Module 2: Vascular Disorders

Question 1

Peripheral Artery Disease (PAD)

Answer 1

Involves thickening of the artery walls and
progressive narrowing of arteries of upper and lower extremities
 Symptomatic age 50 to 70; earlier with diabetes
 In United States, 8.5 million over age 40 have PAD
*  prevalence with blacks

Strongly related to other CVD
Higher risk of mortality, CVD mortality, major
coronary events and stroke

Question 2

Etiology and Pathophysiology of PAD

Answer 2

Atherosclerosis is leading cause in majority of
cases
 Gradual thickening of the intima and media due
to cholesterol and lipid deposits
 Exact cause unknown; inflammation and
endothelial injury play a major role
 Symptoms occur when vessels are 60-75%
blocked

Question 3

Risk Factors for PAD

Answer 3

Risk factors:
 Tobacco use
 Diabetes
 HTN
 High cholesterol
 Age greater than 60
 Multiple risk factors increase the risk of PAD
 Atherosclerosis often affects coronary, carotid, and lower extremity arteries

Question 4

Clinical Manifestations of PAD

Answer 4

Classic symptom of PAD—intermittent claudication
 Ischemic muscle pain that is caused by a constant
level of exercise
* Build up of lactic acid from anaerobic metabolism
 Resolves within 10 minutes or less with rest
 Reproducible
 Occurs in as many as 1/3 of patients with PAD

Paresthesia
 Numbness or tingling in the toes or feet from nerve tissue ischemia
 Neuropathy causes severe shooting or burning pain
 Produces loss of pressure and deep pain sensations from reduced blood flow
 Injuries often go unnoticed by patient

Reduced blood flow to limb
 Thin, shiny, and taut skin
 Loss of hair on the lower legs
 Diminished or absent pedal, popliteal, or femoral
pulses
 Elevation pallor
* Pallor of foot with leg elevation
 Dependent rubor
* Reactive hyperemia of foot with dependent position

Pain at rest
 Progressive disease
 Occurs in feet or toes most often
 Aggravated by limb elevation
 Occurs from insufficient blood flow to distal tissues
 Occurs more often at night
 Pain relief by gravity

Critical Limb Ischemia (CLI)
-Characterized by
 Chronic ischemic rest pain lasting more than 2 weeks
 Nonhealing arterial leg ulcers or gangrene
- At increased risk
 Diabetes
 HF
 History of stroke

Question 5

Complications of PAD

Answer 5

Prolonged ischemia leads to:
 Atrophy of skin and underlying muscles
 Delayed healing
 Wound infection
 Tissue necrosis
 Arterial ulcers over bony prominences

Most serious: Nonhealing arterial ulcers and
gangrene
 Collateral circulation may prevent gangrene
 May result in amputation
 If adequate blood flow is not restored and if severe infection occurs
 Indicated with uncontrolled pain and spreading
infection

Question 6

PAD Diagnostic Studies

Answer 6

Doppler ultrasound
 Segmental blood pressure
 Duplex imaging
 Bidirectional, color Doppler
 Ankle-brachial index (ABI)
 Done using a hand-held Doppler
 Calculated by dividing the ankle systolic BP (SBP) by the higher of the brachial SBPs
 Falsely elevated results can be seen in older patients or those with diabetes

Question 7

Nutrition Therapy for PAD

Answer 7

BMI <25 kg/m2
 Waist circumference is less than 40 in for men
and less than 35 in for women
 3% to 5% weight loss yields reduced
triglycerides, glucose, A1C, and decreased risk
of type 2 diabetes
 Recommend reduced calories and salt for obese
or overweight persons

Question 8

Leg with Critical Limb Ischemia

Answer 8

 Revascularization via bypass surgery using
autogenous vein
-This surgical procedure involves using a vein from the patient’s body (autogenous vein) to create a bypass around the blocked artery in the leg.
The vein is grafted above and below the blocked area, allowing blood to flow around the obstruction.

 Percutaneous transluminal angioplasty (PTA)
-PTA is a less invasive procedure where a small balloon at the tip of a catheter is inserted into the blocked artery.
-Once in place, the balloon is inflated to open the artery, improving blood flow. Stents may also be placed to keep the artery open.

 IV prostanoids (iloprost [Ventavis])
-Iloprost is a type of medication known as a prostanoid, which can help improve blood flow and reduce symptoms.
-While it’s used for CLI, it’s important to note that Iloprost (Ventavis) is not FDA-approved specifically for this condition. It is primarily approved for pulmonary arterial hypertension.

 Continue to decrease CVD risk: statins, antiplatelet, ACE inhibitor, and beta-blocker
Managing overall cardiovascular risk is crucial in the treatment of CLI. This includes medications like:
Statins: To lower cholesterol levels and stabilize plaque in the arteries.
Antiplatelet Agents: Such as aspirin or clopidogrel, to prevent blood clots.
ACE Inhibitors: To lower blood pressure and reduce strain on the heart.
Beta-Blockers: Also to manage blood pressure and reduce the heart’s workload.

Conservative treatment
-Conservative treatment refers to non-surgical approaches that focus on managing symptoms and preventing complications, especially in conditions where surgery might not be immediately necessary, feasible, or the patient’s preference.

 Protect from trauma
This involves safeguarding the affected area (like a limb) from injury or excessive pressure, which can worsen the condition. For example, using protective footwear and avoiding activities that might lead to cuts, bruises, or other injuries.

 Decrease ischemic pain
Pain management is crucial, particularly for conditions that cause ischemic pain (pain resulting from reduced blood flow). This can include medications like analgesics, and in some cases, specific drugs that help improve blood flow and reduce pain.

 Prevent/control infection
Keeping the affected area clean and monitoring for signs of infection is important. In cases where the skin integrity is compromised, such as ulcers or wounds, appropriate wound care and possibly antibiotics may be needed to prevent or treat infections.

 Improve arterial perfusion – healing is unlikely
Enhancing blood flow to the affected area is crucial, as healing is unlikely without adequate perfusion. This can be achieved through lifestyle changes (like smoking cessation and exercise), medications (such as vasodilators or antiplatelet drugs), and in some cases, specific therapies designed to improve circulation without increasing blood flow

 Spinal cord stimulation - pain
In cases where pain is difficult to manage with conventional methods, spinal cord stimulation, a procedure where electrical impulses are used to relieve pain, can be an option.

 Angiogenesis—new blood vessel growth
This involves therapeutic approaches to encourage the formation of new blood vessels in areas with poor circulation. While still an area of active research, certain treatments and medications can promote angiogenesis, potentially improving blood flow in ischemic tissues.

Question 9

Interventional Radiology Procedures
Catheter Based Procedures
Catheterization Lab instead of OR

Answer 9

Pre and postprocedure nursing care—same as for
diagnostic angiography
 Special catheter inserted in femoral artery in all of the following procedures
 Antiplatelet agents given postprocedure to reduce risk of restenosis (clopidogrel or low dose ASA)

Question 10

Interventional Radiology Procedures
Catheter Based Procedures
Percutaneous transluminal angioplasty (PTA)

Answer 10

Catheter has a balloon at the tip
 Balloon is inflated dilating the vessel by compressing atherosclerotic intimal lining
 Stent is placed to hold artery open
* Stent coated with drug (paclitaxel) to limit growth of new tissue in treated area

Question 11

Interventional Radiology Procedures
Catheter Based Procedures
Atherectomy

Answer 11

Removal of obstructing plaque
 Performed using a cutting disc, laser, or rotating
diamond tip

Question 12

Interventional Radiology Procedures
Catheter Based Procedures
Cryoplasty

Answer 12

Combines PTA and cold therapy
 Balloon filled with liquid nitrous oxide that changes to
a gas; the gas expands and cools to 14° F (−10° C)
 Limits restenosis by reducing smooth muscle cell
activity

Question 13

Interprofessional Care
Surgical Therapy
Peripheral Artery Bypass Surgery

Answer 13

-with autogenous vein or synthetic graft to bypass blood around the lesion
 Human umbilical vein or composite sequential bypass graft may be used
 PTA with stenting may also be used in combination with bypass surgery

Question 14

Femoral-popliteal Bypass Grafts (picture)

Answer 14

Question 15

Interprofessional Care
Surgical Therapy
-Endarterectomy
-Patch graft angioplasty
-Amputation

Answer 15

Other surgical options:
 Endarterectomy—open artery and remove plaque
 Patch graft angioplasty—open artery, remove plaque and sew patch to widen the lumen
 Amputation—considered if necrosis, gangrene, or
osteomyelitis develop
* As much of the limb as possible is preserved to improve rehabilitation potential

Question 16

Nursing Care for PAD

Answer 16

Health promotion
 Identification of at-risk patients
 Diet modification
 Proper care of feet
 Avoidance of injuries
 Regular follow-up care

Acute care
 In recovery area, after surgery or radiologic
intervention, frequently monitor
* Skin color and temperature
* Capillary refill
* Presence of peripheral pulses distal to the operative site
 Notify HCP immediately with any changes
* Sensation and movement of extremity
* Pain management

Acute care—after leaves recovery
 Continued circulatory assessment
 Monitor for potential complications
* Report: Increased pain, loss of pulses, pallor or
cyanosis, numbness or tingling
 Avoid knee-flexed positions
 Turn and position frequently, OOB, ambulate; avoid prolonged sitting
 Graduated compression stockings

Ambulatory care
 Management of risk factors
* Smoking cessation
 Long-term antiplatelet/ASA therapy
 Supervised exercise training after revascularization
 Importance of meticulous foot care
 Daily inspection of the feet
 Comfortable shoes with rounded toes and soft
insoles; shoes lightly laced
 Show how to check skin temperature, capillary refill, and palpate pulses
 Patient and caregiver teaching

Question 17

Acute Arterial Ischemic Disorders

Answer 17

Etiology and pathophysiology
 Sudden interruption in arterial blood supply to a
tissue, organ, or extremity
 If untreated, can result in tissue death
 Causes: embolism, thrombosis, or trauma

Most frequent: embolization of thrombus from the
heart related to: infective endocarditis, mitral valve
disease, atrial fibrillation, cardiomyopathies, and
prosthetic heart valves

 Noncardiac causes: aneurysms, ulcerated
atherosclerotic plaque, endovascular procedures,
and venous thrombi

Thrombi from left side of heart may dislodge and
travel anywhere in systemic circulation
 Most block an artery in the leg
 Sudden local thrombosis may occur at site of
atherosclerotic plaque
 Predisposing factors: hypovolemia, hyperviscosity,
and hypercoagulability

Traumatic injury to an extremity may cause
partial or complete blockage
 Acute arterial occlusion may occur with arterial
dissection of the carotid artery or aorta or
procedure-related injury

Question 18

Acute Arterial Ischemic Disorders
6Ps

Answer 18

 Pain
 Pallor
 Pulselessness
 Paresthesia
 Paralysis (late sign)
 Poikilothermia

• Adaptation of limb to environmental temperature (cool)
   Immediate intervention needed to avoid ischemia,
  necrosis, and gangrene – can occur within hours

Question 19

Acute Arterial Ischemic Disorders

Answer 19

Treatment
Early diagnosis and treatment
 Anticoagulant—IV unfractionated heparin
 Restore blood flow—remove thrombus
 Surgical thrombectomy
 Percutaneous catheter-directed thrombolytic therapy
 Percutaneous mechanical thrombectomy with or
without thrombolytic therapy
 Surgical bypass

Percutaneous catheter-directed thrombolytic therapy with alteplase or urokinase preferred if arterial
ischemia is less than 14 days old
* Thrombolytic dissolves clot over 24 to 48 hours
* Requires close monitoring or catheter position and
bleeding at insertion site
 Surgical revascularization—trauma or arterial
blockage
 Amputation—ischemic rest pain and tissue loss
 Long-term anticoagulation recommended if risk for further embolization exists

Question 20

Thromboangiitis Obliterans
Buerger’s Disease

Answer 20

 Nonatherosclerotic, segmental, recurrent
inflammatory disorder of the small and medium
arteries and veins of the arms and legs
 Most common in men younger than 45 years old with history of tobacco and/or marijuana use without other CVD risk factors

Question 21

Thromboangiitis Obliterans
Buerger’s Disease
Phases

Answer 21

Acute phase
 Inflammatory thrombus blocks vessel
 Chronic phase
 Thrombosis and fibrosis causes ischemia
 Symptoms
 Intermittent claudication of feet, hands, or arms; rest pain, ischemic ulcerations, changes in color and
temperature, paresthesia, superficial vein thrombosis and cold sensitivity

Question 22

Thromboangiitis Obliterans
Buerger’s Disease
Diagnosis + Treatment

Answer 22

No specific lab or diagnostic tests
 Based on history and symptoms and exclusion of
other disorders
 Treatment: no smoking tobacco or marijuana; no
nicotine replacements
 Conservative:
 Avoid cold exposure; walking program, antibiotics for ulcers, analgesia for pain, avoid trauma

IV iloprost—promotes vasodilation
 Surgeries
 Lumbar sympathectomy
 Spinal cord stimulator
 Microsurgical flap and omental transfer
 Bypass surgery
 Amputation
 Stem cell therapy

Question 23

Raynaud’s Phenomenon

Answer 23

-Episodic, vasospastic disorder of small cutaneous
arteries; fingers and toes most commonly involved
 More common in women, age 15 to 40 years
 Pathogenesis—abnormalities in vascular,
intravascular, and neuronal mechanisms that cause
vasodilation

May occur alone (primary) or with other diseases
 Contributing factors
 Use of vibrating machinery
 Work in cold environments
 Exposure to heavy metals
 High homocysteine levels
 Diagnosis: persistent symptoms for at least 2 years

Characteristic change in color of fingers, toes, ears,
and nose
 White, blue, and red
 Also: coldness, numbness followed by throbbing,
aching pain, tingling, and swelling
 Several minutes to hours
 Prolonged, frequent attacks causes thick skin, brittle nails, punctate lesions and gangrenous ulcers
 Triggers: cold exposure, emotional upset, tobacco
use and caffeine

Question 24

Raynaud’s Nursing Care

Answer 24

Patient education: prevent episodes
* Avoid temperature extremes; wear appropriate clothing
* No tobacco products; avoid caffeine
* No vasoconstrictor drugs
* Stress management
 Immerse hands in warm water to help decrease
vasospasm

Question 25

Raynaud's Drug Therapy

Answer 25

Drug therapy * Sustained release calcium channel blockers to decrease vasospasm * Vasodilators * Topical nitroglycerin 2% ointment  Digital ulceration or critical ischemia * Prostacyclin infusion, antibiotics, analgesia * Surgical debridement * Botox and statins * Sympathectomy

Question 26

Aortic Aneurism

Answer 26

Aorta is largest artery, supplies oxygen and nutrients to all vital organs Permanent, localized, outpouching, or dilation of wall of aorta  Occur in men more than in women and in whites more often than blacks  Incidence increases with age  May occur in more than one location

Question 27

Aortic Aneurysms Etiology and Pathophysiology

Answer 27

Abdominal aortic aneurysms (AAA)  ¾ occur in abdominal aorta  ¼ occur in thoracic aorta  Most occur below renal arteries  The larger aneurysm, the greater risk of rupture Causes  Degenerative  Congenital  Infectious  Mechanical * Penetrating or blunt trauma  Inflammatory Risk Factors  Age  Male gender  HTN  CAD  Family history  Tobacco use  High cholesterol  Lower extremity PAD  Carotid artery disease  Previous stroke  Obesity

Question 28

Aortic Aneurysms Genetic Link

Answer 28

Familial tendency—congenital anomalies  Bicuspid aortic valve Normally, the aortic valve has three leaflets, but in a bicuspid aortic valve, there are only two. This congenital anomaly can lead to abnormal blood flow, increasing the risk of an aortic aneurysm.  Coarctation of aorta This is a congenital condition where a part of the aorta is narrowed, affecting blood flow. The increased pressure proximal to the coarctation can contribute to the development of an aortic aneurysm.  Turner’s syndrome A genetic disorder in females characterized by the partial or complete absence of one X chromosome. Turner’s syndrome is associated with heart defects, including bicuspid aortic valves and coarctation of the aorta, which can increase the risk of an aortic aneurysm.  Autosomal dominant polycystic kidney disease This genetic disorder is characterized by the development of numerous cysts in the kidneys and can be associated with abnormalities in blood vessels, including an increased risk of aortic aneurysms.  Ehlers-Danlos syndrome A group of disorders that affect connective tissues, characterized by hypermobile joints and elastic skin. Certain types of Ehlers-Danlos syndrome, which involve defects in collagen (a key component of vascular tissue), can lead to weakening of the aorta's walls, predisposing individuals to aneurysms. * Collagen defects  Marfan’s syndrome A genetic disorder affecting connective tissue, Marfan's syndrome is known for causing elongation of the bones and other skeletal anomalies. It also leads to a premature breakdown of the elastic tissue in the aorta, making the aortic wall more susceptible to aneurysm formation. * Premature breakdown of vascular elastic tissue

Question 29

Classification - True Aneurism

Answer 29

A true aneurysm is a type of aneurysm where the bulge or dilation occurs in the wall of an artery and involves at least one of the vessel's intact layers. Wall of artery forms aneurysm In a true aneurysm, the aneurysm is formed by a dilation or ballooning of the arterial wall itself. Unlike a false aneurysm, where the bulge is outside the vessel wall, a true aneurysm involves the actual layers of the artery.  At least one vessel layer still intact For an aneurysm to be classified as true, at least one of the three layers of the artery (intima, media, or adventitia) must still be intact. The structural integrity of the artery is partially maintained, but the weakened area is prone to expansion and potential rupture. Subtypes of True Aneurysm: Fusiform Aneurysm: -This is a type of true aneurysm where the dilation occurs around the entire circumference of the artery. -Fusiform aneurysms are relatively uniform in shape, appearing as a symmetrical bulge that extends around the entire vessel. Saccular Aneurysm: -Saccular aneurysms are pouch-like dilations that protrude from one side of the arterial wall. -They have a narrow neck that connects the bulge to the artery, resembling a small sack or pouch coming off the side of the vessel.

Question 30

Classification - False Aneurism

Answer 30

False aneurysm or pseudoaneurysm  Not an aneurysm  Disruption of all layers of arterial wall * Results in bleeding contained by surrounding structures * From trauma, infection, peripheral artery bypass graft surgery or arterial leakage after removal of cannulae

Question 31

Aortic Aneurism Clinical Manifestations Thoracic aortic aneurysm (TAA)

Answer 31

Often asymptomatic  Most common manifestation * Deep diffuse chest pain * Pain may extend to interscapular area Ascending aorta/aortic arch  Angina  Transient ischemic attacks  Coughing, shortness of breath, hoarseness, and/or dysphagia  If presses on superior vena cava * Decreased venous return  Distended neck veins  Edema of face and arms Abdominal aortic aneurysms (AAA)  Often asymptomatic  Frequently detected * On routine physical exam * When patient examined for unrelated problem (i.e., CT scan, abdominal x-ray)  Pulsatile mass in periumbilical area slightly left of midline  Bruit auscultated over aneurysm AAA  May mimic pain associated with abdominal or back disorders  May cause back pain, epigastric discomfort, altered bowel elimination, intermittent claudication  May spontaneously embolize plaque * Causing “blue toe syndrome” – patchy mottling of the feet and toes in the presence of palpable pedal pulses

Question 32

Aortic Aneurism Complications - Rupture

Answer 32

Rupture—most serious complication Rupture into the Retroperitoneal Space: -The retroperitoneal space is an area in the abdomen behind the peritoneum (the lining of the abdominal cavity). -If an abdominal aortic aneurysm ruptures into this space, the bleeding may be somewhat contained by the surrounding tissues and structures. This containment, known as tamponade, can temporarily prevent massive blood loss (exsanguination). Bleeding May Be Tamponaded: Tamponade in the context of a ruptured aneurysm is a double-edged sword. While it can initially prevent catastrophic blood loss, it can also delay diagnosis and treatment, as the usual signs of internal bleeding may not be immediately apparent. This contained rupture, however, still requires urgent medical attention as it can quickly become unstable and lead to significant blood loss and shock. Symptoms of Rupture: Severe Back Pain: This is a common symptom of a ruptured abdominal aortic aneurysm. The pain is often described as a tearing or ripping sensation and can be severe and sudden in onset. Back/Flank Ecchymosis (Grey Turner’s Sign): In some cases, there may be bruising on the back or flanks. Grey Turner’s sign is the appearance of bruising over the flanks and indicates severe retroperitoneal bleeding. However, this sign may not always be present. Importance of Immediate Medical Attention: A ruptured aneurysm is a medical emergency that requires immediate attention. Even with tamponade, the situation can rapidly deteriorate. Emergency surgery is often necessary to stop the bleeding and repair the ruptured artery.

Question 33

Rupture in Thoracic or Abdominal Cavity

Answer 33

Massive Hemorrhage and Hypovolemic Shock: When an aneurysm ruptures into the thoracic (chest) or abdominal cavity, it can lead to rapid and severe internal bleeding. Hypovolemic shock occurs as a result of this massive blood loss, where there isn't enough blood circulating in the body. This deprives organs of oxygen and nutrients, leading to organ failure. Survival Rate and Emergency Response: Unfortunately, due to the severity of the bleeding, many individuals do not survive long enough to reach a hospital. For those who do make it to medical care, the situation is still extremely critical. Immediate and aggressive resuscitation is necessary to stabilize the patient’s condition. Need for Simultaneous Resuscitation and Immediate Surgery: -Patients who suffer from an aneurysm rupture into the thoracic or abdominal cavity require simultaneous resuscitation and emergency surgery. -Resuscitation efforts focus on stabilizing blood pressure and maintaining organ perfusion by replacing lost blood and fluids. -Surgery is aimed at stopping the bleeding and repairing the ruptured artery. This often involves replacing the damaged section of the artery with a graft. High Mortality Rate: Even with prompt medical intervention, the mortality rate remains high, with around 53% of patients not surviving. This high mortality rate is due to the rapid onset of shock and the complications associated with major surgery under such critical conditions. Importance of Early Detection and Intervention: This situation underscores the importance of early detection and management of aneurysms. Regular monitoring and appropriate treatment of aneurysms can prevent rupture in many cases.

Question 34

Aortic Aneurism Diagnostic Studies

Answer 34

X-rays  Chest—demonstrate mediastinal silhouette and any abnormal widening of thoracic aorta  Abdomen—may show calcification within wall of AAA  ECG—to rule out MI  Thoracic aneurysm or dissection symptoms can mimic angina Echocardiography  Assesses aortic valve function  Ultrasonography  Useful in screening for aneurysms  Monitors aneurysm size  CT scan or MRI  Diagnose and assess location and severity  Angiography  Anatomic mapping of aortic system using contrast

Question 35

Care for Aortic Aneurism

Answer 35

Goal: prevent from rupturing Studies to determine size + location Small aneurysm (size < 5.4 cm)  Conservative therapy used * Risk factor modification * ↓ blood pressure, tobacco cessation, optimize lipid profile, gradual  physical activity * Size 4 to 5.4 cm—ultrasound, CT scan monitoring every 6 to 12 months * Size < 4cm—ultrasound every 3 years Size larger than 5.5 cm—recommend surgical repair  Surgery may occur earlier in:  Patients with a genetic disorder  Rapidly expanding aneurysm  Symptomatic patients  High rupture risk  Identify and correct co-morbidities

Question 36

Surgery for Aortic Aneurism

Answer 36

Surgical therapy  Preop—elective repair * Hydration * Stabilize electrolytes, coagulation, and hematocrit  If ruptures, emergent surgical intervention required * 90% mortality with ruptured AAAs

Question 37

Open Aneurism Repair (OAR)

Answer 37

Open aneurysm repair (OAR)  Incises diseased segment of aorta  Removes thrombus or plaque  Inserts synthetic graft to the aorta proximal and distal to aneurysm  Sutures native aortic wall around graft * Acts as protective cover Iliac artery aneurysms  Replace diseased section with a bifurcated graft  Saccular aneurysms  Repair bulbous section and suture aorta or apply autogenous or synthetic patch graft  All OARs require cross clamping the aorta; proximal and distal to aneurysm  High risk of acute kidney injury if above the renal arteries due to decreased blood flow

Question 38

Endovascular Graft Procedure

Answer 38

Endovascular aneurysm repair (EVAR)  Alternative to OAR (minimally invasive) * Criteria: iliofemoral vessels are safe for graft insertion and vessels are adequate length and width to support graft  Involves placement of sutureless aortic graft into abdominal aorta inside aneurysm Graft * Constructed from Dacron cylinder * Surface supported with rings of flexible wire * Delivered through sheath to predetermined point * Delivered through a femoral artery catheter * Deployed against vessel wall by balloon inflation * Anchored to vessel by series of small hooks Blood then flows through graft, preventing expansion of aneurysm  Aneurysm wall will begin to shrink over time  Post procedure angiography—checks for leaks and confirms patency Benefits * Less invasive * Shorter hospital stay * Fewer complications Potential complications * Endoleak—most common  Seepage of blood into old aneurysm * Aneurysm growth * Aneurysm rupture * Aortic dissection * Bleeding Renal artery occlusion related to  Stent migration  Graft thrombosis  Incisional site hematoma  Site infection Intraabdominal hypertension (IAH)  Potentially lethal complication in emergency repair * Intraabdominal pressure measure with catheter and transducer  Associated with abdominal compartment syndrome * Reduces blood flow to viscera * End-organ perfusion impaired results in multisystem organ failure Intraabdominal hypertension (IAH)  Treatment * Open surgical compression * Percutaneous drainage * Percutaneous drainage combined with thrombolytic infusion Graft dysfunction may require surgical repair  Need for life-long follow-up

Question 39

Signs of Aneurism Rupture

Answer 39

 Diaphoresis (excessive sweating not related to heat and exercise)  Pallor  Weakness  Tachycardia  Hypotension  Abdominal, back, groin or periumbilical pain  Changes in LOC (level of consciousness, AAOx3)  Pulsating abdominal mass

Question 40

Aortic Dissection

Answer 40

Not a type of aneurysm  Result of a false lumen through which blood flows  Between intima and media of arterial wall

Question 41

Aortic Dissection Classification 1 and 2

Answer 41

Aortic dissection is classified based on location of dissection * Type A dissection: Affects the ascending aorta and arch; requires emergency surgery * Type B dissection: Begins in the descending aorta; possible conservative management Classified by duration of onset  Acute—first 14 days  Subacute—14 to 90 days  Chronic—more than 90 days

Question 42

Nontraumatic Aortic Dissection

Answer 42

 Due to weakened elastic fibers in the arterial wall  Chronic hypertension hastens the process  Tear in inner layer allows blood to surge between inner and middle layer  Rupture through outside wall can cause death As heart contracts, each systolic pulsation increases pressure on damaged area making it worse  May occlude major branches of aorta * Cutting off blood supply to brain, abdominal organs, kidneys, spinal cord, and extremities  False lumen may remain patent, become thrombosed, or rejoin true lumen Affects men more than women  Women with aortic dissection are often older and have HF, coma, or altered mental status  HTN—most important risk factor  Other predisposing factors: age, aortic disease, atherosclerosis, blunt trauma, tobacco use, cocaine or methamphetamine use, congenital heart disease, connective tissue disease, family history, previous heart surgery, and pregnancy If aortic arch involved, Neuro deficits might be present

Question 43

Acute Type A Aortic Dissection

Answer 43

Abrupt onset of severe anterior chest pain or back pain Type A and B may overlap  Pain described as “ sharp”, “worst ever,” “tearing,” “ripping,” or ‘stabbing”

Question 44

Acute Type B Aortic Dissection

Answer 44

Back, abdomen, or leg pain Disruption of blood flow in coronary arteries and aortic valve insufficiency Type A and B may overlap  Pain described as “ sharp”, “worst ever,” “tearing,” “ripping,” or ‘stabbing”

Question 45

Dissection Pain vs MI Pain

Answer 45

-more gradual onset with increased intensity  May follow path of dissection with progression  Older patients: less likely to have abrupt onset; see hypotension and vague symptoms  May be painless for some

Question 46

Dissection Clinical Manifestations

Answer 46

-Subclavian artery  BP and arterial pulses different between arms -Aortic progression  Decreased tissue perfusion to abdominal organs and lower extremities

Question 47

Dissection Complications: Cardiac Temponade

Answer 47

Cardiac tamponade  Severe, life-threatening complication of acute ascending aorta dissection  Occurs when blood escapes from dissection into pericardial sac Clinical manifestations include: * Hypotension * Narrowed pulse pressure * Distended neck veins * Muffled heart sounds * Pulsus paradoxus

Question 48

Dissection Complications: Rupture

Answer 48

Aorta may rupture resulting in hemorrhage in mediastinal, pleural, or abdominal cavities  Results in exsanguination and death

Question 49

Dissection Complications: Occlusion of arterial supply to vital organs

Answer 49

 Spinal cord -Aortic dissection can lead to reduced blood flow to the arteries that supply the spinal cord. -This can result in spinal cord ischemia, potentially causing symptoms like severe back pain, muscle weakness, paralysis, or loss of bowel and bladder control. -Spinal cord ischemia is a medical emergency, as it can lead to permanent damage or paralysis.  Renal ischemia -If the dissection involves the renal arteries, it can lead to renal ischemia, affecting kidney function. -This can result in acute kidney injury, characterized by a sudden decrease in kidney function, reduced urine output, and the accumulation of waste products in the blood. -Renal ischemia requires prompt medical attention to restore blood flow and prevent permanent kidney damage.  Abdominal ischemia -When a dissection affects the arteries supplying the abdomen, it can cause abdominal ischemia. -This can affect various abdominal organs, leading to severe abdominal pain, digestive disturbances, and potential damage to organs like the intestines. -Abdominal ischemia is a serious condition that can lead to tissue death (necrosis) and requires immediate medical intervention.

Question 50

Aortic Dissection Diagnostic Studies

Answer 50

H & P  ECG  Chest x-ray  3-D CT scan  MRI  TEE - Transesophageal echocardiography  CT scan

Question 51

Care Goals After Aortic Dissection

Answer 51

HR and BP control * Decreased BP and myocardial contractility to diminish pulsatile forces within aorta * IV -blocker to HR less than 60/min or SBP 100 to 110 mm Hg; alternative is calcium channel blocker  Pain management * Morphine Conservative therapy for acute or chronic Type B without complications  Pain relief  HR and BP control  CVD risk factor modification  Close surveillance with CT or MRI Surgical therapy  Emergency surgery for acute Type A aortic dissection (mortality = 50% within 48 hours of symptom onset)  Considered when drug therapy is ineffective or when complications of aortic dissection are present  Surgery is delayed to allow edema to decrease and permit clotting of blood Involves resection of aortic segment and replacement with synthetic graft material  In-hospital mortality high * Causes of death—aortic rupture, mesenteric ischemia, MI, sepsis, stroke, or multi-organ failure

Question 52

Endovascular Dissection Repair - Post Op Care

Answer 52

horacic endovascular aortic repair (TEVAR)  Standard to treat acute and chronic Type B aortic dissections with complications  Similar to EVAR but fewer post-surgical complications * May have lumbar drain

Question 53

Aortic Dissection Nursing Management

Answer 53

Preoperative  Semi-Fowler’s position & quiet environment to  HR and SBP  Anxiety and pain management * Opioids and sedatives  Titrate IV antihypertensive agents  Continuous BP and ECG monitoring  Frequent VS (every 2 to 3 minutes) -Observation of changes in quality of peripheral pulses  Monitor for * Increasing pain * Restlessness * Anxiety Postoperative  See aneurysm postop care (discussed earlier)  Discharge teaching  Long-term HR and BP control * Antihypertensive drugs and side effects * -blockers or ACE inhibitors  Regular follow-up with CT or MRI  If pain returns or symptoms progress, instruct patient to seek immediate help

Question 54

Phlebitis

Answer 54

Acute inflammation of the walls of small cannulated veins of the hand or arm (related to IV catheter)  Manifestations: pain, tenderness, warmth, erythema, swelling, and palpable cord  Risk factors: irritation from catheter, infusion of irritating drugs, and catheter location (area of flexion)  Avoid IV insertion in these areas whenever possible Rarely infectious  Treatment: remove catheter  Edema * Elevate extremity to promote fluid reabsorption  Pain and inflammation * NSAIDs * Warm, moist hear

Question 55

Venous Thrombosis

Answer 55

Venous thrombosis refers to the formation of a blood clot (thrombus) within a vein, which can be accompanied by inflammation of the vein (thrombophlebitis). This condition can occur in superficial or deep veins and is a significant health concern due to its potential complications.  Most common disorder of the veins Superficial Vein Thrombosis: Occurs in the superficial veins, which are closer to the skin's surface. Most commonly affects the greater or lesser saphenous veins in the legs. Symptoms may include redness, warmth, tenderness, and a palpable, firm vein. While generally less dangerous than deep vein thrombosis, superficial vein thrombosis can sometimes lead to more serious conditions or indicate an underlying medical issue. Deep Vein Thrombosis (DVT): DVT occurs in the deep veins, typically in the lower limbs (iliac and/or femoral veins). It can cause leg pain, swelling, warmth, and redness, but sometimes it may occur without noticeable symptoms. DVT is particularly concerning because the clot can dislodge and travel through the bloodstream to the lungs, leading to a pulmonary embolism (PE), a potentially life-threatening condition. Venous Thromboembolism (VTE): VTE is a preferred term that encompasses both DVT and PE. It represents a spectrum of conditions where a blood clot forms in a vein (usually DVT) and can potentially lead to PE if the clot travels to the lungs. PE can cause symptoms like shortness of breath, chest pain, cough (sometimes with blood), and in severe cases, can result in sudden death. Risk Factors: Risk factors for venous thrombosis include prolonged immobility (like long flights or bed rest), surgery, certain medical conditions, pregnancy, hormone therapy, smoking, and a family history of clotting disorders. Treatment: Treatment for venous thrombosis typically involves anticoagulant medications (blood thinners) to prevent the clot from growing and reduce the risk of further clots. In DVT, compression stockings are often recommended to reduce swelling and prevent long-term complications. In cases of PE, emergency treatment is required to manage the clot in the lungs. Prevention: Preventive measures include regular movement and exercise, especially during long periods of immobility, staying hydrated, and following medical advice for blood clot prevention after surgeries or during high-risk situations.

Question 56

Venous Thrombosis Etiology

Answer 56

Virchow’s triad - 3 key factors that cause venous thrombosis  Venous stasis  Damage to endothelium  Hypercoagulability of blood  Patients at risk for developing VTE usually have predisposing conditions to these 3 factors

Question 57

Venous Stasis

Answer 57

Dysfunctional valves  Inactive extremity muscles  At risk * Obese * Pregnant * Chronic HF or atrial fibrillation * Traveling on long trips without exercise * Prolonged surgery * Prolonged immobility

Question 58

Venous Stasis Endothelial Damage

Answer 58

Endothelial damage  Stimulates platelet activation and starts coagulation cascade, which predisposes patient to thrombus development  Direct damage * Surgery, burns, IV catheter, trauma, prior VTE  Indirect damage * Chemotherapy, diabetes, sepsis

Question 59

Venous Stasis Hypercoagulability of Blood

Answer 59

Occurs with many disorders * Anemia, polycythemia * Cancer * Nephrotic syndrome * High homocysteine levels * Coagulation disorders * Sepsis * Drugs: corticosteroids, estrogens * Smoking Very high risk—women who: * Use tobacco  Smoking increases plasma fibrinogen, homocysteine levels and activates intrinsic coagulation pathway * Are childbearing age and take estrogen-based oral contraceptives * Are postmenopausal and take oral hormone therapy * Are over age 35 * Have family history of VTE

Question 60

VTE (venous thromboembolism) Pathophysiology

Answer 60

-Clot formation occurs when localized platelet aggregation and fibrin entrap RBCs, WBCs, and more platelets.  Clot gets larger and has a “tail” that blocks the lumen of the vein  Partial blockage—endothelial cells cover thrombus and stop growth; lysis or adherence occurs within 5 to 7 days Detached thrombus results in embolus  Travels through venous system to right side of the heart and lodges in pulmonary circulation, becomes a PE  Turbulent blood flow—major factor in embolization

Question 61

Superficial Vein Thrombosis

Answer 61

Superficial leg veins most common  Clinical Manifestations  Palpable, firm, cordlike vein  Itchy, painful, red, and warm  Mild fever, leukocytosis  Often involves varicose veins  Risk Factors -Increased age, pregnancy, obesity, cancer, recent fracture(s), estrogen therapy, recent sclerotherapy, recent surgery or long-distance travel, hypercoagulability, history of CVI or VTE Interprofessional care  Diagnosis—ultrasound  Treatment of clot smaller than 5 cm and not near saphenousfemoral junction * Oral (or topical) NSAIDs * Graduated compression stockings * Warm compresses * Elevate limb above heart * Mild exercise

Question 62

VTE (deep) Manifestations

Answer 62

Deep veins of arms or legs, pelvis, vena cava, and pulmonary system  Manifestations  Lower extremity * Unilateral edema * Pain, tenderness with palpation * Dilated superficial veins * Full sensation in thigh or calf * Paresthesias * Red, warm, Fever greater than 100.4° F (38° C) Manifestations  Inferior vena cava * Legs edematous and cyanotic  Superior vena cava * Similar symptoms of arms, neck, back and face  Some patients are asymptomatic

Question 63

VTE Complications: PTS

Answer 63

Most serious  PE  Chronic thromboembolic pulmonary hypertension  Postthrombotic syndrome (PTS)  Phlegmasia cerulea dolens Post-thrombotic syndrome (PTS)  8% to 70% of patients  Chronic inflammation and venous hypertension; damage to vein walls and valves, venous valve reflux, and persistent venous obstruction  Symptoms * Pain, aching, fatigue, heaviness, swollen sensation, cramps, pruritus, tingling, paresthesia, pain with exercise, and venous claudication PTS: Manifestations * Persistent edema, spider veins, venous dilation, redness, cyanosis, increased pigmentation, eczema, pain during compression, white scar tissue, and lipodermatosclerosis * Venous ulceration with severe PTS * Signs may occur in a few months or years PTS risk factors:  Persistent leg symptoms for more than 1 month after VTE  VTE: Proximal location, extensive, or recurrent  Residual thrombus  Other: obesity, old age, poor INR control, tobacco use, increased D-dimer, increased inflammatory markers, varicose veins, and asymptomatic VTE PTS risk factors:  Persistent leg symptoms for more than 1 month after VTE  VTE: Proximal location, extensive, or recurrent  Residual thrombus  Other: obesity, old age, poor INR control, tobacco use, increased D-dimer, increased inflammatory markers, varicose veins, and asymptomatic VTE

Question 64

VTE Diagnostic Studies

Answer 64

Diagnostic studies  Blood: ACT, aPTT, INR, bleeding time, Hgb, Hct, platelet count, D-dimer, fibrin monomer complex  Noninvasive venous: venous compression ultrasound, duplex ultrasound  Invasive venous: CT venography, MR venography, contrast venography

Question 65

VTE Hospital Interventions

Answer 65

Interventions are based on  Bleeding and thrombosis risk, PMH, current drugs, medical diagnoses, scheduled procedures, and patient preferences -Three VTE measures  Early and progressive mobilization  Graduated compression stockings  Intermittent pneumatic compression devices (IPCs)

Question 66

VTE: Early.+ Aggressive Mobilization

Answer 66

Early and aggressive mobilization  Bed rest—reposition every 2 hours  Flex and extend feet, knees and hips every 2 to 4 hours while awake  OOB to chair  Walk 4 to 6 times/day

Question 67

VTE: Compression Stockings

Answer 67

Graduated compression stockings  Thromboembolic deterrent (TED)  Often used with anticoagulation  Fit and wear correctly: * Toe hole under toes, heel patch over heel; thigh gusset on inner thigh * No wrinkles; don’t roll down, cut, or alter  Not recommended if VTE already exists Intermittent pneumatic compression devices (IPCs) - increased venous return  External pressure from electric pump inflates sleeves or boots to compress calf or thigh and/or foot and ankle  Use with graduated compression stockings  Fit and apply correctly; wear continuously except for bathing, skin assessment, and ambulation  Do not use with active VTE; risk of PE

Question 68

VTE: Drug Therapy

Answer 68

Drug therapy: anticoagulants  VTE prophylaxis: prevent clot formation  Existing VTE: prevent: new clot formation, spread of the clot, and embolization  Three classifications * Vitamin K antagonists (VKA) * Thrombin inhibitors (direct and indirect) * Factor Xa inhibitors Vitamin K antagonists: Warfarin  Inhibits Vitamin K-dependent coagulation factors II, VII, IX, and X and anticoagulant proteins C and S * For long-term or extended anticoagulation * Takes 48 to 72 to be effective; often overlap with parenteral anticoagulant for 5 days * Monitor INR * Antidote: Vitamin K Warfarin (continued)  Do not give with antiplatelet drugs or NSAIDS  Many interactions: See Complementary and Alternative Therapies Box  Avoid vitamin K in diet; alters INR * Green leafy vegetables  Genetic variants may alter response Thrombin inhibitors  Indirect: UH (heparin) and LMWH * Affects intrinsic plasma antithrombin coagulation pathway; inhibits thrombin mediated conversion of fibrinogen to fibrin (Fig. 29-4) * Prophylaxis—subcutaneously * Existing VTE—continuous IV; monitor aPTT Heparin (continued)  Serious side effect: heparin-induced thrombocytopenia (HIT)  Long-term side effect: osteoporosis  LMWH—enoxaparin  More predictable, longer half-life, fewer bleeding complications  Antidote: protamine Direct thrombin inhibitors  Hirudin derivative—bivalirudin (Angiomax) * Binds with thrombin and inhibits function * Continuous IV infusion  Synthetic (Argatroban)— * Hinders thrombin  Both: * Indications: patients with or at risk for HIT having a percutaneous coronary intervention * Monitor aPTT or ACT * No antidote Dabigatran (Pradaxa)—oral * Indications: VTE prevention after elective joint replacement, for stroke prevention in nonvalvular atrial fibrillation, and as a treatment for VTE * Antidote: idarucizumab * Advantages over warfarin  Rapid onset, no monitoring, few drug-food interactions, decreased risk of bleeding, predictable response Factor Xa Inhibitors  Inhibit factor Xa; rapid anticoagulation * VTE prophylaxis and treatment * Fondaparinux (Arixtra)—Subcutaneous  Contraindicated with severe renal disease * Rivaroxaba (Xarelto), apixaban (Eliquis), edoxaban (Savaysa)—oral * Monitoring not required but can use anti-Xa assays (Table 41.11) * Andexant Alfa—reverses rivaroxaban and apixaban

Question 69

Anticoagulant Therapy for VTE Prophylaxis

Answer 69

Anticoagulant therapy for VTE prophylaxis  Hospitalized patient not bleeding For patients in the hospital who are not actively bleeding but are at risk for VTE, prophylactic anticoagulation is often recommended. Commonly used anticoagulants include Unfractionated Heparin (UH), Low Molecular Weight Heparin (LMWH), and Fondaparinux. The choice of agent depends on the patient's risk factors, renal function, and other clinical considerations. Low Risk VTE – No Prophylaxis: Patients considered to be at low risk for VTE may not require prophylactic anticoagulation. In these cases, the risk of bleeding from anticoagulation might outweigh the benefits. Moderate Risk – UH or LMWH: Patients with moderate risk of VTE, such as those undergoing general, gynecological, or urological surgery, are often prescribed Unfractionated Heparin or Low Molecular Weight Heparin for prophylaxis. These medications help prevent the formation of blood clots without significantly increasing the risk of bleeding. High Risk – UH or LMWH: High-risk patients, such as those with trauma, abdominal or pelvic surgery for cancer, or undergoing orthopedic surgery (like hip or knee replacement), are at a greater risk for developing VTE. In these cases, more aggressive prophylaxis with UH or LMWH is often recommended to prevent clot formation. Considerations in Anticoagulant Therapy: The duration of prophylaxis can vary based on the patient’s risk factors and the type of surgery or condition. Regular monitoring and adjustments might be needed, especially in patients with renal impairment or other co-morbidities. Other Preventive Measures: In addition to pharmacological prophylaxis, mechanical methods like compression stockings or intermittent pneumatic compression devices are also used, particularly in patients with contraindications to anticoagulation.

Question 70

Anticoagulation Therapy for VTE Treatment

Answer 70

Anticoagulant therapy is the cornerstone of treatment for Venous Thromboembolism (VTE), which includes Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE). Initial Therapy: Low Molecular Weight Heparin (LMWH): Often used as an initial treatment due to its effectiveness and relative ease of use (subcutaneous injections). LMWH has a predictable effect and doesn't usually require routine blood monitoring. Unfractionated Heparin (UH): May be administered intravenously, especially in hospital settings. It requires close monitoring of blood clotting times to ensure proper dosing. Oral Factor XA Inhibitors: These are newer oral anticoagulants that directly inhibit Factor XA, an important component of the blood clotting process. Examples include rivaroxaban and apixaban. Vitamin K Antagonists (VKA): Warfarin is the most commonly used VKA. It requires regular blood monitoring, with the goal of maintaining an International Normalized Ratio (INR) between 2.0 and 3.0 for effective treatment. Duration of Treatment: Treatment typically continues for at least 3 months. The exact duration depends on the cause of the VTE, the patient's risk factors for recurrence, and their risk of bleeding. Hospitalization for Complex Cases: Patients with co-morbidities, complex medical issues, or a very large VTE may require hospitalization. In these cases, intravenous Unfractionated Heparin is often used initially due to its rapid onset and the ability to quickly adjust the dose as needed. Monitoring and Adjustment: For patients on VKA therapy, regular INR monitoring is crucial to ensure the effectiveness and safety of the treatment. Dosage adjustments are often necessary based on INR results, dietary vitamin K intake, and other medications. Interprofessional Care: Managing VTE often involves an interprofessional team, including physicians, nurses, pharmacists, and possibly specialists in hematology or pulmonology. This team approach ensures comprehensive care, from diagnosis through treatment and follow-up, including patient education about medication management and lifestyle adjustments.

Question 71

Thrombolytic Therapy for VTE Treatment

Answer 71

Thrombolytic therapy is a treatment used in certain medical conditions to dissolve blood clots. It's particularly used in the treatment of acute, extensive, and symptomatic venous thromboembolism (VTE), which includes deep vein thrombosis (DVT) and pulmonary embolism (PE). Here is how it is used for VTE: Thrombolytic Drugs: Medications such as tissue Plasminogen Activator (tPA) or urokinase are used in thrombolytic therapy. These drugs work by breaking down the fibrin component of blood clots, effectively dissolving the clot. Thrombolytic drugs can be administered through a catheter directly at the site of the clot (catheter-directed thrombolysis) or systemically through an intravenous (IV) line. Goals of Thrombolytic Therapy: The primary aim is to quickly dissolve blood clots, which helps reduce acute symptoms. It can improve deep venous flow, reduce valvular reflux (backward flow of blood), and decrease the risk of developing post-thrombotic syndrome (PTS), a long-term complication of DVT. Indications for Thrombolytic Therapy: Thrombolytic therapy is generally reserved for patients with a low risk of bleeding. It's indicated for acute, extensive, symptomatic, proximal VTE, where the clot is located in the larger, proximal veins (like those in the thigh or pelvis). This treatment is considered when the potential benefits of rapidly dissolving the clot outweigh the risks of bleeding. Systemic Anticoagulation: It’s crucial to have systemic anticoagulation before, during, and after thrombolysis. This means that patients will also be given anticoagulants (like heparin) to prevent new clot formation while the thrombolytic therapy is working on dissolving the existing clot. Anticoagulation is continued after thrombolysis to stabilize the clotting process and reduce the risk of recurrent VTE. Risk Assessment: Before administering thrombolytic therapy, a thorough evaluation of the patient’s risk for bleeding is essential. This includes reviewing the patient's medical history, current medications, and any potential contraindications.

Question 72

VTE: Surgical + Interventional Radiology Therapies

Answer 72

Surgical options: * Open venous thrombectomy—incision into vein to remove clot * Inferior vena cava interruption devices—filters placed via right femoral or internal jugular veins to trap clots without impeding blood flow

Question 73

IVC Interruption Device

Answer 73

 Recommended for acute PE or proximal VTE of leg with active bleeding, or if anticoagulation contraindicated or ineffective  Complications: air embolism, improper placement, filter migration, perforation of vena cava with retroperitoneal bleeding, clogged filter

Question 74

VTE: Percutaneous endovascular interventional radiology procedures

Answer 74

Percutaneous endovascular interventional radiology procedures are minimally invasive treatments used in the management of Venous Thromboembolism (VTE), including Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE). These procedures are often performed in a hospital setting by interventional radiologists. Mechanical Thrombectomy: This procedure involves the removal of a blood clot using a catheter-based device. The device is guided to the site of the clot, where it physically breaks up and/or removes the clot. Mechanical thrombectomy can be particularly useful in cases of large or life-threatening clots. Pharmacomechanical Devices: These are advanced tools that combine mechanical thrombectomy with localized delivery of thrombolytic agents (drugs that dissolve clots). The device both breaks up the clot mechanically and administers medication directly to the clot site to help dissolve it. Post-Thrombus Extraction: After removing a clot, additional procedures might be necessary to treat underlying issues that contributed to the clot’s formation, such as narrowing of the veins. Angioplasty and/or Stenting: Angioplasty involves the use of a balloon-tipped catheter to open up narrowed or blocked veins. Stenting involves placing a small, wire mesh tube (stent) into the vein to keep it open. These techniques can be used to improve blood flow in veins that have been narrowed or blocked, which is a common issue after a significant DVT. Use with Catheter-Directed Thrombolytic Therapy: These interventional procedures can be used in conjunction with catheter-directed thrombolytic therapy, where a catheter is used to deliver clot-dissolving medication directly to the site of a thrombus. This combination approach can be highly effective in quickly reducing clot burden and alleviating symptoms. Advantages: Percutaneous endovascular procedures are less invasive than traditional open surgery and usually have shorter recovery times. They allow for targeted treatment, which can be more effective and may reduce the risk of complications.  Nursing care: Maintain catheter systems, monitor for bleeding, embolization, and impaired perfusion; and teach VTE prevention

Question 75

Varicose Veins

Answer 75

Superficial veins in legs become dilated and tortuous from retrograde blood flow and  venous pressure  Risk factors: * Family history of venous problems, female, tobacco use, aging, obesity, multiparity, history of VTE, venous obstruction, phlebitis, leg injury, prolonged sitting or standing

Question 76

Varicose Veins Clinical Manifestations

Answer 76

Most common symptoms: heavy, achy feeling or pain after prolonged standing or sitting; relieved by walking or limb elevation * Other: pressure, itchy, burning, tingling, throbbing, or cramp-like sensation  Complications  Most common: superficial venous thrombosis * Other: rupture of varicosities results in bleeding and skin ulcerations

Question 77

Varicose Veins Diagnosis + Treatment

Answer 77

Diagnosis  Examination  Duplex ultrasound  Interprofessional care  Conservative treatment: * Rest with limb elevation * Graduated compression stockings * Leg-strengthening exercises * Weight loss

Question 78

Varicose Veins Drug Therapy

Answer 78

Venoactive drugs * Antioxidants from plant extracts stimulate release of chemicals to strengthen the circulation and reduce inflammation and edema * Not FDA approved; available OTC and as herbal or dietary supplements  Micronized purified flavonoid fraction  Rutosides (horse chestnut seed extract—see Drug Alert)  Proanthocyanidins (apples and grapes)  Ruscus (butcher’s broom)

Question 79

Varicose Veins Interventional + Surgical Therapies

Answer 79

Sclerotherapy—ablates vein by direct injection of sclerosis agent * Complications: residual pigmentation, matting, thrombophlebitis, and ulcers * Wear compression stocking and limit travel  Transcutaneous laser therapy or high-intensity pulsed light therapy * Complications: pain, blistering, hyperpigmentation, and superficial erosions Endovenous ablation—radiofrequency or laser therapy * Complications: bruising, burns, hyperpigmentation, infection, paresthesia, superficial or deep vein thrombosis, and PE * Graduated compression stockings after Interventional and surgical therapies  Traditional: ligation of vein and branches  Ambulatory phlebectomy  Transilluminated powdered phlebectomy * Complications: bleeding, bruising, and infection

Question 80

Varicose Veins Prevention

Answer 80

Avoid prolonged sitting or standing  Maintain ideal weight  Avoid injury  Avoid restrictive clothing  Walk every day

Question 81

Chronic Venous Insufficiency (CVI) and Venous Leg Ulcers

Answer 81

CVI—abnormalities of venous system include edema, skin changes, and venous leg ulcers  Etiology and Pathophysiology  Primary varicose veins and PTS  Ambulatory venous hypertension * Serous fluid and RBC leak results in edema and chronic inflammatory changes * Hemosiderin—brown skin discoloration * Skin is hard, thick, and contracted Chronic Venous Insufficiency (CVI)