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Definition of AAA 

Abnormal dilaiton of abdominal aortia (1.5>2 x normal) forming a true aneurysm 


Name the branches of the descending abdominal aorta? 

Prostitutes Cause SaggingSwollen Red Testicles [in men] Living In Sin":

  • Phrenic [inferior]
  • Celiac
  • Superior mesenteric
  • Suprarenal [middle]
  • Renal
  • Testicular ["in men" only]
  • Lumbars
  • Inferior mesenteric
  • Sacral 


Aetiology of AAA 

  • atherosclerotic -95% 
  • inflammatory - 5% 



  • older males, positive family history, hypertension, tobacco smoking 
  • 5% of all adults >65 
  • Male to female ratio is 6:1 


Common site 

  • 85% - Infra-renal artery (below levels of the renal arterys 
  • 15%- Extends down to involve the origins of the common iliac arterys 
  • associated with other operipheral aneurysm  


Symptoms of AAA

May be 

  • Asymptomatic (60%) - detected on routine physical examination, plain x-ray or most commonly, abdominal ultrasound scan conducted for another reason 
  • Symptomatic (10%) 
    • pain in the central abdomen, back, loin, illiac fossa 
    • becomes inflamed and compresses surrounding structures (ureter, inferior vena cava) 
    • distal embolisation 
  • Rupture (30%) 
    • ​AAA may rupture in to the retroperitoneum


Signs of AAA

  • hypotension 
  • palpable mass felt at/above umbillicus 
  • bounding femoral pulses 
  • distal pulses inact 


Investigations  of AAA

  • Physical exam 
  • ultrasound (confirm AAA with initially)
  • CT scan (accurate visualisation, size, positioning, and involvement of surrounding structures ) 
  • Angiography 


Complications of AAA

  • free rupture
    • collpase 
    • hypotension 
    • tachycardia 
  • retroperitoneal rupture - abck pain, nausea, vomitting, hypotension 
  • distal embolisation - thrombus from the sac may disperse distally and block the small vessels in the foot and lower leg causing acute ischaemia 
  • aorto-caval fistula - plethora
  • aorto-duodenal fistula - haematemsis, melaena 
  • aortic occlusion 


Screening of AAA

  • All men > 65 years are invited to attend screening
  • screen using ultrasound scan 


Treatment of AAA 

  • Blood pressure control and stop smoking 
  • incidental asymptomatic small AAA
    • repair is deferred until the theortical risk of rupture exceeds the estimated risk of operative mortality - until AAA reaches 5.5cm 
    • ultrasound is only accurate to 0.5cm and will therfore underestimate AA. 
    • Perform CT once 5.0cm is reached 
  • Symptomatic 
    • if the patient is having pain concurrent with their abdominal aortic aneurysms they should always be considered for surgery as pain often preceds rupture 
  • surgical repair - synthetic graft 
  • endovascular graft 


Two types of AAA surgical repair 

  • Open repair 
  • Endovascular aneuryms repair (EVAR) 


Open repair process, adv and disadvantages 

  • involves replacing the anuerysmal segment with a prosthetic graft
  • the graft is straight forward if the aneuryms is confined to the aorta or bifurcated 
  • If there are common iliac anuerysms as well the aorta must be clamped off during surgery


  • increased durability and long term mortality


  • Recovery period is 7-10 days 
  • return to preoperative functional status is 4-6 months 


EVAR process, advantages and disadvantages 

A guidewire is passed through the right common femoral artery. A catheter containing the main body of the stent graft is passed over the guidance wire and placed in position inside the aneurysms. Deployment of main body and right limb of stent graft. Deployment of short leg or stent fraft over second wire guide. Requires two incisions 


  • performed under regional or local anaesthesia 
  • patient is fit to go home with 48 hours 
  • rapid return to preoperative functional status 
  • decreased immediate mortality 


  • decreased durability 
  • expensive 
  • large amount of AAA not suitable 
  • life-long surveillance 
  • no long term survival rates beneft over open repair
  • high re-intervention rate 


Leading cause of postoperative death in a patient undergoing elective AAA treatment> 

Myocardial infarction (MI) 


Normal abdominal aortic diameter 



Possible operative complications 

  • MI 
  • atheroembolism 
  • declamping hypotension 
  • acute renal failure (especially if the anerysm involves the renal arteries) 
  • uretar injury 
  • haemorrhage 
  • colonic ischaemia 


Emergency management of rutured AAA


  • call for senior surgical assistance 
  • transfer to theatre 
  • permissive hypotension- dont worry if not normal BP after fluids as may worsen the rupture 
  • If patient is critically hypotensive, consider calling a peri-arrest cardiac emergency 
  • IV access via two large bore cannulae, catheterize, cross match blood, order FFP and plateles 
  • high flow O2 via a non-rebreather mask 
  • give modest doses of analgesia 
  • alert anaesthesit, theatres, ITU 
  • Witnesses verbal consent for surgery may be the only practical way and is accectable here 


Prognosis of ruputerd AAA

  • risk of rupture relates to maximum AP diameters 
    • <0.5cm per year, <4.0cm 
    • once percent per year-->4-4.5cm
    • over 3% --> >5.5cm 
  • less than 50% of patient with a ruptured AAA may reach hospital alive and the overall mortality of the condition may be as high as 75-95% 


Label the arteries of the leg

  1. abdominal aortia 
  2. ilternal iliac (hypogastric) 
  3. external iliac artery 
  4. common femoral artery 
  5. Deep femoral artery 
  6. Superficial femoral artery 
  7. popliteal artery 
  8. Trifercation 
  9. anterior tibial artery 
  10. peroneal artery 
  11. posterior tibial 
  12. dorsalis pedis artery 


lateral anterior tibial 

Medial posterior tibial 


Acute limb ischaemia features 

6 P's 

  • Pain 
  • parasethesia 
  • pulseless
  • pallor 
  • perishingly cold 
  • paralysis 

Sudden onset of a painful cold lum. Parasthesia indicates severe ischaemia. There is no history or signs of previous vascular insuffiency then an embolus is suspected. 


Management of acute ischaemia 

  • Anticoagulation – IV heparin
  • Urgent embolectomy/thrombectomy/bypass
  • Thrombolysis
  • If above fails or delay in diagnosis leading to dead tissue amputation may be required


Causes/ risk factors of PVD 

  • smoking 
  • diabetes 
  • hypertension 
  • hyperlipidaemia 
  • Old age 


Stages of chronic limb ischaemia 

  • Intermittent claudication:
    • Cramp like pain in the legs, thigh or buttock relived by rest after walking for a given distance 
    • relieved by rest .
    • Pain develops distal to the obstruction. 
    • femoral disease causes calf pain, but blockage of the iliacs causes buttock pain 
  • Critical ischaemia 
    • Rest pain -
    • Implies that the ischaemia is critical and the viability of the leg is threatened. The pain is severe and requires opioid analgesia.
    • Gangrene and ulceration –  in dry gangrene, ischaemia results in death of tissue 
    • foot pain at rest- eg burning pain at night relieved by hanging legs over side of bed 


Claudication + impotence implies 

Leriches syndrome 


Fontaine classification for peripheral arterial disease 

  1. asymptomatic 
  2. intermittent claudication 
  3. ischaemic rest pain 
  4. ulceration/gangrene (critical ischaemia) 


Signs of PVD 

  • absent femoral, popliteal or foot pulses 
  • cold, white leg 
  • atrophic skin 
  • punched out ulcers (often painfu) 
  • postural/dependent colour change 
  • vascular (buergers) angle <20o 
  • capillary filling time >15s are found in severe ischaemia 


Investigations of PVD

  • exclude DM, Arterities (ESR/C RP), FBC (anaemia, polycythaemia), U7E (renal disease); Lipids (dyslipidaemia) 
  • ECG (cardiac ischaemia) 
  • Thombophillia screen and homocysteniine if <50 years 
  • ABPI - 
    • normal 1-1.2,
    • peripheral arterial disease = 0.5-0.9
    • critical limb ischaemia <0.5 
  • imaging 
    • 1st line - doppler duplex USS is 1st line (non invasive and readily available) 
    • 2nd - if considereing intervention MR/CT angiography - extent and location os stenoses and quality of dital vessels 


Treatment of PVD 

  • risk factor modification - quit smoking, treat hypertension and high cholesterol, antiplateles to prevent progression and to reduce CV risk (clopidogrel) 
  • management of claudicaiton - 
    • supervised exercise programmes - reduce symptoms by improving collateral blood flow (2h per week for 3 months ) 
    • vasoactive drugs- nafitifrofuryl oxalate - offer modest beenfit and are recommened only in those who do not wish to undergo revascularsation and if exercise fails to improve symptoms 
  • if conservative management has failed interention required 
    • PTA - percutaenous transluminal angioplasty (disease located to single arterial segment) 
    • surgical reconstruction - atheromatous disease extensive but distal run off is good consider arterial reconstruction with a bypass graft 
      • femoral popliteal 
      • femoral-femoral cross over 
      • aorto-bifemoral bypass grafts 


What is ABPI 

Ankle to brachial index: simply, the ratio of the systolic blood pressure at the ankle to the systolic blood pressure at the arm (brachial artery) 



What ABIs are assocated with normals, claudicators, and rest pain?

  • Normal =>1,0
  • claudicator ABI <0.6
  • rest pain ABI <0.4


Who gets false ABI readings 

patients with calcified arteries, especially those with diabetes 


varicose veins definition 

Long, tortous, dilated veins of the superficial venous system 


Pathology of varicose veins 

  • blood from superficial veins of the leg passes into deep veins via perforator veins and at the sapheno-femoral and sapheno-popliteal junctions 
  • valves prevent blood from passing from deep to superficial veins 
  • if they become incompetent there is venous hypertension and dilation of the superficial veins occus 


Aetiology of varicose veins 

Primary causes 

  • uknown 
  • congential valve absence 

Secondary causes 

  • obstruction: DVT, fetus, ovarian tumour 
  • valve destruction: DVT 
  • ateriovenous malformation (Increase pressure) 
  • constipation 
  • overactive muscle pumps 


Symptoms of varicose veins 

  • my legs are ugly 
  • pain
  • cramps
  • tingling 
  • heaviness
  • restless legs 



Signs of VV

  • oedema - leaking of interstitial fluid. press finger behind medial mallelous release after 10 seconds. Pitting oedema is present if pitting remains 
  • Venous eczema: erythematus scaling skin. Causes crusting and blistering 
  • ulcers - gaiter area is the most common location for venous ulceration. More likely on the medial side, wheras arterial ulcers more common over pressure areas 
  • lipodermatosclerosis - skin hardens from subcutaenous fibrosis cased by chronic inflammation and fat necrosis 
  • inverted champagne bottle- when both lipodermatosclerosis and oedma are present 
  • haemosiderosis - brown skin pigmentation caused by deposits of haemosiderin 
  • atrophie blanche: patches of smooth white skin caused by scar tissue from previous, healed ulcer 


Treatment of vv

criteria for specialist referrral of patents with vvs should be: 

  • bleeding 
  • pain
  • ulceration 
  • superficial thromphlebitis 
  • severe impact of quality of life 


  • treat underlying cause 
  • education:
    • avoid prolonged standing
    • elevate legs whenever pssible 
    • support stockings 
    • lose weight 
    • regular walks  (calf muscle aids venous return) 
  • endovascular treatment 
    • radiofrequency ablation 
    • injection sclerotherapy 
  • surgery- high saphenous ligation 
    • stripping of above knee long saphenous vein 
    • avulsion of veins 
    • ligation of perforator from deep veins 


Radiofreuqncy ablation 

catheter is inserted into the vein and heated to 120o destroying the endotherlium and closing the vein. results are as good as conventional surgery at 3 months 


endovenous laser ablation 

is similar to laser. Outcomes are similar to surgical repair after 2 years 


Injection sclerotherapy 

  • liquid or foam can be used
  • liquid - below the knee, at multple sites and the vein compressed for a few weeks to avoid thrombosis 
  • foam - injected under US at a single site and spreads rapidly throught the veins, damaging the endothelium


Causes of venous ulceration 

prolonged venous hypertension 


History  of venous ulceration

  • present and previous episodes of ulceration 
  • previous thrombotic episodes 
  • revious venous and non-venous surgery to the leg, pelvis and abdomen 
  • diabetes 
  • autoimmune disease 
  • locomotor problems 
  • current mediactions and allergies 



examination of venous ulceration 

  • Age
  • pain 
  • site 
  • lesion characteristics 
    • edge 
    • base 
    • surrounding skin 
  • veins
  • swelling 


Investigations of venous ulceration 

  • dupplex ultrasoud - nature and dsitrubution of superficial and deep venous disease 
  • in patients with absent pulses and/or low ABPO ultrasound can be vaulable 
  • FBC, Biochem, TFTS, blood glucose, lipid profile 
  • bioposies of malignant tissue 


Management of venous ulcers 

all patients with a break in the skin below the knee that has not healed properly within two weeks should be referred to a vascualr surgeon 


  • treat co-morbidities 
  • ulcers colonised with bacteria not infected therefore abx contraindicated 

Dressings - keep clean, change regularly, good hygiene, non adherant 

Compression therapy- with bandaging, compression stockings prescribed for life 

surgical and endovenous therapy