Status Asthmaticus

Background
Acute Exacerbation
Unresponsive
Mild to Severe form
Trend is towards less number of admissions in intensive care1

Han P, Cole RP. Evolving differences in the presentation of severe asthma requiring intensive care unit
admission. Respiration. Sep-Oct 2004;71(5):458-62.
Treatment goals
Reverse airway obstruction
Correct Hypoxemia
Prevent or treat complications like pneumothorax and respiratory
arrest
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 ECP and MBP which induce desquamation of
airway epithelium and expose nerve endings
It leads to further hyper 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.
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
Risk factors
Genetic
GERD
Viral infections
Air pollutants
Medications
Cold exposure
Exercise
Prognosis
Generally good except when combined with heart failure or COPD
Poor prognostic factors include delay in starting treatment especially
steroids
History
Severe dyspnea or hours or days.
Previous intubation and ventilation
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 acute exacerbation
Oxygen saturation below 92% despite supplemental oxygen
Asthma with No Wheezing
Silent chest
Severe obstruction
fatigue
Physical Examination
Tachypnea
Wheezing in early stages
Initially expiratory
Later in both phases, may have absent breath sound in advance stage
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 severe asthma.
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 in one 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, Theophillne level
Chest X-ray
To rule out pneumothorax, pneumomediastinum, heart failure, pneumonia
Complete blood count
CBC with 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 or patient
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 PEF and 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. National Guideline Clearinghouse
Response to treatment
Response to treatment is assessed by Pulse oximetry and spirometry
Impulse Oscillometry Testing
Almost independent of patient cooperation
Valid for all ages from 4 years and older children, adult and geriatric
patients.
Quite breathing i.e Tidal volume breathing for 30 seconds
It measures impedance at different frequencies indicative of central
and peripheral airway resistance.
Bronchodilator therapy often does not reach the peripheral airways.
IOS can provide objective response to drug therapy even when FEV1
can't.
Impulse Oscillometry Testing
Histologic finding
Autopsy of patients dying in few hours showed Neutrophil infiltration
Those who die in days showed Eosinophilic infiltration.
Extensive mucus production and severe bronchial smooth muscle
hypertrophy
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 is discouraged
Oxygen monitoring and therapy
Maintain SatO2 above 92% except in pregnant and cardiac patients where maintain
above 95%.
Endotracheal intubation, ventilation and chest tube placement as needed.
ECMO when needed.
Beta2 Agonists
Albuterol neubulizer continuously 10 15 mg/hour or q5 to 20 min
Albuterol MDI 4 puff with chamber 15 to 30 minute interval
Endotracheal epinephrine has no role.
Intravenous beta2 agonist when inhalation is not possible
Epinephrine 0.3 to 0.5mg subcutaneously (caution in CHF and history
of arrhythmias)
Anticholinergics
Ipratropium bromide every 4 to 6 hours
Synergistic effect with beta2 agonist.
Does not cross blood brain barrier like atropine
Glucocorticoids
Most important treatment in status asthmaticus
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 20 minutes
Sedatives
Usually reserved for intubated patients
In very agitated patients on high bronchodilator therapy a dose of
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
Extracorporeal life support
high risk of developing refractory status asthmaticus.
Patients with a history of multiple incubations
Respiratory failure requiring intubation within 6 hours of admission
Hemodynamic instability
Neurologic impairment at the time of admission
Duration of respiratory failure greater than 12 hours despite maximal medical
therapy.
Practiced in limited centers of the world
references
1. Mikkelsen ME, Pugh ME, Hansen-Flaschen JH, Woo YJ, Sager JS. Emergency extracorporeal life support for asphyxic status
asthmaticus. Respir Care. Nov 2007;52(11):1525-9
2. Coleman NE, Dalton HJ. Extracorporeal life support for status asthmaticus: the breath of life that's often forgotten. Crit Care.
2009;13(2):136
3. Hebbar KB, Petrillo-Albarano T, Coto-Puckett W, Heard M, Rycus PT, Fortenberry JD. Experience with use of extracorporeal life
support for severe refractory status asthmaticus in children. Crit Care. 2009;13(2):R29
Non invasive ventilation
Limited to weaning from ventilation
Not effective in most of the acute cases unlike acute exacerbation of
COPD
Mechanical ventilation
Indications --- already discussed
Considerations
Low volume, lower rate, I:E 1:3-4, addition of PEEP to prevent airway collapse
during expiration (cautiously)
Heavy sedation
Steroids and NMBA can cause prolong paralysis
Monitor flow volume loop, exhaled tidal volume, autoPEEP
Decreased cardiac output due to decreased preload, diastolic hypotension
Fluid and judicious use of noradrenaline / phenylephrine
Arterial line for repeated blood gases
Replace electrolytes
Heliox
Mixture of Helium and Oxygen
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 so the
Oxygen reach to lower airways besides nebulized aerosols.
No effect on caliber of bronchi.