Ch 36 Vascular Disorders

Pathophysiology: Plaque formation that occurs in the blood vessels, most commonly in the distal superficial femoral and popliteal arteries. Tissue hypoxia distal to occlusion causes ischemia and necrosis. Compensatory mechanisms include collateral blood vessels, vasodilation, and anaerobic metabolism.
Risk Factors: Hyperlipidemia, hypertension, diabetes mellitus, chronic kidney disease, and smoking.
Clinical Manifestations: A classic sign is Intermittent claudication: pain with walking, relived by resting. More common on the calf.
Other s/s are rest pain, numbness, coldness, muscle atrophy, pale skin, thickened toenails, hairlessness, shiny scaly skin, and pale gray or yellowish ankle ulcers.
Diagnosis: Most inexpensive is Ankle-brachial index, which compares bp at the ankle with the bp at the arm. Also duplex imaging, and angiography are other methods.
Treatment: Lifestyle changes such as, smoking cessation which is a highest priority, exercise (90 min a week) and claudication medications like cilostazol or pentoxifylline that dialate blood vessels and prevent plalets from clumping.

Pathophysiology: usually froms from a thrombus in the heart. It is associated with infective endocarditis, mitral valve disease, atrial fibrillation, cardiomyopathy, or prosthetic valves or atheromatous plaques.
Clinical Manifestations: decreased or absent pusle, absent bp and posible signs of tissue death (necrosis) in the extremities distal to the obsrtuction.
Diagnosis & Management: Diagnostic confirmation via Doppler ultrasound, MRI, or angiography. Emergency medical therapy includes IV anticoagulants (heparin, warfarin), antiplatelets or thrombolytics.

Pathophysiology: condition in where the veins have difficulty sending blood from the extremities back to the heart. Major factors are age, family hsitory, past DVT, obesity, pregnancy, females, long periods of standing/sitting and tall height.
Clinical Manifestations: edema around the legs, pain, leg cramps, brownish skin descolorations (stasis dermatitis) and ulcers.
Management: Leg elevation, compression stockings (not for arterial), endovenous laser or radiofrequency ablation, wound dressings maintaining a moist bed, hyperbaric $O_2$ therapy, and systemic antibiotics for infection.

Pathophysiology: when a thrombus forms in the presence of phlebitis (inflamation of a superficial vein)
Includes superficial vein thrombosis (SVT, commonly in saphenous vein) and deep vein thrombosis (DVT).
Thrombus formation is driven by Virchow's triad: (1) stasis of blood, (2) vessel wall damage, and (3) hypercoagulability (increased tendency of blood to clot).
Clinical Manifestations: SVT presents as a firm, cordlike, warm, red, tender vein. DVT presents with extremity edema, deep warmth, tenderness, and low-grade fever. Pulmonary embolism is a critical complication causing dyspnea, chest pain, and tachycardia.
Diagnosis & Management: Confirmed via duplex ultrasonography, venography, MRI, and D-dimer blood tests. Managed with IV/oral anticoagulants, thrombolytics, vena cava filters, leg elevation, and warm moist soaks (massage is strictly contraindicated).

Pathophysiology: Dilated, tortuous superficial veins caused by incompetent valves and hereditary vein weakness, exacerbated by aging, pregnancy, obesity, and prolonged standing.
Clinical Manifestations: Oversized purplish veins, dull aching, leg heaviness, nocturnal muscle cramps, ankle edema, and risk of postphlebitic syndrome.
Management: Weight reduction, avoiding prolonged standing/sitting/leg crossing, compression stockings, sclerotherapy, laser therapy, endovenous ablation, or surgical ligation and stripping.
Hourse chestnut can also be used to improve the tone of the veins, making them less fragile and permeable.

Pathophysiology: Non-atherosclerotic, inflammatory thrombotic disorder affecting small blood vessels in hands and feet, occurring almost exclusively in tobacco users around an average onset age of $35$ .
Clinical Manifestations: Intermittent claudication, burning or tingling rest pain, cold digits, cold sensitivity, pale/red/bluish skin, ulcerations, and gangrene.
Management: Absolute smoking cessation is essential. Supportive care includes iloprost, sympathectomy, vasodilators, analgesics, and amputation if gangrene occurs ( $40\%$ amputation rate among persistent tobacco users).

Pathophysiology: Intermittent arteriolar vasospasms affecting the digits. Primary (Raynaud disease) has no known cause; Secondary (Raynaud phenomenon) is secondary to connective tissue disorders (such as lupus, scleroderma, rheumatoid arthritis).
Clinical Manifestations: Cold hands, numbness, tingling, and a triphasic color sequence during spasms: pallor (vasoconstriction) $\rightarrow$ cyanosis (hypoxia) $\rightarrow$ redness (rubor/hyperemia upon resolution).
Management: Cold avoidance, stress management, smoking cessation, warm mittens/socks, calcium-channel blockers, and alpha-blockers. Direct hot water application is contraindicated due to burn risk from sensory loss.

Aortic Aneurysms: Permanent localized dilatation of the aorta (abdominal aortic aneurysm [AAA] or thoracic aortic aneurysm [TAA]), primarily caused by atherosclerosis, hypertension, or genetic conditions (Marfan syndrome, Ehlers-Danlos syndrome).
- Manifestations & Surgical Repair: AAA presents as a pulsating abdominal mass left of the umbilicus; TAA can cause deep chest pain, hoarseness, dysphagia, or superior vena cava compression. Aneurysms $< 5\,cm$ are monitored; larger defects undergo open graft repair, TEVAR, or EVAR.
Aortic Dissection: Intimal tear allowing blood to separate the aortic wall layers. Type A involves the ascending aorta (causing abrupt excruciating anterior chest pain; surgical emergency); Type B involves the descending aorta (causing back/abdominal pain).
- Management: Preoperative semi-Fowler's positioning, sedatives, opioids, and strict antihypertensive therapy to reduce aortic wall stress.

Pathophysiology: Acute bacterial infection and inflammation of lymphatic channels, typically entering via skin wounds, with potential to progress to systemic sepsis if untreated.
Clinical Manifestations: Red streaks tracking up the extremity along lymphatic pathways, tender and enlarged regional lymph nodes (groin, axilla, cervical), fever, weakness, and potential abscess formation.
Management: Systemic IV antimicrobials, limb elevation, warm wet dressings, elastic support hose, and incision and drainage of abscesses.