Peripheral Dz Notecards Flashcards
Types of Aortic Aneurysms:
- arterial
- abdominal aorta: 4-8% in elderly males
- abdominal thoracic: much less common
Types of Arterial Aneurysms:
- cerebral “berry” aneurysms: risk of rupture and SAH
- aortic: risk of rupture and hemorrhage; risk of arterial branch stenosis or occlusion
- peripheral(popliteal/carotid/femoral): emboli/thrombi
Risk of aortic rupture:
- increases a lot after 5cm: 5%/yr
- below 5cm: 1%/yr
AA growth:
1-4 mm/year
Pathopneumonic signs for Marfinoid syndrome:
steinburg and walker murdoch
AA dx:
1- duplex ultrasonography: ID suspect iliac and abdominal aneurysms
2- contrasted CT angiography: to ID branches of iliac arteries
3- MRA- but takes longer
AA clinical sxs:
- not ruptured: asymptomatic
- ruptured: severe hypotension and abdominal pain
- abdominal mass below umbilicus
- iliac aneurysm: hydronephrosis ipsilaterally via compressed ureter
- mural walll thrombis–> emboli in LE
- compress adjacent structures–> abdominal discomfort
Management of AAA rupture:
CV emergency: rq. prompt IV fluids w/ blood, isotonic saline and emergent surgery
AA Risk Factors:
- Atherosclerosis
- Hypertension
- Family history
- Smoking
- Cystic Medial Necrosis (Connective Tissue Disorders of Large Arteries)
- Marfan Syndrome
- Ehlers Danlos Syndrome aka “Rubber Man Syndrome”
- -Rare
- Vasculitis
- Takayasu Arteritis
- Giant Cell Arteritis (i.e. Temporal Arteritis)
- Chronic infection–>Syphilitic Aortitis
- Trauma
Clinical features include of Marfan’s: (7)
- Arachnodactyly (long fingers)
- Subluxation (dislocation) of lens in eye (Ectopia lentis)
- Long slender limbs
- Hx of spontaneous pneumothorax
- Murmurs (Mitral Valve prolapse/Aortic regurgitation)
- AA/Dissection
- degradation of CT of arteries
Marfan’s progression:
Spectrum of clinic severity from isolated features–> rapidly progressive multi-organ dz
Autosomal dominant disorder of CT
Marfan’s Syndrome
Tx of AAA:
- no surgical benefit 4-5.5 cm
- surgical tx: sxs of expansion, occlusion/compression, rupture, rapid expansion >1cm/yr, AAA>5.5cm
Screening for AAA:
one time screening abdominal US for males between 65-75 y.o. who: smoked > 5 packs of cigarettes in their life or with fam hx of AAA
Tx for a AAA >5.5:
Surgical option:
- OPEN (gortex graft within the aneurysm)
- Percutaneous ENDOVASCULAR ANEURYSM REPAIR (EVAR)
Tx for a AAA <5.5:
- Smoking cessation
- Tight BP control
- Beta-blockers helpful in Marfanoid
- CHOL reduction (STATINS)
- Monitoring aneurysm q6-12 months by duplex ultrasound
Acute Aortic Syndromes:
- Aortic Dissection: dissection of blood into the intimal layer resulting in a false lumen parallel to true lumen
- Incomplete Dissection: Tear without dissecting blood
- Intramural hematoma: Due to Vasa vasorum rupture–> hemorrhage in wall of Aorta
- Penetrating Ulcer: Ulceration of plaque penetrating intima
Aortic Dissection Risk Factors:
- Hypertension
- Connective Tissue Diseases (Marfan Syndrome, Ehlers Danlos Syndrome)
- Trauma
- Cocaine use
- Weight lifting
- Prior CABG/Bicuspid Aortic valve
- Preexisting AA
- Aortic Coarctation = narrowing of the aortic arch
- Vasculitides: Takayasu Arteritis or Giant Cell Arteritis
Classification of Aortic Dissection:
Stanford A (ascending/proximal)- 70-75% or Stanford B (descending/distal)- 25-30%
Aortic dissection’s and mortality:
- 1-2% mortality risk/hr during first 24-48 hrs
- Untx Aortic Dissections w/ increasing mortality in real-time:
25% risk of death in first 24hrs
50%: in first 48 hours
75%: in first week
90%: in first month
Clinical Presentation of Aortic Dissection:
- Sudden onset of anterior CP (‘tearing’ quality) and/or back pain (between scapulae)
- Chest pain more common in Type A and back pain and abdominal pain more common in Type B
- Painless dissection is RARE
- Also, Abdominal pain, syncope, and stroke
If dissection involves ascending aorta it can dissect against Coronary Arteries and cause:
MI
If dissection is distal:
it can cause ischemia to lower extremities and result in an ischemic neuropathy
Clinical Presentation of Aortic Dissection:
- Pulse deficits (weak or absent carotid, brachial or femoral pulses)
- Dissection back toward heart can cause Aortic regurgitation diastolic murmur
- CHF
Dx of Aortic Dissection:
- Clinical suspicion: “tearing chest or back pain” in setting of risk factors
- Chest radiograph shows widening of the mediastinum
- CT/MRA Angiography of Chest, Abdomen and Pelvis
- Transesophageal Echo
Tx of Aortic Dissection:
- ICU
- Pain management
-BP reduction to SBP < 120, HR about 60 - IV antihypertensives used (Metoprolol, Esmolol, Labetalol)–Blunts increased HR with vasodilators
- If severe HTN: Beta-blockers + Sodium Nitroprusside
- Stanford Type A (PROXIMAL):
SURGICAL THERAPY (Aortic repair) + Medical Therapy (above) - Standford Type B (DISTAL):
MEDICAL THERAPY (above) - F/u CT scans to check on dissection and antihypertensive therapy with BB
Standford Type B (DISTAL) may need surgery if:
occlusion of major Aortic Branch, persistent pain/HTN, aneurysm development, or worsening of the dissection
suggests dissection back into the heart and bleeding into pericardial space
hypotension and JVD
Suspect Hemopericardium and Cardiac Tamponade w/ these sxs:
- JVD
- Hypotension
- Pulsus paradoxus (large decrease in pulse strength)
AMI Patho:
- arterial embolism
- atherosclerosis
- vasospasm of mesenteric artery
AMI sxs:
- Pain out of proportion on physical exam
- Visceral abdominal pain (poorly localized)
- May have melena or hematochezia
PAD MC
Men and increases with age
PAD RF:
CV RF’s: HTN, hyperlipidemia, DM, smoking
- associated w/ high 10 year CVD risk
PAD sxs:
- only 50% w/ sxs
- intermittent claudication: worsened w/ exercise; improved w/ rest
CAD PE:
- loss of hair
- ulcers
- poor peripheral pulses
- changes in skin color (dusky color, bluish, cool)
Pseudoclaudication is aka..
Lumbar spinal stenosis
Pseudoclaudication sxs:
- unrelated to PAD
- muscle pain and weakness that radiates down the leg; tingling in lower extremities
- exacerbating w/ standing erect
- relief w/ sitting down or flexion at waist w/ walking
PAD hx:
- CVD RF’s: HTN, hyperlipidemia, DM, smoking, age, male sex
- established hx CAD, MI, CVA
PAD claudication occurs where to stenosis?
Distal
LeRiche Syndrome aka…
Aortoiliac Occlusive Dz
LeRiche Syndrome MOA:
Severe atherosclerosis of abdominal aorta and iliac arteries
LeRiche Syndrome sxs:
Claudication of buttock, hips, and thigh
Often associated w/ erectile dysfunction/impotence
LeRiche Syndrome PE:
Poor femoral pulses
LeRiche Syndrome tx:
Aortoiliac bypass graft
Complications of PAD:
1- increased risk for CV event (CVA/AMI): 30%
2- worsening claudication: 25%
3- ischemic ulcers in LE: 10-20%
4- amputations: 5%
PAD dx:
1- clinical suspicion
2- ABI at bedside w/ Duplex Ultrasound
3- CT Ang/MRA of LE
4- if pt. To undergo revascularization for tx- catheter directed angiography
Explain an ABI calculation and how it’s done:
- demonstrates clinical severity of occlusion
- SBP ankle/SBP brachial
- simple and inexpensive method; confirmatory
- pt rests 15-30 min prior
- ultrasound to locate arteries by amplifying sound; BP obtained
- ultrasound works by ID the direction of flow
ABI Classification system for PAD:
> 1.30- noncompressible, calcified vessel
0.91-1.30: normal
0.41-0.90: mild to moderate PAD
<0.40: severe PAD
PAD Rutherford classification system:
Classifies claudication based on mild, moderate, and severe
PAD Fontaine classification system:
Specifies walking distance that provokes claudication (less than or greater than 650 feet)
PAD definitive tx:
- percuteaneous revascularization for areas of small stenosis
- arterial bypass for areas of large stenosis:
—severe claudication (<0.4) w/ sxs refractory to medical management
—ALI: caused by arterial embolus/thrombus in situ; vascular emergency
—LeRiche dz: erectile dysfx
PAD medical management:
- targeted at reducing CV risk for atherosclerosis
- exercise program
- LDL goal <100
- ASA: 81-325 mg QD/Clopidogrel 75 mg QD (mortality benefit)
- Cilostazol (pletal) and Pentoxifylline (trental) for sxs benefit
—Clio: improves walking; C/I in CHF
—Pent: methylxanthine derivative; may improve walking distance
ALI MOA:
Sudden occlusion of LE artery secondary to:
- arterial emboli: LV mural thrombus; atrial thrombus from a fib
- thrombosis in situ: secondary to ruptured plaque
ALI presents with:
Sudden onset of sxs: 6 P’s
Pain, pallor, paralysis, paresthesia, pulseless, poikilothermia
- crescendo pattern: hours to days
ALI PE:
Cyanotic blue/pale, pulseless LE and diminished neuro vascular fx (both motor and sensory)
ALI dx:
- continuos flow Doppler: evidence of pulse?
- ABI: emergently to determine degrees of ischemia
- CTA/MRA
ALI surgical tx:
Duration <14 days w/ small occlusion: - percuteaneous revascularization w/stent - catheter directed thrombolysis Duration >14days w/ larger occlusion: - arterial bypass surgery - endovascular thrombo-embolectomy
ALI medical tx:
- heparin IV
ALI rqs. R/o of:
Gangrene; if present— pain management, abx, amputation, deride, hospitalization
RF’s for Gangrene: (5)
IV drug use Trauma Surgery PAD Diabetics
Gangrene etiology:
Tissue that has lost its blood supply and is undergoing necrosis
Describe dry gangrene:
- often due to PAD
- secondary to tissue ischemia
- tissue undergoing sterile ischemic coag. Necrosis
- well demarcated borders; total tissue death
Describe wet gangrene:
- secondary to stasis of blood, promoting bacterial growth
- Type I: polymicrobial
- Type II: monomicrobial (clostridium perfringens, GA streptococcus, MRSA)
- bacteria release endotoxins and cause systemic manifestation of sepsis and death
- poor prognosis
- moist appearance and blisters
Gas gangrene aka
Myonecrosis
Gas gangrene MC caused by this bacteria
Clostridium perfringens
Gas gangrene early and late presentation sxs:
Early: POP; edema- or skin may appear normal
Later: signs of sepsis (tachycardia, fever, hypotension, tachypnea)
- Bullae
- Palpable crackles
- Watery-brown purulence “dish water discharge”
- Fetid odor
- skin becomes pale and grey- then purple to red
Gas gangrene develops from:
Wound or during surgery in an area that is depleted of blood supply
Gas gangrene can appear deceptively _____ early in it’s course, however it’s associated with ______________
Benign, high mortality
RF’s for Gas gangrene:
NSAID use, alcohol, HIV, immunodeficiency, DM, advanced age, PVD, heart disease, renal failure, chronic skin infx, cancer, IV drug use, decubitus ulcers
Gas gangrene infx can spread up to
1 in/hr
Etiology of gas gangrene:
IV, skin infx, surgery, abscess, insect bite, ulcer
Gas Gangrene dx: (7)
1- clinical suspicion
2- Radiographs: r/o clostridium myonecrosis and osetomyelitis
—X-rays LE
—CTA LE (MC- demonstrates thickening facial planes, subQ gas, and decreased bone integrity)
—MRI LE
—emergent surgical consult
—angiograms
3- CRP and ESR- elevated in osteomyelitis
4- lactate dehydrogenase (elevated w/ ischemia)
5- BMP (common w/ worsened renal fx)
6- CBC (leukocytosis > 15,000)
7- gram stain: gram + bacillus w/ lack of leukocytes is dx for clostridium myonecrosis
Gas gangrene tx: (6)
1- IV fluid resuscitation
2- pRBC transfusion
3- Broad spectrum abx: Clinda/zosyn (targets endotoxins) or Vanc/zosyn
4- Tetanus prophylaxis
5- Emergent surgical debridement or amputation (MAINSTAY OF TX; INITIATED PROMPTLY)
6- Hyperbaric oxygen
Gas Gangrene Pearls (4):
1- clostridium infx w/ POP, tachycardia and fever
2- clindamycin tx may improve survival
3- gram stain yielding gram-positive bacilli w/ a relative lack of leukocytes can confirm clostridium myonecrosis
4- shock and multi-organ failure can be rapidly progressive; mortality in 80-90% if untx; 10-25% w/ tx
AMI etiology:
- 1/3rd Embolism: Cardiac thrombus (e.g. CHF, Atrial Fibrillation)
- MC by emboli to proximal Superior Mesenteric Artery
- Sxs: sudden onset of pain
- 1/3rd Thrombosis:
- Hx of PAD (atherosclerosis) localized plaque rupture develops a thrombus within the mesenteric arteries
- Sxs: Abdominal pain worsens after eating
- 1/3rd Non-occlusive etiology:
- Vasospasm or drop in arterial blood pressure (e.g. shock)
- Sxs: Angina of the gut; pain may vary in presentation and rqs. a high index of suspicion; often over-shadowed by hypotension, CHF or cardiac arrhythmias
Sub-acute mesenteric ischemia (thrombosis) Sxs:
- Intermittient exacerbations of chronic mesenteric ischemia
- Athersclerosis plaque rupture with local thrombus formation
- onset and severitiy of pain depends upon the duration of occlusion and the effectiveness of collateral circulation
- chronic mesenteric ischemia, abdominal pain usually develops after eating, Sitophobia (fear of eating), and unintentional weight loss
Acute mesenteric ischemia (embolic) risk factor?
atrial fibrillation
Acute mesenteric ischemia (embolic) etiology:
Relocation of embolus to the arterial supply of the mesentery
AMI dx:
- Clinical presentation/risk factors
- Most have leukocytosis
- Lactate elevations raises suspicion (sensitivity 96%)
- Diagnostic Imaging- preferred radiographic image CT ABD/PELVIS with contrast
Pathopneumonic radiographic findings of mesenteric ischemia:
- “Thumbprinting” sign on plain x-ray
- Portal venous gas
- Pneumatosis intestinalis
AMI tx:
-Surgical resection of the dead bowel
Arterial Embolus/Thrombosis with Mesenteric Ischemia tx:
- IV hydration
- Pain management
- Vascular Surgery Consultation:
- -Vascular surgical embolectomy
- -Arterial bypass (Aortosuperior mesenteric arterial bypass grafting)
- -Intra-arterial thrombolysis
Chronic Mesenteric Ischemia tx:
- Angioplasty with stent placement
- Surgical bypass
In acute colon ischemia, areas of the colon with less blood supple are most vulnerable:
Splenic flexure and Rectosigmoid junction
Acute colon ischemia sxs:
- Patients do not appear ill
- 90% of patients > 60 years old
- Mild abdominal pain and tenderness
- Rectal bleeding/bloody diarrhea common
Acute colon ischemia risk factors:
Aortic or Iliac artery instrumentation MI Cardiac Bypass Hemodialysis Acquired clotting disorders Extreme exercise Drug side effects
What is vasculitis:
- Inflammation of BV (arteries, veins)
- arteritis and phlebitis
Vasculitis etiology:
Inflammation may be due to:
- Infection (Syphilitic aortitis)
- CT Disorder/Rheumatologic Disorder (ANCA-Associated vasculitis)
- Idiopathic: Buerger Disease
Buerger disease aka…
Thromboangitis obliterans
Buerger disease etiology:
Non-atherosclerotic disease of smaller peripheral arteries, veins, nerves resulting in recurring inflammation and occlusion
Buerger disease commonly seen in this population:
Typically affecting young males < 45 years of age w/ Heavy tobacco addiction
Buerger disease sxs:
- Claudication sxs of feet, legs, arms, and hands with some patients presenting with ischemic changes to the distal portion of the digits
- Pale/dusky (decreased capillary refill)
- Ulcerations
- Necrotic eschar formation
Buerger disease dx:
- based upon presentations in young, smoking male with exclusion of other causes
- Radiographic diagnosis assisted with CTA with run off to extremities: No evidence of atherosclerosis, No evidence of embolic occlusion, Segmental occlusion to small vessels, Cork-screw collaterals (collateral development around segmental occlusion
Buerger disease tx:
- Smoking cessation is the only way to halt the progression of the disease
- Iloprost (Ventavis)- A prostaglandin inhibitor that is a systemic vasodilator
- Vascular surgery (sometimes amputation)
Common, vasospastic disease of small arteries
Raynaud’s phenomenon
Raynaud’s phenomenon etiology:
- Primary Raynaud’s:
- No underlying disorder
- Secondary Raynaud’s
- Scleroderma (CREST Syndrome); Polymyositis; Rheumatoid arthritis; SLE
- Repetitive trauma (e.g. jackhammer operators)
- Buerger Disease
- Drugs (MAOIs, Tricyclic antidepressants, Serotonin agonists, Interferon
Primary Raynaud’s: sex, age of onset, frequency of attacks
female, adolescence, QD attacks
Secondary Raynaud’s: sex, age of onset, frequency of attacks, sxs, autoabs?
- male/female; 20-30’s
- weekly/monthly episodes
- finger edema, periungal erythema, and arthritis common
- +autoab’s
Raynaud’s phenomenon clinical features:
- Recurrent episodes of color changes to toes, fingers, nose, ears due to vasospasm of digital (small) arteries
- Often precipitated by cold and emotional stress
- WHITE (pallor) to BLUE (cyanosis) to RED (reactive hyperemia)
Raynaud’s phenomenon PE:
Repetitive episodes result in digital ulcerations or thickening of fat pads (sclerodactyly)
Raynaud’s phenomenon tx:
Avoidance of triggers (gloves in winter)
Calcium channel blockers
Takayasu Arteritis patho:
- Idiopathic granulomatous vasculitis of Aorta, its branches, and Pulmonary artery
- Granulomatous inflammation in vessel wall results in stenosis and aneurysm formation
Takayasu Arteritis clinical features:
- Early hx of fatigue, weight loss and low-grade fevers
- Cool extremities, extremity claudication or numbness, syncope due to decreased blood flow to the brain
Takayasu Arteritis epidemiology:
-Common in young Asian women
Takayasu Arteritis PE:
- HTN commonly occurs in 80% due to stenosis of renal artery or coarctation of Aorta
- Aortic regurgitation murmur heard along the left sternal boarder
- Bruits can be heard over subclavian arteries, brachial arteries, carotid arteries, renal arteries
- Diminished and asymmetric extremity pulses
Takayasu Arteritis dx:
- Clinical presentation/exam consistent
- Angiographic evidence of stenosis of Aorta or its branches
Takayasu Arteritis tx:
corticosteroids
vascular surg consult
Giant Cell Arteritis (Temporal Arteritis) epidemiology:
- More common in females over age 50
- Males more likely to suffer from blindness
- 40% also have Polymyalgia rheumatica
Giant Cell Arteritis (Temporal Arteritis) pathophysiology:
- Vasculitis of medium/large arteries involving subclavian, axillary, and Aorta arteries as well as branches of these arteries such as Temporal artery
- Dangerous cause of ocular blindness due to occlusion of retinal artery
Giant Cell Arteritis (Temporal Arteritis) PE:
- Tender temporal pulse
- If the pt is having ocular symptoms:
- -Afferent pupillary defect
- -Pale retina with a cherry red spot
- BP difference between two arms suggests subclavian stenosis
Giant Cell Arteritis (Temporal Arteritis) Clinical Features:
- Temporal headache, jaw claudication, unilateral blindness (Retinal Artery Occlusion), low grade fever, shoulder/hip pain
- Syndrome of pain (not weakness) of shoulder/hip girdle (patients with polymyalgia rheumatica)
- Chest pain indicating Aortic Dissection/Aneurysm
Giant Cell Arteritis (Temporal Arteritis) dx:
- Clinical exam & hx
- Elevated ESR and CRP
- Gold Standard: Temporal artery biopsy (which shows lymphocytic and macrocytic (giant cell) infiltration of arterial wall)
Giant Cell Arteritis (Temporal Arteritis) tx:
- HIGH-DOSE Corticosteroids
- Begin tx based on clinical suspicion and elevated sed rate and CRP
- Do not wait for temporal artery biopsy to begin treatment
Describe the E sed rate:
Measure of inflammation
Rate at which erythrocytes (RBCs) sediment (fall down) over 1 hour
Nonspecific test
Inflammatory process causes increase in fibrinogen which allows RBCs to stick together
Abnormal communications shunting blood from arterial system directly into venous system (bypassing capillaries)
Arteriovenous malformations
Arteriovenous Malformations etiology, PE, sxs in bone or brain, dx, tx
- May be congential (AVM) or acquired (AV fistula due to trauma, vascular surgery, or for dialysis)
-Can be seen in several syndromes:
Hereditary Hemorrhagic Telangiectasia (Osler-Weber-Rendu Syndrome)
-PE may denote pulsatile mass if superficial or bruits
-AVM in bone: pathologic fractures
AVM in brain: sz, neuro deficits or even hemorrhage
-Dx Radiographic Studies: CTA or
MRA
-Management is either surgical removal or endovascular embolization (unclear if asymptomatic AVMs should be treated)
dilated, tortuous veins of the lower extremity
Varicose veins
Varicose Veins/Venous Insufficiency etiology:
- Gradually develops and becomes painful
- Hereditary component
- Increase in frequency after pregnancy
- Due to venous insufficiency:
- -Damaged or incompetent venous valves in LE result in failure of venous segments and pooling of blood in LE
- Often due to hx of DVT or phlebitis
- May be due to traumatic history
Venous Insufficiency risk factors:
Smoking History of DVT Post-thrombotic syndrome Family hx of venous disease Age Sedentary lifestyle Obesity hx of LE trauma Pregnancy Presence of AV shunt/malformation
Venous Insufficiency clinical presentation:
Leg pain/heaviness
Skin changes (Stasis dermatitis)
Varicose veins (superficial dilated veins)
LE edema
Ulcerations (venous stasis ulcers)- commonly found on the medial aspect of ankles
Venous Insufficiency dx:
- Clinical exam/history
- Venous duplex ultrasonography
- -Shows retrograde flow of > 0.5 seconds in duration
- -Often combo of superficial and deep insufficiency
- -Excludes concomitant arterial insufficiency (i.e. PAD)
Venous Insufficiency tx:
Leg elevation Exercise Compressions stockings Venous ulcer care Silver dressings (decreased bacterial counts) Escin (Horse Chestnut Seed Extract) (OTC, induces some venocontriction) Hyperbaric oxygen Surgical therapy (ablation, stripping)
is inflammation of vein without thrombus
Superficial phlebitis
inflammation and confirmed thrombosis within a venous tributary
Superficial thrombophlebitis
Superficial phlebitis/Superficial thrombophlebitis sxs:
- Pain, tenderness, redness, swelling along the course of a superficial vein
- Vein feels like a palpable cord
Superficial phlebitis/Superficial thrombophlebitis RF’s:
- Intravenous catheter use (IV sites)
- Medications- IV Potassium
- Varicose veins
- Hypercoagulable Conditions (Pregnancy, Malignancy, Exogenous estrogen use)
- Thrombophlebitis migrans (Trousseau Syndrome)
Thrombophlebitis migrans (Trousseau Syndrome) associated with:
hypercoagulability often due to: Glioma and Adenocarcinoma of pancreas, lung
Migrating thrombophlebitis due to thrombosis of superficial veins in multiple areas of the body at the same time
Thrombophlebitis migrans (Trousseau Syndrome)
Superficial phlebitis/Superficial thrombophlebitis tx:
Pain medications/anti-inflammatory agents
- Removal of catheter if possible
- Warm compresses/Support stockings/wraps
- Abx: Not indicated for uncomplicated superficial thrombophlebitis; If infx thrombophlebitis is suspected, empiric abx
- Surgical removal/stripping may be necessary
Venous Thromboembolism occurs due to disruptions in 1 or more:
.. of Virchow’s Triad:
Endothelial Injury
Venous Stasis
Hypercoagulation
Venous Thromboembolism etiology:
Higher incidence in males, African Americans/Caucasians
Venous Thromboembolism: 2 types
Deep Vein Thrombosis
Pulmonary Embolism
Venous Thromboembolism: Endothelial risk factors
- Trauma
- Surgery
- Prior DVT
- Inflammation
Venous Thromboembolism: venous stasis RFs
- Leg immobilization (cast)
- Inactivity (e.g. long plane ride > 6 hours)
- CHF
- CVA within 3 months
Venous Thromboembolism: hypercoaguable state RFs
- Factor V Leiden mutation (MC hereditary cause of VTE) Prothrombin gene mutation, Antiphospholipid antibody syndrome, and Protein S/C deficiency
- OC pills/HRT
- Pregnancy
- Malignancy (12% of idiopathic VTE)
DVT pathogenesis:
- Commonly originate in the calf
15-30% progress proximally - With proximal progression, the risk of embolus occurring increases:
Risk of PE increases from 10% to 50%
-DVT breaks off section causing embolus–>travels through right heart to pulmonary artery–>Blocks blood flow to lung resulting in hypoxia, decreased preload to left heart, HF, and death
DVT sxs:
Calf pain Calf/leg swelling (edema) Warmth/tenderness/palpable cord Homan’s Sign (pain in calf with dorsiflexion of foot) Cyanosis
PE sxs:
Dyspnea (SOB) Pleuritic chest pain Cough Hemoptysis Tachypnea Hypoxia Tachycardia Fever Syncope (massive PE)
Describe post-thrombotic syndrome:
- Syndrome of venous insufficiency AFTER DVT (extends beyond resolution of thrombosis)
- Pain and swelling in LE affected by DVT
- TX: compression stockings and pain management
- PREVENTION: Compression stockings decrease risk
Describe Well’s Criteria for DVT: (#’s)
- Score of 3 or greater: High Probability
- Score of 1 or 2: Moderate Probability
- Score of 0: Low Probability
If low probablity of DVT: provider should order..
Degradation product of fibrin (i.e. clot)
- If elevated: perform Ultrasound
- If normal: DVT ruled out
If moderate/high probablity of DVT: provider should order..
Venous Doppler Ultrasound of LE
- 95% Sensitivity, Specificity
- Venogram is gold standard (but not done anymore)
- CTA, MRA
Describe Modified Wells Criteria for PE: (#s)
PE likely >4 points
PE unlikely
What are the PERC criteria: (8)
Age < 50 years Heart rate < 100 bpm Oxyhemoglobin saturation > 95% No hemoptysis No estrogen use No prior history of DVT or PE No unilateral leg swelling No surgery/trauma requiring hospitalization within the prior four weeks
Describe the PERC rules:
- PERC rule is only valid in patients with a low clinical probability of PE (gestalt estimate <15%)
- In pts w/ a low probability of PE who fulfill all 8 criteria, the likelihood of PE is low
- No further testing is required
- All other patients should be considered for further testing with D-dimer, CTA or VQ scan
Gold Standard dx test for pts moderate to high probability of PE:
- Gold Standard is Pulmonary Angiogram (CTPA)
- Ordered as CT Angiography (CTA) of chest: (morbidity of 5%)
- -Risk of Contrast Induced AKI
- Sensitivity 90%; Specificity 95%
VQ scan indications:
renal insuffiencey (eGFR <60%)
IV contrast allergy
Morbid obesity
Measures discordance between perfusion and ventilation (no perfusion but ventilation suggests PE)
VQ scan
Pulmonary Embolism: Other Testing (4)
- *EKG w/ Classic: S1-Q3-T3
- MC: Sinus tachycardia
- *ABG: Increased A-a gradient
- Hypoxemia with hypocapnia
- *Chest X-ray: Westermark Sign
- Hampton’s Hump
- *Transthoracic US:
- McConnell sign (Dilation of right ventricle, Kinetic activity of the apex, Puckering of cardiac apex)
Describe Short-term VTE anticoagulation:
- Initial anticoagulation: admin. immediately following dx of acute VTE
- Often given over the first few days (typically from 0 to 10 days) while planning for long term anticoagulation
Describe Long-term VTE anticoagulation:
-Typically administered for a finite period beyond the initial period, usually 3-6 months and occasionally up to 12 months
Treatment of Unstable severe PE:
- Unstable pts with severe PE may need to be tx with tpa therapy
- In hemodynamically unstable patients, in whom the suspicion for severe PE is high, definitive testing is typically considered unsafe
- SBP <90 mmHg for 15 minutes; Cardiac arrest with PEA, or Respiratory arrest
-Transthoracic echocardiogram can be used, although not definitively dx of PE - may indicate presumptive dx of PE prior to the empiric admin of tpa
- Evaluate for right ventricular dysfunction:
McConnell sign (Hypokinetic RV free wall and puckering or contraction at the apex of the RV) - Catheter directed tpa also option for treatment of severe PE: often used to tx pt’s over 65 y/o, with a severe PE and hemodynamic instability, who have a increased risk of IC bleeding
-Pts with low-risk PE should NOT receive fibrinolysis
-Heparin or low-molecular-weight heparin are typically started after the tpa infusion - IVC filters are indicated if anticoagulation CANNOT be done: (ex) cancer pt with the presence of proximal LE clot in conjunction with active bleeding
Short term anticoagulation in VTE includes which drug groups:
*Unfractionated IV Heparin: Severe PE (unstable patients); Used to tx pts with renal failure
*SQ LMWH: enoxaparin (Lovenox) and dalteparin (Fragmin)
–Used for acute tx VTE in stable PE/DVT, pts with malignancy, pregnancy, and for extended txs
–avoided in renal failure pts
*NOACS as mono-therapy approved for DVT and PE: rivaroxaban (Xarelto) Xa inhibitor; apixaban (Eliquis) Xa inhibitor;
edoxaban (Savaysa) Xa inhibitor;
dabigitran (Pradaxa)- DTI
- Can be started in the ED then discharged home to continue therapy long term
- No lab testing required
- Expensive $$$
- Avoid in patients with renal failure
Describe extended therapy VTE anticoagulation:
usually refers to therapy that is administered indefinitely
Subcutaneous LMWH may be preferred in certain populations:
cancer and pregnant
Long term anticoagulation in VTE includes which drug groups:
- LMWH: subQ
- -Avoid in pts with renal failure
- -used as a 5 day overlap to Coumadin
- Coumadin: Inhibits Epoxide Reductase, Vitamin K dependent factors drop in concentration: Factors 2, 7, 9, 10, Protein S, C
- -Inexpensive $
- -Requires lab testing to measure coagulation times (PT/INR)
First proximal DVT or PE due to reversible, precipitating factor:
3 mos. duration of long term anti-coag tx
First DVT/PE unprovoked tx duration:
3-12 months then reassess
Recurrent DVT/PE treatment duration:
indefinite tx
Reassessment following a First DVT/PE unprovoked includes:
- Gender (males w/ higher risk)
- Presence of a clotting disorder
- Obesity
- Chronic leg swelling
- Positive D-dimer test while pt is still on anticoagulation therapy
- Positive D-dimer test 4 weeks after discontinuing anticoagulation therapy
- Residual clot on f/u (Doppler ultrasound)
- Pts with PEs are more likey to have a recurrence of future PEs; Moreso than pt’s with DVTs
