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* From the Departments of Anesthesiology and
Surgery, MetroHealth Medical Center, Case Western Reserve University, Cleveland, Ohio, 44109 USA.
Address correspondence to: Dr. C.E. Smith, Department of Anesthesiology, MetroHealth Medical Center, 2500 MetroHealth Drive, Cleveland, Ohio, 44109 USA. Phone: 216-778-3616; Fax: 216-778-5378; E-mail: ces4{at}po.cwru.edu
| Abstract |
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Clinical Features: A 29-yr-old intoxicated woman suffered a motor vehicle accident. Injuries consisted of multiple abrasions to her head, forehead, and face, right temporal lobe hemorrhage, and complex mandibular fractures with displacement. Mouth opening was < 10 mm. Blood pressure was 106/71 mmHg, pulse 109, respirations 18, temperature 37.3°C, SpO2 100%. Chest and pelvic radiographs were normal and the there was increased anterior angulation of C4-C5 on the cervical spine film. Drug screen was positive for cocaine and alcohol. The initial plan was to perform awake tracheostomy with local anesthesia. However, the patient was uncooperative despite sedation and infiltration of local anesthesia. Sevoflurane, 1%, inspired in oxygen 100%, was administered via face mask. The concentration of sevoflurane was gradually increased to 4%, and loss of consciousness occurred within one minute. The patient breathed spontaneously and required gentle chin lift and jaw thrust. A cuffed tracheostomy tube was surgically inserted without complication. Blood gas showed pH 7.40, PCO2 35 mmHg, PO2 396 mmHg, hematocrit 33.6%. Diagnostic peritoneal lavage was negative. Pulmonary aspiration did not occur. Oxygenation and ventilation were maintained throughout the procedure.
Conclusion: Continuous mask ventilation with sevoflurane is an appropriate technique when confronted with an uncooperative trauma patient with a difficult airway.
| Introduction |
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| Case History |
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Because of increasing somnolence and brief periods of agitation, she was transferred to the operating room for urgent tracheostomy with local anesthesia. Prior to transfer to the operating room, the patient pulled out her Foley catheter and was struggling against the cervical restraints. The patient calmed down with firm reassurance and log-rolled onto the operating room table. The head and neck were immobilized manually and anesthesia monitors were applied. Glycopyrolate, 0.2 mg, iv and titrated midazolam, 4 mg, iv were given and the neck was prepared and draped for surgery. The BP was 140/80 mmHg, heart rate 110 bpm, respirations 30, SpO2 100%. During infiltration of local anesthesia, the patient began to move and an infusion of propofol was started. The propofol infusion was titrated at 150 µgkg1min1. Despite the sedation and local anesthesia, the patient continued to move and could not be calmed down. Sevoflurane, 1%, inspired in oxygen 100%, was administered via face mask. The propofol infusion was discontinued. The concentration of sevoflurane was gradually increased to 4%, and loss of consciousness occurred within one minute. The patient breathed spontaneously and required gentle chin lift, jaw thrust, and assist. End tidal CO2 was 32-38 mmHg. A cuffed tracheostomy tube, I.D. 6.0 mm was surgically inserted without complication. Blood gas analysis after tracheostomy and during controlled mechanical ventilation at eight breathsmin and tidal volume 650 mL showed pH 7.40, PCO2 35 mmHg, PO2 396 mmHg, hematocrit 33.6%. Diagnostic peritoneal lavage was negative.
Subsequent work-up revealed that the right mandibular condyle had been driven up and through the glenoid fossa and was in an intracranial position (Figure 1
). There was a large right temporal lobe hemorrhage (Figure 2
). Other injuries were a displaced left subcondylar mandibular ramus fracture and a right comminuted parasymphseal mandible fracture. Three days later, surgery was performed to remove the condyle from the intracranial fossa, reconstruct the right glenoid fossa with bone graft and temporal muscle flap, and repair the symphysis and left subcondylar fractures. She was discharged to a rehabilitation facility on the 18th postoperative day with independent mobility and activities of daily living, but mild cognitive dysfunction.
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| Discussion |
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The use of deep sedation or general anesthesia has been shown to decrease upper airway tone and cause airway occlusion during spontaneous ventilation.4 Thus, it is not surprising that the patient required a jaw thrust and chin lift maneuver to prevent airway obstruction as the concentration of sevoflurane was increased. Head extension was not done because of suspected cervical spine injury. Transtracheal jet ventilation was the backup plan to oxygenate the patient and ventilate the lungs in an emergency since there was insufficient mouth opening for placement of a Combitube or laryngeal mask airway.
It is recognized that this patient was at increased risk for gastric regurgitation and pulmonary aspiration with deep sedation and general anesthesia by face mask. Despite this increased risk, rapid sequence intubation together with cricoid pressure was not considered because of the inability to open the mouth. The priorities in this patient were to establish a definitive airway by providing optimal conditions for tracheostomy while at the same time preventing hypoxemia. Had regurgitation occurred prior to insertion of the cuffed tracheostomy tube, the plan was to place the patient in a head-down position to permit vomitus to run out of the mouth. Oropharyngeal and tracheobronchial suctioning, including bronchoscopy to remove food particles, would also be necessary. Thorough tracheobronchial suctioning would have awaited placement of the tracheostomy tube. Pharmacologic agents to stimulate gastric emptying (e.g., metoclopramide) were not used, although these agents may be helpful in some patients.
Nasotracheal intubation via a flexible fibreoptic bronchoscope was considered but not done because of the possibility of basilar skull fracture with disruption of the cribriform plate of the ethmoid bone. In these instances, the tracheal tube may traverse the fractured cribiform plate and disrupt the brain substance. Blind nasal intubation was not considered because of the above factors and because this technique may result in loss of the airway due to epistaxis or hematoma.5
Experience with inhalational induction in adults has previously been limited by the relatively slow uptake of halothane and the relatively high noxious nature of the other gases desflurane, isoflurane, and enflurane which produced complications such as excessive secretions, coughing, and laryngospasm during induction. In contrast, sevoflurane has a low blood:gas solubility and is associated with smooth induction of anesthesia with minimal or no airway irritation or cough, rapid control of anesthetic depth, and preservation of spontaneous ventilation.7 Despite the possible adverse effects of volatile anesthetic agents on cerebral autoregulatory capacity, cerebral blood flow, and intracranial pressure,810 sevoflurane has been shown to provide significant neuronal protection in the presence of hypoxia and ischemia.11 Moreover, doses as high as 1.5 MAC sevoflurane do not impair static rate of cerebral autoregulation provided that normocapnia is maintained,12 as occurred in this report. For these reasons, sevoflurane was chosen instead of the other volatile agents. Nitrous oxide was not used because it reduces the inspired oxygen concentration and may enlarge air- containing spaces (e.g., pneumothorax, pneumocephalus). Higher doses of propofol were not used because of the risk of apnea and the desire to maintain spontaneous ventilation. It is acknowledged, however, that in the presence of hypercapnia (PaCO2 50- 66 mmHg), autoregulation is better preserved with propofol than with sevoflurane.12
In summary, inhalation induction of anesthesia using sevoflurane greatly facilitated airway management in an uncooperative, intoxicated multiple trauma patient with a difficult airway. Use of mask anesthesia permitted the performance of a surgical airway in a relatively controlled situation with maintenance of oxygenation and normocarbia.
| Acknowledgments |
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Accepted for publication November 27, 1999.
| References |
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2
Rosenblatt WH, Wagner PJ, Ovassapian A, Kain ZN. Practice patterns in managing the difficult airway by anesthesiologists in the United States. Anesth Analg 1998; 87: 1537.
3 Stene JK, Grande CM, Barton CR. Airway management for the trauma patient. In: Stene JK, Grande CM (Eds.). Trauma Anesthesia, Baltimore: Williams and Wilkins Inc., 1991: 6499.
4 Mathru M, Esch O, Lang J, et al. Magnetic resonance imaging of the upper airway. Effects of propofol anesthesia and nasal continuous positive pressure in humans. Anesthesiology 1996; 84: 2739.[Medline]
5
Shearer VE, Giesecke AH. Airway management for patients with penetrating neck trauma: a retrospective study. Anesth Analg 1993; 77: 11358.
6 Green WB Jr. The ventilatory effects of sevoflurane. Anesth Analg 1995; 81: S236.[Medline]
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9 Engelhard KR, Möllenberg O, Werner CP, Kochs EF. Effects of S + ketamine/propofol and sevoflurane on dynamic cerebrovascular autoregulation in humans. Anesthesiology 1999; 91: A174.
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11 Faberowski LW, Raizada MK, Sumners C. Sevoflurane and desflurane attenuate hypoxia/ischemia-induced neuronal apoptosis. Anesthesiology 1999; 91: A739.
12 McCulloch TJ, Visco E, Lam AM. Graded hypercapnia and cerebral autoregulation during sevoflurane or propofol anesthesia. Anesthesiology 1999; 91: A175.
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