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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Skeletal muscle disuse with space-flight and ground-based models (e.g., hindlimb unloading) results in dramatic skeletal muscle atrophy and weakness. Pathological conditions that cause muscle wasting (i.e., heart failure, muscular dystrophy, sepsis, COPD, cancer) are characterized by elevated "oxidative stress," where antioxidant defenses are overwhelmed by oxidant production. However, the existence, cellular mechanisms, and ramifications of oxidative stress in skeletal muscle subjected to hindlimb unloading are poorly understood. Thus we examined the effects of hindlimb unloading on hindlimb muscle antioxidant enzymes (e.g., superoxide dismutase, catalase, glutathione peroxidase), nonenzymatic antioxidant scavenging capacity (ASC), total hydroperoxides, and dichlorohydrofluorescein diacetate (DCFH-DA) oxidation, a direct indicator of oxidative stress. Twelve 6 month old Sprague Dawley rats were divided into two groups: 28 d of hindlimb unloading (n = 6) and controls (n = 6). Hindlimb unloading resulted in a small decrease in Mn-superoxide dismutase activity (10.1%) in the soleus muscle, while Cu,Zn-superoxide dismutase increased 71.2%. In contrast, catalase and glutathione peroxidase, antioxidant enzymes that remove hydroperoxides, were significantly reduced in the soleus with hindlimb unloading by 54.5 and 16.1%, respectively. Hindlimb unloading also significantly reduced ASC. Hindlimb unloading increased soleus lipid hydroperoxide levels by 21.6% and hindlimb muscle DCFH-DA oxidation by 162.1%. These results indicate that hindlimb unloading results in a disruption of antioxidant status, elevation of hydroperoxides, and an increase in oxidative stress.
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PMID:Hindlimb unloading increases oxidative stress and disrupts antioxidant capacity in skeletal muscle. 1282 51

This report concerns two patients (female, 9 and 6 years) who were diagnosed with megacystis-microcolon-intestinal hypoperistalsis syndrome (MMIHS). Although they exceeded the usual life expectancy of patients diagnosed with MMIHS because of total parenteral nutrition (TPN), they demonstrated progressive neurological deficits and showed histopathological features in the brain. Both patients were diagnosed with MMIHS in the neonatal period and were fed by TPN. The first patient developed visual and gait disturbances at the age of 7 years. Two months later, she developed dysarthria and muscular weakness, and could not maintain her posture. The level of serum selenium was extremely low. The second patient developed flexion and spasticity of the extremities followed by decorticate posture at the age of 3 years. Both patients died of sepsis. The brain weights of the two cases were 880 g and 715 g. In both cases, severe neuronal loss and gliosis were present in the medial convolutions of the occipital lobe, including the visual cortex. The postcentral gyrus and temporal transverse gyrus were also involved. In addition, extensive loss of Purkinje cells and granular neurons, and gliosis were observed in the cerebellum. We measured the selenium content of the brains and livers using the graphite furnace atomic absorption spectrometry method. Selenium was not detected in either brain, although the livers of both cases contained a low level of selenium. On immunohistochemical examination of the anti-oxidative enzymes, histiocyte-macrophage lineage cells in MMIHS cases, including microglia and Kupffer cells, showed only a weak reaction for glutathione peroxidase, of which selenium is an essential component. However, the cells in the control cases were strongly positive. In cases of MMIHS and methylmercury intoxication, the brain features similar lesions, in both their topographical and histopathological aspects. We considered that the brain lesions of the MMIHS patients mainly resulted from oxidative damage of the brain related to the low levels of glutathione peroxidase and other selenoproteins due to selenium deficiency.
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PMID:Encephalopathy in megacystis-microcolon-intestinal hypoperistalsis syndrome patients on long-term total parenteral nutrition possibly due to selenium deficiency. 1284 51

Neuromuscular weakness in critically ill patients is a diagnostic challenge. Critical illness polyneuropathy, an important cause of failure to wean from assisted ventilation is often missed due to lack of suspicion and initiative to undertake regular bedside neurological and electrophysiological examinations in critically ill patients. We report two cases who developed motor weakness while receiving mechanical ventilation in whom axonal neuropathy was diagnosed on electrophysiological studies, establishing a diagnosis of critical illness polyneuropathy. Both patients had evidence of sepsis and multiorgan failure. One case could be successfully weaned off and weakness improved while other succumbed to the underlying illness.
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PMID:Critical illness polyneuropathy: how often do we diagnose it? 1286 41

The amount of muscle that should be retained on the free fibula during harvest is unresolved. Muscle is used to protect the periosteum, but by harvesting a large muscle cuff, the recipient and donor site morbidity increases. A retrospective review of 47 free fibula flaps performed between January 1997 and March 2002 was undertaken. There was an average follow-up of 15 months. The dissection method used for all cases was a muscle sparing technique where the peroneal vessels were skeletonised anteromedially. Only a very thin rim of muscle (1-2 mm) was left attached to the fibula. The recipient and donor vessels were flushed with heparin saline solution intra-operatively and a Dextran 40 infusion was used for four days post-operatively in all cases. Of the 47 flaps, 39 were used for mandible reconstruction, six for maxillary reconstruction and two for long bone reconstruction following trauma. The average age was 47.7 years (range 13-82) and two-thirds (28/43) of the patients were male. There was one post-operative death. The overall failure rate was 10.9% (5/46). Two flaps were lost as a result of arterial thrombosis, one from venous thrombosis, one from sepsis and in one case the cause could not be determined. There were 2 (4.3%) recipient site haematomas. It is suggested that the low recipient site haematoma rate in this series may be related to the limited muscle bulk transferred with the flap. Harvesting less muscle also enables easier insetting and folding of skin flap, and reduces the donor site problems of haematoma and weakness of the foot. The blood supply to the fibula does not appear to be compromised.
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PMID:The fibula free flap: advantages of the muscle sparing technique. 1287 68

With the continuous improvement in the survival of critical patients, new neuromuscular syndromes are being described. The clinical finding is an acute-subacute onset of generalised weakness with difficulty in weaning the patient from the ventilator, due to polyneuropathy, myopathy, prolonged neuromuscular blockade or a combination of these disorders. Although having a multifactorial ethiopathology, the major risk factors in the development of these disorders are multiple organ failure and sepsis for polyneuropathy; corticosteroids and neuromuscular junction blocking agents (NMB) for myopathy; and NMB and renal and liver failure for prolonged neuromuscular blockade. No specific treatment exists, which is why--due to the high incidence of these syndromes and their poor prognosis, with a mortality rate higher than 50%--we should recognise, diagnose and avoid, where possible, the conditions that help the development of these disorders.
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PMID:[Neuromuscular syndromes of the critically ill]. 1287 89

We report a case of subdural empyema and herpes zoster syndrome (Hunt syndrome) complicating routine removal of third molars. Subdural empyema is an extremely rare but life-threatening complication of dental sepsis arising spontaneously or after dental surgery. The clinician should be familiar with its presentation and have a high index of suspicion, because late recognition and delay in its treatment can increase the associated morbidity and mortality. Surgical procedures and in particular maxillofacial surgery have also been known to trigger varicella zoster reactivation resulting in Hunt syndrome. Some patients develop the characteristic rash several days after the onset of facial weakness, so that Hunt syndrome may initially be misdiagnosed as Bell's palsy. We highlight the difficulties in diagnosing Hunt syndrome and argue the case for early treatment of all patients with Hunt syndrome and Bell's palsy with a combination of systemic steroids and antiviral drugs.
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PMID:Subdural empyema and herpes zoster syndrome (Hunt syndrome) complicating removal of third molars. 1470 3

Acute quadriplegic myopathy (AQM; also called "critical illness myopathy") shows acute muscle wasting and weakness and is experienced by some patients with severe systemic illness, often associated with administration of corticosteroids and/or neuroblocking agents. Key aspects of AQM include muscle atrophy and myofilament loss. Although these features are shared with neurogenic atrophy, myogenic atrophy in AQM appears mechanistically distinct from neurogenic atrophy. Using muscle biopsies from AQM, neurogenic atrophy, and normal controls, we show that both myogenic and neurogenic atrophy share induction of myofiber-specific ubiquitin/proteosome pathways (eg, atrogin-1). However, AQM patient muscle showed a specific strong induction of transforming growth factor (TGF)-beta/MAPK pathways. Atrophic AQM myofibers showed coexpression of TGF-beta receptors, p38 MAPK, c-jun, and c-myc, including phosphorylated active forms, and these same fibers showed apoptotic features. Our data suggest a model of AQM pathogenesis in which stress stimuli (sepsis, corticosteroids, pH imbalance, osmotic imbalance) converge on the TGF-beta pathway in myofibers. The acute stimulation of the TGF-beta/MAPK pathway, coupled with the inactivity-induced atrogin-1/proteosome pathway, leads to the acute muscle loss seen in AQM patients.
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PMID:Constitutive activation of MAPK cascade in acute quadriplegic myopathy. 1475 18

There were eleven cases of pure red cell aplasia diagnosed over a period of 2 years (January 2000-December 2001). All the patients had anemia with pallor and weakness being the presenting complaints. Hematological profile depicted normocytic normochromic anemia, reticulocytopenia and marked paucity of erythroid precursors on bone marrow aspiration and biopsy studies. In the present study, one case was of congenital pure red cell aplasia, in one other case of pyrexia of unknown origin, no definitive diagnosis could be made. Other associated diseases seen with pure red cell aplasia were thymoma, septicemia, protein energy malnutrition, non-Hodgkin's lymphoma, juvenile rheumatoid arthritis, acute myeloid leukemia, tuberculosis and hepatitis C. The association of pure red cell aplasia with haematologic malignancies is rare. There are very few case reports on pure red cell aplasia with hepatitis C.
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PMID:Pure red cell aplasia--report of 11 cases from eastern Nepal. 1502 85

Critical Illness Polyneuropathy (CIP) and Myopathy (CIM), either singly or in combination, are a common complication of critical illness. Both disorders may lead to severe weakness and require mechanical ventilation. CIP, as initially described by Bolton et al., in 1984, is a sensorimotor polyneuropathy that is often a complication of sepsis and multiorgan failure. In Japan, Horinouchi et al., first reported a case in 1994. CIM has been referred to by a number of different terms (acute quadriplegic myopathy, thick filament myopathy, acute necrotizing myopathy of intensive care, rapidly evolving myopathy with myosin-deficiency fibers) in the literature. A variety of serious problems (e.g., pneumonia, severe asthma, and lung or liver transplantation) and the concomitant use of high-dose intravenous corticosteroids and nondepolarizing neuromuscular blocking agents predispose to CIM. In Japan, Kawada et al., reported a first case as acute quadriplegic myopathy in 2000. There is no specific treatment for CIP and CIM. Minimizing the use of corticosteroids and nondepolarizing neuromuscular blocking agents in a critical illness setting may prove helpful in preventing the occurrence of these disorders. The prognosis is directly related to the age of the patient and the seriousness of the underlying illness.
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PMID:[Critical illness polyneuropathy and myopathy]. 1515 69

Myasthenic crisis may be defined as respiratory failure or delayed postoperative extubation for more than 24 hours resulting from myasthenic weakness. Myasthenic crisis results from weakness of upper airway muscles leading to obstruction and aspiration, weakness of respiratory muscles leading to reduced tidal volumes, or from weakness of both muscle groups. About one-fifth of patients with myasthenia gravis experience crisis, usually within the first year of illness. Over the last four decades, prognosis from myasthenic crisis has dramatically improved from a mortality rate of 75% to the current rate of less than 5%. Common precipitating factors for myasthenic crisis include respiratory infections, aspiration, sepsis, surgical procedures, rapid tapering of immune modulation, beginning treatment with corticosteroids, exposure to drugs that may increase myasthenic weakness, and pregnancy. Myasthenic crisis should not be fatal, as long as patients receive timely respiratory support and appropriate immunotherapy to reduce myasthenic weakness of the upper airway and respiratory muscles. Myasthenic patients with oropharyngeal or respiratory muscle weakness should receive preoperative plasma exchange or intravenous immunoglobulin therapy to a minimal level of weakness to prevent postoperative complications.
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PMID:Myasthenia gravis: management of myasthenic crisis and perioperative care. 1522 94


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