Lu畉n vn Nghi棚n c畛u 畉c i畛m l但m sng, c畉n l但m sng v k畉t qu畉 ph畉u thu畉t thay van hai l叩 i畛u tr畛 b畛nh van hai l叩 c坦 tng 叩p l畛c 畛ng m畉ch ph畛i n畉ng.B畛nh van hai l叩 l b畛nh tim m畉c ph畉i th動畛ng g畉p 畛 c叩c n動畛c ang ph叩t tri畛n, trong 坦 c坦 Vi畛t Nam. Th動董ng t畛n trong b畛nh van hai l叩 c坦 th畛 l h畉p van hai l叩, h畛 van hai l叩 ho畉c h畉p h畛 van hai l叩 ph畛i h畛p. C坦 nhi畛u nguy棚n nh但n kh叩c nhau g但y b畛nh. V畛i nguy棚n nh但n do th畉p tim, th動董ng t畛n ch畛 y畉u l h畉p van hai l叩 ho畉c h畉p h畛 van hai l叩 ph畛i h畛p, 鱈t khi g但y h畛 van hai l叩 董n thu畉n. C叩c nguy棚n nh但n kh叩c g但y b畛nh van hai l叩 nh動 tho叩i h坦a, vi棚m n畛i t但m m畉c nhi畛m khu畉n, b畛nh m畉ch vnhch畛 y畉u g但y h畛 van hai l叩. Trong 坦 nguy棚n nh但n do th畉p v畉n l ph畛 bi畉n 畛 Vi畛t Nam.
6. BS TU畉N-Ph畉u thu畉t au than kinh toa.pdfPhcThnhTrn
油
integration processing, imparting effective and efficient
asymptomatic place-in-space homeostasis. However, various
peripheral and central pathologies disrupt this required func-
tional adjustment, often leading to persistent visually mediat-
ed vertiginous outputs including impaired correction and ad-
aptation to postural control perceptions of vection and OKS-
mediated ocular motor phases. This proximal impairment in
turn leads to the advancement of the distal outputs of large
postural sway patterns and symptoms of dizziness, vertigo, or
nausea. Peripheral abnormalities, especially involving the ves-
tibular end organ, may result in visual motion hypersensitivi-
ty; individuals become abnormally dependent upon the visual
system for posture and balance control, leading to an exces-
sive response to variations in visual field motions. Central
vestibular abnormalities also are associated with sensitivity
to OKS. Central origin of OKS-related hypersensitivity has
also been reported in those without a diagnosis of a central
disease. Pollak and colleagues reported 37.5% of patients
without neurological, psychiatric, cardiovascular, or pharma-
cological etiology of dizziness and OKS-related hypersensi-
tivity presented with scattered cortical hemispheric white mat-
ter abnormalities compared to 7% in controls without OKS-
related hypersensitivity (p = 0.009) [32]. A potential con-
founder in this study was an age-related increase in prevalence
of white matter lesions in the study population (31% for age
4049 vs 83% for age > 70), as 67% of the OKS-related hy-
persensitivity group was thought to have symptoms related to
a vascular cause [32]. Furthermore, it was theorized that a
global multifocal distribution of white matter abnormalities
was likely more predictive of OKS-related hypersensitivity
than the specific etiology of the white matter lesions them-
selves. However, these findings were not replicated in a recent
imaging trial comparing patients with OKS-related hypersen-
sitivity to healthy controls [33]. OKS-related hypersensitivity
is found in defined central disorders, especially when related
to conditions that cause multifocal brain dysfunction such as
traumatic brain injury [34, 35]. Wright and colleagues found
OKS-related symptoms were greater in patients with mild
traumatic brain injury compared to healthy controls (p =
0.020) [36≒]. Similar to MdDS, psychopathologies such as
depression and anxiety [37, 38] have been associated with
OKS-related hypersensitivity.
OKS-mediated hypersensitivity, also referred to as visual
vertigo (VV), is often confused with other ocular motor-
related symptoms including oscillopsia; differentiating the
two is crucial since their diagnosis and management are quite
distinct [39]. Oscillopsia is also an illusionary disorder; howev-
er, instead of the perception of vection (self-motion) experi-
enced for patients with VV, oscillopsia is the sense that the
visual field is in motion or unstable. The onset of o
6. BS TU畉N-Ph畉u thu畉t au than kinh toa.pdfPhcThnhTrn
油
integration processing, imparting effective and efficient
asymptomatic place-in-space homeostasis. However, various
peripheral and central pathologies disrupt this required func-
tional adjustment, often leading to persistent visually mediat-
ed vertiginous outputs including impaired correction and ad-
aptation to postural control perceptions of vection and OKS-
mediated ocular motor phases. This proximal impairment in
turn leads to the advancement of the distal outputs of large
postural sway patterns and symptoms of dizziness, vertigo, or
nausea. Peripheral abnormalities, especially involving the ves-
tibular end organ, may result in visual motion hypersensitivi-
ty; individuals become abnormally dependent upon the visual
system for posture and balance control, leading to an exces-
sive response to variations in visual field motions. Central
vestibular abnormalities also are associated with sensitivity
to OKS. Central origin of OKS-related hypersensitivity has
also been reported in those without a diagnosis of a central
disease. Pollak and colleagues reported 37.5% of patients
without neurological, psychiatric, cardiovascular, or pharma-
cological etiology of dizziness and OKS-related hypersensi-
tivity presented with scattered cortical hemispheric white mat-
ter abnormalities compared to 7% in controls without OKS-
related hypersensitivity (p = 0.009) [32]. A potential con-
founder in this study was an age-related increase in prevalence
of white matter lesions in the study population (31% for age
4049 vs 83% for age > 70), as 67% of the OKS-related hy-
persensitivity group was thought to have symptoms related to
a vascular cause [32]. Furthermore, it was theorized that a
global multifocal distribution of white matter abnormalities
was likely more predictive of OKS-related hypersensitivity
than the specific etiology of the white matter lesions them-
selves. However, these findings were not replicated in a recent
imaging trial comparing patients with OKS-related hypersen-
sitivity to healthy controls [33]. OKS-related hypersensitivity
is found in defined central disorders, especially when related
to conditions that cause multifocal brain dysfunction such as
traumatic brain injury [34, 35]. Wright and colleagues found
OKS-related symptoms were greater in patients with mild
traumatic brain injury compared to healthy controls (p =
0.020) [36≒]. Similar to MdDS, psychopathologies such as
depression and anxiety [37, 38] have been associated with
OKS-related hypersensitivity.
OKS-mediated hypersensitivity, also referred to as visual
vertigo (VV), is often confused with other ocular motor-
related symptoms including oscillopsia; differentiating the
two is crucial since their diagnosis and management are quite
distinct [39]. Oscillopsia is also an illusionary disorder; howev-
er, instead of the perception of vection (self-motion) experi-
enced for patients with VV, oscillopsia is the sense that the
visual field is in motion or unstable. The onset of o
10. Angiosome
Ph但n v湛ng c畉p m叩u (Angiosome): v湛ng m担
動畛c c畉p m叩u b畛i m畛t ngu畛n M nh畉t 畛nh
Taylor (1987): gi畛i thi畛u l畉n 畉u
Attinger (1997): b董m dung d畛ch m畉u x叩c
畛nh v湛ng c畉p m叩u
S畛 t動董ng quan gi畛a t畛n th動董ng 畛ng m畉ch
v畛i t畛n th動董ng m担 t動董ng 畛ng
10
Attinger C. Vascular anatomy of the foot and ankle. Oper Tech Plast Reconstr Surg 1997;4:183
11. Angiosome
Ton c董 th畛: 40
V湛ng c畛 - bn ch但n: 6
11
Taylor GI, Palmer JH. The vascular territories [angiosomes] of the body:
experimental study and clinical applications. Br J Plast Surg. 1987;40:113
12. Angiosome
T叩i th担ng m畉ch: Angiosome vs. Non Angiosome
12
Alexandrescu et al. J Endovasc Ther 2011;18:376
13. T叩i th担ng m畉ch: Angiosome vs. Non Angiosome
Angiosome
13
T叩c gi畉 Nm N Endpoint Tr畛c ti畉p Gi叩n ti畉p
Attinger et al 2006 56 T畛n th動董ng kh担ng li畛n 9% 38%
Iidia et all 2010 203 B畉o t畛n chi 86% 69%
Valera et all 2010 76 Li畛n v畉t lo辿t 92% 73%
Iidia et all 2012 369 B畉o t畛n chi (Rutherford III) 49% 29%
C叩c k畉t qu畉 nghi棚n c畛u cho th畉y t畛 l畛 thnh c担ng v畛 l但m sng (b畉o t畛n chi) t畛t h董n
r探 r畛t 畛 nh坦m ph畛c h畛i tu畉n hon tr畛c ti畉p 畉n t畛n th動董ng
19. Khi ti畉p c畉n trong l嘆ng / xu担i d嘆ng th畉t b畉i
POBA
19
20. POBA
634 b畛nh nh但n CLI (101 BTK only)
Tu畛i trung b狸nh: 65
Rutherford: 5-6
Chi畛u di t畛n th動董ng trung b狸nh: 21cm
Theo d探i 3 nm sau can thi畛p
20
European Society for Vascular Surgery 2008