Vascular disorders Flashcards
Acute ischemia causes (A++)
I. Intrinsic causes:
1. Arterial embolism
2. Acute Thrombosis
II. Extrinsic causes:
1. Trauma.
2. Neglected tourniquet or tight plaster.
3. Compartment syndrome.
4. Intra-arterial injection.
5. Low flow states.
6. Venous outflow blockade.
7. Drug induced.
Arterial embolism: Sources of emboli:
o Commonest from the heart (left side) in cases of A.F.
o Detached atheromatous patch thrombus.
o Detached thrombus from aneurysm.
o Paradoxical embolus: comes from venous side (right side) through patent foramen ovale.
Acute thrombosis:
o Commoner cause than embolism.
o It is due to the same factors of gradual thrombosis, but it is not known why the onset is sudden!
Investigations of Acute arterial ischemia (A++)
A) Plain X ray chest: For exclusion of thoracic aortic aneurysm as a source of embolism
B) Abdominal ultrasonography and duplex scanning:
1. Exclude abdominal aortic aneurysm (AAA).
2. Can detect the actual site of occlusion and its propagation.
3. Assess the condition of the arteries and atherosclerosis of its wall.
C) Echocardiography: For diagnosis of cardiac source of embolism e.g. left atrial thrombus or mitral valve vegetations.
D) Angiography: It is indicated in:
o Preoperative: If acute thrombosis on top of atherosclerosis is suspected.
o Intra-operative: As a completion angiography.
o Postoperative: When in early postoperative,
the pulsation become absent after being palpable and mild degree of ischemia starts
to appear
E) Laboratory Investigations:
1. CBC for diagnosis of cases with polycythemia and thrombocytosis.
2. Coagulation profile to obtain a baseline for anticoagulant therapy.
3. Renal function to assess the capability of kidney to secrete the dye of
angiography and to compare with its function after reperfusion of the ischemic
limb.
Causes of chronic arterial occlusion (B)
1- Atherosclerosis → the commonest cause
* Aorto-iliac disease. * Femoro- popliteal.
* Tibio-peroneal disease (more in diabetics).
2- Arteritis:
* Thrombangitis obliterans “Burger Disease”.
* Purpura fulminans “Toxic purpuric gangrene”.
* Arteritis of collagen disease: (Polyarteritis nodusa & Scleroderma).
3- Raynaud’s disease “Vasospastic disease”.
4- Pressure from outside as in cervical rib and popliteal entrapment syndrome.
5- Aneurysm due to thrombosis and thrombo-embolisation which may occur.
Short note on Burgers disease (A++)
Aetiology:
* Unknown but smoking is a fixed accompanying feature in almost all cases.
Pathology:
* The artery, the vein and the nearby nerve are incorporated in dense fibrosis with inflammatory reaction.
* Thrombosis will develop and the thrombus will be organized in late stages.
* The net result is ischaemia, phlebitis and perivascular inflammation → severe pain from the nearby sensory nerves.
Clinical Picture:
* It affects the medium sized vessels. Individuals suffer:
1 Phlebitis migrans: in early cases “pass undiagnosed”
2 Pain: due to involvement of:
Artery → ischaemia. Vein → Phlebitis. Nerve → neuritis.
3 Raynaud’s phenomenon.
Treatment:
1 Prohibit smoking.
2 Sympathectomy “lumbar” gives good results.
3 Reconstructive surgery is impossible in most cases
Raynaud’s disease short note (A++)
Definition:
* It is a vasospastic disease showing special Raynaud’s phenomenon (pallor followed by cyanosis then redness).
Aetiology:
* Sympathetic overtone.
* Local arterial fault e.g. endarteritis obliterans.
Pathology:
* The phenomenon can be explained as follow:
1 Exposure to cold or emotional stress → severe arterial spasm → blanching.
2 The anoxia occurs resulting in paralysis of the pre-capillary sphincters → stagnation of anoxic blood in the capillary spaces → cyanosis.
3 When the anoxic blood becomes oxygenated it gives the red colour → redness.
4 The capillary sphincters regain its normal tone → normal colour again..
Clinical Picture:
* The disease usually affect young adult female who is usually emotionally unstable.
* It is usually bilateral & symmetrical affecting the fingers or toes and rarely affect the nose and ears.
* The Raynaud’s phenomenon may occur in other diseases as Burger’s Disease, cervical rib, atherosclerosis & collagen diseases but the patient is usually male of old age and the condition may be unilateral and exposure to cold is not essential as a precipitating factor.
Treatment:
1 Psychotherapy & protection from cold.
2 Bilateral cervical sympathectomy with varying results.
Complaint and examination in chronic ischemia management. (A)
Complaint:
1 Pain = Intermittent claudication.
* Character → cramping pain.
* Site → Depends on the site of obstruction. e.g.
Aortic bifurcation occlusion → pain in the gluteal region.
Femoral artery occlusion → pain the hamstring muscles.
Popliteal artery occlusion → pain in the calf muscles.
* Precipitated by → Exercise
* Relieved by → Rest.
* Claudication time → Duration of pain.
* Claudication distance → the distance before each attack.
The longer the claudication period (time) and the shorter the claudication distance the severe the degree of ischaemia.
* Rest pain → Pain while the patient is in his bed.
It reflects severe degree of ischaemia.
2 Pallor: distal to obstruction. Raynaud phenomenon may be described.
3 Paresthesia: occurs in acute and chronic ischaemia.
4 Cold limb: the level of temperature change detected by examination.
5 Paralysis: = as in acute ischaemia. 6 Sloughing and gangrene.
7 Impotence in aorto-iliac occlusion “LeRiche syndrome” → Impotence + bilateral loss of femoral pulsation.
Examination:
1 Colour changes: pallor, cyanosis, mottling, or Raynaud’s phenomenon.
* Buerger’s angle: i.e. the angle at which pallor occurs.
- It decreases with the increase of ischaemia.
2 Venous refilling: Elevate the limb → the veins will be evacuated.
- Then make the limb dependent again and detect the refilling time.
- It ↑ with ↑ severity of ischaemia.
3 Temperature: Comparing with the healthy side, the level of occlusion can be predicted.
4 Arterial Pulsation:
* All pulsation sites must be examined comparing it with the healthy side.
* State of the artery must be detected.
* If you feel pulsation distal to obstruction it may be from collaterals, so, ask the patient to do exercise, if disappear it is of collateral.
5 Atrophic changes: e.g. ulceration, pigmentation and loss of hairs.
The Ankle Brachial index (ABI) can be calculated by dividing the measured pressure at the tibial vessel over the measured pressure at the brachial artery.
Normally the ABI is more than 1.0. If it decreased below 0.9 this reflects a degree of ischemia. According the ABI chronic ischemia can be classified and the need for surgical reconstruction can be judged.
Gangrene Dry VS moist
- Arterial obstruction.
Sudden with venous spasm VS Gradual with patent veins.
-Infection:
2ry infection. VS No infection.
- Common in:
Diabetic foot VS Senile atherosclerosis - Skin:
Moist and macerated. VS Dry, wrinkled. - Line of demarcation:
ill defined or absent. VS Will defined. - Line of separation:
No time for its occurrence.VS Distal to the line of demarcation.
Etiology types, and DD of aneurysm. (A)
Aetiology:
1. Congenital: usually in circle of Willis.
2. Traumatic:
* True: Following arterial contusion.
* False: Pulsating haematoma.
3. Inflammatory:
* Syphilitic: In thoracic & may be abdominal aorta.
* Mycotic: In small arteries due to septic thrombosis as in S.B.E.
4. Atherosclerosis: Common in abdominal aorta & iliac vessels.
Types:
1- Fusiform: Atherosclerosis, Syphilis
2- Saccular: Traumatic, Mycotic, Congenital
3- Dissecting: Atherosclerosis, Mycotic.
Differential Diagnosis:
* “of pulsating swelling”
1 Connected to an artery → aneurysms.
2 Lying on an artery → transmitted pulsation e.g. Pseudopancreatic cyst over
abdominal aorta.
3 Tumour having rich blood supply: e.g. highly vascular sarcoma &
thyrotoxicosis.
Complications of Aneurysm (A++)
1- Thrombosis and calcification.
2- Distal emobilization → ischaemia.
3- Inflammation: Pyaemia, septicemia → precipitate rupture.
4- Rupture → fatal haemorrhage.
5- Compression of the surrounding:
* Vein → Varicose vein, oedema.
* Artery → Ischaemia.
* Nerve → Paralysis, loss of sensation.
* Bone → Indentation or pathological fracture.
→ Syphilitic aneurysm may erode the bone.
* In thorax → Dysphagia.
- Etiology of Thoracic aortic aneurysm (A)
Aetiology:
* Cystic media degeneration (most common) … Marfan syndrome and Ehler-Danlos syndrome
* Genetic:
Bicuspid aortic valve
Familial thoracic aortic aneurysm syndrome
* Atherosclerosis
* Vasculitis
* Infectious
Classification, Risk factors & DD of aortic dissection. (A++)
Classification:
* De Bakey classification
Type I: Ascending and descending aortic dissection
Type II: Ascending aortic dissection.
Type III: Descending aortic dissection
* Stanford classification
Type A: Ascending aortic dissection
Type B: Descending aortic dissection
Risk factors:
* Increased aortic wall stress
Hypertension
- Severe uncontrolled hypertension
- Pheochromocytoma leads to attacks of severe hypertension due to release of catecholamines
- Cocaine induced hypertension as cocaine blocks the reuptake of norepinephrine and dopamine at the presynaptic adrenergic terminals
- Coarctation of aorta which elevates blood pressure before the coarctation site
Straining during cough or Weightlifting
Trauma or accident
* Aortic media abnormality
Genetic
- Marfan syndrome - Ehler-Danlos syndrome
- Bicuspid aortic valve - Turner syndrome
Vasculitis
- Takayasau vasculitis - Giant cell vasculitis - Behcet syndrome
Others
- Pregnancy - Infections
- Steroids - Immunosuppression
Common differential diagnosis:
* This patient must be management as acute chest pain for differential diagnosis
Common differential diagnosis
* Acute aortic dissection
* Acute coronary syndrome
* Acute pulmonary embolism
* Acute pericarditis
Etiology and clinical picture of AVF (A)
Aetiology:
1 Congenital: 5% it is usually microscopical and leads to local gigantism.
2 Traumatic: 9%.
3 Therapeutic fistula: is done for haemodialysis purposes.
4 Iatrogenic fistula: follow transfixed ligation of vascular pedicles.
Clinical Picture:
1) Local features:
* Pulsating mass.
* Machinery murmur may be auscultated over it.
* Thrill may be felt over it.
* 2ry varicose vein.
2) General feature:
* Hyperdynamic circulation with water hammer pulse.
* Thrill on palpation maximum at the AV communication.
* Systolic murmur.
* Tachycardia but if the fistula is closed by finger compression this will lead to bradycardia (Branham’s sign).
* Distal features of ischaemia due to steal phenomenon and V.V (Fig.).
Discuss Pathogenesis of virchow’s triad (A)
1- Injury of endothelium of vein by infection or trauma.
2- Stagnation of blood by heart disease or prolonged recumbency.
3- ↑ blood viscosity by dehydration or polycythemia
Clarify Risk factors, Clinical picture, types and DD of DVT. (A++++++)
Predisposing Factors and high risk conditions:
1. Age above 40 especially if obese and going to spend long time setting on chair e.g. long-time air travel.
2. Prolonged recumbency in spine diseases or surgery.
3. Hip and knee replacement surgery.
4. Gynaecologic pelvic operations.
5. Pregnancy and labour especially if there is cysteinemia and/or deficiency of antithrombin, protein C and protein S.
6. Contraceptive pills.
7. Patient with malignancy.
8. Patients under chemotherapy or radiotherapy.
9. Thrombophilia either genetic or acquired.
10. The most important risk factor is previous episode of DVT especially if the D- dimer level is still high reflecting ongoing thrombosis and fibrinolysis.
Clinical picture:
1- Puffiness: Edema of the foot or leg.
2- Loss of laxity of the calf when palpated which the knee is in moderate flexion.
3- Pain & tenderness in the sole or the calf.
4- Pyrexia: Postoperative unexplained fever & tachycardia must direct the attention to the possibility of DVT.
5- Positive Homan’s sign: Pain in the calf on dorsi-flexion of the foot.
- This test is painful and may induce pulmonary embolism by pushing the thrombus inside subsoleal vein plexus.
- So, it is mentioned to be avoided.
Clinical types:
A. Isolated sub-soleal plexus venous thrombosis.
B. Femoro-popliteal vein thrombosis.
C. Massive ilio-femoral DVT.
Differential diagnosis:
☑ DVT should be differentiated from all other causes of painful edematous leg:
1. Partial tear of tendo-achilis, it occurs usually during walking with typical history of sudden pain in the calf during activity. Bluish ecchymosis may appear later in
2-3 days.
- This diagnosis possibility should be excluded in any case to avoid worsening of the case if treated by heparin as DVT.
2. Post-traumatic calf hematoma.
3. Deep abscess or cellulites of the leg and foot.
4. Erysipelas of the leg and foot.
5. Complicated gastrocnemius bursae (rupture, hemorrhage, infection).
6. Pelvic mass with compression or invasion of the iliac vein.
Illustrate Anticoagulant therapy regimen, doses and dose adjustment tests. (A)
A. Unfractionated Heparin:
400-800 units/Kg/day continuous infusion for ten days.
Activated partial thromboplastin time can control the dose of heparin.
It should not exceed double of the control value.
It’s antidote is protamine sulphate 1mg for each 100 IU heparin given to the patient .
B. Fractionated Heparin:
Examples: Dalteparin, Enoxapain and Tenzapaine or synthesized fractionated heparin (Fondaparinux).
It carries better results than unfractionated heparin with lower risk of bleeding.
It is given in subcutaneous route for 10 days.
C. Oral anticoagulant (Warfarin, Cumadin & Dendivan):
It should be given with the appropriate dose according to the prothrombin time and concentration and International Normalizing Ratio (INR) of the patient at the time of diagnosis.
The prothrombin concentration should be between 30-60% with INR between 2-3.
The maintenance dose is given for 6 months. Its antidote is vitamin K.
