Chronic subdural hematoma
The essence of chronic subdural hematoma (CSDH) is bleeding from the bridging veins in patients with variously expressed cortical atrophy (elderly patients, alcoholics), as well as in infants. CSDH was first described by Rudolf Virchow in 1857 as "pachymeningitis haemorrhagica interna" , after which Wilfred Totter described the basics of CSDH pathophysiology and thus defined that hemorrhage from the bridging veins is its root cause and named it "subdural hemorrhagic" .
It is important to adequately distinguish CSDH from acute subdural hematoma. Compared with CSDH, acute SDH typically occurs in younger individuals primarily as a result of more severe cranio traumas and is associated with symptomatic compression of the brain parenchyma, which typically manifests within 72 hours. Conversely, in the case of CSDH, bleeding is clinically asymptomatic for a longer period of time, on the order of several weeks or months, most often occurring after minor injuries. The incidence of CSDH in the population is around 1.72 / 100,000 inhabitants per year, in the population aged 70–79 this value increases to 7.35 / 100,000 per year, thus further confirming the fact of a higher risk of developing CSDH in the elderly.
Risk factors[edit | edit source]
The basic risk factors include cerebral atrophy, associated with older age. In direct proportion to aging, the space between the calva and the parenchyma itself increases from the original 6% to 11%. This allows the brain to move sideways, so in the event of trauma, bridging veins can be more easily damaged, resulting in CSDH. . However, trauma alone is not the only cause of CSDH, patients with anticoagulant medication, alcoholism or epilepsy are also affected (up to 10% of patients with CSDH are alcoholics or people with a history of seizures). .
Pathophysiology and symptomatology[edit | edit source]
Damage to the bridging veins (eg in the case of trauma) results in bleeding into the subdural space, with a thin layer of fibrin and fibroblast forming around the hematoma surrounding the hematoma. Fibrin and fibroblasts further proliferate and migrate, forming a kind of membrane (approximately 4 days after the incident), which then progressively enlarges. Some CSDH is resorbed spontaneously, but most grows in volume and results in clinically symptomatic CSDH , neurologically manifested by headache, confusion or, at a more advanced stage, contralateral hemiparesis.
Diagnosis[edit | edit source]
CT is used to image the hematoma. It clearly displays the resulting hematoma. It is typically a hypodense extracerebral bed, see picture.
Therapy[edit | edit source]
In the case of large CSDHs without expansive tendencies and clinically good patient status, it is not necessary to evacuate the hematoma, conservative treatment consists in close monitoring of the patient . In the case of a progressive symptomatic lesion, we indicate a trepanation return, ie the evacuation of covalent blood and the introduction of temporary subdural drainage from the return site under local anesthesia. In some cases, craniotomy is used, especially in patients with recurrent hematomas, resp. in persons showing blood re-accumulation after trenapulation return, or the presence of a solid hematoma. Rehydration of the patient and care for the patency of the drainage under strictly sterile conditions is important, while a control CT is performed after 3 days and the drain is removed if the finding is satisfactory. 
Links[edit | edit source]
Related articles[edit | edit source]
- Craniocerebral trauma
- Acute subdural hematoma
- Subdural hematoma
- Epidural hematoma
- Subarachnoid hemorrhage
References[edit | edit source]
- SAMEŠ, M, et al. Neurochirurgie. 1. edition. Praha : Jessenius Maxdorf, 2005. ISBN 80-7345-072-0.
Reference[edit | edit source]
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