Dr.Hesham Noor, MBBCH,M.Sc.M.D

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Dr.Hesham Noor, MBBCH,M.Sc.M.D

• Assistant Prof. and Consultant Of General Surgery

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• vascular risk factors can usefully be divided
  into fixed (non-modifiable) and modifiable risk
  factors.
• Fixed risk factors include older age, male
  gender, family history, and a South Asian
  background.
• Modifiable risk factors include hypertension.
  hyperlipidaemia. Diabetes, smoking, alcohol,
  exercise, and stress.

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• Having one or more of these risk factors does not
  mean that a person is going to develop
  cardiovascular disease, but merely that he is at
  increased probability of developing it.
  Conversely, having no risk factors is not a
  guarantee that a person is not going to develop
  cardiovascular disease.
• (coronary heart disease, cerebrovascular disease,
  and peripheral vascular disease) often coexist.

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• Modifiable risk factors
• 6. Hypertension. If hypertensive, ask about
  latest blood pressure measurement, time since
  first diagnosis, and any medication being taken.
• 7. Hyperlipidaemia. If hyperlipidaemic, ask about
  latest serum cholesterol level, time since first
  diagnosis, and any medication being taken.
• 8. Diabetes mellitus. If diabetic, ask about
  medication being taken, level of diabetes control
  being achieved, and time since first diagnosis,
  and presence of complications.
• 9. Cigarette smoking. If a smoker or ex-smoker.
  ask about number of years spent smoking and
  average number of cigarettes smoked per day.
• 10. Alcohol. Ask about the number of units of
  alcohol drunk in a day. Note that depending on
  the amount that is drunk, alcohol can be either a
  protective factor or a risk factor.
• 11. Lack of exercise. Ask about amount of
  exercise taken in a day or week. Does the patient
  walk to work or walk to the shops?
• 12. Stress. Ask about occupational history and
  home/social life.

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• Inspection
• o Skin changes atrophy. pallor. Shininess,
  pigmentation, loss of body hair.
• o Scars. Of What?
• o Signs of gangrene blackened skin. nail
  infection, amputated toes.
• Venous and arterial ulcers. Remember to look in
  the interdigital spaces.Why?
• o Oedema.
• o Varicose veins (ask the patient to stand up).
• Do not make the common mistake of asking the
  patient to stand up before having examined for
  varicose veins.

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• Palpation
• o Skin temperature. Compare both legs.
• o Capillary refill. Compress a nail bed for 5
  seconds and let go, It should take less than 2
  seconds for the nail bed to return to its normal
  colour.
• o Peripheral pulses
• o Femoral pulse at the inguinal ligament.
• o Popliteal pulse in the popliteal space (flex
  the knee).
• o Posterior tibial pulse behind the medial
  malleolus.
• o Dorsalis pedis pulse over the dorsum of the
  foot, just lateral to the extensor tendon of the
  great toe.
• o Oedema. Firm "non-pitting" oedema is a sign of
  chronic venous insufficiency or chronic lymphatic
  insufficiency. (compare to the "pitting" oedema
  of cardiac failure).
• o Varicose veins. Tenderness on palpation
  suggests thrombophlebitis.

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• Why you should examine the suprficial venous
  system in lower exterimity periheral arterial
  disease?

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• o Buerger's test
• o Lift both of the patient's legs to a 45 degree
  angle and note the change in skin colour.
• o Ask the patient to dangle his legs over the
  edge of the couch, If the arterial supply is
  normal, the original skin colour should return in
  less than 10 seconds. (elevation pallor and
  dependent rubor)

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• Auscultation for vascular bruit
• o Femoral arteries.
• o Abdominal aorta.
• o Carotid arteries

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• Fixed risk factors
• 1. Age.
• 2. Sex.
• 3 Ethnic background. People from a South Asian
  background are at a notably higher risk of
  cardiovascular disease.
• 4. Family history.
• 5. High levels of fibrinogen coagulation factor.

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• Symptoms and signs of acute limb ischaemia
  Symptoms or signs
• Pain Occasionally absent in complete
  ischaemia
• Pallor Also present in chronic ischaemia
• Pulseless Also present in chronic ischaemia
• Perishing cold Unreliable as ischaemic limb takes
  on ambient
• temperature
• Paraesthesia Leading to anaesthesia (unable
  to feel touch
• on foot or hand)
• Paralysis Unable to wiggle toes or fingers
• Comment
• Anaesthesia and paralysis are the key to
  diagnosing complete ischaemia that requires
  emergency surgical treatment

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• CHRONIC CRITICAL LIMB ISCHAEMIA
• Definition
• Chronic critical limb ischaemia is defined by the
  presence of rest pain or tissue loss (ulceration
  or gangrene) in association with an ankle
  pressure of less than 50 mmHg or an ankle
  brachial pressure index (ABPI) of less than 0.5.

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• Gangrene
• Gangrene most commonly affects the toes and
  heels. Without the presence of infection,
  gangrenous tissue will mummify and demarcate
  This is termed dry gangrene and eventually
  results in auto-amputation if the stump receives
  sufficient blood flow.
• The presence of infection in gangrenous tissue
  results in wet gangrene. This requires surgical
  debridement or amputation to prevent worsening
  sepsis

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• Ulcers
• Ischaemic ulcers most commonly affect the tips of
  the toes, the margins of the foot (e.g. lateral
  to fifth metatarsophalangeal joint) where the
  circulation is poorest, and also at the lateral
  malleolus .
• Ulceration in diabetic patients may have a
  neuropathic component ((Neuro-ishaemic Ulcer

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• Compare and contrast
• Gangrene and necrosis
• Venous and ischemic ulcer
• Dry and wet gangrene
• Embolic and thrombotic acute ischemia
• Acute and chronic ischemia
• Venous and arterial gangrene (extremities and
  (bowel

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Palpation
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Adsons test
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Chronic venous insufficiency and Postphlebitic
syndrome

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• Venous valvular incompetence with distal
  ambulatory venous hypertension. After DVT, the
  involved venous segments eventually recanalize to
  some degree. However, their delicate valves
  remain scarred or trapped by residual organized
  thrombus.
• The loss of valvular mechanism disables the
  venomotor pump. The vein walls become thicker and
  less compliant, increasing resistance to proximal
  blood flow. These factors result in distal venous
  hypertension during walking .  

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• Protein-rich fluids, fibrin, and red blood cells
  and WBC are extravasated and deposited through
  large pores in the distended microcirculation
  during periods of venous hypertension. This
  process leads to inflammation, scarring, fibrosis
  of the subcutaneous tissues.(Lipodermatosclerosis)
  and discoloration by hemosiderin deposition
  ("brawny" edema).
• The resultant inflammatory reaction, scarring,
  and interstitial edema create a further barrier
  to capillary flow and diffusion of oxygen
  adequate nutrition to the skin is inhibited.
  These changes may lead to tissue atrophy and
  (ulceration (venous stasis ulcer

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• Do all patients with DVT develop postphlebitic
  syndrome?
•  No. Recent epidemiologic studies suggest that
  the incidence of venous ulceration is about 5.
  As many as one in five post-DVT patients have
  absolutely no symptoms and maintain the normal
  noninvasive vascular test data.
• The median time for the appearance of a first
  venous stasis ulcer is 2.5 years. Of interest,
  50 of patients with venous ulcers have no
  history of DVT (probably because of previous
  (asymptomatic calf vein DVT.

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• Distinguish between phlegmasia alba dolens and
  phlegmasia cerulea dolens
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• Iliofemoral venous thrombosis is characterized by
  unilateral pain and edema of an entire lower
  extremity, discoloration, and groin tenderness. A
  total of 75 of the cases of iliofemoral venous
  thrombosis occur on the left side, presumably
  because of compression of the left common iliac
  vein by the overlying right common iliac artery
  (May-Thurner syndrome). In phlegmasia alba dolens
  (literally, painful white swelling), the leg
  becomes pale and white. Arterial pulses remain
  normal. Progressive thrombosis may occur with
  propagation proximally or distally and into
  neighboring tributaries.

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• The entire leg becomes both edematous and mottled
  or cyanotic. This stage is called phlegmasia
  cerulea dolens (literally, painful purple
  swelling). When venous outflow is seriously
  impeded, arterial inflow may be reduced
  secondarily by as much as 30.
• Limb loss is a serious concern aggressive
  management (i.e., venous thrombectomy,
  catheter-directed thrombolytic therapy, or both)
  is necessary.

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• What is venous claudication
•  When venous recanalization fails to occur after
  iliofemoral venous thrombosis, venous collaterals
  develop to bypass the obstruction to venous
  outflow. These collaterals usually suffice while
  the patient is at rest. However, leg exercise
  induces increased arterial inflow, which may
  exceed the capacity of the venous collateral bed
  and result in progressive venous hypertension.
  The pressure buildup in the venous system results
  in calf pain commonly described as tight, heavy,
  or bursting (venous claudication). Relief is
  obtained with rest and elevation but is not as
  prompt as with arterial claudication

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• How can one distinguish primary varicose veins
  from secondary varicose veins
•  Primary varicose veins result from uncomplicated
  saphenofemoral venous valvular incompetence and
  have a greater saphenous distribution, positive
  tourniquet test result, no stasis sequelae
  (dermatitis or ulceration), and no morning ankle
  edema ((lymphedema
• Secondary varicose veins are most commonly a
  consequence of deep and perforator venous
  incompetence secondary to postphlebitic syndrome.
  
•  

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• . Aetiology of primary varicose veins
•  The most common cause is congenital absence of
  venous valves proximal to the saphenofemoral
  junction. There are normally no valves in the
  vena cava or common iliac veins and only an
  occasional valve in the external iliac veins.
  Thus, the sentinel valve in the common femoral
  vein just above the saphenofemoral junction is of
  critical importance. However, anatomic studies
  reveal that this valve is absent on one or the
  other side in 30 of patients.