Traumatic and burn shock

Stages of traumatic shock

Traumatic shock develops as a result of massive mechanical damage (soft tissue crushing, limb avulsions, severe fractures), which is generally accompanied by blood loss and wound infection. Its course comprises two main phases:

1. Compensation stage (erectile phase). This is a period of emergency adaptation of the body to hypoxia and blood loss, acting as a component of the general adaptation syndrome. There is a substantial increase in the activity of the sympathoadrenal and adrenocortical systems. Clinically, the patient is in a state of psychomotor agitation, their pupils are dilated (mydriasis), and the skin and mucous membranes turn pale due to the centralization of blood circulation. Hemodynamics is characterized by rising blood pressure, tachycardia, rapid breathing (tachypnea), and increased blood flow velocity. It is important to remember: the more extensive the trauma, the shorter this stage due to the rapid depletion of reserves.
2. Decompensation stage (torpid phase). Occurs when adaptive reactions fail. The effectiveness of neuroendocrine regulation progressively decreases, and organ and system failure begins to mount.

Hemodynamic and systemic disorders

The failure of compensation leads to a cascade of life-threatening changes in the body's internal environment:

• Cardiovascular system: Blood pressure drops precipitously down to collapse. The pulse becomes weak («thready»), heart rate reaches 180–210 beats per minute, and arrhythmias occur with dropped individual pulse waves.
• Water-electrolyte balance: Fluid massively shifts from the vascular bed into the tissues. Hypovolemia develops, circulating blood volume (CBV) critically drops, and the blood itself hemoconcentrates, which is reflected by an increase in hematocrit.
• Hemostasis system: Primary hypercoagulation and generalized microvascular thrombus formation in later stages are replaced by DIC syndrome with activation of fibrinolysis and hemorrhages.
• Blood sequestration: Blood is pooled in the abdominal vessels, spleen, liver, and lungs. This reduces cardiac output and triggers severe hypoxia.

«Shock organ» syndromes

Impaired microcirculation strikes all systems, forming a vicious circle. Without medical assistance, these disorders potentiate each other and lead to death:

• «Shock lung» syndrome: Initiated by an extreme impact. Excess catecholamines cause pre- and postcapillary angiospasm, fluid filtration increases — pulmonary edema occurs. Concurrently, a disbalance of biologically active substances provokes bronchospasm and bronchiolar edema. The result is obstruction, focal atelectasis, and acute respiratory failure (ARF).
• «Shock kidney» syndrome: Hypercatecholaminemia causes vascular spasm, ischemia, and nephron death. Due to impaired systemic circulation, glomerular filtration pressure drops. Sludge phenomenon (sludge) and thrombi form, and casts develop in the tubules. Hypoxia and toxemia directly damage the parenchyma. Acute renal failure and uremia develop.
• «Shock liver» and GI tract: Hemodynamic disorders lead to total hepatic failure and mesenteric ischemia. Intestinal dysfunction triggers autoinfection and autointoxication.

Specifics of burn shock and coma

Burn shock occurs with extensive grade II–III burns. Its pathogenesis is similar to traumatic shock, but has a number of specific features:

• The extremely powerful pain factor dominates (strong afferentation from the burn zone).
• Colossal plasma loss and significant body dehydration occur.
• Pronounced intoxication by tissue breakdown products (toxemia) mounts.
• The erectile phase is extremely brief, while the torpid phase proceeds severely, often complicated by wound infection, sepsis, and the development of «shock kidneys».

An extreme degree of body depression under the action of damaging factors can be coma (from Greek koma — deep sleep). It is characterized by profound depression of nervous activity, prolonged loss of consciousness, hypo- and areflexia, as well as total failure of physiological systems.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Mechanisms of DIC syndrome development in shock
• Pathogenesis of intestinal autoinfection against the background of GI ischemia
• Differences between shock and coma: differential diagnosis
• The role of hypercatecholaminemia in renal parenchymal injury
• Formation of the sludge phenomenon in the microvasculature

Other topics in "Chapter 20. Extreme and Terminal States"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.