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Surgery > Vascular Surgery > Flashcards

Vascular Surgery Flashcards

1
Q

Definition of AAA

A

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

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2
Q

Name the branches of the descending abdominal aorta?

A

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
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3
Q

Aetiology of AAA

A
  • atherosclerotic -95%
  • inflammatory - 5%
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4
Q

Prevalence

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

Common site

A
  • 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
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6
Q

Symptoms of AAA

A

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
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7
Q

Signs of AAA

A
  • hypotension
  • palpable mass felt at/above umbillicus
  • bounding femoral pulses
  • distal pulses inact
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8
Q

Investigations of AAA

A
  • Physical exam
  • ultrasound (confirm AAA with initially)
  • CT scan (accurate visualisation, size, positioning, and involvement of surrounding structures )
  • Angiography
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9
Q

Complications of AAA

A
  • 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
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10
Q

Screening of AAA

A
  • All men > 65 years are invited to attend screening
  • screen using ultrasound scan
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11
Q

Treatment of AAA

A
  • 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
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12
Q

Two types of AAA surgical repair

A
  • Open repair
  • Endovascular aneuryms repair (EVAR)
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13
Q

Open repair process, adv and disadvantages

A
  • 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

Advantages

  • increased durability and long term mortality

Disadvantages

  • Recovery period is 7-10 days
  • return to preoperative functional status is 4-6 months
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14
Q

EVAR process, advantages and disadvantages

A

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

Advantages

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

Disadvantges

  • 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
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15
Q

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

A

Myocardial infarction (MI)

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16
Q

Normal abdominal aortic diameter

A

2cm

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17
Q

Possible operative complications

A
  • MI
  • atheroembolism
  • declamping hypotension
  • acute renal failure (especially if the anerysm involves the renal arteries)
  • uretar injury
  • haemorrhage
  • colonic ischaemia
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18
Q

Emergency management of rutured AAA

A

resuscitation

  • 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
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19
Q

Prognosis of ruputerd AAA

A
  • 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%
20
Q

Label the arteries of the leg

A
  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

LAMP

  • lateral anterior tibial
  • Medial posterior tibial
21
Q

Acute limb ischaemia features

A

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.

22
Q

Management of acute ischaemia

A
  • Anticoagulation – IV heparin
  • Urgent embolectomy/thrombectomy/bypass
  • Thrombolysis
  • If above fails or delay in diagnosis leading to dead tissue amputation may be required
23
Q

Causes/ risk factors of PVD

A
  • smoking
  • diabetes
  • hypertension
  • hyperlipidaemia
  • Old age
24
Q

Stages of chronic limb ischaemia

A
  • 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
25
Q

Claudication + impotence implies

A

Leriches syndrome

26
Q

Fontaine classification for peripheral arterial disease

A
  1. asymptomatic
  2. intermittent claudication
  3. ischaemic rest pain
  4. ulceration/gangrene (critical ischaemia)
27
Q

Signs of PVD

A
  • 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
28
Q

Investigations of PVD

A
  • 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
29
Q

Treatment of PVD

A
  • 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
30
Q

What is ABPI

A

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)

31
Q

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

A
  • Normal =>1,0
  • claudicator ABI <0.6
  • rest pain ABI <0.4
32
Q

Who gets false ABI readings

A

patients with calcified arteries, especially those with diabetes

33
Q

varicose veins definition

A

Long, tortous, dilated veins of the superficial venous system

34
Q

Pathology of varicose veins

A
  • 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
35
Q

Aetiology of varicose veins

A

Primary causes

  • uknown
  • congential valve absence

Secondary causes

  • obstruction: DVT, fetus, ovarian tumour
  • valve destruction: DVT
  • ateriovenous malformation (Increase pressure)
  • constipation
  • overactive muscle pumps
36
Q

Symptoms of varicose veins

A
  • my legs are ugly
  • pain
  • cramps
  • tingling
  • heaviness
  • restless legs
37
Q

Signs of VV

A
  • 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
38
Q

Treatment of vv

A

criteria for specialist referrral of patents with vvs should be:

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

treatment

  • 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
39
Q

Radiofreuqncy ablation

A

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

40
Q

endovenous laser ablation

A

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

41
Q

Injection sclerotherapy

A
  • 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
42
Q

Causes of venous ulceration

A

prolonged venous hypertension

43
Q

History of venous ulceration

A
  • 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
44
Q

examination of venous ulceration

A
  • Age
  • pain
  • site
  • lesion characteristics
    • edge
    • base
    • surrounding skin
  • veins
  • swelling
45
Q

Investigations of venous ulceration

A
  • 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
46
Q

Management of venous ulcers

A

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

Medical

  • 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

Surgery (24 decks)

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