Vascular Surgery Notes PDF

‫تفريغات‬ Vascular Surgery 5th Y e a r Edited by: H.A.S  Contents Anatomy of arterial system 1 Acute limb ischemia 3 Chron...

‫تفريغات‬ Vascular Surgery 5th Y e a r Edited by: H.A.S  Contents Anatomy of arterial system 1 Acute limb ischemia 3 Chronic limb ischemia 9 Raynaud’s disease 15 Burger’s disease 16 A-V fistula 17 Diabetic foot 20 Aneurysm 25 Anatomy of venous system 32 CVI 34 Varicose Vein (VV) 35 DVT 41 Post-Phlebetic Syndrome (PPS) 45 Lymphedema 47 Differential Diagnosis 51 َ ‫طريقا يَبتَغي فيه ِعلما‬ ‫س َّهل هللا له طريقا إلى‬ َ ‫ « َمن‬:‫قال ﷺ‬ َ ‫سلَ َك‬.»‫الجنة‬ ‫ فالعلم الذي‬.‫ علم الدين وعلم الدنيا‬:‫ "إنما العلم علمان‬:‫قال الإمام الشافعي‬."‫للدين هو الفقه والعلم الذي للدنيا هو الطب‬  Anatomy of arterial system - Aorta passes through the diaphragm at T12 ➦ divides into 2 common Iliac arteries ➦ each gives internal iliac and external iliac branches. ➜ Median sacral artery is the continuation of the aorta. ➜ External iliac branch is the continuation of the common iliac. ➜ Internal iliac supplies the pelvis and divides into anterior and posterior divisions. -External iliac artery becomes the common femoral artery at mid-inguinal point (midway between ASIS and symphysis pubis) against head of femur. -Common femoral artery gives superficial epigastric, superficial external pudendal and superficial circumflex iliac arteries. ➜ Ends by dividing into superficial femoral (the continuation) and deep femoral arteries. -Deep femoral (profunda femoris) artery passes laterally and gives most of arterial supply to thigh. -Superficial femoral passes through the femoral triangle then through the subsartorial canal to become the popliteal artery at the adductor hiatus in the adductor magnus muscles. ➜ SFA only gives a genicular branch before ending. -Popliteal artery * Has 2 parts: A part passes supra genicular felt against the popliteal surface of femur between medial and lateral epicondyles A part passes infra genicular felt against popliteal fascia * Then popliteal gives the trifurcation (anterior tibial [the highest branch] and tibio-peroneal trunk which gives the peroneal and posterior tibial arteries). -Anterior tibial artery becomes the dorsalis pedis artery which is felt in the foot against 1st metatarsal bone lateral to extensor hallucis longus (dorsiflex the big toe to be prominent). 1 -Posterior tibial artery passes behind the medial malleolus. ➜ Its pulsation felt in that site or against calcaneus. ➜ More important than anterior tibial because it gives medial and lateral planter arteries. 2  Acute limb ischemia ❖ Definition Sudden or rapid cessation of the blood flow to a limb that threated its viability. ❖ ETIOLOGY Arterial embolism “most common cause” Cardiac 90% “most common” Non-cardiac 10% 1. Atrial fibrillation (AF) “most common” 1. Dislodgment of atheroma 2. left atrial myxoma. 2. Air embolism 3. Subacute bacterial endocarditis 3. Mural thrombi (SABE) 4. Fat embolism 4. Recent myocardial infarction (MI) 5. Parasitic embolism 5. Mitral stenosis. 6. Paradoxical embolism Acute thrombosis “2nd most common”: which may be On top of chronic arterial disease (e.g. atherosclerosis). As a complication of aneurysm. Massive ileo-femoral DVT “the only type of DVT cause arterial ischemia”. Trauma Direct: stap. Indirect: fracture bone. Intra-arterial injection. Acute aortic dissection. Severe vaso-spastic disorders: Raynaud’s disease. Compartmental syndrome ➤ due to Muscle edema with neurovascular (NV) compression. ❖ Pathophysiology Sudden occlusion ➜ anoxia of tissue ➜ first *nerves affected* ➜ second *muscles affected* ➜ necrosis (within 6-8 hours) ➜ gangrene in 50% of cases. ❖ Prognosis Depends on: Collateral circulation Prognosis of acute on top of chronic is better than acute from the start, as there are collaterals in acute on top of chronic. Presence or absence of arterial pathology Proximity of occlusion more proximal occlusion has worse prognosis. Heart condition: better prognosis is good cardiac output. 3 ❖ C/P Personal history: ◆ Age (old): Atherosclerosis ‫أفكر في‬ ◆ Special habits: smoking. Complaint (6 P) 1. Pain The earliest and main presentation. Acute severe cramp-like or burning in characters. Start at the point of occlusion then shoots distally (in the most peripheral part of the limb). Not respond to analgesics Increased by movements, warmth or elevation. Rarely absent in some patients due to rapid onset of sensory loss. “Bad prognosis” 2. Pallor 3. Pulseless Absent pulsation distal to the site of occlusion (embolism). 4. Paresthesia The earliest manifestations of nerve ischemia. Start with loss of touch then progress to loss of deep sensation. 5. Paralysis Due to ischemia of distal muscles. Paralysis of intrinsic muscles occur first. 6. Poikilothermia (coldness) Progressive coldness of the limb as there is poor capillary refilling. ❖ Complications/fate Resolution if small emboli with efficient collaterals. Gangrene. Chronic ischemia. Volkmann’s ischemic contracture if affecting upper limb ➜ muscle contraction. 4 ❖ DD Causes of acute limb pain: Trauma Inflammation Vascular Neurological Fracture Rheumatoid arthritis DVT Peripheral neuropathy Low flow stasis (shock) Acute occlusion of popliteal or femoral aneurysm Phlegmasia cerula dolens Arterial spasm after trauma Acute Acute thrombosis on top embolism of atherosclerosis History Arrhythmia or Recent MI Intermittent claudication Source of emboli Usually present e.g. cardiac Absent Radial pulse Usually irregular as (AF) Usually regular Skin color white Dusky Severity More severe Less Manifestations Absent Present of chronic (no trophic changes) (trophic changes) ischemia Limb nutrition Normal Picture of chronic ischemia ▪ Sharp cut-off of the ▪ Tapering stenosis. Duplex & artery. ▪ Extensive collaterals arteriography and distal run-off. ▪ Minimal collaterals. ▪ Diffuse atherosclerosis. Medical thrombolysis, TTT Embolectomy, warfarin bypass. Acute Ischemia Chronic ischemia Age young Old Other manifestations of History Cardiac problems Atherosclerosis Source of emboli Present Absent Preceding claudication Absent Present Motor function Absent (no collaterals) present 5 ❖ Classifications class Prognosis Sensory Motor Arterial Venous loss deficit Doppler Doppler I Limb viable, None None audible audible not immediately threatened Limb marginally threatened, Minimal (toes), II a salvageable if promptly Or None Inaudible Audible treated. none Limb immediately threatened, More than toes, II b salvageable with immediate Rest pain Mild/moderate Inaudible Audible revascularization Limb irreversibly damaged, Major tissue loss Profound, Profound, Or Anesthetic Paralysis Inaudible inaudible III permanent nerve damage (rigor) inevitable ❖ Investigations leukocytosis & acidosis occur as ischemic Laboratory: nerve secretes these metabolites. CBC Acidosis with raised creatine phosphokinase (CPK) and WBCs indicate muscle necrosis. High hemoglobin, BUN and creatinine indicate intravascular hypovolemia. Due to fluid sequestration in the limb. K blood test. For the cause: ECG Abdominal U/S for Aortic aneurism. Echocardiogram (Echo) to detect source of emboli. X-RAY to detect fracture. For the site of occlusion: Arterial Duplex: “1st investigation” Localize and identify emboli or thrombosis. For injury of the artery or vein, A-V fistula, pseudoaneurysm. Show sharp cut-off. Doppler: Blood flow distal to site of occlusion is absent in embolus and present in thrombosis. N.B Arterial duplex is enough to diagnose acute ischemia. 6  CT angiography (CTA): “Gold standard” Done only before surgery. Detect: 1. Site of occlusion. 2. Proximal inflow. 3. Distal run-off. 4. Collaterals. MRA ❖ TTT Hospitalization Preoperative measures: Resuscitation & Bleeding control. Immediate IV Heparin to prevent propagation of thrombus. Analgesics e.g. Opiates/Opioids. Fogarty catheter IV fluid To Correct dehydration if present. Care of cardiac condition. Surgery: Embolism ➜ Urgent Embolectomy + fasciotomy Done early by Fogarty catheter. ➤ Technique: ▪ Exploration the artery (at the first absence of pulse) ▪ Close the arteriotomy: ✓ primary if transverse arteriotomy. ✓ with patch if longitudinal arteriotomy. to avoid stenosis Compartmental syndrome ➜ Fasciotomy.  to release the involved compartment. Acute thrombosis:  Thrombectomy By Fogarty catheter  Thrombolytic therapy In marginally threatened stage. By intra-arterial catheter, Inject (streptokinase - urokinase – TPA).  Revascularization procedure. By: 1. Bypass graft in cases of acute ischemia on top chronic. 2. Thromboendarterectomy if localized thrombus. 7  Trauma: i. Resuscitation ii. Exposure iii. Control according to pathological types: ▪ Partial tear: If < ½ circumference: ✓ Direct (Lateral) repair with proline suture for transverse tear. ✓ Repair using Venous patch for longitudinal tear. If > ½ circumference: ✓ Cut it and deal with it as complete tear. ▪ Complete tear: ✓ End to end anastomosis for near gap. ✓ Interposition graft for wide gap. ✓ Ligate if small artery. ▪ Puncture ➜ direct repair. ▪ Pseudoaneurysm ➜ excision with interposition graft. ▪ A-V fistula: ✓ Excision of tract between the artery & the vein. ✓ repair the artery and the vein. Acute Aortic dissection: ✓ EVAR (Endovascular aortic repair) by insertion of covered stent. Artery spasm ➜ muscle relaxant e.g. Papaverine. Postoperative: ‫ي‬ ‫ وبعد ين مشي علي‬follow up If thrombotic ➜ Anticoagulant “more related to vein” If trauma ➜ Antiplatelets “more related to artery” ------------------------------------------------------------------------------------------ N.B. To differentiate between acute ischemia from acute on top of chronic, we search for collaterals (if present, it is acute on top of chronic / if not, it is acute from the start). N.B. DVT never causes acute ischemia, but there is only one special type can cause acute arterial ischemia & this type is phlegmasia cerulea dolens (iliofemoral DVT) 8  Chronic limb ischemia ❖ Definition Gradual progressive decrease in limb perfusion causing a potential threat to limb viability. Early clinical evaluation is crucial to allow early interference & obtain best results. ❖ Epidemiology Prevalence of peripheral vascular disease in general population is 12-14%. ❖ Risk factors Major Minor 1. Obesity Non-modifiable Modifiable 2. Physical inactivity 1. HTN 1. ↑ Age 3. Stress 2. DM 2. Male > female 4. Alcohol ↑ risk of atherosclerosis 2-4 folds. 3. Black race 5. Estrogen deficiency 3. Smoking 4. Family history ↑ risk of atherosclerosis 10 folds. Most modifiable risk factors. 4. Hyperlipidemia ❖ Etiology Vaso-occlusive: Vasospastic: Atherosclerosis. Raynaud's disease: “Most common” Paroxysmal recurrent attacks of digital Buerger's disease. vasoconstriction. Vasculitis with stenosis. more in upper limbs of young females (18-30) Thrombosis ↑ with cold and stress. Consists of 3 phases of color changes: "‫ "بالترتيب‬Pallor, Cyanosis, Redness Acrocyanosis:  It’s a functional peripheral arterial disease, characterized by painless bluish discoloration of hands & feet.  Caused by spasm of the small blood vessels. Ergotism Livedo reticularis 9 ❖ C/P 70-80 % of affected individuals are Asymptomatic.  only a minority ever require revascularization or amputation. Symptoms: Intermittent claudication's: Crampy like pain affecting certain group of muscles according to level of obstruction. Level of obstruction Affected site Aorto-iliac Buttocks, Thigh, Calf CFA and SFA Calf, Foot Tibial Foot Initiated by walking for certain distance & Relieved by rest for few minutes.  Claudication distance: Mild claudication Moderate claudication Severe claudication >300 m 100-300 m 150 m II Moderate claudication II Moderate-Severe 2 b claudication 600 ml/min ‫ أكيد في‬MCQ ‫سؤال‬ 2. Vein diameter >6 mm Rule of 6 ‫االمتحان من‬ 3. Vein wall thickness >0.6 mm 4. Distance between vein and skin 6 cm 6. Duration after 6 weeks of creation 18 ❖ Complications Early (first 30 days of creation) Infection of the wound Thrombosis Fluid collection: hematoma, seroma Ischemic monomeric neuropathy “very rare”. Late (after 30 days of creation) Thrombosis True and false aneurysms (Pseudo-aneurysm) Bleeding (rupture) Steal phenomena occurs in A-V Fistula & means distal ischemic changes Hand edema from central stenosis ------------------------------------------------------------------------------------------------------------- Exam Question ‫ والمطلوب‬end stage renal disease ‫ المريض‬Case scenario ‫ ومكتوب في الـــ‬Arm ‫ صورة‬ ‫؟‬Shunt ‫تحديد نوع الـــ‬ ‫ ألنها الوحيدة اللي بتتعمل تحت‬Radio-cephalic female Female > Male Male = female -Commonly bilateral -Commonly unilateral -Usually unilateral Site -Involving whole limb -Below knee ◆ According to Findings in Development of Lymph Vessels: 1. Aplasia: No lymph vessels are demonstrated. 2. Hypoplasia: The number of lymph vessels is reduced in the affected limb & underdeveloped. e.g. In the thigh there one or two vessels instead of the usual five or more. 3. Varicose Lymphatics (Hyperplasia): The condition is often associated with incompetent valves. Lymph vessels are dilated and tortious. Secondary (Acquired) Common Inflammatory: a. Non-specific infection: Recurrent cellulitis ”Commonest cause of lymphedema in Egypt”. Recurrent non-specific Lymphangitis & Erysipelas. b. Specific infection: Filariasis “commonest cause of lymphedema worldwide” & TB. Traumatic: Surgical excision of LNs which drain the limb (e.g. after radical mastectomy). Irradiation ➜ fibrosis Neoplastic: Obstruction of lymphatic by malignant tumors: 1. 1ry as lymphoma. 2. 2ry as lymph nodes metastasis. 47 ❖ Incidence Female > male. Lower limb > Upper limb. Unilateral lower limb edema > Bilateral lower limb edema. ❖ Pathology Lymphatic obstruction ➜ retention of fluid rich in protein in the tissue space. The protein initiates foreign body reaction (as protein is irritant) ➜ fibrosis of S.C. tissue ➜ more obstruction. Recurrent attack of lymphangitis ➜ more lymphatic obstruction.  Pathological changes: Swelling: At first due to accumulation of fluids ➜ pitting edema. Later: swelling due to fibrous tissue replacing S.C. fat ➜ non-pitting edema. Skin changes: “More in 2ry causes” Thickened and hyperkeratosis, lymphatic vesicles may appear in the skin. In severe case skin develop huge bulges (elephantiasis). ❖ C/P History of 2ry causes Edema: Slowly progressive. ↑ by standing, ↓ by elevation then become refractory. N.B. In lymphedema, edema ↑ by standing & ↓ by limb elevation like venous system, but lymphedema differs from venous disorders that lymphedema become refractory. Spared ankle (ankle has no edema), with buffalo hump of foot. first is pitting then become non-pitting. Severe grade cause disability e.g. elephantiasis. Positive stemmer’s sign. Stemmer's Sign A thickened skin fold at the base of the second toe or second finger that is a diagnostic sign for lymphedema. ✓ negative result: if you can pinch and lift the fold of skin. ✓ positive result: if you are unable to pinch and lift the skin. Skin: Skin is thick with area of hyperkeratotic and lymphatic vesicles may appear. multiple ulcerations. Heavy limb, Deep flexion creases, Recurrent infections. 48 ❖ Clinical classifications (Burner) Grade Clinical features (Burner) latent Excess Interstitial fluid and histological abnormalities of lymphatics but no clinical lymphedema. I Edema pits on pressure and swelling disappears on elevation and bed rest. II Edema does not pit or reduce on elevation. III Edema is associated with irreversible skin changes, fibrosis, watery overgrowths and increased fat deposits (elephantiasis) ❖ Complications 1. Recurrent cellulitis & lymphangitis. 2. Lymphangiosarcoma. “Rare” 3. Elephantiasis Arm or leg becomes so hardened with thickened skin that you have difficulty to move it. 4. Lymphatic ulcer. 5. Lymphatic fistula. 6. Chyluria. ❖ Investigations Laboratory: Night blood film: may show microfilaria Analysis of protein content of edema: show high protein content (>1.5 gm %) CBC, CRP, Serum albumin, Renal function test (RFT) Radiological: Lymphoscintigraphy “Gold standard” Using Tc99 with antimony sulfide are injected in lymphatic vessels Rate of disappearance of radioactivity is estimated (normally 40% disappear after 90 minutes). Lymphangiography “Not done now” Injection of dye in lymphatic vessels Then taken serial X-ray to visualize the level of lymphatic obstruction. LN biopsy to exclude neoplastic cause 49 ❖ TTT Conservative “in early stage” Leg elevation, Elastic stocking & Leg care. Drugs: diuretics & long-acting penicillin. Prophylactic antibiotics to prevent cellulitis. Diethyl carbamazine for active filarial infection. Surgical: Physiological operations: “to enhancement of lymph drainage” a. Enteromesentric bridge operation. b. Free omental flap. c. Lymphatico–Venous Anastomosis (LVA). d. Lympho–Venous Anastomosis. Excisional operations: “reduce the bulk” a. Charles: excision of skin and S.C. tissue then covering the limb by skin graft. b. Sistrunk: excision of ellipse of skin and S.C. tissue then direct closure of defect. Physiological and excisional: a. Thompson (Swiss roll): excision of S.C. tissue then implantation of skin flap between muscles. 50 DIFFERENTIAL DIAGNOSIS  Chronic leg ulcers ◆ Definition of ulcer Loss in the continuity of the covering epithelium (skin or mucus membrane). ◆ Leg ulcers Vascular ulcers: Incidence of leg ulcers 1. Venous ulcer (varicose ulcer). 2. Arterial ulcer (ischemic ulcer). 1. Venous ulcer. “commonest” 3. Lymphatic ulcer. 2. Ischemic ulcer. Non-Vascular ulcers: 3. Neuropathic ulcer. 1. Diabetic ulcer. " ‫"بالترتيب‬ 2. Traumatic ulcer. 3. Inflammatory ulcer. 4. Malignant ulcer. ----------------------------------------------------------------------- ❖ Vascular ulcers Ischemic ulcer Venous ulcer Etiology Ischemic disease CVI Pain More pain, relieved by foot Less pain, relieved by foot elevation dependency Swelling No leg swelling Marked leg swelling Between the toes, in the -In the ulcer bearing area (Gaiter area) Site dorsum of the foot or around the malleoli -just above the medial malleolus At first irregular, sloping & serrated Edge Punched out then punched out Margin Hyperemic Skin around the ulcer is pigmented Infected ulcer ➜ dirty granulation tissue (pus). floor Non infected ulcer ➜ healthy granulation tissue. Base Difficult to be palpated Indurated (hard) Depth Deep Superficial Healing Difficult Rapid (by conservative treatment) Associations Ischemic manifestations VV manifestations Lymphedema ulcer: Cause: rupture of an infected bulla. 51 ❖ Neuropathic (Trophic) ulcers Cause: Skin anesthesia in some neurological diseases e.g. peripheral neuritis, nerve injuries or DM. Pathology: Skin anesthesia ➜ trauma not felt by the patient ➜ callosity and adventitious bursae ➜ infection of bursae ➜ separation ➜ deep penetrating ulcer to bone and joints. Characters: It’s painless Patient is Unaware. Site: usually over bony prominence (over pressure points) e.g. over heal, head of 1st metatarsal and base of 5th metatarsal. Size: variable Margin: callosity of skin. Edges: sloping. Center: deeply penetrating or even penetrates the foot to change into perforating ulcer. TTT: Conservative treatment: rest, elevation & dressing. Amputation if destroyed bone or joints. ❖ Traumatic ulcer Cause: Direct destruction of epithelium by trauma with 2ry infection. Characters: Site: commonest over tibia “most liable to trauma”. Number: single. Shape: variable. Floor: granulation tissue “healthy if healed & unhealthy if recent”. Edge: punched out, but if healthy ➜ slopping. Discharge: serous or sero-purulent. Base: indurated. Inguinal lymph nodes: firm & tender. Treatment: Rest, elevation, dressings and antibiotics. Grafting may be needed. 52 ❖ Inflammatory ulcers 1. Syphilitic Ulcer Rare nowadays. Characters: Site: upper part of leg. Number: solitary or multiple. Edge: punched out. Floor: covered with yellowish (wet wash leather) slough. Base: fixed to bone, indurated, painless. 2. TB Ulcer Cause: Usually secondary to tuberculous arthritis or osteitis. Characters: Edge: undermined. Margin: thin cyanotic. Floor: covered with pale granulation tissue. Base: slight induration. ❖ Neoplastic ulcers 1. 1ry skin tumors: SCC, BCC, Ulcerating melanoma. 2. Marjolin’s ulcer Definition: SCC on top of chronic ulcer or scar (e.g. venous ulcer or burn) Characters: It has raised everted edge & hard fixed base. It grows slowly as scar is avascular. Painless as scar tissue contain no nerves. Late L.Ns metastasis as fibrosis affect lymphatic vessels. -----------------------------------------------------------------------  Most common type of leg ulcers is venous ulcer.  Most common type of diabetic ulcers is trophic ulcer.  Site of venous ulcer is gaiter area (the same area of medial kockett’s perforators).  Ischemic & venous ulcer are painful.  Shape of venous ulcer is oval & rounded. 53  DD of pulsating swelling 1. Aneurysm Gives expansile pulsation and systolic bruit. 2. A-V fistula Gives Machinery murmur (systolic & diastolic murmur). 3. Swelling over an artery Gives transmitted pulsation. Pressure on proximal artery doesn’t affect the size of swelling. 4. pulsating tumors (e.g. osteosarcoma) Irregular in shape & consistency, not compressible, ill-defined & not overlie the line of main artery. 5. Abscess If aneurysm becomes clotted infected may misdiagnosed. 6. Serpentine arteries especially in common carotid artery. DD of unilateral LL edema 1. Cellulitis “most common” 2. DVT. 3. Ruptured baker cyst. 4 ‫األهم بالرتتيب أول‬ 4. Lymphedema. 5. VV. 6. Calf Hematoma. 7. Rupture of gastrocnemius. DD of bilateral LL edema 1. Bilateral DVT 2. Heart failure 3. Renal disease 4. Liver disease 5. Angioneurotic 54