Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hemorrhagic shock and encephalopathy syndrome (HSES) is a devastating symptom complex that affects previously healthy infants and is associated with significant mortality and neurologic morbidity. The syndrome was first reported less than ten years ago, and there continues to be debate regarding whether HSES actually represents a distinct clinical entity or instead is a manifestation of heat illness, occult sepsis or endotoxic shock, or perhaps toxic ingestion. Nevertheless, the signs and symptoms described as HSES present in a typical fashion in the emergency department with sudden onset of shock, encephalopathy, seizures, and coagulopathy. Even with the initiation of intensive support in the ED, the outcome is probably dismal. We describe a case of HSES and review the presentation, proposed etiologies, and management of this catastrophic illness.
 ...
PMID:Hemorrhagic shock and encephalopathy syndrome. 174 41

A retrospective study was done on infants and children hospitalized from January 1, 1988 to December 31, 1988 at the Pediatric Ward of Dr. Pirngadi Hospital, Medan. In this period a total of 3370 patients had been hospitalized and 1356 (40.24%) had gastroenteritis of whom 96 patients (7.08%) died. The causes of death as the complications were encephalopathy in 27 patients (28.12%), bronchopneumonia in 32 (33.33%), shock in 27 (28.12%), sepsis in 6 (6.25%) and acidosis in 4 (4.17%). Fifty one (53.12%) of those 96 patients who died were in the age group of under one year. The age specific mortality rate was highest in the age group of 1 month (14.28%). Of those 1356 patients with gastroenteritis 566 (41.74%) were well nourished of whom 8 patients died (1.42%); mildly malnourished in 532 patients of whom 36 (6.77%) died; and severely malnourished in 258 patients of whom 52 (20.16%) died. As far as the duration of illness was concerned 43 patients (12.73%) who died had a history of illness at home of 1 day. Beside the complications of the disease it seemed that the nutritional factors might have interfered with the mortality of patients with gastroenteritis.
 ...
PMID:Factors influencing the mortality of children with gastroenteritis at the Pediatric Ward of Dr. Pirngadi Hospital, Medan. 185 66

Clinical and postmortem findings of a case that had combined alcoholic pellagra encephalopathy and Wernicke disease are described. This 51-year-old malnourished and chronic alcoholic man presented with progressive mental deterioration, pellagra dermatitis, hypertonus of the neck and other musculatures, myoclonic jerks with bizarre involuntary movements, in addition to total external ophthalmoplegia and gait disturbance. After administration of multivitamins, including thiamine and nicotinamide, these neurologic abnormalities were dramatically improved in a few days. However, the patient died thereafter because of sepsis associated with pneumonia. Postmortem examination revealed marked abnormalities in CNS, characterized by diffuse atrophy of gray matter and widespread neuronal degeneration and characteristic central chromatolysis in pontine nuclei, dentate nuclei, cranial nerve nuclei in the brain stem, Betz cells of the cerebral cortex, and Clarke's column and anterior horn cells of the spinal cord. There were also atrophy and gliosis of the mammillary bodies, degeneration and vascular proliferation of periaqueductal gray matter, and massive gliosis around the third ventricle. These neuropathological changes were compatible with symptoms of both alcoholic pellagra encephalopathy and Wernicke's disease, but they were also strongly suspected on clinical grounds.
 ...
PMID:Alcoholic pellagra encephalopathy combined with Wernicke disease. 188 55

From October 1986 to March 1989, a total of 7 patients who had preoperative profound shock underwent surgical treatment at the National Taiwan University Hospital for a ruptured aorta or vena cava. All 7 patients were men. Their age ranged from 21 to 70 years with a mean of 45 years. Emergency operations were performed due to a ruptured abdominal aortic aneurysm in 2, a ruptured dissecting thoracic aneurysm in 1, a penetrating injury which transected the intrahepatic vena cava in 2, and blunt chest injury which resulted in acute traumatic aortic transection in 2. One of these 7 patients died of acute tubular necrosis, anoxic encephalopathy and secondary sepsis, in spite of successful restoration of circulation. Two patients had postoperative complications. One had a transient paraparesis after an aortic cross-clamp, and the other had a transient impairment of the hepatic function due to the penetrating hepatic injury and the hypoxic hepatic damage. All 6 survivors were restored to an excellent state of health and had minimal post-resuscitation sequelae. We emphasize the importance of aggressive surgical treatment for those patients with the threat of impending death due to massive hemorrhage from a ruptured great vessel.
 ...
PMID:Emergency surgery of patients with ruptured great vessels and profound shock. 197 58

Recent studies in alcoholic hepatitis have proposed a role for the cytokine tumour necrosis factor-alpha (TNF-alpha) a mediator of endotoxic shock in sepsis. In this study plasma levels of the closely related cytokine interleukin-6 (IL-6) were assayed in 96 samples from 58 patients with severe alcoholic hepatitis, and 69 patients in control groups (21 normal, 10 alcoholic without liver disease, 10 inactive alcoholic cirrhosis, 18 chronic liver disease, 10 chronic renal failure). Plasma IL-6 levels were markedly elevated in patients with alcoholic hepatitis when compared with all control groups (P less than 0.001). IL-6 levels were higher in patients who died (P = 0.04) and correlated with the features of severe disease including: increased grade of encephalopathy, increased neutrophil count, increased prothrombin ratio, hypotension, increased serum creatinine and increased serum bilirubin. Surprisingly, no correlation was found between levels of plasma IL-6 and plasma TNF-alpha or endotoxin, or the presence of infection; an inverse correlation was found between plasma IL-6 and serum globulins. These findings provide further evidence that the IL-6/TNF cytokine system is activated in severe alcoholic hepatitis and may mediate hepatic or extra-hepatic tissue damage.
 ...
PMID:Elevated plasma interleukin-6 and increased severity and mortality in alcoholic hepatitis. 204 24

Complications that can lead to death during shigellosis include intestinal as well as systemic manifestations. The former include intestinal perforation, toxic megacolon, and dehydration, and the latter include sepsis, hyponatremia, hypoglycemia, seizures and encephalopathy, hemolyticuremic syndrome, pneumonia, and malnutrition. Data on the frequency of these complications come primarily from hospital-based studies, in which sepsis-either with Shigella or with other Enterobacteriaceae-and hypoglycemia are the most common causes of death. Management of these two complications requires broad-spectrum empiric antibiotic treatment of all severely ill, malnourished patients with shigellosis as well as frequent feedings to prevent hypoglycemia. Unfortunately, in developing countries, access to parenteral broad-spectrum antimicrobial agents is often limited, and frequent feedings are often precluded by the severe anorexia that is characteristic of shigellosis. Realistic approaches to the reduction of mortality from shigellosis must continue to focus on prevention and early antimicrobial therapy rather than on treatment of established complications.
 ...
PMID:Potentially lethal complications of shigellosis. 204 57

Physicians and surgeons have long recognized that septic illness may be accompanied by abnormal brain functions; however, no systematic, comprehensive study has been done to define the clinical and laboratory features of the syndrome of sepsis-associated encephalopathy. We undertook such a prospective study in a tertiary care hospital and found that of 69 patients with fever and microbial cultures, 32 had marked brain dysfunction, 17 showed mild encephalopathy, and 20 were clinically nonencephalopathic. Severe cases showed obtundation and paratonic rigidity while milder cases showed confusion, inappropriate behavior, inattention, disorientation, and writing errors. There were no focal neurological deficits. The following factors correlated with the severity of brain dysfunction: adult respiratory distress syndrome; fatal outcome; certain types of EEG abnormality; axonal peripheral neuropathy; elevated peripheral white blood cell count; elevated serum levels of alkaline phosphatase, bilirubin, creatinine, phosphate, potassium, and urea; reduced blood pressure and reduced serum albumin level. Our data suggest that brain functions fail with dysfunction of other organs in septic illness. Pathogenetic mechanisms are discussed. The brain dysfunction should be regarded as potentially reversible, even in severely encephalopathic cases. Prompt control of the infection is the most important measure in controlling the encephalopathy and in preventing the increased mortality found with severely encephalopathic patients.
 ...
PMID:The encephalopathy associated with septic illness. 207 9

Clinical features of bilirubin encephalopathy vary depending on the age of the infant and the degree of hyperbilirubinemia. In term infants with hyperbilirubinemia, three distinct clinical phases are apparent in the first weeks of life, and long-term consequences include extrapyramidal disturbances (particularly athetosis), hearing loss, gaze abnormalities (particularly limitation of upward gaze), and, in a minority, intellectual deficits. In term infants with moderate hyperbilirubinemia, minor delay in motor development during the first year has been demonstrated, but with longer follow-up this delay is not apparent. Associated conditions such as sepsis, anoxia, and acidosis may increase the likelihood of neurotoxicity of bilirubin in these infants. The clinical consequences of moderate hyperbilirubinemia in premature infants are unclear. No acute clinical syndrome is recognizable during the first weeks. The results of follow-up studies are variable. Hearing loss is the commonest consequence. Follow-up through age 2 years in one large study suggests that static encephalopathy may be a sequel. Longer follow-up is needed to understand the clinical consequences of moderate hyperbilirubinemia in this important group of infants.
 ...
PMID:Clinical features of bilirubin encephalopathy. 219 35

We elected to test the hypothesis that the metabolic encephalopathy associated with systemic sepsis may have a pathogenesis that is similar to hepatic encepathology, ie, as the consequence of hepatic dysfunction that induces alterations in synthesis of catecholic and noncatecholic neurotransmitters. Eleven patients with septic encephalopathy were compared with nine patients with septic encephalopathy and nine normal controls with respect to blood and cerebrospinal fluid (CSF) amino acid profile, phenylethylamine and its metabolite phenylacetic acid, and blood ammonia. Blood and CSF levels of phenylacetic acid increased markedly in septic and hepatic encephalopathy while CSF phenylethylamine levels were not increased in either condition, presumably due to rapid turnover. The CSF concentrations of all the aromatic amino acids were increased in hepatic encephalopathy, whereas in the patients with sepsis, only phenylalanine levels were increased. Evidence of stimulated neutral amino acid transport into brain was demonstrated in hepatic not septic encephalopathy and appeared to correlate with the CSF glutamine concentration. Blood ammonia levels were increased in hepatic but not in septic encephalopathy. Our data support the hypothesis that metabolites of phenylethylamine contribute to encephalopathy in systemic sepsis and hepatic failure; however, the entities differ in other respects.
 ...
PMID:Septic encephalopathy. Evidence for altered phenylalanine metabolism and comparison with hepatic encephalopathy. 230 19

To identify cortical and subcortical structures in the brain which are associated with septic encephalopathy, local cerebral glucose utilization (LCGU) in the 31 discrete regions were evaluated with a quantitative (14C)-2.deoxyglucose autoradiographic method in the septic rat model. Sepsis was produced by cecal ligation and punctures. Forty rats were subjected to behavioral study and divided into two groups (control, n = 15; sepsis, n = 25). Septic rats died within 36 h, and the rats developed behavioral depression, and showed EEG slowing and an increase in pain threshold. The latter was evaluated by a tail flick method within 8 h after the surgical procedures, while control rats did not show significant change in either behaviors or pain threshold. In another study, LCGU was measured when behavioral depression, increase in pain threshold, and EEG slowing developed in the sepsis group (n = 7). In this group, the mean LCGU in auditory and parietal cortices, lateral geniculate, superior colliculus, hippocampus, and locus ceruleus was 95, 74, 67, 69, 72, and 53 mumol.100 g-1.min-1, being lower by 23%, 22%, 18%, 19%, 14%, and 27% than that in the sham-operated control group (n = 7), respectively. However, the mean LCGU in septal and raphe nuclei was 52 and 84 mumol.100 g-1.min-1, being significantly higher by 27% and 33% than that in the control group, respectively. These results suggest that septic encephalopathy is associated with metabolic changes in the discrete brain regions, which are related to the serotonergic or noradrenergic system.
 ...
PMID:Local cerebral glucose utilization in septic rats. 231 53


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>