- Clinical Findings & Diagnostic Criteria
- Risk Factors
- Etiology
- Pathology
- Epidemiology
- Management & Treatment
- Prevention
- Complications
- Prognosis
- Research Frontier
- Clinical Case Studies
- Study Questions
Symptoms
Signs
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- Most frequently it is a result of valvular dysfunction.
- Valvular dysfunction may be primary or secondary (result of trauma, deep venous thrombosis [DVT], or May-Thurner syndrome).
- It may affect deep system (i.e., femoral veins), superficial system (i.e., saphenous vein), or both.
- The superficial system is involved in 88% of cases either alone or in conjunction with the deep system.
- Dysfunction leads to loss of compartmentalization of veins, leading to distention and increased pressure (Figures 52-1 and 52-2).
Varicose veins of posterior calf without hemosiderin deposition, lipodermatosclerosis, or ulceration. (Courtesy of Maureen K. Sheehan, MD.)- Increased pressure in veins is transmitted to microvasculature leading to basement membrane thickening, increased capillary elongation, and visual skin changes (Figures 52-3 and 52-4).
Chronic Venous Insufficiency
Results from prior DVT or venous valvular incompetence and manifests as chronic dull ache in leg that worsens with prolonged standing, edema, and superficial varicosities.
May lead to erythema, hyperpigmentation, and recurrent cellulitis; ulcers may appear at medial and lateral malleoli.
Chronic exposure to elevated venous pressure by the postcapillary venules in the legs leads to leakage of fibrinogen and growth factors into the interstitial space, leukocyte aggregation and activation, and obliteration of the cutaneous lymphatic network. These changes account for the brawny, fibrotic skin changes observed in patients with chronic venous insufficiency, and the predisposition toward skin ulceration, particularly in the medial malleolar area.
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Treatment includes graduated compression stockings and leg elevation.
Complications of Injecting Drug Use
- Local problems—Abscess (Figures 240-2
and 240-3; Abscess), cellulitis, septic thrombophlebitis, local induration, necrotizing fasciitis, gas gangrene, pyomyositis, mycotic aneurysm, compartmental syndromes, and foreign bodies (e.g., broken needle parts) in local areas.2A 32-year-old woman with type 1 diabetes developed large abscesses all over her body secondary to injection of cocaine and heroin. Her back shows the large scars remaining after the healing of these abscesses. (Courtesy of Richard P. Usatine, MD.)
- IDUs are at higher risk of getting methicillin-resistant Staphylococcus aureus(MRSA) skin infections that the patient may think are spider bites (Figure 240-4).
- Some IDUs give up trying to inject into their veins and put the cocaine directly into the skin. This causes local skin necrosis that produces round atrophic scars (Figure 240-5).
- IDUs are at risk for contracting systemic infections, including HIV and hepatitis B or hepatitis C.
- Injecting drug users are at risk of endocarditis, osteomyelitis (Figures 240-6and 240-7), and an abscess of the epidural region. These infections can lead to long hospitalizations for intravenous antibiotics. The endocarditis that occurs in IDUs involves the right-sided heart valves (see Chapter 50, Bacterial Endocarditis).2 They are also at risk of septic emboli to the lungs, group A β-hemolytic streptococcal septicemia, septic arthritis, and candidal and other fungal infections.
Venous insufficiency, or improperly functioning valves in the venous system, can lead to variety of symptoms, including, but not limited to, heaviness and/or swelling in the legs with prolonged standing, leg fatigue or aching, bleeding from leg varices, skin changes, and ulcerations.
Venous stasis ulcer in the typical location around the medial malleolus. (Courtesy of Maureen K. Sheehan, MD.)
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Content 11
Question 1 of 1
A 42-year-old African-American man has been diagnosed with hypertension for the past 10 years and treated with medication. One morning, he is found unresponsive by his wife. He is taken to the emergency department and pronounced dead by the physician. An autopsy revealed cardiac hypertrophy and a narrowing of the aorta just distal to the ligamentum arteriosum, with dilation of the intercostal artery's ostia. How could the death have possibly been prevented?