Open lumbar spine surgery - Part I
Types of tables:
- Jackson with OSI frame: standard setup that we use - has table with the rails and the pads for chest, hips, thighs. can adjust level of rods at each end so you get extra T or reverse-T - if you're doing say an L5-S1 fusion and the sacral slope is really steep, you can get feet up so you're working horizontally, etc etc. When putting people on OSI, put chest pad on upper chest- not directly against chin, not too low for women. Some people think you should straighten knees relative to hips so you avoid hypothetical risk of fusing people in hip flexion position, however in real life this is rarely a problem.
- Jackson table with Wilson frame: forced flexion over the arc. Gets you better access to the disc, which is useful if you're doing a discectomy, however can give you a false sense of security about how much decompression you have achieved. Like you feel nerve roots, you think they are decompressed because they are in forced flexion, but then when back goes straight everything closes off and then you're not decompressed anymore. Also as a note - if you're gonna use a Wilson frame, better to do Jackson table because its' lower - Wilson frame is high, unless you're really tall you're gonna be on 4 steps.
- Jackson table w Axis frame - can bend in half. Most useful for XLIF/DLIF when you position patient laterally, really opens up space between iliac crest and and ribs.
- Jackson flattop - useful vs standard table because its radiolucent and also no giant pedicle in the middle- so if you're doing an ALIF you have an easier time getting C-arm under table.
Arm positioning :
- up for middle T/L - make sure no hyperextension of arms back or too anterior, keep elbows soft, 90 degrees; protect against axillary nerve injury
- down/wrapped for C and upper T
Setting up the room:
- head towards anesthesia, scrub nurse at legs, surgeon on each side of back.
- assuming the pathology doesn't have laterality, choose the side of patient that doesn't have the base of the C-arm on it, so you're not moving your steps/foot pedals around every time the C-arm moves.
- when you move c-arm out of the way, move it towards anesthesia/patient head - because your scrub nurse is by patient's legs and you don't want the c-arm between you
General principles
- Look at CT scan before every case; look at anatomy - planning on lami, make sure there is actually lamina at every level. Some people have big facets, and there may be no lamina to take at a given level, or some atypical scoliosis, such that you have to drill at an angle. if you meant to do a lami, without a fusion, and you violate the facet capsule or worse drill facet when you didn't mean to, then you're hosed because you've destabilized that level.
- determine pedicle sizes on scan, pick out screw size and length beforehand, write them on the board
Process:
- localize level first with c-arm.
- mark incision
- prep and drape wide
- 15 blade through skin
- buzz through fat with impunity
- put finger in and feel for the spinous processes - directly above spinous process is fascia. every time. every time. that's where it is. lateral to spinous process will be bumps for paraspinous muscle.
- take cobb and scrape last bit of fat off fascia. In everyone except super old frail people with terrible fascia, you can scrape and you will not accidentally break through as long as you're not jabbing aggressively
- cut on either side of spinous process. Take cobb, put raytech on it, and scrape down along spinous process. you should be sub-periosteal. if you are not, you will be in muscle - it will bleed like crazy and the patient will have a lot more postop pain. alternative to cobb is bovie down bone (but be careful directly lateral to lamina- there lie nerve roots). problem with bovie is it will cause paraspinal muscles to tighten and fight you - option to ask anesthesia for short-acting muscle relaxant. if someone has pacemaker or otherwise can't tolerate electrocautery, then you have to do the bipolar and cut thing which sucks.
- your cobb will then land on lamina. scrape ROSTRAL and LATERAL - next you will land on a valley of bone which is the superior aspect of pars, between the superior facet and the lamina. then scrape your cobb more rostral and more lateral - you will go over a bump, this is the facet capsule, and then you will land on the transverse process. If you're only doing a lami, you don't need to see TP but if you're doing a fusion you will need to expose a lot of the TP.
- THE PEDICLE IS ROSTRAL TO THE SPINOUS PROCESS. once you find the spinous process, you have to go rostral to find pedicle. this is especially true in thoracic spine - if you try to take shortcuts and aren't thoughtful, and you go for the pedicle directly next to the spinous process, you will put the screw in the wrong level.
- the anatomy is as such: from rostral to caudal superior facet, TP/pedicle, lamina, inferior facet, with the pars representing the bridge of bone connecting superior to inferior facet
NB
- if you're doing a lami, you cannot drill all the way lateral - if you take pars, you destabilize
- you cannot bovie with impunity directly lateral to the spinous process/lamina - that's where the nerve roots come out. (if patient jumps and they are not paralyzed, its because your electrocautery hit a nerve root). this is why we don't paralyze spine cases.
- there is often a large artery next to pars - if it starts bleeding like crazy, don't dive after it with electrocautery, as you might hit nerve roots.
- if someone has giant, super hypertrophied facets, you might need to drill off the inferior aspect of facet to access entry point for pedicle screw - be careful - you can only drill approx 1/3 of facet joint before you destabilize
Thoughts on cervical decompression
- if most of someone's compression is coming from disk, you can do ACDF
- if there is a hypertrophied ligamentum flavum or facet arthropathy, you can get a lot more decompression of spinal cord if you come from the back
Thursday, August 18, 2016
Wednesday, August 17, 2016
Cranioplasty
- just like for a decompressive hemicrani - when you're making a giant trauma flap incision, you have to think about positioning such that you can reach the back of the head/most posterior aspect of incision. If someone has excellent neck mobility, you can just put them flat and turn head all the way over. If someone doesn't have good neck mobility (ie. c-collar, really old, arthritis, contractures) then you put a bump under the shoulder to get you access to back of head. similar principle for shunt - shoulder bump to straighten out neck for optimal tunneling.
- putting someone on a horse-shoe means that you can reach more posterior around their head more easily - think about your hand/wrist position relative to head vs them being flat on a table, and having the table block you
- shave around the incision area only
- cover eyes well with tegaderm, and then again with the 1000 drape, put drape as low across brow as you can to get the biggest field, but make sure to shield eyes - chlorhexadine is very caustic to corneas
- stuff xeroform into the ears only if you intend to use a chlorhexadine prep - it is ototoxic. if you are painting betadine or using alcohol only this step is skiappable
- prep and drape wide - you will have to tunnel a drain out of your flap
- feel bone edges under incision - if you have bone under incision you can cut all the way down. if you do not, you have to be careful - go thru skin with knife and then carefully bovie/dissect because its scalp - dura - brain. you will definitely not have any bone over the squamous temporal bone, because if you did a good decompression originally, you put a burr hole right at the pterion/over root of zygoma, and you kerrison'd all the way flush to the floor of the middle fossa for good temporal lobe decompression.
- for temporalis muscle, carefully dissect it off the dura - if you don't dissect between temporalis muscle and scalp, you can have a better chance of not causing a frontalis palsy. this is also a good place to find the bone edge and begin to develop the plane between periostium and dura.
- if you are lucky, there will be a good plane between periostium and dura, and you can follow that plane all the way around - you are not done until you see all bone edges. Put screws into the bone flap, push it flush all the way against anterior aspect of bone. if temporalis muscle is large and healthy, you can just close (fascia on fascia) anterior temporalis muscle against posterior. If its kind of bad looking, consider putting in a mesh over the cranial defect where temporal bone used to be, to buttress it and prevent a hollowing defect later on.
- if you are not lucky, the whole thing will be scarred down and socked in and you just have to create a plane - find the bone, do not violate dura.
- leave a subgaleal drain, use hemovac (same width of drain all the way around vs JP which is a wider drain; HMV hurts less coming out, creates a smaller hole to close when removed). Always leave drain because it will bleed a lot and you will not be able to use aggressive electrocautery because otherwise it won't heal well.
- tunnel your drain before you close, tunnel it outside of your flap becusae it will heal better. do not sew in drain until you finish closing, otherwise you'll shift the position of the drain in head and where you tunnel it out may not be as sterile as the rest of your field so do that last.
- close galea with 3-0 vicryl with C-23 needle
- close skin with either absorbable sutures or staples - for healthy people who will heal well, choose absorbable - it looks nicer, plus you don't have to hurt people 2 weeks later when you take them out. If there is any question about whether someone will heal an incision though, use staples - you can hypothetically leave staples in forever. also they are faster.
- if you are struggling to close, either because scalp is really scarred or tight, consider nylon sutures with horizontal mattress- you can use it to pull the scalp incrementally closer together
- just like for a decompressive hemicrani - when you're making a giant trauma flap incision, you have to think about positioning such that you can reach the back of the head/most posterior aspect of incision. If someone has excellent neck mobility, you can just put them flat and turn head all the way over. If someone doesn't have good neck mobility (ie. c-collar, really old, arthritis, contractures) then you put a bump under the shoulder to get you access to back of head. similar principle for shunt - shoulder bump to straighten out neck for optimal tunneling.
- putting someone on a horse-shoe means that you can reach more posterior around their head more easily - think about your hand/wrist position relative to head vs them being flat on a table, and having the table block you
- shave around the incision area only
- cover eyes well with tegaderm, and then again with the 1000 drape, put drape as low across brow as you can to get the biggest field, but make sure to shield eyes - chlorhexadine is very caustic to corneas
- stuff xeroform into the ears only if you intend to use a chlorhexadine prep - it is ototoxic. if you are painting betadine or using alcohol only this step is skiappable
- prep and drape wide - you will have to tunnel a drain out of your flap
- feel bone edges under incision - if you have bone under incision you can cut all the way down. if you do not, you have to be careful - go thru skin with knife and then carefully bovie/dissect because its scalp - dura - brain. you will definitely not have any bone over the squamous temporal bone, because if you did a good decompression originally, you put a burr hole right at the pterion/over root of zygoma, and you kerrison'd all the way flush to the floor of the middle fossa for good temporal lobe decompression.
- for temporalis muscle, carefully dissect it off the dura - if you don't dissect between temporalis muscle and scalp, you can have a better chance of not causing a frontalis palsy. this is also a good place to find the bone edge and begin to develop the plane between periostium and dura.
- if you are lucky, there will be a good plane between periostium and dura, and you can follow that plane all the way around - you are not done until you see all bone edges. Put screws into the bone flap, push it flush all the way against anterior aspect of bone. if temporalis muscle is large and healthy, you can just close (fascia on fascia) anterior temporalis muscle against posterior. If its kind of bad looking, consider putting in a mesh over the cranial defect where temporal bone used to be, to buttress it and prevent a hollowing defect later on.
- if you are not lucky, the whole thing will be scarred down and socked in and you just have to create a plane - find the bone, do not violate dura.
- leave a subgaleal drain, use hemovac (same width of drain all the way around vs JP which is a wider drain; HMV hurts less coming out, creates a smaller hole to close when removed). Always leave drain because it will bleed a lot and you will not be able to use aggressive electrocautery because otherwise it won't heal well.
- tunnel your drain before you close, tunnel it outside of your flap becusae it will heal better. do not sew in drain until you finish closing, otherwise you'll shift the position of the drain in head and where you tunnel it out may not be as sterile as the rest of your field so do that last.
- close galea with 3-0 vicryl with C-23 needle
- close skin with either absorbable sutures or staples - for healthy people who will heal well, choose absorbable - it looks nicer, plus you don't have to hurt people 2 weeks later when you take them out. If there is any question about whether someone will heal an incision though, use staples - you can hypothetically leave staples in forever. also they are faster.
- if you are struggling to close, either because scalp is really scarred or tight, consider nylon sutures with horizontal mattress- you can use it to pull the scalp incrementally closer together
Saturday, June 25, 2016
Differential Diagnosis of Intra-Axial Brain Tumor based on appearance in Adults
Intra-axial: 75% astrocytic tumor or mets
Tumors that invade the corpus callosum and cross midline
- GBM (rarely has leptomeningeal spread)
- Lymphoma (can have leptomeningeal spread, typically homogenously enhancing but in immunocompromised hosts can appear ring-enhancing or heterogenous)
- Mets (can have leptomeningeal enhancement, often cystic)
Multiple lesions
- usually mets
- multifocal GBM - rarer but exists
- gliomatosis cerebri
- lymphoma can appear as multiple lesions
- CNS metatstases - i.e. medulloblastoma, ependymoma, oligodendro
Genetic diseases that cause multiple tumors :
- NF1 (optic glioma, astrocytoma)
- NF2 (meningiomas, schwannoma, ependymoma of brain and spinal cord)
- Tuberous Sclerosis (SEGA, ependymoma)
- VHL (cerebellar/retinal/spinal cord hemangioblastomas, endolymphatic sac tumor)
Cortical-based
Oligodendro
- often cortical/subcortical, and are shown on MRI "extending all the way to the cortex"
- classically frontal but can be in any lobe.
- 70-90% calcified.
- usually T1 dark, T2 bright (except calcified areas - which will show up as T2 dark/T2* blooming
- 50% will enhance with Gad - usually heterogenously. Gad enhancement is not a reliable indicator of grade.
- Typically do not restrict on DWI. Often older people (40-50s+)
Ganglioglioma
- mix of glial and neuronal cells (if the glial component de-differentiates it turns into a GBM; if the neuronal component de-differentiates it turns into a neuroblastoma).
- 45% of the time it will appear as a cyst with mural nodule in a cortical area, but it can be very variable in appearance--- simple cyst with small mural nodule, complex cyst with large, heterogenous mural nodule, solid tumor only.
- The mural nodule has variable enhancement - sometimes enhances vividly
- not much edema.
- Usually affects children and young adults.
DNET:
- arise from cortical or deep grey matter.
- Predilection for temporal lobes.
- often associated with cortical dysplasia
- often cause intractable seizures.
- May be cyst with mural nodule.
- Enhances 20-30% of the time.
- T1 isodense, T2 bright with sometimes "bubbly" appearance
- not much peritumoral edema.
- Rarely grow in size over time, excellent oncologic prognosis but often removed because of the intractable seizures they cause - seizures often stop when the tumor is resected.
- Typically affects children and young adults.
Of note: in clinical practice, DNETs and GG often appear very similar radiographically, are both T1-dark, T2-bright tumors that rarely enhance (DNET can sometimes appear as ring-enhancing but not commonly, GG are a little more likely to be cystic with mural nodule, etc), with predilections for the temporal lobe, cause seizures, and have excellent seizure freedom outcomes with resection. See this retrospective series from Turkey with 52 patients.
PXA:
- cortical tumors with cystic component and vivid enhancement with Gad.
- 98% supratentorial. Mostly temporal.
- Often low grade/slow growing without much edema.
- T1 iso/hypointense. 50-60% cyst with mural nodule that enhances strongly. T2 - cyst often looks different than CSF due to proteinacious content.
- Avascular on angio despite vidid enhancement.
- Often affects kids and young adults.
Contain T1-bright tissue that resembles fat
Lipoma
- always located in subarachnoid spaces - believed to be from maldevelopment of meninx primativa (subarachnoid precursor)
- pericallosal (can wrap around corpus callosum - associated with agensis of corpus callosum in 50% of cases) - 45%
- quadrigeminal cistern (associated with underdevelopment of inferior colliculus) - 35%
- suprasellar cistern - 15%
- CP angle - 10%
- sylvian fissure - 5%
Dermoid:
- Can be thought of as on the spectrum from epidermoid (only squamous epithelial tissue) to dermoid (ectodermal only) to teratomas (contain tissue from all 3 embryonic layers)
- They appear bright on T1 but there is actually no fat in them. They contain squamous epithelial tissue + ectodermal appendages like hair follicles, sweat glands, sebaceous glands - which secrete sebum which looks T1 bright (from cholesterol and other things). Technically no adipose tissue, because that is from mesenchymal tissue so it would technically be a teratoma if there was mesenchyme
- Often midline - suprasellar, subfrontal, cerebellar vermis
- They can rupture and cause a chemical meningitis - leptomeningeal enhancement
- Very rarely will transform into squamous carcinoma
Teratoma - contains tissue from all 3 embryonic layers.
- rare in general population - however 25-50% of fetal brain tumor
- usually pineal or suprasellar
- T1 bright from fat, can enhance
Sources:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3876643/
http://www.radiologyassistant.nl/en/p47f86aa182b3a/brain-tumor-systematic-approach.html
http://radiopaedia.org/articles/dysembryoplastic-neuroepithelial-tumour
http://radiopaedia.org/articles/ganglioglioma
http://radiopaedia.org/articles/pleomorphic-xanthoastrocytoma
http://radiopaedia.org/articles/intracranial-dermoid-cyst-1
http://radiopaedia.org/articles/gliomatosis-cerebri
http://radiopaedia.org/articles/leptomeningeal-enhancement
Intra-axial: 75% astrocytic tumor or mets
Tumors that invade the corpus callosum and cross midline
- GBM (rarely has leptomeningeal spread)
- Lymphoma (can have leptomeningeal spread, typically homogenously enhancing but in immunocompromised hosts can appear ring-enhancing or heterogenous)
- Mets (can have leptomeningeal enhancement, often cystic)
Multiple lesions
- usually mets
- multifocal GBM - rarer but exists
- gliomatosis cerebri
- lymphoma can appear as multiple lesions
- CNS metatstases - i.e. medulloblastoma, ependymoma, oligodendro
Genetic diseases that cause multiple tumors :
- NF1 (optic glioma, astrocytoma)
- NF2 (meningiomas, schwannoma, ependymoma of brain and spinal cord)
- Tuberous Sclerosis (SEGA, ependymoma)
- VHL (cerebellar/retinal/spinal cord hemangioblastomas, endolymphatic sac tumor)
Cortical-based
Oligodendro
- often cortical/subcortical, and are shown on MRI "extending all the way to the cortex"
- classically frontal but can be in any lobe.
- 70-90% calcified.
- usually T1 dark, T2 bright (except calcified areas - which will show up as T2 dark/T2* blooming
- 50% will enhance with Gad - usually heterogenously. Gad enhancement is not a reliable indicator of grade.
- Typically do not restrict on DWI. Often older people (40-50s+)
Ganglioglioma
- mix of glial and neuronal cells (if the glial component de-differentiates it turns into a GBM; if the neuronal component de-differentiates it turns into a neuroblastoma).
- 45% of the time it will appear as a cyst with mural nodule in a cortical area, but it can be very variable in appearance--- simple cyst with small mural nodule, complex cyst with large, heterogenous mural nodule, solid tumor only.
- The mural nodule has variable enhancement - sometimes enhances vividly
- not much edema.
- Usually affects children and young adults.
DNET:
- arise from cortical or deep grey matter.
- Predilection for temporal lobes.
- often associated with cortical dysplasia
- often cause intractable seizures.
- May be cyst with mural nodule.
- Enhances 20-30% of the time.
- T1 isodense, T2 bright with sometimes "bubbly" appearance
- not much peritumoral edema.
- Rarely grow in size over time, excellent oncologic prognosis but often removed because of the intractable seizures they cause - seizures often stop when the tumor is resected.
- Typically affects children and young adults.
Of note: in clinical practice, DNETs and GG often appear very similar radiographically, are both T1-dark, T2-bright tumors that rarely enhance (DNET can sometimes appear as ring-enhancing but not commonly, GG are a little more likely to be cystic with mural nodule, etc), with predilections for the temporal lobe, cause seizures, and have excellent seizure freedom outcomes with resection. See this retrospective series from Turkey with 52 patients.
PXA:
- cortical tumors with cystic component and vivid enhancement with Gad.
- 98% supratentorial. Mostly temporal.
- Often low grade/slow growing without much edema.
- T1 iso/hypointense. 50-60% cyst with mural nodule that enhances strongly. T2 - cyst often looks different than CSF due to proteinacious content.
- Avascular on angio despite vidid enhancement.
- Often affects kids and young adults.
Contain T1-bright tissue that resembles fat
Lipoma
- always located in subarachnoid spaces - believed to be from maldevelopment of meninx primativa (subarachnoid precursor)
- pericallosal (can wrap around corpus callosum - associated with agensis of corpus callosum in 50% of cases) - 45%
- quadrigeminal cistern (associated with underdevelopment of inferior colliculus) - 35%
- suprasellar cistern - 15%
- CP angle - 10%
- sylvian fissure - 5%
Dermoid:
- Can be thought of as on the spectrum from epidermoid (only squamous epithelial tissue) to dermoid (ectodermal only) to teratomas (contain tissue from all 3 embryonic layers)
- They appear bright on T1 but there is actually no fat in them. They contain squamous epithelial tissue + ectodermal appendages like hair follicles, sweat glands, sebaceous glands - which secrete sebum which looks T1 bright (from cholesterol and other things). Technically no adipose tissue, because that is from mesenchymal tissue so it would technically be a teratoma if there was mesenchyme
- Often midline - suprasellar, subfrontal, cerebellar vermis
- They can rupture and cause a chemical meningitis - leptomeningeal enhancement
- Very rarely will transform into squamous carcinoma
Teratoma - contains tissue from all 3 embryonic layers.
- rare in general population - however 25-50% of fetal brain tumor
- usually pineal or suprasellar
- T1 bright from fat, can enhance
Contain Calcifications
- Oligodendro - rare, but often calicfied
- Astrocytoma - common, but infrequently calcified
- Pinealcytoma - are not calcified in and of themselves, but contain the inherent calcifications of the pineal gland
- Craniopharyngioma - suprasellar
Cystic lesions with same intensity as CSF
- Arachnoid
- Neurenteric cyst
- Neurenteric cyst
- Enlarged virchow-robin space
Bright on T1
- most tumors are isodense or slightly hypodense on T1. T1 hyperintensity implies presence of one of the elements which are hyperintense on T1, which include the following:
- Fat -> Lipoma, Teratoma
- Cholesterol -> Craniopharyngioma, Dermoid, colloid cyst
- Melanin -> Melanoma met
- Subacute blood (intracellular or extracellular metHb) -> Hemorrhagic tumor - melanoma met, breast/lung (uncommonly bleed), follicular thyroid met, renal cell met, choriocarcinoma met. pituitary apoplexy
- Mineralization with paramagnetic divalent cations ( Ca, Copper, manganese )
- Proteinaceous fluid - neurentetic cyst
Dark on T2
- Most tumors are bright on T2 dude to high water content. Low T2 signal implies:
- hypercellularity -> PNET/medullo, lymphoma, mucinous adenoCA mets, high-cellularity parts of GBM (although GBM is usually T2 bright)
- calcifications -> oligo, astro, craniopharyngioma
- many flow voids -> hemangioblastoma
Contrast enhancement:
- Fundamentally based on the integrity of the BBB
Tumors that do not have a BBB will enhance vividly
- extra-axial masses like meningioma, schwannoma
- non-CNS tumors like lymphoma, metastatic lesions (breast, lung, etc)
- CNS tumors derived from tissue that does not have a BBB - pituitary, pineal (including germinoma and other pineal gland tumors), choroid plexus
Homogenous enhancement
- Mets
- Lymphoma (non immunocompromised)
- Meningioma - and its great mimics, hemangiopericytoma and dural based MALT lymphomas
- Schwannoma/neurofibroma
- Mural nodule of hemangioblastoma, JPA
- Germinoma, other pineal gland tumors
- Pituitary adenoma
- Ganglioglioma
Patchy Enhancement
- Mets
- GBM
- Non tumor things (like radiation necrosis)
Ring Enhancement
- MAGICALDR
- Mets
- Abscess
- GBM
- Ischemia (subacute stroke), Infection (neurocystercercosis, toxoplasma, TB, blasto/histo/crypto, nocardia, listeria)
- Contusion
- Alternative weird stuff (sarcoid, vasculitis, behcets)
- Lymphoma
- Demyelination (MS, ADEM)
- Radiation necrosis
Leptomeningeal Enhancement
- leptomeningeal carcinomatosis (breast, lung, melanoma, leukemia/lymphoma)
- from CNS tumors - GBM, medullo/PNET, ependymoma, choroid plexus carcinoma.
- infectious - meningitis (bacterial, viral, crypto, TB)
- sarcoid
- post-LP (<5%), post-surgery/hemorrhage/trauma
Sources:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3876643/
http://www.radiologyassistant.nl/en/p47f86aa182b3a/brain-tumor-systematic-approach.html
http://radiopaedia.org/articles/dysembryoplastic-neuroepithelial-tumour
http://radiopaedia.org/articles/ganglioglioma
http://radiopaedia.org/articles/pleomorphic-xanthoastrocytoma
http://radiopaedia.org/articles/intracranial-dermoid-cyst-1
http://radiopaedia.org/articles/gliomatosis-cerebri
http://radiopaedia.org/articles/leptomeningeal-enhancement
Friday, June 24, 2016
Bright
|
Dark
|
|
T1
|
- contrast
- fat/cholesterol (lipoma, teratoma, dermoid, lipomatous ependymoma, cholesteatoma) ** to differentiate fat from other T1-bright lesions, look for chemical shift artifact (dark band at edge of fat on one side, light band at the other)
- melanin
- early subacute blood
(intracellular metHb 3-7 days) and late
subacute blood (extraceullar metHb, 1-4 weeks)
- subacute thrombus (i.e.
venous sinus)
- protein-rich fluid
(colloid, rathke’s cleft, ectopic posterior pituitary, craniopharyngioma –
also cholesterol and blood)
- minerals (microcalcifcations,
iron, manganese – hepatic encephalopathy, copper)
- laminar necrosis (from
global hypoxemia or immunosuppression – appears 2 weeks after insult) – may
appear as cortical ribbon
- slowly flowing fluid
|
- CSF
- Edema
- flow voids
- calcium (bone) –
although microcalcifications often appear as bright on T2 due to their
interaction of water molecules
|
T2
|
- Edema (from tumor, infection,
inflammation, ischemia, vasculitis, radiation-induced, chemo-induced, migraines, etc)
- late subacute blood (extracellular metHb)
- CSF (virchow robin spaces)
- Demyelination
- Myelinolysis - Degeneration |
- contrast
- acute blood (deoxy Hb)/early subactue blood (intracellular
metHb), chronic blood
(hemosiderin)
- melanin
- mucous/protein (i.e.
colloid/rathke cyst
- hypercellular tumors
(high nucleus to cytoplasm ratio – medullo, lymphoma, highest grade parts of
high grade gliomas) ** - tends to be dark but not black
- minerality (iron,
copper, calcium)
- flow voids/turbulent flow
– of blood and CSF (jets can appear
dark)
- air
- fibrous
tissue/bone
|
Diffusion
|
- T2 shine through
- acute ischemia (<2-3 weeks)
- highly cellular tumors (lymphoma, medullo/PNET,
meningioma, chordoma, germinoma, hemangiopericytoma, pinealblastoma, cortical
part of high-grade gliomas – cyst part typically does not restrict in
gliomas)
- abscess (cystic part restricts 2/2 pus)
- mucinous metastasis like breast or colon adenocarcinoma (mucus restricts)
- epidermoid
- prion disease (CJD, kuru – cortical ribboning)
- toxic (carbon monoxide, methanol, Wernicke, maple syrup
urine, gluteric aciduria, methyl malonic aciduria other inborn errors of
metabolism diseases)
- adrenoleukodystrophy
|
- old stroke (> 3 weeks)
- necrosis (i.e. core of GBM/mets)
|
GRE/SWI
|
Blooming
- air
- blood of any age
- mineralization
- inflammation
|
Source papers:
Monday, June 6, 2016
Sympathetic storming
Epidemiology
- Typically occurs in young patients with significant/diffuse brain injury - TBI/DAI, SAH, big IPH, etc.
- Archetypally a young male with bad DAI -- likely no true gender predilection but rather trauma tends to affect male > female. And perhaps age predilection because young people have a more robust sympathetic response, or maybe because the degree of neurological injury that is typically associated tends to be mortal in older adults, or maybe because high grade SAH or IPH or diffuse injury occurs more in middle age than late age
Pathophys
- Poorly understood
- Originally believed to be exclusively a function of deep white matter injury; however its also seen in bilateral/diffuse cortical injury
- Perhaps decrease in the dampening signals? exaggerated sympathetic response to all stim, instead of only to severe/noxious stim.
Clinical Presentation
- Paroxysmal bouts of tachycardia, hypertension, diaphoresis, fever, mydriasis
- Characteristically waxing/waning, rather than constant (i.e. alcohol withdrawal)
- Typically occurs 3-5 days after the initial injury, and resolves on the scale of days to weeks but can start as early as immediately after the injury and last for years
Treatment
- Very severe (i.e. uncontrollable blood pressures leading to problematic sequelae) - precedex gtt and/or esmolol gtt
- Less severe/transitioning off gtts/on the floor - clonidine, propanolol, gabapentin (especially useful for controlling storming that directly follows stim - like turning/bathing/etc)
- Some people believe that opiates like morphine are an integral part of treating storming, some people don't.
- You can always snow people into the ground with propofol or drips of benzos or narcotics, but it's an inelegant solution and some people believe that they are suboptimal ways of treating storming.
Epidemiology
- Typically occurs in young patients with significant/diffuse brain injury - TBI/DAI, SAH, big IPH, etc.
- Archetypally a young male with bad DAI -- likely no true gender predilection but rather trauma tends to affect male > female. And perhaps age predilection because young people have a more robust sympathetic response, or maybe because the degree of neurological injury that is typically associated tends to be mortal in older adults, or maybe because high grade SAH or IPH or diffuse injury occurs more in middle age than late age
Pathophys
- Poorly understood
- Originally believed to be exclusively a function of deep white matter injury; however its also seen in bilateral/diffuse cortical injury
- Perhaps decrease in the dampening signals? exaggerated sympathetic response to all stim, instead of only to severe/noxious stim.
Clinical Presentation
- Paroxysmal bouts of tachycardia, hypertension, diaphoresis, fever, mydriasis
- Characteristically waxing/waning, rather than constant (i.e. alcohol withdrawal)
- Typically occurs 3-5 days after the initial injury, and resolves on the scale of days to weeks but can start as early as immediately after the injury and last for years
Treatment
- Very severe (i.e. uncontrollable blood pressures leading to problematic sequelae) - precedex gtt and/or esmolol gtt
- Less severe/transitioning off gtts/on the floor - clonidine, propanolol, gabapentin (especially useful for controlling storming that directly follows stim - like turning/bathing/etc)
- Some people believe that opiates like morphine are an integral part of treating storming, some people don't.
- You can always snow people into the ground with propofol or drips of benzos or narcotics, but it's an inelegant solution and some people believe that they are suboptimal ways of treating storming.
Tuesday, May 31, 2016
Aging of stroke
|
Time
|
DWI
|
ADC
|
T2
|
CT
|
|
30 mins
|
First becomes visible -
bright
|
First starts to become
visible – dark – in animal stroke models ADC changes visible in < 5 mins
|
Invisible
|
invisible
|
|
6-8 hours
|
Clearly Bright
|
Clearly Dark
|
First starts to become
visible – bright (edema)
|
First start to become
visible - loss of grey-white, insular ribbon, etc
|
|
24 hours
|
Clearly Bright
|
Clearly Dark
|
Clearly bright
|
Clearly dark
|
|
1-4 days
|
Clearly Bright
|
Max darkness
|
Clearly bright
|
Clearly dark
|
|
7 days
|
Max brightness
|
Clearly dark
|
Clearly bright
|
Clearly dark
|
|
10-15 days
|
Signal starts to fade
|
Reverses from dark to
bright, sometimes becomes invisible
|
Clearly bright
|
Clearly dark
|
|
2-3 weeks
|
Signal fading/reversing
|
Becomes bright
|
Clearly bright
|
Clearly dark
|
|
>30 days
|
Dark
|
bright
|
Max brightness
|
Clearly dark
|
Sunday, December 20, 2015
UCAS (prospective)
- 2001-2004 in Japan
- N=5720 patients, 6697 aneurysms (3050 : treatment before rupture @ median of 48 days, 3647: not treated before rupture)
- Rupture rate of 0.95% per aneurysm-year ; rupture rates associated with 35% mortality, 29% mRS 3-5
Whereas ISUIA found increased rates in all posterior circulation aneurysms, UCAS found higher rupture rates with Acomm and Pcomm (but not more with say, BTAs..... however the total number of VA/BTA aneurysms was small (see below chart)
Graphical representations of rupture rates by location and size:
Multivariate analyses of predictors of rupture:
*smoking status (former or current) not associated with rupture rate!
*previous SAH not predictive of rupture - however only 3% of the cohort had ever had a SAH
Criticisms:
- Japanese population: which has the same incidence of aneurysm, but a higher risk of SAH compared to the rest of the world. Unclear if this data can be applied to US or european populations.- Same selection bias as ISUIA - non-randomized data; the aneurysms believed to be high risk were all treated.
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