Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
What is the indication for the procedure?
Diagnosis
Preoperative staging
Therapy
Define the problem.
What is the diagnostic question that is to be answered?
Which study can best answer the question (ultrasound [US], computed tomography [CT], magnetic resonance imaging [MRI], angiography)?
Patient history, interview, examination
Review chart
Key data: signs and symptoms
Previous vascular surgery/interventions
Previous studies
Laboratory values
Other medical illnesses
Pulse examination
Explanation of the procedure to the patient
Obtain informed consent
Assess risk versus benefit (there are no absolute contraindications to angiography).
Approach and access
Coagulopathy?
Renal insufficiency?
What are alternative options?
Preprocedural orders
Appropriate laboratory samples drawn (i.e., prothrombin time [PT]/partial thromboplastin time [PTT])?
Appropriate medication withheld (i.e., Coumadin [warfarin])?
Intravenous (IV) access present?
Hydration
Clear liquids only
Premedication if necessary
Right femoral artery
Left femoral artery
Left axillary artery
Right axillary artery
Translumbar aorta
Brachial arteries
Antegrade femoral artery
Through a surgical graft
Easily accessible for manipulations and hemostasis
Large-caliber vessel
Well-defined landmarks exist.
Most angiographers are right-handed.
Low complication rate compared with other approaches
Double-wall technique is preferred.
Advantages of “single-wall” puncture are only theoretical.
Use fluoroscopy to determine puncture level.
Artery entry: midfemoral head
Skin entry: inferior margin of femoral head
Local anesthesia at skin entry site: 1%–2% lidocaine
Palpate artery above site
Advance 18-gauge Seldinger needle (45–60 degree angle) to bone.
Remove central stylet and withdraw slowly.
Advance guidewire through needle while good pulsatile flow jets out of the hub.
Always use fluoroscope when advancing a guidewire.
Never advance guidewire against resistance.
Exchange needle over wire for dilator or catheter.
Inflow can be assessed by obtaining pull-down pressures.
Should complications arise (i.e., emboli, thrombosis), they will affect the already compromised extremity.
Conversion to antegrade approach is possible if necessary.
May interfere with surgical procedure if complication develops (e.g., hematoma)
If a severe stenosis is present, a catheter may obturate the vessel completely.
Main indication for this approach is nonpalpable femoral pulses (i.e., aortic occlusion)
Left-sided approach is preferred.
Easier to access descending aorta
Left-sided approach crosses fewer central nervous system (CNS) arteries.
3J wire is preferred.
Disadvantages:
Difficult to compress
Relatively high incidence of complications (e.g., stroke, bleeding, thrombosis)
Brachial plexus injury
Always check for blood pressure (BP) differential to detect occult arterial disease.
Main indication for this approach is nonpalpable peripheral pulses.
High TLA is preferred: above abdominal aortic aneurysm (AAA), grafts, diseased distal aorta
Disadvantages:
Patient must lie prone for entire study.
Higher incidence of bleeding (debatable)
More difficult to manipulate catheters
Use an 18-gauge needle/sheath system
The main indication for this approach is a distal extremity intervention (e.g., percutaneous transluminal angioplasty [PTA] of the superficial femoral artery [SFA]).
Retrograde catheterization may be converted to antegrade access with a Simmons 1 catheter and a 3J or angled guidewire.
Difficult to manage in obese patients
There are four types of complication:
Puncture site complications (e.g., groin hematoma)
Contrast agent complications (e.g., anaphylactoid reaction)
Catheter-related complications (e.g., vessel dissection)
Therapy-related complications (e.g., CNS bleeding during thrombolysis)
Problems with the puncture site and contrast media are the most frequent complications during angiography. Puncture site problems depend on coagulation status, size of catheter, patient body habitus, and compliance issues. The overall incidence of death related to angiography is very low (<0.05%).
Minor hematoma, >5%
Major hematoma that requires surgical therapy, <0.5%
Arteriovenous fistula (AVF), 0.05%
Pseudoaneurysm, 0.01%
Vessel thrombosis, 0.1%
Neuritis
Infection
Renal failure
Cardiac failure
Phlebitis (venography)
Anaphylactoid reactions (rare with arteriography)
Cholesterol emboli
Thromboembolism
Cerebrovascular accident (CVA)
Arterial dissection
Complications can be limited by:
Careful preangiography assessment (e.g., correct coagulopathies)
Appropriate approach (e.g., history and pulse examination)
Good technique (e.g., trained angiographer)
Risk factors for development of AVF or pseudoaneurysm:
Low puncture
Heparinization
Large catheters
Most puncture site complications can be prevented by good manual compression and correction of coagulopathies before angiography.
Always reassess patient after the procedure.
Diagnostic catheters
High-flow catheters with side holes are used for central vessels (>10 mL/s).
Low-flow catheters with end holes are used for selective arterial work.
Therapeutic catheters
Balloon catheters (percutaneous transluminal angioplasty [PTA] and balloon occlusion)
Atherectomy catheters
Coaxial infusion catheters
Embolization catheters
Outer diameter (OD): catheter size is determined by the OD and given in “French” size. French (Fr) = the circumference in millimeters. Divide French size by 3 to obtain OD in millimeters.
Inner diameter (ID): measured in 1/1000 of an inch
Length: measured in centimeters. 65 cm is commonly used for abdominal studies. 100 cm is usually used for arch and carotid studies.
Location | Catheter | Injection a | Comments |
---|---|---|---|
Thoracic aorta | Pigtail | 25/50 | |
Abdominal aorta | Pigtail/tip occluded straight | 20/40 | Tip occluded straight catheter for iliac pressures |
Celiac | C2, S2 | 5/50 | Variations in anatomy common |
Renals | C2, S2 | 4/8 | Multiple vessels in 25% |
SMA | C2, S2 | 5/50 | IA tolazoline (Priscoline) for venous phase |
CT portography | In SMA | 3/120 | Helical CT |
IMA | S2, C2 | 3/30 | |
Splenic | Variable | 5/50 | Good splenic vein opacification |
Hepatic | Variable | 5/50 | Dual (artery, portal) blood supply; variable anatomy |
Aortic bifurcation/pelvic | Pigtail | 10/20 | Position above bifurcation |
Internal iliac | C2, S2 | 5/25 | |
One leg runoff | Straight tip | 4/48 | Positioned in external iliac |
Two leg runoff | Pigtail | 6/72 | Position above bifurcation |
Arm | H1 | Variable | LOCA (reduces pain) |
IVC | Pigtail | 20/30 | |
Pulmonary | Pigtail | 20/40 | |
Aortic arch | Pigtail | 30/60 | Higher injections in young patients |
CCA | Davis A1 | 8/10 | 60% HOCA or LOCA |
ICA | Davis A1 | 6/8 | 60% HOCA or LOCA |
ECA | Davis A1 | 2/4 | 60% HOCA or LOCA |
Vertebral | Davis A1 | 6/8 | 60% HOCA or LOCA |
Coronary | Judkins | 4/8 | LOCA |
Thermoplastic materials (polyurethane and polyethylene) are very commonly used for catheter manufacturing.
Nylon: combined with polyurethane to manufacture high-flow, small French catheters
Teflon: very stiff, low-friction material
Braided catheters: internal wire mesh improves torquability.
Rate and volume of contrast are reduced for digital subtraction angiography.
Rate and volume always depend on rate of blood flow and size of vessel observed under fluoroscopy.
Shorter catheters allow for higher flow rates and easier exchangeability.
The larger the ID, the better the flow dynamics.
It is good practice to size catheters, sheaths, and wires before their use; considerable discrepancy of dimensions may occur (variable among manufacturers).
Maximum flow rate and pressure tolerance of catheters are specified by manufacturer on package or insert.
All nonspecialty guidewires have a similar construction:
Central stiff steel core with a distal taper
Wire coil spring wound around core
Thin filamentous safety wire holding the other two components together
Most wires are coated with Teflon to decrease friction.
Length: 145 cm is the standard length and allows exchanges of 65-cm catheters. “Exchange length” wires are 220–250 cm in length and are used for long catheters.
OD: guidewires are designated by OD in 1/1000 of an inch: 0.018–0.038 is the most common size range.
J tip: refers to the radius of wire curvature in millimeters (i.e., a 3J wire has a 3-mm distal curvature)
Wire | Major Use/Comments |
---|---|
3J | Tortuous and diseased vessels, avoids selecting branch vessels |
15J | Large vessels: femoral, aorta, IVC |
Straight wire | Dissection is more common |
Rosen | Exchanges/PTA |
Amplatz stiff | Exchanges, tortuous iliac arteries |
Bentson | Long, flexible taper (floppy end) |
Terumo | Slippery hydrophilic coating; glides well, torque guide |
Dosage a | Use | Comments | |
---|---|---|---|
Vasodilator | |||
Nitroglycerin | 50–300 µg | Peripheral spasm | Direct muscle relaxant |
Verapamil | 1–10 mg in 10 mL saline | Peripheral spasm | Calcium channel blocker; More potent, longer acting than nitroglycerin |
Vasoconstrictor | |||
Vasopressin (Pitressin) | 0.2–0.4 U/min | GI bleeding | Contraindication: CAD, HTN, arrhythmias |
a See manufacturer's package insert for specific rates of administration.
Hemorrhage
Gastrointestinal (GI) bleeding
Varices
Traumatic organ injury
Bronchial artery hemorrhage
Tumors
Postoperative bleeding
Vascular lesions
Arteriovenous malformation (AVM) or fistula (AVF)
Pseudoaneurysms
Preoperative devascularization
Renal cell carcinoma (RCC)
AVM
Vascular bone metastases
Other
Hypersplenism
Gonadal varices
Hepatic chemoembolization
Proximal occlusion is equivalent to surgical ligation. It does not compromise collateral flow. For this reason, it may be ineffective to control bleeding if collaterals continue to supply the bleeding site.
Distal embolization usually infarcts tissue and is followed by necrosis.
Temporary versus permanent embolization: tumors, vascular lesions, varices, and preoperative embolizations are usually permanent occlusions. GI bleeding is best treated with Gelfoam at first (if vasopressin has failed).
Be as selective as possible (i.e., use tracker catheter).
Prevent reflux of embolic material into other vessels.
Document preangiographic and postangiographic appearance.
Temporary
Surgical gelatin (Gelfoam): not U.S. Food and Drug Administration (FDA)–approved for embolization. Pledgets are cut to size or occlude large vessels; Gelfoam powder occludes distal vessels and causes infarction.
Permanent
Steel coils of variable sizes are commercially available; coils obstruct proximal vessels.
Microcoils (platinum) are used to occlude more distal vessels.
Detachable balloons are used for large vessel occlusion. FDA restricted. Useful for pulmonary AVF, carotid cavernous fistula (CCF).
Polyvinyl alcohol (Ivalon): small particles for distal occlusion. 200–1000 µm. Suspend in albumin–contrast agent mixture.
Absolute ethanol: causes tissue necrosis. Used with proximal balloon occlusion to minimize shunting and reflux. Useful for solid organ necrosis (i.e., malignant tumors).
Plastic polymers: glue, tissue adhesives
Material | Occlusion | Primary Use |
---|---|---|
Temporary Agents | ||
Autologous blood clot | 6–12 hr | Rarely used currently |
Gelfoam | Weeks | Upper GI, hemorrhage, pelvic, trauma |
Permanent Agents | ||
Ethyl alcohol (1 mL/kg) | Permanent | Tumors (causes coagulative necrosis) |
Steel/platinum coils | Permanent | Large vessel, aneurysm, tumor |
Polyvinyl alcohol (200–1000 m) | Permanent | Tumors |
Tris-acryl gelatin microspheres (embospheres) | Permanent | Uterine embolization |
Balloons | Permanent | High-output AVF |
Cyanoacrylate (glue) | Permanent | AVM |
Postembolization syndrome (fever, elevated white blood cell [WBC] count), 40%
Infection of embolized area (administer prophylactic antibiotics)
Reflux of embolic material (nontarget embolization)
Alcohol causes skin, nerve, and muscle infarction if used in the periphery; its use should be restricted to parenchymal organs.
Palliative only; prolonged survival or relief of endocrine symptoms
Dual hepatic/portal supply allows for arterial embolotherapy
Agents: Gelfoam or Ethiodol mixed with chemotherapeutic agents; drug-eluting microspheres
Tumors: hepatocellular carcinoma (HCC), ocular melanoma, metastatic endocrine tumors
Ytrium-90 (Y-90) radioembolization of hepatic artery (HA) is an effective treatment for unresectable HCC. It is a form of brachytherapy.
Y-90 is a pure beta emitter with a short half-life (64 hr). The size of the microspheres ranges between 20 and 40 µm (sufficient for local trapping).
Basic requirements
Absent surgical or ablative options
Absent other conventional treatment options
Preserved liver function
Adequate general condition
Liver dominant tumor burden
Life expectancy >3 months
Arterial graft thrombosis
Native vessel acute thrombosis
Before percutaneous intervention
Hemodialysis AVF or graft
Venous thrombosis
Axillosubclavian
Portal vein (PV), superior mesenteric vein (SMV)
Inferior vena cava (IVC)
Always obtain a diagnostic angiogram before thrombolysis.
Streptokinase is no longer used (antigenic side effects).
Recombinant tissue plasminogen activator (r-tPA) is no more effective than urokinase (UK) but is much more expensive.
Favorable prognostic factors for thrombolysis:
Recent clot (<3 months)
Good inflow/outflow
Positioned in thrombus
End points of thrombolytic therapy:
No lysis present after 12 hours of infusion
Major complication develops
Severe reperfusion syndrome
Progression to irreversible ischemia
Successful thrombolysis is defined as:
>95% lysis of thrombus
Clinical reperfusion
Always treat underlying lesions.
Overall success:
Grafts, 90%
Native arteries, 75%
Heparinize concomitant with UK infusion
Monitor in intensive care unit (ICU)
No good correlation among success, complications, and blood tests
SK | UK | r-tPA | |
---|---|---|---|
Source | Streptococcus culture | Renal cell culture | DNA technology |
Dosage | 5000 U/hr | 100,000 U/hr | 0.001–0.02 mg/kg per hr a |
Half-life | 20 min | 10 min | 5 min |
Treatment time | 24–48 hr | 24 hr | 6 hr |
Bleeding cost | 20% | 10% | 10% |
Cost | Inexpensive | Expensive | Very expensive |
a Dosage not to exceed 10 mg for a single bolus; total dose should be <40 mg.
Low-dose technique (constant)
100,000 U/hr of UK
Repeat angiogram after 12 hours
High-dose technique (graded)
250,000 U/hr × 4 hours of UK
Repeat angiogram and then 125,000 U/hr
Pulse spray ultrahigh dose
600,000 U/hr in 5000 U of UK bolus doses
Aliquots every 30 s
Catheter placement
Coaxial dual infusion is best.
5-Fr catheter lodged in proximal thrombus
T3 or infusion wire (Katzen) coaxially into distal thrombus
Split infusion of UK into proximal and distal catheters
Secure skin entry site
Tissue plasminogen activator (tPA) infusion
tPA (arterial): infuse at 1 mg/hr total dose divided among infusion sites. Total maximum dose per patient is 100 mg. tPA has half-life of 6 min.
tPA (venous): same infusion rate as arterial, lower bleeding complication rate
tPA (line clearance): 0.5 mg/hr × 3–4 hours
Absolute
Active bleeding
Intracranial lesion (stroke, tumor, recent surgery)
Pregnancy
Nonviable limb
Revascularization of nonviable limb will cause acute renal failure and cardiovascular collapse because of lactic acid and myoglobin
Infected thrombus
Relative
Bleeding diathesis
Cardiac thrombus
Malignant hypertension (HTN)
Recent major surgery
Postpartum
Complications
Major hemorrhage requiring termination of UK, surgery, or transfusion (e.g., intracranial hemorrhage, massive puncture site bleed), 7%
Minor hemorrhage, 7%
Distal embolization
Pericatheter thrombosis
Overall, termination of therapy is required in 10%.
PTA is a method to fracture the vascular intima and stretch the media of a vessel by a balloon ( Fig. 8.2 ). Atherosclerotic plaques are very firm and are fractured by PTA. Healing occurs by intimal hyperplasia.
Claudication or rest pain
Tissue loss
Nonhealing wound
Establish inflow for a distal bypass graft
Hemodialysis AVF or grafts
Premedication with aspirin and 10 mg of nifedipine
Ipsilateral approach is preferred.
Heparinize (5000–10,000 U) after the lesion is crossed.
Diagnostic angiogram is obtained before PTA.
Measure pressure gradients with borderline lesions.
Significant gradient >10 mm Hg at rest; >20 mm Hg after vasodilator; >10% systolic BP
Pharmacologic adjuncts
Intraarterial (IA) nitroglycerin or tolazoline for vasospasm and provoked pressure measurements
Balloon size: sized to adjacent normal artery
Common iliac artery: 8–10 mm
External iliac artery: 6–8 mm
Superficial femoral artery (SFA): 4–6 mm
Renal artery: 4–6 mm
Popliteal artery: 3–4 mm
Wire should always remain across lesion
Repeat angiogram and pressure measurements after angioplasty.
Postprocedure heparin with “limited flow” results (dissection, thrombus)
Large vessels/proximal lesions respond better than small vessel/distal lesions.
Stenoses respond better to PTA than occlusions.
Short stenoses respond better to PTA than long stenoses.
Isolated disease responds better to PTA than multifocal disease.
Poor inflow or poor outflow decreases success.
Limb salvage interventions have a poor prognosis.
Diabetics have a poorer prognosis than nondiabetic patients.
Iliac system
95% initial success
70%–80% 5-year patency
Femoral-popliteal
90% initial success
70% 5-year patency
Renal artery
95% initial success
Fibromuscular dysplasia (FMD): 95% 5-year patency
Atherosclerosis: 70%–90% 5-year patency
Ostial lesions have a poorer prognosis.
Acute failures are due to thrombosis, dissection, or inability to cross a lesion.
Recurrent stenosis
Intimal hyperplasia (3 months–1 year)
Progression of disease elsewhere (>1 year)
Groin complications (same as diagnostic angiography)
Distal embolism
Arterial rupture (rare)
Renal infarction or failure (with renal PTA)
Metallic stents have an evolving role in interventional angiography. Two major types of stents:
Balloon-expandable stent (Palmaz, Genesis, Omniflex, Herculink, Crown)
Balloon mounted; usually made of nitinol
Placement is precise; shortens slightly
Less flexible (minimal elastic deformation because of hoop strength), limited by balloon size
Should not be placed at sites where extrinsic forces could crush the stent
Thoracic outlet veins
Dialysis graft
Self-expandable (Wallstent, Protégé, Luminex, Symphony, SMART, Dynalink)
Bare; usually made of stainless steel
Placement is less precise; can have large diameters
Considerable elastic deformity (flexible)
Useful in tortuous vessels and tight curves
Gianturco zigzag stent (Cook)
Stent grafts (metallic stents combined with synthetic graft material) are used in aortic aneurysms and dissections (AneuRx, Ancure, Gore [descending thoracic] are FDA-approved).
Unsuccessful PTA
Recurrent stenosis
Venous obstruction, thrombosis
Transjugular intrahepatic portosystemic shunt (TIPS)
Long-segment stenosis
Total occlusion
Ineffective or unsuccessful PTA:
Residual stenosis >30%
Residual pressure gradient >5 mm Hg rest, >10 mm Hg posthyperemia
Hard, calcified plaque
Large post-PTA dissection flap
Recurrent stenosis after PTA
Ulcerated plaque
Renal ostial lesions
Iliac artery: over 90% 5-year patency (better than PTA)
Renal artery and other vessels: limited long-term data
Portal HTN with variceal bleeding that has failed endoscopic treatment
Refractory ascites
Hepatic pleural effusion (hydrothorax)
Budd-Chiari syndrome
Pretransplant
Hepatorenal syndrome
Venoocclusive disease
Confirm PV patency before procedure (US, CT, or angiography).
Preprocedure paracentesis may be helpful.
Right internal jugular vein (RIJV) is the preferred access vessel.
Goal: portosystemic gradient <10 mm Hg, decompression of varices
Absolute
Severe right-sided heart failure with elevated central venous pressure
Severe polycystic liver disease
Uncontrolled systemic infection or sepsis
Liver abscess
Unrelieved biliary obstruction
Portal HTN from arterioportal fistula
Relative
Severe encephalopathy
PV thrombosis
Hepatic vein obstruction/thrombosis
Severe coagulopathy (INR >5)
Thrombocytopenia (<20,000/cm 3 )
Moderate pulmonary HTN
Severe stenosis or occlusion of celiac or HA
Large liver hypervascular tumor (hepatoma)
Severe liver failure (TIPS have unclear survival benefit)
RIJV approach
Obtain wedged hepatic pressure and venogram
Create tract from right hepatic vein to PV with 16-gauge needle
Advance catheter over wire into portal venous system
Obtain portal venogram
Measure portal pressures
Dilate tract with PTA balloon (8 mm)
Deploy metallic stent (Palmaz or Wallstent) or stent graft
Dilate stent until gradient <10 mm Hg
Coil embolization of varices optional
Patency: 50% at 1 year
Recurrent bleeding in 10%
Hepatic encephalopathy 10%; more likely when residual gradient is <10 mm Hg
Bleeding
Shunt thrombosis or stenosis
Right-sided heart failure
Renal failure
No flow
Low-velocity flow (<50–60 cm/s) at portal venous end of shunt
Reversal of flow in hepatic vein away from IVC
Hepatopedal flow in intrahepatic PV
Reaccumulation of ascites; varices; recanalized umbilical vein
Direct intrahepatic portocaval shunt (DIPS)–modified TIPS with intravascular US guidance
Balloon-occluded retrograde transvenous obliteration (BRTO)–gastric varices
Partial splenic embolization (PSE)–variceal hemorrhage
These techniques increase portal venous pressure and may result in worsening of untreated varices
May be preferred over percutaneous liver biopsy in patients with bleeding disorders and when a hepatic venous pressure gradient (= wedged – free hepatic venous pressure) is desired.
RIJV approach preferred.
Right hepatic vein is selected with wire/catheter, and sheath advanced.
Core biopsy device (18- to 19-gauge) is advanced into the liver parenchyma.
Device | Purpose/Situation |
---|---|
External tunneled catheter (silicone or polyurethane) | Continuous use, multiple simultaneous uses |
Implantable port | Intermittent use; immunocompromised patient |
High-flow catheter | Temporary hemodialysis; pheresis |
Peripherally inserted central catheter | Short-term use, usually <2–3 months; infrequent blood drawing |
The catheters are typically inserted through axillary (subclavian), internal jugular, or arm vein. Pneumothorax, symptomatic vein stenosis, and thrombotic complications are less common with jugular than subclavian vein approaches. Internal jugular approach preserves subclavian for future fistula/graft. For the axillary vein puncture, the entry site should be lateral to the ribs in the subcoracoid region ( Fig. 8.4 ). This approach eliminates the possibility of pneumothorax and also ensures that the catheter is well within the subclavian vein as it passes through the costoclavicular space. If the catheter is extravascular at this site, chronic compression may occur and lead to catheter erosion and fracture—“pinch-off syndrome.” For IJV puncture, a site on the midneck above the clavicle is selected. The vein is punctured under transverse US guidance, ensuring that the carotid artery is avoided.
Pneumothorax
Arterial puncture
Hemorrhage or hematoma
Occlusion
Mechanical problems
Air embolism
This usually occurs when venous dilator is removed from peel-away sheath to be replaced with the catheter. The embolism can be avoided by covering the opening with a gloved finger and removing the dilator with patient in suspended deep inspiration.
If air does get sucked in, perform fluoroscopy of the chest. If there is air in the pulmonary artery (PA) do the following:
Place patient in left lateral decubitus position to keep air in the right chamber.
Suck out air with Swan-Ganz balloon catheter.
Administer supplemental O 2 and monitor patient.
Frequency shift = 2 × transducer frequency × velocity of blood × cosine of angle × 1/speed of sound (1540 m/s). Cos of 90 degrees = 0 and cos of 0 degrees = 1. The optimal angle between the probe and the vessel is less than 60 degrees ( Fig. 8.5 ).
Performed with a pencil probe. No static image is produced, as the machine does not stop to listen. If one vessel is located behind the other, one cannot use continuous wave Doppler because it will reveal both waveforms.
Frequently used for interrogating arteries and veins; duplex Doppler refers to the fact that one gets gray scale and Doppler images.
The operator can set the machine to listen only to those Doppler shifts coming from a particular depth. This is called Doppler gate or sample volume.
Color flow is used to determine the direction of flow (by convention, red is toward the transducer and blue is away), as well as magnitude of shift.
Color machines do not display velocity, because angle of insonation is not used to assign color; the color indicates magnitude of frequency shift. The greater the shift, the lower the saturation of color. In simple terms, in a tortuous vessel the frequency shifts and angle of insonation changes; thus change in color is due to frequency shift even though velocity is the same.
The color image is a display of average frequency shift and not peak frequency shift. Calculations of stenosis from Doppler data are based on peak frequency shift or peak velocity.
The signal is related to the number of moving targets (usually red blood cells [RBCs]).
This technique ignores velocity and direction of flow. Used to detect flow and has high sensitivity.
Aliasing is the result of flow velocity exceeding the measuring ability of pulsed wave Doppler. By Doppler imaging, this is seen as a wraparound with high velocity below the bottom of the scale rather than on the top. By color imaging, aliasing becomes evident by inversion of color (blue within an area of red and vice versa). Ways for reducing aliasing:
Pulse repetition frequency (PRF) can be increased by raising the scale.
The Doppler shift can be reduced by manipulating variables of equation, thus either a greater angle (reduced cosθ value) or a lower frequency can be used.
Color aliasing refers to wrapping of signal displayed as areas of color reversal.
Changes because of vessel tortuosity can also change colors, but in that case color changes are marked by a band of black, thus red to blue with black (no signal) in between. Artifacts due to 0 = 90 degrees.
Because the US machine typically only displays either gray scale or color information, there is competition as to which signal is displayed. If the gray scale gain setting is high, the color image is suppressed when flow is low, giving the impression of absent flow or smaller lumen.
Two main noncontrast MR angiography (MRA) techniques: time of flight (TOF) MRA and phase contrast (PC) MRA. Both techniques can be acquired in either two dimensions (2D) or three dimensions (3D).
TOF-MRA
Maximizes contrast between flowing blood and stationary tissue; flow-related enhancement repetition interval (TR) < T1
3D has higher signal-to-noise ratio (SNR) and shorter imaging times than 2D.
Works well for high-flow arterial systems
Limitations for imaging: slow flow vessels (especially venous system), tortuous vessels, poor background resolution
PC-MRA
Flowing spins encoded with a bipolar gradient
Velocity encoding gradient setting critical
Speed or flow images
2D good for slow flow
3D has better spatial resolution.
Less saturation effects
Flow velocity information
Longer imaging times
A perfectly timed Gd contrast agent injection with 3D spoiled gradient-echo (SPGR) produces high SNR MRA covering extensive regions of vascular anatomy within a breathhold. Compared with noncontrast techniques, signal does not depend on inflow of blood, is not subject to problems of flow saturation, and reduces intravoxel dephasing. The IV-administered Gd shortens the T1 of blood to <270 ms (T1 of fat), so all bright signal essentially originates from vessels. Images are reconstructed as maximum-intensity projections (MIPs). Technique:
Dose: two or three bottles (20 mL each) of the Gd (about 0.3 mmol/kg Gd)
Timing: perfect contrast agent bolus timing is crucial to ensure that the maximum arterial Gd occurs during the middle of the acquisition, when central k-space data are acquired. Begin injecting Gd immediately after starting the scan. Finish the injection just after the midpoint of the MR acquisition. To ensure full use of the entire dose of contrast, flush the IV tubing with 20 mL of normal saline.
Spinal AVF/AVM is a potentially devastating disease that is often overlooked. MRA can be an excellent screening examination in suspected patients and for preangiographic planning. Patients usually present with pain and weakness of the extremities. On MRI, there is often an abnormal T2-weighted (T2W) signal change in the cord, most commonly near the conus (congestive phenomenon), which can be reversible if the AVF/AVM is treated. Small flow voids can also be seen on T2W sagittal images. MRA protocol:
Acquire MRA in the coronal plane unless there is extensive scoliosis; then, the sagittal plane is preferred.
Timing run: axial image, one slice centered on the aorta at L2; 2 mL of Gd bolus (usually about 17 s)
Acquisition: 30 mL of contrast followed by 30 mL of saline push with number of averages (NEX) = 1 (no repetition) to ensure arterial phase
Look for early enhancing tortuous venous structures, usually posterior to the spinal cord.
Technique | Application |
---|---|
Multiplanar reformation | Routine |
MIP | Overall survey; identify areas of further interest |
Targeted MIP | Isolate vessel of interest; reduce background signal |
Curved reformations | Obtain vessel measurements |
Shaded surface display | Convey depth perception |
Volume rendering | Convey anatomic relationship |
Subtraction | Eliminate background; produce pure venous images |
Catheter in central venous structure; a combined large volume and high concentration of contrast agent is given as a bolus.
Adequate results in only 70% of patients
Invasive study
Advantages: lower iodine concentration required than that for cut radiograph, less pain, speedy
Disadvantages: less resolution, motion, and bowel gas artifacts
Venous blood is obtained from bilateral inferior petrosal veins (which drain the cavernous sinus) to detect lateralization of hormones produced by pituitary tumors (very sensitive test). Simultaneous tracker catheters are advanced into the inferior petrosal veins. Simultaneous samples are obtained to distinguish paraneoplastic/endocrine production of hormones from pituitary sources and localize the abnormality to left or right.
Isosulfan blue, 1 mL, injected between 1st–2nd and 4th–5th toes; wait 10 min for lymphatic uptake.
Cutaneous cutdown to the fascia (dorsum of foot)
Isolate a lymphatic; pass a silk suture above and below.
Milk the blue dye into the vessel.
Puncture lymphatic with a 30-gauge needle lymphography set.
Hook up needle to pump and inject oily contrast medium (Ethiodol)
Obtain initial images of lymphatic vascular phase and later of the nodal phase.
Form of sedation in which the patient is given sedation and pain medication but should remain easily arousable. The following parameters are continuously monitored:
BP
Oxygenation using a pulse oximeter
Electrocardiogram (ECG) and heart rate (HR)
Conscious sedation is usually achieved by small aliquot dosing of midazolam and fentanyl.
IV Dosage | Total Dose | Duration (hr) | Comments | |
---|---|---|---|---|
Benzodiazepines | ||||
Diazepam | 1–5 mg | 10–25 mg | 6–24 | Long-acting |
Lorazepam | 0.5–2.0 mg | 2–4 mg | 6–16 | |
Midazolam | 0.5–2.0 mg | <0.15 mg/kg | 1–2 | Good amnesic effect; short-acting |
Flumazenil | 0.2 mg | May repeat q 1 min up to 1 mg | 0.5–1 | For benzodiazepine reversal |
Narcotic Analgesics | ||||
Morphine | 1–5 mg | <0.2 mg/kg | 3–4 | Histamine release |
Meperidine | 12.5–25 mg | 0.5–1 mg/kg | 2–4 | MAOI interaction |
Fentanyl | 15–75 µg | 1–3 µg/kg | 0.5–1 | Immediate onset |
Naloxone | 0.4–0.8 mg | Repeated as needed | 0.3–0.5 | For narcotic overdose |
Antiemetics | ||||
Metoclopramide | 10 mg | 0.5–1 mg/kg | 1–2 | Stimulates GI motility |
Ondansetron | 4 mg | 8 mg | 4–8 | |
Prochlorperazine | 2.5–10 mg | 10 mg | 4–6 | Adjust dosage for age |
Promethazine | 12.5–25 mg | 25 mg | 4–6 | CNS depressant effects |
Droperidol | 0.625–1.25 mg | Higher dose: sedation | 4–6 | Potent antiemetic at low doses |
a See manufacturer's packet insert for specific rates of administration.
Warfarin interferes with vitamin K-dependent synthesis of clotting factors.
Heparin inactivates thrombin by combining with antithrombin III.
PTT is the time required for 1 mL of recalcified whole blood to clot. It therefore reflects the intrinsic clotting axis.
PT is the time required for 1 mL of recalcified whole blood to clot in the presence of thromboplastin (phospholipid extract); it therefore reflects the extrinsic clotting axis.
Clotting Parameter | Normal Value | Causes of Abnormal Values |
---|---|---|
Prothrombin time (extrinsic coagulation system) | <3 s of control | Warfarin, heparin, liver disease |
Coagulopathy (DIC, thrombolytic therapy) | ||
Vitamin K deficiency (parenteral nutrition, biliary obstruction, malabsorption, antibiotics) | ||
PTT (intrinsic coagulation system) | <6 s of control | Lupus anticoagulant |
Hemophilia | ||
Bleeding time | <8 min | Platelet count <50,000/mm 3 |
Qualitative: uremia, NSAIDs, | ||
von Willebrand disease |
Interventions (biopsy, aspiration, drainage) should not be performed if coagulation times are markedly prolonged (i.e., beyond above values); correction of coagulopathies (see table) can often be achieved in several hours.
Anticoagulant | PT/PTT | Antidote | Normalization |
---|---|---|---|
Heparin | Both prolonged | Stop heparin | 3–6 hr |
IV protamine titration | Minutes | ||
Warfarin | Both prolonged | IV vitamin K for 3 doses | Days |
Fresh frozen plasma | Minutes | ||
Aspirin | Normal (platelet aggregation reduced) | Platelet concentrates Stop aspirin |
Minutes, week |
Activated clotting time (ACT) is the method of choice for monitoring heparin therapy.
Preheparin administration: <120 s
Heparin drip: <300 s
Catheter and percutaneous transluminal coronary angioplasty (PTCA): >200 s
Postprocedure/sheath removal: <200 s
Mechanism of action: Potentiates the action of antithrombin III and thereby inactivates thrombin (as well as activated coagulation factors IX, X, XI, XII, and plasmin) and prevents the conversion of fibrinogen to fibrin; heparin also stimulates release of lipoprotein lipase (lipoprotein lipase hydrolyzes triglycerides to glycerol and free fatty acids). Half-life: 1–2 hours, depending on route. Stop 2 hours before procedure.
Mechanism of action: Interferes with hepatic synthesis of vitamin K-dependent coagulation factors (II, VII, IX, X). Duration of action is 2–5 days. Stop 4 days before procedure.
Low-molecular-weight heparin. Subcutaneous (SC) dose, once daily after the loading dose. Duration: >12 hours; half-life: 2–5 hours. Stop the dose 24 hours before procedure.
Direct thrombin inhibitor, IV infusion; half-life: 39–51 min. Stop 4 hours before procedure.
Factor X inhibitor; half-life: 17–21 hours, SC dose once. Stop 24 hours before procedure.
Platelet aggregation inhibitor. Pharmacodynamic/kinetic peak effect: 75 mg/day; bleeding time: 5–6 days. Platelet function: 3–7 days; half-life: ~8 hours. Discontinue 7 days before procedure.
Glycoprotein IIb/IIIa inhibitor. IV dosage. Pharmacodynamic/kinetic half-life: ~30 min. Platelet function returns to normal 24–48 hours after discontinuation of infusion. Antiplatelet effects can be reversed with platelet transfusions.
Aspirin, cilostazol, dipyridamole, eptifibatide, ticlopidine, tirofiban. Stop most of the antiplatelet agents 5 days before procedure.
All biliary, renal, and other nonvascular interventions
Stent placements, TIPS, ports
(Chemo)embolizations
Patients with increased risks: endocarditis, transplant
G-tube in patients with head and neck cancer
Solid organ biopsies
Diagnostic angiography
Vena cava filter
Regular G-tube (nonhead and neck cancer patients)
Simple biopsies: thyroid, subcutaneous
Paracentesis and thoracentesis
Procedure | Antibiotic |
---|---|
All routine procedures | Ampicillin (1 g IV) and gentamicin (80 mg IV or 40 mg IV if creatinine elevated) |
Ampicillin allergy (low cost) | Clindamycin (Clindacin, 600 mg IV) and gentamicin (80 mg IV or 40 mg IV if creatinine elevated) |
Ampicillin allergy (higher cost) | Levofloxacin (Levaquin, 500 mg IV or 250 mg if creatinine elevated) |
Septic patients | Consider adding metronidazole (Flagyl, 500 mg IV) to above combination of ampicillin and gentamicin |
Tube injection | Levofloxacin (Levaquin, 500 mg PO) |
G-tube (HN CA) | Cefazolin (Ancef, 1 g, IV) followed by 5 days cephalexin (Keflex 500 mg BID PO) |
Prostate biopsy | Gentamicin (80 mg IM on day of procedure) and ciprofloxacin (Cipro, 500 mg PO for 7 days including day before procedure) |
Transplant patients | Piperacillin and tazobactam (Zosyn, 3.375 mg IV) |
Indwelling catheter and continued resistant growth | Consider giving vancomycin (500 mg IV) instead of gentamicin. Consult resistance tests. |
The normal ascending aorta is always larger in diameter than the descending aorta.
Branches:
Great vessels
Intercostal arteries
Bronchial arteries
Normal great vessel configuration, 70% (see Fig. 8.7 ). Variants occur in 30%:
Bovine arch, 20%: common origin of brachiocephalic and left common carotid artery (CCA)
Left vertebral artery (LVA) comes off aortic arch (AA) between left CCA and subclavian artery (SA), 5%
Common carotid trunk, 1%
Arteria thyroidea inferior mesenteric artery (IMA) to thyroid isthmus
Intercostal arteries are usually paired from 3rd–11th intercostal spaces; these arteries may give rise to spinal arteries.
Bronchial artery configuration is quite variable. Most common configurations are:
Single right bronchial artery
Multiple left bronchial artery
Superior vena cava (SVC) congenital variants
Persistent left SVC (most common variant)—right SVC may be normal, small, or absent
Right upper lobe partial anomalous pulmonary venous return—one or more pulmonary veins drain into the systemic venous system or right atrium (RA) instead of the left atrium (LA)
SVC aneurysm—asymptomatic, caused by congenital weakness in the SVC wall or muscular layer of the tunica adventitia
Indications:
Diagnosis and surveillance of aneurysms
Aneurysm rupture
Aortic dissection
Spiral CT is currently expanding CT indications.
CT is not yet validated as the sole evaluation of traumatic arch injuries.
Indications:
Diagnosis and surveillance of aneurysms
Aortic dissection
Allows evaluation of the aortic root better than CT
MRA of great vessels is gaining in diagnostic importance.
Indications:
Preoperative aneurysm assessment
Traumatic arch injury
Equivocal CT or MRI
Remains the gold standard diagnostic tool but is rarely the initial diagnostic examination for the thoracic aorta.
Indications:
Aortic dissection
Associated cardiac disease (aortic insufficiency [AI], left ventricle [LV] dysfunction)
Not validated to evaluate traumatic aortic injury
Catheter: 7- to 8-Fr pigtail
Contrast: Hypaque 76 or nonionic equivalent
Rate: 30–40 mL/s × 2 s (total: 60–80 mL)
Fast filming: 3/s × 3. Higher rate for DSA.
Always perform imaging in at least two orthogonal views.
True aneurysms contain all three major layers of an intact arterial wall. False aneurysms lack one or more layers of the vessel wall; false aneurysms are also called pseudoaneurysms. Most thoracic aortic aneurysms are asymptomatic and are detected incidentally. Clinical symptoms usually indicate large size, expansion, or contained rupture.
Atherosclerosis
Dissection
Cystic medial generation
Connective tissue diseases (Marfan, Ehlers-Danlos)
Syphilis
Posttraumatic pseudoaneurysm
Mycotic aneurysm
Aortitis
Takayasu arteritis
Giant cell aortitis
Collagen vascular diseases (rheumatoid arthritis, ankylosing spondylitis)
True aneurysms tend to be fusiform.
False aneurysms tend to be saccular.
Posttraumatic, mycotic, and postsurgical aneurysms are false aneurysms.
Bicuspid aortic valve is a risk factor for thoracic aortic aneurysm
Ascending aorta aneurysm associated with annuloaortic ectasia, syphilis, postoperative aneurysm, aortic valve disease, or aortitis.
thoracic aortic aneurysm mimics: ductus diverticulum, aortic spindle
90% of these aneurysms are fusiform because thoracic atherosclerosis is usually circumferential; 10% are saccular. A saccular shape should therefore raise the suspicion of a false aneurysm (pseudoaneurysm). Atherosclerotic thoracic aneurysm is more common in the descending aorta and has a high incidence of concomitant AAA.
Expansion
Pain
Hoarseness, dysphagia
Aortic insufficiency
Rupture (uncommon if <5 cm)
Rupture into pericardial or pleural space, trachea, mediastinum, esophagus
Rupture into SVC (aortocaval fistula), PA (aortopulmonary fistula)
Angiography ( Fig. 8.8 )
Most useful in preoperative assessment of asymptomatic patients
Appearance
Fusiform > saccular
Determine proximal and distal extent (often thoracoabdominal)
Determine branch involvement
Coexistent aneurysmal or occlusive disease
Not accurate in determining aneurysm size because of:
Magnification
Layering of contrast
Thrombus in the lumen
An indicator of an impending rupture is focal ectasia (so-called pointing aneurysm, or nipple of aneurysm)
Mural thrombus well seen
Dual energy CT (DECT) may be helpful in characterizing plaques by generating calcium and iodine images
Extraluminal extent and contained rupture better seen than by angiography
Signs of rupture (see also AAA below)
High attenuation crescent in the mural thrombus
Draped aorta sign—posterior aortic wall closely apposed to the spine
Penetrating ulcer
Hemothorax
Degenerative process of the aortic muscular layer (media) causing aneurysms of the ascending aorta. Commonly involves aortic sinuses and sinotubular junction, also resulting in aortic insufficiency. Causes:
HTN
Marfan, Ehlers-Danlos, homocystinuria (structural collagen diseases)
Symmetric sinus involvement (“tulip bulb”)
Ascending aorta is most commonly involved.
Dissection is a frequent complication.
Calcifications are rare.
Syphilitic aneurysms are a delayed manifestation of tertiary syphilis 10–30 years after primary infection. Infectious aortitis occurs via vasa vasorum. 80% of cases involve the ascending aorta or the AA.
Asymmetric saccular sinus involvement
Tree-bark calcification is common.
Dissections are rare.
Mycotic aneurysms are saccular pseudoaneurysms located in the ascending aorta or isthmus. Organisms: Staphylococcus, Streptococcus, Salmonella . CT often reveals perianeurysmal inflammation. Associations include:
Immunocompromised patients
Intravenous drug abuse (IVDA)
Endocarditis
Postsurgical
Idiopathic
Treatment with resection and extraanatomic bypass.
Aortic dissection represents a spectrum of processes in which blood enters the muscular layer (media) of the aortic wall and splits it in a longitudinal fashion. Most dissections are spontaneous and occur in the setting of acquired or inherited degeneration of the aortic media (medial necrosis). Medial necrosis occurs most commonly as an acquired lesion in middle-aged to older adult hypertensive patients. Dissections (spontaneous) almost exclusively originate in the thoracic aorta and secondarily involve the abdominal aorta by extension from above. Aortic dissection results in the separation of two lumens by an intimal flap. The false lumen represents the space created by the splitting of the aortic wall; the true lumen represents the native aortic lumen. “Dissecting aortic aneurysm” is somewhat of a misnomer because many dissections occur in normal-caliber aortas. In chronic dissections the false channel may become aneurysmal.
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