The vascular system and stroke - Varicose veins, DVT and leg ulcers Flashcards
1
Q
What is the gold standard imaging modality for assessing the competence of venous valves
A
Duplex ultrasound
2
Q
a) What is a varicocele
b) Describe the presentation
c) Describe the complications
d) Describe the treatment
A
a) Enlargement of the scrotal veins
b) Often asymptomatic but may cause an ache or heavy feeling within the scrotum
c) Impaired fertility
d) If asymptomatic they require no treatment. If they are causing pain or infertility they can be treated using embolization or surgery. I
3
Q
a) What is a thrombus?
b) What is it composed of?
A
a) A thrombus is a mass of normal blood constituents formed inappropriately within the circulation
b) Composed of fibrin and platelets with entrapped red and white blood cells
4
Q
What are the 3 consequences of thrombus?
A
- May obstruct lumen of the vessel which it forms
- May form in cardiac chamber or vessel
- May break off, travel in circulation, and obstruct a vessel elsewhere - embolus/thromboembolus
5
Q
Which process is thrombosis identical to? and define that process.
A
Haemostasis - a physiological response to injury of blood vessels
6
Q
The process involved in thrombosis are identical to those involved in haemostasis. Describe the mechanisms of haemostasis.
A
- Injury to blood vessels leads to loss of the lining endothelial cells, which normally prevent haemostasis
- Exposure of underlying extracellular matrix (collagen), activates platelets forming a primary haemostatic plug
- Coagulation cascade activated
- Thrombin produced, fibrin deposited around fused platelets, producing secondary haemostatic plug
7
Q
Name the 3 main components of controlled haemostasis
A
- Endothelial cells
- Platelets
- Coagulation system
8
Q
a) What are endothelial cells?
b) List 3 properties of endothelial cells and provide 1-2 examples for each property
A
a) Normal interrupted sheet of cells with anti-thrombotic properties
b)
1. Antiplatelet properties - Prostacyclin and nitric oxide
- Anticoagulant properties - Antithrombin III and thrombomodulin-activated protein C/S
- Profibronyltic properties - tissue plasminogen activator (tPA)
9
Q
a) What are platelets produced by?
b) How is it activated?
A
a) Produced by megakarocytes
b) Activated on exposure to sub endothelial extracellular matrix
10
Q
a) What is the coagulation cascade?
b) Name the 2 pathways
c) What is the common pathway between the two pathways you mentioned above?
A
a) Cascade of protein converted from inactive pro-enzyme to active enzymes and cofactors
b)
1. Intrinsic pathway - Hageman factor (XII)
- Extrinsic pathway - tissue factor (thromboplastin)
c) Common pathway - Fibrinogen to fibrin
11
Q
Name the 3 predisposing factors for thrombus information (Virchow’s triad)
A
- Change in blood flow
- Change in vessel wall
- Change in blood constituents
12
Q
Name 5 causes of altered blood flow
A
- Narrowing caused by atherosclerosis
- Aneurysms
- Infarcted myocardium
- AF
- Abdominal cardiac rhythm
- Valvular heart disease
- Stasis
13
Q
What does the
disruption of laminar flow cause?
A
- Causes platelets to come into contact with endothelium
- Leads to injury or activation of endothelium
- Impaired removal of pro-coagulant factors/impaired delivery of anti-coagulant factors
14
Q
Name 3 causes that results in a change of vessel wall
A
- Endothelial cell injury or activation
- Coronary artery thrombosis
- myocardial infarction
15
Q
Name 5 reasons for endothelial cell injury or activation
A
- Ischaemia hypoxia
- Infection of blood vessels
- Physical e.g., atheroma, crushed veins, hypertension
- Chemical e.g., lipids, cigarette toxins
- Immunological deposition of immune complexes
16
Q
Changes in constituents of blood can be genetic or acquired
a) Provide 2 examples of genetic changes in constituents
b) Provide 5 examples of acquired changes in constituents
A
a)
1. Antithrombin II deficiency
2. Protein C
b)
1. Tissue damage
2. Pre-operative
3. Malignancy
4. Cigarette smoke
5. Elevated blood lipids
6. Oral contraceptives
17
Q
Describe the possible fate of thrombus
A
18
Q
a) What is an embolism?
b) Name the 5 types of embolism
A
a) An abnormal mass of undissolved material which is transported from one part of the circulation to another
b)
1. Thrombus
2. Gas - air, nitrogen
3. Fat
4. Tumour
5. Miscellaneous - foreign bodies (drug addicts), amniotic fluid, therapeutic
19
Q
Name 3 ways that pulmonary thromboembolism may occur
A
- Saddle embolus
- Smaller emboli in peripheral arterial tree
- Paradoxical embolus
20
Q
What is a saddle embolus?
A
Occludes both pulmonary arteries
21
Q
What is paradoxical embolus?
A
An embolus that moves through intraatrial (e.g., patent foramen) or inter ventricular cardiac defect to gain access to systemic circulation. Following this, it may lead to an arterial embolus and associated sequelae (DVT like symptoms followed by the development of ALI)
22
Q
a) Emboli can travel from the left side of heart or aorta will enter the systemic arterial system. What organs can it affect?
b) What is the consequence of this?
c) What is the consequence if the emboli is infected?
A
a) Brain, kidney, spleen, gut and legs
b) Ischaemia or infarction
c) Infected emboli may give rise pyaemia and absence formation
23
Q
Air may enter the circulation, known as an air embolus. Give 2 reasons that could lead this to
A
- During obstetric procedures
- In chest wall injury
24
Q
a) When do nitrogen embolus’ occur?
b) Describe how this occurs
c) What is this also known as and what organs can it affect?
A
a) Occurs in deep sea divers on rapid ascent
b) Occurs when nitrogen expands, bubbling out of tissues into the blood to form a painful gas emboli
c)
Decompression sickness (the bends). It can affect the skeletal muscle, brain, heart and lungs
25
What may persistent gas emboli in skeletal system lead to?
May lead to multiple foci or ischaemic necrosis in heads of femur, tibia ad humerus - Caisson disease
26
a) When may microscopic fat globules be found in the circulation?
b) Describe the presentation of fat embolism
a) After
- Fractures of long bones
- Soft tissue trauma
- Burns
b)
- Tachypnoea
- Tachycardia
- Dyspnoea
- Diffuse petechial rash in 20-50%
- Irritability and restlessness
- Thrombocytopenia
27
a) When does an amniotic fluid embolus occur?
b) Describe the presentation of amniotic fluid embolism
a) Occurs when there is infusion of amniotic fluid into maternal circulation from placental tear and rupture of uterine veins
b)
- Dyspnoea
- Cyanosis
- Hypotension
- Disseminated intravascular coagulation (IDC - a disorder which the protein that control blood clotting become overactive)
- Seizures
- Shock
28
Define 'leg ulcer'
A leg ulcer is defined as the loss of skin below the knee on the leg or foot, which takes more than 2 weeks to heal
29
Name the 4 categories of ulcers
1. Venous ulcers
2. Arterial ulcers
3. Mixed ulcers
4. Other ulcers - diabetic foot ulcers and pressure ulcers
30
Describe the epidemiology of ulcers
- More common with increasing age
- More common in females
- More common if prior ulcer
31
Name 3 diseases involved in the pathophysiology of venous ulcers
- Deep venous disease
- Superficial venous disease
- Perforator disease
32
List 6 risk factors of venous ulcers
- Obesity
- Immobility
- Varicose veins
- Previous DVTs
- Age
- Previous trauma to the leg
33
Describe the investigations for a venous ulcer
1. ABPI - assess arterial disease (as compression stockings/bandaging is contraindicated in PAD)
2. Blood tests - assess for infection and co-morbidities
3. charcoal swabs
4. Skin biopsy
34
Describe the management of venous ulcers
1. Conservative (lifestyle) - keep ulcer clean, encourage mobility, weight reduction, leg elevation at rest
2. Emollient treatment on the leg
3. Compression bandage (mainstay)
4. Pentoxifylline (if failing to respond to initial treatment)
5. Surgery - ablation of superficial incompetence (mainstay), debridement and skin grafting
35
Name 4 complication of venous ulcers
- Immobility - due to pain
- Infection and sepsis
- Osteomyelitis
- Decreased QoL
36
Name 4 complication of venous ulcers
- Immobility - due to pain
- Infection and sepsis
- Osteomyelitis
- Decreased QoL
37
Describe the pathophysiology of arterial ulcers
- Result of peripheral arterial disease (stage IV involvement is ulceration and/or gangrene)
- Atherosclerosis
- Endothelial cell injury
38
Describe the epidemiology of arterial ulcers
More common in males
39
Describe the presentation of arterial ulcers
- Tips of toes/over the toes, in-between toes, above lateral malleolus or the sides of feet or soles
- Punched out, well-defined edges
- Wound is covered with slough and necrotic tissue
- Low level of exudate
- Severe pain
- Not much oedema
- Can have gangrene
- Thin, dry, cool and hairless leg
- Thickened toenails
- No or weakened foot pulses
40
Describe investigation for arterial ulcers
- ABPI to check for PAD
- Buerger's test
- Arterial duplex scan
41
When should you refer a patient with a venous ulcer to a leg ulcer clinic or vascular specialist?
If the venous leg ulcer has not healed after 2 weeks of primary care treatment
42
Describe the management of arterial ulcers
- Urgent referral to vascular to consider surgical revascularisation
- Debridement and compression are NOT used in arterial ulcers
43
What pressure should compression bandaging/stocks be at?
40 mmHg
44
Describe the differences between venous and arterial ulcers
45
Neuropathic ulcers
a) Epidemiology
b) Risks
c) Presentation
d) Investigations
e) Management
a)
- Neuropathy presents in 50% diabetes
- Type 2 > type 1
- 15% diabetics have a neuropathic ulcer
b)
- Poor blood glucose control
- Smoking
- Anatomic foot deformity e.g., bunions, charcot
- Previous amputation
- Previous ulcer
c)
- Appear in weight-bearing/pressure areas e.g., heel, metatarsal heads, tips of toes
- Punched out
- Painless - may experience burning/tingling in legs
d)
- ABPI
- Blood glucose levels
e)
- Diabetic foot clinic
- Control of diabetes
- Manage infection/osteomyeletitis
46
What are varicose veins?
Dilated, tortuous, superficial veins that are > 2mm
47
Describe the pathophysiology of varicose veins
- The deep and superficial veins are connected by vessels called perforating veins (perforators), which allow blood to flow from the superficial veins to the deep veins
- When the valves are incompetent in the perforations, blood flows from the deep veins back into the superficial veins and causing increased venous pressure
- This leads to dilation and engorgement of the superficial veins, causing varicose veins
48
Describe chronic venous insufficiency
- When blood pools in the distal veins, the pressure causes the veins to leak small amounts of blood into the nearby tissues. The haemoglobin in this leaked blood breaks down to haemosiderin, which is deposited around the shins in the leg. This gives a brown discolouration
Pooling of blood in the distal tissues results in inflammation. The skin becomes dry and inflamed, referred to as venous eczema
The skin and soft tissue become fibrotic and tight, causing the lower legs to become narrow and hard, referred to as lipodermatosclerosis
49
Name the most widely used classification for varicose veins
CEAP
50
Describe the different stages of CEAP
51
Describe the risk factors of varicose veins/chronic venous insufficiency
- Increasing age
- Family history
- Female
- Pregnancy
- Obesity
- Prolonged standing
- DVT
52
Describe the presentation of varicose veins
- Pain/tenderness
- Itching
- Aching
- Muscle cramps
- Oedema
- Phlebitis - inflammation in vein
- Thrombophlebitis - clot in vein
- Bleeding ulceration
53
Describe the investigations for varicose veins
- Pulses
- ABPI
- Tourniquet test/tredelenburg test
- Cough impulse test
- Perthe's test
- Venous duplex ultrasound
- If prior DVT particularly iliac/femoral then magnetic resonance venography (MRV)
54
Describe the indications for patient referral to vascular injury
- Pain
- Symptomatic primary or recurrent varicose veins
- Skin changes (hyperpigmentation, lipodermatosclerosis, venous eczema) related to chronic venous insufficiency
- Superficial vein thrombosis and suspected venous incompetence
- Active/healed venous ulcer
55
Describe the management of varicose veins
1. Conservative
- Advice
- Weight loss/excercise
- Exacerbating factors e.g., Avoid prolonged standing/sitting, keep leg elevated
- Compression stockings - offered once arterial disease is excluded
2. Intervention
- Radiofrequency ablation: radiofrequency energy heats up wall of vein so that is collapsing. Vein closes and seals up and blood directed to healthy veins
- Foam scleropathy: vein injected with irritant foam causing closure of the vein
- High ligation and stripping: long saphenous vein is tied (ligated) and pulled out of leg 9stripped)
56
Venous thromboembolism compasses two conditions. Name the two conditions
Deep vein thrombosis (DVT)
Pulmonary embolism (PE)
57
a) Describe what a deep vein thrombosis
b) Describe what a pulmonary embolism is
a) Acute/chronic occlusion of deep vein(s). Commonly affects the lower limbs through the formation of a clot forms (thrombus)
b) Acute/chronic occlusion of pulmonary arteries. Occurs when a thrombus breaks off from the deep veins, through the right side of the heart and travels to the lungs (emboli). This blocks blood flow to areas of the lung.
58
Describe how a pulmonary embolism forms
Occurs when a thrombus breaks off from the deep veins, through the right side of the heart and travels to the lungs(emboli). This blocks blood flow to areas of the lung.
59
Virchow's triad or the triad of Virchow describes the three broad categories of factors that are thought to contribute to thrombosis. Name the 3 categories and provide examples
Stasis (slowing of blood flow) - heart failure, immobility
Endothelial injury - trauma, phlebitis, chemotherapy
Hypercoaguable state (aka thrombophilia is an increased tendency to develop blood clots) -
60
What scoring criteria is used to predict the risk of a patient presenting with symptoms having a DVT or PE
Wells scoring criteria
61
What Wells score is considered a low, moderate and high risk of DVT
b) Total score 0 – low risk of DVT
Total 1 or 2 – Moderate risk of DVT
Total score 3 - High risk of DVT
62
Describe the next steps if a patient has a wells score of:
a) Low/moderate score ( 2)
a)
- Proceed to d-dimer testing.
- If test is positive proceed to proximal leg vein ultrasound testing.
- If test is negative ultrasound not required, GP informed, telephone follow-up at 3 months
b)
- Straight to proximal leg vein ultrasound within 4 hours, without need for D-dimer.
- Alternatively, request D-dimer, give interim anticoagulation and arrange ultrasound within 24 hours
63
Describe the aetiology of VTE
Provoked - transient or persistent risk factors. Factor usually easily removed. Typically within three months of event
Unprovoked - no readily identifiable risk factor for VTE. Not easily correctable
64
Describe the risk factors of VTE split into major and minor risk factors
Major risk factors
- Major surgery
- Late pregnancy
- Lower limb fracture
- Malignancy
- Reduced mobility
- Previous DVT
Minor risk factors
- Congenital heart disease
- Cardiac failure
- Hypertension
- Central venous catheter
- Oral contraceptive/HRT
- Long distance sedentary travel
- Thrombotic disorders
- Obesity
- COPD
- Intravenous drug abuse
65
Describe the presentation of a DVT
- Unilateral calf or leg swelling
- Oedema
- Pain or tenderness
- Colour changes (red)
- Venous insufficiency and ulceration
- Dilated superficial veins
- Homan's sign (tenderness on passive dorsiflexion)
- Cyanosis
66
Name 5 differential diagnosis of DVT
- Cellulitis (always suspect if unilateral swelling)
- Ruptured popliteal cyst
- Muscle tear/haematoma
- Fracture
- Lymphoedema
- Hypoproteinaemia
67
Name the pain presentation of an oleo-femoral DVT
Phlegmasia - cyanosed limb or white cold pulseless limb
68
a) Describe the symptoms of a PE
b) Describe the signs of a PE
a)
- Short of breath
- Palpitations
- Pleuritic chest pain - worse on inspiration
- Cough
- Haemoptysis (coughing of blood)
- Arrhythmias
- Syncope (fainting/passing out)
- Sudden death
b)
- Classically tachypnoea, tachycardia and hypoxia is present
- May be low-grade pyrexia
- A small PE may result in a normal examination
- A massive PE may present with hypotension, cyanosis and signs of right heart strain (e.g., raised JVP, parasternal heave and loud P2)
69
Describe the investigations for a DVT and PE and the clinical findings
FBC - Hb, WCC, platelets (in PE patient may be anaemic due to haemoptysis
D-dimer - non-specific but good negative predictive value so useful in ruling out a PE if negative
Coagulation screen - may show prolonged PT
Troponin - can be raised in PE
ABG - hyperaemia, respiratory failure
ECG - sinus tachycardia, right axis deviation, ST changes (PE)
70
What is the gold standard imaging modality for a DVT
Doppler/duplex ultrasound (95% sensitive and specific to DVT)
71
Describe the imaging modalities for a PE
CT pulmonary angiography (diagnostic)
Ventiliation-perfusion (VQ) scan - nuclear medicine scan that may be utilised in pregnancy or renal impairment
Lower limb duplex - helpful if a DVT is thought to be the cause of the PE (1st line investigation before a CTPA in pregnancy)
Bedside echocardiogram - assessment of right ventricular strain/failure in patients with suspected ‘massive’ PE and to assess suitability of thrombolysis
CXR - exclude any obvious alternative pathology that may explain symptoms
72
Describe the initial management of a DVT/PE
- Anticoagulation: Apixaban or rivaroxaban should be started immediately
- If not suitable (e.g, post-operative) LMWH for 5 days then offer edoxaban/warafin
- LMWH for pregnant woman/renal dysfunction
- Consider thrombolysis if symptomatic ileofemoral DVT and significant symptoms lasting 14 days days / massive PE
- Inferor vena cava (VC) filter if cannot have anticoagulation (rarely used)
- Thrombophilia screen – protein C+S, factor V Leiden, Anti-thrombin 3, antiphospholipid, homocysteine
- Compression therapy to reduce oedema and leg elevation
73
Describe the long term management of a DVT/PE
- Provoked DVT/PE: anticoagulation with DOAC, warfarin or LMWH
- Unprovoked DVT/PE / recurrent VTE / irreversible underlying cause such as thrombophilia): anticoagulation for 6 months
- 3-6 months in active cancer (then review)
74
Describe the investigation pathway and management of a suspected DVT
75
Describe the investigation pathway for a suspected PE
76
Describe the investigation and management of an unprovoked DVT/PE
Review the medical history, baseline blood results and physical examination for an underlying cause:
- Thrombophilia tests - antiphospholipid syndrome, hereditary thrombophilias (only if they have 1st degree relative also affected by a DVT or PE)
- Cancer
77
Thromophilia are conditions that predispose patients to develop blood clots. Name 3 examples of these
- Antiphospholipid syndrome – associated with recurrent miscarriage
- Factor v leiden - most common thrombophilia
- Antithrombin deficiency
- Protein C or S deficiency
- Hyperhomocysteinaemia
- Prothombin gene variant
- Activated protein C resistance
78
What are the two broad causes of a swollen leg
Central cause
Peripheral cause
79
A painful swollen leg could be bilateral or unilateral.
State whether a central and peripheral cause leads to a bilateral/unilateral swelling
Central cause - bilateral
Peripheral cause - unilateral
80
List 8 differential diagnosis of a central cause of a painful swollen leg
Cardiac – Congestive cardiac failure (CCF), pericarditis
Renal – nephrotic syndrome
Hepatic – cirrhosis, portal hypertension
Venous – outflow obstruction
Endocrine – myxoedema (swelling of the skin and underlying tissues giving a waxy consistency, typical of patients with underactive thyroid glands)
Allergic – angio-oedema
Nutrition – hypoproteinaemia
Drugs
Obesity – lipoedema
81
List 6 differential diagnosis of a peripheral cause of a painful swollen leg
Lymphatic – filariasis, radiation, surgery, compression from tumour
Trauma – bruise, sprain, tendon rupture
Infection – cellulitis
Gout
Venous
AV malformation
Hereditary – Milroy’s disease (congenital lymphatic abnormality)
82
a) Describe the management of a painful swollen leg
b) What is the goal of management?
a)
Treat the underlying cause
- If no contraindication such a cellulitis then start compression therapy
b) To maintain a healthy skin and prevent ulceration
83
What must you look for when examining varicose veins
- surgical scars
- Venous ulcers
- medical equipments e.g., compression stockings and wound dressings
- Vital signs
- Prescriptions
- Venous eczema
- Lipodermatosclerosis
- Saphena varix - localised dilation of long saphenous vein at the saphenofemoral junction
- Arterial disease
- Varicose veins
- Oedema
84
What must feel for when examining varicose veins
- Temperature
- Palpate any visible varicosities
85
a) What is the role of the percussion (tap test)
b) Describe the percussion (tap test) for varicose veins
a) Provides a crude assessment of lower limb venous valve competency
b)
1. Place one finger, with a small amount of pressure, onto the saphenofemoral junction (SFJ) which is located 4cm inferior-lateral to the pubic tubercle.
2. Tap the varicose vein you are assessing, which should be located lower down the leg.
3.If your finger over the SFJ detects a thrill, this suggests that there is continuity of the vein due to incompetent venous valves (normally the venous valves should prevent the thrill transmitting along the entirety of the vessel).
86
a) What is the role of the cough impulse test?
b) Describe the cough impulse test for varicose veins
a) To determine if there is a saphena varix
b)
1. Place your hand over the saphenofemoral junction and ask the patient to cough.
2. If you feel an impulse over the SFJ this indicates a saphena varix (dilatation of the saphenous vein at the SFJ).
87
a) What is the role of the Perthe's test in varicose veins?
b) Describe the Perthe's test
c) Describe the interpretation
a) Perthe’s test is used to distinguish between venous valvular insufficiency in the deep, perforator and superficial venous systems.
b)
1. Apply a tourniquet at the proximal mid-thigh level whilst the patient is standing.
2. Ask the patient to walk around the room (or continually alternate between standing on tip-toes and flat feet) for 5 minutes.
c)
- If the varicose veins become less distended, it suggests that there is no deep venous valvular insufficiency, because the calf muscle is able to empty the varicose veins by pumping blood from the superficial venous system to the deep venous system. This result would suggest there is a primary problem with the superficial veins.
- If the varicose veins remain distended (or become more distended) it suggests there is also a problem with the deep venous system, preventing the drainage of blood from the superficial varicose veins. In this circumstance, the patient may also experience pain in the leg due to venous hypertension.
88
a) What is the role of the troedelenburg (tourniquet) test in varicose veins
b) Describe the troedelenburg (tourniquet) test
a) Identifies main site of reflux
b)
1. Position the patient lying flat on the examination couch.
2. Lift the patient’s leg up (as far as the patient is comfortable with) and empty the superficial veins by milking the leg towards the groin (SFJ).
3. Place a tourniquet over the saphenofemoral junction (SFJ)
4. Ask the patient to stand and observe for filling of the veins:
- At this point, if the veins have not filled and remain collapsed, it indicates the incompetent venous valve(s) was/were at the level of the SFJ.
- If the veins have filled up again, it indicates the incompetent valve(s) is/are inferior to the SFJ (i.e. perforator veins – veins that drain venous blood from superficial to deep veins within the muscle).
5. Repeat the test with the patient lying down, placing the tourniquet 3cm lower than the previous position.
6. Ask the patient to stand and observe venous filling once again.
7. Repeat this sequence until filling stops and the location of the incompetent venous valves is localised.
89
Describe handheld doppler scanning for varicose veins and its interpretation
1. Place a doppler at saphenofemoral junction and squeeze calf. A whooshing side will be heard
2. When the calf is let go no sound should be heard
3. However, if there is a second backward whooshing sound then this is a sign of fluxing of the deep vein back into the superficial long saphenous vein. This indicates there is incompetence of the saphenofemoral junction
90
a) What is a d-dimer?
b) What does the absence signify?
c) What is the advantage of using a d-dimer to test for a DVT/PE?
a)
Degradation products of cross-linked fibrin. It is released when the fibrinolytic system attacks the fibrin matrix of fresh venous thromboemboli.
b) Absence of a raised concentration of D-dimer implies that there is no fresh thromboembolic material undergoing dissolution in the deep veins/pulmonary arterial tree.
c) Has a high negative predictive value in those with low clinical probability
91
In patients with recurrence of a VTE on warfarin. What should the target INR be increased from and to?
Increased from 2-3 INR to 3-5
92
Describe the management of patients with thrombophilia
Anti-coagualation for life
93
a) What are the signs of a massive PE?
b) What is the emergency management of patient with a massive PE?
a) Tachycardia, low BP (<60/90), right heart strain (raised JVP, parasternal heave, loud P2) - haemodynamically unstable as in shock
b) Thrombolysis (IV alteplase)
94
Why is a D-dimer test not useful in a pregnant women?
D-dimer is usually elevated in pregnancy
95
a) How long are patients with a provoked PE treat with an anticoagulant for?
b) How long are patients with a provoke PE treated with an anticoagulant for?
a) 3 months (as provoking factor would of been resolved by then)
b) Up to 6 months
96
What is the management for massive DVTs
Percutaneous mechanical thrombectomy
97
How long should patients with active cancer with a DVT be anti-coagulated for?
3-6 months
98
How long should patients with a recurrent DVT be anti-coagulated for?
Consider life-long therapy
99
What are the clinical features of a PE that is:
a) Non-massive
b) Sub-massive
c) Massive
a) Non-massive: haemodynamically stable and no evidence of right heart strain
b) Sub-massive: haemodynamically stable, but evidence of right heart strain on imaging (e.g. CT, ECHO) or biochemistry (e.g. elevated troponin)
c) Massive: haemodynamic instability. Defined as persistently low BP (< 90 mmHg or fall > 40 mmHg) for > 15 minutes or hypotension that requires inotropic support not explained by another cause.
100
What are the signs of a right heart failure in PE?
- Hypotension (BP < 90 mmHg or drop > 40 mmHg)
- Elevated JVP
- Tricuspid regurgitation (pansystolic murmur)
- Split second heart sound: elevated pulmonary pressure leads to delay in pulmonary valve closure.
101
Describe the signs on an ECG that indicates a PE
Common: sinus tachycardia, non-specific ST or T wave abnormalities
Classical: S1Q3T3 pattern (deep S wave V1, Q wave in V3 and T wave inversion in V3)
Right heart strain: right bundle branch block, ST depression and T wave inversion anteriorly (V1-V4) and/or inferiorly (II, III, aVF)
Alternative diagnosis (e.g. acute coronary syndrome)
102
After excluding contraindications to thrombolysis, what are the indications of a patient with a PE?
Cardiac arrest with confirmed or suspected PE
Confirmed PE with deterioration despite anticoagulation (i.e. worsening right ventricular strain, increasing oxygen requirements)
Haemodynamic instability (BP < 90 mmHg for > 15 minutes), AND
High clinical suspicious of PE
Confirmed PE within 14 days
103
Describe and diagnose this ulcer
Venous ulcer
- Medial gaiter area
- Small, shallow
- Mix of slough and granulation in base
- Surrounding haemosiderin staining
104
Describe and diagnose this ulcer
Neuropathic/neuroischaemic ulcer
- Plantar over metatarsal heads
- Deep, probes to bone
- Punched out
105
- 25 years male
- Small ulcer right medial malleolus
- No PMH
- Varicose LSV
- Palpable foot pulses
a) What is the likely cause of this ulcer?
b) What investigations would you request?
a) Venous ulcer due to superficial venous insufficiency
b) ABPI and venous duplex scan
106
- 60 years male
- Painful ulcer on right shin
- PMH HTN
- Smoker
- Absent popliteal and foot pulses
a) What is the likely cause of this ulcer?
b) What investigations would you request?
a) Arterial ulcer
b) ABPI and arterial duplex scan or CT angiogram
107
- 85 years lady
- Painful ulcer in left medial gaiter area
- PMH CKD
- Swollen leg
- Varicose veins
- Absent popliteal and foot pulses
Questions
a) What is the likely cause of this ulcer?
b) What investigations would you request?
a) Mixed arterial and venous ulcer
b) ABPI, arterial and venous duplex scans
108
- 25 years male
- Small ulcer right medial malleolus
- No PMH
- Varicose LSV
- Palpable foot pulses
- ABPI=1.1
- Venous duplex scan shows incompetent Saphenofemoral junction and long saphenous vein with normal deep veins
a) How would you treat this ulcer?
- Venous ulcer
- Full compression bandage
- Long saphenous vein radiofrequency ablation
109
- 35 years male
- Painless plantar ulcer over - 1st MTPJ
- PMH T1DM
- Absent foot pulses
- Reduced sensation
- ABPI=1.4
- MRA shows multifocal stenoses of anterior and posterior tibial arteries
How would you treat this ulcer?
- Neuropathic ulcer
- Pressure offloading
- Tibial angioplasty or popliteal-pedal bypass surgery
110
- 60 years male
- Painful ulcer on right shin
- PMH HTN
- Smoker
- Absent popliteal and foot pulses
- ABPI=0.3
- CTA shows long superficial femoral artery occlusion with two vessel run-off
How would you treat this ulcer?
Superficial femoral artery angioplasty +/- stenting or femoro-popliteal bypass surgery
