Vascular Diseases of the Extremities

INTERNAL MEDICINE II
FACILITATOR: Jonah L. Amora, MD, FPCP, FPCC DATE: December 12, 2016

OUTLINE

• Peripheral Artery Disease • Venous and Superficial vein Thrombosis

• Thromboangiitis Obliterans • Cardiac manifestations of systemic diseases
• Acute arterial occlusion

PERIPHERAL ARTERY DISEASE (PAD)

• The most common disease entity that can affect our PATHOLOGY
extremities and vasculature is Peripheral Artery Disease.
• Stenosis or occlusion in the aorta or arteries of the limbs
• Number 1 cause in individuals 40 and above:
ATHEROSCLEROSIS
§ 2016: It is a lifelong process but for people with risk factors,
atherosclerosis may progress faster and more advance even if
they are younger
§ Other causes include embolism, thrombosis,
vasculitis, trauma
• Highest prevalence occurs in 60 and 70+ because
atherosclerosis is a lifelong process
• Risk factors – The risk factors for PAD are the same as those
for CAD
§ SMOKING
§ DIABETES MELLITUS
§ HYPERCHOLESTEROLEMIA
§ HYPERTENSION
§ HYPERHOMOCYSTEINEMIA
§ 2016: This risk factors contributes to accelerate the process of On the atherosclerotic artery (right), a plaque has been formed which
atherosclerosis which may increase the chance to develop PAD leads to stenosis. There is a decreased blood flow but there is no
§ 2016: The first four are the most important and are the MAJOR presence of total occlusion. Take note that there is a difference
RISK FACTORS between saying that “may baradong ugat” and “may masikip na
ugat”. Masikip na ugat means that there is just stenosis but there is
RISK FACTORS still blood flow. Baradong ugat means that there is total occlusion.
They are two different things and they have different implications for
• 2-4x increase in prevalence of PAD in CURRENT SMOKERS the patient. So again just take note that atherosclerosis can lead to
compared to never smokers decreased blood flow because of the stenosis.
• DIABETES MELLITUS patients have 2-4x increased risk and
often have extensive and severe PAD • Segmental lesions in large and medium-sized vessels
§ 2016: greater propensity for arterial calcification • 2016: Scenario: Patient goes to emergency room with chest pain.
• HYPERCHOLESTEROLEMIA: Increase in total and LDL Would you consider CAD as most likely cause of chest pain for the
cholesterol increases risk for PAD and claudication patient?
• HYPERTENSION increases risk for PAD by 1.3 to 2.2 § Base on the concept of risk factors for advance atherosclerosis,
it would be the LEAST consideration for the chest pain in
§ 2016: People who smoke has a greater risk than
individuals around 23-32 years old
hypertension people in developing atherosclerosis § BUT if patient is 60 above, smoker, non-compliant with
• The magic number here is “2”. Almost all the risk factors give a hypertensive meds, you have a 90% of being right that this
twofold increase in developing PAD. is PAD

PRIMARY SITE OF INVOLVEMENT (you have to remember this)

FEMORAL AND 80-90%

POPLITEAL ARTERIES
DISTAL VESSELS 40-50%
(ex. posterior tibial a.,
anterior tibial a., dorsalis
pedis a.)
ABDOMINAL AORTA 30% of symptomatic
AND ILIAC ARTERIES patients

• Arterial branch points - most commonly affected due to

stress of blood flow

1 | DLSHSI COLLEGE OF MEDICINE Batch 2018

 • Distal vasculature involvement most common in elderly and § Do not mistake the edema for a venous problem. Edema
DM can also be a manifestation of an arterial obstruction,
§ Lesions are composed of plaques with calcium deposition not just venous congestion/thrombosis.
§ Most patients with PAD prefer putting their legs in the
SYMPTOMS dependent position and so they develop peripheral
• > 50% are ASYMPTOMATIC, more common in lower edema.
extremities • Ischemic neuropathy
§ However, it can also occur in the upper extremities (ex. § Numbness and hyporeflexia
brachial a., distal hand a., radial a.) albeit less § Blood supply to peripheral nerves is compromised.
commonly.
• INTERMITTENT CLAUDICATION – MOST COMMON
symptom
§ “Pain on the lower extremities upon exertion”
§ Intermittent claudication refers to pain, ache, cramp
numbness, sense of fatigue, or other discomfort that
occurs in the affected muscle group during exercise,
and relieved by rest
w Classic symptoms of PAD
w If you notice, angina is very similar in description.
They refer to intermittent claudication as “ angina
of the legs”.
w 2016: Angina is pain located in chest while
claudication is pain located in lower extremities. Extensive gangrene and necrosis; very chronic and severe. Note also
w 2016: Same pathophysiology: Decreased oxygen the swollen / edematous dorsum, the secondary skin changes: the
supply during exertion creating the pain and skin is shiny and the nails are thick. Since the distal toes are affected,
the lesion is probably at the level of the popliteal artery.
discomfort. Symptoms disappear at rest.
§ Site of claudication is distal to the occlusion
DIAGNOSIS/NON-INVASIVE TESTING
w Buttock, hip, or thigh claudication typically
occurs in patient with obstruction of the aorta
• Usually history and PE are sufficient
and iliac arteries
• In the presence of significant stenoses, systolic BP in the
w Calf claudication is caused by femoral or
legs is decreased
popliteal artery stenoses

• CRITICAL LIMB ISCHEMIA (CLI) NONINVASIVE TESTING

§ Develops in patients whose circulation is significantly • Ankle : Brachial index (ABI)
compromised § One of the easiest noninvasive test is ABI testing.
§ In patients with severe disease such that resting blood § Arterial pressure recorded by BP cuffs
flow cannot accommodate nutritional needs of the § Use Doppler device to auscultate or record blood flow
tissues, CLI may develop. § < 1 in patients with PAD
§ Rest pain, cold, numbness in the feet and toes § < 0.5 in severe ischemia
(remember that!) § Normal ABI > 1
w There is pain even at rest because the tissues are
already compromised. • Segmental pressure and pulse volume recordings
w Heart equivalent: Unstable Angina § Pressure gradients between sequential cuffs
§ Occur at night when legs are horizontal § Records your pulse waveforms and will record the
§ Symptoms improve when legs are dependent difference in pressures (gradients) between sequential
w Due to the effect of gravity that augments the levels
circulation towards the legs.
• Duplex ultrasonography
PHYSICAL FINDINGS § Used to detect stenotic lesions
• Decreased or absent pulses distal to the obstruction § 2016: The idea is to look for the sites of obstruction in the
• (+) Bruit over the narrowed artery blood vessels
§ “Murmur over the artery”, “Murmur outside the heart”
§ Bruit is defined as murmur on peripheral vessels or • Treadmill Exercise Test (TET)
murmur outside the heart due to decreased lumen § Some patients will develop symptoms only when they
causing turbulence of blood flow exercise so you can record the patient’s Stress ABI.You
• Muscle atrophy can detect any changes in pressure.
§ Due to the decrease oxygen perfusion leading to § 2016: Assess functional limitations
decrease nutrient delivery § 2016: Used for both cases of PAD and Coronary Artery
• Secondary skin changes Disease (CAD)
§ Hair loss, thickened nails § 2016: You can stage at what point of exertion the patient
§ Smooth and shiny skin develops symptoms
§ Reduced skin temperature § 2016: In treatment, TET is used to measure if there is a
§ Pallor or cyanosis response to the drug. There should be prolongation of
• Critical Limb Ischemia (CLI) the amount of activity that the patient is able to do
§ Ulcers or gangrene before the patient becomes symptomatic
w The lesions are necrotic and there might even be
secondary infections
• Leg elevation à PALLOR
• Legs dependent à RUBOR or reactive hyperemia
• Peripheral edema

2 | DLSHSI COLLEGE OF MEDICINE Batch 2018

 Duplex Ultrasonography
Here you can see the demonstration of the color flow which means
that there is no significant obstruction. You can demonstrate the
presence of plaques here (whitish lesions).

Ankle-Brachial Index OTHER IMAGING STUDIES

Normally, the lower extremities give you a higher blood pressure – • Magnetic resonance angiography
which is why a normal ABI is more than 1. If the pressure in the lower • CT angiography
extremities is lower than that of the upper extremities, your ABI will • Conventional contrast angiography
be less than 1 – which is diagnostic of PAD. • NOT for routine diagnosis
• Performed before planned revascularization

Conventional Angiography
An example of an angiographic view demonstrating the iliacs and its
major branches. You can see some narrowing here, but it’s not really
that significant.
Sample picture of segmental pressure measurements with
PROGNOSIS
corresponding waveforms.
• CAD commonly coexists in symptomatic PAD
§ If the vessels in the extremities are already affected,
then most likely the coronary vessels are also affected
because they have smaller calibers.
§ 33% to 50% of PAD have evidence of CAD, based on
symptoms and ECG
w 2016: PAD patients die more of cardiovascular
events rather than PAD, due to same
pathophysiology (atherosclerosis)
§ > 50% have significant CAD based on coronary
angiogram
• 2-6x increased risk of death from CAD
§ Prognosis of these patients is greatly influenced by the
presence of CAD
Segmental Pressure and PVRs
§ CAD is the most common cause of death in PAD, with
up to 6x increased risk of death due to CAD.
§ If a patient presents with leg pain and you diagnose
him/her PAD, you should automatically work him/her up
for CAD.
• Severe PAD: highest mortality rates
§ Severe PAD: those with gangrene, ulcers, critical limb
ischemia
§ Be more aggressive with treatment

3 | DLSHSI COLLEGE OF MEDICINE Batch 2018

 • Critical Limb Ischemia § Physical activity is actually more beneficial than the
§ 25-30% of patients with critical limb ischemia undergo absence of exercise in cases of PAD, according to
amputation within 1 year studies
§ Worse prognosis: smokers, DM § Patients are advised to exercise regularly and
progressively
TREATMENT • MEDICATIONS
§ CILOSTAZOL, a phospodiesterase inhibitor with
• Risk factor modification vasodilator and antiplatelet properties
§ Hypertension: ACE-I, Beta blockers w Can increase claudication distance by 40-60%
w B-blockers are especially beneficial for patients and improves measures of quality of life
with CAD w Highly recommended by the guidelines
§ Hypercholesterolemia: statins to lower LDL § PENTOXIFYLLINE: increases blood flow to
<100mg/dL microcirculation, increases duration of exercise
§ 2016: You can advise the patient to stop smoking, control the w Evidence is not as strong for this drug compared to
hypertension with medication, modify/control the
cilostazol
hyperglycemia and decrease the cholesterol
• REVASCULARIZATION
• Anti-platelet therapy (Aspirin, Clopidogrel)
§ Catheter-based and surgical interventions
§ To prevent future clot formation; take note that this is
§ For patients with disabling, progressive or severe
not only for the legs but also for CAD.
symptoms despite medical therapy
§ ASA and clopidogrel reduce adverse CV events (e.g.
§ Percutaneous Transluminal Angioplasty (PTA) and
MI, stroke)
stenting of iliac: higher success rates
§ Dual antiplatelet not more effective
w You can give just one of the two. Either aspirin or w Stenting the iliac has a higher success rate
clopidogrel. compared to stenting more distal vasculature
• Therapies for intermittent claudication and critical limb § Surgical: aortobifemoral bypass
ischemia include:
§ Supportive measures
w Meticulous foot care
w Well-fitting and protective shoes
S Avoid injury since it may lead to an infection
later on.
w Avoid elastic support hoses
S If a patient with varicose veins discovers
that he/she has PAD, then she cannot use
these anymore.
• Exercise
§ Supervised training programs, 3-5x / week for at least
12 weeks prolong walking distance Stent Placement
w The patients can walk a further distance without
feeling any symptoms.

FIBROMUSCULAR DYSPLASIA

• Hyperplastic disorders affecting medium-size and small

arteries
§ Not due to atherosclerosis, rather it is because your
arteries are thickening.
• Predominantly in females
• Usually involves RENAL and CAROTID arteries
§ If extremities are involved; the ILIAC arteries are
the most commonly affected
• Medial fibroplasia: most common type
§ Medial fibroplasia: thinned media and
fibromuscular ridges.
§ Other types: intimal fibroplasia, medial dysplasia,
adventitial hyperplasia.
• Angiography: string of beads appearance

String of beads appearance due to areas of thick fibromuscular

ridges. Very classic.

THROMBOANGIITIS OBLITERANS

• Buerger’s disease § Unknown mechanism but epidemiology showed

• INFLAMMATORY occlusive vascular disorder involving small relationship to smoking
and medium sized arteries and veins in the distal upper • Triad:
and lower extremities § Claudication
• Frequently in men <40 years, high prevalence in Asians § Raynaud’s phenomenon
• Definite relationship to SMOKING § Migratory superficial vein thrombophlebitis
§ 2016 Mnemonics: si CLAUdine & Raymart nag Buerger.

4 | DLSHSI COLLEGE OF MEDICINE Batch 2018

 • Claudication confined to calves and feet or forearms and
hands
§ Again, because the distal vessels are most commonly
affected
• DIAGNOSIS: confirmed by EXCISIONAL BIOPSY
§ Excisional biopsy: inflammatory infiltrate with preserved
IEL.
• The only treatment is CESSATION OF SMOKING
§ But of course if there is frank infection, frank gangrene –
then there is no choice but to amputate the limb or digits.

The leftmost toe shows Raynaud’s phenomenon. Thickened nails,

ulcerations on digits.

ACUTE ARTERIAL OCCLUSION (AAO)

• AN ACUTE EVENT! Much like an acute MI.
• Sudden cessation of blood flow to an extremity
• Two principal causes/soruces:
§ EMBOLISM and
§ THROMBUS IN SITU
ARTERIAL EMBOLISM
• Most common sources of arterial emboli are the (1) heart, (2)
aorta, and (3) large arteries
• Cardiac sources: Atrial Fibrillation (AF), Acute myocardial
infarction (AMI), cardiomyopathy (CMP), aneurysm,
endocarditis, myxoma, prosthetic valves
§ 2016: If you have any of these, then the high chance that you
could develop an event due to embolism.
• Emboli commonly lodges in your bifurcations/branches.
§ Most common location on lower extremities for
arterial embolism: femorals
w Common femoral, deep femoral, superficial
femoral – the femoral artery has several
bifurcations kaya dito siya nagbabara.
ARTERIAL THROMBUS (IN SITU )
• Atherosclerotic vessels
o The cap of an unstable plaque might be peeled off
and it will work like an acute MI.
o The ruptured plaque leads to the formation of a clot
• Bypass grafts
2016: In patients with any occlusion, there are only 2 causes. You
have to do your history and PE, to detect whether it is an embolism or
thrombus in situ.

CARDIAC SOURCE DESCRIPTION/PATHOPHYSIOLOGY

for ARTERIAL
EMBOLISM
ATRIAL • Irregular rhythm leads to the formation of a blood clot in the left atrium or left ventricle.
FIBRILLATION • These clots can then embolize to the other distal arteries.

2016:
• These patients do not have atrial contraction.
• Remember the cardiac cycle?
§ EARLY diastole: rapid inflow of blood from the atrium to the ventricle, because of
momentum.
§ LATE diastole: – Atrial contraction. This contributes to about 30% of the cardiac
output.
• So in patients with atrial fibrillation, they lose about 30% of the CO.
• But the problem with patients with atrial fibrillation that predispose them to embolism is that
they have a dilated left atrium.
• Since they do not have atrial contraction, and they have a dilated left atrium, these patients
are predisposed to blood clot or thrombus formation due to STASIS inside the left and the
right atrium.
• Once there is a blood clot in the left atrium, it can be dislodged and will move into the left
ventricle and into the systemic circulation.
§ Patients with AF have a common complication of cerebral vascular infarct because of the
emboli lodge in the cerebral arteries.
• Common complication: HYPOTENSION
§ Because atrial fibrillation commonly appears with rapid ventricular response – a fast
heart rate will compromise the diastolic filling of blood plus the lost of 30% of CO due to
absence of atrial contraction.
ACUTE • The heart is enlarged and dilated, there could be an aneurysm.
MYOCARDIAL • A blood clot can form in the aneurysm because of stasis and this clot can then once again
INFARCTION embolize to other areas.

2016:
• A portion of the left ventricle dies.
• A heart is basically a pump. When 40% of the left ventricle dies and only 60% is left, so the
portion with MI is actually dead, so there is stasis of blood.

5 | DLSHSI COLLEGE OF MEDICINE Batch 2018

 • Infarction = STASIS or CELL DEATH.
• Common complication: HEART FAILURE – because the heart cannot pump adequately
anymore as efficient as before.
• The area which is infracted: there is no movement of the ventricle, stasis of blood so it is prone
to blood clot formation and then embolism once it moves out of the left ventricle.
§ Portion of left ventricle pump is contracting and the portion that is not contracting would
predispose to blood clot or thrombus formation.
CARDIOMYOPATHY 2016:
• Systolic dysfunction because of blood stasis.
• The heart is basically a pump, when you are looking at the short axis of the heart in an
echocardiogram, the left ventricle decreases in cavity during systole, BUT in patients with
CMP, the heart barely moves the left ventricle.
• So the reason for the predisposition of patients with CMP to blood formation is that the heart is
hardly moving due to systolic dysfunction.
ANEURYSM 2016:
• Whether the aneurysm is in the ventricle of large arteries, the stasis of blood would cause
blood clot formation.
ENDOCARDITIS • There is a septic embolus or vegetation that dislodges which can embolize and occlude your
distal arteries

2016:
• Vegetation
§ One of the criteria in the diagnosis of endocarditis.
§ Once it is dislodged from one of the valves that affected it can move into any artery and
cause infarct of the brain and can even cause MI (unusual)
MYXOMA 2016:
• A big tumor that if dislodged, can cause fatal infarction
• Most common location: LEFT ATRIUM.
PROSTHETIC • Can be a nidus for clot formation leading to embolism.
VALVES
2016:
• Because it is a foreign body in the heart, it can predispose to thrombus or blood clot formation.
§ Patients taking warfarin or coumadin should monitor their Protime monthly to
decrease embolism.

SYMPTOMS OF AAO
• Severe pain, paresthesia, numbness, coldness of extremities
§ 5Ps: Pain, paresthesia, pallor, poikilothermia,
pulselessness
• Paralysis may occur with severe and persistent ischemia
• Loss of pulses, cyanosis, mottling, decreased skin
temperature, muscle stiffening, weakness
§ Common symptoms on patients with arterial
hypoperfusion
§ We do not see the secondary skin changes in AAO
because this is an acute event.
• Diagnosis usually obvious from clinical presentation
• Most patients will require:
§ MRA (Magnetic Resonance Angiogram),
§ CTA (Computerized Tomography Angiogram),
§ Conventional arteriography
§ The diagnostic tools to fully investigate the location and
extent of obstruction.
• The end effect of ARTERIAL OCLUSSION whether it is ACUTE
or CHRONIC would be NECROSIS or GANGRENE of a portion
of the extremity.
6 | DLSHSI COLLEGE OF MEDICINE Batch 2018
• Image: Necrosis involving the two digits. There is also
hypoperfusion (decrease of blood flow) since the color of some
digits is pale.
• Sometimes they would remove the fingers and preserve the big
toe to minimize the disability of the patient.
TREATMENT FOR ACUTE ARTERIAL OCLUSSION
• Anticoagulation with INTRAVENOUS HEPARIN to prevent
propagation of the clot.
§ 2016: Heparin is an anticoagulant so the purpose is
prevent the formation of further clots and prevent
propagation of clot. Wag ng lumaki at wag ng
madagdagan.
• IMMEDIATE ENDOVASCULAR / SURGICAL
THROMBOEMBOLECTOMY OR ARTERIAL BYPASS
• INTRA-ARTERIAL THROMBOLYSIS
§ with recombinant tissue plasminogen activator (rTPA),
reteplase, tenecteplase
§ Effective when occlusion due to thrombus in bypass
graft or atherosclerotic vessel
§ You can inject all of these in order to save the limb.
§ 2016: Same pathophysiology with coronary artery disease,
treatment is also related or the same in a way: the idea is to
lyse the thrombus causing the acute arterial occlusion
§ 2016: If you are talking about acute arterial occlusion then a
role of a thrombolytic drug is more appropriate. Sudden, and if
you have a chance in saving the extremities, you should
dissolve that clot or thrombus as early as possible.
§ 2016: And if that medical treatment is not successful, you can
do other intervention like catheter-based interventions.
• AMPUTATION when limb is not viable
§ You do the first 3 only when the limb is still viable. If it is
not viable, then you would have to amputate the limb
already.
RAYNAUD’S PHENOMENON
• “Episodic sequential digital ischemia”
• Episodic digital ischemia, manifested by sequential
development of
§ Digital blanching
w Vasospasm of digital arteries, causing ischemia
§ Cyanosis
w Capillaries and venules dilate
§ Rubor of fingers or toes
w Rewarming, reactive hyperemia
#THROWBACK:
Remember Pathology? Dr. Pascual’s mnemonic for the sequence in
Raynaud’s Phenomenon: WeBeR -> white, blue, red. It even came out in
our Evals back then! Okay. Enough reminiscing, back to work...
§ This phenomenon usually occurs after cold exposure
and subsequent rewarming.
w 2016: The postulated mechanism is the SPASM of
the arteries.
RAYNAUD’S DISEASE
• When secondary causes of Raynaud’s phenomenon are
excluded
§ DO NOT BE CONFUSED. Raynaud’s disease is the
idiopathic form (an actual disease) – diagnosed when
you have ruled out all other secondary causes.
§ Raynaud’s phenomenon is a sign that can be seen in
several other diseases
• Female preponderance, 20-40 y/o
• FINGERS more involved than toes
SECONDARY CAUSES (of Raynaud’s Phenomenon)
• Systemic sclerosis
§ Up to 90% of patients with Sscle have Raynaud’s
Phenomenon
• SLE
§ Up to 20% of patients with SLE have Raynaud’s
Phenomenon
• Atherosclerosis: men >50 y/o
• Thromboangiitis obliterans (Buerger’s Disease)
• Blood dyscrasias
• Drugs: beta-blockers, ergot derivatives, vinblastine, cisplatin,
bleomycin
VENOUS THROMBOSIS & SUPERFICIAL VEIN THROMBOSIS
VENOUS THROMBOSIS
• Presence of thrombus within a superficial or deep
vein, with inflammatory response
§ Usually there is an event that provokes venous
thrombosis
• VIRCHOW’S TRIAD: Stasis, vascular damage,
hypercoagulability
• It is commonly observed in patients that
undergo/have:
§ Orthopedic surgeries, abdominal or thoracic
operations – stasis + endothelial injury
§ Neoplasms (pancreas, lungs, GUT, stomach,
breast) – hypercoagulable state
§ Any condition where there will be stasis or
vascular damaged or hypercoagulability
there’s a high chance of developing venous
thrombosis.
• Risk of thrombosis is increased after TRAUMA &
IMMOBILIZATION
• Increase incidence during PREGNANCY
7 | DLSHSI COLLEGE OF MEDICINE Batch 2018
TREATMENT
• Avoid unnecessary cold exposure
• Avoid tobacco use
§ What disease is treated only by cessation of smoking????
BUERGER’S DISEASE! Correct!
• Calcium channel blockers in severe cases
• Alpha-1 adrenergic antagonists: prazosin
• Topical nitrates
§ For frequently symptomatic or severe cases
2016 NOTES
• In patient who are persistently asymptomatic: CALCIUM
CHANNEL BLOCKERS in severe cases.
§ Calcium channel blockers are indicted since it is use for
VASODILATOR of the ARTERIES
w Prevent the spasm and cause dilation of the
smooth muscles in the arteries located in the
tunica media, and
w Prevents the entry of calcium for muscle
contraction.
§ 2016: Why would Calcium-channel blockers be used?
What are the most common indication of the use of
calcium-channel blockers? HYPERTENSION. And the
reason we use these for hypertension is because it dilate
the arteries
§ Examples: 1st gen CCB - Nifedipine, Verapamil,
Diltiazem
w The problem with Nifedipine is it is short acting so
you have to give it every 6 or every 8 hours.
§ 2016: CCB drugs that are most commonly used in
treatment of hypertension: Amplodipine, Phyllodipine,
Nacidiphine
§ 2016: These are long acting vasodilator CCBs, you give it
once a day and usually it is enough to control the
hypertension.
• Raynaud’s phenomenon. Blanching and cyanosis
• It is something that is paroxysmal / episodic. But for patients
with short periods of Raynaud’s phenomenon, you do not need
to treat them only those patients with severe.
SUPERFICIAL VEIN THROMBOSIS
• Thrombosis of the greater saphenous vein or
lesser saphenous veins or their tributaries
§ Can also be in the visible veins in your hands,
visible veins in your extremities, varicosities
• Does NOT result in pulmonary embolism
• Associated with IV catheters and infusions
• Occur in varicose veins or associated with deep vein
thrombosis
§ So you should also workup the patient for DVT
• Migrating superficial vein thrombosis is often a
marker for carcinoma
• Patients complain of pain localized to site of
thrombus
• Physical exam shows reddened, warm, tender
cord extending along a superficial vein (which
represents the thrombus)
 TREATMENT
2016 NOTES (not part of the latest PPT)
• Primary therapy consists of clot dissolution with
thrombolysis or removal of PE (Pulmonary
Embolism) by embolectomy
§ The most serious complication of Venous
Thrombosis is Pulmonary Embolism. The
mortality for PE is very high.
• Anticoagulation with heparin and warfarin or
placement of an IVC filter constitutes secondary
prevention of recurrent PE.
2016 NOTES
if PERIPHERAL ARTERY DISEASE: temp-COLD and ↓PULSE
if SUPERFICIAL VEIN THROMBOSIS: red, warm and tender cord
VARICOSE VEINS
• Dilated, tortuous superficial veins
• Primary:
§ Originate in superficial system
§ More frequent (23x) in women
• Secondary:
§ Result from deep venous insufficiency and
incompetent perforating veins
• These result from defective structure and function of the valves
of the saphenous veins or intrinsic weakness of the vein wall.
CLINICAL FINDINGS
• Dull ache or pressure sensation after prolonged standing
• Extensive varicosities may cause skin ulcerations near the
ankle
• Mild ankle edema
• May rarely rupture and bleed
• Patients usually complain of the cosmetic appearance. “Hala,
hindi na flawless” L
CARDIAC MANIFESTATIONS OF SYSTEMIC DISEASES
DIABETES MELLITUS (DM)
• DM is a strong, independent risk factor for CAD
§ Just like how you are a strong, independent woman. J
§ CAD is the most common cause of death in DM.
• “CAD EQUIVALENT”
§ 2016: DM is a major CORONARY risk factor. But DM has been
elevated to a coronary artery disease equivalent, meaning if
you are diabetic, you are treated as somebody who already has
MI (more serious than a risk factor). So the treatment must be
more aggressive.
§ 2016: If the patient already had MI, you are talking about
SECONDARY prevention: Prevent another MI, death, unstable
angina.
§ 2016: Same goes for DM patients. We will still be applying
SECONDARY PREVENTION, not primary, because it is
assumed that the patient already has a CAD, which can
potentially lead to MI.
§ 2016: Again, for emphasis, CAD equivalent means that a
patient with DM is considered one who also has CAD, and
therefore must be treated in a similar manner.
• Incidence of CAD relevant to the duration of DM and level of
glycemic control
§ The longer you are diabetic, the more uncontrolled your
blood sugar is, the higher your chances of having a
coronary event in the future.
8 | DLSHSI COLLEGE OF MEDICINE Batch 2018
• Primarily supportive
§ Bed rest with leg elevation
w BUT be careful. Make sure that the
patient does not have a concomitant
PAD.
§ Warm compress
• NSAIDs: for analgesia
• Anti- coagulant therapy in severe cases: if
thrombosis extends to deeper system
§ Since it is deeper, it is more likely to evolve into
a deep venous thrombosis
TREATMENT
• Supportive
§ Leg elevation, elastic support hose
§ External compression stockings
w These stockings have particular sizes and
pressures. You don’t just use whatever stockings
you want.
• Sclerotherapy
§ Injecting of sclerosing solution
• Radiofrequency or laser ablation
• Surgery
§ Ligation and vein stripping
§ There is a direct relationship between duration of disease
and the adequacy of glycemic control and the incidence
of CAD.
§ There should be a low threshold in suspecting CAD in DM
patients.
• DM patients are more likely to have myocardial infarction
and if they do get an MI, the infarct size is larger and would
have more post infarct complications
• CAD is the most common cause of death in adults with DM
• Diabetic patients present with:
§ ATYPICAL ISCHEMIC SYMPTOMS
w Typical symptoms: Angina: chest pain on exertion,
relieved by rest, MI: retrosternal, crushing,
heaviness
w DM patients having an MI can present with
dyspnea, vomiting, epigastric pain, nausea. So be
very careful! You might mistake it for a
gastrointestinal episode.
§ “SILENT ISCHEMIA” from dysautonomia
w They do not have any form of symptoms but when
you screen them with your treadmill test, stress
echo, or stress perfusion imaging you would be
able to demonstrate ischemia.
 w 2016: Patients with DM will have abnormalities in their
sensory perception so that a lot of them would have
symptoms referable to an angina occurrence but they
are not aware of it that is why it is called “silent
ischemia.”
w DM patients actually have CAD but they are
asymptomatic, but it does not mean that they don’t
have the disease.
w If you have patient with DM, don’t rely on chest pain
alone, you look other symptoms that would suggest the
presence of CAD.
w Implication of larger infarct size: higher incidence of
heart failure, higher mortality.
w 2016: If two patients developed Myocardial Infarction,
and one patient had a larger infarct size (particularly in
the left ventricle)
S The probability of cardiogenic shock is much
higher in an individual who have larger infarct.
w 2016: Again, the larger the infarct size, the higher
probability in developing heart failure or complications
of myocardial infarction.
• Treatment is a similar to non-diabetic in terms of controlling
the risk factors.
• Higher morbidity and mortality rates associated with
revascularization
§ L
§ May be due to the increased number of comorbidities
• Increased risk of restenosis after PCI
§ You should be more aggressive in giving antiplatelet
therapy.
• SURGICAL BYPASS (CABG) probably has improved
survival vs. PCI (Percutaneous Coronary Intervention) in
multi-vessel involvement (more than 1 coronary artery)
§ If at least 3 vessels in the coronary circulation are
affected (left anterior descending a., circumflex a., right
coronary a.) then CABG would be preferred as compared
to PCI because again the risk of restenosis in PCI is high.
§ In CABG, the extent of revascularization is more
complete and you improve the circulation even to the
unaffected vessels.
§ 2016: If you are asked: How would you revascularize in patients
with DM?
§ 2016: You do SURGERY: Coronary artery by-pass grafting
(better than angioplasty in patient with Diabetes who have
CAD, usually angioplasty is not successful in a patient who has
diabetes).

OTHER SYSTEMIC DISEASES

OBESITY • Increased CV mortality and morbidity
• Associated with increased prevalence of hypertension, glucose intolerance and
atherosclerotic CAD
• Abdominal obesity or central adiposity – sign of insulin resistance and glucose intolerance
§ Thin chest but big belly
• Distinct cardiac abnormality: increased total and central blood volume, increased CO,
elevated LV filling pressure.
§ They also have eccentric left ventricular hypertrophy
§ 2016: ↑CO = ↑WORKLOAD on the heart and this means that you are exposing the
heart to an earlier cardiovascular event.
2
§ 2016: Cut-off for obesity: >30 kg/m2; overweight: >25 kg/m
• Weight reduction – most effective therapy but should NOT be rapid to prevent
electrolyte abnormalities.
§ Gradual weight reduction is recommended BUT BUT BUT make sure that the patient
does not have a CAD. If you make a CAD patient exercise, he/she might have a
sudden cardiac death! They cannot tolerate much exercise.
§ 2016: Arrhythmias may develop as well as sudden cardiac death due to electrolyte
abnormalities
§ 2016: When you reach the age of 30, it’s much harder to lose weight. Start now!

THYROID DISEASE HYPERTHYROIDISM

• Palpitations, systolic hypertension, fatigue
• Sinus tachycardia – 40% (because of the increase in metabolism), MOST COMMON
vascular sign
• Atrial fibrillation – 15%
• Hyperdynamic precordium, widened pulse pressure in PE, increased S1 and P2
§ Widened pulse pressure due to increased blood volume
§ Most common cardiac condition that presents with widened pulse pressure: Aortic
regurgitation (has a diastolic blood pressure of ZERO.
• Increased incidence of mitral valve prolapse
§ Due to the effect of the hormone on the mitral valve structure
§ You may hear a midsystolic click
• Means- Lerman scratch
nd
§ Systolic pleuropericardial friction rub at the L 2 ICS
§ Due to hyperdynamic cardiac motion

HYPOTHYROIDISM
• Reduced cardiac output, stroke volume, heart rate, blood pressure, and pulse pressure.
• Pericardial effusion in 1/3 of patients even pleural effusions
§ They retain a lot of fluids
§ In patients who have hypercholesterolemia and apparently not responding to the
treatment (statin), then check for the thyroid function test because hypothyroidism
present also with elevated cholesterol and triglycerides.
§ Patients with hypothyroidism need to undergo echocardiogram for documentation,
because 33% have pericardial effusion
• ECG: sinus bradycardia, low voltage, QT prolongations, conduction disturbances
• Elevated cholesterol and triglycerides

9 | DLSHSI COLLEGE OF MEDICINE Batch 2018

COLLAGEN VASCULAR • Rheumatoid arthritis: pericarditis, pericardial effusions, coronary arteritis
DISEASES • Seronegative arthropathies (problems with arteries) are associated with pancarditis and
proximal aortitis, aortic insufficiency
• Systemic lupus erythematosus
§ Pericarditis
§ Libman-Sacks endocarditis – nonseptic vegetations; left-sided valves, may
embolize or become infected (infective endocarditis)

Use at your own risk.

Good luck, Batch 2018!

MERRY CHRISTMAS!!!

10 | DLSHSI COLLEGE OF MEDICINE Batch 2018