Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study is to report 18 cases of membranous laryngotracheobronchitis (MLTB) and to review 143 published cases in order to accurately characterize the epidemiology, presentation, clinical course, treatment, and outcome of patients with this disorder. The male:female ratio was 2:1; mean age was four years. Most patients presented with acute onset of respiratory distress with fever, toxicity, and stridor after a prodrome of upper respiratory tract infection lasting a few days. White blood cell counts varied over a wide range, and blood culture results were rarely positive. Respiratory cultures commonly yielded Staphylococcus aureus or Haemophilus influenzae. Diagnosis was usually confirmed by airway radiographs or endoscopy. An artificial airway was required in 83% of patients. Complications included respiratory failure, toxic shock syndrome, anoxic encephalopathy, and death. MLTB is a serious, potentially fatal cause of acute infectious airway obstruction in infants and children that requires an organized approach to diagnosis and management.
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PMID:An approach to the diagnosis and treatment of membranous laryngotracheobronchitis in infants and children. 178 20

A case of toxic shock syndrome occurring during a menstrual period, and associated with severe hypophosphataemia, is reported. The patient was a 21-year old woman using tampons. On the fourth day, she developed encephalopathy with decreased consciousness and hyperventilation. Severe hypophosphataemia was noted. A phage-group-1 Staphylococcus aureus, producing TSST-1 and enterotoxin A, was isolated from vaginal, pharyngeal and skin sites. Pathogenesis and role of hypophosphataemia in toxic shock syndrome are emphasized.
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PMID:[Severe hypophosphoremia in a toxic shock syndrome]. 334 18

Your recent lead article on toxic shock and tampons (November 1, p. 1161) prompts me to report a case of pelvic infection and staphylococcal septicemia 8 days after the insertion of a Lippes loop. Pelvic infection is a recognized complication of IUDs; although there have been 2 reports of endocarditis occurring in susceptible patients following the insertion of an IUD, septicemia is rare. A previously healthy 31-year old married woman had a loop inserted at a family planning clinic. 3 days later she developed sweating, vomiting, confusion, and cough and during the following 48 hours became disoriented with hallucinations. She was referred to the hospital with suspected encephalitis and on admission was febrile (38.8 degrees Celsius) and stuporose but responded to simple commands. Blood pressure was 95/60 mmHg but there were no other abnormal signs. Hemoglobin was 12.2 g/dl, white blood count 4.0x109/1 (80% neutrophils), erythrocyte sedimentation rate 70mm in the 1st hour; cerebrospinal fluid normal. Chest x-ray examination revealed patchy consolidation in the upper lobes of both lungs and an electroencephalogram showed bilateral nonspecific abnormality. 3 blood cultures taken on admission yielded penicillin-resistant Staphylococcus aureus. She was treated with high-dose intravenous cloxacillin and 24 hours after starting the antibiotic had improved markedly and the IUD was removed. Culture from the coil and also from a high vaginal swab yielded Staph aureus with a similar antibiogram to that of the organism cultured from the blood. Subsequent recovery was uneventful, although repeat chest x-ray examination showed small abscess cavities in the upper lobes of both lungs. The patient was discharged 4 weeks after admission and serial chest radiographs have confirmed complete resolution of the pneumonia and abscesses. There is little doubt that this patients' septicemia with lung abscess formation and encephalopathy originated in the genital tract. The patient was both toxic and shocked but was different from patients with the recently described toxic shock syndrome in that her blood culture was positive for Staph aureus. The case provides another example of the importance of this organism as a cause of infection associated with the insertion of foreign bodies into or through the vagina.
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PMID:Staphylococcal septicaemia after insertion of an intrauterine contraceptive device. 744 49

Toxic Shock Syndrome (TSS) is a potentially fatal illness caused by a particular strain of Staphylococcus aureus. The clinical presentation is similar to that of septic shock. The incidence of TSS peaked in the late 1970s and early 1980s, probably as a result of availability of super absorbent tampons. Although most commonly associated with menstruation, the overall incidence of menstrual and nonmenstrual TSS in men and women ranges from 1 to 3 per 100,000. There are almost equal numbers of menstrual and nonmenstrual cases of TSS identified annually. S aureus, the causative microorganism in cases of TSS, has been isolated from many body tissues. Toxic shock syndrome presents as a flu-like illness with high fever, vomiting, diarrhea, general malaise, and muscle weakness. Nursing and medical management focus on controlling or preventing potentially serious complications, such as adult respiratory distress syndrome, renal failure, electrolyte imbalances, disseminated intravascular coagulation, encephalopathy, and cardiomyopathy. Judicious use of tampons and barrier contraceptive devices may decrease the risk of developing TSS.
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PMID:Toxic shock syndrome: an opportunity for nursing intervention. 865

Renal failure occurs commonly in children with shock, coagulopathy and multi-organ failure. Successful management of these patients requires not only management of the renal failure, but recognition and treatment of the underlying process. In addition to common and well-recognised causes of renal failure and shock, such as Gram-negative sepsis, there are a number of syndromes which are either less well recognised or confined to specific geographic locations. This article reviews the clinical and epidemiological features of the syndromes with shock and renal failure, focusing on the more recently recognised syndromes such as staphylococcal and streptococcal toxic shock syndrome, haemorrhagic shock and encephalopathy syndrome and viral haemorrhagic fevers.
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PMID:Syndromes with renal failure and shock. 801 5

Toxic shock syndrome (TSS) is a well-defined clinical syndrome attributed to certain exotoxins produced by Staphylococcus aureus. The acute episode is often characterized by a toxic encephalopathy, possibly caused by direct neurotoxicity of these exotoxins, although this mechanism has never been proven. We describe a patient who developed TSS, meningitis and cauda equina syndrome simultaneously several days after lumbar laminectomy. A space-occupying lesion was excluded. Enterotoxin C-producing S. aureus was cultured from the surgical wound and the cerebrospinal fluid (CSF). The patient recovered from TSS but remained partially paralyzed. Presumably the cauda equina syndrome was caused by neurotoxic effects of the intrathecally produced S. aureus exotoxins. This case provides evidence for the neurotoxic effects of TSS-associated S. aureus exotoxins.
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PMID:Postoperative cauda syndrome caused by Staphylococcus aureus. 822 30

Urgent critical condition during acute course of infectious diseases can be developed in early terms and suddenly with fast irreversible changes in vital organs and systems. In connection with generality of pathogenesis of many groups of infectious diseases the critical conditions characterized by stereotyped clinical syndromes. They include infective toxic shock, infective toxic encephalopathy and cerebral hypertension, acute dehydration, acute respiratory, cardiac, hepatic, adrenal and renal insufficiency. Urgent therapeutic measures can be standardized with reference to that or other syndromes of critical conditions. In their number--prescription of glucocorticosteroids, diuretics, neuroleptics, antipyretic preparations, solutions of various applicability. Application of antimicrobic preparations and specific antitoxic serums, antimalarial preparations requires care in connection with possible development of complications of toxic or allergic character.
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PMID:[Emergency care for infectious disease patients]. 925 65

A diffuse macular erythroderma and subsequent desquamation after 1 to 2 weeks are two of the five major diagnostic criteria of toxic shock syndrome (TSS). We present the case of a 15-month-old girl with TSS, but without erythroderma or desquamation. She was admitted with high fever, shock, and multiorgan involvement. Minimal or no cutaneous signs were present. Initially the diagnosis of the syndrome of hemorrhagic shock and encephalopathy was made. After 7 days, a TSS toxin 1-producing strain of Staphylococcus aureus was cultured from an inguinal lymph node, where inflammation had already been noticed on admission. Moreover, the girl had no antibodies against this toxin. The serum cytokine profile during the acute phase of her illness showed high levels of tumor necrosis factor-alpha, interleukin-6 and interferon-gamma, as is seen during activation of the immune system by TSS toxin 1. Other possible causes for the patient's illness were excluded. We conclude that the patient had TSS without rash. Without the evidence implicating a TSS toxin 1-producing strain of S. aureus as the cause of her disease, a diagnosis of syndrome of hemorrhagic shock and encephalopathy would have been made. It is possible that some cases of syndrome of hemorrhagic shock and encephalopathy represent a variant of TSS in small children.
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PMID:Toxic shock syndrome without rash in a young child: link with syndrome of hemorrhagic shock and encephalopathy? 967 39

To probe encephalopathy pathogenesis during toxic shock syndrome (TSS), we investigated the fate of bloodborne TSS toxin-1 (TSST-1) as it moves through the choroid plexus epithelium that forms the main blood-cerebrospinal fluid (CSF) barrier and the effect that TSST-1 has on choroidal barrier properties and on cultured neuronal cell viability. TSST-1 showed a slow, diffusional movement across a cellular model of the blood-CSF barrier but did not compromise the integrity of the barrier. Relevant to the acute symptoms of TSS, a combination of human leukocytes and the toxin induced a decrease in CSF clearance of the pyrogenic prostaglandin E(2) (PGE(2)). The direct effects that TSST-1 had on primary cortical neuron cultures and a neuronal cell line involved elevated caspase 3/7 levels, which correlated with an increase in neuronal cell death. The results of the present study suggest that TSST-1 can affect the brain, by inducing both an intracerebral increase in PGE(2) concentration and caspase-dependent neuronal death, which are possibly relevant to long-term intoxication.
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PMID:Toxic shock syndrome toxin-1 challenges the neuroprotective functions of the choroidal epithelium and induces neurotoxicity. 1682 82

We report a case of acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) associated with toxic shock syndrome caused by burns. A one-year-old girl was admitted to our hospital for treatment of severe burns. On day 3, she exhibited a fever, generalized rash and multiple organ failure. She was diagnosed with toxic shock syndrome after burns. She had seizures with fever twice on the same day, followed by secondary seizures on day 8 and transient deterioration of the gross motor functions involved in sitting alone and rolling over. On day 9, MRI diffusion-weighted images showed bright tree appearance (BTA). We conclude that she developed AESD.
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PMID:Acute encephalopathy with biphasic seizures and late reduced diffusion associated with staphylococcal toxic shock syndrome caused by burns. 2711 86


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