Acute Severe Asthma

OVERVIEW

• increased prevalence worldwide
• significant morbidity and mortality -> related to underestimation of severity
• improved outpatient management + more inhaled corticosteroids have meant less serious presentations
• aetiology: ?’hygiene hypothesis’, IgE dependent inflammatory response:

Characteristics:

• reversible obstruction
• inflammation
• mucous formation

Resulting in:

1. increased WOB – increased airway resistance and decreased pulmonary compliance -> hypercapnic respiratory failure
2. V/Q mismatch – from airway narrowing and closure -> impaired gas exchange and increase WOB to compensate
3. adverse cardiorespiratory interactions – increase venous return because of high intrapleural pressures, but also increased afterload -> pulsus paradoxus

HISTORY

• SOB
• cough
• wheeze
• chest tightness
• status asthmaticus = anyone failing to respond to nebulised bronchodilators
• acute severe asthma (90%) – chronic presentation with previous poor control
• hyperacute, fulminating asthma (10%) – onset over<3h

• previous intubations
• previous control
• multiple admissions
• poor psychological circumstances
• poor response to treatments

Triggers

• specific: URTI, housemite, pollen, animal, aspirin, beta-blockers
• non-specific: cold air, exercise, atmospheric pollutants, stress, emotion

EXAMINATION

• RR
• SpO2
• suprasternal retraction
• upright posture
• sweating

Markers of severe episode

• accessory muscle use
• pulsus paradoxus > 25mmHg
• HR >110
• RR > 25-30
• phrases and words
• PEFR < 50%, < 100L/min
• SpO2 < 92%

Markers of imminent respiratory arrest

• altered mental status
• paradoxical respiration
• bradycardia
• quiet chest
• absence of pulsus paradoxus

INVESTIGATIONS

• ABG: initially respiratory alkalosis -> with tiring CO2 rises -> metabolic lactic acidosis from salbutamol/adrenaline (beta adrenergic stimulation -> increases glycolysis and increased pyruvate+lactate production)
• – CXR: perform in severe asthma, LRTI or barotrauma expected
• – monitor K+
• – Mg2+

DIFFERENTIALS TO CONSIDER

• LVF
• anaphylaxis
• aspiration
• upper airway obstruction (vocal cord dysfunction, tracheal stenosis)
• inhaled foreign body
• PE
• hyperventilation syndrome
• pneumothorax
• parodoxical motion of the vocal cords

MANAGEMENT

Established Treatments

• O2 – titrated to SpO2 92%
• Beta-agonists – salbutamol nebulised/MDI/IV – bolus 250mcg (5-10mcg/kg) -> 1-20mcg/min
• Anticholinergics – ipratropium bromide 500mcg Q2-6 hourly nebulized
• Corticosteroids – hydrocortisone 200mg Q6hrly -> prednisone 0.5mg/kg/day
• Aminophylline – 6mg/kg load -> 0.5mg/kg/hr (check levels daily, aim 30-80micromol/L)

Non-established Treatments

• Adrenaline – nebulised 5mg, SC 0.5mg, IV – load with 1mg -> 1-20mcg/min
• MgSO4 – 5-10mmol over 20min (up to 80mmol have been given)
• Heliox – reduces turbulent air flow, 70:30 (He:O2)
• Ketamine – 0.5-2mg/kg/hr
• Inhalational agents – sevoflurane, anaesthetic machine or custom fitted ventilator required
• Leukotriene anatagonists – some benefit in chronic asthma
• BAL – can clear mucous plugging but transiently worsens bronchospasm

RAPID SEQUENCE INTUBATION

• induction agent:
  — ketamine preferred due to bronchodilation
  — propofol is an alternative, but beware hypotension
• consider a ‘delayed sequence intubation’ approach using ketamine and non-invasive ventilation for pre-oxygenation if experienced
• avoid drugs that cause histamine release and may worsen
• intubated asthma patients are prone to post-intubation hypotension due to dynamic hyperinflation (‘stacking’), hypovolaemia, induction drugs and tension pneumothorax (SH!T)
• initially provide gentle BVM post-intubation then transition to mechanical ventilation with appropriate settings (see below) when stable

VENTILATION

Dynamic Hyperinflation

• slow expiratory airflow -> incomplete exhalation of gas during normal expiratory times -> gas trapping

Dynamic Hyperinflation on controlled MV

• the gas trapping = dynamic hyperinflation
• this continues until an equilibrium point is reached where the exhaled volume matches inspired volume to:

(1) increases small-airway calibre (2) increases lung elastic recoil pressure

-> improvement in expiratory airflow -> allows inspired tidal volume to be exhaled in the available expiratory time available

Assessing DHI in the Mechanically Ventilated

• plateau airway pressure (Pplat) = airway pressure after transient expiratory occlusion at the end of inspiration
• inspiratory hold function on ventilator
• this pressure is directly proportional to degree of DHI
• should be maintained at < 25cmH2O

Other techniques:

• end-inspiratory lung volume – not routinely used but is good predictor of complications during MV
• assessment of change in BP and CVP during ventilator disconnection – disconnect for 1-2 min or decrease rate to 4/min
  -> increase in MAP and CVP if DHI present

Auto-PEEP or PEEPi

• the gas trapped at the end of expiration exerts a positive pressure on the alveoli (intrinsic positive end-expiratory pressure – PEEPi or auto-PEEP)
• during expiration sequential closure of the most severely obstructed airway occurs with only the less obstructed airway remaining in communication with the airway
  -> measured PEEPi underestimates the true magnitude of PEEPi.
  -> the only way to infer whether the patient has occult Auto PEEP is the presence of a elevated Pplat and low Auto PEEP
  -> there must be occult Auto PEEP that is not accounted for when measuring the end-expiratory pressure from gas trapping.

Assessing PEEPi in the Mechanically Ventilated

• = this is the airway pressure during occlusion of expiratory flow at the end of expiration
• end-expiratory hold function on ventilator
• this measurement is known to underestimated PEEPi as a consequence of small airway closure during expiration (occult PEEPi) -> thus this measurement can only be used to show the presence of DHI but not to regulate mechanical ventilation.)
• ideally should be < 12cmH2O but exact safe level unknown.

Non-invasive Ventilation

Advantages

• helps overcome PEEPi from gas trapping -> reduces inspiratory WOB
• augmentation of inspiration -> decreases WOB, increases TV and minute ventilation
• can decrease expiratory work by opposing dynamic airway compression and allowing more expiration with less gas trapping and hyperinflation
• reduce V/Q mismatch
• decreased hospitalisation rate
• significant increase in FEV1
• significant decrease in hospital admission rates
• titrate to patient comfort and decrease in WOB

Disadvantages

• claustrophobia
• agitation
• gastric distension
• dyssynchrony
• increased expiratory work and hyperinflation

Management

• test patients response by starting with CPAP of 5cmH2O and then titrate IPAP and EPAP to patients comfort.
• there is no role for NIV in patients with respiratory or cardiac arrest or those who are uncooperative or can’t protect their airway

Invasive Ventilation

• life saving but associated with major mortality and morbidity

Indications

• arrest
• severe hypoxia
• altered mental state
• failure to respond to treatment

Procedure

• load with IVF and have inotropes ready to go
• large ETT
• RSI with ketamine/propofol
• slow hand ventilation
• attention to possible complications

Ventilator settings

• goals: avoid DHI and hypoventilation

• MV 100mL/kg/min (<8L/min in adult)
• TV 6mL/kg
• RR 10
• short inspiratory time (flow rate 80-100L/min) -> high peak airway pressure but low plateau pressure -> decreased barotrauma
• I:E of 1:>4
• hypercapnia will result -> sedation and often paralysis initially
• PEEP
  – traditionally no PEEP was used out of fear of exacerbating Auto PEEP
  -> but it is now known that PEEP should be set at 60-80% of Auto-PEEP to augment distal airway emptying through splinting airways open

Adjustment of Ventilation

• adjust ventilation to degree of DHI (not PaCO2 or pH)
• if Pplat > 25cmH2O or cardiovascular suppression -> reduce rate
• if Pplat < 25cmH2O -> ventilation can be liberalised with increase in RR and reduction in sedation
• hypercapnia is well tolerated but can consider bicarbonate if pH < 7.1

COMPLICATIONS

HYPOTENSION -> PEA ARREST

• causes:

(1) sedation (2) DHI (3) pneumothorax with tension (4) arrhythmias (5) hypovolaemia (rare) (6) endobronchial intubation (7) myocardial depression from prolonged hypoxia (8) reversal of pleural pressures impairing venous return

-> disconnect from ventilator -> slow RR and load with fluid -> auscultate the chest -> check ETCO2 and ECG -> urgent CXR -> treat cause -> fluids + inotropes -> heliox -> ECMO

PNEUMOTHORAX

-> decrease ventilation to protect other lung -> if hypotensive -> decompress -> if not hypotensive -> urgent CXR as signs not reliable

ACUTE NECROTISING MYOPATHY

• caused by prolonged, deep sedation, steroids +/- paralysis
• results in prolonged weakness and rehabilitation
  -> try to avoid!

References and Links

Journal articles

• Holley AD, Boots RJ. Review article: management of acute severe and near-fatal asthma. Emerg Med Australas. 2009 Aug;21(4):259-68. doi: 10.1111/j.1742-6723.2009.01195.x. Review. PubMed PMID: 19682010. [Free Full Text]
• Stanley D, Tunnicliffe. Management of life-threatening asthma in adults. Contin Educ Anaesth Crit Care Pain (2008) 8 (3): 95-99. doi: 10.1093/bjaceaccp/mkn012 [Free Full Text]
• Wener RR, Bel EH. Severe refractory asthma: an update. Eur Respir Rev. 2013 Sep 1;22(129):227-35. doi: 10.1183/09059180.00001913. Review. PubMed PMID: 23997049. [Free Full Text]