Resolution is not the end: the Macklin effect after chest tube removal in a trauma patient with aging and comorbidities: a case report
Article information
Abstract
Pneumomediastinum is an uncommon complication in cases of blunt chest trauma but can signal severe underlying issues. This report discusses a 69-year-old male patient with preexisting conditions of obesity, sleep apnea, and asthma, who experienced delayed pneumomediastinum and pneumopericardium following the removal of a chest tube. This tube had been placed to address a traumatic hemopneumothorax, which had resolved. The removal of the chest tube triggered a series of events, exacerbated by the patient's chronic health conditions. The patient was managed conservatively with close monitoring and physiotherapy, which successfully resolved the condition without the need for further invasive procedures. The multifactorial nature of the Macklin effect illustrates that even routine procedures such as chest tube removal can trigger a chain reaction in susceptible patients. The choice of conservative management, rather than immediate invasive interventions, underscores the delicate balance necessary in trauma care.
INTRODUCTION
Pneumomediastinum occurs in up to 10% of blunt chest trauma cases. While most instances are benign, a small percentage presents significant morbidity and mortality risks [1,2]. The decision to intervene in cases of pneumomediastinum and pneumopericardium has been a subject of ongoing debate. Even a century after its initial description, the significance of the Macklin effect continues to be recognized, particularly with the routine use of computed tomography (CT) and x-rays. These imaging advancements have further fueled discussions on finding the right balance between overtreating and undertriaging pneumomediastinum in trauma patients [3].
The Macklin effect can be triggered by various conditions and activities beyond the context of trauma [4]. These include bronchial asthma, respiratory tract infections, strenuous physical activity, and events associated with the Valsalva maneuver, such as forceful coughing or vomiting [5]. Additionally, the Macklin effect has been linked to other conditions such as diabetic ketoacidosis, forceful straining during exercise, drug inhalation, and childbirth [4].
In this case report, we describe a patient who developed pneumomediastinum and pneumopericardium following the removal of a chest tube, which had been placed to resolve a traumatic pneumothorax. The patient's comorbidities, such as obesity, sleep apnea, and asthma, likely played a role in the development of these complications. The discussion emphasizes the importance of recognizing the Macklin effect in similar cases.
CASE REPORT
A 69-year-old male patient with a history of hypertension, diabetes mellitus, and asthma was involved in a severe motor vehicle accident. The accident, characterized by a high-speed rollover, resulted in multiple fatalities among the passengers, including family members. The patient, who was not wearing a seatbelt, was ejected from the vehicle and sustained multiple traumatic injuries. Initially, he received treatment at a small rural hospital located approximately 2 hours from King Saud Medical City (Riyadh, Saudi Arabia). At that facility, a chest tube was inserted to manage a hemopneumothorax that was identified on a chest x-ray. Throughout this period, his vital signs remained stable.
Due to the severity of his injuries and the limited resources available at the rural hospital, the patient was transferred to our level I trauma center for advanced care. Upon his arrival, the initial assessment indicated that he was stable, although decreased air entry was noted on the left side during auscultation, consistent with a hemopneumothorax. He remained hemodynamically stable, and his airway was secured with a cervical collar. The secondary survey revealed multiple minor external lacerations, including one on the head and another on the right forearm. Additionally, a cast had been placed on his right leg prior to transfer. A chest x-ray performed upon arrival (Fig. 1A) and an electrocardiogram (ECG) were part of the initial evaluation. The ECG results suggested left ventricular hypertrophy and possible strain. Further diagnostic imaging with a pan CT scan identified multiple traumatic injuries. These included fractures of the left occipital condyle, a T9 vertebral body lesion suggestive of a bone hemangioma, a T4 vertebral body compression fracture, several rib fractures, and a manubrium fracture (Fig. 1B). Orthopedic injuries were extensive, featuring a comminuted distal third fibular fracture with an open wound and a posterior dislocation of the left femoral head accompanied by a comminuted fracture of the acetabular posterior column, which was surgically addressed on the day of presentation.
Imaging findings related to the patient's initial presentation. (A) The initial chest x-ray shows the chest tube (white arrow) used to manage the hemopneumothorax. (B) A computed tomography scan reveals pneumothorax (yellow arrow), sternal fracture, rib fractures, hemothorax, chest tube (black arrow).
The patient was admitted to the intensive care unit for further monitoring and management. Serial chest x-rays were conducted (Fig. 2A, B), and chest physiotherapy was initiated along with pain management. By the third day, the pneumothorax had resolved (Fig. 2C), as confirmed by imaging, and the chest tube was removed, secured with a stitch. Although there were no immediate complications, extensive subcutaneous emphysema began to develop by the fourth day and continued to spread over the subsequent days (Fig. 2D–F), affecting the chest wall and neck.
Serial chest x-rays and computed tomography (CT) imaging of the patient throughout the intensive care unit stay following traumatic hemopneumothorax (before and after chest tube removal). (A) The chest tube (white arrow) effectively manages the hemopneumothorax on day 1. The resolution of the pneumothorax on (B) day 2 and (C) day 3, with the chest tube (white arrows) still in place. After the chest tube removal on day 3, the patient developed extensive surgical emphysema (orange arrows), which are progressively depicted in (D) day 4, (E) day 5, and (F) day 6 chest x-rays. (G) A CT scan performed on day 6 reveals additional complications, including pneumomediastinum (purple arrow) and pneumopericardium (blue arrow), along with widespread subcutaneous emphysema (orange arrows). (H) The conservative management approach resulted in gradual improvement, as evidenced by day 12 chest x-ray. The orange arrows indicate surgical emphysema. (I) By day 22, the emphysema had completely resolved.
Initially, the patient's oxygen requirement escalated from 2 to 3 L via nasal cannula to 5 L via face mask as his condition deteriorated, evidenced by increasing surgical emphysema that extended from the neck to the left flank. Subsequent chest x-rays indicated further worsening (Fig. 2F), leading to a CT scan of the chest. This scan revealed the presence of pneumomediastinum and pneumopericardium (Fig. 2G, H). Despite these findings, the patient's respiratory status remained stable. Consequently, it was decided to manage his condition conservatively, employing aggressive chest physiotherapy and close monitoring.
Subsequent cardiac evaluation through echocardiography was performed, as it was deemed necessary to assess potential cardiac injury resulting from the pneumopericardium and the patient's sternal fracture. The echocardiogram revealed mild tricuspid regurgitation, moderate concentric left ventricular hypertrophy, mild asymmetric left ventricular hypertrophy, and an ejection fraction of 55%. These findings are consistent with hypertrophic cardiomyopathy and left ventricular outflow obstruction. Additionally, systolic anterior motion of the mitral valve was noted, along with severe mitral regurgitation.
Over the next several days, the subcutaneous emphysema and pneumomediastinum began to resolve (Fig. 2H). Throughout this period, the patient maintained stable hemodynamics. He was successfully downgraded from the intensive care unit to the general ward in stable condition, having recovered from these complications without the need for further invasive procedures. Subsequent management of his injuries was coordinated by other involved teams, and he was referred to pulmonology for management of obstructive sleep apnea. A follow-up chest x-ray on day 22 confirmed the ongoing resolution of the complications (Fig. 2I). The patient was discharged home in his usual state of health.
Ethics statement
Written informed consent for publication of the research details and clinical images was obtained from the patient.
DISCUSSION
It has been nearly eight decades since Charles Macklin, a Canadian pulmonologist, published his initial experimental investigation on the phenomenon now known as the Macklin effect [3]. The pathophysiology underlying this observation remains critically important in an era dominated by diagnostic imaging [1]. The Macklin effect involves alveolar rupture, allowing air to escape into the perivascular and peribronchial interstitial tissues (Fig. 3A, B) [3,6]. Once air escapes the alveoli, it travels along the bronchovascular sheaths toward the lung root (Fig. 3C, D), eventually accumulating in the mediastinum (Fig. 3E–H) [3]. The stretching and subsequent leaking of alveolar walls, which may be caused by barotrauma from positive pressure ventilation, high-speed trauma, or even something as simple as the Valsalva maneuver, triggers this effect [4,7]. Another mechanism involves the thinning of alveolar walls, which weakens them. This can occur in conditions like asthma and aging, or from factors that reduce elasticity, such as emphysema or smoking [8,9]. Although rare, this effect is often responsible for excessive investigations and management in trauma contexts [1,2].
Pathophysiology of the Macklin effect (illustrated by Fayez G. Aldarsouni). (A) The normal bronchovascular bundle in the lung displays intact alveoli, arterioles, and venules, with no signs of air leakage. (B) With an increase in intrathoracic pressure, the bronchioles become distended, leading to chronic thinning of the alveolar walls and eventual rupture of the alveoli. (C) After the alveoli rupture, air starts to dissect along the bronchovascular sheaths. (D, E) The air then progressively tracks along these sheaths toward the mediastinum. (F, G) This accumulation of air continues to spread through the lung interstitium and into the mediastinal space. (H) The process ultimately results in the development of pneumomediastinum, characterized by the presence of air within the mediastinal space.
The balance in trauma management is precarious, with very high stakes. A false-positive investigation is often more justifiable than missing a true-negative injury, particularly in the rare cases of tracheobronchial injuries or esophageal tears. This rationale has long been accepted as a fundamental principle in trauma [1]. The conclusion that iatrogenic trauma is the primary cause of aerodigestive tract injuries within the thorax was reached after careful consideration [10]. The size of these structures and their protected position generally shield them from most traumatic injuries [1]. However, some argue that, despite their rarity, these injuries carry significant morbidity and mortality if overlooked, making pneumomediastinum both a hallmark of aerodigestive trauma and a persistent concern for trauma surgeons. We concur with the review by Muckart et al. [1], which describes the benign nature of pneumomediastinum and pneumopericardium following blunt chest trauma. Thus, we chose conservative management for our patient.
Our patient was a 69-year-old obese male patient with multiple comorbidities. As previously mentioned, these comorbidities, coupled with the patient's age, are risk factors for the pathophysiological processes of loss of elasticity and wall thinning. It appears that the patient was not fully aware of or compliant with the management of his comorbidities. We observed that he was frequently sleepy, leading us to suspect obstructive sleep apnea (OSA). Although an ECG was performed in the emergency room, it showed no specific changes. The echocardiogram findings suggest long-term sequelae of OSA [11], even though OSA does not directly affect elasticity. Typically, OSA causes fluctuations in intrathoracic pressure that can suddenly stretch the alveoli. This occurs as a result of breathing against a blocked airway, where rapid and intense pressure changes can stretch the alveoli, contributing to leakage. A similar mechanism has been noted to increase the risk of barotrauma in patients using continuous positive airway pressure [12]. It appears that the onset of surgical emphysema occurred when we removed the chest tube, a procedure that can cause similar shifts. Novoa et al. [13] recommended removing the chest tube at the end of expiration during a Valsalva maneuver, corresponding to when the difference between the atmospheric and pleural pressure is lowest. Although this practice is not a fixed rule and remains controversial, it is the standard procedure at our center.
Interestingly, our case involved a pneumopericardium similar to that described by Nowitz et al. [7], where a Valsalva maneuver triggered the condition. Closure following chest tube removal can be achieved either through an occlusive dressing or by placing a suture [14]. Although a case-by-case approach is preferred, obesity—as noted in our case—has been identified as a risk factor for chest-related complications; therefore, special consideration should be given to such patients [15].
In trauma care, no procedure can be considered truly routine. The Macklin effect serves as a reminder that complications can still arise even after a pneumothorax has resolved, particularly in patients with obesity, sleep apnea, and asthma. In our case, what seemed like a straightforward chest tube removal became a catalyst for unexpected events such as pneumomediastinum and pneumopericardium. The process involves more than just the removal of the tube; it requires careful consideration of timing, technique, and a thorough understanding of the patient's medical history. Every decision, no matter how seemingly minor, can influence the outcome, tipping the scales between complication and recovery. Although the Macklin effect is often benign, it remains a persistent concern in trauma care, serving as a reminder that dangers that are not immediately apparent can be just as threatening as those that are visible.
Notes
Author contributions
Conceptualization: all authors; Methodology: all authors; Investigation: all authors; Supervision: ZT, EA, MA, TA, KT, GZAR; Writing–original draft: FGA, SA, HMA; Writing–review & editing: all authors. All authors read and approved the manuscript.
Conflicts of interest
The authors have no conflicts of interest to declare.
Funding
The authors received no financial support for this study.
Data availability
Data sharing is not applicable as no new data were created or analyzed in this study.