Status asthmaticus

Status asthmaticus

1. Status Asthmaticus in
Children
Soumya Ranjan Parida
Basic B.Sc. Nursing 4
th
year
Sum Nursing College

2. Chronic inflammatory disorder of the medium and small
airways.
These airways are hypersensitive to certain “triggers” in
the environment.
Intermittent and recurrent episodes of...
–Wheezing
–Shortness of breath
–Chest tightness
–Cough - night, early morning
Usually reversible
Asthma cannot be cured but its symptoms can be
controlled with proper environmental changes and
medication.
What is Asthma ?

3. Status Asthmaticus in
Children
Definition: Status Asthmaticus is a
life threatening form of asthma
defined as “a condition in which a
progressively worsening attack is
unresponsive to the usual appropriate
therapy with adrenergic drugs and
that leads to pulmonary
insufficiency.”

4. Epidemiology
Pathophysiology
Presentation and Assessment
Treatment
Topics Covered

5. Risk factors for fatal asthma
Medical
–Previous attack with rapid/severe
deterioration or respiratory failure or
seizure/loss of consciousness
Psychosocial
–Denial, non-compliance
–Depression or other psychiatric disorder
–Dysfunctional family
: Epidemiology: Epidemiology

6. Status Asthmaticus in
Children
Epidemiology
Pathophysiology
–Cytokines
–Airway pathology
–Autonomic nervous system
–Pulmonary mechanics
–Cardiopulmonary interactions
–Metabolism
Presentation and assessment
Treatment

7. Pathophysiology
Asthma is primarily an
inflammatory disease
Mucous pluggingMucous plugging
Smooth muscle Smooth muscle
spasmspasm Airway edemaAirway edema

8. Inflammatory cytokines
Activated mast cells and
lymphocytes produce pro-
inflammatory cytokines
(histamine, leukotrienes,
PAF,PGD2), which are increased
in asthmatics’ airways and
bloodstream
:: Pathophysiology Pathophysiology

9. Airway
The irritable and inflamed airway is
susceptible to obstruction
triggered by
–Allergens
–Infections
–Irritants including smoke
–Exercise
–Emotional stress
–GE reflux
–Drugs
–Other factors
Pathophysiology

12. Irritable and damaged
airway
HypersecretionHypersecretion
Epithelial damage with
exposed nerve endings
Epithelial damage with
exposed nerve endings
Hypertrophy of goblet
cells and mucus glands
Hypertrophy of goblet
cells and mucus glands
Pathophysiology

13. Autonomic nervous system
BronchodilationBronchoconstriction
SympatheticSympathetic
Circulating catecholamines Circulating catecholamines
stimulate ß-receptorsstimulate ß-receptors
--
ParasympatheticParasympathetic
Vagal signals stimulate Vagal signals stimulate
bronchodilating Mbronchodilating M
2 2 - -
receptorsreceptors
Vagal signals stimulate Vagal signals stimulate
bronchoconstricting Mbronchoconstricting M
33--
receptorsreceptors
Nonadrenergic-Nonadrenergic-
noncholinergic noncholinergic
(NANC)(NANC)
Release of bronchodilating Release of bronchodilating
neurotransmitters (VIP, NO)neurotransmitters (VIP, NO)
Release of tachykinins Release of tachykinins
(substance P, neurokinin A)(substance P, neurokinin A)
Pathophysiology

14. Lung mechanics
Hyperinflation
–Obstructed small airways cause
premature airway closure, leading to air
trapping and hyperinflation
Hypoxemia
–Inhomogeneous distribution of affected
areas results in V/Q mismatch, mostly
shunt
Pathophysiology

15. Severe airflow Severe airflow
obstructionobstruction
Incomplete Incomplete
exhalationexhalation
Increased lung Increased lung
volumevolume
Increased elastic Increased elastic
recoil pressurerecoil pressure
Increased Increased
expiratory flowexpiratory flow
Expanded small Expanded small
airwaysairways
Decreased expiratory Decreased expiratory
resistanceresistance
Compensated:Compensated:
Hyperinflation, Hyperinflation,
normocapnianormocapnia
Decreased expiratory Decreased expiratory
resistanceresistance
Decompensated: Decompensated:
Severe hyperinflation, hypercapniaSevere hyperinflation, hypercapnia
Worsening Worsening
airflow airflow
obstructionobstruction
Pathophysiology

16. Cardiopulmonary
interactions
Left ventricular load
–Spontaneously breathing children
with severe asthma have negative
intrapleural pressure (as low as -35
cmH
2
O) during almost the entire
respiratory cycle
–Negative intrapleural pressure
causes increased left ventricular
afterload, resulting in risk for
pulmonary edema
Pathophysiology

17. Cardiopulmonary
interactions
Right ventricular load
–Hypoxic pulmonary vasoconstriction and
lung hyperinflation lead to increased
right ventricular afterload
Pathophysiology

18. Cardiopulmonary
interactions
Pulsus paradoxus
–P. paradoxus is the clinical correlate of
cardiopulmonary interaction during asthma. It
is defined as exaggeration of the normal
inspiratory drop in systolic BP : normally < 5
mmHg, but > 10 mmHg in pulsus paradoxus.
ExpirExpir Inspir
NlNl
P. P.
paradoxusparadoxus
InspirExpirExpir
Pathophysiology

19. Pulsus paradoxus correlates
with severity
All patients who presented with
FEV
1
of < 20% (of their best FEV
1
while well) had pulsus paradoxus
Pathophysiology

20. Cardiopulmonary
interactions
Negative intrapleuralNegative intrapleural
pressurepressure
Pulmonary edemaPulmonary edema Pulsus paradoxusPulsus paradoxus
HyperinflationHyperinflation
HypotensionHypotension
Altered hemodynamicsAltered hemodynamics
Pathophysiology

21. Metabolism
V/Q mismatchV/Q mismatch
HypoxiaHypoxia
DehydrationDehydration
LactateLactate KetonesKetones
Metabolic acidosisMetabolic acidosis
Increased workIncreased work
of breathingof breathing
Pathophysiology

22. Presentation
Cough
Wheezing
Increased work of breathing
Anxiety
Restlessness
Oxygen desaturation
Chest tightness
Shortness of breath
Audible wheezes : reasonable airflowAudible wheezes : reasonable airflowAudible wheezes : reasonable airflowAudible wheezes : reasonable airflow
““Silent chest” : ominous!Silent chest” : ominous!““Silent chest” : ominous!Silent chest” : ominous!
Pathophysiology

23. Assessment
Findings consistent with impending
respiratory failure:
–Altered level of consciousness
–Inability to speak
–Absent breath sounds
–Central cyanosis
–Diaphoresis
–Inability to lie down
–Marked pulsus paradoxus

24. Clinical Asthma Score
0 1 2
Cyanosis or None In air In 40%
PaO
2
>70 in air < 70 in air <70 in 40%
Inspiratory B/SNl Unequal or Absent
decreased
Expir wheezingNone Moderate Marked
Cerebral Nl Depressed Coma
function Agitated
³ ³ 5 = impending resp failure5 = impending resp failure

25. Chest X-Ray
–Not routinely indicated
–Exceptions:
Patient is intubated/ventilated
Suspected barotrauma
Suspected pneumonia
Other causes for wheezing are being
suspected
Assessment

26. ABG
–Early status asthmaticus: hypoxemia,
hypocarbia
–Late: hypercarbia
–Decision to intubate should not depend
on ABG, but on clinical assessment
–Frequent ABGs are crucial in the
ventilated asthmatic
Assessment

27. Differential Diagnosis of
wheezing
Bronchiolitis
Pneumonia-viral, bacterial, atypical
Congenital abnormalities: larnygotrachelmalacia, vocal cord
paralysis, tracheal or bronchial stenosis, gastro-esophageal
reflux, vascular ring.
Enlarged lymph nodes from infection or tumor
Foreign bodies in trachea, bronchus, or esophagus
Cystic Fibrosis
Aspergillus
Anaphylaxis
Toxic fume exposure

28. Oxygen
Deliver high flow
oxygen, as severe
asthma causes V/Q
mismatch (shunt)
Oxygen will not suppress respiratory drive
in children with asthma
Treatment

29. Fluid
Judicious use of IV fluid necessary
–Most asthmatics are dehydrated on
presentations - rehydrate to euvolemia
–Overhydration may lead to pulmonary
edema
–SIADH may be common in severe asthma
Treatment

30. Antibiotics
Most infections precipitating asthma
are viral
Antibiotics are not routinely
indicated
??
Treatment

31. ß-Agonists
ß-receptor agonists stimulate ß
2
-
receptors on bronchial smooth
muscle and mediate muscle
relaxation
Epinephrine
Isoproterenol
Terbutaline
Albuterol
Relatively ßRelatively ß
22 selective selective
Significant ßSignificant ß
11 cardiovascular cardiovascular
effectseffects
Treatment

32. ß-Agonists
Less than 10% of nebulized drug
reach the lung under ideal conditions
Drug delivery depends on
–Breathing pattern
–Tidal volume
–Nebulizer type and gas flow
Treatment

33. ß -Agonists
Delivery of nebulized
drug
–Only particles between
0.8 - 3 mm are
deposited in alveoli
–Correct gas flow rate is
crucial
–Most devices require
10-12 L/min gas flow to
generate correct
particle size
Treatment

34. •ß -Agonists
Continuous nebulization superior to
intermittent nebulization
–More rapid improvement
–More cost effective
–More patient friendly
Treatment

35. ß -Agonists
Dosage
–Intermittent nebulization
O.1-2.5mg (0.5% solution), dilute with NS to
3 ml
High dose: use up to undiluted 0.5% solution
–Continuous nebulization
0.5mg/kg/hr
High dose: up to undiluted 5% solution (≈ 150
mg/hr)
Treatment

36. ß -Agonists
Intravenous ß - Agonist
–Consider for patients with severe air
flow limitation who remain unresponsive
to nebulized albuterol
–Terbutaline is i.v. ß-agonist of choice
–Loading dosage :10mcg/kg in 10 min
–Maintenance Dosage: 0.5 – 5.0
mcg/kg/min
Treatment

37. ß -Agonists
Side effects
Tachycardia
Agitation, tremor
Hypokalemia
Treatment

38. ß -Agonists
Cardiac side effects
–Myocardial ischemia known to occur with
i.v. isoproterenol
–No significant cardiovascular toxicity
with i.v. terbutaline (prospective study in
children with severe asthma)
–Tachycardia (and tremor) show
tachyphylaxis, bronchodilation does not
Treatment

39. Steroids
Asthma is an inflammatory
disease
Steroids are a mandatory
element of first line therapy
regimen (few exceptions only)
Treatment

40. Steroids
Hydrocortisone 4-8 mg/kg x 1,
then 2-4 mg/kg q 6°
Methylprednisolone 2 mg/kg x1,
then 0.5-1 mg/kg q 4-6°
Treatment

41. Steroids
Significant side effects
–Hyperglycemia
–Hypertension
–Acute psychosis
–Unusual or unusually severe
infections
Steroids contraindicated with
active or recent exposure to
chickenpox
–Allergic reaction
Reported with
methylprednisolone, hydrocortisone
and prednisone*
Treatment

42. Anticholinergics - Ipratropium
Quaternary atropine derivative
Not absorbed systemically
Thus minimal cardiac effects
(may find a fixed/dilated pupil if the nebulizer mask slips
over an eye!)
Treatment

43. Anticholinergics
Change in FEV
1
is significantly greater
when ipratropium was added to ß-
agonists (199 adults)
Highly significant improvement in
pulmonary function when ipratropium
was added to albuterol (128 children).
Sickest asthmatics experienced
greatest improvement
Treatment

44. Ipratropium
Dose-Response Curve in Children (n=19,
age 11-17 yrs)
0
0.1
0.2
0.3
0.4
7.5 25 75 250
Dose (micrograms)Dose (micrograms)
Average increase in FEVAverage increase in FEV
11 (over 4 hrs) (over 4 hrs)
Treatment

45. Ipratropium
Nebulize 250 - 500 mg every 6 hours
Treatment

46. Intubation, Ventilation
Absolute indications:
–Cardiac or respiratory arrest
–Severe hypoxia
–Rapid deterioration in mental state
–Respiratory acidosis does not dictate
intubation
Treatment

47. Why hesitate to intubate
the asthmatic child?
Tracheal foreign body
aggravates
bronchospasm
Positive pressure
ventilation increases
risk of barotrauma and
hypotension
> 50% of morbidity/mortality during severe
asthma occurs during or immediately after
intubation
Treatment

48. Intubation
Preoxygenate, decompress stomach
Sedate (consider ketamine)
Neuromuscular blockade (may avoid
large swings in airway/pleural
pressure)
Rapid orotracheal intubation
(consider cuffed tube)
Treatment

49. Immediately after
intubation
Expect hypotension, circulatory
depression
Allow long expiratory time
Avoid overzealous manual breaths
Consider volume administration
Consider pneumothorax
Consider endotracheal tube
obstruction (++ secretions)
Treatment

50. Mechanical ventilation
Positive pressure ventilation
worsens hyperinflation/risk of
barotrauma
Thoughtful strategies include:
–Pressure-limited ventilation, TV 8-12
ml/kg, short T
i
, rate 8-12/min
(permissive hypercapnia)
–Pressure support ventilation using
PS=20-30 cmH
2
O (may decrease
hyperinflation by allowing active
exhalation)
Treatment

51. Ketamine
Dissociative anesthetic with strong
analgesic effect
Direct bronchodilating action
Useful for induction (2 mg/kg i.v.) as
well as continuous infusion (0.5 - 2
mg/kg/hr)
Induces bronchorrhea, emergence
reaction
Treatment

52. Inhalational anesthetics
Halothane, isoflurane have
bronchodilating effect
Halothane may cause hypotension,
dysrhythmia
Requires scavenging system,
continuous gas analysis
Treatment

53. Theophylline
Role in children with severe asthma
remains controversial
Narrow therapeutic range
High risk of serious adverse effects
Mechanism of effect in asthma
remains unclear
Treatment

54. –Loading Dosage :6-7mg/kg
–Maintenance Dosage; as per age
–6wk-6mth :0.5mg/kg/hr
–6mth-1yr : 0.7mg/kg/hr
–1yr-9yr : 1mg/kg/hr
–9yr-12yr : 0.9mg/kg/hr
–12yr-ad : 0.7mg/kg/hr
Theophylline
Treatment

55. Theophylline
May have a role in selected,
critically ill children with asthma
unresponsive to conventional
therapy:
–Randomized, placebo-controlled, blinded trial
(n=163) in children with severe status
asthmaticus
–Theophylline group had greater improvement in
PFTs and O
2
saturation
–No difference in length
– of PICU stay
–Theophylline group had signifi-
– cantly more N/V
0
10
20
30
40
50
60
P rior 6 hr 12 hr 24 hr
FEV 1 (% )
Placebo
Theophylline
Treatment

56. Magnesium
Smooth-muscle relaxation by
inhibition of calcium uptake
(=bronchodilator)
Dosage recommendation: 25 - 75
mg/kg i.v. over 20 minutes
Treatment

57. Magnesium
Several anecdotal reports
Only one randomized pediatric
trial
–Randomized, placebo-controlled, blinded trial (n=31)
in children with acute asthma in ER (MgSO
4
25
mg/kg i.v. for 20 min)
–Magnesium group had significantly greater
improvement in FEV
1
/PEFR/FVC
–Magnesium group more likely
– to be discharged home
–No adverse effects
0
10
20
30
40
50
60
50 min 80 min 110 min
Placebo
M agnesium
Treatment

58. Helium - Oxygen (Heliox)
Helium lowers gas density (if at least
60% helium fraction)
Reduces resistance during turbulent
flow
Renders turbulent flow less likely to
occur
Treatment

59. Heliox
Helium-oxygen (80:20) decreased
pulsus paradoxus and increased PEFR in
a controlled trial of adult patients
Heliox may worsen dynamic
hyperinflation
Treatment

60. Bronchoscopy, bronchial
lavage
Marked mucus plugging may render
bronchodilating and anti-inflammatory
therapy ineffective
“Plastic bronchitis” has been
described in asthmatic children
Combined bronchoscopy/lavage has
been used in desperately ill asthmatic
children
Treatment

61. Summary
Severe asthma in children is increasing in
prevalence and mortality
Aggressive treatment with ß-agonist, steroids and
anticholinergic is warranted even in the sick-
appearing child
Avoid intubation if possible
Mechanical ventilation will worsen bronchospasm
and hyperinflation
Use low morbidity approach to mechanical
ventilation

64. Management of Asthma Exacerbations in Acute Care Setting
Initial Assessment
• History, physical examination (auscultation, use of
accessory muscles, heart rate, respiratory rate, PEF or
FEV1, oxygen
saturation, arterial blood gas if patient in extremis)
Initial Treatment
• Oxygen to achieve O2 saturation ≥ 90% (95% in
children)
• Inhaled rapid-acting 2-agonist continuously for one hour.
• Systemic glucocorticosteroids if no immediate response,
or if patient recently took oral glucocorticosteroid, or if
episode is severe.
• Sedation is contraindicated in the treatment of an
exacerbation.

65. Reassess after 1 Hour
Physical Examination, PEF, O2 saturation and other tests as needed
Criteria for Moderate Episode:
• PEF 60-80% predicted/personal
best
• Physical exam: moderate
symptoms, accessory muscle use
Treatment:
• Oxygen
• Inhaled 2-agonist and inhaled
anticholinergic every 60 min
• Oral glucocorticosteroids
• Continue treatment for 1-3 hours,
provided there is improvement
Criteria for Severe Episode:
• History of risk factors for near fatal
asthma
• PEF < 60% predicted/personal best
• Physical exam: severe symptoms at rest,
chest retraction
• No improvement after initial treatment
Treatment:
• Oxygen
• Inhaled 2-agonist and inhaled
anticholinergic
• Systemic glucocorticosteroids
• Intravenous magnesiu
Reassess after 1 Hour
Physical Examination, PEF, O2 saturation and other tests as needed

66. Good Response within 1-2
Hours:
• Response sustained 60 min after
last
treatment
• Physical exam normal: No
distress
• PEF > 70%
• O2 saturation > 90% (95%
children
Incomplete Response within 1-2
Hours:
• Risk factors for near fatal asthma
• Physical exam: mild to moderate signs
• PEF < 60%
• O2 saturation not improving
Improved: Criteria for Discharge Home
• PEF > 60% predicted/personal best
• Sustained on oral/inhaled medication
Home Treatment:
• Continue inhaled 2-agonist
• Consider, in most cases, oral
glucocorticosteroids
• Consider adding a combination inhaler
• Patient education: Take medicine
correctly
Review action plan
Close medical follow-up
Poor Response within 1-2 Hours:
• Risk factors for near fatal asthma
• Physical exam: symptoms severe,
drowsiness, confusion
• PEF < 30%
• PCO2 > 45 mm Hg
• P O2 < 60mm Hg

67. Admit to Acute Care Setting
• Oxygen
• Inhaled 2-agonist ― anticholinergic
• Systemic glucocorticosteroid
• Intravenous magnesium
• Monitor PEF, O
Admit to Intensive Care
• Oxygen
• Inhaled 2-agonist + anticholinergic
• Intravenous glucocorticosteroids
• Consider intravenous 2-agonist
• Consider intravenous theophylline
• Possible intubation and mechanical
ventilation
Reassess at intervals
Poor Response (see above):
• Admit to Intensive Care
Incomplete response in 6-12 hours
(see above)
• Consider admission to Intensive Care
if no improvement within 6-12 hours
Improved: Criteria for Discharge Home
• PEF > 60% predicted/personal best
• Sustained on oral/inhaled medication
Home Treatment:
• Continue inhaled 2-agonist
• Consider, in most cases, oral
glucocorticosteroids
• Consider adding a combination inhaler
• Patient education: Take medicine
correctly
Review action plan
Close medical follow-up
Improved