Pneumothorax is usually diagnosed when signs of life-threatening tension pneumothorax develop. The case report describes novel data derived from miniature superficial sensors that continuously monitored the amplitude and symmetry of the chest wall tidal displacement (TDi) in a premature infant that suffered from pneumothorax. Off-line analysis of the TDi revealed slowly progressing asymmetric ventilation that could be detected 38 min before the diagnosis was made. The TDi provides novel and valuable information that can assist in early detection and decision making.
Pneumothorax (PTX) is a life-threatening complication, with higher incidence in very low birth weight infants. PTX is usually diagnosed when signs of tension PTX develop, and when life-saving surgical drainage must be performed. The estimated median time delay from PTX onset to diagnosis and treatment is 127 min.1 The prevalence of associated neurological complications, such as intracranial bleeding or diffuse cerebral damage is high, with mortality rates as high as 43%.2 Therefore, preventing the development of tension PTX is essential in order to avoid serious consequences.
Our group has described the feasibility of monitoring the amplitude and symmetry of lung ventilation with three miniature motion sensors attached to both sides of the chest wall and to the upper abdomen.3, 4, 5 These sensors sense the local chest wall tidal displacement (TDi), as well as the vibrations and breath and heart sounds. A 20% change in the TDi from the patient's established baseline TDi, measured by any of the sensors, defined a significant trend deviation.
We describe a case of a premature male newborn, second of twins, born at 32 weeks+3 days, with a birth weight of 1369 g. The infant initially received respiratory support by nasal continuous positive airway pressure, but later required mechanical ventilation, provided by high-frequency oscillatory ventilation (HFOV) and surfactant replacement therapy (Curosurf, Chiesi Pharmaceuticals, Parma, Italy). On day 1 of life, the newborn developed a left PTX and a chest-tube (CT) was inserted to drain it. On day 3, following parental consent, the baby was recruited to a feasibility study of TDi monitoring in our neonatal intensive care unit, (approved by the Carmel Medical Center institutional review board, CMC 0012-08, and registered at U.S. National Institutes of Health, NCT00702169). Three miniature motion sensors were attached to both sides of the chest and to the upper abdomen. The patient was monitored with the Pneumonitor (Pneumedicare, Yokneam, Israel) and recordings and printouts of the medical follow-up sheets were collected for off-line analysis.
On day 3, the infant was stable while being ventilated on HFOV, the CT was clamped for 4 h, chest x-ray and transillumination were performed and were negative for free air, and the drain was removed. One hour later, blood-gas analysis revealed an increase in PaCO2 from 39.8 mm Hg before the CT extraction to 50.5 mm Hg, while being ventilated with HFOV with 30% FiO2. Transillumination of the chest revealed a large PTX (Figure 1). Surgical drainage via a CT was performed, and successful drainage was validated by x-ray. Off-line analysis of the TDi from the moment of tube extraction revealed progressive development of asymmetric ventilation (Figure 2), significantly before diagnosis of PTX (denoted by ‘T’ in Figure 2). The TDi in the left chest, the side of the PTX, progressively decreased with a concomitant increase in the TDi in the contralateral right side. Overt asymmetric ventilation with a 20% increase in the right TDi developed 38 min before the diagnosis of PTX (denoted by ‘R’ in Figure 2). A 20% decrease in the left TDi was recorded 31 min before the diagnosis of PTX (denoted by ‘L’ in Figure 2). The abdominal sensor also revealed a progressive increase in the abdominal TDi, escalating to a 20% change from baseline 24 min before the diagnosis of PTX (denoted by ‘A’ in Figure 2). The changes in the TDi at the epigastric area may result from the increase in the PTX and larger tidal displacement of the diaphragm.
It is important to note that diagnosis of progressing PTX via development of asymmetric TDis was performed in the presence of normal SpO2, and before development of cardiovascular decompensation.
Two days later (on day 5), the baby was clinically stable and the endotracheal tube was removed, whereas the CT was left in place. In addition, he received high-flow therapy through a nasal cannula (Vapotherm, Stevensville, MD, USA).
On day 7, the baby was breathing spontaneously with 25% FiO2, and was hemodynamically stable and asymptomatic. An x-ray obtained following clumping of the CT revealed a residual, moderate size, non-tension PTX and malposition of the chest drain. The malpositioned CT was removed and the non-tension PTX was conservatively monitored for the next 3 days. The infant was breathing spontaneously, asymptomatic and the subsequent x-rays demonstrated slow resolution of the PTX.
Following resolution, off-line analysis of the monitor trends (TDi) revealed stable symmetric readings of the TDi on both chest sides. Breath rate was 41.3±8.0 breaths per minute, and a good correlation (R2=0.75) was found between breathing rate measured by impedance monitor (MP40 Philips, Philips, Boeblingen, Germany) and by the motion sensors. The mean TDi was 0.93±0.42 mm and 1.11±0.48 mm, on the right and left chest sides, respectively.
This non-invasive modality assesses the symmetry of lung function and changes in the magnitude of the tidal volume. It enables detection of progressing PTX, significantly before the development of respiratory distress. In addition, it provides tight monitoring of the respiratory function in the presence of non-tension PTX. Symmetric, quiet, spontaneous breathing associated with slow resolution of the PTX was observed.
The probability of detecting a progressing PTX early enough is low with available methods. Auscultation, transillumination, x-rays and blood gases are intermittent procedures. Pulse oximetry, end-tidal and transcutaneous PCO2 monitors, alarm, in most situations, only when a tension PTX is already established.1, 3
The suggested technology has already been used for early detection of deteriorating ventilation in premature infants during HFOV, but did not involve any cases of PTX.4 In about half the cases, the deteriorations were owing to airway obstruction by secretions or decline in lung compliance, and these conditions were detected 22.4±18.7 min before the detection of hypoxemia.4
This first demonstration in humans is corroborated by our previous preclinical studies on the effect of PTX on chest wall dynamics.3, 5 TDi provided the earliest sign of PTX when progressive PTX was induced in rabbits,3 by injecting 1 ml min−1 of air into the pleural space. A decrease in SpO2 below 90% was detected after 46.6±11.3 min, whereas 20% decreases in the TDi was detected after 16.1±7.2 min.3
In summary, the progressive and rapid decrease in TDi on the PTX side, enabled detection of asymmetric ventilation, as shown in the present case.
Continuous monitoring of the TDi enables detection of asymmetric ventilation and provides novel and valuable information that can be translated for early detection of progressing PTX, as well as tight monitoring of an already present non-tension PTX. This intuitive physiological index can assist in decision making and management of PTX.
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Chest wall dynamics were measured by the equipment provided by Pneumedicare Ltd.
DW, SK, AF, ICK and AL are involved in the development of a respiratory function monitor within a collaborative effort between the Technion—Israel Institute of Technology, Clalit Health Services and Pneumedicare Ltd. The remaining authors declare no conflict of interest.
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Waisman, D., Landesberg, A., Kohn, S. et al. Chest dynamics asymmetry facilitates earlier detection of pneumothorax. J Perinatol 36, 157–159 (2016). https://doi.org/10.1038/jp.2015.172
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