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Subdural hematoma overview

Subdural Hematoma on CT

Acute and Chronic Subdural Hematoma on CT: Pathogenesis and findings Brain shrinkage with age or alcohol misuse Head trauma Congenital or acquired coagulopathy (i.e. anticoagulant use) Other (i.e. brain mass) Stretching & tearing of bridging cortical veins that cross from the cortex to dural sinuses Crescent shape Blood accumulation in the potential space between the dura mater & the arachnoid mater As the blood clots over time, its appearance varies on CT and is measured as different radiodensities (MRI may be needed to detect subtle bleeds) Acute < 3 days Subacute 3 days to 3 weeks Chronic > 3 weeks Acute on Chronic Acute blood (50-60 HU) is hyperdense to the surrounding cortex As blood clot ages and protein degradation occurs, the density drops to 35-40 HU The collection of blood becomes hypodense (~0 HU) to adjacent cortex Both hypodense & hyperdense collections visible forming a hematocrit level Hounsfield units (HU) are a measure of radiodensity (Air -1000 HU appears black, CSF is 0 HU appears dark, and cortical bone is >1000 HU appears white) Hypodense collection A pre-existing chronic hematoma Hematocrit level Fluid-fluid level in the case of an acute bleed into a pre-existing chronic subdural collection. This can also be seen in patients with coagulopathy as blood clots improperly, allowing for dependent blood layering Hyperdense collection Acute blood sinks inferiorly (as CT is taken with patient supine) Authors: Nameerah Wajahat, Aly Valji, Omer Mansoor Reviewers: Reshma Sirajee, Tara Shannon, Mao Ding, Petra Cimflova* *MD at time of publication Subdural hemorrhages spread past suture lines to take on a crescent shape (seen bilaterally on this CT), but limited by dural reflections (falx cerebri, tentorium) R Intracranial pressure ↑ Mass effect on the brain tissue Midline shift Shift of brain tissue across the center line of the brain (dashed line shows ideal midline) Ventricular effacement (partial) Ventricles appear smaller as some cerebrospinal fluid (CSF) is pushed out Sulcal effacement CSF filled sulci become less apparent as CSF is squeezed out and gyri are lying on each other Herniation Protrusion of brain through rigid membranes or foramina of skull Axial CT Head: Acute on Chronic Bilateral Subdural Hematoma showing features of both acute and chronic bleeding. Image Source: Radiopaedia.org Legend: Pathophysiology Mechanism Radiographic Findings Complications Published May 10, 2023 on www.thecalgaryguide.com

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

Acute Subdural Hematoma

Acute Subdural Hematoma (SDH): Clinical Presentation Subdural Hematoma Authors: Cora Laidlaw Reviewers: Braxton Phillips Shahab Marzoughi Sina Marzoughi* * MD at time of publication Ischemia of cranial nerve tissue in brainstem Cranial nerve palsies ↓ Level of consciousness Generalized or focal seizures Uncal herniation Compression of oculomotor nerve (CN III) – responsible for eye movement (adduction, elevation, and depression) and parasympathetic tone Eyes fixed outwards and down with pupillary dilation ↑ Pressure compresses intracranial tissue Compression of brain structures Compression of arterial vasculature in brain ↓ Global perfusion to intracranial tissue Uncus (mediobasal aspect of temporal lobe) herniates into the infratentorial via the tentorial notch Cerebellar tonsils (part of posterior lobe of cerebellum) herniates through foramen magnum (opening in base of skull) Cerebellar tonsil herniation Tonsils compress brainstem Brainstem loses ability to control vital functions of life (such as respiration, heart rate, blood pressure) Coma or death Blood accumulation results in ↑ intracranial pressure (Bleeding within potential space between dura and arachnoid meningeal layers ) Compression of nociceptors in meninges and meningeal vasculature Headache Compression of medulla (contains emetic center) Stimulation of emetic centers Loss of function of primary sensory cortex (posterior to central sulcus) Contralateral hemisensory loss (including proprioception, fine touch, and two point discrimination) Loss of function of primary motor cortex (anterior to central sulcus) Contralateral hemiparesis (upper motor neuron) Ischemia and necrosis of brain parenchyma Cerebral disturbances altering neuronal networks Vomiting Nausea See Calgary Guide slide - Chronic Subdural Hematoma (SDH): Clinical Presentation Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Oct 4, 2024 on www.thecalgaryguide.com