Injury Metrics for Assessing the Risk of Acute Subdural Hematoma in Traumatic Events

Worldwide, the ocurrence of acute subdural hematomas (ASDHs) in road traffic crashes is a major public health problem. ASDHs are usually produced by loss of structural integrity of one of the cerebral bridging veins (CBVs) linking the parasagittal sinus to the brain. Therefore, to assess the risk of ASDH it is important to know the mechanical conditions to which the CBVs are subjected during a potentially traumatic event (such as a traffic accident or a fall from height). Recently, new studies on CBVs have been published allowing much more accurate prediction of the likelihood of mechanical failure of CBVs. These new data can be used to propose new damage metrics, which make more accurate predictions about the probability of occurrence of ASDH in road crashes. This would allow a better assessement of the effects of passive safety countermeasures and, consequently, to improve vehicle restraint systems. Currently, some widely used damage metrics are based on partially obsolete data and measurements of the mechanical behavior of CBVs that have not been confirmed by subsequent studies. This paper proposes a revision of some existing metrics and constructs a new metric based on more accurate recent data on the mechanical failure of human CBVs.

Microvascular proliferation in the clots: The key finding of acute subdural hematoma transforming into chronic subdural hematoma?

Background: Despite extensive investigations, the exact etiology of chronic subdural hematoma (CSDH) remains elusive. Organized CSDHs are a distinct but less-understood type of CSDH. Case Description: A 50-year-old hypertensive woman experienced headache without any previous head injury. At presentation, the patient showed no focal neurological deficits. Cranial computed tomography (CT) revealed a slightly compressive subdural hematoma that spontaneously regressed and no intracranial vascular lesions. Cerebral magnetic resonance imaging identified a non-enhancing nodular lesion in the subdural hematoma. After the patient presented disorientation and aphasia on post hospitalization day 14, CT showed a considerable enlargement of the subdural hematoma. Partial removal of the bi-layered hematoma was performed through a parietal craniotomy. Histological examination revealed microvascular proliferation in both the outer membrane and the nodular lesion. On postoperative day 35, CT demonstrated a remarkable resolution of the residual hematoma. Conclusion: Development of microvascular proliferation in the clots of an acute subdural hematoma may lead to its rapid enlargement as an organized CSDH. Organized CSDH can be managed by partial removal of the outer membrane and hematoma through a craniotomy.

Clinical and Laboratory Markers in Determination of Treatment Modalities and Short-Term Prognosis in Patients with Traumatic Acute Subdural Hematoma: Original Study

Objective In patients with traumatic acute subdural hematoma (ASH), it has not been yet fully elucidated which patients can benefit from surgery or from clinical follow-up. This study was constructed to predict treatment modality and short-term prognosis in patients with ASH using their clinical, radiological, and biochemical laboratory findings during admission to hospital. Methods Findings of patients with ASH determined on their CT scan between 2015 and 2018 were evaluated. Patients were grouped in terms of ASH-FOL (patients followed-up without surgery, n = 13), ASH-OP (patients treated surgically, n = 10), and ASH-INOP (patients considered as inoperable, n = 5) groups. They also were divided into “survived (n = 14)” and “nonsurvived (n = 14)” groups. Results ASH developed as a result of fall from a height in 15 patients and traffic accidents in 13 patients. In deciding for surgery, it was determined that Glasgow coma scale (GCS) scores < 8, midline shift (MLS) level > 5 mm, MLS-hematoma thickness ratio > 0.22, leukocyte count > 12730 uL, and presence of anisocoria could be used as predictive markers. It was determined that GCS scores < 8, hematoma thickness value > 8 mm, and the presence of anisocoria could be considered as biomarkers in prediction of mortality likelihood. Conclusion It could be suggested that GCS scores, MLS level, MLS-hematoma thickness ratio, presence of anisocoria, and leukocyte count value could help in determination of the treatment modality in patients with ASH. Additionally, GCS scores, hematoma thickness value, and presence of anisocoria could each be used as a marker in the prediction of early-stage prognosis and mortality likelihood of these patients.

A fatal case of traumatic brain injury with severe coagulopathy due to Rhabdophis tigrinus (yamakagashi) bites: a case report

Background Yamakagashi venom is a prothrombin activator, leading to disseminated intravascular coagulation. We report a fatal case of severe coagulopathy from head trauma assumed to be caused by a yamakagashi bite. Case presentation An 80-year-old man fell and developed systemic tonic–clonic convulsions. Head computed tomography revealed brain contusion and acute subdural hematoma. Physical examination revealed two bite marks with persistent bleeding on the right lower leg. The patient stated that he had been bitten by some creature 3 days prior, but the bite was left untreated. Laboratory tests showed fibrinogen levels below the detection limit. Although eighteen units of fresh frozen plasma were administered for coagulopathy, fibrinogen levels did not improve. He died about 18 h after a head injury. Conclusion In this case of a yamakagashi bite with active bleeding due to trauma, early administration of yamakagashi antivenom should be considered to control coagulopathy.