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

The HELLP syndrome (hemolysis, elevated liver enzymes, low platelet count) is a severe complication of pre-eclampsia with high risk for mother and fetus. During the last 40 months 27 parturients met the diagnostic criteria for HELLP syndrome in the University Hospital of Kiel (Tables 1-3). In 24 cases cesarean section was performed. Fetal mortality was 17.2%. In 13 women an uneventful clinical course resulted, all other patients developed complications: renal insufficiency (11 cases), disseminated intravascular coagulation (DIC) (4), intracerebral hemorrhage (1), cerebrovascular ischemia (1), eclamptic convulsions (3), reoperation due to intra- or extra-abdominal hemorrhage (4), severe blood loss ex vagina following spontaneous delivery (1), and liver rupture (1). Despite these severe complications no maternal death was observed. DIC, intrauterine death, and a rapid increase in liver enzymes are considered to be serious prognostic factors that could help to identify high-risk patients. The following recommendations for therapy of parturients suffering from HELLP syndrome are given: epidural anesthesia is not an appropriate method in HELLP syndrome because of the risk of epidural hemorrhage due to thrombopenia. At the present time general anesthesia seems to be the method of choice. Inhalation anesthetics such as halothane, enflurane, or isoflurane should probably be omitted in view of the preexisting hepatopathy. The high risk and the unpredictable postpartum course strongly indicate intensive care for parturients with HELLP syndrome. Antihypertensive, antieclamptic therapy and prophylactic measures to avoid renal insufficiency or hemorrhage (e.g. early substitution of erythrocytes, thrombocytes, and coagulation factors) deserve special attention. Co-operation between obstetrician and anesthesiologist is essential to obtain optimal therapy for these high-risk patients.
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PMID:[Anesthesia and intensive therapy of pregnant women with the HELLP syndrome]. 231 3

Lupus anticoagulants and anticardiolipin antibodies are antiphospholipid antibodies (APLAb) with related antigenic specificities and are newly recognized markers for an increased risk of thrombosis. We studied 48 patients who presented with cerebral or visual dysfunction associated with APLAb to help clarify the diagnostic, clinical, laboratory, radiologic, and pathologic features in these patients. Most patients presented with transient cerebral ischemia or cerebral infarction. Recurrent and stereotypic events were frequent. Visual disturbances resulted from amaurosis fugax, retinal arterial or venous occlusion, occipital ischemia, diplopia, and migraine-like disturbances. Three patients presented with severe atypical classic migraine. Recurrent infarcts of brain and eye were significantly associated with the presence of cigarette smoking, hyperlipidemia, and a positive antinuclear antibody. During 44.4 patient-years of prospective follow-up, the combined stroke and systemic thrombotic event rate was 0.27 events per patient-year and was 0.54 events per patient-year if TIA and death were included. Forty (83%) of the patients did not have systemic lupus erythematosus (SLE). Thrombocytopenia was present in 15 (31%) and a false-positive VDRL in 11 (23%) of the patients. Cerebral angiography was normal or revealed large-vessel occlusion or stenosis without changes suggestive of vasculitis. Patients with only transient dysfunction generally had normal radiologic studies, including angiography. Organs and arterial vessels studied pathologically revealed thrombotic occlusive disease without vasculitis. APLAb are strongly associated with an immune-mediated thrombotic tendency, generally in the absence of SLE. Other stroke risk factors may add to the risk of recurrent ischemic events in patients with APLAb.
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PMID:Cerebrovascular and neurologic disease associated with antiphospholipid antibodies: 48 cases. 238 25

The presence of a lupus anticoagulant (LA) is paradoxically associated with a high incidence of arterial and venous thrombosis. In a patient with a lupus-like systemic disease, having received phenindione for 11 years, LA was discovered in association with recurrent deep venous thrombosis, a right atrial thrombus, coronary occlusion, arterial hypertension, thrombopenia, and anticardiolipin antibodies without anti-DNA antibodies. Renal cortical ischemia was detected by a tomographic scan. Renal biopsy showed glomerular ischemia and diffuse interstitial fibrosis. After a one-year anticoagulant and steroid therapy, LA has disappeared despite a high level of anticardiolipin antibodies, and renal function remains normal.
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PMID:[Renal cortex ischemia, right atrial thrombosis and coronary occlusion in anti-phospholipid antibody syndrome]. 251 17

Thrombocytopenia and platelet dysfunction are commonly seen after cardiopulmonary bypass. In addition, the microvascular bed of ischemic myocardium is a potent stimulus for platelet deposition and microvascular plugging. Thus, it would appear theoretically advantageous to provide pharmacologic protection of platelets by inhibiting their response to activating agents and thereby preventing their loss into the extracorporeal circuit; this would further inhibit myocardial platelet deposition and the deleterious effects therein. Twenty-one mongrel dogs were placed on cardiopulmonary bypass with 30 minutes of normothermic global ischemia. They were randomly assigned to receive pretreatment with an infusion of saline (control, n = 8), a thromboxane synthetase inhibitor (RO-22-4679, n = 5), or a prostacyclin analogue that does not produce hypotension (ZK 36,374, n = 8). The platelet count in those animals treated with ZK 36,374 was significantly higher at the end of the experiment than in the control group (102.8 +/- 10.7 X 10(3) versus 69.7 +/- 10.6 X 10(3), p less than 0.01); the animals treated with RO-22-4679 had a platelet count between the other two groups (92.8 +/- 14.8 X 10(30)), which was not significantly different from either. Myocardial platelet deposition was measured with indium 111-labeled platelets. Those animals treated with ZK 36,374 had a much lower level of platelet deposition than the group of controls; again the RO-22-4679 group had values between the other two. Finally, myocardial blood flow after global ischemia and cardiopulmonary bypass, measured with radioactive microspheres, was significantly higher in the ZK 36,374 group than in the control group. We conclude that ZK 36,374 prevents platelet consumption during cardiopulmonary bypass over and above that seen with inhibition of thromboxane synthesis alone. It also prevents deposition of platelets into the myocardium after global ischemia and we presume by that mechanism increases myocardial blood flow.
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PMID:Amelioration of the deleterious effects of platelets activated during cardiopulmonary bypass. Comparison of a thromboxane synthetase inhibitor and a prostacyclin analogue. 257 91

Renal vein thrombosis in early infancy is a complication of dehydration and prolonged hypotension. The onset is usually acute and the most common clinical signs are uni- or bilateral frank masses, hematuria, proteinuria and thrombocytopenia. In most cases, with conservative management, the late outcome is favorable. In the adult, renal vein thrombosis is often a silent complication of the nephrotic syndrome, the hypercoagulability of which may be an important factor in the pathogenesis of the thrombosis. Clinically, the presentation of a sudden complete occlusion is that of severe abdominal and lumbar pain with hematuria and loss of function of the kidney that suffers hemorrhagic infarction. Physical examination often reveals an enlarged kidney. With gradual occlusion, renal function is preserved. The initial diagnostic approach is with ultrasound studies and computed tomography; definitive diagnosis is established by renal venography or by selective renal arteriography. In general, a conservative approach including the use of anticoagulant treatment is preferred to surgical intervention. Priapism is a persistent painful penile erection due to ischemic or non-ischemic causes; therapeutic intracavernosal injection of papaverine is becoming the most common cause. In early and mild stages, aspiration of blood from the corpora cavernosa supplemented with intracavernosal irrigation with alpha-stimulating agents is the procedure of first choice; in late and severe ischemia, a shunt procedure may become necessary. Hepatic vein thrombosis occurs in association with a number of conditions considered predisposing factors including the use of oral contraceptives. The clinical picture may be that of an acute illness with abdominal pain, hepatomegaly, ascites and hepatic failure as well as early death. More often, the onset is insidious with slowly developing ascites and wasting. For the diagnosis, hepatic scintigraphy may be helpful but, at present, ultrasonography, computed tomography and magnetic resonance scanning are procedures of choice. There is, as yet, no adequate treatment. A fatal outcome may be prevented by surgical decompression of the congested liver and, in recent years, liver transplantation has been employed. Portal vein thrombosis, in children, is usually considered a complication of umbilical sepsis or a result of a congenital abnormality of the portal vein. In adults, the most frequent causes are hepatic cirrhosis and neoplasia. Clinically, there may be a sudden appearance of ascites with resolution in a symptom-free interval until the onset of other features of portal hypertension occur. Currently, ultrasound real-time imaging supplemented with Doppler capability, computed tomography and magnetic resonance scanning provide the necessary diagnostic information. Variceal hemorrhage is often the first major complication requiring treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Thrombosis in particular organ veins. 268 Aug 53

The aim of this chapter was to highlight the major components of PAF actions which lead to a state of shock, i.e. inadequate perfusion of essential organs which if sustained over a critical period of time, leads to irreversible damage in essential organs and eventually death. The heart, the pulmonary vessels and the microcirculation seem to be the primary target organs to PAF-induced hypotension. The effects of PAF on the pulmonary airways in some species (bronchoconstriction) might lead to hypoxemia and further exacerbate organ function. Thrombocytopenia, leukopenia and activation of the complement system are also important in PAF-induced shock by promoting thrombi formation and generation of multiple secondary mediators (e.g. histamine kinins, TXA2, leukotrienes, oxygen radicals). Identification of PAF production during specific or generalized pathophysiological processes is a critical step to implicate this vasoactive lipid in disease processes. So far, only limited information has been derived from studies involving immune responses (anaphylaxis) or bacterial endotoxins. Yet, the growing number of selective and potent PAF antagonists provide important information on the potential role of PAF in shock states. Such evidence, summarized in table I, is of great importance in designing new therapeutic strategies to a highly complex and lethal disease such as septicemia. However, the data summarized in table I clearly show that little is known on the mechanism of action of the various PAF antagonists. It is also important to note that PAF-induced shock and death can be prevented by drugs which are not necessarily PAF antagonists. For example, dexamethasone is extremely efficient in preventing PAF-induced shock and death in the mouse [24, 39] and thyrotropin releasing hormone in the guinea pig [15]. Therefore, it is conceivable that pathological conditions in which PAF might play a fundamental role might be reversed by pharmacological interventions which activate physiological mechanisms which can overcome and reverse the pathological processes activated by PAF. In conclusion, PAF is a powerful vasoactive lipid which can produce severe derangements in essential biological functions which can lead to death. The role of PAF in pathological processes in vivo is well supported in conditions such as anaphylaxis and endotoxemia. Yet, direct proof for PAF production in other shock states, such as multiple trauma, ischemia, inflammation and hemorrhage, is still missing. Furthermore, it is important to keep in mind that in shock, trauma or inflammation, multiple mediators in addition to PAF are formed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Platelet-activating factor and shock. 304 32

Two patients with the lupus anticoagulant exhibited unusual cutaneous manifestations. They both fulfilled four criteria for systemic lupus erythematosus and had experienced deep venous thrombosis. The first patient suffered from a leg ulcer that resembled a pyoderma gangrenosum. The second patient presented erythematous and purplish macules on the fingertips. The histologic studies showed only microthrombosis in the dermal vessels without vasculitis, although such lesions in systemic lupus erythematosus are usually attributed to vasculitis. The association of these cutaneous lesions with lupus anticoagulant has never been reported. It is likely that this association is not fortuitous. After a review of the literature, it seems possible to individualize a new syndrome characterized by the presence of a subgroup of antiphospholipid antibodies. Thrombosis, spontaneous abortions, neurologic manifestations, pulmonary hypertension, positive results of a Coombs' test, and thrombocytopenia can be included in this syndrome, which overlaps with systemic lupus erythematosus. Certain cutaneous symptoms are associated with the presence of lupus anticoagulant or other antiphospholipid antibodies: leg ulcers, distal cutaneous ischemia, widespread cutaneous necrosis, and livedo. They can be considered as the dermatologic manifestations of this syndrome.
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PMID:Cutaneous manifestations associated with the presence of the lupus anticoagulant. A report of two cases and a review of the literature. 309 56

The Authors report a series of 21 cases of heparin induced thrombocytopenia (HIT) observed in a Department of Cardiovascular Surgery. The indication for heparin treatment was a cardiac procedure in 12 cases, peripheral arterial reconstructive surgery in 3 cases and in 6 cases a prevention of embolism. Two routes were used for heparin administration: subcutaneous and intravenous injections. The diagnosis was biological on low platelet counts (p.c.) in 4 cases, in 7 cases a deep venous thrombophlebitis and in 9 cases an acute arterial ischemia complicated the heparin treatment. From the 7th to 15th day after heparin treatment the p.c. had risen to the average value of 46,857/mm3. The diagnosis was clinical in 3 cases, biological with a positive aggregation test in the presence of heparin in 11 cases out of 14 biological tests performed and pathological with observation of white clots in 11 cases. The related mortality rate to HIT was 28.5% of the cases (6 cases). HIT is a rare but severe complication often associated with thrombo-embolic complications. The routine check of p.c. before and after the first week of heparin treatment is reasonable. The negative aggregation test in the presence of heparin does not permit to confirm this diagnosis. The drop in the p.c. between the 6th to 10th day after heparin treatment required an immediate arrest of this type of anticoagulation and replacement with Coumadin. The low molecular weight Heparin may induce cross matching reactions with heparin and therefore is not used as treatment for HIT. In emergency, cardiac surgery with the use of the extra-corporeal circulation device can be performed with success with heparin (2 cases).
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PMID:Cardiovascular surgery and heparin induced thrombocytopenia. 319 76

Thirty-three patients hospitalized as they presented with cerebral vascular lesions during anticoagulant therapy (25 intracerebral hemorrhages, 7 subdural hematoma, and one ischemia lesion). Frequency of intra-cerebral hemorrhages along with anticoagulant therapy was about 11 p. 100, this of subdural hematoma ranged from 12 to 38 p. 100. Intra-cerebral hemorrhages failed to show any peculiar topography and volume was variable. A predisposing factor thus existed in about 50 p. 100 of cases: high blood pressure or arterial aneurysm. Previous cranial traumatism was only demonstrated in 48 p. 100 patients presenting with a subdural hematoma. Prognosis as for these intracranial hemorrhages might be compared to this of hemorrhagic lesions appearing under other etiologic conditions. Ischemia lesion was secondary to a severe thrombopenia to heparin.
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PMID:[Cerebral vascular accidents in anticoagulant therapy]. 381 86

During a 5-year period (1979 to 1983), 50 consecutive patients undergoing continuous intraaortic balloon (IAB) pumping were transferred from Evanston Hospital to Northwestern Memorial Hospital (16 miles), where they underwent cardiac operation. All patients had cardiac catheterization before transfer. Indications for IAB were cardiogenic shock (9 patients), postinfarction angina (18 patients), unstable angina (9 patients), evolving myocardial infarction (3 patients), accelerating angina or hemodynamic instability during cardiac catheterization (9 patients) and prophylactic insertion for high-grade left main stenosis (2 patients). Transportation after stabilization was uneventful in all patients. All patients underwent operative coronary revascularization. There was concomitant mitral valve replacement in 3 patients, acute ventricular septal defect repair in 1 patient, aortic valve replacement in 1, and ventricular aneurysmectomy in 1. Three patients (5%) died postoperatively. Nine patients (20%) had complications directly related to IAB insertion. One patient required femoral-femoral arterial bypass preoperatively, 4 patients had postoperative lower limb ischemia treated by IAB removal or thrombectomy and 1 patient had thrombocytopenia (less than 60,000/mm3), 1 false aneurysm, 1 anterior compartment syndrome and 1 prolonged bleeding at the insertion site. Interhospital transfer with IAB pumping in progress should not be restricted to patients with cardiogenic shock, but can be effectively used for all patients who require preoperative IAB insertion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interhospital transport of patients with ongoing intraaortic balloon pumping. 387 35


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