Brainscape's Knowledge GenomeTM

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


See full index

2a Conditions- Cardio > Vascular Diseaese: Embolisms, PVD, DVT > Flashcards

Vascular Diseaese: Embolisms, PVD, DVT Flashcards

1
Q

What is an pulmonary embolism?

A

Pulmonary embolism (PE) refers to obstruction of the pulmonary vasculature, secondary to an embolus.

Pulmonary embolism is a consequence of thrombus formation within a deep vein of the body, most frequently in the lower extremities.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the epidemiology of a PE?

A
  • ## There were 47,594 cases of PE between 2013 and 2014 in the UK
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the aetiology of a PE?

A

Virchow’s triad causing clots:

  • Hypercoagulability: cancer, surgery (activates clotting cascade), oestrogen (pregnancy, contraceptive pill, HRT), nephrotic syndrome, sepsis, thrombophilia (factor V leiden mutation, protein C and S deficiency, antiphospholipid antibody syndrome)
  • Venous stasis: recent surgery, DVT, immobility (long-haul travel/ hospitilisation), >60 yrs of age, obesity, other co-morbidities e.g. heart failure
  • Endothelial damage: lower limb trauma, previous VTE, venous surgery, infections, toxins e.g smoking
  • Rarer causes:
    • Right ventricular thrombus (post-MI)
    • Septic emboli (right-sided endocarditis - bacterial vegetation)
    • Fat embolism (due to long bone fracture)
    • Air embolism
    • Amniotic fluid embolism
    • Neoplastic cells
    • Parasites
    • Foreign material during IV drug misuse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the main aetiology of PE?

A

Virchow’s triad is the main aetiological model for venous thromboembolism.

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

What is the pathophysiology of

A
  • Clots usually form in the deep venous system of the lower extremities and embolise.
  • The pathophysiology is therefore directly related to that of deep vein thrombosis (DVT).
  • DVT in the upper extremities is associated with a lower incidence of PE.
  • PE occurs when a thrombus dislodges and becomes trapped in the pulmonary vasculature.
  • This obstruction increases pulmonary vascular resistance (PVR), increasing the work of the right ventricle.
  • The right ventricle compensates by increasing heart rate using the Frank-Starling preload reserve via dilation.
  • Further increases in PVR overcome the right ventricular (RV) compensatory mechanisms, leading to over-distension of the right ventricle, increased RV end-diastolic pressure, and decreased RV cardiac output.
  • Decreased RV output leads to decreased left ventricular (LV) preload.
  • As left ventricle filling and cardiac output decrease, lowered mean arterial pressure progresses to hypotension and shock.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Missed detailed pathophysiology

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the symptoms of PE?

A

Only asmall minority of patients (approximately 10%) present with the characteristic features of pleuritic chest pain, dyspnoea and haemoptysis.

In fact, a pulmonary embolism can be very difficult to diagnose and can present with an array of different cardiorespiratory features.

  • Pleuritic chest pain
  • Dyspnoea
  • Syncope: a red flag symptom
  • Cough +/- haemoptysis
  • Fever
  • Fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the signs of PE?

A
  • Hypoxaemia (Lower than normal arterial blood oxygen level)
  • Hypoxia (hypoxia refers to low levels of oxygen in the tissues of your body)
    • Cyanosis may be present
  • Hypotension: SBP <90 mmHg suggests a massive PE
  • Syncope
  • Tachypnoea and tachycardia
  • Deep vein thrombosis: swollen, tender calf
  • Pyrexia may be present
  • Crackles
  • Elevated JVP: suggests cor pulmonale
  • Right parasternal heave: suggests right ventricular strain

The PERC scoreuses some of these data to assist clinicians in ruling out a PE.

Below are the relative frequencies of themost common clinical featuresassociated with a pulmonary embolism:

  • Tachypnoea(RR >16/minute): 96%
  • Crackles: 58%
  • Tachycardia(HR >100): 44%
  • Fever(temp >37.8°C): 43%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the wells score?

A

Wells Two-Level score, in conjunction with clinical judgement, is utilised to determine the probability of PE.

> 4: high probability of PE

≤ 4: low probability of PE

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

What are the clinical features of the wells score?

A

Clinical signs and symptoms of a DVT - 3.0
PE is the number 1 diagnosis or equally likely - 3.0
Tachycardia (>100BPM) - 1.5
Immobilisation for more than three days or surgery in the previous four weeks -1.5
Previous, objectively diagnosed PE or DVT - 1.5
Haemoptysis
Malignancy with treatment within the last 6 months, or palliative

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

What are the primary investigations for PE?

A
  • CXR:performed to rule out alternative pathology. It is typically normal in a PE, although a wedge-shaped opacification may be seen
  • Computed tomographic pulmonary angiography (CTPA)
    • Highlights the pulmonary arteries to demonstrate any blood clots.
    • CTPAperformed if high probability (Wells score > 4)
    • If there is a delay in CTPA, anticoagulate patients until the scan is performed
  • D-dimer:detect fibrin breakdown products
    • D-dimerperformed if low probability (Wells score ≤ 4); has ahigh sensitivity(95-98%) butpoor specificity
  • ECG
    • Sinus tachycardiais the most common finding
    • RBBBandright axis deviationsuggest right heart strain
    • S1Q3T3: large S wave in lead I; large Q wave in lead III; inverted T-wave in lead III (a classic finding but only in 20% of patients)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are other investigations for PE?

A
  • ABG:to quantify the degree of hypoxaemia; Also respiratory alkalosis if there is hyperventilation that gets rid of CO2. Not performed in all patients.
  • V/Q scan: involves using radioactive isotopes and a gamma camera to reveal areas of the lung that are ventilated but not perfused.
    • Done in patients allergic to contrast, with severe renal impairment and also considered in pregnancy
  • Pulmonary angiography:gold-standardbut more invasive and has higher complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the investigations for cancer (PE)?

A
  • All patients:all patients with an unprovoked PE should be examined and have a full set of blood tests
  • Most recent guidance suggests that patientsdo not need further investigationunless they have signs or symptoms of cancer. This is in contrast to previous guidance which advised CT imaging in those above 40 years of age.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are investigations for thrombophilia?

A
  • Antiphospholipid antibodies:considered in people who have an unprovoked DVT and where there is a plan to stop anticoagulation
  • Thrombophilia screen:considered in people who have an unprovoked DVT anda first-degree relative who has had DVT and there is a plan to stop anticoagulation
  • Aprovoked PEis associated with a transient risk factor within theprevious 3 months, such as significant immobility, surgery, trauma or pregnancy.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the algorithm for investigating a PE?

A

Full blood count

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the managements for a massive PE?

A
  • Thrombolysis e.g. alteplase: injecting a fibrinolytic medication that rapidly dissolves clots.
    • Offer to patients with a suspected massive PE as evidenced by haemodynamic instability (e.g. SBP < 90 mmHg).

Can be done:

  • Intravenouslyusing a peripheral cannula.
  • Directly into thepulmonary arteriesusing a central catheter.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the management for non-massive PE?

A

Anticoagulation:

  • Provoked:consider stopping anticoagulation at 3 months
  • Unprovoked:consider continuing anticoagulationbeyond3 months.
  • Interim anticoagulation: if a PE islikely(Well’s score >4) and investigations cannot be performed immediately, offer interim anticoagulation; if a PE isunlikely(Well’s score ≤4) and a D-dimer cannot be obtained within 4 hours, offer interim anticoagulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the anticoagulation options?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the alternative treatments for PE?

A
  • Inferior vena cava filter:to stop clots from potentially moving into the heart and then the lungs
    • Consider in patients with recurrent PEs despite anticoagulation, or if anticoagulation is contraindicated
  • Surgical embolectomy:performed if thrombolysis is contraindicated or has failed
    • Percutaneous catheter-directed thrombolysisis an alternative
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the prevention for PE?

A
  • Compression stockings
  • Frequent calf exercises during long periods of sitting still
  • Prophylactic treatment with low molecular weight heparin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the supportive management for PE?

A
  • Supportive management
    • Admission to hospital
    • Oxygen, as required
    • Analgesia, if required
    • Adequate monitoring for any deterioration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the complications for PE?

A
  • Cor pulmonale
    • Pulmonary vasculature obstruction can lead to pulmonary hypertension with subsequent right heart strain
  • Pulmonary infarction
    • Obstruction of the pulmonary vasculature can result in tissue necrosis
  • Heparin-associated thrombocytopaenia:a side-effect of heparin therapy
  • Cardiac arrest
  • Acute bleeding during treatment
  • Sudden death
    • If a large pulmonary thromboembolism happens at the pulmonary saddle, then it blocks blood from going to both lungs and can cause sudden death
  • Respiratory alkalosis
    • Hyperventilation as a response to the embolism causes rapid release of CO2 which can make the blood more alkali
  • Embolic stroke
    • If patient has an atrial septal defect, embolus may enter left atrium and then left ventricle and travel to other parts of the body, including the brain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the risk factors for PE?

A
  • Increasing age
  • Diagnosis of deep vein thrombosis (DVT)
  • Obesity
  • Surgery within the last 2 months
  • Significant immobility: hospitalisation
  • Active cancer
  • Pregnancy
  • Lower limb trauma
  • Previous venous thromboembolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the prognosis for PE?

A
  • Less than 5 to 10% of symptomatic pulmonary embolisms are fatal within the first hour of symptoms.
  • Hemodynamically stable patients have a lower mortality rate compared to those who present with cardiorespiratory arrest, which is associated with a very poor prognosis.
  • Ultimately, the overall mortality at 3 months for an acute pulmonary embolisms is 17%.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Why is a CTPA / V/Q offered?

A
  • CTPA vs. V/Q scanAs per NICE, for a patient with a suspected PE:
    • Offer aCTPAimmediately if possibleOR
    • V/Q SPECT scan: should be considered forpeople with anallergyto contrast media, severerenal impairment(creatinine clearance <30 ml/min) or are at a high risk fromirradiationOR
    • V/Q planar scan: used if a V/Q SPECT scan is not available, as an alternative to a CTPA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is Peripheral Vascular Disease?

A

Peripheral vascular disease is a large umbrella term that describes a large number of circulatory diseases. It is a slow and progressive circulation disorder.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Which part of the body is most commonly affected by PVD?

A

The legs

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

Which arteries are affected in PVD?

A
  • Which artery is affected?
    • If there is hip or buttocks painThe aorta or iliac arteries.
    • The thighThe common femoral artery
    • The upper 2/3rd of the calfThe superior femoral artery
    • The lower 2/3rd of the calfThe popliteal artery
    • The footThe tibial or peroneal artery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the four stages of chronic limb ischaemia?

A
  • Stage 1 - Asymptomatic
  • Stage 2 - Intermittent claudication
  • Stage 3 - Rest pain / Nocturnal pain
  • Stage 4 - Necrosis / gangrene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Define peripheral arterial disease?

A

Peripheral arterial disease (PAD) is a major circulatory disorder characterised by arterial obstruction, leading to reduced blood supply and ischaemia in the lower limbs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the epidemiology for PAD?

A
  • PAD affects around 13% of the Western population aged over 50 years old
  • 60% of patients have co-existing ischaemic heart disease
  • M>F
  • Prevalence increases with advancing age
  • Commonly caused by atherosclerosis and usually affects the aorta-iliac and infra-inguinal arteries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the aetiology for peripheral arterial disease?

A

The arterial obstruction, mainly due to atherosclerosis and thrombosis

  • Blockage - atherosclerosis
  • Narrowing,blockage, or spasms in a blood vessel can also cause peripheral vascular disease
  • Injury to the arms or legs
  • Irregular anatomy of muscles or ligaments
  • Infection
33
Q

What is the pathophysiology for PAD?

A
  • Atherosclerotic plaque builds up slowly on the inside of arteries.
  • The arteries compensate for the plaque buildup by dilating to preserve flow through the vessel.
  • Eventually, the artery cannot dilate any further, and the atherosclerotic plaque starts to narrow the arterial flow lumen.
  • Emboli
    • In some cases, the cause of sudden ischemia may be emboli either of cardiac origin or from atherosclerotic disease of the aorta.
    • Emboli tend to be most common at sites of arterial bifurcation or where vessel branches have an abrupt takeoff.
    • The femoral artery is the most common site for emboli, followed by the iliac arteries, aorta and the popliteal arteries.
  • When the plaque ruptures, this results in thrombosis that obliterates the vascular lumen, triggering the acute syndrome.
  • However, because new-formed collateral circulation has often taken place prior to the rupture of the plaque, acute ischemia is tolerated better than when the underlying cause of the acute ischemia is of embolic origin.
34
Q

What is the Fontaine classification of PAD?

A

Stage - symptoms - signs

1 asymptomatic - low ABPI (<0.90) or lack of palpable pulse
2 intermittent claudication
3 critical limb ischaemia
4 tissue loss; ulceration of gangrene

35
Q

What does it mean to be asymptomatic?

A

symptoms may be masked by a inability to wake (e.g. severe heart failure) or due to pain insensitivity (e.g. diabetic neuropathy)

36
Q

What are the symptoms of intermittent claudication?

A

Aching or burning in the muscles of the leg:
Stage 2A: after more than 200m of walking
Stage 2b: after less than 200m of walking
Relieved within minutes on rest
Never present at rest

37
Q

What are the symptoms of critical limb ischaemia?

A

Rest pain
Dangling leg over the edge of the bed for pain relief (night pain)
Imminent risk of limb loss

38
Q

What do you examine for in stage 2,3,4?

A
  • temperature differences
    Skin changes e.g.g ulceration
    Thin shiny skin
    Skin discoloration
    Tissue loss on the heel or between the toes
    Hair loss
    Bruits: aortic, femoral, carotid

Beuerger’s test:
Lie the patient flat
Elevate the leg to 45 for 1 minute
A positive test suggests PAD: elevation pallor and reactive hyperaemia

39
Q

What does the site of claudication imply?

A

Implies site of disease

  • Common iliac:unilateral buttock
  • Common femoral:unilateral thigh
  • Superficial femoral:unilateral calf
  • Aortoiliac (Leriche syndrome)may cause the triad of:
    • Bilateral buttock and thigh claudication
    • Absent or decreased femoral pulses
    • Erectile dysfunction
40
Q

What are the features of an arterial ulcer?

A
  • Site: lower legs and tops of feet or toes
  • Symmetrical shape, well-defined borders, ‘punched-out appearance’
  • Painful, particularly at night
  • Minimal bleeding when touched or knocked
41
Q

What are the symptoms and signs of PAD?

A
  • Symptoms
    • Cramping pain in calves, thighs and buttocks when walking
    • Pain relieved by rest.
  • Signs
    • Absent pulses
    • Punched out ulcers
    • Postural colour changes
      • Buerger’s test - foot turns white when elevated, red when lowered
    • 6 P’s of limb ischaemia
      • Pain
      • Pallor
      • Pulseless
      • Perishing cold
      • Paraesthesia
      • Paralysis
42
Q

What are the 1st investigations to order for PAD?

A
  • Ankle brachial pressure index (ABPI)Record systolic blood pressure with an appropriately sized cuff in both arms and in the posterior tibial, dorsalis pedis, and, where possible, peroneal arteries; always interpretin the context of signs and symptoms
    • Normal is 1 - 1.2
    • Peripheral arterial disease is 0.5-0.9
    • ABPI interpretation
  • Colour duplex USSDuplex ultrasound:first-line imaging, offering some information on the location and severity of stenosis.
    • Quick and non invasive
    • Can show vessels and blood flow within them
  • Assessment of cardiovascular risk factors: ECG, FBC, U&E, random glucose or HbA1c, serum cholesterol and lipid profiles

History and examination, assessment of risk factors, family history of thrombosis and impact of symptoms on work, daily living, and socialising

43
Q

What are the other investigations for PAD?

A

Other investigations:

  • Exercise ABPI: for people in whom the diagnosis is uncertain on the basis of resting ABPI (e.g. normal resting ABPI despite exertional claudication)
  • Computed tomography angiography: vital if surgical management is being planned as it is more accurate than ultrasound in determining the precise anatomy and degree of stenosis
    • To identify stenosis and quality of vessels
  • Magnetic resonance angiography:performed**as an alternative to CT angiogram if it is contraindicated, e.g. in pregnant women or those in mild to moderate chronic kidney disease
    • To identify stenosis and quality of vessels
  • Auscultation bruit
    • Bruits are blowing vascular sounds resembling heart murmurs.
44
Q

What are management for PAD grouped into?

A

Exercise programs
Risk factor modification
Medications
Surgical intervention

45
Q

What are some exercise programs for management of PAD?

A
  • Can be supervised or unsupervised exercise programme
    • Supervised exercise programme: first-line and should be offered to all patients with PAD. Defined by NICE as ‘community-based exercise including hospital or gym-based exercise programmes supervised by healthcare professionals.’ 2 hours per week for up to 3 months
    • Unsupervised exercise training: offered when supervised programme not available. 30 minutes three to five times a week
46
Q

What are the risk factor modifications for management of PAD?

A
  • Risk factor modificationAims to reduce risk of death from myocardial infarction or stroke and relieve symptoms
    • Smoking cessation therapy: excess cardiovascular risk halved within one year of cessation; the risk is the same as for a non-smoker within 5 years of quitting
      • Quit smoking
    • Blood pressure control:target <140/90 mmHg
      • Treat hypertension
    • Lipid modification
      • NICE recommends secondary prevention therapy with atorvastatin 80mg OD
      • Lower cholesterol
    • HbA1c control:target <48 mmol/mol
      • improve diabetes
    • Diet and weight management
      • Improve diet
    • Management of cardiovascular risk factors: smoking cessation, HbA1c control, BP control, diet and weight management, lipid modification (statins), antiplatelet agents (e.g. clopidogrel)
47
Q

What are the medication managements for PAD?

A
  • Medications
    • Antiplatelet therapy
      • Clopidogrel 75mg: first-line antiplatelet therapy and has been found to be better than aspirin for the prevention of cardiovascular complications
    • Lipid modification
      • NICE recommends secondary prevention therapy with atorvastatin 80mg OD
    • Consideration of naftidrofuryl oxalate: vasodilator
      • If supervised exercise has not led to satisfactory improvement,andthe patient prefers not to be referred for consideration of angioplasty or bypass surgery.
48
Q

What is the surgical intervention options for management for PAD?

A
  • Surgical interventionReferral to a vascular surgeon is required if quality of life does not improve after a 3-month course of supervised exercise therapyPercutaneous transluminal angioplasty or surgery if severely stenosed.
    • Surgical intervention:
      • Referral to a vascular surgeon is required if quality of life does not improve after a 3-month course of supervised exercise therapy
      • Endovascular procedurese.g. balloon dilatation (angioplasty), stents, and atherectomy
        • Performed on lesions that are deemed to be haemodynamically significant and stenosis has a reasonable likelihood of limiting perfusion to the distal limb
        • Long term patency is greater in the aortoiliac than femoropopliteal segment
      • Bypass surgery: diverts blood around blocked artery
        • Superficial femoral and proximal popliteal arteries are the most common anatomical sites of stenosis or occlusion
        • Femoral-popliteal bypassis one of the most common bypass procedures
49
Q

What are the complications of PAD?

A
  • Critical limb ischaemia and acute limb ischaemia
  • Ulceration and gangrene
  • Infection and poor tissue healing
    • Poor wound healing
  • Amputation (loss of a limb)
  • Multiorgan dysfunction may occur, especially in people with acute limb ischaemia
  • Restricted mobility due to pain or discomfort
  • Severe pain in the affected extremity
  • Stroke (3 times more likely in people with PVD)
50
Q

What are the modifiable risk factors of PVD?

A

Risk factors that may be changed or treated include:

  • Smoking
    • Thesingle greatest risk factorand is thought to confer more than a 4-fold increased risk of PAD
    • Smoking or use of tobacco products
  • Diabetes Mellitus
  • Hypertension
    • Associated with 3x increased risk of PAD
  • Hypercholesterolaemia
    • Dyslipidemia (An abnormal level of cholesterol and other lipids)
  • Overweight and physical inactivity
  • Coronary artery disease
51
Q

What are the non-modifiable risk factors for PVD?

A

Risk factors that you can’t change:

  • Advancing Age (especially older than age 50)
    • PAD affects 1% of people in their 40s, compared to 15% of those over 70 years old
  • Male gender
    • Men are affected at a younger age than women
  • Chronic kidney disease
  • High serum homocysteine
  • History of heart disease
  • Postmenopausal women
  • Family history of high cholesterol, high blood pressure, or peripheral vascular disease
52
Q

What is the prognosis for PVD?

A
  • The course of peripheral arterial disease is not always predictable. It can progress gradually or suddenly.
  • Over a 5-year-period, patients withintermittent claudicationoften continue to have stable symptoms, whilst 10-20% develop worsening symptoms and 5-10% develop critical limb ischaemia.
  • Amputation is eventually required in 1-2% of these patients.
  • Critical limb ischaemia carries a high risk of amputation and premature death.
  • Most patients with peripheral arterial disease also have atherosclerotic disease affecting the brain or heart and are three times more likely to die of cardiovascular causes.
53
Q

What is DVT?

A

A deep vein thrombosis (DVT) is the formation of a blood clot in the deep veins of the leg or pelvis (as opposed to the superficial veins).

  • What is it?Deep vein thrombosis (DVT) is a blood clot that develops within a deep vein in the body, usually in the lower leg.
54
Q

What is the epidemiology of deep vein thrombosis?

A
  • DVT is a very common medical condition, with the incidence increasing with age.
  • 65% of below-knee DVTs are asymptomatic and these rarely embolise to the lung
55
Q

What is the aetiology for DVT?

A

Venous thrombosis causes

  • Circumstantial (immobility)
    • Surgery
    • Immobilisation
      • Hospitalisation / bed bound
    • Long haul flights
  • Genetic
    • Factor V Leiden
    • Antithrombin deficiency
  • Acquired
    • Antiphospholipid syndrome
    • Lupus anticoagulant
  • Virchow’s triad: hypercoagulability, venous stasis, endothelial damage
56
Q

How is virchow’s triad a venous thrombosis cause?

A

Aetiology image

57
Q

What is the pathophysiology of DVT?

A

Factors that leads to DVT are: VIRCHOW’s triad

  1. slowed blood flow (stasis)
  2. hypercoagulation (altered amount of clotting factors, during surgery damage to the vessels, medications such as birth control pills)
  3. damage to blood vessels lining —> could be because of infections, chronic inflammation, or toxins eg cigarettes

Most blood clots that develop in the deep venous system of the leg begin to form just above and behind a venous valve.

Once a thrombus has developed, it can travel (embolise) from the deep veins, through the right side of the heart and into the lungs, where it becomes lodged in the pulmonary arteries. This blocks blood flow to areas of the lungs and is called a pulmonary embolism (PE).

If the patient has a hole in their heart (for example, an atrial septal defect), the blood clot can pass through to the left side of the heart and into the systemic circulation. If it travels to the brain, it can cause a large stroke.

58
Q

what are the symptoms of DVT?

A
  • Symptoms
    • Unilateral calf pain,
    • Redness
    • Swelling
59
Q

What are the signs of DVT?

A

DVTs are almost always unilateral. Bilateral DVT is rare and bilateral symptoms are more likely due to an alternative diagnosis such as chronic venous insufficiency or heart failure.

  • Unilateral swelling
  • Oedema
  • Calf or leg swelling
  • Distention (Dilated) of superficial veins
  • Tenderness to the calf (particularly over the site of the deep veins)
  • Erythematous
    • Colour changes to the leg
  • Phlegmasia cerulea dolens: occurs in a massive DVT, resulting in obstruction of venous and arterial outflow (rare). This leads to ischaemia and a blue and painful leg
60
Q

What does the wells score do?

A

The Wells score calculates the risk of DVT and determines how the patient is investigated and managed. Those with a score ≥ 2 are deemed high risk.

61
Q

What are the clinical features of the wells score for DVT?

A
62
Q

What are the investigations of DVT dependent on?

A

Examination: measure the circumference of the calf 10cm below the tibial tuberosity. More than 3cm difference between calves is significant.

The investigation and management of a DVT depend on the patient’s Wells score:

63
Q

What are the investigations and management id DVT is likely and unlikely?

A
  • DVT likely: Wells score ≥ 2Duplex ultrasound of leg within 4 hours: this is diagnostic (offer a D-dimer if the scan is negative); if an ultrasound is not possible to arrange within 4 hours:
    • Perform a D-dimerAND
    • Offer interim anticoagulation for 24 hours (ideally in a form that can be easily continued)AND
    • Arrange the ultrasound for the following day
  • DVT unlikely: Wells score ≤ 1D-Dimer with a result available within 4 hours: if D-Dimer results cannot be obtained within 4 hours, offer interim anticoagulation until the result is available
    • If D-Dimer is raised: perform a duplex ultrasound within 4 hours
    • If D-Dimer is normal: a DVT is unlikely and alternative diagnoses should be consideredD-dimer is sensitive not specific
64
Q

What are the investigations for a positive D-dimer test result and negative proximal leg vein ultrasound scan?

A
  • Positive D-dimer test result and negative proximal leg vein ultrasound scan
    • Stopinterim therapeutic anticoagulation
    • Offer arepeat proximal leg vein ultrasound scan 6 to 8 days later
      • Ifpositive: continue or startanticoagulation
      • Ifnegative:stopanticoagulation and think about alternative diagnoses
  • Negative proximal leg vein ultrasound scan and a negative D-dimer test result:
    • Stopinterim therapeutic anticoagulation think about alternative diagnoses
65
Q

What blood tests do you do when starting interim anticoagulation?

A
  • Blood tests when starting interim anticoagulation
    • Baseline bloods tests: FBC, U&Es, LFTs, PT and APTT
    • Donotwait for the results of baseline bloods before starting anticoagulation
    • Review and, if necessary act on, baseline blood results within 24 hours of starting interim anticoagulation
66
Q

What are the investigations for cancer?

A
  • All patients:all patients with an unprovoked DVT should have a full history, be examined and have blood tests (FBC, U&Es, LFTs, PT and APTT)
  • Patientsdo not need further investigationunless they have signs or symptoms of cancer
67
Q

What are the investigations for thrombophilia?

A

Donottest if the patient is on lifelong anticoagulation

  • Antiphospholipid antibodies:considered in people who have an unprovoked DVTandwhere there is a plan to stop anticoagulation
  • Thrombophilia screen:considered in people who have an unprovoked DVTanda first-degree relative who has had DVTandwhere there is a plan to stop anticoagulation
68
Q

What are other investigations for DVT?

A
  • D-dimer: normal excludes diagnosis
    • Positive does not confirm diagnosis – surgery/ pregnancy/ infection can provide positive D-dimer (useless for inpatients in hospital)
  • Ultrasound compression test proximal veins
  • Venogram for calf, recurrence, uncertain
69
Q

What is the management for DVT?

A

Once a DVT is confirmed on ultrasound, the patient requires long term anticoagulation.

70
Q

What is the management for no renal impairement for DVT ?

A
  • No renal impairment
    • Offer apixaban or rivaroxaban
    • If neither suitable, offerone of:
      • LMWH for at least 5 days followed by dabigatranoredoxaban
      • LMWH and warfarin for at least 5 days (or INR stable at 2.0), then warfarin alone
    • Offer anticoagulation treatmentfor at least 3 months to people with confirmed proximal DVT or PE
71
Q

What is the management for renal impairement for DVT?

A
  • Renal impairment (estimated creatinine clearance <15 ml/min)
    • Offerone of:
      • LMWH
      • Unfractionated heparin (UFH)
      • LMWHorUFH and warfarin for at least 5 days (or INR stable at 2.0), then warfarin alone
    • Offer anticoagulation treatmentfor at least 3 months to people with confirmed proximal DVT or PE
72
Q

What is the management for active cancer DVT?

A
  • Active cancer (receiving treatment, diagnosed in past 6 months, recurrent, metastatic or inoperable)
    • Consider a DOAC (e.g. rivaroxaban)
    • Offer anticoagulation for 3 to 6 months, taking into account tumour site, drugs and bleeding risk
    • If a DOAC is not suitable, considerone of:
      • LMWH
      • LMWH and warfarin for at least 5 days (or INR stable at 2.0), then warfarin alone
    • Offer anticoagulationfor 3 to 6 months, taking into account tumour site, drugs and bleeding risk
73
Q

What are the treatments for DVT?

A

DVT treatment

  • Oral warfarin
  • LMW (low molecular weight) heparin
  • DOAC (direct oral anticoagulant)
  • Compression stockings
  • Treat underlying cause – malignancy, thrombophilia
  • Other
    • Inferior vena cava filters: devices inserted into the inferior vena cava designed to filter the blood and catch any blood clots traveling from the venous system towards the heart and lungs.
74
Q

What is the prevention for DVT?

A
  • Compression stockings
  • Frequent calf exercises during long periods of immobilisation
  • Prophylactic anticoagulation with LMW heparin (LMWH) e.g. in patients who have had surgery and will be immobilised for a long period of time
  • Mechanical – hydration and early mobilisation, compression stockings, foot pumps
75
Q

What are the complications for DVT?

A
  • Pulmonary embolism:increased pressure in the vein can cause a part of the main clot to break free.
    • Therefore, there is a risk of an embolism to the lungs.
    • A significant proportion of pulmonary emboli arise from a DVT
      • Pulmonary embolism can be diagnosed with a CT pulmonary angiogram or ventilation–perfusion (VQ) scan.
  • Post-thrombotic syndrome:this is a long term complication caused by chronic obstruction of venous blood, leading to venous hypertension, with pain, swelling, and ulceration
  • Increased risk of bleeding:patients on anticoagulation are at risk of bleeding
  • Phlegmasia cerulea dolens: occurs in a massive DVT, resulting in obstruction of venousandarterial outflow (rare). This leads toperipheral limb ischaemiaand a blue and painful leg
  • Embolic stroke: in patients with an atrial septal defect, the clot may travel to the left atria and then the left ventricle. The clot can then embolise to any part of the body, including the brain causing an embolic stroke
  • Bleeding during initial treatment
  • Osteoporosis due to heparin treatment
76
Q

What are some differential diagnosis for DVT?

A
  • Differential diagnosis
    • Cellulitismakes your skin painful, hot and swollen
    • Calf muscle haematoma
    • Calf muscle tear/Achilles’ tendon tear
77
Q

What are the risk factors for DVT?

A

The risk factors for DVT are dependent onVirchow’s triad:

- **Virchow's triad:** hypercoagulability, venous stasis, endothelial damage

MISSED IMAGE

    An abnormality in**any one** of the three components can result in thrombus formation.
  

- Advanced **age**: the risk of DVT is greater after 40 years old
- **Immobility**: surgery, hospitalisation, long-haul travel and bed-bound
    - Long haul flights
- **Trauma**
- **Thrombophilia**
    - Hypercoagulability (pregnancy, cancer, inherited thrombophilic disorders)
        - Thrombophilia e.g. antiphospholipid syndrome, antithrombin deficiency, protein C or S deficiency, Factor V Leiden
        - Inherited thrombophilia – genetic predisposition (Caucasian)
- **Malignancy**
- **Smoking**
- **Pregnancy**
- **Drugs**: combined oral contraceptive pill, hormone replacement therapy, tamoxifen

---

- Venous flow stasis from any cause (e.g. cardiac failure, chronic venous insufficiency)
- Injury (trauma, surgery, child birth)
- Sickle cell disease
- Polycythaemia
- SLE
78
Q

What is the prognosis for DVT?

A

Patients are at an increased risk of future venous thromboemboli, with a 30% risk of recurrence in the subsequent 5 years.

Fatality in these patients is usually either related to a subsequent pulmonary embolism or major haemorrhage as a result of anticoagulation.

79
Q

DOACs vs traditional anticoagulants?

A
  • DOACs vs traditional anticoagulantsTraditional anticoagulants: warfarin, coumarin and heparinNewer anticoagulants, novel oral anticoagulants (NOACs) aka directly acting oral anticoagulants (DOACs): direct thrombin inhibitor (dabigatran) and factor Xa inhibitor (rivaroxaban and apixaban)

2a Conditions- Cardio (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions