Acute failure in open pneumothorax
In open internal pneumothorax, a functioning communication persists between the bronchial tree, lung tissue, and the pleural cavity. As a result, the inhaled gas begins to make "pendulum-like movements" synchronous with respiration, circulating between the affected side and the healthy lung. In this case, the pleural cavity acts as an extensive "dead space".
This leads to catastrophic consequences for gas exchange. The patient rapidly develops hypercapnia (excess carbon dioxide in the blood) and hypoxemia (critical oxygen deficiency). Acute ventilatory respiratory failure develops, which is soon joined by cardiovascular system failure due to increasing hypoxia. Externally, this manifests as pronounced dyspnea, forced posture of the patient, and acrocyanosis.
The cascade of valvular (tension) pneumothorax
The most severe variant in blunt chest trauma is considered to be internal valvular, or tension, pneumothorax. Damaged tissues begin to act as a one-way valve: during inspiration, air is freely sucked into the pleural cavity, but upon expiration, this tissue valve slams shut, preventing the gas from escaping outward.
Intrathoracic pressure rises rapidly, triggering a pathogenetic cascade of disorders:
- Progressive collapsing (collapse) of the damaged lung occurs.
- Mediastinal organs are displaced to the opposite, healthy side.
- Due to the displacement, the tidal volume of the remaining intact lung sharply decreases.
- The great vessels of the mediastinum (primarily the venae cavae) undergo compression and kinking.
- A sharp deficit in venous blood inflow to the heart occurs.
Clinically, this condition manifests as tachycardia, rapid thready pulse, and collapse (drop in blood pressure). A real threat of fatal pleuropulmonary shock arises. The condition is classified as extremely severe and requires emergency intensive care in an intensive care unit (ICU) with immediate drainage of the pleural cavity.
Hemothorax and subcutaneous emphysema
Chest injuries are often accompanied not only by the ingress of air, but also by the accumulation of blood in the pleural cavity — hemothorax. The source of bleeding can be torn intercostal arteries, branches of the subclavian artery and aorta, as well as vessels of the damaged lung parenchyma. With massive blood loss (exceeding 1000 ml), the patient's condition is assessed as severe, pallor occurs, the pulse quickens, and relief is brought only by a forced semi-sitting position.
Of particular danger is clotted hemothorax. Normally, the shed blood first clots and then, under the action of pleural enzymes, is defibrinated and becomes liquid again. This physiological lysis is disrupted in:
- Simultaneous shedding of too large a volume of blood;
- Post-traumatic parietal pleural dysfunction;
- High overall coagulant activity;
- Release of tissue thromboplastin from destroyed structures (activates local clotting factors).
As a result, dense blood clots remain in the cavity, resistant to lysis.
Another common complication is subcutaneous emphysema. Air is pumped into the subcutaneous adipose tissue of the chest wall through the parietal pleura torn by rib fragments. If emphysema primarily occurs in the neck rather than above the fracture site, it serves as a diagnostic marker of mediastinal organ damage. In tension pneumothorax, subcutaneous emphysema is characterized by an extremely rapid spread over a large area.
Iatrogenic complications in diagnostics
The management of patients with pneumothorax is associated with risks when treatment tactics are incorrectly chosen. It is strictly not recommended to perform diagnostic pleural puncture in the absence of clear clinical and instrumental signs of pneumo- or hemothorax. Performing a puncture "blindly" (without prior radiography, CT, or ultrasound with dopplerography) carries a huge risk of iatrogenic injuries.
A complication of such a blind puncture can be accidental injury to the diaphragm. In this case, gastric or intestinal contents may end up in the syringe, which will highly likely lead to the development of severe purulent-inflammatory complications in the pleural cavity. Any drainage requires prior visualization of the contents.
The pathogenesis of tension pneumothorax is easy to remember using the "LDSV" rule: Lung collapse → Displacement of the mediastinum → Decrease in tidal volume → Compression of the venae cavae.
Class and exam questions
Why does blood pressure drop sharply in tension pneumothorax?
Due to increasing intrapleural pressure, the mediastinum shifts and compresses the major venae cavae. This leads to a sharp deficit of venous return to the heart and subsequent collapse (drop in BP).
What is the pathophysiological danger of open internal pneumothorax?
In this form, the inhaled air makes pendulum movements between the healthy lung and the pleural cavity, which turns into a functional "dead space". This rapidly leads to severe hypercapnia and hypoxemia.
Why doesn't blood in hemothorax resorb, but instead clots?
The formation of clotted hemothorax occurs when fibrinolysis processes are disrupted. This is promoted by the outpouring of a large volume of blood, pleural dysfunction, general hypercoagulation, and massive release of tissue thromboplastin from damaged tissues.
What else to study on this topic
- Detailed radiological picture: visceral pleural line and the level of the collapsed lung edge
- Comparative percussion and auscultatory diagnostics of pneumothorax and hemothorax
- Changes in blood gas composition during respiratory failure
- Technique and sites for performing pleural puncture
- Features of pain syndrome: mimicking the clinical presentation of myocardial infarction in mediastinal emphysema
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