Vasculopathies - Aortic Aneurysm, Peripheral Vascular Disease, Ulcers Flashcards
Pathophysiology of atherosclerosis
Endothelium damaged by sheer stress
Monocytes adhere and penetrate to damage => macrophages
- absorb oxLDL => foam cells => die and form lesion core
- cytokine release => aggregation of more macrophages, SM proliferation
SM forms fibrous cap
Plaque rupture => thrombosis, coronary artery block
Peripheral arterial disease
- disease progression and presentation
- diagnosis and investigations
- management
SMOKING - GREATEST RISK FACTOR
Intermittent claudication - 0.5-0.9
- pain on exertion (few mins) relieved by rest
-feet, calf, thigh, bottom
- cold, dry skin, no hair
- weak pulses
Management
- CV risk optimisation (statin, smoking cessation, clopidogrel)
- supervised exercise programme
- angioplasty/bypass surgery
Critical limb ischemia - U0.5
- burning pain on rest
- arterial ulcers, gangrene
- cold, dry skin, no hair
- no pulses
Management
- analgesia
- angioplasty if U10cm stenosis
-bypass if 10cm+
-distal aorta + bilateral common iliac occlusive disease - aorto bifemoral bypass
-amputation if gangrenous
Pulse check
ABPI - ankle BP:brachial BP
Duplex US - confirm diagnosis
Aortic dissection
- pathophysiology
- risk factors
Tear in intima => weakens aortic wall => rupture
-occlusion of branching vessels => ischemia of affected areas
STRONGEST - HTN, connective tissue disorders
-CV risk factors
Aortic dissection
- presentation and signs
- investigation and diagnosis
Sudden, severe tearing pain between shoulder blades
Chest/back pain
SOB
RR/RF delay
BP difference between both arms
If unstable => ALS, A-E resus
HOE
B
- ECG - can be some non specific changes
B
-FBC, U&E, G&S and crossmatch
I
-CXR - wide mediastinum
-CT angio - false lumen
-Transesophageal echo if too unstable for CT
Aortic dissection
-types and the management
Type A (most common) - proximal to LSC
SURGICAL REPLACEMENT OF AA
-permissive hypotension, IV labetolol
- transfusion
Type B - distal to LSC
CONSERVATIVE MANAGEMENT
- bedrest, analgesia, IV labetolol
- consider TEVAR
Abdominal aortic aneurysm
- pathophysiology
- risk factors
Dilation of all 3 layers => 3cm+
MOST COMMONLY - infrarenal
CV risk factors
Connective tissue disorders
Abdominal aortic aneurysm
- presentation and signs
- investigation and diagnosis
Back, abdo pain
Abdo pulsation
Bruit on auscultation
Grey-Turners
SHOCKED => RUPTURE!
Diagnostic - Abdo USS
HOE
B
-ECG
B
-FBC, U&E, CRP, G&S and crossmatch
I
-CT angio, MRI
Abdominal aortic aneurysm
- screening
- management
Screening
65+ males US
U3cm - :)
3.0-4.4cm - yearly
4.5-5.5 - 3monthly
5.5+ - 2w vascular referral
Surveillance - CV risk optimisation
Elective surgical repair
-5.5+, asymptomatic
-4cm+ and grown by 1cm in 1 year
Urgent surgical repair
-symptomatic/ruptured
What are ulcers
Abnormal breaks in skin or mucous membranes
Venous ulcers
-risk factors
-pathophysiology
Most common ulcer
Increased venous pooling => reduced venous return => uneven, impaired tissue perfusion => ulceration, delayed healing
Age
Existing/Hx venous problems
-VTE
-varicose veins
Pregnancy, obesity, physical inactivity
Leg trauma
Venous ulcer
-presentation
Before ulcers appear - Aching, itching
Painful
Superficial, irregular borders
Gaiter region
Leg edema
Varicose veins
Infection prone (cellulitis)
Hemosiderin staining - hemosiderin pools in veins
Venous eczema
Lipodermatosclerosis - wine bottle
Atrophie blanche - white scar after ulcer heals
Venous ulcer
-investigations
Clinical diagnosis
Investigation only confirms findings
-insufficiency confirmed by duplex
-ABPI to check whether there is sufficient arterial flow
If infection present - swabs and ABx
Venous ulcer
-management
Definitive - compression bandaging until ulcer has healed
Compression stockings to prevent recurrence of ulcers
Conservative - leg elevation, increased physical activity
-weight reduction
ABx if infection found
Arterial ulcer
-risk factors
-pathophysiology
CV risk factors
Reduction in arterial blood flow => reduced perfusion and poor healing
Arterial ulcer
-presentaton
Existing intermittent claudication or critical limb ischemia
Develops over long period of time with v little healing
Small deep lesions
Well demarcated
Long CRT
Patient may sleep in a chair, increase blood flow to legs
Distal to trauma sites
Pressure areas
Cold limbs
Reduced/no pulse
Thick, necrotic toes
Hair loss
Shiny taut skin
Arterial ulcer
-investigations
Clinical diagnosis but confirm location and severity with investigations
ABPI - measure severity of PAD
1 = :)
0.5-0.9 = PAD
U0.5 = critical limb ischemia
Duplex => assess location of arterial disease leading to distal ischemia
Arterial ulcer
-management
Vascular review needed if ulcers present (critical limb ischemia)
Conservative - CV risk lifestyle changes
Medical - lipid modification, aspirin, HTN, DM
Surgical - if extensive disease
-angioplasty, stenting if U10cm
-femoral artery bypass if 10cm+
Neuropathic ulcer
-risk factors
-pathophysiology
Result of peripheral neuropathy
-loss of protective sensation => unnoticed injuries resulting in painless ulcers on pressure points
Healing complicated by concurrent vascular disease
Most common causes
-DM
-B12 deficiency
Ulcer risk made worse by existing foot deformity, PVD
Neuropathic ulcer
-presentation
Hx of peripheral neuropathy
-burning, tingling, pain in legs
-weakness, balance issues
-length dependent neuropathy
Hx of PVD
Punched out appearance of ulcers on pressure sites
Warm feet, pulses unless concurrent arterial disease
Difference between wet and dry gangrene
-management
Gangrene - tissue death from ischemia
Management - debridement, amputation if needed
Dry - chronic ischemia without infection
-cannot be saved
Wet - ischemia leading to necrosis + bacterial infection
Neuropathic ulcers
-investigations
Glucose check
B12 check
Assess for arterial disease - ABPI, duplex
If infection - swab
Assess extent of peripheral neuropathy with tuning fork
Neuropathic ulcers
-management
Optimise diabetic control
-HbA1c
-diet, exercise
Optimise CV risk factors
Regular chiropody
foot hygiene
good footwear
Signs of infection - ABx
Ischemic/necrotic tissue - debride or amputate
If painful - neuropathic agents
Duloxetine - unless eGFR U30
Amitriptyline - safe in renal impairment
Gabapentin
Pregabalin
What is Charcot’s Foot
Loss of joint sensation => continuous joint trauma leading to foot deformity
-increased risk of neuropathic ulcers
Swollen, distorted, painful foot
Specialist review needed
offload abnormal weight
immobilise joint in plaster
Lymphodema
-causes
-investigations and diagnosis
-management
Cancer treatment
Cellulitis - damages lymphatics
Inflammatory conditions
Venous insufficiency
Obesity, immobility, trauma
Clinical diagnosis
-confirmed with lymphoscintigram
Supportive - skin care
Definitive - compression garments
-elevation, exercise, weight reduction
Mesenteric ischemia
-presentation
-definitive diagnosis
Minimal clinical signs
Distended abdo
Diffuse tenderness
No guarding => no peritonitis
Tympanic abdo
Abdo pain out of proportion to clinical findings
High LACTATE!
CT angiogram
Mesenteric ischemia
-management
Quick restoration of blood flow
-keep laparotomy open for 2nd look
Remove necrotic bowel
Manage ends of healthy bowel with stoma
Short gut syndrome management
Peripheral arterial disease
-3 types
Intermittent claudication
Critical limb ischemia
Acute limb-threatening ischemia
Acute limb-threatening ischemia
-presentation
-investigations
6Ps
-pale
-pulseless
-pain
-paralysed
-paraesthetic
-perishingly cold
Handheld arterial Doppler
ABPI
Differentiating between thrombus and embolus in acute limb ischemia
Thrombus
-known claudication with sudden deterioration
-no clear source of emboli
-reduced/no pulses in other limb
-evidence of widespread CVD
Embolus
-sudden onset pain
-no Hx of claudication, PAD
-clear source of emboli
Acute limb ischemia
-initial management
-definitive management
Initial
-A-E
-IV opioids, heparin
-vascular review
Definitive
-intra-arterial thrombolysis
-surgical embolectomy
-angioplasty
-bypass
-amputation is irreversible
