Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A number of patients admitted to intensive care units for non-neurological disorders develop neuromuscular complications. These patients present with an acute flaccid generalized weakness that may or may not be accompanied by sensory symptoms. There are two main conditions, namely critical illness polyneuropathy and neuromuscular disorder related to the use of neuromuscular blocking agents. These conditions differ in several ways. Critical illness polyneuropathy occurs usually after long stays (weeks) in intensive care units. It concerns patients presenting with a multiple organ dysfunction syndrome, and often sepsis. The polyneuropathy is axonal and implies both sensory and motor fibres. Its pathophysiology remains unclear. Mortality is as high as 60 p.cent and relates to the medical, rather than to the neurological condition. In survivors recovery may be complete, although over a period of months. Neuromuscular disorder related to the use of neuromuscular blocking agents occurs on average after 10 days. It most often concerns patients admitted to intensive care units for acute respiratory failure, mainly asthma or adult respiratory distress syndrome, that may require mechanical ventilation, use of neuromuscular blocking agents and steroids. A purely motor deficit is usually first noticed when curarisation is discontinued. Electromyography discloses fibrillation potentials in all muscles, as well as myopathic changes. Muscle biopsy demonstrates necrosis and a deficit in myosin filaments. In severe cases, injury to distal motor axons probably occurs. Recovery is usually excellent over a few weeks. Recently, replacement of neuromuscular blocking agents by sedatives has notably reduced the occurrence of this disorder. Critical illness neuropathies often cause difficulty in weaning patients from the respirator. They prolong the stay in the intensive care unit, thereby increasing the risks of complications for the patients. Course of these neuromuscular disorders is usually favorable, however sometimes with sequelae.
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PMID:[Critical illness neuropathies]. 1197 88

IVIg is a safe and effective adjunctive treatment for myasthenia gravis, but there are no well established guidelines for the use of IVIg in this disease, lacking controlled randomized trials to assess its efficacy in homogeneous group of patients. The main advantages of IVIg are the rapid onset of the effect, the lack of long-term toxicity, and the possibility to reduce the required doses of immunosuppressive drugs. IVIg appears to have a role as an acute treatment in rapidly progressive myasthenia gravis weakness, particularly in situations when therapeutic apheresis is not feasible. In addition, IVIg is safer than plasma exchange (PE) in patients with hypotension or autonomic instability, in children, in patients of older age (>65 years), and in those suffering from sepsis. For these reasons, at present, IVIg are recommended during crises of myasthenia gravis in older patients when PE is contraindicated or not feasible IVIg can be also used as a chronic maintenance therapy when other immunosuppressive treatments have failed or cannot be used. Periodic administration of IVIg on a bimonthly or monthly basis may be able to stabilize chronic, nonresponding patients.
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PMID:High-dose intravenous immunoglobulin G treatment of myasthenia gravis. 1203 83

The respiratory and limb skeletal muscles become weakened in sepsis, congestive heart failure, and other inflammatory diseases. A potential mediator of muscle weakness is tumor necrosis factor (TNF)-alpha, a cytokine that can stimulate muscle wasting and also can induce contractile dysfunction without overt catabolism. This study addressed the latter process. Murine diaphragm and limb muscle (flexor digitorum brevis [FDB]) preparations were used to determine the relative sensitivities of these muscles to TNF-alpha. Intact muscle fibers were isolated from FDB and microinjected with indo-1 to measure changes in sarcoplasmic calcium regulation. We found that TNF-alpha depressed tetanic force of the diaphragm and FDB to comparable degrees across a range of stimulus frequencies. In isolated muscle fibers, TNF-alpha decreased tetanic force without altering tetanic calcium transients or resting calcium levels. We conclude that (1) TNF-alpha compromises contractile function of diaphragm and limb muscle similarly, and (2) TNF-alpha decreases force by blunting the response of muscle myofilaments to calcium activation.
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PMID:Respiratory and limb muscle weakness induced by tumor necrosis factor-alpha: involvement of muscle myofilaments. 1218 24

We presented atypical manifestations in tuberculous meningitis (TbM) and herpes simplex encephalitis (HSE), lymphocytic dominant cerebrospinal fluid pleocytosis in bacterial meningitis, and a hitherto easily overlooked critical illness polyneuropathy (CIP) associated with sepsis. 1) We presented 2 TbM patients with atypical manifestations. One patient was a 25-year-old man who exhibited polymorphonuclear (PMN) dominant pleocytosis in CSF throughout his clinical course. He died the next day after a CSF culture yielded the growth of tuberculous bacilli, before receiving appropriate anti-TBM therapy. This was a rare TbM example of persistent PMN dominant CSF pleocytosis. The other patient was a 39-year-old woman whose CSF pleocytosis changed from lymphocytic dominant to PMN dominant about 1 month after the initiation of antituberculous chemotherapy. This CSF change was followed by multiple cerebral infarcts due to vauculitis caused by TbM. Administration of prednisolone caused marked improvement of the patient's symptomatology. Tuberculomas appeared transiently during anti-TbM therapy, consistent with paradoxical progression of tuberculoma. 2) A few patients with HSE may show atypical CSF findings such as PMN dominant pleocytosis, absence of pleocytosis, and low sugar value. Our national survey of HSE patients showed following percentages of these atypical findings: PMN dominant pleocytosis observed in 10% of the patients in the early stage and at the time of exacerbation, no pleocytosis in 0.9% (1 patient), and low sugar value in 4%. 3) Bacterial meningitis typically causes PMN dominant CSF pleocytosis. However, Listeria meningitis (LM) may cause lymphocytic dominant pleocytosis in 30% of the patients, particularly in elderly ones. We showed one such 69-year-old patient with persistent lymphocytic dominant CSF pleocytosis throughout the clinical course. 4) CIP, septic encephalopathy and critical illness myopathy are 3 major complications associated with sepsis. CIP is a frequent cause of neuromuscular weakness due to axonal dysfunction, which occurs to critically ill patients with sepsis, particularly when multiple organ dysfunctions are present. We showed our CIP patient associated with acute bacterial endocarditis and multiple organ failure. We should bear in mind these atypical manifestations, and frequent and important complications associated with sepsis such as CIP, to provide appropriate management to patients with neuro-infection and sepsis.
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PMID:[Neuro-infections to be borne in mind]. 1223 30

Sepsis, excessive inflammation, multiple organ failure and weakness prolong the need for intensive care in critically ill patients. Furthermore, the risk of death is high in the prolonged critically ill patient (20% after two weeks and 30% after 3 weeks). In prolonged critical illness, protein hypercatabolism and relative preservation of adipose tissue with fatty infiltration of vital organ systems is present. In view of the crucial role of the hypothalamus-pituitary axis for metabolic homeostasis, we have studied this endocrine organ in the context of critical illness. The initial "adaptive" neuroendocrine response to critical illness illness consists primarily of activated anterior pituitary function. In the chronic phase of critical illness, a uniformly reduced pulsatile secretion of anterior pituitary hormones has been observed, whereby impaired function of target organs. A reduced availability of thyrotropin (TSH)-releasing hormone (TRH), gonadotropin (LH)-releasing hormone (GnRH), the endogenous ligand of the growth hormone (GH)-releasing peptide (GHRP) receptor (ghrelin) and, in very long-stay critically ill men also of GH-releasing hormone (GHRH), inferrentially appears involved. Pulsatile secretion of GH, TSH and LH can be re-amplified by relevant combinations of releasing factors which also substantially increases circulating levels of insulin-like growth factor (IGF)-I, GH-dependent IGF-binding proteins, thyroxine (T4), triiodothyronine (T3) and testosterone. Anabolism is only evoked when GH-secretagogues, TRH and GnRH are administered together whereas the effect of single hormone treatment is minor and accompanied by side effects. A remarkable observation was that a high serum concentration of IGF-binding protein 1 predicts death in the ICU. This observation challenged the classical dogma of adaptive hyperglycemia during critical illness. In a large prospective randomized clinical study (1548 patients), we showed that ICU mortality was reduced by 42% with strict normalization of glycemia using exogenous insulin infusion (N Engl J Med 2001). This was due to prevention of typical ICU complications such as sepsis, multiple organ failure and need for prolonged invasive organ support and intensive care. We conclude that the new concept of reduced stimulation of pituitary function in prolonged critically ill patients opens new therapeutic perspectives to reverse the paradoxical 'wasting syndrome' but that maintenance of strict normoglycemia with insulin is crucial to also increase the chances of survival of these patients.
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PMID:Endocrinology in intensive care medicine: new insights and therapeutic consequences. 1223 41

Abortion is called the invisible plague of all countries and cultures in the twentieth century. It is by far the most important method of birth control in the world today. For every 200 babies born there are at least 100 abortions. In the rich world, a woman who wants to end her pregnancy goes to an abortionist, but for millions of poor women, abortion happens spontaneously in their own homes induced by poor nutrition, sheer physical weakness, and too many pregnancies too close together. In countries where abortion is illegal, millions of women die each year as a result of severe illness or the botched handiwork of backyard operators. The most common complications are massive hemorrhaging, perforation of the uterus, laceration, sepsis, and renal failure. The experience of a great many countries shows that simply legalizing abortion can lead to a dramatic drop in death and illness. Relaxation of abortion laws can save lives, money, and misery for mothers and children. Illegal abortion has become a major problem in Africa there are 3 main types of women who enter hospitals with complications after abortions: 1) the teenager who is away from home; 2) the young woman, often educated, working, and with financial responsibilities, who is ambitious for herself, her husband, or her family; and 3) the woman in her thirties, illiterate, a rural worker, married most of her reproductive life, and pregnant most years. The third type of woman may abort because her system is utterly depleted. Such women must be shown that there is a good chance of survival for her children so that she will not have so many.
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PMID:Abortion: the hidden plague. 1230 49

Neuromuscular weakness commonly develops in the setting of critical illness. This weakness delays recovery and often causes prolonged ventilator dependence. An axonal sensory-motor polyneuropathy, critical illness polyneuropathy (CIP), is seen in up to one third of critically ill patients with the systemic inflammatory response syndrome (usually due to sepsis). An acute myopathy, critical illness myopathy (CIM), frequently develops in a similar setting, often in association with the use of corticosteroids and/or nondepolarizing neuromuscular blocking agents. These patients are often difficult to evaluate due to the limitations imposed by the critical care setting and may be further complicated by the presence of both CIP and CIM in varying degrees. This paper reviews the clinical and electrophysiologic features of these disorders, as well as the putative pathophysiology. In the case of CIM, an animal model has provided evidence that weakness in this disorder is caused by muscle membrane inexcitability due to altered membrane sodium currents and loss of myosin thick filaments.
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PMID:Critical illness myopathy and polyneuropathy. 1235 8

Critical illness polyneuropathy (CIP) is a syndrome that was first extensively described in the early 1980s, mainly in patients with failure to wean from mechanical ventilation. The syndrome is further characterized by limb muscle weakness, usually more pronounced distally than proximally, and is often accompanied by atrophy. The facial musculature is often strikingly spared. Reduced or absent deep-tendon reflexes and loss of peripheral sensation to light touch and pin prick often accompany the syndrome. Involvement of the phrenic nerve has been shown to further contribute to delayed weaning from the ventilator in many patients. The electrophysiologic studies are consistent with a predominantly motor and, often to a lesser extent, sensory axonal polyneuropathy. The incidence of CIP is high, with often more than 50% of patients in major medical and surgical critical care units suffering from the syndrome. The systemic inflammatory response syndrome (SIRS) is strongly associated with CIP and, among the multiorgan failure often seen in SIRS, CIP is thought to represent a neurologic manifestation of SIRS. The neurologic effects of SIRS are thought to be mediated by released mediators like cytokines and free radicals, affecting the microcirculation of the central and peripheral nervous system. Examination of the peripheral nervous system is often unreliable, and the only way to establish a definitive diagnosis is by performing electrophysiologic studies. Morbidity and mortality rates are high. If the underlying problem causing sepsis and/or SIRS can be treated successfully, full recovery from CIP can occur. This recovery often occurs in a matter of weeks in milder cases and in months in more severe cases. Knowledge of CIP is essential for intensivists and other specialists who care for critically ill patients. This review summarizes the current available literature on this topic.
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PMID:Critical illness polyneuropathy. 1238 90

In sepsis contractile weakness of the diaphragm is a major cause of the onset of respiratory failure. This muscular weakness is the result of haemodynamic and metabolic disorders secondary to sepsis and also the damaging effects of inflammatory mediators, among which oxygen free radicals play a crucial role. This role is demonstrated by the protective effect of various exogenous anti-oxidants on diaphragmatic contraction. Early in the course of sepsis there is, in animal models and in man, an increased production of oxygen free radicals and nitric oxide (NO) in the diaphragm, principally within the mitochondria. The formation of peroxinitrite as the result of the action of NO on superoxide anions impairs mitochondrial respiration and consequently the energy production necessary for diaphragmatic contraction. Among the endogenous anti-oxidant systems haem oxygenase, which splits haemoglobin into bilirubin, iron and carbon monoxide, is an effective system for the protection of diaphragmatic function by limiting the damage of oxidant stress. Nevertheless a transient deficiency of local anti-oxidant defences during the early stages of sepsis, when the production of oxygen free radicals is intense, encourages the onset of contractile weakness.
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PMID:[Diaphragmatic weakness in sepsis: the role of oxidant stress]. 1247 46

A 4-month-old Maltese puppy and a 7.5-year-old Collie were diagnosed with septicemia associated with Citrobacter freundii. The puppy died soon, after developing weakness and mucohemorragic diarrhea. The Collie had immune-mediated hemolytic anemia and thrombocytopenia and was treated with immunosuppressive drugs before being euthanized. Gross examination of the puppy revealed mucohemorrhagic intestinal contents. Focal necrotic hepatitis, fibrinous peritonitis, interstitial pneumonia, and hemorrhagic gastrointestinal contents were observed in the older dog. Histologically, there was a diffuse, moderate, histiocytic meningitis in the puppy and a focal fibrinonecrotic hepatitis in the adult dog. Lesions in both dogs contained numerous gram-negative rods. Citrobacter freudii is a potential cause of monomicrobic bacteraemia-septicemia in puppies or immunocompromized adult dogs. The gastrointestinal tract is probably the main site of entry.
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PMID:Citrobacter freundii septicemia in two dogs. 1273 57


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