We report a case of retropharyngeal hematoma caused by minor injury. An 83-year-old man stumbled and hit his face on the floor at home. He called the emergency services because of facial pain. He was able to talk when the ambulance crew contacted him, but his condition soon deteriorated and he lost consciousness, with decreased percutaneous oxygen saturation. On admission, his Glasgow Coma Scale score was E1V1M4. He also had difficulty breathing, indicating upper airway obstruction. Swelling of the posterior wall of the pharynx due to hematoma was observed during intubation. Cervical CT revealed a retropharyngeal hematoma causing upper airway obstruction, which was managed conservatively by tracheostomy. The patient was discharged on the 25th hospital day. Based on this case, even a minor injury, such as that sustained from a fall, may induce retropharyngeal hematoma causing upper airway obstruction, which can lead to unconsciousness, respiratory failure, and even death without emergency treatment.
A 31-year-old man had a car accident and was transported to our hospital. His blood pressure was 99/66 mmHg and heart rate was 94 bpm, and the FAST test was positive on arrival. We diagnosed liver injury with extravasation by enhanced CT and performed transcatheter arterial embolization. CT on the 3rd day of hospitalization revealed portal vein thrombosis in the posterior medial segment and heparin was started on the 7th day. As the platelet count started decreasing on the 11th day, we suspected heparin-induced thrombocytopenia (HIT). Although we stopped administering heparin, treatment for HIT was delayed, causing new vein thrombosis. Several recent clinical studies suggested that severe trauma can cause HIT. When HIT is suspected in trauma cases, appropriate alternative anticoagulant treatment should be performed as soon as possible after achieving hemostasis.
Vertebral artery injury (VAI) is rare. However, the neurological prognosis is serious in patients that develop stroke. The stroke incidence and mortality rate are high, especially for Denver scale Grade IV (occlusion). The efficacy of anticoagulant therapies and interventional radiology (IVR) has been reported, but treatment methods remain controversial.
We diagnosed a patient with VAI (Grade IV) associated with cervical spine trauma. He developed vertebrobasilar infarction after surgery for cervical spine injury.
As cervical spine trauma is frequently associated with VAI, we should detect VAI on computed tomography angiography. In addition, multidiscipline cooperation is important to consider treatments such as IVR.
We describe the case of a 9-year-old girl who was in a motor vehicle accident. She was in shock on hospital arrival. Endovascular treatment was performed for intra-abdominal hemorrhage from hepatosplenic injury. Although pancreatic head injury was suspected on trauma pan scan, the patient demonstrated hemodynamic improvement ; therefore, conservative treatment was applied in the form of ascites drainage using a catheter. Hyper-amylase ascites was drained until day 9. After the start of meals on day 10, her serum amylase level increased. Cystic fluid collection around the pancreatic head was noted on magnetic resonance imaging on day 17. No worsening abdominal symptoms were noted ; therefore, she was discharged on day 24 and followed up in an outpatient setting. The pancreatic pseudocyst gradually shrank and spontaneously disappeared on day 52. Thus, conservative therapy with ascites drainage was suggested to be useful for pediatric pancreatic head trauma with suspected main pancreatic duct injury.
A 50-year-old man was admitted to our hospital after a motorcycle accident. Although his vital signs demonstrated slight tachycardia, blood pressure was maintained throughout resuscitation. Since contrast enhanced abdominal CT showed extravasation of enhancement medium in the splenic injury, we decided to perform transcatheter arterial embolization to control the bleeding. The pseudoaneurysm in the splenic hilum and hemorrhage inside the injured splenic viscera were embolized using gelatin sponges. Since progressive anemia was observed, arterial coiling was added to the splenic artery on the next day. On the 27th hospital day, contrast enhanced CT demonstrated giant liquefaction. We managed the lesion with cautious observation for infection or spontaneous rupture. The size of the liquefaction got smaller on the 66th day. When no complications or concomitant symptoms are observed, giant liquefaction after splenic infarction can be treated conservatively even if the size of the liquefaction exceeds the splenic viscera.