The precise mechanism involved in DIC and delayed traumatic subarachnoid hemorrhage (DT-SAH) remains unclear in multiple-trauma patients. Hereby, we describe a polytraumatized patient with DIC who died due to DT-SAH. A 75-year-old female patient was admitted to our Emergency Department complaining of abdominal pain and drowsiness after a pedestrian accident. Her initial brain computerized tomography (CT) finding was negative for intracranial injury. However, her abdominal CT scan revealed a collection of retroperitoneal hematomas from internal iliac artery bleeding after a compressive pelvic fracture. This event eventually resulted in shock and DIC. An immediate angiographic embolization of the bleeding artery was performed along with transfusion and anti-thrombin III. Her vital signs were stabilized without neurological change. Fourteen hours after admission, she suddenly became comatose, and her follow-up brain CT scan revealed a dense DT-SAH along the basal cisterns with acute hydrocephalus. This event rapidly prompted brain CT angiography and digital subtraction angiography, which both confirmed the absence of any cerebrovascular abnormality. Despite emergency extraventricular drainage to reverse the hydrocephalus, the patient died three days after the trauma. This paper presents an unusual case of DT-SAH in a polytraumatized patient with DIC.
Abdominal Pain ; Aged ; Angiography ; Angiography, Digital Subtraction ; Arteries ; Brain ; Coma ; Dacarbazine ; Disseminated Intravascular Coagulation* ; Drainage ; Emergencies ; Emergency Service, Hospital ; Female ; Follow-Up Studies ; Hematoma ; Hemorrhage ; Humans ; Hydrocephalus ; Iliac Artery ; Multiple Trauma ; Shock ; Sleep Stages ; Subarachnoid Hemorrhage, Traumatic* ; Tomography, X-Ray Computed ; Vital Signs

Like other bodily materials, lipids such as plasma triacylglycerol, cholesterols, and free fatty acids are in a dynamic state of constant turnover (i.e., synthesis, breakdown, oxidation, and/or conversion to other compounds) as essential processes for achieving dynamic homeostasis in the body. However, dysregulation of lipid turnover can lead to clinical conditions such as obesity, fatty liver disease, and dyslipidemia. Assessment of “snap-shot” information on lipid metabolism (e.g., tissue contents of lipids, abundance of mRNA and protein and/or signaling molecules) are often used in clinical and research settings, and can help to understand one's health and disease status. However, such “snapshots” do not provide critical information on dynamic nature of lipid metabolism, and therefore may miss “true” origin of the dysregulation implicated in related diseases. In this regard, stable isotope tracer methodology can provide the in vivo kinetic information of lipid metabolism. Combining with “static” information, knowledge of lipid kinetics can enable the acquisition of in depth understanding of lipid metabolism in relation to various health and disease status. This in turn facilitates the development of effective therapeutic approaches (e.g., exercise, nutrition, and/or drugs). In this review we will discuss 1) the importance of obtaining kinetic information for a better understanding of lipid metabolism, 2) basic principles of stable isotope tracer methodologies that enable exploration of “lipid kinetics” in vivo, and 3) quantification of some aspects of lipid kinetics in vivo with numerical examples.

The precise mechanism involved in DIC and delayed traumatic subarachnoid hemorrhage (DT-SAH) remains unclear in multiple-trauma patients. Hereby, we describe a polytraumatized patient with DIC who died due to DT-SAH. A 75-year-old female patient was admitted to our Emergency Department complaining of abdominal pain and drowsiness after a pedestrian accident. Her initial brain computerized tomography (CT) finding was negative for intracranial injury. However, her abdominal CT scan revealed a collection of retroperitoneal hematomas from internal iliac artery bleeding after a compressive pelvic fracture. This event eventually resulted in shock and DIC. An immediate angiographic embolization of the bleeding artery was performed along with transfusion and anti-thrombin III. Her vital signs were stabilized without neurological change. Fourteen hours after admission, she suddenly became comatose, and her follow-up brain CT scan revealed a dense DT-SAH along the basal cisterns with acute hydrocephalus. This event rapidly prompted brain CT angiography and digital subtraction angiography, which both confirmed the absence of any cerebrovascular abnormality. Despite emergency extraventricular drainage to reverse the hydrocephalus, the patient died three days after the trauma. This paper presents an unusual case of DT-SAH in a polytraumatized patient with DIC.
Abdominal Pain ; Aged ; Angiography ; Angiography, Digital Subtraction ; Arteries ; Brain ; Coma ; Dacarbazine ; Disseminated Intravascular Coagulation ; Drainage ; Emergencies ; Emergency Service, Hospital ; Female ; Follow-Up Studies ; Hematoma ; Hemorrhage ; Humans ; Hydrocephalus ; Iliac Artery ; Multiple Trauma ; Shock ; Sleep Stages ; Subarachnoid Hemorrhage, Traumatic ; Tomography, X-Ray Computed ; Vital Signs