Fentanyl-Induced Wooden Chest Syndrome Masquerading as Severe Respiratory Distress Syndrome in COVID-19

G. I. Judd, R. W. Starcher, D. Hotchkin
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引用次数: 1

Abstract

Introduction: Wooden chest syndrome (WCS) is a rare and often fatal reaction to fentanyl where airways and chest wall musculature become rigid through α1-noradrenergic activation and cholinergic modulation causing ineffective ventilation.1-4 This dose-independent response is more easily diagnosed in non-ventilated patients either in the operating room or who overdose recreationally.2,4,5 In ventilated patients with acute respiratory distress syndrome (ARDS) it can be difficult to distinguish from poor lung compliance. We describe a case of a previously healthy male with COVID-19 on mechanical ventilation who developed WCS.Case: A 47-year-old previously healthy male was admitted for COVID-19 pneumonia requiring high-flow nasal cannula. On hospital day 11, he was intubated and placed on lung protective ventilation for moderate ARDS (PaO2/FiO2 192). On ventilator day (VD) 2 a fentanyl infusion was started. After 36 hours, hypoxemia improved but plateau pressures were consistently <30 cm H2O necessitating a decrease to 4 cc/kg after minimizing dead space within the ventilator circuit. A trial of airway pressure release ventilation worsened hypercarbia and bronchoscopy did not reveal mucous plugging, airway collapse, or purulent secretions. Worsening lung compliance (PPlat 50 on 4 cc/kg) without change in oxygenation raised suspicion for WCS, so fentanyl was discontinued. Within one hour, plateau pressures nadired at 16 and the ventilator was changed to pressure support. The patient was successfully extubated on VD 10.Discussion: Differentiating low lung compliance in classical ARDS from disproportionately compliant hypoxemia in COVID-19-induced ARDS is an ongoing point of research in the thoracic community.6-9 The novelty of this paradigm allows potential to overlook less common, if not rare, complications such as fentanyl-induced WCS. Our patient's poor compliance despite relatively quick improvement in oxygenation countered available evidence on COVID-19 lung physiology, prompting suspicion for an alternative explanation for his poor ventilation. With descriptions of WCS limited to case reports we found that onset and severity of initial signs (contraction of the chest wall, diaphragm, and abdominal and laryngeal muscles2) can be masked in mechanically ventilated patients. Inadequate ventilation can be interpreted as manifestations of high airway and alveolar pressure making it difficult to differentiate it from classical ARDS and ultimately increasing ventilator use duration. To our knowledge, this is the first report of WCS in a patient with COVID-19 associated ARDS. It demonstrates that when mechanically ventilated COVID-19 patients receiving fentanyl have poor lung compliance and oxygenation improves disproportionately faster than ventilation, WCS should be considered.
芬太尼诱发的木胸综合征伪装成COVID-19严重呼吸窘迫综合征
木胸综合征(WCS)是一种罕见且通常致命的芬太尼反应,气道和胸壁肌肉组织通过α - 1-去甲肾上腺素能激活和胆碱能调节而变得僵硬,导致无效通气。1-4这种与剂量无关的反应更容易在非通气的患者中诊断出来,无论是在手术室还是因娱乐而过量用药。2,4,5在急性呼吸窘迫综合征(ARDS)患者中,很难将其与肺顺应性差区分开来。我们描述了一例先前健康的男性COVID-19患者在机械通气后出现WCS。病例:一名47岁健康男性因COVID-19肺炎入院,需要高流量鼻插管。住院第11天,患者因中度ARDS (PaO2/FiO2 192)插管并给予肺保护性通气。在呼吸机日(VD) 2开始芬太尼输注。36小时后,低氧血症得到改善,但平台压一直为30 cm H2O,需要在最小化呼吸机回路内的死区后降至4 cc/kg。气道压力释放通气的试验加重了高碳化,支气管镜检查未发现粘液堵塞、气道塌陷或化脓性分泌物。肺顺应性恶化(4 cc/kg时ppl50)而氧合没有改变,这引起了对WCS的怀疑,因此停用芬太尼。1小时内,平台压力降至16,呼吸机改为压力支持。患者在VD 10上成功拔管。讨论:区分经典ARDS的低肺顺应性与covid -19诱导的ARDS的不成比例的顺应性低氧血症是胸医学界正在进行的研究点。这一范例的新颖性使我们有可能忽略不太常见的并发症,如芬太尼诱发的WCS。尽管氧合改善相对较快,但患者的依从性较差,这与COVID-19肺部生理学的现有证据相悖,促使人们怀疑其通气不良的另一种解释。由于对WCS的描述仅限于病例报告,我们发现机械通气患者的初始症状(胸壁、膈肌、腹部和喉部肌肉收缩2)的发作和严重程度可能被掩盖。通气不足可解释为气道和肺泡压力高的表现,使其难以与典型的ARDS区分,并最终增加呼吸机使用时间。据我们所知,这是首例与COVID-19相关的ARDS患者出现WCS的报告。这表明,当机械通气后接受芬太尼治疗的COVID-19患者肺顺应性较差,氧合改善明显快于通气时,应考虑WCS。
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