Chapter 15: Peripheral Vascular

Disease
Patient Evaluation
The Vascular Diseases
15
 PERIPHERAL VASCULAR DISEASE

The podiatric physician should be able to decide whether the patient is at

risk for developing complications based on arterial and venous insufficiency
to the tissues of the foot. The podiatrist should be able to evaluate whether
there is sufficient blood flow entering the foot and leg to sustain its normal
nutrition, to heal, and to sustain nutrition following surgery.
The lower extremity is predisposed to the development of vascular disease.
Some of the causes are: hypertension, hypercoagulability of blood,
the natural aging of the blood vessel walls, diet, tobacco use, oral
contraceptives, prostaglandins and even gravity. A misdiagnosis of vascular
disease may result in significant morbidity.

Patient Evaluation
1. Vascular History: the chief complaint and history of the present illness
often preclude the immediate diagnosis of vascular disease. Some clues to
follow:
a. Attempt to establish time relationships accurately (date of onset, etc.)
b. Attempt to separate symptoms that appear to be superficially similar
c. Try to identify the exact location of the symptom
d. Characterize the symptom as to type and severity
e. Delineate factors that aggravate or alleviate symptoms
f. Determine the effect of self-treatment or treatment by other physicians
g. Determine the progression/rate of symptoms
h. Evaluate the amount of disability imposed by the symptoms
i. Analyze any associated conditions or complaints
j. Document any previous studies and their results

NOTE* A study by Hershey et al (1984) revealed that majority of patients

with PVD undergoing major vascular reconstruction will have
concomitant problems: 60% had an abnormal EKG, 20% had a previous
Ml, 7% had CHF, 4% had previous arrhythmia and 7% had a previous
CVA. Thus, PVD occurs most frequently in the older population or as
part of conditions that compromise vascular integrity (such as diabetes
mellitus)
2. Pain: Arterial, venous, and even lymphatic diseases present with
manifestations, however, painful extremities are not necessarily a
manifestation of a disturbance in peripheral circulation.
a. History: Mode of onset, characteristics, progression, location, duration,
excerbating and alleviating factors, pain on walking flat surfaces/hills,
distance walked
b. Ischemic Pain: Severe persistent pain associated with ulcerated or
gangrenous ischemic tissue is indicative of a more severe arterial disease.
Ischemic complaints in order of frequency are pain, numbness,
coldness, tenderness, burning, fullness, and pallor, more severe during
excercise and localized in the muscles
c. Intermittent Claudication: The classic pain associated with chronic arterial
insufficiency is that of intermittent claudication. This symptom is defined as
a transient, exercise induced ischemic myalgia, characterized by aching,
cramping, tiredness, or tightness of the affected muscle group. Most
often seen in the calf muscles.
The extent of claudication is determined by measuring the number of blocks
walked, prior to the onset of symptoms (a treadmill can be substituted -set at
120 steps/minute and claudication time measured). Generally with arterial
blockage, the lesion occurs one joint or level above the muscle group in
which the symptoms manifest.
The differential diagnosis of intermittent claudication is- musculoskeletal
disorders, venous claudication, shin splints, tendonitis, Morton's neuralgia,
vitamin B1 deficiency, metabolic disorders (McCardle's disease),
and pseudoclaudication of spinal disease.
Intermittent claudication generally is not an indication for reconstructive
surgery unless the symptoms are debilitating.
d. Rest Pain: As the disease and ischemic changes progress, rest pain develops,
usually insidiously.
 Rest pain reflects severe ischemia.
Rest pain is produced by the body's shunting blood from the periphery to a
more central circulation when the person is sleeping. A buildup of
metabolites occurs in the muscles, resulting in pain.
Usually the patient is awakened every night at the same time, and must
get up or dangle the feet to alleviate the pain, sometimes these patients
sleep in a recliner to avoid this pain;

Note* No podiatric elective surgery should be done in patients with these

symptoms.

e. Ischemic neuropathy: Ischemia due to chronic/acute arterial occlusion will

result in an hypoxic condition of the peripheral nerves.
Pain is sharp, shooting, poorly localized, radiating throughout the entire
extremity following no distinct nerve root.
Pain described as tearing, pulling, or agonizing discomfort.
 Areas of occurence of intermittent claudication
Clinics in Podiatric Medicine and Surgery: Peripheral Vascular Disease, January 1992, Volume 9:1,
Saunders, Philadelphia, with permission

3. Edema: Can be a manifestation of many diseases, so must be carefully

evaluated as to whether it is bilateral from systemic disease or unilateral
from a regional condition, is the edema pitting (can be graded) or
nonpitting, and when/if does the edema disappear. The edema
associated with systemic disease is generally pitting and bilateral,
involving the entire lower leg/foot/toes
 Common causes of Edema in the lower Extremity
a. Systemic: CHF, nephritis, nephrosis, hypervolemia, hypoproteinemia,
hypothyroid, hyperadrenalism, lymphedema
b. Local: lymphangiectasis, lymphatic obstruction (filaria, tumors), pelvic or
abdominal masses, varicose veins, venous stasis, thrombophlebitis,
popliteal vein obstruction
c. Drug induced: corticosteroids, estrogen, progesterone, androgens,
phenylbutazone, MAO inhibitors, hydralazine, methyldopa
d. Other causes: angioneurotic edema and pretibial myxedema, Milroy's
disease

4. History of Emboli: Arterial emboli should be suspected whenever there

is a sudden and marked decrease in circulation to an extremity, with
sudden cyanosis of the foot or toes;
a. The source of arterial embolus is the heart in over 90% cases.
b. Conditions associated with emboli are:
i. mitral stenosis
ii. acute MI
iii. bacterial endocarditis iv. prosthetic valves v. aneurysms vi. stroke

5. Color and Temperature Changes: The color of the skin is directly

proportional to the degree of perfusion of arterial blood and oxygen
saturation of hemoglobin in the subpapillary venous plexus.
a. Pallor associated with sudden arterial occlusion, results from the absence of
arterial perfusion
b. Cyanosis occurs with decreased arterial perfusion of chronic arterial
insufficiency
c. Red/warm skin of erythromelalgia is the vasodilatory effect of the disease
d. Petechiae or pinpoint areas of cutaneous bleeding indicate capillary
fragility, which may arise in a number of conditions
e. Purpura, bluish/black areas of subcutaneous bleeding is the result of clotting
abnormalities or other diseases (see section Dermatology)
f. Telangectasias are visible dilations of capillaries which can result from
arterial or venous insufficiency
g. A drop in skin temperature of 6-8 degrees may indicate ischemia

6. Trophic Changes and Hair Growth: The nutritional changes of the skin and
appendages is directly affected by cutaneous circulation. Alterations in
arterial- flow can cause thickening, brittleness, longitudinal ridging and
slow growth of the nails. This can be confused with onychomycoses. The
disappearance of hair on the foot can be indicative of reduced arterial flow.

7. Past Medical History: Ten risk factors have been associated with
arteriosclerosis- chronic cigarette smoking, hypertension, diabetes mellitus,
hypercholesterolemia, hyperlipidemia, obesity, stress, lack of exercise, age,
and genetics.
a. Family history: Of any of the above
b. Medications/allergies
c. Medical care
d. Social factors
e. Past medical history: Important to assess the healing ability. Factors that
reduce the healing potential are anemia, alcoholism, uncontrolled diabetes,
neuropathy, rheumatoid arthritis, SLE, scleroderma, severe pulmonary
disease, polycythemia, sickle cell disease, treatment with antineoplastic
drugs, radiation therapy, high doses of prednisone, dialysis, and poor
nutrition.

Note* Adequate blood flow does assure adequate healing potential, but
inadequate blood flow will contribute to poor healing

8. Ulcerations: Commonly, ulcerations of the lower extremity may be the

first sign of PVD, however, they may occur secondary to hematologic,
endocrinic, dermatologic or systemic disease. Vascular ulcerations can be
due to ASO, venous stasis, thromboangiitis obliterans, acute arterial
occlusion, Raynauds phenomenon, emboli, and systemic hypertension.
(See Section Dermatology)

9. Gangrene: Due to impairment in circulation, can be either wet or dry.

Remember, pedal gangrene is not a diagnosis, but it is a symptom.

An adequate workup is required to determine the causes

a. Drugs- amphetamines, amobarbital, pentobarbital, meperidine HCL,
hydroxyzine HCL, sodium thiopental, propoxyphene HCL and ergotamine
(oral). When injected IV to the tissues these can produce extensive
necrosis.
b. Infectious Processes- meningococcic, staphylococcic or streptococcic
bacteremia (SBE), cholera, typhus fever, typhoid fever, pneumonia, and
trichinosis can produce gangrene of the digits.
c. Spontaneous Acute Occlusive Arterial Disorders- arterial embolism
(arteriosclerosis), spontaneous arterial thrombosis (thromboangiitis
obliterans, CHF, cardiac arrthymias)
d. Venous Thrombosis
e. Trauma to blood vessels
f. Compartment Syndrome
g. Exposure to low temperatures- frostbite
h. Mechanical, neurotrophic and metabolic factors
i. Vasospastic disease
j. Connective tissue diseases

10. Palpation of Peripheral Pulses: Peripheral pulses that are evaluated

are the radial, femoral, popliteal, posterior tibial, anterior tibial (dorsalis
pedis), and peroneal. These pulses should be graded according to rhythm,
symmetry, and amplitude.
a. Factors that reduce pulse amplitude: CHF, rapid atrial fibrillation,
numerous premature contractions, paroxymal tachycardia, aortic stenosis,
shock, and myocarditis.
Also included are: coarctation of the aorta, Leriche's syndrome, dissecting
aneurysm of the aorta, tumors of the abdominal cavity compressing
arteries, and edema overlying the artery.
Also included are: Vasospasm (Raynaud's disease, acrocyanosis, livedo
reticularis, later stages of frostbite, causalgia, post-traumatic vasomotor
disorders, disuse atrophy), chronic occlusive arterial disorders affecting the
large arteries, acute occlusion of large arteries, organic occlusion of small
arteries, congenital/acquired A-V fistula, Monckeberg's sclerosis, and
trauma to large arteries
b. Factors that increase pulse amplitude: Hyperthyroidism, hypertension,
aortic insufficiency, marked anemia, fever, physical exertion, and
erythromelalgia.
Also included are: lumbar sympathectomy, early stage of causalgia, Paget's
disease of Bone.
Also, Quincke's pulse is seen in the toenails in cases of aortic regurgitation,
patent ductus arteriosis, very slow heart rate with increased central pressure,
extreme increase in venous return and extreme dilatation of the small
arteries and arterioles. In cases of coarctation of the aorta, Quincke's
capillary pulsations are seen in the fingernails (dueto the increased pressure
above the coartation) but not in the toenails (due to the decreased
pressure below the coarctation)

Note* Please refer to Chapter 33: Anatomy, for description of the

complete circulation of the foot, however, some important arterial
anatomic facts are presented here:
1. The posterior tibial is the largest of the three pedal arteries and bears
major responsibility for perfusing all the plantar intrinsic muscles.
2. The dorsalis pedis is second in importance and is responsible for perfusing
the dorsum of the foot.
3. Ten percent of the normal population does not have a dorsalis pedis
artery, so the perforating peroneal can take its place.
4. Lack of pedal pulses may suggest anatomic variation rather than PVD, if no
other suggestions of vascular insufficiency are present

Palpation of peripheral pulses and corresponding arteriograms

(femoral and popliteal)
Palpation of peripheral pulses and corresponding arteriograms
(anterior and posterior tibial)

Note* When the PT is absent the DP can function as primary artery of the foot.
The entire foot can even be perfused by one pedal artery since they all
interconnect (an important concept in vascular reconstruction). Each toe
has 4 digital arteries, with the plantar arteries being larger than the dorsal
ones.
The lateral plantar digital artery of the hallux is larger than the medial
plantar digital artery of the hallux.
The medial plantar digital artery of the lesser toes is larger than their lateral
plantar diqital artery.
 Vascular anatomy to foot showing alternate circulation with
absent DP artery
Clinics in Podiatric Medicine and Surgery: Peripheral Vascular Disease, January 1992, Volume 9:1,
Saunders, Philadelphia, with permission

11. Non-Invasive Measurements of Arterial Flow: The most important

measurements of arterial inflow are easy to perform and consist of the
following
a. Ankle/Arm Pressure (Ankle/Brachial Index)- is the measurement obtained
by dividing the ankle systolic pressure by the arm systolic pressure. Use a
8MHz Doppler

Ankle/Arm Ratio Clinical Finding

A/A ratio=NOTE*
0.96 orFalsely
more elevated
Normal ankle pressures are seen with diabetes mellitus. This
A/A ratio=is0.71-0.95
due to either ASO Mild
or obstruction
Monckeberg's (intermittent
medial calcific
claudication)
sclerosis. The ABI
A/A ratio=should
0.31-0.70
not be the Moderate
sole criteria
obstruction
for vascular
(intermittent
assessment in these patients.
claudication/rest pain)
A/A ratio= 0.00-0.30 Severe obstruction (rest pain/impending
gangrene)
Note* If there is doubt about whether the ABI is falsely elevated, the
modified Carter exercise test can be used to differentiate.
Additionally, listen to the sounds of the artery, it should be either bi
b. Segmental or triphasic. Any abnormal swishing sound would indicate a
Pressures- proximal obstruction.
taken at the upper thigh, lower thigh, upper calf, and ankle. The ABI is
noted.
The criteria for this test are based on the 1-10-20-30 Rule of Thumb.

Note* The ABI index if less than 1 may indicate an obstruction.

The upper thigh pressure should be greater than 10mmHG greater than
the brachial pressure, if less there may be an obstruction. Pressure
differences between adjacent cuff sites on the same leg that exceed
20mmHg may indicate obstruction (some sources use a 30 mmHg
drop between sites).
Pressure differences of 30mmHg over the entire leg may indicate
obstruction.

c. Doppler Signal- Doppler recordings reflect flow velocity in a specific

vessel, the frequency of the emitted beam is altered by any object moving
faster than 6 cm/sec. If waveforms are being recorded, the faster the blood
can flow, the steeper is the recorded waveform. The qualitative audible
Doppler signal, when made into a tracing, shows that the normal arterial
pattern is a triphasic picture. A monophasic sound indicates arterial
pathology.
d. Photoplethysmography- is a modality used to provide an indication of
skin blood flow. The emitted beam of the PPG sensor is reflected by
hemoglobin molecules located in the cutaneous microcirculation. A
photoelectric detector measures this reflected beam and the signal is
transformed to be displayed as a recorded waveform looking more like a
narrow teepee. This waveform is representative of pulsatile flow in the
subpapillary plexus of the skin. This test should be correlated with digital
Doppler tests, noting discrepancies in the waveforms.
e. Digital Blood Pressure- this is obtained by placing an appropriate-sized cuff
around the digit, staying away from the joint. In normal digits without any
pathology the pressure is generally between 70-110 mmHg, and have
waveforms that look more like teepees than igloos.
f. Pulse volume recording (PVR)- pulse volume recording, reflects the volume of
blood that pulses under a sensor cuff, obtained by placing cuffs filled to 60
mmHg pressure around the parts to be measured. The PVR closely corresponds
to direct intra-arterial recordings at the level being tested. The waveforms
look like high teepees with a dicrotic notch. Changes in waveform
morphology between segments reflect severe stenosis or occlusions. The
waveforms should be analyzed for changes existing between segments and
for differences between left and right.
g. Five-Minute Reactive Hyperemia Test- used to aid in the differentiation of
vasospastic foot pathology from organic disease. In vasospastic disease,
blood flow is limited by increased tone of smooth muscles surrounding the
blood vessels; in organic disease by material clogging the lumen of the
vessels. This test can also be used to predict the success of a contemplated
sympathectomy.
 12. Invasive Measurements of Assessing Arterial flow:
a. Angiography for PVD is generally performed as a preoperative or
screening evaluation of the arterial tree in patients with non-healing ulcers,
rest pain, severe claudication, gangrene, and absence of pulses. Non-
invasive examinations should precede angiography to select the
appropriate candidates since this test is not without its potential
complications. The compounds used are either ionic or nonionic, both
with high iodide contents for its radiodensity. They cannot be done in
anyone who has iodine allergy. History of use of similar compounds (such
as an IVP for renal studies) and of thyroid disorders/medications is necessary,
with appropriate consultations.

Ionic Contrast vs. Nonionic Contrast

More painful on injection
Use in patients < 60
Less painful
Patients > 60
Use with patients with previous contrast reaction, history of
asthma, allergy to shellfish, cardiovascular disease, renal
failure, a diabetes

Both are toxic and can cause renal failure, hypotension, direct myocardial depression,
pulmonary edema, bronchospasm, convulsions and even stroke

NOTE* Adequate preparation of the patient is essential with hydration to

prevent renal complications. This involves infusing approx. 1000cc b.
sterile fluids within 24 hours of the procedure. Also given is Mannitol
(12.5 g) in patients with an elevated creatinine to effect an osmotic
diuresis to minimize nephrotoxicity. Oblique and lateral views are taken.
Digital substraction angiography (DSA) is a method of performing
angiography that uses computerized techniques to enhance contrast
visualization. The image before contrast injection is electronically
subtracted from the contrast images, leaving only opacified vessels on
the final image. A DSA image can only be obtained at one position per
injection of contrast. DSA complements regular angiography.

13. MRI: This study is now being done to assess distal runoff in the foot
when angiography is questionable or to double check angiography when
attempting to save a limb.

The Vascular Diseases

1. Treatment of Chronic Arterial Occlusive Disease: Patients with chronic
lower extremity ischemia should be divided into those with claudication
and those with limb-threatening ischemia.
a. Claudicators: Treatment can consist of conservative management
including exercise, elimination of tobacco/caffeine etc., control of
medical conditions. Pharmacological management includes Trental
(pentoxifylline) which alters blood flow characteristics by "softening" the
RBC.
b. Limb Threatening Ischemia: Gangrene, rest pain, or tissue loss is an
indication for revascularization. Options for revascularization include
endarterectomy, balloon angioplasty, atherectomy, and bypass grafting
(in-situ autologous vein or prosthetic material-Gortex).

NOTE* In diabetics the most common site of occlusion is just above the trifurcation
in the leg.
Femoral popliteal and popliteal-peroneal bypasses are most common
procedures in these individuals.

The treatment goal is to bypass all hemodynamically significant disease

down to the level of a continuous outflow artery to the foot.

2.. Venous Disease: The venous system is characterized by low pressure,

distensibility and high capacity. It is driven by the effects of respiration
on intraabdominal pressure, the calf muscle pump, and the venous valves.
Veins are superficial or deep, connected, by perforators. a. Venous
Thrombosis (DVT): Conditions predisposing a patient to DVT include
prolonged immobilization, bedrest with a recent MI, women confined to bed
during pregnancy or post Caesarean section, obesity, an underlying
malignancy, use of a tourniquet, a history of ulcerative colitis and Behcet's
syndrome, inherited hypercoagulative states and oral contraceptives.
Patients can present with pain and swelling of the leg, but additionally DVT's
can be silent. A patient with suspected DVT should undergo venography for
a definitive diagnosis. Treatment is with heparin initially (full anticoagulation
via IV administration), then coumadin to prevent pulmonary emboli, and to
inhibit further DVT

NOTE* Treatment with heparin is as follows: after drawing blood for a

coagulation profile, 5000 to 10,000 U of intravenous heparin is A
given followed by a constant infusion of 1000 to 1500 U/hour. The
activated thromboplastin time is kept at 2-2.5 times the baseline.
DVT prophylaxis is with subcutaneous heparin Q 8-12 hours.
long term sequelae of DVT is postphlebitic syndrome characterized by failure
of the calf muscle pump, increased ambulatory venous pressure, pain, edema,
skin and soft tissue changes, and ulceration.
b. Pulmonary Embolism: A potentially lethal complication of DVT. Heparin
coagulation is the treatment of choice. There are vena cava devices to
prevent pulmonary embolism while the patient is being treated for DVT.
c. Superficial Venous Insufficiency: Results in primary varicose veins.
d. Deep Venous Insufficiency: Results in secondary varicose veins are
related to incompetent perforator veins or deep venous system
insufficiency.

3. Diabetes and PVD: Diabetes is the seventh leading cause of death in the
United States. Vascular complications of diabetes are accelerated by
hypertension, cigarette smoking, hypercholesteremia, hyperglycemia, the
duration of diabetes, and the degree of blood sugar control.
a. Pathogenesis: The three most important factors that influence the
vascular complications of diabetes are- the duration of diabetes after
puberty, elevated blood sugar levels, and blood pressure. Diabetic
microangiopathy is a result of metabolic abnormalities caused by an
absolute or relative insulin deficiency. The development of neuropathy is a
critical factor in the rapid progression of peripheral arterial disease with
the concurrent development of autonomic denervation.

b. Pathophysiology: Microangiopathy is characterized by the thickening of

the basement membrane and arteriovenous shunting.
Hypercoagulability of blood components is recognized as a significant
factor in diabetic angiopathy. Hypertension can cause a threefold
increase in atherosclerosis in the diabetic.

Note* The use of Beta blockers for the treatment of hypertension is

contraindicated in the diabetic because of the unopposed alpha c. Signs
action. Calcium channel blockers or ACE inhibitors are the end
recommended drugs for diabetics.
Symptoms: Pain is the most common symptom. The three signs are-
blenching of the foot upon elevation, delayed venous filling time after
elevation, end rubor on dependency. Other signs end symptoms ere
pulseless feet, subcutaneous fat tissue atrophy, shiny skin, absent hair
growth on the lower extremities, and thickened nails.
d. Treatment: Exercise and diet, cholesterol control, cessation of cigarette
smoking, daily aspirin (?) (suppress prostaglandin production in
platelets/suppresses platelet aggregation), blood sugar control, blood
pressure control, drugs (PV dilators).

Note* Treatment for venous stasis ulceration is almost always conservative, 'with
compression therapy with graduated elastic compression stockings (30-40 mm
Hg), Unna Boot with DuoDERM hydroactive dressings etc., or the "Oregon
Protocol".

4. Vasospastic Disorders:
a. Raynaud's Vasospasticity: Divided into Raynauds phenomenon,
syndrome and disease. Phenomenon is the clinical presentation of the
discoloration sequence of pallor, cyanosis, end rubor accompanied by
paresthesias. Syndrome is the bilateral end symmetric recurrence of the
phenomenon that persists for longer periods of time with each incident,
and is associated with an underlying collagen or autoimmune disorder, or
with organic arterial disease. Disease is the state of a consistent
recurrence of discoloration with associated paresthesias upon exposure to
cold or emotional crisis that has not been identified to coexist with any
other disorder 2 to 3 years after the original presentation. All of these
forms of vasospesticity ere precipitated by exposure to cold water, ice,
cold ambient temperature, cold humid air, or a chilly wind.
b. Acrocyanosis: A condition characterized by persistent uniform cyanosis
of the feet and toes end associated plantar hyperhidrosis. Unlike
Raynaud's, the vesospesticity extends proximally beyond the digits.
c. Livedo Reticularis: A condition involving the arterioles of the skin
presenting with livid discoloration in a reticular pattern (mottled or lace-
like red-blue discoloration). Has an annular form, livedo annularis, and a
grape-like form, livedo annularis racemosa
d. Medications: The traditional vasodilators, isoxsuprine, pepavarine, niacin
are used in Raynaud's cases. Nitroglycerine 2% ointment applied in a
0.75 inch strip on the dorsum of the foot Q 5 hours has been beneficial
when oral vasodilators have failed. Calcium channel blockers (nifedipine
end diltiezem) have recently been studied for these disorders.
5. Lymphatic Diseases: Can be either primary or secondary lymphedema a.
Primary lymphedema: The classic indication of primary lymphedema is soft
tissue swelling as a result of lymph accumulation. This swelling arises without
cause and may not present bilaterally. It is associated with aplasia,
hypoplasia, or hyperplasia of the lymphatic channels, trunks, or nodes.
i. Milroy's Disease: Congenital/hereditary form of lymphedema, with the
edema noted at birth to be firm but pitting, chronic, permanent, and
confined to the lower extremity.
ii. Congenital Lymphedema: Congenital although no family history is
determinable, more prevalent than Milroy's disease, edema may be present
in the lower or upper extremities.
iii. Lymphedema Praecox: Hereditary, noncongenital manifesting itself in
early life (ages 9-25), seen predominantly in girls, a rapid onset
involving one foot and ankle, progresses to a nonpitting form. Treatment is
with an intermittent compression pump and compression stockings.
b. Secondary Lymphedema: Results from acute, repetitive or chronic
lymphangitis secondary to a known cause. The inflammation may be due
to direct trauma, foreign bodies, infection, or as a complication of venous
insufficiency with associated venous hypertension. It also may result as an
extention of acute cellulitis or deep thrombophlebitis.
i. Traumatic Lymphedema: From direct impact or lacerating injury to the large
pre- and post nodal collecting lymphatics, nodes, and major trunks.
ii. Infectious Lymphedema: From bacterial or filarial infections
iii. Neoplastic and Foreign Body Lymphedema
iv. Postphlebitic Lymphedema
v. Neuroplegic Lymphedema
c. Direct Lymphangiography: The gold standard of lymphatic system
imaging