Trauma is the usual inciting event. Risk factors for developing SDH include cerebral atrophy, which causes stretching of bridging veins and increases the risk of tearing a vein with trauma, and the use of antiplatelets and anticoagulation. Cerebral atrophy increases with age and is prominently seen in patients who chronically abuse alcohol. The incidence of SDHs increases with age, likely due to increased cerebral atrophy and higher incidence of antiplatelet and anticoagulation use.
All SDHs start as an acute SDH and, depending on multiple factors including size of hematoma, rate of hematoma growth, and baseline cerebral atrophy, may present in the acute period or may go undiagnosed and progress to a chronic SDH.
Patients who present in the acute period often do so after a precipitating traumatic event and have typical traumatic brain injury symptoms including depressed mentation, confusion, vomiting, and balance deficits, depending on the size and location of the hematoma. Acute SDH is seen in 10%-20% of patients with head injuries.
Patients with chronic SDH typically present several weeks following injury. However, approximately 30%-40% of patients will not report a memorable traumatic incidence. They may describe an insidious onset of symptoms, which may include gait disturbance, hemiparesis, headaches, confusion, incontinence, somnolence, or seizures.
I62.00 – Nontraumatic subdural hemorrhage, unspecified
S06.5X0A – Traumatic subdural hemorrhage without loss of consciousness, initial encounter
95453001 – Subdural intracranial hematoma
Differential Diagnosis & Pitfalls
Drug Reaction Data