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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors recently treated three patients showing rather marked complications following sclerosing injections for varicose veins. In the first case, the intra-arterial injection brought about a tissular necrosis in the form of a distal-based triangle. The preservative treatment, undertaken 4 weeks after the injection, did not make it possible to save three toes, that had to be amputated. The second patient was sent to use after an injection in the posterior tibial artery. Acute ischemia was treated on an emergency basis with a lumbar sympathectomy. I believe that the approach we took allowed us to cure the trophic problems and to loose only one small phalanx. The third case reported on concerns a patient brought to us in a state of shock after a massive pulmonary embolism. She had been given a sclerosing injection in a large varicose vein of the leg 48 hours previously. The leg had rapidly increased in volume and was apparently the site of a deep veinous thrombosis.
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PMID:[Complications of sclerotherapy]. 48 71

The case of a 75 year old white male, with severe ischemia of the left lower limb and gangrene of its fifth digit, is presented. Because of early post-operative thrombosis after insertion of an autogenous composite femoro-popliteal venous by-pass graft and recurrence of symptoms, a fresh frozen human varicose vein allograft procedure was performed. A pseudo-aneurism which occurred along the graft on the 13th postoperative day was successfully treated by segmental excision with "end-to-end" reconstruction of the allograft itself. This was followed by plastic reconstruction of his foot with primary healing and complete disappearance of symptoms. The patient is now eight months post- op with excellent functional result. Only twenty two similar cases were gathered from the literature. All problems associated with allograft transplantation of fresh and frozen veins are discussed. This case further supports the facts that bloodgroup incompatibility is not a major problem and that reinterventions on such grafts are feasable.
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PMID:[On frozen vena saphena magna as an allograft in peripheral vascular surgery. Report of a case]. 111 77

The balance between prostacyclin and thromboxane has been suggested to be of great importance for the maintenance of patency in veins. In order to investigate prostacyclin and thromboxane release, segments from the human saphenous veins were investigated in 53 patients. Twenty-seven patients (10 males, 17 females) underwent surgery for varicose veins. Twenty-six patients (14 nondiabetics, 12 diabetics) underwent surgery for lower limb ischemia (rest pain or gangrene) with use of the saphenous vein as arterial conduit. Vein segments were gently excised and perfused ex vivo for five 15 minute periods, with a balanced salt solution and determination of the stable degradation products 6-keto-PGF1 alpha and TxB2. Saphenous veins from patients with varicose veins had an initial prostacyclin release of 61 +/- 13 pg/mm2/15 min declining to 4 +/- 1 pg/mm2/15 min after 60 min (p < 0.001) and increasing after addition to arachidonic acid to 37 +/- 7 pg/mm2/15 min (p < 0.001). Segments from nondiabetic patients with lower limb ischemia did not differ from those of varicectomy patients, but diabetic segments had a significantly lower prostacyclin release than both these groups, 34 +/- 11 pg/mm2/15 min, 1 +/- 1 pg/mm2/15 min, and 7 +/- 5 pg/mm2/15 min, respectively (p < 0.05). The addition of arachidonic acid failed to increase the prostacyclin release in diabetics. Three patients from each group were studied regarding thromboxane release and there was almost no detectable thromboxane in any group. These findings suggest that diabetics have a lowered prostacyclin release from the saphenous vein and that the deficiency is at the cyclo-oxygenase level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prostacyclin release from the human saphenous vein in diabetics in lower than in nondiabetics. 145 86

Transperineurial and epineurial vessels are innervated by plexuses of unmyelinated axons. Human sural nerve biopsies were examined ultrastructurally and immunocytochemically with an antibody which recognizes a neuronal and neuroendocrine protein, PGP 9.5, to characterize perivascular axons of these plexuses. Diabetics exhibited a greater degree of abnormal innervation of the vasa nervorum than nondiabetics with and without neuropathy. Abnormal innervation included: a reduction in the percentage of vessels exhibiting perivascular axons and a concomitant increase in the percentage of vessels having denervated Schwann cell units, particularly around vessels confined to perineurial compartments, and remaining axons in nerves from diabetics exhibited fewer varicosities. Denervated arterioles of diabetics also displayed structural changes indicating injury. The arteriolar structural defects and loss of neurogenic control of neural blood flow may lead to or aggravate endoneurial ischemia or hypoxia. The patchy, focal endoneurial fiber loss that is prominent in proximal nerves and associated with the distal myelinated fiber loss of some diabetic patients may be due in part to perivascular denervation of the vasa nervorum.
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PMID:Innervation of the vasa nervorum: changes in human diabetics. 148 91

Hemorrhages caused by gastric varices are a real therapeutic problem in cirrhotic patients. We resort to gastric devascularization in such cases. In 5 of our patients, this devascularization was subtotal, preserving only the pyloric pedicle. Two patients died of liver failure, one immediately after the operation and the other during the second month. The other patients are still living and have not bled again after 9, 12 and 17 months, respectively. Three of the 5 operated patients presented with ischemia of the gastric mucosa postoperatively. In our opinion, the principle of gastric devascularization to an extent still to be defined seems to be an interesting way of treatment these hemorrhages, which are caused by the rupture of gastric varices due to overall portal hypertension.
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PMID:[Subtotal gastric devascularization for hemorrhage caused by the rupture of gastric varices in cirrhotic patients]. 226 18

Endoscopic variceal ligation (EVL) was performed in 14 consecutive patients who had recently bled from esophageal varices. None was actively bleeding at initial treatment. Ligations were accomplished using an endoscopic ligating device and an overtube. There were no procedural complications. 132 varix ligations were performed during 44 separate EVL sessions. Two patients were lost to follow-up and two died; neither death resulted from hemorrhage or treatment complications. Variceal rebleeding occurred in 2 noncompliant patients (14.3%) and was successfully controlled with emergent EVL. Ten patients achieved complete variceal eradication with from 1 to 6 (mean, 3.9) EVL sessions. No major complications (perforation, secondary bleeding, deep ulceration) resulted and there were no treatment failures. Follow-up of 10 surviving patients ranged from 240 to 370 (mean, 280) days. Endoscopic observation suggested that varices were obliterated by a process of mechanical strangulation, ischemia, superficial ulceration, and scar formation. Preliminary data indicate that EVL is a safe and effective treatment for esophageal varices.
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PMID:Endoscopic esophageal varix ligation: preliminary clinical experience. 325 95

Thirty-four adult patients with portomesenteric venous occlusion (PVO) were reviewed. In 11 with hepatic cirrhosis, PVO was usually heralded by worsening ascites often with varix hemorrhage; mortality was high. Four with isolated portal block had varix hemorrhage without ascites. All of these patients survived despite recurrent hematemesis when portal decompression was not feasible in two patients. Eight others (5 agnogenic and 3 with hypercoagulability), experienced sudden abdominal pain with a clot typically propagated into mesenteric tributaries with ileojejunal infarction; survival was related to the promptness of operation and the extent of bowel ischemia. Of five patients with intraabdominal sepsis and pylephlebitis, only one survived. In the final six patients, PVO occurred with intraabdominal carcinoma. Five had progressive ascites, cachexia, and an early death. Imaging techniques included plain and contrast roentgenograms, ultrasonography, and for definitive diagnosis direct portography (operative or splenoportogram), indirect portography (splanchnic arteriovenogram), and computed tomography. Thirteen of 34 patients had ascites, and in nine of 11 patients examined, protein concentration of ascitic fluid was extremely low (less than 0.6 g/dl). Clinical presentation of PVO varies, depending on acuteness and extent of visceral venous blockade, severity of portal hypertension, auxiliary venous collateralization, and regional lymph flow. Inciting factors include endothelial damage and blood hypercoagulability from trauma, infection, stagnant circulation, blood dyscrasia, and malignancy. Improved imaging now allows early diagnosis.
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PMID:Protean manifestations of pylethrombosis. A review of thirty-four patients. 387 12

Surgical treatment of varicose veins occasionally can be followed by severe limb ischemia either after surgery or sclerotherapy. We report here two cases with the clinical features and the therapeutic strategy. The first case concerned a woman operated by venous stripping. A post-operative acute ischemia occurred and was treated by femoro-femoral bypass and lumbar sympathectomy. However this procedure did not avoid persistent chronic ischemia, sciatica paralysis and equinus ankle blockage. A secondary arterial procedure associated with intensive physiotherapy and ankle arthrodesis led to a poor functional result, partly because of an irreversible algodystrophia. The second case concerned a woman treated by sclerotherapy. An injection of the drug in the retro-malleolar area was immediately followed by an acute foot ischemia. Heparin, xylocaine and sodium nitroprusside perfusion avoided a foot amputation, however osteoporosis and algodystrophia occurred. A sympathectomy was necessary two years later. These dramatic complications although unusual, may occur even with experienced physicians. Therefore a great attention is always necessary during these simple procedures. In case of acute ischemia, early diagnosis and aggressive treatment are necessary, but prevention remains more secure.
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PMID:[Arterial complications following surgery or sclerotherapy of varices]. 394 17

Portal hypertension is defined as an increase of the portal venous pressure over 20 cm H2O or 7 mm Hg, respectively. It may be induced by different types of portal venous stenosis or obstruction, primarily by cirrhosis and fibrosis of the liver and, less frequent by posthepatic disorders such as the Budd-Chiari-syndrome or congestive heart failure. Portal hypertension is followed by ectasia and phlebosclerosis of the portal vein, by splenomegaly, ascites and by various types of collateral circulation. Among these, oesophageal varices, are most important since they often lead to acute upper gastrointestinal haemorrhage, the major complication of portal hypertension. Bleeding from oesophaeal varices is essentially based on atrophy of the squamous epithelium, caused by ischemia from local hypoxia and venous stasis. Portal hypertension and the frequently compromised blood clotting mechanism due to reduced synthesis of clotting factors in the liver aggravate the bleeding. Atrophy of the esophageal mucosa presents an area of decreased resistance likely to ulcerate with easy erosion of the varices--usually lying very superficially--; with mechanical irritation by food or peptic erosion from gastroesophageal reflux being frequent inducers of hemorrhage.
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PMID:[Pathologic-anatomic reflections on portal hypertension (author's transl)]. 624 21

One-hundred twenty-five cases of upper extremity internal arteriovenous and graft fistulas were reviewed. Clinical problems requiring study were poor fistula flow during dialysis, difficulty in cannulation, diminished graft pulsations, extremity edema or varicosities, the appearance of pulsatile or nonpulsatile masses in the graft or fistula, and distal ischemia. Angiography demonstrated venous occlusion (13 cases), venous stenosis at or near the anastomotic site (32 cases), thrombi within shunts (9 cases), venous aneurysms or pseudoaneurysms related to either proximal obstruction or traumatic dialysis (23 cases), distal venous overdistention due to proximal obstruction or overcirculation (15 cases), and radial artery steal of blood from the distal extremity (15 cases). The causes and predisposing factors leading to the complications are presented along with a discussion of the angiographic techniques that were used.
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PMID:Angiography of upper extremity access fistulas for dialysis. 646 Oct 26


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