Cardiac - AAA, AD, DVT and PE Flashcards

1
Q

Aortic dissection

Most common location of dissection
Classification systems
Use of classification

A

Ascending aorta dissection 2x more common than descending aorta

Right lateral wall of ascending aorta is most common site of aorta dissecction

DeBakey classification
- Type 1: involves ascending aorta, aortic arch, descending thoracic aorta
- Type 2: involves ascending aorta only
- Type 3a: involves descending aorta distal to left subclavian artery and proximal to celiac artery
- Type 3b: involves thoracic and abdominal aorta distal to left subclavian artery

Stanford classification Type A: (60%)
- involves ascending aorta, may progress to aortic arch and abdominal aorta
- Life threatening, requires emergency surgical repair

Stanford classification type B:
- involves descending thoracic and abdominal aorta
- Usually managed medically unless dissection into end-organ vessels leading to ischemia, or concomitant aortic aneurysm with high risk of rupture

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2
Q

Acute aortic syndromes

Definition
Types/ variants

A

Definition:
- spectrum of life-threatening aortic conditions
Includes aortic dissection, intramural haematoma, penetrating aortic ulcers, intimal tear without haematoma, periaortic haematoma

Aortic intramural haematoma:
- 5-20% of acute aortic syndrome
- Focal haematoma confined between intima and media layer due to spontaneous rupture of vasa vasorum without detectable intimal tear or dissection flap due to hypertension, trauma or iatrogenic injury
- ascending type managed surgically
- descending type managed medically unless >1cm thick, aorta diameter >4cm or progression on serial imaging

Penetrating aortic ulcer:
- Aortic ulcer penetrating adventitia with subadventitial haematoma
- lead to aortic dissection or perforation

Limited intimal tear without haematoma:
- stellate or linear intimal tear with exposure of underlying aortic media or adventitia

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3
Q

Aortic dissection

Risk factors
Pathophysiology

A

Risk factors:
- Hypertension
- Collagen disorders: Marfan syndrome, Ehlers-Danlos syndrome
- Aortic aneurysm
- Bicuspid aortic valve
- Family history of aortic dissection

Pathogenesis:
- Tear in aortic intima
- Blood flow into aortic media and creates false lumen by separating intima layer
- False lumen dilatation depends on BP, size of entry tear, depth of dissection plane within media and percentage of aortic circumference involved
- True lumen may collapse due to pressure differential, exacerbated by muscular elements within dissection flap

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4
Q

Aortic Dissection

S/S

A

S/S

Acute pain:
-Site: Anterior for type A, Back/ abdomen for type B
- Onset: abrupt
- Character: Sharp, tearing, knife-penetrating
- Radiation: generalized in thorax or abdomen

Pulse deficit:
- Weak of absent peripheral pulses due to impaired flow

BP:
- Hypertension: Type A 35%, Type B 70%
- Hypotesion: Type A 25%, Type B 5%
- Hypotension due to Aortic regurgitation, Cardiac tamponade, Acute MI, Haemothorax, Haemoperitoneum

Aortic regurgitation: Early diastolic decrescendo murmur with wide pulse pressure

Focal neurological deficits
o Paraplegia (spinal cord)
o Altered level of consciousness (carotid artery)
o Horner’s syndrome (superior cervical ganglion)
o Hoarseness (left recurrent laryngeal nerve

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5
Q

Aortic dissection

Investigations
D/dx

A

Differential diagnosis
 Pneumothorax
 Pulmonary embolism
 Pericarditis
 Acute pancreatitis
 Acute myocardial infarction (AMI)

Investigations:
Biochemical: Cardiac enzymes: cTnT, cTnI, CK-MB

Radiological:
Chest X-ray (CXR) features: differentiate from pneumothorax
o Irregular or wavy aortic outline
o Widening of aortic silhouette
o Widening of mediastinum (erect PA = 6 cm and supine AP = 8 cm) (unable to see the aortic knuckle and descending aorta)

ECG: Differentiate from AMI

ECHO: for AR, pericardial effusion, dissection flap

CT angiography/ Contrast CT Aortogram (stable): compressed true lumen, identify false lumen

Transesophageal echocardiography (TEE) (unstable): AR. pericardial effusion, dissection flap, ture and false lumens

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6
Q

Aortic dissection

Management options

A

General care:
- ICU or coronary care unit CCU admission, complete bed rest
- NPO with IV saline, morphine analgesics

Medical: Uncomplicated type B patients: medical therapy + long term antihypertensives
- Sodium nitroprusside (give second): vasodilator to control systolic BP to 100-120mmHg
- Labetalol (give first): B-blocker to control HR at 60/min

Surgical:
- All type A patients
- Complicated type B patients (end-organ hypoperfusion)

Surgical treatment options:
- Open dissection repair: excision of intimal tear, obliteration of entry into false lumen, reconsitution of aorta by synthetic vacular graft, repair/ replace AV
- Endovascular repair: endovascular stent grafting

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7
Q

Aortic dissection

Complications

Prognosis

A

Type A
* Dissection in aortic valvular annulus - Aortic regurgitation
* Dissection into pericardium - Cardiac tamponade
* Dissection in coronary artery ostia - Myocardial infarction
* Focal neurological deficits related to cerebrovascular ischemia

Type B
* Dissection into abdominal aortic branches  Celiac/ Renal/ LL ischemia
* Focal neurological deficits related to spinal ischemia

Mortality of Type B dissections
* 10% at 30 days
* 25% at 3 years
* 50% at 5 years

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8
Q

AAA

Risk factors

A

↑ Risk of AAA
 Elderly + Caucasian + Male
 Smoking
 Atherosclerosis
 Hypertension
 Family history of AAA
 Presence of large artery aneurysm
* Iliac artery aneurysm
* Femoral aneurysm
* Popliteal aneurysm

↓ Risk of AAA
 Non-Caucasian females
 Diabetes

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9
Q

AAA

Investigations

A

CBC with differentials
* Anemia: Hypochromic microcytic anemia due to acute blood loss
* Leukocytosis: Infected or inflamed aneurysm

Clotting profile: Disseminated intravascular coagulopathy (DIC)
o ↑ (Prolongation) of PT, APTT, TT
o ↓ Coagulation inhibitor (e.g. anti-thrombin)
o ↓ Platelet count
o ↓ Fibrinogen level from consumption of coagulation factors and platelets
o ↑ Fibrin degradation products especially D-Dimers (Clot lysis indicator)

Inflammatory markers: ↑ ESR and CRP
o Infected or inflamed aneurysm

Arterial blood gas (ABG): Metabolic acidosis
o Acute blood loss leading to shock

Imaging:
- USG abdomen/ Focused Assessment with Sonography in Trauma (FAST) exam
- CT angiography (CTA): for urgent surgical planning for symptomatic patients
- MR angiography (MRA): for contrast contraindications

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10
Q

AAA

Treatment options
Indication for surgery

A

Non-operative management
Monitoring with USG/ CTA yearly
Lifestyle modification
o Smoking cessation
o Control of hypertension
o Exercise
o Treatment of COPD

Indications for surgery of uncomplicated AAA
* Symptomatic aneurysm of any size
* ALL AAA > 5 cm (5.5 cm in Caucasians) unless patient is medically unfit or limited life expectancy
* Rapidly expanding AAA > 1.0 cm/ year or > 0.5 cm/ 6 months
* Saccular aneurysm

Surgical options:
* Open surgical repair
* Endovascular aneurysm repair (EVAR)

Ruptured AAA:
- IV fluid resuscitation (crystalloids/ colloids/ blood) to maintain organ perfusion
- Allows permissive hypotension (SBP < 100 mmHg). avoid over-resuscitation causing dilution of clotting factor and thrombus destabilization
- Emergency EVAR repair

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11
Q

Open surgical AAA repair

Procedure
Approaches

A

Replacement of diseased aortic segment with a tube or bifurcated prosthetic graft

Transabdominal or retroperitoneal approach
Transabdominal: Midline abdominal incision
Retroperitoneal: Left retroperitoneal incision
- Advantageous in patients with previous intraabdominal surgery, obese patients,
COPD patients
- Proximal suprarenal or supraceliac control of aorta is more easily achieved by retroperitoneal approach

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12
Q

Open surgical AAA repair

Complications

A

CVS: Arrhythmia/ AMI

Vascular: Intraoperative hemorrhage/ LL ischemia/ Distal embolization/ Aortoduodenal fistula
- LL ischemia prevented by minimizing manipulation of aneurysm before clamping, use Fogarty balloon catheter to remove distal emboli

UG: Acute renal failure/ Sexual dysfunction
- Related to use of IV contrast, inadequate hydration, hypotension or renal ischemia
from a period of aortic clamping above renal arteries or embolization to renal
arteries
- Sexual dysfunction and retrograde ejaculation resulting from damage to sympathetic plexus during dissection near the proximal left common iliac artery

CNS: Paraplegia due to spinal cord ischemia

GI: Bowel ischemia/ Prolonged paralytic ileus
- Ischemic colitis from ligation of IMA without adequate collateral circulation
Necrosis limited to mucosa: IV Abx and bowel rest
Necrosis through muscularis propria: segmental stricture needs delayed resection
Transmural necrosis: immediate resection of necrotic colon and end colostomy

Infection: wound or graft

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13
Q

EVAR

Procedure

A

Placement of modular graft components delivered via the iliac or femoral arteries to line the aorta
and exclude the aneurysm sac from the circulation

Lifelong surveillance is required to assure integrity of the repair

Close FU with CT scan every 6 months for 1 year and then yearly is essential to maintain long-term clinical success with this technique

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14
Q

EVAR

Selection criteria

A

Aortic neck diameter at the lowest renal artery:
- Required endograft diameter is calculated by adding an additional 15 – 20% of aortic neck diameter to provide sufficient radial force to prevent device migration
- Commercially available devices have endograft diameter largest at 36 mm which allows EVAR to a maximal aortic neck diameter of 32 mm
- Undersizing will lead to inadequate seal and failure to exclude the aneurysm
- Oversizing will lead to incomplete expansion of endograft with infolding and inadequate seal, kinging of device, thrombus formation, endoleak

Aortic neck length: Distance from lowest renal artery to the origin of aneurysm
- at least 10 – 15 mm to provide an adequate proximal landing zone

Aortic neck angulation: < 60o
- Angle formed between points connecting the lowest renal artery, origin of aneurysm and aortic bifurcation

Cone-shaped neck/ Reverse tapered aortic neck:
- Diameter of aorta 15 mm below the lowest renal artery is ≥ 10% larger than diameter of aorta at lowest renal artery

Iliac artery and access vessel morphology in distal landing zone: minimal amount of tortuosity and calcification and no significant stenosis or mural thrombus

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15
Q

EVAR

Complications

A

Systemic complications
- Vascular injury (e.g. iliac or femoral artery) at entry site
- Arterial dissection
- Bowel ischemia
- Acute renal failure: Secondary to embolization or renal artery occlusion, or contrast-induced nephropathy

Complications related to endografts
- Endoleaks* (Type I and III NOT acceptable): Defined as failure to exclude the aneurysmal sac from arterial blood flow
- Graft infection/ thrombosis/ migration
- Mechanical failures: Graft kinking, separation of components, stenosis, collapse

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16
Q

EVAR

Endoleak types

A

Type 1: Not acceptable leak at graft attachement site
- A: Inadequate seal at proximal end of endograft
- B: Inadequate seal at distal end of endograft
- C: Inadequate seal at iliac occlude plug

Type 2: Close observation for static aneurysm, embolization if expanding
- Backflow of blood from aortic collaterals (lumbar arteries and IMA) into aneurysm sac

Type 3: Not acceptable leak though graft defect
- A: Junctional leak or disconnect of endograft components
- B: Holes in the endograft fabric (minor < 2 mm; major ≥ 2 mm)

Type 4: Leak through graft fabric as a result of graft porosity

Type 5: Flow visualized but source unidentified

17
Q

AAA

Complications
Prognosis

A

Complications
Rupture of aneurysm
* Intraperitoneal (Free)
* Retroperitoneal - Retroperitoneal hematoma
* Duodenum (Aortoduodenal fistula) - GI bleeding
* Inferior vena cava (Aortocaval fistula) - Heart failure
Thrombosis and embolism
Infection and inflammation
Pressure effects

Risk of rupture at 5 years
 Aneurysm < 5 cm = 20%
 Aneurysm > 5 cm = 50%

18
Q

DVT

  • Cause of mortality
  • Subclass
A

DVT is commonly associated with pulmonary embolism (PE)
Patients with PE usually die from right heart failure (cardiogenic shock) rather than hypoxemia

DVT of lower extremity is subdivided into 2 categories
1. Proximal vein thrombosis
o Thrombi involves popliteal, femoral or iliac veins
o Clinically more significant as it more commonly associates with PE

  1. Distal (Calf) vein thrombosis
    o Thrombi involves deep calf veins
19
Q

DVT and PE

Risk factors

A

Medical history
- Malignancy (Hypercoagulability)
o Especially adenocarcinoma which secretes mucin
o Myeloproliferative neoplasm (MPN)
o Gynecological malignancy obstructing LL veins

  • Stroke
  • Obesity
  • Prior venous thromboembolism
  • Trauma of lower extremity

Immobilization
* Prolonged hospitalization or bed rest
* Occupational immobilization
* Air travel

  • Recent surgery
  • Pregnancy or post-partum, Oral contraceptives or hormone replacement therapy (HRT)

Inherited conditions
* Anti-thrombin III deficiency
* Protein C deficiency
* Protein S deficiency
* Factor V Leiden

Acquired conditions
* Lupus anticoagulants
* Antiphospholipid syndrome

Others
* Paroxysmal nocturnal hemoglobinuria
* Homocysteinemia
* Nephrotic syndrome

20
Q

DVT and PE

Pathogenesis

A

Virchow’s triad: Stasis + Endothelial injury + Hypercoagulability

  • Stasis = Prolonged bed rest/ Air travel > 6 hours/ Congestive heart failure (CHF)/ Cerebrovascular accident within 3 months
  • Endothelial injury = Surgery/ Trauma/ Prior DVT/ Central catheter placement
  • Hypercoagulability
21
Q

DVT and PE

S/S

A

Features of involved extremity
* Unilateral pitting edema
* 腫: Swelling with difference in calf diameters
* 紅/熱: Erythema/ Warmth
* 疼: Pain/ Tenderness of calf or thigh (along distribution of deep veins)

Signs suggesting PE
* Cough
* Pleuritic chest pain
* Dyspnea on exertion: Secondary to pleural effusion
* Hemoptysis: Tissues become anoxic or hypoxic in pulmonary infarction
* Shock: Obstructive shock, Hypotension due to decrease in venous return (VR) in venous thrombosis and decrease cardiac output (CO) in pulmonary artery blockage

Vital signs
* Sinus tachycardia
* Hypotension (Obstructive shock if massive)
* Fever

Respiratory examination
* Tachypnea (> 70%)
* Cyanosis
* Pleural friction rub
* Crepitations

CVS examination
* Elevated JVP
* Right-sided S3
* Graham Steell (PR) murmur

22
Q

DVT

D/dx

A
  • Muscle strain/ tear/ twisting/ injury to leg
  • Cellulitis
  • Superficial thrombophlebitis
  • Lymphangitis
  • Lymphedema
  • Venous valvular insufficiency
  • Ruptured Baker’s cyst
23
Q

DVT and PE

Diagnostic criteria

A
24
Q

DVT and PE

Biochemical/ bloods Investigations

A

CBC with differentials: any Polycythemia, Thrombocytosis

Clotting profile
* Prothrombin time (PT)
* Activated partial thromboplastin time (APTT)
* D-dimer
o Sensitive but NOT specific and also increase in MI, pneumonia, sepsis or malignancy
o Only used to rule out venous thrombosis if absence
o Consider age-specific cutoff: 500 if < 50 years old; 10 x age if ≥ 50 years old

Thrombophilia screen
* Anti-thrombin III deficiency
* Protein C deficiency
* Protein S deficiency
* Factor V Leiden
* Antiphospholipid syndrome: Lupus anticoagulant antibody

LRFT

Arterial blood gas (ABG)
* Hypoxemia/ Hypocapnia/ Respiratory alkalosis/ ↑ A-a gradient
* Type I Respiratory failure in pulmonary embolism

Urinalysis

25
Q

DVT and PE

Radiological investigations

A

ECG
Sinus tachycardia

S1Q3T3
o S1: Right-axis deviation or deep S wave in lead I
o Q3: Q wave in lead III
o T3: Inverted T wave in lead III

Evidence of right heart strain
o R-axis deviation
o T inversion in V1 – 4
o Incomplete or complete RBBB

CXR
- Hampton’s hump (Wedge-shaped infarction)
- Westermark sign: Avascularity distal to the PE, Demonstration of a sharp cut-off of pulmonary vessels with distal hypoperfusion
- Pleural effusion
- Atelectasis: Decreased ventilation in alveoli that is deprived of blood supply to improve V/Q ratio, or collapse of segment which is infarcted due to embolism

Venous Duplex USG in LL for DVT, Loss of vein compressibility

CT pulmonary angiogram (CTPA): for filling defects in pulmonary trunk

Ventilation-perfusion (V/Q) scan

Echocardiogram (Transthoracic/ Transesophageal): for saddle, left main or right main PE; RV volume and dysfunction;
- McConnell’s sign: Hypokinesis of RV free wall + Normal or hyperkinetic motion of RV apex

26
Q

DVT and PE

Treatment objectives
Treatment options

A

Treatment objectives
 Prevent further clot extension
 Prevention of acute pulmonary embolism
 Reduce risk of recurrent thrombosis
 Treatment of massive ilio-femoral thrombosis causing LL ischemia and venous gangrene
 Limiting development of late complications
* Post-thrombotic syndrome
* Chronic venous insufficiency
* Chronic thromboembolic pulmonary HT

Medical:
Parenteral therapy (UFH/ LMWH/ Fondaparinux) bridged to warfarin
Parenteral therapy (UFH/ LMWH/ Fondaparinux) bridged to NOAC

Surgical:
- Catheter-directed fibrinolytics with thrombus fragmentation or aspiration
- Catheter-based embolectomy ± Adjunctive catheter-based thrombolysis
- Surgical embolectomy
- IVC filter placement

27
Q

Medical therapy for DVT and PE

Options
Indication
Timing

A

Short-term options: Continued for ≥ 5 days
LMWH: SC Enoxaparin/ SC Dalteparin
o Indicated for cancer patients

Unfractionated heparin (UFH)
o Indicated for before thrombolysis or catheter based treatment; renal failure, extreme obesity, hemodynamic instability, bleeding risk
o e.g. IV UFH 80 U/kg bolus&raquo_space; 18 U/kg/hr and titrate to APTT 1.5 – 2.5x

Fondaparinux: SC Fondaparinux 5 – 10 mg QD

Long-term options:
Wafarin
* Initiated simultaneously with heparin with initial dose = 5 mg/day and overlap for ≥ 5 days with parenteral anticoagulants until INR ≥ 2.0 for ≥ 24 hours
* Prolong INR to a target of 2.5
Heparin product can be discontinued on day 5/6 when INR has been therapeutic for two
consecutive days

NOAC
* Initial oral anticoagulants in patients with acute VTE (OR)
* Initiate after ≥ 5 days of parenteral coagulation for edoxaban and dabigatran
* Direct thrombin (factor IIa) inhibitors: Dabigatran
* Direct factor Xa inhibitor: Rivaroxaban/ Apixaban/ Edoxaban

Complications:
Thrombolytic (Fibrinolytic) agents: tPA/ Streptokinase
- Indication: Hemodynamically unstable PE, Massive ilio-femoral thrombosis, RV dilatation

28
Q

DVT and PE treatment

Compare Unfractionated and LMWH

A
29
Q

DVT and PE

Surgical treatment options
Indications
Procedures

A

Catheter-directed intervention: Fibrinolytics with thrombus fragmentation or aspiration
- Indication: extensive DVT and to decrease post-thrombotic syndrome, PE with hemodynamic compromise or high risk and not candidate for systemic lysis or surgical thrombectomy

Thrombectomy (Embolectomy)
- Indicated in patients with obstructive or cardiogenic shock or evidence of RV dysfunction
- Catheter-based embolectomy ± Adjunctive catheter-based thrombolysis, (OR) Surgical embolectomy

IVC filter placement
- Indicated for Chronic recurrent embolism with pulmonary PE, High risk for proximal vein thrombosis or PE, Recurrent thromboembolism despite adequate anticoagulation, Contraindicated or failure to anticoagulant therapy

30
Q

DVT and PE prophylaxis

A

Screening of malignancy
Compression stocking
Posturing, avoid prolonged stasis
Low-dose heparin

31
Q

AAA

Physical exam features

A

General examination
Vital signs
o Fever
o Tachycardia
o Hypotension

Ecchymosis: Extensive retroperitoneal hematoma causing extravasation of blood into subcutaneous tissues
o Grey-Turner sign: Flank ecchymosis
o Cullen’s sign: Periumbilical ecchymosis
o Fox’s sign: Proximal thigh ecchymosis
o Bryant’s sign: Discoloration of scrotum

Abdominal examination (Aortic bifurcation = Umbilicus - L3/4 level)
* Expansile (displace sideways) pulsatile (displace vertically) mass
* Abdominal distension
* Abdominal tenderness

Vascular examination: Other peripheral artery aneurysms
o Femoral aneurysm
o Popliteal aneurysm

Evidence of distal embolization and ischemia

32
Q

AAA

S/S for non-ruptured/ ruptured AAA
D/dx

A

Non-ruptured AAA (75%)
- Abdominal, back, flank or pelvic pain due to rapid expansion, rupture, compression or erosion, inflammation in mycotic aneurysm
- Limb ischemia: acute arterial insufficiency, 6Ps
- Atherosclerotic thrombus dislodgement and emboli: stroke, PE, MI…
- Constitutional symptoms (infected or inflammatory aneurysm/ DIC)

Ruptured AAA
- Hypotension, signs of hypovolemic shock
- Haemoperitoneum: Abdominal distension. Abdominal pain (severe and acute), Grey-turner, Fox’s, Bryant’s, Cullen’s
- Back or flank pain for juxtarenal aneurysm
- Low abdominal/ pelvic pain radiating to groin/ thigh for infrarenal aneurysm
- Focal back pain for retroperitoneal haematoma, ubsidization of pain after hematoma stabilizes

Differential diagnosis
 Aortic dissection
 Ulcerated aortic plaque
 Acute pancreatitis
 Acute peritonitis
 Acute myocardial infarction (MI

33
Q

AAA

Pathogenesis

A

Majority (90%) of AAA are degenerative in origin and the remaining are inflammatory (5%) and
idiopathic

Alterations in vascular wall biology leading to progressive thinning and weakening of aortic wall
and enlargement of aortic diameter
* Transmural inflammatory changes
* Abnormal collagen remodelling and cross-linking
* Loss of elastin and smooth muscle cells

34
Q

AAA

  • Clinical definition
  • Size cut-offs
  • Locations of aneurysm
A

Clinical definition:
- Segmental, full-thickness (intima, media and adventitia) dilation of a blood vessel that is > 50% greater than the normal aortic diameter (i.e. 3 cm)
- Rapidly expanding = > 1.0 cm/ year

Different size of aneurysm
Normal aortic diameter = 2.0 cm
Aortic diameter > 3.0 cm is considered aneurysmal
o Small aneurysm: Diameter < 4.0 cm
o Medium aneurysm: Diameter = 4.0 cm – 5.5 cm
o Large aneurysm: Diameter > 5.5 cm
o Very large aneurysm: Diameter ≥ 6.0 cm

Locations:
* Suprarenal AAA: Aneurysm originates above renal arteries
* Pararenal AAA: Aneurysm originates from an aneurysmal aorta (i.e. involves aorta at
the level of renal arteries)
* Juxtarenal AAA: Aneurysm originates at level of renal arteries but aorta at the level of
renal arteries is normal
* Infrarenal AAA (most common) (85%): Aneurysm originates below renal arteries