AVM - CT
AVM - CT
Search Pattern Assist ?Exam
Purpose
- Developmental or acquired intradural vascular malformations are divided between those with AV-shunting and those that don't. Both have to be distinguished from other lesions, like vascular tumors that also exhibit AV-shunting.
- Intradural AV shunting malformations are divided between direct AV-fistulae and AV malformation some of which primarily involve the dura and are fed by meningeal vessels versus intraaxial AVM's supplied by intraaxial arteries. In some case AVM's can include both a pial & meningeal components.
- There is another form of CNS AV malformation that exhibits focal areas of AV shunting of individual small vessels all clustered together. There is brain tissue interposed between these microfistulae. These lesions are often multicentric. The label we use to describe these AVM's is "angiomatous transformation." they seldom hemorrhage and present most often with seizures.
- Dural AVM's are really mostly complex or racemose dural AV fistulae that lack a distinct nidus, but do have both afferent and efferent components. Dural AVM's add a distinct hemorrhage risk, when they drain into pial veins.
- Intraaxial AVM's have afferent arterial, efferent venous, and a distinct anomalous nidus components. Some pial AVM's have internal, high flow, fistulous components as well, which focally enlarge some efferent veins and can produce venous aneurysms. Some pial AVM's with high flow can generate saccular type aneurysms off proximal feeding arteries.
- Primary CNS AV fistulae are mostly evident in neonates and children. They represent high flow, high pressure AV shunts involving pial or perforating arteries. The most common are the Galenic AV fistulae and direct pial artery AV fistulae. Most present either as heart failure as neonates, or later with failure to thrive, seizures, etc.
- Non-shunting developmental vascular malformations include mainly developmental venous anomalies (i.e. DVA's), cavernous malformation (single sporadic) or familial cavernous malformation (multicentric). Also in this category are the AVM's that have thrombosed with no residual AV shunting. These are often confused with brain tumor or metastatic lesions, since they often have marginal enhancement.
- Detection of acute hydrocephalus includes: rapidly progressive ventricular enlargement, plus features of raised CSF pressure: transependymal fluid accumulation, effacement of sulci and cisterns, optic hydrops and eventually downward incisural and tonsillar herniation. The hydrocephalus can be related to either an internal or an external CSF resorption block. Ventriculomegaly (in general) grading scale is 1 (NL for age) to 4 (gross vent enlargement)/4. In other words, Grade 1.1/4 is the very first detection of lateral ventricular enlargement. Grade 4/4 is massive ventriculomegaly with virtually no remaining brain. Everything else is in between. Ex vacuo ventriculomegaly is not under pressure and can be any grade. In acute hydrocephalus ventriculomegaly can only reach 2/4 before fatal brain herniation occurs. Therefore, the ventriculomegaly in hydrocephalus can only go from 1.1/4 to 2/4. In between are 10% interval, i.e. 1.1/4 1.2/4, 1.3/4 and so on up to 2/4. Concurrently, there will be other features of rising CSF pressure: transependymal fluid accumulation, tight ependymal margins, papiiledema, exaggerated CSF pulsations, and finally brain herniation at grade 2/4. In terms hydrocephalus acuity rating Grade 1.1 to grade 1.3/4 represent early or mild hydrocephalus; grades 1.4-to 1.6 are moderate hydrocephalus, grade 1.7 to 1.8 are serious hydrocephalus and grades 1.8 to 2 represent critical (impending herniation) hydrocephalus. If ventriculomegaly reaches exceeds grade 2/4 then the hydrocephalus is more likely subacute or chronic compensated hydrocephalus (which has slowly progressing ventricular enlargement) or may have stabilized (arrested hydrocephalus). Ex vacuo (brain loss) conditions can be any grade but lacks any of the features of raised intracranial pressure; ex vacuo ventricular enlargement should NOT be described as hydrocephalus.
Findings
Initial CT findings
There is evidence of focal parenchymal hemorrhage. [Yes/No]
There is evidence of intra ventricular bleeding. [Yes/No]
There is evidence of concurrent parenchymal plus SAH to suggest a sentinel aneurysm bleed. [Yes/No]
There is evidence of only trace amount of blood in occipital horns, posterior intrasylvian sulci, or foramen cecum part of the interpeduncular fossa. [Yes/No]
There is evidence of intercurrent obstructive hydrocephalus. [Yes/No]
There is evidence of subarachnoid, pial or subpial bleed adjacent to cortical veins or dural sinuses. [Yes/No]
There is evidence of SAH near falx (possibly post traumatic in origin). [Yes/No]
There is evidence of vertex sulcal blood (possibly reversible vasoconstrictive vascular disorders). [Yes/No]
There is evidence of focal cytogenic edema related to intercurrent hemorrhagic stroke. [Yes/No]
There is evidence of thrombosed pial artery/vein as a cause for intraaxial hemorrhage. [Yes/No]
There is evidence of thrombosed vascular malformation. [Yes/No]
There is evidence of focal subarachnoid blood, possibly from saccular aneurysm associated with an AVM. [Yes/No]
There is evidence of hemorrhagic met or other tumor as basis for SAH. [Yes/No]
There is evidence of multicentric bleeding sites consistent with coagulopathy as cause for bleeding. [Yes/No]
There is evidence of visibly enlarged pial or deep veins representing the venous egress of a pial AVM. [Yes/No]
There is evidence of visibly enlarged dural sinuses, or enlarged orbital/pial veins with proptosis representing the venous egress of a dural AVF. [Yes/No]
There is evidence of markedly enlarged pial or deep veins representing the venous egress of a direct AV fistula. [Yes/No]
There is evidence of markedly enlarged internal cerebral veins and vein of Galen consistent with Galenic AV malformation. [Yes/No]
Other abnormality. [Yes/No]
