We reviewed the recent advances in the coagulation and fibrinolytic responses to trauma. At first we highlighted the main differences between the physiological and pathological hemostatic responses to trauma. The physiological coagulation and fibrinolytic changes after trauma occurs for the purpose of hemostasis and wound healing. The abnormal pathological responses to trauma are called disseminated intravascular coagulation (DIC), which has been recognized as one of the most important causes of posttrauma multiple organ dysfunction syndrome (MODS). During the 1990s, evidence has been accumulating demonstrating the existence of bidirectional crosstalk between coagulation and inflammation. Both the coagulation and inflammation exert effects on each other, thus leading to DIC and systemic inflammatory response syndrome (SIRS), which give rise to MODS in patients with trauma. We then discussed some factors such as hypothermia, severe metabolic acidosis, and dilution which affect the coagulation and fibrinolytic responses after trauma. In this section we contend that dilutional coagulopathy can be prevented by administering sufficient coagulation factors to the patients using fresh frozen plasma in an acute phase of major trauma resuscitation. Finally, we introduced new treatment strategies for posttrauma DIC and exsanguinating hemorrhaging with special reference to a worldwide prospective randomized controlled trial (CRASH2) and recombinant human factor VIIa (rFVIIa) therapy for severely injured trauma patients. We believe that this review will help to provide medical specialists with greater knowledge regarding the managements of posttrauma coagulation and fibrinolysis.

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The patient was a 62-year-old male. The patient had collapsed an estimated 5 days before being discovered and was transported to our hospital after first being brought to another hospital. The patient was treated in the ICU for hyperglycemic coma and infectious disease. On the third day of hospitalization, sudden respiratory arrest occurred following suction induced irritation, and nasal intubation was performed. Antificial ventilation was undertaken. Following those clinical course, stimulation evoked worsening rigidity and autonomic dysfunction in the limbs. On the seventh day of hospitalization, tetanus was diagnosed and treatment for tetanus was begun. Under intensive care, the patient's status improved. On the 82nd day of hospitalization, the patient changed hospitals for rehabilitation. Even though clinical signs indicating tetanus were present from the first day of hospitalization, it was very difficult to establish correct diagnosis due to comorbid conditions. This case showed the importance of early diagnosis of tetanus from the clinical symptoms, anticipation of the condition worsening and early treatment.

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Consecutive assessments of the anteroposterior distance (AP distance) of the epiglottis with ultrasonography may provide useful information regarding airway management in patients with inhalational burn or acute epiglottis. The AP distance of the epiglottis was ultrasonographically measured in 3 adult patients with inhalational burn. Two adult male patients had an AP distance of 0.35 and 0.25cm, respectively and both were intubated at ICU admission. The distance gradually decreased to<0.2cm by the sixth ICU day. One adult female had a low AP distance (0.08-0.14cm) and was not intubated. These results indicate that non-invasive consecutive ultrasonographic assessments of the AP distance of the epiglottis can assist with evaluation of laryngeal edema in patients with suspected inhalational burn.

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