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

Patients with sepsis-induced multiple organ failure often experience muscle fatigue in both locomotive and respiratory muscles. Muscle fatigue extends intensive care unit stay, mostly in the form of prolonged weaning from the ventilator, and the recovery period after intensive care unit treatment due to general muscle fatigue. Muscle mitochondria are the main determinant of muscle fatigue and fatigability. Derangements in mitochondrial function in locomotive muscles have been described extensively both in animal models and patients with sepsis. Also, in respiratory muscle, mitochondrial function and content are impaired during sepsis. However, in septic patients with multiple organ failure, in locomotive muscle, lower levels of energy-rich compounds accompany the decreased mitochondrial content, whereas in respiratory muscle, the decreased mitochondrial content has no effect on cellular energy metabolism.
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PMID:Mitochondrial function in sepsis: respiratory versus leg muscle. 1771 92

A 35-year-old female with malabsorption syndrome who underwent a pancreatoduodenectomy for multiple endocrine adenomatosis 13 years prior was admitted to our hospital with diarrhea, general fatigue, high fever, and eruption in the lower legs. The patient had consumed raw shrimp a few days before onset and presented systemic inflammatory response syndrome at the time of hospitalization. Vibrio vulnificus was isolated from a blood culture performed before admission to the intensive care unit. We excised necrotizing tissue in the legs after improvement of her general condition. During the treatment process, glucose, catecholamine, and appropriate antibiotics were administered for hypoglycemia, hypotension, and high fever, respectively. The patient was discharged 107 days after contracting the disease. Of 18 septic patients with V. vulnificus infection admitted to our hospital, this was the first to develop septicemia in the absence of a previous liver dysfunction. In order to prevent this type of fatal infection, public education for immuno-compromised individuals as well as those with liver disease is essential. For early diagnosis and appropriate treatment, more effective strategies are required, such as the establishment of a network system where family physicians and emergency hospital staff could discuss information regarding high-risk patients.
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PMID:Survival case of Vibrio vulnificus infection with multiple endocrine neoplasia type I. 1797 78

In 1892 Osler described 'rapid loss of flesh' in prolonged sepsis. Thereafter, for years, limb weakness was attributed to cachectic myopathy, and difficulty weaning from mechanical ventilation was attributed to diaphragmatic fatigue. In 1961 Mertens described 'coma-polyneuropathies', and in 1971 Henderson and colleagues described polyneuropathy in patients with burns. In 1984 Bolton and colleagues, in a series of reports, defined the clinical, electrophysiological and morphological features of septic encephalopathy and critical illness polyneuropathy. Evidence suggested that polyneuropathy was due to the 'toxic' effects of sepsis. Polyneuropathy was a common cause of difficulty in weaning when lung and cardiac cause had been excluded. Since 1984, cases of critical illness polyneuropathy have been reported from several countries. Moreover, a number of investigators reported instances of critical illness myopathy. Comprehensive studies by Latronico and colleagues indicated that polyneuropathy and myopathy often occurred together in the same patient. With successful treatment of sepsis, improvement often occurred in encephalopathy, polyneuropathy and myopathy, except in very severe cases.
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PMID:The discovery of critical illness polyneuropathy. 1828 19

We report a case of Yersinia pseudotuberculosis (Y. pseudotuberculosis) septicemia in a healthy 22-year-old woman with clinical manifestations including high fever and general fatigue. The patient's ferer sudden elevation of her fever, and, liver damage and elevated inflammatory markers were indicated. General fatigue and appetite loss were noted on hospitalization. Exanthema was recognized, and all oral medications, including antibiotics, was stopped. The fever continued and high inflammatory parameters developed. After chemotherapy with imipenem, subjective symptoms ameliorated. Membranous desquamation without itching appeared between the fingers of both hands but improved naturally. Y. psuedotuberculosis septicemia was diagnosed as Y. psuedotuberculosis isolated from blood and elevated serum antibody titer against Y. psuedotuberculosis 4b detected at 1:160.
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PMID:[Yersinia psuedotuberculosis septicemia in a healthy young woman]. 1841 66

Streptococcus suis, a major global porcine pathogen, is an emerging zoonosis in Southeast Asia that triggered a 2005 outbreak in China. S. suis causes meningitis, sepsis, and endocarditis in both pigs and humans and involves significant mortality. We report the case of a previously healthy 50-year-old dairy farmer who developed S. suis type 2 endocarditis complicated by pulmonary embolism and spondylitis. He experienced a high fever, chills, fatigue, and worsening low back pain in the 6 weeks prior to admission. On physical examination, he had lumbar spine tenderness and weakness of the left leg. Blood culture identified penicillin-sensitive S. suis type 2. Echocardiography showed vegetation on the tricuspid valve, and magnetic resonance imaging (MRI) showed signs of spondylitis. The man reported sudden chest pain several days after admission, which computed tomography (CT) showed what was diagnosed as a septic pulmonary embolism. He was treated with penicillin G for 4 weeks and gentamicin for the first 2 weeks, followed by 2 weeks of oral amoxicillin, after which his symptoms gradually improved. The infection source was probably his dairy herd, since calves often bit his fingers while feeding and S. suis was found in their oral mucus. Over 400 cases of human S. suis infection have been reported globally, but this is, to our knowledge, the first known case of bovine transmission. All of Japan's 8 other cases involved occupational swine exposure, 5 of whom had injuries to their fingers. This emerging situation should be made known to all possibly involved in unprotected direct contact with swine and cattle, particularly when the skin could be compromised by cuts or abrasions.
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PMID:[A case of Streptococcus suis endocarditis, probably bovine-transmitted, complicated by pulmonary embolism and spondylitis]. 1986 Feb 57

This flu season, health care providers must be prepared to treat patients who have the seasonal flu and also those who have contracted a novel strain of the H1N1 influenza virus. Although H1N1 flu is sometimes incorrectly called "swine flu," the virus is transmitted from person to person; it cannot be contracted from pigs or from eating pork products. Symptoms of the H1N1 flu include fever, chills, nausea, vomiting, body aches, lethargy, and fatigue, which usually appear in rapid succession. People at high risk include children, pregnant women, and those with certain medical conditions. The most common cause of death from the virus is respiratory failure, but other causes of mortality include sepsis, dehydration, and electrolyte imbalance. The first line of defense against H1N1 flu is vaccination. Treatment includes use of antiemetics, antipyretics, and respiratory support.
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PMID:The enigma of the H1N1 flu: are you ready? 1996 71

A 64-year old hospitalized male for severe bronchial asthma began to complain fatigue and appetite loss. His asthma had been treated with oral bethamethasone. The Chest CT at this time revealed a bilateral consolidation of the lower lung. Despite a week of treatment with antibiotics and anti-fungals, the patient expired from DIC progression. His premortem sputum and blood culture grew Cryptococcus Neoformans. We concluded his diagnosis as cryptococcal pneumonia and sepsis. Sepsis by Cryptococcus neoformans is a rare clinical event, and only 20 cases have been reported in Japan. Although 16 of the 20 had preexisting medical conditions, a case with underlying bronchial asthma has never been reported. A comparison of the reported cases of the US and Europe to that of Japan revealed differences in the patients' underlying conditions. We report a case with a brief review of the literature and summarize the 20 cases that have been reported in Japan.
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PMID:[Cryptococcemia with a severe bronchial asthma: case report and review of the literature]. 2016 72

Sphingomyelinase (SMase) hydrolyzes membrane sphingomyelin into ceramide, which increases oxidants in nonmuscle cells. Serum SMase activity is elevated in sepsis and heart failure, conditions where muscle oxidants are increased, maximal muscle force is diminished, and fatigue is accelerated. We tested the hypotheses that exogenous SMase and accumulation of ceramide in muscle increases oxidants in muscle cells, depresses specific force of unfatigued muscle, and accelerates the fatigue process. We also anticipated that the antioxidant N-acetylcysteine (NAC) would prevent SMase effects on muscle function. We studied the responses of C2C12 myotubes and mouse diaphragm to SMase treatment in vitro. We observed that SMase caused a 2.8-fold increase in total ceramide levels in myotubes. Exogenous ceramide and SMase elevated oxidant activity in C2C12 myotubes by 15-35% (P < 0.05) and in diaphragm muscle fiber bundles by 58-120% (P < 0.05). The SMase-induced increase in diaphragm oxidant activity was prevented by NAC. Exogenous ceramide depressed diaphragm force by 55% (P < 0.05), while SMase depressed maximal force by 30% (P < 0.05) and accelerated fatigue--effects opposed by treatment with NAC. In conclusion, our findings suggest that SMase stimulates a ceramide-oxidant signaling pathway that results in muscle weakness and fatigue.
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PMID:Sphingomyelinase stimulates oxidant signaling to weaken skeletal muscle and promote fatigue. 2057 98

Fatigue is a common symptom of advanced cancer limiting one's activity and affecting the quality of life. It is a multidimensional symptom complex with subjective and objective components. Hence, its definition and assessment seems arbitrary, incomplete, and elusive. Components of fatigue often merge with other 'disease states' as anemia, depression and so on, compounding difficulty to assess it separately. Fatigue has a high prevalence rate, and lasts longer in chronic diseases like cancer. Its association with treatment modalities like chemotherapy, radiotherapy alongside the primary disease process makes it seemingly ubiquitous in many cases. Systemic manifestation of cancer causes excess demand on body resources on cell repair, uncontrolled growth with metabolite accumulation causing fatigue. Co-morbid conditions of organic and psychological nature causes fatigue. There are many assessment tools for fatigue with different uses and objectives, simple and reproducible tools like Brief Fatigue Inventory, Edmonton Symptom assessment scale seem feasible in everyday practice. Management of fatigue is not straightforward and rewarding. Although treatment of cause appears to be an attractive option, it is not possible in all cases. Therapeutic agents targeting cytokine load is in early stages of study and available results are not favorable. Specific measures aimed at pain relief, prevention/treatment of sepsis, management of depression, avoidance of drugs causing fatigue, restoring the metabolic profile are important. Methyl phenidate, megestrol, and modafinil are some drugs with promising effect to treat fatigue, though confirmatory studies are yet to be established. Non-pharmacological methods are also helpful. Forewarning patients on upcoming fatigue, active regular exercise, and stress management are some of them. Fatigue being a multidimensional entity, single mode of therapy is insufficient. Combined modality tailored to individual patient need and understanding may be the right way to battle this ill-understood symptom. This review article examines the etiopathogenesis and management strategies of fatigue in cancer.
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PMID:Fatigue in cancer: a review of literature. 2060 51

The systemic capillary leak syndrome (SCLS) is a rare disease of reversible plasma extravasation and vascular collapse accompanied by hemoconcentration and hypoalbuminemia. Its cause is unknown, although it is believed to be a manifestation of transient endothelial dysfunction due to endothelial contraction, apoptosis, injury, or a combination of these. Fewer than 150 cases of SCLS have been reported, but the condition is probably underrecognized because of its nonspecific symptoms and signs and high mortality rate. Patients experience shock and massive edema, often after a nonspecific prodrome of weakness, fatigue, and myalgias, and are at risk for ischemia-induced organ failure, rhabdomyolysis and muscle compartment syndromes, and venous thromboembolism. Shock and edema reverse almost as quickly as they begin, at which time patients are at risk for death from flash pulmonary edema during rapid fluid remobilization. Diagnosis is made clinically and by exclusion of other diseases that cause similar symptoms and signs, most notably sepsis, anaphylaxis, and angioedema. Acute episodes are treated with vasopressor therapy and judicious fluid replacement, possibly with colloid solutions for their osmotic effects, to prevent the sequelae of underperfusion. Between episodes, patients may be treated with theophylline and terbutaline, which clinical experience suggests may reduce the severity and frequency of acute episodes. Prognosis is uncertain, but patients who survive an initial severe SCLS episode are estimated to have a 10-year survival rate greater than 70%. Much remains to be learned about SCLS, and clinicians should consider the diagnosis in patients with unexplained edema, increased hematocrit, and hypotension.
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PMID:Narrative review: the systemic capillary leak syndrome. 2113 5


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