Systemic responses to trauma are influenced by various factors, including soft tissue injuries, long bone fractures, and blood loss. The pathophysiology of traumatic shock differs significantly from that of purely hemorrhagic shock. Patients with traumatic shock are more likely to develop multiple organ dysfunction syndrome (MODS). During the pathophysiological process of traumatic shock, ischemia-reperfusion injury triggers damage-associated molecular patterns (DAMPs), which activate and bind to cell surface receptors. This interaction initiates intracellular signal transduction with a cascading amplification effect, ultimately resulting in the release of various cytokines and chemokines, leading to shock.
Treatment
The focus of treatment for traumatic shock involves controlling the progression and aggravation of systemic inflammatory responses. Measures include:
- Hemorrhage control, fluid resuscitation to restore blood volume, correction of tissue hypoxia, and timely management of soft tissue injuries. Blood volume reduction in traumatic shock is often caused by the accumulation of blood clots and inflammatory exudates in body cavities and deep tissues, making fluid resuscitation frequently necessary during emergency care.
- Use of appropriate analgesics and sedatives.
- Proper temporary immobilization (stabilization) of injured body parts.
- Implementation of necessary emergency interventions for life-threatening injuries, such as open or tension pneumothorax and flail chest.
Surgical interventions and more complex treatments are generally conducted after blood pressure has stabilized or shown initial recovery, which distinguishes the management of traumatic shock from that of solely hemorrhagic shock. This approach aligns with the principles of damage control surgery. Following shock secondary to trauma or major surgery, the use of antibiotics is recommended to prevent secondary infections.