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

The clinical hallmark of myasthenia gravis (MG) is fluctuating, painless weakness of muscles that most often affect extraocular, lower bulbar, or limb musculature. Predicting the probability of successful treatment for the patient assumes that the physician has made an accurate diagnosis. In this review, the practical differential diagnosis of MG is reviewed from the perspective of conditions (at presentation of symptoms and signs) that may mimic the disorder. The differential diagnosis includes disorders that limit eye movements (with or without associated diplopia), cause false-positive laboratory studies, and mimic MG but have normal eye movements. The differential diagnosis includes disorders that affect the upper brainstem, cranial nerves, neuromuscular junction, muscles, or local orbit anatomy. Nonneurological systemic diseases (i.e., encephalopathy, sepsis) can produce fluctuating ptosis or eye movements that can occasionally be confused with MG. Although MG is considered often in the differential diagnosis of weakness or fatigue symptoms that lack a correlate on neurological examination (subjective fatigue, breakaway weakness, chronic fatigue syndrome), MG is almost never found.
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PMID:Myasthenia gravis: diagnostic mimics. 1525 10

Three 8-week-old kittens were presented with a history of acute, generalized weakness and severe fever. One cat was dead upon presentation, and necropsy findings were supportive of a group G Streptococcus spp. septicemia. During their clinical courses, two of the three kittens developed a progressive, marked swelling of one or more limbs. One moribund and severely hypothermic cat was euthanized a few hours after presentation, and necropsy was also supportive of a group G Streptococcus spp. septicemia. One kitten recovered. Group G streptococcal toxic shock-like syndrome was suspected because of the fulminant progression of the septicemia.
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PMID:Group G streptococcal toxic shock-like syndrome in three cats. 1534 23

Infection of gravid Nya: NYLAR (NYLAR), C57BL/6J (C57), and BALB/c mice with Toxoplasma gondii, on gestation day 7, resulted in fetal resorptions, abortions, and stillbirths. Fetal wastage (estimated) was 35 and 40% in the NYLAR and C57 strains and 55% in the BALB/c strain. Postnatally, pups were cachectic and growth-retarded, with some developing hind limb weakness, petechial lesions on ears and tail, and a blood-tinged nasal exudate. Only 13 of 97 BALB/c pups, 14 of 41 C57 pups, and 46 of 153 NYLAR pups survived the first month of life. At necropsy, swollen, blotched livers, enlarged spleens, pallid kidneys and pulmonary hemorrhages were observed. Cysts of T. gondii were detected in every pup, via press-smears of brain. Histologic examination revealed mineralizing cavitations, ventricular deformations, and periventricular edema in the central nervous system; extensive liver pathology marked by hepatocellular necrosis and calcification, sinusoidal dilatation, and giant cell granulomas; congestion of the spleen with blurring of red and white compartments and cavitations in the white pulp; and tubule and glomerular necrosis and calcification in the kidney. The pulmonary hemorrhages and dermal petechial lesions may reflect a bleeding diathesis due to hepatic insufficiency. The pathogenesis of congenital toxoplasmosis, in the 3 strains of mice, appears due to microvascular dysfunction characterized by dysregulation of hemostasis, perfusion failure, and multiple organ dysfunction, rather than to parasite-mediated cytopathology. We suggest that hematogenous dissemination and endothelial invasion by the parasite induced a systemic inflammatory response syndrome (i.e; toxoplasmic sepsis) leading to the microvascular dysfunction.
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PMID:Multiple organ dysfunction in congenital murine toxoplasmosis. 1547 41

ICU-acquired limb and respiratory muscle weakness is a common, serious ICU syndrome, increasing in frequency with prolonged ICU stay and sepsis. A systematic approach facilitates precise localization of the problem within central or peripheral nervous system. Most cases relate to critical illness polyneuropathy or myopathy or a combination of both (critical illness neuromyopathy). Within the latter entity, the relative contribution of neuropathy versus myopathy varies considerably among affected patients. Muscle enzyme testing, electromyography-nerve conduction and muscle biopsy are valuable investigative tests. Nerve biopsy is less commonly needed, but is useful when vascultis is suspected.
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PMID:A stronger approach to weakness in the intensive care unit. 1556 79

A 75-year-old woman with infective endocarditis developed critical illness polyneuropathy (CIP) with quadriplegia after cardiac surgery. The quadriplegia resolved gradually after aggressive treatment of the underlying infection and with rehabilitation. However, a MEDLINE search of the English-language literature failed to yield results matching quadriplegia and infective endocarditis. CIP is a complication of septic syndrome and sepsis. This complication has been largely unrecognized in intensive care units owing to difficulties in performing a clinical examination or electrophysiologic studies. Difficulty in weaning from the ventilator is an important early manifestation of CIP. Electroneuromyography (ENMG) should be routinely performed to establish the diagnosis. We suggest that any septic patients with unexplained muscle weakness, paralysis, or difficulty in weaning from the ventilator should be evaluated for CIP.
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PMID:Acute quadriplegia complicating critical illness polyneuropathy in a patient with infective endocarditis: a case report. 1566 18

Botryomycosis is a rare bacterial infection of the skin and, rarely, viscera that is characterized by the formation of characteristic hyaline grains. We encountered a patient with Erysipelothrix rhusiopathiae endocarditis who developed visceral botryomycosis. He was a 54-year-old black man who presented in sepsis with a history of progressive weakness and severe weight loss. He died 10 hours after admission. At autopsy, endocarditis was identified, along with infarcts of the spleen and kidneys. Microscopically, visceral botryomycosis was seen. With these bacteria, an animal source is usually identified, although one was not found in this man. Erysipelothrix rhusiopathiae is an organism that is becoming identified in a range of infections in humans, the manifestations and pathophysiology of which are still being discovered.
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PMID:Visceral botryomycosis in a case of Erysipelothrix rhusiopathiae endocarditis. 1571 90

Thirteen cases of feline primary hyperaldosteronism were diagnosed based on clinical signs, serum biochemistry, plasma aldosterone concentration, adrenal imaging and histopathology of adrenal tissue. Two cases presented with blindness caused by systemic hypertension, whilst the remaining 11 cases showed weakness resulting from hypokalaemic polymyopathy. Elevated concentrations of plasma aldosterone and adrenocortical neoplasia were documented in all cases. Seven cases had adrenal adenomas (unilateral in five and bilateral in two) and six had unilateral adrenal carcinomas. Three cases underwent medical treatment only with amlodipine, spironolactone and potassium gluconate; two cases survived for 304 and 984 days until they were euthanased because of chronic renal failure, whilst the third case was euthanased at 50 days following failure of the owner to medicate the cat. Ten cases underwent surgical adrenalectomy following a successful stabilisation period on medical management. Five cases remain alive at the time of writing with follow-up periods of between 240 and 1803 days. Three cases were euthanased during or immediately following surgery because of surgical-induced haemorrhage. One cat was euthanased 14 days after surgery because of generalised sepsis, whilst the remaining cat was euthanased 1045 days after surgery because of anorexia and the development of a cranial abdominal mass. It is recommended that primary hyperaldosteronism should be considered as a differential diagnosis in middle-aged and older cats with hypokalaemic polymyopathy and/or systemic hypertension and should no longer be considered a rare condition.
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PMID:Primary hyperaldosteronism in the cat: a series of 13 cases. 1592 24

The aim of the study was to the clinical features and long term follow up after treatment with Cladarbine in a tertiary care hospital. Seven patients with hairy cell leukemia were diagnosed between January 1990 till December 2003. Diagnosis in all the patients was established by bone marrow aspirates and trephine biopsy along with TRAP. In two patients the diagnosis was supplemented by flowcytometry and in another two patients by splenectomy. Six patients were male while one was female. Mean age was 47.7 years (range 36-64). Most common presenting features were pallor and weakness (n=5). All patients had splenomegaly. Blood count at presentation revealed that one patient had bicytopenia, two had isolated thrombocytopenia, and three had pancytopenia. Treatment responses were evaluable in seven patients. Complete response was seen in six patients (85.7%). One patient died after two months due to sepsis while 3 (50%) patients relapsed. Those who relapsed received another course of CDA and have maintained remission with a median duration of response of 48 months (20-48). From this small series we can conclude that CDA is an effective treatment for HCL and even it works very well in relapsed cases.
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PMID:Hairy cell leukemia: clinical presentation and long term follow up after treatment with 2-chlorodeoxyadenosine (2-CdA). 1596 Feb 89

Myopathies occurring in critically ill patients have gained increasing interest during the past years. For the patient, they represent a crucial factor for prolonged intensive care unit treatment and secondary complications. Critical illness myopathies (CIMs) seem to be related to various pathogenic factors. Among those, the septic inflammatory response syndrome seems to play a major role. It has been suggested that, similar to sepsis-related multiorgan failure, CIM might be considered a failure of the organ muscle. Muscle function might be impaired by proposed "myotoxic" humoral factors. These could be endogenously produced during the innate immune response to sepsis. This article follows up recent evidence for such active fractions in the blood serum of CIM patients. To explain muscle weakness in CIM, serum fractions acutely modified membrane excitability and subcellular Ca2+ regulation in an animal model. From the differential serum effects, early-phase CIM seems to involve a reduction in the overall force generation in muscle but also a compensation by the membrane, increasing the excitability. Different animal models will help to elucidate the underlying mechanisms accounting for the specific proteolytic activities found in different forms of CIM. CIM represents a systemic rather than a local disorder. Humoral factors might initiate the local reaction of skeletal muscle clinically seen as muscle weakness, altered excitability, and proteolysis of contractile proteins. Establishing the interactions in the excitation-contraction cascade in CIM is a challenging task, not only to clarify its pathomechanism but also to deduce clinical interventions.
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PMID:Understanding critical illness myopathy: approaching the pathomechanism. 1598 71

Three infants with infant botulism are presented to illustrate how atypical, early, and severe features may obscure or delay diagnosis. Two boys aged 6 weeks and 20 days, respectively, presented with rapid deterioration after brief periods of poor feeding, one with an apparent life-threatening event at home and the other with a full cardiopulmonary arrest. Initial abnormal laboratory findings of coagulopathy suggested sepsis in the first infant. In the second infant, severe acidosis and hypoglycemia suggested an underlying metabolic disorder. A third infant, aged 1 month, was hospitalized originally with an admitting diagnosis of "pharyngitis" resulting from his inability to take adequate feedings. He received intravenous fluids and antibiotics. One week later he suffered a respiratory arrest. Laboratory findings of severe hyponatremia and acidosis at the time of his arrest suggested a metabolic etiology. Even retrospectively, none of these infants had the typical initial complaint of constipation, and none were noted to have ptosis or facial weakness before catastrophic collapse. However, in each case, the parent had initially brought the child to the physician for "poor feeding" or "poor suck," which was not recognized by medical personnel as a result of bulbar weakness. Ultimately, all 3 infants were found to have infant botulism. All 3 had received antibiotics before catastrophic collapse, possibly contributing to the rapidity of the deterioration. Each recovered, although the delay in diagnosis made them ineligible for treatment with botulism immunoglobulin.
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PMID:Catastrophic presentation of infant botulism may obscure or delay diagnosis. 1614 Jun 90


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