Kei Ishimaru

Superficial Thrombophlebitis of the Lower Limbs in Patients with Varicose Veins

AbstractPurpose. This study reviews 51 consecutive patients with superficial thrombophlebitis (STP) among 710 patients treated for varicose veins in our department. Methods. An assessment was made of various factors involved. Results. Of these 51 patients, 21 (41.1%) had systemic disorders, including 4 (7.8%) with malignant diseases. Six patients (11.8%) had deep vein thrombosis (DVT) and five (9.8%) had pulmonary embolism (PE). All of the patients with DVT and/or PE had a thrombus in either the greater saphenous vein or the lesser saphenous vein; however, none of the patients with STP and a thrombus in the distal saphenous branch had either DVT or PE. The levels of coagulofibrinolytic markers such as fibrin degradation product-D dimer, plasmin α2 plasmin inhibitor complex, and thrombin antithrombin III complex were elevated in patients with STP or DVT, compared with those with varicose veins only. The level of C-reactive protein (CRP) was also elevated in the patients with STP or DVT. These findings indicate that STP is not necessarily a localized disease, but may be a symptom of systemic disease. In addition to duplex scanning, the measurement of coagulofibrinolytic markers as well as CRP may be useful for detecting STP and/or DVT prior to the treatment of varicose veins.

Pancreatic proteases and inflammatory mediators in peritoneal fluid during splanchnic arterial occlusion and reperfusion.

Pancreatic enzymes in the ischemic intestine are involved in the production of in vivo inflammatory mediators. These mediators stimulate cells in the cardiovascular system during shock and initiate multiorgan failure. An important aspect that controls the extent of the inflammation is the dispersion of these mediators from the ischemic intestine. In the past, two pathways for dispersion of these inflammatory mediators have been identified, absorption into the intestinal venous circulation and uptake into the lymphatics. We hypothesize here that the inflammatory mediators produced by pancreatic digestive enzymes in the lumen of the intestine may also be released directly into the peritoneal space. To assess the presence of inflammatory mediators in the peritoneal cavity in response to splanchnic arterial occlusion (90 min) and reperfusion (SAO shock), we measured the ability of fluid collected from this cavity to activate naïve donor granulocytes. After SAO in control rats, peritoneal lavage fluid caused activation of naïve donor granulocytes when tested in vitro. In contrast, when the lumen of the small intestine was flushed with a broad-acting pancreatic enzyme inhibitor (6-amidino-2-naphtyl p-guanidinobenzoate dimethanesulfate), the fluid no longer caused leukocyte activation. Reduction of the levels of inflammatory mediators in the peritoneal fluid was associated with an attenuation in the fall of blood pressure after SAO shock. These results indicate that the inflammatory mediators, which are produced by pancreatic digestive enzymes, can be absorbed directly into the systemic circulation via a transperitoneal route and play a part in the development of multiorgan failure.

Automated Bedside Measurement of Penile Blood Flow Using Pulse-Volume Plethysmography

PurposeTo evaluate the efficiency of the form PWV/ABI (pulse wave velocity/ankle brachial pressure index) for measuring penile blood pressure (PBP) and the penile brachial pressure index (PBI).MethodsWe measured PBP and the PBI using both form PWV/ABI and Doppler ultrasonography in 40 men with surgical disorders.ResultsBy using pulse-volume recording, the form PWV/ABI can simultaneously measure PBP and bilateral brachial artery pressure, and calculate the PBI automatically. The data obtained showed strong correlations with those obtained by the conventional Doppler ultrasound technique. Moreover, measurements were completed within 5 min at the bedside and the data were stored in the devices memory.ConclusionThe form PWV/ABI is a useful tool for assessing pelvic hemodynamics and diagnosing vasculogenic impotence.

Videodensitometric blood flow analysis of abdominal aortic aneurysm and intravascular coagulation

OBJECTIVE We investigated the relation between flow pattern in abdominal aortic aneurysm (AAA) and intravascular coagulopathy characterized by increased fibrin degradation product d-dimer (FDP-DD) or thrombin-antithrombin complex (TAT). Materials and methods The ratio of AAA maximum endoluminal diameter (diameter of flow channel) (n = 23) to diameter of the aorta between the superior mesenteric and renal arteries (R ratio) was measured with three-dimensional computed tomography angiography. Digital subtraction angiography was performed with 20 mL (10 mL/s) of contrast agent injected from the suprarenal portion of the abdominal aorta. The duration between the time when average gray scale in the AAA reached maximum and average region of interest gray scale decreased to half-maximum (bolus transit time in AAA [BTT(AAA)]) was calculated. RESULTS Single correlation coefficient with statistic significance was detected between R ratio and BTT(AAA) (BTT(AAA) = 2.54 x R ratio + 3.65; r(2) =.30; P =.042). Among the three-dimensional morphologic and videodensitometric variants, BTT(AAA) was the most determinant factor associated with FDP-DD (FDP-DD = - 8.647 + 2.029 x BTT(AAA); r(2) =.448; P =.005). The most efficient predictors for TAT were maximum AAA endoluminal diameter (R(endomax)) and BTT(AAA) (TAT = - 14.007 + 2.102 x BTT(AAA) + 0.296 x R(endomax), r(2) =.360; P =.0069). CONCLUSIONS Our findings suggest a close link between abnormal flow pattern in AAA and activation of the coagulation-fibrinolysis system. Videodensitometric blood flow analysis can be useful in investigation of the pathophysiology of phenomena related to abnormal flow field in AAA.