- -

Vascular Surgery Prometric Test

|Io] gjo |Io] gjo |Io] gjo |Io] gjo
1. Rutherford's Vascular Surgery, 6th Edition.
2. Current Therapy in Vascular Surgery, 4th Edition.
|Io] uI aoL |Io] uI aoL |Io] uI aoL |Io] uI aoL


ea m n|m j ea m n|m j ea m n|m j ea m n|m j ulo mlI uo eja ulo mlI uo eja ulo mlI uo eja ulo mlI uo eja s] ulo s] ulo s] ulo s] ulo
drmohtaha@gmail.com ulo c|E]o uj j uj almj u |mj n|jI ulo c|E]o uj j uj almj u |mj n|jI ulo c|E]o uj j uj almj u |mj n|jI ulo c|E]o uj j uj almj u |mj n|jI



- -


1. Injury of the nerve passing with anterior bial artery causes what of the following:
a- loss of planter flexion of the foot
foot drop - b
c- loss of sensations at the foot and leg
d- loss of sensations at the sole
2. One of the following structures crosses the bifurcation of common carotid artery:-
common facial vein - a
b- vagus nerve
c- hypoglossal nerve
d- recurrent laryngeal nerve

The common facial vein branch of the internal jugular vein marks the site of the carotid bifurcation. After
dividing the facial vein, the internal jugular vein is retracted posteriorly to expose the carotid bifurcation.
The hypoglossal nerve crosses the vessels superior to the bifurcation.




- -

3. One of the following muscles present at the deep posterior group of the leg:
a- soleus
b- gastrocnemius
popliteus - c
d- tibialis anterior

4. One of the following muscles present at the superfascial posterior group of the leg:-
soleus - a
b- Flexor digitorum
c- tibialis posterior
d- popliteus

Muscles of the Posterior Fascial Compartment of the Leg
Superficial Group
Gastrocnemius Plantaris Soleus
Deep Group
Popliteus Flexor digitorum longus Flexor hallucis longus Tibialis posterior


- -

5. One of the structures that present during exposure of the subclavian artery at
supraclavicular approach:-
a- scalenus posterior muscle
b- recurrent laryngeal nerve
phrenic nerve - c
d- hypoglossal nerve


Branches of Subclavian artery
1st part 1. The vertebral artery 2. The thyrocervical trunk:
(a) inferior thyroid artery (b) transverse cervical artery (c) suprascapular artery
3. The internal thoracic artery
2nd part :- the costocervical trunk (supplying deep structures of the neck via its deep
cervical branch, and the superior intercostal artery, which gives o the 1st and 2nd
posterior intercostal arteries). 3rd part gives no constant branch.
Branches of Axillary artery
1st part: 1. superior thoracic artery
2nd part: 1. acromiothoracic artery 2. lateral thoracic artery
3rd part: 1. subscapular artery 2. anterior circumex humeral artery
3. posterior circumex humeral artery


- -

6. The vertebral artery is divided into V1, V2, V3, and V4, V4 passes through
intracranial - a
b- from the origin ll C6
c- from C6 ll C2
d- from C1 to the dura
Vertebral Artery


Internal Carotid Artery

- -


7. Which of the following is a branch from axillary artery:-
a- vertebral artery
acromial artery - thoraco - b
c- costocervical trunck
d- superior thyroid
8. The commonest vein anomaly is in:-
a- right renal vein
left renal vein - b
c- SVC
d- IVC
Left renal vein anomalies or variants:-
circumaortic and retroaortic

IVC anomalies:-
duplication, left IVC and absent hepatic portion

The left vertebral artery is usually larger and carries more blood.

9. The most common site for embolus impaction is in:-
a- common femoral artery
b- popliteal artery
c- iliac bifurcation
d- aortic bifurcation
10. The most common site for peripheral aneurysm is:-
a- external iliac artery
b- common femoral artery
c- superficial femoral artery
d- popliteal artery
11. ABI is more than 1 in the following disease:-
a- Burger disease
b- Raynaud,s disease
c- Diabetes patient
d- Cardiac patient
12. Ligaon of left renal vein during AAA repair can cause:-
a- frequently asymptomatic
b- 20% renal failure
c- 5% renal dysfuncon
d- should be avided

- -

13. Valves of the lower limb veins are composed of :-
a- 3 leaets b- intima only
c- intima and media d- intima, media and adventitia

Risk Factors for AAA
A type I endoleak (periprosthetic) occurs at the proximal or distal attachment
zones (or at both).
A type II endoleak is caused by retrograde flow from patent lumbar or inferior
mesenteric arteries.
A type III endoleak arises from a defect in the graft fabric, an inadequate seal, or
disconnection of modular graft components.
A type IV endoleak is due to graft fabric porosity, which often results in a
generalized mild blush of contrast material within the aneurysm sac.

- -

14. in AAA incidence in rst degree relaves:-
a- 5 15%
b- 3 5%
c- 10 20%
d- more than 20% (NB in Rutherford 15 25%)
N.B. Although popliteal aneurysms are the most common aneurysms of the lower
extremity and account for 70% of all lower extremity aneurysms, they are relavely
uncommon. Popliteal artery aneurysm is almost exclusively a disease of men.
Contralateral aneurysms were found in 50% and aorc aneurysms in 36%.
Takayasu arteritis
can be divided into the following 6 types based on angiographic involvement :
Type I - Branches of the aortic arch
Type IIa - Ascending aorta, aortic arch, and its branches
Type IIb - Type IIa region plus thoracic descending aorta
Type III - Thoracic descending aorta, abdominal aorta, renal arteries, or a combination
Type IV - Abdominal aorta, renal arteries, or both
Type V - Entire aorta and its branches
Classification criteria The American College of Rheumatology has established classification
criteria for Takayasu arteris (3 of 6 criteria are necessary). The presence of any 3 or more
criteria yields a sensivity of 90.5% and a specicity of 97.8%.

The criteria are as follows:
Age of 40 years or younger at disease onset
Claudication of the extremities
Decreased pulsaon of 1 or both brachial arteries
Dierence of at least 10 mm Hg in systolic blood pressure between arms
Bruit over 1 or both subclavian arteries or the abdominal aorta
Arteriographic narrowing or occlusion of the entire aorta, its primary branches, or
large arteries in the upper or lower extremities that is not due to arteriosclerosis,
fibromuscular dysplasia, or other causes.
Patterns of disease have also been described by geographic region. Stenotic lesions are
thought to be more common in Japan, whereas aneurysmal disease is more frequent in
India,Thailand, and Mexico.
Cardiac manifestations of TA are common. Coronary artery involvement occurs in 6% to
16% of patients with TA and may lead to ischemic symptoms or congestive heart failure.
Hypertension is one of the most common presenting signs in patients with TA and occurs
in 33% to 60% of paents. Bilateral stenosis of the subclavian arteries occurs in up to 92%
of patients with TA and can mask hypertension. Blood pressure measurements of both
upper and lower extremities should be performed in any patient suspected of having TA.
Congestive heart failure is the most common cause of death in patients with TA.

- -

Classification of Takayasus Arteritis


15. The least presentation of AAA is:-
a- colonic obstruction
b- hematuria and hydronephrosis
c- vomiting of bile
d- massive GIT bleeding
16. Warfarin's anticoagulant effect is inhibited by one of these drugs
a- ciprofloxacin b- metronidazole
c- rifampicin d- propranolol
N.B. The commonest cause of renal fistula is kidney biopsy.



- -

Statins
Statins decrease hepatic cholesterol synthesis, leading to the upregulation of LDL
receptors on the surface of hepatocytes. This increase in hepatocyte LDL receptors results
in increased clearance of LDL cholesterol particles from the serum, ultimately lowering
total serum LDL cholesterol levels.
Adverse Effects
a. 1.4% incidence of elevated hepac transaminases, Dose-dependent phenomenon that is
usually reversible
b. Myopathy (myalgias, myositis, rhabdomyolysis) c. Incident diabetes
d. Neuropathies e.Hemmorhagic stroke f. memory loss
When the FDA approved the rst stans in the late 1980s, doctors were told to do periodic
blood tests on anyone taking a statin to look for early signs of liver trouble. Millions of
statin users later, its clear that liver damage is extremely rare. It also cant be predicted by
checking liver tests every few months.
The FDA now says that you should have a liver function test soon after starting to take a
statin or after switching to a new one. If everything is fine, no further blood test is needed
unless a problem arises.
16. One of the following concerned to stans
a- the paent must check for liver funcons at 3,6,9 months
b- follow up for GB function
c- can cause myopathy
Angiotensin Converting Enzyme Inhibitors
Adverse Effects
Hypotension
Renal Insufficiency (if bilateral renal artery stenosis)
Hyperkalemia special group of patients (Na restricted, on K-sparing diuretic, COX
inhibitors)
Cough (20 %)
Angioedema
With captopril especially: neutropenia, nephrotic syndrome, skin rash, taste disturbances
(SH group- related).
Therapeutic Uses
Anti-hypertensive
Prevent or reverse LVH
Protect against sudden death and second myocardial infarction after acute MI
Improve survival and hemodynamics in patients with congestive heart failure
Protect against progression of diabetic and non-diabetic nephropathy

Additional Beneficial Effects of ACE Inhibitors:-
Cardioprotective
Reduce incidence of second heart attack
Reduce cardiovascular complications in patients with risk factors
Reduce incidence of diabetes in high risk patients
Reduce complications in diabetic patients

- -

17. ACE inhibitors are effective treatment in patients with PVD, in all except:-
a- good control of hypertension b- control of CHF
c- improve renal function in renal artery stenosis
d- decreases risk of MI
18. Self expanding stents, All are correct except:-
a- precise placement site b- used in tortuous arteries
c- foreshortening on deployment d- overriding
19. During excision of carotid body tumor more than 5 cm, to decrease intra-operative
bleeding do:-
a- preoperative radiotherapy
b- balloon in CCA
c- preoperative embolization of ECA
20. Carod duplex for heterogenous plaques, can show all except:-
a- hemorrhage
b- necrosis
c- calcification
d- ulceration
21. Smoking affect bleeding profile through:-
a- increase of blood viscosity
b- decrease in bleeding time
c- increase in coagulation time
d- increase in platelet function and platelet aggregation
POPLITEAL ARTERY ENTRAPMENT SYNDROME
This is a rare disorder with an esmated prevalence of 0.16% that occurs with a male-to
female rao of 15:1. Concomitant popliteal vein impingement occurs in up to 30%.
Twenty-five percent of cases are bilateral.
Five types of anatomic entrapment have been defined:-
I Popliteal artery is displaced medially around a normal medial head of the gastrocnemius
II Medial head of gastrocnemius, which arises lateral to popliteal artery
III Popliteal artery is compressed by an accessory slip of muscle form the medial head
IV Entrapment by a deeper popliteus muscle
V Any of the above plus popliteal vein
VI Functional entrapment
Noninvasive studies with ankle-brachial indices should be performed with the knee
extended and the foot in a neutral, forced plantar, and dorsiflexed position. A drop in
pressure of 50% or greater or dampening of the plethysmographic waveforms in plantar or
dorsiflexion is a classic finding. Although CT and MRI have been used, angiography
remains the most widely used test. Angiography performed with the foot in a neutral
position may demonstrate classical medial deviation of the popliteal artery or normal
anatomic positioning. Coexisting abnormalities may include stenosis, luminal irregularity,
delayed flow, aneurysm, or complete occlusion. Diagnostic accuracy is increased with the
use of ankle stress viewactive plantar flexion and passive dorsiflexion. The treatment of
popliteal artery entrapment consists of surgical decompression of the impinged artery
with possible arterial reconstruction.

- -


Range of diameters of normal arteries in adults.


Aneurysms in children are uncommon, tend to be congenital, and usually involve the
aorta. They are associated with a variety of anomalies, such as tuberous sclerosis, aortic
coarctation, and Marfans syndrome.
Aneurysms due to Developmental Anomalies:-
1. persistent sciac arteries
2. aberrant right subclavian artery and an associated Kommerell diverculum.
Common femoral artery aneurysms are most commonly pseudoaneurysms that occur after
percutaneous arterial puncture.
Popliteal aneurysms are the most common peripheral aneurysms.
Visceral Aneurysms
The most common of the visceral artery aneurysms is renal, and they represent 0.3% of
aneurysm repairs overall in our series versus 0.1% for the other visceral vessels.
Renal artery aneurysms are associated with fibromuscular dysplasia, arteritis, and
dissections, although they are most commonly degenerative.


- -


The splenic and mesenteric arteries are most commonly affected by aneurysm, followed
by the hepatic and celiac vessels. Visceral aneurysms can also occur in association with
diseases such as polyarteritis nodosa.
Splanchnic artery aneurysms
splenic artery, 60% hepac artery, 20%; SMA, 6%; celiac artery, 4%.
Splenic artery aneurysms, the most common type of splanchnic aneurysm, occur
predominantly in women during the sixth decade of life.
Infected aneurysms

Infected aortoiliac aneurysms

The most prevalent form of infected aneurysm was a post-traumatic infected false
aneurysm, the predominant infecng organism has been S. aureus (30%).

The predominant microorganisms associated with microbial arteritis leading to aneurysms
are Escherichia coli and Salmonella and Staphylococcus species.

Incidence of Cranial Nerve Dysfunction after Carotid Endarterectomy

22. 50% stenosis of an artery denong reducon of the cross-sectional area of the artery
by:- a- 50% b- 75% c- 90% d- 25%


- -

Estimation of Internal Carotid Artery Stenosis.
A PSV of 125 cm/sec recorded from a proximal diseased ICA segment is the
threshold for greater than or less than 50% stenosis.
Artery Diameters and Peak Systolic Velocities in Healthy Subjects
Duplex Classification of Peripheral Artery Occlusive Disease




- -

23.The following test does not need to be checked before convenonal angiography:-
a- bleeding time
b- PTT
c- PT
d- platelet count

Aspirin
Aspirin irreversibly acetylates the active site of cyclooxygenase, which is required for the
producon of thromboxane A2, a powerful promoter of platelet aggregaon.
Anplatelet therapy, principally with aspirin, reduced stroke by about 25%.
Antiplatelet therapy, principally with aspirin, increases the absolute risk of hemorrhagic
stroke by 3 per 10,000 treated paents.

Additive Benefits of Aspirin and Statins in
Secondary Prevention of CVD. Aspirin reduces risk of a first myocardial infarction by about
1/3 but unl then any decision to use aspirin in primary prevention should be an individual
clinical judgement by the healthcare provider. Aspirin and clopidogrel are not licensed for
primary prevention. For Secondary Prevention of CVD Clopidogrel monotherapy should
not be used first-line, but can be considered for patients with aspirin hypersensitivity.
Possible Additional Beneficial Mechanisms of Action of Higher Doses of Aspirin on CVD
Enhance nitric oxide formation,Decrease inflammation and Stabilize enadothelial function.
New data show that when clopidogrel and omeprazole are taken together, the
effectiveness of clopidogrel is reduced. Patients at risk for heart attacks or strokes who use
clopidogrel to prevent blood clots will not get the full effect of this medicine if they are
also taking omeprazole.

- -

Platelet activation leads to platelet aggregation. Various classes of antiplatelet therapies
act by disparate mechanisms to reduce platelet activation and clot formation. Aspirin
inhibits platelet aggregaon by inhibing the producon of thromboxane A2.
The thienopyridines, clopidogrel and ticlopidine, bind and inhibit adenosine diphosphate
(ADP) receptors on platelets thereby inhibiting glycoprotein IIb/IIIa-receptor activation
and preventing platelet aggregation. Dipyridamole interferes with platelet stimulating
factors like collagen through various mechanisms including the inhibition of
phosphodiesterase and inhibition of cellular uptake of adenosine. Dipyridamole may also
cause vasodilation.
Dipyridamole is currently available in two forms:
An immediate-release form, usually given as 50 to 100 mg three mes per day
A proprietary formulaon containing both aspirin (25 mg) plus extended-release
dipyridamole (200 mg), given two mes per day. Headache is a well known side effect of
dipyridamole and also may cause Gastric upset and/or diarrhea.
American College of Cardiology/American Heart Association guideline for the
management of patients with chronic stable angina recommend avoidance of
dipyridamole in patients with stable angina.

Glycoprotein IIb/IIa inhibitors directly interfere with platelet binding of fibrinogen, the
final step in platelet aggregation.
The thienopyridines, clopidogrel and ticlopidine, selecvely and irreversibly bind P2Y12,
one of the adenosine diphosphate (ADP) receptors on platelets. This binding inhibits ADP-
induced platelet glycoprotein IIb/IIIa-receptor activation and prevents platelet
aggregation.
Side effects of ticlopidine : The most serious complication of ticlopidine therapy is severe
neutropenia, which occurs in approximately 1 percent of paents. Thus, for the rst three
months of treatment, patients must undergo biweekly complete blood counts. This side
effect limits the utility of ticlopidine. Other common side effects, which occur more
frequently with ticlopidine than aspirin, are rash and diarrhea.
Cilostazol The antiplatelet agent cilostazol is a phosphodiesterase 3 inhibitor that is
used mainly for intermittent claudication in patients with peripheral artery disease and
also significantly reduced the risk of stroke .
24. Mechanism of acon of Clopidogrel is :-
a- inhibits AMP
b- inhibition of phosphodiesterase
c- inhibition of cyclooxygenase
d- inhibits ADP-induced platelet glycoprotein IIb/IIIa-receptor activation
25. Classicaon used in carod body tumor:-
a- Charlls classification b- Debakey classification
c- Shamblin classification d- Levels classification

- -

26. For the paent with the following angiography, the procedure of choice is:-


a- carotid-subclavian bypass
b- aorta-subclavian bypass
c- subclavian endarterectomy
d- Percutaneous angioplasty and stenting
Subclavian steal syndrome
The term "subclavian steal" refers to a phenomenon of flow reversal in the vertebral
artery ipsilateral to a hemodynamically significant stenosis or occlusion of the subclavian
artery. In most cases, subclavian steal is asymptomatic, does not warrant invasive
evaluation or treatment, and represents an appropriate physiological response to
proximal arterial disease. Subclavian steal syndrome implies the presence of significant
symptoms due to arterial insufficiency in the brain (ie, vertebrobasilar insufficiency) or
upper extremity which are supplied by the subclavian artery.
Coronary-subclavian steal
A coronary-subclavian steal phenomenon has been described in patients who have
undergone prior coronary artery bypass surgery (CABG) utilizing the internal mammary
artery (IMA). In the presence of a hemodynamically significant subclavian artery stenosis
proximal to the origin of the ipsilateral IMA, flow through the internal mammary artery
may reverse and "steal" flow from the coronary circulation during upper extremity
exercise. Coronary and graft angiography demonstrate retrograde flow in the involved
IMA during selective catheterization of the grafted coronary artery. Simultaneous
coronary and cerebrovascular ischemia have also been reported. Identification of a
significant subclavian artery stenosis prior to CABG can prevent this important problem.
Those patients with a high-grade subclavian artery stenosis should be treated
(percutaneously or surgically) prior to CABG.


- -

ETIOLOGY
Atherosclerosis is the most common cause of subclavian steal syndrome which is more
common on the left side, possibly due to a more acute origin of the left subclavian artery,
resulting in accelerated atherosclerosis from increased turbulence.
Other cause Takayasu arteritis
Extra-anatomic revascularization (eg, carotid-subclavian bypass, carotid transposition) is
the most common form of surgical correction for symptomatic subclavian artery stenosis.
The approach to therapy of subclavian steal associated with symptoms varies with the
clinical setting. In many patients, symptoms improve over time without treatment.
Interventional treatment is not usually warranted in patients with asymptomatic
subclavian stenosis/occlusion. Symptomatic patients with proximal subclavian artery
ulcerative occlusive disease complicated by embolization, in the absence of other
significant cerebrovascular disease, can be successfully treated by surgical removal or
exclusion of the proximal subclavian lesion. Percutaneous angioplasty and stenting (with
embolic protection) for embolism related to proximal subclavian artery is appropriate for
patients with short stenosis/occlusion at the origin of the subclavian artery.
AAA
Rupture risk is directly related to aneurysm size.
Acute expansion is considered an immediate precursor of rupture.
A triad of chronic abdominal pain, weight loss, and elevated erythrocyte sedimentation
rate in a patient with an AAA is highly suggestive of an inflammatory aneurysm, occur
predominantly in males in the 5th and 6th decades of life. The diagnosis is made
preoperavely on abdominal CT scan in approximately 50% of paents. The treatment of
IAAA is resection and grafting. Ureterolysis is fraught with danger and seldom indicated.
Administration of beta-blocking medications may offer the first effective nonsurgical
therapy for AAA. The classic triad of abdominal pain, cardiovascular collapse and
a pulsatile abdominal mass may often be present in patients with ruptured AAA.
Stent Characteristics
Ballon- expandable stents are the preferred choice for eccentric, heavily calcified lesions.
Self- expanding stents may require postdilation, not for ostial lesions but can be used for
tortuous arteries.

- -

Carotid body tumor
The carotid body is a collection of chemoreceptor cells in the adventitia of carotid
bifurcation for control of Ph, and is supplied by ascending pharyngeal artery from ECA and
Glossopharyngeal nerve .The commonest type of cervical paraganglionoma, derived from
neural crest ectoderm, occurs in the fourth and fifth decades.
Carod body tumor occurs more in femals, 5% bilateral, 5% locally malignant
5% systemacally malignant, 10% familial, 1% of neck tumors. The risk of malignancy is
greatest in young patients with familial tumors.
Diagnostic Evaluation
Carotid body tumors are usually detected by clinical examination, and the diagnosis is
confirmed by basic imaging. Diagnostic biopsy is avoided because paragangliomas are so
highly vascular, rarely malignant, and easily diagnosed with routine imaging modalities.
Ultrasound, computed tomography (CT), and magnetic resonance imaging (MRI) are all
effective for diagnosis; bilateral imaging is advocated to rule out multicentricity.
On ultrasound examination, carotid body tumors usually appear as solid, well-defined,
hypoechoic, hypervascular masses that characteristically splay the carotid bifurcation.
The tumor itself may exhibit a very active mixed signal pattern representing the extensive
vascularity of the tumor.
MRI and CT show a hypervascular tumor that does not invade the carotid. Positron
emission tomography is being used to diagnose paragangliomas with a diameter of less
than 1 cm and may be helpful in diagnosing small or mulcentric tumors.

Selective carotid angiogram demonstrating the classic characteristics of a carotid body
tumor. The bifurcation is widened by the tumor; note the contrast density of the tumor
blush, which illustrates the highly vascular nature of these tumors.
N.B. Glomus vagale causes splaying of ICA and ECA.


- -


Shamblins classification of carotid body tumors based on the degree of difficulty of
resection. Type I tumors are localized and easily resected. Type II tumors include tumors
adherent to or partially surrounding vessels. Type III tumors intimately surround or encase
the vessels and nerves. ECA, external carotid artery; ICA, internal carotid artery.
Treatment
Resection in subadventitial plane
Conservative in old age with small lesion
Preoperative embolization of ECA or covered stent within the first few centimeters of ECA
Recurrence 5%.

Risk Factors for AAA rupture
Available data suggest that, For a given sized AAA, female gender, hypertension, COPD,
current smoking status, and wall stress seem to be independent risk factors for rupture.

Family history for AAA and rapid expansion are probably risk factors for rupture, whereas
the influence of thrombus content and diameter ratio are less certain.
Other factors:-DM eccentric or saccular aneurysms. Large AAA diameter and
hypertension should increase wall tension and rupture risk. maximum
Transverse diameter remains the standard method of risk assessment for aneurysm
rupture.

- -

GRADING OF CAROTID DISEASE
B-mode imaging is the most appropriate method to evaluate the degree of narrowing, if
the degree of lumen diameter reducon is less than 50%.
In the ECST trial, the degree of stenosis was measured by comparing the residual lumen
diameter with the estimated diameter of the carotid bulb, whereas the NASCET trial
compared the residual lumen diameter with the diameter of the normal distal ICA.

The percentage diameter reduction can be estimated from diameter measurements as
follows:


- -

Classification of lower extremity arterial stenosis


Classification of renal artery stenosis



Bypass Graft Failure
1. <30 days technical error, hypercoagulable state, or inadequate outflow
2. 1- 6 months residual lesion
3. 6 -24 months myoinmal hyperplasia
4. >24 months progression of atherosclerosis


- -

Observable characteristics of venous thrombus

27. Paent with aorto-iliac occlusive disease, angiography revealed bilateral external iliac
and inferior mesenteric occlusion, the procedure of choice is :-
a- aorto- bifemoral bypass graft, end of graft to side of aorta
b- aorto- bifemoral bypass graft, end of graft to end of aorta
c- axillo-bifemaral bypass
Aorto- bifemoral bypass
For most patients, an end-to-end aortic anastomosis is preferred for several reasons. First,
because all blood flows through the graft, there is less chance of competitive flow through
the native aortoiliac vessels that may potentially increase the incidence of graft limb
thrombosis. Second, an end-to-end anastomosis is theoretically a hemodynamically
superior configuration. It is associated with less perianastomotic turbulence and therefore
a smaller likelihood of developing recurrent atheroma or an anastomotic aneurysm. In
addition, the end-to-end anastomosis is less likely to cause distal atheromatous
embolization and is easier to cover with retroperitoneal tissue after implantation than the
end-to-side anastomosis, which tends to protrude anteriorly off the aorta. This
consideration may reduce the potential for late graft-enteric fistula formation.
End-to-Side Aortic Anastomosis
in patients with either a sizable accessory renal artery arising from the infrarenal aorta or
a large, patent inferior mesenteric artery. Although these branch vessels may be preserved
by reimplanting them into the body of an end-to-end graft, it is clearly easier to achieve
this objective with the end-to-side aortic anastomosis that maintains the native antegrade
aortic blood flow. More commonly, an end-to-side is used in patients in whom most of
their occlusive disease is located in the external iliac arteries. An end-to-side graft
configuration that maintains antegrade pelvic circulation via the hypogastric systems is
clearly desirable in these circumstances.
28. For stenting of SFA after balloon angioplasty, the following is true:-
a- indicated if there is a small dissection. b- stenting is done every time after PTA
c- if there is a remaining stenosis more than 30%

- -

29. 9 months aer femoro-popliteal bypass by saphenous vein graft, the most important
cause of graft failure is :-
a- intimal hyperplasia b- technical defect
c- progression of the underlying cause d- residual lesion

30. Type I endoleak after EVAR is:
a- leak occurs at the proximal or distal attachment zones (or at both).
b- caused by retrograde flow from patent lumbar or inferior mesenteric arteries
c- leak from defect in graft fabric
d- endoleak is due to graft fabric porosity
31. Type II endoleak aer EVAR is caused by:-
a- leak occurs at the proximal or distal attachment zones (or at both).
b- leak from defect in graft fabric
c- leak from collateras
d- endoleak is due to graft fabric porosity
32. Duplex ndings in carod body tumor include the following except:-
a- deviation of both ICA and ECA
b- hypoechoic lesion
c- intra tumor thrombus
d- hypervascular lesion
33. In angiography for proximal subclavian artery stenosis, loss of dye in vertebral artery
means :-
a- improper collaterals from innominate artery
b- incomplete circle of Willis
c- occluded vertebral artery
d- Flow reversal in vertebral artery
34. Sclerosing agents that may cause skin necrosis:-
a- Sodium tetradecyl sulphate
b- Polidocanol
c- Sodium morrhuate
d- Ethanolamine oleate
35. For good resoluon during angiography and angioplasty for distal lesions :-
a- increase the rate of dye injection
b- increase the dye concentration
c- increase sequence
d- use of ????
36. The skin lesion in Lymphangiosarcoma after cancer breast surgery is :-
a- skin pigmentation
b- blue skin nodules
c- skin ulceration

- -

37. In patients with superficial venous reflux, the following is true :-
a-venous stripping can worse the patient if there is deep venous reflux
b- GSF stripping to just below the knee can improve the patient
c- Trendelenberg operation is the operation of choice
38. One of the following is concerning the saphenous nerve:-
a- leaves the GSV at the knee
b- enter the saphenous opening with the GSV
c- accompanies GSV all through its course till saphenous opening
d-supply ankle and foot
39. The most common complicaon of long standing lymphedema is:-
a- Angiosarcoma
b- deep venous insufficiency
c- pitting edema
40. Male paent, 45 years, heavy smoker is showing the following picture, the most
possible diagnosis is:-

a- Reynaud's disease
b- Burger's disease
c- Scleroderma
d- Takayasu disease
41. Male paent, 50 years, heavy smoker is showing the following angiography

a- Marfan syndrome b- Takayasu disease
c- Burger's disease d- popliteal entrapment

- -

42. The most common disease causes congenital aneurysm is:-
a- Marfan syndrome
b- Takayasu disease
c- Fibromuscular dysplasia
43. The most common artery affected by Fibromuscular dysplasia is:-
a- renal artery
b- internal carotid artery
c- retinal artery
d- external iliac artery
44. Clinical picture of Pseudoxanthom elasticum include all except:-
a- GIT bleeding
b- hematuria
c- constrictive pericarditis
d- ischemic heart disease
45. Absence of pedal pulse on knee exion occurs in :-
a- popliteal entrapment
b- Burger's disease
c- popliteal cystic adventitial disease
N.B. Angiography in popliteal cystic adventitial disease
Scimitar sign
46. in polytrauma paent with vascular injury, the following item mandates direct push to
O.R. without investigations:-
a- palpable thrill at the groin
b- history of massive bleeding at scene
c- weak pulse if compared to contralateral extremity
d- Peripheral nerve deficit
47. Paent with gunshot injury at the leg , but there is palpable pulse, the following
investigation is needed to exclude vascular injury:-
a- CT Angiography
b- Conventional angiography
c- MRA
d- Duplex

48. Paent with chronic L.L. ischemia operated with synthetic graft for bypass, he can take
first generation cephalosporin during:-
a- as long as IV cannula is present
b- during the operation only
c- the rst 24 hours post-operative


- -

49. The most common risk factors for AAA rupture, includes all except:-
a- hypertension
b-positive family history for AAA
c- male gender
d- COPD

50. male paent with severe blunt chest trauma with fracture ribs, the following
angiography was done , what is the diagnosis?

a- type A aortic dissection
b- type B aortic dissection
c- descending aortic aneurysm


- -


51. male paent with severe blunt chest trauma, the following angiography was done ,
what is the diagnosis?

a- Coincedental thoracic aortic aneurysm
aortic disruption at the aortic isthmus - b
c-injury and leak in right subclavian artery
d- injury and leak in innominate artery
52. What is the second most common cause of synthetic graft failure in renal dialysis
patients:-
a- pseudoaneurysm
infection - b
c- arterial steal
d- Thrombosis
Vascular Access Associated Steal Syndrome
Constructing vascular access for hemodialysis causes changes in
blood flow to the extremity, which can lead to distal ischemia.
Ischemic steal syndrome is manifested by pain; weakness; pallor;
and, in severe cases, ulceration and tissue loss. Severe ischemia,
requiring reintervention, has an incidence of 5%, although some
degree of ischemia causing pain or parasthesias occurs in 10% to
20% of paents following access construcon.
Pathophysiology may be on the basis of inadequate arterial collateral
inflow due to occlusive disease, particularly involving the mediumsized
vessels, or high flow in a fistula exceeding the inflow capacity in
the absence of intrinsic occlusive disease of the inflow arteries.
Predicting steal remains difficult, although certain patient characteristics
and preoperative techniques can help identify those patients in whom
arteriovenous fistulas have an increased risk of causing steal. Patients with

- -

diabetes, multiple access procedures, and constructions based on proximal
arteries are more prone to ischemia.
Operative techniques for correcting steal include arteriovenous
fistula ligation, percutaneous transluminal angioplasty, banding or
restrictive procedures, and distal revascularization interval ligation
or modifications of this technique.

Operative intervention for ischemic steal syndrome successfully
resolves ischemia in 80% to 95% of paents.Some paents can have
persistent pain despite healing of ulceration. Blood flow can reverse in the
distal vascular bed so that retrograde flow will be present in the artery just
distal to the stula in 80% to 90% of all AV stulas. Reversal of distal
arterial flow usually occurs when the diameter of the fistula opening
exceeds the diameter of the inflow artery. Distal pulses are frequently
diminished or absent. Despite these physiological changes, clinically evident
ischemia may not be present.
AV grafts typically develop steal immediately following surgery.
Ischemia caused by autologous fistulas presents later as the vein
matures and dilates, allowing increased blood flow.
Compression of the shunt often relieves symptoms temporarily and
augments the distal pulse.
Classification of Steal Symptoms in Patients with Arteriovenous Shunts

Treatment
1. DRIL
2. Revision using distal inflow (RUDI).
3. Proximalization of the arterial inflow.
4. Simple ligation of the brachial artery without
revascularization. Blood flow distal to the ligation was
maintained by collateral blood vessels.
5. Simple arterial bypass graft from the artery just
proximal to the fistulas to a site just distal to the
fistula (without arterial ligation).

Banding, partial suturing, application of a clip, or other methods to
restrict shunt diameter remain accepted procedures for reducing
blood flow in the graft, although one must be careful because
thrombosis frequently complicates this approach.



- -


53. Cysc medial necrosis (CMN) is associated with :-
a- Marfan's syndrome
b- Turner syndrome
c- Dawn syndrome

Cystic medial necrosis (CMN) is a disorder of large arteries, in particular the aorta,
characterized by an accumulation of basophilic ground substance in the media with cyst-
like lesions. CMN is known to occur in certain connective tissue diseases such as Marfan
syndrome, Ehlers-Danlos syndrome, and annuloaortic ectasia, which usually result from
degenerative changes in the aortic wall. The relationships between CMN and congenital
heart defects as well as other disorders have been evidenced.

54. Heterogenous carod plaques by duplex, means all except:-
a- hemorrhage
b- necrosis
c- calcification
d- ulceration


55. The best management of retrohepac IVC injuries is :-
a- IVC ligation b- liver resection and repair
c-extensive mobilization of the liver and repair
d- perihepatic packing and observation










- -

IVC Injuries
The IVC is the most commonly injured abdominal vessel and accounts for about 25% of
abdominal vascular injuries. Blunt trauma is responsible for about 10% of IVC injuries, and
it usually involves the retrohepatic part of the vein.
Infrarenal IVC
Many injuries to the IVC, especially those involving the infrarenal IVC, present with stable
hematomas. As a rule, all hematomas due to penetrating trauma should be explored. An
exception to this approach is stable retrohepatic hematomas. The infrarenal and
juxtarenal IVC are best exposed by mobilization and medial rotation of the right colon, the
hepatic flexure of the colon, and the duodenum.
Exposure of the retrohepatic IVC is technically challenging and usually requires
extensive mobilization of the liver by dividing its ligaments and extending the incision to
include a right subcostal incision, right thoracotomy, or sternotomy. In our experience, a
subcostal incision provides excellent exposure and is preferred. A median sternotomy is
performed if an atriocaval shunt is anticipated. These additional incisions should be
considered only if perihepatic packing is not effective in controlling the hemorrhage.
In cases in which packing is not effective and the additional incisions are not sufficient for
adequate visualization and repair of the IVC or hepatic veins, other more radical
maneuvers may be considered. Such maneuvers include hepatic vascular isolation, an
atriocaval shunt, or division of the liver.
Hepatic Vascular Isolation. Hepatic vascular isolation involves cross-clamping the
infradiaphragmatic aorta, suprahepatic IVC, infrahepatic IVC above the renal veins, and
portal triad.

56. Evaluation of carotid shunt function during CEA to ensure that antegrade flow is
present :-
a- carotid stump pressure
b- EEG
c- Transcranial Doppler
d-application of a hand held Doppler probe to the shunt tubing


Interactions of Warfarin with Drugs and Food

Many drugs and foods interact with warfarin, including antibiotics, drugs affecting the
central nervous system, and cardiac medications. Many of these drug interactions increase
warfarin's anticoagulant effect.
Warfarin's anticoagulant effect was potentiated by 6 anbiocs (cotrimoxazole,
erythromycin, uconazole, isoniazid, metronidazole, and miconazole); 5 cardiac drugs
(amiodarone, clofibrate, propafenone, propranolol, and sulfinpyrazone); phenylbutazone;
piroxicam; alcohol (only with concomitant liver disease); cimetidine; and omeprazole.
Three patients had a hemorrhage at the time of a potentiating interaction (caused by
alcohol, isoniazid, and phenylbutazone).
Warfarin's anticoagulant effect was inhibited by 3 anbiocs (griseofulvin, rifampin, and
nafcillin); 3 drugs acve on the central nervous system (barbiturates, carbamazepine, and
chlordiazepoxide); cholestyramine; sucralfate; foods high in vitamin K; and large amounts
of avocado. Alcohol increases the metabolism of Warfarin (decreases the effect).


- -


COAGULATION
Antithrombin
Antithrombin is a serine protease inhibitor of thrombin and also inhibits factors IXa, Xa,
XIa, and XIIa. Thrombin is irreversibly bound by antithrombin and prevents thrombins
action on fibrinogen, on factors V, VIII, and XIII, and on platelets. This anticoagulant is
synthesized in the liver and endothelial cells, and has a half-life of 2.8 days.
Protein C, S and Z
Protein C is a vitamin K dependent anticoagulant protein that, once activated by thrombin,
will inactivate factors Va and VIIIa, thereby inhibiting the generation of thrombin.
Additionally, activated protein C stimulates the release of t-PA. It is produced in the liver
and is the dominant endogenous anticoagulant with an eight-hour half-life. Protein S is
also a vitamin K dependent anticoagulant protein that is a cofactor to activated protein C.
Additionally, protein S appears to have independent anticoagulant function by directly
inhibiting procoagulant enzyme complexes.
Protein Z Mediates thrombin adhesion to phospholipids and stimulates degradation of
factor X by ZPI (Protein Z-related protease inhibitor).

Coagulation begins almost instantly after an injury to the blood vessel has damaged the
endothelium (lining of the vessel). Exposure of the blood to proteins such as tissue factor
initiates changes to blood platelets and the plasma protein fibrinogen, a clotting factor.
Platelets immediately form a plug at the site of injury; this is called primary hemostasis.
Secondary hemostasis occurs simultaneously: Proteins in the blood plasma, called
coagulation factors or clotting factors, respond in a complex cascade to form fibrin
strands, which strengthen the platelet plug.

It is now known that the primary pathway for the initiation of blood coagulation is the
tissue factor pathway. The pathways are a series of reactions, in which a zymogen(inactive
enzyme precursor) of a serine protease and its glycoprotein co-factor are activated to
become active components that then catalyze the next reaction in the cascade, ultimately
resulting in cross-linked fibrin.

Tissue factor pathway (extrinsic)
Following damage to the blood vessel, FVII leaves the circulation and comes into
contact with tissue factor (TF which was formerly known as factor III or
Thromboplastin) forming an activated complex (TF-FVIIa).
TF-FVIIa activates FIX and FX.
FVII is itself activated by thrombin, FXIa, FXII and FXa.
The activation of FXa by TF-FVIIa is almost immediately inhibited by tissue factor
pathway inhibitor (TFPI).
FXa and its co-factor FVa form the prothrombinase complex, which activates
prothrombin to thrombin.
Thrombin then activates other components of the coagulation cascade, including
FV and FVIII.



- -



Contact activation pathway (intrinsic)
The contact activation pathway begins with formation of the primary complex on collagen
by high-molecular-weight kininogen (HMWK), prekallikrein, and FXII (Hageman factor).
Prekallikrein is converted to kallikrein and FXII becomes FXIIa. FXIIa converts FXI into FXIa.
Factor XIa activates FIX, which with its co-factor FVIIIa form the tenase complex, which
activates FX to FXa. The minor role that the contact activation pathway has in initiating
clot formation can be illustrated by the fact that patients with severe deficiencies of FXII,
HMWK, and prekallikrein do not have a bleeding disorder. Instead, contact activation
system seems to be more involved in inflammation. Patients without FXII (Hageman
factor) suffer from constant infections.
Final common pathway
Thrombin has a large array of functions. Its primary role is the conversion of fibrinogen to
fibrin, the building block of a hemostatic plug.
Cofactors
Calcium
Phospholipid
Vitamin K
Regulators
Protein C
Antithrombin
Tissue factor pathway inhibitor (TFPI).
Plasmin
Prostacyclin (inhibits platelets activation)


- -


Laboratory Tests of Thrombosis
Hypercoagulable Disorders


Nonlipid Lowering Effects of Statins



- -

57. Female paent with thigh supercial thrombophlebis, the most proper
management:-
a- surgery
b- venous duplex
c- antibiotic, anti-inflammatory and compression
d- anticoagulation with Warfarin

58. Male paent with a venous ulcer of 3 years duraon, duplex revealed incompetent
saphenous vein, the treatment should be:-
a- GSV stripping
b- GSV endovenous ablation
c- compression
d-skin graft

Percutaneous Transluminal Angioplasty in femoropopliteal
artery disease
Despite the higher immediate success, routine stenting was not associated with
a significant reduction in the rate of restenosis or target vessel revascularization (TVR).
Current data do not support use of routine stenting as the primary endovascular
treatment for short SFPA lesions. TASC II recommends PTA as the initial preferred option
for endovascular treatment of symptomatic SFPA lesions, reserving provisional stenting
for salvage therapy after a suboptimal or failed result from balloon dilation.

Endovascular stenting avoids the problems of early elastic recoil, residual stenosis, and
flow-limiting dissection after balloon angioplasty and can thus be used for the treatment
of long and calcified lesions. In contrast, SFPA is subject to longitudinal stretching, external
compression, torsion, and flexion, which may lead to stent fractures and eventually to
restenosis.

Immediate technical success after PTA was defined as residual stenosis less than 30%
without flow-limiting dissection. PTA with provisional stenting should remain the
preferred endovascular therapy for patients with SFPA disease.

Iliac Artery Angioplasty
Percutaneous angioplasty is widely used for the treatment of iliac artery occlusive disease.
Stent placement is used in lesions not amenable to balloon angioplasty, in complications,
and recurrences. Evidence suggests that balloon angioplasty is the procedure of choice for
iliac artery occlusive lesions. Stent placement should be reserved for angioplasty failures.
However, primary stent placement is indicated in total occlusions. Lesion morphology is an
important determinant of immediate success and long-term patency. TASC lesions
type A and B are best treated with angioplasty and stenting, while TASC lesions type C and
D show better results with surgical treatment.

The technical success of the intervention is judged not only by the angiographic
appearance, but most importantly by measurement of the pressure gradient across the
lesion. Less than 20% residual stenosis and < 10 mm Hg systolic pressure gradient is
considered a technical success. When in doubt, the pressures are measured following
vasodilator injection distal to the lesion (200 mg of nitroglycerin or 15-25 mg of tolazoline)
: more than 15mmHg systolic pressure gradient represents a technical failure. The decision
for successful PTA should be based on the translesional pressure gradient measurement ;
angiographic criteria are not reliable.

- -


Stent placement is indicated to address a technical failure, or a complication of PTA ;
heavily calcified and eccentric lesions do not respond to PTA alone. Elastic recoil is another
cause of PTA failure. Recurrent stenosis after PTA and flow-limiting dissection are
indications for stenting. Primary stenting is the practice of using stents as the initial
treatment modality instead of trying to achieve successful results with PTA alone.
Chronic occlusions are best managed by primary stenting. In the case of lesions suspected
as sources of emboli, stenting is indicated to trap embolic material between the arterial
wall and the stent mesh. Nevertheless, the efficacy of this practice still remains unproven.


CEAP Classification of Lower Extremity Chronic
Venous Disease













- -


Historic and New Anatomic Terms of Lower Extremity Veins






Anatomy of the superficial veins of the lower extremity





- -

Risk Factors for Varicose Veins





Pathophysiology of CVI
There are three basic mechanisms that lead to raised AVP and the symptoms and signs of
CVI: (1) muscle pump dysfuncon, (2) valvular reux, and (3) venous obstrucon.
Reflux is present in more than 90% of paents with CVI; 5% to 10% have isolated deep,
30% to 50% isolated supercial, and 50% to 60% combined. In general, superficial reflux
has a better prognosis than deep reflux (especially when the latter is postphlebitic), and
proximal reflux has a better prognosis than distal reflux.

59. During supraclavicular approach of the subclavian artery, one of the following
structures is not found:-
a- scalenus anterior
b- vagus nerve
c- phrenic nerve
d- vertebral artery

60. During distal exposure of ICA, which of the following structures is divided:-
a- internal jugular vein
b- lingual artery
c- posterior belly of digastrics muscle
d- hypoglossal nerve

61. The lowest infecon rate occurs in:-
a- carotid endarterectomy with patch closure
b- fem-fem bypass
c- Axillo-bifemoral bypass
d- aorto-bifemoral bypass




- -

62. Patient with stab wound in the zone I of the neck, the next step in management is:-
a- immediate exploration
b- observation
c- Angiography
d- duplex US

63. Patient with a stab wound in a limb with external bleeding, the best treatment is:-
a- tourniquet
b- external compression followed by wound exploration at OR
c- Extension of the wound
d- control of bleeding at ER

64. The most common organism found in synthetic graft infection is:-
a- Staphylococcus aureus
b- Pseudomonas aeruginosa
c- Staphylococcus epidermidis
d- Escherichia coli
Vascular Graft Infections
Early-appearing gra infecons occur within the rst 4 months following vascular
bypass surgery and are associated with virulent pathogens. Patients present with classic
signs of graft sepsis, such as fever, leukocytosis, and bacteremia. The pathogens are easily
identified by cultures of blood or perigraft tissues. S. aureus continues is the most
prevalent pathogen.
Gram-negative bacteria are also implicated in early graft infection. Pseudomonas
aeruginosa infection is most commonly associated with anastomotic bleeding. Graft
healing complications, such as graft-enteric erosion or fistula, typically involve infection
with gram-negative enteric bacteria and can develop in both the early and late
postoperative periods.
Late-appearing infections are most frequently the result of graft colonization by
Staphylococcus epidermidis or other coagulase-negative staphylococci. These indolent
infections manifest themselves months to years after implantation and have replaced
early graft infections as the most common presentation in vascular patients

Zones of the Neck




- -

The widely accepted pracce is that zone 2 injuries are explored in the operating room,
whereas zone 1 and 3 injuries require angiography.
Hard signs of vascular injury (active bleeding, expanding hematoma,
bruit/thrill, pulse deficit, central neurologic deficit).
Patients with zone 2 penetrang neck wounds can be safely and accurately evaluated by
physical examination alone to confirm or exclude vascular injury.

Preoperative arteriography is recommended in all patients with zone 1 penetraon if they
are hemodynamically stable and do not have evidence of active hemorrhage.
It is recommended because these injuries are frequently clinically occult and their
exposure technically challenging. Angiography appears to be essenal in zone 3
neck wounds because of the potential inaccessibility of distal vascular injuries.

Ultrasonography has been used for penetrating neck trauma, but its utility is limited to
zone II neck injuries. In addition, subcutaneous air, fragments, and hematomas make
ultrasound less reliable.
Angiosarcoma (Lymphangiosarcoma)
Stewart-Treves syndrome is a rare, deadly cutaneous angiosarcoma that develops in long-
standing chronic lymphedema. Most commonly, this tumor is a result of lymphedema
induced by radical or conservative mastectomy to treat breast cancer.
Chronic lymphedema from other causes may also be associated with Stewart-Treves
syndrome. The skin in patients with Stewart-Treves syndrome tends to become atrophic
and eventually pachydermatous, with prominent wrinkle lines. At times, hyperkeratoses
and telangiectasias can be observed.
Aer an interval of 1-30 years, a purplish patch appears that then develops into a plaque
or nodule in the area of chronic lymphedema. Other initial lesions of Stewart-Treves
syndrome may include a palpable subcutaneous mass or a poorly healing eschar with
recurrent bleeding and oozing.

The lesions of Stewart-Treves syndrome typically appear as multiple reddish blue macules
or nodules that may become polypoid. Around these nodules, small satellite areas can
develop and become confluent, forming an enlarging lesion. Sometimes, a bullous
component may be seen. Thus, the morphology may be heterogeneous, with
hematomalike lesions, multiple bluish-reddish nodules, and asymptomatic nodules.

As the angiosarcoma continues to grow and expand, the overlying atrophic epidermis may
ulcerate, producing recurrent episodes of bleeding and infection. Necrosis may be evident
in advanced cutaneous tumors.

Ultimately, extensive cutaneous nodules and systemic metastases appear. These nodules
most commonly occur in the lungs and cause the patient's death. Not every tumor in an
area of lymphedema is an angiosarcoma.
Lymphangiosarcoma is a misnomer because this malignancy seems to arise from blood
vessels instead of lymphatic vessels. A more appropriate name is hemangiosarcoma.
Lymphangiosarcomas are extremely aggressive tumors with a high local recurrence rate
and a tendency to metastasize early to many areas. Long-term survivors are the
exceptions.


- -

65. The Treatment of Hyperhomocysteinemia is:-
a- Folic acid
b- Zinc
c- Vit. A
d- Iron
N.B. oral supplementaon with the combinaon of folic acid, B6-, and B12-vitmains
substantially lowers circulating homocysteine levels.

66. Measurement of toe pressure is more accurate than ABPI:-
a- D.M. and ESRD
b- PVD
c- Burger's disease
d-Popliteal entrapment syndrome

67. Patient presented by bilateral LL edema, scrotal swelling, hematuria. Diagnosis is:-
a- IVC obstruction
b- Left renal artery thrombosis
c- Left renal vein thrombosis
d- Portal vein thrombosis

N.B. IVC obstruction: The classic presentation of IVCT includes bilateral lower extremity
edema with dilated, visible superficial abdominal veins.
Renal Vein Thrombosis
Although renal vein thrombosis (RVT) has numerous etiologies, it occurs most commonly
in patients with nephrotic syndrome (ie, >3 g/d protein loss in the urine,
hypoalbuminemia, hypercholesterolemia, edema). The syndrome is responsible for a
hypercoagulable state. The excessive urinary protein loss is associated with decreased
antithrombin III, a relative excess of fibrinogen, and changes in other clotting factors; all
lead to a propensity to clot.
The renal vein may also contain thrombus after invasion by renal cell cancer. Other less
common causes include renal transplantation, Behet syndrome, hypercoagulable states,
and antiphospholipid antibody syndrome.

68. Paent with past history of CABAG harvested both GSV, now the paent need Fem-
distal bypass, which graft can be used?
a- ePTFE
b- Dacron
c- Upper limb veins
d- Umblical vein graft

69. Usual presentaon of isolated iliac aneurysm:-
a- deep pelvic pain b- sepsis
c- sudden pain and collapse d- distal embolization

70. Reperfusion aer acute L.L. ischemia:-
a- hyperkalemia b- hypercalcemia c- hypermagnesemia d- hypernatremia

71. Management of aorto-caval fistula:-
a- complete separation between aorta and IVC B- shunt in IVC
c- closure of the fistula from within the aneurysm sac


- -

Ischemia-Reperfusion Injury
Ischemic effects are due to not only the lack of oxygen as seen during ischemia, but also
due to the absence of whole blood with its scavenging properties.The leukocyte-
endothelial cell interactions appear to be a key element in the pathophysiology of I/R
injury. The cellular damage and capillary leak result from oxygen free radical and
neutrophil activity.

Endothelium is damaged by ischemia resulting in an increase in capillary permeability.
Under these conditions, white cells marginate and become activated. The superoxides and
other substances so released further increase capillary permeability and can cause direct
tissue damage and the condition may end in microvascular perfusion failure.
There are two components to the reperfusion syndrome, which follows extremity
ischemia. The local response, which follows reperfusion, consists of limb swelling with its
potential for aggravating tissue injury and the systemic response, which results in multiple
organ failure and death. It is apparent that skeletal muscle is the predominant tissue in the
limb but also the tissue that is most vulnerable to ischemia. Physiological and anatomical
studies show that irreversible muscle cell damage starts aer 3 h of ischemia and is nearly
complete at 6 h. These muscle changes are paralleled by progressive microvascular
damage.
Critical tissue ischemic times

No reflow phenomenon
Assessment of limb ischemia tolerance times is confused by the no-reflow phenomenon
the observation that when muscle ischemia is advanced there is permanent closure of the
nutrient vessels. As a result there is controversy as to whether the no reflow phenomenon
occurs as a consequence of cell muscle death or whether the no-flow injury results in a
perfusion deficit that subsequently leads to muscle death. The post ischemic no reflow is
due to intravascular hemoconcentration and thrombosis, swelling of capillary endothelial
cells, plugging of the capillaries by leukocytes, and increased extravascular tissue pressure
caused by interstitial edema formation.

Heparin anticoagulation protects the microcirculation from further thrombosis, lessens the
risk of venous thromboembolism and decreases microvascular permeability and
interstitial edema in the reperfused area. Moreover, heparin in adequate dosage sufficient
to stop local propagating thrombus will shut down the local inflammatory response,
improve collateral blood flow, and lower the level of demarcation even in limbs in which
there has been irreversible damage.



- -


Laboratory findings in Crush syndrome
Urinalysis that is dipstick positive for blood with few or no red blood cells on microscopic
examination is highly suggestive of rhabdomyolysis. Urine myoglobin is usually positive
and pigmented casts may be seen. Elevated serum creatine phosphokinase is the most
sensitive marker of muscle damage in rhabdomyolysis. Muscle cell death also leads to
hyperkalemia, hyperuricemia,acidosis and hyperphosphatemia. Hypocalcemia secondary
to production of calcium phosphate salts commonly follows hyperphosphatemia.

Aorto caval fistula (the bursting heart syndrome)
Spontaneous rupture of abdominal aortic aneurysm into the inferior vena cava is rare but
it is the most common form of spontaneous AVF encountered. The incidence of ACF ranges
from 0.2% to 1.3% of paents with AAAs and 3% to 4% of those with ruptured aneurysms.
Patients with ACFs are predominantly male, with an average age of 65 years.
The clinical presentation is highly variable, and the diagnosis can be difficult, often being
made only at operation. Hematuria in association with an abdominal aortic aneurysm
should raise the suspicion of an aortocaval fistula. The aortocaval fistula results in a large
left-to-right shunt, which can cause cardiac failure (high output congestive cardiac failure
with warm peripheries). Once the diagnosis is made, treatment is by surgical closure of the
fistula and repair of the aneurysm with a graft.
Diagnosis of an aortocaval fistula before operation is helpful to plan operative strategy
and to prepare for blood loss caused by hemorrhage. Both ultrasonography, either B-
mode or duplex, and CT scanning have been used to demonstrate the fistula.
During surgery for ruptured AAA:-
Rarely, venous bleeding, which can be secondary to an aortocaval fistula, will continue to
fill the opened aneurysm. Direct digital pressure or the use of proximal and distal sponge
sticks is recommended for control of the vena cava above and below the fistula. Suture of
the fistula from within the aneurysm is then performed either directly with interrupted
polypropylene sutures or with a prosthetic patch. The aneurysm is then repaired with a
tube or bifurcated prosthetic graft in the standard fashion. It is important to not generate
an air embolism or push thrombus or other aortic debris into the vena cava during this
repair. Attempts to dissect the vena cava proximally and distally will greatly increase the
chance of a venous injury.

Intraoperative maneuvers used to control bleeding from an aortocaval fistula. A, Vessel
loop constriction; B, digital compression; C, sponge stick compression.





- -

Combined Vascular Malformations (Hemolymphatic Malformations)
Klippel-Trenaunay-Weber syndrome
(KTWS) is characterized by a triad of:
1. port-wine stain (CM),
2. varicose veins and lymphedema (VM & LM)
3. bony and so tissue hypertrophy involving an extremity.
Parkes Weber syndrome (PWS)
the triad above with the addition of arteriovenous malformation.
Other Regional vascular syndromes
Sturge-Weber: facial CM, intracranial CM, VM and AVM

PHACE syndrome: neurocutaneous syndrome with CM in 5th Cranial N.
distribution. Posterior fossa abnormalities (brain malformations) Hemangioma,
Arterial anomalies, Cardiac anomalies and Coarctation of the Aorta, Eye anomalies
Rendu-Osler-Weber syndrome (heriditary hemorrhagic telangiectasia), Visceral
AVMs.
N.B. The commonest congenital vascular defect is PDA.

72. The main blood supply of the ureter:-
a- aorta b- renal arteries c- iliac arteies d- gonadal arteries
Chopart Amputation (midtarsal joint amputation)
- Chopart amputation removes the forefoot and midfoot, saving talus and calcaneus;
- Chopart amptutations should not performed for ischemia;
- this is a very unstable amputation, noting that most of the tendons which act around
the ankle joint have lost their insertion into foot and the heel remains unstable.
Syme's Amputation
- includes ankle disarticulation, removal of malleoli, & anchoring heel pad to the wt
bearing surface) allows execellent gait with a cosmetic prosthesis;
- symes amputations will not heal w/o palpable posterior artery pulse
Ray Amputation
Ray resection consists of longitudinal amputation of a toe and its corresponding
metatarsal head.


Lisfranc Amputation
tarso-metatarsal amputation

Amputations Through the Midfoot
Lisfranc and Chopart amputations


- -

Isolated iliac aneurysms
Before the era of widespread use of CT and MRI, larger isolated iliac aneurysms were more
often initially found to have ruptured, with a high resultant mortality rate. Today they are
often identified incidentally during abdominal imaging studies performed for
other reasons.
Larger aneurysms may have vague findings, typically caused by compression of adjacent
pelvic structures. In symptomatic patients, the diagnosis is frequently delayed until the
aneurysm is large and imaging studies finally reveal the cause of the complaint. Local
compression or erosive problems that affect adjacent pelvic structures can lead to ureteral
obstruction, hematuria, iliac vein thrombosis, bowel obstruction, or neurologic deficit.
Surgical treatment is appropriate for aneurysms larger than 3 cm.

Critical Limb Ischemia
The term critical limb ischemia should be used for all patients with chronic ischemic rest
pain, ulcers or gangrene attributable to objectively proven arterial occlusive disease. The
term CLI implies chronicity and is to be distinguished from acute limb ischemia. The
common major manifestations of CLI are rest pain and ischemic ulceration or gangrene of
the forefoot or toes, representing a reduction in distal tissue perfusion below resting
metabolic requirements. The clinical diagnosis is confirmed by a fall in ankle pressure to
less than 50 mm Hg, toe pressure to less than 30 mm Hg, or ABI to less than 0.40.







- -

Pharmacotherapy for symptoms of intermittent claudication
A 3- to 6-month course of cilostazol (Pletal) should be firstline pharmacotherapy for the
relief of claudication symptoms, as evidence shows both an improvement in treadmill
exercise performance and in quality of life [A].
Naftidrofuryl (Praxilene) can also be considered for treatment of claudication symptoms.




Smoking



- -





Toe pressure
Normal toe systolic pressure ranges from 90-100 mm Hg and is 80-90% of brachial systolic
pressure (30 mmHg less than the ankle pressure) and a toe-brachial index of <0.70 is
abnormal.

Primary lymphedema
Congenita (onset <2 years old): sporadic
Congenita (onset <2 years old): familial (Milroys disease)
Praecox (onset 235 years): sporadic
Praecox (onset 235 years): familial (Meiges disease)
Tarda (onset aer 35 years of age)





- -

Ideal Characteristics of an Aneurysm for EVAR
Neck length (mm) >15
Neck diameter (mm) >18, <32
Aortic neck angle () <60
Neck mural calcification (% circumference) <50
Neck luminal thrombus (% circumference) <50
Common iliac artery diameter (mm) between 8 20
Common iliac artery length (mm) >20
External iliac artery diameter (mm) >7

Features that are severe as relative contraindications to the procedure include
short (<25mm) and wide (>14mm) common iliac arteries and the presence of mural
thrombus in the aneurysmal sac. Funnel-shaped necks and excessive calcification are
absolute contraindications to endovascular repair.

Complications of Hemodialysis Access Fistulae and Grafts
THROMBOTIC COMPLICATIONS
ACCESS SITE INFECTION
Infection is the most common reason for hospitalization and the second most
common cause of death in hemodialysis patients. Infecon accounts for 12% of
mortality in this group, exceeded only by cardiovascular causes.
The vast majority of graft infections are caused by gram-positive cocci, with
Staphylococcus aureus accounng for approximately 70% and Staphylococcus
epidermidis responsible for only 10% in one series. Infection is commonly seen in patients
with synthetic grafts (5%) but is an uncommon complication of autogenous fistulae.

Treatment of Infection of Dialysis AV Grafts



Treatment of Infection of Primary AV Fistulae





- -

HEMODYNAMIC COMPLICATIONS
Arterial insufficiency or steal syndrome
Venous Hypertension
Congestive Heart Failure
OTHER COMPLICATIONS
Pseudoaneurysm
Pseudoaneurysm formaon secondary to gra infecon or trauma occurs in 2 to
10% of patients and is more commonly seen in prosthetic grafts. Pseudoaneurysm
formation at the arterial anastomosis is often due to local infection, with
partial disruption of the suture line. This complication may lead to anastomotic
disruption or graft rupture, with resultant exsanguination.


Access Aneurysm
True aneurysms are more likely to occur in native AVFs.




Venous hypertension
Venous hypertension is an uncommon complication of dialysis angioaccess. Two clinical
syndromes may be recognized. The first occurs in the setting of a side to- side fistula and
affects the extremity distal to the fistula. High-pressure arterial blood flows into the low-
resistance venous bed results in venous hypertension, which is manifest as progressive
extremity swelling, hyperpigmentation, induration, cyanosis, andif allowed to
progressskin ulceration. The hand is most commonly affected. The clinical appearance is
similar to that seen in chronic lower extremity venous insufficiency. Resolution is typically
seen following ligation of the vein distal to the anastamosis, converting the side-to-side
anastomosis to a functional side-of-artery to end-of-vein configuration.

The second syndrome of venous hypertension is related to venous outflow obstruction.
This more common form of venous hypertension may present acutely when an
arteriovenous anastomosis is constructed distal to an unrecognized proximal venous
stenosis or occlusion. More often, however, venous hypertension develops chronically in
the extremity with a patent AV fistula and proximal venous obstruction. The most
common site of venous obstruction is at the axillary subclavian vein level. If the
subclavian vein occlusion is located proximal to the internal mammary vein, ipsilateral
breast edema may be seen. Chronic subclavian vein occlusions are more difficult to treat
successfully.




- -


Treatment of Central Vein Stenosis

When complete subclavian or brachiocephalic occlusion is encountered in a patient whose
contralateral extremity is free of any contraindications for use as an AV access site, the
most reliable method to eliminate venous hypertension in the involved extremity is simple
fistula ligation.

Carotid siphon stenosis
CALCIFICATION of the carotid siphon or intracranial internal carotid artery occurs
frequently, but significant stenosis of this segment is less common. Stenosis of the carotid
siphon has been estimated to be about one-sixth as common as disease of the carotid
bifurcation. Patients with carotid siphon or MCA stenosis who were treated medically
had an annual stroke rate of 10%.More common in Asian patients. Patients with
symptomatic intracranial vertebral artery or basilar stenosis are at a higher risk of stroke,
MI, or sudden death. Symptomatic atherosclerotic intracranial stenosis is a high-risk
condition. Aspirin is safer and as effective as warfarin for preventing recurrent strokes.
Angioplasty and stenting cannot be justified in paents with < 70% stenosis. Females are
at the highest risk for strokes. 30-40% of patients had subsequent ischemic events, and
more than half of these events were ipsilateral to the siphon stenosis. Although carotid
siphon stenosis seemed to be associated with a higher risk of late death, it did not alter
the short- and long-term stroke morbidity rates after carotid endarterectomy significantly.
Transcranial Doppler sonography seems to be a valuable tool for noninvasive detection of
intracranial lesions of the middle cerebral artery and carotid siphon.

The presence of a tandem lesion infrequently alters the surgeon's decision to perform an
endarterectomy. However, the importance of detecting tandem stenoses cannot be
underestimated, since they may have important implications for long-term medical
management in symptomatic patients. Carotid siphon calcification was correlated with the
occurrence of lacunar infarction.

Venous Leg Ulcer
From 70% to 80% of ulcers healed aer 6 months of compression therapy.
Patients with chronic venous insufficiency (CVI) who have lower extremity ulceration
develop have difficult conditions to treat even after ulcer healing because of the frequency
of ulcer recurrence. The incidence rate of recurrent ulceration after wound healing with
nonoperative techniques has been reported as 28% at 2 years, 38% at 3 years, and 57% at
4 years in various studies. The incidence rate of recurrence is markedly increased by
associated deep venous insufficiency.








- -

Transcutaneous oxygen tension (TcpO2) measurements
normal, 45 mm Hg; mild ischemia, 40-45 mm Hg;
moderate ischemia, 20-39 mm Hg; severe ischemia 20 mm Hg.
Skin Perfusion Pressure
Chronic extremity wounds with an SPP < 30 mmHg have a low probability of healing.




Acute Mesenteric Ischemia





Nonocclusive Mesenteric Ischemia (NOMI)
(Severe mesenteric vasoconstriction)
NOMI accounts for more than 10% to 20% of cases of acute mesenteric ischemia. The
prognosis is poor, despite the absence of organic obstruction in the principal arteries.
Visceral ischemia can occur due to low-flow states, especially in conjunction with intestinal
atherosclerotic disease. NOMI most commonly occurs secondary to cardiac disease,
particularly severe congestive heart failure. Atrial fibrillation, commonly a cause of cardiac
thrombi and visceral embolization, can also induce NOMI by reducing left ventricular
function and causing low cardiac output.
Other risk factors for NOMI include hypovolemia, systemic vasoconstrictors, vasoactive
drugs (e.g., digoxin, -adrenergic agents, -receptor blocking agents, cocaine), aortic
insufficiency, cardiopulmonary bypass, abdominal and cardiovascular surgery, and liver
failure.


N.B. in all cases the surgeon should proceed with revascularization before resecting any
intestine unless faced with an area of frank necrosis or perforation and peritoneal soilage.

Operative exposure of the infrapancreatic superior me
SMA Embolectomy
The proximal SMA is vented to allow any clot to be expelled without the use of an
embolectomy catheter if possible. When necessary, catheter
performed with 3 or 4 Fr balloon
pulsatile inflow should be expected.
or 3 Fr, is employed. Great care must be taken to avoid damage
mesenteric arteries. Difficulty p
complexity of the distal embolectomy. An alternative or adjunct to
of the distal mesenteric vessels is for
mesentery and milk thrombotic material out of the vessels.

- -
in all cases the surgeon should proceed with revascularization before resecting any
intestine unless faced with an area of frank necrosis or perforation and peritoneal soilage.
Operative exposure of the infrapancreatic superior mesenteric artery (SMA).
SMA Embolectomy
vented to allow any clot to be expelled without the use of an
embolectomy catheter if possible. When necessary, catheter embolectomy is typically
or 4 Fr balloon catheter. With extraction of the embolus, torrential and
inflow should be expected. Distally, a smaller embolectomy catheter, typically
3 Fr, is employed. Great care must be taken to avoid damage or rupture of the fragile
mesenteric arteries. Difficulty passing a catheter down multiple small branches adds to the
of the distal embolectomy. An alternative or adjunct to balloon embolectomy
of the distal mesenteric vessels is for the surgeon to place a hand on either side of the
thrombotic material out of the vessels.



in all cases the surgeon should proceed with revascularization before resecting any
intestine unless faced with an area of frank necrosis or perforation and peritoneal soilage.
senteric artery (SMA).
vented to allow any clot to be expelled without the use of an
embolectomy is typically
extraction of the embolus, torrential and
Distally, a smaller embolectomy catheter, typically 2
or rupture of the fragile
a catheter down multiple small branches adds to the
balloon embolectomy
the surgeon to place a hand on either side of the

- -

Raynauds syndrome.
Raynauds syndrome is intermittent digital ischemia occurring in response to cold or
emotional stress. Most patients describe tricolor changes, with the fingers initially turning
white, then blue or purple, and finally red after rewarming. The traditional division of
Raynauds patients was into Raynauds phenomenon and Raynauds disease, where
phenomenon refers to patients with a diagnosed associated disease and disease refers to
those with episodic digital ischemia in the absence of a diagnosed associated disease.




Acrocyanosis
Acrocyanosis may be confused with Raynauds disease but it is painless and not episodic. It
tends to affect young women and the mottled cyanosis of the fingers and/or toes may be
accompanied by paraesthesia and chilblains.

Livedo reticularis
Livedo reticularis is a vascular condition characterized by a purplish discoloration of the
skin, usually on the legs. This discoloration is described as lacy or net-like in appearance
and may be aggravated by cold exposure. Most often livedo reticularis causes no
symptoms and needs no treatment. But it can be associated with serious underlying
disorders, such as lupus, anti-phospholipid syndrome or Sneddon's syndrome. A rare
complication of chronic renal dialysis known as calciphylaxis may first present with a
livedo reticularis pattern. In addition, livedo reticularis may occur as a side effect of certain
medications, such as hydroxyurea.




- -




Clinical Features Distinguishing Primary from Secondary Raynauds Syndrome



- -


Hypothenar Hammer Syndrome


Arteriogram of the hand of a carpenter. Note the aneurysm of the ulnar artery
(arrow) caused by repetitive trauma from using the hand as a hammer.


- -



Renal Artery Stenosis
Renal Artery Stenosis more than 60% =
PSV more than 180 cm/s
A rao of PSV in Renal artery to PSV in Aorta, 3.5 or more

Etiology of Renal Artery Stenosis (greater than 60% luminal narrowing)
Atherosclerosis (70%)
Usually involves the ostium and/or proximal third (the proximal 2 cm of the main renal
artery, with non-ostial lesions comprising only 10% of cases. 10-15% progress to occlusion.
Fibromuscular dysplasia (30%) (Medial Fibroplasia) more in femals and younger age and
usually bilateral involves distal 2/3 and branches and progression is less common. Never
leads to occlusion and loss of renal function is rare.Responds well to PTA.
Polyarteritis Nodosa
Radiation-induced
Takayasus arteritis

23% of malignant hypertension is the result of renovascular causes
Not all patients with RAS are hypertensive as a result
Found in 2-5% of all cases of hypertension
The majority of patients are unlikely to benefit from renal revascularization, but optimal
medical therapy is appropriate for all patients.
Renal stenting has become the initial technique of choice to revascularise an
atherosclerotic RAS and has replaced PTA and surgery.

- -


Indications for Renal Artery Revascularization
Angiography criteria
Fibromuscular dysplasia lesion
Pressure gradient >20 mmHg
Aected/unaected kidney renin rao >1.5:1
Clinical criteria
Refractory or rapidly progressive hypertension
Hypertension associated with flash pulmonary edema without coronary artery
disease
Rapidly progressive deterioration in renal function
Intolerance to antihypertensive medications
Chronic renal insufficiency related to bilateral renal artery occlusive disease or
stenosis to a solitary functioning kidney
Dialysis-dependent renal failure in a patient with renal artery stenosis but without
another definite cause of end-stage renal disease
Recurrent congestive heart failure or flash pulmonary edema not attributable to
active coronary ischemia

The indications for endovascular treatment for renal artery occlusive disease
include 70% or greater stenosis of one or both renal arteries and at least one of the
following clinical criteria:
Inability to adequately control hypertension despite appropriate antihypertensive
regimen.
Chronic renal insufficiency related to bilateral renal artery occlusive disease or
stenosis to a solitary functioning kidney.
Dialysis-dependent renal failure in a patient with renal artery stenosis but without
another definite cause of end-stage renal disease.
Recurrent congestive heart failure or flash pulmonary edema not attributable to
active coronary ischemia.

Choice of Conduit for Infrainguinal Bypass Grafting
Autogenous vein is superior to prosthetic conduits for all infrainguinal bypasses, even in
the AK position. This preference is applicable not only for the initial bypass but also for
reoperative cases. For long bypasses, ipsilateral great saphenous vein (GSV), contralateral
GSV, small saphenous vein, arm vein, and spliced vein are used, in decreasing order of
preference.

Retroperitoneal Hematomas
Particularly after blunt trauma, intact retroperitoneal hematomas are a common finding
during laparotomy. If such hematomas are not bleeding actively or expanding, they should
not be explored right away. Other injuries can be treated first if needed and if sufficient
time is available, additional diagnostic work-up pursued. Hematomas with
signs of active bleeding and those that appear to be expanding rapidly should be left intact
until proximal and distal control is achieved.

Because of their propensity to contain major vessel damage, it is recommended to explore
most hematomas in the midline.

- -


Lateral hematomas found after blunt injury should be left intact, but after penetrating
injury, lateral hematomas should be explored because they are more often associated
with major vessel damage. It is recommended, however, is to leave all nonexpanding
lateral hematomas, regardless of trauma mechanism. Instead, the patient should undergo
CT, IVP, or angiography to rule out major vessel injury and urinary leaks.

The most common cause of pelvic hematomas after blunt trauma is pelvic fracture.
Hematomas in this area should not be explored routinely. Even if the pelvic hematoma is
expanding, it is often better to pack the pelvic area and continue the work-up with
arteriography. For penetrating trauma, on the other hand, it is usually wise to explore
pelvic hematomas after securing proximal control to exclude vessel damage.

Contrast Agents
Iodinated Contrast Agents
Ionic contrast agents
When iodinated contrast agents dissolve, their osmolality doubles because of the presence
of two ions. The osmolality of these agents ranges from 1500 to 1700 mOsm, thus making
them significantly more hyperosmolar than plasma (285 mOsm).
Non-ionic contrast agents
Have considerably less osmolality but the osmolality remains half that of ionic contrast
agents.
Toxic side effects of iodinated contrast agents
The toxic side effects of iodinated contrast agents are primarily thought to be due to
hyperosmolality. The most common adverse symptoms are nausea, vomiting, and pain in
the distribution of the specific arterial bed that is injected.
Other adverse systemic effects:- urticaria, laryngeal edema or bronchospasm,
cardiopulmonary arrest.
Reduction in adverse reactions from 12.6% to 3.1% when using ionic, high-osmolality
contrast agents as opposed to non-ionic, low-osmolality agents.
Cardiac Toxicity:- The most common hemodynamic effects are a decrease in heart rate and
blood pressure, usually temporary and self-limited. Use of low-osmolality agents has been
shown to reduce the incidence of such adverse hemodynamic effects.
Hematologic Toxicity:- inhibit multiple coagulation factors and antithrombin activity, as
well as exhibit antifibrinolytic properties. There is some evidence that use of non-ionic
contrast agents may reduce these adverse hematologic effects.
Nephrotoxicity:- Contrast-induced nephropathy is perhaps the most commonly cited and
studied adverse reaction to iodinated contrast agents and carries with it significant
morbidity and mortality. It continues to be the third leading cause of acute renal failure in
hospitalized patients. there is no difference in such occurrence with ionic and non-ionic
contrast agents. There does, however, appear to be reduced risk with the use of low-
osmolality contrast agents as opposed to those with high osmolality.
Neither the type of contrast agent used nor the total volume infused seems to play a
significant role in the development of this complication in patients with normal renal
function. Although administering contrast agents to patients already suffering from
complete renal failure may be done without fear of inducing nephropathy, these patients
are at risk for hyperosmolar volume overload and should be scheduled for dialysis after
the angiography procedure. The principal site of contrast-induced nephropathy
is the renal tubule secondary to transient local ischemia.

- -

The incidence of contrast-induced nephropathy in patients with normal renal function is
only 1% to 2%. This risk increases to 10% in paents with creanine levels of 1.3 to
1.9 mg/dL (115 mol/L to 168 mol/L) and to 62% in patients with levels greater than 2
mg/dL (177 mol/L). The incidence of contrast-induced nephropathy is high in the diabetic
population. Paents with type 1 diabetes are more prone to the development of contrast-
induced nephropathy than are paents with type 2 diabetes. Diabetics taking metformin
(dimethylbiguanide), an oral hypoglycemic agent, require special consideration when
receiving iodinated contrast material.

Carbon Dioxide Arteriography
Another contrast agent with novel properties and applications is CO2. Injection of this gas
with its decreased radiodensity creates radiographic contrast by transiently displacing
blood from the artery being imaged. Historically, CO2 arteriography has had limited use
because of poor imaging quality in comparison to conventional contrast agents. However,
with improved equipment, technology, and image-processing software, coupled with the
significant number of vascular patients who have compromised renal funcon, use of CO2
arteriography has expanded to a wide variety of cases, and it can be used with much less
reservation and hesitation than in the past.

Unfavorable Carotid Angiographic Appearance in Which Carotid
Stenting Should Be Avoided:-
Extensive carotid calcification
Polypoid or globular carotid lesions
Severe tortuosity of the common carotid artery
Long segment stenoses (>2 cm in length)
Carotid artery occlusion
Severe intraluminal thrombus (angiographic defects)
Extensive middle cerebral artery atherosclerosis

Treatment of air embolism
Oxygen, and left lateral decubitus in the Trendelenburg position. Because death may be
due to an airlock that obstructs the pulmonary outflow tract, this maneuver keeps the air
within the apex of the right ventricle.

Widened mediastinum
Widened mediastinum is a mediastinum with a measured width greater than 8 cm on PA
chest X-ray, A widened mediastinum can be indicative of several important pathologies:-
aortic aneurysm
aortic dissection or disruption
hilar lymphadenopathy
esophageal rupture - presents usually with
mediastinal mass
cardiac tamponade
pericardial effusion
thoracic vertebrae fractures in trauma patients.

- -


Widened mediastinum due to Aortic Pseudoaneurysm




ANTICOAGULANTS
Vitamin K antagonists
These oral anticoagulants are a class of pharmaceuticals that antagonize the effects of
vitamin K. Examples include warfarin. It takes at least 48 to 72 hours for the ancoagulant
eect to develop. Approved for clinical use in 1955
Where an immediate effect is required, heparin must be given concomitantly. These
anticoagulants are used to treat patients with deep-vein thrombosis (DVT), pulmonary
embolism (PE), atrial fibrillation (AF), and mechanical prosthetic heart valves.
I. Coumarins Warfarin - Approx. 6 8 generic forms - Best to order coumadin
II. Indandiones - Phenindione - Differ slightly from the coumarins - Same Mech. of action -
No therapeutic advantages
Warfarin inhibits hepac synthesis of vit. K dependent coagulaon factors, 2-7-9-10 and
decreases synthesis of protein C and S.

Adverse effects
1.Paents aged 80 years or more may be especially suscepble to bleeding complicaons
with a rate of 13 bleeds per 100 person-years.
2.These oral ancoagulants are used widely as poisons for mammalian pests, especially
rodents.
3.Depleon of vitamin K by coumadin therapy increases risk of arterial calcicaon and
heart valve calcification, especially if too much vitamin D is present.
4. Warfarin skin necrosis.

Heparin and derivative substances
Heparin is a biological substance, usually made from pig intestines. It works by activating
antithrombin III, which blocks thrombin from clotting blood. Heparin can be used in vivo
(by injection), and also in vitro to prevent blood or plasma clotting in or on medical
devices.

- -

UFH
Direct and indirect (through Antithrombin) actions.
Anti Xa = Anti IIa Excreted by kidneys.
Heparin catalyzes the inactivation of thrombin by plasma cofactor II which acts
independently of Antithrombin.
Heparin suppresses platelet function and increases vascular permeability.
About 1/3 of dose binds to AT III
To form the AT III:Heparin:Clotting Factor Complex- requires at least18
saccharides
Unique high affinity pentasaccharide heparin sequences catalyze inhibition of Xa
by AT

Mechanism of action Only about one third of an administered dose of heparin
binds to AT, and this fraction is responsible for most of its anticoagulant effect.
The remaining two thirds has minimal anticoagulant activity at therapeutic
concentrations, but at concentrations greater than usually obtained clinically, both
high-affinity and low-affinity heparin catalyze the AT effect of a second plasma
protein, heparin cofactor II

The role of heparin cofactor II is insignificant except at very high heparin concentrations.
The heparin-AT complex inactivates a number of coagulation enzymes, including thrombin
factor (IIa), factors Xa, IXa, XIa, and XIIa. Of these, thrombin and factor Xa are most
responsive to inhibion, and human thrombin is about 10-fold more sensitive to inhibition
by the heparin-AT complex than factor Xa
By inactivating thrombin, heparin not only prevents fibrin formation but also inhibits
thrombin-induced activation of factor V and factor VIII.

Unfractionated heparin (UFH) and LMWH also induce secretion of tissue factor pathway
inhibitor by vascular endothelial cells that reduce procoagulant activity of tissue factor
VIIa complex, and this could contribute to the antithrombotic action of heparin and
LMWH.

Heparin binds to platelets, and depending on the experimental conditions in vitro, can
either induce or inhibit platelet aggregation.

In addition to its anticoagulant effect, heparin increases vessel wall permeability, inhibits
the proliferation of vascular smooth muscle cells, and suppresses osteoblast formation
and activates osteoclasts that promote bone loss. Each of these effects is independent of
its anticoagulant activity, but only the osteopenic effect is likely to be relevant clinically.

Anticoagulant Properties of Heparin
1. Inhibits the thrombin-mediated conversion of fibrinogen to fibrin
2. Inhibits the aggregation of platelets by thrombin
3. Inhibits activation of fibrin stabilizing enzyme
4. Inhibits activated factors XII, XI, IX, X and II




- -


Heparin Dose
1. IV- 5,000 Units bolus, then 30,000-35,000 units/24 hrs
2. 80 Units/kg bolus, then 18 Units/kg/hr to maintain aPTT in therapeutic
range. Aer IV the half me is 90 minutes and aer SC the peak 4-6 hours
and lasts about 12 hours.
Protamin sulphate
Up to 50 mg slow iv (1-2 mg per 100 IU heparin).

Low molecular weight heparin
Low molecular weight heparin is a more highly processed product that is useful as it does
not require monitoring of the APTT coagulation parameter (it has more predictable plasma
levels) and has fewer side effects.
Binds to Antithrombin with no direct action.
The Anti Xa is more than the Anti IIa
Less effect on platelet function. Less frequent HIT and Osteoprosis.
Doesnt change the APTT (much) an increased APTT may signify an overdose of LMWH or
some other influence on the APTT (platelet antibodies)
Difficult to reverse with protamine sulfate (antidote for UFH)
Cleared through the kidneys
Enoxaparin (Lovenox and Clexane) twice daily.
Tinzaparin (Innohep) once daily. Amp. 0.5 (10000 IU),0.7(14000 IU),0.9 ml(18000 IU) and
multidose vial 20000 IU 175 IU per Kg per day
Who should be monitored for LMWH?
Patients with kidney problems (need to check creatinine clearance)
Patients that are obese or have a very low body weight
Children, burn patients
How should LMWH be monitored?
Monitor with an anti-Xa method, using LMWH calibrators and controls.
Samples should be drawn 4 hours aer dosing.

Synthetic pentasaccharide indirect inhibitors of factor Xa
Fondaparinux
(Arixtra) is a synthetic sugar composed of the five sugars (pentasaccharide) in heparin that
bind to antithrombin. It is a smaller molecule than low molecular weight heparin.
A synthetic analog of the antithrombin-binding pentasaccharide sequence found on
heparin or LMWH.
Fondaparinux binds antithrombin with high affinity. Once bound, fondaparinux evokes
conformational changes in the reactive center loop of antithrombin that enhance its
reactivity with factor Xa. Fondaparinux is a catalytic inhibitor; thus, after promoting the
formation of the factor Xa/antithrombin complex, fondaparinux dissociates from
antithrombin and is available to activate additional antithrombin molecules.

- -

With excellent bioavailability after SC administration and a plasma half-life of 17 hours,
fondaparinux is administered subcutaneously once daily. Systemic fondaparinux is
excreted unchanged via the kidneys. Therefore, fondaparinux must be used with caution
in patients with renal insufficiency.
When given SC in fixed doses, fondaparinux produces a predictable anticoagulant
response. Consequently, routine coagulation monitoring is unnecessary. If necessary,
fondaparinux can be monitored with antifactor Xa levels using a chromogenic assay.
Fondaparinux has no effect on routine tests of coagulation, such as the activated partial
thromboplastin time or activated clotting time. Does not produce heparin associated
antibodies or bind to platelets. Not associated with HIT

Arixtra SC Once daily 7.5 mg for treatment and 2.5 mg for prophylaxis.


Idraparinux
A second-generation synthetic pentasaccharide, idraparinux is more negatively charged
than fondaparinux . Consequently, idraparinux binds to antithrombin with an affinity
higher than that of fondaparinux. Because it binds antithrombin so tightly, idraparinux
has a plasma half-life similar to that of antithrombin, about 80 hours. With this long half-
life, idraparinux is administered SC on a once-weekly basis. Like fondaparinux, idraparinux
exhibits excellent bioavailability after SC injection and produces a predictable
anticoagulant response, thereby obviating the need for routine coagulation monitoring.
Its anticoagulant activity is reversible with Novo Seven (r FVIIa)

Heparinoid
Danaparoid
Danaparoid sodium (Orgaran) is an anticoagulant that works by inhibiting activated factor
X (factor Xa). IV and SC
Danaparoid is considered a "low molecular weight heparin" by some sources, but is
chemically distinct from heparin and thus has little cross-reactivity in heparin-intolerant
patients. It has also been described as a heparinoid.
It is used to prevent deep venous clots, particularly in situations with a high risk of clot
formation, such as after hip surgery.
It is also used as a heparinoid substitute in heparin-induced thrombocytopenia (HIT).
SIDE EFFECTS
Bleeding problems
Low platelets, due to a low level of structural similarity between danaparoid
and heparin
Asthma exacerbations, due to allergies to sulfites contained within the medicine


- -


Direct thrombin inhibitors
Another type of anticoagulant is the direct thrombin inhibitor. Current members of this
class include:-
Hirudin (Thrombex) & Recombinant hirudins like lepirudin (Refludan)
and bivalirudin (Angiomax).
Argatroban (Argatroban injection or Novastan).
Oral direct thrombin inhibitors:- dabigatran (Pradaxa) and ximelagatran (Exanta).
Ximelagatran

The first oral, direct thrombin inhibitor, ximelagatran is a prodrug of melagatran , a 429-
dalton dipeptide that fits within the active-site cleft of thrombin and blocks the enzymes
interactions with its substrates. Thus, melagatran is a stoichiometric inhibitor of thrombin
that forms a reversible 1:1 complex with the enzyme. Melagatran exhibits poor
bioavailability aer oral administraon. Ximelagatran, which has a molecular mass of 474,
was developed to overcome this problem.
An oral direct thrombin inhibitor, ximelagatran (Exanta) was denied approval by the Food
and Drug Administration (FDA) in September 2004 and was pulled from the market
enrely in February 2006 aer reports of severe liver damage and heart attacks.
The New Oral Anticoagulants

Dabigatran (Pradaxa)
Direct thrombin inhibitor
Approved by FDA on 10/20/2010
The first and only new oral anticoagulant that is currently approved in the US
The only FDA approved indication prevention of stroke in atrial fibrillation (RE-LY
trial)
Several large phase III trials are either completed or ongoing for dabigatran in DVT
prophylaxis and acute VTE treatments
75,110 and 150mg capsules. bid

Rivaroxaban (Xarelto 10mg tab.)
A direct factor Xa inhibitor once daily
Approved in Canada and Europe for DVT prophylaxis for after total knee and hip
replacement, based on RECORD trial 1-4 Not yet approved in the US.

Apixaban ( Eliques tablets)
Direct factor Xa inhibitor
The recommended dose is 5 mg orally twice daily.

- -

HIT
Venous thrombosis itself is the most common complication of HIT.
HIT is a thrombotic storm
HIT occurs in approximately 1-5% of paents receiving heparin.
The diagnosis of this condion is clinical. Platelet counts drop below 100000/uL or there is
more than a 50% drop of the baseline platelet count following the administraon of
heparin, independent of the route of administration.
The incidence of HIT may be lower with LMWHs. The morbidity and mortality rates are so
high, that failure to diagnose early can result in catastrophic complications.
HIT can be defined as any clinical event (or events) best explained by platelet-activating
anti-platelet factor 4 (PF4)/ heparin antibodies (HIT antibodies) in a patient who is
receiving, or who has recently received, heparin.
Types of HIT
Type I (HAT) due to direct (nonimmune) effect of heparin on platelet activation, occurs
within the first two days and often normalizes with continued heparin administration.
Type II (HIT-T) Characterized by formation of antibodies against the heparin-platelet factor
4 complex (immune mediated syndrome). Occurs aer 5-10 days aer starng heparin.
CONTRAINDICATIONS:
Warfarin, Platelet Transfusions, Vena Caval Filters

ALTERNATIVE NON HEPARIN ANTICOAGULANTS
Five alternative nonheparin anticoagulants have a rational basis for use in managing
HIT.10 Three (lepirudin, argatroban, bivalirudin) are direct thrombin inhibitors (DTIs),
whereas two can be classifi ed as indirect (antithrombin
[AT]-dependent) inhibitors of activated factor X (Xa), either predominantly (danaparoid) or
exclusively (fondaparinux). Lepirudin and argatroban are approved by the U.S. Food and
Drug Administration (FDA) for treatment of HIT, whereas danaparoid is approved for this
indication in Canada and Europe (but not in the United States).



- -