Cardiac - AAA, AD, DVT and PE Flashcards
Aortic dissection
Most common location of dissection
Classification systems
Use of classification
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
Acute aortic syndromes
Definition
Types/ variants
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
Aortic dissection
Risk factors
Pathophysiology
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
Aortic Dissection
S/S
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
Aortic dissection
Investigations
D/dx
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
Aortic dissection
Management options
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
Aortic dissection
Complications
Prognosis
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
AAA
Risk factors
↑ 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
AAA
Investigations
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
AAA
Treatment options
Indication for surgery
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
Open surgical AAA repair
Procedure
Approaches
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
Open surgical AAA repair
Complications
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
EVAR
Procedure
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
EVAR
Selection criteria
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
EVAR
Complications
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
EVAR
Endoleak types
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
AAA
Complications
Prognosis
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%
DVT
- Cause of mortality
- Subclass
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
- Distal (Calf) vein thrombosis
o Thrombi involves deep calf veins
DVT and PE
Risk factors
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
DVT and PE
Pathogenesis
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
DVT and PE
S/S
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
DVT
D/dx
- Muscle strain/ tear/ twisting/ injury to leg
- Cellulitis
- Superficial thrombophlebitis
- Lymphangitis
- Lymphedema
- Venous valvular insufficiency
- Ruptured Baker’s cyst
DVT and PE
Diagnostic criteria
DVT and PE
Biochemical/ bloods Investigations
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
DVT and PE
Radiological investigations
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
DVT and PE
Treatment objectives
Treatment options
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
Medical therapy for DVT and PE
Options
Indication
Timing
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»_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
DVT and PE treatment
Compare Unfractionated and LMWH
DVT and PE
Surgical treatment options
Indications
Procedures
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
DVT and PE prophylaxis
Screening of malignancy
Compression stocking
Posturing, avoid prolonged stasis
Low-dose heparin
AAA
Physical exam features
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
AAA
S/S for non-ruptured/ ruptured AAA
D/dx
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
AAA
Pathogenesis
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
AAA
- Clinical definition
- Size cut-offs
- Locations of aneurysm
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
