cardiovascular conditions Flashcards

1
Q

subarachnoid haemorrhage presentation

A

thunderclap headache, very high intensity, may have had an episode of a sentinel headache: leading up to event less intense one, meningism: photophobia and neck stiffness
nausea and vomiting

can also have ECG changes such as ST elevation

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2
Q

most common cause of subarachnoid haemorrhage

A

trauma
otherwise its spontaneous

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3
Q

most common pathophysiology of spontaneous subarachnoid haemorrhage

A

berry aneurism

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4
Q

condiitons associated with berry aneurism

A

polycystic kidney disease

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5
Q

conditions associated with spontaneous sub haem

A

cardiovscular disease such as ehlers danlos syndrome and coarctation of the aorta

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6
Q

first line investigation for subarachnoid haemorrhage

A

non contrast ct head

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7
Q

if CT is normal?

A

if done within 6 h of symptom onset then NO LP and you trust the CT

if more than 6 hours after you need to do a lumbar puncture

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8
Q

how many hours after symptom onset can you preform LP?

A

AT LEAST 12 HOURS After
to allow the development of xanthochromia (the result of red blood cell breakdown).
xanthochromia helps to distinguish true SAH from a ‘traumatic tap’ (blood introduced by the LP procedure).

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9
Q

what finding other than xanthochromia is characteristic of Subarach haem on LP?

A

NORMAL or raised opening pressure

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10
Q

next steps after identifying subarach ahem on non contrast ct?

A

referral urgent to neuro
CT intracranial angiogram (to identify a vascular lesion e.g. aneurysm or AVM)
+/- digital subtraction angiogram (catheter angiogram)

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11
Q

management of subarachnoid haemorrhage

A

supportive
bed rest
analgesia
venous thromboembolism prophylaxis
discontinuation of antithrombotics (reversal of anticoagulation if present)
vasospasm is prevented using a course of oral nimodipine
intracranial aneurysms are at risk of rebleeding and therefore require prompt intervention, preferably within 24 hours
most intracranial aneurysms are now treated with a coil by interventional neuroradiologists, but a minority require a craniotomy and clipping by a neurosurgeon

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12
Q

complications of subarachnpoid haem

A

re-bleeding
happens in around 10% of cases and most common in the first 12 hours
if rebleeding is suspected (e.g. sudden worsening of neurological symptoms) then a repeat CT should be arranged
associated with a high mortality (up to 70%)
hydrocephalus
hydrocephalus is temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculoperitoneal shunt
vasospasm (also termed delayed cerebral ischaemia), typically 7-14 days after onset
ensure euvolaemia (normal blood volume)
consider treatment with a vasopressor if symptoms persist
hyponatraemia (most typically due to syndrome inappropriate anti-diuretic hormone (SIADH))
seizures

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13
Q

Important predictive factors in SAH:
for prognosis

A

conscious level on admission
age
amount of blood visible on CT head

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14
Q

cardiac tamponade presentation

A

becks triad- hypotension, raised jvp, muffled heart sounds
(think- 1 thing before heart picks up blood, one thing while heart holds blood, one thing after it sends it away)

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15
Q

other features of cardiac tamponade

A

dyspnoea, tachycardia, pulsus paradoxus- frop in bp during inspiration!!! important differentiator to restrictive pericarditis
ecg: electrical alternans: when QRS complex alternates form tall to short ect.

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16
Q

cardiac tamponade management

A

urgent pericardiocentesis

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17
Q

anaphylaxis DEFINING features

A

ABC features SO
airway (throat and tongue swelling)
and/OR breathing (wheeze and dyspnoea)
and/OR circulation problems (hypotensive, tachycardic)

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18
Q

additional possible anaphylaxis symptoms

A

generalised pruritus
widespread erythematous or urticarial rash

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19
Q

adrenaline dose used for dif ages

A

under 6 months 100-150 microoog
6mo-6y 150 μg
6-12 y 300 μg
500 microog over 12 yrs

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20
Q

after how long can you repeat IM Adrenaline if needed

A

5 mins

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21
Q

anaphylaxis management after stabilisation

A

1) non sedating oral antihistamines
2) serum tryptase taken to confirm anaphylaxis when unsure since can remain high up to 12 h after
3) new diagnosis: allergy clinic referral
4) adrenaline injector 2 autoinjectors given

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22
Q

discharge approach for anaphylaxis

A

2 hours post symptoms resolution in best case scenario

6 h minimum if 2 doses of adrenaline needed or PREVIOUS biphasic reaction

12h minimum if
> 2 doses req
severe asthma
possible ongoing reaction (slow release meds)
late night
difficult emergency access

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23
Q

what is refractory anaphylaxis

A

when doesnt resolve after 2 IM adrenaline
iv fluids given for shock
specialist help to consider IV adrenaline

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24
Q

most common causes of anaphylaxis

A

food
drug
venom

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25
Q

how to categorise tachyarrhythmias

A

1) SUPRAVENTRICULAR arrhythmias and ventricular

2) supraventricular arrhythmias: AF (the only irregularly irregular arrhythmia), SVTs: regularly irregular, Atrial flutter, WPW syndrome

3) ventricular: monomorphic VT, polymorphic VT, ventricular fibrillation

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26
Q

which is the most common sustained (it stays and you have it all the time) arrhythmia?

A

AF

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27
Q

AF pathophysiology

A

the atria depolarise spontaneously in a RAPID and UNCOORDINATED fashion often > 300bpm and the AV node filters this and so some beat signals are passed on to ventricles but not with any pattern so ventricular beat usually falls< 200 so around 100-150 but is IRREGULARLY IRREGULAR

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28
Q

classification of AF

A

Paroxysmal AF - When it terminates spontaneously or due to intervention within 7 DAYS
Presistent AF when mosre than 7 days
permanent AF- when its accepted to be permanent and no further attempts to restore sinus rhythm are made

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29
Q

ECG findings of AF

A

missing P waves and irregularly irregular rhythm and tachycardic

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30
Q

clinical presentaton of AF

A

non specific can have many forms
-fast irregular palpitations of “cardiac nature” (meaning defined onset, duration and offset)

  • effort intolerance ect sometimes only recognised after treated
  • sometimes present with stroke
  • syncope rare (more a bradyarrhythmia thing)
  • congestive heart failure
  • asymptomatic and only picked up from heart rate
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31
Q

management principles of AF

A

anticoagulation (arguably most important)
rate control
rhythm control

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32
Q

when is anticoagulation considered in AF

A

for all types, even if paroxismal bla bla ALWAYS!

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33
Q

How to assess if someone needs anti coagulation in AF?

A

CHA2DS2-VASc score

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34
Q

what are the categories in CHA2DS2-VASc score

A

congestive heart failure
hypertension
age>/= 75 (And age 65-74 is 11 point)
diabetes
prior stroke TIA or Thromboembolism

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35
Q

what is the anticoagulation strategy based on the chadvasc score?

A

0 No treatment
1 Males: Consider anticoagulation
Females: No treatment (this is because their score of 1 is only reached due to their gender)
2 or more Offer anticoagulation

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36
Q

what do you need to ensure if chadvasc score suggests no anticoagulatoin is required?

A

transthoracic echo has been done to exclude valvular disease which in combo with af would be absolute INDICATION for anticoagulatio

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37
Q

what is the scoring system used to assess bleeding risk for people receIving anticoagulation for AF

A

ORBIT score

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38
Q

list orbit score criteria

A

Haemoglobin <130 g/L for males and < 120 g/L for females, or haemtocrit < 40% for males and < 36% for females 2
Age > 74 years 1
Bleeding history (GI bleeding, intracranial bleeding or haemorrhagic stroke) 2
Renal impairment (GFR < 60 mL/min/1.73m2) 1
Treatment with antiplatelet agents 1

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39
Q

what is the classification of bleeding risk based on ORBIT score?

A

ORBIT score Risk group Bleeds per 100 patient-years
0-2 Low 2.4
3 Medium 4.7
4-7 High 8.1

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40
Q

first and second line anticoagulants used for AF

A

DOACS first

warfarrin second for ex in someone with prosthetic valve or other contraindic of doac

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41
Q

rate/ rhythm management of someone presenting with AF that is haemodynamically unstable

A

electrical cardioversion

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42
Q

rate/ rhythm management of someone presenting with AF that is haemodynamically stable

A

if <48 hours rhythm control
if >48 hours or uncertain rate control

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43
Q

what needs to be ensured if patient considered for long-term rhythm control

A

ensure anticoagulated for min 3 weeks

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44
Q

rate control drugs

A

beta blocker
calcium channel blocker
digoxin

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45
Q

important contraindication for beta blocker?

A

asthma

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46
Q

rhythm control drugs

A

beta blockers
dronedarone: second-line in patients following cardioversion
amiodarone: particularly if coexisting heart failure

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47
Q

when is catheter ablation used in AF

A

for those with AF who have not responded to or wish to avoid, antiarrhythmic medication.

48
Q

anticoagulation in catheter ablation

A

should be used 4 weeks before and during the procedure
it should be remember that catheter ablation controls the rhythm but does not reduce the stroke risk, even if patients remain in sinus rhythm. Therefore, patients still require anticoagulation as per their CHA2DS2-VASc score
if score = 0: 2 months anticoagulation recommended
if score > 1: longterm anticoagulation recommended

49
Q

catheter ablation outcome

A

notable complications include
cardiac tamponade
stroke
pulmonary vein stenosis
success rate
around 50% of patients experience an early recurrence (within 3 months) of AF that often resolves spontaneously
longer term, after 3 years, around 55% of patients who’ve had a single procedure remain in sinus rhythm. Of patients who’ve undergone multiple procedures around 80% are in sinus rhythm

50
Q

SVT pathogenesis

A

its re-entrant circuit due to an additional electrical oathway
1) AVNRT
2) AVRT

51
Q

ecg diagnosis of SVT

A

reggularly irregular,
present p waves abnormally shaped
150-200bpm
NARROW COMPLEX

52
Q

treatment of SVT

A

1) vagal manoeuvres
2) drugs: adenosine rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18

53
Q

what is contraindication of IV adenosine and alternative used?

A

contraindicated in asthmatics - verapamil is a preferable option

54
Q

last resort of SVT treatment

A

electrical cardioversion

55
Q

A flutter characteristics

A

saw tooth
atrial depol occur 300bpm and conduction to ventricles is limmited to every decond, third or fourth dep, most commonly 2nd so hr is exact 150 bpm

may be asymtomatic or breathless and palpitations and can occur with AF commonly

56
Q

atrial flutter treat

A

radiofreq ablation is safe and good success

57
Q

types of ventricular tachycardias

A

monomorphic
polymorphic
ventricular fibrillation

58
Q

important suvbtype of POLYMORPHIC VT and what triggers it?

A

torsades des pointes triggered by QT prolongation

59
Q

cAUSES of prolonged QT

A

Congenital:
Jervell-Lange-Nielsen syndrome (includes deafness
Romano-Ward syndrome (no deafness)

DRUGS:
amiodarone, sotalol, class 1a antiarrhythmics
tricyclic antidepressants, fluoxetine
chloroquine
terfenadine
erythromycin

OTHER:
electrolyte:
HYPO
K+
CA2+
Mg2+

-acute myocardial infarction
-myocarditis
-hypothermia
-subarachnoid haemorrhage

60
Q

WHEN do you use DC cardioversion in VTs?

A

when adverse signs: systolic BP < 90 mmHg, chest pain, heart failure

and if none of these signs but drugs (Antiarrhythmics) were given failed

61
Q

antiarrhytmic drugs used in VT

A

amiodarone: ideally administered through a central line
lidocaine: use with caution in severe left ventricular impairment
procainamide

62
Q

WHAT ELSE is done in the case that antiarrhythmics fail in VT?

A

If drug therapy fails
electrophysiological study (EPS)
implant able cardioverter-defibrillator (ICD) - this is particularly indicated in patients with significantly impaired LV function

63
Q

what drug cant be given as antiarrhytmhic in VT

64
Q

what condition does the exam buzzword “pink frothy sputum” point to?

A

heart failure

65
Q

what are the 3 classifications of peripheral arterial disease

A

1) intermittent claudication
2) critical limb ischemia
3) acute limb threatening ischemia

66
Q

presentation of intermittent claudication

A
  • aching or burning in the leg muscles following walking
  • patients can typically walk for a predictable distance before the symptoms start
  • usually relieved within minutes of stopping
  • not present at rest
67
Q

Assessment for intermittent claudication (investigations)

A

check pulses (femoral, popliteal, posterior tibialis and dorsalis pedis)

check ABPI

duplex ultrasound is first line investigation

magnetic resonance angiography (MRA) should be performed prior to any intervention

68
Q

treatment for peripheral arterial disease

A

statin and clopidogrel
and a supervised EXERCISE program: exercise training

69
Q

treatment options of critical limb ischemia or severe PAD

A

endovascular revascularisation (for <10 cm aortic iliac disease and high risk patients

surgical revascularisation: > 10 cm lesions, multifocal, lesions of the common femoral artery and purely infrapopliteal disease

70
Q

diagnosis of critical limb ischemia

A

if theres one or more of the following features:

  • rest pain in foot for more than 2 weeks
  • ulceration
  • gangrene

ABPI: <0.5
(patients often report sleeping with legs hanging of bed to aleviate pain)

71
Q

acute limb threatening ischaemia features

A

one or more of the 5P+C

PULSELESS
painful
paralysed
pale
paraesthetic

COLD

72
Q

acute limb threatening ischaemia initial investigations

A

handheld arterial Doppler examination

if doppler signals are present then you do an ABPI to check

73
Q

once acute limb- threatening ischaemia is confirmed what aspect is it also good to establish?

A

whether its caused by a thrombus or an embolus

an embolus doesnt have any previous pain in leg or difficulties in past and also more unilateral and no vascular disease
maybe indication of a clear cause eg AF tips you towards that for sure

74
Q

initial management of limb threatening ischaemia presentation

A

ABC approach
analgesia : IV opioids often used
IV unfractioned heparin - prevent thrombus propagation especially if patient not suitable for immediate surgery
vascular review

75
Q

definitive management of acute limb threatening ischaemia

A

intra arterial thrombolysis
surgical embolectomy
angioplasty
bypass surgery
amputation if irreversible

76
Q

how to organise the types of peripheral venous disease

A

1) the disease that causes progressive venous problems and incompetence is termed:
chronic venous insufficiency - this can be in deep or superficial veins with dif problems in each

2) classification system for progression of venous disease: CEAP classification based on clinical presentation of the disease

3) think about different pathologies in DEEP vein insufficiency and superficial vein insufficiency

77
Q

presentation of varicose veins (SYMptoms)

A

itchyness, painful, swollen, can feel heavy, burning or throbbing pain

78
Q

risk factors of varicose veins

A

old age , prolonged immobility or standing still for long, obesity, female!, pregnant!

79
Q

management of varicose veins

A

most cases dont require surgery just compression stockings and putting feet up when resting ect

weight loss
exercise

80
Q

when is surgery indicated for varicose veins?

A

when theres significant symptoms or some form of complication: ulcer (HEALED or active) , bleeding, superficial thrombophlebitis, skin change (pigmentation or eczema)

81
Q

what are the possible invasive treatment options of varicose veins

A

endothermal ablation: using either radiofrequency ablation or endovenous laser treatment
foam sclerotherapy: irritant foam → inflammatory response → closure of the vein
surgery: either ligation or stripping

82
Q

abdominal aortic aneurism presentation

A

USUALLY asymptomatic!!!
if there are symptoms its non specific abdo pain or expansile mass on examination with both hands ect

83
Q

screening for AAA

A

males when they turn 65! single abdominal ultrasound

84
Q

screening classifications based on size of AAA

A

< 3cm normal and no further action

3-4.4 small 0 rescan yearly

4.5-5.4- medium rescan every 3 months

for small and medium also minimise cardiovascular risk factors

> /= 5.5 is large OR
if rapidly enlarging: > 1cm / year (regardless of actual size)

refer urgently (2 weeks) to vascular surgery for probable intervention

85
Q

presentation of RUPTURED abdominal aortic aneurism

A

severe, central abdominal pain radiating to the back
pulsatile, expansile mass in the abdomen
patients may be shocked (hypotension, tachycardic) or MAY HAVE COLLAPSED

86
Q

MANAGEMENT OF ruptured AAA

A

IMMEDIATE vascular review with a view to emergency repair

in haemodynamically unstable patients no CT straight to theatres

if frail consider paliative as they may die either way

haemodynamically stable may be sent for CT angio where diagnosis in doubt - also to assess the suitability of endovascular repair

87
Q

most common site of venous ulceration

A

above the medial malleolus- in gaiter area of leg: aka: between ankle and mid calf

88
Q

investigations to do if a venous ucer is not healing

A

ankle-brachial pressure index (ABPI) is important in non-healing ulcers to assess for poor arterial flow which could impair healing

89
Q

what is an abnormal ABPI and what does it indicate

A

a ‘normal’ ABPI may be regarded as between 0.9 - 1.2. Values below 0.9 indicate arterial disease.

90
Q

in what case could someone hace an ABPI >1.3 ?

A

values above 1.3 may also indicate arterial disease, in the form of false-negative results secondary to arterial calcification (e.g. In diabetics)

91
Q

management of venous ulceration

A

compression bandaging, usually four layer (only treatment shown to be of real benefit)

oral pentoxifylline, a peripheral vasodilator, improves healing rate

92
Q

what elements do you need to check when examining an ulcer

A
  • Location
  • Size
  • Shape
  • Depth
  • Edge
  • Base
  • Signs of infection–
    redness/discharge
93
Q

arterial ulcer presentation

A

very painful
well demarcated
deep

on sites of pressure commonly!! more LATERAL maleoli and toes or heels

94
Q

investigations for arterial ulcer

A

diagnosis usually clinical but to confirm you do

Ankle-brachial pressure index (ABPI): An ABPI less than 0.9 suggests peripheral arterial disease.

Doppler ultrasound: Doppler ultrasound is used to assess blood flow and identify any blockages or narrowing in the arteries.

95
Q

management of arterial ulcers

A

Consider referral for angiography or duplex ultrasound if ABPI is less than 0.8 or if there are signs of severe ischaemia.
Endovascular procedures or bypass surgery may be necessary based on the severity of peripheral artery disease.

wound care
pain management
lifestyle (cardio rf)

96
Q

dry vs wet gangrene compare and contrast

A

1) cause + progression: dry is by chronic ischaemia due to PAD - sloww progression
vs wet is sudden lack of blood supply combined with bacterial infection - fast progression and can lead to systemic sepsis

2) Appearance: dry shrivelled and blackened + clear demarcation between necrotic and healthy
VS swolen, moist, blistered tissue with foul odour

3) pain: painless in dry and painful in wet

97
Q

what is gas gangrene

A

Caused by infection with Clostridium bacteria, which produce gas and toxins.

98
Q

gas gangrene presentation

A

Severe pain and swelling at the site of infection.
Crepitus due to gas production by Clostridium bacteria.
Rapid onset of systemic symptoms, including tachycardia, hypotension, and shock.

99
Q

what is necrotising fascitis

A

A severe form of gangrene involving the fascia and subcutaneous tissues.
Caused by mixed bacterial infections, often including Streptococcus pyogenes and Staphylococcus aureus.

100
Q

necrotising fasciitis presentation

A

Intense pain disproportionate to the visible signs.
Rapid progression of erythema, swelling, and tissue necrosis.
Systemic signs of sepsis, such as fever, tachycardia, and hypotension

101
Q

management of gangrene principles

A

control infection
restore blood supply
remove necrotic tissue

102
Q

surgical interventions in gangrene

A

Debridement: Surgical removal of necrotic tissue to prevent the spread of infection.
Amputation: In severe cases, partial or complete amputation of the affected limb may be necessary.
Revascularisation: Procedures such as angioplasty or bypass surgery to restore blood flow in cases of arterial occlusion.

103
Q

antibiotics when needed in gangrene what are they

A

Empirical broad-spectrum antibiotics initially, followed by targeted therapy based on culture results.
For gas gangrene, high-dose penicillin and clindamycin are often recommended.

104
Q

what is another thing used in some cases of gas gangrene

A

Hyperbaric oxygen therapy:
Used in some cases of gas gangrene to enhance oxygen delivery to ischaemic tissues and inhibit anaerobic bacterial growth.

105
Q

what are the clinical features outlined in two level DVT wells score

A

risk factor related:
- active cancer
- paralysis paresis or recent plaster
immobilisation of lower extremities
- recently bedridden for >3 d or major
surgery requiring any anaesthesia
- previously documented DVT

Symptom related
- localised tenderness along the distribution of the deep venous system
- entire leg swollen
- calf swelling >3cm larger than normal leg
- pitting oedema only on symptomatic leg
- collateral superficial veins (non varicose)

alternative diagnosis equally likely is -2 points

106
Q

clinical probability definition based on wells score

A

> /= 2 likely
1 or less unlikely

107
Q

what is done if wells>/=2

A

a proximal leg vein ultrasound needs to be done

108
Q

what is don if wells</= 1

109
Q

what happens if any of the needed investigations cant be done within 4 hours in DVT

A

give interim anticoagulation

110
Q

what happens if negative proximal leg vein US?

A

need to do d dimer, if thats positive:

repeat scan in 6-8 days and stop anticoagulation

111
Q

what if wells <1 and dvt positive

A

you do proximal leg vein us scan

112
Q

how should blood be obtained for d dimer

A

recommend either a point-of-care (finger prick) or laboratory-based test

113
Q

d dimer cut offs used

A

age-adjusted cut-offs should be used for patients > 50 years old

114
Q

management of confirmed dvt

A

DOAC even for cancer patientss

115
Q

who doesnt get doac in DVT management?

A

if renal impairment is severe (e.g. < 15/min) then LMWH, unfractionated heparin or LMWH followed by a VKA
if the patient has antiphospholipid syndrome (specifically ‘triple positive’ in the guidance) then LMWH followed by a VKA should be used

116
Q

length of anticoagulation

A

3 months if provoked (maybe 3-6 if active cancer)

6 months if unprovoked