Acute Severe

Asthma
Critical Care
Management
LOKESH TIWARI
AIIMS PATNA
Objectives

 General management principals status

asthmaticus

 Assessment
 Pharmacologic Therapies
 Respiratory Management
Pathophysiology

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

 Status asthmaticus
 Reversible
 Recurrent
 Diffuse
 Obstructive
Pathophysiology status asthmaticus

 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
Clinical Definition

 Severe asthma that fails to respond to inhaled β2

agonists, oral or IV steroids, and O2, and that
requires admission to the hospital for treatment
Presentation

Varies by severity, asthmatic trigger, and patient

age.
 Cough
 Wheezing
 Increased work of breathing.
 The noisy chest

The degree of wheezing does not correlate well with

severity of the disease.
Assessment: do not forget PALS

Initial Assessment (PAT)

 Colour
 Breathing
 Circulation

Primary assessment
 Airway
 Breathing
 Circulation
 Disability
 Exposure

Secondary assessment (Focused history and examination)

Predict it

High risk factors for asthma severity and fatality

 Previous severe sudden deterioration,

 Past PICU admissions
 Previous respiratory failure
 Need for mechanical ventilation.
Presentation ‘Red-alerts’

Severe respiratory compromise:

 ‘Silent Chest’ with increased respiratory efforts usually
precede respiratory failure.
 Agitation or dyspnea
 Altered consciousness
 Inability to speak >1-2 words at a time
 Central cyanosis
 Diaphoresis
 Inability to lie down
 Pulsus paradoxus >25 mmHg
 PaCO2 normalization or hypercapnia (ominous)
 Bradycardia
 Severe Hypoxia
Assessment of severity

 Becker Asthma score

 A score >4 is moderate status asthmaticus

 score 7 and above is severe and needs ICU
admission
 Assessment of severity

 Clinical Asthma score

 A score >4 is impending Resp failure

 Score 7 and above is Resp failure
Oxygen therapy

 100% oxygen
 Oxygen saturation monitoring
 Other monitors
Pulsus paradoxus
Cardiopulmonary
Interactions
 Severe the attack, more negative intrapleural
pressure
 Increased left ventricular afterload
 Increased transcapillary filtration of edema fluid
into airspaces resulting in a high risk for pulmonary
edema.
 Overhydration increases microvascular
hydrostatic pressure and further worsens
pulmonary edema.
Cardiopulmonary
Interactions
 High right ventricular afterload due to
 Hypoxic pulmonary vasoconstriction,

 Acidosis

 Increased lung volume.

Chest Radiography

Limited role but indicated in-

 First time wheezers

 Clinical evidence of parenchymal disease
 Those requiring admission to PICU.
 Suspected air leak or pneumonia
 When the underlying cause of wheezing is in
doubt
Arterial blood gas

 In all children at baseline

 Subsequently as indicated
 Hypocarbia in early stage
 Normalization of CO2 with persistent respiratory
distress indicates impending respiratory failure.

 A PaO2<60 mm Hg and a normal or increased

PaCO2 (>45 mm Hg) indicates the presence of
respiratory failure
PICU Admission

 Comfortable environment
 IV access
 Maintain euvolemia
 Continuous cardio-respiratory monitoring
 Avoid sedation
 Monitor potassium
 Antibiotics, if indicated
 If ventilated -arterial and central venous access
Fluid

 Restoration of euvolemia
 Isotonic fluid like normal saline or Ringer’s lactate
 Fluid balance
 Avoid overhydration; Risk of pulm edema
 Serum potassium monitoring
Antibiotics

 Not routinely indicated

 Reserved for children with evidence of bacterial
infection
 High fever

 Purulent secretions

 Consolidation on X ray film or

 Very high leucocyte counts

Pharmacologic Targets

 Improving oxygen delivery

 Relaxation of bronchial smooth muscles

 B2 receptors

 M1 receptors

 Attenuating underlying inflammation

 Instituting vigorous pulmonary toilet

Pharmacologic Therapies

 Oxygen
 β2 agonists
 Steroids
 Anticholinergics
 Magnesium Sulfate
 Aminophylline
 Ketamine
 Heliox
Inhaled β2 agonists

 The mainstay of therapy

 Inhaled, intravenous, subcutaneous, or oral routes
 Salbutamol and terbutaline have relative β2-
selectivity.

 No difference in clinical response to treatment

with racemic salbutamol vs lev-salbutamol in
acute severe asthma in children

Qureshi F. et al. Ann Emerg Med. 2005;46:29–36.

Inhaled β2 agonists

 Continuous nebulization
 0.15–0.5 mg/kg/hr, or 10– 20 mg/hr (Use an infusion
pump)
 Intermittent back-to-back nebulization
 0.15 mg/kg (weaning from cont neb)
 MDI
 4-8 puffs (100 mcg each) per dose

 MDI with a holding chamber is at least as effective

as nebulized salbutamol in young children with
moderate to severe asthma exacerbations

Castro-Rodriguez JA et al J Pediatr. 2004;145:172–7.

Intravenous β2-agonists

 Not to give routinely in acute

exacerbations
Travers A. et al. Cochrane Database Syst Rev. 2001; (2): CD002988.

 Use in patients unresponsive to inhaled β2-agonists

 Those in whom nebulization is not feasible
 Intubated patients,
 patients with poor air entry

 IV Terbutaline
 Loading 10 mcg/kg IV over 10 min, followed by
continuous infusion at 0.1–10 mcg/kg/min.
Subcutaneous β2 agonist

 Primarily used for children with no IV access

 As a rapidly available adjunct to inhaled β2
agonist.
 Subcutaneous terbutaline 0.01 mg/kg/dose (max
of 0.3 mg)
 May be repeated every 15–20 min for up to three
doses.
Adverse effects of β2- agonists

 Cardiovascular system
 Tachycardia

 Increased QTc interval

 Dysarrhythmia

 Hypertension

 Diastolic hypotension.
Adverse effects of β2- agonists

 Excessive CNS stimulation

 Hyperactivity,
 Tremors
 Nausea with vomiting
 Hypokalemia
 Hyperglycemia
Corticosteroids

 First line of therapy

 Early during their hospital visit
 Parenteral: preferred for critically ill children.
 Oral: equal efficacy if it can be given
 Aerosolized: limited role in status asthmaticus
 Effect starts in 1–3 h and reach at max in 4–8 h.
 Corticosteroids

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

 Dosing:
 Hydrocortisone: 10 mg/kg followed by 5 mg/kg 6hrly
 Methylprednisone: 0.5–1 mg/kg IV q 6h (2-4 mg/kg/day)
 Dexamethasone: 0.15 mg/kg/dose 4-6 hrly
 Prednisolone: 1-2 mg/kg/day
 Duration 5-7 days

 In status, steroids should be administered IV to assure adequate

drug delivery in a timely manner
Corticosteroids: Side effects

 Short-term use of high-dose steroids

 Hyperglycemia
 Hypertension
 Acute psychosis
 Prolonged steroid
 Immunosuppression
 Hypothalamic-pituitary-adrenal axis suppression,
 Osteoporosis
 Myopathy
 Weakness
 Anticholinergic Agents

Ipratroprium Bromide
 Mechanism:
 Muscarinic agonist (anticholinergic)
 M1 receptor  decrease cGMP  decreases intracellular Ca2+
 125–500 mcg inhaled every 20 min for up to three doses.
 Subsequently every 4–6 h.
 Dry mouth, bitter taste, flushing, tachycardia, and dizziness.
 Caution: Sometimes unilateral pupillary dilation (local effect)
 Magnesium Sulfate

 Mechanism:
 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

 50 mg/kg IV over 20-30 min with max of 2 gm

 Repeat once or twice after 4–6 h.
Magnesium -Side effects

 Hypotension
 CNS depression,
 Muscle weakness
 Flushing

 Very high serum magnesium levels (usually >10–12

mg/dL).
 Cardiac arrhythmia/ complete heart block,
 Respiratory failure due to severe muscle weakness
 Sudden cardiopulmonary arrest

 Treatment: IV Calcium Gluconate

Aminophylline

•  Mechanism
•  Xanthine derivative

•  Decreases intracellular Ca2+

•  Inhibits TNF-alpha and leukotriene synthesis

•  Loading dose: 6 mg/kg over 20 min IV

•  Continuous infusion: 0.6–1 mg/kg/min IV

•  Limited rolein children unresponsive to steroids, inhaled and IV

β2 agonist, and O2 with status asthmaticus
• Ream RS et al. Chest 2001;119:1480–8.
Aminophylline Toxicity

 Nausea and vomiting

 Tachycardia
 Agitation

 Severe toxicity (high serum concentrations)

 Cardiac arrhythmias,
 Hypotension,
 Seizures
 Death

 Monitor drug level in blood:

 Level q8hr after drug initiation and then every morning.
 Therapeutic levels are 10 – 20 mcg/ml.
Mechanical Ventilation

Indications

 Poor response to initial therapy

 Severe hypoxia
 Rapid deterioration in mental state
 Rising PCO2
 Cardiopulmonary arrest
Intubation Tips

 Preoxygenate with 100% oxygen

 Anticipate hypotension
 Cuffed ET tube with the largest appropriate
diameter
 Avoid histamine-producing agents like morphine
or atracurium
 Ketamine: preferred induction agent due to its
bronchodilatory action.
 Use atropine, Benzodiazepam and by a rapid-
acting muscle relaxant (vecuronium).
Ventilation Principles

 Maintain adequate oxygenation,

 permissive hypercarbia with arterial pH of >7.2
 Adjust minute ventilation
 Slow ventilator rates
 Avoid air trapping:
 Prolonged expiratory phase, short inspiratory time
 Minimal PEEP (debatable)
Stewart TE, Slutsky AS. Crit Care Med. 1996;24:379–80
 Attempt extubation as soon as possible.
Typical Ventilator Setting

 VT of 5–6 mL/kg,
 RR approximately half of the normal for age,
 I: E ratio of 1:3
 PEEP of 2–3 cm of H2O.

 In infants, pressure controlled ventilation: adjust

PIP to achieve adequate ventilation;
Complications

 Hypotension
 Oxygen desaturation
 Pneumothorax/ subcutaneous emphysema,
 Cardiac arrest

 Suspect tension pneumothorax and treat

promptly
Sedation, Analgesia and Muscle Relaxants

 Is sedation needed at all?

 Non ventilated in agitation ?? sedation

 Ketamine
 Fentanyl vs morphine
 Vecuronium vs atracurium
Ketamine

 Mechanism:
 “Dissociative” anesthetic

 Bronchodilates by intrinsic catecholamine release

 Decreases airway resistance and maintains laryngeal tone &
reflexes

 0.5–1 mg/kg IV
 Continuous infusion 1-2 mg/kg/hr
Heliox

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

 Adjunct therapy
 For children unresponsive to conventional therapy
 Children on high-pressure mechanical ventilatory support

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

 No systemic side effects

-Colebourn CL et al. Anaesthesia 2007;62:34–42.

Noninvasive Mechanical Ventilation

 An alternative to conventional mechanical

ventilation in early phase

 While weaning off conventional ventilator

-Carroll CL, Schramm CM. Ann Allergy Asthma Immunol.

2006;96:454–9.
Chest Physiotherapy

 Useful in children with segmental or lobar

atelectasis.
 In others no therapeutic benefit in the critically ill
patient with status asthmaticus.
Leukotriene Modifiers

 Little data to suggest a role for leukotriene

modifiers in acute asthma
 It is not part of standard management of status
asthmaticus

Silverman RA et al. Chest 2004;126:1480–9.

TodiVK, Lodha R, Kabra SK. Arch Dis Child. 2010;95:540–3.
Summary
Indian J Pediatr (2010) 77:1417–1423
Indian J Pediatr (2010) 77:1417–1423
Indian J Pediatr (2010) 77:1417–1423
Indian J Pediatr (2010) 77:1417–1423
Thank you