Module 2: Vascular Disorders Flashcards
Peripheral Artery Disease (PAD)
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
Etiology and Pathophysiology of PAD
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
Risk Factors for PAD
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
Clinical Manifestations of PAD
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
Complications of PAD
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
PAD Diagnostic Studies
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
Nutrition Therapy for PAD
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
Leg with Critical Limb Ischemia
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.
Interventional Radiology Procedures
Catheter Based Procedures
Catheterization Lab instead of OR
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)
Interventional Radiology Procedures
Catheter Based Procedures
Percutaneous transluminal angioplasty (PTA)
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
Interventional Radiology Procedures
Catheter Based Procedures
Atherectomy
Removal of obstructing plaque
Performed using a cutting disc, laser, or rotating
diamond tip
Interventional Radiology Procedures
Catheter Based Procedures
Cryoplasty
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
Interprofessional Care
Surgical Therapy
Peripheral Artery Bypass Surgery
-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
Femoral-popliteal Bypass Grafts (picture)
Interprofessional Care
Surgical Therapy
-Endarterectomy
-Patch graft angioplasty
-Amputation
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
Nursing Care for PAD
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
Acute Arterial Ischemic Disorders
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
Acute Arterial Ischemic Disorders
6Ps
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
Acute Arterial Ischemic Disorders
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
Thromboangiitis Obliterans
Buerger’s Disease
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
Thromboangiitis Obliterans
Buerger’s Disease
Phases
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
Thromboangiitis Obliterans
Buerger’s Disease
Diagnosis + Treatment
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
Raynaud’s Phenomenon
-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
Raynaud’s Nursing Care
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
Raynaud’s Drug Therapy
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
Aortic Aneurism
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
Aortic Aneurysms
Etiology and Pathophysiology
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
Aortic Aneurysms
Genetic Link
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
Classification - True Aneurism
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.
Classification - False Aneurism
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
Aortic Aneurism
Clinical Manifestations
Thoracic aortic aneurysm (TAA)
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
Aortic Aneurism Complications - Rupture
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.
Rupture in Thoracic or Abdominal Cavity
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.
Aortic Aneurism Diagnostic Studies
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
Care for Aortic Aneurism
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
Surgery for Aortic Aneurism
Surgical therapy
Preop—elective repair
* Hydration
* Stabilize electrolytes, coagulation, and hematocrit
If ruptures, emergent surgical intervention required
* 90% mortality with ruptured AAAs
Open Aneurism Repair (OAR)
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
Endovascular Graft Procedure
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
Signs of Aneurism Rupture
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
Aortic Dissection
Not a type of aneurysm
Result of a false lumen through which blood flows
Between intima and media of arterial wall
Aortic Dissection
Classification 1 and 2
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
Nontraumatic Aortic Dissection
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
Acute Type A Aortic Dissection
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”
Acute Type B Aortic Dissection
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”
Dissection Pain vs MI Pain
-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
Dissection Clinical Manifestations
-Subclavian artery
BP and arterial pulses different between arms
-Aortic progression
Decreased tissue perfusion to abdominal organs and lower extremities
Dissection Complications: Cardiac Temponade
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
Dissection Complications: Rupture
Aorta may rupture resulting in hemorrhage in
mediastinal, pleural, or abdominal cavities
Results in exsanguination and death
Dissection Complications: Occlusion of arterial supply to vital organs
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.
Aortic Dissection Diagnostic Studies
H & P
ECG
Chest x-ray
3-D CT scan
MRI
TEE - Transesophageal echocardiography
CT scan
Care Goals After Aortic Dissection
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
Endovascular Dissection Repair - Post Op Care
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
Aortic Dissection Nursing Management
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
Phlebitis
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
Venous Thrombosis
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.
Venous Thrombosis Etiology
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
Venous Stasis
Dysfunctional valves
Inactive extremity muscles
At risk
* Obese
* Pregnant
* Chronic HF or atrial fibrillation
* Traveling on long trips without exercise
* Prolonged surgery
* Prolonged immobility
Venous Stasis
Endothelial Damage
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
Venous Stasis
Hypercoagulability of Blood
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
VTE (venous thromboembolism) Pathophysiology
-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
Superficial Vein Thrombosis
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
VTE (deep) Manifestations
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
VTE Complications: PTS
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
VTE Diagnostic Studies
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
VTE Hospital Interventions
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)
VTE: Early.+ Aggressive Mobilization
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
VTE: Compression Stockings
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
VTE: Drug Therapy
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
Anticoagulant Therapy for VTE Prophylaxis
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.
Anticoagulation Therapy for VTE Treatment
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.
Thrombolytic Therapy for VTE Treatment
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.
VTE: Surgical + Interventional Radiology Therapies
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
IVC Interruption Device
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
VTE: Percutaneous endovascular interventional radiology procedures
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
Varicose Veins
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
Varicose Veins Clinical Manifestations
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
Varicose Veins Diagnosis + Treatment
Diagnosis
Examination
Duplex ultrasound
Interprofessional care
Conservative treatment:
* Rest with limb elevation
* Graduated compression stockings
* Leg-strengthening exercises
* Weight loss
Varicose Veins Drug Therapy
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)
Varicose Veins Interventional + Surgical Therapies
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
Varicose Veins Prevention
Avoid prolonged sitting or standing
Maintain ideal weight
Avoid injury
Avoid restrictive clothing
Walk every day
Chronic Venous Insufficiency (CVI)
and Venous Leg Ulcers
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)
