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VASOSPASTIC DISORDERS
AND GANGRENE
BY
DR H SURESH CLEMENT
PROFESSOR
PHYSIOLOGY OF ARTERIES:
It transports the blood.
Blood is a connective tissue made of plasma and cellular components
which carries the oxygen, nutrients and helps in expelling the nitrogen
end products and carbon di oxide.
It is dense and viscous than water.
Temp: 38 C that is 1 C higher than rectal temperature.
• Bright red due to oxygenated blood
• Dark red due to deoxygenated blood.
• Blood constitutes 8% of total body weight and 20% of Extra cellular fluid.
• Of the whole blood contents plasma 55%, 44% cellular part, 1% platelet.
• Of the 55% plasma 7% is made up of proteins of which 54% is albumin, 38%
globulin and 7% fibrinogen and 95% of plasma is made up of water and
electrolyte and nutri.ents and gases and waste products.
• Hematocrit :
Is the percentage of RBC in the whole blood.
Normal value in men 40 – 54% avg - 47%.
Normal value in Women 38 – 46% avg – 42%.
Proteins:
• Albumin – Produced by liver which helps in transportation of steroids,
hormones and fatty acids.
• Globulins – Produced by liver and plasma cells, mostly from β
lymphocytes, these produce immunoglobulins and anti biotics.
• Fibrinogen mostly helps in clotting mechanism.
RBC:
• Normal value is 5.4 Million/μL in men.
• Normal value is 4.8 Million/μL in women.
• 1 drop of blood is about 50 μL.
Platelets:
• Developed from the megakaryocytes from red bone marrow.
• Normal count is 1.5L to 4L /μL of blood.
• Size to 2 – 4 μm.
• Life span is 5 – 9 days.
• In the year 1900 Dr. Carl Landsteiner identified the blood groups A,B,AB,O, in
the year 1939 Dr. Philip and Dr. Profus identified the concept of Rhesus (Rh+)
Different types of Blood transfusions:
• Whole blood transfusion – stored for 6 weeks, RBC live for 24 hours,
remaining survive for 6 weeks except for factor 5 and 8.
• Fresh Whole blood transfusion – Drawn and transfused in 24 hours,
advantage is full of RBC, WBC and Coagulative factors.
• Packed RBC’s – Obtained by centrifuge, only RBC are transfuse,
advantage is less sensitization, no overloading with cations (ca2+,
na+, etc.,)
• Platelet Transfusion – When the counts falls below 1 lakh/μL of blood.
• Fresh Frozen Plasma – Derived from the freshly drawn blood, usually
in DIC and massive bleeding.
• Blood Loss:
• Class 1 – 15% of blood is lost that is about 750 ml.
• Class 2 – 15% - 30% of blood is lost that is about 750 ml – 1500ml.
Patient will have tachycardia and decreased pulse pressure.
• Class 3 – 30% - 40% of blood is lost that is about 1500 ml – 2000ml.
Patient will have features of hypovolemia.
• Class 4 – >40% of blood is lost that is >2000ml which is life threatening.
• Blood Pressure is generated by the contraction of the left ventricle which
produces hydrostatic pressure on the blood vessels.
• BP is determined by cardiac output, blood volume and vascular resistance.
• BP monitored by 1. Direct – Canulization of aorta.
2. Indirectly – Sphygmomanometer.
• Cuff should be 40% of circumference of limb.
• Doppler stethoscope by audible sounds.
• Pulse oximeter.
• Piezoelectrical crystal operators.
• Photoplethysmography using infrared operators, which is operated by micro
processor using the laser technology.
• Direct method of recording BP is by intraarterial canulization and connecting it
to SGT (strain gauze transducer).
Arteries:
• Name derived from air and terry meaning carrier, which function is
hemostasis, carry oxygen and nutrients, etc.,.
• Left side heart pumps blood approximately 1 Lakh km or 60,000 miles.
Types are:
• Elastic arteries: also called conducting arteries which are rich in elastic
fibers in tunica media, when ventricles pump blood in them, they
swell up due to elasticity of vessels which will convert the potential
energy generated by ventricles into kinetic energy which will help in
blood moving forwards or periphery. ex: Aorta, Pulmonary trunk,
Brachiocephalic, Common carotid, Subclavian and Common iliac.
• Muscular Arteries:
They are medium size, they have more muscular tissue than elastic
tissue. Ex: Femoral artery, Popliteal artey, etc.,.
• Anastomotic Arteries:
Also called collateral arteries giving alternate blood supply.
• End arteries
• Arterioles are microscopic vessels which regulate the flow in capillary
network, size is 15 micro meters to 300 micro meters.
• There are 400 million arterioles are present.
• Meta Arterioles is the end part of arterioles which connect the capillary
network.
• Capillaries is the junction between meta arterioles and capillaries is guarded
by the capillary sphincter which will regulate the flow to the capillaries.
• Capillus means hair, size is 5 – 10 μmwhich connects with the venous plexus.
• There are about 20 Billion capillaries present in the body, it is in the
capillaries where the exchange of blood and interstitial fluid occurs,
extensive capillary network is seen when oxygen is more required like
in brain and kidney, and absent in cornea and cartilage.
• Capillaries have only intima layer, no tunica media and tunica externa,
therefore exchange of blood and interstitial fluid occurs.
• One meta arteriole give 10 – 100 capillaries.
• The precapillary sphincter blood controls the blood into the venules.
• Fenestration Capillaries many small pores present through which
blood enters the superficial system, size is 70 – 100nm in diameter.
• Myocardial contraction is by myocardial cells (also called myocytes).
• Acute Limb Ischemia (ALI) :
• Ischemia of limb is classified into Acute limb ischemia and Chronic
limb ischemia, intermittent claudication is due to arterial obstruction
is increased by the exercise and decreased by the relaxation.
Classification of OCCLUSIVE DISEASES OF VESSEL:
Fountain Classification:
1. Patient is asymptomatic.
2. Mild to severe claudication.
3. Rest pain.
4. Complications like ulcer, gangrene.
• Rutherford classification:
Grade 1 : Asymptomatic.
Grade 2 : Claudication.
Grade 3 : Tissue loss.
Grade 4 : Gangrene.
• Boyd Classification of ischemic limb:
Grade 1 : Patient has claudication, still can walk.
Grade 2 : Claudication present, still can walk with pain and strain.
Grade 3 : Patient has to take rest
• Causes of Claudication:
1. Chronic Compartment syndrome
2. Venous Claudication
3. Nerve Compression
4. Symptomatic Baker’s cyst
5. Hip Arthritis
6. Spinal Cord Compression
7. Coaractation of Aorta
8. Popliteal Aneurysm.
9. Popliteal Entrapment
10. Takayasus disease
11. Thromoangitis Obliterans.
• ABI – Ankle Brachial Index:
• Record the BP in the Upper arm and take highest systolic BP, now
record the BP at ankle joint, in anterior and posterior tibial artery with
doppler pencil probe.
• Now, Ankle pressure is divided by the arm systolic,
• normal being >1
• if <0.9 – ischemic changes will set in
• 0.7 – 0.5 – claudication will start
• 0.3 – 0.5 – rest pain will start
• <0.3 – impending gangrene.
Causes of Chronic Limb Ischemia:
1. Atherosclerosis.
2. Arteriopathies – buerger’s disease
Raynaud’s Disease
Takayasu Disease
3. Diabetes
4. Scleroderma
5. Trauma, radiation arteritis, Temporal arteritis.
• Features of Arterial Stenosis and block:
1. Intermittent claudication
2. Rest pain
3. Cold periphery
4. Numbness
5. Paresthesia
6. Color changes
7. Ulceration
8. Gangrene
9. Altered Sensation
10. Decreased mobility
11. Low Volume Pulse or No Pulse
12. Thrill or Bruit over the stenosed artery
13. Delayed Venous filling.
14. Marked pallor to blue color
15. Thinning of skin
16. Diminished hair
17. Loss of subcutaneous fat
18. Brittle nails with transverse ridges
19. Ulceration in digits
20. Wasting of Muscle.
And Limb may go into Gangrene.
Line of DEMARCATION:
It’s the line between viable tissue and dying tissue, indicated by band
of hyperemia, its also called final separation line.
Clinical Signs of Ischemic Limb:
1. Delayed capillary filling – Pulp of the finger and the nail bed
circulation on compression delayed filling will be seen.
2. Delayed Venous Filling: It is called Harvey sign – Empty the vein with 2 fingers,
above finger towards the heart is removed followed by the distal finger, slow
filling will be observed.
3. Crossed Leg Test also called Fuchsig’s test: Put the limb in a cross leg position
that is popliteal fossa on knee of other side and see for oscillations as the
popliteal artery is compressed.
4. Beurger’s Postural Test: Patient lying on the couch as the patient to
raise the limb
a. If no insufficiency the limb will stay pink even after raising above 90
degrees.
b. If ischemia is present, marked pallor and emptiness of veins is
observed, the angle in which the pallor develops is called as angle
of insufficiency, if this angle is <30 degrees it indicates severe limb
ischemia, it may turn into gangrene.
5. Systolic Bruit is heard over arterial stenosis particularly carotid
artery, renal artery and femoral artery.
Palpation of Blood Vessels:
• Dorsalis pedis artery felt in the foot against navicular and middle
cuneiform bones, it is absent on 10% cases.
• Posterior tibial artery felt against the calcaneum just behind the
medial malleolus and between it and tendon achilless.
• Anterior Tibial artery is felt anteriorly between 2 malleoli against the
lower end of tibia just above the ankle, lateral to extensor hallucis
longus tendon.
• Popliteal artery is felt in prone position with knee flexed at 90 to 130
degrees, relaxing the popliteal fascia pressing against the upper end of
tibia.
• Femoral artery felt in the groin between ASIS and pubic symphysis, flex
the hip joint 10 – 15 degress.
• Radial artery at the wrist on the lateral aspect of lower end and in
front of the radius.
• Common Carotid artery is felt medial to the sternomastoid at the
level of thyroid cartilage against the carotid tubercle (chassaigne
tubercle of transverse process of 6th cervical vertebra in the carotid
triangle).
• Superficial temporal artery is felt in front of the tragus against the
zygomatic bone.
• Investigations for Arterial diseases:
1. Blood test :
Hb
Rbs
Lipid profile
2. Hand Held Doppler
3. Duplex scan – Combination of B mode of USG and Doppler study.
• That is difference between transmitted beam from ultrasound and
reflected beam is called doppler shift.
• Which are converted into audible signals, which will tell site, extent,
severity of block and status of collaterals.
• Turbulence sounds indicate stenosis.
• Absence of audible sounds indicate complete block.
• With a doppler probe BP’s can be monitored at different levels.
• Angiogram:
1. Retrograde transfemoral seldinger angiography
2. Transbrachial Angiography
3. Transaortic angiogram
4. Other Angiograms are Ciliac superior Mesenteric Angiogram and
Coronary Angiogram
• Seldinger Technique –
• Arterial canula passed in the femoral artery,
• needle is removed,
• guide wire is passed through the canula,
• then canula is removed,
• arterial catheter is passed over the guide wire,
• Arterial catheter is insitu, guide wire is removed.
• Water Soluble Iodine dye (Sodium diatrizoate)
Is pushed, x-rays are taken or observed on C – Arm.
• Complications of Retrograde Angiogram
Bleeding
Dissection of vessels
Hematoma Formation
Thrombosis
Infection and Anaphylaxis
DSA – Digital Subtraction Angiography
• Here vessels are delineated in a better way through the computer
system, dye is injected in to artery or vein and films are taken nearby
tissue are concealed by computer subtraction.
Digital Subtraction Angiography
CT Angiogram:
By injecting the dye or contrast in the vein or artery, the sequential films are
taken and interpreted to make a diagnosis.
Risk Factors for Arteriopathies:
1. Hypercholesterolemia
2. Hyperlipidemia
3. Hypertriglyceridemia
4. Cigarette smoking
5. Diabetes mellitus
6. Elderly People
7. Obesity and Sedentary Life
ThromboAngitisObliterans:
• It was described by Urology professor Leo buerger in the year 1908.
• Seen only in males, not seen in women.
• Usually starts in the lower limb may involve upper limb also.
• Usually medium sized arteries are seen, sometimes affecting superior
mesenteric artery.
• Associated with the cell mediated sensitivity to the type 1 and type 3 collagen.
Buerger’s disease affecting Lower Limb
Buerger’s disease affecting Upper Limb
Pathogenesis:
Smoke contains CO and nicotinic acid
↓
Causes vasospasm and hyperplasia of intima
↓
Thrombosis and obliteration of vessels
↓
Panarteritis
↓
Eventually vein and nerve also involved
↓
Involvement of Nerve give rest pain
↓
Features of ischemia appear clinically
↓
As obliteration takes place collaterals develop
Therefore it’s called Compensatory Peripheral Vascular Disease.
As patient continue smoking limb will go into Decompensatory
Peripheral Vascular Disease, eventually results in ischemia.
Smoker’s Index :
No. of cigarettes smoked per day X No. of years of smoking
If >300 = Patient is at risk.
Pack Year Index
• No. of years of smoking X No. of packets of cigarettes per day
• If >40 patient is at risk.
Clinical Features:
Pain in the limb
Intermittent Claudication
Rest pain ,Ulceration
Gangrene, Clinically absence of pulses
Recurrent migratory superficial thrombophlebitis and all the features of
chronic limb ischemia will be seen and ABI will be less than 1.
Investigations:
Hb
Blood sugar levels
Doppler study
Duplex study
Transfemoral Angiogram
Transbrachial Angiogram
Features seen are:
• Arterial block.
• Cork screw appearance of the vessel due to dilatation of vasa vasorum.
• Inverted tree appearance due to collaterals.
• Corrugated/rippled appearance due to severe vasospasm.
• Distal run off – amount dye filling in the main vessel distal to the obstruction
through collaterals, if the dye appears good distal to the obstruction it’s
compensated, if the dye doesn’t appear meaning its decompensated.
• Nerve and vein biopsy to confirm.
• Treatment is:
conservative,
stop smoking,
limb care,
buerger’s position and exercise,
regular graded exercise up to the point of claudication will improve the
collaterals then limb will become compensated.
• buerger’s Exercise: Raising the heel.
• Drugs:
Vasodilators like nifedipine 30mg BID
Pentoxyphylline 400mg BID
Low dose Aspirin 75mg OID
Clopidogrel 75mg OID
Atorvastatin 10mg OID
Cilostazol 100mg OID (more effective)
SURGERIES:
• Lumbar Sympathectomy – Open and chemical(usg guided).
• Radio frequency ablation of lumbar sympathetic ganglion (usually L3, L4
ganglion are removed).
• Ligation of Profounda femoris artery so that blood will be diverted into
popliteal arteries.
• If Ganglion is there, amputation is done.
• Gene therapy – Intramuscular injection of Vascular Endothelial Growth
factor which promotes the angiogenesis.
GANGRENE
• It’s a type of cell death which is classified into
1. Apoptosis
2. Cell Necrosis
3. Gangrene.
Apoptosis:
• It’s a programmed, non inflammatory cell death which occurs normally in
the body in a controlled manner by which body destroys unneeded and
abnormal cells.
• Features:
Non Inflammatory, single cell involved, cell shrinkage occurs
membrane intact, usually macrophages clear in a non inflammatory
mechanism. The process of destruction occurs in a step ladder pattern.
Cell Necrosis:
• It’s a cell death which is associated with the molecular death of the
cell.
• Features are:
Always associated with the inflammation.
Group of cells are involved.
Membrane of cell ruptures, nuclear damage occurs, inflammatory
cells like wbc’s are present, a diffuse pattern of destruction occurs
and is always pathological.
Gangrene
• Death of macroscopic portion of tissue which involves large portion of
tissue and lastly in truns from various colors to black color due to
break down of Hb giving rise to iron sulphite.
• The usual causes are:
Ischemia ex: TAO, Atherosclerosis, Venous obstruction.
Infection ex: Gas Gangrene, Fournier’s gangrene, Influenza, Dengue,
Hypernatremia, Plague.
• Traumatic ex: Crush injury and vessel rupture.
• Physical causes ex: Frost bite, electrocution, radiation and thermal bite.
Varieties of Gangrene are:
1. Dry Gangrene.
2. Wet Gangrene.
3. Internal Gangrene.
4. Necrotizing Fasciitis.
Dry Gangrene
• Causes are usually chronic arterial obstruction.
• It is characterized by local drainage, colour changes from pallor, grey,
purple then dark brown finally greenish black and black.
• Line of demarcation is present due to line of inflammation.
• Putrefaction is little, bacterial count is very low and less chances of
septicaemia and prognosis is better.
Wet Gangrene
• Usually due it bacterial infection.
• Associated with venous obstruction.
• Swelling with the blisters present.
• Rotten smell present.
• Usually dark in colour.
• Putrefaction is more due to congestion as organ is filled with the blood.
• No line of demarcation.
• Bacteria thrives and may result in septicaemia and SIRS, MODS and
shock.
• Prognosis is bad.
GAS GANGRENE
• Also known as Myonecrosis/ Clostridial Myonecrosis.
• Usually caused by clostridium perfringes which produce exotoxins.
• Sometimes caused by klebsiella pneumoniae.
• Gas is made of 6% Hydrogen, 3.4% CO2, 74.5% N2 and 16.1% O2.
• Discharge is usually sweety putrid.
• Toxins are called IOTA toxins & ALFA toxins which is heamolytic exotoxins.
TREATMENT
• Antibiotics
• Fluid management
• Debridement
• Maggots treatment
• Bi – pass graft
• Angioplasty
• Hyperbaric Oxygen is giving 100% oxygen to a patient, it is given in a
oxygen chamber.
Can be given through mask or ET tube in a chamber creating a
pressure between 250 – 280 kpa which is equal to 15 – 18m of water
depth, time is 45 – 300 min with 100% oxygen.
• Kpa named after blaise pascal.
• 101 Kpa is equal to 1 atmospheric pressure.
• In hyperbaric oxygen 20 times more oxygen is supplied than normal.
• Gases in the ratio of normal atmosphere.
• 78% nitrogen
• 20% oxygen
• 0.9% Arganon
• 0.1% other gases.
• Fasciotomy.
• Debridement and skin grafting.
• If inevitable amputation is the last resort.

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vasospastic.pptx

  • 1. VASOSPASTIC DISORDERS AND GANGRENE BY DR H SURESH CLEMENT PROFESSOR
  • 2. PHYSIOLOGY OF ARTERIES: It transports the blood. Blood is a connective tissue made of plasma and cellular components which carries the oxygen, nutrients and helps in expelling the nitrogen end products and carbon di oxide. It is dense and viscous than water. Temp: 38 C that is 1 C higher than rectal temperature.
  • 3. • Bright red due to oxygenated blood • Dark red due to deoxygenated blood. • Blood constitutes 8% of total body weight and 20% of Extra cellular fluid. • Of the whole blood contents plasma 55%, 44% cellular part, 1% platelet. • Of the 55% plasma 7% is made up of proteins of which 54% is albumin, 38% globulin and 7% fibrinogen and 95% of plasma is made up of water and electrolyte and nutri.ents and gases and waste products.
  • 4. • Hematocrit : Is the percentage of RBC in the whole blood. Normal value in men 40 – 54% avg - 47%. Normal value in Women 38 – 46% avg – 42%.
  • 5. Proteins: • Albumin – Produced by liver which helps in transportation of steroids, hormones and fatty acids. • Globulins – Produced by liver and plasma cells, mostly from β lymphocytes, these produce immunoglobulins and anti biotics. • Fibrinogen mostly helps in clotting mechanism.
  • 6. RBC: • Normal value is 5.4 Million/μL in men. • Normal value is 4.8 Million/μL in women. • 1 drop of blood is about 50 μL.
  • 7. Platelets: • Developed from the megakaryocytes from red bone marrow. • Normal count is 1.5L to 4L /μL of blood. • Size to 2 – 4 μm. • Life span is 5 – 9 days. • In the year 1900 Dr. Carl Landsteiner identified the blood groups A,B,AB,O, in the year 1939 Dr. Philip and Dr. Profus identified the concept of Rhesus (Rh+)
  • 8. Different types of Blood transfusions: • Whole blood transfusion – stored for 6 weeks, RBC live for 24 hours, remaining survive for 6 weeks except for factor 5 and 8. • Fresh Whole blood transfusion – Drawn and transfused in 24 hours, advantage is full of RBC, WBC and Coagulative factors. • Packed RBC’s – Obtained by centrifuge, only RBC are transfuse, advantage is less sensitization, no overloading with cations (ca2+, na+, etc.,)
  • 9. • Platelet Transfusion – When the counts falls below 1 lakh/μL of blood. • Fresh Frozen Plasma – Derived from the freshly drawn blood, usually in DIC and massive bleeding.
  • 10. • Blood Loss: • Class 1 – 15% of blood is lost that is about 750 ml. • Class 2 – 15% - 30% of blood is lost that is about 750 ml – 1500ml. Patient will have tachycardia and decreased pulse pressure. • Class 3 – 30% - 40% of blood is lost that is about 1500 ml – 2000ml. Patient will have features of hypovolemia. • Class 4 – >40% of blood is lost that is >2000ml which is life threatening.
  • 11. • Blood Pressure is generated by the contraction of the left ventricle which produces hydrostatic pressure on the blood vessels. • BP is determined by cardiac output, blood volume and vascular resistance. • BP monitored by 1. Direct – Canulization of aorta. 2. Indirectly – Sphygmomanometer. • Cuff should be 40% of circumference of limb. • Doppler stethoscope by audible sounds. • Pulse oximeter.
  • 12. • Piezoelectrical crystal operators. • Photoplethysmography using infrared operators, which is operated by micro processor using the laser technology. • Direct method of recording BP is by intraarterial canulization and connecting it to SGT (strain gauze transducer).
  • 13. Arteries: • Name derived from air and terry meaning carrier, which function is hemostasis, carry oxygen and nutrients, etc.,. • Left side heart pumps blood approximately 1 Lakh km or 60,000 miles.
  • 14. Types are: • Elastic arteries: also called conducting arteries which are rich in elastic fibers in tunica media, when ventricles pump blood in them, they swell up due to elasticity of vessels which will convert the potential energy generated by ventricles into kinetic energy which will help in blood moving forwards or periphery. ex: Aorta, Pulmonary trunk, Brachiocephalic, Common carotid, Subclavian and Common iliac.
  • 15. • Muscular Arteries: They are medium size, they have more muscular tissue than elastic tissue. Ex: Femoral artery, Popliteal artey, etc.,. • Anastomotic Arteries: Also called collateral arteries giving alternate blood supply. • End arteries
  • 16. • Arterioles are microscopic vessels which regulate the flow in capillary network, size is 15 micro meters to 300 micro meters. • There are 400 million arterioles are present. • Meta Arterioles is the end part of arterioles which connect the capillary network. • Capillaries is the junction between meta arterioles and capillaries is guarded by the capillary sphincter which will regulate the flow to the capillaries. • Capillus means hair, size is 5 – 10 μmwhich connects with the venous plexus.
  • 17. • There are about 20 Billion capillaries present in the body, it is in the capillaries where the exchange of blood and interstitial fluid occurs, extensive capillary network is seen when oxygen is more required like in brain and kidney, and absent in cornea and cartilage. • Capillaries have only intima layer, no tunica media and tunica externa, therefore exchange of blood and interstitial fluid occurs. • One meta arteriole give 10 – 100 capillaries.
  • 18. • The precapillary sphincter blood controls the blood into the venules. • Fenestration Capillaries many small pores present through which blood enters the superficial system, size is 70 – 100nm in diameter. • Myocardial contraction is by myocardial cells (also called myocytes).
  • 19. • Acute Limb Ischemia (ALI) : • Ischemia of limb is classified into Acute limb ischemia and Chronic limb ischemia, intermittent claudication is due to arterial obstruction is increased by the exercise and decreased by the relaxation.
  • 20. Classification of OCCLUSIVE DISEASES OF VESSEL: Fountain Classification: 1. Patient is asymptomatic. 2. Mild to severe claudication. 3. Rest pain. 4. Complications like ulcer, gangrene.
  • 21. • Rutherford classification: Grade 1 : Asymptomatic. Grade 2 : Claudication. Grade 3 : Tissue loss. Grade 4 : Gangrene.
  • 22. • Boyd Classification of ischemic limb: Grade 1 : Patient has claudication, still can walk. Grade 2 : Claudication present, still can walk with pain and strain. Grade 3 : Patient has to take rest
  • 23. • Causes of Claudication: 1. Chronic Compartment syndrome 2. Venous Claudication 3. Nerve Compression 4. Symptomatic Baker’s cyst 5. Hip Arthritis 6. Spinal Cord Compression
  • 24. 7. Coaractation of Aorta 8. Popliteal Aneurysm. 9. Popliteal Entrapment 10. Takayasus disease 11. Thromoangitis Obliterans.
  • 25. • ABI – Ankle Brachial Index: • Record the BP in the Upper arm and take highest systolic BP, now record the BP at ankle joint, in anterior and posterior tibial artery with doppler pencil probe.
  • 26. • Now, Ankle pressure is divided by the arm systolic, • normal being >1 • if <0.9 – ischemic changes will set in • 0.7 – 0.5 – claudication will start • 0.3 – 0.5 – rest pain will start • <0.3 – impending gangrene.
  • 27. Causes of Chronic Limb Ischemia: 1. Atherosclerosis. 2. Arteriopathies – buerger’s disease Raynaud’s Disease Takayasu Disease 3. Diabetes 4. Scleroderma 5. Trauma, radiation arteritis, Temporal arteritis.
  • 28. • Features of Arterial Stenosis and block: 1. Intermittent claudication 2. Rest pain 3. Cold periphery 4. Numbness 5. Paresthesia 6. Color changes
  • 29. 7. Ulceration 8. Gangrene 9. Altered Sensation 10. Decreased mobility 11. Low Volume Pulse or No Pulse 12. Thrill or Bruit over the stenosed artery 13. Delayed Venous filling.
  • 30. 14. Marked pallor to blue color 15. Thinning of skin 16. Diminished hair 17. Loss of subcutaneous fat 18. Brittle nails with transverse ridges 19. Ulceration in digits 20. Wasting of Muscle.
  • 31. And Limb may go into Gangrene. Line of DEMARCATION: It’s the line between viable tissue and dying tissue, indicated by band of hyperemia, its also called final separation line. Clinical Signs of Ischemic Limb: 1. Delayed capillary filling – Pulp of the finger and the nail bed circulation on compression delayed filling will be seen.
  • 32. 2. Delayed Venous Filling: It is called Harvey sign – Empty the vein with 2 fingers, above finger towards the heart is removed followed by the distal finger, slow filling will be observed. 3. Crossed Leg Test also called Fuchsig’s test: Put the limb in a cross leg position that is popliteal fossa on knee of other side and see for oscillations as the popliteal artery is compressed.
  • 33. 4. Beurger’s Postural Test: Patient lying on the couch as the patient to raise the limb a. If no insufficiency the limb will stay pink even after raising above 90 degrees. b. If ischemia is present, marked pallor and emptiness of veins is observed, the angle in which the pallor develops is called as angle of insufficiency, if this angle is <30 degrees it indicates severe limb ischemia, it may turn into gangrene.
  • 34. 5. Systolic Bruit is heard over arterial stenosis particularly carotid artery, renal artery and femoral artery. Palpation of Blood Vessels: • Dorsalis pedis artery felt in the foot against navicular and middle cuneiform bones, it is absent on 10% cases. • Posterior tibial artery felt against the calcaneum just behind the medial malleolus and between it and tendon achilless.
  • 35. • Anterior Tibial artery is felt anteriorly between 2 malleoli against the lower end of tibia just above the ankle, lateral to extensor hallucis longus tendon. • Popliteal artery is felt in prone position with knee flexed at 90 to 130 degrees, relaxing the popliteal fascia pressing against the upper end of tibia. • Femoral artery felt in the groin between ASIS and pubic symphysis, flex the hip joint 10 – 15 degress.
  • 36. • Radial artery at the wrist on the lateral aspect of lower end and in front of the radius. • Common Carotid artery is felt medial to the sternomastoid at the level of thyroid cartilage against the carotid tubercle (chassaigne tubercle of transverse process of 6th cervical vertebra in the carotid triangle). • Superficial temporal artery is felt in front of the tragus against the zygomatic bone.
  • 37. • Investigations for Arterial diseases: 1. Blood test : Hb Rbs Lipid profile 2. Hand Held Doppler 3. Duplex scan – Combination of B mode of USG and Doppler study.
  • 38. • That is difference between transmitted beam from ultrasound and reflected beam is called doppler shift. • Which are converted into audible signals, which will tell site, extent, severity of block and status of collaterals. • Turbulence sounds indicate stenosis. • Absence of audible sounds indicate complete block. • With a doppler probe BP’s can be monitored at different levels.
  • 39. • Angiogram: 1. Retrograde transfemoral seldinger angiography 2. Transbrachial Angiography 3. Transaortic angiogram 4. Other Angiograms are Ciliac superior Mesenteric Angiogram and Coronary Angiogram
  • 40. • Seldinger Technique – • Arterial canula passed in the femoral artery, • needle is removed, • guide wire is passed through the canula, • then canula is removed, • arterial catheter is passed over the guide wire, • Arterial catheter is insitu, guide wire is removed.
  • 41. • Water Soluble Iodine dye (Sodium diatrizoate) Is pushed, x-rays are taken or observed on C – Arm. • Complications of Retrograde Angiogram Bleeding Dissection of vessels Hematoma Formation Thrombosis Infection and Anaphylaxis
  • 42. DSA – Digital Subtraction Angiography • Here vessels are delineated in a better way through the computer system, dye is injected in to artery or vein and films are taken nearby tissue are concealed by computer subtraction.
  • 44. CT Angiogram: By injecting the dye or contrast in the vein or artery, the sequential films are taken and interpreted to make a diagnosis.
  • 45.
  • 46. Risk Factors for Arteriopathies: 1. Hypercholesterolemia 2. Hyperlipidemia 3. Hypertriglyceridemia 4. Cigarette smoking 5. Diabetes mellitus 6. Elderly People 7. Obesity and Sedentary Life
  • 47. ThromboAngitisObliterans: • It was described by Urology professor Leo buerger in the year 1908. • Seen only in males, not seen in women. • Usually starts in the lower limb may involve upper limb also. • Usually medium sized arteries are seen, sometimes affecting superior mesenteric artery. • Associated with the cell mediated sensitivity to the type 1 and type 3 collagen.
  • 48.
  • 51. Pathogenesis: Smoke contains CO and nicotinic acid ↓ Causes vasospasm and hyperplasia of intima ↓ Thrombosis and obliteration of vessels ↓ Panarteritis ↓
  • 52. Eventually vein and nerve also involved ↓ Involvement of Nerve give rest pain ↓ Features of ischemia appear clinically ↓ As obliteration takes place collaterals develop Therefore it’s called Compensatory Peripheral Vascular Disease.
  • 53. As patient continue smoking limb will go into Decompensatory Peripheral Vascular Disease, eventually results in ischemia. Smoker’s Index : No. of cigarettes smoked per day X No. of years of smoking If >300 = Patient is at risk.
  • 54. Pack Year Index • No. of years of smoking X No. of packets of cigarettes per day • If >40 patient is at risk.
  • 55. Clinical Features: Pain in the limb Intermittent Claudication Rest pain ,Ulceration Gangrene, Clinically absence of pulses Recurrent migratory superficial thrombophlebitis and all the features of chronic limb ischemia will be seen and ABI will be less than 1.
  • 56. Investigations: Hb Blood sugar levels Doppler study Duplex study Transfemoral Angiogram Transbrachial Angiogram
  • 57. Features seen are: • Arterial block. • Cork screw appearance of the vessel due to dilatation of vasa vasorum. • Inverted tree appearance due to collaterals. • Corrugated/rippled appearance due to severe vasospasm. • Distal run off – amount dye filling in the main vessel distal to the obstruction through collaterals, if the dye appears good distal to the obstruction it’s compensated, if the dye doesn’t appear meaning its decompensated.
  • 58. • Nerve and vein biopsy to confirm. • Treatment is: conservative, stop smoking, limb care, buerger’s position and exercise, regular graded exercise up to the point of claudication will improve the collaterals then limb will become compensated.
  • 59. • buerger’s Exercise: Raising the heel. • Drugs: Vasodilators like nifedipine 30mg BID Pentoxyphylline 400mg BID Low dose Aspirin 75mg OID Clopidogrel 75mg OID Atorvastatin 10mg OID Cilostazol 100mg OID (more effective)
  • 60. SURGERIES: • Lumbar Sympathectomy – Open and chemical(usg guided). • Radio frequency ablation of lumbar sympathetic ganglion (usually L3, L4 ganglion are removed). • Ligation of Profounda femoris artery so that blood will be diverted into popliteal arteries. • If Ganglion is there, amputation is done.
  • 61. • Gene therapy – Intramuscular injection of Vascular Endothelial Growth factor which promotes the angiogenesis.
  • 62. GANGRENE • It’s a type of cell death which is classified into 1. Apoptosis 2. Cell Necrosis 3. Gangrene.
  • 63. Apoptosis: • It’s a programmed, non inflammatory cell death which occurs normally in the body in a controlled manner by which body destroys unneeded and abnormal cells. • Features: Non Inflammatory, single cell involved, cell shrinkage occurs membrane intact, usually macrophages clear in a non inflammatory mechanism. The process of destruction occurs in a step ladder pattern.
  • 64. Cell Necrosis: • It’s a cell death which is associated with the molecular death of the cell. • Features are: Always associated with the inflammation. Group of cells are involved. Membrane of cell ruptures, nuclear damage occurs, inflammatory cells like wbc’s are present, a diffuse pattern of destruction occurs and is always pathological.
  • 65.
  • 66. Gangrene • Death of macroscopic portion of tissue which involves large portion of tissue and lastly in truns from various colors to black color due to break down of Hb giving rise to iron sulphite. • The usual causes are: Ischemia ex: TAO, Atherosclerosis, Venous obstruction. Infection ex: Gas Gangrene, Fournier’s gangrene, Influenza, Dengue, Hypernatremia, Plague.
  • 67. • Traumatic ex: Crush injury and vessel rupture. • Physical causes ex: Frost bite, electrocution, radiation and thermal bite. Varieties of Gangrene are: 1. Dry Gangrene. 2. Wet Gangrene. 3. Internal Gangrene. 4. Necrotizing Fasciitis.
  • 68. Dry Gangrene • Causes are usually chronic arterial obstruction. • It is characterized by local drainage, colour changes from pallor, grey, purple then dark brown finally greenish black and black. • Line of demarcation is present due to line of inflammation. • Putrefaction is little, bacterial count is very low and less chances of septicaemia and prognosis is better.
  • 69. Wet Gangrene • Usually due it bacterial infection. • Associated with venous obstruction. • Swelling with the blisters present. • Rotten smell present. • Usually dark in colour. • Putrefaction is more due to congestion as organ is filled with the blood.
  • 70. • No line of demarcation. • Bacteria thrives and may result in septicaemia and SIRS, MODS and shock. • Prognosis is bad.
  • 71. GAS GANGRENE • Also known as Myonecrosis/ Clostridial Myonecrosis. • Usually caused by clostridium perfringes which produce exotoxins. • Sometimes caused by klebsiella pneumoniae. • Gas is made of 6% Hydrogen, 3.4% CO2, 74.5% N2 and 16.1% O2. • Discharge is usually sweety putrid. • Toxins are called IOTA toxins & ALFA toxins which is heamolytic exotoxins.
  • 72. TREATMENT • Antibiotics • Fluid management • Debridement • Maggots treatment • Bi – pass graft • Angioplasty
  • 73. • Hyperbaric Oxygen is giving 100% oxygen to a patient, it is given in a oxygen chamber. Can be given through mask or ET tube in a chamber creating a pressure between 250 – 280 kpa which is equal to 15 – 18m of water depth, time is 45 – 300 min with 100% oxygen. • Kpa named after blaise pascal. • 101 Kpa is equal to 1 atmospheric pressure.
  • 74.
  • 75.
  • 76. • In hyperbaric oxygen 20 times more oxygen is supplied than normal. • Gases in the ratio of normal atmosphere. • 78% nitrogen • 20% oxygen • 0.9% Arganon • 0.1% other gases.
  • 77. • Fasciotomy. • Debridement and skin grafting. • If inevitable amputation is the last resort.