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Massive Subcutaneous Emphysema During Emergence from Anesthesia Followed by Seizures

Oberoi, Mohinder P. MD; Amayam, Ahmed MD; Ganta, Raghuvender MD; Maddineni, Venkata R. MD, PhD

Letter to the Editor

Department of Anesthesiology, The University of Oklahoma College of Medicine, Oklahoma City, OK 73152.

To the Editor:

A 17-yr-old male, ASA physical status I, had open reduction and internal fixation of the left femur under general endotracheal anesthesia. Prior to tracheal extubation, he started coughing and developed massive subcutaneous emphysema of the face, neck, abdomen, and scrotum with 20% bilateral pneumothoraces. Some subcutaneous air was vented during placement of chest tubes, with consequent reduction in swelling and peak airway pressure. At that time, the vital signs were stable and O2 saturation remained greater than 94%. Fiberoptic bronchoscopy revealed no tracheal or oropharyngeal injury. The trachea was extubated in the postanesthesia care unit after the patient became responsive to verbal commands. Five minutes after tracheal extubation, the patient developed focal seizures in his left arm progressing to grand mal seizures, which were treated with diazepam. He was tracheally reintubated and ventilated due to irregular respiration. An arterial blood gas showed mild hypercarbia but good oxygenation. Computed tomography scan of the head showed no abnormality. Repeat bronchoscopy, electroencephalogram, and neurological examination were normal. A day after extubation, he was discharged on phenytoin; on reexamination for up to 9 mo, he reported no further seizures or neurologic deficits.

Anesthesia-related causes of subcutaneous emphysema include esophageal/hypopharyngeal perforation from traumatic intubation or laryngoscopy, high airway pressures as in the Valsalva maneuver due to faulty anesthetic circuits and resuscitation bags, an inappropriately closed pop-off valve, positive pressure ventilation, and coughing against a closed airway [1]. Air can be forced through a break in the mucosal lining of the trachea or bronchi due to an increase in intraluminal pressure from such activities as nose blowing, sneezing, coughing, or bag and mask ventilation [2]. After alveolar rupture into the pulmonary interstitium, air dissects along the pulmonary vasculature and eventually into the mediastinum [3]. Once air reaches the mediastinum, it continues to dissect along the tissue planes offering the least resistance [3].

We postulate that perivascular alveoli could have ruptured from coughing with the endotracheal tube in place, thus forming a bronchovenous fistula, leading to a systemic air embolism as discussed by Graham et al. [4]. If air goes into the cerebral circulation, seizures may occur [5]. This probably was the cause of seizures in our patient. Nonfatal cerebral air injury may be associated with a prolonged convalescence, yet complete recovery, compared to embolism from debris or clot, which offers a poorer prognosis [6]. Since our patient had a complete neurological recovery, it is likely that he had a cerebral air embolism.

Mohinder P. Oberoi, MD

Ahmed Amayam, MD

Raghuvender Ganta, MD

Venkata R. Maddineni, MD, PhD

Department of Anesthesiology

The University of Oklahoma College of Medicine

Oklahoma City, OK 73152

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© 1996 International Anesthesia Research Society