Acute asthma

INTRODUCTION

• Most attacks reversible and improve within minutes to hours of treatment with symptom-free intervals
• Many patients develop chronic airflow limitation, which impacts on diagnosis, management and prevention of further attacks
• 8% of population
• Most common chronic disease of childhood (7%)
• 50% develop before age 10 and another 1/3 before age 40

PATTERNS

• Acute severe asthma (80-90%)
  • Progression over hours or days often with b/g of poor control and recurrent presentations
  • Majority female
  • URTI more common precipitants
  • Responds slowly to therapy
• Hyperacute fulminating asphyxic asthma (10-20%)
  • Onset of symptoms to intubation <3 hours
  • Mostly younger men
  • High bronchial reactivity with relatively normal lung function at rest
  • Responds rapidly to therapy

PATHOPHYSIOLOGY

• Reduction in airway diameter due to smooth muscle contraction, bronchial wall oedema, vascular congestion and thick secretions
• Continuum from acute bronchospasm to chronic airway inflammatory remodelling with non-reversible loss of lung function
• Increased airway responsiveness secondary to viral infection may last 2-8 weeks
• Medication triggers
  • Aspirin/NSAID’s, beta-blockers (inc. topical), sulfating agents, tartrazine dyes and food additives/preservatives
• Changing levels of oestradiol and progesterone can alter airway responsiveness in normal cycle or pregnancy

PATHOPHYSIOLOGY

• Increased WOB
  • Increased airway resistance and reduced pulmonary compliance with high lung volumes
  • Lung volume can reach TLC with severe mechanical disadvantage
• VQ mismatch
  • Airway narrowing, closure and impaired gas exchange

PATHOPHYSIOLOGY

• Cardiopulmonary effects
  • Critical negative intrapleural pressures increase venous return to right heart, but high pulmonary pressures due to hypoxic pulmonary vasoconstriction causes impaired RV outflow and LV filling
  • Also get increased LV afterload due to critical negative intrapleural pressure further limiting LV outflow
  • Get septal shift to LV, further reducing LV output during inspiration
  • Pulsus paradoxus results with SBP drop of 10mmHg during inspiration
  • Lose pulsus paradoxus with fatigue as unable to generate the same negative intrapleural pressures

CLINICAL

• History
  • Symptoms – cough, wheeze, SOB, sputum, fever
  • Pattern – Perennial/seasonal, continual/episodic, onset, duration, severity, triggers
  • Age at onset, chronic management, steroid use, ICU/intubation
• Risk factors for death
  • Past history of severe exacerbation
  • 2 or more hospitalisations for asthma in the past year
  • >3 ED visits for asthma each year
  • >2 canisters per month of SABA
  • Difficulty perceiving airflow limitation or severity
  • Low SES or inner-city resident
  • Illicit drug use
  • Psychiatric disease or medical comorbidities

CLINICAL

• Dyspnoea + wheeze + cough
• Accessory muscle use indicates diaphragmatic fatigue
• Paradoxical respiration (chest deflation and abdominal protrusion on inspiration) indicates pending ventilatory failure
• Directed exam
  • Hyperresonance, decreased breath sounds, prolongation of expiratory phase, usually with wheeze
  • Pulsus paradoxus (inspiratory drop in SBP >20mmHg) indicates severe asthma
  • Normal HR, RR and lack of pulsus paradoxus does not indicate complete relief of airway obstruction

SEVERITY OF ACUTE EPISODE

ASTHMA MIMICS

• CCF
• Upper airway obstruction
• Multiple PE
• Aspiration
• Tumors/disorders causing endobronchial obstruction
• Interstitial lung disease
• Vocal cord dysfunction syndrome
• Anaphylaxis

DIAGNOSIS AND MONITORING

• FEV 1 or PEF provide direct measure of large airway obstruction
  • Sequential measures help guide therapy
  • Patient cooperation for this is essential and may not be possible in critical asthma
• ABG should be reserved for suspected Type 2 failure
  • In critical asthma, normal or slightly elevated PaCO2 indicates extreme airway dysfunction and fatigue
• CXR indicated if suspected pneumothorax, pneumomediastinum, pneumonia or CCF
  • Less than 1/3 of admitted asthma patients have CXR findings

BETA-AGONISTS

• Beta-1 agonism: Positive chronotrope/inotrope, reduced small intestinal tone and motility
• Beta-2 agonism: Bronchodilation, vasodilation, uterine relaxation and skeletal muscle tremor
  • Cause bronchodilation through stimulation of adenyl cyclase converting ATP to cAMP, which enhances binding of Ca to cell membranes, reducing myoplasmic calcium concentration and subsequent relaxation
  • Also inhibit mediator release and promote mucociliary clearance
  • Salbutamol is a racemic 50:50 R and S isomer mix with R isomer responsible for bronchodilation and S isomer having no bronchodilatory effect but long half-life (12 hours)

BETA-AGONISTS

• MDI with spacer delivers the most drug to target airways, better than nebulised
• Maximum 15-20% of drug dose delivered to airways, irrespective of method
• IV infusions carry no benefit and have increased risk
• Nebulised salbutamol carries greater side effect profile
• In severe asthma, 33% of nebulised dose is actually inspired and 20% reaches bronchioles
• Mild/moderate
  • 6-12 puffs 100mcg MDI via spacer every 20-30min or sooner as needed for 3 doses then as often as required with slow titration
• Severe
  • 12 puffs via spacer or 5mg nebs q20min for three doses then 2.5-10mg every 1-4 hours as required
• Life-threatening
  • 2x5mg nebs continuously until dyspnoea improves

IPRATROPIUM BROMIDE

• Anticholinergic effect on large, central airways (vs. salbutamol effect on smaller airways)
• Act by inhibiting post-ganglionic vagal stimulation on larger airways + reduce cGMP concentrations
• Add if poor response to SABA
• 500mcg neb or 8x18mcg puffs via spacer q20min for three doses, then q4-6hr
• Not been shown to have benefit once patient is hospitalised

SYSTEMIC CORTICOSTEROIDS

• Prednisone
  • 40-80mg/day in one or two divided doses until PEFR >70% predicted or best as inpatient
  • Same for 5-10 days for outpatient
  • Aus asthma handbook states 37.5 – 50mg continued 5-10 days OR hydrocortisone 100mg q6h
• Prednisolone preferred for children as more palatable
• IV hydrocortisone 200mg q6h
  • Start reducing dose at 1-3 days according to severity
• Peak anti-inflammatory effect at 4-8 hours after IV or PO administration
• If given within 1 hour of arrival, reduces hospitalisation
• Inhaled agents recommended for all mild persistent asthma or more severe asthma
  • Should provide script for this on discharge if meeting criteria

STATUS ASTHMATICUS

• Acute severe asthma that does not improve with usual doses of inhaled SABA and steroids
• Magnesium
  • Recommended for acute, very severe asthma (FEV1<25% predicted; one word)
  • 5-10mmol over 20 minutes
  • 1.2-2g IV over 20-30 minutes (50mg/kg in children)
  • Target serum level 1-1.5
  • Nebulised magnesium is effective and can follow beta-agonist and steroid therapy – 384mg neb MgSO4 in sterile water
  • May block calcium channels and possibly Ach release at NMJ leading to smooth muscle relaxation and bronchodilation
  • Does not reduce admission rates but improves lung function
• Ketamine
  • Inhibits reuptake of noradrenaline
  • IV 0.2mg/kg bolus then 0.5mg/kg/hr infusion (14mg bolus then 35mg/hr in 70kg adult)
  • Good for RSI and sedation

STATUS ASTHMATICUS

• Adrenaline
  • Often overlooked in status asthmaticus
  • IM 0.5mg in adults for refractory cases may benefit
  • IV 1mg slow load over 5 minutes then 1-20mcg/min
• IV salbutamol
  • 250mcg bolus then 1-20mcg/min
  • No clear evidence of benefit and significant side effect profile
  • Theoretical advantage in reaching lung units with severe airflow limitation
  • Results in lactic acidosis in 70% of patients and can worsen respiratory acidosis and respiratory distress

NIV

• Improves airflow and respiration compared to usual care
• Decreases need for intubation, results in clinical improvement and decreases need for hospitalisation
• Do not initiate if intubation indicated (except as stop-gap while preparing) or suspected pneumothorax
• Can start at EPAP 5 and IPAP 8-10cmH20 with target of RR <25 and Vt 7mL/kg
• Can increase EPAP to 7-10cmH20 if difficulty initiating flow-triggered breaths (to match auto-PEEP/PEEPi) and can increase IPAP if Vt low
• Concerns around PEEP/EPAP above 5cmH20 are less than in mechanically positive-pressure ventilated patients as in spontaneously ventilated patients, matching autoPEEP allows a reduction in work of breathing through decreasing the negative pressures having to be generated to initiate flow

MECHANICAL VENTILATION

• Absolute indications for intubation
  • Deteriorating consciousness
  • Severe exhaustion
  • Arrest
• If severe respiratory acidosis but consciousness remains – continue with maximal therapy
• Hypercarbia may not be tolerated by those with myocardial depression
• More likely to be required in acute severe asthma vs. hyperacute asthma and should consider this when making decision to intubate
• If complaining of exhaustion or deteriorating despite therapy – intubate early
• Mucous plugging is frequent leading to increased airway resistance, atelectasis and pulmonary infection, air trapping and increased residual volume (iPEEP)

MECHANICAL VENTILATION

• Use rapid inspiratory flow rates (80-100L/min), RR <12 and long I:E (>1:4) may alleviate this, expiratory time >=4s is ideal
• Volume control ventilation is commonly used with frequent checking of pressures
• PEEP
  • Oh’s states to use ZEEP initially as PEEP will further increase lung volume
  • In reality, PEEP is usually set to 0-5cmH20 to compensate for resistance of ventilatory circuit
  • Higher PEEP risks raising overall airway pressures above safe levels
  • This is different to spontaneously ventilating patients in whom attempts to match autoPEEP reduce the work of breathing by reducing the negative pressure needing to be achieved to initiate flow
• Permissive hypercarbia with pH >7.2 tolerated
  • Risk of raised ICP, impaired myocardial contractility, vasodilation, pulmonary vasoconstriction
• Ongoing paralysis will be required
• Use largest ET possible and limit circuit length (take out any unnecessary components)
• Load with IV fluids and have vasopressors ready
• Target Pplat <25 and PEEPi <12

CIRCULATORY ARREST WITH ELECTROMECHANICAL DISSOCIATION

• Recognised complications within 10 minutes of intubation
• 20% of patients set to safe levels of initial mechanical ventilation can suffer this due to rapid DHI
• Immediate disconnection for 60-90 seconds
• Heliox or ECMO may be required

POST-INTUBATION HYPOXIA

• DOPES
  • Displaced ETT
  • Obstructed ETT
  • Pneumothorax
  • Equipment
• Mucous plugging is common
• If PTX causing hypoxia, likely to be visible even on supine CXR

PNEUMOTHORAX

• Almost always tension due to severe airflow obstruction
• May be due to positive pressure ventilation, DHI, subclavian line or intercostal catheter insertion for ‘pneumothorax’ during arrest
• Pneumothorax on one side leads to impaired ventilation of that side and subsequent worsened DHI on other side with consequent bilateral PTX
• As soon as PTX identified, reduce RR to reduce risk to other lung
• Insert ICC’s by blunt dissection only

IF BECOMES HYPOTENSIVE?

• DDx – Sedation drugs, DHI, PTX, hypovolaemia, right main intubation, arrhythmias, myocardial depression or positive pressure ventilation impaired venous return
• Steps
  • Disconnect for 60 seconds
  • Slow RR
  • Fluid load
  • Auscultate
  • Check etCO2 and ECG
  • Urgent CXR (not USS as not reliable if minimal air movement)
  • Treat cause
  • Consider heliox/ECMO

MECHANICAL VENTILATION

OTHER AGENTS

• Heliox (80% helium/20% O2)
  • Lowers airway resistance
  • Does not reliably avert intubation, change ICU or hospital admission rates/duration or decrease mortality
• Methylxanthines
  • Risk of seizures and cardiac dysrhythmias but consider for life-threatening asthma
  • Aminophylline 6mg/kg load then 0.5mg/kg/hr (targeting levels of 30-80micromol/L)
• Mast cell modifiers (Cromolyn and nedocromil)
  • Neither indicated for acute bronchospasm
• Leukotriene receptor antagonists (montelukast)
  • No indication in ED

OTHER AGENTS

• Anaesthetic gases
  • Halothane, isoflurane and enflurane
  • Risk of myocardial depression, hypotension and arrhythmias
  • Isoflurane first-line due to least myocardial depression and arrhythmic effects

DISPOSITION AND FOLLOW-UP

• Good response to therapy
• Observed for at least 1 hour after dyspnoea/respiratory distress has resolved
• PEFR or FEV1 >70% predicted or best
• No risk factors for death
• Educated re: spacer and ICS requirement
• Asthma action plan
• Close GP follow-up
• Good social situation
• Compliance with medications
• If not meeting above, SSU or admission is warranted

RISK FACTORS FOR ADMISSION

• Systemic steroid use at time of ED presentation
• Pregnancy is not considered a risk factor for admission despite the slightly increased risk of maternal complications and perinatal mortality

Last Updated on March 8, 2023 by Andrew Crofton