Extubation Algorithm after Thyroidectomy Surgery

Laura Cavallone, M.D.,
Most of the dreaded events related to thyroid surgery are manifested in the post-op period, which include, but are not limited to Hemorrhage, Laryngeal edema, RLN damage, Superior laryngeal nerve damage and Tracheomalacia.
The American Society of Anesthesiologists practice guidelines for management of the difficult airway recommend that, in addition to planning for intubation, the anesthesiologist should have a preformulated strategy for extubation of such patients.
Laura Cavallone, M.D., has designed the “Extubation Algorithm” major neck and upper airway surgery. In herrecent review article, she tried to summarize some of the practical recommendations; however, the evidence behind different extubation strategies and techniques remains sparse.
Extubation Algorithm for Major Neck and Upper Airway Surgery | Society for Head and Neck Anesthesia:
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Ten Golden Rules of Extubation after Thyroidectomy:
1. Easy versus difficult intubation: the rationale for a differentiated strategy at extubation
When the airway is considered difficult [at intubation] there should be consideration for a staged extubation. The [Difficult Airway] Task Force regards the concept of an extubation strategy as a logical extension of the intubation strategy.
 2. Use of steroids in major neck upper airway surgery Controversial and scarce data from specific literature:
 Data from studies in ICU setting suggest that steroids administration prior to extubation decreases the odds ratio for laryngeal edema and subsequent need for reintubation;
 Dexamethasone 8 mg pre-operatively improves post-op nausea, vomiting, pain, subjective vocal function after thyroidectomy
3. Deep asleep versus fully awake extubation
Pros = patient still anesthetized avoids coughing and fighting ventilator which would lead to increased risk of re-bleeding at the site of surgery (due to increased venous pressure and straining on sutures.)
Cons = lack/decrease of protective airway reflexes may lead to increased risk for aspiration and airway obstruction;
 Caveats=easy intubation and mask ventilation are important prerequisites; increased risk of laryngospasm if performed during transition between deep anesthetized state and awake state
Fully awake
Pros = complete recovery of airway protective reflexes and effective spont. breathing are present and may increase safety in the presence of possible difficult re-intubation.
Cons = active protective airway reflexes may lead to increased risk of re-bleeding at the site of surgery (increased venous pressure and straining on wound).
Caveats= if pt. awake but NOT calm and cooperative, safe extubation procedures (e.g. flexible laryngoscopy, positioning of tube exchanger) may be extremely difficult
4. Use of airway exchange catheter for protected extubation
In the presence of a “difficult airway”, use of an Airway Exchange Catheter should be considered
5. Use of CPAP after upper airway surgery
Not always best choice/feasible:
Impaired access for suction
 Impaired possibility to monitor site of surgery
 Fit of mask may be changed after surgery (edema)
 Increased risks of post-op upper airway aspiration
6. Cuff leak test: validated methods
Measurements of expiratory tidal volumes after 4 complete respiratory cycles with the ETT cuff deflated;
 Measurements of expiratory tidal volumes with cuff deflated ONLY at the end of the end-  inspiratory pause
Proposed cut-off values:
 10-12% of the TV that was measured before cuff deflation (average-adult population);
 110-130 ml (average – adult population)
7. Direct laryngoscopy/video-assisted laryngoscopy/fibreoptic for pre-extubation airway exam
Scarce data from literature; considered marginally useful in ICU setting to predict post extubation laryngeal edema
 In the context of upper airway and neck surgery, where factors modifying airway anatomy and physiology and affecting post-extubation airway patency may have intervened intraopeartively, a thorough airway exam prior to extubation is advised.
8. Alternatives to early extubation (re-evaluation at 24-48 hrs versus temporary tracheostomy)
In selected groups of patients, early extubation after upper airway and neck surgery should be avoided and prolonged intubation or temporary tracheostomy should be considered as alternatives
9. Risk of vocal cord paralysis after major neck and upper airway surgery
A significant number of patients experience temporary or permanent vocal cord paralysis after thyroidectomy caused by RLN injury
Reported rates of RLN injury vary greatly in literature; rate reported also depends on the method of examining the larynx (e.g. temporary palsy: 1.4% to 38%)
 • Uncertain role of nerve monitoring during thyroid, PPV 40% and NPV 100%
 Thyroid surgery remains the most common cause of bilateral vocal fold immobility; non-thyroid surgeries (other neck, intracranial and intra-thoracic procedures) are the main cause of iatrogenic monolateral vocal cord paralysis
   Monolateral paralysis more than 50% of times is asymptomatic; bilateral presents with stridor/airway obstruction.
10. Flexible laryngoscopy for post-extubation airway exam
Recommend as “the gold standard method to examine the larynx after thyroidectomy”
Strategies to treat laryngospasm at extubation
Laryngospasm is most commonly seen in the post-extubation phase of anaesthesia, either in theatre or in the recovery area
1 Call for help.
2 Apply continuous positive airway pressure with 100% oxygen using a reservoir bag and facemask whilst ensuring the upper airway is patent. Avoid unnecessary upper airway stimulation
3 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
4 Low-dose propofol e.g. 0.25 mg.kg−1 intravenously may help If laryngospasm persists and/or oxygen saturation is falling:
5 Propofol (1–2 mg.kg−1 intravenously) Whilst low doses of propofol may be effective in early laryngospasm, larger doses are needed in severe laryngospasm or total cord closure
6 Suxamethonium 1 mg.kg−1 intravenously. Worsening hypoxia in the face of continuing severe laryngospasm with total cord closure unresponsive to propofol requires immediate treatment with intravenous suxamethonium succinylcholine. The rationale for 1 mg.kg−1 is to provide cord relaxation, permitting ventilation, re-oxygenation and intubation should it be necessary
7 In the absence of intravenous access suxamethonium can be administered via the intramuscular (2–4 mg.kg−1), intralingual (2–4 mg.kg−1) or intra-osseous (1 mg.kg−1) routes
8 Atropine may be required to treat bradycardia
9 In extremis, consider a surgical airway.
Management of post-obstructive pulmonary oedema:
The negative intrathoracic pressure created by forceful inspiratory efforts against an obstructed airway can lead to post-obstructive (non-cardiogenic) pulmonary oedema. The commonest cause is laryngospasm (> 50%), but post-obstructive pulmonary oedema. Post-obstructive pulmonary oedema occurs after 0.1% of all general anaesthetics. It is more common in young muscular adults (male:female ratio 4:1)
Negative pleural pressures are generated by forceful inspiratory efforts, which increase the hydrostatic pressure gradient across the pulmonary capillary wall and cause fluid leak into the interstitial space. Efforts to exhale against airway obstruction are protective as they result in PEEP, which reduces the capillary wall pressure gradient and fluid leak into the interstitium; PEEP also counters alveolar collapse and de-recruitment.
Negative intrathoracic pressure results in increased venous return (preload) to the right ventricle and increase in the pulmonary capillary blood volume. Hypoxic pulmonary vasoconstriction facilitates fluid shifts into the interstitium. Right ventricular afterload also increases as hypoxia, acidosis and negative intrathoracic pressure increase pulmonary vascular tone. This may result in a shift of the interventricular septum into the left ventricular outflow tract, increasing left ventricular diastolic dysfunction and promoting pulmonary oedema.
Together with reactive catecholamine release, hypoxia, hypercarbia and acidosis cause systemic and pulmonary vasoconstriction, increasing left and right ventricular afterload. Increased hydrostatic pressure in the pulmonary capillaries causes disruption of the alveolar capillary membrane (stress failure), increasing permeability, and may contribute to the development of pulmonary oedema, or cause frank bronchial bleeding, although the generally benign nature and rapid resolution of post-obstructive pulmonary oedema suggest that this is not the predominant mechanism
Management of post-obstructive pulmonary oedema:
1 Treat the cause: relieve the airway obstruction
2 Administer 100% O2 with full facial CPAP mask. In addition to relieving upper airway obstruction, CPAP may reduce oedema formation by increasing mean intrathoracic pressure and minimise alveolar collapse by increasing functional residual capacity, improving gas exchange and reducing the work of breathing
3 Nurse the patient sitting upright
4 If there is fulminant pulmonary oedema with critical hypoxaemia, tracheal intubation and mechanical ventilation with PEEP are necessary. Less severe hypoxia responds to supplemental oxygen and/or non-invasive ventilation, or CPAP [200]
5 Intravenous opioids may help reduce subjective dyspnoea
6 Chest radiography may exclude other complications of difficult airway management and causes of hypoxia (gastric aspiration, pre-existing infection, pneumothorax, barotrauma, pulmonary collapse)
7 Frank haemoptysis may necessitate direct laryngoscopy and/or flexible bronchoscopy
8 Diuretics are often administered, but their efficacy is unproven.
References :
1. Extubation Algorithm for Major Neck and Upper Airway Surgery. Presented by Laura Cavallone, M.D., Washington University School of Medicine in St. Louis, Missouri. Society for Head and Neck Anesthesia.
2. Guidelines: Difficult Airway Society Guidelines for the management of tracheal extubation. Anaesthesia. Volume 67, Issue 3 March 2012 Pages 318–340.

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