Arterial and Venous Diseases Session 5 PDF
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Shahid Sadoughi University of Medical Sciences
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This document provides an overview of arterial and venous diseases, focusing on peripheral vascular diseases, aortic diseases, aortic aneurysms, and types of aortic aneurysms. It discusses structural changes in vessel walls, narrowing of the vascular lumen, and spasms of smooth vascular muscles as potential causes. The document details the aspects of aortic aneurysms, including size, growth rate, and risk of rupture.
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**Peripheral Vascular Diseases**: This term encompasses various pathological conditions affecting arteries, veins, and lymphatic vessels. Peripheral vascular diseases arise from processes that can be categorized into three groups: 1. **Structural Changes in Vessel Walls**: Due to degenerative condi...
**Peripheral Vascular Diseases**: This term encompasses various pathological conditions affecting arteries, veins, and lymphatic vessels. Peripheral vascular diseases arise from processes that can be categorized into three groups: 1. **Structural Changes in Vessel Walls**: Due to degenerative conditions, infections, or inflammation, leading to dilation, aneurysm, dissection, or rupture. 2. **Narrowing of Vascular Lumen**: Resulting from atherosclerosis, thrombosis, or inflammation. 3. **Spasms of Smooth Vascular Muscles**. **Aortic Diseases**: The aorta is the largest vessel in the vascular system. In adults, its diameter at the base of the heart is about 3 cm. The ascending aorta, 5-6 cm long, leads to the aortic arch, from which three main branches emerge: the brachiocephalic trunk (branching into the right common carotid and right subclavian arteries), the left common carotid, and the left subclavian arteries. As the descending aorta continues from the arch, its diameter in healthy adults decreases to 2-2.5 cm. When the aorta pierces the diaphragm, it becomes the abdominal aorta, supplying visceral arteries before dividing into the left and right common iliac arteries, which supply the pelvis and lower limbs. **Aortic Aneurysm**: An aortic aneurysm is an abnormal localized dilation of the artery. In the aorta, aneurysms are distinct from ectasia, which is a generalized increase in the aorta's diameter. Aneurysm is localized, while ectasia is diffuse. The term “aneurysm” is used when a part of the aorta’s diameter increases by at least 50% compared to normal, approximately 4.5 cm. **Types of Aortic Aneurysm**: 1. **True Aneurysm**: Involves dilation of all three layers of the aorta, creating a large bulge in the vessel wall. True aneurysms can be fusiform or saccular: - **Fusiform Aneurysm**: The more common type, involving symmetrical dilation of the entire vessel circumference. - **Saccular Aneurysm**: A localized outpouching affecting only part of the vessel circumference. 2. **Pseudoaneurysm (False Aneurysm)**: A limited tear in the vessel wall occurs when blood leaks from the vessel lumen through a hole in the intimal and medial layers, contained by a layer of adventitia or organized perivascular thrombus. The aorta Is susceptible to mechanical damage due to constant exposure to high pulsatile pressure and stress. The prevalence of elastin in its wall (2:1 over collagen) allows the aorta to expand during systole and propel blood forward during diastole. As people age, the elastic component of the aorta and its branches deteriorates, and collagen prominence stiffens the arteries. Thus, systolic blood pressure (SBP) tends to increase with age because less energy is absorbed by the aorta during left ventricular contraction. **Degeneration, fibrillin gene disorder causing imbalance of elastin and collagen**: Typically involves the ascending aorta. Commonly seen with infections like Salmonella, Staph, and Strep. **Clinical Presentation and Diagnosis**: - Most aneurysms are asymptomatic, but some patients, especially those with abdominal aortic aneurysms, might notice a pulsating mass. - Symptoms related to compression of adjacent structures by an expanding aneurysm can also appear. - **Thoracic Aortic Aneurysm**: May compress the trachea or main bronchus, leading to cough, dyspnea, or pneumonia. - **Esophageal Compression**: Can cause dysphagia. - **Recurrent Laryngeal Nerve Involvement**: May result in hoarseness. - **Ascending Aortic Aneurysm**: Can dilate the aortic ring, causing aortic regurgitation and symptoms of congestive heart failure. - **Abdominal Aortic Aneurysm**: May cause abdominal or back pain or nonspecific gastrointestinal symptoms. - Aortic aneurysms are often suspected when vascular dilation is observed on chest or abdominal radiographs, especially if the wall is calcified. Abdominal aortic aneurysms or large peripheral arteries may also be detected through careful palpation during a physical exam. - Definitive diagnosis is confirmed by ultrasound, contrast-enhanced computed tomography (CT), or magnetic resonance imaging (MRI). **Most Devastating Outcome**: - **Rupture**: Can be fatal. Aneurysms might leak slowly or rupture suddenly, causing blood loss and hypotension. - **Thoracic Aortic Aneurysm**: May rupture into the pleural space, mediastinum, or bronchus. - **Abdominal Aortic Aneurysm**: May rupture into the retroperitoneal space or abdominal cavity or erode into the intestines, leading to massive gastrointestinal bleeding. **Key Aspects of Aneurysms**: - **Size and Growth Rate**: Risk of rupture correlates with the aneurysm size, as predicted by Laplace’s law (wall tension is proportional to the product of pressure and radius). The average growth rate for thoracic and abdominal aortic aneurysms is 0.1 and 0.4 cm per year, respectively. - **Screening**: The US Preventive Services Task Force (USPSTF) recommends one-time ultrasound screening for men aged 65 to 75 who have ever smoked to identify abdominal aortic aneurysms among those at highest risk. Aortic aneurysms clearly demand careful monitoring and timely intervention. Is there anything else you’d like to explore? **Treatment**: **Aortic Aneurysm Treatment**: - Treatment depends on the aneurysm size, patient’s overall medical condition, and comorbidities. - **Surgical Intervention**: Recommended for ascending aortic aneurysms larger than 5.5 cm. - **Follow-up**: - **5-5.5 cm**: Every 6 months with ultrasound or CT angiography. - **4-5 cm**: Annually with ultrasound. - **3-4 cm**: Every 2 years with ultrasound. - **Patients with Marfan and Loeys-Dietz Syndromes**: Higher risk of rupture. Surgical repair is considered if the diameter exceeds 5 cm in Marfan and 4.5 cm in Loeys-Dietz. - Smaller aneurysms growing more than 1.0 cm per year also warrant surgical consideration. **Medical Management**: - **Risk Reduction**: Quit smoking, treat hypertension. - **Medication**: Given that abdominal aortic aneurysms are comparable to atherosclerotic coronary artery disease, treatment with aspirin and statins is generally recommended. - **β-blockers and Angiotensin II Receptor Antagonists**: Reduce blood pressure and inhibit TGF-β, potentially slowing the expansion of thoracic aortic aneurysms in Marfan syndrome patients. Their efficacy for other causes or types of aneurysms is uncertain. **Aortic Dissection**: - **Definition**: A life-threatening condition where blood enters the vessel wall through an intimal tear, spreading along the artery. - **Other Acute Syndromes**: Intramural hematoma, penetrating aortic ulcer, and aortic rupture. **Etiology, Pathogenesis, and Classification**: - **Aortic Dissection**: Arises from a peripheral or transverse tear in the intimal layer, allowing blood to enter the media layer under systemic pressure, spreading along the muscular plane. - **Potential Origin**: Rupture of vasa vasorum with subsequent bleeding into the media, forming an arterial wall hematoma that eventually ruptures through the intima into the vessel lumen. - **Prevalence**: More common in the sixth and seventh decades of life, predominantly affecting men. Over two-thirds have a history of hypertension. - **Sites**: - **Thoracic Aorta**: 65% - **Descending Thoracic Aorta**: 20% - **Aortic Arch**: 10% - **Abdominal Aorta**: 5% - **Stanford Classification**: - **Type A (Proximal Dissection)**: Involves the ascending aorta and/or aortic arch, regardless of the initial tear location. - **Type B (Distal Dissection)**: Involves only the descending thoracic and abdominal aorta. - **Acute vs. Chronic Dissection**: Acute dissection presents symptoms within 2 weeks. **Clinical Diagnosis**: - **Aortic Dissection**: The most common symptom is sudden, severe, tearing pain in the chest (typically Type A dissections) or between the shoulder blades (Type B dissections). While painless dissection is rare, it occurs in about 6.4% of cases. High blood pressure is often noted, either as an underlying cause or resulting from the sympathetic nervous system’s response to severe pain or reduced renal blood flow activating the renin-angiotensin system. **Clinical Presentation and Diagnosis**: Diagnosis of aortic dissection should not be delayed as it can rapidly lead to catastrophic complications or death. Confirmatory imaging techniques include contrast-enhanced CT, transesophageal echocardiography (TEE), MR angiography, and contrast angiography. In emergencies, CT or TEE can be obtained quickly and provide high sensitivity and specificity for diagnosis. **Treatment**: - The aim of acute treatment is to prevent the progression of the dissection channel. Acute aortic dissection requires immediate medical management to lower blood pressure (target systolic pressure 100-120 mmHg) and reduce the force of left ventricular contraction, thereby minimizing aortic wall shear stress. Useful pharmacological agents include beta-blockers (to reduce contraction force and heart rate, and lower blood pressure) and vasodilators like sodium nitroprusside (for rapid blood pressure reduction). - **Surgical Repair**: Early surgical correction improves outcomes in proximal dissections (Type A). Surgery involves repairing the intimal tear, suturing the edges of the false channel, and, if necessary, placing an artificial aortic graft. - **Type B Dissections**: Initially managed with aggressive medical therapy. Surgical intervention, such as stenting, may be required for complications. **Peripheral Arterial Disease (PAD)**: - **Definition**: PAD is defined by the presence of a flow-limiting lesion in an artery that supplies blood to the limbs. The main causes of such arterial narrowing or blockage are atherosclerosis (most common), thromboembolism, and vasculitis. - **Clinical Manifestations**: Symptoms result from reduced perfusion to the affected limb. **Etiology and Pathogenesis**: - The most common cause of PAD is atherosclerosis, affecting about 4% of individuals over 40 and 15-20% of those over 70. Approximately 40% of PAD patients have significant coronary artery disease (CAD). *Systemic Atherosclerosis**: - Patients with PAD (Peripheral Arterial Disease) face a cardiovascular mortality risk that is 2-5 times higher compared to those without the condition. - The degree of blood flow reduction is closely related to the extent of arterial narrowing, the length of the stenosis, and blood viscosity. Vessel diameter has the greatest impact. **Summary**: - Atherosclerotic lesions create narrowings in peripheral arteries, limiting blood flow to the affected limb. - Mechanisms typically compensating for increased demand, such as the release of endogenous vasodilators during exercise and the recruitment of microvessels, fail due to endothelial dysfunction and reduced flow velocity. Consequently, increased oxygen demand is not met, leading to limb ischemia. - Adaptations to ischemia involve changes in muscle fiber metabolism and muscle fiber loss. These physical and biochemical changes weaken the lower limb, causing ischemic discomfort during exercise. - Severe peripheral atherosclerosis can reduce limb blood flow so much that it cannot meet resting metabolic needs, resulting in critical limb ischemia that may lead to tissue necrosis and gangrene, posing a threat to limb viability. **Clinical Presentation and Diagnosis**: - PAD predominantly affects the lower limbs, impacting the iliac, femoral, popliteal, and tibio- peroneal arteries. Therefore, patients with PAD may experience discomfort in the hips, thighs, or calves that is exacerbated by walking and relieved by rest, a classic symptom known as intermittent claudication. - However, intermittent claudication occurs in only about one-third of PAD patients. Another third present with atypical symptoms, and the remaining third are asymptomatic. - In severe PAD, patients may experience pain at rest, usually affecting the feet or toes. Chronic reduced blood flow predisposes the limb to ulcers, infections, and skin necrosis, which may lead to amputation. Smokers and diabetics are at higher risk for these complications. - **Intermittent Claudication**: Characterized by increased pain with activity and pain relief with rest. Powerful information. Anything more specific you’d like to translate or expand upon? **Foot Ulcers**: - **Figure A**: An ulcer affecting the foot in a patient with diabetes and peripheral artery disease (PAD). Caused by arterial occlusion, typically dry and pale. - **Figure B**: Venous insufficiency ulcer near the right inner ankle (medial malleolus). Note the venous stasis pigmentation around the ulcer. Caused by venous insufficiency, typically moist and pigmented, often on the medial or lateral malleolus. **Key Points**: - The location of symptoms is always one segment below the site of narrowing. If the narrowing is in the aorta and iliac arteries, pain is felt in the pelvis. If in the femoral artery, pain is in the calf. If in the subclavian artery, pain is in the arm. **Physical Examination**: - Given the diversity of symptoms in PAD patients, precise physical examination is crucial. Palpate the femoral, popliteal, and pedal pulses symmetrically. Pulse ratings: 0 (absent), 1 (diminished), 2 (normal). - **Bruits**: Audible turbulence sounds over areas of turbulent blood flow may be heard in the abdomen (due to narrowing of mesenteric or renal arteries) or over iliac, femoral, or subclavian artery stenosis. - **Severe Chronic Ischemia**: Leads to muscle atrophy, pallor, cyanotic discoloration, hair loss, and sometimes gangrene and necrosis of the foot and toes. **Spectrum of PAD Symptoms**: 1. Asymptomatic 2. Intermittent Claudication 3. Rest Pain Ischemia 4. Ulcers and Necrosis **Diagnostic Methods**: - **Ankle-Brachial Index (ABI)**: Measures the ratio of the highest systolic pressure at the ankle (anterior or posterior tibial artery) to the systolic pressure at the brachial artery. For ABI measurement, the patient should lie down for 10 minutes, with head and heels fully supported. A Doppler ultrasound probe detects flow in the brachial, posterior tibial (PT), and dorsalis pedis (DP) arteries. - **Segmental Systolic Pressure Measurement** - **Pulse Volume Recording** - **Duplex Ultrasonography** - **MR Angiography** - **CT Angiography or Contrast Intra-arterial Angiography**: Most accurate. ABI Ranges**: - **Normal**: Between 1.0 and 1.4 - **Borderline**: Between 0.9 and 1.0 (requires further evaluation) - **Mild**: 0.7 to 0.9 - **Moderate**: 0.4 to 0.7 - **Severe**: Less than 0.4 **Treatment**: - **Lifestyle Modifications**: Smoking cessation, managing diabetes, and controlling hypertension. - **Atherosclerosis Risk Factor Modification**: - Platelet inhibitors such as aspirin and clopidogrel. - Rivaroxaban (an oral anticoagulant that inhibits factor Xa), at a low dose combined with aspirin, can reduce cardiovascular and limb events compared to aspirin alone, though it also increases bleeding risk. - **Specific PAD Treatments**: - Supportive foot care to prevent trauma and ulcers. - Regular exercise, especially walking. - Medications sometimes help treat claudication. For example, **cilostazol**, a selective phosphodiesterase inhibitor, increases cyclic adenosine monophosphate (cAMP), has vasodilatory and platelet-inhibiting properties, and has been shown to improve exercise capacity in PAD patients. - **Mechanical Revascularization**: Indicated when medication therapy for disabling claudication is unsuccessful and as the first-line treatment in cases of critical limb ischemia.