2<92%, PaO2<8 kPa, 'normal' PaCO2(4.6-
6.0 kPa).
Differential diagnosis
• In children
• Viral infections, bronchiolitis
• Foreign body
• Congestive heart failure
• Extrinsic compression, lymph node, tumor, blood vessel
• Tracheomalacia, primary or secondary
• Inhalational injury
• Other diagnosis, like cystic fibrosis, bronchiectasis etc
Workup
• Blood test
• CBC,ABG, Electrolytes, RBS,Theophillnelevel
• Chest X-ray
• Torule out pneumothorax, pneumomediastinum, heart failure, pneumonia
Complete blood count
• CBCwith differential to evaluate for pneumonia,ABPA, Churg-Strauss
vasculitis
• It could vary because of treatment as well with or without
neutrophilia
• Serum lactate level
Arterial blood gases
• If peak expiratory flow rate is less than 30% of predicted orpatient
best
• Signs of fatigue or progressive airflow obstruction
• Stages of progression
4 stages of blood gas progression with status
asthmaticus
PaCO2 PaO2
Stage 1 Decrease Normal
Stage 2 Decrease Decreased
Stage 3 NORMAL Decreased
Stage 4 High Decreased
Electrolytes and glucose
• Hypokalemia as a result of medications
• Hyperglycemia and in infants hypoglycemia
Need for hospitalization
• If after treatment PEFand FEV1 is between 50% to 70%
• If less than 50% then intensive care admission is indicated

National Heart, Lung, and Blood Institute. Managing exacerbations of asthma. In: National
Asthma Education and Prevention Program (NAEPP). Expert panel report 3: guidelines for
the diagnosis and management of asthma. NationalGuideline Clearinghouse
Treatment goals
• Reverse airway obstruction
• Correct Hypoxemia
• Prevent or treat complications like pneumothorax andrespiratory
arrest
Treatment
• Mainstay of treatment of status asthmaticus are beta 2 agonist, systemic
steroids and theophyllines.
• Pregnant and non pregnant are treated in the same manner
• Fluid replacement, hypokalemia and hypophosphatemia are important to
treat.
• Routine use of antibiotics isdiscouraged
• Oxygen monitoring and therapy
• Maintain SatO2 above 92% except in pregnant and cardiac patients where maintain
above 95%.
• Endotracheal intubation, ventilation and chest tube placementas needed.
• ECMO whenneeded.
Beta2 Agonists
• Albuterol neubulizer continuously 10 – 15 mg/hour or q5 to 20min
• Albuterol MDI 4 puff with chamber 15 to30 minute interval
• Endotracheal epinephrine has no role.
• Intravenous beta2 agonist when inhalation is not possible
• Epinephrine 0.3 to 0.5mg subcutaneously (caution in CHFand history
of arrhythmias)
Anticholinergics
• Ipratropium bromide every 4 to 6hours
• Synergistic effect with beta2 agonist.
• Does not cross blood brain barrier like atropine
Glucocorticoids
• Most important treatment in statusasthmaticus
• decrease mucus production
• Improve oxygenation
• Reduce beta-agonist or theophylline requirements
• Decrease bronchial hypersensitivity
• Help to regenerate the bronchial epithelial cells.
• Oral and IV have same onset of action
• No role of nebulized steroids
• Name any ten Adverse effects of steroids
Bronchodilators
• Methylxanthines theophylline, aminophylline
• bronchodilatation, increased diaphragmatic function, and central
stimulation of breathing
• Narrow therapeutic index, needs monitoring
• Smokers and patients on phenytoin need higher doses
• Side effects, nausea, vomiting, palpitation
• 6mg/kg loading followed by 1mg/kg/hour
Bronchodilators
• Magnesium Sulfate
• relax smooth muscle and hence cause bronchodilation
• Usually 1 gm to 2.5gm is administered as a single dose.
• No studies on repeated doses
• More effective in children. 40mg/kg over 20minutes
Sedatives
• Usually reserved for intubated patients
• In very agitated patients on high bronchodilator therapy a doseof
lorazepam 0.5mg to 1mg intravenous
Therapies for severe and resistant status
despite mechanical ventilation
• Ketamine
• Inhaled anesthetic agents
• NMBA
• Other treatments in case reports and personal experiences
Non invasive ventilation
• Limited to weaning from ventilation
• Not effective in most of the acute cases unlike acute exacerbationof
COPD
Mechanical ventilation
• Indications --- already discussed
• Considerations
• Low volume, lower rate, I:E 1:3-4, addition of PEEPto prevent airway collapse
during expiration (cautiously)
• Heavy sedation
• Steroids and NMBA can cause prolong paralysis
• Monitor flow volume loop, exhaled tidalvolume, autoPEEP
• Decreased cardiac output due todecreased preload, diastolic hypotension
• Fluid and judicious use of noradrenaline / phenylephrine
• Arterial line for repeated bloodgases
• Replace electrolytes
Heliox
• Mixture of Helium andOxygen
• Effective when percentage of Helium is at least 60%, so limiting its use
when FiO2 requirement is high
• It has more laminar flow and less turbulence in small airways sothe
Oxygen reach to lower airways besides nebulized aerosols.
• No effect on caliber of bronchi.
A word about transfer, prevention and long
term care
• Features of stability
• Monitorting FEV1 andIOS
Complications
• Slow compartments vs fast compartments
• Respiratory alkalosis vs hypercarbia
• Cardiac arrest
• Respiratory failure or arrest
• Hypoxemia with hypoxic ischemic central nervous system (CNS)injury
• Pneumothorax or pneumomediastinum
• Toxicity from medications
Prognosis
• Generally good except when combined with heart failure orCOPD
• Poor prognostic factors include delay in starting treatment especially
steroids