Due to high-pressure boilers, chemical substances, or gas explosions, and during wartime, due to high explosives or nuclear detonations, enormous energy can be released instantaneously, causing a sharp increase in pressure and temperature at the blast center, which rapidly propagates outward, forming a supersonic high-pressure wave known as a shock wave. The continuous overpressure-negative pressure of air shock waves or underwater shock waves acts on the human body, causing rapid compression and expansion of the chest and abdomen, leading to a series of hemodynamic changes that result in injuries to the heart, lungs, and blood vessels. Gases within the body produce an implosion effect under the overpressure-negative pressure, causing injuries to gas-containing tissues (such as alveoli). When pressure waves pass through tissues of different densities, reflection at interfaces causes a shattering effect, resulting in injuries. Additionally, tissues of varying densities subjected to the same pressure wave experience different speeds due to varying inertia, leading to tearing and bleeding at connecting points. The injuries caused directly by the shock wave itself acting on the human body are referred to as blast injuries.

bubble_chart Etiology

The injury caused directly by the blast wave acting on the human body is called blast injury. At the same time, the dynamic pressure of the blast wave (the impact force of high-speed airflow) throws and strikes the human body, causing indirect injury after acting on other objects. The high temperature of the blast wave can cause burns on the body surface or respiratory tract. The blast wave can injure all tissues and organs of the human body, with gas-containing organs being particularly susceptible. The severity of tissue and organ injury depends on the magnitude of the peak pressure, the duration of the positive pressure, and the rate of pressure rise. Clinical characteristics of blast injury: ① Multiple injuries, often polytrauma or combined injuries, with complex conditions; ② External mildness but internal severity, where the body surface may appear intact but with obvious symptoms and severe internal organ injuries; ③ Rapid progression, usually peaking within 6 hours post-injury, though it may also develop within 1–2 days. Once the body's compensatory function fails, the condition can deteriorate rapidly, making treatment difficult. Theoretically, blast injury includes both the direct injury caused by the overpressure-negative pressure of the blast wave (i.e., blast injury) as well as injuries caused by dynamic pressure and burns. However, in clinical practice, blast injury and blast injury are often conflated.

The main pathological changes of pulmonary blast injury are alveolar rupture and intra-alveolar hemorrhage, followed by pulmonary edema and emphysema, sometimes accompanied by lung rupture. Pulmonary hemorrhage can range from patchy to diffuse, with severe cases showing parallel linear hemorrhages in the lung parenchyma corresponding to the intercostal spaces. Rupture of blood vessels in the lung parenchyma can form hematomas, and even blood clots may block the trachea, leading to rapid death. Mild pulmonary edema may present as interstitial or small amounts of fluid in the alveolar spaces, while severe cases can show large amounts of edema fluid overflowing into the bronchi and even the trachea, often mixed with blood, appearing as bloody frothy fluid. Pulmonary hemorrhage and edema can lead to atelectasis. Pulmonary emphysema can be interstitial or alveolar, with severe cases developing bullae containing blood and air under the pleural membrane. When lung rupture occurs, it can cause hemothorax or hemopneumothorax.

bubble_chart Clinical Manifestations

The clinical manifestations of pulmonary blast injury vary depending on the severity of the condition. Mild cases may only present with brief chest pain, chest tightness, or a feeling of suffocation. In moderately severe cases, symptoms such as cough, hemoptysis, or blood-streaked sputum may appear within 1 to 3 days after the injury, with a few patients experiencing dyspnea. Auscultation may reveal scattered and variable moist rales or crepitations. Severe cases can exhibit significant dyspnea, cyanosis, bloody frothy sputum, and are often accompanied by shock. Physical examination may show lung hyperresonance and signs of hemopneumothorax in addition to pulmonary rales. Additionally, manifestations of injury to other organs are often present. Chest X-rays may reveal thickened lung markings, patchy shadows, reduced radiolucency, or even large dense shadows, as well as signs of atelectasis and hemopneumothorax. Blood gas analysis may show varying degrees of abnormal results.

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Based on the history of blast injury, clinical manifestations, and X-ray examination, pulmonary blast injury is easy to diagnose. However, attention should be paid to its characteristics of being externally mild but internally severe, rapidly progressing, and often accompanied by combined injuries, so as to avoid misdiagnosis and confusion with fistula disease.

bubble_chart Treatment Measures

The treatment of pulmonary blast injury focuses on maintaining respiratory and circulatory functions, including ensuring airway patency, administering oxygen, performing tracheostomy when necessary, and assisting with mechanical ventilation as well as blood transfusion and fluid resuscitation to counteract shock. Closed thoracic drainage should be performed as early as possible for those with hemopneumothorax. Hemostatic medications should be administered. Sufficient antibiotics should be used to prevent infection. Appropriate measures should be taken for concurrent injuries to other organs.