Vascular Surgery Flashcards
Pathophysiology of PAD
Atherosclerosis
Stable clots may be asymptomatic or ass w stable claudication. Unstable clots can cause sx such as rapid onset progressive claudication, CLTI or ALI.
- Accelerated atherosclerosis 40-55y
- Precocious atherosclerosis <40
- Hypercoagulable states (Antiphospholipid syndrome, hyperhomocysteinaemia, cancer)
- Vasculatides (Scleroderma, RA, SLE, Takayasu)
- Popliteal entrapment syndrome
- Anterior compartment syndrome
- Fibromascular dysplasia
- Iliac endofibrosis in cyclists
- HIV related PID
Etiology of acute limb ischaemia
Embolism (Cardio embolism and arterial embolism)
Thrombosis (Vascular graft thrombosis, Instent thrombosis, natives artery thrombosis, peripheral aneurisms)
Trauma (blunt or penetrating)
Iatrogenic injury (post catheterisation, following surgery)
Malperfusiom (aortic dissection, isolated PAD -dissection)
Thrombophilia
Which drugs are contraindicated in patients undergoing thrombolysis after acute limb ischemia
IM opiates
Heparin alone in acutethreatened limb- give calcium heparin (potential for immediate reversal with protamine)
Which aneurysm are likely to rupture
Aortic aneurysms
Which aneurysms are likely to develop thrombotic or thromboembolic complications
Non aortic
Triad of ruptured AAA
Sudden onset of severe backache
Shock
Pulsatile abdo mass
Hard man risk index in assessing for mortality rate in surgery for ruptured AAA
- Age >79
- Systolic <90 persistently
- Creatinine >179
- HB <9
- ECG showing ischemia
If 3 or more of these present 100% mortality with surgery
If 2 70% mortality
Differential for Charcot osteoarthropathy
Gout
Cellulitis
Osteomyelitis
How do you examine the foot
- Pulses
- Trophic changes (hair, muscles, skin, nails)
- Features of CLTI (Buergers test and Goldfam test)
- Peripheral neuropathy (sensory, reflexes, deformities claw/hammer)
- Chronic venous disorder (DVTs- claudation, swelling, hyperpigmentation)
- Musculoskeletal disorders (spine tenderness, swollen joints)
- Unusual skin lesions (Rheumatoid nodules etc)
- Peripheral aneurisms
Basically : Neuropathy, Ischemia and Deformity (callus, swelling, ulcer, infection, necrosis)
Normal ABI
Normal percutaneous oxygen
ABI 0.9 to 1.3
O2: >55mmHg
What foot deformities are found in diabetic feet patients
Skin cracks, fissures from dry skin
Callus
Claw/ hammer toes
Fixed flexion deformities of PIPs
Pes cavus
Rocker bottom feet
Hallux valgus and hallux rigidis
Charcot foot
Leads to bony prominence leading to high pressure and ulceration
Pathophysiology of DVTs
Virchows triad!
Coagulation cascade = prothrombin factors + antithrombotic modulation
DVT develops when there is an imbalance in prothrombotic direction (more clotting)
Virchows triad=
1. Hypercoagulability/ Thrombophilia (procoagulant process within blood)
2. Damage to vessel wall (chemical or physical)
3. Slow blood flow
Outline the types of thrombophilias according to the inherited and acquired groups
Inherited
Reduced anticoagulants : Protein C, Protein S, Antithrombin
Increased procoagulants: Factor 5 Leiden (mutation)
-Elevated clotting factors (7, 9, 11, Fibrinogen)
-Hyperhomocysteinaemia
-Lipoprotein
Acquired
-Antiphospholipid syndrome
-Malignancy
-Pregnancy
-Exogenous hormones
Which DVTs are proximal and which are distal
Proximal: iliac, femoral, popliteal
Distal: deep calf
Risk factors for DVTs
PV 276
Which models can we use to predict likelihood of someone having a DVT
Wells Score - based on Clin features and hx
Prev DVT
Active ca tx
Major surgery within 12weeks requiring general or spinal, or recently bedridden for 3days
Recent plaster immobilisation of lower extremety, or paralysis or paresis
Entire leg swollen
Localised tenderness all on deep venous system distribution
Calf swelling atleast 3cm larger than asymptomatic side
Putting oedema confined to symptomatic side
Collateral superficial veins
Alternative dx atleast likely as DVT
How to diagnose DVTs
- Wells score (2 or more, DVT likely)
- D-dimer (presence of fibrin from degradation of cross linked fibrin by plasmin. sensitive for dx of thromboembolism- seen in malignancy, infection,DiC, trauma)
- Duplex Ultrasonography (diagnostic test of choice): can distinguish among non vascular pathologies eg bakers cysts, abscess, hematoma
- CT and MRI (when US isn’t adequate)
- Invasive venography (for intervention not dx) contrast injected into vein
Early and late complications of DVT
Early
1. PE
2. Threatened limb
Late
1. Pulmo HPT
2. Post-thrombotic syndrome
Initial treatment of DVTs
- Immobilisation and elevation
- Anticoagulation:
-IV Unfractured heparin (5-10days then oral anticoagu) or High dose subcutaneous LMWH (better, outpatient)
-DOAC (for factor Xa eg Rivaroxaban and Apixaban) - Early thrombus removal
—endovascular using thrombolysis teleplase
Long term tx of DVTs
- Extended anticoagulation
Was initially Vit K antagonist now DOAC - Elastic stockings for prevention of post thrombotic syndrome (pressure 20-30mmHg or > at ankle)
- Vena cava filters (if anticoag doesn’t work)
INR 2-3 should be achieved 24-48 hrs before heparin is discontinued
Usual starting dose of warfarin is 5g -10g
Which anticoagulants are effective in cancer patients
LMWH and DOAC
VitKA ineffective
Factors associated with/w poor outcome in AMI mx
Age
Comorbidities
Extensive of necrosis
Perforation and peritonitis bowel
Management of PAD
Risk factor modification
-weight loss
smoking cessation
hypertension control
DM control
Antiplatelet
Lipid lowering
Proper foot care
Pharmacological
-Antiplatelet therapy: Asprin 81mg-150mg
-Anti-lipid therapy: Simvastatin 40mg or Rovustatin 10mg (target LDL<2.6 or 1.8 in prev MI, DM, PAD)
Pharmacotherapy of Claudation
Cilostazol: phosphodiesterase type 3 inhibitor, increases CAMP. Vasodilatory+ platelet inhibitory
Naftodrofuryl
L-carnitine and propionyl-L-carnitine
What do we take into consideration when deciding Ethernet surgical and end ova sculpt management in PAD
(PLAN approach)
Patient fitness and life expectancy
Extent of Limb lesion
Anatomical distribution of occlusive disease in affected limb
