Download STATUS ASTHMATICUS Definition Status asthmaticus is a life

STATUS ASTHMATICUS
S. Agarwal, MD, S. Kache, MD
Definition
Status asthmaticus is a life-threatening form of asthma in which progressively
worsening reactive airways are unresponsive to usual appropriate therapy that leads
to pulmonary insufficiency.
Epidemiology
In 1994, the prevalence of status asthmaticus was 7.4% in children ages 5-14 years
old with asthma. The rate of death was noted to be 3.7 per 1 million children aged
5-14 years in 1995.
The risk factors for death in adults include:
• Male gender
• Presentation with severe mixed acidosis with extreme hypercapnia (pCO2=
97+/- 31)
• Silent chest exam on admission
The risk factors for death in children include:
• Requiring intubation
• Prior admission to intensive care unit for asthma
• Chronic use of oral corticosteroids
• More than 2 hospitalizations for asthma in the past year, more than 3
Emergency visits to the hospital or health professional’s office in the past year
• History of non-compliance
• History of family disturbances
• Living in poverty
• Underestimating severity of acute attack (American Academy of Allergy,
Asthma, and Immunology (2000). Allergy Report).
Pathophysiology
Status asthmaticus is a reversible, recurrent, diffuse obstructive pulmonary disease
process caused by airway inflammation and hyper-reactivity.
The primary pathophysiology includes:
• Smooth muscle spasm
• Mucosal edema
• Mucous plugging.
These changes in the airway cause airflow obstruction leading to premature airway
closure on expiration which causes hypercarbia and dynamic hyperinflation. This
dynamic hyperinflation or “air-trapping” also leads to ventilation / perfusion (V/Q)
mismatching causing hypoxemia.
Clinical Presentation
The primary signs & symptoms of asthma are cough, dyspnea, and wheezing. SA
patients may be unresponsive to treatment, have minimal respiratory reserve and
have a deteriorating clinical condition. Upper respiratory tract infections are often
found concomitantly and exacerbate the acute reactive airway process. The
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presence or absence of wheezing while examining a child with SA requires special
attention. The clinical exam of wheezing changes as the disease progresses:
- Expiratory wheeze: airways only obstruct during expiration
- Inspiratory and expiratory wheeze: airways are obstructed throughout
Disease
the respiratory cycle
Progression
- Little air movement heard (“tight”): complete airway obstruction occurs
despite maximal patient effort suggesting impending respiratory failure
Other
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exam findings that signify severe respiratory function compromise include:
Retractions
Prolonged expiratory phase
Pulsus paradoxus - systolic blood pressure drop of more than 18 mmHg with
inspiration in teenagers or more than 10 mmHg in children
Evidence of cyanosis/hypoxemia - PaO2 less than 60mmHg, change in
consciousness
Hypercapnia - PaCO2 greater than 40mmHg in presence of dyspnea and
wheezing
Metabolic acidosis
FEV1 or PEFR (peak expiratory flow rate) less than 20% predicted with little or
no response to acute therapy
Differential Diagnosis
The differential for wheezing in the pediatric population is extensive and should be
considered in a patient presenting with wheezing for the first time. Some of the
more common diagnoses include laryngotracheomalacia, other congenital
malformations, vocal cord dysfunction, foreign body, infection (croup, bronchiolitis,
pneumonia), and cardiac disease. “Not all wheezing is asthma.”
Diagnostics
• A chest radiograph should be obtained to define the extent of the associated
parenchymal disease and to rule out other diagnoses (e.g. foreign body,
infiltrate). Hyperinflation and peribronchial thickening are common findings.
• Laboratory tests to evaluate the degree of acidosis and for a potential
infection are beneficial.
• Spirometry can be useful to also assess severity of disease. A fall in FEV1 has
been shown to correlate well with the degree of airway obstruction and
hypoxemia in status asthmaticus.
• Blood gases: Although, blood gases are often discussed in asthma
management, they should not be used to determine the need for intubation.
The patient’s clinical status should be the grounds for intubation – see
intubation section below. An attempt at a blood gas often only agitates the
patient further exacerbating the reactive airway process. Therefore, the need
for a blood gas should be determined prior to acquiring one.
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General Principles of Management
1. An initial drop in O2 saturation may occur once treatment is initiated. After the
initial bronchospasm, as the disease progresses, hypoxic vasoconstriction
causes shunting of blood away from poorly ventilated lungs. With treatment,
the vascular smooth muscle presumably dilates first causing intra-pulmonary
shunting and a transient desaturation. This drop in O2 saturation quickly
resolves and bronchial constriction improves.
2. If it is necessary to assist a patient with status asthmaticus with positive
pressure ventilation (bag-valve-mask or ventilator), use the slowest rate
required to maintain appropriate oxygenation allowing for a long expiratory
time. It must be recognized that intubation is not a treatment for asthma, but
merely temporizes the respiratory failure as other treatments take effect and
the inflammatory process resolves.
3. Declining oxygen saturations is a marker of impending respiratory failure.
Normal O2 saturations however do not indicate adequate respiratory reserve.
Treatment
Intravenous Fluids: Patients in SA are inevitably dehydrated due to poor oral intake,
tachypnea, and often emesis. The dehydration often causes a metabolic acidosis as
well increasing their work of breathing. Rehydration prevents thickening of mucous
secretions and begins to treat the metabolic acidosis.
Albuterol: first line therapy
• Mechanism of action: a β2 agonist responsible for smooth muscle relaxation
• Dosing: Continuous nebulization - 10-20 mg/hr (or 0.5-0.6 mg/kg/hour) with
an oxygen flow rate of 10 – 12L/min
• Advantages: rapid acting and can be rapidly administered
• Disadvantages: tachycardia, hyperglycemia, hypokalemia.
• Other: Nebulization is preferred to MDI
Ipratropium bromide (Atrovent):
• Mechanism of action: anticholinergic, muscarinic – M1, receptors mediate
bronchoconstriction
• Dosing: 0.25 – 0.5 mg nebulized
o Q20 min X 3 doses with continuous albuterol has proven effective in
acute management
o Every 6- 8 hrs with Albuterol for chronic treatment
• Advantages: has no systemic anticholinergic action
• Other: unilateral pupillary dilation can occur with local med entry
Corticosteroids – Solu-medrol
• Mechanism of action: effective in controlling or preventing the sustained
inflammatory phase which occurs 6-8 hours after allergen exposure
• Dosing: Methyl-prednisone
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•
o Loading dose: 2 mg/kg IV
o Maintenance dose: 0.5mg/kg IV q 6hr
Other: Steroids should be administered IV to SA patients to assure adequate
drug delivery in a timely manner. Given the risk of emesis and differential
absorption enterally, the drug should not be administered orally.
Magnesium Sulfate
• Mechanism of action: smooth muscle relaxant
• Dosing: 50 mg/kg IV over 20 min with max of 2 gm
• Advantages: has been shown to be effective in “severe” (FEV1<25%
predicted) asthma
• Disadvantages / Side effects: rarely noted; hypotension, respiratory
depression & muscle weakness can be treated with IV Calcium Gluconate
• Other: respiratory depression & muscle weakness are noted only at levels
>12mg/dL. Normal Mg levels are 1.5-2mg/dL and minimal increase in level is
noted with a single dose of magnesium. Therefore, there should be little
concern by the practitioner of causing respiratory depression with a single
dose of magnesium sulfate.
Terbutaline
• Mechanism of action: IV β2 agonist
• Dosing:
o Loading dose: 5 - 10mcg/kg IV over 10 min
o Continuous infusion: 0.4 - 4 mcg/kg/min IV
• Advantages: effectively reaches areas of lung by intravenous infusion that
Albuterol does not due to airway obstruction
• Disadvantages / side effects: tachycardia, hyperglycemia, hypokalemia,
(rhabdomyolysis & cardiac ischemia – rarely)
• Other: the continuous infusion can be increased every 20-30 minutes by
0.4mcg/kg/min until the patient’s symptoms begin to subside.
Aminophylline
• Mechanism of action: phosphodiesterase inhibitor which allows for smooth
muscle relaxation and augments mucociliary clearance
• Dosing:
o Loading dose: 6 mg/kg over 20 min IV
o Continuous infusion: 0.6 - 1 mg/kg/min IV
• Advantages: may prove very effective in patients resistant to above
treatments given the different mechanism of action
• Disadvantages / side effects: nausea, vomiting, agitation, arrhythmias,
seizures
• Other: A theophylline level needs to be checked 8 hours after drug initiation
and then every morning. Therapeutic levels are 10 – 20 mcg/ml. Beginning a
new medication should prompt a recheck of the level since multiple drugs may
affect the level.
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Heliox
• Mechanism of action: It is a low-density gas that increases laminar flow and
decreases turbulent flow. can be used concomitantly with Albuterol (may
improve delivery), and may be given in intubated or non-intubated patients.
• Dosing: only effective with 60% or greater helium. Patients requiring greater
than 40% FiO2 cannot be placed on heliox.
• Advantages: has no systemic side effects (except causing high pitched voice)
• Other: The data to date is not conclusive, but small studies have shown both
objective and subjective improvements in patients receiving heliox along with
the prevention of intubation. In intubated patients, heliox has been shown to
decrease the PIP requirements.
Ketamine
• Mechanism of action: a “dissociative” anesthetic that bronchodilates by
intrinsic catecholamine release, decreases airway resistance, and maintains
laryngeal tone & reflexes
• Dosing: 0.5-1 mg/kg IV, 1 time doses
• Advantages: Ketamine should be the drug of choice for induction should a
patient with SA requires intubation (see Chapter 11 – Airway Management).
Along with providing sedation for intubation, it also treats the underlying
reactive airway disease
• Disadvantages: increases intracranial pressure
• Other: it can be considered in SA patients with severe agitation, but be
prepared to intubate the patient should it cause hypoxia. Be cautious of
agitation however since it often precedes respiratory failure.
Mechanical Ventilation
The two primary indications to intubate an SA patient are:
• Severe hypoxia
• Depressed level of consciousness
Other potential indications for mechanical ventilation include:
• Obvious life-threatening respiratory distress not responding to bronchodilator
therapy – impending respiratory failure
• Hemodynamic compromise, including bradycardia, severe pulsus paradoxus
• Lactic acidosis associated with increased work of breathing
• Apnea or near-apnea
• Peak flows <40% of predicted
The decision to intubate a patient with asthma should not be taken lightly since:
1) patients are at risk for severe decompensation during intubation
2) mechanical ventilation doesn’t directly help with expiration (which is the
primary problem in a patient with status asthmaticus)
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Potential complications include:
• Pneumothorax / tension pneumothorax – introduction of positive pressure into
hyper-inflated lungs, i.e. air-trapping
• Hemodynamic instability – since they are often volume depleted
Induction meds:
• Anesthetics: Ketamine (for reasons discussed above) & midazolam
• Paralytics: Rocuronium or another rapid onset paralytic (carry out as rapid
sequence intubation)
• Other: Volume to prevent any hemodynamic instability; Lidocaine & Atropine
to prevent any bronchospasm that maybe associated with laryngoscopy
General guidelines for mechanical ventilation management:
1. Start with low tidal volume, permissive hypercapnia strategy.
• Tidal volume 4-7 ml/kg (prevents barotrauma / volutrauma, minimize
lung distension)
• Low Ventilatory rate 10-14 breaths per minute
• I:E ratio 1:4 to 1:6 (avoid air trapping by allowing for complete
exhalation)
• Tolerate hypercapnia
• Goal pH>7.25 (may require HCO3)
• Peak pressures <30-35
2. Keep well sedated – consider ketamine and versed infusions.
3. Prevent bronchoconstriction with suctioning by providing adequate sedation
and Lidocaine.
4. As the patient is on steroids, limit use of paralytics (to avoid myopathy)
5. Bronchoscopy- Maybe effective in patients with signs of large mucus plugs,
e.g. lobar atelectasis in CXR. Particularly seen in African-American, heavy set
adolescent patients.
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