Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sternothyroid muscle biopsy specimens, obtained during tracheostomies from 15 patients with acute stroke and respiratory failure, were examined immunohistochemically to immunoreactivity to myoglobin (Mb). A marked decrease or lack of Mb immunoreactivity in association with hyaline degeneration was observed in 0.8 to 44.4% of the muscle fibers on both the paretic and non-paretic sides of all patients. The percentages of negative staining for Mb were less than 3.1% in 5 patients with acute respiratory failure due to causes other than stroke. The pattern and incidence of attenuated Mb immunoreactivity in the muscle fibers was found to be distinctively different in the two patients groups. In one group of 5 patients, a large number of muscle fibers (24.8 +/- 15.6%) had no Mb staining and were clearly bordered and grouped. In another 10-patient group, only a limited number of muscle fibers (3.3 +/- 2.5%) had no staining for Mb and these fibers were scattered. Four patients in the former group had catastrophic outcomes, while all the patients in the latter group survived. Ischemia, produced by an increase in catecholamines, and the consequent vasoconstriction, rather than hypoxemia seemed to be the cause of the negative immunoreactivity for Mb in the group pattern. In contrast, hypoxemia may have caused the scattered pattern of negative Mb immunoreactivity. It was concluded that negative immunostaining for Mb in muscle fibers represents a common and characteristic complication in acute stroke patients.
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PMID:Lack of immunoreactivity for myoglobin in skeletal muscle of acute stroke patients. 902 93

A 61-year-old man with pulmonary emphysema was admitted due to acute exacerbation of chronic respiratory failure and a complaint of chest pain. A chest CT scan on admission showed aneurysmal dissection from the ascending aorta to the descending aorta. Analgesia was noted below the fourth thoracic vertebra, which supplies the accessory respiratory muscles including the intercostal muscles. Even after recovery from circulatory failure, his chest muscles were weak and he could not be removed from mechanical ventilation. An autopsy revealed ischemia of the spinal cord at the T4 level. In contrast, The C3 level of the spinal cord, which supplies the diaphragm, was intact. Paralysis of accessory respiratory muscles including intercostal muscles may have caused the continuation of the respiratory failure. This case shows the importance of accessory respiratory muscles in maintaining chest wall movement in patients with chronic pulmonary emphysema.
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PMID:[Spinal cord ischemia caused by dissecting aortic aneurysm in a patient with acute exacerbation of pulmonary emphysema]. 907 Nov 61

Cardiac and circulatory failure are the main causes of hypoxic hepatitis. In a prospective study of 142 cases of hypoxic hepatitis collected during a 10-year period, we encountered two cases resulting from extreme arterial hypoxemia without congestive heart failure, cor pulmonale, or circulatory failure. Both patients were morbidly obese women admitted to the intensive care unit for carbonarcosis. Oxygen arterial saturation was very low, less than 35% in both patients, but there was no history of cardiac or respiratory failure and no clinical evidence of circulatory failure. Cardiac function, evaluated by isotopic scintigraphy, was normal. After the episode of hypoxic hepatitis, a diagnosis of obstructive sleep apnea was made clinically and confirmed by performing nocturnal oximetry, which showed multiple episodes of oxygen desaturation in both patients. Polysonography could be performed in one case and was typical of obstructive sleep apnea. Liver ischemia is the main mechanism leading to hypoxic hepatitis. More recently, the role of passive congestion of the liver has been emphasized. Arterial hypoxemia, however, is generally considered to be a minor factor. Our two cases support the hypothesis that severe arterial hypoxemia may lead to hypoxic hepatitis even in the absence of cardiac and circulatory failure.
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PMID:Hypoxic hepatitis caused by severe hypoxemia from obstructive sleep apnea. 925 50

We treated a neonate in intractable cardiac failure due to a vein of Galen malformation. She manifested severe multiple organ failure. Perioperative problems are cardiac failure, respiratory failure, renal as well as hepatic dysfunction, and coagulopathy. Direct clipping of the feeding arteries improved her symptoms. Anesthetic problems encountered in this patient are massive bleeding and drastic circulatory changes while clipping the feeding arteries, increased intracranial pressure and brain ischemia, and other underlying complications; hepatic and renal dysfunction, respiratory failure and coagulopathy.
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PMID:[Anesthetic and perioperative management of a neonatal vein of Galen malformation with multiple organ failure]. 928 69

Animal models of arteriovenous carbon dioxide removal (AVCO2R) have achieved lung rest during treatment of severe respiratory failure, with total CO2 removal at arteriovenous shunt flow rates of 10% to 25% of cardiac output (CO). Previously, no statistically significant changes were reported in heart rate, cardiac output, mean arterial pressure, or pulmonary arterial pressure during prolonged (7 days) AVCO2R with shunt flows to 25% of CO. In this study, to determine the effect of various shunt levels on organ blood flow, colored microspheres were used in a conscious ovine model of AVCO2R. A low resistance 2.5 m2 oxygenator was placed in a simple carotid-to-jugular arteriovenous circuit. The AVCO2R flow (Qb) was incrementally increased to 5%, 10%, 15%, 20%, and 25% of baseline CO. After equilibration, colored microspheres were injected into a left atrial catheter while reference blood was withdrawn from an arterial line at a constant rate. Organ blood flow obtained by measuring microspheres in the tissues, showed approximately a 10-20% decrease at a 5% shunt, but remained relatively unchanged thereafter at up to a 25% shunt, and was well tolerated without hemodynamic sequelae or evidence of end organ ischemia. It was concluded that AVCO2R can achieve lung rest during respiratory failure at flow rates of 10-25% CO, with a resultant mild decrease in critical organ blood flow that appears well tolerated.
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PMID:Organ blood flow during arteriovenous carbon dioxide removal. 936 Jan 61

This article reviews controversies associated with the selection of patients for extracorporeal membrane oxygenation (ECMO) and their management. Although there has been a raging debate regarding the use of ECMO in the management of hypoxic respiratory failure in the near-term and term newborn, the authors maintain that this issue is resolved and that ECMO is now a standard of care and should be offered to every neonate who is likely to fail conventional treatment. It is the authors' contention, that there is no apparent increase in morbidity associated with the use of ECMO and that better results might be achieved if ECMO were employed earlier in the patient's course, before hypoxic-ischemia organ damage occurs.
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PMID:Extracorporeal membrane oxygenation. Controversies in selection of patients and management. 952 79

The inhalation of racemic adrenalin is an important part of the treatment of inflammatory airway obstruction in children. In Norway during the last few years there have been several cases of adrenal solutions intended only for inhalation being accidentally administered as intravenous injections. The solution for inhalation contains an adrenalin concentration 110 times greater than the adrenalin intended for emergency use (0.1 mg/ml). The instant consequences of intravenous injections of inhalation adrenalin include arterial hypertension followed by hypotension, cardiac ischemia and cardiac insufficiency, pulmonary oedema, and respiratory failure and the need for artificial ventilation. The clinical picture in the three patients we describe was very dramatic. The injected doses were 0.16-1.1 mg l-adrenalin per kg body weight. All children survived without sequelae. In order to reduce the risk of accidentally administering intravenous injections of adrenalin intended for inhalation a set of guidelines is being proposed.
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PMID:[Accidental administration of racemic adrenaline. Three life-threatening cases after intravenous injection in children]. 953 34

Up to 10% of patients who arrive at the hospital with acute myocardial infarction (AMI) present with or develop cardiogenic shock. Some patients, despite inotropes and intra-aortic balloon pump (IABP) placement, are not hemodynamically stable enough to undergo emergent revascularization. The use of percutaneous extracorporeal life support (ECLS) can stabilize patients to allow effective therapy. In a retrospective review of the first 100 patients emergently placed on ECLS by a nurse-supported physician insertion technique at Sharp Memorial Hospital, 10 patients underwent placement of ECLS after out-of hospital AMI. All AMI patients required intubation for respiratory failure and temporary CPR for cardiovascular collapse before initiation of ECLS. Of the 10 AMI patients placed on ECLS, four (40%) are currently long-term survivors (5.1 +/- 4.2 years; range, 6 months to 11 years). All survivors underwent successful revascularization after placement on ECLS. The cause of death in the other six patients was neurologic insufficiency in two, ineffective ECLS in two, and recurrent cardiovascular collapse after weaning from bypass in two. Total CPR time before initiation of cardiopulmonary bypass was 17 +/- 10.3 minutes for the survivors and 54.2 +/-11.1 minutes for the nonsurvivors (p < 0.001). The average time on ECLS was 29 +/- 26 hours for the survivors and 30 +/-67 hours for the nonsurvivors (p = NS). Leg complications were common among long-term survivors, associated with the use of ECLS (three ischemia, one infection). After AMI and cardiovascular collapse, insertion of ECLS may permit long-term patient survival.
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PMID:Long-term survival with use of percutaneous extracorporeal life support in patients presenting with acute myocardial infarction and cardiovascular collapse. 1059 95

Despite marked improvements in early survival, long-term outcome after lung transplantation is still threatened by obliterative bronchiolitis (OB). Thought to be a manifestation of chronic allograft rejection, OB affects up to 65% of patients at 5 years after surgery and produces a relentless airflow obstruction. Early and late acute rejection are the primary risk factors for OB, but cytomegalovirus infection and airway ischemia may also play a role. In most patients, OB responds poorly to augmented immunosuppression and eventually leads to infectious complications and terminal respiratory failure. Because early diagnosis is associated with better prognosis, every effort should be made to detect OB in a preclinical stage. This may be best achieved by combining several techniques, such as surveillance transbronchial biopsy and bronchoalveolar lavage, measurements of ventilation distribution and exhaled nitric oxide, and expiratory computed tomography.
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PMID:Obliterative bronchiolitis after lung transplantation. 1074 73

The abdominal compartment syndrome (ACS) causes dysfunctions of various organs through a progressive unphysiologic increase of the intraabdominal pressure. While the primary ACS is a result of the underlying disease/injury, secondary ACS is caused by surgical interventions. In the severely injured patient intra- and/or retroperitoneal bleeding, edema of viscera due to systemic ischemia reperfusion injury following hemorrhagic shock, abdominal/pelvic packing, and laparotomy closure under tension lead to ACS. The clinical signs of ACS are a tense abdomen with a decreased abdominal wall compliance. Early signs of ACS are a rise in inspiratory pressure and oliguria. Manifest ACS results in anuria, respiratory failure, reduced intestinal perfusion, and low cardiac output syndrome. If untreated, patients die due to left ventricular failure. Diagnosis of ACS is made using the patient's history including the injury pattern, the symptoms, the time period between injury and the occurrence of organ dysfunctions, and the physiologic response to decompression. Frequent determinations of the bladder pressure represent the "golden standard" for early recognition of ACS. Decompressive laparotomy should be performed with a bladder pressure > or = 20 mmHg and rapidly restores impaired organ functions. In the case of a multiple injured patients in shock or with associated severe head injury decompressive laparotomy may even be carried out at a lower bladder pressure. The abdomen is left open. In most patients staged laparotomy is necessary. The final closure of the abdominal wall is carried out after the edema have resolved between day 6 and 8 after primary laparotomy.
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PMID:[The abdominal compartment syndrome]. 1149 Sep 47


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