Pathophysiology
Summary
Epidural hematomas (EDH) occur between the skull and dura mater, and often result from traumatic injury to the middle meningeal artery, a branch of the external carotid artery located beneath the skull. Skull fractures are common in EDHs, particularly at the pterion.
On a non-contrast CT, EDH manifests as a hyperdense lens shaped mass. This unique shape is due to the dura's strong adhesion to suture lines, which prevents the hematoma from expanding laterally.
As the hematoma expands inwardly, it can lead to a midline shift, compressing and displacing the brain parenchyma and increasing intracranial pressure (ICP). The increase in ICP leads to symptoms such as severe headache, nausea, vomiting, altered mental status, & syncope.
EDH take time to expand, and can exhibit a lucid interval immediately follow injury, which is followed by rapid deteriorating as the hematoma expands. If unchecked, the elevated ICP can lead to uncal herniation, resulting in compression of the parasympathetic fibers in the oculomotor nerve and a consequent ipsilateral ‘blown’ pupil. In acute scenarios, burr holes can be drilled into the skull to alleviate intracranial hypertension.
A subdural hematoma (SDH) is the result of bleeding into the potential space between the dura and arachnoid mater. SDHs most commonly arise from injury to the bridging veins due to sudden acceleration-deceleration forces. Factors heightening SDH risk include chronic anticoagulation (e.g., with warfarin, especially in the elderly), and conditions causing cerebral atrophy (e.g., aging, neurodegenerative diseases, and chronic alcoholism). Such atrophy elongates bridging veins, escalating their rupture risk. SDHs are prevalent in shaken baby syndrome due to the susceptibility of thin-walled bridging veins.
On non-contrast CT, SDH exhibits a hyperdense crescent shape spreading along the skull's curvature. Unlike EDH, SDH is not constrained by suture lines. A chronic SDH might become hypodense (dark) due to the degradation of blood and proteins, resulting in a less dense fluid. Nevertheless, any rebleeding, or ‘acute on chronic hemorrhage will manifest as new hyperdense regions.
Chronic SDH causes a slow onset of neurological symptoms, including headaches, seizures, and cognitive decline. Over time, fibroblasts may surround the hematoma, forming a protective membrane, resulting in an organized subdural hematoma.
Subarachnoid hemorrhage (SAH) is marked by bleeding in the CSF space situated between the arachnoid and pia mater. SAHs predominantly occur due to the rupture of a saccular (berry) cerebral artery aneurysm. Clinically, individuals with SAH frequently report an abrupt and intense thunderclap headache, which many describe as the ‘worst headache of my life.’ Accompanying symptoms include fever, nausea & vomiting, and photophobia, as well as a reflexive spasm of the neck extensor muscles triggered by irritation of the meninges known as meningismus,
If left untreated, SAH can results in expansion of the subarachnoid space, leading to intracranial hypertension. Furthermore, the breakdown products of hemoglobin in the CSF post-SAH can induce vasospasm that can cause ischemic stroke, which typically arise ~1 week after the initial bleed.
Diagnostic measures for SAH include a non-contrast CT scan that reveals hyperdense (white) material in the subarachnoid space, especially near the circle of Willis. Lumbar puncture shows elevated RBC count in the CSF and the presence of xanthochromia, a pinkish-yellow tint due to hemoglobin breakdown. Nimodipine, a dihydropyridine calcium channel blocker, is used to treat vasospasm.
Cerebral aneurysms predominantly form in the anterior circle of Willis, especially at the conjunction of the anterior cerebral artery and anterior communicating artery, and are the main instigators of SAH. Risk factors for cerebral aneurysm includes smoking, alcohol abuse, vascular Ehler-Danlos syndrome, and autosomal dominant polycystic kidney disease (ADPKD). Cerebral aneurysms are more common in postmenopausal women due to a decline in estrogen levels, resulting in reduced collagen production and weakened vessel walls.
Lesson Outline
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FAQs
Epidural hematomas form between the dura mater and the skull and often result from a traumatic injury to the middle meningeal artery. Subdural hematomas develop in the space between the dura and arachnoid mater and are primarily caused by the tearing of bridging veins from sudden acceleration-deceleration injuries. Subarachnoid hemorrhages involve bleeding between the arachnoid and pia mater, predominantly due to a ruptured cerebral artery aneurysm.
On non-contrast CT, an epidural hematoma appears as a hyperdense or bright lesion with a biconvex or lens-like shape, constrained by the dura's suture lines. This hematoma can expand, potentially compressing and displacing the brain tissue, leading to a midline shift.
Increased intracranial pressure from hematomas can manifest as severe headaches, nausea, vomiting, altered mental status, and occasionally syncope. In advanced cases, it can result in uncal herniation, characterized by the downward displacement of the medial temporal lobe. This can compress the oculomotor nerve, leading to ipsilateral pupillary dilation known as a ‘blown’ pupil.
A subarachnoid hemorrhage is characterized by bleeding in the cerebrospinal fluid space between the arachnoid and pia mater. On a non-contrast CT scan, it presents as a hyperdense or white material filling the subarachnoid space, especially prominent around the circle of Willis.
Risk factors for cerebral artery aneurysms include smoking, excessive alcohol consumption, and specific conditions like vascular Ehler-Danlos syndrome and autosomal dominant polycystic kidney disease. Postmenopausal women are particularly vulnerable due to reduced estrogen levels, which decrease collagen production, leading to weakened vessel walls.
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