Notes in Vascular

Surgery

Dr. Joel Arudchelvam.

Contents
Anatomy............................................................................................. 1
Arteries of lower limb .................................................................... 1
Femoral artery ............................................................................ 1
The popliteal artery .................................................................... 1
Anterior tibial artery .................................................................. 2
Occlusive Arterial Disease (OAD) .................................................. 3
Extremity Vascular Trauma ............................................................... 8
Compartments of the leg .............................................................. 13
Varicose veins. ................................................................................. 14
Veins of lower limb ..................................................................... 14
Wounds (ulcers) ............................................................................. 19
Wound dressings .............................................................................. 24
Acute limb ischemia ........................................................................ 28
Deep Vein Thrombosis (DVT) ........................................................ 31
Examination of Haemodialysis access (Arterio Venous Fistula) .... 42
Arterial aneurysms - Abdominal Aortic Aneurysm (AAA) ............. 44
Anatomy

Arteries of lower limb

Femoral artery
Femoral artery is the main artery supplying the lower limb.it is
the direct continuation of external iliac artery beyond inguinal
ligament and lies at the mid inguinal point i.e. midway between
anterior superior superior iliac spine and pubic symphysis.

Branches;

 From common femoral;

o Superficial epigastric artery
o Superficial circumflex iliac artery
o Superficial external pudendal artery
o Deep external pudendal artery

 From profunda;
o Lateral circumflex femoral
o medial circumflex femoral
o Perforating branches.

It divides into superficial femoral and profunda (deep) femoral

artery. The part of femoral artery prior to this division is called
common femoral artery.

The popliteal artery

It is the continuation of the femoral beyond adductor hiatus in
the Adductor magnus and runs downward and laterallyin the
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popliteal fossa and divides into anterior and posterior tibial
arteries at the lower border of popliteus muscle.

Branches

 Muscular
 Cutaneous
 Genicular
 Terminal – anterior and posterior tibial

Anterior tibial artery

This is the artery of anterior compartment of the leg originates
from the popliteal artery passes forward into the anterior
compartment of leg through interosseous membrane.

It runs on the interosseus membrane and lies lateral to tibialis

anterior tendon in the lower leg. Flexor hallucis tendon crosses
the artery from lateral to medial at lower leg. The artery
crosses anterior to ankle joint to become dorsalis paedis artery.

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 Occlusive Arterial Disease (OAD)
 What are the peripheral vessels?
o Vessels outside thoracic cavity.

 Peripheral Vascular Disease (PVD)

o Arterial
 OAD
 Aneurysmal
 Trauma
o Venous

 Presentation of an arterial disease;

 Asymptomatic
 Claudication
 Rest pain
 Gangrene / ulcer
 Claudication
o Pain while walking
o Not present during rest
o Does not appear with first few steps
o Appears after walking some distance (Claudication
distance - CD)
o CD is reproducible

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 o CD decreases while climbing up and increases
while climbing down ( opposite happens in
neurogenic claudication)
o Relived after resting for few minutes ( does not
disappear instantly after stopping walking, and can
be relieved even by standing)
 Rest pain,
o Pain while resting
o pain relieved by putting leg down and worsened by
elevating the limb
o Not responding to usual analgesics (have to give
narcotic analgesics)

Grading of occlusive arterial disease(Fontaine

classification)

I. Asymptomatic - Incidental findings

II. Claudication
a. IIA – claudication >100 m
b. IIB – claudication <100 m
III. Rest pain
IV. Tissue loss – ulcer / gangrene

Commonest pathology causing chronic arterial occlusion is

Atherosclerosis, but there are other rare causes especially in
young patients with no risk factors for atherosclerosis
(Buerger’s, vasculitis)

 Risk factors for atherosclerosis are age, DM,

Hyperlipidemia, hypertension, smoking, etc.
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 In addition atherosclerosis affects other arteries as well.
Therefore in patient evaluation other systemic vascular
status also should be assessed i.e;
o Cerebrovascular – stroke, Transient ischaemic
attacks
o Cardiovascular – angina, cardiac failure
o Mesenteric ischaemia – development of abdominal
pain following meals. This occurs constantly every
time after a delay of 15 to 20 minutes.
o Impotence – Leriche syndrome – due to occlusion
of lower aorta or bilateral internal iliac arteries.

Documentation of pulse in a pulse chart

 Normal - A

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 Distal disease – B
 Femoro-popliteal disease - C
 Aorto iliac disease - D

 ABPI- Ratio between ankle pressure and brachial pressure,

denominator is brachial pressure, normal value is between
0.9-1.3
 If the value is below 0.9 it indicates occlusive arterial
disease
 If the value is higher than 1.3 it indicates there is non
compressible artery as seen in DM.

Investigations

Imaging
 USS + Doppler
o Shows vessel wall, narrowing, velocity changes
o difficult to visualiseintrabdomial vasculature
 Angiography
o CT and conventional catheter angiograms(in CT
arteriogram the contrast is injected into the vein
and scanning is done in arterial phase and
arteriogram is reconstructed, whereas in
conventional angiogram the contrast is directly
injected into the desired artery and X ray
imaging done. In DSA the bone image is
subtracted from the conventional arteriogram by
a computer program. )
o accurate display of occlusion / narrowing, and
its extent
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Management

 Patients with disabling claudication (grade IIB), rest

pain (grade III) and with tissue loss ( ulcer and
gangrene – grade IV ) needs interventions ( open /
endovascular )
 All patients needs modification of risk factors and
optimization of associated co- morbidities

Medical management

 Stop smoking
 Optimization of underlying disease (DM, HTN,
Hyperlipidemia, etc.)
 Foot care / footwear modification
 Drugs such as Aspirin, Statins, Phosphodiestaerse
inhibitors (Cilostazol)

Interventions

 Radiological and surgical

 Radiological - angioplasty / stents.
 Surgical interventions - Bypass, endarterectomy.
 Conduits used in bypass
o synthetic (PTFE, Dacron)
o Natural - Saphenous vein( RSVG )

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Extremity Vascular Trauma

Vessels are injured due to Blunt or Penetrating trauma (due

to gunshot, stab etc.)

 Blunt injuries- e.g. dislocations, fractures, direct

impact, etc.
 Penetrating trauma – e.g. - gunshot, stab, cut, etc.)

These mechanisms lead to cut, transection(Generally sharp

weapons), laceration, contusion (generally due to blunt
trauma), etc. on the vessels.

Signs of a vessel injury

 Hard signs
o Active bleeding
o Thrills, Bruits
o Signs of distal ischemia
 Absent pulse
 Pain
 Pale
 Perishing Cold
 Paresthesia / anaesthesia
 Paresis / Paralysis

o Expanding hematoma
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  Soft signs
o Hematoma
o Injury close to a known neurovascular bundle

Out of the features of ischaemia paresis/ paralysis and

paresthesia / anaesthesia are late signs. Paresis and paresthesia
indicates that the viability of the limb is in immediate threat
and anaethesia and paralysis indicate that the limb is not viable.

Management

 Patients with vascular injury often have associated

injuries therefore assessment and resuscitation should
be done together.
 If patient has hard signs and fit for surgery, send to OT
immediately.
 If there is only soft signs image
o CT angiography preferred in trauma.
 General consideration in vascular repair
o Assess the viability and the need for fasciotomy
o Proximal and distal control of vessel
o Trimming of damaged vessel segment
o tension free repair – if healthy ends of vessel
can be approximated without tension then direct
repair, if the gap is long , therefore cannot be
approximated without tension then use
interposition graft ( Reversed Saphenous Vein
Graft – RSVG)

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 o in any situation if the patient is not fit for
vascular repair due to associated trauma, then
the surgery should be delayed and the limb
shroud be reevaluated for viability when the
patient become fit for vascular surgery.

Complications of vascular injury and reperfusion

 immediate
o hemorrhage
o death
o compartment syndrome
o reperfusion injury / post perfusion
syndrome
o arteriovenous fistula
o false aneurysm
 late
o ischemic contracture

Reperfusion effects

 Reperfusion injury
 Post perfusion syndrome

Reperfusion injury

During ischaemia the cells in the undergo anaerobic

metabolism, which results in depletion of ATP and
accumulation of lactic acid. In addition depletion of ATP

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results in reduced function of ion pumps and activation of
certain enzymes and alteration of cell membranes.
When these cells are reperfused there is production of oxygen
free radicals by the activated enzymes and there is adhesion of
platelets and neutrophils to the endothelium. These events
results in death of already dying cells and intravascular
thrombosis. This paradoxical death of already dying cells when
reperfused is called a Reperfusion injury.

at the same time dead and dying cells release intracellular ions
(i.e.K+,myoglobin, ect.), lactic acid, activated enzymes,
activated neutrophils , ect are released into circulation resulting
in myocardial depression, acute kidney injury, hypotension,
DIC, ARDS, lactic acidosis,hyperkalaemia,ect. These systemic
effects of reperfusion is called post perfusion syndrome.

Compartment syndrome

Reduced organ perfusion due to increased intra compartment

pressure.

Causes;
 Trauma (fracture, muscle contusion)
 Haematoma
 Reperfusion
 Tissue oedema
 Intracompartmental extravasation of fluids
 Tight bandage, cast
 Burn
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Clinical features
 Excessive pain
 Numbness at the area of nerve distribution travelling
through compartment(e.g. anterior compartment - often
involved first in leg - results in numbness at first toe
web i.e. deep peroneal nerve distribution)
 Tense compartment
In unconscious patients some of these features cannot be
elicited – then need to measure intra-compartmental pressure

Prevention and treatment

 Fasciotomy (therapeutic / prophylactic) – in hospital

where vascular repair cannot be done do fasciotomy
before transferring.
 elevation
 maintaining blood pressure and oxygenation (because
compartment perfusion pressure (PF) depends on mean
arterial pressure (MAP) and intra-compartmental
pressure (ICP) (PF = MAP – ICP)

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Compartments of the leg

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Varicose veins.
Varicose veins are abnormal, tortuous, dilated, elongated
superficial veins.

Veins of lower limb

Venous system of lower limb is divided into superficial and
deep systems (i.e. superficial and deep to deep
fascia).superficial system is formed by long and short
saphenous veins (LSV/ SSV).superficial veins carry only 10%
of blood.

The LSV originates from the medial aspect of the dorsal

venous arch and ascends anterior to the medial malleolus. It
travels proximally on the medial aspect of the leg posterior to
medial border of tibia and with saphenous nerve ,then about
one hand breadth behind knee joint and the thigh within the
subcutaneous tissues. In the groin region, the LSV passes
through the saphenous opening to join the femoral vein ( about
3- 4 cm inferolateral to pubic tubercle). Here it receives several
venous tributaries

• superficial circumflex iliac

• superficial epigastric

• deep and superficial external pudendal veins

• anterolateral vein of thigh

the LSV and SSV communicates with the deep venous system
through a number of perforating veins (about 90 ) present
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along the medial aspect of the thigh ( Dodd ) and calf (Boyd)
and ankle (Cockett).usually these perforators connect to
posterior arch vein (Leonardo’s vein ) in the leg which
subsequently drain into LSV.

A communicating vein may pass from saphenous vein in thigh

and runs posteroinferiorly to communicate with SSV
(Giacomini).

SSV originates from the lateral aspect of the dorsal venous

arch and ascends posterior to the lateral malleolus with the
sural nerve. The vein travels along the middle of the calf,
pierces the popliteal fascia, and passes between the two
heads of gastrocnemius about 2 – 5 cms below knee joint.

o .

Grading of severity.

CEAP (clinical-etiological-anatomical-pathophysiological
grading)

Clinical

1. Thread veins, venous spider.

2. Varicose veins
3. oedema
4. pigmentation
5. healed ulcer
6. active ulcer

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Examination of varicose veins

Short history
 findout indications for intervention and exclude
DVT in past

Inspection

 Ask the patient to stand

 expose
 Site(above or below knee)
 Affected veins (long / short saphenous veins)
 Edema
 Skin changes

Palpation

Tapping test

Patient on supine position.

 Distal pulse.
 Oedema
 Lipodermatosclerosis
 Palpate along the vein for any depression .which
indicate fascial defect due to perforator
incompetence (button hole).
 Keep hand at SFJ. (Just medial to the femoral
pulse.3- 4 cms below and lateral to the pubic

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 tubercle.)Ask the patient to cough and palpate
cough impulse.

Special test

Tourniquet test

Raise the leg to empty the veins. Tie 3 tourniquets at the

levels of midthigh, below knee, mid-leg. Ask the patient
to stand .observe. If veins are getting filled within 30 sec
while tourniquet is on that indicates perforator
incompetence inbetween tourniquets.Untie the
tourniquets from distal to proximal. See whether the
veins are refilled which indicate which indicated LSV /
SSV incompetence.

Indications for intervention.

 symptomatic
 Cosmetic concerns.
 complications
o Ulceration.
o AtrophyBlanche.
o Lipodermatosclerosis.
 Bleeding

Interventions

Interventions are directed towards addressing sapheno-femoral

(SFI) / sapheno-popliteal junction incompetence, long

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saphenous (LSV)/ short saphenous vein reflux and varicosities
and perforators.

 SFI
o sapheno-femoral junction Ligation – SFL
o Endo venous laser ablation (EVLA)
 LSV
o Stripping
o EVLA
o Sclerotherapy
 Varicosities
o Avulsions
o Sclerotherapy
After intervention compression stocking/ dressings are
applied ( check distal pulse before applying)

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Wounds (ulcers)
A full thickness breach in the continuity of the skin is
called a wound.

Partial thickness breach(epidermis) is called an

Abrasion

Skin Anatomy

Skin consists of an epidermis, dermis and subcutaneous tissue.

Wound healing

Wound healing occurs through four stages i.e.

 Haematoma formation

 Inflammation/ debridment

 Proliferation

 Remodelling / maturation

 Haematoma formation occur always following injury.

 Inflammatory stage - Within 24 hours inflammatory

cells (mainly neutrophils) migrate into the injured area
and they remove bacterial growth and remove dead
tissue

 Proliferation –during this stage fibroblasts migrate into

wound and start to produce collagen and other
connective tissue elements. New capillaries grow into it
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 from adjacent blood vessels. This results in granulation
tissue formation. After the wound is filled with
granulation tissue it is covered with epithelium from
peripheral areas of wound.

 Remodelling – after the completion of granulation

formation, organisation of fibres and change in fibre
types occurs (e.g. type III to type I collagen) this results
in increasing strength of wound. The amount of
capillaries also reduce resulting in relatively avascular
scar tissue.

Abrasion heals br regeneration of epithelium only and it does

not result in scarring.

Chronic ulcers

Ulcers not showing signs of healing by 6 weeks arecalled

chronic ulcers.

Causes for non-healingulcers.

1. Local causes

-Repeated trauma
-Presence of foreign body / slough
-ongoing infection / osteomyelitis

2. Regional causes

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 -Venous
-Arterial
-Neuropathic

3. Systemic causes

-Diseases- diabetes mellitus, renal failure, etc.

- Drugs- immunosuppressive drugs,
cytotoxic
-Nutritional deficiencies- hypo-albuminaemia,
anaemia, vitamin and mineral

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Differentiating Arterial, Venous and Neuropathic Ulcers

Venous Arterial Neuropathic

ulcer

Site Over the Tips of the Pressure areas

medial / toes and (heel, under Neath
lateral distal foot metatarsal heads)
malleolar
area - Gaiter

Size varying size Varying Varying size

size

Shape varying varying varying shape

shape shape

Surroundin Features of Shiny Loss of

g skin chronic atrophic sensation,Charcot’
venous skin, loss s joint, clawing of
hypertensio of hair foot, flat foot
n

Wall Sloping punched out

Base pink No Bone may be

granulation granulatio exposed
tissue n tissue,
bone may

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 be exposed

temperature Warm/ Cold normal

normal

Pain Painless / Extremely Painless

painful painful

Pulses present absent Present

Treatment for chronic ulcers

Treat for the causes accordingly.

Local

 Wound toilet

o Process of removal of slough, dead tissue,

foreign bodies and draining pus.

o Following a wound toilet the wound base is

made suitable for future granulation and
epithelialisation.

Regional causes

 Arterial- revascularization

 Venous- Strapping (i.e. multilayer compression - two or

three layers with cotton wool, crape bandage and

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 elasto-plaster. Can be made 4 layers by adding a
cohesive bandage in between crape and elasto-plaster –
the idea of applying multiple layers instead of single
tight layer is to provide sustained firm compression.
The amount of pressure applied should be maximum at
foot level and minimum at calf level thus providing a
graduated compression)

 Neuropathic- off loading

Systemic causes

 Correct anaemia, vitamin deficiency and other

nutritional deficiencies.

 Optimization of underlying comorbidities.

 Role of antibiotics in wound - indicated only in patients

with evidence of local or systemic infection.

Wound dressings
The material which is applied to the surface of wound to cover
it is called a dressing.

 Primary dressing - The material which directly

touches the wound

 Secondary dressing - The material which covers the

primary dressing

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Ideal wound dressing
Dressings are applied to wounds for the following reasons;

 To provide a protective cover

 To maintain moisture

 To reduce pain

 To absorb exudates

 Etc.

In addition to above functions an ideal dressing should have

the following features;

 does not induce pain or itching

 easy to change
 Allows gaseous exchange
 Cheap
 Freely available

Types of Wound dressings

1. Gauze
a. advantages
i. cheap
ii. freely available
b. disadvantages
i. allows wounds to dry

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 ii. causes pain while removing
2. Low adherent dressing: does not induce pain on
removal. e.g.
a. Vaseline

3. Hydrocolloids: methylcellulose, gelatin, pectin, and

adhesives mixed together to make a sheet. E.g.Comfeel,
a. Advantages
i. Provides Protective barrier
ii. Absorbs exudates – can be applied on
oozing wounds
iii. Does not induce pain on removal
4. Hydrogels: e.g. – Intrasite
a. Hydrogels promote wound hydration and
promote debridement by autolysis – applied on
necrotic dry wounds.
5. Alginates: produced from calcium and sodium salts of
alginic acid found in seaweed. E.g. – SeaSorb
a. Highly absorbent –used in oozing wounds
b. Used in cavities
6. Semi permeable filmsE.g.Tegaderm, Opsite
a. Advantages
i. Keep moisture

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 ii. Do not adhere to wound
iii. Allows inspection without removing
7. Antimicrobial dressings
a. Silver dressings- Acticoat, Atruman silver
b. Iodine - Iodosorb
8. Negative-pressure wound therapy (NPWT): application
of negative pressure to wound
a. Suck out exudates
b. Reduce size of cavities and prevent collections
developing - – can be applied for oozing and
deep cavity wounds.
c. Promotes wound healing by various processes at
tissue level.

How often do you have to change the dressing?

There is no fixed duration for dressing change. The

dressing is changed when it is soaked of when it has to be
removed for other reasons e.g. wound inspection,
discomfort to the patient etc.

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Acute limb ischemia
Sudden interruption of blood supply to limb resulting in threat
to the limb viability.

Sudden interruption of a vessel may be due to,

 Compression from outside

o Tight bandage, cast, tourniquet
o Compartment syndrome
o Burn
 on the wall of vessel
o Thrombosis
o trauma
o Dissection
 Inside the vessel
o embolus

Patient presentation

With evidence of ischaemia(P’s)

 pain - which is severe and sudden onset

 pallor

 Perishing cold

 Pulselessness

 Paresis / paralysis

 Paraesthesia / anaesthesia.
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Differentiating thrombosis and embolism

Embolism Thrombosis

Sudden onset pain Sub acute onset

Young patient Elderly patient

Has a source of emboli* No source of emboli

No history of occlusive History of occlusive arterial

arterial disease disease

Other pulses are present Other pulses may be absent

*Sources of emboli;

 Heart – recent MI, Atrial fibrillation, Valvular heart

disease.

 Blood vessels – aneurysms

An embolus gets stuck at sites of bifurcation as the diameter of

the vessels reduces at these places.

Management

 Start unfractionated heparin

o Loading dose 75 – 100 IU/Kg ( approximately
5000 IU )

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 o Followed byInfusion of heparin -18U/kg
(approximately -1000U/hr)
o Keep APTT between 60 to 80s
 Pain relief
 Keep fasting
 Urgent ECG,FBC, INR
 Check the Viability of the limb – refer to viability
assessment in vascular trauma section of the note.

Interventions:-

 Embolectomy – using balloon tipped Fogarty catheter

 + /- Fasciotomy
 Continue heparin (infusion 18U/kg) until the INR is 2-
3 for 2 days
 Start warfarin – adjust dose to keep INR between 2-3
 Monitor distal pulse and for effects of reperfusion

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Deep Vein Thrombosis (DVT)
Thrombosis - formation of solid material with the components
of the blood inside the vessels of a living person

Causes

Virchow’s triad e.g.

1.endothelial damage femoral venous line

2 .Stasis prolonged immobilization,

pregnancy, pelvic masses

3. Hypercoagulability Pregnancy, carcinoma,

primary thrombophilia

Presentation

 Calf pain
 Swelling

Differential Diagnosis - cellulitis

Diagnosis

1) Duplex scan ( USS + Doppler)

USS shows solid material inside vessel and non

compressibility,with reduced / absent flow, no
augmentation and no phasic variation

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 2) D dimer

Originate from clot lysis. Increase even in post surgical

thrombosis. Therefore doboth duplex scan & D dimer
together.

 USS +ve- start treatment

 USS –ve& D dimer also -ve- no treatment/ find
alternative causes
 USS –ve& D dimer +ve- repeat USS in 1 week if
again -vethink of alternative causes

Wells score
 Low risk – DVT unlikely, think of alternative causes
 High risk – Do Duplex and D- Dimer

Treatment

 unfractionated heparin
o Loading dose 75 – 100 IU/Kg ( approximately
5000 IU )
o Followed Infusion of heparin -18U/kg
(approximately -1000U/hr)
o Effect is monitored with APTT.Keep APTT
between 60 to 80s

 Also start
o warfarin 10 mg D1
10 mg D2
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 5 mg D3
Target INR is in between 2 - 3. Adjust the dose accordingly.
When INR between 2 - 3 for 2 days omit heparin.

 LMWH (low molecular weight heparin) – e.g.

Enoxaparin (1 mg/kg twice daily SC), dalteparin,
tinzaparin

o Can be started instead of unfractionated heparin.

Advantages include;
o
 Has prolonged half life therefore patient
does not require infusion. Can be
administered subcutaneous once or twice
daily therefore patient can be treated as
outpatient ( not yet done in Sri Lanka)
 Does not need monitoring with frequent
APTT.( effect is monitored with factor X
level. Which need not be done)

How long warfarin should continue?

o 3 - 6 months

When a person below 50 yrs without risk factors presented

with DVT should be screened for thrombophilia.
All patients who had DVT should wear compressive stockings
for at least 2 years to reduce stasis & to augment the blood
flow and to prevent post thrombotic syndrome.

Complications

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  Pulmonary embolism - immediate
 Post thrombotic syndrome – long term

Post thrombotic syndrome

The development of features of chronic venous insufficiency

following an episode of DVT.

Following DVT the thrombus may undergo;

 propagation and get detached (leading to embolism)

 lysis
 organisation and become fibrosed

When the thrombus gets lysed the valves may get damaged and
become incompetent. When it gets organized the veins become
blocked. Both these events lead to venous incompetent and
venous hypertension leading to chronic venous hypertension.
Patient develops oedema, pigmentation, lipodermatosclerosis
and ulcers.

Prevention;
 initial treatment of DVT
 prevention of recurrence
 compression stocking

Warfarin

Warfarin is an anticoagulant derived from coumarin(found in

sweet clover-based animal feeds). Warfarin inhibits the
vitamin K-dependent synthesis of coagulant factors II, VII, IX
and X and also protein C and S. it is used in the treatment and
34 | P a g e
prevention of thrombosis and embolism.in the initial phase of
warfarin therapy there is rapid reduction of protein C but the
reduction of factor II effect takes four to five days, thus there is
an increased risk of thrombosis initially. Therefore warfarin is
started with Heparin.

Advice to patient

 What is warfarin – refer above

 How does it act – refer above

 Why is it given to patient – tell the indication

 Dose to be taken, How to and how frequently to

monitor

o Same dose everyday at the same time ( i.e. 6pm)

of the day in empty stomach ( fast 1 hour before
and take meal one hour after – to make
absorption consistent)

o INR testing – refer below.

o INR range – keep between 2-3.

 Difference Between Brands – take same brand

 Avoid or do not take certain food in increased amount

(cauliflower, cabbage, beetroot and other green leafy
vegetables, liver, vitamin supplements – because these
35 | P a g e
 contain vitamin K which will interfere with action of
warfarin – reduce INR)

 Get the advice of the doctor when starting new drugs –

because of drug interactions.

 Drugs usually interacting with warfarin

o Aspirin, NSAIDS
o Antibiotics, anti TB
o antidepressants - fluoxetine
o antifungals - fluconazole , miconazole, and
others
o herbal products
o Anti epileptics- carbamazepine (Tegretol),
phenobarbital, phenytoin (Dilantin).

 Side effects
o Nausea, loss of appetite
o Bleeding - bleeding from the
gums,haematuria,bleeding per rectum, melaena,
epistaxis
o Advice to stop and report immediately.

 Pregnancy – not suitable in first trimester (warfarin

embryopathy), plan.

 Surgeries and dental procedures – report to doctor,

needs to be stopped and heparin started

 Avoid getting injections into the muscles; it should be

given in the arm
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  Do not miss doses. If a dose is missed and if you
remember on the same day (within 12 hours), take it as
soon as you remember. If you remember on the next
day, skip the missed dose and take the usual dose. Do
not take double dose inform the doctor if 2 or more
doses are missed in a row (need to check INR and if
low have to start with heparin again).

 How to monitor INR

Every 2 – 3 days Until INR within therapeutic range on

2 consecutive INR checks

Then every weekly for one month

Then monthly.

 How long to continue warfarin?

Depends on indication e.g. DVT – 3 months, heart valves -

lifelong

Management of High INR

 Current INR > 5–8 , without bleeding

1. Stop warfarin

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 2. Test INR daily until it has returned to the therapeutic
range

3. Restart warfarin with a reduced dose when INR < 5

 Current INR is > 8, without bleeding

1. Stop warfarin therapy

2. Give vitamin K 2.5 – 5 mg, orally

3. Measure INR in 24 hours

4. Restart warfarin with a reduced dose when INR < 5

If major bleeding occurs (at any high INR)

1. Stop warfarin
2. Give vitamin K 10 mg, slow IV
3.give prothrombin complex/ FFP
3. Refer to secondary care

If there is bleeding with therapeutic range INR look for

secondary course. E.g. – colonic tumour, bladder tumour

INR Dose adjustment Next INR test

≤ 1.5 Increase weekly dose by 7 days

15%

1.6– 1.9 Continue current dose-If 7 days

repeat INR falling or low
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 for 2 consecutive INRs,
increase weekly dose by
10%

2–3 Continue current dose Refer above

3.1–3.9 Continue current dose, 7 days

If repeat INR rising or
high for 2 consecutive
INRs, reduce weekly dose
by 10%

4.0–5.0 Omit warfarin dose for 1 7 days

day, reduce weekly dose
by 10%

≥ 5.0 Refer above

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Below knee amputation as a short case

History:

 age

 What is the reason for amputation?

 When it was done?

 What is the current situation of the patient and the

amputated limb?

 Comorbidities

 Using a prosthetic limb or not

Examination:

Proper exposure of the amputated stump compare with contra-

lateral limb

Inspection

o side

o type

o BKA / AKA

o In BKA – flap

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  Long posterior, skew, equal

o Scar

o Stretched (protruding bone),Hypertrophy, sinus

o Skin changes to suggest prosthetic limb usage.

o Knee joint contractures

o Thigh muscle wastage

Palpation;

o Flap tight or soft.

o Tenderness over the scar.(neuroma)

o Ask the patient to flex and extend the knee joint

and the hip joint.Look for range of movement.

o check for pulse – femoral and popliteal

o examine the other limb

o Ask the patient to sit up and transfer and if the

patient is using crutches / prosthesis to
demonstrate walking.

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Examination of Haemodialysis access (Arterio Venous
Fistula)

History

 When it was created – takes about 6 weeks to become

mature and to use for dialysis.
 Is it being used for dialysis –how many times per week
 Any problems during dialysis
o Can the patient get adequate dialysis during
specified time – patients often know
o Pain during dialysis
o Any abnormality in venous and arterial side
pressure during dialysis - patients often know
o Prolonged bleeding after removal of cannula
(indicate venous hypertension)
o Features of heart failure
o Previous interventions – fistulogram,
fistuloplasty, surgery.

Inspection

 inspection of the entire limb, the neck and chest

o Describe the type of fistula – e.g. Radio
Cephalic (scar at wrist), Brachio Cephalic and
BrachioBasilic (scar at elbow crease level).
 Fistula
o Skin overlying the fistula - normal / signs of
infection.
o Veins are easily visible/ not, and of adequate
diameter ( 6mm)
o Adequate length of vein for cannulation ( 8 to
10 cms)
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 o Cannulation sites – should only have scabs and
no evidence of inflammation.
o Aneurysm

 Arm swelling and dilation of veins at chest wall and

neck – indicate central venous stenosis

Palpation

 Begin at the anastomosis

 Thrill – should be continuous, examine the entire length
of vein
 Veins are distinctly palpable for an adequate length (
about 8 to 10 cms for cannulation)
 Distal circulation – signs of distal ischemia – due to
steal phenomenon

Auscultation

 If there is no thrill auscultate along the fistula

 For features of heart failure

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Arterial aneurysms - Abdominal Aortic Aneurysm (AAA)
An aneurysm is defined as an abnormal focal dilatation of a
vessel of more than 50 percent of its normal diameter.(in case
of abdominal aorta more than 3 cms – normal diameter is about
2 cms)

A focal dilatation between normal size and 50% is called an

ectasia and when this is diffuse it is called arteriomegaly.

Types of aneurysm

 Based on wall characteristics

o True – all layers of the vessel wall is involeved
o False – all layers are not involved. Doed not
have intima and the wall is formed by fibrous
surrounding surrounding tissues or by organize
haematoma. Occur following vascular trauma
and vessel wall infection (Mycotic) leading to
focal rupture of wall and formation of
haematoma. The center of which remains as a
false aneurysm.

 Based on morphology
o Fusiform
o Fusiform – spherical and only involves part of
vessel wall.

 Based on location –e.g. aortic, femoral,popliteal, ect.

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45 | P a g e
Abdominal Aortic Aneurysm (AAA)

Epidemiology

Common in males (1:4) and white men. Prevalence increases

with age.

Causes
 Atherosclerosis and weakening of vessel wall –
commonest cause
 Cystic medial necrosis
 Aortitis
 Collagen vascular disease – Marfan’s. Ehlers- danlos
 Infection

Presentation

 Incidental finding – Asymptomatic

 Self-felt lump
 Symptomatic – pin due to erosion of vertebrae,
infection and rapid expansion.
 Complications
o Rupture
o Thrombosis
o Embolism – blue toe syndrome
o infection

Imaging
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  USS Abdomen – helps to confirm the diagnosis and in
follow-up and screening.
 CT scan of abdomen and pelvis with CT aortogram –
helps to measure the exact diameter of aneurysm
(maximum) the extent (supra/infra renal, Aortic, Aorto
iliac, length and angulation of neck, etc. which helps to
plan the intervention – surgical/ endovascular) and also
helps to detect leak.

Management

Indication for intervention include

 Diameter more than 5.5cms

 Symptomatic
 Complicated

Available modalities include;

 Surgical – inlay repair with synthetic vascular grafts

(PTFE, Polyester)
 Endo Vascular Aneurysm Repair (EVAR) – for
patient who are unfit for open repair. Very
expensive.
Patients with smaller aneurysms are followed up with
regular USS.

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Management of leaking aortic aneurysm

This is a surgical emergency. Therefore the resuscitation and

treatment should go hand in hand

 Grouping and DT and transfuse to keep the

blood pressure just enough to keep vital organs
perfused,
 Prepare for emergency surgery ( inform
surgeon, anaesthetist, theatre, ICU)
 Explain the risk of surgery to the patient and the
relatives
 Surgical intervention is similar to non ruptured
aneurysm repair, but in actively bleeding patient
proximal aorta is clamped first to reduce the
bleeding and then the patient is transfused to
elevate the blood pressure and then the surgeon
proceed with the rest of the surgery.

Complications of AAA repair

In addition to common complications following any major

surgery AAA repair is associated with:
 Large bowel ischaemia – inferior mesenteric artery is
often involved with the aneurysm sac. If the artery is
not implanted to graft there is risk of left sided bowel
gangrene

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 Embolisation / trash foot fo lower limbs – during
clamping and unclamping of aorta thrombus in the
aortic sac may embolise into lower limb.

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