Intraoperative ultrasonography, especially transesophageal echocardiography, is commonly used by anesthesiologists in patients with cardiovascular instability. Intraoperative lung ultrasonography, although simpler to perform, is less commonly discussed in the anesthesia literature. Yet, bedside lung ultrasound is useful for rapid diagnosis of conditions relevant to anesthesiologists such as pleural effusions/hemothorax, pulmonary edema, and pneumothorax.1–3
In the present case, intraoperative lung ultrasonography played a key role in the timely management of sudden cardiopulmonary decompensation.
The patient provided written consent for the publication of his case.
A 78-year-old man with locally advanced non-small-cell lung cancer presented for palliative core-out laser excision of intrabronchial lesions and Y-stent placement. A carinal mass (Fig. 1) was invading the airways and partially obstructing both mainstem bronchi and the distal trachea. Clinically, the patient had expiratory wheezing and was unable to lie flat without desaturation despite receiving 12 L/min supplemental oxygen via facemask.
Recognizing the risk of complete airway obstruction after paralysis, the anesthesia team first induced inhaled general anesthesia with sevoflurane under spontaneous mask ventilation. After the patient’s condition proved stable under positive-pressure ventilation, he was paralyzed, and his trachea was intubated uneventfully. Subsequently, rigid bronchoscopy was performed, and laser-assisted excision of the lesions was begun. High-frequency jet ventilation was applied to the side port of the rigid scope (TwinStream; Carl Reiner GmbH, Vienna, Austria) with the following settings: frequency, 450/min; amplitude, 0.5 (dimensionless proportion of power dedicated to producing flow oscillations); and FiO2, 1.0 to 0.38. After 10 minutes of jet ventilation, arterial blood gas analysis produced the following findings: pH, 7.33; pCO2, 63; and pO2, 287.
Suddenly, the patient’s oxyhemoglobin saturation decreased, prompting the team to reintubate with a cuffed 8.5 endotracheal tube (ETT) to provide positive-pressure ventilation and allow for bronchoscopy. However, only very small tidal volumes could be achieved despite high airway peak pressures exceeding 50 mm Hg. Flexible bronchoscopy showed that a portion of the excised tumor was obstructing the ETT during exhalation. Although the bronchoscope could be pushed past the endotracheal and endobronchial tumors into the right mainstem bronchus, the team was unable to advance the 8.5 ETT over the scope. With an Eschmann stylet, the 8.5 ETT was exchanged for a 6.5 ETT, which appeared to pass more distally.
During this time, the patient’s pulse oximetric oxyhemoglobin saturation decreased to approximately 40%. The patient had concomitant severe junctional bradycardia (approximately 30 beats/min) and hypotension; mean arterial blood pressure was approximately 30 mm Hg, and the end-tidal CO2 level was low. After 5 minutes of cardiopulmonary resuscitation and 2 mg of epinephrine, spontaneous circulation was restored. Rigid bronchoscopy was attempted once more and led to the successful removal of a large portion of the tumor floating in the trachea and mainstem bronchi. However, after tracheal reintubation with an 8.5 ETT, high airway pressures (up to 60 mm Hg) persisted, as did marginal ventilation and hemodynamic instability requiring intermittent epinephrine boluses. Flexible bronchoscopy revealed that the tracheal obstruction was gone and that the tumor burden obstructing both mainstem bronchi was lower than it had been preoperatively, but the operative team assumed that more distal tumor, swelling, and blood clots were responsible for the ventilatory difficulties. However, further bronchoscopy, attempted to confirm this assumption, was tolerated poorly.
Ultrasonography was then performed, producing normal findings in the left chest but abnormal findings in the right chest (Fig. 2; Video 1, Supplemental Digital Content 1, http://links.lww.com/AA/B39). The anesthesia team recognized a lack of lung sliding throughout the entire right chest. Furthermore, no lung pulse or B-lines could be detected. A cursory search also did not reveal a lung point. Considering the clinical setting, these findings supported the diagnosis of pneumothorax (detailed in Discussion below).
Immediate needle decompression in the second intercostal space (midclavicular line) caused an audible release of air; subsequent placement of a chest tube rapidly resolved the cardiopulmonary instability. Before the patient was transported to the intensive care unit, and while the chest tube continued to show a small intermittent leak, ultrasonography was repeated, now showing a lung sliding over the right chest. A portable chest radiogram confirmed the chest tube placement and showed no evidence of pneumothorax. The patient’s trachea was extubated the next day, and the patient was discharged to the floor while receiving supplemental oxygen.
Unbeknownst to the operative team, the patient had developed a tension pneumothorax, probably because of vigorous ventilation and air-trapping when the tracheal tumor was obstructing exhalation into the ETT. When the patient’s condition did not stabilize even after removal of the large tracheal tumor, the operative team considered 3 possible causes:
- Pieces of tumor or clot might have been dislodged and pushed distally, which would explain the high ventilation pressures.
- Swelling of residual tumor due to surgical manipulation might have impeded ventilation.
- A tension pneumothorax might have developed.
The possibility of a pneumothorax should always be considered when high airway pressures become necessary. When hemodynamic instability ensues, the clinician may suspect tension pneumothorax and have to perform presumptive needle decompression and chest tube placement even before chest radiography can confirm the diagnosis. In this case, however, there were plausible alternate diagnoses to consider. In addition, empiric needle decompression carries a high risk of creating a pneumothorax if one is not already present. This surely would have complicated the course if the high airway pressures had been due to the residual tumor and not a tension pneumothorax.
Lung ultrasonography provided immediate information that helped guide management in this deteriorating patient. Including the time required to transport and set up the ultrasound machine, the ultrasound examination can be completed in a matter of minutes. A chest radiogram with immediate image display would have been a feasible alternative, but this would require rearranging the video bronchoscopy equipment in the operating room to maneuver the radiograph arm into place. Unlike chest ultrasonography, using radiography would have required the surgeon to interrupt the procedure, a delay that might have been critical. In the absence of an ultrasonogram or radiogram, the clinical examination alone (auscultation, chest movement, and tracheal deviation) and the clinical setting could have led to the correct diagnosis and treatment, albeit with less diagnostic certainty.
The diagnosis of pneumothorax with lung ultrasonography has recently been addressed by an international consensus conference and can be approached by using an algorithm that integrates 4 ultrasonography artifacts.4 These artifacts are lung sliding, B-lines, lung pulse, and lung point (Fig. 3).
Lung sliding occurs when the visceral pleura slides on the parietal pleura during normal ventilation, as seen in the left lung in Video 1 (Supplemental Digital Content 1, http://links.lww.com/AA/B39). In critically ill patients whose lungs are being mechanically ventilated, the detection of lung sliding has been shown to exclude pneumothorax with a sensitivity of 95% and a negative predictive value of 100%.5 When the lungs have an increased fluid content at their surface such as in pulmonary edema, other ultrasound artifacts called B-lines, or comet-tail artifacts, can be seen. Here, the fluid pockets abutting the visceral pleura cause multiple internal reflections of the ultrasound waves before they return to the transducer. The inherent delays are interpreted as signals returning from deeper structures, thus creating the impression of narrow rays progressing into the deeper ultrasound field. B-lines prove that the parietal and visceral pleura are in apposition, thus excluding pneumothorax with a negative predictive value of 100%.6
Another sign, lung pulse, consists of small shuddering movements at the pleural interface that are detected by M-mode ultrasonography even when gross lung sliding is not detectable. This sign is useful when pleural adhesions or atelectasis prevent pleural sliding. M-mode can also be useful for confirming lung sliding initially seen on 2-dimensional ultrasonography; the typical “sandy beach” sign represents the pleural interface (Fig. 2).
An additional sign, the “lung point,” is the only sign with a high specificity for pneumothorax. The lung point occurs when the ultrasound probe is positioned directly over the transitional zone, where normal lung sliding alternates with lack of lung sliding where the pneumothorax begins. Video 2 (Supplemental Digital Content 2, http://links.lww.com/AA/B40) shows an example of lung point obtained from a different patient. In our case, this sign was sought, but not found. The lung was probably completely collapsed, so no contact between parietal and visceral pleura would be expected anywhere over the affected thorax.
Thus, because there were no sonographic signs that would exclude pneumothorax, and because the patient’s unstable condition precluded waiting for a chest radiogram, the anesthesia team considered it very likely that a tension pneumothorax was present and elected to apply needle decompression, which immediately stabilized the patient.
Our case report joins a report by Ueda et al.7 that describes the successful use of intraoperative lung ultrasonography to detect pneumothorax in a laparoscopic case and a trauma patient with rib fractures. Our case further supports the utility of lung ultrasonography, especially when competing differential diagnoses must be considered, such as endobronchial obstruction due to tumor, rapidly evolving edema due to surgical irritation, or clots.
In summary, ultrasonography is familiar to anesthesiologists as a tool to guide central line and regional block placement. Detection of pneumothorax with the same ultrasound transducer can be easily taught, even in an online format, as recently demonstrated by Cuca et al.8 This case suggests that acquiring this easily learned skill is beneficial.
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