Vascular Surgery Flashcards
1
Q
What are the 6 Ps of acute limb ischaemia?
A
Pale Pulseless Pain Paralysis Parasthesia Perishingly cold
2
Q
What is the best management for acute limb ischaemia?
A
Surgical intervention
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
4
Q
What is acute limb ischaemia?
A
A sudden decrease in limb perfusion that is a potential threat to viability of the limb
5
Q
How common is acute limb ischaemia?
A
Affects 1 in 6000 people
6
Q
What are the 2 main pathophysiologies of acute limb ischaemia?
A
- Acute thrombosis of a vessel with pre-existing atherosclerosis
- Emboli
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
8
Q
What proportion of acute limb ischaemia is caused by acute thrombosis of an already atherosclerosed vessel?
A
60%
9
Q
What factors predispose a patient to acute thrombosis -> acute limb ischaemia?
A
Dehydration Hypotension Malignancy Polycythaemia Inherited pro-thrombotic states
10
Q
How do the majority of emboli form?
A
Cardiac causes e.g. AF, MI, ventricular aneurysm
11
Q
Where are the common sites of impaction of an embolus?
A
Brachial artery
Common femoral artery
Popliteal artery
Aortic bifurcation
12
Q
When does irreversible tissue damage occur to a limb?
A
After 6 hours of severe ischaemia
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.
14
Q
What blood tests do we request for acute limb ischaemia?
A
FBCs U+Es Troponin Clotting Glucose Group and save
15
Q
How can you assess limb viability?
A
Look for pulses, temperature, appearance of skin, limb power, sensation, and cap refill
16
Q
How does irreversible limb ischaemia appear?
A
Fixed mottling of skin, petechial haemorrhages, wood hard muscles
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
18
Q
How is irreversible limb damage managed definitively?
A
Amputation
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
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
21
Q
Which limb does chronic ischaemia occur in most commonly?
A
Lower limb
22
Q
What are the causes of chronic limb ischaemia?
A
Atherosclerosis
Arteriosclerosis
23
Q
How do we classify lower limb ischaemia?
A
The Fontaine classification
24
Q
What are the 4 levels of Fontaine classification?
A
I - asymptomatic
II - intermittent claudication
III - Rest pain
IV - Ulcers/Gangrene
25
Which Fontaine classifications are critical limb ischaemia?
III and IV
26
What are the stats on intermittent claudication?
1/3 improve, 1/3 stable, 1/3 deteriorate
4% require intervention
27
What are the clinical features of IC?
Muscle pain on exercise (worse with increased intensity). Relieved by rest. Usually in calf muscle.
28
What are the differentials for IC?
- Spinal stenosis (usually while walking down stairs/hill, rather than up)
- OA (esp. of hip joint)
- Nerve root entrapment e.g. sciatica
29
How is IC diagnosed?
Clinical (not based on imaging)
| Post exercise fall in ABPI
30
How is IC treated?
- Risk factor modification
- Pt should walk through pain -> angiogenesis -> establish collaterals
- Endovascular treatment
- Surgery
31
What are the risk factors for IC?
```
HTN
Hyperlipidaemia
DM
Smoker
FH
```
32
What is critical limb ischaemia?
Severe obstruction of the arteries which markedly reduces blood flow to the extremities which has progressed to severe rest pain +- ulcers.
33
How long must rest pain be present for to diagnose critical limb ischaemia?
2 weeks or more + no relief with simple analgesia
34
When is th pain usually worst with critical limb ischaemia?
At night i.e. when the pt is lying down
35
How is critical limb ischaemia diagnosed?
Clinically
36
How is critical limb ischaemia diagnosed?
- Identify risk factors to modify
| - Identify vessels affected location and severity
37
How is criticla limb ischaemia treated?
```
REVASCULARISE as much as possible.
Treat proximal disease before distal disease.
Analgesia
Angioplasty +- stent in proximal disease
Surgery - bypass or amputation
```
38
What's an aneurysm?
An abnormal localised blood vessel dilation by more than 50% of its original diameter
39
What is the definition of an AAA?
Dilation of the abdominal aorta greater than 3cm
40
What are the risk factors for AAA?
```
Smoking
HTN
Hyperlipidaemia
FH
Male
Increasing age
```
41
What are the clinical features of AAA?
Mostly asymptomatic.
If not:
- Abdominal pain
- Back/loin pain
- Distal embolisation
- Aortoenteric fistula
42
What can be found O/E of a pt with AAA?
Pulsatile mass felt in the abdomen (above umbilical level)
43
How has the mortality rate of AAA decreased recently?
Screening programme!!
44
Who does the AAA screening programme screen?
Men in their 65th year
45
If a man is found to have an AAA on screening, what happens next?
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
46
How frequently should a small aneurysm be monitored?
Every 12 months
47
How frequently should a medium aneurysm be monitored?
Every 3 months
48
What are the differentials for AAA?
(If symptomatic) renal colic.
Other abdominal pathology
49
What happens after an USS confirms an AAA?
CT with contrast for anatomical details to determine if suitable for endovascular procedures
50
What can we modify for AAA and why?
Smoking cessation
BP control
Statin and aspirin therapy
Weight loss
Reduce risk of progression and mortality
51
Which AAA pts should be considered for surgery?
- AAA >5.5cm
- AAA expanding at >1cm/year
- Symptomatic AAA in otherwise fit pt
52
How can AAAs be repaired?
- Open repair
| - Endovascular repair
53
Why do we offer surgery to pts with AAA over 5.5cms?
The risk of surgery becomes equal to risk of not having surgery at 5.5cm
54
Which procedure has better outcomes for AAA?
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.
55
What are the complications of AAA?
***Rupture***
Retroperitoneal leak
Embolisation
Aortoduodenal fistula
56
What factors are associated with an increased risk of AAA rupture?
Smoker, HTN (especially if uncontrolled), FHx, atherosclerosis
57
What is the rate of AAA rupture in pts with an AAA over 5.5cm?
3% per year
58
How many pts whose AAAs rupture reach hospital alive?
Less than 50%
59
What is the mortality rate for ruptured AAA?
75-95%
60
What are the symptoms of a ruptured AAA?
Severe epigastric &/or back/loin pain, collapse, Hx of AAA under surveillance
61
What are the signs of a ruptured AAA?
Sudden onset hypotension, pain, and sweating, pulsatile abdominal mass (often hard to feel due to pain causing pt to contract abdo wall muscles).
62
If a ruptured AAA is a distinct possibility, what should we not do in resus?
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).
63
How is a ruptured AAA managed?
Surgically!
64
What are the possible complications of ruptured AAA surgical repair?
Death (that's a biggy, like 50% of those operated on die), MI, renal failure, lower limb embolism, gut ischaemia, abdominal compartmet syndrome
65
What is carotid disease a risk factor for?
TIAs or CVAs
66
Who do we investigate for carotid disease?
Pts who have had a TIA or CVA in the past 6 months
67
How do we investigate carotid disease?
With a colour duplex scan. If this is inconclusive, MRA or CT angiography
68
What is a CEA and who is it offered to?
Carotid endarterectomy, offered to pts smptomatice with more than 70% stenosis of ICA, or more than 50% if recent TIA/CVA
69
What is the most common outcome of diabetic vascular complications?
Foot ulceration
70
What are the 4 key features of the diabetic foot?
Ulceration, sensory neuropathy, loss of ability to heal small injuries, and infection.
71
What are the risk factors for diabetic foot ulceration?
Previous ulceration, neuropathy, peripheral arterial disease, altered foot shape, callus, visual impairment, living alone, renal impairment
72
What % of diabetic foot ulceration is due purely to sensory neuropathy?
45%
73
What % of diabetic foot ulceration is due purely to ischaemia?
10%
74
What is the remaining 45% of diabetic ulceration due to?
Mixed neuropathic and ischaemic
75
How does a purely neuropathic ulcered foot present?
Warm foot with palpable pulses, evidence of sensory loss, normal or high ABPI
76
How does a mixed neuropathic/ischaemic ulcered foot present?
Cool, absent pulses, ulcers situated on toe, heel, or metatarsal head, ABPI may be high.
77
How do we manage diabetic ulcers (general steps)?
Prophylaxis, Surveillance, Treat infection, revascularise, amputate
78
What prophylactic steps can we take to prevent diabetic foot ulcers?
Diabetic nurse/clinic checkups regularly, appropriate footwear, chiropody, keep feet cool, don't walk around barefoot
79
If there is infection present in a diabetic foot, what imaging should we do and why?
X-ray to look out for osteomyelitis
80
How do we attempt to revascularise a pt with diabetic foor tulcers?
Angioplasty, femorodistal bypass grafts
81
What are varicose veins?
Tortuous and dilated segments of veins, associated with valvular incompetence
82
Give me the stats for varicose veins.
Affects 35% of the population, M=F
83
What causes varicose veins?
Congenital, idiopathic (majority), or econdary to pelvic masses or pelvic venous abnormalities
84
What pelvic masses can cause varicose veins?
Pregnancy, uterine fibroids,, ovarian mass, pelvic tumour.
85
What are the clinical features of varicose veins?
Often just cosmetic concerns, but can cause pain, itchiness, swelling, aching, oedema, and can be worse under certain conditions.
86
What complications should we screen for when a pt presents with varicose veins?
Eczema, phlebitis, lipodermatosclerosis, ulceration, and bleeding.
87
What is the gold standard test for diagnosing venous valve incompetence?
Colour duplex
88
Why do DVTs occur?
Due to abnormalities vein wall, blood flow, or blood components i.e. Virchow's triad
89
What are some risk factors that cause vein compression and stasis tht can lead to DVT?
```
Immobility
Trauma
Mass
Surgery
Paralysis
Long distance travel (including airline)
```
90
What are some of the inherited risk factors for DVT?
Factor V Leiden
Protein C insufficiency
Protein S insufficiency
Antithrombin insufficeincy
91
What are some acquired hypercoagulable states that increase the risk of DVT?
```
Smoking
Surgery
Malignancy
Polycythaemia
HRT
OCP
Dehydration
```
92
What are the clinical features suggestive of a DVT?
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
What are the complications of a DVT?
PE and venous gangrene
94
What are the clinical features of a PE?
Dyspnoea, pleuritic chest pain, haemoptysis, dizziness, sncope, hypoxia, cyanosis, hypotension, pleural effusion, tachycardia
95
What tool do we use to work out a pts risk of having a DVT?
Well's score
96
What risk does a pt with a score of 0 have of having a DVT? What should we do now?
5% - a D-dimer should be done. If negative, DVT is ruled out.
97
What risk does a pt with a score of 1-2 have of having a DVT? What should we do now?
17% - With a positive D-dimer, a USS should be done.
98
What risk does a pt with a score of 3 or more have of having a DVT? What should we do now?
17-53% - very likely. Diagnostic USS should be done.
99
If we are suspicious of PE, what should we do?
VQ scan or CTPA (most sensitive).
100
Even though once a pt has a DVT we need to treat, what is better than treatment?
Effective prophylaxis
101
What conservative measures can we do for a DVT?
Elevate the limb and ensure good hydration
102
What determines the treatment for a DVT?
If it is complicated or uncomplicated.
103
How do we treat an uncomplicated DVT?
LMWH in hospital (or as outpatient, DVT clinic decides), then follow-up with warfarin for 3-6 months.
104
How do we treat a complicated DVT?
IV unfractionated heparin initially, or LMWH to convert to warfarin.
105
Do we do thrombolysis for DVT?
Only if severe thrombosis with venous gangrene
106
What can we do for a pt who has recurrent PE despite treatment?
A vena caval filter
107
What can occur aas a complication of extensive or recurrent DVTs?
Chronic venous insufficiency
108
What is the risk of thrombolysis?
Hameorrhage or stroke
109
What thrombolysis agents are there?
Streptokinase
tPA
Urokinase
110
Which thrombolytic is usually used?
Streptokinase
111
Tell me about streptokinase.
Cheap
Acts systemically
27 minute half life
S/Es include anaphylaxis, fever, and antibody resistance, which limits repeated use.
112
How quickly does a AAA need to be growing to be a high enough risk for surgery?
More than 1cm per year
113
If a patient has sudden arterial occlusion, what does the outcome depend on?
Timely intervention and state of collateral supply
114
When might a patient with acute limb ischaemia have good collateral supply?
Pre-existing chronic occlusive disease causing increased collateral supply
115
A patient who has had a tibial fracture suddenly develops acute limb ischaemia. What is the likely pathophysiology?
Compartment syndrome
116
Why is a red limb in acute limb ischaemia misleading?
It can be misdiagnosed as gout or cellulitis (some kind of inflammation)
117
Why can limb ischaemia cause red flushing of the limb?
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
What surgery is indicated for acute limb ischaemia?
Angioplasty (or open surgery)
119
If acute limb ischaemia is embolic in origin, what surgical intervention can be performed?
Embolectomy
120
Post-embolectomy, should a patient be anticoagulated considering they have just undergone vascular surgery?
Yes, usually wait until 6 hours post-surgery.
121
What is the management of irreversible ischaemic limb?
Amputation
122
Other than surgery, how should vascular disease be managed?
Lifestyle modicifcation - diet, exercise, smoking cessation.
| Modification of underlying disease - chiefly cholesterol, HTN, diabetes.
123
A patient is discharged from hospital following surgery for peripheral arterial disease. What main medications should they be discharged with?
Long term dual antiplatelet therapy (aspirin and clopidogrel), ACE inhibitor, and statin.
124
What are the complications of acute limb ischaemia?
- Reperfusion injury
- Chronic pain
- Loss of limb
125
Describe the pathophysiology of reperfusion injury?
- Neutrophils migrate to reperfused tissue
| - Increased capillary permeability due to inflammatory mediators causing limb swelling leading to compartment syndrome.
126
What is an ABPI below one indicative of?
Periperal arterial disease
127
Why is it important to do an ABPI on patients with venous ulcers?
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
What is a normal ABPI?
1.0 - 1.2.
129
What does an ABPI >1.2 signify?
Calcified, stiff arteries, usually associated with old age or T2DM.
130
What is an acceptable ABPI?
>0.9
131
What is the cut off for compression bandaging in terms of ABPI?
Compression bandaging is ok for anyone with ABPI >0.8
132
Describe a venous ulcer.
Large, shallow, painless, situated over medial or lateral malleoli.
133
Other than venous ulcers, what are the signs of venous hypertension?
```
Varicose veins
Varicose eczema
Haemosiderin pigmentation
Oedema
Skin thickening
```
134
What is the definition of an leg ulcer?
Loss of skin below the knee on the leg or foot
135
Which rheumatological condition is associated with increased risk of venous ulcers?
Rheumatoid arthritis
136
How is an arterial ulcer different to a venous ulcer?
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
Describe a neuropathic ulcer.
Painless
Deep
Overlying keratosis
Sites of nerve supply loss and recurrent trauma
Common in diabetics and chronic alcoholics
138
What kind of ulcers do RA patients get?
Rheumatoid ulcers as well as venous ulcers.
139
Describe a rheumatoid ulcer.
Sharp, deep, and well demarctaed.
Punched-out appearance.
Usually on foot and calf.
140
Do all venous ulcers need swabbing to rule out infection?
No, only those with markers of infection such as cellulitis.
141
When is a biopsy of a venous ulcer indicated?
If they have an atypical appearance or fail to heal afte 12 weeks of active treatment.
142
How can venous ulcers be managed?
- Graduated compression (after ruling out arterial insufficiency)
- Debridement and cleaning
- Dressings
- Antibiotics if infected
- Management of complications
143
What kind of dressings are used on venous ulcers?
- Occlusive hydrocolloidal dressings
- Alginate dressings
- Dressings containing topical growth factor
144
What improves prognosis of venous ulcer?
Increased mobility
No significant co-morbidities
Ability to walk
145
When should a venous ulcer be referred from primary care?
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
What is osteomyelitis?
Infection of the bone marrow, which may spread to the bone cortex and periosteum.
147
What does osteomyelitis lead to if it is untreated?
Inflammatory destruction of bone and periosteum causing necrosis.
148
How does chronic osteomyelitis lead to deformity?
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
What are the 2 types of osteomyelitis?
Haematogenous (bacterial seeding from remote source) and Direct (contiguous) osteomyelitis.
150
Which is the most common organism causing osteomyelitis?
Staph aureus
151
Why is the incidence of osteomyelitis increasing?
Increasing prevalence of risk factors such as diabetes mellitus and peripheral arterial disease.
152
Which demographic group is haematogenous osteomyelitis common in?
Children
153
A diabetic patient has a chronic persistent diabetic foot ulcer. What does this mean they are at high risk of?
Developing underlying osteomyelitis
154
How does osteomyelitis present?
- Fever, pain, and erythema
- Hx of accidental injury or surgical trauma
- -Long term overlying diabetic ulcer present
155
Why can osteomyelitis go undiagnosed in diabetic patients?
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
What are the differentials for osteomyelitis?
- Cellulitis
- Trauma
- Gout
- MSCC
- Acute sickle cell crisis
- Other causes of limp
157
What lab tests can confirm osteomyelitis?
- FBC with raised WCC
- Positive blood cultures - should ALWAYS be done
- Cultures of any discharge
- Bone culture is gold standard for diagnosis
158
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?
MRI - allows good visualisation of subtle abnormalities.
159
What are the main aspects of management for osteomyelitis?
Abx for 4-6 weeks
Surgical debridement
Analgesia
160
What complications can arise due to osteomyelitis?
- Bone abscess
- Sepsis
- Fracture
- Septic arthritis
- Cellulitis
- Chronic infection
161
What is peripheral arterial disease?
Significant narrowing of arteries distal to arch of aorta, usually due to atherosclerosis.
162
What are the degrees of peripheral arterial disease?
- Asymptomatic
- Intermittent claudication
- Critical limb ischaemia
- Skin ulceration and gangrene
163
Can the upper limbs be affected by peripheral arterial disease?
Yes - usually the subclavian artery and brachiocephalic trunk.
164
How common is peripheral arterial disease?
Very - 15-20% of people over 70 are affected.
165
What are the big risk factors for peripheral arterial disease?
- Smoking
- DM
- HTN
- Hyperlipidaemia
- Physical inactivity
- Obesity
166
A patient presents with intermittent claudication. What other areas in the body are at risk of vascular disease, and should be screened for?
- Coronary arter disease
- Cerebrovascular disease
- Aortic aneurysm
- Kidney/bowel
- Upper and lower limbs
167
How is a diagnosis of PAD confirmed?
Doppler ultrasonography
168
Why are ACE inhibitors needed but closely monitored in pateints with PAD?
To manage HTN and reduced cardiovascular morbidity and mortality, but 25% of PAD patients have co-existing renal artery stenosis.
169
What is angioplasty?
Endovascular surger where a balloon is used to widen narrowed or obstructed arteries or veins.
170
What is gangrene?
Death and decay of body tissue due to lack of blood supply.
171
What are the 2 main types of gangrene?
Dry and wet
172
What is dry gangrene?
Death and decay of tissues due to diminished lood supply, usually due to peripheral arterial disease.
173
Other than peripheral arterial disease, what can cause dry gangrene?
Vasculitis and other conditions that cause vasculitis
174
What is the pathophysiology of wet gangrene?
Tissue infection causing swelling -> inflammation -> blockage of blood vessels -> tissue death -> gangrene associated with infection and discharge.
175
Which parts of the body are usually affected by gangrene?
Extremities most often, but also rest of limbs and the GI tract.
176
What are the symptoms of wet gangrene?
- Systemic upset
- Swelling
- Erythema
- Pin
- Discharge
- Foul-smelling
- Blackening of skin
177
What are the symptoms of dry gangrene?
- Systemic upset
- Erythema
- Coldness and pallor
- Numb
- No discharge
- Brown then black skin
178
What imaging is used with gangrene, and why?
X-ray - detect gas.
CT/MRI - detect extent of local involvement.
179
Are antibiotics used to manage gangrene?
Yes, however they won't penetrate the dead tissue but will help prevent the spread of infection
180
How is wet gangrene managed?
- Analgesia
- Broad spec abx
- Surgical debridement
- Amputation may be necessary
- Management of risk factors
181
How is dry gangrene managed?
- Restoration of blood supply
- Amputation may be required
- Management of risk factors
182
What is the main complication associated with gangrene?
Sepsis
183
What kind of gangrene is gas gangrene?
Life-threatening Wet gangrene
184
What organism most commonly causes gas gangrene following trauma or surgery?
Clostridium perfringens
185
What organism species most commonly causes gas gangrene?
Clostridium species
186
How does gas gangrene occur?
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
What can predispose someone to gas gangrene?
Anything that means a tissue might not be in best condition e.g. alcohol abuse, malnutrition, trauma, DM, steroid use, malignancy.
188
How does the appearance of gas gangrene differ to other gangrene?
It appears cellulitic at first then progresses to dark purple with vesicles and bullae.
Sub-cut air may be present on palpation.
189
How should gas gangrene be managed?
- Supportive
- Surgical debridement
- Abx
190
Which dermatological condition affects vessels?
Vasculitis (and conditions that cause vasculitis).
191
What can cause vasculitis?
- Idiopathic (aound half)
- Infection
- Inflammatory disease
- Drug-induced
- Neoplastic
192
How is vasculitis classified?
According to what it affects
193
How does medium-sized vessel vasculitis present?
- Ulcers
- Digital infarcts
- Nodules
- HTN due to renal vessle damage
194
How does small-sized vessel vasculitis present?
- Palpable purpura
- Splinter haemorrhages
- Urticaria
- Vasicles
195
What is an aortic dissection?
Disruption of medial layer of wall of aorta due to intramural bleeding, leading to separation of aortic wall layers.
196
What is the main associated disease with aortic dissection?
Hypertension
Classically though all the usual vascular risk factors apply.
197
What inherited conditions and congenital issues increase risk of aortic dissection?
- Ehlers-Danlos syndrome
- Marfan's syndrome
- Congenital aortic valve problems
198
How are aortic dissections classified?
Into Stanford A and Stanford B
199
What is the difference ebtween a Stanford A and a Stanford B aortic dissection?
A affects ascending aorta, and B does not.
200
How does aortic dissection present?
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
How do patients classically describe aortic dissection pain?
Ripping pain, usually in back or chest.
Sudden onset.
Usually migrates as the dissection progresses.
