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Surgery > Vascular Surgery > Flashcards

Vascular Surgery Flashcards

1
Q

What are the 6 Ps of acute limb ischaemia?

A 
Pale
Pulseless
Pain
Paralysis
Parasthesia
Perishingly cold
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2
Q

What is the best management for acute limb ischaemia?

A

Surgical intervention

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3
Q

How is ABPI calculated?

A

ABPI = the highest pressure in either the posterior tibial artery or dorsalis pedis artery in ONE foot divided by the highest pressure in the brachial artery from either arm

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4
Q

What is acute limb ischaemia?

A

A sudden decrease in limb perfusion that is a potential threat to viability of the limb

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5
Q

How common is acute limb ischaemia?

A

Affects 1 in 6000 people

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6
Q

What are the 2 main pathophysiologies of acute limb ischaemia?

A
  • Acute thrombosis of a vessel with pre-existing atherosclerosis
  • Emboli
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7
Q

Name some other rare causes of acute limb ischaemia?

A
  • Aortic dissection
  • Trauma
  • Iatrogenic injury
  • Peripheral aneurysm (esp. popliteal)
  • Intra-arterial drug use
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8
Q

What proportion of acute limb ischaemia is caused by acute thrombosis of an already atherosclerosed vessel?

A

60%

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9
Q

What factors predispose a patient to acute thrombosis -> acute limb ischaemia?

A 
Dehydration
Hypotension
Malignancy
Polycythaemia
Inherited pro-thrombotic states
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10
Q

How do the majority of emboli form?

A

Cardiac causes e.g. AF, MI, ventricular aneurysm

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11
Q

Where are the common sites of impaction of an embolus?

A

Brachial artery
Common femoral artery
Popliteal artery
Aortic bifurcation

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12
Q

When does irreversible tissue damage occur to a limb?

A

After 6 hours of severe ischaemia

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13
Q

How is acute limb ischaemia managed initially?

A

Emergency management - give 100% O2, IV access and consider crystalloids if dehydrated, blood tests, CXR and ECG. Opiate analgesia, refer upwards.

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14
Q

What blood tests do we request for acute limb ischaemia?

A 
FBCs
U+Es
Troponin
Clotting
Glucose
Group and save
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15
Q

How can you assess limb viability?

A

Look for pulses, temperature, appearance of skin, limb power, sensation, and cap refill

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16
Q

How does irreversible limb ischaemia appear?

A

Fixed mottling of skin, petechial haemorrhages, wood hard muscles

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17
Q

How does limb ischaemia appear if it is saveable but needs immediate treatment?

A

Muscles tender to palpation, swollen, loss of power and loss of sensation

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18
Q

How is irreversible limb damage managed definitively?

A

Amputation

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19
Q

How is severe limb ischaemia (requires immediate treatment) managed definitively?

A

Prevent systemic complications of muscle necrosis (acidosis, hyperkalaemia, AKI).

Surgery to revascularise the limb + perform fasciotomy

Consider amputation

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20
Q

How is severe limb ischaemia (requires prompt treatment after investigation) managed definitively?

A

Heparinisation
Angiogram/Duplex/CT to determine location of disease
Thrombolysis
Surgery

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21
Q

Which limb does chronic ischaemia occur in most commonly?

A

Lower limb

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22
Q

What are the causes of chronic limb ischaemia?

A

Atherosclerosis

Arteriosclerosis

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23
Q

How do we classify lower limb ischaemia?

A

The Fontaine classification

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24
Q

What are the 4 levels of Fontaine classification?

A

I - asymptomatic
II - intermittent claudication
III - Rest pain
IV - Ulcers/Gangrene

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25
Q

Which Fontaine classifications are critical limb ischaemia?

A

III and IV

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26
Q

What are the stats on intermittent claudication?

A

1/3 improve, 1/3 stable, 1/3 deteriorate

4% require intervention

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27
Q

What are the clinical features of IC?

A

Muscle pain on exercise (worse with increased intensity). Relieved by rest. Usually in calf muscle.

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28
Q

What are the differentials for IC?

A
  • Spinal stenosis (usually while walking down stairs/hill, rather than up)
  • OA (esp. of hip joint)
  • Nerve root entrapment e.g. sciatica
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29
Q

How is IC diagnosed?

A

Clinical (not based on imaging)

Post exercise fall in ABPI

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30
Q

How is IC treated?

A
  • Risk factor modification
  • Pt should walk through pain -> angiogenesis -> establish collaterals
  • Endovascular treatment
  • Surgery
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31
Q

What are the risk factors for IC?

A 
HTN
Hyperlipidaemia
DM
Smoker
FH
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32
Q

What is critical limb ischaemia?

A

Severe obstruction of the arteries which markedly reduces blood flow to the extremities which has progressed to severe rest pain +- ulcers.

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33
Q

How long must rest pain be present for to diagnose critical limb ischaemia?

A

2 weeks or more + no relief with simple analgesia

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34
Q

When is th pain usually worst with critical limb ischaemia?

A

At night i.e. when the pt is lying down

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35
Q

How is critical limb ischaemia diagnosed?

A

Clinically

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36
Q

How is critical limb ischaemia diagnosed?

A
  • Identify risk factors to modify

- Identify vessels affected location and severity

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37
Q

How is criticla limb ischaemia treated?

A 
REVASCULARISE as much as possible.
Treat proximal disease before distal disease.
Analgesia
Angioplasty +- stent in proximal disease
Surgery - bypass or amputation
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38
Q

What’s an aneurysm?

A

An abnormal localised blood vessel dilation by more than 50% of its original diameter

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39
Q

What is the definition of an AAA?

A

Dilation of the abdominal aorta greater than 3cm

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40
Q

What are the risk factors for AAA?

A 
Smoking
HTN
Hyperlipidaemia
FH
Male
Increasing age
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41
Q

What are the clinical features of AAA?

A

Mostly asymptomatic.

If not:

  • Abdominal pain
  • Back/loin pain
  • Distal embolisation
  • Aortoenteric fistula
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42
Q

What can be found O/E of a pt with AAA?

A

Pulsatile mass felt in the abdomen (above umbilical level)

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43
Q

How has the mortality rate of AAA decreased recently?

A

Screening programme!!

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44
Q

Who does the AAA screening programme screen?

A

Men in their 65th year

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45
Q

If a man is found to have an AAA on screening, what happens next?

A

If it is small (3.0-4.4cm) or medium (4.5-5.4cm), invite for ongoing US surveillance.

If large (>=5.5 cm) refer for surgical repair

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46
Q

How frequently should a small aneurysm be monitored?

A

Every 12 months

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47
Q

How frequently should a medium aneurysm be monitored?

A

Every 3 months

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48
Q

What are the differentials for AAA?

A

(If symptomatic) renal colic.

Other abdominal pathology

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49
Q

What happens after an USS confirms an AAA?

A

CT with contrast for anatomical details to determine if suitable for endovascular procedures

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50
Q

What can we modify for AAA and why?

A

Smoking cessation
BP control
Statin and aspirin therapy
Weight loss

Reduce risk of progression and mortality

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51
Q

Which AAA pts should be considered for surgery?

A
  • AAA >5.5cm
  • AAA expanding at >1cm/year
  • Symptomatic AAA in otherwise fit pt
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52
Q

How can AAAs be repaired?

A
  • Open repair

- Endovascular repair

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53
Q

Why do we offer surgery to pts with AAA over 5.5cms?

A

The risk of surgery becomes equal to risk of not having surgery at 5.5cm

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54
Q

Which procedure has better outcomes for AAA?

A

Endovascular has better short term outcomes, but worse long term. Open repair is reccommended in younger, fit pts as 2 year mortality is the same for both procedures.

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55
Q

What are the complications of AAA?

A

Rupture
Retroperitoneal leak
Embolisation
Aortoduodenal fistula

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56
Q

What factors are associated with an increased risk of AAA rupture?

A

Smoker, HTN (especially if uncontrolled), FHx, atherosclerosis

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57
Q

What is the rate of AAA rupture in pts with an AAA over 5.5cm?

A

3% per year

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58
Q

How many pts whose AAAs rupture reach hospital alive?

A

Less than 50%

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59
Q

What is the mortality rate for ruptured AAA?

A

75-95%

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60
Q

What are the symptoms of a ruptured AAA?

A

Severe epigastric &/or back/loin pain, collapse, Hx of AAA under surveillance

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61
Q

What are the signs of a ruptured AAA?

A

Sudden onset hypotension, pain, and sweating, pulsatile abdominal mass (often hard to feel due to pain causing pt to contract abdo wall muscles).

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62
Q

If a ruptured AAA is a distinct possibility, what should we not do in resus?

A

Chase a normal BP because that would risk worsening the rupture (unless pt is dangerously hypotensive, in which case call a peri-arrest cardiac emergency).

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63
Q

How is a ruptured AAA managed?

A

Surgically!

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64
Q

What are the possible complications of ruptured AAA surgical repair?

A

Death (that’s a biggy, like 50% of those operated on die), MI, renal failure, lower limb embolism, gut ischaemia, abdominal compartmet syndrome

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65
Q

What is carotid disease a risk factor for?

A

TIAs or CVAs

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66
Q

Who do we investigate for carotid disease?

A

Pts who have had a TIA or CVA in the past 6 months

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67
Q

How do we investigate carotid disease?

A

With a colour duplex scan. If this is inconclusive, MRA or CT angiography

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68
Q

What is a CEA and who is it offered to?

A

Carotid endarterectomy, offered to pts smptomatice with more than 70% stenosis of ICA, or more than 50% if recent TIA/CVA

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69
Q

What is the most common outcome of diabetic vascular complications?

A

Foot ulceration

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70
Q

What are the 4 key features of the diabetic foot?

A

Ulceration, sensory neuropathy, loss of ability to heal small injuries, and infection.

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71
Q

What are the risk factors for diabetic foot ulceration?

A

Previous ulceration, neuropathy, peripheral arterial disease, altered foot shape, callus, visual impairment, living alone, renal impairment

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72
Q

What % of diabetic foot ulceration is due purely to sensory neuropathy?

A

45%

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73
Q

What % of diabetic foot ulceration is due purely to ischaemia?

A

10%

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74
Q

What is the remaining 45% of diabetic ulceration due to?

A

Mixed neuropathic and ischaemic

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75
Q

How does a purely neuropathic ulcered foot present?

A

Warm foot with palpable pulses, evidence of sensory loss, normal or high ABPI

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76
Q

How does a mixed neuropathic/ischaemic ulcered foot present?

A

Cool, absent pulses, ulcers situated on toe, heel, or metatarsal head, ABPI may be high.

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77
Q

How do we manage diabetic ulcers (general steps)?

A

Prophylaxis, Surveillance, Treat infection, revascularise, amputate

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78
Q

What prophylactic steps can we take to prevent diabetic foot ulcers?

A

Diabetic nurse/clinic checkups regularly, appropriate footwear, chiropody, keep feet cool, don’t walk around barefoot

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79
Q

If there is infection present in a diabetic foot, what imaging should we do and why?

A

X-ray to look out for osteomyelitis

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80
Q

How do we attempt to revascularise a pt with diabetic foor tulcers?

A

Angioplasty, femorodistal bypass grafts

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81
Q

What are varicose veins?

A

Tortuous and dilated segments of veins, associated with valvular incompetence

82
Q

Give me the stats for varicose veins.

A

Affects 35% of the population, M=F

83
Q

What causes varicose veins?

A

Congenital, idiopathic (majority), or econdary to pelvic masses or pelvic venous abnormalities

84
Q

What pelvic masses can cause varicose veins?

A

Pregnancy, uterine fibroids,, ovarian mass, pelvic tumour.

85
Q

What are the clinical features of varicose veins?

A

Often just cosmetic concerns, but can cause pain, itchiness, swelling, aching, oedema, and can be worse under certain conditions.

86
Q

What complications should we screen for when a pt presents with varicose veins?

A

Eczema, phlebitis, lipodermatosclerosis, ulceration, and bleeding.

87
Q

What is the gold standard test for diagnosing venous valve incompetence?

A

Colour duplex

88
Q

Why do DVTs occur?

A

Due to abnormalities vein wall, blood flow, or blood components i.e. Virchow’s triad

89
Q

What are some risk factors that cause vein compression and stasis tht can lead to DVT?

A 
Immobility
Trauma
Mass
Surgery
Paralysis
Long distance travel (including airline)
90
Q

What are some of the inherited risk factors for DVT?

A

Factor V Leiden
Protein C insufficiency
Protein S insufficiency
Antithrombin insufficeincy

91
Q

What are some acquired hypercoagulable states that increase the risk of DVT?

A 
Smoking
Surgery
Malignancy
Polycythaemia
HRT
OCP
Dehydration
92
Q

What are the clinical features suggestive of a DVT?

A

There may not be any

Local features of venous engorgement and stasis such as limb swelling, pain, erythema, relative warmth, fever/tachycardia.

Also features of complcications.

93
Q

What are the complications of a DVT?

A

PE and venous gangrene

94
Q

What are the clinical features of a PE?

A

Dyspnoea, pleuritic chest pain, haemoptysis, dizziness, sncope, hypoxia, cyanosis, hypotension, pleural effusion, tachycardia

95
Q

What tool do we use to work out a pts risk of having a DVT?

A

Well’s score

96
Q

What risk does a pt with a score of 0 have of having a DVT? What should we do now?

A

5% - a D-dimer should be done. If negative, DVT is ruled out.

97
Q

What risk does a pt with a score of 1-2 have of having a DVT? What should we do now?

A

17% - With a positive D-dimer, a USS should be done.

98
Q

What risk does a pt with a score of 3 or more have of having a DVT? What should we do now?

A

17-53% - very likely. Diagnostic USS should be done.

99
Q

If we are suspicious of PE, what should we do?

A

VQ scan or CTPA (most sensitive).

100
Q

Even though once a pt has a DVT we need to treat, what is better than treatment?

A

Effective prophylaxis

101
Q

What conservative measures can we do for a DVT?

A

Elevate the limb and ensure good hydration

102
Q

What determines the treatment for a DVT?

A

If it is complicated or uncomplicated.

103
Q

How do we treat an uncomplicated DVT?

A

LMWH in hospital (or as outpatient, DVT clinic decides), then follow-up with warfarin for 3-6 months.

104
Q

How do we treat a complicated DVT?

A

IV unfractionated heparin initially, or LMWH to convert to warfarin.

105
Q

Do we do thrombolysis for DVT?

A

Only if severe thrombosis with venous gangrene

106
Q

What can we do for a pt who has recurrent PE despite treatment?

A

A vena caval filter

107
Q

What can occur aas a complication of extensive or recurrent DVTs?

A

Chronic venous insufficiency

108
Q

What is the risk of thrombolysis?

A

Hameorrhage or stroke

109
Q

What thrombolysis agents are there?

A

Streptokinase
tPA
Urokinase

110
Q

Which thrombolytic is usually used?

A

Streptokinase

111
Q

Tell me about streptokinase.

A

Cheap
Acts systemically
27 minute half life
S/Es include anaphylaxis, fever, and antibody resistance, which limits repeated use.

112
Q

How quickly does a AAA need to be growing to be a high enough risk for surgery?

A

More than 1cm per year

113
Q

If a patient has sudden arterial occlusion, what does the outcome depend on?

A

Timely intervention and state of collateral supply

114
Q

When might a patient with acute limb ischaemia have good collateral supply?

A

Pre-existing chronic occlusive disease causing increased collateral supply

115
Q

A patient who has had a tibial fracture suddenly develops acute limb ischaemia. What is the likely pathophysiology?

A

Compartment syndrome

116
Q

Why is a red limb in acute limb ischaemia misleading?

A

It can be misdiagnosed as gout or cellulitis (some kind of inflammation)

117
Q

Why can limb ischaemia cause red flushing of the limb?

A

Re-establishment of arterial supply after a period of reduced perfusion causes rapid vasodilation of arterioles in order to increase the metabolic waste removal that builds up during the period of reduced perfusion.

This can be seen when performing Buerger’s test.

118
Q

What surgery is indicated for acute limb ischaemia?

A

Angioplasty (or open surgery)

119
Q

If acute limb ischaemia is embolic in origin, what surgical intervention can be performed?

A

Embolectomy

120
Q

Post-embolectomy, should a patient be anticoagulated considering they have just undergone vascular surgery?

A

Yes, usually wait until 6 hours post-surgery.

121
Q

What is the management of irreversible ischaemic limb?

A

Amputation

122
Q

Other than surgery, how should vascular disease be managed?

A

Lifestyle modicifcation - diet, exercise, smoking cessation.

Modification of underlying disease - chiefly cholesterol, HTN, diabetes.

123
Q

A patient is discharged from hospital following surgery for peripheral arterial disease. What main medications should they be discharged with?

A

Long term dual antiplatelet therapy (aspirin and clopidogrel), ACE inhibitor, and statin.

124
Q

What are the complications of acute limb ischaemia?

A
  • Reperfusion injury
  • Chronic pain
  • Loss of limb
125
Q

Describe the pathophysiology of reperfusion injury?

A
  • Neutrophils migrate to reperfused tissue

- Increased capillary permeability due to inflammatory mediators causing limb swelling leading to compartment syndrome.

126
Q

What is an ABPI below one indicative of?

A

Periperal arterial disease

127
Q

Why is it important to do an ABPI on patients with venous ulcers?

A

Bceause compression banaging is one of the main treatments but if a patient has peripheral arterial diesase this will do more harm than good.

128
Q

What is a normal ABPI?

A

1.0 - 1.2.

129
Q

What does an ABPI >1.2 signify?

A

Calcified, stiff arteries, usually associated with old age or T2DM.

130
Q

What is an acceptable ABPI?

A

> 0.9

131
Q

What is the cut off for compression bandaging in terms of ABPI?

A

Compression bandaging is ok for anyone with ABPI >0.8

132
Q

Describe a venous ulcer.

A

Large, shallow, painless, situated over medial or lateral malleoli.

133
Q

Other than venous ulcers, what are the signs of venous hypertension?

A 
Varicose veins
Varicose eczema
Haemosiderin pigmentation
Oedema
Skin thickening
134
Q

What is the definition of an leg ulcer?

A

Loss of skin below the knee on the leg or foot

135
Q

Which rheumatological condition is associated with increased risk of venous ulcers?

A

Rheumatoid arthritis

136
Q

How is an arterial ulcer different to a venous ulcer?

A

Indicated by absent or weak peripheral pulses.
Located in areas of poor blood supply e.g between toes, over tibia.
Painful and deep.
Signs of peripheral cyanosis + claudication

137
Q

Describe a neuropathic ulcer.

A

Painless
Deep
Overlying keratosis
Sites of nerve supply loss and recurrent trauma
Common in diabetics and chronic alcoholics

138
Q

What kind of ulcers do RA patients get?

A

Rheumatoid ulcers as well as venous ulcers.

139
Q

Describe a rheumatoid ulcer.

A

Sharp, deep, and well demarctaed.
Punched-out appearance.
Usually on foot and calf.

140
Q

Do all venous ulcers need swabbing to rule out infection?

A

No, only those with markers of infection such as cellulitis.

141
Q

When is a biopsy of a venous ulcer indicated?

A

If they have an atypical appearance or fail to heal afte 12 weeks of active treatment.

142
Q

How can venous ulcers be managed?

A
  • Graduated compression (after ruling out arterial insufficiency)
  • Debridement and cleaning
  • Dressings
  • Antibiotics if infected
  • Management of complications
143
Q

What kind of dressings are used on venous ulcers?

A
  • Occlusive hydrocolloidal dressings
  • Alginate dressings
  • Dressings containing topical growth factor
144
Q

What improves prognosis of venous ulcer?

A

Increased mobility
No significant co-morbidities
Ability to walk

145
Q

When should a venous ulcer be referred from primary care?

A

If it fails to respond after 2 weeks of treatment, or if the patient has a co-morbidity or the ulcer is suspicious of malignancy

146
Q

What is osteomyelitis?

A

Infection of the bone marrow, which may spread to the bone cortex and periosteum.

147
Q

What does osteomyelitis lead to if it is untreated?

A

Inflammatory destruction of bone and periosteum causing necrosis.

148
Q

How does chronic osteomyelitis lead to deformity?

A

Dead bone from necrosis detaches to form a sequestrum. This remains in situ, and the viable bone underlying it starts to form new bone aorund it, causing remodelling and deformity.

149
Q

What are the 2 types of osteomyelitis?

A

Haematogenous (bacterial seeding from remote source) and Direct (contiguous) osteomyelitis.

150
Q

Which is the most common organism causing osteomyelitis?

A

Staph aureus

151
Q

Why is the incidence of osteomyelitis increasing?

A

Increasing prevalence of risk factors such as diabetes mellitus and peripheral arterial disease.

152
Q

Which demographic group is haematogenous osteomyelitis common in?

A

Children

153
Q

A diabetic patient has a chronic persistent diabetic foot ulcer. What does this mean they are at high risk of?

A

Developing underlying osteomyelitis

154
Q

How does osteomyelitis present?

A
  • Fever, pain, and erythema
  • Hx of accidental injury or surgical trauma
  • -Long term overlying diabetic ulcer present
155
Q

Why can osteomyelitis go undiagnosed in diabetic patients?

A

The pain may be masked by diabetic peripheral neuropathy, and there may not be any local signs of infection.

It does however often cause recalcitrant hyperglycaemia.

156
Q

What are the differentials for osteomyelitis?

A
  • Cellulitis
  • Trauma
  • Gout
  • MSCC
  • Acute sickle cell crisis
  • Other causes of limp
157
Q

What lab tests can confirm osteomyelitis?

A
  • FBC with raised WCC
  • Positive blood cultures - should ALWAYS be done
  • Cultures of any discharge
  • Bone culture is gold standard for diagnosis
158
Q

A patient has ?osteomyelitis, and a foot x-ray is done. The report agrees that osteomyelitis is possible.Which imaging modality is gold standard for the diagnosis be confirmed?

A

MRI - allows good visualisation of subtle abnormalities.

159
Q

What are the main aspects of management for osteomyelitis?

A

Abx for 4-6 weeks
Surgical debridement
Analgesia

160
Q

What complications can arise due to osteomyelitis?

A
  • Bone abscess
  • Sepsis
  • Fracture
  • Septic arthritis
  • Cellulitis
  • Chronic infection
161
Q

What is peripheral arterial disease?

A

Significant narrowing of arteries distal to arch of aorta, usually due to atherosclerosis.

162
Q

What are the degrees of peripheral arterial disease?

A
  • Asymptomatic
  • Intermittent claudication
  • Critical limb ischaemia
  • Skin ulceration and gangrene
163
Q

Can the upper limbs be affected by peripheral arterial disease?

A

Yes - usually the subclavian artery and brachiocephalic trunk.

164
Q

How common is peripheral arterial disease?

A

Very - 15-20% of people over 70 are affected.

165
Q

What are the big risk factors for peripheral arterial disease?

A
  • Smoking
  • DM
  • HTN
  • Hyperlipidaemia
  • Physical inactivity
  • Obesity
166
Q

A patient presents with intermittent claudication. What other areas in the body are at risk of vascular disease, and should be screened for?

A
  • Coronary arter disease
  • Cerebrovascular disease
  • Aortic aneurysm
  • Kidney/bowel
  • Upper and lower limbs
167
Q

How is a diagnosis of PAD confirmed?

A

Doppler ultrasonography

168
Q

Why are ACE inhibitors needed but closely monitored in pateints with PAD?

A

To manage HTN and reduced cardiovascular morbidity and mortality, but 25% of PAD patients have co-existing renal artery stenosis.

169
Q

What is angioplasty?

A

Endovascular surger where a balloon is used to widen narrowed or obstructed arteries or veins.

170
Q

What is gangrene?

A

Death and decay of body tissue due to lack of blood supply.

171
Q

What are the 2 main types of gangrene?

A

Dry and wet

172
Q

What is dry gangrene?

A

Death and decay of tissues due to diminished lood supply, usually due to peripheral arterial disease.

173
Q

Other than peripheral arterial disease, what can cause dry gangrene?

A

Vasculitis and other conditions that cause vasculitis

174
Q

What is the pathophysiology of wet gangrene?

A

Tissue infection causing swelling -> inflammation -> blockage of blood vessels -> tissue death -> gangrene associated with infection and discharge.

175
Q

Which parts of the body are usually affected by gangrene?

A

Extremities most often, but also rest of limbs and the GI tract.

176
Q

What are the symptoms of wet gangrene?

A
  • Systemic upset
  • Swelling
  • Erythema
  • Pin
  • Discharge
  • Foul-smelling
  • Blackening of skin
177
Q

What are the symptoms of dry gangrene?

A
  • Systemic upset
  • Erythema
  • Coldness and pallor
  • Numb
  • No discharge
  • Brown then black skin
178
Q

What imaging is used with gangrene, and why?

A

X-ray - detect gas.

CT/MRI - detect extent of local involvement.

179
Q

Are antibiotics used to manage gangrene?

A

Yes, however they won’t penetrate the dead tissue but will help prevent the spread of infection

180
Q

How is wet gangrene managed?

A
  • Analgesia
  • Broad spec abx
  • Surgical debridement
  • Amputation may be necessary
  • Management of risk factors
181
Q

How is dry gangrene managed?

A
  • Restoration of blood supply
  • Amputation may be required
  • Management of risk factors
182
Q

What is the main complication associated with gangrene?

A

Sepsis

183
Q

What kind of gangrene is gas gangrene?

A

Life-threatening Wet gangrene

184
Q

What organism most commonly causes gas gangrene following trauma or surgery?

A

Clostridium perfringens

185
Q

What organism species most commonly causes gas gangrene?

A

Clostridium species

186
Q

How does gas gangrene occur?

A

Organism (usually Clostridium species) enters through wound, usually after contact with soil -> already devitalised tissue -> anaerobic respiration and endotoxin release -> tissue destruction, rhabdomyolysis, AKI, red cell destruction, and shock.

187
Q

What can predispose someone to gas gangrene?

A

Anything that means a tissue might not be in best condition e.g. alcohol abuse, malnutrition, trauma, DM, steroid use, malignancy.

188
Q

How does the appearance of gas gangrene differ to other gangrene?

A

It appears cellulitic at first then progresses to dark purple with vesicles and bullae.
Sub-cut air may be present on palpation.

189
Q

How should gas gangrene be managed?

A
  • Supportive
  • Surgical debridement
  • Abx
190
Q

Which dermatological condition affects vessels?

A

Vasculitis (and conditions that cause vasculitis).

191
Q

What can cause vasculitis?

A
  • Idiopathic (aound half)
  • Infection
  • Inflammatory disease
  • Drug-induced
  • Neoplastic
192
Q

How is vasculitis classified?

A

According to what it affects

193
Q

How does medium-sized vessel vasculitis present?

A
  • Ulcers
  • Digital infarcts
  • Nodules
  • HTN due to renal vessle damage
194
Q

How does small-sized vessel vasculitis present?

A
  • Palpable purpura
  • Splinter haemorrhages
  • Urticaria
  • Vasicles
195
Q

What is an aortic dissection?

A

Disruption of medial layer of wall of aorta due to intramural bleeding, leading to separation of aortic wall layers.

196
Q

What is the main associated disease with aortic dissection?

A

Hypertension

Classically though all the usual vascular risk factors apply.

197
Q

What inherited conditions and congenital issues increase risk of aortic dissection?

A
  • Ehlers-Danlos syndrome
  • Marfan’s syndrome
  • Congenital aortic valve problems
198
Q

How are aortic dissections classified?

A

Into Stanford A and Stanford B

199
Q

What is the difference ebtween a Stanford A and a Stanford B aortic dissection?

A

A affects ascending aorta, and B does not.

200
Q

How does aortic dissection present?

A

Very variable. Can present with chest pain, MI symptoms, congestive heart failure, syncope, pleural effusions, neurological symptoms, or with rupture and signs of shock.

201
Q

How do patients classically describe aortic dissection pain?

A

Ripping pain, usually in back or chest.

Sudden onset.

Usually migrates as the dissection progresses.

Surgery (11 decks)

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