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

The sonograms of 12 infants aged 2 days to 7 months were evaluated to determine if the torcular Herophili could be demonstrated routinely on cranial sonography. Sonography, which was performed for a variety of indications (prematurity, seizures, hydrocephalus, sepsis, congenital anomalies, and subarachnoid hemorrhage) demonstrated the torcular Herophili in all cases. It appeared as a variable-sized, anechoic, and triangular or elongated structure inferior to the occipital lobes, posterior to the cerebellum, and just inside the cranial vault. Correlation with computed tomographic scans was available in four patients. A detailed description of the normal anatomy of the torcular Herophili is provided. Knowledge of the variable sonographic appearance of the torcular Herophili is important to distinguish it from a pathologic entity.
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PMID:Sonographic appearance of the torcular Herophili. 351 38

Prospective screening of an extremely high risk group of 137 infants cared for in the Newborn Intensive Care Unit of the James Whitcomb Riley Hospital for Children was undertaken during 1983. Auditory brain stem responses (ABR) were obtained utilizing a clinical evoked potential system (Madsen 2250). Patients were selected for screening prior to discharge or transfer to the referring hospital on the basis of one or more of the following criteria: birth weight less than 1250 grams; birth weight less than 1500 grams and ventilatory support; significant depression at birth (Apgars less than 3 and 6 at 1 and 5 minutes, respectively); seizures, meningitis, and/or sepsis. Of the original 137 infants tested, 82 passed the initial ABR, 22 conditionally passed, and 34 failed. Eighty-two infants had follow-up behavioral and audiometric testing while 20 infants died and 35 were lost to follow-up. Four infants had severe sensorineural hearing loss, each of whom had failed the initial ABR. None of the infants who initially passed or conditionally passed the ABR had sensorineural hearing loss on follow-up testing. High risk factors for sensorineural hearing loss in the neonatal period included: intraventricular/periventricular hemorrhage, apnea, family history, major malformations of the head and neck, and possibly hyperbilirubinemia and congenital infection. No relationship of sensorineural hearing loss with very low birth weight, hyponatremia, infection, seizures, or medications was found. On the basis of these data, it is suggested that electrophysiologic hearing screening of a high risk population may be delayed until 3 to 6 months of age to improve specificity of testing.
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PMID:Hearing screening of high risk newborns. 355 7

One hundred twenty-five infants underwent surgical intervention for necrotizing enterocolitis between 1972 and 1984. Sixty-three infants, who survived more than 30 days postoperatively, were evaluated for long-term complications. There were 28 girls and 35 boys (mean birth weight 1,725 +/- 890 g; gestational age 32 +/- 4 weeks). Associated problems included hyaline membrane disease (43), cardiac anomalies (25), and trisomy 21(2). Thirty-six survivors required long-term ventilatory support. Fifty-nine infants underwent bowel resection and enterostomy, 3 decompressing enterostomies without resection, and 1, exploratory laparotomy only. Enterostomies were closed at four months. Twenty four had short bowel syndrome. Fifteen infants subsequently died for a late mortality rate of 23%. Mortality was related to sepsis (3), respiratory failure (5), cardiac anomalies (3), cardio-respiratory arrest (2), and TPN related liver failure (2), and was common with gestational age less than 31 weeks and birth weight less than 1,000 g. Medical problems included cholestasis (17), TPN induced cirrhosis (3), meningitis (3), seizures (8), and nutritional rickets (6). Significant developmental and intellectual delays were observed.
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PMID:Long-term follow-up after surgical management of necrotizing enterocolitis: sixty-three cases. 372 6

Neonates are susceptible to infection since several elements of the immune system are deficient. At present, the most common pathogens are Group B streptococci and Escherichia coli. Prolonged rupture of membranes with amnionitis is a high-risk setting. Clinical signs suggesting neonatal sepsis include respiratory distress, poor feeding, hypothermia, seizures and hypotonia. After the sepsis work-up is completed, the initial choice of antibiotics is based on the prevailing organisms and antibiotic sensitivities within the community.
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PMID:Neonatal sepsis. 389 74

From 1974 through 1982, fulminant hepatitis was diagnosed in 34 patients at our institution. Of these patients, only two survived (survival rate, 6%). This syndrome was caused by viruses (B and non-B hepatitis and herpes simplex) in 23 patients, hepatotoxic drug in 6, Wilson's disease (hepatolenticular degeneration) in 3, and industrial poisons in 2. Most of the patients died within 10 days after the onset of encephalopathy. The poor prognosis in our group of patients was probably related to the preponderance of older patients and cases caused by non-B hepatitis virus. In our patients, the clinical course was complicated by renal failure, ascites, bleeding, sepsis, pancreatitis, and seizures. The major cause of death was hepatic failure.
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PMID:Fulminant hepatitis: Mayo Clinic experience with 34 cases. 392 80

Lactate concentrations in the cerebrospinal fluid of 104 patients were determined by the Monotest Lactate Kit. Lactate values were found higher in cases of bacterial meningitis than in patients not suffering from acute CNS disorders. Elevated lactate levels were also found in patients suffering from aseptic meningitis, septicemia, CNS trauma and cerebrovascular accidents, seizures and diabetes mellitus. The highest levels were found in cases of bacterial meningitis, but there was considerable overlapping between the groups. CSF lactate thus appears to have limited diagnostic value in the differential diagnosis between bacterial meningitis and other diseases with meningeal involvement.
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PMID:Value of CSF lactate in the differential diagnosis between bacterial meningitis and other diseases with meningeal involvement. 398 42

During a 12-month prospective study there were 125 visits to the Harlem Hospital Emergency Room for symptomatic hypoglycemia. Sixty-five patients had obtundation, stupor, or coma; 38 had confusion or bizarre behavior; 10 were dizzy or tremulous; 9 had had seizures; and 3 had suffered sudden hemiparesis. Diabetes mellitus, alcoholism, and sepsis, alone or in combination, accounted for 90% of predisposing conditions; others included fasting, terminal cancer, gastroenteritis, insulin abuse, and myxedema. Average blood glucose levels were lower among comatose than among obtunded patients, but overlap was considerable, and overall there was little correlation among cause, blood glucose levels, and symptoms. Although mortality was 11%, only one death was attributable to hypoglycemia per se, and only four survivors had focal neurological residua.
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PMID:Hypoglycemia: causes, neurological manifestations, and outcome. 400 66

Twelve fatal cases of encephalopathy associated with sepsis were examined in a ten-year retrospective study. The sources of infection and organisms isolated were variable. Six of the patients had focal neurologic signs; five had seizures. The level of consciousness varied from drowsiness to deep coma, and electroencephalograms revealed diffuse or multifocal abnormalities. Computed tomographic head scans and cerebrospinal fluid examinations were usually unremarkable. Eight patients had disseminated microabscesses in the brain at autopsy. Four patients had proliferation of astrocytes and microglia in the cerebral cortex, a feature associated with metabolic encephalopathies. Additional findings included cerebral infarcts, brain purpura, multiple small white matter hemorrhages, and central pontine myelinolysis. Although sepsis may cause encephalopathy by producing disturbances in cerebral synaptic transmission and cerebral energy production through a toxic mechanism, bacterial invasion of the brain with the formation of disseminated microabscesses is also an important cause.
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PMID:The encephalopathy of sepsis. 408 65

Bacterial infections are frequent events in premature and newborn infants. The reason is a defective specific and nonspecific defence of bacterial organisms. Some immunoglobulins like IgM and IgA including secretory IgA are absent. Premature infants also show a decreased level of IgG. Cellular immunity is anatomically intact but functionally defective. A number of complement factors are lacking, the activation of the alternative pathway is impaired. Newborn infants with perinatal problems like asphyxia or difficult delivery, show defects of leucocyte function like decreased deformability, defective chemotaxis and defective killing of ingested bacteria. Certain diseases, like hypoxia and malformations of immature organ functions in this age group (decreased acid production in the stomach), facilitate bacterial colonization of surface epithelia and the invasion of tissues. Consequences of these pathogenetic mechanisms are an unimpaired propagation of bacterial organisms into the blood and meninges without localization of the infecting organisms at the entry site. Bacterial meningitis is not considered a separate disease entity but a complication of bacteremia and sepsis. Clinical symptoms are nonspecific at the onset of the infection. Fever is frequently absent; decreased appetite, vomiting, a bloated abdomen, diarrhea, tachycardia, tachypnea are early signs of a bacterial infection, a grey mottled appearance, cyanosis, jaundice, petechiae, apneic spells, seizure activity and a metabolic acidosis are symptoms of advanced infection. Successful treatment at this stage is often not possible. Every sign of a decreased well being of a newborn of premature infant warrants laboratory and bacteriologic work up for septicemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Chemotherapy of severe bacterial infections in pediatrics]. 631 69

A survey of 89 patients with subdural empyema was conducted to assess the incidence of late seizures and morbidity in this disease. Twenty-four patients died during the acute stage of the illness and, of the 65 survivors, 13 were lost or had incomplete follow-up review. Hemiparesis occurred in 48 of the survivors during the acute stage, and all but nine recovered completely. Thirteen patients had a visual field deficit and all recovered; in three of these 13 who had speech disorders the deficits persisted. Recovery from neurological morbidity was not related to the type of surgical treatment; however, the mortality rate was improved by craniotomy. The same incidence of early seizures occurred in those who died (62%) as in those who survived (63%). Of those who had no early seizures, 42% had late seizures, the majority appearing within 16 months. Of those who had early seizures, 71% did not have subsequent attacks. The highest incidence of seizures occurred in patients who had their empyema in the second and third decades of life. The incidence of late seizures was not influenced by the method of surgical treatment, the degree of deterioration of consciousness during the acute stage of the illness, nor by occurrence of early seizures. A significantly increased incidence of early seizures was associated with paranasal sepsis, but not with late seizures.
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PMID:Late seizures and morbidity after subdural empyema. 640 70


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