Vocal cord dysfunction causing hypoxaemia in the postanaesthesia care unit

Abstract

Hypoxaemia in the postanaesthesia care unit is common and the majority is caused by hypoventilation or upper airway obstruction due to the (residual) effects of anaesthetic and analgesic agents. We present a case of upper airway obstruction caused by vocal cord dysfunction, a less frequently occurring aetiology. The patient’s case suggests a notable relationship between procedural laryngeal stimulus and the onset of symptoms. Approach to the diagnosis and flexible laryngoscopy to either rule-in or rule-out several relevant differentials are discussed.

Background

Vocal cord dysfunction (VCD) is a disorder that refers to paradoxical adduction of the vocal cords during inhalation and sometimes during exhalation. During normal inhalation, the vocal cords are completely abducted (open). In VCD, the vocal cords are inappropriately adducted (closed), which limits the air flow.^1–3 This may cause stridor, shortness of breath, hyperventilation and wheezing and in severe cases alveolar hypoventilation and hypoxaemia.

Hypoxaemia due to hypoventilation and acute upper airway obstruction is common in the postanaesthesia care unit.³ Central respiratory drive and airway muscle tonus are depressed by a wide range of commonly administered anaesthetic and analgesic agents. Most episodes are self-limiting or resolve by basic techniques such as verbal stimulation, proper positioning, airway manoeuvres and devices or administration of specific antagonists or supplemental oxygen.³

Differential diagnosis

While these aetiologies are responsible for most episodes, other aetiologies occur nonetheless. These may be more difficult to diagnose, differentiate or treat as symptoms (including but not limited to: dyspnoea, wheezing or stridor) can show significant overlap or their pathophysiology is less well understood. Other causes of hypoxaemia in the postanaesthesia care unit include laryngospasm, asthma, angio-oedema, foreign body aspiration, vocal cord paralysis, postoperative bleeding, (airway) oedema or arytenoid subluxation and dislocation.⁴

We describe a case of VCD, a less frequently occurring cause of hypoxaemia and respiratory distress in the postanaesthesia care unit. Its diagnostic challenge, management and background in the context of perioperative care are discussed.

Case presentation

A woman in her 20s with a known history of migraine, depression and attention deficit disorder presented to the emergency department with fever, chills and rigours. In the past few days, an apparent abscess (7×5 cm) had formed in the subcutaneous tissue of the abdominal lower left quadrant. The diagnosis was confirmed by ultrasound and a diagnostic punction was performed after which antibiotic therapy (cefuroxime 1500 mg) was initiated.

The patient was transferred to the operating theatre where she was prepared for surgical incision and drainage. On clinical examination she was alert but anxious, her respiratory rate was 20 breaths per minute and she had a sinus tachycardia of 122 beats per minute with a blood pressure of 128/68 mm Hg. A notable discrepancy in her patient file regarding allergies was discussed with the patient. The patient file reported a severe allergy for amoxicillin/clavulanic acid (angio-oedema, swelling of the tongue), however she denied these side effects and stated she only suffered from mild side effects (gastrointestinal discomfort and nausea).

General anaesthesia was induced with 200 mg propofol, 100 mg lidocaine and 10 μg sufentanil. Apart from a slightly elevated body mass index of 28.7, she presented with no clinical risk factors for difficult mask ventilation and bag-mask ventilation was easily achieved. An initial attempt was made to place a laryngeal mask. However, due to a light plane of anaesthesia, the patient did not tolerate the placement of the laryngeal mask, and an additional 150 mg of propofol had to be given. In a second attempt, the laryngeal mask was placed with ease and anaesthesia was maintained with sevoflurane. After incision and drainage and uneventful anaesthesia, the patient was transferred to the recovery room. The patient was alert and stable, her breathing was sufficient.

After 20 min she developed severe hypoxaemia (SpO₂ reading dropped to 57%), basic airway manoeuvres were employed by the recovery nurse (jaw thrust, nasopharyngeal airway) and her ventilation was supported using a Water’s set (FiO₂ 1.0).

Investigations

Chart review showed she had not received any additional sedatives or opioids so far. The patient experienced and reported dyspnoea and a tight throat. She was able to produce audible speech and her breathing pattern was shallow and paradoxical. There were no visible signs of swelling or (angio)-oedema, however she did develop erythema/rash mainly on her chest. There was a mild intermittent audible stridor depending on breathing effort and breath sounds were normal on auscultation. Airway manoeuvres did not have any positive effect. These episodes recurred several times with accompanying hypoxaemia for which additional oxygen was given.

A chest X-ray and lung ultrasonography showed no abnormalities. Venous blood gas sampling was consistent with mild alveolar hypoventilation (pH 7.32, pCO₂ 55 mm Hg).

The clinical picture was suspect for VCD. However, because of the severity of the hypoxaemia, uncertain allergy history combined with the rash that had developed and recent airway instrumentation other pathologies had to be ruled out. Therefore, transnasal flexible laryngoscopy was performed. It showed almost complete, inappropriate adduction of the vocal cords during inspiration (figure 1, online supplemental file 1). There were no signs of trauma or oedema.

Figure 1.

(A) Flexible laryngoscopy—inappropriate and full adduction (closure) of the vocal cords seen during inspiration. (B) Flexible laryngoscopy—vocal cords during expiration.

Treatment

Flexible laryngoscopy findings were most consistent with VCD. She was reassured and instructed to perform specific breathing exercises (nose-to-mouth breathing, pursed lip breathing) but attempts were terminated as she was unable to fully cooperate and there was no significant clinical effect. A low dose of benzodiazepine (midazolam 1 mg intravenous) was administered as second-tier therapy whereafter her breathing pattern normalised.

Outcome and follow-up

Because of the initial hypoxaemia (SpO₂ readings in 50s), further postoperative observation was performed at the medium care unit. The next morning, she was admitted to the normal ward as she had not shown any further paradoxical breathing or hypoxaemia.

There was no known history of VCD in the patient. It is noteworthy that she experienced a similar episode of dyspnoea and discomfort after a gastroscopy under mild sedation (midazolam) performed in the gastro-enterology department later that year. These symptoms were significantly milder and did not cause hypoxia.

Given the apparent clarity of the trigger for the patient’s VCD, we opted against further diagnostics or follow-up. However, we advised the patient to promptly contact us if symptoms recurred outside a treatment setting. We also emphasised the importance of her informing any treating physicians about this condition and it was documented in her patient file for future reference.

Discussion

VCD is a rare cause of hypoxaemia or respiratory distress in the perioperative period.^{5 6} One should consider the possibility of VCD in case of (recurring) unexplained respiratory distress or hypoxaemia with features of upper airway obstruction. Especially in patients with predisposing characteristics and known possible triggers such as stress and airway instrumentation.^{1 7}

The exact pathophysiology and underlying mechanism of VCD is currently unclear. The disease is primarily regarded as a functional disorder. Some authors suggest that laryngeal hypersensitivity and increased responsiveness play a central role. The increased sensitivity is associated with various factors such as local irritation, gastric reflux disease, viral (upper respiratory tract) infection and emotional stress.^{8 9} Our patient experienced isolated episodes of VCD after procedures that included airway manipulation. This observation suggests that in our patient, who had predisposing factors, a laryngeal stimulus or possibly mild trauma (such as the use of a laryngeal mask or a gastroscope) could potentially trigger an episode of VCD.

The true prevalence of VCD is unknown as uniform diagnostic criteria are absent and there is significant overlap with symptoms of other diseases. Originally, it was thought to occur more frequently in young female patients with psychiatric comorbidity.¹⁰ While younger age and absence of other objective diagnosis increase the likelihood of VCD, it is important to realise that VCD can co-exist with other pathology such as asthma or upper respiratory tract infection.^{1 11 12} Cases that fail to respond to perceived adequate treatment should trigger the physician to consider VCD as a possible cause.¹² Not considering the diagnosis may lead to inadequate or unnecessary treatment ranging from nebulisation of bronchodilators and steroid and adrenalin administration to even (repeated) intubation or tracheostomy with consequent ICU admissions.^{7 13}

Diagnosing VCD can be challenging and in case of severe acute respiratory distress and hypoxaemia supportive therapy has first priority. Subsequently, most common and life-threatening disorders must be ruled out first. In this case, we had to exclude airway trauma after (failed) laryngeal mask placement and angio-oedema since the patient developed a rash and had an ambiguous history for antibiotic allergy. Fibre optic laryngoscopy should be considered as first-line diagnostic as it is able to rule out other supraglottic pathology and aids to confirm a definitive diagnosis while visualising the vocal cords during an episode.¹ During laryngoscopy, attention must be paid to observing both the inspiratory and expiratory phases. This is crucial for detecting the paradoxical adduction of the vocal cords that typically occurs during inspiration. Stridor or paradoxical breathing occurs simultaneously with the adduction of the vocal cords. While alternatives like ultrasonography, CT and MRI can be employed to assess vocal cord motion, fibre optic laryngoscopy continues to be the gold standard.^14–18 It is important to note that these alternative imaging modalities may necessitate specialised expertise for accurate interpretation and are still subject of debate.¹⁸ Spirometry is another non-invasive diagnostic modality which can also play a role in supporting the diagnosis.^{1 3}

When considering the onset of symptoms such as stridor and dyspnoea, we speculate about the role of the patient’s respiratory drive during the early postanaesthesia recovery phase. Given the potential for residual sedation to diminish respiratory drive, it is conceivable that VCD was present but asymptomatic immediately after surgery. As the effects of sedation and analgesia gradually subsided, the patient’s respiratory drive likely increased. Increased respiratory drive along with increased inspiratory flow rates might have led to a relative narrowing of the airway at the vocal cord level causing stridor and sensation of dyspnoea. Notably, the onset of dyspnoea itself could further escalate respiratory drive, creating a feedback loop that exacerbates both the sensation and the physical symptoms of respiratory distress.

The aetiology of the rash remains uncertain. Its morbilliform nature, together with the delayed onset, >1 hour after the last intravenous drug administration, argue against but does not exclude a classic type I IgE-mediated or non-IgE-mediated (anaphylactoid) reaction. When faced with the challenge of securing a definitive diagnosis, measuring tryptase levels may serve as a helpful (retrospective) tool for either excluding or including anaphylaxis as a potential diagnosis. It is important to emphasise that this should not delay the initiation of anaphylaxis treatment when clinical suspicion is high. In our specific case, we did not assess tryptase levels as flexible laryngoscopy provided a conclusive diagnosis.

Once the diagnosis of VCD is established, therapeutic breathing techniques can be used in an attempt to undo or alleviate the VCD.⁷ If these are unsuccessful or cannot be performed, non-invasive positive-pressure ventilation or helium-oxygen therapy can be used to relief symptoms.¹⁵ Sedatives and benzodiazepines may be effective, but could cause respiratory suppression and therefore must be used with caution.⁷ It must be noted that evidence on acute management is scarce. Long-term treatment and recurrence may require a more multidisciplinary approach including otolaryngology and speech therapy consultation.¹⁸ Predisposing factors or pathology should be addressed.

This case underscores the efficiency of diagnosing VCD when personnel capable of visualising the vocal cords are present during an episode. However, it is important to acknowledge that cases with less evident triggers, particularly those presenting in emergency settings, may pose unique challenges. These scenarios may necessitate a more extensive diagnostic workup by specialised physicians and a multidisciplinary approach to treatment.

Conclusion

VCD may occur in the postanaesthesia care unit and the diagnosis should be considered in case of poorly understood hypoxaemia or upper airway obstruction. Flexible laryngoscopy, within the skill-set of for instance an anaesthesiologist or otolaryngologist, can help to either rule-in or rule-out the VCD and other more severe differentials.

Learning points.

• Vocal cord dysfunction should be considered in case of unexplained dyspnoea, upper airway obstruction or hypoxaemia.

• Vocal cord dysfunction may mimic alternative and more severe causes of upper airway obstruction in the recovery room such as laryngospasm and angio-oedema or anaphylaxis.

• Flexible laryngoscopy aids the physicians in securing the diagnosis while excluding other differentials.

Ethics statements

Patient consent for publication

Consent obtained directly from patient(s).