Objectives:
• TO UNDERSTAND THE NATURE OF OCCLUSIVE ARTERIAL DISEASE AND ITS
ASSOCIATED SYMPYOMS AND SIGNS
•TO ABLE TO ASSESS ACUTE AND CHRONIC ARTERIAL INSUFFICIENCY AND
KNOW TREATMENT OPTIONS.
•TO KNOW ABOUT GANGRENE AND ITS MANAGEMENT
•TO KNOW OTHER ARTERIAL DISEASES LIKE ANEURYSMS,
ARTERITIS AND VASOSPASTIC DISEASES & AVFistula
Arterial Occlusion
Occlusive arterial disease
Types
 Acute arterial occlusion
 Chronic arterial occlusion
ACUTE ARTERIAL OCCLUSION
CAUSES EMBOLIC
 THROMBOTIC
 Heart diseases-Atrial fibrillation,mural thrombus, Post MI
 Rheumatic valvular heart diseases
 Paradoxical embolism- venous thromboembolism due to patent
foramen ovale
 Arterio- arterial embolism- dislodgement of atheromatous
plaques
 Angiographic procedures
 Accidental- intraarterial injection- Ergot,thiopental
 Trauma.

Embolism
 Brain-MCA
 Retina-Amaurosis fugax
 Mesenteric vessel-
 Spleen
 Kidneys
 Lungs-pulmonary embolism
ACUTE ARTERIAL OCCLUSIONEmbolism





C/F FIVE Ps
PAIN
PARALYSIS
PALLOR
PULSELESSNESS
PARAESTHESIA
Relation ship of symptoms to the site of obstruction
Aorto-iliac obstruction
Iliac obstruction
 Caludication in both buttocks,thighs & calves. Femoral &
distal pulses absent in both limbs. Impotence.bruit over
aortoiliac region.
 U/l claudication in thigh & calf buttocks.
 Bruits over iliac region
Femoro-popliteal obstruction
 U/L absence of femoral or distal pulses.
Distal obstruction
 U/L claudication in calf. Femoral pulse palpable with
absent u/l distal pulses
 Femoral & Popliteal pulse palpable
ankle pulses absent

claudication in calf & foot
Arterial Stenosis
Investigations:
GeneralCBC,ESR,
PLASMA -fibrinogen, protein, electrophoresis,
Glucose- blood n urine.
Lipid profile
 Doppler -USG blood flow detection
 Duplex imaging.
 Echocardiography
 Arteriography
 DSA
 ECG
Hand held Doppler
COLOUR DUPLEX
ARTERIOGRAM
DSA
Angioscope
Treatment.
Embolic arterial occlusion is an emergency!!!
 THROMBOLYSIS – Immediate -Intra Venous Heparin 5000U
to prevent distal and proximal extension of thrombus.
Contraindications
Recent stroke
Active peptic ulcer
Bleeding disorders
Pregnancy
 Hydration
 EMBOLECTOMY
 THROMBECTOMY.
 Fogarty catheterization- for removing proximal and distal







extension of thrombus.
Postoperatively- heparin and oral anticoagulation
Intrarterial Thrombolysis
Only if ischemia is not so severe that immediate operation
is mandatory, it is possible to treat thrombus or embolus by
intra arterial thrombolysis
Agents-TPA-tissue plasminogen activator**
Streptokinase
Urokinase
Identify and treat the basic cause.
SFA thrombolectomy
Removed thrombus
Arterial Catheters
Chronic Arterial Insufficiency
Etiology
 Atherosclerosis
 Buerger’s disease
 Artritis
 Arterisclerosis
 Diabetes
Risk Factors
 Hypertension
 Diabetes
 Strong family history
 Smoking
 Lipid abnormalities
Chronic Limb Ischemia
 Ischemia of the lower limb may be minimal to critical
 Also called Chronic arterial insufficiency or
Peripheral Vascular disease-PVD.
Clinical presentationIntermittant Claudication-commonest complaint. Fatigue,
aching or crampy pain occuring with exertion and relieved
by rest, reproducible at the same distance.
Claudication distance- distance at which the pain appears
Rest pain
Critical ischemia- severe ischemia with actual or potential
tisssue loss.
Signs of chronic ishemia
 Loss of muscle mass/bulk
 Loss of subcutaneous fat
 Skin shiny
 Loss of hair
 Brittle nails
 Gangrene and ulcers of foot.
???
GANGRENE
 Def: death, often with putrifaction of macroscopic portion of
tissues.
 VARIETIES ACCORDING TO THE CAUSE-
Secondary:
 Thrombus in atherosclerotic artery.
 ATRIAL FIBRILLATION-embolus.
 Arteritis from NEUROPATHY
 BUERGERS DISEASE
 RAYNAUDS DISEASE/ERGOTISM- causing arterial shutdown
 INTRARTERIAL INJECTIONS- thiopentone & cytotoxic
materials.
GANGRENE
Primary:
 INFECTIVE- boils, carbuncles, gas gangrene, gangrene of
scrotum (Fournier’s gangrene)
 TRAUMATIC- crush, pressure sores & constriction grooves
 PHYSICAL- burns, scalds,frostbite,chemical irradiation &
electricity.
 VENOUS



C/F
Pulseless,painnless,funtionless, with colour change.
Lacks capillary refill and venous return.
Black,brown, greenish black.
GANGRENE
 CLINICAL TYPES- DRY & MOIST
 DRY gangrene dessicated tissues,part becomes dry and wrinkled.





Wrinkled ,discolourd from disintegration of Hb. & greasy
to touch.
MOISTgangrene:
when venous & arterial obstruction is present, when artery
is suddenly occluded by a ligature or embolus & in
diabetes..
Infection & putrifaction is present.
Part is swollen& discoloured.
Crepitus may be present.
GANGRENE
SEPERATION OF GANGRENE SEPERATION BY DEMARCATION
 SEPERATION WITHOUT DEMARCATION.
 Vague DEMARCATION & skip lesions.
TREATMENT OF GANGRENE GENERAL PRINCIPLES- limb saving attitude.
 Cardiac failure
 Atrial fibrillation anaemia. Nutritious diet.
 Control of diabetes.
 Analgesics.
 LOCAL TREATMENT dry.protection of pressure areas. Cleanniess.
VARIETIES OF GANGRENE
DIABETIC GANGRENE- three factors Trophic changes from peripheral neuritis.
 Atheroma of artries causing ischemia
 Excess sugar –decreases resistance to infections esp. fungal infection
 DIRACT TRAUMATIC GANGRENE
 BEDSORES-(Decubitus Ulcers) 5 factors
1.
2.
3.
4.
5.
Pressure
Injury
Anemia
Malnutrition
Moisture
Pressure Sore
Gangrene
INDIRECT TRAUMATIC GANGRENEInterference with blood vessels from pressure by a
fractured bones
/ strangulation
Thrombosis of an artery
Ligation of an artery
poor technique for digital anesthesia
ERGOT- claviceps purpurea.
Fingers,nose & ears .
Seen in migrane suffers.
PHYSICAL AND CHEMICAL CAUSE
OF GANGRENE
.
 FROST BITE- cold+wind. Damage to Vessel wall with
transudation & edema. Pain initially later painless &
gangrene
 TRENCH FOOT-cold+ moist+ muscular inactivity.
 Ill fitting boots.
 I/V INJECTION OF THIOPENTONE
 DRUG ABUSE
 CHEMICAL GANGRENE- carbolic acid(phenol).
Frost bite
ANEURYSMS
 ANEURYSMS- dilatation of a localised segment of the
arterial system.
 True- all three layers involved.
 False- single layer of fibrinous tissue as the wall of the sac.
 According to the shape
-fusiform
-Saccular
-Dissecting
Eti0logy-traumatic/atherosclerotic/syphilitic/collagen
disease(Marfan,syndrome), mycotic(bacterial)
ANEURYSMS
 Symptoms- due to expansion, thrombosis, rupture or release of
emboli.
 Symptom relate to the vessel affected, the site supplies or the
tissue compressed.
Clinical features
Intrinsic-expansile pulsation along the course of an artery.
proximal compression decreases pulsations
 Palpation- thrill
 Auscultation-bruits??
Extrinsic- neighboring or distal structures are affected.
 Nerve
 Veins
 Tubes-trachea ,esophagus
D/D
 Swelling under an artery- cervical rib(subclavian)
 Swelling over an artery-pancreatic cyst
 Pulsatile tumors-sarcoma,osteoclastoma & metastsis
from hypernephroma.
 abscess
 serpentine artery- innominate,carotid.
ANEURYSMS
Abdominal aortic aneurysm Commonest large vessel aneurysm
 2% population
 95% atherosclerotic
 95% below the renal arteries
 Symptomatic/asymptomatic
 Symptoms-back pain, sudden – mild-sudden severe.
ANEURYSMS
Ruptured AAA Anterior
 Posterior
 Free bleeding into the peritoneal cavity(20%)
 Retroperitoneal hematoma(80%)
 Profound hypotension
 Severe pain
ANEURYSMS
 Investigation:
 USG abdomen
 CT Chest & abdomen.
 AORTOGRAM
ANEURYSMS
Procedure
 Open surgical procedure
 Endoluminal stent graft procedure.
Complications:
Respiratory
H’ge
Colonic ischemia
Renal failure
Infection of the graft.
Sexual dysfunction
Fistula formation.
Spinal cord ischemia.
Peripheral aneurysms
 Popliteal aneurysms- most common
 Femoral
 Iliac
 Ascending aorta & arch
AVF:
 Communication between an artery & vein.
 Congenital
 Acquired-






trauma, penetrating wound or sharp blow, surgical
for renal failure.
Structural effect- arterialized veins. Dilated tortuous veins
Physiological effect- Increased VR, Increased VP, Increased HRIncreased CO.
PP-HIGH
LVF
Cardiac failure
Cong Fistula- Overgrowth of limb.
Persistent ulcer due to distal ischemia.
???
AVF
Clinical signs:
 Pulsatile swelling
 Thrill on palpation
 Bruits on ausculatation
 Dilated veins
 Nicoladoni-Branham’s test- Decreased thrill, reduction in
size and bradycardia on pressing the artery proximal to
fistula
Treatment
 Embolization
 Ligation of feeding artery???
 Surgery- Separation of artery & vein
ARTERITIS
 Thromboangitis obliterans/ Buerger’s disease
Small & medium sized arteries.Occlusive disease
2. Thrombophebitis of superficial/ deep veins.
3. Raynauds syndrome, male, young patients
1.
VASOSPASTIC CONDITIONS:
Reynaud's syndrome:
 Primary/ idiopathic form.
 Secondary




Pallor- blanching
Blue- cyanosis
Redness-red engorgement.
Accompanied by pain.
Treatment - conservative
Tab. nicotinamide
Secondary Reynaud's syndrome due to some other problem like-collagen disease, atherosclerosis, thoracic
outlet syndrome, carpal tunnel syndrome