Computed tomography changes of alveoli and airway collapse after laryngospasm.
An eight-month-old girl underwent a computed axial tomographic
study of the chest and neck for investigation of expiratory stridor.
Following the scout scan, severe laryngospasm developed. While no cause
for the laryngospasm was found, the computed axial tomographic chest
study showed marked changes in the lungs consistent with absorption
atelectasis which we postulate occurred secondary to laryngospasm.
Key Words: anaesthesia, complications, laryngospasm, absorption atelectasis
|Article Type:||Case study|
Respiratory tract diseases (Diagnosis)
Respiratory tract diseases (Care and treatment)
Respiratory tract diseases (Case studies)
Anesthesia (Health aspects)
von Ungern-Sternberg, B.S.
|Publication:||Name: Anaesthesia and Intensive Care Publisher: Australian Society of Anaesthetists Audience: Academic Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2011 Australian Society of Anaesthetists ISSN: 0310-057X|
|Issue:||Date: Sept, 2011 Source Volume: 39 Source Issue: 5|
|Geographic:||Geographic Scope: Switzerland Geographic Code: 4EXSI Switzerland|
An eight-month-old girl weighing 8 kg had been taken to the general practitioner by her mother who described respiratory symptoms since birth. The child had been born at 33.5 weeks by spontaneous vaginal delivery. She was discharged from hospital on day 13, having had apnoeas in the first few postnatal days without requirement for respiratory support. In subsequent months she had attended her general practitioner several times with a history of stridor and cough. A later neck radiograph suggested a prevertebral or retropharyngeal abnormality but otherwise was normal. A computed axial tomographic (CT) scan of the chest and neck was ordered for further evaluation.
General anaesthesia to facilitate imaging was planned. At the pre-anaesthetic assessment, the patient was completely healthy with no recent history of an upper respiratory tract infection. Other than the presenting history of stridor she was asymptomatic. Stridor was not evident at the time of examination and auscultation of the chest revealed normal air entry with no added sounds.
General anaesthesia was induced with inhalation of sevoflurane 8% in a mixture of oxygen and nitrous oxide (30:70%) and maintained with 1 minimum alveolar concentration of sevoflurane and an inspiratory oxygen fraction of 0.4. Pulse oximetry and electrocardiographic monitoring were applied. An endotracheal tube was avoided so as not to interfere with imaging. A size 1.5 laryngeal mask airway (LMA ProBreathe-Well Lead Medical, Guangzhou, China) was inserted on the second attempt and the LMA was tested for leakage around the cuff by ausculation during manual ventilation with pressures up to 35 cm[H.sub.2]O. A recruitment manoeuvre was performed by giving 10 slow breaths up to 35 cm[H.sub.2]O followed by a positive end-expiratory pressure of 5 cm[H.sub.2]O (1). Following the scout CT scan, the patient developed laryngospasm. Sevoflurane was continued with 100% oxygen and continuous positive airway pressure (CPAP) was applied. Despite the immediate application of CPAP, the oxygen saturation dropped to a nadir of 70%. Eventually the laryngospasm was overcome with CPAP alone and rapid return of normal saturations occurred. Suxamethonium or propofol were not administered. The remaining subsequent scanning, emergence from anaesthesia and recovery were without incident.
The CT scan did not reveal a cause for the history of expiratory stridor. However marked changes in the lungs were noted which had not been present on the previous chest X-ray or during the scout CT scan.
Figure 1 shows bilateral dependent atelectasis predominantly involving the posterior segments of both lower lobes and a minimal area of the posterior parts of both upper lobes.
There was minimal atelectasis in the inferior parts of the anterior segments of both upper lobes. Changes were symmetrical and pleural based. In both upper lobes there were several perihilar areas of lower attenuation when compared to the peripheral lung. This was most likely due to mucous plugging with localised gas trapping. Tracheal and bronchial morphology were normal. There was a small amount of mucous in the upper trachea. Even though similar changes are commonly seen during general anaesthesia, these can be reversed with a recruitment manoeuvre as performed here prior to the initial CT scan. Since the initial scout scan undertaken prior to the laryngospasm was normal, we speculate that the atelectasis and the air trapping were consequent to the laryngospasm. There were no changes suggestive of negative pressure pulmonary oedema as commonly seen following a severe laryngospasm.
[FIGURE 1 OMITTED]
Laryngospasm is defined as glottic closure because of reflex contraction of laryngeal muscles. It can involve the true cords alone or closure of the true and false vocal cords (2). It is seen more commonly in the paediatric population undergoing anaesthesia, especially on emergence from anaesthesia (3). This patient however developed laryngospasm following induction of anaesthesia while the first CT images were taken. Causative factors for the development of laryngospasm include irritating inhalational agents, excessive secretions in the airway, light anaesthesia or manipulation of the airway. The use of a laryngeal mask airway has been shown to be an independent risk factor for the development of laryngospasm (4,5). Laryngospasm can result in rapid desaturation as occurred in our patient.
Respiratory effort against a closed glottis may generate large negative intrapleural pressures. These pressures may result in large fluid shifts from the vascular compartment into the interstitium and subsequently into the alveoli as the rate of removal of fluid by the lymphatic system is greatly exceeded (6,7). This is termed negative pressure pulmonary oedema and is a well known potential complication of laryngospasm. However, our patient did not show the typical signs of negative pressure pulmonary oedema. The CT appearances showed marked alveolar and airway collapse in both lungs including air trapping.
The possibility of aspiration as a cause of the respiratory event in this patient needs to be considered. That the oxygen saturation of our patient rapidly returned to a normal range makes aspiration unlikely in the setting of the degree of radiological change seen in this patient. With clinical and imaging signs of aspiration absent, aspiration is highly unlikely in the differential diagnosis.
How can the atelectasis be explained following laryngospasm? After induction of anaesthesia, atelectasis is a common finding in children, especially in the dorso-caudal areas of both lungs (1). The pattern of atelectasis seen in this patient differs from that distribution and was not seen on the scout image. Therefore a likely explanation for the changes seen in this case is absorption atelectasis; during laryngospasm (complete occlusion of the laryngeal inlet) oxygen was still absorbed from the lungs into the circulation, resulting in a reduction of lung volume and consequent atelectasis. Furthermore, this process is likely to be accelerated in the presence of an expiration reflex (i.e. forceful expiration without preceding inspiration), an additional laryngeal reflex response often occurring in association with laryngospasm (9) leading to an immediate reduction of the lung volume.
We conclude that the larygnospasm led to a significant degree of atelectasis. Surprisingly, the oxygen saturation returned to normal values despite the extensive changes on CT. We speculate that the changes seen on the CT could have been reversed with another recruitment manoeuvre following the laryngospasm prior to the continuation of the CT scan. Therefore, anaesthetists should be aware of the marked changes in the lungs that can occur even after a short period of laryngospasm. Since atelectasis has been shown to resolve with a recruitment manoeuvre followed by CPAP1, recruitment manoeuvres and the application of CPAP/positive end-expiratory pressure should therefore be considered to reverse atelectasis following a laryngospasm, even if the oxygen saturation has returned to normal values.
(1.) Tusman G, Boehm SH, Tempra A, Melkun F, Garcia E, Turchetto E et al. Effects of recruitment maneuver on atelectasis in anesthetized children. Anesthesiology 2003; 98:14-22.
(2.) Miller RD. Millers Anaesthesia, 7th ed. Chapter 50: Physiology and Pathophysiology of the Upper Airway. Churchill Livingstone, Philadelphia 2009.
(3.) Olsson GL, Hallen B. Laryngospasm during anaesthesia. A computer-aided incidence study in 136,929 patients. Acta Anaesthesiol Scand 1984; 28:567-575.
(4.) Flick RP, Wilder RT, Pieper SF, van Koeverden K, Ellison KM, Marienau MES et al. Risk factors for laryngospasm in children during general anesthesia. Paediatr Anaesth 2008; 18:289-296.
(5.) von Ungern-Sternberg BS, Boda K, Chambers NA, Rebmann C, Johnson C, Sly PD et al. Risk assessment for respiratory complications in paediatric anaesthesia: a prospective cohort study. Lancet 2010; 376:773-783.
(6.) Halter JM, Steinberg JM, Schiller HJ, DaSilva M, Gatto LA, Landas S et al. Positive end-expiratory pressure after a recruitment maneuver prevents both alveolar collapse and recruitment/derecruitment. Am J Respir Crit Care Med 2003; 167:1620-1626.
(7.) Krodel DJ, Bittner EA, Abdulnour R, Brown R, Eikermann M. Case scenario: acute postoperative negative pressure pulmonary edema. Anesthesiology 2010; 113:200-207.
(8.) von Ungern-Sternberg BS, Wallace CJ, Stick S, Erb TO, Chambers NA. Fibreoptic assessment of paediatric sized laryngeal mask airways. Anaesth Intensive Care 2010; 38:50-54.
(9.) Oberer C, von Ungern-Sternberg BS, Frei FJ, Erb TO. Respiratory reflex responses of the larynx differ between sevoflurane and propofol in pediatric patients. Anesthesiology 2005; 103:1142-1148.
M. KEATING *, J. JOHNSON ([dagger]), T. O. ERB ([double dagger]), B. S. von UNGERN-STERNBERG ([section])
Department of Anaesthesia, Princess Margaret Hospital for Children, Perth, Western Australia, Australia
* M.D., Registrar.
([dagger]) M.D., F.A.N.Z.C.A., Consultant.
([double dagger]) M.D., M.H.S., Consultant, Division of Paediatric Anaesthesia, University Childrens Hospital, Basel, Switzerland.
([section]) M.D., Ph.D., D.E.A.A., Chair of Paediatric Anaesthesia.
Address for correspondence: Professor B. S. von Ungern-Sternberg, Department of Anaesthesia, Princess Margaret Hospital for Children, Roberts Road, Subiaco, WA 6008. Email: Britta.regli-vonungern@health. wa.gov.au
Accepted for publication on May 28, 2011.
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