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KC Cardio Module-1 > Peripheral Dz Notecards > Flashcards

Peripheral Dz Notecards Flashcards

1
Q

Types of Aortic Aneurysms:

A
  • arterial
  • abdominal aorta: 4-8% in elderly males
  • abdominal thoracic: much less common
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2
Q

Types of Arterial Aneurysms:

A
  • 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
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3
Q

Risk of aortic rupture:

A
  • increases a lot after 5cm: 5%/yr

- below 5cm: 1%/yr

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4
Q

AA growth:

A

1-4 mm/year

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5
Q

Pathopneumonic signs for Marfinoid syndrome:

A

steinburg and walker murdoch

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6
Q

AA dx:

A

1- duplex ultrasonography: ID suspect iliac and abdominal aneurysms
2- contrasted CT angiography: to ID branches of iliac arteries
3- MRA- but takes longer

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7
Q

AA clinical sxs:

A
  • 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
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8
Q

Management of AAA rupture:

A

CV emergency: rq. prompt IV fluids w/ blood, isotonic saline and emergent surgery

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9
Q

AA Risk Factors:

A
  • 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
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10
Q

Clinical features include of Marfan’s: (7)

A
  • 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
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11
Q

Marfan’s progression:

A

Spectrum of clinic severity from isolated features–> rapidly progressive multi-organ dz

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12
Q

Autosomal dominant disorder of CT

A

Marfan’s Syndrome

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13
Q

Tx of AAA:

A
  • no surgical benefit 4-5.5 cm

- surgical tx: sxs of expansion, occlusion/compression, rupture, rapid expansion >1cm/yr, AAA>5.5cm

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14
Q

Screening for AAA:

A

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

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15
Q

Tx for a AAA >5.5:

A

Surgical option:

  • OPEN (gortex graft within the aneurysm)
  • Percutaneous ENDOVASCULAR ANEURYSM REPAIR (EVAR)
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16
Q

Tx for a AAA <5.5:

A
  • Smoking cessation
  • Tight BP control
  • Beta-blockers helpful in Marfanoid
  • CHOL reduction (STATINS)
  • Monitoring aneurysm q6-12 months by duplex ultrasound
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17
Q

Acute Aortic Syndromes:

A
  • 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
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18
Q

Aortic Dissection Risk Factors:

A
  • 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
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19
Q

Classification of Aortic Dissection:

A

Stanford A (ascending/proximal)- 70-75% or Stanford B (descending/distal)- 25-30%

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20
Q

Aortic dissection’s and mortality:

A
  • 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
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21
Q

Clinical Presentation of Aortic Dissection:

A
  • 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
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22
Q

If dissection involves ascending aorta it can dissect against Coronary Arteries and cause:

A

MI

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23
Q

If dissection is distal:

A

it can cause ischemia to lower extremities and result in an ischemic neuropathy

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24
Q

Clinical Presentation of Aortic Dissection:

A
  • Pulse deficits (weak or absent carotid, brachial or femoral pulses)
  • Dissection back toward heart can cause Aortic regurgitation diastolic murmur
  • CHF
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25
Q

Dx of Aortic Dissection:

A
  • 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
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26
Q

Tx of Aortic Dissection:

A
  • 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
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27
Q

Standford Type B (DISTAL) may need surgery if:

A

occlusion of major Aortic Branch, persistent pain/HTN, aneurysm development, or worsening of the dissection

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28
Q

suggests dissection back into the heart and bleeding into pericardial space

A

hypotension and JVD

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29
Q

Suspect Hemopericardium and Cardiac Tamponade w/ these sxs:

A
  • JVD
  • Hypotension
  • Pulsus paradoxus (large decrease in pulse strength)
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30
Q

AMI Patho:

A
  • arterial embolism
  • atherosclerosis
  • vasospasm of mesenteric artery
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31
Q

AMI sxs:

A
  • Pain out of proportion on physical exam
  • Visceral abdominal pain (poorly localized)
  • May have melena or hematochezia
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32
Q

PAD MC

A

Men and increases with age

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33
Q

PAD RF:

A

CV RF’s: HTN, hyperlipidemia, DM, smoking

- associated w/ high 10 year CVD risk

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34
Q

PAD sxs:

A
  • only 50% w/ sxs

- intermittent claudication: worsened w/ exercise; improved w/ rest

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35
Q

CAD PE:

A
  • loss of hair
  • ulcers
  • poor peripheral pulses
  • changes in skin color (dusky color, bluish, cool)
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36
Q

Pseudoclaudication is aka..

A

Lumbar spinal stenosis

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37
Q

Pseudoclaudication sxs:

A
  • 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
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38
Q

PAD hx:

A
  • CVD RF’s: HTN, hyperlipidemia, DM, smoking, age, male sex

- established hx CAD, MI, CVA

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39
Q

PAD claudication occurs where to stenosis?

A

Distal

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40
Q

LeRiche Syndrome aka…

A

Aortoiliac Occlusive Dz

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41
Q

LeRiche Syndrome MOA:

A

Severe atherosclerosis of abdominal aorta and iliac arteries

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42
Q

LeRiche Syndrome sxs:

A

Claudication of buttock, hips, and thigh

Often associated w/ erectile dysfunction/impotence

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43
Q

LeRiche Syndrome PE:

A

Poor femoral pulses

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44
Q

LeRiche Syndrome tx:

A

Aortoiliac bypass graft

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45
Q

Complications of PAD:

A

1- increased risk for CV event (CVA/AMI): 30%
2- worsening claudication: 25%
3- ischemic ulcers in LE: 10-20%
4- amputations: 5%

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46
Q

PAD dx:

A

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

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47
Q

Explain an ABI calculation and how it’s done:

A
  • 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
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48
Q

ABI Classification system for PAD:

A

> 1.30- noncompressible, calcified vessel
0.91-1.30: normal
0.41-0.90: mild to moderate PAD
<0.40: severe PAD

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49
Q

PAD Rutherford classification system:

A

Classifies claudication based on mild, moderate, and severe

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50
Q

PAD Fontaine classification system:

A

Specifies walking distance that provokes claudication (less than or greater than 650 feet)

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51
Q

PAD definitive tx:

A
  • 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
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52
Q

PAD medical management:

A
  • 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
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53
Q

ALI MOA:

A

Sudden occlusion of LE artery secondary to:

  • arterial emboli: LV mural thrombus; atrial thrombus from a fib
  • thrombosis in situ: secondary to ruptured plaque
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54
Q

ALI presents with:

A

Sudden onset of sxs: 6 P’s
Pain, pallor, paralysis, paresthesia, pulseless, poikilothermia
- crescendo pattern: hours to days

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55
Q

ALI PE:

A

Cyanotic blue/pale, pulseless LE and diminished neuro vascular fx (both motor and sensory)

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56
Q

ALI dx:

A
  • continuos flow Doppler: evidence of pulse?
  • ABI: emergently to determine degrees of ischemia
  • CTA/MRA
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57
Q

ALI surgical tx:

A 
Duration <14 days w/ small occlusion:
- percuteaneous revascularization w/stent
- catheter directed thrombolysis
Duration >14days w/ larger occlusion:
- arterial bypass surgery
- endovascular thrombo-embolectomy
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58
Q

ALI medical tx:

A
  • heparin IV
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59
Q

ALI rqs. R/o of:

A

Gangrene; if present— pain management, abx, amputation, deride, hospitalization

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60
Q

RF’s for Gangrene: (5)

A 
IV drug use
Trauma
Surgery
PAD
Diabetics
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61
Q

Gangrene etiology:

A

Tissue that has lost its blood supply and is undergoing necrosis

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62
Q

Describe dry gangrene:

A
  • often due to PAD
  • secondary to tissue ischemia
  • tissue undergoing sterile ischemic coag. Necrosis
  • well demarcated borders; total tissue death
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63
Q

Describe wet gangrene:

A
  • 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
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64
Q

Gas gangrene aka

A

Myonecrosis

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65
Q

Gas gangrene MC caused by this bacteria

A

Clostridium perfringens

66
Q

Gas gangrene early and late presentation sxs:

A

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

67
Q

Gas gangrene develops from:

A

Wound or during surgery in an area that is depleted of blood supply

68
Q

Gas gangrene can appear deceptively _____ early in it’s course, however it’s associated with ______________

A

Benign, high mortality

69
Q

RF’s for Gas gangrene:

A

NSAID use, alcohol, HIV, immunodeficiency, DM, advanced age, PVD, heart disease, renal failure, chronic skin infx, cancer, IV drug use, decubitus ulcers

70
Q

Gas gangrene infx can spread up to

A

1 in/hr

71
Q

Etiology of gas gangrene:

A

IV, skin infx, surgery, abscess, insect bite, ulcer

72
Q

Gas Gangrene dx: (7)

A

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

73
Q

Gas gangrene tx: (6)

A

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

74
Q

Gas Gangrene Pearls (4):

A

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

75
Q

AMI etiology:

A
  • 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
76
Q

Sub-acute mesenteric ischemia (thrombosis) Sxs:

A
  • 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
77
Q

Acute mesenteric ischemia (embolic) risk factor?

A

atrial fibrillation

78
Q

Acute mesenteric ischemia (embolic) etiology:

A

Relocation of embolus to the arterial supply of the mesentery

79
Q

AMI dx:

A
  • Clinical presentation/risk factors
  • Most have leukocytosis
  • Lactate elevations raises suspicion (sensitivity 96%)
  • Diagnostic Imaging- preferred radiographic image CT ABD/PELVIS with contrast
80
Q

Pathopneumonic radiographic findings of mesenteric ischemia:

A
  • “Thumbprinting” sign on plain x-ray
  • Portal venous gas
  • Pneumatosis intestinalis
81
Q

AMI tx:

A

-Surgical resection of the dead bowel

82
Q

Arterial Embolus/Thrombosis with Mesenteric Ischemia tx:

A
  • IV hydration
  • Pain management
  • Vascular Surgery Consultation:
  • -Vascular surgical embolectomy
  • -Arterial bypass (Aortosuperior mesenteric arterial bypass grafting)
  • -Intra-arterial thrombolysis
83
Q

Chronic Mesenteric Ischemia tx:

A
  • Angioplasty with stent placement

- Surgical bypass

84
Q

In acute colon ischemia, areas of the colon with less blood supple are most vulnerable:

A

Splenic flexure and Rectosigmoid junction

85
Q

Acute colon ischemia sxs:

A
  • Patients do not appear ill
  • 90% of patients > 60 years old
  • Mild abdominal pain and tenderness
  • Rectal bleeding/bloody diarrhea common
86
Q

Acute colon ischemia risk factors:

A 
Aortic or Iliac artery instrumentation
MI
Cardiac Bypass
Hemodialysis
Acquired clotting disorders
Extreme exercise
Drug side effects
87
Q

What is vasculitis:

A
  • Inflammation of BV (arteries, veins)

- arteritis and phlebitis

88
Q

Vasculitis etiology:

A

Inflammation may be due to:

  • Infection (Syphilitic aortitis)
  • CT Disorder/Rheumatologic Disorder (ANCA-Associated vasculitis)
  • Idiopathic: Buerger Disease
89
Q

Buerger disease aka…

A

Thromboangitis obliterans

90
Q

Buerger disease etiology:

A

Non-atherosclerotic disease of smaller peripheral arteries, veins, nerves resulting in recurring inflammation and occlusion

91
Q

Buerger disease commonly seen in this population:

A

Typically affecting young males < 45 years of age w/ Heavy tobacco addiction

92
Q

Buerger disease sxs:

A
  • 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
93
Q

Buerger disease dx:

A
  • 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
94
Q

Buerger disease tx:

A
  • 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)
95
Q

Common, vasospastic disease of small arteries

A

Raynaud’s phenomenon

96
Q

Raynaud’s phenomenon etiology:

A
  • 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
97
Q

Primary Raynaud’s: sex, age of onset, frequency of attacks

A

female, adolescence, QD attacks

98
Q

Secondary Raynaud’s: sex, age of onset, frequency of attacks, sxs, autoabs?

A
  • male/female; 20-30’s
  • weekly/monthly episodes
  • finger edema, periungal erythema, and arthritis common
  • +autoab’s
99
Q

Raynaud’s phenomenon clinical features:

A
  • 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)
100
Q

Raynaud’s phenomenon PE:

A

Repetitive episodes result in digital ulcerations or thickening of fat pads (sclerodactyly)

101
Q

Raynaud’s phenomenon tx:

A

Avoidance of triggers (gloves in winter)

Calcium channel blockers

102
Q

Takayasu Arteritis patho:

A
  • Idiopathic granulomatous vasculitis of Aorta, its branches, and Pulmonary artery
  • Granulomatous inflammation in vessel wall results in stenosis and aneurysm formation
103
Q

Takayasu Arteritis clinical features:

A
  • 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

104
Q

Takayasu Arteritis epidemiology:

A

-Common in young Asian women

105
Q

Takayasu Arteritis PE:

A
  • 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
106
Q

Takayasu Arteritis dx:

A
  • Clinical presentation/exam consistent

- Angiographic evidence of stenosis of Aorta or its branches

107
Q

Takayasu Arteritis tx:

A

corticosteroids

vascular surg consult

108
Q

Giant Cell Arteritis (Temporal Arteritis) epidemiology:

A
  • More common in females over age 50
  • Males more likely to suffer from blindness
  • 40% also have Polymyalgia rheumatica
109
Q

Giant Cell Arteritis (Temporal Arteritis) pathophysiology:

A
  • 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
110
Q

Giant Cell Arteritis (Temporal Arteritis) PE:

A
  • 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
111
Q

Giant Cell Arteritis (Temporal Arteritis) Clinical Features:

A
  • 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
112
Q

Giant Cell Arteritis (Temporal Arteritis) dx:

A
  • Clinical exam & hx
  • Elevated ESR and CRP
  • Gold Standard: Temporal artery biopsy (which shows lymphocytic and macrocytic (giant cell) infiltration of arterial wall)
113
Q

Giant Cell Arteritis (Temporal Arteritis) tx:

A
  • 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
114
Q

Describe the E sed rate:

A

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

115
Q

Abnormal communications shunting blood from arterial system directly into venous system (bypassing capillaries)

A

Arteriovenous malformations

116
Q

Arteriovenous Malformations etiology, PE, sxs in bone or brain, dx, tx

A
  • 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)
117
Q

dilated, tortuous veins of the lower extremity

A

Varicose veins

118
Q

Varicose Veins/Venous Insufficiency etiology:

A
  • 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
119
Q

Venous Insufficiency risk factors:

A 
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
120
Q

Venous Insufficiency clinical presentation:

A

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

121
Q

Venous Insufficiency dx:

A
  • 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)
122
Q

Venous Insufficiency tx:

A 
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)
123
Q

is inflammation of vein without thrombus

A

Superficial phlebitis

124
Q

inflammation and confirmed thrombosis within a venous tributary

A

Superficial thrombophlebitis

125
Q

Superficial phlebitis/Superficial thrombophlebitis sxs:

A
  • Pain, tenderness, redness, swelling along the course of a superficial vein
  • Vein feels like a palpable cord
126
Q

Superficial phlebitis/Superficial thrombophlebitis RF’s:

A
  • Intravenous catheter use (IV sites)
  • Medications- IV Potassium
  • Varicose veins
  • Hypercoagulable Conditions (Pregnancy, Malignancy, Exogenous estrogen use)
  • Thrombophlebitis migrans (Trousseau Syndrome)
127
Q

Thrombophlebitis migrans (Trousseau Syndrome) associated with:

A

hypercoagulability often due to: Glioma and Adenocarcinoma of pancreas, lung

128
Q

Migrating thrombophlebitis due to thrombosis of superficial veins in multiple areas of the body at the same time

A

Thrombophlebitis migrans (Trousseau Syndrome)

129
Q

Superficial phlebitis/Superficial thrombophlebitis tx:

A

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
130
Q

Venous Thromboembolism occurs due to disruptions in 1 or more:

A

.. of Virchow’s Triad:
Endothelial Injury
Venous Stasis
Hypercoagulation

131
Q

Venous Thromboembolism etiology:

A

Higher incidence in males, African Americans/Caucasians

132
Q

Venous Thromboembolism: 2 types

A

Deep Vein Thrombosis

Pulmonary Embolism

133
Q

Venous Thromboembolism: Endothelial risk factors

A
  • Trauma
  • Surgery
  • Prior DVT
  • Inflammation
134
Q

Venous Thromboembolism: venous stasis RFs

A
  • Leg immobilization (cast)
  • Inactivity (e.g. long plane ride > 6 hours)
  • CHF
  • CVA within 3 months
135
Q

Venous Thromboembolism: hypercoaguable state RFs

A
  • 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)
136
Q

DVT pathogenesis:

A
  • 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
137
Q

DVT sxs:

A 
Calf pain
Calf/leg swelling (edema)
Warmth/tenderness/palpable cord
Homan’s Sign (pain in calf with dorsiflexion of foot)
Cyanosis
138
Q

PE sxs:

A 
Dyspnea (SOB)
Pleuritic chest pain
Cough
Hemoptysis
Tachypnea
Hypoxia
Tachycardia
Fever
Syncope (massive PE)
139
Q

Describe post-thrombotic syndrome:

A
  • 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
140
Q

Describe Well’s Criteria for DVT: (#’s)

A
  • Score of 3 or greater: High Probability
  • Score of 1 or 2: Moderate Probability
  • Score of 0: Low Probability
141
Q

If low probablity of DVT: provider should order..

A

Degradation product of fibrin (i.e. clot)

  • If elevated: perform Ultrasound
  • If normal: DVT ruled out
142
Q

If moderate/high probablity of DVT: provider should order..

A

Venous Doppler Ultrasound of LE

  • 95% Sensitivity, Specificity
  • Venogram is gold standard (but not done anymore)
  • CTA, MRA
143
Q

Describe Modified Wells Criteria for PE: (#s)

A

PE likely >4 points

PE unlikely

144
Q

What are the PERC criteria: (8)

A 
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
145
Q

Describe the PERC rules:

A
  • 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
146
Q

Gold Standard dx test for pts moderate to high probability of PE:

A
  • 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%
147
Q

VQ scan indications:

A

renal insuffiencey (eGFR <60%)
IV contrast allergy
Morbid obesity

148
Q

Measures discordance between perfusion and ventilation (no perfusion but ventilation suggests PE)

A

VQ scan

149
Q

Pulmonary Embolism: Other Testing (4)

A
  • *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)
150
Q

Describe Short-term VTE anticoagulation:

A
  • 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
151
Q

Describe Long-term VTE anticoagulation:

A

-Typically administered for a finite period beyond the initial period, usually 3-6 months and occasionally up to 12 months

152
Q

Treatment of Unstable severe PE:

A
  • 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
153
Q

Short term anticoagulation in VTE includes which drug groups:

A

*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

154
Q

Describe extended therapy VTE anticoagulation:

A

usually refers to therapy that is administered indefinitely

155
Q

Subcutaneous LMWH may be preferred in certain populations:

A

cancer and pregnant

156
Q

Long term anticoagulation in VTE includes which drug groups:

A
  • 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)
157
Q

First proximal DVT or PE due to reversible, precipitating factor:

A

3 mos. duration of long term anti-coag tx

158
Q

First DVT/PE unprovoked tx duration:

A

3-12 months then reassess

159
Q

Recurrent DVT/PE treatment duration:

A

indefinite tx

160
Q

Reassessment following a First DVT/PE unprovoked includes:

A
  • 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

KC Cardio Module-1 (7 decks)

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