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Alex > Vascular > Flashcards

Vascular Flashcards

1
Q
A
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2
Q

Describe the pathophysiology of acute limb ischaemia

A

Acute phase:

  • Insufficient substrate (glucose) delivery and insufficient oxygen delivery
  • Local anaerobic metabolism leads to lactic acidosis
  • Failure of ATP pumps: cellular damage with K+ release, cytokine release, and oedema due to increased membrane permeability
  • Oedema further impairs oxygen delivery, bacterial infections may be superimposed, especially in the context of pre-existing disease
  • Compartment syndrome is caused when local compartmental pressure becomes greater than perfusion pressure.

Reperfusion phase:

  • Generation of oxygen free radicals; attach to FAs in the phospholipid membrane and cause mechanical and functional derangements
  • Proteins (including myoglobin) are released and washed into general circulation
    • Myoglobin may cause ARF
    • K+ may cause arrhythmias
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3
Q

Discuss the aetiology of limb ischaemia

A
  • Embolic (~30%)
    • Cardiac source (AF, myxoma, endocarditis)
    • Aneurysmal source (aorta, iliac)
    • Atherosclerotic plaque proximal vessel
  • Thrombosis (~60%)
    • Atherosclerosis with acute rupture
    • Bypass graft occlusion
  • Rarer causes
    • Large vessel arteritis (Takayasu, Buerger’s, PAN)
    • Small vessel disease (DM, Raynaud’s, CT disorder)
  • Miscellaneous
    • Dissection
    • Trauma/external compression
    • Compartment syndrome
    • Frost-bite
    • Cold agglutinins
    • Myeloproliferative disorders
    • Drug-related (e.g. Norad)
    • Sepsis (e.g. Meningcoccaemia)
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4
Q

What solution is used for “Heparin flushes” in vacular surgery?

A

5000 units of Heparin in 500ml of 0.9% saline.

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5
Q

Prior to arterial clamping, what anticoagulation should be given?

A

70units of Heparin per kg given 2 minutes prior to arterial clamping.

In complex procedures liasion with anaesthetics based on dynamic coagulation profiles (e.g. Thromboelastography) is preferable.

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6
Q

Describe the technical considerations made in arterial repair.

A
  • Use non-absorpable monofilament sutures (PDS)
  • Use the finest suture for the job;
    • 3-0 for the aorta
    • 4-0 for the iliacs
    • 5-0 for the femoral
    • 6-0 for the popliteal
  • Use double armed sutures
  • Always use rubber shods on clamps
  • Include all layers of the vascular wall
  • Do not invert!
  • Do NOT tie knots at the apex of a patch
  • Start patch repairs at one side of the patch
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7
Q

Describe your technique of end-to-end repair of a small artery.

A
  • Accomplished most safely by applying the principles of triangulation;
    • Join the vessels with a suture placed in the centre of the deepest aspect of the anastamosis
    • Place two more sutures so as to divide the anastamosis into three equal segments
    • Place all knots on the outside
    • Use interupted sutures
    • Use the three stay sutures to rotate the anastamosis as neeed.
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8
Q

Describe your technique of end-to-side vascular anastamosis

A
  • The spatulation should result in a diameter 2-2.5 times the length of the diameter
  • The toe of the spatulated end should be slightly rounded
  • Place a double ended suture at heel of the anastamosis
  • Inside to outside on artery
  • Outside to inside on graft
  • Secure heel, then 1/3 circuference, then 2/3 circumference to finish around the toe.
  • If parachuting is required, 8 loops is the maximum number to parachute, and lubrication and a nerve hook may be required.
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9
Q

Describe the classification and subsequent treatment of hydatid cysts.

A

WHO Cystic Echinococcus classification

Based on USS appearance.

PAIR = percutaneous aspiration, injection, re-aspiration

Peri-operative/peri-procedural Albendazole

Surgery only indicated for (II, IIIb, or complex cysts)

  1. Cystectomy (recurrence 15-20%)
  2. Pericystectomy (higher risk to biliary tree)
  3. Segementectomy (more definitive)
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10
Q

Describe the epidemiology of abdominal aortic aneurysms

A
  • Present in 3-5% of population 65-80 years of age
  • M:F ratio of 5:1
  • Smoking 8:1 ratio
  • 50% of patients with femoral/popliteal aneurysms have AAA
  • Infra-renal 90%
  • Some familial tendency (10% FDR)
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11
Q

Briefly describe screening for AAA

A

A one-time screening for AAA is recommended for men ages 65 to 75 who have smoked, and in men ages 65 to 75 who have never smoked but who have a first-degree relative who required repair of an AAA or died from a ruptured AAA.

Approximately 800 men needed to be invited to screening to prevent one death in five years and approximately 210 men needed to be invited to screening to prevent one death in 13 to 15 years.

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12
Q

What are the indications for repair of an Abdominal Aortic Aneurysm?

A
  • Rupture/leak
  • Symptomatic AAA
  • >5.5cm AAA
  • AAA increasing in size (>0.5cm/6 months)
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13
Q

Describe the pathophysiology of diabetic foot sepsis.

A

Describe in terms of effects on vasculature, effects on neurology, and local effects of hyperglycaemia.

Vasculature

  • Microvascular disease
    • Hyperglycaemia causes vasoconstriction, inflammation, and thrombosis
    • Reduced endothelial NO, increased ROS, “advanced glycation products” all cause thickened capillaries
  • Macrovascular disease
    • Diabetes often part of the metabolic syndrome that drives macrovascular disease

Neurology

  • Sensory neuropathy
    • Disease of the vasa nervorum from microvascular disease
  • Autonomic neuropathy
    • Denervation of sweat glands causes dry skin and cracks
    • Inability to vasodilate in response to infection
  • Motor neuropathy
    • Atrophy of small muscles causes change in weight distribution and eventual dislocation of MTP heads
  • Visual impairment
    • ​Contributes to trauma and ulceration

Tissue effects in hyperglycaemia

  • Impaired chemotaxis and phagocytosis
    • Due to chronic glycosylation of neutrophils
  • Ideal bacterial substrate
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14
Q

What is the pathophysiology and treatment of Charcot foot?

A

Charcot neuropathy is characterised by bone and joint destruction, fragmentation, and remodelling.

It occurs due to a combination of mechanical and vascular factors resulting from diabetic peripheral and autonomic neuropathy and metabolic abnormalities of bone.

Treatment is based on

  1. Offloading ALL mechanical pressure off the foot
  2. Minimising the inflammatory cascade (NSAIDS)
  3. Minimising osteoclastic activity (Pamidronate)
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15
Q

Describe your treatment approach to Raynaud’s phenomenon

A
  1. Exclude primary causes
    • Systemic sclerosis, malignancy, SLE, drugs etc.
  2. Lifestyle modification
    • Gloves, warm socks, hand and foot warmers
    • Stop smoking
  3. Medication
    • Oral Nifedipine
    • IVI Prostaglandin
      • Iloprost 6 hours per day for 3-5 days
  4. Surgery
    • Sympathectomy for lower limb ONLY.
    • Amputation of non-viable digits/limbs.
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16
Q

What is thoracic outlet syndrome?

Outline the treatment options.

A

Thoracic outlet syndrome is characterised by neurovascular symptoms associated with repetitive use of the affected arm. Neurological symptoms, including pain, parasthesia, and weakness, are more common than vascular complications (such as ischaemia or VTE) which only occur in ~5%.

Treatment options include postural change and physiotherapy for neurological symptoms. Vascular symptoms or complications often require surgery; a trans-axillary, supra- or infra-clavicular approach may be used to resect the first +/- cervical rib/s. Where there is arterial stricture and post-stenotic dilatation, bypass is required.

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17
Q

What are the indications for repair of varicose veins?

Outline the treatment options.

A
  • Venous ulceration
  • Bleeding
  • DVT
  • Symptomatic skin complications of varicose vein disease; lipodermatosclerosis etc.
  • Symptoms due to disease, not responsive to non-operative management.

Treatment options are all forms of ablative venous destruction; surgical, thermal, or chemical.

Traditionally, surgical stripping of the GSV with SFJ ligation and stab phlebectomy has been considered the gold standard. Recently (last 5-10 years) advanced thermo-ablative techniques have seen comparable results with office-based procedures and quicker return to work. These advanced techniqes (and chemical foam ablation) require training and technology which is expensive at the outset.

18
Q

Describe the treatment of lymphoedema.

A
  • General measures
    • Maintain healthy weight
    • Optimum skin hygiene
    • Avoid triggers; IVLs, gardening gloves etc.
  • Compression
    • Gradiated compression aim for Grade IV
  • Physiotherapy
    • Manual lymphatic massage
  • Surgery
    • For primary disease or failure of above
    • Either physiological or debulking
      • Physiological transplant of lymphatic tissue or omentum including bypass of basins.
      • Debulking surgery has poor healing rates and is a last resort.
19
Q

Describe the pathophysiology of mesenteric ischaemia.

A
  1. Mucosal ischaemia, characterised by visceral pain without clinical signs
  2. Disruption of microvascular integrity — capillaries become damaged, increase mucosal permeability, blood may extravasate causing haemorrhagic foci and bowel wall thickening
  3. Progressive mucosal injury, leakage of protein, fluid and electrolytes — gas-producing organism, translocation of bacteria, pneumatosis, portal venous gas and peritonitis
  4. Reperfusion — more damaging production of free radicals, neutrophil infiltration, anaerobic metabolism leading to lactic acidosis.
20
Q

What are the causes of an acutely swollen leg?

A
  1. Deep vein thrombosis
  2. Cellulitis or erysipelas
  3. Necrotizing soft tissue infection
  4. Lymphoedema
  5. Musculotendinous rupture
  6. Ruptured Baker’s cyst
21
Q

What is an ulcer?

A
  1. A breach in the epithelium of a tissue
  2. A dimished ability of the tissue to heal
  3. Acute and chronic inflammation
22
Q

Describe the pathophysiology of atheromata

A

Described in histological terms:

  1. Fatty streaks
    • Focal thickening of the intima with accumulation of lipid-laden macrophages (foam cells) and extracellular matrix
  2. Fibrous cap
    • Lesion becomes a well defined lipid core with a fibrous cap
  3. Vasa-vasorum
    • Eventually the vasa-vasorum from nearby adventitia in-grows to supply to lesion, weakening the walls and causing remodelling
  4. Fibrous plaque
    • Smooth muscle hypertrophy and consolidation of the deep lipid core characterises the fibrous plaque, which may have a relatively thin surface, vulnerable to rupture
  5. Intra-plaque haemorrhage
    • Plaque neovascularization results in spontaneous haemorrhage and subsequent rupture with thrombo-embolism.
23
Q

Outline the options for treatment of a threatened limb with ischaemia.

A

Both surgery and thrombolysis seem effective and the choice should be made on an individual basis for each patient, taking into account the skills and local experience in vascular surgery. All patients should receive Heparin or LMWH to prevent propagation while considering options.

Thrombolysis

  • Achieved by stimulating plasminogen into plasmin to degrade fibrin plug.
  • Can use t-PA or Urokinase (both preferred to Streptokinase)
  • Advantage of concurrent angiography during procedure
  • Minor haemorrage in 40%
  • Always perform catheter angiogram at end of case

Balloon Catheter Embolectomy

  • Transverse arteriotomy easier to close
  • 4-5Fr balloon tip catheter
  • Always perform a catheter angiogram
  • Consider fasciotomies
24
Q

Describe the range of values and implications for Ankle-Brachial Pressure Index.

A

0.9 - 1.3

Normal

0.4-0.9

Claudication

<0.4

Rest pain

<0.3

Ulceration

25
Q

What are normal and abnormal toe pressures?

A

An absolute toe pressure >30 mmHg is favorable for wound healing, although toe pressures >45 to 55 mmHg may be required for healing in patients with diabetes.

26
Q

Classify the aetiology of aneurysms

A

Congenital

  • Weak areas e.g. berry aneurysm
  • Weak material within walls e.g. Ehlers Danlos
  • Arterial dilatation associated with AV fistula

Acquired

  • Trauma (often pseudoaneurysm)
  • Infection
  • Degeneration
    • Atherosclerosis
    • Cystic medial necrosis
27
Q

Describe AAA size with relation to risk of rupture per year.

How should AAAs be followed up?

A
  1. 0-3.9cm - 0.4%
  2. 0-4.9cm - 1.1%
  3. 0-5.9cm - 3.3%
  4. 0-6.9cm - 9.4%

7.0-7.9cm - 24%

AAA that are 4.0-5.5cm should be followed up 6 monthly

AAAs that are 3-4cm should be followed up 2-3 yearly

28
Q

What are the criteria for EVAR for AAA?

A

Originally developed for patients too comorbid for open repair, the current indications for EVAR are less clear.

  • Relative indications include a hostile abdomen, a patient who cannot undergo open surgery, or inflammatory AAAs.
  • EVAR requires compatible AAA morphology;
    • Healthy AAA neck; 15mm in length, >30mm diameter
    • Limited angulation
    • Iliacs >7mm to fit delivery apparatus
    • IMA expendable

Approximately 55-75% AAA patients are suitable for EVAR.

29
Q

What is an endoleak?

How is classified?

How is treated?

A

Endoleak refers to persistent blood flow outside the lumen of the endoluminal graft but within the aneurysm sac or adjacent vascular segment being treated by the device.

Treat all type I endoleaks immediately. Type II and III leaks require revision to repair if enlarging or complicated.

30
Q

How are aortic dissections classified?

A

The Stanford Classification (focuses on part affected)

  • Type I - Ascending aorta
  • Type II - Descending aorta

The DeBakey Classification (focuses on origin)

  • Type I - Asc. Ao + Arch + Desc. Ao
  • Type II - Asc. Ao only
  • Type III - Desc. Ao distal to subclavian artery.

Stanford more commonly used;

Type I requires surgery.

Type II usually managed medically, although they often require surgery for organ ischaemia.

31
Q

How is peripheral arterial disease classified?

A

Using the (more widely used) Fontaine Classification or the (less used, more detailed) Rutherford Classification.

32
Q

What are the different classes of gradiated compression stocking available?

What class do we typically use?

What are the contraindications?

How do we use them?

A

Patients almost never tolerate class III or IV; anecdotally vascular surgeons typically prescribe calss II for all.

PVD; ABPI of less than 0.8

Stockings are worn continuously when not in bed, washed every 1-2 days so cycle several pairs, need to be replaced every 6 months.

33
Q

How is lymphoedema classified in terms of severity?

A

Grade I

  • Subclinical
  • 3% volume change
  • Not visible

Grade II

  • Mild
  • 5-8% volume change
  • Visible and symptomatic

Grade III

  • Moderate
  • >8% volume change
  • Proliferative fibrosis

Grade IV

  • Severe elephantiasis
34
Q

Classify the causes of lymphoedema

A

Primary

  • Congenital (<1 year)
    • Familial i.e Millroy’s disease
    • Non-familial
  • Praecox (<35 years)
    • Familial
    • Non-familial
  • Tarda (>35 years)

Secondary

  • Malignant disease and its treatment
    • Malignant infiltration of lymphatics
    • Surgical excision or interruption of lymphatics
    • Radiation therapy causing fibrosis of lymphatics
  • Infection
    • Parasitic filariasis most common infection
    • Tuberculosis
    • Recurrent bacterial cellulitis
  • Vascular
    • Arterial surgery to lymph node basin
    • Venous disease
35
Q

How can patients with TIA be stratified for risk of stroke?

A

By using the ABCD2 score; a score of 6-7 portends a stroke risk of ~10% within 7 days; consider inpatient repair!

A = Age

  • >60 (1 point)

B = Blood pressure

  • Systolic >140 or diastolic >90 (1 point)

C = Clinical features

  • Unilateral weakness (2 points)
  • Speech disturbance only (1 point)

D = Duration of symptoms

  • >60 minutes (2 points)
  • 10-59 minutes (1 point)

D = Diabetes

  • Yes (1 point)
36
Q

Which patients with carotid artery stenosis should be offered surgery?

A

All patients being considered for surgery must have a life expectancy over 5 years and have favourable anatomy for carotid endarterectomy.

  • Symptomatic patients with stenosis >70%
    • NNT of 16
  • Symptomatic patients with stenosis 50-69%
    • NNT of 22
  • Asymptomatic patients with stenosis >80%
    • NNT of 33
37
Q

What are the hard and soft signs of vascular injury?

A

Hard signs of vascular injury

  • Active pulsatile bleeding
  • Shock with ongoing bleeding
  • Absent distal pulses
  • Symptoms and signs of acute ischaemia
  • Expanding or pulsatile haematoma
  • Bruit or thrill over the area of the injury

Soft signs of vascular injury

  • History of severe bleeding
  • Diminshed distal pulse
  • Injury of anatomically related structures
  • Small non-expanding haematoma
  • Multiple fractures and extensive soft itssue injury
  • Injury in the anatomical area of a major blood vessel
38
Q

What is vascular access steal syndrome?

How is it classified?

A

Steal refers to the relative loss of arterial supply to the digits following creation of an AVF; it is caused in two ways; high flow steal is caused by lowered peripheral resistance causing ischaemia and low flow steal is caused by stenosis of the AVF.

39
Q

How are vascular anomalies classified?

A

Vascular Tumours

  • Congenital haemangioma
    • Present at birth
    • Some resolve, some are permanent.
  • Infantile haemangioma
    • “Strawberry birthmarks” appear in first 2 months
    • 50% resolved by 5 years, 90% by 9 years
  • Sub-glottic haemangioma
    • Requires careful follow up as 60% have associated with airway haemangioma
  • Parotid gland haemangioma
  • PHACE syndrome
    • Posterior fossa, Haemangiomas, Arterial abnormalities, Cardiac defects, and eye abnomrmalities.

Vascular Malformations

  • Low flow malformations (sclerotherapy)
    • Capillary malformations e.g Port wine stain
    • Venous malformations e.g Labial VM
    • Lymphatic malformations
  • High flow malformations (embolisation)
    • Arteriovenous
    • Arteriolovenous
    • Arteriolovenulous
40
Q

What threshold do you repair aneurysms?

A

AAA - 5.5cm

Iliac - >4cm

Popliteal - >2-3cm, or if lined with thrombus or if distal ischaemia (high likelihood of becoming symptomatic)

Splenic - >3cm

41
Q

What are the venous tributaries to the GSV?

A
  1. Superficial inferior epigastric vein
  2. Superficial circumflex iliac vein
  3. Supeficial anteriolateral thigh vein
  4. External pudendal vein
  5. Supeficial external pudendal vein
  6. Supeficial posteriomedial vein
42
Q

List some of the key markers of a successful fistula that can be assessed post-operatively.

A
  • At 6 weeks:
    • Diameter of 6mm
    • Depth of no more than 6mm
    • Flow rate of 600ml/min
    • Access length of 5-6cm for two dialysis needles.

Alex (36 decks)

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