ACUTE ASTHMA EXACEBATIONS
Dr. Ogunkoya John Omotola. MBBS, MWACP, FMCP, Human
Genetics (Cert.)
Senior Lecturer/ Consultant Pulmonologist, Benjamin Carson Snr.
College of Health and Medical Sciences, Babcock
University/Babcock University Teaching Hospital, Ilishan Remo,
Ogun Sate, Nigeria.
Case presentation
• 22 year old man from Okitipupa, Ondo State
• Presents with tight chest, sudden onset breathlessness
and wheezing, occasional dry cough
• Previous episodes, subsided spontaneously
• No TB contact
• No allergies
• Positive family history of similar presentation in maternal
grandmother
• +ve history of triggers
• No important previous medical history
• Not cyanotic
• No clubbing
• Severely distress
Respiratory system
• Tachycardia> 110bpm
• Tachypnea >35cpm
• Rib retraction
• Trachea central
• Reduced breath sounds bilaterally but right more than left
• Expiratory rhonchi
• Audibly wheezing
• Not able to speak in sentences
• Diaphoretic
• 30min after presentation, he became the family member noticed
?very little respiration and non responsive
• Your examination found R/R= 8cpm, diminished chest movement,
now cyanotic.
• What is your impression/diagnosis?
• Highlight your goals of management
• Highlight the steps you will take to ensure
survival of your patient
Which of these is/are the hallmark(s) of your management
• Salbutamol IV
• Solumedrol IV
• Intubation/ mechanical ventilation
• Intranasal oxygen
• Iv aminophylline
• Nebulized salbutamol/ ipratropium bromide
• At this stage very little ventilation right and
hyper-resonant on percussion
Prevalence of acute asthma
• Estimated prevalence in South Africa
– 10 – 15%
• Most asthmatics have mild to moderate
disease, with severe asthma thought to
affect less than 10% of asthmatics.
Levin M.S A Resp r J 2006;12(1) 14- 18.
Moore WC J Allergy Clin Immunol l 2006; 17: 487-494
• Acute attacks of asthma come on
suddenly.
• May occur in patients with well-controlled
asthma, but usually are an indication of
failure of the long-term management plan.
• Acute severe asthma is one of the most
common medical emergency
Status asthmatics
“Defined as wheezing which does not
respond to initial treatment with inhaled
bronchodilators “
Mannix R, Bachur R: Status asthmaticus in children. Curr Opin
Pediatr 2007, 19:281-7.
Werner HA: Status asthmaticus in children. Chest 2001,
119:1913-29.
Acute Asthma Exacerbations :
Definition
• Exacerbations is acute or sub-acute
worsening of symptoms and lung function
from the patients usual status, or in some
cases, a patient may present for the first
time during an exacerbation.
• The terms “attacks”, “episodes” and
“acute severe asthma” are often used, but
they have variable meanings.
• The term “flare-up” is prefarable for use in
discussions with most patients.
Classification of acute asthma
exacerbations
What factors define a severe acute
attacks?
• Disturbance in level of consciousness
• Inability to speak and/or feed
• Severely diminished or absent breath sounds
• Central cyanosis.
• Use of accessory muscles while breathing.
• Increased respiratory (>35 cycles/min.) and
cardiac rate (HR>110 beats/min.)
• Non-invasive objective measures, which aid in
the assessment of the patient with acute asthma
include:
– peak expiratory flow rate (PEF) < 30% of predicted
– pulse oximetry: SPO2<80%
Who are at risk for fatal asthma
• Previous ICU admission for asthma, especially if
mechanical ventilation required
• Current or very recent treatment with prednisone
• Hospitalization or emergency department visit for
asthma in the past year
• Not currently using inhaled corticosteroids
• Excessive use of short-acting inhaled ß2 agonist
• Chronic severity with impaired lung functions
Cardiopulmonary interactions
• Marked changes in lung volume and pleural pressures
impact on the function of both left and right ventricles.
• Spontaneously breathing children with severe asthma
have negative intrapleural pressures
• Mean pleural pressure becomes more negative with
increasing severity of the attack.
• Negative intrapleural pressure causes increased left
ventricular afterload and favors transcapillary filtration of
edema fluid into airspaces resulting in a high risk for
pulmonary edema.
• Right ventricular afterload is increased secondary to
hypoxic pulmonary vasoconstriction, acidosis, and
increased lung volume.
Pulses paradoxus
• This actually inappropriate term describes an
exaggeration of the normal inspiratory drop in
arterial pressure (normally < 5 mm Hg, but < 10
mm Hg in pulses paradoxus).
• Pulsus paradoxus is the result of a marked
inspiratory decrease in left sided cardiac output,
caused by decreased left atrial return from
increased capacitance of the pulmonary vascular
bed, and increased left ventricular afterload from
negative pleural pressures.
Is this asthma?
• (1) Cystic fibrosis
• (2) Primary ciliary dyskinesia
• (3) Bronchiolitis obliterans
• (4) Congenital or acquired airway abnormalities
• (5) Extrinsic allergic alveolitis;
• (6) Inhaled foreign body;
• (7) Gastro-oesophageal reflux;
• (8) Vocal cord dysfunction;
• (9) Hyperventilation/panic disorder
Blood gasses
• Hypoxemia and the increased work of breathing
may result in anaerobic muscle work and
accumulation of lactate.
• During an asthma attack, metabolic acidosis
may initially be compensated for by
hyperventilation and a respiratory alkalosis
• But as respiratory failure develops, increasing
arterial CO2 will result in a respiratory acidosis
and a further decrease in arterial pH
• Increasing levels of CO2 is a ominous sign
• Hypocarbia → Normal PCO2 = trouble
Chest X-ray in severe asthma
• Relevant in search for underlining
complications
– Pneumonia
– Air leakages
– Collapse
• Ventilated patients
Basic treatment of acute asthma
• Repeated doses of short acting B2 agonist
– driven by oxygen
– repeated doses every 15 – 30 min
• Systemic corticosteroids
– The earlier they are administered the better
the outcome
• Oxygen
Oxygen
• Oxygen must be considered as a drug in a
situation of acute asthma
– reducing hypoxic pulmonary vasoconstriction
– ventilation-perfusion mismatch
• Recent guidelines recommend that oxygen
saturation should be kept above 95%
Global Strategy for Asthma Management and Prevention
2008 (update) [http://www.ginasthma.org]
Inhaled bronchodilators
• Inhaled bronchodilators
– B2 agonists
– Adrenaline
– Anticholinergics
• Additional treatment
– IV theophylline
– IV b2-agonists
– IV magnesium sulphate
Inhaled B2 agonists
• There is evidence suggesting that continuous
administration of nebulised β2-agonists may
have a better and prolonged bronchodilatory
effect compared to intermittent therapy
• A sustained stimulation of β2-receptors is
accomplished, and a possible rebound
bronchoconstriction reported during intermittent
therapy is prevented
• An often used rule of thumb is that β2-agonist
should be administered until development of
significant side effects, a strategy requiring close
monitoring
Carroll W, Lenney W: Drug therapy in the management of
acute asthma. Arch Dis Child Educ Pract Ed 2007, 92(3):ep82-ep86
• Nebulizes Salbuterol, 2.5 mg (diluted to 4
mL), in uncomplicated asthma, double the
concentration in severe cases
• Undiluted drug for severe status
asthmaticus.
Werner HA. Chest 2001 ; 119:1913-1929
Nebulized vs MDI B2 agonist
• A meta-analysis performed in 491 children
under 5 years of age with acute
exacerbations.
• Patients who received b-agonists by MDI
and valved holding chamber showed a
significant decrease in the admission rate
compared with those receiving nebulizer
treatments [odds ratio (OR), 0.42;95% CI,
0.24–0.72)]
Castro-Rodriguez JA et al. J Pediatr 2004; 145:172–177.
• Patient may use an empty MDI during an acute
exacerbation.
• Even with adequate supervision, correct MDI
technique, and a full MDI device, hospitalized
children may benefit from nebulized b-agonists
over MDI forms.
• The potential for suboptimal MDI technique may
increase with increasing severity of
exacerbations.
• The nebulized route allows continuous
bronchodilator administration,
Ipratropium bromide
• The combination of nebulised IB with a nebulised ß2
agonist has been shown to result in greater
bronchodilatation than a ß2 agonist alone.
• The most severely affected patients benefit the most,
and IB should be considered in combination with inhaled
ß2 agonists :
– More severe forms of asthma
– Early in the acute attack,
– If there is an incomplete response to inhaled ß2 agonists on their
own
• May be repeated every 20 min for the first hour and
every four hours thereafter
Plotnick LH et al. Cochrane library issue 3 2001
Nebulised adrenaline
• Both the a-agonist and b-agonist effects of adrenaline
might be beneficial, with the a-effect decreasing oedema
and the b-effect responsible for bronchodilation
• In infants and young children with acute asthma and
mucosal oedema and secretion may dominate the
pathophysiology
• Inhaled β2-agonists may be less efficient.
• Nebulised adrenaline has a rapid but short acting effect on
mucosal oedema and may be of value as initial treatment
also in severely obstructed older children, before
administration of inhaled β2-agonists.
Carlsen KH, Carlsen KCL: Pharmaceutical treatment strategies
for childhood asthma. Curr Opin Allergy Clin Immunol 2008,
8(2):166-17
IV aminophylline
• The positive effect from theophylline infusion on acute
asthma is well documented, as are the potential for side
effects and severe or even fatal complications
• May be used in cases of near fatal or life threatening
asthma in the intensive care unit.
• Inhaled drugs may have limited effect in patients with
nearly complete airway obstruction and have practical
limitations in ventilated patients.
• A reasonable starting point is a 6-mg/kg
aminophylline load followed by a 1-mg/kg/h
infusion.
Steroid therapy
• Steroid tablets or liquid are effective as injected steroids.
– Effect after 3-4 hours
• But patient must be able to swallow and not vomit
• Usual dose of oral prednisone or prednisolone is
2mg/kg/day
• Hydrocortisone of 4 mg/kg or methylprednisolone 0.5 -
1.0 mg/kg every 4-6 hour are alternatives to oral
steroids, but may be reserved for children unable to
receive oral administration due to severity or low age
• A prolonged course of treatment may be particularly
necessary if the exacerbation is the result of
longstanding untreated bronchial inflammation.
BTS guidelines 2005
• Higher steroid doses do not appear to offer a
therapeutic advantage, and because the risk of
myopathy is significant, especially in the ventilated
patients
• The concomitant use of systemic corticosteroids and
paralytic agents should be avoided if at all possible.
• There is some suggestion that for patients with
severe symptoms i.v. corticosteroid therapy might
have an early effect (within 1–6 h) by reversing
b2-receptor down regulation seen in chronic
b2-agonist use.
Ellul-Micallef R, Fenech FF. Effect of intravenous prednisolone in
asthmatics with diminished adrenergic responsiveness. Lancet
1975; 2: 1269–71.
Adrenaline
• Adrenaline 0.01 ml/kg of a 1:1000 solu-
tion administered subcutaneously may be
used in patients who are moribund on
presentation to the ED, or where in- haled
therapy is not available.
Magnesium sulphate
• Magnesium cause smooth muscle relaxation secondary to inhibition
of calcium uptake.
• A single dose of IV magnesium sulphate has been shown to be safe
and effective in those patients with acute severe asthma who have
had a poor response to initial therapy.
• The response to magnesium appears to be best in patients who
present with very severe illness.
• The recent GINA-guidelines suggest that iv magnesium may be
considered in acute moderate and severe asthma with incomplete
response to initial treatment during the first 1-2 hours
• The dose is 25 - 50 mg/kg/dose (maximum 2 g) by slow IV infusion.
Ciarallo L et al. J Pediatr 1996;129809-814
Global Strategy for Asthma Management and Prevention
2008 (update) [http://www.ginasthma.org]
IV fluids
• It is inadvisable to overhydrate patients
with acute asthma, and the recommended
IV fluid volume should not exceed 50
ml/kg/24 hours.
• Risks
– Pulmonary oedema
– SIADH
OTHER
• Heliox
– 80:20 mixture of helium-oxygen is most effective, and heliox
loses most of its clinical utility when the FiO2 is greater than
40%, reducing the percentage of helium to less than 60%
• Leukotriene antagonists
– montelukast intravenousl
– administered in the ED to patients presenting with acute
asthma resulted in improved FEV1 within20 min of
administration.
– Patients treated with montelukast tended to receive less
b-agonists and have fewer treatment failures than patients
receiving placebo.
Camargo CA Jr, Smithline HA, Malice MP, Green SA, Reiss TF.
A randomized controlled trial of intravenous montelukast in
acute asthma. Am. J. Respir. Crit. Care Med. 2003; 167: 528– 33.
Intubation
• Intubation and positive pressure ventilation of an
asthmatic may:
– increase bronchoconstriction,
– Increase the risk of airway leakage
– has disadvantageous effects on circulation and cardiac
output
• < 1% of asthmatic admitted to a hospital and 5 to 10% of
asthmatic patients intensive care require intubation.
When to intubate
• Absolute indications for intubation:
– include severe hypoxia
– cardiopulmonary arrest
– severe deterioration of the mental status of the child.
• Relative indications:
– are progress of respiratory failure
– increasing CO2 despite adequate utilisation of all
available treatment measure
– Global initiative for asthma suggests PC02 > 45 mmHg
is an indication for ICU admission
Decision should not only depend on blood gas , but
should be made on clinical grounds
Asthma complications
• Pneumothorax
• Pneumomediastinum
• Pneumopericardium
• Pulmonary interstitial emphysema
• Pneumoretroperitoneum
• Cardiac arrhythmias
• Myocardial ischaemia or infarction
• Mucus plugging
• Atelectasis
• Pneumonia
• Electrolyte disturbances
– Hypokalaemia
– Hypomagnesaemia
– hypophosphataemia)
• Lactic acidosis
• Hyperglycaemia
• Theophylline toxicity
Acute severe asthma
1.Oxgen
Duration of treatment + 1 hour
2.B2 agonist plus IB allowed before next step
3. Steroids
Improvement
No improvement
Risk factors
plus danger
IV magnesium signs
sulphate
Long term
No improvement management
ICU admission for
IV salbutamol or IV aminophyllin
No improvement
Inhalation gas
Intubation plus ventilation HFOV ?
Add Ketamine infusion ECMO?
Use muscle relaxant No improvement
