Assessment of Shock in Trauma Patients

Hemorrhagic shock: most common in trauma patients

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  Bleeding from lacerations

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  Bleeding in the soft tissue of the extremity injuries

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  Fractures: due to bleeding at fracture sites

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    Pelvic fractures: 2000–3000 mL

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    Femur shaft fracture: 1000–1500 mL

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    Tibia fracture: 500–1000 mL

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    Humerus: up to 750 mL

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    Radius/ulna: 250–500 mL

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  Retroperitoneal bleeding

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  Intraperitoneal bleeding

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  Intrathoracic bleeding in severe chest injuries

Nonhemorrhagic shock

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  Hypovolemia: due to volume loss

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    Severe burns

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    Other causes of volume loss

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  Obstructive shock: due to physical obstruction in the heart or great vessels

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    Cardiac tamponade

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    Tension pneumothorax

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    Massive pulmonary embolism

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  Cardiogenic shock: due to failure of the cardiac pump.

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    Cardiac contusion

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    Myocardial infarction

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    Dysrhythmias

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    Blunt cardiac injury

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  Distributive shock: impaired utilization of oxygen and failure of energy production by cells

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    Neurogenic shock

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    Septic shock

Exsanguinating hemorrhage

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  Major thoracic injuries

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  Major abdominal injuries

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  Retroperitoneal vascular injuries

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  Pelvic injuries

Tension pneumothorax

Cardiac tamponade

Cardiogenic shock

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  Cardiac contusion

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  Myocardial infarction

Neurogenic shock

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  Cervical or upper thoracic spinal cord injury

American College of Surgeons (ACS) classification: based on the quantity of blood loss

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  Class I: <15% blood loss

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  Class II: 15%–30% blood loss

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  Class III: 30%–40% blood loss

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  Class IV: >40 % blood loss

Based on response to initial crystalloid infusion:

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  Rapid responder

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    Patients with <20 % blood loss

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    Patent becomes hemodynamically stable after receiving the initial crystalloid bolus.

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    May require surgical intervention

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  Transient responder

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    Responds briefly to crystalloid bolus

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    Ongoing bleeding, 20%–40% blood loss

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    Blood and blood product transfusions are indicated.

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    Surgical intervention is indicated.

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  Minimal or nonresponder

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    Failure to respond to crystalloid or blood infusions

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    Emergent surgical intervention is required.

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    Shock may be due to nonhemorrhagic causes.

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      Cardiogenic shock: blunt cardiac injury, myocardial infarction

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      Cardiac tamponade

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      Tension pneumothorax

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      Neurogenic shock: cervical or upper thoracic spinal cord injury

Low ventricular filling pressure

Decreased cardiac output, leading to hypotension

Increased systemic vascular resistance (SVR)

Tachycardia, except in patients on beta blockers, and athletes

Increased cardiac contractility

Vasoconstriction due to catecholamine release:

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  Skin pallor

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  Reduced capillary refilling

Cellular hypoxia leading to cellular death and organ failure

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  Skin and muscles

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    Anaerobic metabolism causing lactic acidosis

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  Kidney

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    Initially reduced cortical function followed by renal failure

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  Bowel

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    Cellular damage

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    Failure to transport nutrients from bowel mucosa

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    Bacterial translocation from gut to portal circulation

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    Bowel may remain ischemic after flow is reestablished in the macro circulation, because of the occlusion of capillary networks caused by edema.

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  Liver

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    Hypoglycemia

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    Coagulopathy

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    Cellular necrosis

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    The liver may remain ischemic after flow is reestablished in the macro circulation, because of the occlusion of capillary networks caused by edema.

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  Lungs

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    Impaired functions to filter for toxic metabolites, inflammatory mediators released by ischemic cells, and translocated gut bacteria

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    Acute lung injury

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    Increased pulmonary resistance leading to right heart failure

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  Heart

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    Myocardial ischemia leading to hypotension and heart failure

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    Low pulse pressure

Reduced platelet activities

Activated protein C:

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  Inactivate factors V and VIII

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  Increases plasmin activities

Release of tPA

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  Hypothermia

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  Large-volume crystalloid infusion

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    Dilution of coagulation factors

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    Acidosis

Local thrombosis by platelet activation

Fibrinogen to fibrin conversion

Shedding of glycocalyx barrier of the endothelial cells

Increased plasmin activity resulting in fibrinolysis

Reperfusion following hemorrhagic shock causes release of toxic mediators into the circulation, causing immune modulation and resulting in failure of nonischemic organs (liver, lung, heart, brain, endocrine, and bone).