You are on page 1of 21

Status Asthmaticus

PICU RESIDENT LECTURE SERIES


LUCILE PACKARD CHILDRENS HOSPITAL

(UPDATED: JUNE 2014)


Objectives

General principals

Pathophysiology

Pharmacologic Therapies

Respiratory Management
Relevance

Asthma affects 6 million children in the United


States, making it the most common chronic disease
of childhood.1,2
Up to 10 % have severe disease unresponsive to typical
therapeutic interventions.

Annually, childhood asthma accounts for 4 million


outpatient visits, 600,000 emergency department
visits, 150,000 hospitalizations, and 75 deaths.3
Pathophysiology

Primary pathophysiology
Airway inflammation & hyper-reactivity
Smooth muscle spasm
Mucosal edema & plugging

Status asthmaticus
Reversible
Recurrent
Diffuse
Obstructive
Pathophysiology

Pathologic changes in the airway airflow


obstruction premature airway closure on
expiration dynamic hyperinflation hypercarbia

Dynamic hyperinflation or air-trapping also leads


to ventilation / perfusion (V/Q) mismatching
causing hypoxemia

PaO2 = FiO2(Patm PH2o) paCO2/0.8


Pathophysiology

Hypersecretion
Hypersecretion

Epithelial
Epithelial damage
damage
with
with exposed
exposed nerve
nerve
Epithelium

endings
endings

Hypertrophy
Hypertrophy of
of goblet
goblet
cells
cells and
and mucus
mucus glands
glands
Interstium

Equals airway
obstruction and
resultant air trapping
Pharmacologic Targets

Relaxation of bronchial smooth muscles


B2 receptors
M1 receptors

Improving oxygen delivery

Attenuating underlying inflammation

Instituting vigorous pulmonary toilet


Pharmacologic Therapies

Albuterol
Atrovent
Methylprednisone/Decadron
Magnesium Sulfate
Terbutaline
Aminophylline
Heliox
Ketamine
Oxygen
Epineprhine
Albuterol

MOA:
Inhaled B2 agonist
B2 receptor activates adenylate cyclase increases cAMP activates protein kinase
A inhibits of myosin-light chain phosphorylation and decreases intracellular Ca 2+

Dosing: Continuous nebulization 1020 mg/hr with an O 2 flow rate of


1012 L/min
Superior to intermittent nebulization Rapid improvement, cost effective, patient
friendly 4,5

Advantages: rapid acting, rapidly administered, easily titrated

Disadvantages: tachycardia (B 2 effects on heart), hyperglycemia


(glycogenolysis & gluconeogenesis), hypokalemia (intracellular shunting).
Ipratroprium Bromide

MOA:
Muscarinic agonist (anticholinergic)
M1 receptor decrease cGMP decreases intracellular Ca2+

Dosing: 0.250.5 mg nebulized q 4h

Advantages: no systemic anticholinergic action

Disadvantages: unilateral pupillary dilation can


occur with local medication entry
Corticosteroids

MOA:
Systemically reduce inflammation, decrease mucus production, and
enhance the effects of B2-agonists.2
Prevents the sustained inflammatory phase which occurs 6-8 hours
after allergen exposure

Dosing:
Methylprednisone: 0.51 mg/kg IV q 6h (2-4 mg/kg/day), duration 5-7
days
Decadron6: 0.30.6 mg/kg IM x 1

Steroids should be administered IV to assure adequate drug


delivery in a timely manner
Magnesium Sulfate

MOA:
Inhibits Ca2+ influx into cytosol smooth muscle relaxant
Increases B2 agonist affinity for its receptor, thereby potentiating its effect
Inhibits histamine release from mast cells

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: rarely noted: hypotension, respiratory depression &


muscle weakness can be treated with IV Calcium Gluconate
Respiratory depression & muscle weakness are noted at levels >12 mg/dL.
(normal Mg levels are 1.5-2 mg/dL and minimal increase in level is noted with a
single dose)
Terbutaline

MAO:
IV B2 agonist
B2 receptor activates adenylate cyclase increases cAMP activates protein kinase
A inhibits of myosin-light chain phosphorylation and decreases intracellular Ca 2+

Dosing:
Loading dose: 510 mcg/kg IV over 10 min
Continuous infusion: 0.44 mcg/kg/min IV (incr by 0.4 mcg/kg/min q 30 mins)

Advantages: effectively reaches areas of lung by IV infusion that


Albuterol does not due to airway obstruction

Disadvantages / side effects: tachycardia, hyperglycemia, hypokalemia,


(rhabdomyolysis & cardiac ischemia rarely)
Aminophylline

MAO:
Xanthine derivative
competitive nonselective phosphodiesterase inhibitor increase cAMP (by preventing its
degradation) activates PKA inhibits myosin-light chain kinase and decreases intracellular
Ca2+
Inhibits TNF-alpha and leukotriene synthesis

Dosing:
Loading dose: 6 mg/kg over 20 min IV
Continuous infusion: 0.61 mg/kg/min IV

Advantages: may prove very effective in patients resistant to above treatments


given the different MOA

Disadvantages / side effects: N/V, agitation, arrhythmias, seizures


Level q8hr after drug initiation and then every morning.
Therapeutic levels are 10 20 mcg/ml.
Heliox

MOA:
Low-density gas that increases laminar flow of oxygen and
decreases turbulent flow.

Dosing: 60%/40% or 80%/20% helium/O2

Advantages: has no systemic side effects

Other: Data suggests prevents intubation. In


intubated patients, heliox has been shown to decrease
the PIP requirements.
Ketamine

MAO:
Dissociative anesthetic
Bronchodilates by intrinsic catecholamine release
Decreases airway resistance and maintains laryngeal tone & reflexes

Dosing: 0.51 mg/kg IV, 1 time doses or continuous infusion.

Advantages: Ketamine should be the drug of choice for intubation


induction.

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.
ABG

ABGs generally not indicated in an asthmatic

Early status asthmaticus: hypoxemia, hypocarbia


Late status asthmaticus: hypercarbia

Decision to intubate should not depend on ABG, but on clinical


assessment.

Frequent ABGs are crucial in the ventilated asthmatic.


Management

The use of mechanical ventilation during an asthma


exacerbation is associated with significant morbidity
and increased risk of death.

The decision to intubate a patient should not be


delayed until respiratory failure is imminent. If
progressing toward respiratory muscle fatigue, NPPV
may avoid intubation by easing WOB while awaiting
maximal therapeutic effects of pharmacotherapy. 9
Intubation

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
Intubation

General guidelines for mechanical ventilation management:


Start with low tidal volume, permissive hypercapnia strategy.
Tidal volume 4-7 ml/kg (prevents barotrauma / volutrauma, minimize lung
distension)
Goal pH>7.25 (may require HCO3)
Low ventilatory rate 10-14 breaths per minute
I:E ratio 1:4 to 1:6 (avoid air trapping by allowing for complete
exhalation)
PEEP match intrinsic
Peak pressures <30-35 (prevent barotrauma)
Keep well sedated consider ketamine and versed infusions.
As the patient is on steroids, limit use of paralytics (to avoid myopathy)
References

1. National Asthma Education and Prevention Program. Expert panel report 3


(EPR-3): Guidelines for the diagnosis and management of asthma-summary
report 2007. J Allergy Clin Immunol. 2007;120(suppl 5): S94S138
2. Scarfone RJ, Friedlaender E. Corticosteroids in acute asthma: past, present,
and future. Pediatr Emerg Care. 2003;19(5):355361
3. Akinbami et al. Pediatrics. 2009;123(suppl 3):S131S145.
4. Papo MC. Crit Care Med 1993;21:1479-86
5. Ackerman AD. Crit Care Med 1993;21:1422-4
6. Keeney et al. Pediatrics. 2014;133(3):493-499.
7. http://peds.stanford.edu/Rotations/picu/pdfs/14_status_asthmaticus.pdf
8. Howell J. Acute severe asthma exacerbations in children: Intensive care unit
management, www.uptodate.com
9. Mansel et al. Mechanical ventilation in patients with acute severe asthma,
Am J Med. 1990;89(1):42-8