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Clinical Surgery > Vascular Surgery > Flashcards

Vascular Surgery Flashcards

1
Q

Definition/Epidemiology/Pathophysiology of an Abdominal Aortic Aneurysm (AAA)?

A
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2
Q

Presentation of Abdominal Aortic Aneurisms?

A

~ 75% of aortic aneurysms are asymptomatic and are discovered incidentally either as a pulsatile abdominal mass on physical examination or on abdominal imaging done for another reason.

A small proportion will present with symptoms related to pressure on adjacent structures:

  • Back/flank pain
  • Ureteric compression
  • Caval compression (tachycardia, diaphoresis, nausea, vomiting, pallor, weakness, lightheadedness, and dizziness)

Most of the clinical symptoms due to aortic aneurysm are related to aneurysm rupture or embolism of mural thrombus

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3
Q

Risk Factors for Abdominal Aortic Aneurisms?

A
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4
Q

Complications of AAA?

A
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5
Q

Investigations for AAA?

A
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6
Q

Surveillance of Asymptomatic AAA?

A
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7
Q

Types of Operation and Indications for AAA Repair?

A

Open Surgical Repair (OSR) or Endovascular Aneurysm Repair (EVAR)

  • Elective: when the aneurysm size is exceeding the 5.5 cm threshold or when the rate of growth is >1cm per year
  • Emergency: Rupture/Symptomatic
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8
Q

Method/Complications of OSR of AAA?

A

Open Surgical Repair (OSR) is done through midline incision (laparotomy) with mortality around 5%. The aneurysm is replaced with a synthetic graft

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9
Q

Method/Complications of EVAR of AAA?

A

In Endovascular Aneurysm Repair (EVAR) a stent graft is delivered through groin incisions to exclude the aneurysm. Done using radiation and nephrotoxic contrast is used. No Aortic clamping is needed, less early postoperative mortality than OSR, but higher re-intervention rate due to endoleak which requires lifelong surveillance with US or CTA

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10
Q

What is the principle of Permissive Hypotension

A

Following aortic rupture, systolic BP is kept between 70-80 mmHg to maintain vital organs perfusion.

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11
Q

Stroke vs. TIA?

A
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12
Q

~ 80% of strokes are _______ and 20% ______

~ 80% of ischaemic strokes affect the _____________. The main cause of which is _____________________.

A

~ 80% of strokes are ischaemic and 20% hemorrhagic (intracerebral/subarachnoid)

~ 80% of ischaemic strokes affect the carotid territory the main cause of which is thromboembolism of the internal carotid artery (ICA)

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13
Q

Risk Factors for Stroke?

A
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14
Q

Clinical Presentation of a Stroke?

A

80% of strokes are ischaemic of which 80% are in the carotid territory.

Carotid territory classical symptoms:

  • Hemimotor/hemisensory signs
  • Monocular visual loss (Amaurosis Fugax: sudden, short-term, painless loss of vision in one eye)
  • Higher cortical dysfunction (dysphasia, visuospatial neglect etc.)

General:

  • Facial drooping
  • Arm weakness
  • Speech difficulties
  • Time to call emergency services.
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15
Q

Investigations for Stroke?

A
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16
Q

Medical Treatment of Asymptomatic Stroke

A

Asprin

clopidogrel

Statins

Smoking Cessation

Control of BP/Diabetes

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17
Q

Surgical/Endovascular Treatment of Stroke

  • Complications?
  • Contraindications?
A
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18
Q

What is Acute Lower Limb Ischemia?

A

Sudden decrease in limb perfusion that threatens limb viability

Acute lower limb ischaemia is associated with high risk of limb loss, up to 30-50% at 30 days.

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19
Q

Causes of Acute Lower Limb Ischemis

A
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20
Q

Clinical Features of Acute Lower Limb Ischemia?

A

6 P’S

  • Pain
  • Pallor
  • Pulselessness
  • Perishing Cold
  • Paresthsia
  • Paralysis
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21
Q

Classification of Acute Lower Limb Ischemia?

A

Rutherford’s CLassification

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22
Q

Initial Management of Acute Lower Limb Ischemia?

A
  • If there is clear evidence of acute ischemia on history and exam, do not delay definitive treatment and give IV heparin 5000 units bolus
  • Give O2
  • IV access and fluids if dehydrated
  • Bloods – FBC, U&E, coagulation profile, troponin, glucose, group & save
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23
Q

Management Options for Category III Lower Limb Iscehmia?

A

III Irreversible Leg Ischemia

Resuscitate and stabilize before considering amputation

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24
Q

Management Options for Category IIb Lower Limb Ischemia?

A

IIb Immediately Threatened

Start initial management with urgent Computed Tomography Angiography (CTA) followed by urgent revascularization with surgery (thromboembolectomy +/- bypass surgery)

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25
Q

Management Options for Category I/IIa Lower Limb Ischemia?

A

Category IIa (threatened) and Category I (viable) limb

Revascularization options include endovascular catheter-directed thrombolysis in addition to open surgical thromboembolectomy and bypass.

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26
Q

Complications of Reperfusion and their treatments

A

Mostly occur after delayed revascularization

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27
Q

Causes of Peripheral Arterial Disease

A

Atherosclerosis (Primary Cause)

Popliteal Artery Entrapment

Fibromuscular Dysplasia

Vasculitides (Buerger’s Disease, Takayasu Arteritis)

28
Q

Symptoms of Peripheral Arterial Disease

A
29
Q

Classical Triad of Aortoiliac occlusion?

A
30
Q

Risk Factors for Peripheral Arterial Disease

A
31
Q

Classification of Peripheral Arterial Disease

A
32
Q

Differential Diagnoses to Consider Apart from Intermittent Claudication

A
  • Spinal stenosis
  • Osteoarthritis
  • Symptomatic Baker’s Cyst
  • Nerve root entrapment (e.g. Sciatica)
33
Q

Examination/Investigations of Peripheral Arterial Disease

A

Examination

  • Inspection: trophic changes and scars of previous surgery
  • Palpation: of all pulses and capillary refill time
  • Buerger’s test and sign

Investigations

  • Ankle-Brachial Pressure Index (ABPI): ratio of peak systolic doppler ankle pressure to arm pressure
  • Duplex ultrasound
  • CT Angiogram/ MR Angiogram
  • DIgital Subtraction Angiogram (DSA)
34
Q

Medical/Surgical Intervention for Peripheral Arterial Disease

A
35
Q

Causes of Ulcers?

A
36
Q

Arterial Ulcer

  • Pulses
  • Skin Perfusion
  • ABPI
  • Ulcer Location
  • Ulcer Margin
  • Depth
  • Size
  • Base
  • Exudate
  • Skin
  • Edema
  • Pain
A
  • Pulses: Absent
  • Skin Perfusion: Cool, Prolonged Cap. Refill
  • ABPI: Reduced
  • Ulcer Location: Pressure/Friction Areas (heel/toes)
  • Ulcer Margin: ‘Punched out’ well defined
  • Depth: Deep
  • Size: Small
  • Base: Black Necrotic Tissue (dry/wet)
  • Exudate: Minimal
  • Skin: Pale, Thin, Hairless, Friable
  • Edema: Minimal
  • Pain: Ischemic Rest Pain
37
Q

Neuropathic Ulcer

  • Pulses
  • Skin Perfusion
  • ABPI
  • Ulcer Location
  • Ulcer Margin
  • Depth
  • Size
  • Base
  • Exudate
  • Skin
  • Edema
  • Pain
A
  • Pulses: Present
  • Skin Perfusion: Normal/Warm
  • ABPI: Normal
  • Ulcer Location: Pressure Areas
  • Ulcer Margin: ‘Punched out’ well defined
  • Depth: Deep
  • Size: Small
  • Base: Clean, Granulating Pink Wound
  • Exudate: Minimal
  • Skin: Healthy
  • Edema: Minimal
  • Pain: Insensate
38
Q

Venous Ulcer

  • Pulses
  • Skin Perfusion
  • ABPI
  • Ulcer Location
  • Ulcer Margin
  • Depth
  • Size
  • Base
  • Exudate
  • Skin
  • Edema
  • Pain
A
  • Pulses: Present
  • Skin Perfusion: Normal/Warm
  • ABPI: Normal
  • Ulcer Location: Medial Malleolus
  • Ulcer Margin: Irregular ‘sloped’
  • Depth: Superficial
  • Size: Large
  • Base: Yellow/Wet
  • Exudate: Large
  • Skin: Signs of Venous Hypertension (vericocities, Hemosiderin deposits)
  • Edema: Severe
  • Pain: Painful
39
Q

Arterial Ulcers

  • Pathophysiology
  • Causes
  • Investigations
  • Management
A

Pathophysiology: Poor arterial supply resulting in tissue hypoxia. Decreased perfusion also leaves these prone to infection with poor healing ability.

Causes:

  • PVD
  • Diabetes Mellitus (Micro/Macrovascular occlusion)
  • Arterial Trauma
  • Arterial Embolism
  • Vasculitis

Investigations:

  • Wound swab
  • ABPI
  • Arterial Duplex
  • +/- CT/MR angiogram

Management: Correction of poor tissue perfusion as per chronic PVD in patients with critical limb ischemia

40
Q

Neuropathic Ulcers

  • Pathophysiology
  • Causes
  • Investigations
  • Management
A

Pathophysiology: Limb prone to injury without detection given reduced sensation. There may be associated chronic joint destruction and malformation (Charcot’s joint’)

Causes:

  • Diabetes
  • Ischemic neuropathy
  • Alcoholic Neuropathy
  • Vit B12 Defficiency
  • Medications

Investigations:

  • Wound swab
  • +/-Nerve conduction studies for initial diagnosis
  • +/-ABPI if pulses are not palpable

Management:

  • Relieve pressure areas
  • Treat infection
  • Generally irreversible
  • Good diabetic control
41
Q

Venous Ulcers

  • Pathophysiology
  • Causes
  • Investigations
  • Management
A

Pathophysiology: Chronic venous hypertension leads to tissue oedema with venous congestion. The skin is vulnerable to minor trauma or spontaneous breakdown with poor healing ability.

Causes:

  • Venous Hypertension
  • Varicose Veins
  • DVT
  • Congenital absence of deep veins (Klippel- Trenaunay syndrome)

Investigations:

  • Wound swab
  • Venous Duplex
  • +/-ABPI

Management:

  • Compression bandage
  • Leg elevation
  • Class II stocking when healed
  • +/-Skin graft
  • Treat infection
  • VV surgery if possible once ulcer healed to reduce recurrence rate
42
Q

Pathophysiology of Diabetic Foot

A
43
Q

Risk Factors for Diabetic Foot

A
44
Q

Clinical Features/Investigations of Diabetic Foot

A
45
Q

Management of Diabetic Foot

A

Best done at specialty clinic

Regularly inspect feet/Nail Care

Apriately fitting footwear

If INfected Ulcer:

  • Broad Spectrum Antibiotics
  • Debridement of dead tissue
  • Amputation of non-viable digits
  • XRAY/MRI to rule out osteomyelitis
46
Q

Pathophysiology of Charcot’s Foot?

A
  • Neuropathic arthropathy – loss of protective joint and sensory reflexes allows minor trauma and chronic pressure maldistribution to go undetected.
  • Joints (ankle and foot- metatarsal-phalangeal) become painlessly destroyed resulting in deformity, osteoarthropathy and new bone formation
  • Motor neuropathy – muscle wasting and loss of arch architecture, in-drawing of toes (‘hammer’ or ‘claw’ toes)
  • Autonomic neuropathy – shunting of blood away from skin. Feet are dry and prone to callus formation over pressure areas.
47
Q

Clinical Features of Charcot Foot?

A

Clincal Features

  • Sensory neuropathy – pin-prick & light touch, loss of temperature sensation, loss of proprioception and vibration sense
  • Grossly deformed, swollen ankle joint
  • Fallen arches ‘flat foot’
  • +/- ulceration
  • Acute - warm, red, swollen, painful (can be confused with cellulitis)
48
Q

Definition of varicose veins?

A

Subcutaneous superficial veins that are tortuous and dilated measuring >3mm when examined in the standing position. They are the result of underlying venous incompetence.

Venous incompetence: dysfunctional venous emptying, leading to venous hypertension, most commonly associated with underlying valvular failure

49
Q

Epidemiology of Vericose Veins

A
50
Q

Risk Factors for vericose veins

A
51
Q

Pathophysiology and Common Location of Vericose Veins

A

Pathophysiology: Functioning deep and superficial veins permit outflow of blood from the lower limb. In normal anatomy this anti-gravitational effect occurs using a system of one-way valves, which prevent reflux of blood and the muscle pump (muscular contraction which propagates venous blood towards the heart). Chronic failure of these systems results in an increased peripheral vessel hydrostatic pressure => increases permeability of peripheral venules => extravasation and chronic interstitial inflammation. This inflammatory cascade causes peripheral oedema, skin damage and subsequently ulceration.

Deep veins traverse the leg and connect with the Great Saphenous Vein (GSV) at the groin (saphenofemoral junction) and the Small Saphenous Vein (SSV) in the popliteal fossa (saphenopopliteal fossa):

  • GSV runs along the medial aspect of the leg from the groin to the medial malleolus
  • SSV runs down the centre of the calf from the popliteal fossa to the lateral malleolus.

Incompetence of these veins typically leads to varicose veins and as such they are the focus of surgical treatment.

52
Q

Signs/Symptoms of Vericose Veins?

A
53
Q

Investigation for Venous Incompetence

A
54
Q

Treatment of Varicose Veins

A

Conservative: aims to reduce effects of chronic venous hypertension

  • Leg elevation
  • External Compression stocking (Class 2: compress to greater extent at ankle while reducing proximally)
  • Multilayer compression bandaging (Provided arterial circulation is adequate)

Surgical: focus on removing the incompetent superficial venous system (either GSV or SSV) redirecting flow through a functioning deep system

  • Ligation at either the Sapheno-Popliteal junction (SPJ) or Sapheno-Femoral junction (SPF)
  • Stripping of the SSV is rarely performed due to the risk of sural nerve injury

Endovenous Intervention

  • First line, performed under local anesthesia
  • involve cannulation of the target vessel using ultrasound and insertion of a probe into the GSV or SSV to a point 3cm distal to the junction with the deep vein

Thermal Ablation (Radiofrequency Ablation or Laser Ablation)

  • Involves the passage of a heater probe into the GSV or SSV => induces venous endothelial injury, inflammation and subsequent vessel thrombosis
  • Alternatively mechanochemical ablation induced endothelial injury can be inflicted via trauma/chemical irritation to the vein wall while cyanoacrylate glues the vessel closed
55
Q

Complications of Venous Interventions?

A
56
Q

Risk Factors for DVT

A
57
Q

Commonly affected site for DVT

A
58
Q

Which Surgeries are at a particular high risk of DVT?

A

Trauma, orthopaedic and pelvic interventions

Prophylaxis using low molecular weight
heparin (LMWH) should always be considered unless contraindicated

59
Q

Presentation of DVT

A
60
Q

Differential diagnosis of the acutely swollen leg

A
61
Q

Investigations for DVT

A
62
Q

Classification used to assess the clinical risk of DVT

A

Wells Score

3 or more = high risk

1-2 = intermediate risk

0 = low risk

63
Q

Treatment of DVT

Timeframes for treatment

A
64
Q

Prophylaxis for DVT in Hospital

A
65
Q

Complications of DVT

A

Clinical Surgery (20 decks)

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