Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Junior surgery > Vascular > Flashcards

Vascular Flashcards

1
Q

What are the signs of critical limb ischemia?

A
  1. Pulseless
  2. Pallor
  3. Perishing with cold
  4. Paralysis
  5. Pain
  6. Paraesthesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 2 causes of intermittent claudication?

A

Vascular

Neurological

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Name 3 ways that intermittent claudication can be diagnosed

A
  1. USS doppler
  2. ABPi
  3. Angiography
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 3 causes of acute limb ischemia?

A
  1. Trauma
  2. Thrombosis in situ
  3. Embolus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are some of the complications of acute limb ischemia?

A
  1. Reperfusion injury
  2. Compartment syndrome
  3. Amputation
  4. Sepsis (secondary to infected gangrene)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How do you diagnose rhabdomyolysis?

A
  • Measure CK and LDH in blood
  • Clincal Triad of:
    • myalgia
    • weakness
    • myoglobinuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are some of the long term management things you can do after a patient has had acute limb ischemia?

A
  1. Promote regular exercise
  2. Smoking cessation
  3. Weight loss
  4. Most cases should start anti-platelet: aspirin or clopidogrel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

AAA’s can rupture anteriorly and posteriorly. Which has a better prognosis and why?

A

Posterior has better prognoses due to tamponade by neighbouring structures e.g. vertebrae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What size of AAA needs surgical management?

A

AAA >5.5 cm

or AAA expanding at a rate of 1cm p/year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How often do AAA <5.5cm need monitoring?

A

If small: 3-4.4cm = annually

If medium= 4.5-5.4cm = every 3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What steps can you take to improve outcomes in those with small AAA?

A
  • Smoking cessation
  • Improve BP control
  • Statin and aspirin therapy
  • Weight loss and exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are some of the signs and symptoms patients can present with if they have AAA?

A
  • Abdominal pain
  • Back or loin pain
  • Distal embolus can cause limb ischemia
  • Aortoenteric fistula
  • Pulsatile mass flet in the abdomen
  • If ruptured
    • degree of shock or syncope
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are some of the signs of venous insufficiency?

A
  • Venous eczema
  • Haemosiderin staining
  • Venous ulcer
  • Lipdermasclerosis
  • White atrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What imaging should be done if suspecting acute limb ischemia?

A

CT angiogram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How should acute limb ischemia be managed?

A
  • Surgical emergency: tissue damage occurs within 6 houts
  • Resucitate patient
  • Start on IV heparin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are ulcers?

A

Abnormal breaks in the skin or mucous membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do venous ulcers appear?

A
  • Shallow with irregular borders
  • granulating base
  • Characteristically over the medial malleolus
  • Prone to infection so can present with cellulitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Briefly explain the pathophysiology of venous ulcers

A
  • Valvular incompetence or venous flow obstruction leads to impaired venous return
  • Results in venous hypertension which traps white blood cells and forms a fibrin cuff around vessels
  • White cells release inflammatory mediators which leads to poor wound healing and necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Give some risk factors for developing venous ulcers?

A
  • Increasing age
  • Pre-existing venous incompetence e.g. varicose veins, hx of venous thromboembolism
  • Pregnancy
  • Obesity or physical inactive
  • Severe leg injury or trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do venous ulcers present clinically (signs and symptoms)

A
  • Painful particularly at the end of the day
  • Associated symptoms of chronic venous disease before ulcers appear
    • aching
    • itching
    • burning
  • Leg or ankle oedema
  • Varicose eczema or thrombophlebitis
  • Haemosiderin skin staining
  • Lipdermatosclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How should venous ulcers be investigated?

A
  • Duplex ultrasound
  • ABPi
  • Swab cultures if suspecting isolated infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How should venous ulcers be managed?

A
  • Leg elevation
  • Increased exercise - aids venous return
  • Lifestyle changes
    • weight reduction
    • improved nutrition
  • Abx if evidence of wound infection
  • Multicomponent compression bandaging (30-75% will heal after 6 months)
  • Appropriate dressings and emollients required
  • If there are concurrent varicose veins treat with endovenous or open surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are arterial ulcers?

A

Ulcers caused by a reduction in arterial blood flow leading to decreased perfusion of the tissues and subsequent poor healing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How do arterial ulcers appear clinically?

A
  • Small, deep lesions
  • Well defined borders
  • Necrotic base
  • Occur distally at sites of trauma or pressure
  • Likely have a preceding history of intermittent claudication or critical limb ischemia
  • Develop over a long period of time with no healing
  • O/E: limbs are cold and have reduced/ absent pulses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Give some of the risk factors for arterial ulcers

A
  • Peripheral arterial disease risk factors
  • Smoking
  • Diabetes mellitus
  • Hypertension
  • Hyperlipaemia
  • Increasing age
  • FHx
  • Obesity
  • Physical inactivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What investigations should be done if suspecting arterial ulcers?

A
  • ABPI
    • ​>0.9 = normal
    • 0.9-0.8 = mild
    • 0.8-0.5 = moderate
    • <0.5 = severe
  • Duplex ultrasound
  • CT angiograpphy +/- MR angiogram
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How should arterial ulcers be managed?

A

Conservative: smoking cessation, weight loss, increase exercise

Medical: CV risk factor modification, statin therapy, antiplatelet, optimised BP and glucose

Surgical: angioplasty +/- stenting or bypass gradting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are neuropathic ulcers? How do they form?

A

Ulcers that form as a result of peripheral neuropathy

There is a loss of protective sensation which leads to repetitive stress and unnoticed injuries forming on pressure points of the limb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are some of the risk factors for developing peripheral neuropathy?

A
  • Diabetes Mellitus
  • B12 deficiency
  • Any foot deformity
  • Peripheral vascular disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the clinical features of neuropathic ulcers?

A
  • Hx of peripheral neuropathy (although may be unaware)
  • Burning/ tingling legs
  • Single nerve involvement
  • Amotrophic neuropathy (painful wasting of proximal quadriceps)
  • Peripheral neuropathy in glove and stocking distribution
  • Ulcers are variable in size and depth - have a ‘punched out’ appearance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What investigations should be done if suspecting an ulcer is neuropathic?

A
  • Blood glucose
    • HbA1C or random blood glucose
  • Serum B12 levels
  • Concurrent arterial disease assessed with ABPI and duplex
  • Microbiology swab for sites of infection
  • Deep infection may warrant X-Ray to assess for osteomyelitis
  • 10g monofilament and 128Hx tuning fork foot assessment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How are neuropathic ulcers managed?

A
  • Optimise Diabetic control
    • Target HbA1c <7%
  • Improve diet
  • Increase exercise
  • Manage any CV risk factors
  • Ensure regular chiropody
  • Maintain good food hygeine
  • Appropriate footwear
  • Swab any signs of infection and treat with antibiotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is Charcot’s foot?

A
  • Neuropathic ulcers can be seen alongside Charcot’s foot
  • Loss of sensation in the join leads to continual unnoticed trauma and deformity
  • Presents with swelling, distortion, pain, loss of function and ‘rocker bottom’ sole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is carotid artery disease?

A

The build up of atherosclerotic plaque in one or both common and internal carotid arteries causing stenosis or occlusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

How can carotid artery disease be classified?

A

Radiologically by the degree of stenosis

Mild - <50% diameter reduction

Moderate 50-69% diameter reduction

Severe 70-99% diameter reduction

Total occlusion 100% diameter reduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How does carotid artery disease present clinically?

A
  • Usually asymptomatic
  • Can present as a focal neurological deficit
    • TIA
    • Stroke
  • O/E - may hear a carotid bruit
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the differential diagnoses for carotid artery disease?

A
  • Carotid dissection - typically patients <50yrs with underlying connective tissue disease
  • Thrombotic Occlusion of Carotid Artery - can only be differentiated to plaque on imaging
  • Fibromuscular dysplasia - a non-atheromatous stenotic angiopathy causing hypertrophy of the vessel wall
    • typically <50 years, female, also affects renal arteries
  • Vasculitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What investigations should be done for suspected ischemia or haemorrhagic stroke?

A
  • Urgent non-contrast CT head
  • Bloods: FBC, U&E, clotting, lipid profile, glucose
  • ECG
  • Once diagnosis of ischemic stroke/ TIA made… screen carotid arteries with duplex ultrasound scans
  • Lesions within the carotid artery can be classified further with CT angiography
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How should patients admitted with potential stroke be managed?

A
  • High flow oxygen
  • Blood glucose optimised (4-11mmol target)
  • Initial managment depends on nature of stroke
    • Ischemic - IV alteplase (r-tPA) within 4.5hrs of symptoms and 300mg aspirin
    • Haemorrhorrhagic stroke - correction of any coagulopathy and refer to neurosurgery
  • Thrombectomy indicated in patients with confirmed acute ischemic stroke and confirmed occlusion of the proximal anterior circulation on angiography
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the long term management of patients with known ischemic stroke or TIA?

A

Cardiovascular risk management

  • Antiplatelet 300mg aspirin for 2 weeks then clopidogrel 75mg OD
  • Statin - ideally high dose atorvastatin
  • Aggressive management of HTN / diabetes
  • Smoking cessation
  • Regular cardiovascular exercise
  • Weight loss
  • SALT team referall for any dysphagia
  • PT/OT for any mobility issues
  • Carotid endacarterectomy for all patients with acute non-disabling stroke
41
Q

What is a carotid endarterectomy?

A
  • Removal of atheroma and associated damaged intima of the carotid vessels
  • Reduces risk of future strokes or TIAs
42
Q

What are some of the main risks of carotid endarterectomy (CEA) surgery?

A
  • Stroke 2-3%
  • Nerve damage to the hypoglossal, glossopharyngeal or vagus nerve
  • Myocardial infarction
  • Local bleeding
  • Infection
  • Post op haematoma which can threaten the airway
43
Q

Explain the principles of the AAA screening programme

A
  • Offered to all men in their 65th year
  • Shown to have approx 50% reduction in aneurysm related mortality
  • 1.1% of those screened are diagnosed with AAA
  • Most men with detected AAA need 3-5 years surveillance prior to reaching the threshold for elective AAA repair
44
Q

How are AAA routinely investigated?

A
  • Outpatient abdominal ultrasound scan
  • If AAA confirmed follow up with CT scan with contrast
45
Q

When is surgical intervention offered for AAA?

A
  • AAA >5.5 cm diameter
  • AAA expanding at >1cm/year
  • Symptomatic AAA in a patient who is otherwise fit
46
Q

What are the 2 treatment options for AAA repair?

A
  • Open repair
    • midline laparotomy or long transverse incision exposing the aorta
    • segment removed and replaced with prosthetic graft
  • Endovascular repair
    • graft introduced by the femoral artery to fix a stent across the aneurysm
    • Has improved short term outcomes
      • decreased hospital stay
      • 30 day mortality lower
    • However higher rate of re-intervention
  • Both options have similar long term outcomes
47
Q

What is an important complication of endovascular AAA repair?

A

Endovascular Leaking

  • Where an incomplete seal forms around the aneurysm causing blood to leak into the graft
  • Often asymptomatic therefore rgular surveillance (USS) is needed
  • If left untreated aneurysm can expland and subsequently rupture
48
Q

Describe the management of a patient with suspected AAA rupture

A
  • High flow O2
  • IV access - x2 large bore cannulae
  • Urgent bloods (FBC, U&E, clotting)
  • Crossmatch for minimum 6 units
  • Treat any shock very carefully
    • ​raising BP too much will dislodge any clot and may precipitate further bleeding
    • Aim to keep BP <100mmHg (permissive hypotension) to prevent excessive blood loss
  • Transfer to local vascular unit
49
Q

What are the different layers of arterial wall?

A
  • tunica intima (innermost)
  • tunica media (middle)
  • tunica adventitia (outermost)
50
Q

What is an aortic dissection?

A

A tear in the intimal layer of the aortic wall causing blood to flow between the tunica intima and tunic media and cause the layers to split apart

51
Q

What are the 2 systems used to classify aortic dissections?

A

De Bakey Classification

Stanford Classification

52
Q

What time span are aortic dissections classified as either acute or chronic?

A

Acute - diagnosed in <14 days

Chronic diagnosed >14 days

53
Q

In which directions can aortic dissections progress?

A
  • Anterograde - propogate towards the iliac arteries
  • Retrograde dissections propogate towards the aortic valve
54
Q

Explain the De Bakey Classification of aortic dissections

A

Type 1: originates in the ascending aorta and propogates to the aortic arach

Type 2: confined to the ascending aorta

Type 3: originate distal to the subclavian artery in the descending aorta

  • 3a extends to the diaphragm
  • 3b extend beyond the diaphragm into the abdominal aorta
55
Q

Explain the Stanford classification of aortic dissection

A

Group A - involves the ascending aorta

Group B - dissections do not involve the ascending aorta

56
Q

Give some risk factors for aortic dissection

A
  • Hypertension
  • Atherosclerotic disease
  • Male
  • Connective tissue disorder e.g. Marfan’s or Ehler’s Danlos
  • Bicuspid aortic valve
57
Q

How do aortic dissections present clinically?

A
  • Tearing chest pain
  • Radiates to the back
  • Tachycardia
  • Hypotension (secondary to hypovolaemia)
  • Aortic regurgitation murmur
  • Signs of end organ hypoperfusion
    • reduced urine output
    • paraplegia
    • abdominal pain
    • deteriorating concious level
58
Q

What investigations should be done if suspecting aortic dissection?

A
  • Baseline bloods (FBC, U&E, LFT, Troponin, coagulation)
  • Crossmatch at least 4 units of blood
  • ABG
  • ECG to rule out any cardiac pathology
  • CT angiogram - 1st line imaging
  • Transoesophageal ECHO - can be used but very user dependent
59
Q

How are aortic dissections managed?

A
  • High flow O2
  • IV access - x2 large bore cannuals
  • Fluid resuscitate cautiously
  • Stanford Type A - managed surgically
  • Uncomplicated Stanford Type B - managed medically
  • Lifelong antihypertensive therapy
  • Surveillance imaging 1,3 and 12 months post discharge and every 6-12 months thereafter
60
Q

How are aortic dissections managed medically?

A
  • Uncomplicated Type B dissections only
  • Manage hypertension - IV Beta blockers (labetalol) or CCB 2nd line
    • aims to lower systolic BP and pulse rate to minimise stress of dissection
61
Q

What complications can arise from aortic dissections?

A
  • Aortic rupture
  • Aortic regurgitation
  • Myocardial ischaemia
  • Cardiac tamponade
  • Stroke or paraplegia
    • 2ndry to cerebral artery or spinal artery involvement
  • Mortality (20% die before hospital)
62
Q

What is an aneurysm?

A

A persistant, abnormal dilatation of an artery to 1.5x its normal diameter

63
Q

How does the location of pain change depending on the location of a thoracic aneurysm?

A
  • Ascending aorta - pain in the anterior chest
  • Aortic arch - pain in the neck
  • Descending aorta - pain between the scapulae
64
Q

What signs and symptoms might you get in thoracic aneurysms and why?

A
  • Back pain - due to spinal compression by descending or thoracic aneurysm
  • Hoarse voice - in arch aneurysms compressing left recurrent laryngeal nerve
  • Distended neck vein - from SVC compression
  • Symptoms of HF - involving aortic valve
  • Dyspnoea and cough - secondary to tracheal or bronchial compression
65
Q

Which imaging is used to detect thoracic aneurysms?

A
  • CXR - widened mediastinum, enlarged aortic knob, possible trachea deviation but not typically sensitive enough
  • CT scan with contrast - preferred choice
  • Tranoesophageal echocardiography - can detect any concurrent aortic insufficiency or dissection
66
Q

What classification system is used to assess acute limb ischemia?

A

Rutherford classification

67
Q

How should acute limb ischemia be managed?

A
  • Early surgical input
  • High flow O2
  • IV access
  • Therapuetic heparin
  • Rutherford 1 or 2a can be managed conservatively
    • prolonged course of heparin
  • Rutherford 2b +
    • surgical intervention
68
Q

What are the complications of acute limb ischemia?

A
  • Mortality 20%
  • Reperfusion injury - sudden increase in capillary permeability can result in
    • compartment syndrome
    • Release of substances from damaged cells
      • K+ causing hyperkalaemia
      • H+ causing acidosis
      • Myoglobin causing AKI
69
Q

What are the stages of chronic limb ischemia?

A

Stage 1 : asymptomatic

Stage 2 : Intermittent claudication

Stage 3 : Ischemic rest pain

Stage 4: Ulceration or gangrene

70
Q

Explain Buerger’s test and why it is used

A
  • Position patient supine
  • Raise legs until they go pale and lowe them until colour returns or they become hyperaemia
  • The angle that the limb goes pale is Buerger’s angle
    • Angle of <20 degrees indicates severe ischaemia
71
Q

What is Leriche syndrome?

A

Form of peripheral artery disease affecting the aortic bifurcation specifically presents with buttock or thigh pain and associated erectile dysfunction

72
Q

What are the 3 ways that critical limb ischaemia can be defined?

A
  • Ischemic rest pain for >2 weeks (requiring opiate analgesia)
  • Presence of ischemic lesions or gangrene
  • ABPI <0.5
73
Q

What might you find on examination in critical limb ischemia?

A
  • Pale
  • cold
  • Weak or absent pulses
  • Hair loss on limb
  • Skin changes - atrophic skin, ulceration, gangrene
  • Thickened nails
74
Q

What are the 2 major differential diagnosis of a patient presenting with limb ischemia symptoms?

A
  • Spinal stenosis- neurogenic claudication
    • pain radiates from back down lateral aspect of leg
    • symptoms on initial movement, relieved by sitting rather than standing
  • Acute limb ischemia
    • clinical features <14 days duration
    • often present within hours
75
Q

Why should an ABPI of >1.2 be interpreted with caution?

A

Calcification and hardening of the arteries by cause a falsely high ABPI

76
Q

At which ABPI do you get foot pain at rest?

A

0.5

77
Q

Give some of the common causes of acute mesenteric ischaemia

A
  • thrombosis in situ
  • embolism
  • non-occlusive causes
  • venous occlusion and congestion
78
Q

What investigations can be done if suspecting acute mesenteric ischemia?

A
  • ABG - urgent! to assess degree of acidosis and serum lactate
  • Routine bloods: FBC, U&E, clotting, amylase, LFTs
  • Imaging - CT scan with IV contast triple phase scan
    • initially shows as oedematous bowel then progresses to loss of bowel wall enhancement then penumatosis
79
Q

How should acute mesenteric ischemia be managed?

A
  • IV fluids
  • Catheter inserted and fluid balance chart started
  • Start broad spectrum abx - due to risk of faecal contamination
  • Surgical intervention either:
    • ​Revascularisation of the bowel - removal of any thrombus by radiological intervention
    • ​Excision of necrotic/ non viable bowel if revascularisation not suitable
      • post op will need intensive care. most patients end up needed covering loop or end stoma
80
Q

What is chronic mesenteric ischemia and how does it arise?

A

Reduced blood flow to the bowel which gradually deteriorates over time as a result of atherosclerosis of the coeliac trunk, SMA +/- IMA

81
Q

What are the clinical features of chronic mesenteric ischemia?

A
  • Postprandial pain 10mins-4hrs after eating
  • Weight loss - combination of decreased calorie intake due to pain and malabsorption
  • Concurrent vascular co-morbidities - previous stoke, MI, PVD
  • Change in bowel habit
  • N+V
82
Q

What is a pseudoaneurysm?

A

A ‘false’ aneurysm that occurs when there is breach to the arterial wall causing blood to accumulate between the tunica media and tunica adventitia

There is a direct communication betwen the vessel lumen and aneurysm which causes them to increase in size

83
Q

How do pseudoaneurysms typically occur?

A

Following damage to the vessel wall e.g.

  • puncture following cardiac catheterisation
  • repeaded injections e.g, IVDU
  • trauma
  • regional inflammation
  • vasculitis
84
Q

What are the most common locations of pseudoaneurysms?

A
  • Femoral artery (most common)
  • Radial artery
  • Carotid
  • Abdominal/ thoracic aorta
85
Q

How do pseudoaneurysms present clinically?

A
  • Pulsatile lump
    • can be tender or painful
  • Most commonly at femoral artery
  • Distal arterial occlusion leading to limb ischemia
  • If infected: erythematous and tender, may have pruluent discharge, features of sepsis
86
Q

How are pseudoaneurysms managed?

A
  • Smaller ones can be left alone
  • Larger or symptomatic pseudoaneurysms treated by ultrasound guided compression or thrombin injection
  • USS guided thrombin tehcnique involves thrombin directly injected into the lumen of pseudoaneurysm to form a thrombus to close off the pseudoaneurysm
  • Endovascular stents can be used but often not possible due to location
87
Q

How are infected pseudoaneurysms treated?

A
  • High risk of perforation which can cause significant haemorrhage means they need intervention
  • Pressure dressing applied and urgent imaging needed
  • Surgical ligation definitive treatment - occasionally a bypass graft is required (vein or bovine graft preferred)
88
Q

What are varicose veins?

A

Tortuous dilated segments of vein that arise from incompetent valves causing venous hypertension and dilation

89
Q

Give some risk factors for developing variose veins

A
  • Prolonged standing
  • Obesity
  • Pregnency
  • Family Hx
90
Q

What investigations can be done for varicose veins?

A
  • Ultrasound duplex doppler is the gold standard
    • can be done bedside and assess valve competence
91
Q

What are the treatment options for varicose veins?

A

Non invasive:

  • patient education: avoid prologed standing, weight loss, increase exercise
  • compression stocking only if interventional treatment is not appropriate
  • any venous ulceration requires four layer bandaging

Surgical treatment

92
Q

When is surgery offered for varicose veins?

A
  • Symptomatic primary or reccurent varicose veins
  • Lower limb changes e.g. pigmentation, eczema
  • Superficial vein thrombosis - appearance of hard, painful veins
  • Venous leg ulcer
93
Q

What are the surgical options for treating varicose veins?

A
  • Vein ligation, stripping and avulsion
    • responsible vein is tied off and stripped away
  • Foam scleotherapy
    • injection of a sclerosing (irritating) agent directly into affect vein causing a inflammatory response that closes off the vein
  • Thermal ablation
    • heating the vein from the inside via radiofrequency or lasers causing irreverible damage to the vein which closes it off
94
Q

What are some complications of varicose vein surgery?

A
  • Haemorrhage
  • Thrombophlebitis
  • DVT
  • Disease recurrence
  • Nerve damage - especially saphenous or sural nerves
95
Q

What is Deep Venous Insufficiency (DVI)

A

A chronic disease that occurs a result of the failure of the venous system causing valvular reflux, venous hypertension and obstruction

96
Q

What are the causes of Deep Venous Insufficiency?

A

Primary:

  • an underlying defect in the vein wall or valvular component
  • includes congenital defects and connective tissue disorders

Secondary:

  • defects occur secondary to damange
  • includes post thrombotic disease, post-phlebitic disease, venous outflow obstruction, trauma
97
Q

How do patients with Deep Venous Insufficiency present clinically?

A
  • Chronically swollen lower limbs
  • Itching, aching and painful
  • Venous claudication - bursting pain and tightness on walking that resolves with leg elevation
  • O/E may have signs of
    • varicose eczema (dry and scaly)
    • thrombophlebitis
    • haemosiderin skin stainig
    • lipderamtoslerosis
    • atrophie blanche
98
Q

What is post thrombotic syndrome?

A
  • Occurs in patients with prior DVT
  • heaviness
  • cramps
  • pain
  • pruritis
  • paraesthesia
  • pre-tibial oedema
  • skin induration
  • hyperpigmentation

Junior surgery (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions