Transcript peripheral vascular disease and abdominal aortic aneurysm

DR SURIANI SULAIMAN
UKM FMS TRAINEE
OBJECTIVES

1. To recognize the symptoms of peripheral vascular
disease (PVD) and AAA
2. To perform complete assessment of patient with
PVD and AAA
3. Know the urgency and indication to refer patient to
hospital
4. Give appropriate advice to prevent progression and
complications of PVD
WHAT IS PVD?

 Also known as Peripheral Artery Disease (PAD) or
PAOD
 Occlusive disease of the arteries of the lower
extremity
 Most common cause:
 Atherothrombosis
 Others: arteritis, embolism
 Has both ACUTE and CHRONIC presentation
How common is PVD?

 Affects about 1 in 20 people over the age of 50, or 8
million people in the US
 PVD is only diagnosed in 50% of the population
 Symptomatic PVD carries at least a 30% risk of death
within 5 years and almost 50% within 10 years,
primarily due to MI (60%) or stroke (12%).
Pathophysiology

Risk Factors

Chronic PVD
SYMPTOMS

Asymptomatic or atypical leg pain — 20 to 50 %
Intermittent claudication — 10 to 35 %
Critical limb ischemia — 1 to 2 %
Chronic PVD
SYMPTOMS

INTERMITTENT CLAUDICATION
• Derived from the Latin word ‘to limp’
• “Reproducible pain on exercise which is
relieved by rest”
• Discomfort felt at 1 level below the occlusion
• Pain can also be reproduced by elevating the
leg
• “my legs get sore at night and feel better when
I hang them over the edge of the bed”
30% Buttock & Hip Claudication

±Impotence – Leriche’s Syndrome
Thigh Claudication
60% Upper 2/3 Calf Claudication
Lower 1/3 Calf Claudication
Foot Claudication

2. ATYPICAL LEG PAIN
- 20 to 50%
- Exertional lower extremity pain that
does not occur with consistent level of
exertion
- Takes longer time to resolve with rest

3. Other Symptom/Signs:
• A burning or aching pain in the feet
(especially at night)
• Cold skin/feet
• Increased occurrence of infection
• Non-healing Ulcers
• Gangrene
DDx of Leg Pain
1. Vascular
a)
b)
DVT (as for risk factors)
PVD (claudication)

2. Neurospinal
a)
b)
Disc Disease
Spinal Stenosis (Pseudoclaudication)
3. Neuropathic
a)
b)
Diabetes
Chronic EtOH abuse
4. Musculoskeletal
a)
b)
OA (variation with weather + time of day)
Chronic compartment syndrome

Physical Examination:
Examination:
What do to:
Inspection
•
•
•
•
•
•
Thick Shiny Skin
Hair Loss
Brittle Nails
Colour Changes (pallor)
Ulcers
Muscle Wasting
Palpation
•
•
•
•
Temperature (cool, bilateral/unilateral)
Pulses: ?Regular, ?AAA
Capillary Refill
Sensation/Movement (paraesthesia/paralysis)
Auscultation
•
Femoral Bruits
Ankle Brachial
Index (ABI)
= Systolic BP in ankle
Systolic BP in brachial artery
Buerger’s Test
•
•
Expose the skin
and look for:
•

Elevate the leg to 45° - and look for pallor
Place the leg in a dependent position 90°& look
for a red flushed foot before returning to normal
Pallor at <20° = severe PAD.
NEUROPATHIC
FOOT ULCER
ISCHAEMIC FOOT
ULCER
VENOUS FOOT
ULCER
Site
Pressure points,
toes,plantar surface
Dorsum of foot, toes,
pressure points
Gaiter distribution
Appearance
Well-demarcated
granulation base,
diabetic foot changes
Punch out,irregular,
sharp border, poor
granulation tissue, dry
gangrene
Shallow, irregular,
granulated, flat
margin/slight steep
elevation
Foot temperature Warm
Cold
Warm
Colour
Pink foot
Blanching on elevation,
red when dependent
Pink foot
Sensation
Pain
Reduced/absent
Painless ulcer
Preserved
Painful ulcer
Preserved
Medium pain;
reduced with leg
elevation
Pulses
Callus
ABSI
Other findings
Well palpable
Present around ulcer
>0.9
Charchot foot, hammer
toe
Absent
No callus
<0.9
Trophic changes
Well palpable
No callus
>0.9
Hyperpigmentation,
dermatitis, oedema


What is ABPI

ABI
What does the ABI
mean?

Clinical Correlation
>0.9
Normal Limb
0.5-0.9
Intermittent Claudication
<0.4
Rest Pain
<0.15
Gangrene
CAUTION:
Patient’s with Diabetes, + Renal Failure
They have calcified arterial walls which can falsely elevate their ABI.
Therefore REFER TO VASCULAR TEAM for further evaluation (toe
pressure)

A normal resting ABI is 1 or 1.1.
An index of 0.9 or less indicates the presence
of obstructive disease.
0.5 or less suggests multiple-level arterial
disease.
An ABI of less than 0.26 indicates severe,
limb-threatening arterial compromise.
Investigations:
BLOOD TESTS:
1. FBC : infection, polycythemia
2. Blood sugar (FBS, HBA1C)
3. Fasting Lipids
4. Renal Profile

Wound Swab
1. Culture and sensitivity
Imaging
1. Foot X-ray : Osteomyelitis changes
2. Duplex Scan
3. CT Angiography
4. MRA
WHEN TO IMAGE:
1. To image = to intervene
2. Pt’s with disabling symptoms where revascularisation is considered
3. To accurately depict anatomy of stenosis and plan for PCI or Surgery
4. Sometimes in pt’s with discrepancy in hx and clinical findings
NON INVASIVE:
 Duplex Ultrasound
  normal is triphasic  biphasic  monophasic 
absent

ANGIOGRAPHY:
Non-invasive:
•
CT Angiogram
•
MR Angiogram

Invasive:
•
Digital Subtraction Angiography
 Gold Standard
 Intervention at the same time
Treatment:

1. RISK FACTOR MODIFICATION:
a)Smoking Cessation
b)BP reduction
c)Rigorous BSL control: HbA1c close to 6
d)Lipid Lowering Therapy :
- LDL 2.6mmol/L with PAD
- LDL<1.8 with ATH in other vessels
Treatment:

2. EXERCISE:
a)Claudication exercise
rehabilitation program
b) Walking beyond the
claudication distance : daily
or 3x/week
c)ABPI and PPG will be
measured
d)Usually within 3 months
Treatment:

3. MEDICAL MANAGEMENT:
a)Antiplatelet therapy e.g.
Aspirin/Clopidogrel
b)Pentoxyphylline – improves blood flow
c)Phosphodiesterase Inhibitor e.g.
Cilostazol – has antiplatlet activity
d)Foot Care
NO ROLE OF MEDICATIONS ONCE THE PATIENT
DEVELOPS CRITICAL LIMB SCHEMIA
REVASCULARIZATION

Indications for Revascularization in Peripheral Artery
Disease
Symptoms refractory to exercise and claudication drug
therapy
Presence of severe disability or serious impairment of
functional status
Anticipated natural history of progression of the disease
Absence of other comorbidities (such as angina or
respiratory disease)
that would explain limitation of functional status
Lesion amenable to
probability of success
revascularization
with
high

ENDOVASCULAR THERAPY
1. Angioplasty
2. Stenting
BYPASS SURGERY – for lesion that is not amenable to
angioplasty and when long segments are involved
AMPUTATION – last resort


 Mr. XX – a 60 yr old gentleman with a
very painful leg.
 He tells you that he woke up this
morning with an excruciating pain in
his left leg and has never felt this
pain before.
MUST RULE OUT
ACUTE LIMB
ISCHEMIA
 ? Embolism (AF/Recent
Infarct/Aneurysm)
 ? Thrombosis of native
vessel or graft
 ?Trauma

What are the features of an
acute ischemic limb?

REMEMBER
THE
6 P’S
History & Exam Findings
Further Hx:
• Smokes 20cigs/day for 30 years
• 4 months of ‘leg cramps’ in BOTH legs
• 2-3 weeks of intermittent chest palpitations
• Has not seen a Dr. in the last month

Examination:
Inspection:
o LLL: below the knee is pale
Palpation:
o Irregularly irregular pulse
o LL Capillary return is sluggish
o No pulses palpable below L femoral artery
o All pulses palpable but appear reduced in R leg
o Normal Sensation + Movement bilaterally
Impression?
60yo male with a L Acute Ischemic limb on the background of
heavy smoking, untreated AF and symptomatic PVD.

What will you do now?
1. CALL THE VASCULAR REGISTRAR
2. ORDER INVESTIGATIONS
a) FBC
b) BUSE/creatinine
c) Coagulation Studies
d) GSH
e) 12 Lead ECG
f) Chest XR

Simple measures to improve
existing perfusion:
• Keep the foot dependant
• Avoid pressure over the heel
• Avoid extremes of temperature
(cold induces vasospasm)
• Maximum tissue oxygenation
(oxygen inhalation)
• Correct hypotension
3. INITIATE ACUTE MANAGEMENT:
a) Analgesia
b) Commence IV heparin 5000u bolus with 1000u/hr infusion
afterwards
c) Angiography if limb still viable
d) Discuss with registrar:
i) Thrombotic cause  ?catheter induced thrombolysis
ii) Embolic cause  ?embolectomy
iii) All other measures not possible  Bypass/Amputation
Mr. X’s Complication
-
Angiogram is done in radiology
Shows acute thrombosis of L popliteal artery
Catheter induced urokinase and heparin infusion is started

…. 3-4 hours later
-Severe calf pain in the reperfused limb
-All pulses are present
-Leg is swollen, tense and +++ tender
REPERFUSION INJURY!
-Restored blood flow can lead to unwanted local + systemic effects
oMetabolic Acidosis
oHyperkalemia
oARF (myoglobinuria)
Compartment Syndrome =
oMay need fasciotomy

ABDOMINAL AORTIC
ANEURYSM

Aneurysm = abnormal
dilatation of an artery >1.5x
of normal vessel size
EPIDEMIOLOGY

> 32,000 cases in US every year
15,000 deaths per year in USA
Men are at 4-6 times greater risks of
developing AAA
Incidence increases with age
- Affects 2-5% of men >50 y.o, rare in
patient < 50 y.o
RISK FACTORS

75% aneurysms > 4cm in diameter can be
positively linked to a history of SMOKING
Positive FAMILY HISTORY OF AAA can
double the risk
- 15-20% AAA patients fave1st degree relative
with AAA
- 69% risk of AAA in offspring of women with
AAA
HYPERTENSION, DYSLIPIDEMIA
Marfan’s, Ehlers-Danlos
Infection (Syphilis, Salmonella, etc)
MORPHOLOGY

TRUE ANEURYSM
- Saccular
- Fusiform
- Dissecting
FALSE or PSEUDO-ANEURYSM = a
pulsatile hematoma
Pathophysiology
AAA develops as a chronic aortic
wall inflammations

Arterial injury
- Hypertension
- Hyperlipidemia
- Toxins (nicotines)
Inflammation
Degradation of elastin
AAA growth & rupture

95% of AAA are infrarenal
25% of AAA involve iliac arteries
Isolated iliac aneurysms are rare –
(<1%)
Suprarenal aneurysms are rare unless
they have an associated thoracic or
infrarenal component
Femoral or popliteal aneurysms seen
in 3.5% of patients with AAA
AAA seen in 30-40% of patients with
popliteal aneurysms

PRESENTATION

ASYMPTOMATIC
Pain
– dull, vague pain in the abdomen, back or flank
- Can be acute and severe in ruptured AAAs
Mass
- Sensation of pulsatile mass in the abdomen
Hypotension
- usually manifested as syncope
- In cases of ruptured AAAs
INITIAL DIAGNOSIS OF AAA
 38% patients AAAs initially detected by PE

 62% found incidentally on x-ray studies done for other
indications
 AAAs detected by PE had lower BMIs but there was no
difference in AAA size
 43 % of AAAs detected on radiologic examination had
palpable AAAs that should have been detected on PE.
 23% AAAs were not palpable on preoperative PE, even
when the diagnosis was known.
 Obese patients had only 15% of AAAs detected by PE,
and only 33% were palpable.
Role of physical examination in detection of abdominal aortic aneurysms. Surgery 1995 Apr;117(4):454-7
Chervu A; Clagett GP; Valentine RJ; Myers SI; Rossi PJ
Physical Exam:
 If <5cm in diameter, then cannot
be detected by routine physical
exam
 Deep palpation
 Above umbilicus
 LEFT of midline
 Continuous over several
heartbeats

AAA NOT detected on exam for
tenderness or lower abdominal
masses!

Radiographs:
Calcified wall. Can
determine size in 2/3
Cannot rule out and
AAA
AAA DIAGNOSIS

Ultrasound
Establishes diagnosis easily
Accurately measures infrarenal diameter
Difficult to visualize thoracic or
suprarenal aneurysms
Difficult to establish relationship to renal
arteries
Technician dependent
Widely available, quick, no risk, cheap
CT Scan
Very reliable and reproducible
Can image entire aorta
Can visualize relation ship to visceral
vessels
Longer to obtain and is more costly
than U/S
Most useful
Requires contrast agent - renal toxicity


MRA
Now widely available
More expensive than CT
No contrast agent required
Little if any advantage over CT

Complications of AAA
Thrombosis
Distal embolization
Rupture
Size
5-6 cm
Yearly
Rupture
Rate
5-10%
5 Year
Risk
25-50%
6-7 cm
7-15%%
30-75%
>7 cm
20-30%
>90%
Rupture Risks

Patients with COPD and HTN have increased
risk of rupture
Emphysema, smoking, hypertension increase
likelihood of rupture (Cronenwett 1985)
Larger aneurysm more likely to rupture
Rate of enlargement:
 0.5 cm/ year
Survival
 50% die prior to reaching hospital, and an
additional 24% prior to repair
TREATMENT OPTIONS

Observation: Small aneurysms < 5cm
Repair:
- Open surgical repair
- Endovascular (“stent-graft”) repair

Aortic Aneurysms
Indications for Treatment

Presence of an infrarenal aneurysm > 5cm
without associated co-morbid medical
conditions
Repair smaller aneurysms if rate of enlargement
is greater than expected
Repair all symptomatic aneurysms
If co-morbid conditions exist wait until risk of
repair and rupture are equal (approx. 6 cm)
Surgical repair

3-5% mortality (elective
cases)
Small risk of MI,
pulmonary complications,
renal failure, limb
ischemia, colon ischemia,
etc
Repair effectively
permanent
Endovascular repair

Quick recovery, less
trauma, possibly lower
mortality
“Endoleaks” about 20%
need further procedures
Requires very tight
follow-up
Expensive procedure
Endovascular vs. Open
Repair

Open
• Health status predicts
ability to withstand
surgery
• Health status predicts
chance of 5-10 yr survival
“good”
• Likely to be difficult to
maintain follow-up
• Renal “cuff”, iliacs
preclude EVAR
Endo (EVAR)
• Unusual risk for open
surgery
• Limited life expectancy
• Likely to be compliant
with follow-up
• “Friendly” anatomy of
renal “cuff” and iliac
arteries

TREATMENT
ALGORITHM

SCREENING FOR
AAA?

 Lancet. 2002;360:1531-1539 “Multicentre aneurysm
screening study (MASS): cost effectiveness analysis
of screening for abdominal aortic aneurysms based
on four year results from randomised controlled
trial”
 Routine ultrasound screening of men older than 65
years for abdominal aortic aneurysm (AAA)
reduced aneurysm-related mortality by 50%
U.S. Preventive Services Task Force
Screening for Abdominal Aortic
Aneurysm: A Best-Evidence
Systematic Review

Conclusion: For men age 65 to 75
years with any tobacco exposure, AAA
screening reduces AAA-related
mortality.
Ann Intern Med 2005;142:203-11
Their Current Medicare
Policy

 Men over 65 with any smoking history
 Single screening ultrasound
 Must be ordered at initial “Welcome to Medicare”
examination
 Patients with Family History of AAA
 (Exam my be ordered in any patient with suggestive
physical findings, or known AAA
In Malaysia

Due to lack of data on the prevalence
of AAA in Asia, the role of AAA
screening in Asia is uncertain

85.3% of patients had not heard off
both PAD
lead on to delayed presentation
Great effort is warranted to educate
patients with CAD
Prevalence of Peripheral Arterial Disease and AbdominalAortic Aneurysm among Patients with ACS: Med J
Malaysia Vol 68 No 1 February 2013;;Benjamin Dak Keung Leong

Thank you