B115 intracranial hmorrhages Flashcards

1
Q

What causes intra-parenchymal/intracerebral hemorrhage, and what is the specific term for this

A

Apoplexia

Causes:

  • Hypertension is the main source
    • Arteriolosclerosis, hyaline deposition in the walls makes them fragile
    • Narrowed lumen and increased pressure
    • Forms Charcot-Bouchard aneurysms - microaneurysms of the cerebral vessels
    • These eventually rupture and cause a hemorrhagic stroke.
  • Vascular malformation rupture
    • Arteriovenous malformations - most common
    • Cavernous angiomas
    • Capillary telangiectasias
    • Venous angiomas
  • Purpura cerebri - small clinically insignificant
    • result from thrombopathies/coagulopathies/vasculopathies
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2
Q

What are the types of intracranial non-parenchymal bleeding?

A

Sub-ependymal hemorrhage

Subarachnoid hemorrhage

Subdural hemorrhage

Epidural hemorrahge

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3
Q

Describe Sub-ependymal hemorrhage

A
  1. Seen in immature babies.
  2. Bleeding under the ependyma, which is a thin epithelial membrane, which lines
    the ventricular system.
  3. Due to incomplete development of the cerebral vascular, making it very sensitive to pH and PaO2 changes.
  4. With superimposed IRDS, the PaO2 is diminished, which in turn results in a
    hypoxic state which provokes the sub‐ependymal hemorrhage.
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4
Q

Describe Subarachnoid hemorrhage, cause and pathogenesis

A

Caused by:

  • Rupture of a berry aneurysm aka saccular aneurysms found on the arteries in the subarachnoid space, overlying the brain parenchyma.
  • Can occur spontaneously at any time, but are initiated in 1/3rd of cases by an abrupt increase in intracranial pressure, often during an orgasm or bowel movement.
  • Risk factors of berry aneurysms include disorders of ECM (e.g. Marfan syndrome)
    and autosomal dominant polycystic kidney disease, and hypertension
  • Saccular aneurysms are most common at branch points of arteries.
  • multiple aneurysms are present in 20-30%
  • aneurysms larger than 1 cm are particularly vulnerable and should be excised, have a 50% chance to rupture each year.

Pathogenesis:

  • Blood under arterial pressure is forced into the subarachnoid space,
  • Sudden, excruciating headache
  • Quickly lose conciousness from increased intracranial pressure
  • 25 ‐ 50% of people die shortly after the initial rupture and bleeding, although those who survive typically improve and recover consciousness in minutes.
  • There is also significant risk of ischemia in other regions of the brain, due to vasospasm of other vessels.
  • Recurrent bleeds are common if they survive, with a higher chance of death each time.
  • The organizing phase after the bleed causes fibrosis in the subarachnoid space, and this may cause obstruction and possible hydrocephalus.
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5
Q

Describe subdural hemorrhage,

cause, pathogenesis, progression

A

Caused by:

  1. Acceleration-deceleration injury, of the braincauses trauma and stretching of the bridging veins extending from the cerebrum through the subarachnoid space and joining to the dural sinuses.
    • seen in car crashes
    • falls, especially in alcoholics
  2. Severe dehydration and CNS cell shrinking
  3. Very young and old patients are at greatest risk, having the weakest cerebral veins.

Either of these injuries can tear the bridging veins, and cause venous bleeding into the subdural space.

  • Slow accumulation of venous blood in the subdural space
  • Causes a prolonged asymptomatic lucid period, and then appearnace of symptoms hours, days, or even weeks later.
  • The blood compresses the brain but interdigitates around the gyri.
  • Repetitive/chronic subdural hematomas can cause granulation tissue to form, from repeated organization of the hematomas, leading to a permanent subdural mass.

Symptoms:

  • Headache.
  • Confusion.
  • Change in behavior.
  • Dizziness.
  • Nausea and vomiting.
  • Lethargy or excessive drowsiness.
  • Weakness.
  • Apathy.
  • Compression, herniation
    • sensory losses, focal ischemia, coma
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6
Q

Describe epidural hemorrhage

A

Pathogenesis:

Caused by skull fracture and rupture of a dural artery.

Most often rupture of the middle meningeal artery

Rapid accumulation of arterial blood in the epidural space, and a very brief lucid period before onset of symptoms.

The hematoma is convex and sharply bordered, not following the gyri of the brain and causing compression, herniation.

Epidural hematomas are a surgical emergency and are rapidly life threatening.

Symptoms:

  • Confusion
  • Dizziness
  • Nausea or vomiting
  • Drowsiness or altered level of alertness
  • Blown pupil in one eye
  • Severe headache
  • Loss of conciousness, coma
  • Weakness in part of the body, usually on the opposite side from the side with the enlarged pupil
  • Herniations, their symptoms, coma, death.
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7
Q

Morphology/histology of intraparenchymal hemorrhage

A

Morphology:

Gross:

  • Encephalomalacia rubra, hemmorrhagic necrosis
  • Encephalomalacia flava
  • Cysta post encephalomalacia

Histology:

The microscopic picture and evolution of hemorrhagic
infarction parallel those of ischemic infarction, with the
addition of blood extravasation and resorption

  • Early changes: 12-24 hours
  • acute neruonal change, shrinking and eosinophilia
  • nuclear pyknosis and karyorrhexis
  • similar changes occur to a lesser degree in astrocytes and oligos
  • Subacute changes: 1 day - 2 weeks
  • neutrophils invade areas of damaged tissue
  • vascular proliferation
  • reactive gliosis
  • Repair
  • replacement of infarcted regions by fibrotic glial scar.
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