SEARCH RESULTS FOR: Chronic-Subdural-Hematoma

Chronic Subdural Hematoma

Chronic Subdural Hematoma (SDH): Pathogenesis and Clinical Features Atraumatic SDH risk factors Authors: Cora Laidlaw Reviewers: Braxton Phillips Shahab Marzoughi Gary Michael Klein* * MD at time of publication For more information on acute subdural hematoma, see Calgary Guide slide - Acute Subdural Hematoma (SDH): Traumatic SDH mechanisms Intoxication leading to decreased balance and coordination Neurodegenerative disease causes cerebral atrophy (such as ALS, MS, and dementia) General cerebral atrophy with increased age Chronic alcohol use dilates blood vessels, thinning the walls Thinner, developing vessels in infants Age related risks: decreased vision, decreased mobility, decreased balance Low Impact trauma such as minor falls Child abuse Increased tension on bridging veins as ↓ brain volume ↑ distance they must span Bridging veins are more delicate Abusive head trauma Cytokines increase the leaky nature of vessels Blood degradation over time releases proinflammatory cytokines Atraumatic risk factors combined with traumatic mechanisms results in the breaking of bridging veins Low pressure venous blood slowly accumulates between the dura and arachnoid meningeal layers (increased with anticoagulation, hypertension, or other bleeding risk factors) Damaged tissue release inflammatory factors that promote angiogenesis through secondary intention (the use of granular tissue to fill in the non-approximated edges of the blood vessels) As the vessels are not approximated (connected to be rejoined), the granular tissue does not create a solid blood vessel wall Vessels are partially repaired and leaky in nature Recurrent bleeding due to small traumas and fluid accumulation due to leaky vessels results in expansion Chronic Subdural Hematoma (Bleeding within potential space between dura and arachnoid meningeal layers present >14 days) Dural attachments limits fluid expansion Local increased pressure and a mass effect on underlying brain tissue Cerebral atrophy (specific areas and therefore symptoms will depend on lesion location) Mesial temporal lobe Impaired memory (including verbal) Acute blood is present in small volumes with larger volume chronic hematoma Damaged tissues release proinflammatory cytokines from immune cells (astrocytes, peripheral immune cells, neurons, and microglial cells) Acute blood appears hyperintense on T2 MRI Chronic blood appears hypointense on T2 MRI Cytokines inflame nociceptive neurons (such as the trigeminal neuron) Recurrent headaches Altered mental status (confusion) Personality changes Damage to neuronal tissue Mass compression of underlying vasculature Hypoperfusion of brain tissue T2 MRI Brain shows lesions with hyperintensive cores surrounded by hypointensive Pressure placed indirectly onto cerebellum with inferior displacement of brain mass Gait ataxia Frontal lobe atrophy (specifically in orbitofrontal area) Orbitofrontal area Prefrontal cortex Impaired working memory (short term memory used for rapid executive, phonological visuospatial thought processes) Atrophy of focal brain structure Contralateral homonymous hemianopsia (loss of the half visual fields in both eyes) Somatic motor cortex Contralateral hemiplegia (inability to move the body opposite to the side of lesion) Primary visual cortex Pontine micturition centre Urinary incontinence (uncontrolled leakage of urine) Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Oct 4, 2024 on www.thecalgaryguide.com