PERIPHERAL VASCULAR MEDICINE 2014 -2015

Dr. Deduyo CARDIOLOGY

PERIPHERAL VASCULAR MEDICINE 35% - stable claudication
Definition 9% - chronic critical limb ischemia
a clinical disorder in which there is a stenosis or occlusion in 3% - acute limb ischemia
the aorta or arteries of the limbs
emboli or thrombus-> occlusion/stenotic -> blood flow is
compromised, pwedeng mag stuck sya,di nakapag flow ng
maayos ->results to manifestations of dec blood flow such
as ischemia -> claudications (leg pain)

Causes
Atherosclerosis patients >40 years old
Thromobosis
Embolus
Vascultits
Fibromuscular dysplasia Figure 1. PAD Statistics
Entrapment (Masmarami pa ang asymptomatic kaysa sa may
Cystic adventitial disease mga symptoms)
Trauma
Sixth and seventh decades of life The most common symptom is intermittent claudication
Patients with atheros of the coronary and defined as a pain, ache, cramp, numbness or a sense of
cerebral vasculature fatigue in the muscles; it occurs during exercise and is
relieved by rest
Increased risk of developing PAD in : o The site of claudication is distal to the location of
Cigarette smokers the occlusive lesion
DM Sumasakit ang legs on prolonged
Hypercholesterolemia walking tapos nawawala kapag
HPN nagpapahinga
Hyperhomocysteinemia o For example, buttocks, hip and thigh discomfort
occur in patients with aortoiliac dse, whereas calf
Pathology: claudication develops in px with femoral popliteal
Segmental lesions causing stenosis or occlusion dse.
are usually localized to large and medium sized Buttocks pain is least to be
vessels noticed,minsan akala UTI
Foot pain and leg pain are the MOST
The pathology of the lesion includes: COMMON MANIFESTATION in the
elderly, sometimes mistaken as arthritis
1. Atheros plaque with calcium deposition
2. Thinning of the media DIAGNOSIS
3. Patchy destruction of muscle and elastic fibers
4. Fragmentation of the internal elastic lamina I. HISTORY
5. Thrombi composed of platelets and fibrin Individuals with Asymptomatic PAD
Identified in order to offer therapeutic interventions
The primary sites of involvement: known to diminish their increased risk of MI, stroke and
death
1. Femoral and popliteal arteries (80-90% of px) A history of walking impairment, claudication and ischemic
2. The more distal vessels, including the tibial and peroneal arteries rest pain
(40-50% of px)
3. The abdominal aorta and iliac arteries (30% of symptomatic px) II. ROS

Atheros lesions occur preferentially: Recommended as a required component of a standard ROS for:
1. Adults >/ 50 yrs who have atheros R/F
1. Arterial branch points 2. Adults >/ 70 yrs
2. Sites of increased turbulence
3. Altered shear stress, and internal injury Key Components of the Vascular Review of Systems and Family
4. Involvement of the distal vasculature is most History
common I elderly individuals and px with DM 1. Any exertional limitation of the lower extremity
muscle or any hx of walking impairment
Manifestations of PAD o Claudication of this limitation:
Fatigue
53% - asymptomatic PAD Aching
o We need to identify this (since silent assassin ito) Numbness
o If patient has CAD+PAD -> worse prognosis Pain
o Patient has PAD+ CVD -> worse prognosis too

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PERIPHERAL VASCULAR MEDICINE 2014 -2015

Dr. Deduyo CARDIOLOGY

o Primary sites of discomfort Pag binaba, ok na ulit ang kulay ng paa,
Buttocks same color na
Thigh
Calf IV. LABORATORY
Foot
2. Any poor healing or nonhealing wounds of the legs or 1. Routine
feet a. CBC with platelets
3. Any pain at rest localized to the lower leg or foot and b. FBS
its assoc with the upright or recumbent position c. HBA1c levels
4. Postprandial abdominal pain that reproducibly is d. Renal fxn (BUN and creatinine)
provoked by eating and is assoc with weight loss e. Fasting lipid profile
5. Family hx of a first degree relative with an AAA f. UA (for microalbuminemia
g. 12 lead ECG
III. PE
V. HEMODYNAMIC NON-INVASIVE TESTING
Key components of the vascular PE a. Resting Ankle Brachial Index (ABI)
b. Exercise ABI
1. Measurement of BP in both arms and notation of any c. Segmental pressure exam
interim asymmetry d. Pulse volume recordings
2. Palpation of the carotid pulses and notation of the carotid
uprstroke and amplitude and presence of bruits 1. ANKLE BRACHIAL INDEX
3. Auscultation of the abdomen and flank for bruits
4. Palpation of the abdomen and notation for the presence of ***ABI =
aortic pulsation and its maximal diameter Lower extremity systolic pressure
5. Palpation of pulses at the brachial, radial, ulnar, femoral, Brachial artery systolic pressure
popliteal, dorsalis pedis and posterior tibial sites.
Performance of Allens test when knowledge of hand The ABI is 95% sensitive and 99% specific for PAD
perfusion is needed. Establishes the PAD dx
6. Auscultation of both femoral arteries for the presence of Identifies a pop at high risk of CV ischemic events
bruits Pop at risk can be clinically and epidemiologically defined:
7. Pulse intensity should be assessed and should be recorded o Exertional leg sx, non healing wounds, age >70
numerically as follows: years, age >50 years with hx of smoking and DM
o 0 - absent Toe brachial index (TBI) useful in individuals with non
o 1 diminished compressible pedal pulses
o 2 normal
o 3 bounding ABI Classification System (this is the new classification) Only used
8. The shoes and socks should be removed, the feet inspected, for prognosticating and staging of PAD:
the color, temp and integrity of the skin and intertriginous >1.4 incompressible
areas evaluated, and the presence of ulcerations recorded o Di na accurate ang ABI,present in DM and old age
9. Additional findings suggestive of severe PAD should o Calcified arteries present, abnormal vessel
be sought and recorded. This includes: o Get other important modalities
a. Distal hair loss 1.0-1.4 normal
b. Trophic skin changes 0.91 0.99 equivocal/borderline
c. Hypertrophic nails o Do an exercise ABI to unmask the PAD
0.70 0.90 mild to mod
MANIFESTATIONS OF SEVERE PAD 0.40 0.69 - mod to severe
<0.40 severe -> requires amputation (ito yung isasagot
Acute limb ischemia natin sa part ng management pag binigyan tayo ng case
Pain tapos ganito na ang ABI nya,so goodbye legs/paa )
Pallor
Pulselessness ** ABI alone can diagnose the patient. Get BP of the brachial artery of
Paresthesia both right and left and the BP of dorsalis pedis or posterior tibial
Paralysis artery r and l. Get the higher of both upper and lower ex and divide.
Polar Example: BP in upper ex R-130, L-120
Chronic limb ischemia Bp lower ex R-120 L-130
Sustained- severe decrease in blood flow in the legs which
if untreated would lead to pain even at rest, ulceration and ABI= 130/130 -> (1)
incipient limb loss ABI of 1 falls under the normal range
At elevation dependency test (like a straight leg test):
o Elevation- pallor results 2. EXERCISE ABI
Pag tinaas,asymmetric ang kulay ng paa Confirms the risk for PAD
o Dependent- rubor Done to unmask the PAD that is normal at rest pero after
exercise lumalabas

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Dr. Deduyo CARDIOLOGY

Assess the final severity of classification PROGNOSIS
Fall ABI after exercise
1/3 of patients with PAD have CAD
Over of CAD cases are confirmed by arteriography
Patients with PAD have 15-30% mortality rate in 5 years and
2-6x increase if present CAD
Mortality is highest in severe PAD
The likelihood of symptomatic progression of PAD appears
less than succumbing CAD (it only means mas ikinamamatay
talaga ang CAD kesa sa PAD)
Approx 70-80% of non DM patients with mild or moderate
claudications remain stable
25-30% of patients with critical limb ischemia will go
amputation within 1 year
Prognosis is worse if patient is SMOKING and those with DM

Figure 2. Natural History of PAD

3. HAND DOPPLER (not in the slide pero demonstrated by doc in

class, si Linuel yung subject.Remember? )
Easiest way to assess PAD
Normal arterial sound- rifling sound, TRIPHASIC
Flat sound- SUGGESTIVE of PAD

4. ARTERIAL DUPLEX SCAN

Detects areas of stenosis and blood flow
Normal: triphasic
Abnormal: absence of downward shift
Can visualize stenotic vessels

Figure 4. PAD Screening and algorithm

TREATMENT
Patient with PAD should receive therapies to
o Reduce the risk of associated CV events such as
MI and death
o Improve limb symptoms
o Prevent progression to critical limb ischemia
o Preserve limb viability
Risk factor modification and antiplatelet therapy should
be initiated to improve CV outcomes
BP control (ACE-I, B-blockers)
Treatment of hypercholesterolemia (statins, recommends
tx to reduce LDL, cholesterol to <100mg/dl )
Platelet inhibitors
o Aspirin sse: bleeding ->so do not give to px with
PUD. If given in px with PUD, give PPI muna then
aspirin
o Clodipogrel- proven MORE effective than aspirin
o Insufficient evidence if dual therapy (aspirin +
clodipogrel) is effective
Figure 3. Arterial duplex scan imaging and arteriography o Warfarin is NOT given because it does not
In the second picture, kita dito yung part na may stenosis and after improve outcome in patients with PAD
the part with stenosis, turbulent na yung blood flow. o Voraxapar
New drug
Dec limb ischemia but increases risk of
bleeding -> so it is not given in px with
bleeding disorders

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Dr. Deduyo
Glycemic Control in DM patients
A. Diabetes control and complications trial
o Aggressive glycemic control resulted to dec
progression of carotid IMT
B. UKPDS subgroup study
o Reductaion in HBA1c by 7% resulted in 18%
reduction in MI, 15% reduction in stroke and
4.2% reduction in PAD
* lower HBA1C <6.5 -> leads to hypoglycaemia
Diabetes Treatment in PAD
o Intensive glycemic control
o HbA1c <7.0%
o No clear benefit on limb events
BP Control
1. ACE Inhibitor
Hope: Ramipril significantly reduced the rates of
death, MI and styroke in px at high risk for CV
events independent of antihypertensive impact
2. Beta blockers
Do not aversely affect the walking capacity of
intermittent claudication with mild to mod PAD
Supportive measures
1. Meticulous care of the feet, which should be kept
clean and protected against excessive drying, apply
moisturizing creams.
2. Well fitting and protective shoes are advised to
reduce trauma
3. Elastic support hose should be avoided as they reduce
BF to the skin
4. Supervised exercise training programs for 30-45 mins
session, 3 to 5 times per week atleast 12 weeks,
prolong walking distance
5. Drugs such as:
a. Alpha adrenergic antagonist
b. CA channel blockers
c. Papaverine and other vasodilators : effective
in px with PAD
d.
Cilostazol: a phosphodiesterase inhibitor with vasodilator and
antiplatelet properties, increases claudication distance by 40-60% and
improves measures of quality of life
Pentoxifylline: a substituted xanthine derivative, has been reported
to decrease blood viscosity and to increase red cell flexibility, thereby
increasing blood flow to the microcirculation and enhancing tissue
oxygenation
Statins and propionyl-L-carnitine: a drug that affects skeletal muscle
metabolic fxn, appear promising for tx of intermittent claudication in
initial clinical trial
** cilostazol + aspirin + clodipogrel -> can improve quality of walking
SE: headache, fluid retention
If patient has CAD, give nitrates to relieve HEADACHES
If patient has CHF, do not give nitrates,give a diuretic first
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CARDIOLOGY
Emerging therapies
o Naftidrofuryl
o Proprionyl levocarnitine
o L-arginine
o Prostaglandins
o Gene induced angiogenesis
** Stem cell study conducted in India -> improves claudication but
does not decrease size of stenosis, just open up small collaterals, not
the bigger vessels
Newer modalities
o Long term parenteral administration of
vasodilating prostaglandins decreases pain and
facilitates healing of ulcer in px with chronic limb
ischemia
o Intramuscular transfer of DNA encoding
endothelial GF, FGF, Hepatocyte GF or hypoxia
inducible factor 1 and also admin of endothelial
progenitor cells, may promote collateral BV
growth in px with critical limb ischemia
Revascularization
o Catheter based surgical interventions are usually
indicated for px with disabling, progressive or
severe sx of intermittent claudication despite
medical therapy and for those with critical limb
ischemia
o Nonoperative interventions include PTCA, stent
placement and atherectomy
o PTA and stenting of iliac artery are associated
with with higher success rates that PTA and
stenting of femoral arteries
o 90-95% of iliac PTA are initially successful in the 3
yr patency rate is >75%
o Patency rates may be higher if placed in the iliac
artery. The initial success rates for femoral-
popliteal PTA and stenting are approx 80%, with
60% 3 yr patency rate
o Patency rates are influenced by pretreatment
stenoses, the prognosis of occlusive lesions is
worse that nonocclusive lesions
o The role of drug eluting stents in PAD is helpful
o Operative procedures for aortoiliac dse are the ff
Aortobifemoral bypass
Axillofemoral bypass
Femoral-femoral bypass
Aortoilac endarterectomy
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PERIPHERAL VASCULAR MEDICINE 2014 -2015

Dr. Deduyo CARDIOLOGY

*** PTA has higher success rates if artery is bigger.It is not Thrombosis
useful if we are going to target small vessels o No obvious cardiac source
Surgery is better option for small arteries o History of claudication
*** stents are used (metal) are used above the knee level o Abnormal pulses in the contralateral limb
Cotton stents are used if below the knee.If very small o Angiography: diffuse atherosclerosis with well
vessels, use the balloon developed collaterals

PROGNOSIS
ACUTE LIMB ISCHEMIA Amputation rate: 6-20%
6% if revascularized within 12 hours
Acute limb ischemia 12% if revascularized within 12-24 hours
Results from sudden cessation of blood flow to the 20% if revascularized after 24 hours
extremity. The severity of the ischemia and the viability of Mortality rate: 6-12%
the extremity depend on the location and the extent of
occlusion and the presence and subsequent development of HISTORY
collateral BV
2 principal causes of occlusion: History of claudication
o embolism thrombus in situ History of heart disease
from proximal sites of atherosclerosis Interventions for poor circulation
and aneurysm of the aorta and large Has other cardiovascular risk factors
vessels
arterial emboli tend to lodge at DIAGNOSIS
bifurcations ** ABI is not of use anymore
most frequently lodge in the femoral
artery, followed by the iliac artery, aorta 1. Physical examination
and popliteal and tibioperoneal arteries
o thrombus
entered the systemic circulation via a
patent foramen ovale or other septal
defect

INCIDENCE
Scanty information available
Estimate at 140 per 100,00
Decreased ALI incidence secondary embolism
Increase incidence of thrombotic acute limb ischemia

ETIOLOGY
Etiology of Arterial Occlusion

Thrombotic vs Embolic
o Embolic Sources
Cardiac- 75 %
Atrial Fibrillation- 51%
Acute Mi- 24%
o Non-Cardiac- 10%
Atheromathous Debris 5%
Aneurysmal 5%
Post CV Surgery 7%
2. Electrocardiogram
3.Standard chemistry
Emboli impact at branching points in arterial tree
4.Complete blood count
Femoral Artery 45%
5.Prothrombin time
Aorta and Iliac Artery -26%
6.Partial thromboplastin time
Poplitial Artery 15%
7.Creatinine phosphokinase level
Tibial Artery -1%
Hypercoagulable state will need additional studies
Clinical differentiation between thrombosis and embolism
Anticardiolipin antibodies
Embolism
Homocysteine concentration
o Obvious cardiac source
Antibody to platelet factor IV
o No history of claudication
o Normal pulses in the contralateral limb
o Angiography: may have minimal atherosclerosis
with few collateral noted

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Dr. Deduyo CARDIOLOGY

Arterial Doppler signals assess level of obstruction and severity of 1. Unfractionated heparin
ischemia
Pedal signals allow time for conventional arteriography and Intravenous heparin at full anticoagulant dosage should be
proper patient preparation given as soon as the diagnosis of acute limb ischemia has
ABI is not of value in acute ischemia been made,provided that heparin is not contraindicated
If it can be measured, the limb is not threatened Conventional Anticoagulation
o Unfractionated adjusted dose
IMAGING STUDIES o IV or subcutaneous Heparin
o Target PTT: 1.5 x control
1. Arteriography o Dosing: Bolus 80-100u/kg
Localize obstruction, visualize distal arterial tree o Drip 15-20 u/kg/h (Rashke Protocol)
Assists in distinguishing patients who will benefit more from o If HIT is present,do not give heparin
percutaneous treatment than from embolectomy or open 2. Analgesia- tramadol, morphine
revascularization procedures 3. Keep foot dependent
Patients with high clinical probability of embolic ischemia 4.Avoid heel pressure
DO NOT need angiography 5.Avoid extreme temperatures- no aircon muna
2. Computed topographic angiography (CTA) 6.Maximum tissue oxygenation
3. Magnetic resonance angiography (MRA) 7.Correct Hypotension- not to sacrifice peripheral veins, give
Diagnose and delineate disease extent inotropics
Advantage of speed, convenience, ability for cross-sectional 8. Treat other co-morbid conditions
imaging of vessel

TREATMENT
** identify first the level of acute ischemia because treatment is
based on the level of the dse

Figure 5. Algorithm of treatment for px with ALI.

Factors for consideration in choosing intervention for acute

limb ischemia

Choice as to which intervention should be used for

acute limb ischemia should be based on
o Location and anatomy of lesion
o Duration of acute limb ischemia
o Type of clot
o Patient-related risks
o Surgery-related risks
o Contraindications to thrombolysis

Pharmacologic thrombolysis

Treatment of choice if degree of severity allows time

i.e. severity levels I and IIa
Recent advances in endovascular devices and
techniques allow rapid clot removal
Permit treatment of more advanced degree of
** measure then the level of bleeding before giving drugs. After
ischemia
giving the drug measure the PTT. Once drug is given, measure PTT
Thrombolytic therapy reduces risk of endothelial
every 6 hours and it should reach >1.5
trauma & clot lysis in branch vessels too small for

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Dr. Deduyo
embolectomy balloons
Systemic thrombolysis has no role in the treatment of
patients with ALI
Absolute Contraindications to pharmacologic thrombolysis
o Established cerebrovascular event (excluding TIA
within previous 2 months)
o Active bleeding diathesis
o Recent gastrointestinal bleeding (within previous
10 days)
o Neurosurgery (intracranial, spinal) within previous
3 months
o Intracranial trauma within previous 3 months
Catheter-directed thrombolysis
Intra-arterial medications: Urokinase, tPA, alteplase,
reteplas Injection technique variable
o Lacing
o Pulse-spray dosing
o Low continuous dose
o May need 4-24 hrs of thrombolytics
o Intracranial hemorrhage rate: 1-2%
Thrombolysis after arteriography in acute limb ischemia
If the decision is made to proceed with thrombolysis
afterarteriography, the intrathrombus infusion method
should be used
o Percutaneouos aspiration thrombolectomy (PAT)
and percutaneous mechanical thrombolectomy
(PMT)
PMT is the one to use if the thrombus is
organized and if thrombus cannot be
aspirated anymore
o Alternative non-surgical modalities for ALI
o Combination with pharmacologic thrombolysis
may substantially speed up clot lysis
Important in more advanced ALI where
time to revascularization is critical
Percutaneous aspiration thrombectomy (PAT)
Uses thin-wall, large lumen catheters and suction with a
50-ml syringe to remove embolus or thrombus from native
arteries, bypass grafts and run-off vessels
Adjunct to thrombolysis in acute arterial occlusion or can
be used as salvage therapy to remove distal emboli
Percutaneous aspiration thrombectomy as rapid and
effective way of removing thrombus in thromboembolic
occlusions of the limb arteries below the inguinal ligament
and can be a very good alternative to surgery in selected
patients.
Percutaneous mechanical thrombectomy (PMT)
Hydrodynamic recirculation
Efficiency depends mainly on age of thrombus
Fresh thrombus responds better than older organized clot
Small Clinical series have demonstrated short term (30
day) salvage of 80-90%
Only Angiojet MTD approved for peripheral arterial use
Percutaneous mechanical thrombectomy (PMT) with thrombolysis
Reduce thrombus burden
Reduce length of time and total dose of thrombolytic
therapy
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CARDIOLOGY
Decrease hemorrhagic complications and improve
outcome
Complications
o Hemolysis
o Possible renal failure secondary to release of
free haemoglobin
Surgery
For profoundly ischemic limb ( class IIb)
For profound sensory and motor deficits of very short
duration
o Revascularization completed within a few hours
after onset of severe symptoms may produce
remarkable recovery
Previously, urgency of treatment made surgery the treatment of
choice in many cases
In suprainguinal occlusion (no femoral pulse), open surgery
may be the preferred choice of treatment
o E.g. large embolus in common proximal iliac
artery or distal aorta may most effectively be
treated with catheter embolectomy
Suprainguinal graft occlusion may best be treated with
surgery
Done if involved limb has no underlying atherosclerosis
Intraoperative assessment of adequacy of clot removal
require
o completion angiography
o Ultrasound-based methods
Distal clot may be treated by intraoperative thrombolysis
with instillation of high doses of thrombolytic agents for a
brief period followed by irrigation or additional passages of
balloon catheter
Repeat angiography followed by clinical & Doppler
examination should be performed on the operating table
Limits of thromboembolectomy
Leaves residual thrombus (35-85%)
Cannot clear branch vessel occlusion
Causes endothelial injury
Unless there is good evidence that adequate
circulation has been restored, intraoperative
angiography should be performed to identify any
residual occlusion or critical arterial lesions requiring
further treatment
Studies regarding surgery as treatment (additional readings)
1. Rochester Series
Prospective, randomized, single-center study with 114
patients
Intra-arterial urokinase versus surgical revascularization
Results:
o Outcome @12 months:
o Lower 1-year amputation rate with thrombolytics
(16%) versus surgery (42%)
Conclusion: Especially in medically compromised group, ALI
of <7 days duration should receive thrombolytics
Ouriel K, Shortell CK, DeWeede JA et al J Vasc Surg 1994
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Dr. Deduyo
2. Surgery or Thrombolysis for the Ischemic Lower Extremity (STILE)
Prospective, randomized, multi-center study with 393
patients
Intra-arterial thrombolytics (r-TPA, urokinase) versus
surgical revascularization
Limb ischemia patients with symptom duration <6months
(mean duration was 6 weeks) not necessarily acute limb
ischemia
Death and amputation rates similar in both groups
3. SURGERY OR THROMBOLYSIS FOR THE ISCHEMIC LOWER
EXTREMITY
SUBGROUP ANALYSIS:
o Native artery vs. Graft occlusion
o 10% amputation rate in native artery treated with
lysis vs. 0% treated with surgery (p=0.0024)
o Amputation rate lower in graft occlusions treated
with lysis vs. Surgery (p=0.026)
CONCLUSION
o Lysis more beneficial in acute graft occlusion < 14
days
o Symptoms < 14 days duration: thrombolytics
yielded lower amputation rate at 1 year
o Symptoms > 14 days duration: thrombolytics
yielded no difference in amputation rate but had
higher recurrent ischemia rate at 1 year
o If symptom duration <14 days: Thrombolytics,
otherwise surgery
o If bypass graft occlusion: Thrombolysis,
especially if symptom duration <14 days
4. THROMBOLYSIS or PERIPHERAL ARTERIAL SURGERY ( TOPAS )
Similar amputation- free survival rate at 1 year:
thrombolysis (65%) vs. Surgery (70%)
Half of thromboytic patients averted need for open
revascularization procedure
Rate of intracranial hemorrhage with thrombolytics in first
62 patients= 4.8%
Subsequent intracranial hemorrhage rate with
thrombolytics (without heparin)= 1.6%
5. COMPARISON OF CATHETER-DIRECTED THROMBOLYSIS AND
SURGICAL REVASCULARIZATION IN TREATMENT OF LIMB ISCHEMIA
All studies proved that surgery is superior to CDT.
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CARDIOLOGY
** amputation is done if there is increased bleeding in use of
anticoagulants. This could be done in stage I and II if there is
anticoagulant failure
COMPARTMENT SYNDROME
Increased pressure within a limited space compromise the
circulation and function of the tissues within that space -
Mates, 1980
First described by Malgaigne
First medical reference by Volkmann, 1881
Compartment pressures can be measured
o Pressures of greater or equal to 20mmHg are
clear indication for fasciotomy
PATHOPHYSIOLOGY
Extremity reperfusion ->Increased capillary permeability ->Local
edema -> Compartment hypertension -> Regional venule obstruction
-> Nerve dysfunction ->Capillary and arteriolar obstruction -> Muscle
and nerve infarction
CLINICAL PRESENTATION
Pain out of proportion to physical signs
Paresthesia
Edema
TREATMENT
Treatment of choice
four-compartment fasciotomy
BUERGERS DISEASE
Thromboangiitis Obliterans (Buergers Disease)
A vasculopathy involving distal arteries and veins of both
upper and lower extremities with a distinctive thrombus at
sites of vessel wall inflammation in its acute face
nd th
A disease of 2 thru 4 decades seen predominantly in
men
Tobacco use is universally associated with the active phase
but the exact etiologic mechanisms are not defined
It causes clauditication and a significant incidence Of digit
and limb loss in the young (nagkakatanggalan ang digits)
PATHOGENESIS
Definitive etiology is unknown
Occurs in active smokers and cessation of smoking brings
remission
Genetic predisposition and immunologic mechanisms were
implicated
HLA typing done and patterns vary with ethnic population
Autoimmune disease remains the most plausible cause:
o Cytokine production altered production of IL-6,
IL-12, IL-10, the increased apoptosis, and elevated
levels of circulating immune complexes could be
the reason for persisting immune inflammation
o Anticardiolipin autoantibodies- seen in some
patients with Buergers disease
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PERIPHERAL VASCULAR MEDICINE
Dr. Deduyo
o Plasma Endothelin 1- plays a role in exacerbation
of clinical symptoms nd endothelial injury is
connected with increase in concentration of
selecting P in patients serum
o T cell mediated inflammation was a significant
event in the development of Buergers disease
Gross features of TAO in amputated limbs
focal, segmental, and sometimes long thrombotic
occlusions of arteries and adjacent vein, involvement of
digital arteries, presence of normal vessels proximally, and
absence of atheroscierosis
Acute phase/lesion
Considered diagnostic
artery or vein is modestly swollen
moderate infiltration of adventitia and media
lumen is occluded by a highly cellular, unique thrombus
with microabscesses
lymphocytes and occasionally giant cells and eosinophils
Subacute phase/lesion
less cellularity and thrombus
disappearance of microabscesses
recanalization has begun
Late Phase
organized and recanalized thrombus in fibrotic, small
vessels
intact architecture of vessel wall, internal elastic membrane
no necrosis seen
TAO in chronic stage
Theres marked increase in elastic lamina and near total
occlusion of the lumen by fibrotic, partly recanalized
thrombus with mixed inflammatory cell infiltrates
CLINICAL ASPECTS
Diagnosis should be considered in all tobacco users (male
and female) presenting with:
o digital ischemia of feet or hands
o distal claudication
o migratory superficial thrombophlebitis or
o Raynauds phenomenon
Angiography and biopsy, when feasible, used for
confirmation or clarification
Bilateral involvement is usual, involving 3 or 4 limbs; begins
distally and progresses cephalad.
Interval from onset o tissue loss is only 2-5 years; foot
claudication, upper extremity involvement, superficial
phlebitis, and Raynauds phenomenon are common but rare
in atherosclerotic diseases of the limb
Onset is between 19 and 45 years of age (median = 30-
35years)
Initial presentation:
cold sensitivity, dysesthesias, coolness and rubor or
cyanosis of food (33%)
rest pain (10-80%)
digital ulceration or gangrene (18-60%)
pedal claudication (15-25%)
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CARDIOLOGY
LABORATORY
Laboratory Tests Exclude:
risk factor of hyperlipidemia and DM
collagen vascular disease test for ANA, complement, ESR,
VDRL
clotting disorders and dysproteinemias
serum electrophoresis, CBC platelet count
hypercoagulable state antiphospholipid antibody, protein
C and S, antithrombin lll, etc.
Vascular Lab:
Digital artery pressures and waveforms Segmental
Doppler pressure and waveforms of the limbs
Arterial duplex ultrasound
Laser flow velocities; assess occlusive disease of thefingers
and potential response to sympathetic block
Thallium-202 scan-determine healing potential of distal
ischemia
TREATMENT
Cornerstone of tx total abstinence from tobacco use halt
the progress & prevent recrudescence
Adequate pain control dysesthesia & minor lesions (OPD
Tx) but with rest pain, ulceration, or infection warrant
hospitalization
o continuous IV narcotics or epidural anesthesia
o periodic debridement of wound
Anticoagulation during acute phase due to thrombus
formation.
Antiplatelet agents chronic cases(?)
Prostaglandins provide dual benefits of vasodilation and
antiplatelet activity.
Vasodilators (ca channel and aadrenergic blockers)
greatest on vasomotor changers; efficacy on ischemic pain
and wound healing?
Pulse-therapy with glucocortucoids and cyclophosphamide
- anti-inflammatory effect (decrease BVAS, ESR, CRPV and
lowers frequency of amputations)
RAYNAULDS PHENOMENON
Raynauds phenomenon is characterized by episodic
digital ischemia, manifested clinically by the sequential
development of digital blanching, cyanosis, and rubor
of the fingers or toes following cold exposure and
subsequent rewarming.
Emotional stress may also precipitate Raynauds
phenomenon
The color changes are usually well demarcated and
confined to fingers and toes
o when patient is exosed to a cold env or touch
cold obj.
o The blanching, pallor represents ischemic
phase of the phenomenon and results from
vasospasm of digital arteries.
paresthesia of digits often accompanies the phases of pallor
and cyanosis
With rewarming, the digital vasospasm resolves, and blood
flow into the dilated arterioles and capillaries increases
dramatically.
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In addition to rubor and warmth, patients often experience
a throbbing, painful sensation during the hyperemic phase
PRIMARY RAYNUADS DISEASE
Vasospastic disease reversible, localized or diffuse
vasoconstriction of arteries or smaller blood vessels; may
cause irreversible damage in prolonged attacks.
Idiopathic or primary type unknown cause; usually benign
with little permanent ischemic damage
Prevalence
General population: 3.7 30%
Higher prevalence in cooler climates
PATHOLOGY
Mild disease: normal digital arteries
Severe disease: intimal hyperplasia, narrowing or total
occlusion of digital arteries, or presence of thrombi;
inflammatory destruction of the capillary bed or fibrinoid
degeneration of capillaries and abnormalities in basement
membrane
Pathophysiology
Normal subjects:
o Digital blood flow is controlled by sympathetic
nervous system
Decreased by activation of SNS
increased by withdrawal of SNS activity
o Reflex sympathetic digital vasoconstriction results
from body coolng or application of cold to other
body parts
o AV anastomoses shunts allow large food flow to
the digits in warm conditions but close during cold
exposure.
Raynauds disease:
Decreased finger blood flow or vasospastic attack is
unknown
2 classic theories:
o Local fault (abnornmality at the level of digital
artery)
o Overactivity of the SNS
DIAGNOSIS
Criteria to Distinguish Primary from Secondary Type:
1.) Vasospastic attack precipitated by exposure to cold or emotional
stimuli
2.) Bilateral involvement of the extremities
3.) Absence of gangrene, or if present, limited to the skin of fingertips
4.) No evidence of underlying disease
5.) A history of symptoms for the last 2 years
Diagnostic Modalities to Distinguish Primary from Secondary Type:
1.) Hand perfusion scintigraphy with 99Tc-DTPAObjectively reflects
global and regional microcirculatory abnormalities in the hand and
provides quantitavie data for follow up.
2.) Nailfold capillaries visualized using microscope opthalmoscope
o Normal pattern in primary Rd
o Decrease number of capillaries that are enlarge
and deformed with avascular areas in the
scleroderma, mixed CT disease, dermatomyositis
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TREATMENT
TREATMENT
1.) Conservative Therapy
Keep fingers warm (mittens better than gloves)
Avoid pressure or exposure to cold
Avoid smoking
2.) Drug Therapy
Calcium Channel Blockers; several small RCTs of CCBs for
primary RD showed clinical improvement in frequency and
severity of attacks.
Reserpine and guanethedine interfere with sympathetic
vasoconstriction and shown to increase digital capillary
blood flow (no RCT)
Prazocin (Alpha1-Adreneceptor Antagonist) shown to
decrease frequency, duration or severity of vasospasm
NTG (direct acting vasodilator) is used as transdermal paste
but with variable results Prostaglandins induce vasodilation
and inhibit platelet aggregation but with variable results
Thyroid preparation decrease frequency, duration and
severity vasospasm but caused increase BP and PR.
3.) Sympathectomy
sympathectomy of upper extremity may benefit 50-60% of
patients but vasospastic attacks often recur within 6
months to 2 years
More success with digital sympathectomy in severe disease
Lumbar sympathectomy for RD in the toes have >80%
success rate
CHRONIC VENOUS DISEASE
Normal Venous Anatomy and Function
Functions as a reservoir to store blood and as a conduit
to return blood to the heart
Carries blood from the legs up to the heart
Proper functioning depends on a series of valves and
muscle pumps
Blood that enters into the lower extremity venous
system must travel against gravity and against
fluctuating thoracoabdominal pressures to return to
the central circulation in a person in an erect position
Peripheral Venous System
Superficial Venous System
Deep Venous System
Perforator Veins
Perforator Veins
Connects the superficial venous to the deep venous
system
Located in the thigh and legs
Contain one- way valves that prevent reflux of blood
from the deep veins into the superficial system
Bicuspid Valves (venous valve)
Located throughout the deep and superficial veins and
ensure that:
Blood moves in the cephalad direction
Prevent the return of blood toward the feet
while in the upright posture
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Dr. Deduyo CARDIOLOGY

Frequency increases from proximal to the
distal leg to prevent an increase in pressure
within the distal veins resulting from the
effects of gravity
The venous pressure is neutral while lying down,
increases by 50% while sitting down, it increases by
100% while standing up.
Professions that entail prolonged standing will
eventually have venous insufficiency.
White blood cell trapping in the capillaries or
postcapillary venules
Adhesion of WBCs with activation releases
inflammatory mediators and proteolytic
enzymes with endothelial damage that may
increase permeability or impede flow leading
to occlusion
Classify your patients from C0 to C6

A Damaged Vein
If heredity, an injury, or a blood clot weakens a vein,
the wall near the valve begins to sag. The valve may no
longer close fully, allowing blood to move in both
directions when the muscle relaxes.
Most vein problems begin with damaged veins
Dapat kasi, your bicuspid valve, meron syang
preferential flow going up. When this valve weakens, it
leads to a bidirectional flow due to gravity.

Two components that determine venous pressure

Hydrostatic Component
Related to the weight of the column of blood
from the right atrium to the foot
Hydro dynamic Component
Related to pressures generated by
contractions of the skeletal muscles of the
leg and the pressure in the capillary network
Yung calf pump? on the normal limb. So yung calf
pump mo, nagsstop pag umuupo ka, when you walk, it C0 no venous disease)
leads to a good circulation kaya narerelieve ka while But at this level, meron ka ng symptom leg
walking. heaviness (first manifestation)
In PAD, meron kang claudication, magkakaroon ka ng C1 you develop telangiectasia and reticular veins, better
symptoms when walking. lookat your legs, kungmeron ka ng makikitang bluish
Sa venous disease, baliktad, you have the symptoms discoloration at maliliit na veinscalf mo
while lying still(pagnakaupo or nakatayo ka) when you C2 pag malaki na ung blood vessel mo, varicose veins na
walk, the leg heaviness will be relieved. Ang tawag sya.
dun, reverse claudication C3 pag meron ka ng varicose + telangiectasia + edema
C4 skin changes/discoloration sa foot and distal legs
Venous pathology ascribed to be venous disease
Develops when venous pressure is increased and C5 healed ulcer
return of blood is impaired C6 active ulcer
Mechanism
Valvular incompetence (deep, superficial, perforator) Risk Factors
Venous obstruction ( previous DVT, venous stenosis, Age
May-Thumer syndrome) Gender
Combination of both Occupation(prolonged standing)
Macrocirculatory hemodynamic disturbance Sedentary Lifestyle
Exacerbated by muscle pump dysfunction Long Flights or automobile journeys (more than3 hours)
Venous microangiopathy Sports that increase intra-abdominal pressure(weightlifting
and wresling)
VENOUS MICROANGIOGRAPHY Tight clothig(skinny jeans)
Mechanisms: High heels(the higher the heels the higher the chance)
Fibrin cuff formation Pregnancy
Accumulation of fluid containing fibrin into Immobility
the pericapillary space Heredity
Increase diffusion barrier, inhibit repair Obesity
process
Maintain the inflammatory process Symptoms
Growth factor trapping by fibrin and other Cramping
macromolecules, making them unavailable to facilitate Burning pain
healing Heaviness

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Fatigue Reticular Veins
Itching Dilated bluish subdermal veins usually
Tension from 1mm to < 3mm in diameter
Throbbing pain Generally tortuous
Restless legs Excludes normal visible veins in people
Tingling with transparent skin
Prevalence: about 50% (male
Signs andfemale)
Dermatitis C2
Hemorrhage Varicose veins
Superficial Thrombophlebitis Subcutaneous dilated veins > or equal to 3mm in
Ulceration diameter in the upright position
Usually tortuous
Lipodermatosclerosis
Prevalence: 10-15% of total population of which
Atrophic blanche
67% have symptoms
C3
Other causes:
Edema
Acute venous problems such as DVT
Perceptible increase in volume of fluid in the skin
Systemic causes of edema such as:
and subcutaneous tissue characterized by
Heart failure
indentation with pressure
Nephrosis
Usually occur in the ankle region, but may extend
Liver Disease
to the leg and foot
Endocrine Disorders
Prevalence: 5-10% ; 85% have symptoms
Side effect of a medication such as CCB, NSAIDS,
C4
oral hypoglycaemic agents
Skin changes ascribed to venous disease
Differentials: if meron kang lower extremity edema,
A. Pigmentation
meron ba yang systemic cause?
Brownish darkening of the skin initiated
Meron ba yang venous insufficiency?
by extravasated blood, which usually
Meron ba yang DVT?
occurs in the ankle region, but may
Meron ba yang PAD?
extend to the leg and foot darkening is
extensive which starts at thefoot then
Other regional considerations:
goes upwards
Ruptured popliteal cyst
B. Eczema
Soft tissue hematoma or mass Erythematous dermatitis which may
Chronic exertional compartment syndrome progress to a blistering, weeping or
Cellulitis scaling eruption of the skin of the leg
Arthritis of the knee or ankle joint Often located near varicose veins
Swelling following recent hip or knee surgery C. Lipodermatosclerosis
Gastrocnemius tear Localized chronic inflammation and
Lymphedema fibrosis of the skin and subcutaneous
Neurogenic pain tissue sometimes associated with
scarring or contracture of the Achilles
Classification of chronic lower extremity venous disease tendon
C Clinical stage (grade 0-6) Sometimes preceded by diffuse
Supplemented by: inflammatory edema of the skin, which
(A) for asymptomatic may be painful and which is often
(S) for symptomatic referred to as hypodermatitis
E Etiological Classification(Congenital, Primary, Secondary ) Can be differentiated from cellulitis by
A Anatomic Distribution(Superficial, Deep, or Perforator, the absence of fever
alone or in combination ) A sign of severe chronic venous disease
P Pathophysiologic Dysfunction(Reflux or Obstruction, alone D. Atrophied Blanche or White Atrophy
or in combination) usually found at the area of the distal
leg
C0S Localized, often circular, whitish and
No visible or palpable signs of venous disease atrophic skin areas surrounded by
Prevalence is 15-20% in the total population dilated capillary spot and sometimes
First level of the classification and was especially hyperpigmentation
created to emphasize that symptoms have to be A sign of severe chronic venous disease
considered as the first signal of the disease C5
C1 Skin changes with healed ulcer
Telangiectasia Full thickness defect of the skin most frequently
A confluence of dilated intradermal at the ankle that fails to heal and is spontaneously
venules of <1mm in caliber sustained by chronic venous disease

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C6 Move your toes with your legs slightly
Skin changes with active ulcer raised and extended: alternately bend
Most severe manifestation of CVD and unbend your toes(up to 20
Increase markedly with age times)Other basic measures
Prevalence: C4 to C6 is 0.3% -1% ; 78 % are Reverse bicycle
Symptomatic Other Basic Measures
Do:
Leg ulcers Wash in cold water after shower
Regular deep breathing exercises
Arterial ulcer most likely nasa toes and plantar aspect Appropriate sports:walking, swimming,
Mixed type - + venous and arterial disease mahirap itreat cycling, running on soft ground
Arterial appearance atropic, dry, shiny, hairloss signs of severe Avoid:
arterial disease Saunas
Restrictive clothing, girdles
Weight-lifting, skiing, tennis, marathons,
immobile sunbathing

Sclerotherapy
Is the most commonly performed treatment
option for patients with venous telangiectasia and
reticular veins often for cosmetic reasons alone
Injection of a sclerosing agent direct into the
vessel
Pwede injection at pwede laser, mawawala sya
pero it will recur because you do not address the
primary problem. The primary problem is the
pathology in your deep vein.
Treatment Majority of the treatment failure in sclerotherapy
Chronic Venous Disease is due to the failure to use compression stockings
General measures after the treatment
Leg elevation pag mabigat yung legs mo, itaas
mo sya para mabawasan ung pain or gawin mo Sclerotherapy complications:
yung exercise na ginagawa saeroplano, or para Pain or cramping
mas mabilis, ilakad mo sya para mabawasan ung Hyperpigmentation
symptom Telangiectatic matting
Control of body weight Blistering or necrosis
Exercise of calf muscles with periodic flexion of Superficial thrombophlebitis
ankles and transfer of weight Deep vein thrombosis
Avoid heat (mas matagal exposure sa heat, mas Urticaria
madadamage ung vein. Hot showers pwede.) Edema
Avoid standing for long periods
Cold showers to delay progression of disease Laser therapy
Lying flat on the healthy side in the presence of much better compared to doing your injectable
unilateral varicose veins sclerotherapy
Controlling vein problems Indications:
When you sleep, you need to elevate your legs Superficial, fine-caliver venous telangiectasia
with 2-3pillows Telangiectatic matting
Raise your feet above heart level Patient afraid of needles
Elevate your feet at work to prevent worsening of Poor responders to sclerotherapy
leg edema Adverse side effects from sclerotherapy
Anti-stasis exercises Application of laser and light source indirectly over the
Exercises to improve venous circulation vessels
Walk on your heels Pero not allpatients will respond to laser therapy, mas
Stand on tiptoe maliit, mas magrerespond, the larger the varicose veins, di
Rock from your toes to your heels tatalab ung laser hanggang telangiectasia lang sya saka
Point your toes together and then apart reticular veins saka it will also depend on the type of the
Cycling movement: move your legs with laser that you are using.
energetic movements (15-20 times). Older lasers (5yrs ago) will not work lesser treatment
Cross and uncross your legs in a scissors success compared to the ones that came out 2-3 years ago
movement(10-15 times) Endovascular laser therapy(EVLT)
Move each leg in a small circle up to 10 Newer modality
times You need to puncture your femoral vein, papasok
ung ___?sa femoral vein tapos papasok sa greater

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Dr. Deduyo
saphenous vein kasi ultrasound guided din sya
hanggang umabot sya dun sa bleeding vein. Once
the bleeding vein is identified, mag aapply sya ng
laser, pwede syang sound frequency, pwededin
syang laser tapos iisclerose mo na yung
telangiectasia saka ung reticular veins
Kaya ng EVLT ang varicose veins.
Although maramipa rin ang gumagawa ng vein
stripping, Better success rate pa rin ang EVLT
Other causes(hindi to binanggit pero sinali ko na rin just in
case)
Obstruction of the deep veins
DVT with inadequate recanalization
Venous stasis
Extrinsic compression, as in may
thumer syndrome(compression of the
left common iliac vein as is traverses
between the right common iliac artery
and the lumbosacral region)
Dysfunction of muscle pumps
Neuro muscular conditions or muscle
wasting syndromes
Conservative management
Toreduce symptoms and help prevent the
development of secondary complications and the
progression of disease
Behavioural measures such as elevating the legs
to minimize edema and reducing intraabdominal
pressure should be advocated
The use of compressive stocking is the mainstay
of conservative treatment
Prescription for elastic stockings includes
information about the tension and length. The
tension is based on the clinical severity:
20-30mmHg for CEAP 2-3 venous
insufficiency
30-40mmHg for ceap 4-6dvt or
recurrent ulcer
40-50mmHg for recurrent ulcers
Pagpostsclerotherapy, you have to use your
stockings
Pwede ka mag start out using your lower compression
stockings, pag ____yung symptoms, you need yo give your
higher compression
The problem lang, pag nasa tropical country, a lot of
patients will complain na lalo silang nagpapawis when using
the compression stockings
If the problem is only on the bifurcation vessles, you will
need to wear your below the knee stockings
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CARDIOLOGY
But if the problem is yung from the femoral downwards,
kailangan talaga na thigh stockings ung susuotin
Instruct the patient to wear the stockings immediately sa
moring and remove it at night
Compression stockings will last approximately 6 months
then eventually, kasi stockings yan so ung elasticity nya
nawawala, Elastic bandage pwede pa kaso mas matagal
sya ikabit
Elastic stockings
They should be worn daily
Put other socks over them if youre concerned
about their appearance
Elastic stockings: tips for wear and care
Once your stockings are on, make sure the top of
the stockings is about two fingers width below
the crease of the knee or the groin. If a stocking is
too high, it will cut off blood flow
Wound and skin care
Progressive CVI may lead to compromised skin
integrity, it is important to keep the affected area
well moisturized to reduce the risk of skin
breakdown and possibility of infection
Development of stasis dermatitis needs to be
treated with a topical steroid
With venous ulcers, bacterial overgrowth control
and aggressive wound care are required to
minimize infections complications
Pharmacologic therapy
Four groups of drugs evaluated for CVI:
Coumarins(alpha-benzopyrones)
Flavonoids (gamma-benzopyrones)
Saponosides (horse chestnut extracts)
Rutosides
With venoactive properties, widely used in Europe but not
approved for use in the USA
Principle for use of venoactive drugs: improve venous tone
and capillary permeability.
Yung available lang sa market natin ay ung Daflon and ung
generic nya
Sa Europe merong antistax = main component red leaf
Antistax vs daflon
Daflon-better symptom control - 1tab 2x per day
In patients with hemorrhoids, 2tabs 2x per day
In some patients with severe venous insufficiency,
2 tabs 2xper day.
Best response for venous insufficiency daflon 3-6 months
plus your compression stockings
2 months of treatment with daflon will be equivalent to a
pair of compression stockings O_O
Depends on the type ofcompression stockings.
Care for your stockings
You just need to wash them with ordinary soap
and water wag mo silang ilalagay sa washing
machine at wag ibilad sa araw..
STEF AND SHAY