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Review Question - QID 108269

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QID 108269 (Type "108269" in App Search)
An 18-year-old male is brought in by fire rescue. The patient was an unrestrained passenger in a motor vehicle crash and was ejected from the vehicle after collision. Upon arrival to the trauma bay, the patient has a Glasgow coma scale (GCS) of 6. He is rapidly intubated, and vitals are a temperature of 99.5°F (37.5°C), pulse of 130 bpm, and blood pressure of 83/64 mmHg. He is noted to have multiple ecchymoses over his body, as well as petechiae and purpura. He has a laceration over his clavicle that continues to bleed despite a pressure bandage. Radiographs of his lower extremity show multiple long bone fractures. Two large bore IV lines are placed, and the patient oozes from around the sites of venepuncture. Labs are notable for a WBC of 20,000/mm^3, Hb of 10.1g/dL, platelets of 48,000/mm^3, and prolongation of the PT and aPTT. This patient's presentation can best be explained by which of the following diagnoses?

Fat embolization

3%

12/353

Air embolization

1%

3/353

Tension pneumothorax

0%

1/353

Disseminated intravascular coagulation

80%

281/353

Coagulopathy of trauma

6%

21/353

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This patient presenting with hypotension, tachycardia, prolonged bleeding from lacerations, petechiae and low platelets in the setting of trauma is concerning for disseminated intravascular coagulation (DIC).

DIC is a consumptive coagulopathy, characterized by simultaneous activation and degradation of fibrin products. The system dysregulation of the endothelial control of clotting results in activation of platelets and consumption of platelets and clotting factors. Patients can present with simultaneous evidence of thrombotic and hemorrhagic sequellae such as prolonged bleeding, kidney and microvascular damage, and multiple organ systems failure.

Levi et al. review DIC and the pathophysiology of this coagulopathy. DIC is prevalent in 30 percent of trauma patients, with particular risk of occurrence in individuals with CNS trauma. Pathogenesis is due to exposure of blood to one or more procoagulants (thromboplastins) such as tissue factor, fat embolism, amniotic fluid embolism, lipopolysaccharides from GN bacteria, as well as others. The syndrome accelerates as coagulation factors are consumed, and normally trivial endothelial tears result in further activation and platelet consumption.

Hess et al. review coagulopathies in the trauma patient, in particular comparing and contrasting coagulopathy of trauma (COT) and DIC. COT is a syndrome which presents in trauma patients, in particular hemorrhagic trauma, which is characterized by dilution of clotting factors by resuscitation, acidosis, hypothermia, and platelet dysfunction. The loss of hemostasis occurs as a result of the inability of clotting factors and platelets to function either because of loss in concentration or function due to acidemia and hypothermia.

Incorrect Answer:
Answer 1: Fat embolization is possible, especially in the setting of long bone fracture; however, this alone would not describe the constellation of hemostatic dysfunction.

Answer 2: Air embolization alone would not account for the findings in this patient.

Answer 3: Tension pneumothorax would not account for the hemostatic dysfunction in this patient.

Answer 5: Coagulopathy of trauma is a possible etiology, however, this patient has no record of extensive resuscitation or hypothermia, and has a markedly decreased platelet count.

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