Chapter 138 - Thromboangiitis obliterans Flashcards
Thromboangiitis obliterans define
1) Buerger disease 2) von Winiwarter-Buerger syndrome 3) inflammatory affecting infrapopliteal and infrabrachial medium small arteries and veins 4) age < 50 5) smoking related 6) male > female (5-10x more in men) 7) middle east, asia, mediterranean, eastern europe
Treatment for Buerger disease
1) smoking cessation 2) iloprost 3) endothelin receptor antagonist 4) immunoadsorption 5) growth factors 6) gene and stem therapy 7) bone fenestration to mobilize bone marrow
First full description of thromboangiitis obliterans
Buerger 1924 - the circulatory disturbances of the extremities
Risk factors for Buerger disease
1) smoking 2) low SES 3) poor oral hygiene 4) nutritional deficit 5) fungal/viral infection 6) cold injury 7) sympathomimetic drug abuse 8) arsenic intoxication
Possible pathways of immune-mediated injury in thromboangiitis obliterans
1) active smoking (urinary cotinine) 2) increased cellular sensitivity to collagen type I, III, IV 3) circulating immune complex 4) TNFalpha, IL1beta, IL5, IL6, IL12, IL17, IL23 increase 5) reduced IL10 6) Increased HMGB1, MMP9, ICAM1
Autoantibodies associated with TAO
1) antiphospholipid syndrome 2) anticardiolipin 3) antineutrophil cytoplasmic antibodies (ANCA) (controversial) 4) anti-endothelial cell antibodies
Genes associated with TAO
1) England: HLA-A9 and HLA-B5 2) Israel: HLA-DR4 and low HLA-DRW6 3) India: HLA-DRB1*1501
Hypercoagulable states in TAO
controversial 1) lower levels of urokinase-plasminogen activator 2) lower levels of plasminogen activator inhibitor 1 3) elevated platelet contractile force
Associated infectious cause of TAO
1) Treponema denticola 2) porphyromonas gingivalis 3) actinobacillus actinomycetemcomitans
Pathogenesis of TAO
1) endothelial cell damage 2) activation of APC 3) cellular and humoral inflammation 4) thrombotic occlusion
Which layer is affected in TAO
restricted to intima = endarteritis
Differentiating TAO from atherosclerosis in histology
Internal elastic lamina and architecture of vascular wall preserved in TAO
Three stages of TAO
1) acute phase: inflammation of small-medium (1-5mm) artery/vein - occlusive - cellular arterial thrombus - polymorphonuclear cell infiltrate - leukocytoclasis - giant cells - microabscess - inflammation of entire vessel wall - neurovascular bundle 2) intermediate/subacute phase: organization of occlusive thrombus - disappearance of microabscesses - CD3 pan, CD4 T cells, CD20 panB cells against internal elastic lamina - CD68 macrophage and S100 dendritic cells in intima - IgG, IgM, IgA, complement 3d 4c on internal elastic lamina 3) Chronic phase/end-stage: thrombus organization and recanalization - prominent vascularization of media - perivascular fibrosis
Phlebitis saltans define
Migrating phlebitis in 40-65% of TAO patients
How often are venous involvements in TAO
60% mostly superficial, DVT unusual
Symptoms of TAO and rate
TABLE 138.2
Late signs of TAO
1) trophic nail changes 2) ischemic ulcerations 3) digital gangrene 4) superinfections 5) joint manifestations 6) splinter hemorrhages 7) psych conditions
TAO rate of 2, 3, 4 limb involvement
2 limb - 16% 3 limbs 41% 4 limbs 43%
TAO rate of UE vs LE involvement
LE only 75% UE only 5% both 20%
Distribution of TAO in LE named vessels
AT 41% PT 40% DP 21% peroneal 18% pop 18% digital 11% plantar 9%
Distribution of TAO in UE named vessels
Ulnar 11.5% digital 8% radial 7% palmar arch 4.5% brachial 0.8%
Shionoya 5 major criteria for TAO
No criteria is universally accepted 1) smoking history 2) onset < 50 years age 3) infrapopliteal arterial occlusive lesion 4) UE involvement or phlebitis migrans 5) absence of atherosclerotic risk factors (besides smoking)
Olin’s criteria on TAO
1) age < 45 2) recent smoking 3) distal extremity ischemia on imaging 4) exclusion of autoimmune, hypercoabulable, DM 5) exclusion of proximal emboli 6) consistent arteriographic findings
Martorell sign
snake or dot sign Monophasic waveform pattern within corkscrew shaped collaterals
ESR and CRP in TAO
normal or slightly elevated
Percentage of TAO with corkscrew collaterals
27%
Corkkscrew collaterals in other disease besides TAO
1) Scleroderma 2) CREST 3) SLE 4) rheumatoid vasculitis 5) antiphospholipid-antibody syndrome
CREST syndrome define
1) calcinosis 2) Raynaud phenomenon 3) esophageal disease 4) sclerodactyly 5) telangiectasia
Arteriographic findings in TAO
1) small and medium arteries 2) segmental occlusive lesion 3) more severe distally 4) tapering or abrupt cutoff with corkscrew 5) normal proximal artery
Types of corkscrew
Type 1: artery > 2mm, large hlical sign Type 2: 1.5-2mm, medium helical sign Type 3: 1-1.5 mm, small helical sign Type 4: <1 mm, tiny helical sign
TAO mean life expectancy
52.2 +/- 8.9 years
TAO risk of amputation any
25% 5 years 38% 10 years 46% 20 years
TAO risk of major amputation
11% at 5 years 21% at 10 years 23% at 20 years
TAO survival long term
97% 5 years 94.4% 10 years 92.4% 20 years 83.8% 25 years
Length of smoking cessation in TAO to eliminate risk of amputation
8 years
Regular exercise regimen for TAO
30 min 3-5x/week
Improvement in claudication in TAO with exercise
180% pain-free walking time 120% max walking time
Pharmacological treatment of TAO
1) calcium channel blocker - help vasospasm 2) iloprost - vasodilator and antiplatelet, antiproliferation, anti-chemotaxis 3) cilastazol (PDE3 inhibitor) 4) PDE5 inhibitor (sildenafil, tadalafil) - offlabel use 5) Bosentan - dual endothelin 1 receptor antagonist 6) thrombolytics 7) folate supplement 8) statins 9) analgesia no clear evidence
Nerve treatment of TAO
1) regional sympathetic blockade 2) spinal cord stimulation 3) lumbar/thoracic sympathectomy no clear evidence helps with neurogenic but not somatic
Surgical treatment of TAO
1) bypass 2) pedicled omental graft 3) distal venous arterialization 4) hyperbaric oxygen therapy
Immunoadsorption in TAO key points
1) selective removal of circulating immunoglobulin and antibodies 2) treat pain, improve walking distance and improve tissue perfusion
