Vascular & Haematology Flashcards
What is difference between thrombus and embolus?
Thrombus is a blood clot in a vein
An embolus is an plug of material e.g. clot, foreign body, bacterial clump, piece of tumour, air
Describe the different Central Venous Catheters (CVC) and their advantages/disadvantages.
Non-Tunneled CVC
Direct Protrusion of Catheter
Placed at Bedside
Tunneled CVC
Passed Under Skin to Separate Site
Placed by IR or in OR
*Lower Infection Risk
Peripherally Inserted Central Catheter (PICC)
Longer Line Placed Peripherally in an Arm Vein
Less Invasive & Lower Infection Risk
Smaller Caliber Lumens
Often Used if Anticipating Long-Term Need (TPN or ABX)
Subcutaneous Port
Completely Tunneled with No Exposed Ports
Placed Under Anesthesia
Lower Infection Risk than Tunneled or Non-Tunneled CVC
Longer Patency – Ideal for Chemotherapy
What is the preferred site for CVC placement and why?
Right internal jugular vein as has a straight path the the subclavian (less likely to cause intimal damage and technically easier to place than left) and in neck is lower risk of infection and DVT than groin (c.f. femoral). The IJV is also easier to compress to stop bleeding than directly into subclavian vein.
NB: if patient already has a pneumothorax and chest drain then strongly consider placing CVC on ipsilateral side. (already has the Ptx and drain so a ‘free shot’ so to speak at placing the CVC).
Describe the approach for blind placement of IJV, subclavian and femoral CVCs.
Internal Jugular (IJ) Vein
Insertion:
Anterior Approach: Along the Medial Border of the SCM, 2-3 Fingerbreadths Above the Clavicle
Central Approach: The Apex of the Bifurcation of the SCM Heads
Angle: 30-45 Degrees
Aim: Ipsilateral Nipple
*Palpate the Carotid Artery During Placement (Vein Should be Lateral to Pulse)
Subclavian Vein
Insert: 2-3 cm Below Midpoint of Clavicle (1-2 cm Lateral of Bend)
Aim: Just Deep to Suprasternal Notch
If Clavicle is Hit, Withdraw and March Down
Femoral Vein
Insert: 1-2 cm Below Inguinal Ligament & 1 cm Medial to the Femoral Artery Pulse
Angle: 30-45 Degrees
Describe the Seldinger technique for CVC placement.
Puncture Vein with Hollow Introducer Needle
Attach Syringe with Gentle Negative Pressure During Advancement
Dark Non-Pulsatile Blood Confirms Venipuncture (Caution: Arterial Blood in Hypoxic Patients May Also be Dark)
Pass Guidewire Through the Needle
Always Maintain Control of the Guidewire During Placement – Should Never Completely Enter the Vein
Withdraw Needle
Make Small Skin Incision at the Entry Site
Pass Dilator Over the Guidewire & Remove the Dilator
Pass CVC Over the Guidewire
Withdraw Guidewire
Suture CVC to Skin & Place Sterile Dressing
Always Obtain Post-Procedure Chest XR to Confirm Appropriate Positioning & Look for Pneumothorax
(CVC: 1-2 cm Above the Right Atrium-SVC Junction
Seen as Just Above the Carina on CXR)
What are some possible complications of CVC placement and how would you treat them?
Carotid Cannulation (Arterial Injury)
Can Cause Life-Threatening Hemorrhage
Reduce Risk by Using Ultrasound-Guidance for Placement
Diagnosis:
ABG
Pressure Transducer Showing Arterial Waveform
CXR Showing Line to the Left of the Spine
Treatment:
Cannulation with Probe Needle Only: Remove & Hold Pressure for 5-10 Minutes
Cannulation with Dilator or Catheter: Remove in OR
Malposition
Tip Abutting into the Wall of the Superior Vena Cava
Risk for SVC Puncture
Treatment: Retract to the Innominate Vein (Do Not Advance)
Tip in Right Atrium
Risk for Atrial Wall Puncture
Treatment: Retract to the Right-Atrium-SVC Junction
Pneumothorax (PTX)
Risk: 1-6.6% (Higher Risk in Emergency Setting or if Multiple Needle Passes are Required to Find the Vein)
*See Trauma: Pulmonary Trauma
Cardiac Tamponade
From Puncture of the Right Atrium
*See Trauma: Cardiac Trauma
Thrombosis
*See Vascular: Deep Venous Thrombosis (DVT)
Treatment:
If Catheter Not Needed: Remove & Heparin
If Catheter Needed: Systemic Heparin or tPA Down the Line
Air Embolism
*See Vascular: Other Venous Emboli
Central Line-Associated Bloodstream Infection (CLABSI)
Also Known as Catheter-Related Bloodstream Infection (CRBSI)
Risk Increases with Duration of Placement (However there is No Indication for Routine Catheter Changing Based on the Number of Days)
Most Common Source: Skin Colonization
Most Common Organisms:
S. epidermidis (Most Common)
S. aureus (Second Most Common)
Enterococci
Candida
Presentation:
Inflammation & Purulence at the Catheter Insertion Site
Fever
Sepsis (Often Sudden Onset)
Complications:
Septic Thrombophlebitis
Infective Endocarditis
Treatment: Antibiotics & Catheter Removal
If Clinically Unable to Remove the Catheter – Consider Exchange Over a Guidewire
What are indications for anticoagulation in atrial fibrillation.
Anticoagulation Indications:
Postoperatively Persists > 48 Hours
If Requires Cardioversion
CHADS-VASC Score ≥ 1-2
CHF History (+1)
HTN History (+1)
Age ≥ 65 (+1) or ≥ 75 (+2)
DM History (+1)
Stroke/TIA/Thromboembolism History (+2)
Vascular Disease History (MI, PAD or Aortic Plaque) (+1)
Sex Female (+1)
DVT treatment
VTE provoked by a reversible risk factor, or a first unprovoked isolated distal (calf) deep vein thrombosis (DVT), has a low risk of recurrence and is usually treated for 3 months.
VTE associated with active cancer, or a second unprovoked VTE, has a high risk of recurrence and is usually treated indefinitely.
Describe the ligamentous attachments of the spleen.
Gastrosplenic
- hilum to greater curvature of stomach.
- contains short gastrics and left gastroepiploic artery.
Lienorenal (splenorenal)
- hilum to left kidney
- contains splenic artery & vein
- contains tail of pancreas
Splenocolic
- inferior pole to colon
- avascular
Splenophrenic
- superior pole to diaphragm
- avascular
Phrenicocolic - not directly attached to spleen but does cradle/support the spleen to some extent.
What is the normal function of the spleen?
Red pulp and white pulp function differently.
Red pulp filters and removes aged/damaged RBC debris.
- Arteries bring blood to the cords
- cords filter and drain into sinuses
- sinuses drain into venous system.
White pulp immunologic function in IgM antibotides and the malpighian corpuscles contain B cells (lymphoid follicles) and T cells (Periarteriolar lymphoid sheaths (PALS)).
What is an accessory spleen?
An additional segment of splenic tissue at an ectopic site.
What are the most common sites for accessory spleens?
Splenic hilum
Pancreatic tail
Greater omentum
Along splenic artery
Gastrosplenic ligament
Splenocolic ligament
Retroperitoneum
Greater curve of the stomach
Gastrocolic ligament
Small bowel mesentery
How do accessory spleens usually present?
Assymptomatic/incidental finding
Can be prone to torsion
Can be ‘symptomatic’ as a relapse of ITP post splenectomy.
What are these and their relevance?
These are Howell Jolly bodies.
They are left over nuclear remnants that are usually removed when red blood cells are in the spleen.
Presence of Howell Jolly bodies indicates asplenism (anatomically or functionally).
What are these and their relevance?
Schistocytes (red arrow) and helmet cells (blue arrow) are common in any disease where there is shearing or mechanical destruction of the red cells. This includes, disseminated intravascular coagulation, thrombotic thrombocytopenic purpura and aortic stenosis.
What are these and their relevance?
Target cells (AKA codocytes) appear as bullseyes, as seen here. These can be seen in liver disease, alpha/beta thalassemia, hemoglobin C disease and in asplenia.
What is the spleens role in hereditary spherocytosis?
Hereditary spherocystosis is an inherited mutation in one of a number of different genes responsible for vertical linkages in RBCs that contribute to its deformable biconcave disc shape.
The mutations lead to abnormally shaped RBCs.
In the spleen haemolysis occurs of these RBCs due to the spherocytic shape, splenic microenvironment and splenic macrophages phagocytosing the RBCs and ‘conditioning them’ to progressively more spherical shape which in turn further impairs passage through the narrow splenic cords
A splenectomy can in select mod-severe cases of HS resolve the haemolysis.
Describe the haemostatis products available and their uses broadly speaking.
Haemostatic agents can be used as adjuncts to control diffuse, non-brisk bleeding.
Agents are either physical or biologically active.
Examples of physical agents are dry matrix, oxidised regenerated cellulose e.g. Surgicel, microfibrillar collagen, microporous polysaccharide or gelatin matrix. Generally these agents create a passive substrate on which clotting can occur.
Biologically active agents enhance coalugation and include topical thrombin combined with gelatin matrix e.g. floseal, fibrin sealents e.g. tisseal and tranexamic acid.
What are some potential complications or adverse reactions to topical haemostatic agents?
- doesn’t work well (i.e. bleeding too brisk or poor application).
- peels off and lifts clot away when you remove sponge
- air/gas embolism if sprayed too close or at pressures exceeding recommendations
- surgical infection - some agents take months to absorb and especially if excessive amounts used can form a nidus for infection
- inflammation reaction and granuloma formation can impair healing
- hypotension and anaphylaxis largely to bovine collagen products.
- blood-borne diseases theoretically possible though none documented
- vascular thrombosis - need to avoid injecting into blood vessels and don’t use with cellsavers.
- immune mediated coagulopathy in patients with prior use of bovine products they have been shown to develop antibodies to it.
What is a haemopatch?
It is a haemostatic adjunct. It is an absorbable, collagen and polyethylene glycol based pad that provides firm tissue attachment to seal the bleeding surface and provides a scaffold and initiates the platelets and plasma factors to form fibrin and thus a clot forms.
Absorbs in 6-8 weeks.
What rate of bleeding is required for visualisation on a CT-A and a red cell-labelled nuclear medicine scan?
1ml/min and 0.1ml/min respectively.
Which named veins are valveless?
Portal vein, SVC, IVC, common iliacs.
What are the layers of a blood vessel?
From inside to out;
- Tunica intima (endothelium)
- Tunica media (smooth muscle, collagen, elastic fibres)
- Tunica adventitia (collagen and elastic fibres)
What is the bovine variant of aortic anatomy?
Common origin of innominate & left common carotid.
Describe the anatomy of the subclavian artery.
Right side comes off innominate and originates as common carotid comes off. The left originates from the aortic arch directly. They both are divided into 3 by the anterior scalene muscle. See diagram. 1st part gives 3 branches, 2nd 2 and 3rd bit 1 branch.
Subclavian Branches: “VITamin C & D”
First Part – VIT
Vertebral Artery
Internal Thoracic Artery (Internal Mammary Artery)
Thyrocervical Trunk
Second Part – C
Costocervical Trunk
Third Part – D
Dorsal Scapular Artery
What is Virchow’s triad?
- Venous stasis
- Hypercoagulability
- Endothelial wall injury
(the 3 factors that contribute to pathophysiology of venous thromboembolism)
How do you treat a DVT?
First episode & proximal DVT:
- Provoked - 3-6m anticoagulation
- Unprovoked >12m
- If hypercoagulable disorder present consider lifelong.
First episode & distal DVT:
- sympotmatic gets anticoagulation
- assymptomatic serial USS 2 weeks.
Phlegmasia Cerulea Dolens:
- Non threatened (use Rutherfords classification) then can use catheter directed thrombolytics
- Threatened limb then thrombectomy.
Second Episode: Long-Term (> 12 Months) Anticoagulation
Third Episode: Life-Long Anticoagulation
What is May-Thurner syndrome?
When right iliac artery compresses the left iliac vein can lead to increased risk of DVT in left leg and if DVT in left leg occurs due to May-Thurner syndrome then may need angioplasty & stenting in addition to thrombolysis/ anticoagulation.
When would you consider deploying an IVC filter?
Goal of IVC filter is to prevent DVTs becoming PEs.
Indications:
- acute proximal DVT or PE in a patient with absolute contraindication to anticoagulation e.g. active bleeding, acute intracranial haemorrhage, major trauma, high-bleeding risk surgery.
OR
- recurrent DVT despite therapeutic anticoagulation
How and where is an IVC filter placed?
Using interventional/ endovascular techniques preferred to be placed using right internal jugular vein as is the straightest pathway.
Preferred location is infrarenal to prevent occlusion of renal veins but suprarenal is preferred in renal vein thrombosis or pregnancy to avoid gravid uterus.
What is ABPI and how is it interpreted?
Ankle-Brachial pressure index.
It is a bedside test using a blood pressure cuff on upper arm and ankle to ascertain a systolic ratio (ankle/brachial)
> 1.2 = calcification
0.9 -1 = normal
<0.9 = PVD
<0.5 = critical disease
What are your landmarks for a below knee amputation?
Spot diagnosis. What is it and how is it treated?
Thromboangitis obliterans (Buergers disease)
Small vessel thrombi in hands and feet in young usually men <50yo with no other risk factors for atherosclerosis other than smoking.
Treatment is smoking cessation. (smoking reduction and NRT is not sufficient).
Can use iloprost (prostaglandin vasodilator).
What is Buerger’s test?
Bedside examination that can be conducted to assess for peripheral arterial disease. i.e. is the arterial supply able to overcome gravity.
Describe differences in ulcers with arterial vs venous eitiology.
In performing a high ligation of the great saphenous vein for varicose vein surgery what tributaries may you encounter?
Superficial inferior epigastric vein
Superficial External Pudendal vein
Superficial circumflex iliac vein
Anterolateral accessory saphenous vein
Posteromedial accessory saphenous vein
What is the pathogenesis of the diabetic foot?
- Peripheral Neuropathy
– Somatic Neuropathy
Causes Loss of Protective Sensation
> Delayed Detection of Injury
– Autonomic Neuropathy
Decreased Sweating with Dry & Fragile Skin - Charcot Neuropathic Osteoarthropathy (Charcot Foot)
– “Rocker-Bottom” Foot with Midfoot Collapse
– Uncontrolled Inflammation Causes Osteolysis with Progressive Fracture and Dislocation
– Increases Risk of Ulceration from Altered Patterns of Mechanical Stress & Pressure - Peripheral Arterial Disease – Causes Both Macrovascular & Microvascular Disease
– Macrovascular Changes –
> Infrapopliteal Occlusive Disease (Tibial and Peroneal Arteries)
> Generally Spares Aorto-Iliac and Femoral Arteries
– Microvascular Changes –
> Dysfunction of Autoregulation
> Endothelial Damage
> Increased Flow
Edema
> Arteriovenous Shunting
> Impaired Oxygen Diffusion
> Impaired Leukocyte Migration
