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YEAR 2 > Vascular > Flashcards

Vascular Flashcards

1
Q

What is acute limb ischaemia?

A

Sudden hypoperfusion threatening limb viability < 2 weeks

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2
Q

What are the 6Ps of acute limb ischaemia?

A

Pain
Pallor
Pulselessness
Poikilothermia
Paralysis
Paraesthesia

Limb initially marble white -> mottles blue/pink = salvageable
Dark, non-blanching mottling = blistering and liquefactions = gangrene = non-salvageable

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3
Q

What are key investigations for acute limb ischaemia?

A

Doppler ultrasound
ABPI - if pulse present
CT angiogram - best if thrombotic cause

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4
Q

What suggests the cause of acute limb ischaemia is thrombotic over embolic?

A

Previous claudication with sudden deterioration
Develops within hours to days
Reduced or absent pulses elsewhere in the body
Incomplete ischaemia - presence of collaterals
Palpation of artery = hard, calcified
Widespread evidence of vascular disease
Bruits

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5
Q

What suggests the cause of acute limb ischaemia is embolic rather than thrombotic?

A

Sudden onset of painful leg < 24 hours
No history of claudication
Complete ischaemia - no collaterals
Evidence of emboli - MI, AF
No evidence of widespread vascular disease
Normal palpation of artery

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6
Q

What is the initial management of acute limb ischaemia?

A

Analgesia
Oxygen
IV fluids
IV heparin - bolus followed by continued infusion

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7
Q

How does compartment syndrome occur as a complication of revascularisation?

A

Reperfusion of ischaemic muscle → muscle oedema → swelling due to failure of cellular membrane function and capillary leakage → increase in volume leads to increase compartmental pressure → pressure rises = tissue perfusion decreases

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8
Q

How does reperfusion injury occur as a complication of revascularisation?

A

Products of cell death released when blood flow to ischaemic limb is restored - can result in rhabdomyolysis, cardiac dysrhythmia, acute kidney injury, ARDS, multi-organ failure and DIC.

Release of myoglobin from damaged muscle cells - reddish/brown urine - lead to AKI

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9
Q

What is the triad of Leriche Syndrome?

A
  1. Claudication of the buttocks and thighs
  2. Impotence erectile dysfunction - due to paralysis of the L1 nerve
  3. Loss of femoral pulses
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10
Q

At what % of stenosis is normally symptomatic?

A

> 70%

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11
Q

At which artery site is there occlusion for buttock and hip pain?

A

Aortoiliac artery

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12
Q

At which artery site is there occlusion for thigh pain?

A

Aortoiliac or common femoral artery

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13
Q

At which artery site is there occlusion for upper 2/3 of calf pain?

A

Superficial femoral artery

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14
Q

At which artery site is there occlusion for lower 2/3 of calf pain?

A

Popliteal artery

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15
Q

At which artery site is there occlusion for foot claudication?

A

Tibial/peroneal artery

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16
Q

What artery is most commonly affected first in lower limbs?

A

Superficial femoral artery

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17
Q

Why do symptoms of patients with PAD initially improve/stabilise before they deteriorate again?

A

Collateral vessels enlarge and develop when blood supply through main vessels are blocked. Ensure adequate blood supply which minimises symptoms.

Eventually collaterals become atherosclerosed and damaged = deterioration and worsening of symptoms

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18
Q

What are symptoms in PAD?

A

Intermittent claudication
Reduced skin temperature - cold limbs
Reduced hair and nail growth - shiny skin
Weak pulses and loss of sensation
Ischaemic rest pain
Reduced capillary refill
Non-healing ulcerations
Gangrene - dry or wet

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19
Q

What is ischaemic rest pain in PAD?

A

Associated with critical limb ischaemia

worse when patient is supine and better when hanging leg over bed

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20
Q

What are features of intermittent claudication in PAD?

A

-Exercise-induced muscle pain - Increased oxygen demand from exercise - unable to meet requirements = ischaemic pain - cramp/weakness

  • Most commonly in the calf, thighs, buttocks
  • Worse walking uphill or hurrying
  • Normally specific, consistent reproducible pain at same distance = claudication distance
  • Relieved by rest < 10 minutes
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21
Q

What is the Fontaine classification in PAD?

A

I - asymptomatic
IIa - mild claudication
IIb - moderate to severe - short distance claudication
III - ischaemic rest pain
IV - ulceration or gangrene

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22
Q

What are the ABPI measurements indicative of?

A

> 1.2 = Diabetes
0.9 - 1.2 = Normal
< 0.8 = PAD
< 0.5-0.8 - Moderate PAD
< 0.3 = Severe PAD

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23
Q

What is gold standard investigation in PAD?

A

MR angiography > CT angiography
(duplex ultrasound and ABPI first)

when needing to visualise for revascularisation

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24
Q

What is the conservative management in PAD?

A

Smoking cessation
Supervised exercise programme
Weight management
Diet

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25
Q

What is the medical management in PAD?

A

Anti-platelet - clopidogrel 75mg
Atorvastatin 80mg
Diabetic control
HTN control

Should get response within 6 months - 1 year to continue with medical management > surgical

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26
Q

What can medication can be used for pain relief in PAD when revascularisation options are not wanted?

A

Naftidrofuryl oxalate - vasodilator
Cilostazol

(also when exercise not effective)

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27
Q

What are endovasular revascularisation treatments for PAD?

A

Percutaneous transluminal angioplasty with balloon or stent
Atherectomy

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28
Q

What are the guidelines of stenosis for eligibility of surgical revasculrisation (bypass)

A

Aortoiliac stenosis > 10cm
Multifocal lesions
Lesions in common femoral artery

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29
Q

What are endovascular revascularisation treatments in acute limb ischaemia?

A

Thrombolysis - urokinase, alteplase - intra-arterial

Percutaneous transluminal angioplasty with balloon
Percutaneous mechanical thrombus extraction

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30
Q

What are the indications for endovasular revascularisation treatments in PAD?

A

Single, short segment uniform occlusions

Aortoiliac and femoropopliteal disease = < 10cm stenosis or if chronic/calcified stenosis <5cm

Also if no autologous vein for graft and life expectancy is less than 2 years

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31
Q

What are indications for surgical bypass in PAD and which vein is normally grafted?

A

Great saphenous vein
(prosthetic veins carry higher risk of infection)

Stenosis > 10cm
Large, extensive and multi-focal stenosis
and must be medically fit enough to handle surgery

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32
Q

What is the triad of symptoms of critical limb ischaemia?

A
  1. Ischaemic rest pain
  2. Gangrene
  3. Non-healing wounds/foot and leg ulcers
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33
Q

What are differentials for intermittent claudication?

A

Nerve root compression - sharp pain radiating down leg
Cauda equina syndrome
Hip arthritis
Spinal stenosis - relieved by flexing forward
Foot and ankle arthritis
Symptomatic Baker’s cyst
Venous obstruction

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34
Q

What is the difference between amputation and disarticulation?

A

amputation = removal of limb
disarticulation = removal of joint (more energy consumption)

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35
Q

Indications for amputation?

A

Gangrene - wet or dry
Uncontrolled sepsis of lower limb, necrotising fasciitis
Severe rest pain with no reconstruction option
Paralysis with contractures
Trauma

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36
Q

What are the 2 main complications of amputations?

A

Phantom limb pain
Wound breakdown - skin infections

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37
Q

Amputation levels:

A

Below knee - transtibial

Above knee - transfemoral

Above elbow - transhumeral

Congenital - transverse/longitudinal limb deficiency

Stump - residual limb

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38
Q

Difference between prosthesis and orthosis?

A

Prosthesis - artificial substitute or replacement of part of the body

Orthosis - device externally applied to body segment to improve

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39
Q

What are the K activity levels: K0-K4

A

K0 - Non ambulatory - bed bound

K1 - Limited to transfers or limited household ambulator

K2 - Unlimited household but limited community ambulator

K3 - Unlimited community ambulator

K4 - High energy activities - sports, work

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40
Q

Rehab timeline post amputation?

A

1 week - weight bearing on other limb between parallel bars

10 days - walk with pneumatic walking aid

3 weeks - trial of temporary prosthesis, final fitting of the artificial limb must await shaping and firming of the stump

-Once stump healed
- Elasticated compression stump socks fitted to shrink stump to an acceptable size for fitting for prosthesis
- Limb fitting usually delayed until >6/52 post-op to allow stump oedema to subside

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41
Q

What is Buerger’s Disease - Thromboangiitis obliterans?

A

Non-atherosclerotic, inflammatory vasculitis - segmental occlusions of small and medium sized arteries - typically in hands and feet

cigarette smoking - direct endothelial cell toxicity by tobacco + hereditary susceptibility
(Young males who smoke, Mediterranean and Middle Eastern origin)

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42
Q

What is the management of Buerger’s disease?

A

Smoking cessation
Nifedipine - vasodilate to improve blood flow

Escalate if turned into critical limb ischaemia

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43
Q

Presentation of Buerger’s disease?

A

Ischaemia of extremities - positive Allen test
Cold sensitivity in hands - raynauds
Severe pain, even at rest + night - neural involvement
Chronic ulceration of toes, feet, fingers - can lead to gangrene
Superficial thrombophlebitis
Wrist and ankle pulses usually absent - but brachial and popliteal pulses palpable

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44
Q

What is seen on arterial duplex and angiography in Buerger’s Disease?

A

Corkscrew collaterals are dilated vasa vasorum of the occluded main artery (Martorell’s sign)

Normal non-atherosclerotic proximal arteries and shows occluded distal small and medium-sized vessels

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45
Q

What is the guideline for aneurysm screening?

A

Single abdominal ultrasound for males 65+

< 3cm - discharged and no further action
3-4.4cm - rescan every 12 months
4.5-5.4cm - rescan every 3 months
> 5.5cm - 2 week referral to surgeon

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46
Q

What are the 3 separate criteria for 2 week referral to a vascular surgeon considering aneursyms?

A

If symptomatic
If grown > 1cm in a year
If > 5.5cm

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47
Q

What is the most common site for an AAA?

A

Between renal and inferior mesenteric arteries

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48
Q

Risk factors for AAA?

A

Atherosclerosis - mainly cause AAA
Hypertension - mostly associated with aneurysms of ascending aorta
Marfan Syndrome - defective synthesis of fibrillin
Ehlers-Danlos Syndrome - defective type III collagen synthesis
Vitamin C Deficiency - altered collagen cross-linking
Trauma
Infections - mycotic aneurysms - syphilis
Vasculitis
Congenital - berry aneurysms in circle of willis

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49
Q

What are the 2 main forms of an aneurysm?

A

Fusiform - symmetrical bulging on both walls of artery
Saccular - only one side of wall bulges outward (more likely to be false)

True aneurysm = dilation of all 3 tunica layers

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50
Q

What is a false aneurysm and how can it occur?

A

Defect in vascular wall - accumulation of blood within tunica media and adventitia layers

  • risk of thrombosis
  • common at radial, femoral, anastomotic site - where doctors make holes
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51
Q

How can syphilis cause an aneurysm?

A

Syphilis causes inflammation of vasa vasorum
Ischaemic injury of aortic media and aneurysmal dilation

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52
Q

Four pathophysiological ways infection can lead to mycotic aneurysms?

A
  1. Embolisation of septic thrombus, (usually as complication of IE = secondary mycotic aneurysm)
  2. Extension of an adjacent suppurative process
  3. Circulating organisms directly infecting the arterial wall
  4. Infection of prosthetic grafts = infected anastomotic aneurysms
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53
Q

Pathogenesis of vascular wall compromise leading to aneurysm formation?

A
  1. Poor quality of the vascular wall and connective tissue (Marfans, Ehlers-Danlos, Vitamin C deficiency)
  2. Altered balance of collagen degradation and synthesis is altered (Local inflammatory infiltrates → production of destructive proteolytic enzymes )
  3. Vascular wall is weakened through loss of smooth muscle cells (HTN or atherosclerosis)
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54
Q

What 4 ways can aneurysms cause symptoms?

A
  1. expansion - compression on adjacent structures
  2. rupture
  3. distal embolisation
  4. thrombosis
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55
Q

How does atherosclerosis cause aneurysms?

A

Atherosclerotic plaque in the intima compressed the underlying media → compromises nutrient and waste diffusion from the vascular lumen into the arterial wall → ischaemia - media undergoes degeneration and necrosis → arterial wall weakness and consequent thinning

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56
Q

What environmental changes can increase risk of rupture of an aneurysm?

A

Low atmospheric pressure
Colder weather

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57
Q

Symptoms in AAA

A

Pain - chest, belly, flanks, back, groin
Pulsatile abdominal mass
Blue toe syndrome - clot
Claudication
Acute limb ischaemia

58
Q

Symptoms in ruptured AAA?

A

Severe, central abdominal pain radiating to back
Sudden cardiovascular collapse - shock, hypotension, tachycardia
Pulsatile abdominal mass

59
Q

What are the anatomical requirements of an aneurysm for EVAR?

A
  1. Good iliac access - latent, diameter, toruosity
  2. Neck of aneurysm - infrarenal
  3. Aneurysm shape - cylindrical > conical/angulated
  4. Aneurysm size 15<30
60
Q

What are patient factors when deciding open repair over EVAR for aneurysm repair?

A

If patient is medically fit enough to handle open surgery.
More invasive, risks and longer recovery

61
Q

What are complications of EVAR?

A

Contrast and radiation toxicity
Wound haemotoma, infection, damage to access vessels
Endoleaks
Likely to need secondary intervention in the future
Rupture

62
Q

What are the 5 types of endoleaks?

A
  1. Inadequate anastamoses - leak between attachement site
  2. Retroleak - aneurysm sac filling via branch vessel
  3. Leak through defect in graft fabric
  4. Graft wall porosity
  5. Endotension - not actual leak - sac expansion > 5mm
63
Q

Acute initial management of ruptured AAA?

A

ABCDE

BP control - to reduce bleed (DO NOT give fluids, permissive hypotension at 80-100 systolic)

Pain control

Major haemorrhage protocol
- 2 units of packed red cells O negative
- 2 units FFP
- Cryoprecipitate
- Tranexamic acid

Immediate vascular review - take for CT

64
Q

What are 4 mechanisms of physiological survival from ruptured AAA?

A

Rupture into retro-peritoneum which tamponades the leak

Intense vasoconstriction of nonessential circulatory beds

Patient develops intensely pro-thrombotic state

Blood pressure drops limiting blood loss - permissive hypotension

65
Q

What are the driving restrictions for aneurysms in a normal car?

A

<6cm - continue as normal
6-6.4cm - must notify DVLA
>6.5cm - must stop driving

66
Q

What are driving restrictions for bus/lorry drivers within aneurysms?

A

<5.5cm - must notify DVLA
>5.5cm - must stop driving

67
Q

Management of small aneurysms?

A

Pharmacology
- Antiplatelet
- Statin
- Treatment of blood pressure
Smoking cessation
Surveillance

68
Q

Management of large aneurysms?

A

Whilst waiting for 2 week referral to surgeons

No driving if > 6.5cm
No strenuous exercise
Keep BP low

69
Q

Indications for surgery of popliteal aneurysm?

A

Asymptomatic
- Diameter > 2-3 cm
- Significant lining thrombus

Symptomatic
- Thrombosis - causing acute limb ischaemia
- Distal embolisation - chronic limb ischaemia or blue toe syndrome
- DVT - from compression of popliteal vein

70
Q

What surgery is done in popliteal aneurysms?

A

Popliteal artery bypass graft with aneurysm exclusion

  • Ligated above and below to exclude from circulation → femoro-popliteal bypass performed to restore blood flow to the foot
  • Using long saphenous vein
71
Q

Risks of popliteal aneurysms?

A

Distal embolisation and acute thrombosis
Can compress the popliteal vein and present as DVT

72
Q

Complications of thoracic aortic aneurysms?

A
  • Compress SVC - Superior vena cava syndrome
  • Aortic valve dilation and regurgitation
  • Compress recurrent laryngeal nerve and phrenic nerve - hoarseness, diaphragm paralysis, wheezing
73
Q

What % of popliteal aneurysms are bilateral?

A

50%

74
Q

What is a big risk factor for thoracic ascending aortic aneurysms?

A

Connective tissue disorders - Marfan’s, Ehler’s Danlos

75
Q

What is an aortic dissection?

A

Rupute of the intima - allowing blood to leak through between intima and media to create a false lumen

76
Q

What is type A and type B Stanford Classification of aortic dissections?

A

Type A - ascending aorta, proximal to left subclavian
Type B - distal to left subclavian, descending aorta

77
Q

Which Stanford classification of an artery would you get a Radio-radial delay?

A

Type A
(and difference in BP between arms > 20)

78
Q

Which Stanford classification of an artery would you get a Radio-femoral delay

A

Type A and B

79
Q

What is a complication if the false lumen of an aortic dissection grows too big?

A

False lumen can narrow and occlude the true lumen of the artery - leading to organ ischaemia

80
Q

What are 3 further complications from the spread of blood in an aortic dissection?

A
  1. Can extend along the aorta retrograde toward the heart - pericardial tamponade
  2. Rupture through adventitia - massive haemorrhage into mediastinum
  3. Pressure from false lumen creates a second tear in intima and blood reenters true lumen
81
Q

What is the DeBakey Classification of aortic dissections?

A

Type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally

Type II - originates in and is confined to the ascending aorta

Type III - originates in descending aorta, rarely extends proximally but will extend distally

82
Q

What can chest x-ray show in an aortic dissection?

A

widened mediastinum

83
Q

Risk factors for aortic dissection?

A

Hypertension - MAIN
Connective tissue disease e.g. Marfan’s syndrome
Coarctation
Pregnancy
Valvular heart disease
Cocaine/amphetamine use

83
Q

What can an ECG show in aortic dissection?

A

Ischaemia - ST elevation, if dissection extends to coronary arteries

84
Q

What is the management of Type A aortic dissection?

A

Surgical management - open surgery
BP controlled to 100-120 systolic

85
Q

What is the management of Type B aortic dissection?

A

Analgesia
Strict control of BP with IV labetalol
Nitroprusside

If complicated - TEVAR to cover entry tear

86
Q

What are features and associated signs of an arterial ulcer?

A

Begin as minor wounds that fail to heal
Deep, punched out lesions
Painful
Deep green or back with no granulation tissue - dry
Over lateral side or bony prominences

Associated symptoms - shiny and col skin, local hair loss, reduced pulses, intermittent claudication

87
Q

How does pooling of blood lead to venous ulcers?

A

Venous insufficiency → stasis of blood → increase venous pressure → tissue ischaemia → breakdown of tissues

88
Q

How does venous insufficiency lead to venous ulcers?

A

Chronic Venous Insufficiency
- Reflux - due to valvular incompetence
- Outflow obstruction
- DVT

89
Q

Common risk factors of venous ulcers?

A
  • Venous hypertension
  • Varicose veins
  • Female
  • Obesity
  • Standing for prolonged periods of time
  • Immobility
  • Previous DVT
  • Pregnant
90
Q

Features and associated signs of venous ulcers?

A
  • Shallow, Irregular borders
  • Yellow, fibrinous exudate
  • Mild pain
  • Gait area, medial malleolus

Associated with oedema, venous stasis eczema, lipdermatosclerosis, haemosidren deposition

91
Q

How do you treat venous ulcers?

A

Compression therapy/stockings - MUST exclude PAD - do ABPI
Leg elevation
Weight reduction
Emollients
Treatment of varicose veins

92
Q

What is the referral guidelines for venous ulcers?

A

Refer to vascular specialist if venous leg ulcer not healed after 2 weeks of primary care

Surgery options - debridement, skin grafting, vein transplant

93
Q

Features of a neuropathic ulcer?

A

Punched out appearance
Painless
Decreased sensation around area
Commonly over plantar surface of metatarsal head and plantar surface of hallux

94
Q

Features of venous insufficiency?

A
  • Phlebitis - inflammation in vein
  • Thrombophlebitis - clot in vein
  • Venous stasis
  • Oedema
  • Lipodermatosclerosis - upside champagne bottle sign
  • Haemosiderin deposition - hyperpigmentation
  • Bleeding
  • Ulceration
95
Q

What is the CEAP classification of varicose veins C0-C6?

A

C0 - No visible or palpable varicose veins
C1 - Telangectasia
C2 - Varicose veins
C3 - Swollen ankle (oedema)
C4 - Skin damage/changes
C5 - Healed venous leg ulcer
C6 - Venous leg ulcer

96
Q

What are conservative managements of varicose veins?

A
  • Leg elevation
  • Weight loss
  • Reduce long periods of standing
  • Regular exercise, walking
  • Manual Compression
  • Compression Stocking
97
Q

What are surgical intervention options for varicose veins?

A

Radio-frequency ablation - destruction of the endothelium of the vein via high RF
Injection sclerotherapy - injection of sclerosant substance at several points in the vein leading to occlusion

98
Q

What are indications for surgical referral in vascular surgery?

A
  • Significant pain and symptomatic varicose veins
  • Skin changes secondary to chronic venous insufficiency
  • Superficial thrombophlebitis
  • Venous leg ulcer
99
Q

What are varicose veins?

A

Abnormally dilated, tortuous veins > 2mm … normally superficial veins of upper and lower leg

Leads to incompetent venous valves - pressure changes in legs leads to structural defect of vein walls

100
Q

What changes occur in the venous walls in varicose veins?

A

Retrograde flow and pooling of blood in the superficial venous system → increased venous pressure leads to…
Marked proliferation of collagen matrix and decreased elastin = distortion and disruption of muscle fibre layers

101
Q

What is a varicocele and how does it occur?

A

Varicose veins of scrotal veins…

  • Left testicular veins drain blood into left renal vein at 90 degree angle BUT Blood can back up and venous blood pools in testicle → Testicular vein enlarges and becomes tortuous
  • Can be a result of compression of the gonadal vein from renal cell carcinoma
102
Q

What is the presentation of a varicocele?

A

Looks like a bag of worms - Larger when standing and smaller when lying flat
Ache or heavy feeling within the scrotum
Causes testicular temp to rise - testicular atrophy and poor quality sperm + infertility

(can be treated if causing pain or infertility otherwise fine to leave)

103
Q

What health condition is thought to be a protective against abdominal aortic aneurysms?

A

diabetes
?? due to metformin ??

104
Q

Differentials for ruptured AAA?

A
  • MI
  • Dissections
  • Perforated duodenal ulcer
  • Acute pancreatitis

check amylase to rule out GI differentials

105
Q

What blood test is helpful to rule out differentials in a ruptured AAA?

A

Amylase
(increased in pancreatitis)

106
Q

Differentials for unilateral leg swelling?

A
  • Lymphatic - filariasis, radiation, surgery, compression from tumour
  • Trauma - bruise, sprain, tendon rupture
  • Infection - cellulitis, erysipelas, osteomyelitis
  • Gout
  • Venous insufficiency
  • DVT
  • AV malformation
107
Q

Differentials for bilateral leg swelling?

A
  • Cardiac - CCF, pericarditis, pulmonary hypertension
  • Renal - nephrotic syndrome
  • Hepatic - cirrhosis, portal hypertension
  • Venous - outflow obstruction
  • Endocrine - myxoedema
  • Allergic - angio-oedema
  • Nutrition - hypoproteinaemia
  • Drugs - CCB, steroids, NSAIDs
  • Obesity - lipoedema
108
Q

What is Virchow’s Triad?

A
  1. Abnormal vessel wall
    • Endothelial cell damage promotes thrombus formation, usually at venous valves
  2. Abnormal blood flow - stasis
    • Poor blood flow and stasis result in valvular damage and promote thrombus formation
  3. Abnormal coagulability
    • Altered amounts of clotting factors - genetics, surgery, medications
109
Q

What is a paradoxical embolus?

A

DVT that passes through PFO or cardiac defect to gain access to systemic circulation

110
Q

What is a saddle embolus?

A

Occludes both pulmonary arteries

111
Q

What is a positive Homan’s sign in DVT?

A

Homan’s sign - calf pain at dorsiflexion of the foot

112
Q

What are features of Ilio-femoral DVT?

A

Cyanosed, white, cold, pulseless limb

113
Q

What is the triad of symptoms in PE?

A
  • Sudden onset SOB
  • Pleuritic chest pain
  • Haemoptysis
114
Q

What are features of a massive PE

A

Shock - hypotension, cyanosis, signs of right heart strain - raised JVP, parasternal heave, loud P2

115
Q

What are the guidelines of Well’s score for treatment and investigation in DVT?

A

> 2 = DVT likely → diagnostic imaging
<2 = DVT unlikely → d-dimer

116
Q

What does a Well’s score of 2+ in DVT indicate and what should be done next?

A

Likely DVT

  1. Leg ultrasound within 4 hours
    (If US cannot be done within 4 hours - take a D-dimer and give DOAC - if eventually US is negative = stop DOAC)

If US positive = give DOAC 3-6 months

117
Q

What should be done if an ultrasound scan is negative in suspected DVT and d-dimer is positive?

A

Stop any DOACs that were started on the interim
Repeat ultrasound in 6-8 days

118
Q

What does a Well’s Score of <1 indicate and what should be done?

A

DVT is unlikely

D-dimer should be done first

  • If positive - then do an ultrasound within 4 hours
  • If negative - consider alternative diagnosis
119
Q

What are the time frames for DOAC treatment in VTE?

A

3 months if provoked
6 months if unprovoked

120
Q

What intervention can be done in recurrent PE?

A

Inferior vena cava filter

121
Q

What are ECG changes that can be seen from a pulmonary embolism?

A

S1Q3T3
large S wave in lead I, large Q wave in lead III, inverted T wave in lead III

rbbb, right axis deviation
sinus tachycardia

122
Q

What does a Well’s score of 4+ mean in PE and what should be done?

A

PE likely

  1. Arrange CTPA
    (if delay, give interim DOAC)
  • If positive = diagnosed - continue with DOAC treatment
  • If negative - consider leg US if DVT suspected
123
Q

What does a Well’s score of <4 mean in PE and what should be done?

A

PE is unlikely

  1. Arrange d-dimer
  • If positive - arrange CTPA (if delay - give DOAC)
  • If negative - consider alternate diagnosis
124
Q

What does a Well’s score of <4 mean in PE and what should be done?

A

PE is unlikely

  1. Arrange d-dimer
  • If positive - arrange CTPA (if delay - give DOAC)
  • If negative - consider alternate diagnosis
125
Q

What modality of choice should be done in suspected PE for pregnant patients or in renal impairment or in iodine allergies?

A

V/Q scan

126
Q

What is the PERC score in PE?

A

Pulmonary Embolism rule out Criteria
(used in patients already low probability)

if all are absent = PE probability < 2%
1. Age<50
2. HR > 100
3. Oxygen sats < 94%
4. Previous DVT, PE
5. Recent surgery or trauma in past 4 weeks
6. Haemoptysis
7. Unilateral leg swelling
8. Oestrogen use

127
Q

What is the Well’s Score for PE?

A

Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) - 3
An alternative diagnosis is less likely than PE - 3
Heart rate > 100 beats per minute - 1.5
Immobilisation for more than 3 days or surgery in the previous 4 weeks - 1.5
Previous DVT/PT - 1.5
Haemoptysis - 1
Malignancy (on treatment, treated in the last 6 months, or palliative) - 1

128
Q

What is the Well’s Score for DVT?

A

Active cancer (treatment ongoing, within 6 months, or palliative) - 1
Paralysis, paresis or recent plaster immobilisation of the lower extremities - 1
Recently bedridden for 3 days or more or major surgery within 12 weeks requiring general or regional anaesthesia - 1
Localised tenderness along the distribution of the deep venous system - 1
Entire leg swollen - 1
Calf swelling at least 3 cm larger than asymptomatic side - 1
Pitting oedema confined to the symptomatic leg - 1
Collateral superficial veins (non-varicose) - 1
Previously documented DVT - 1
An alternative diagnosis is at least as likely as DVT: (-2)

129
Q

what is the treatment for massive PE with circulatory failure / shock?

A

Thrombolysis

130
Q

What is post-thrombotic syndrome?

A

Complication of DVT - increased pressure on vein walls damages valves

131
Q

Features of post-thrombotic syndrome?

A
  • Aching or cramping
  • Feeling of heaviness in the limb
  • Swelling
  • Discolouration of the skin
  • Hardening of the skin
  • Varicose veins
  • Venous ulcers
132
Q

Management of Post-thrombotic syndrome?

A
  • Leg elevations
  • Compression stockings
  • Regular exercise
  • Weight loss
  • NSAIDs
133
Q

What are risk factors for post-thrombotic syndrome?

A
  • DVT location: Risk of PTS is higher (two- to threefold) after proximal (especially with involvement of the iliac or common femoral vein) than distal (calf) DVT
  • Previous ipsilateral DVT
  • Preexisting primary venous insufficiency: up to twofold increased risk of PTS
  • Elevated body mass index (BMI): obesity (BMI >30) more than doubles the risk of PTS
  • Older age increases the risk of PTS; reported increased risk from 30% to threefold
  • Inadequate level of anticoagulation for tx of DVT
134
Q

What is superficial venous thrombophlebitis and what are common causes in upper and lower limbs?

A

Inflammation due to a blood clot in a superficial vein.

Lower leg - Varicose veins
Upper limb - IV catheters, infusions

135
Q

How can DVTs cause superficial venous thrombophlebitis?

A

DVTs can push and compress on superficial veins - stasis in superficial vein leading to a clot and inflammation

136
Q

What is the presentation of superficial venous thrombophlebitis?

A
  • Gradual onset
  • Redness following line of vein
  • Warm and tender, pain
  • Distal oedema
  • Cyanosis
  • Superficial vein dilation
  • Swelling
137
Q

What is the management in superficial venous thrombophlebitis?

A
  • Warm compress
  • Elevate legs
  • Oral NSAIDs 8-12 days
  • Compression stockings - if appropriate ABPI
  • LWMH prophylactic dose 30 days
138
Q

What is subclavian steal syndrome?

A

Occlusion of the subclavian artery proximal to the vertebral artery

  • when the arm is used -> blood is stolen from the posterior circulation (retrograde flow via vertebral artery) = results in decrease in cerebral blood flow

(3x more common on left side)

139
Q

When are patients with subclavian steal syndrome symptomatic?

A

Symptomatic mainly when arm is used…

  • Dizziness
  • Vertigo
  • Diplopia
  • Dysphagia, dysarthria
  • Cortical blindness
  • Collapse/Syncope
  • Arm claudication - pain or paraesthesia

YEAR 2 (8 decks)

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