Traumatic aortic dissection is a rare but extremely high-risk vascular emergency characterized by rapid hemodynamic deterioration and a significant risk of mortality without urgent intervention. Type A dissections, which involve the ascending aorta, are particularly lethal due to the potential for cardiac tamponade, severe aortic regurgitation, myocardial infarction, or catastrophic rupture. While blunt trauma infrequently causes aortic dissection, elderly individuals with hypertension and vascular fragility are predisposed-even after relatively minor injuries. This report details a case involving a 75-year-old male with a history of hypertension who sustained polytrauma in a two-wheeler road traffic accident. Upon presentation to the emergency department, he was hemodynamically unstable with evidence of head and lower limb trauma, transient loss of consciousness, and clinical shock. After an initial primary survey, the airway was patent, and oxygen was administered via a non-rebreather mask. Given the risk of deterioration (due to low GCS and unstable vital signs), rapid sequence intubation was performed using ketamine, succinylcholine, and vecuronium to facilitate mechanical ventilation. Ventilatory support was maintained with volume-controlled settings (FiO₂ 100%, tidal volume 460 mL, PEEP 5 cm H₂O). Vascular access was secured with two large-bore IVs; aggressive fluid resuscitation and a massive transfusion protocol were initiated. The patient received 4 units of packed red blood cells and 4 units of fresh frozen plasma as haemoglobin dropped precipitously (7.17 g/dL to 3.24 g/dL). Neurological assessment (GCS, pupillary response) and glucose measurement (200 mg/dL) were performed. Physical examination revealed significant left thigh swelling suggestive of femoral fracture. Initial arterial blood gas analysis demonstrated profound metabolic acidosis (pH 6.978, HCO₃⁻ 12.3 mmol/L, lactate 10.79 mmol/L). Despite initial stabilization, the patient developed pulseless electrical activity (PEA) arrest, but return of spontaneous circulation (ROSC) was achieved after two cycles of CPR. CT angiography confirmed Stanford Type A ascending aortic dissection with associated retroperitoneal haemorrhage. Vasopressin and sodium bicarbonate infusions were initiated for refractory shock and severe acidosis. Multidisciplinary teams were mobilized for emergent surgical intervention, but persistent shock and worsening acidosis ensued. Ultimately, the patient suffered intraoperative cardiac arrest and could not be resuscitated. This case underscores the critical importance of rapid, systematic trauma assessment, early airway control, prompt activation of transfusion protocols, and coordinated multidisciplinary management. It also highlights that, despite optimal emergency care, outcomes remain poor in cases of devastating physiologic compromise.
Pooja Vijay (Fri,) studied this question.