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196
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PERIPHERAL ANEURYSM
Peripheral aneurysms are less common compared to aneu-
rysms in the cavity. Such surface aneurysms are easily visible
and better amenable for clinical examination. But same time it
may be mistaken for abscess and inadvertent wrong attempt
of incision and drainage can occur leading to disastrous
consequences.
Popliteal type is the most common one. Peripheral aneurysms
occur in descending order of frequency in popliteal, femoral,
subclavian, axillary and carotid arteries.
Expansile pulsation which is confirmed using two finger
SRB’s Manual of Surgery
placement with thrill and bruit is typical. Infection, thrombosis
make it less pulsatile mimicking an abscess.
Erosion into adjacent bone and skin, rupture are known to
Popliteal Aneurysm
It is most common (70%); 65% are bilateral; 25% cases
are associated with abdominal aortic aneurysm; 75% cause
complications in 5 years.
Presentations:
¾
Swelling in popliteal region which is smooth, soft, pulsatile, well-localised, warm, compressible, often with thrill
and bruit. It may mimic a pyogenic abscess.
¾
Thrombosis and emboli from popliteal aneurysm can
cause distal gangrene which may spread proximally and
may lead to amputation.
¾
Rupture may cause torrential haemorrhage, but rupture
is very rare.
occur. Distal emboli may lead into digital gangrene.
Pressure on the affected artery proximally reduces the size,
and eliminates the thrill/bruit; pressure distal to aneurysm
increases the prominence of the aneurysm swelling with
bounding pulsation.
False aneurysm is common in femoral artery. It is treated with
thrombin injection if size is <3 cm; if size is >3 cm surgical
repair of artery with or without graft is indicated. True femoral
aneurysms are uncommon; when it occurs complications are
also rare (<3%).
X-ray, arterial Doppler, angiogram, echocardiogram are needed.
Treatment is open repair using arterial graft or endovascular
stenting.
Fig. 1.358: Popliteal aneurysm about to rupture. It is the most
common peripheral aneurysm.
Investigations: Duplex scan; CT or MR angiogram or DSA;
echocardiography; evaluation of abdominal aorta.
Treatment: Indications for surgery: Popliteal aneurysm >2
cm; symptomatic aneurysm; aneurysm which has caused
emboli. Surgeries are—exclusion with bypass inlay Dacron
graft through medial approach; aneurysmectomy and graft if
there is neurovascular compression. If there is thromboses
aneurysm, intra-arterial thrombolysis is needed using Fogarty
catheter but amputation rates are very high (>50%).
Fig. 1.356: Femoral artery aneurysm with impending rupture—
needs emergency surgical intervention. It is rare type.
Fig. 1.357: Radial artery aneurysm.
CAROTID ARTERY ANEURYSM (EXTRACRANIAL)
Incidence is less than 4% of peripheral aneurysms.
Most common site: Common carotid artery bulb, often
extends into the internal carotid artery.
Fig. 1.359: Carotid aneurysm.
Causes: Atherosclerosis, trauma; Syphilis, Marfan’s
syndrome; Ehler-Danlos syndrome; Congenital.
CLINICAL FEATURES
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B
x 10% bilateral
x Swelling in the neck at the level of the thyroid cartilage, below the
angle of mandible, Pulsatile (expansile pulsation), Smooth, soft,
nontender, horizontally mobile, with bruit
x Neurological features due to embolic episodes (50%)
x Hoarseness of voice, Horner’s syndrome
x Dysphagia due to swelling extending into the tonsillar bed.
Differential diagnosis: Carotid body tumour; Neurofibroma
arising from the vagus; Abscess in neck.
A B
Figs. 1.360A and B: Basilar artery aneurysm—angiogram
(Courtesty: Dr Muralidhar Pai, MCh, Mangaluru).
I. Classification (DeBakey’s)
x Type I: Dissection begins in ascending aorta extends into
descending thoracic aorta (70%)
x Type II: Dissection originates in ascending aorta and extends
only up to the origin of the major vessels. It is safer type with
less complications
x Type III: Dissection begins in the descending thoracic aorta
beyond the origin of the left subclavian artery
Stanford classification
II.
x Proximal—includes DeBakey’s Type I and II
x Distal—includes DeBakey’s Type III
Dissecting aneurysm can be:
III.
x Acute
x Chronic
x Healed dissecting aneurysm which communicates distally again
to aorta as double barrelled aorta
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CHAPTER 1L General Surgery: Arterial Diseases
Complications: Rupture; Thrombosis; Hemiplegia.
Investigations: Doppler of neck, carotid angiogram; DSA,
CT angiogram.
Treatment:
¾
Reconstruction of the artery using vascular graft.
¾
Ligation of the bulb as a life-saving procedure, but results
in haemiplegia.
¾
Intravascular stents.
DISSECTING ANEURYSM
It is a misnomer. It is not an aneurysm, only an aortic dissection.
It is the dissection of media of the aorta after splitting
through intima creating a channel in the media of the vessel
wall.
Causes: Hypertension (It is associated in 80% of dissecting
aneurysms); Cystic medial necrosis; Marfan’s syndrome and
collagen diseases; Trauma; Weakening of the elastic layers
of the media due to shear forces.
Features:
¾
It is always seen in thoracic aorta, common in ascending
aorta (70%).
¾
It is uncommon in other parts of aorta or other vessels.
¾
It can occur in aortic arch or thoracic descending aorta.
¾
This dissected aortic channel gets lined by endo thelium,
often reopens distally into the aorta causing double-
barrelled aorta which, in fact, prevents complications.
¾
It is commonly associated with aortic insufficiency.
Atherosclerosis is not a usual cause for dissecting aneurysm.
Fig. 1.361: Dissecting aneurysm.
COMPLICATIONS
B
x Acute: Rupture into the pericardium or pleura—dangerous type
x Chronic: Blockage of coronary vessels and major vessels like
carotid and subclavian arteries with aortic insufficiency
¾
Pain in the chest, back which is excruciating.
¾
Features of ischaemia due to blockage of different vessels.
Investigations: Chest X-ray shows mediastinal widening;
Arterial Doppler; CT angiogram.
Treatment:
¾
Antihypertensives.
¾
Surgery: Using Dacron graft reconstruction of aorta has
to be done with cardiopulmonary bypass.
INDICATIONS FOR SURGERY
B
x Progressive disease x Impending rupture
x Significant ischaemia x Type A aortic dissection
Imagination is the highest kite one can y.
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ERYTHROMELALGIA (ERYTHRALGIA)
SCLERODERMA/SYSTEMIC SCLEROSIS
It is also called as Mitchell’s disease; an episodic attack
precipitated by heat, exertion and stress; common in lower
limbs. Primary type is familial and autosomal dominant.
Secondary type is seen in gout, erythrocyanosis frigida,
polycythaemia, viral infection, mushroom poisoning, drug
induced (verapamil, ergots, fluoroquinolones). There is
microvascular and neuropathic changes.
There is severe burning pain in the limbs with redness and
sensation of heat. Warmness in the skin; often excoriation or
ulceration, flushing, prominent veins, severe hyperesthesia
SRB’s Manual of Surgery
are the usual features.
Treatment: Mechanical cooling by elevating the limb (Note:
Should not place the affected limb in cold water which may
flare up the problems); aspirin; pregabalin, gabapentin, IV
lignocaine are different drugs used in this condition.
LIVEDO RETICULARIS
It is a condition with arteriolar spasm along with obstruction of
capillaries by tiny blood clots with dilatation of venules, causing
lace like purplish discoloration. Persistent, mottled, reddish-blue
dermal streaks that do not blanche is typical. It may be idiopathic
or related to vasculitis due to autoimmune conditions along
with SLE or drug induced. Condition worsens by cold. Treating
the cause; PUVA bath; warming the limb; exercise are different
therapies.
POLYARTERITIS NODOSA
It is a necrotising inflammatory reaction with commonly
microscopic polyarteritis and nodule formation, often of
small and medium-sized arteries (not capillaries), causing
ischaemia of lower and upper limb.
Visceral arterial (mesenteric) involvement (70%) can cause
abdominal pain, GI bleed; mucosal ulceration and perforation of small bowel. Massive hepatic infarction, cholecystitis
can develop.
Renal artery can cause loin pain, haematuria, and renal
hypertension.
Coronary artery also can get involved causing myocardial
infarction.
Disease is common at bifurcation of medium/small sized
arteries leading to localised aneurysms.
It is common in males (3:1); fever, weakness, myalgia,
arthralgia are early features.
Presents with localised small aneurysms, like multiple 5–10 mm
nodules, palpable along the course of the artery.
In late stage presents with myocardial infarction, renal failure,
sepsis, GI bled.
HBsAg is positive in 40% patients of polyarteritis nodosa.
Angiogram of renal, mesenteric, peripheral arteries will show
aneurysms at branching points.
Biopsy of tender nodule, tender muscle is useful for diag-
nosis.
Treatment is prednisolone 60 mg daily with cytotoxic drugs.
Prognosis is poor with rapid death in early years.
It is a progressive disease causing fibrosis of skin, GI tract,
lungs, heart and kidney.
It is common in females (4:1) at 4th/5th decade.
It is considered as vasculitis even though earlier considered
as collagen disease.
Pathology consists of cytotoxic endothelial injury causing
interstitial oedema, severe fibroblast proliferation causing
fibrosis of affected vessels, and dilatation and proliferation
of remaining capillaries as telangiectasis.
Thin epidermis, thick dermis with more collagen with absence
of appendages and rete pegs are typical.
Lower 2/3rd oesophagus is sclerosed (50%) with increased
collagen in submucosa with atrophied mucosa and muscu-
laris. Dysphagia is common.
Diffuse interstitial fibrosis, thickening of alveolar membrane
and pulmonary hypertension occurs.
Synovial thickening causes arthritis; fibrosis of skeletal
muscles; interstitial myocardial fibrosis causes bundle branch
block, pericardial effusion.
Glomerulosclerosis in kidney is common (50%). Renal failure
is common.
Fibrosis of thyroid, periodontal membrane can occur.
Malabsorption syndrome is common due to small bowel
involvement.
Involvement of digital arteries present as Raynaud’s phenom-
enon.
Calcinosis, Raynaud’s, oesophageal hypomotility, sclero-
dactyly, and telangiectasia are the presentation of CREST
syndrome.
Investigations—anaemia, raised ESR, elevated IgG, presence
of antinuclear antibodies and anticentromere antibodies (in
CREST)—are different laboratory findings. Skin and periph-
eral arterial biopsy is confirmative.
Treatment—is difficult. Drugs like D pencillamine, colchi-
cines, p amino benzoic acid, vitamin E, dimethyl sulfoxide,
ranitidine are tried at various levels. Vasodilators, warming
and massaging skin, avoiding detergent soaps, oil and hydro-
philic ointment application are used.
Steroids, oxygen therapy for irreversible pulmonary fibrosis;
haemodialysis for renal failure; digitalis and other drugs for
cardiac failure are needed later.
Death is due to cardiac/pulmonary/renal failure.
ACROCYANOSIS (CRURUM PUELLARUM FRIGIDUM)
It is persistent, painless cyanosis seen in fingers and often in
legs with paraesthesia and chilblains affecting young females.
It is chronic persistent arteriolar constriction with slow rate
of blood flow.
Trophic changes and ulcerations are not seen.
Cyanosis which is persisting may aggravate on exposure
to cold.
It may be associated with endocrine dysfunction.
Treatment: Vasodilators; Cervical sympathectomy (effective).
Raynaud’s phenomenon Acrocyanosis
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• Episodic • Persistent
• Painful • Painless
• Acute arteriolar spasm • Chronic constriction
• Ischaemic changes are
common
• Ischaemic changes are not
seen
GANGRENE
If the tips of (the patient’s) fingers are falling off and are black, he
will die.
—(Anonymous), circa 2000 BC
It is macroscopic death of tissue in situ (in continuity with
adjacent viable tissue) with putrefaction (there will be loss
of function also).
Sites: Limbs; Appendix; Bowel; Testes; Gallbladder.
Causes
Secondary to arterial occlusion like athero sclerosis, emboli,
diabetes, TAO, Raynaud’s disease, ergots.
Infective: Boil, carbuncle, gas gangrene, Fournier’s gangrene,
cancrum oris.
Traumatic: Direct, indirect.
Physical: Burns, scalds, frostbite, chemicals, irradia tion,
electrical.
Venous gangrene.
Clinical Features
Colour changes: Pallor, greyish, purple, brownish black due
to disintegration of haemoglobin to sulphide.
Absence of pulse, loss of sensation, loss of function.
Line of demarcation between viable and dead tissue by a band
of hyperaemia and hyperaesthesia along with development
of a layer of granulation tissue.
A
B
Figs. 1.364A and B: Gangrene of foot and leg. Note the line of
demarcation. But skip lesion proximally shown signifies more proximal
spread of gangrene which may need above knee amputation.
In dry gangrene the separation occurs by aseptic ulceration
with minimum infection and the gangrene is dry and mummified.
In wet gangrene, separation takes place by septic ulcera-
tion. Often demarcation is vague with skip lesions more
proximally and so landing with higher level of amputations.
Even after amputation skin flap may show die back process,
leading to failure of taking up of flap of amputation and so
requiring still higher level of amputation.
Proximal ischaemic features may be present with rest pain,
colour changes, hyperaesthesia—pregangrene.
TYPES OF GANGRENE
B
x Dry gangrene is due to slow, gradual loss of blood supply to the
part causing dry, desiccated, wrinkled, mummified part with proper
line of demarcation from the viable adjacent tissues
x Wet gangrene is due to infection with putrefaction, causing
oedematous, swollen, discoloured part, spreading proximally,
with vague line of demar cation from the adjacent viable tissues
Investigations
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CHAPTER 1L General Surgery: Arterial Diseases
Fig. 1.362: Gangrene foot with ischaemic ulcer.
Fig. 1.363: Dry gangrene—great toe.
Today well lived makes every yesterday, a dream of happiness and tomorrow, a vision of hope.
Hb%, blood sugar.
Arterial Doppler, angiogram (Seldinger technique), CT
angiogram.
US abdomen to find out the status of aorta.
Fig. 1.365: Ischaemic features of right hand; compare to left side
which is normal.
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Differences between dry gangrene and wet gangrene
T
Dry gangrene Wet gangrene (Moist)
Clear line of demarcation is seen Line of demarcation is vague
Dry, shriveled, mummified Oedmatous, putrified, discoloured (H
Slow, gradual loss of blood supply Sudden loss of blood supply
Separation is by aseptic ulceration Septic ulceration causes separation
Limits to the demarcation Can extend proximally rapidly
Causes are atherosclerosis, thromboangiitis obliterans (TAO) Emboli, trauma are the causes
S)
2
Treatment
SRB’s Manual of Surgery
Limb saving methods:
Drugs: Antibiotics, vasodilators, pentoxiphylline, praxilene,
dipyridamole, small dose of aspirin, ticlopidine.
Care of feet and toes:
¾
The part has to be kept dry.
¾
Any injury has to be avoided.
¾
Proper footwear is advised (microcellular rubber footwear, MCR).
¾
Measures for pain relief is taken.
¾
Nutrition supplementation is done.
¾
The limb should not be warmed.
¾
Pressure areas has to be protected.
¾
Localised pus has to be drained.
Cause is treated; Diabetes is controlled.
Surgeries to improve the limb perfusion: Lumbar sympathec-
tomy, omentoplasty.
Profundaplasty, femoropopliteal thrombectomy or endarter-
ectomy, arterial graft bypass are done according to the need.
Life-saving procedures:
Amputations may have to be done ofen.
Level of amputation is decided on skin changes, temperature,
line of demarcation, Doppler study.
Below-knee amputation is a better option as BK prosthesis
can be fitted better and also the move
ments of knee joint are
retained. There is no need of external support and limp is absent.
In above-knee amputation range of movements are less, limp
is present, and often requires third (stick) support to walk.
Different amputations done are Ray amputation, below-knee
amputation (Buerger’s amputation), Gritti-Stokes transgenial
amputation, above-knee amputation.
Lisfranc’s, Chopart’s, Symes’, modified Symes’ amputations
are not commonly used in ischaemic limb as flaps will not survive.
DIABETIC FOOT AND DIABETIC GANGRENE
Foot is a complex structure with many layers of muscles, ligaments, joints, arches, fat, thick plantar fascia, vascular arches,
neurological system which maintains weight-bearing, gravity,
normal walk, stability and gait (swing and stance phases).
Problems in diabetic foot: Callosities, ulceration, Abscess
and cellulitis of foot, Osteomyelitis of different bones of foot
like metatarsals, cuneiforms, calcaneum, Diabetic gangrene,
Arthritis of the joints
MEGGITT’S CLASSIFICATION OF DIABETIC FOOT
B
x Grade 0: Foot symptoms like pain, only
x Grade 1: Superficial ulcers
x Grade 2: Deep ulcers
x Grade 3: Ulcer with bone involvement
x Grade 4: Forefoot gangrene
x Grade 5: Full foot gangrene
Pathogenesis of Diabetic Foot/Gangrene
High glucose level in tissues is a good culture media for
bacteria. So infection is common.
Diabetic microangiopathy causes blockade of micro-
circulation leading to hypoxia.
Diabetic neuropathy: Due to sensory neuropathy, minor
injuries are not noticed and so infection occurs. Due to motor
neuropathy, dysfunction of muscles, arches of foot and joints
occurs. And loss of reflexes of foot occurs causing more
prone for trauma and abscess. Due to autonomic neuropathy,
skin will be dry, causing defective skin barrier and so more
prone for infection.
Diabetic atherosclerosis itself reduces the blood supply and
causes gangrene. Thrombosis can be pre
causing infective gan
grene. Blockage occurs at plantar, tibial,
and dorsalis pedis vessels.
Increased glycosylated haemoglobin in blood causes defec-
tive oxygen dissociation leading to more hypoxia. At tissue
level there will be increased glycosylated tissue proteins,
which prevents proper oxygen utilisation and so aggravates
hypoxia.
Features:
¾
Pain in the foot; Ulceration; Absence of sensation.
¾
Absence of pulsations in the foot (posterior tibial and
dorsalis pedis arteries); Loss of joint movements.
¾
Abscess formation; Change in temperature and colour
when gangrene sets in.
¾
Patient may succumb to ketoacidosis, septicaemia or
myocardial infarction.
Investigations:
¾
Blood sugar, urine ketone bodies.
¾
Blood urea and serum creatinine.
¾
X-ray of part to look for osteomyelitis.
¾
Pus for culture and sensitivity.
cipitated by infection
¾
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Doppler study of lower limb to assess arterial patency.
¾
Angiogram to look for proximal blockage.
¾
Ultrasound of abdomen to see the status of abdominal
aorta.
¾
Glycosylated haemoglobin estimation.
Treatment:
Foot can be saved only if there is good blood supply.
¾
Antibiotics—decided by pus C/S.
¾
Regular dressing.
¾
Drugs: Vasodilators, pentoxiphylline, dipyridamole, low
dose aspirin.
¾
Diabetes is controlled by insulin only.
¾
Diet control, control of obesity.
¾
Surgical debridement of wound.
¾
Amputations of the gangrenous area. Level of amputation has to be decided by skin changes and temperature
changes or Doppler study.
¾
Care of feet in diabetic:
–
Any injury has to be avoided.
–
MCR footwears must be used (microcellular rubber).
–
Feet has to be kept clean and dry, especially the toes
and clefts; Hyperkeratosis has to be avoided.
¾
Warm drinks, analgesics, paravertebral injections to
sympathetic chain, hyperbaric oxygen are effective.
¾
If gangrene develops, amputation is needed.
AINHUM
Ainhum also known as ‘dactylolysis spontanea’ is a painful
constriction of the base of the fifth toe frequently (occasionally other toes also) followed by bilateral spontaneous autoamputation a few years later. Grooving → pain → constriction
deepens → tendon, nerve and vessel involvement → bone gets
cut spontaneously without any bleeding (auto-amputation) in
many (2–5) years.
Commonly affects males (can also occur in females).
Common in blacks, in Negroes.
History of running barefoot in childhood is common.
Fifth toe is commonly affected.
A fissure develops at the interphalangeal joint which becomes
a fibrous band, that encircles the digit causing necrosis
(Gangrene of little toe).
Often it can be bilateral.
201
CHAPTER 1L General Surgery: Arterial Diseases
Fig. 1.366: Gangrene of 3rd and 5th toes in a diabetic. Patient
already underwent amputation of 4 the toe earlier for gangrene.
FROSTBITE
It is due to exposure to cold wind or high altitude.
It is common in old age during cold spells.
Damage to vessel wall occurs causing oedema, blistering,
gangrene formation.
Part is painless and waxy.
Cells get frozen at – 5°C. Initially redness and oedema (1st
degree); blister formation (2nd degree); skin necrosis (3rd
degree); gangrene (4th degree) develops gradually.
Treatment:
¾
Gradual warming is done. Part should be wrapped with
cottonwool and rested. Warming is gradually done with
44°C in 30 minutes with warm water. Limb elevation is
done to reduce oedema. Intra-arterial vasodilators may
help.
Fig. 1.367: Bilateral Ainhum involving 4th and 5th toes of both feet.
Note the constriction ring in the toes.
Treatment: It is early “Z” plasty. Amputation is often required
later. Most often autoamputation occurs.
Note:
Yoruba people of Nigeria named ainhum.
ENDOVASCULAR SURGERIES
It is mainly used in peripheral vessels like femoropopliteal, renal,
coronary, cerebral vessels.
INDICATIONS
B
x Aneurysm for stenting and grafting
x Aortoiliac constrictive disease
x Renal artery stenosis; Carotid occlusive disease
x AV fistulas; Management of pseudoaneurysm
Balloon angioplasty: It is useful in short segment stenosis in
large vessles like renal vessels, iliofemoral, coronary vessels.
It is less effective compared to open surgery.
Intravascular stenting: Balloon expandable and self-expanding
stents are used at stenosed area.
Don’t wait for your ship to come; swim out to it.
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Endovascular grafts (PTFE, DACRON).
Endovascular atherectomy.
Angioscopy: Flexible, small, fibreoptic scopes to visualise
vessel wall with sufficient irrigation to avoid opacifi
by blood.
Intravascular ultrasound: To evaluate the vessel wall
morphology.
Complications: Thrombosis; Rupture; Sepsis; Fluid overload;
Air embolism.
UPPER LIMB ISCHAEMIA
It is a rare uncommon entity compared to lower limb ischaemia
SRB’s Manual of Surgery
but important because of its difficulty in managing. Higher-level
amputations are rare in upper limb ischaemia. Its incidence
is rare (5%) due to abundant collateral supply, infrequency
of atherosclerosis, decreased metabolic demand and smaller
muscle mass. It mostly affects distal small arteries (90%).
Symptoms are usually delayed.
Types of upper limb ischaemia: Acute; Chronic.
a. Acute type
Causes:
Embolism—common: 30% of the peripheral emboli lodge in
upper extremity.
of brachial artery (40%); next common is at axillary artery
(12%). Embolism is due to:
¾
Cardiac origin (70%)—valvular lesions (atrial fibrillation,
endocarditis), IHD, paradoxical.
¾
Others—aneurysms, thoracic outlet syndrome, plaque.
Trauma—most common: Brachial artery injury is seen in
30% of civilian trauma with arterial injuries, blunt injuries,
fractures and dislocations, penetrating injuries.
Iatrogenic.
The most common site is at the bifurcation
cation
Atherosclerosis—most common cause in USA.
TAO of upper limb.
Others—fibromuscular dysplasia; postirradiation—lung,
breast; occupational injuries; vibration injury, hypothenar
hammer syndrome; hypercoagulable states; APLA, polycythemia, cold agglutinins.
Raynaud’s phenomenon and disease.
Symptoms of chronic ischaemia
x Upper limb ‘Claudication’
x Weakness and wasting
x Digital ischaemia—ulcer, gangrene in finger tips
x Raynaud’s phenomenon
Signs of chronic ischaemia
x Wasting of arm, forearm and hand muscles
x Ischaemic changes in skin; tapering of finger tips
x Drop in systolic pressure >20 mmHg
x Proximal thrill or bruit
x Mass in the neck, thrill and bruit in the neck in supraclavicular
region
x Adson test, hyperabduction (Halsted) test, Roos test, Allen’s
tests are important
SYMPTOMS OF ACUTE ISCHAEMIA
B
x Pain, pallor, poikilothermia, paraesthesia, paralysis.
Fig. 1.368: Upper limb ischaemia with gangrene extending
proximally towards elbow joint.
b. Chronic Type
Causes:
Arteritis—aortoarteritis, Takayasu arteritis, giant cell arteritis,
connective tissue disease/vasculitis—scleroderma, SLE, RA,
PAN, etc.
Fig. 1.369: Gangrene of left index finger. Patient has undergone
cervical sympathectomy.
Investigations in Upper Limb Ischaemia
Laboratory tests for vasculitis, hypercoagulable states, and
atherosclerotic risk factors.
X-rays—for cervical rib; clavicular and first rib fractures;
fractures and dislocations in extremity; pulmonary lesions
of connective tissue disorders.
Arterial Doppler study.
Angiogram (subclavian angiogram)—CT/MR; conventional.
CT scan neck and thorax.
Blood sugar, lipid profile, cardiac evaluation.
Fig. 1.370: Upper limb angiogram showing blocks in
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subclavian artery.
Management of Upper Limb Ischaemia
Treatment of the cause.
Treatment of Embolus
Time since the first symptom is very important.
Clinical assessment of extent of ischaemia, immediate antico-
agulation with heparin, Doppler study and angiogram of the
arterial system, evaluation for the source of embolus—are
the protocols.
Embolectomy
¾
Brachial embolectomy: Local/regional/general anaes-
thesia is used. Longitudinal incision in the arm is used
for proximal embolus; Lazy S-shaped incision across the
elbow is done for embolus extending into the bifurcation
and to expose the branches.
Cilostazol—suppresses cAMP phosphodiesterase III rise in
cAMP levels with antiplatelet, antithrombotic effects; induces
vasodilatation; increases plasma HDL cholesterol; decreases
plasma triglycerides.
Catheter-based interventions
¾
Atherectomy.
¾
Angioplasty + stenting by conventional or subintimal
approach.
¾
Stent grafts.
¾
Cryoplasty.
Surgery
¾
Endarterectomy; Bypass surgery; Sympathectomy, extraperiosteal resection of the cervical rib.
Bypass Surgeries in Upper Limb Ischaemia
Conventional bypass
¾
Aorto-subclavian/axillary bypass.
¾
Subclavian-Axillary/brachial bypass.
¾
Brachiodistal bypass.
Extra-anatomical bypass
¾
Carotid: Subclavian/Axillary bypass.
¾
Subclavian: Subclavian bypass.
¾
Axillary: Axillary bypass.
Subclavian: Carotid transposition.
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CHAPTER 1L General Surgery: Arterial Diseases
Treatment in Trauma
General evaluation and resuscitation.
Control of bleeding in open wound: Pressure bandage/manual
compression (DO NOT USE TOURNIQUET).
Time since the event and clinical assessment of limb perfusion.
Stabilisation of fractures and dislocations.
Doppler study of arterial system, angiogram if required.
Arterial repair; bypass graft either venous or synthetic.
Treatment of Chronic Ischaemia
Medical management
¾
Risk modification—diabetes, hypertension, dyslipidemia,
smoking, homocystinaemia, exercise training.
¾
Antiplatelets—aspirin/ticlopidine/clopidogrel.
¾
Anticoagulants—heparin/warfarin.
¾
Xanthines/pentoxiphylline/cilostazol.
A B
Figs. 1.371A and B: (A) Carotid subclavian bypass;
(B) Subclavian carotid transposition.
Treatment of Raynaud’s Phenomenon
Avoiding triggering agents.
Drugs (vasodilators)—calcium channel blockers, angiotensin
II receptor blockers, alpha-1 adrenergic blockers, Sildenafil,
prostaglandin E1.
Surgery—sympathectomy.
Note:
Individual topics about causes of upper limb ischaemia are discussed in
different places.
He who attempts the absurd can achieve the impossible.
204
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UPPER LIMB ISCHAEMIA
B
x Trauma/cervical rib are the common causes
x Opposite limb, lower limbs should be examined
x Cardiovascular system should be examined
x Neck should be examined
x Wasting/girth should be checked
x All relevant clinical methods are equally significant
x Auscultation over neck/axilla/carotids for bruit are important
x Doppler; angiogram; nerve conduction studies; CT neck and
thorax are essential investigations
x Arterial repair; therapy for cervical rib; scalenotomy; cervical
SRB’s Manual of Surgery
sympathectomy are the different modalities of treatment
x Digital amputation may be required
ARTERIAL SUBSTITUTES
Ideal arterial substitute is not yet developed. Ideal arterial substitute should be strong, durable for patient’s life, biocompatible,
nonthrombogenic, should be resistant for infection, easily available, should have a long-term patency rate, and should have
elastic property of normal artery.
Classication of Arterial Substitutes
Arterial allograft—not used.
Arterial autograft—internal mammary artery (common),
internal iliac artery.
Arterial xenograft—bovine carotid artery graft—not used.
Venous autograft—long saphenous vein (common), small
saphenous vein, basilic vein, cephalic vein.
Venous allograft—umbilical vein graft.
Prosthetic grafts
¾
Textile grafts
–
Dacron graft—knitted or woven or crimping or velour
types. Dacron is polyethylene terephthalate.
–
Teflon graft—knitted or woven crimping or velour
types.
¾
Non-textile semi-inert polymer graft:
–
ePTFE graft—expanded polytetrafluoroethylene graft.
Preclotting the noncoated knitted or woven Dacron graft is done
to seal the graft and to prevent leak, and to create a smooth
lining at graft—blood interface. This step is not necessary for
PTFE or newer grafts.
Features of ideal graft
T
Strong Should be leak proof on restoration
of blood flow
Durable for patient’s life Should not chemically or physically
degenerate
Nonthrombogenic Should not cause any abnormal
reaction to surrounding tissues
Biocompatible Should not occlude when flexed
Resistant to infection Should not damage blood contents
Flexible
Should maintain long-term
patency
Should have elastic property
of normal artery
Carrel and Guthrie first did venous autograft into arteries of dogs.
They did extensive histological study of viable and nonviable
grafts. Lexer in 1907 used saphenous vein for axillary artery
repair. Murray started to use intraoperative heparin. Enaz Moniz
and dos Santos originated technique of arteriography. Gross and
his colleagues in 1948 started to use viable arterial allografts.
Later it was found that, as of graft is considered tissue viability
is not essential for success of graft uptake.
Complications of Graft
Neointimal fibrous hyperplasia at suture lines of the graft
is due to surgical trauma, PDFG, arterial smooth muscle
proliferation.
Graft infection—incidence is 2%. It is more in lower limb graft
than abdominal graft. Peroperative cephalosporin administration reduces the rate of graft infection. If infection occurs
graft should be removed and revascularisation is achieved
using a saphenous vein graft.
Graft failure is rare but can occur. It is due to fiber degenera-
tion, manufacturing defect, diffuse dilatation of graft (is due
to expansion of the knit in knitted Dacron).
Anastomotic false aneurysm (3%) occurs just adjacent to
suture line towards host artery. It is tearing of the artery
adjacent to suture line due to mismatched graft artery compliance, improper suture placement, and arterial degeneration.
There will be partial or total separation of the graft from the
host with blood collection in a covering of fibrous capsule.
Eventually it will rupture/may cause thrombosis and embolism. Treatment is graft—artery reanastomosis with insertion
of additional piece of graft.
M. Vascular Lesions
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C hapter Outline
·
Vascular Anomalies
·
Haemangioma
·
Vascular Malformations
VASCULAR ANOMALIES
It is a collective term used for haemangioma and vascular
malformations.
Haemangioma is a benign tumour containing hyperplastic
endothelium with cellular proliferation and increased mast
cells. Growth in tissue culture is observed. It is absent at
birth, seen by 1 month in 30%. It usually shows biphasic
growth phase with slow involution. 95% of cases achieve
spontaneous involution. Fast growing type can cause platelet
trapping and thrombocytopenia. Associated skeletal changes
are not common but can occur. But bone erosion by the lesion
can occur. It is common in girls (3:1).
Vascular malformations are single layer endothelium lined
spaces derived from arterial, capillary, venous or lymphatic
system. There is no growth in tissue culture. Raise in mast
cells is not seen. 90% cases are seen at birth; only few at later
period. It is equal in both sexes (1:1). Quiescent endothelium
with vessels showing progressive ectasia is the feature. Intravascular coagulation and mild thrombocytopenia can develop.
Skeletal changes and overgrowth are common. Spontaneous
involution is not common.
Disfigurement, tissue destruction, deformity, dysfunction,
telangiectasia, skin scarring are common.
Szilagyi classification—(1) Cavernous haemangioma; (2)
Microfistulous AV communications; (3) Macrofistulous
communications; (4) Anomalous mature vascular channels.
Humburg classification—(1) Predominantly arterial/venous/
lymphatic defects with aplasia or obstructive dilatation which
·
Cirsoid Aneurysm
·
Arteriovenous Fistula
is limited or infiltrative; (2) Predominantly AV shunting
defects with deep/superficial limited or infiltrating lesions;
(3) combined vascular defects—arterial, venous and haemolymphatic which may be limited or infiltrating.
Diagnosis is made clinically and by radiological imaging—
coloured Doppler, DSA, MRI. MRI is better than CT to identify
the flow (MR angiogram is ideal). Haemangiomas show
intense parenchymal staining; vascular malformations show
ecstatic vessels without much parenchyma; AVM shows rapid
venous shunting.
HAEMANGIOMA
It is the most common tumour in children (in 10% of term
deliveries).
It is benign vascular endothelial tumour, common in girls
(3 : 1).
It shows cellular endothelial hyperplasia with increased mast
cells.
Onset is few weeks after birth with biphasic growth showing
initial rapid growth with gradual involution over 5–7 years.
It is commonly seen in skin and subcutaneous tissue but
can occur anywhere in the body like in liver, brain, lungs or
other organs.
It grows rapidly in first year and 70% involutes in 7 years.
Early proliferative lesion is bright red, irregular; deep lesion
is bluish coloured. Involution causes colour fading, softness,
shrinkage leaving crepe paper like area.
Commonly it is central; common in head and neck region
(60%).
Often large haemangiomas may be associated with visceral
anomalies. Head and neck haemangioma is associated with
ocular and intracranial anomalies; sacral with spinal dysraphism. Multiple cutaneous haemangiomas may be associated
with haemangioma of liver causing hepatomegaly, cardiac
failure (CCF), anaemia.
You may be disappointed if you fail, you are doomed if you don’t try.
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