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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The critical illness polyneuropathy has an acute onset and an axonal predominantly motor nature. It occurs in sepsis or in multiple organ failure usually requiring mechanical ventilation in critical care units. Electroneuromyography corroborates the diagnosis. Usually it courses satisfactorily. We report on a 35-year-old female patient who, after a permanence in a critical care unit due to sepsis and removal of a dead phetus, developed tetraparesis. She had an important improvement in four months. Electromyography showed reduction of amplitude of motor and sensory action potentials, positive waves and fibrillations. The sural nerve biopsy showed axonmyelinic neuropathy. These findings are consistent with those in literature and we believe they support the diagnosis of critical illness neuropathy.
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PMID:[Critical illness polyneuropathy: case report]. 1041 38

Critical illness neuropathy is an axonal polyneuropathy recognized more frequently in adult intensive care patients with sepsis and multiple organ dysfunction. In children the diagnosis is rarely made. Within 1 year the authors observed two children with critical illness neuropathy. Both patients, a male 6 years, 6 months of age with a brain contusion and a male 2 years, 6 months of age who underwent craniectomy for Crouzon's disease, required prolonged mechanical ventilation and developed sepsis with multiple organ dysfunction. Three to 4 weeks after successful treatment of the sepsis, a flaccid tetraparesis was noticed in both patients. Laboratory investigations of blood and cerebrospinal fluid and spinal magnetic resonance imaging revealed normal results. Electrophysiologic examinations were indicative of an axonal polyneuropathy. Spontaneous improvement occurred within several months. It is likely that critical illness neuropathy occurs more often in critically ill children than previously thought. Careful neurologic examination and early electrophysiologic investigations are necessary to establish the diagnosis. Important differential diagnoses of acquired lower motor neuron weakness in pediatric intensive care medicine are discussed.
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PMID:Critical illness neuropathy in pediatric intensive care patients. 1058 Aug 91

We summarize clinical, laboratory and pathologic details regarding a patient who presented with extrahepatic disease manifestations of hepatitis C virus (HCV) infection, including cryoglobulinemic leg ulcers due to cutaneous vasculitis, peripheral sensorimotor neuropathy, and recurrent pulmonary infiltrates. The patient had evidence for B-cell lymphoproliferation, diagnosed as extranodal lymphoma on initial (though not subsequent) bone marrow examination, retroperitoneal lymphadenopathy, and the presence of a Type II IgM6 monoclonal rheumatoid factor which became cryoprecipitable on complexing to IgG. Chronic hepatitis was mild on liver biopsy, though fibrotic changes developed over a three-year period of follow-up. She had consistently normal liver function tests, except for a brief rebound effect on discontinuing interferon-alpha, and preterminally. Symptoms were only partially responsive to trials of corticosteroids, cytotoxic agents, plasmapheresis and interferon, and the patient ultimately died at The Mount Sinai Hospital of sepsis. We review current information regarding the spectrum of extrahepatic HCV infection, including pathogenic factors relevant to its overlapping autoimmune, rheumatic and lymphoproliferative disease manifestations. The exact prevalence of these HCV-related syndromes among the 1% of the world population estimated to be infected by this virus remains to be delineated. Chronicity of infection, and lack of efficacy of currently available therapy in effecting sustained clearance of the virus from the host, have made this an important public health problem that is likely to increase in significance. Possible relationships to non-Hodgkin's lymphoma may present novel opportunities to delineate the basis for oncogenesis in HCV infection.
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PMID:Hepatitis C virus, autoimmunity and lymphoproliferation. 1074 67

Diabetic nephropathy is a leading cause of end-stage renal disease, and its prevalence and incidence vary greatly from country to country, being highest in the United States and Japan. In the United States, diabetic nephropathy accounts for approximately 40% of patients beginning renal replacement therapy. Type 2 diabetes is the largest and fastest-growing single disease that requires dialytic therapy. Most patients succumb to cardiovascular causes, including coronary artery disease and myocardial infarction, sudden death, cardiac failure, and stroke. The survival from cardiovascular complications is relatively better in East Asian countries and to a lesser extent in Mediterranean countries compared with countries that traditionally have higher cardiovascular death rates. Peripheral vascular disease and sepsis contribute to increased morbidity and mortality. Amputation of limbs secondary to peripheral vascular disease in particular has adverse effects on rehabilitation. Asymptomatic hypoglycemia may develop in hemodialysis patients. Such hypoglycemia is not associated with a hormonal balance but is postulated to be due to blunted hormonal response to hypoglycemia. Diabetic muscle infarction is another rare complication attributable to diabetic microangiopathy; magnetic resonance imaging may help in the diagnosis. Risk factors for increased mortality include advanced age, poor glycemic control before starting dialysis, smoking, left ventricular hypertrophy, hypoalbuminemia, and neuropathy, in particular, autonomic dysfunction. In addition to adequate dialysis, it is advisable to achieve tight blood pressure control (at least <140/90 mm Hg and preferably much lower), better blood glucose control (hemoglobin A(1c), <7%), correction of nutritional status, and appropriate foot care.
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PMID:Hemodialysis in diabetic patients. 1157 54

Approximately 3 to 5% of patients with chronic lymphocytic leukemia (CLL) develop an aggressive large cell non Hodgkin's lymphoma (NHL) known as Richter's syndrome (RS). RS has a poor prognosis and a response rate of < 10% with fludarabine-based or other cytotoxic combination regimens. The aim of this study was to evaluate the efficacy and toxicity of the hyperCVXD regimen in RS. Twenty-nine patients, median age 61 years (36-75) 23 males, were treated. Prior diagnosis was CLL in 26 patients, NHL in 2, and Prolymphocytic leukemia in 1. Treatment consisted of fractionated cyclophosphamide, vincristine, daunoXome and dexamethasone. Six patients (20%) died while receiving study therapy, 4 (14%) during the first cycle of whom 2 had started therapy with overt pneumonia. Grade 4 granulocytopenia occurred in all 95 cycles of therapy with a median time to recovery of 14 days. Twenty three (24%) cycles were complicated by fever, and 15 (15%) by pneumonia. Sepsis was documented in 8 (8%) cycles, and neuropathy in 5 (5%) of cycles. Twenty three patients had a platelet count < 100 x 10(9)/l prior to therapy: a greater than 50% decrease in platelet count over pre-therapy level occurred in 79% of first cycles, overt bleeding occurred in 4 (4%) of all cycles. Eleven of 29 (38%) patients achieved complete remission (CR), 4 of whom have relapsed after 5, 6, 9, and 12 months of remission. Two of 11 CR patients presented with RS without any prior CLL therapy. One patient had a partial remission. Thus the overall response rate was 12/29 (41%). Overall median survival was 10 months, 19 months in patients who achieved CR, 3 months in those who did not (p = 0.0008). A landmark analysis performed at 2 months from start of therapy comparing patients alive in CR versus patients alive but not in CR showed a median survival of 19 months versus 6 months, respectively (p 0.0017). In conclusion the hyper CVXD regimen has a relatively high response rate, significant toxicity and a moderate impact on survival in RS.
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PMID:Fractionated cyclophosphamide, vincristine, liposomal daunorubicin (daunoXome), and dexamethasone (hyperCVXD) regimen in Richter's syndrome. 1169 97

Sepsis may cause not only failure of parenchymal organs but can also cause damage to peripheral nerves and skeletal muscles. It is now recognized that sepsis-mediated disorders of the peripheral nerves and the muscle, called critical illness polyneuropathy (CIP) and critical illness myopathy, are responsible for weakness and muscle atrophy occurring de novo in intensively treated patients. CIP represents an acute axonal neuropathy that develops during treatment of severely ill patients and remits spontaneously, once the critical condition is under control. The course is monophasic and self-limiting. Among the critical illness myopathies, three main types have been identified: a non-necrotizing "cachectic" myopathy (critical illness myopathy in the strict sense), a myopathy with selective loss of myosin filaments ("thick filament myopathy") and an acute necrotizing myopathy of intensive care. Clinical manifestations of both critical illness myopathies and CIP include delayed weaning from the respirator, muscle weakness, and prolonging of the mobilization phase. The pathogenesis of these neuromuscular complications of sepsis is not understood in detail but most authors assume that the inflammatory factors that mediate systemic inflammatory response and multiple organ failure are closely involved. In thick filament myopathy and acute necrotizing myopathy, administration of steroids and neuromuscular blocking agents may act as triggers. Specific therapies have not been discovered. Stabilization of the underlying critical condition and elimination of sepsis appear to be of major importance. Steroids and muscle relaxants should be avoided or administered at the lowest dose possible.
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PMID:Neurological complications of sepsis: critical illness polyneuropathy and myopathy. 1175 54

Iliacus hematoma causing femoral neuropathy are mostly seen as a result of anticoagulation. Hematoma can occur even while correctly managed anticoagulant treatment because of drug interactions and/or coagulopathies caused by liver disease. Between 1999 and 2001 a 81 and a 68-year-old man were treated in our department because of retroperitoneal hematoma on the left side. Spinal disease and discus abnormalities were excluded with abdominal ultrasound, CT and MRI. The hematomas were operated on because of the progressive complaints and in one patient because of fever and sepsis. After the operation the patients were fast mobilised with help. To decrease the damage and to be cost-effective, hematomas causing neuropathy or other complications should be drained or operated on as soon as possible.
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PMID:[Femoral neuropathy caused by retroperitoneal hematoma]. 1193 May 63

We evaluated 85 children with congenital chronic intestinal pseudoobstruction (CIP) over the past 10 years. Twelve (14%) were born prematurely. One had a family history of CIP. Six had systemic diseases. Thirty-five (41%) had urinary bladder involvement. Manometric features were consistent with myopathy in 32, neuropathy in 48, and mixed disease in 5. Of 48 patients with neuropathy, 6 had urinary bladder involvement (12.5%) (P < 0.0001 vs myopathy), and 10 had malrotation (21%) (P = NS vs myopathy). Upon referral, 53 (62%) were dependent on partial or total parenteral nutrition (PN). At the time of chart review (median 25 months after evaluation), 22 patients had died, 14 of whom were on total PN, 13 of them died because of PN-related complications and 1 died of sepsis. Three others died of sepsis while on partial PN (P = 0.007 vs mortality in patients fed enterally) and five died after small bowel transplantation. In conclusion, in children with congenital CIP, the risk for prematurity is increased twofold, the majority of cases are sporadic, abnormal bladder function is more common in myopathic CIP, and complications related to parenteral nutrition are the main cause of death in children with CIP.
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PMID:Long-term outcome of congenital intestinal pseudoobstruction. 1239 3

Neuropathic complication often occurs in critically ill patients, and changes in the microcirculation of the peripheral nerve have been suggested to play a role in the pathogenesis of the nerve lesion. We report the results of a pathological and immunohistochemical study of superficial peroneal nerve biopsy specimens in a series of 22 critically ill patients with sepsis and neuromuscular disorders. Eight patients had histopathological features of axonal neuropathy compatible with critical illness polyneuropathy (CIP). The nerve lesions ranged in severity from mildly reduced myelin-fiber density with sporadic axonal degeneration to marked fiber loss with abundant degenerative changes. In no patient did we detect evidence of primary demyelinization or inflammatory infiltrates. We analyzed the immunohistochemical expression of E-selectin, vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor alpha (TNF-alpha) in nerve microvessels. Expression of E-selectin was significantly increased in endothelium of epineurial and endoneurial vessels, suggesting endothelial cell activation. These findings again confirm axonal degeneration as the major pathological feature of CIP. Our immunohistochemical data provide first evidence that activation of the endothelial cells of the microvessels in the endoneurium of human peripheral nerve does occur during sepsis. This specific activation might have implications with the mechanisms responsible for the axonopathy in critically ill patients.
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PMID:Enhanced expression of E-selectin on the vascular endothelium of peripheral nerve in critically ill patients with neuromuscular disorders. 1269 64

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


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