Abstract
Extubation and emergence are high-risk phases of anaesthesia which accounted for 28% of the anaesthesia cases reported to the Fourth National Audit Project of the Difficult Airway Society and the Royal College of Anaesthetists. Problems generally relate to the patient’s anatomy, physiology or to the context in which extubation is carried out. Minor issues such as coughing and breath-holding are common, more serious complications such as aspiration, laryngospasm, post-obstructive pulmonary oedema and hypoxic brain injury are often preventable with proper planning. In this chapter we discuss how to formulate an extubation strategy including risk stratification, planning, awake and deep extubation and modifications aimed at reducing the risk of complications. An awake extubation is suitable for most patients but special techniques such as supraglottic airway exchange, remifentanil infusion or the use of an airway exchange catheter may be helpful in high-risk situations. Post-operative care does not end when the tracheal tube has been removed, handover and documentation are essential components of the extubation plan.
Introduction
Extubation is a critical moment which few anaesthetists approach with total confidence, fearing patient harm and the potential for professional embarrassment. Until recently, discussions about airway management have concentrated on laryngoscopy and intubation. Complications associated with extubation were either ignored or thought to be unavoidable. Minor issues such as coughing and breath-holding are common; more serious complications are rare and often preventable with proper planning. Maintaining oxygenation of the patient’s lungs is the priority during and after extubation.
Prevalence of Problems
The UK 4th National Audit Project (NAP4) reported that 28% of very serious airway complications occurred at emergence or following extubation. Of the 38 reported cases, 5 patients suffered a hypoxic cardiac arrest, 10 required an emergency surgical airway and 13 had post-obstructive pulmonary oedema.
Adverse respiratory events are the leading cause of malpractice claims in the USA, disproportionately leading to death and brain injury. The American Society of Anesthesiologists’ Closed Claims database identified 18 claims associated with extubation either in the operating or recovery area. Most of the claims subsequent to extubation were associated with a difficult airway, obesity or obstructive sleep apnoea (OSA) and sadly the data fail to demonstrate any reduction in claims relating to extubation between 1985–92 and 1993–9.
Failed extubation (i.e. the necessity to reintubate shortly after) occurs in approximately 0.1–0.2% of general anaesthetics administered for a wide range of surgical procedures involving adults. The prevalence increases roughly 10-fold for patients having procedures involving their airway and 10-fold again for patients extubated in critical care areas. Patients with OSA may be at 10 times the risk of requiring reintubation.
The Nature of Problems at Extubation
Although removal of the tracheal tube is usually uneventful, a smooth extubation is of special importance for some patients and in particular situations. Airway obstruction after extubation is the commonest cause of major complications at this time. There is increased risk in patients with obesity or sleep apnoea, residual anaesthesia or muscle weakness, surgery which involves the airway or compromises respiratory mechanics, prior airway difficulties and prolonged head-down positioning. Airway stimulation may result in the activation of reflexes such as coughing, laryngospasm or breath-holding. In some patients, even transient hypertension, tachycardia, increased pressures (venous, intra-gastric, intraocular or intracranial) may be problematic. Thus, the risks involved and the strategies chosen to achieve an uneventful extubation depend on the clinical context.
Problems Related to Reduced Airway Tone and Impaired Airway Reflexes
A number of factors may contribute to reduced pharyngeal tone, causing collapse and airway obstruction. This is a particular problem in obese patients, especially when accompanied by OSA with increased sensitivity to opioids and residual anaesthesia. Protective laryngotracheal reflexes are impaired after extubation for several hours and vomiting or regurgitation may result in aspiration. Blood in the airway, especially when concealed in the nasopharynx (‘coroner’s clot’) increases the risk as inhalation of blood clots can cause complete airway obstruction.
Inadequate Reversal of Neuromuscular Blockade
Inadequate reversal of neuromuscular blockade increases the incidence of post-operative respiratory complications. Train of four (TOF) ratios of less than 0.9 are associated with adverse respiratory events. Clinical tests and qualitative assessment of TOF recovery after neostigmine reversal are unreliable and may result in incomplete neuromuscular recovery. As clinicians cannot detect fade with a TOF ratio > 0.7 and cannot distinguish clinically between ratios of 0.4 to 0.7 there is a strong argument for routine use of quantitative neuromuscular monitoring to ensure adequate reversal whenever a neuromuscular blocking agent is used. Sugammadex provides rapid and effective reversal of neuromuscular blockade.
Aspiration
Patients with increased gastric volume, reduced gastrointestinal motility, reduced lower oesophageal sphincter tone or impaired reflexes are at greater risk of aspiration. It is a leading cause of adverse respiratory complications.
Problems Related to Airway Stimulation
Any noxious stimulus applied during emergence from general anaesthesia can trigger laryngospasm, a sustained adduction of the true vocal cords, vestibular folds and/or aryepiglottic folds. Children are particularly predisposed to this maladaptive response (see Chapter 23).
Laryngospasm is an exaggeration of the normal glottic closure reflex, usually in response to airway stimulation. Although animal studies have suggested that hypoxia and hypercapnia may have an inhibitory effect on laryngospasm, it is untrue that the vocal cords will open before brain injury or death occurs.
Partial laryngospasm presents with a characteristic inspiratory ‘crowing’ sound but complete obstruction is silent. Laryngospasm may lead to post-obstructive pulmonary oedema and can progress to hypoxic cardiac arrest and death.
The risk of laryngospasm is greatest if extubation is attempted in a lighter plane of anaesthesia (i.e. between deep anaesthesia and being fully awake). Before extubation, airway suction should be performed under direct vision with the patient deeply anaesthetised, to clear the airway of debris. Further stimulation should be avoided until the patient is awake. Topical lidocaine sprayed onto the vocal cords at induction can reduce the risk after short procedures. Airway reactivity varies with anaesthetic agent, with sevoflurane and propofol being the least irritating. Treatment is shown in Box 21.1.
Initial actions
Call for help
Apply continuous positive airway pressure with 100% oxygen using a reservoir bag and face mask, ensuring the upper airway is patent. Avoid airway stimulation
Larson’s manoeuvre: place the middle finger of each hand in the ‘laryngospasm notch’ between the posterior border of the mandible and the mastoid process whilst also displacing the mandible forward in a jaw thrust. Deep pressure at this point may help relieve laryngospasm
Low-dose propofol e.g. 0.25 mg kg−1 intravenously
Low-dose suxamethonium 0.1 mg kg−1 intravenously
If laryngospasm persists and⁄or oxygen saturation is falling:
A larger dose of propofol may be needed (1–2 mg kg−1 intravenously)
Suxamethonium 1 mg kg−1 intravenously
In the absence of intravenous access suxamethonium can be given intramuscularly (2–4 mg kg−1), intralingually (2–4 mg kg−1) or intraosseously (1 mg kg−1)
Atropine may be required to treat bradycardia
In extremis, a front of neck airway is indicated
Post-obstructive Pulmonary Oedema
Post-obstructive pulmonary oedema occurs after 0.1% of all general anaesthetics, more commonly in young muscular adult males. Forceful inspiratory efforts against an obstructed airway create high negative intrathoracic pressure which can lead to pulmonary oedema. The commonest cause is laryngospasm, but it can also occur if a patient forcibly bites on a tracheal tube or supraglottic airway (SGA) occluding its lumen. It presents with dyspnoea, agitation, cough, pink frothy sputum and low oxygen saturations. The radiograph may show diffuse, bilateral alveolar opacities consistent with pulmonary oedema. Prompt recognition and management usually result in rapid resolution. Death is rare and usually attributable to hypoxic brain injury.
A bite block should always be used during emergence to prevent post-obstructive pulmonary oedema. If the patient does bite down on the tube, deflating the cuff may enable some inward gas flow and reduce the extent of subatmospheric intrathoracic pressure. Management of post-obstructive pulmonary oedema is shown in Box 21.2.
Box 21.2 Management of post-obstructive pulmonary oedema
Relieve the airway obstruction
Administer 100% oxygen with full facial continuous positive airway pressure (CPAP) mask
Sit the patient upright
Tracheal intubation and ventilatory support may be required
Opioids and diuretics may provide comfort and accelerate recovery
A chest X-ray should be obtained to exclude other airway complications
Critical care admission may be required
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