Vascular Flashcards
1
Q
What are the signs of critical limb ischemia?
A
- Pulseless
- Pallor
- Perishing with cold
- Paralysis
- Pain
- Paraesthesia
2
Q
What are the 2 causes of intermittent claudication?
A
Vascular
Neurological
3
Q
Name 3 ways that intermittent claudication can be diagnosed
A
- USS doppler
- ABPi
- Angiography
4
Q
What are the 3 causes of acute limb ischemia?
A
- Trauma
- Thrombosis in situ
- Embolus
5
Q
What are some of the complications of acute limb ischemia?
A
- Reperfusion injury
- Compartment syndrome
- Amputation
- Sepsis (secondary to infected gangrene)
6
Q
How do you diagnose rhabdomyolysis?
A
- Measure CK and LDH in blood
- Clincal Triad of:
- myalgia
- weakness
- myoglobinuria
7
Q
What are some of the long term management things you can do after a patient has had acute limb ischemia?
A
- Promote regular exercise
- Smoking cessation
- Weight loss
- Most cases should start anti-platelet: aspirin or clopidogrel
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
9
Q
What size of AAA needs surgical management?
A
AAA >5.5 cm
or AAA expanding at a rate of 1cm p/year
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
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
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
13
Q
What are some of the signs of venous insufficiency?
A
- Venous eczema
- Haemosiderin staining
- Venous ulcer
- Lipdermasclerosis
- White atrophy
14
Q
What imaging should be done if suspecting acute limb ischemia?
A
CT angiogram
15
Q
How should acute limb ischemia be managed?
A
- Surgical emergency: tissue damage occurs within 6 houts
- Resucitate patient
- Start on IV heparin
16
Q
What are ulcers?
A
Abnormal breaks in the skin or mucous membranes
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
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
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
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
21
Q
How should venous ulcers be investigated?
A
- Duplex ultrasound
- ABPi
- Swab cultures if suspecting isolated infection
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
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
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
25
Give some of the risk factors for arterial ulcers
* Peripheral arterial disease risk factors
* Smoking
* Diabetes mellitus
* Hypertension
* Hyperlipaemia
* Increasing age
* FHx
* Obesity
* Physical inactivity
26
What investigations should be done if suspecting arterial ulcers?
* ABPI
* **\>0.9 = normal**
* **0.9-0.8 = mild**
* **0.8-0.5 = moderate**
* **\<0.5 = severe**
* Duplex ultrasound
* CT angiograpphy +/- MR angiogram
27
How should arterial ulcers be managed?
**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
28
What are neuropathic ulcers? How do they form?
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
29
What are some of the risk factors for developing peripheral neuropathy?
* Diabetes Mellitus
* B12 deficiency
* Any foot deformity
* Peripheral vascular disease
30
What are the clinical features of neuropathic ulcers?
* 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
31
What investigations should be done if suspecting an ulcer is neuropathic?
* 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
32
How are neuropathic ulcers managed?
* 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
33
What is Charcot's foot?
* 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
34
What is carotid artery disease?
The build up of **atherosclerotic plaque** in one or both **common** and **internal carotid arteries** causing stenosis or occlusion
35
How can carotid artery disease be classified?
Radiologically by the degree of stenosis
## Footnote
**Mild** - \<50% diameter reduction
**Moderate** 50-69% diameter reduction
**Severe** 70-99% diameter reduction
**Total occlusion** 100% diameter reduction
36
How does carotid artery disease present clinically?
* Usually **asymptomatic**
* Can present as a focal neurological deficit
* TIA
* Stroke
* O/E - may hear a carotid bruit
37
What are the differential diagnoses for carotid artery disease?
* **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**
38
What investigations should be done for suspected ischemia or haemorrhagic stroke?
* **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**
39
How should patients admitted with potential stroke be managed?
* 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
40
What is the **long term management** of patients with known ischemic stroke or TIA?
**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
What is a carotid endarterectomy?
* Removal of atheroma and associated damaged intima of the carotid vessels
* Reduces risk of future strokes or TIAs
42
What are some of the main risks of carotid endarterectomy (CEA) surgery?
* 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
Explain the principles of the AAA screening programme
* 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
How are AAA routinely investigated?
* Outpatient abdominal **ultrasound scan**
* If AAA confirmed follow up with **CT scan with contrast**
45
When is surgical intervention offered for AAA?
* AAA **\>5.5 cm** diameter
* AAA expanding at **\>1cm/year**
* **Symptomatic** AAA in a patient who is otherwise fit
46
What are the 2 treatment options for AAA repair?
* **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
What is an important complication of endovascular AAA repair?
**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
Describe the management of a patient with suspected AAA rupture
* 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
What are the different layers of arterial wall?
* tunica intima (innermost)
* tunica media (middle)
* tunica adventitia (outermost)
50
What is an aortic dissection?
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
What are the 2 systems used to classify aortic dissections?
De Bakey Classification
Stanford Classification
52
What time span are aortic dissections classified as either acute or chronic?
**Acute -** diagnosed in \<14 days
**Chronic** diagnosed \>14 days
53
In which directions can aortic dissections progress?
* **Anterograde** - propogate towards the iliac arteries
* **Retrograde dissections** propogate towards the aortic valve
54
Explain the De Bakey Classification of aortic dissections
**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
Explain the Stanford classification of aortic dissection
**Group A** - involves the **ascending aorta**
**Group B** - dissections **do not** involve the ascending aorta
56
Give some risk factors for aortic dissection
* Hypertension
* Atherosclerotic disease
* Male
* Connective tissue disorder e.g. Marfan's or Ehler's Danlos
* Bicuspid aortic valve
57
How do aortic dissections present clinically?
* 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
What investigations should be done if suspecting aortic dissection?
* **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
How are aortic dissections managed?
* 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
How are aortic dissections managed **medically?**
* 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
What complications can arise from aortic dissections?
* 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
What is an aneurysm?
A **persistant, abnormal dilatation** of an artery to 1.5x its normal diameter
63
How does the location of pain change depending on the location of a thoracic aneurysm?
* **Ascending aorta** - pain in the **anterior chest**
* **Aortic arch** - pain in the **neck**
* **Descending aorta** - pain **between the scapulae**
64
What signs and symptoms might you get in thoracic aneurysms and why?
* **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
Which imaging is used to detect thoracic aneurysms?
* **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
What classification system is used to assess acute limb ischemia?
Rutherford classification
67
How should acute limb ischemia be managed?
* 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
What are the complications of acute limb ischemia?
* 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
What are the stages of chronic limb ischemia?
**Stage 1 :** *asymptomatic*
**Stage 2 :** *Intermittent claudication*
**Stage 3 :** *Ischemic rest pain*
**Stage 4:** Ulceration or gangrene
70
Explain Buerger's test and why it is used
* 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
What is Leriche syndrome?
Form of peripheral artery disease affecting the **aortic bifurcation** specifically presents with **buttock or thigh pain** and associated **erectile dysfunction**
72
What are the 3 ways that **critical limb ischaemia** can be defined?
* **Ischemic rest pain for \>2 weeks** (requiring opiate analgesia)
* **Presence of ischemic lesions** or **gangrene**
* **ABPI \<0.5**
73
What might you find on examination in critical limb ischemia?
* Pale
* cold
* Weak or absent pulses
* Hair loss on limb
* Skin changes - atrophic skin, ulceration, gangrene
* Thickened nails
74
What are the 2 major differential diagnosis of a patient presenting with limb ischemia symptoms?
* **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
Why should an ABPI of \>1.2 be interpreted with caution?
Calcification and hardening of the arteries by cause a falsely high ABPI
76
At which ABPI do you get foot pain at rest?
_0.5_
77
Give some of the common causes of acute mesenteric ischaemia
* thrombosis in situ
* embolism
* non-occlusive causes
* venous occlusion and congestion
78
What investigations can be done if suspecting acute mesenteric ischemia?
* 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
How should acute mesenteric ischemia be managed?
* 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
What is chronic mesenteric ischemia and how does it arise?
Reduced blood flow to the bowel which gradually deteriorates over time as a result of **atherosclerosis** of the coeliac trunk, SMA +/- IMA
81
What are the clinical features of chronic mesenteric ischemia?
* **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
What is a pseudoaneurysm?
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
How do pseudoaneurysms typically occur?
Following **damage** to the vessel wall e.g.
* puncture following cardiac catheterisation
* repeaded injections e.g, IVDU
* trauma
* regional inflammation
* vasculitis
84
What are the most common locations of pseudoaneurysms?
* **Femoral artery** (most common)
* Radial artery
* Carotid
* Abdominal/ thoracic aorta
85
How do pseudoaneurysms present clinically?
* 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
How are pseudoaneurysms managed?
* 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
How are infected pseudoaneurysms treated?
* 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
What are varicose veins?
Tortuous dilated segments of vein that arise from **incompetent valves** causing venous hypertension and dilation
89
Give some risk factors for developing variose veins
* Prolonged standing
* Obesity
* Pregnency
* Family Hx
90
What investigations can be done for varicose veins?
* **Ultrasound duplex doppler** is the gold standard
* can be done bedside and assess valve competence
91
What are the treatment options for varicose veins?
**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
When is surgery offered for varicose veins?
* **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
What are the surgical options for treating varicose veins?
* **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
What are some complications of varicose vein surgery?
* Haemorrhage
* Thrombophlebitis
* DVT
* Disease recurrence
* Nerve damage - especially saphenous or sural nerves
95
What is Deep Venous Insufficiency (DVI)
A chronic disease that occurs a result of the **failure of the venous system** causing valvular reflux, venous hypertension and obstruction
96
What are the causes of Deep Venous Insufficiency?
**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
How do patients with Deep Venous Insufficiency present clinically?
* **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
What is post thrombotic syndrome?
* Occurs in patients with prior DVT
* heaviness
* cramps
* pain
* pruritis
* paraesthesia
* pre-tibial oedema
* skin induration
* hyperpigmentation
