5. Asthma exacerbation was not confined to
patients with severe disease or higher levels of
treatment, hence the risk of exacerbation
reflect individual susceptibility
6. Asthma account for ¼ of ED visits per year in
USA.
More than 330 millions have BA worldwide
14% of children has asthma symptoms
4.5% of young adults has asthma
7. 4000 Americans die yearly due to asthma
Females account for 65% of asthma deaths
350.000-400.000 die yearly due asthma
worldwide
8. Oxygen
O2 is mandatory in ASA
Previously it was used liberally
Then to achieve SpO2 94-98%
Now, to achievs SpO2 more than 92%
May be accepted of 88%
9. B-agonists
Salbutamol was discovered by David Jack et al
1966
Salbutamol “albuterol” is the cornerstone of
therapy in ASA, it has immdiate actions 1-5
min “ with 4-6 hours duration
10. Initial dose of salbutamol is 2.5- 5mg every 20
minutes for an hour“ total 7.5 – 15mg” by
nebulization, then 4-6 hours
Doses up to 75-150 mg per hour cause no
more benefits
11. Continuous nebulzation may be used with little
side of efffects, but more cubbersome and
annoying, hence intermittent use is preferred
12. IV salbutamol has no more advantage
exception:
Excessive cough
Moribund patient
Exhaustion
13. B-agnist
Adrenaline dose:
0.01 mg/kg of 1/1000 in 3 divided doses with
20 min. interval. For simplicity 0.3mg for 2
doses with maximum 3 doses
14. Adrenaline is better they selective 2 agonists in
its alpha adrenergic effect that cause
vasoconstriction and decreased airway edema
15. Some authors prefer iv salbutamol to
decreased time of misery and distress of
asthmatics in ASA
21. No more than 200mg / 8 hours of
hydrocortisone or equivalent as no more
efficacy, but more myopathy esp. in MV
patients on NMBA.
Oral steroids equal parenteral except if non
functioning gut
22. IV steroids may have their effect within 4-6
hours
This may occur in one hour thought
1. Reversing down regulation of B-receptions
2. Post transcription epigenetic effect
23. Nebulized high dose ICS in ASA is
controversial, it is helpful in ED Not ICU
Don’t stop ICS in ASA receiving systemic
steroids
24. Ipratropium
Ipratropium needs up to 20 minutes for
its onset of action
Ipratropium is added in 0.25-0.5 mg every 4-6
hours
25. Ipratropium has mild additional bronchodilator
effect on B-agonists
it is reserved for ASA
27. Adding Aminophylline increase both efficacy
and side effects of B-agonist
Side effects are being more prominent
28. Mg so4
Mg So4 is helpful in ASA refractory to B2 –
agonists and steroids
It is not consistently effective
29. Dose of Mg So4
IV route preferred than inhalation
1-2 gm / 20 min / 2 doses
25- 75 mg/kg usual 40 mg /kg”
1g Mg So4 = 98 mg elemental Mg
30. 20 minutes is an empirical choice, as Mg So4
can be given 1gm /min up to 4gm in
preeclampsia
31. Rapid infusion may cause transient
hypotension flushing , or mild drowsiness and
muscle weakness with overdose
32. Mg is an adenyl cyclase stimulator leading to
decreased Ca influx with resultant smooth
muscle relaxation
33. Ketamine
Ketamine dose:
0.1-2 mg / kg loading then
0.1-2 mg / kg / hours “usually 0.5mg”
Duration of action of bolus dose is 10-15 min
The response is rapid in 1-5 minutes
34. First report for ketamine in asthma:
Betts and Parkin, 1971
35. Mode if action of ketamine:
1- Vagolytic effect
2- Increased presynaptic catecholamines
3- Antagonize bradykinins
4- Antagonize inducible NOS
36. Ketamine is not a primary treatment for
asthma in ICU
The worst, the MV patients, are the most
benefited
It may be used in patients with cardiac injury
37. Ketamine may cause
Laryngospasm
Transient increase in ICP
Increased muscle tone
Apnea; if rapid infusion or high dose
Nystagmus, rare
38. Ketamine
ketamine increases airway secretion
How to resolve
1. antisialogogues”: atropine, and
glycopyrrolate.
2. Benzodiazepines is the best to prevent this,
but reserved to MV patient
3. May be used in lowest dose 0.1mg /kg t
minimize this
39. Howton et al, 1996, concluded that there was
no outcome or functional gain for ketamine
over routine treatment except for some
subjective satisfaction
41. Furosemide
Bronchodilator effect of furosemide:
Release of bronchodilator PG “I2”
Blockade of bronchoconstrictor PG “F2alpha”
Counteracting chloride transport in epithelial cells
by blockade of NA-K/CL2 cotransporter
Blockade of inflammatory mediator releases
Inhibit neuropeptide release they by NCNA system
42. Most furosemide studies are small with
conflicting results
Large scale studies are needed
Till now, insufficient evidence, but may be
used as salvage treatment.
43. The antiiflammatory action of furosemide is
not through its diuretic effect.
Furosemide has no anti asthma effect when
used orally or parenterally
Anti Asthma dose of inhaled furosemide is 20-
40 mg / dose / 4-6 hours.
44. Results for furosemide in ASA are mixed
One study showed that inhaled furosemide for
10-28 weeks has steroid sparing effect in
severe steroid dependent asthma
45. No study showed any side effects of inhaled
furosemide or diuretic effect
46. Heparin
Heparin : endogenous glucosaminoglycan
Discovered by Mcleen 1916
First repost as asthma therapy by Dolowitz and
dougherty 1960 With 90% symptoms relief
with IV heparin
Bardona et al 1969, were the first to use
inhaled heparin with mixed result
47. Mechanism of action of heparin
1. Heparin binds and inhibits many
inflammatory mediators including ECP and
peroxidase
2. Heparin increase binding of SLPI with N.
elastase and Cathepsin G reducing their
activity
3. Heparin inhibit lymphocyte activation,
smooth muscle growth, vascular tone and
reduce complement activation
48. The most effective results of heprins are in
preventing antigen induced bronchial
obstruction
The usual dose by inhalation 5000-10000 per
dose – maximize is 100.000 U Being more
effective than cromolyn or placebo
49. No adverse effects of use of up to 80.000 U
heparin by inhalation or any effect on bleeding
profile
Heparin is not absorbed systemically though
bronchial mucosa
51. Heliox
Heliox (70/30) (80/20) (60/40) may delay the
need for MV and give time for other
medicatins to have effect
52. The most commoly used heliox 70/30 may not
help to alleviate hypoxemia
Its best action is only in the 1st hour of use
Heliox may be used as a vehicle for nebulized
therapy
53. In conclusion: Heliox is used only as a trial
therapy, till now
55. They may cause : hypotension and arrhythmia
esp in hypoxemic patient
They may need anaesthesia machine and their
use is complex
56. Ether enema was fist used by Maytum 1931
Then by Kahn 1935
50% efficacy was noticed with repeated doses
of SC ephedrine
Morphine was used in the study
57. IM longterme ether was used by Kahn 1937-
1939
The study included COPD patients with
perplexing effects.
Last vague mention for ether was in Canadian
guidelines of Asthma 1999
Conclusion : do not use
58. Montelukast
IV montelukast was not more effective than
placebo in children with ASA as regard FEV1,
symptoms of hospital admission.
One small study showed rapid small FEVI
59. No approved muco-active drug in ASA
No mention for lidocaine in any asthma
guidelines
Inhaled lidocaine alone or with B2 agonist
protect against histamine induced broncho-
spasm
60. Glucagon
Role of glucagon is extermely limited in ASA
In 1990, one study showed that IMG IV
glucagon reversed ASA in 8/ 14 patients within
10 minutes with no complication
It is a salvage treatment in asthma
In 2000, Wiber et al found no role for glucagon
alone in ASA