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Vascular Anomolies Flashcards

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1
Q

What is the first order classification of vascular anomalies?

A

Vascular tumors
vascular malformations

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2
Q

What is the sub-classification of vascular tumours?

A

infantile hemangioma
hemangioendothelioma
angiosarcoma
Misc

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3
Q

What is the sub-classification of vascular malformations?

A

Slow-flow
capillary malformation CM
lymphatic malfomation LM
venous malformation VM

Fast flow
arterial malformation

Combined

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4
Q

What is the most common location for infantile hemangiomas?

A

head and neck

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5
Q

Describe what slow flow CM are and treatment.

A

Red macular lesions seen at birth and persist throughout life
Laser tx for cosmesis

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6
Q

Names three diseases associated with SF CM.

A

sturge weber
cutis marmorata telangiectatica congenita
Macrocephaly-CM

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7
Q

Describe what SF VM look like and treatment.

A

Bluish compressible swellings
Can be painful
Can be extensive and lead to leg length discrepancy
At risk for systemic coagulopathy after trauma
Tx OR can have significant blood loss
tourniquet

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8
Q

Names three diseases associated with SF VM.

A

Glomuvenous malformation
Cutaneomucosal venous malformation
Blue rubber bleb nevus syndrome

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9
Q

Describe what SF LM are and treatment.

A

Microcystic cmor combined
Tx lenticular excision
Dissect off skin, not malignant need not excise everything
May need to remove associated viscera
Post op, suction drainage

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10
Q

Name types of fast flow VM.

A

AVF
AVM

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11
Q

What are symptoms of AVF?

A

LE—edema, hypertrophy, trophic changes
UE—pain, digital ischemia, discoloration of the digits

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12
Q

What is an AVM?

A

Center call nidus has feeding vessels, micro and macro AVFS and ecstatic veins

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13
Q

Where are AVM most commonly found?

A

Intracranial, followed by limbs, trunk and viscera

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14
Q

How do you stage AVM?

A

I quiescence
Cutaneous blush, warmth (av shuntung on Doppler)
Stage II expansion
Bruit, audible pulsation, expanding lesion
Stage II destruction
Pain ulceration, bleeding, infection
Stage IV decompensation
Cardiac failure

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15
Q

What are indications to treat AVM?

A

pain ulceration, functional impairement, soft tissue and bony destruction and bleeding.
CHF

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16
Q

What is treatment for AVM?

A

Embolization alone or in combo
Embo nidus then resection next few days

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17
Q

What are variation of combine VM?

A

fast or slow
any combo of C, L, V, A

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18
Q

What is klippel-trenaunay syndrome?

A

slow flow Capillary-lymphaticovenous malformation
Large and small CM extremities and buttock
Lymphedema and LM in LE
Limb hypertrophy present at birth

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19
Q

What are side effects of KTS?

A

Infections, PE, thrombophleb, GI, constipation, bladder outlet obstruction , hematuria

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20
Q

What is parks weber?

A

Fast flow capillary arteriovenous malformation CAVM or CLAV<
Usually LE and trunk
Cutaneous flushing wih underlying multiple micro AVFS

large, flat, pink stains on the skin, and because of their color are sometimes called “port-wine stains

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21
Q

What is most common tumour of infancy?

A

infantil hemangioma

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22
Q

What is infantile hemangioma?

A

benign tumor of the endothelium
most common neoplasm of infancy
gros rapidly in first year then growth plateaus then shrinkage
bright color fades becomes less tense.
last phase complete by 4 yo

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23
Q

What is most common site of infantile hemangioma?

A

liver
can cause hepatomeg, IVE compression

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24
Q

How to diagnose infantile hemangioma?

A

US or MRI

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25
What is treatment of infantile hemangioma?
conservation topical steroid laser embolic only for CHF excision only if at risk for injury and blood loss
26
What is the cause of primary raynauds?
idiopathic
27
What are connective tissue causes of secondary raynauds?
systemic sclerosis inflammaroty muscle disease Lupus Sjogren's syndrome Vasculitis
28
What drugs can cause secondary raynauds?
BB clonidine ergotamine vinyl chloride
29
What occupational cause can cause raynauds?
HAVS TOS
30
What illness that impair digital perfusion can cause secondary raynauds?
paraproteinemia cryoglobulinemia malignancy
31
What are some large vessel disease that can cause secondary raynauds?
athero thromboangitis obliterans
32
What are proposed pathogenic cases of raynauds?
``` vascular impaired vasod (impaired NO and prostacyclin) increased vasoconstriction (overproduction of ATII, ET-1) structural vascular abnormalities ``` Neural impaired vasod (calcitonin gene related peptide) increased vasoc (abnormal adrenergic function) central (stress induced) Intravascular factos (plt WBC activation, increased thrombin generation) Genetic
33
What are important questions on hx?
tissue loss CTD (difficulty swallowing, photosensitivity, mouth ulcers) asymmetry what drugs occupational hx fam hx RF for athero bruits, pulses
34
What investigations to do for raynauds?
nailfold cappilaroscopy (abnormalities) angio/NIV for large vessel Thermography (normal thermal gradients at room temp for PRP but not for sclerosis)
35
What is medical therapy for raynauds?
remove triggers CCB ACEi phosphodiesterase inhibitors topical NO, nitrate
36
When to do sx? what sx options for raynauds?
when medical treatment fails ulcer debridement cervical sympathectomy (symptoms may return) periarterial symapthectomy Balloon angio arterial reconstruction excision of calcific deposits amputation botox injections
37
What is the angio anatomic classification of raynauds?
type I: occlusion of R or U artery, decreased flow in level 2-3 arteries type II: as I but with stenosis of R or U artery type IIIa: main disorder in common digital or digital arteries type IIIb: rare, occlusion of the digital arteries to index finger caused by vibration type IV: all level stenotic Type V: global ischemia, paucity of vessels, scant flow on angio
38
What is the technique for digital sympathectomy?
bruner Z-shaped incision stripp adventitia of common digital artery
39
How many neurone are in the motor sympathetic route?
3
40
Where is the thoracic sympathetic trunk located?
in the middle of the intercostal space either bottom edge of top rib or top edge of bottom rib
41
Name indications for cervicothoracic sympathectomy
essential hyperhidrosis ischemia of the hand CRPS Long QT syndrome Raynauds
42
What are surgical approaches to sympathectomy?
paravertebral transthoracic supraclavicular VATS (gold standard)
43
What is the target for CRPS vascular disease and raynauds?
stellate, G2 and G3
44
What are results of sympathectomy for raynauds?
50% dissatifaction 60% compensatory hyperhidrosis may no longer be recommended
45
What are results of sympathectomy for CRPS?
Success 85% needs to be done early
46
What are common complications to sympathectomy?
Compensatory sweating Segmental atelectasis Penumo Subcut emphysema
47
What are rare complications of sympathectomy?
Horners Hemo Effusion Injry to vagus, phrenic, scla, sclv
48
What are causes of failure of sympathectomy?
Incomplete denervation Regeneration Functional reorganization
49
What arête appears to be preferentially affected in secondary raynauds?
Ulnar
50
What is FMD?
Non-athersclerotic noninflamm angiopathy of unknown cause. Medium sized vessels
51
What are complication of carotid FMD and how many get comps?
10% Decreased lumen size Formation distal embolization of thrombus Dissection/rupture
52
What is the most common pathophys for cFMD?
medial fibroplasia 90%
53
What are most common concurrent lesion with cFMD?
ipsi bifurcation 20% extracranial CA anerusy. CA dissection vert artery FMD intracranial aneurysm/occlusive RA FMD
54
What are diagnostic methods?
duplex-may miss distal dz angio--best, string of beads CT-better then MRA MRA-signal dropout may appear to be beads
55
What are therapeutic challenges for cFMD?
Difficult to quantify severity of disease If concurrent lesion, difficult to determine which is causing symptoms If ipsi sympto and contra asympto, difficult to know what to do with contra side May have nonfocal symptoms due to global ischemia Intracranial aneurysms may alter surgical approach HTN from RA FMD may complicate sx on carotid FMD
56
What is conservative therapy for cFMD?
Antiplt Monitor q6 months Rule out involvement in other arterial beds Avoid chiro
57
What are invasive treatment strategies?
Open surgical dilatation Rigid dilators disrupt obstructive webs May need to ivied belly of digastric muscle Start with 1.5mm Back bleed Stroke 3% 10 year patency, stroke-free and survival all about 90% Dilatation mainstay of treatment Stenting Durability of PTA/stent unknown May need to use external to get sheath/balloon up Balloon should cover entire lesion and be slightly undersized to avoid dissection Stent only if needed
58
What is the classification of FMD?
intimal fibroplasia medial dysplasia medial fibrosis perimedial medial hyperplasia adventitial fibroplasia
59
What is the most common type of FMD?
medial
60
What are proposed cause of FMD?
May be hormonal factors Occlusion of vaso vasorum Long straight segs without branches are affected CA and RA also get a lot of motion damaging VV. Right renal longer so this may be why its affected more Smoking Familial EDS
61
What are most common patterns of involvement?
Uni Right Bilat renal Uni left Carotid/vert Multiple
62
How common a cause of HTN is r FMD
2nd most common cause
63
What is the natural hx of r FDM?
About 25% of asympto devel HTN within 4 years 40% angio progression decrease of renal funcition less frequent then with athererosclerotic
64
What are best tools for diagnosis?
DUS/CT/MRA are screening only because limited resolution for distal renal vessels angio for diagnosis
65
What are indication for interventions for rFMD?
renal to aortic P gradient of 0.9 change in kidney size of 1 cm refractory HTN impaired renal function size difference of \>1.5cm pressure gradient across stenosis of 10mmhg
66
What are indications for evaluation of secondary HTN?
\>3 anti-HTN sudden acceleration of CR or HTN increased CR with ACEi \<30 yo spontaneous hypoK unexplained pulm edema bruit
67
What are medical treatments for rFMD?
ASA, statins Anti-htn treatment \<140/90
68
What are surgical options for rFMD?
aortorenal bypass autotransplantation
69
When to consider autotransplantation in rFMD?
if reop failed endo multiseg single kidney with stenosis in several RA
70
What is Takayasu's?
immune arteritis causing inflammation of aorta, its major branches, and pulmonary arteries.
71
What are proposed aetiologies of Takayasu?
``` genetic (HLA-Bw52) immune mediated (cell and antibody) ```
72
What is histology of TA?
panarteritis (3 layers) with skip area excessive ground substance in intima
73
What are clinical features of TA?
claudication (UE\>LE) diminished pulses MSK symptoms constitutional symptoms H/A CVI symptoms' HTN common
74
What are findings on duplex?
thickened wall
75
Describe the1994 Tokyo international conference angiographic classification for TA?
Type I aortic arch branches alone type II ascending, arch, branches Type III ascending, arch branches and descending
76
Describe the1994 Tokyo international conference angiographic classification for TA?
Type I aortic arch branches alone type II ascending, arch, branches Type III ascending, arch branches and descending Type IV abdominal aorta and branches Type V entire aorta
77
What are features of active disease?
fever, myalgias elevated ESR vascular ischemia (claudication) typical angio features
78
What is medical treatment?
glucocorticoids first line treatment methotrexate, cyclophosphamide, azathioprine
79
What is invasive treatment strategies?
dont operate on active disease endo poor results bypass good patency
80
What are RF for TAO?
male smoking
81
What are features of the chronic phase of TAO?
organization of occlusive thrombus with recanalization perivascular fibrosis
82
What are features of the intermediate/subacute phase phase of TAO?
partial recanalizations disappearance of microabcess deposition of immunoglobulins
83
What are features of the acute phase of TAO?
panvasculitis of small and medium vessels occlusive, highly cellular arterial thrombus with microabcess
84
What are diagnostic criteria for TAO (shinoya criteria)?
smoking history/cocaine use onset before 50 infrapop occlusive disease upper limb involvement or phlebitis migranc absence of other atherosclerotic RF
85
What are angiographic features of TAO?
Segmental occlusive lesions more severe disease distally involvement of digital arteries, normal proximal arteries without evidence of atherosclerosis collateralization around areas of occlusion with corkscrew-shaped collaterals (Martorell’s sign, also described as “tree root” or “spider leg” collaterals)
86
What are angiographic features of TAO?
Segmental occlusive lesions more severe disease distally involvement of digital arteries, normal proximal arteries without evidence of atherosclerosis collateralization around areas of occlusion with corkscrew-shaped collaterals (Martorell’s sign, also described as “tree root” or “spider leg” collaterals)
87
What are life style changes for TAO?
smoking cessation exercise training foot care
88
What are medical treatments for TAO?
ABX and NSAIDS for superficial phlebitis CCB for vasospams regional sympathetic block statin cilostazol
89
What are medical treatments for TAO?
ABX and NSAIDS for superficial phlebitis CCB for vasospams regional sympathetic block statin cilostazol
90
What are therapeutic options for TAO?
PCA debride flaps amp

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