Emergency Medicine · Trauma and Resuscitation
The facts most likely to be tested
Class III hemorrhagic shock is defined by a heart rate >120 bpm and a significant decrease in systolic blood pressure.
Damage control resuscitation prioritizes a 1:1:1 ratio of packed red blood cells, fresh frozen plasma, and platelets to prevent coagulopathy of trauma.
Permissive hypotension (target systolic blood pressure 80–90 mmHg) is indicated in patients with penetrating trauma to minimize exsanguination until surgical control is achieved.
Tranexamic acid must be administered within 3 hours of injury to improve mortality in patients with significant hemorrhage.
Focused Assessment with Sonography for Trauma (FAST) is the initial diagnostic modality to detect hemoperitoneum in the hemodynamically unstable patient.
Hypothermia, acidosis, and coagulopathy constitute the lethal triad of trauma that must be aggressively corrected to improve survival.
Massive transfusion protocol is triggered by a positive Assessment of Blood Consumption (ABC) score or clinical evidence of hemodynamic instability.
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A 24-year-old male is brought to the emergency department following a high-speed motor vehicle collision. He is tachycardic at 135 bpm, tachypneic, and has a systolic blood pressure of 82 mmHg. Physical exam reveals a distended abdomen and cool, clammy extremities. A FAST exam is positive for free fluid in the Morison pouch. The patient remains hypotensive despite initial crystalloid bolus.
What is the most appropriate next step in the management of this patient?
Initiation of a massive transfusion protocol (MTP) with a 1:1:1 ratio of blood products.
The patient is in Class III/IV hemorrhagic shock; the most appropriate management is immediate activation of MTP to address the lethal triad and prevent coagulopathy, as tested by the 1:1:1 ratio and MTP trigger criteria.
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Etiology / Epidemiology
Caused by acute blood loss (trauma, GI bleed, ruptured ectopic). Hypovolemia leads to decreased preload and cardiac output.
Clinical Manifestations
Presents with tachycardia, hypotension, and narrow pulse pressure. Look for cool, clammy skin.
Diagnosis
Clinical diagnosis based on ATLS classification. Lactate and base deficit are key markers of tissue hypoperfusion.
Treatment
Control hemorrhage, then isotonic crystalloids (max 1L) followed by packed red blood cells (PRBCs). Avoid excessive crystalloid.
Prognosis
Mortality correlates with the lethal triad: acidosis, coagulopathy, and hypothermia.
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Epidemiology & Etiology
Commonly secondary to blunt or penetrating trauma, gastrointestinal hemorrhage, or obstetric emergencies. Class IV shock represents >40% blood volume loss, requiring immediate intervention. Early identification of the source is critical to prevent irreversible organ failure.
Pertinent Anatomy
The vascular compartment is the primary site of volume loss. Significant hemorrhage into the retroperitoneum, thorax, abdomen, or pelvis can be occult and fatal. Assessment must include the FAST exam to identify these hidden spaces.
Pathophysiology
Decreased venous return reduces preload, causing a drop in stroke volume and cardiac output. The body compensates via the sympathetic nervous system, increasing heart rate and systemic vascular resistance. Prolonged ischemia leads to anaerobic metabolism, resulting in lactic acidosis and cellular death.
Clinical Manifestations
Early signs include tachycardia and tachypnea. Narrow pulse pressure is a classic sign of compensatory vasoconstriction. Altered mental status and anuria are late, ominous signs of end-organ hypoperfusion.
Diagnosis
Diagnosis is clinical, categorized by ATLS shock classification. Serum lactate >2.5 mmol/L or a base deficit < -6 are sensitive indicators of shock. The FAST exam is the gold standard for rapid identification of free intraperitoneal fluid.
Treatment
Initiate 1:1:1 massive transfusion protocol (PRBCs, FFP, platelets) for severe hemorrhage. Avoid aggressive crystalloid resuscitation as it dilutes clotting factors and worsens coagulopathy. Use tranexamic acid within 3 hours of injury to reduce mortality.
Prognosis
Survival depends on reversing the lethal triad: acidosis, coagulopathy, and hypothermia. Monitor urine output (>0.5 mL/kg/hr) as a surrogate for adequate end-organ perfusion.
Differential Diagnosis
Cardiogenic shock: elevated JVP and pulmonary edema
Neurogenic shock: bradycardia and warm, dry skin
Septic shock: fever and bounding pulses
Obstructive shock: Beck's triad (tamponade) or tension pneumothorax
Anaphylactic shock: urticaria and wheezing