Vascular System - VV, DVT, Leg Ulcers Flashcards
Thrombus definition
Mass of normal blood constituents formed inappropriately within the circulation during life
What are thrombus’ composed of
Fibrin
Platelets
Entrapped R/WBC
Where can thrombus’ form
Cardiac chamber
Vessels
Microscopy of thrombus’
Laminations visible, called Lines of Zahn
Haemostasis vs thrombosis production
Haemostasis is a physiological response to injury of blood vessels
Thrombus production is a pathological repose (activated inappropriately)
Mechanisms of haemostasis
Injury –> loss of lining endothelial cells
Exposure of underlying ECM, activates platelets –> 1’ haemostatic plug
Coagulation cascade activates
Thrombin and fibrin produce 2’ haemostatic plug
Main components of controlled haemostasis
Endothelial cells
Platelets
Coagulation cascade
Anti-thrombotic properties of endothelial cells
Antiplatelet
Anticoagulant
Profibrinolytic
Antiplatelets in endothelial cells
Prostacyclin
NO
Anticoagulants in endothelial cells
Antithrombin III
Thrombomodulin-activated proteins C/S
Profibrinolytic in endothelial cells
Tissue plasminogen activator
When do endothelial cells exert a prohaemostatic effect
If injured or activated
Pro-platelet
Pro-coagulant
Anti-fibrinolytic
Pro-platelet factors in endothelial cells
Von-Willebrand factor
Platelet activating factor
Pro-coagulant factors in endothelial cells
Tissue factor
Anti-fibrinolytics in endothelial cells
Plasminogen activator inhibitors
What are platelets produced by
Megakaryocytes in blood
What are platelets activated by
Exposure to sub endothelial ECM
What happens after platelets are activated
Adhesion
Platelet release reaction
Platelet aggregation
Types of coagulation pathways
Intrinsic
Extrinsic
Common
Virchow’s Triad
Change in blood flow
Change in vessel wall
Change in blood constituents
What does disruption to laminar flow cause
Platelets to come into contact with endothelium
Injury or activation of endothelium
Impaired removal of pro-coagulant factors/ impaired delivery of anti-coagulant factors
Causes of altered blood flow
Atherosclerosis (narrowing) Aneurysm Infarcted myocardium Abnormal cardiac rhythm Valvular heart disease
Changes in blood flow are seen in which condns
Following MI
AF
Rhemuatic heart disease, following Group A strep infection
How does an MI change the blood flow
Fibrotic (healed) myocardium may dilate forming ventricular aneurysm and turbulent blood flow
How does AF cause changes to blood flow
Irregularly irregular rhythm of heart can cause blood to pool in atria –> thrombus formation
Can also embolise into systemic circulation
How can rheumatic heart disease cause changes to blood flow
Following Group A strep infection, can destruct mitral valve
Turbulent flow as blood passes through slit like valve
Causes of altered blood flow - veins
Usually stasis
What can cause stasis in veins
Immobilisation
Compressed veins e.g. bed rest
Varicose veins
Increased blood viscosity e.g. sickle cell, dehydration
Factors causing endothelial cell injury
Ischaemia hypoxia
Infection of blood vessels
Physical - atheroma, crushed veins, HTN
Chemical - lipid, cigarette
Immunological deposition of immune complexes
Genetic changes in constituents in blood leading to thrombosis
Antithrombin II deficiency
Protein C
Acquired changes in constituents in blood leading to thrombosis
Tissue damage Post-op Malignancy Cigarette smoke Elevated blood lipids Oral contraceptives
What are the options of a thrombus remains attached
Lysis
Retraction and recanalisation
Organisation
Infection
What happens if a thrombus detaches
Embolises - either sterile, infected or septic
Embolus
Abnormal mass of undisolved material which is transported from one part of circulation to another
Types of emboli
Thrombus Gas - air, nitrogen Fat Tumour Misc - foreign bodies (drug addicts), amniotic fluid
What can happen if emboli lodge in pulmonary artery
Hypoxia Reduced cardiac output Pulmonary infarction Pulmonary HTN Right heart failure Death
Size of thromboembolism determines symptoms
Sequelae to PE
Sudden death R sided heart failure - 60% of circulation is obstructed Organisation of embolism Pulmonary infarction Pulmonary HTN
PE - saddle embolus
Occludes both pulmonary arteries
PE - paradoxical embolus
Passes through interatrial or interventricular cardiac defect to gain access to systemic circulation
Effects of emboli - arterial
Emboli from L side of heart will enter systemic arterial system
Iscahemia/ infarction occurs
Bacterial endocarditis vegetation on inner surface of aortic valves
What may infected emboli give rise to
Pyaemia and access formation
Pyaemia
Type of sepsis leading to widespread abscesses of metastatic nature
Caused by pus-forming bacteria
How may air enter circulation
During obstetric procedures
In chest wall injuries
When does air in the circulation have a clinical effect
More than 100cc
Effect of air embolus
Bubbles coalesce to form frothy masses with may occlude major vessels
Who do nitrogen emboli occur in
Deep sea divers on rapid ascent
When can fat globules be found in circulation
Fracture of long bones
Soft tissue trauma
Burns
Symptoms of fat embolism
Tachypnoea Tachycardia Dyspnea Irritability and restlessness Diffuse petechial rash (20-50%) Thrombocytopenia
What is seen with amniotic fluid embolus
Dyspnoea, cyanosis, HTN
DIC, seizures, shock
Mortality >80%
Leg ulcer definition
Loss of skin below the knee on the leg/foot, which takes >2 wks to heal
Break in continuity of covering epithelium
Epidemiology of ulcers
1% will suffer from leg ulceration at some point
Prevalence 1.5 to 3 per 100 and increases with age
Aetiology of leg ulcers
Venous insufficiency (60-85%) PAD (10-20%) Mixed arterial and venous disease Neuropathic diabetic ulcer RhA Systemic vasculitis Lymphoedema Trauma Malignant ulcer Infection
Vascular causes of leg ulcerations
Venous
Arterial
Mixed arterial and venous aetiology
Lymphatic
Vascular causes of leg ulceration - venous
Venous insufficiency
Varicose veins
Post-phlebitis
post sclerotherapy
Vascular causes of leg ulceration - arterial
Atherosclerosis Buerger's disease Vasculitis Raynaud's Diabetic foot ulceration
Types of veins in LL
Superficial
Deep
Perforator
Superficial veins of LL
Long saphenous vein
Short saphenous vein
Deep veins of LL
Anterior & posterior tibial veins
Peroneal veins
Popliteal vein
Femoral veins (Profunda femoris and superficial femoral vein)
VV definition
Dilated, tortuous,superficial veins > 2mm diameter
Main cause of VV
Increased venous pressure –> valvular incompetence
What can cause post-ambulatory HTN
Ineffective calf muscle contraction
Incompetent valve
Veins that aren’t patent
Normal post-ambulatory venous pressure
<25mmHg
As the pressure increases as does incidence of venous leg ulcers
Causes of venous HTN
Superficial venous reflux
Deep venous reflux & occlusion
Perforating vein reflux
Cause of primary deep venous reflux & occlusion
Idiopathic
Cause of secondary deep venous reflux & occlusion
Caused by DVT or injury
Causes of perforating vein reflux
Abnormal calf pump
Neurological
MSK
What do incompetent valves in the calf lead to
Backflow of blood and the veins elongate and become tortuous
Increase in pressure –> leakage of blood particles and fluid
Overload of lymphatic system –> oedema
Leads to lymphovenous oedema
Venous insufficiency
Irreversible skin damage as the result of sustained ambulatory venous HTN
In which group of people, do venous ulcers take longer to heal
People from lower socioeconomic groups
Also have higher recurrence rates
When do venous leg ulcers become chronic
If they remain unhealed after 4 weeks
Risk factors for venous leg ulcers
Obesity Immobility Personal of Fhx of VV Personal hx of DVT Arteriovenous fistula Increasing age Hx of leg fracture or trauma Prolonged standing Late pregnancy
Most important factors causing venous HTN
Venous insufficiency
Obesity
Immobility
Causes of secondary valvular incompetence
Post-phlebitis Venous obstruction Muscle pump dysfunction Aging/ leg pathologies Valvular hypoplasia/agenesis
Hypothesis of microvascular pathophysiology of venous ulcers
White cell trapping hypothesis
Fibrin cuff hypothesis
Atherosclerosis development and progression
Fatty streak
Fibrous plaque
Complicated plaque - haemorrhage, ulcerated plaque, calcified plaque
Neuroischaemic (diabetic) foot ulcers are seen in what % of DM pts
1–25%
Pathophysiology of diabetic foot ulcers
Neuropathy predisposed foot to ulceration through its effect on the sensory, motor and autonomic nerves
Loss of protective sensation (pressure, pain & temp) render pt vulnerable to physical, thermal and chemical trauma
Link between sensory neuropathy and ulceration
Increase risks of ulceration by 7x
Motor neuropathy and ulceration
Motor neuropathy –> weakness and atrophy of foot muscle –> altering foot structure –> deformity and altered biomechanics
Autonomic neuropathy and ulceration
Autonomic neuropathy is associated with dry skin –> fissures, cracking, and callus
Clinical hx of leg ulcers
Mode of onset/ precipitating event Duration of ulcer Symptoms (pain, discharge, systemic features) Risk factors Peripheral ischaemic symptoms Previous interventions
Clinical assessment of leg ulcers
Hx
Clinical exam of ulcer and surroundings
Vascular system exam (arterial and venous)
Neurological examination if diabetic foot ulcer suspected
Clinical exam of ulcer and surroundings
Number Site Size Shape Floor Edge/ margin Base Discharge? Depth Surrounding skin Exam of arterial, venous and neurological systems Exam of nutritional status or anything that may prolong healing
Venous hx for ulcer
VV DVT/ thrombophlebitis Previous ulceration Previous treatments (e.g. foam sclerotherapy) Oedema Pain or lack of? Precipitating factors Co-existence - PVD, DM, RhA
Arterial hx for ulcer
IC
Ischaemic rest pain
Risk factors for PAD
Previous arterial intervention
Stages of venous leg ulcers
Exudative phase
Granulation stage
Chronic infl and scar formation
What are you looking for in a venous clinical exam
VV Oedema Skin changes Healed ulcers Active ulcers
Skin changes seen in venous disease
Varicose eczema
Haemosiderin staining
Lipodermatosclerosis
Atrophie blanche
Neuroischaemic clinical exam
Inspection - dry skin, absence of hair, ingrown nails, calluses, fissures
Hammer toe deformity
Charcot’s deformity
10g monofilament test
128Hz tuning fork
Ix - venous ulcer suspected
Venous duplex
CT venogram
MR venography
Standard venography
Ix - arterial ulcer suspected
Arterial duplex
CT peripheral angiogram
MR angiography
DSA
Mainstay of ulcer management
Treat underlying cause
Mx of venous leg ulcer
Compression for 3/12 (only if no arterial insufficiency and no infection)
Determine whether deep, superficial or functional problem
Consider surgery if superficial
Consider skin grafting if fails to heal
Surgery for superficial venous ulcers
Endovenous radio frequency ablation
Endovenous laser ablation
Endovenous foam sclerotherapy
What does mx of venous leg ulcer involve
Cleaning and dressing the ulcer Compression therapy Wound swab and abx - if infected Arranging follow up for reassessment Referring to specialist if hasn't healed after 2 wks in primary care
Deep venous procedures
Catheter-directed thrombolytic therapy for DVT
Self-expandable metallic stent placement of pt has significant post-thrombotic complications
Complications of venous leg ulcers
Immobility due to pain Infection Sepsis Contact dermatitis Sinus formation and fistula -ve impacts of QoL OM
What is suggestive of sepsis in ulcer pt
Tachycardia
Fever
Chills
What is suggestive of OM in an ulcer pt
Fever
Disproportionate pain
Systemically unwell
Bone at base at wound
Mx of arterial ulcers
Revascularisation
Treating mixed aetiology leg ulcers
Arterial component must be treated first
ABPI<0.8 means pts needs lower levels of compression (modified compression)
Mx of diabetic foot ulcers
MDT approach Good BM control Treat infection Revascularise Off-load ulcer
Preventing recurrence of venous ulcers
Education and lifestyle changes
Wearing appropriate compression stockings for 5 hrs
Follow up every 6/12 - 12/12 to identify risk factors
Doppler APBI every 6/12
Preventing recurrence of arterial/ neuroischaemic ulcers
Report worsening symptoms Keep skin moist Never walk barefoot Ensure shoes are well fitting Give up smoking Exercise
Prognosis of venous ulcers
Healing rates of 70% have been achieved
Factors associated with failure of venous ulcer to heal within 24 wks
Initial size of ulcer Longer ulcer duration at px
Hx of surgical treatment for VV
Hx of hip or knee replacement
ABPI < 0.8
When is the prognosis of arterial ulcers good
If revascularisation procedures are successful, pt modifies lifestyle and takes antiplatelets and statins
What do we call thrombosis in superficial veins
Superficial thrombophlebitis
Treatment of DVT in pregnancy
LWMH as DOACs and warfarin can cross placenta
Where does the long saphenous vein start
In front of MM
Does the SSV run behind or in front of LM
Behind
SFJ
Sapheno-femoral junction
Where long saphenous vein drains into femoral vein
SPJ
Sapheno-popliteal junction
Where the short saphenous veins drains into popliteal vein
Found posterior
Where can valvular incompetence in the leg be
4 diff areas
SFJ
Mid thigh perforators
SPJ
Mid calf perforators
When can you not refer a DVT to VTE clinic
If there is a suspected PE
Most common artery to stenose in leg
SFA
Leg cellulitis vs a/c DVT
Much warmer
Redness expands over time
If limited to anterior aspect, most likely leg cellulitis
How can impacts of serious illnesses be grouped
Practical and domestic Emotional Social Spiritual Financial
Kubler-Ross grief
Denial Anger Bargaining Depression Acceptance
Open family systems
Communicate freely
Flexible boundaries
Rules are up to date and promote growth
Closed family systems
Indirect/ restricted communication
Overly dependent on one another
Inflexible rules
Roles of carers for those w/ terminal illnesses
ADL
Mediating
Nursing tasks
Issues of concern for carers
Ability to provide care Stress Uncertainty Fear Conflict Altered role and lifestyle Own physical health Finances
Problems faced by carers
Extra demands on time/ energy
Changing roles/ responsibilities
Changing ability to work
Pressure to continue caring and have life outside
Effective palliative care
Symptom control Psychological support Communication Info Practical support End of life care Bereavement support
Families at risk of struggling with being a carer
Other children/ family members already disabled Single parent families Families separating/ divorcing 'Dysfunctional families' PMH mental health problems Cultural/ lang difficulties
Signs of a struggling family
Frequent call outs to GP or district nurse Illness of carer Rship breakdowns within family Symptoms not responding to treatment Psychological distress in carers or pt 'I can't cope'
Recommendation for carers
Take breaks Take care of self Understand limits Get help Professional support e.g. palliative care
Where can families get help with symptom control
GP
Specialist nurse
Palliative care specialists
Where can families get help with Nursing
District/ community nurse
Where can families get domestic support from
Social services
Where can families get psychosocial support
GP
Macmillan nurse
Bereavement counsellors
Where can families get support with aids and appliances
OT/ PT
Where can families get financial support from
Social worker
Macmillan benefits officer
Condns caused by thrombotic problems
MI
Stroke
PAD
Deep venous occlusion
Major risk factors for venous thrombosis
Major surgery Late pregnancy LL fracture Malignancy Reduced mobility Previous DVT
Minor risk factors for venous thrombosis
Congenital heart disease Cardiac failure HTN Central venous catheter Oral contraceptives option/ HRT Thrombotic disorder Obesity, COPD
LL DVT clinical features
Painful, swollen hot LL
Prominent superficial veins
Acute onset
Ddx of DVT
Cellulitis Ruptured popliteal cyst Muscle tear/ haematoma Fracture Lymphoedema Hypoproteinaemia
Where else can DVTs occur
Cerebral sinuses
Arms
Retina
Mesentery
Ix for LL DVT
Ascending venography
Ultrasound
Nuclear med, CT, MR plethysmography
D-dimer
Ultrasound for DVT
Normal veins are compressible and demonstrate venous pattern flow
Thrombus may be visible
When would you repeat a CT for a suspected DVT if unsure
3-5 days
What is D-dimer
Degradation products of cross-linked fibrin
When is D-dimer released
When the fibrinolytic system attacks the fibrin matrix of fresh venous theromboemboli
What does the absence of a raised conc of D-dimer imply
There is no fresh thromboembolic material undergoing dissolution in the deep veins/ pulmonary artery tree
What can cause false +ve in D-dimer test
Cancer PAD Many infl/ infective conditions Post-op Increasing age
Clinical features part of Well’s score
Active cancer Paralysis/ LL immobilisation Bedridden/ major surgery <4 wks Localised tenderness along deep venous system Calf swelling Pitting oedema Dilated collateral superficial veins Pregnancy
Lose 2 points if alternative dx is as likely
Measuring calf swelling in DVT
Measure circumference 10cm below tibial tuberosity
Significant is >3cm difference
Wells’ score of 1 or 2
Moderate possibility of DVT
Check D-dimer, if high venous duplex ultrasound
Well’s score of 3/3+
High probability of DVT
LL ultrasounds requested without need for D-dimer
Low Well’s score and low D-dimer
No ultrasound
GP informed
Telephone follow up @ 3/12
Cause of PE
Venous thrombus breaks off from LL veins and moves through venous circulation
Can get stuck in pulmonary arteries and cause pulmonary infarction
Symptoms of PE
Breathlessness Pleuritic chest pain Haemoptysis Arrhythmias Sudden death
What’s seen in PE
Zone of lung which is ventilated but not perfused
PE - ix
ECG ABG D-dimer Chest radiograph Ventilation-perfusion (VQ) scan CT pulmonary angiogram Catheter pulmonary angiography
Treatment of PE
Anti-coagulate
Possible edges/margins of ulcers
Punched out (arterial)
Sloping (venous)
Heaped-up (cancerous)
Undermined (pressure)
What might the surrounding skin of ulcers look like
Cellulitis (red)
Haemosiderin staining (brown)
Congested (blue)
Ischaemic (pale)
Best ix for suspected neuroischaemic ulcer
MR angiography
What is CTangio contraindicated in
Those with poor renal function e.g. CKD
Dye used is nephrotoxic
What can venous ultrasound duplex scans show you
Thrombosis Valvular incompetence (reflux)
When is catheter-directed thrombolytic therapy used for DVT
Acute ilio-femoral DVT to prevent post-phlebitic limb
Women on OCP are good candidates due to possible complications
What is the sign of complete occlusion in DVT
Cyanotic discolouration of limb
Severe oedema
What location of DVT is more likely to cause of PE
Iliofemoral compared to DVT below knee
Post phlebitis syndrome and its link to DVT
Ulceration of a limb caused by chronic venous obstruction (DVT)
Presents with single swollen limb
