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Anesth Analg 2008; 107:226-228
© 2008 International Anesthesia Research Society
doi: 10.1213/ane.0b013e3181770a45
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NEUROSURGICAL ANESTHESIOLOGY

Pseudomeningocele: An Unusual Cause of Intraoperative Tracheal Compression and Expiratory Obstruction

Randal S. Blank, MD, PhD, Christine S. Waldrop, MD, and Philip J. Balestrieri, MD

From the Department of Anesthesiology, University of Virginia Health System, Charlottesville, Virginia.

Address correspondence to Randal S. Blank, MD, PhD, Department of Anesthesiology, University of Virginia Health System, P.O. Box 800710, Charlottesville, VA 22908-0710. Address e-mail to rsb8p{at}virginia.edu.

Abstract

Cerebrospinal fluid leak resulting from spine surgery has been associated with postoperative upper airway obstruction and the need for emergent airway management. We report a case of a known pseudomeningocele resulting in acute intraoperative compression of the intrathoracic trachea and an unexpected variable expiratory obstruction.

Severe airway compromise associated with anterior cervical spine surgery may be attributable to a variety of surgical etiologies, most commonly pharyngeal edema and hematoma1–3 and rarely, pseudomeningocele formation.4 This phenomenon usually involves upper airway obstruction, develops postoperatively, and is related to the size of the expanding cerebrospinal fluid (CSF) collection. We report the case of a patient with an existing pseudomeningocele without respiratory symptoms who developed acute severe expiratory obstruction of the trachea after induction of general anesthesia.

CASE DESCRIPTION

The patient was a 58-yr-old man with a history of hypertension, Grave's disease, obstructive sleep apnea, and an extensive history of spine procedures, including six lumbar laminectomies, an anterior cervical discectomy and fusion at C3–4 and C5–6 and, within 2 wk before presentation, a C3–7 laminectomy with instrumentation from C2 to T2. This procedure was complicated by a CSF leak. Repair of the pseudomeningocele with ventriculostomy was scheduled.

The patient was initially encountered while sitting upright on a stretcher with his legs outstretched. He denied discomfort, dyspnea, wheezing, and stridor. His vital signs were stable and laboratory studies were unremarkable, except for a mild anemia (hemoglobin concentration 10.9 g/dL). Upon removal of the patient's cervical collar, a moderate bulge on the left anterior neck was observed, but there was no gross displacement of the trachea and the patient appeared comfortable in the supine position before induction.

An inhaled induction with 8% inspired sevoflurane was performed, and endotracheal intubation with an 8.0-mm endotracheal tube was performed easily with a Bullard indirect laryngoscope used to minimize neck movement. Immediately after intubation, his breath sounds were clear bilaterally and expired end-tidal CO2 was present. Within 5 min, however, an increase in peak and plateau ventilator pressures were noted, and auscultation of lung fields revealed diffuse expiratory wheezes bilaterally. Our initial treatment consisted of deepening the inhaled anesthetic with IV administration of lidocaine 100 mg, propofol 100 mg, and paralysis was provided with rocuronium 30 mg. Albuterol was also administered via the breathing circuit with no resolution in wheezing. Dynamic compliance, as indicated by dramatically increasing peak airway pressures, continued to worsen and within several minutes his systolic blood pressure had decreased to 70, despite vasopressor treatment with ephedrine and phenylephrine. Because of increasing evidence of air-trapping, the breathing circuit was disconnected from the endotracheal tube, and flexible fiberoptic bronchoscopy was subsequently performed to identify possible sources of tracheal obstruction. The examination revealed a normal appearing proximal trachea but soft tissue filled the tracheal space approximately 5 cm distal to the vocal cords. Although no channel past the obstruction was visualized, the bronchoscope advanced easily past the obstruction and the endotracheal tube was then advanced over the bronchoscope beyond the obstruction and to within approximately 1–2 cm of the tracheal carina. An immediate increase in expiratory flow was noted, the patient's airway pressures and hemodynamics returned to normal and wheezing ceased.

Examination of a computerized tomography scan taken 24 h before the procedure revealed a large fluid collection originating at the C6–7 level in the retropharyngeal space extending anterolaterally with anterior displacement of the cricoid cartilage and supraglottic structures (Fig. 1). The inferior extent of this fluid can be seen within the thoracic cavity in close apposition to the posterior membranous trachea (Fig. 2).


Figure 136
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Figure 1. Computerized tomographic scan of neck at level of hyoid bone showing cerebrospinal fluid collection within dotted line. T = trachea; V = vertebra. Note that fluid collection is large and displaces airway structures.

 

Figure 236
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Figure 2. Computerized tomographic scan of upper thorax showing cerebrospinal fluid collection within dotted line. T = trachea; V = vertebra. Note that fluid collection extends posterior to airway and displaces esophagus anteriorly into apposition with posterior tracheal wall.

 

The procedure included decompression of the pseudomeningocele (200 mL CSF was drained). On emergence, the endotracheal tube was gradually withdrawn with the bronchoscope in place and only a small bulge at the site of prior obstruction was observed. After extubation, the patient had an uneventful recovery and was discharged to home without complication.

DISCUSSION

Airway obstruction after anterior cervical spine surgery has been attributed to a variety of surgical and nonsurgical causes including edema,1–3 angioedema,5 compression by surgical hardware,6 and CSF leak or pseudomeningocele.4 The true incidence of airway complications is not known, but a clinical series suggests a rate of 6%, of which approximately one-third require reintubation.1 Compression of the upper airway is most common and edema is the presumed mechanism. Clinically significant airway compromise usually occurs within 23–36 h postoperatively. To our knowledge, this is the first report to document an intraoperative tracheal obstruction due to a pseudomeningocele.

The anatomic relationship between the site of the known pseudomeningocele and the subsequent tracheal obstruction was not completely clear. Radiographic data obtained before the surgery demonstrated a fluid collection originating at C6–7 with extension inferiorly to the mid T1 level. Given that prior instrumentation included the T2 vertebra, it is likely that alterations in tissue planes resulting from these procedures may have extended inferiorly beyond T2, potentially permitting fluid access to the posterior mediastium at this level. Although evidence from prior reports and series indicate a clearer anatomic relationship between the cause of airway compression and subsequent clinical signs, the clinical evidence in this case points to compression of the intrathoracic trachea by fluid and/or soft tissue, resulting in a variable intrathoracic expiratory obstruction.

The nature of the variable obstruction itself strongly suggests an intrathoracic location. There is a variable expiratory obstruction when airway caliber is increased by negative intrathoracic pressure or applied positive pressure during inspiration but decreased during forced or passive expiration. Additionally, our postinduction bronchoscopic examination revealed intrathoracic tracheal obstruction by what appeared to be soft tissue. Most likely, this was herniation of soft tissue or fluid mass into the membranous posterior tracheal wall. The obstructing tissue was completely absent during bronchoscopic examination after surgical evacuation of the pseudomeningocele. Furthermore, evaluation of the computed tomography scan postoperatively eliminated the possibility of an occult mediastinal mass acting independently.

Variable intrathoracic obstruction can result from tumor invasion of the airway or from extrinsic compression of the tracheobronchial tree, which may be exaggerated by physiological and positional changes associated with anesthesia. Intraluminal tumors commonly result in expiratory flow limitation and not complete obstruction since full airway collapse is usually limited by the firmness of the tumor mass and the actual lumen is stented open by the tumor. In the presence of extraluminal compression, as in this case, complete luminal obstruction is quite possible.

Risk factors for perioperative cardiorespiratory complications in patients with mediastinal masses include stridor, orthopnea, cyanosis, jugular venous distension, superior vena cava syndrome, tracheal compression of 50% or more, and a combined obstructive and restrictive pattern on pulmonary function testing.7 Our patient did not exhibit any of the above signs or symptoms and, hence, pulmonary function testing was not performed. Thus, it is unknown whether the patient would have exhibited signs of a variable intrathoracic obstruction preoperatively. Intraoperative events lead us to the following conclusion. A relatively large CSF collection (200 mL aspirated by surgeons) in the context of tissue plane alterations from multiple prior spinal procedures resulted in the anterior herniation of soft tissue into the posterior membranous trachea resulting in expiratory obstruction of the trachea.

Pseudomeningocele size may also have been increased by intraoperative factors affecting CSF pressure. Body position affects CSF flow kinetics between the brain and spinal cord, with lower intracranial CSF volume in the upright position.8 Postural change in a canine model from a supine to upright position has been shown to result in decreased cervical and increased lumbar CSF pressures,9 reflecting craniolumbar redistribution of CSF. Additionally, an increase in intrathoracic pressure associated with positive pressure ventilation may also increase CSF pressure by impeding venous return to the thorax. The application of continuous positive airway pressure in healthy volunteers has been shown to increase CSF pressure.10 Given the potential effects of supine positioning and positive intrathoracic pressure on CSF pressure and, hence, pseudomeningocele size, it is conceivable that a positive feedback loop between pseudomeningocele enlargement, tracheal obstruction, and consequent increasing airway and intrathoracic pressures was established, resulting in the observed severe intrathoracic tracheal obstruction.

This report indicates that a seemingly innocuous and asymptomatic pseudomeningocele occurring after spine surgery may lead to a catastrophic airway emergency.

ACKNOWLEDGMENTS

The authors thank Dr. Thomas J. Gal for his insight and helpful comments and Mr. David Alpern for his help with this manuscript.

Footnotes

Accepted for publication March 18, 2008.

The authors have no relationships with any company or organization with a vested interest in the outcome of this work.

Reprints will not be available from the author.

REFERENCES

  1. Sagi HC, Beutler W, Carroll E, Connolly PJ. Airway complications associated with surgery on the anterior cervical spine. Spine 2002;27:949–53[Web of Science][Medline]
  2. Terao Y, Matsumoto S, Yamashita K, Takada M, Inadomi C, Fukusaki M, Sumikawa K. Increased incidence of emergency airway management after combined anterior-posterior cervical spine surgery. J Neuro Anesth 2004;16:282–6
  3. Emery SE, Smith MD, Bohlman HH. Upper-airway obstruction after multilevel cervical corpectomy for myelopathy. J Bone Joint Surg Am 1991;73:544–51[Abstract/Free Full Text]
  4. Chang HS, Kondo S, Mizuno J, Nakagawa H. Airway obstruction caused by cerebrospinal fluid leakage after anterior cervical spine surgery. J Bone Joint Surg Am 2004;86:370–2[Free Full Text]
  5. Krnacik MJ, Heggeness MH. Severe angioedema causing airway obstruction after anterior cervical surgery. Spine 1997;22:2188–90[Web of Science][Medline]
  6. Riew KD, Sethi NS, Devney J, Goette K, Choi K. Complications of buttress plate stabilization of cervical corpectomy. Spine 1999;24:2404–10[Web of Science][Medline]
  7. Bechard P, Letourneau L, Lacasse Y, Cote D, Bussieres JS. Perioperative cardiorespiratory complications in adults with mediastinal mass. Anesthesiology 2004;100:826–34[Web of Science][Medline]
  8. Alperin N, Hushek SG, Lee SH, Sivaramakrishnan A, Lichtor T. MRI study of cerebral blood flow and CSF flow dynamics in an upright posture: the effect of posture on the intracranial compliance and pressure. Acta Neurochir Suppl 2005;95:177–81[Medline]
  9. Carlson GD, Oliff HS, Gorden C, Smith J, Anderson PA. Cerebral spinal fluid pressure. Effects of body position and lumbar subarachnoid drainage in a canine model. Spine 2003;28:119–22[Web of Science][Medline]
  10. Hormann C, Mohsenipour I, Gottardis M, Benzer A. Response of cerebrospinal fluid pressure to continuous positive airway pressure in volunteers. Neurosurg Anesth 1994;78:54–7




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2008 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press