Microangiopathy of cutaneous blood and lymphatic capillaries in chronic venous insufficiency (CVI).

The severity of microangiopathy in patients with chronic venous insufficiency (CVI) determines the extent of the trophic disturbances of the skin. Resulting from valvular incompetence of deep and/or perforating veins and the accompanying venous outflow obstruction caused by deep venous thrombosis (DVT), the increased ambulatory venous pressure heads are transmitted retrograde into the microvasculature of the skin at the ankle region. In the present study, we have assessed the changes in the cutaneous microvasculature by dynamic fluorescence video microscopy, fluorescence microlymphography, and transcutaneous oxygen tension (tcPO2) measurements. In mild forms of CVI, capillary density, morphologic characteristics, and tcPO2 are still normal. Fluorescent light intensity is, however, significantly increased, indicating an increased transcapillary diffusion of sodium fluorescein (NaF) as a marker for enhanced leakage of the capillaries in the early stage of the disease. The pericapillary halo diameters are significantly enlarged, compared to controls (p < 0.01). In the severe stages of CVI and in patients with venous ulcers, capillary thromboses, probably caused by endothelium-blood cell interactions, may lead to a reduced capillary density. In order to enlarge the exchange surface area, the remaining skin capillaries become tortuous (capillary tufts). Parallel to the reduced capillary number, tcPO2 decreases and can be extremely low at the ulcer rim or at white atrophy spots. Fibrin cuffs are not a specific finding for venous ulceration and do not significantly impair oxygen diffusion. Fluorescence microlymphography permits visualization of the lymphatic capillaries of the superficial skin. In severe stages of CVI, the lymphatic capillary network at the medial ankle area is destroyed, and the remaining lymphatic capillary fragments have an increased permeability to FITC-dextran with a molecular weight of 150,000. These findings demonstrate a special lymphatic microangiopathy in CVI, suggesting an additional lymphatic component in the edema formation

Lymphatic microangiopathy of the skin in systemic sclerosis

METHODS: The cutaneous capillary lymphatic system in patients with systemic sclerosis was investigated using fluorescence microlymphography. The distal upper limbs of 16 healthy controls (mean age 62.3+/-13.1 yr) and 16 patients with systemic sclerosis (mean age 58.9+/-13.6 yr) were examined and the following parameters were evaluated: (a) single lymphatic capillaries; (b) lymphatic capillary network and cutaneous backflow; (c) extension of the stained lymphatics; (d) diameter of single lymphatic capillaries. RESULTS: At the finger level, lymphatic capillaries were lacking in five patients, while they were present in all controls (P < 0.05). Extension of the stained lymphatics was increased in 11 patients (8.1+/-6.0 mm) compared to the 16 healthy controls (2.0+/-1.2 mm) (P < 0.0001). Cutaneous backflow was observed in three patients (P < 0.05). At the hand level, lymphatic network extension was significantly different between patients (3.8+/-2.4 mm) and controls (1.2+/-0.8 mm) (P < 0.01); however, no significant differences were found at the forearm level. CONCLUSION: Lesional skin in patients with systemic sclerosis exhibits evidence of lymphatic microangiopath

Inflammatory aneurysm of the splenic artery

The case of a middle-aged man is described, who was admitted because of intermittent back pain and a high sedimentation rate. Abdominal sonography and arteriography showed a large aneurysm of the splenic artery, but failed to recognize the aneurysm as of inflammatory origin. However, the inflammatory nature of the aneurysm was evident on computer tomography scan. Intraoperatively the inflammatory origin of the aneurysm was confirmed. A saphenous vein graft was implanted and marsupialization of the aneurysm performed. Histology could clearly verify the diagnosis of an inflammatory aneurysm. This report indicates the possibility of inflammatory changes occurring in connection with a visceral artery rather than solely with the abdominal aorta