Abstract

A 3-month-old male infant underwent rigid bronchoscopy with manual jet ventilation due to persistent right upper lobe collapse under capnographic surveillance. The CO₂ waveform abruptly vanished soon after application of jet ventilation, while breath sounds decreased gradually until the left side breath sounds were barely audible. Progressive abdominal distension with protruding umbilicus was also detected at the same time. Under the impression of bilateral tension pneumothorax, emergent needle decompression was carried out. In this case, the sudden onset of CO₂ waveform change was the first warning sign of pneumothorax, which is the most common complication of jet ventilation. Therefore, we strongly recommend that continuous capnographic surveillance be applied during bronchoscopy with jet ventilation.

Keywords

capnography; high-frequency jet ventilation; pediatrics; pneumothorax;

1. Introduction

Compared with conventional mechanical ventilation, jet ventilation is more frequently used in preterm infants, especially in those with respiratory distress syndrome. This practice is due to the fact that high frequency jet ventilation (HFJV) functionally causes fewer air leaks and decreases the chance of a chronic lung disease going into rapid progression.¹ Furthermore, rigid bronchoscopy combined with HFJV is valuable in diagnostic and therapeutic procedures for very small premature infants with lung atelectasis.² However, due to the comparatively higher incidence of barotrauma associated with jet ventilation, its clinical application in children is controversial.³

In applying jet ventilation in children, adequate monitoring is especially important to guard against complications. Although the incidence of barotrauma as a result of jet ventilation is rather high,⁴ the overall benefit of HFJV would appear to outweigh its complications (which include subcutaneous emphysema, pneumomediastinum, pneumothorax, and pneumoperitoneum).

In this case, the disappearance of capnographic waveform was the first warning sign of pneumothorax. Early diagnosis with proper management should be the focus of discussion for this complication.

2. Case Report

Since birth, this 3-month-old male infant (5 kg, ASA class III) had suffered from persistent right upper lobe (RUL) collapse with respiratory syncytial virus infection, and had been repeatedly hospitalized due to intermittent tachypnea and fever (Figure 1). He was scheduled to receive jet ventilation for the RUL collapse and rigid bronchoscope examination. Induction of anesthesia was by spontaneous breathing of sevoflurane, and the maintenance of anesthesia was by ventilating sevoflurane through the sidearm of the rigid bronchoscope (Karl Storz, Culver City, CA, USA). Copious mucus secretion in the right upper bronchus was noted bronchoscopically. Initially, the otolaryngologist used epinephrine:saline (1:200,000) for bilateral bronchial lavage, and then manipulated jet ventilation for the collapsed RUL (Monsoon Deluxe Jet Ventilator; Acutronic, Hirzel, Switzerland) via a 2.0-mm suction tube at 20 psi for approximately 20 times. Unfortunately, sudden disappearance of the CO₂ waveform on the capnogram was noted after RUL jet ventilation.

The rigid bronchoscope was withdrawn and we tried to maintain oxygenation by mask ventilation with pure oxygen, but we could not see any capnographic display and the patient’s breathing sounds became fainter and fainter. Bronchospasm was first suspected to be the cause, so aminophylline 10 mg with succinylcholine 5 mg was administered, but without any effect. One minute later, we observed that the patient’s oxygen saturation had rapidly decreased from 95% to 50%, and his heart rate had dropped from 160 to 90 beats/min. Intravenous atropine 0.2 mg was given and emergent endotracheal intubation was established. However, right side breath sounds were inaudible and left side breath sounds could barely be heard. After another 1 minute, SaO₂ was 57% and heart rate was 150 beats/min. Meanwhile, we noted abdominal distension with protruding umbilicus and absent bilateral breath sounds. Bilateral tension pneumothorax was thus highly suspected and decompression with the insertion of a 21-gauge needle through the left second intercostal space was performed. Oxygen saturation was rapidly restored to 85−90% and vital signs returned to normal limits within a few seconds.

Emergent chest radiography showed tension pneumothorax and pneumoperitoneum (Figure 2). After bilateral placement of chest tubes (Figure 3), he was transferred to the ICU, where he exhibited stable vital signs (SaO₂, 92%; heart rate, 164 beats/min). Extubation and removal of bilateral chest tubes took place the next day. He was returned to the general ward 3 days later, where he was placed under close observation. Subsequent chest radiographs were unremarkable.

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Figure 1 Chest computed tomography shows a minimal air collection at the ventral peripheral portion of the right upper lobe (arrowheads), ruling out atelectasis.

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Figure 2 Chest radiography of left side tension pneumo- thorax after emergent chest tube insertion and emergent intubation. Prominent pneumoperitoneum (arrowheads) and free air collection in the pleural space with total collapse of the right lung. Right side tension pneumoth- orax (arrowheads) and pneumoperitoneum are noted.

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Figure 3 Status after bilateral chest tube insertion; free air in the peritoneum is still present.

3. Discussion

The causes of changes in the CO₂ waveform on capnography are diverse and sometimes difficult to sort out with regard to a particular disorder and its differential diagnoses, especially in pediatric patients. However, when applying rigid bronchoscopy with HFJV, end-tidal partial pressure of carbon dioxide (petCO₂) could still be a powerful and useful monitoring parameter in clinical practice. The use of capnography as routine monitoring is strongly recommended, especially when applying HFJV for instrumentational bronchoscopy.⁵ From this case, we benefited from its use and therefore emphasize its importance in therapeutic jet ventilation.

In this case, the right side pneumothorax might have occurred as a result of jet ventilation manipulations, and as the positive pressure ventilation persisted, air leakage might have encroached on the left lung insidiously and progressively. Tension pneumothorax developed and progressed quickly to deter CO₂ exchange, causing changes in the capnographic display. The possible reasons for barotrauma are excessive inspiratory time and hyperinflation of the targeted lobe.^6,7 We emergently treated the pneumothorax with insertion of a venous catheter, which also served as a powerful diagnostic method.⁸ Not only bilateral pneumothorax but also pneumoperitoneum were detected. Following barotrauma, massive alveolar rupture occurs, and the leaked air will travel along the perivascular sheaths and enter the peritoneum to induce pneumoperitoneum.⁹ Another report pointed out that large tidal volume (volotrauma), high peak expiratory pressure or high peak inspiratory pressure may induce barotrauma to cause pneumothorax and pneumoperitoneum.¹⁰

In summary, we should be prepared for complications (such as hypertension, hypotension, bronchospasm, hypoxia or barotrauma) when applying jet ventilation in pediatric patients; sophisticated monitoring and immediate management are indispensable to prevent catastrophic outcome. It is strongly recommend that end-tidal CO₂ monitoring be employed as it could provide the first warning of barotrauma during HFJV. It is also suggested that when applying HFJV, lower driving pressure should be used, and then gradually increased in order to prevent complications, including barotrauma.