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

Multivisceral transplants are gaining acceptance worldwide for patients with chronic gastrointestinal failure with or without irreversible total parenteral nutrition (TPN)-related liver failure. We describe our experience with nine multivisceral harvests reporting our in vivo technique. Multivisceral grafts included stomach, duodenum, pancreas, small bowel, and part of large intestine with or without the liver. After a careful evaluation of the liver and the bowel, we isolated the superior mesenteric artery origin. Then we identified the distal part of the graft isolating the middle colic vein and stapling the transverse colon to its left. After esophagus isolation and stapling, we mobilized the graft, starting from the spleen to the pancreaticoduodenal block, near the celiac trunk. After cross-clamping and cold perfusion, we created an aortic patch including the superior mesenteric artery and celiac trunk as a multivisceral harvest without the liver. A total hepatectomy is added for a liver multivisceral graft. We harvested four multivisceral grafts without the liver and five multivisceral grafts with the liver. We performed seven multivisceral transplants on adult recipients, four without the liver and three with the liver, as well as two liver and one isolated small bowel transplants. Postreperfusion hemostasis was always satisfactory with a mean ischemia time of 6.5 hours. Four recipients died: there was one intraoperative death due to disseminated intravascular coagulopathy. Another patient underwent graftectomy 1 day after transplantation due to vascular thrombosis. In conclusion, our in vivo technique allows a shorter ischemia time with a minimal postreperfusion bleeding and reduced production of lymphatic ascites, without jeopardizing organ function.
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PMID:Multivisceral harvest with in vivo technique: methods and results. 1618 98

An Hypothermia is defined as a decrease in core temperature below 35 degrees C. The well-described deleterious effects of accidental hypothermia on outcome in multiple-trauma patients contrast the beneficial effect of controlled hypothermia on organ function during ischemia in elective surgery. Experimental studies have shown that induced hypothermia during hemorrhagic shock might have beneficial effects on outcome. The beneficial effects of induced hypothermia appear to be partly mediated by the prolongation of the "golden hour" with prevention of hypoxic organ dysfunction. However, hypothermia also has been thought to have an impact on the immunologic response after trauma and elective surgery. Induction of hypothermia seems to decrease the release of pro-inflammatory cytokines believed to influence distant organ damage positively, and is mediated by the interaction of polymorphonuclear leucocytes (PMNL) and capillary endothelial cells. Nevertheless, the incidence of posttraumatic infectious complications may be increased after induction of hypothermia due to an overexpression of anti-inflammatory cytokines. Together with this immunosuppressive profile, coagulopathy and bleeding might limit the use of induced hypothermia after multiple trauma and elective surgery. The purpose of this Chapter is to highlight current knowledge regarding the interaction of hypothermia and posttraumatic immune reactivity. A better understanding of these mechanisms would assist the introduction of preventive and therapeutic strategies into clinical practice.
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PMID:Impact of hypothermia on the immunologic response after trauma and elective surgery. 1652 53

Brain death is associated with complex hemodynamic, endocrine, and metabolic dysfunction that can lead to major complications with the potential donor. Untreated, this can progress to cardiovascular collapse with loss of valuable organs for transplantation. We hypothesized that brain death-related complications would have no effect on the number of organs donated if an aggressive donor management protocol was in place. We identified all successful organ donations between January 2000 and December 2003 and evaluated them for brain death-associated complications (defined as vasopressor requirement, coagulopathy, diabetes insipidus, cardiac ischemia, lactic acidosis, renal failure, and acute respiratory distress syndrome) and donated organs per donor. Sixty-nine organ donors were identified. Complications identified were as follows: intravenous vasopressor requirement in 97.1 per cent, coagulopathy in 55.1 per cent, thrombocytopenia in 53.6 per cent, diabetes insipidus in 46.4 per cent, cardiac ischemia in 30.4 per cent, lactic acidosis in 24.6 per cent, renal failure in 20.3 per cent, and acute respiratory distress syndrome in 13 per cent. There was no significant effect of complications on the average number of organs harvested, with the exception of an increase in organs harvested in the presence of diabetes insipidus. With the implementation of an aggressive organ donor management protocol, these complications can be effectively managed with no impact on the number of organs harvested for transplant.
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PMID:Complications of brain death: frequency and impact on organ retrieval. 1671 88

Non-arteritic anterior ischemic optic neuropathy is caused by a transient optic nerve ischemia and results in permanent vision loss. Currently, there is no effective treatment for this ischemic optic nerve injury. This study characterized the duration and extent of ischemia induced after a coagulopathy injury to the optic nerve of adult rats. Acute ischemia was induced in adult rats by intravenous injection of Rose Bengal dye, followed by argon green laser treatment of the vessels at the optic disc. Rats were assessed in the short-term for hypoxyprobe-1 binding and expression of hypoxia inducible factor-1alpha (HIF-1 alpha) and fractin, markers of neuronal injury. Five months after injury, optic axon number was quantified. The coagulopathy injury resulted in short-term hypoxia in the optic nerve and retina. Tissues were hypoxic within 15 min of the coagulopathy injury, but normoxic by 24 h as measured by hypoxyprobe-1 staining. Both HIF-1alpha and fractin were upregulated in ganglion cells variably across the retina. Five months after the ischemic injury, there was a 71% reduction in optic axon number compared to controls. It is critical to have a reproducible and relevant method for producing transient hypoxia in order to test therapeutic strategies for rescuing injured neurons. The coagulopathy induced in this study resulted in a reproducible and transient ischemic optic nerve injury and long-term axonal loss. This ischemia shows similar, although not identical, morphological and physiological changes to those seen in the human eye after optic nerve ischemia. We are currently testing therapeutic strategies to protect ganglion cells from degeneration after this ischemic injury.
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PMID:Histological and morphometric evaluation of transient retinal and optic nerve ischemia in rat. 1673 Mar 39

Ischemic optic neuropathy (ION) is a common disorder caused by disruption of the arterial blood supply to the optic nerve. It can result in significant loss of visual acuity and/or visual field. An ischemic optic nerve injury was produced in rats by intravenous injection of Rose Bengal dye followed by argon green laser application to the retinal arteries overlying the optic nerve, causing a coagulopathy within the blood vessels and disruption of optic nerve and retinal perfusion. The effect of brimonidine tartrate eye drops on survival of retinal ganglion cell axons in this experimental paradigm was studied. One eye was treated and the contralateral eye served as a control. Four groups of animals were used for this study. Group 1 received 7 days of treatment with 0.15% brimonidine tartrate eye drops twice a day prior to the ischemic injury. Group 2 animals received 0.15% brimonidine tartrate eye drops twice a day for 14 days after photocoagulation injury. Animal groups 3 and 4 received eye drops of 0.9% NaCl twice a day either daily for 7 days before injury or daily for 14 days, respectively. All rats were sacrificed 5 months after the injury to ascertain long-term optic axon survival. Coagulopathy-induced optic nerve ischemia resulted in a 71% loss of optic axons. Treatment with brimonidine daily for the 7 days prior to the injury resulted in a greater survival of optic axons, with only a 56.1% loss compared to control. Brimonidine treatment every day for 14 days after the ischemic injury did not result in a significant rescue of optic axons compared to injury alone. In summary, the application of brimonidine eye drops for one week prior to an ischemic injury resulted in a statistically significant increase in survival of optic axons within the injured optic nerves. Brimonidine treatment of the eye after the ischemic injury did not result in axon rescue, and axon loss was similar to the injured optic nerves treated with saline only. These results suggest that brimonidine may have potential use for prevention of ION in at-risk patients.
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PMID:Neuroprotective effects of brimonidine treatment in a rodent model of ischemic optic neuropathy. 1711 77

Neutropenic enterocolitis or typhlitis (from the Greek word typhlon, meaning cecum) is a clinical syndrome that occurs in the setting of disease or chemotherapy-induced neutropenia. The disease is characterized by an inflammatory process involving colon and/or small bowel, and it can result in ischemia, necrosis, bacteremia, hemorrhage, and perforation. The classic clinical features include fever and abdominal pain. The diagnosis is supported by the findings of bowel wall thickening on ultrasonography or CT imaging. The management of neutropenic enterocolitis is controversial. Neither prospective nor high-quality retrospective studies concerning medical or surgical therapies are available. Most authors will recommend initial conservative management with bowel rest, intravenous fluids, total parenteral nutrition, broad-spectrum antibiotics and normalization of neutrophil counts. Surgical intervention is recommended in the setting of obstruction, perforation, persistent gastrointestinal bleeding despite correction of thrombocytopenia and coagulopathy, and clinical deterioration.
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PMID:Neutropenic enterocolitis: current issues in diagnosis and management. 1732 48

Traditionally, hypothermia has been thought of and used perioperatively as a presumptive strategy to reduce cerebral and myocardial tissue sensitivity to ischemia. Evidence, however, is mounting that maintenance of perioperative normothermia is associated with improved outcomes in patients undergoing all types of surgery, even cardiac surgery. Ambient environmental temperature is sensed by free nerve endings in the dermal and epidermal layers of the skin, which are the axonal extensions of thermosensitive neurons found in the dorsal root ganglia. Free nerve endings in the skin, by means of transient receptor ion channels that are specifically thermosensitive, also may directly sense environmental temperature. This information is transmitted to the preoptic/anterior hypothalamic region of the brainstem, which coordinates efferent responses to abnormal temperature deviation. People have evolved a highly integrated thermoregulatory system that maintains core body temperature in a relatively narrow temperature range. This system, though, is impaired by the stress of regional and general anesthesia, and the added exposure that occurs during the surgical procedure. When combined, these factors can lead to unwanted thermal disturbances. In a cold operating room environment, hypothermia is the usual perioperative consequence; however, hyperthermia is more dangerous and demands immediate diagnosis. Intraoperative hypothermia usually develops in three phases. The first is a rapid decrease in core temperature following anesthetic induction, which mostly results from redistribution of heat from the core thermal compartment to the outer shell of the body. This is followed by a slower, linear reduction in the core temperature that may last several hours. Finally, a core temperature plateau is reached, after which core temperature remains virtually unchanged for the remainder of the procedure. The plateau can be passive or result from re-emergence of thermoregulatory control in patients becoming sufficiently hypothermic. Mild hypothermia in the perioperative period has been associated with adverse outcomes, including impaired drug metabolism, prolonged recovery from anesthesia, cardiac morbidity, coagulopathy, wound infections, and postoperative shivering. Perioperative temperature monitoring devices vary by transducer type and site monitored. More important than the specific device is the site of temperature monitoring. Sites that are accessible during surgery and give an accurate reflection of core temperature include esophageal, nasopharynx, bladder, and rectal sites. Core temperature also may be estimated reasonably using axillary temperature probes except under extreme thermal conditions. Rather than taking a passive approach to thermal management, anesthesiologists need to be proactive in monitoring patients in cold operating rooms and use available technology to prevent gross disturbances in the core temperature. Various methods are available to achieve this. Prewarming patients reduces redistribution hypothermia and is an effective strategy for maintaining intraoperative normothermia. Additionally, forced-air warming and circulating water garments also have been shown to be effective. Heating intravenous fluids does not warm patients, but does prevent fluid-induced hypothermia in patients given large volumes of fluid. This article examined the evolutionary adaptations people possess to combat inadvertent hypothermia and hyperthermia. Because thermal disturbances are associated with severe consequences, the standard of care is to monitor temperature during general anesthesia and to maintain normothermia unless otherwise specifically indicated.
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PMID:Perioperative thermoregulation and temperature monitoring. 1734 66

Activated C protein resistance is a common coagulation defect caused by factor V Leiden mutation and is associated with an augmented risk of predominantly venous thrombosis. Augmented tendency to arterial thrombosis is sporadically reported. This case report describes femoropopliteal thrombosis in a young patient with heterozygous V Leiden factor mutation. Progressive thrombotic occlusion required amputation of the forefoot which resulted in stump dehiscence. Poor blood supply to the perilesional substrate delayed wound healing. An optimal though not yet definitive result was achieved after months of accurate medication. The criticality of lower limb ischemia in an otherwise healthy young patient underscores the grave impact this condition can have on the patient's quality of life and on health care costs.
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PMID:[Femoropopliteal arterial thrombosis in a young patient with heterozygous V Leiden factor mutation. Case report]. 1737 84

Atherosclerotic cardiovascular disease (CVD), which includes coronary heart disease (CHD) and stroke, is now the most common cause of death in the middle aged and elderly in all parts of the world except subSaharan Africa. The direct cause of death is frequently an acute thrombotic arterial occlusion. Because atherosclerosis is a diffuse disease, patients with CHD also have a high risk of ischemic stroke. The hemostatic process is a needed defense mechanism to control hemorrhage after injury but at same time, if overactive, may have the potential to precipitate diseases such as myocardial infarction or stroke in the setting of atherosclerosis. In approximately 1% of all patients with ischemic stroke, and in up to 4% of young adults with stroke, the major precipitant of brain ischemia is a hematologic disorder or coagulopathy that predisposes to thrombosis. von Willebrand factor (vWF) plays an important role in platelet adhesion to subendothelial structures and in the intrinsic pathway of coagulation. It is regarded as an indirect measure of endothelial dysfunction. Deficiency of vWF in von Willebrand's disease is well established. However, much less is known regarding the pathophysiologic implications of an elevated level of vWF, particularly in relation to CVD and cerebrovascular disease. The importance of vWF in the pathogenesis of this disease is poorly defined and information is limited and inconsistent. Elevated levels of vWF have been variably linked with risk of CHD; causal criteria are not fully met. Relationships with stroke risk are even less well established. Measurement of vWF adds little to risk prediction after considering the major risk factors--age, sex, smoking, raised blood cholesterol, and hypertension. vWF may have a greater role in predicting outcome in subjects with acute coronary syndromes (ACS), stroke, and perhaps atrial fibrillation. Investigation of the use of vWF level to guide treatment of ACS or stroke is ongoing; however, there is no compelling evidence to date.
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PMID:von Willebrand Factor in CHD and stroke: relationships and therapeutic implications. 1760 81

This report deals with the perioperative management of ten patients with acute superior mesenteric artery occlusion. All ten patients survived after the surgery. Anesthesia in six patients were maintained with isoflurane, and in four patients with propofol, fentanyl and ketamine (PFK). Total intravenous anesthesia with PFK may provide stable anesthetic managements in superior mesenteric artery occlusion. After the operation patients were treated to control severe infection, multiple organ failure and coagulopathy. Three patients who have only 7, 10 or 5 cm of jejunum are undergoing home parenteral nutrition for short bowel syndrome. Early treatment of intestinal ischemia is essential because necrosis may develop as the condition progresses. The intestine should be preserved to the great extent possible in surgery for acute superior mesenteric arterial occlusion to obtain good long-term quality of life.
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PMID:[Ten cases of acute superior mesenteric artery occlusion]. 1796 19


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