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

Some conditions that predispose to ventilatory failure increase the work of breathing (chronic obstructive pulmonary disease [COPD], obesity, kyphoscoliosis), whereas others cause severe respiratory muscle weakness. Specific reasons for muscle weakness include critical illness (electrolyte imbalance, acidemia, shock, sepsis), chronic illness (poor nutrition, cachexia), and neuromuscular diseases. Inspiratory muscle weakness from mechanical disadvantage to the diaphragm is characteristic of asthma and COPD. The increased work of breathing combined with muscle weakness increases the pressure needed to inspire a breath and decreases maximal inspiratory pressure. When this pressure exceeds 0.4, dyspnea and inspiratory muscle fatigue ensue. One way to lower this pressure and avert fatigue is to lower the tidal volume. Ventilatory drive is high, not low, in ventilatory failure. Concomitant shortening of inspiration and breath duration cause the small tidal volume and increased respiratory rate. Gas exchange is compromised by ventilation/perfusion imbalance, and the ratio of dead space to tidal volume is also increased by rapid, shallow breathing. Reduction in tidal volume minimizes dyspnea, but the small tidal volume is inadequate for gas exchange. Acute treatment of respiratory muscle failure involves respiratory muscle rest through mechanical ventilation and removal of noxious influences (infection, metabolic disarray), whereas chronic treatment involves rebuilding the contractile apparatus by nutritional repletion and training.
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PMID:Respiratory muscles and ventilatory failure: 1993 perspective. 850 1

Thirty-four patients with advanced malignant melanoma were treated with recombinant alpha-interferon (IFN) and chemotherapy consisting of carboplatin, vinblastine, and bleomycin (CVB). CVB was given for four cycles and IFN for 1 year or until progression. Of the 34 analyzed patients, 17 (50%) achieved an objective response, including two complete (6%) and 15 partial responses (44%). Responses were noted in cutaneous, lymph node, and pulmonary sites, with a median time to disease progression of 5 months (range, 3-20 months). The median survival from onset of therapy was 8 months (range, 1-22 months) for the 34 patients. Ninety-four percent of the patients experienced flu-like symptoms and 82% fatigue or weakness. Leukopenia grade 3-4 was observed in four patients (12%). There were two toxicity-related deaths (6%); one from bleomycin-induced pneumonitis and one from neutropenic sepsis. It is concluded that the addition of IFN to CVB regimen, in this study, showed no apparent advantage on response rates, disease-free interval, or survival. The observed treatment-related mortality was unacceptably high. IFN administered as maintenance therapy following CVB conferred no survival benefit.
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PMID:Recombinant interferon ALFA-2A in combination with carboplatin, vinblastine, and bleomycin in the treatment of advanced malignant melanoma. 863 45

Horton giant cell arteritis can present with an atypical clinical picture that often resembles other diseases. In the case described below, the patient initially demonstrated clinical and laboratory evidence of a Candida albicans sepsis, and therefore we started antimycotic treatment with amphotericin B. Because of an adverse reaction to that drug, we added parenteral steroids before every administration of the antimycotic which led to an unexpected improvement of symptoms. This result caused us to reconsider some clinical aspects that could have been interpreted also as vasculitis, in particular for a giant cell arteritis: throbbing temporal headache, diffuse weakness, important rise in ESR, myoarthralgias. We performed a biopsy of the temporal artery that confirmed our diagnosis.
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PMID:[An atypical presentation of a case of Horton's giant-cell arteritis]. 868 82

Onion bulb formations involving cranial nerves are an unusual pathologic feature. We report the postmortem neuropathologic findings in a 69-year-old man with a longstanding neuropathy characterized by progressive muscle weakness, sensory ataxia and multiple cranial nerve abnormalities. Electrodiagnostic testing disclosed features of an acquired demyelinating polyneuropathy. Treatment with corticosteroids and plasmapheresis resulted in no change in his neurologic status, and the patient died after repeated episodes of pneumonia and sepsis. Autopsy showed widespread onion bulb formation in cranial nerves III, IV, V, VI, X, XI and XII, anterior and posterior spinal nerve roots, dorsal root ganglia and multiple peripheral nerves, some of which also had foci of epineurial perivascular inflammation. Muscle sections revealed severe neurogenic atrophy. This case demonstrates that, in longstanding acquired demyelinating neuropathy, the cranial nerves also undergo repetitive cycles of demyelination and remyelination resulting in severe weakness of the bulbar musculature and histologic features of hypertrophic neuropathy.
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PMID:Severe cranial nerve involvement in longstanding demyelinating polyneuropathy: a clinicopathologic correlation. 883 44

An acute myopathy of intensive care occurs in critically ill patients treated with intravenous corticosteroids and neuromuscular junction-blocking agents. The full clinicopathological spectrum is uncertain. We evaluated the clinical, electrodiagnostic, and histopathological features of 14 patients who developed acute myopathy of intensive care after organ transplantation or during treatment of severe pulmonary disorders and sepsis. Patients received high-dose intravenous corticosteroids, usually in conjunction with relatively low to moderate doses of neuromuscular junction-blocking agents. After discontinuation of the latter drugs, most had diffuse, flaccid weakness with failure to wean from mechanical ventilation. Electrodiagnostic findings were consistent with a necrotizing myopathy. Muscle histopathology revealed myopathy with loss of thick filaments in 79%, mild myopathic changes in 14%, and atrophy of type 1 and type 2 fibers in 7%. Loss of thick filaments was identified in muscle biopsy specimens obtained 30 +/- 11 days (mean +/- standard deviation) after intravenous corticosteroid treatment but not in those obtained earlier (12 +/- 2 days). Critically ill patients, including those receiving organ transplants, may develop acute myopathy of intensive care after exposure to intravenous corticosteroids and neuromuscular junction-blocking agents, although the exposure to the latter drugs may be minimal. Selective loss of thick filaments is common in acute myopathy of intensive care, especially if the muscle biopsy specimen is obtained 2 weeks or more after intravenous corticosteroid exposure.
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PMID:Acute myopathy of intensive care: clinical, electromyographic, and pathological aspects. 922 99

Thirty-one patients (26 males, 5 females) with mean age 35 +/- 19 years (range 8 to 85 years) were diagnosed as non-traumatic rhabdomyolysis by clinical findings and elevation of serum creatine kinase (CK) between January 1989 and December 1993. Causes, laboratory measures, clinical courses, and outcome were reviewed retrospectively. Drug abuse, seizure, and excessive activity are the most common etiologies for non-traumatic rhabdomyolysis. Twelve patients presented with muscular pain and seven patients with muscle weakness. Twenty eight patients had urinalysis and five of them (18%) had negative orthotolidine dipstick test. Only seven patients (25%) were detected positive orthotolidine test without microscopic hematuria. Patients with acute renal failure had higher levels of potassium and uric acid. The patients who developed acute renal failure after admission had significantly higher levels of uric acid. The peak levels of CK did not correlate with development of acute renal failure. There was no episode of hyercalcemia. Seventeen patients (55%) had acute renal failure. Hemodialysis was required in nine cases. All survivors recovered with normal renal function except one who needed maintenance hemodialysis after two months follow-up. Two patients died of multi-organ failure and sepsis.
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PMID:Non-traumatic rhabdomyolysis and acute renal failure. 893 69

Critical illness polyneuropathy (CIP) is a recently identified entity for which reliable data is unavailable and of which the prevalence is unknown. Although the percentage of patients suffering CIP is low, more cases, including subclinical ones, are likely to be detected through the use of electroneurography. Any aged patient may be affected by CIP. It usually occurs a long stay in the intensive care unit (ICU) and is generally associated with sepsis, severe trauma and so-called multiple organ failure. The main clinical sign is distal weakness in the lower extremeties, although finding one or more of the following signs is not uncommon: quadriparesis, quadriplegia, difficult weaning, loss of osteo-tendon reflexes and muscle atrophy. The pathophysiology of CIP is unknown, although such mechanisms as cell dehydration, increased proteolysis and the activation of certain cytokins have been suggested. Before diagnosing CIP, other neuromuscle diseases and several recently described toxic myopathies must be ruled out. Electroneuromyographic study of axonal lesions may be of great utility, whereas analyses have low specificity. Histologic examination, when possible, allows axonal lesions (but never demyelinization) to be observed along with the non specific changes of myopathy. Although no specific treatment is available, the long-term prognosis is good if the underlying disease that gave rise to ICU admission is controlled, and if rehabilitation therapy is started early.
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PMID:[Critical illness polyneuropathy]. 899 88

Chronic inflammatory demyelinating polyneuropathy (CIDP) is a progressive or relapsing immune-mediated neuropathy usually responsive to plasma exchange, intravenous gammaglobulin or steroids, with some patients being refractory to these conventional therapies. We report a patient with CIDP who had spontaneous improvement after an episode of sepsis, but subsequently relapsed with severe generalized weakness; he was unresponsive to the conventional treatments for CIDP but had dramatic improvement following treatment with interferon-alpha 2A. Nerve conduction studies following treatment showed improved distal compound muscle action potential amplitudes without change in the degree of conduction block. The mechanism of action of interferon-alpha is unknown, but it may modulate proinflammatory cytokines that have a role in immune-mediated demyelination. Interferon-alpha may be an effective alternative therapy in patients with CIDP who relapse or are refractory to conventional treatments.
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PMID:Improvement following interferon-alpha 2A in chronic inflammatory demyelinating polyneuropathy. 906 66

Critical illness polyneuropathy (CIP) is a recognized cause of muscle weakness and failure of weaning from a ventilator. In order to characterize the features of CIP, we have examined 28 consecutive surgical patients with severe sepsis using bedside electrophysiology. Of the 28 patients (median APACHE II score 31), 20 developed moderate to severe CIP, as shown by the presence of moderate to severe denervation activity on resting EMG. The median nerve compound muscle action potential (CMAP) amplitudes were reduced to 3.24 (SEM 0.48) mV, while sensory nerve action potential (SNAP) amplitudes obtained from the same nerve were normal (13.1 (1.9) microV). In approximately 50% of these patients, the reduction in CMAP exceeded 50% of the lower limit of normal. Similar results were obtained from stimulation of the ulnar nerve. We conclude that CIP is a major complication in patients with severe sepsis and prolonged artificial ventilation. It predominantly involves motor fibres and thus markedly interferes with weaning from the ventilator.
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PMID:Predominant involvement of motor fibres in patients with critical illness polyneuropathy. 938 83

The main manifestations of neuromuscular disease in the newborn period are hypotonia and weakness. Infants with severe hypotonia but only marginal weakness usually do not have a disorder of the lower motor unit. These infants may have genetic conditions, metabolic disturbances, congenital heart disease, hypothyroidism, sepsis, or other systemic disorders. Early on, neonates with central nervous system pathology may present with profound hypotonia, decreased reflexes, and moderate to severe but transient weakness. However, they also tend to have seizures, obtundation, cranial nerve signs, or history of perinatal asphyxia.
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PMID:Neuromuscular disorders in the newborn. 939 65


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