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

Neuropathological examinations were carried out at necropsy on 83 very pre-term babies who died during their first hospital admission. Forty seven (57%) babies had evidence of cerebral damage-39 with ischaemic white matter damage. The time of onset of ischaemic lesions was thought to be prenatal in 12 cases (31%) and postnatal in a further 12 (31%). The exact timing of damage could not be determined in 15 (38%) cases. Maternal and neonatal case notes were reviewed to ascertain clinical associations of ischaemic white matter damage. There were no clear associations between adverse clinical factors and prenatal ischaemic white matter damage. In contrast, pre-eclampsia, intrauterine growth retardation, and delivery without labour were associated with postnatal damage as were neonatal sepsis, necrotising enterocolitis, and seizures. The absence of a clear association between the timing of adverse clinical factors and the timing of ischaemic cerebral damage suggests that cerebral damage in very preterm babies may result from a sequence of events rather than one specific insult.
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PMID:Clinical associations and time of onset of cerebral white matter damage in very preterm babies. 879 52

Sixty-seven patients with brain abscess were managed over 19 years (1975-1993). Our series had a 2.5 to 1 male predominance; the age distribution was from 3 days to 81 years. The underlying conditions of hematogenic brain abscesses (n = 33; 49%) included lung infections (n = 16), heart disease (n = 4), sepsis (n = 10), and other foci (n = 3). Otolaryngologic infections led to the abscess in 10 cases; there were 9 traumatic abscesses. The causes remained unknown in 15 cases. There were 47 solitary abscesses (70%) and 20 multiple abscesses. The most frequent presenting signs and symptoms were neurologic deficits (n = 17), disturbances of consciousness (n = 14), seizures (n = 6), and headaches, meningism and vomiting (n = 13). Causative organisms were isolated in 39 cases (58%) and included staphylococci (n = 6), streptococci (n = 6), enterobacteriae (n = 2), and anaerobic pathogens (n = 9). The most reliable laboratory sign of inflammation was an elevated ESR (52/59 patients). With the advent of computed tomography, burr hole aspiration of the abscess with or without drainage was possible in 30 cases; the mortality in this subgroup was 9%. All 4 patients with surgical excision in the pre CT-era died. The mortality of patients treated with antibiotics only was 62% (18/29). Overall mortality was 37% (25/67), including 5 cases with post mortem-diagnosis of brain abscess. Good recovery was achieved in 29/42 survivors. Predictors of a poor outcome were the patient's age, the level of consciousness, multiple abscesses, polybacterial cultures, and a hematogenic etiology, but not the size of the abscess.
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PMID:[Bacterial brain abscess--experiences with 67 patients]. 880 80

Cerebrovascular disease may be secondary to various disorders including hypothyroidism, sepsis, neoplasia, hypertension, vascular malformation, and coagulopathy. Brain infarction or hemorrhage should be suspected in an animal with a sudden onset of a focal brain lesion. The recent availability of CT and MRI has improved our ability to diagnose cerebrovascular disease in animals. Treatment is directed at maintaining adequate oxygenation of the brain, controlling elevations of ICP, treating seizures, and identifying and treating any underlying disease. With appropriate care, many animals can recover.
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PMID:Cerebrovascular disease. 881 57

Thirty-one patients (26 males, 5 females) with mean age 35 +/- 19 years (range 8 to 85 years) were diagnosed as non-traumatic rhabdomyolysis by clinical findings and elevation of serum creatine kinase (CK) between January 1989 and December 1993. Causes, laboratory measures, clinical courses, and outcome were reviewed retrospectively. Drug abuse, seizure, and excessive activity are the most common etiologies for non-traumatic rhabdomyolysis. Twelve patients presented with muscular pain and seven patients with muscle weakness. Twenty eight patients had urinalysis and five of them (18%) had negative orthotolidine dipstick test. Only seven patients (25%) were detected positive orthotolidine test without microscopic hematuria. Patients with acute renal failure had higher levels of potassium and uric acid. The patients who developed acute renal failure after admission had significantly higher levels of uric acid. The peak levels of CK did not correlate with development of acute renal failure. There was no episode of hyercalcemia. Seventeen patients (55%) had acute renal failure. Hemodialysis was required in nine cases. All survivors recovered with normal renal function except one who needed maintenance hemodialysis after two months follow-up. Two patients died of multi-organ failure and sepsis.
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PMID:Non-traumatic rhabdomyolysis and acute renal failure. 893 69

A female infant presented with cyanosis, respiratory distress and unique to-and-fro murmur which she had since the age of 1-month-old. Absent pulmonary valve syndrome was diagnosed by echocardiography. She developed seizure disorders with hypocalcemia and pneumonia at the age of 2-month-old. The patient died from sepsis, intractable respiratory and heart failure. The postmortem study confirmed the diagnosis of congenital absent pulmonary valve associated with DiGeorge syndrome.
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PMID:Absent pulmonary valve syndrome associated with DiGeorge syndrome: report of one case. 894 31

Previous studies found that seizures in orthotopic liver transplantation (OLT) herald a catastrophic neurologic event, but the studies were done of patients who later died and came to autopsy. We studied 630 OLT patients. Laboratory values, electroencephalography, neuroimaging, and levels of cyclosporine or FK506 were reviewed. Neurotoxicity from immunosuppression was considered a trigger for seizures when toxic blood level or increases > or = to 100% were documented, or when white matter lesions or confusional state or tremors were present. Generalized tonic-clonic seizures occurred in 28 of 630 patients (4%). In 7 patients seizures were part of an agonal event (central nervous system infection [n = 3], anoxic encephalopathy [n = 1], cerebral edema with fulminant hepatic failure [n = 1], intracranial hemorrhage [n = 1], and sepsis [n = 1]. In 17 patients cyclosporine (n = 11) or FK506 (n = 6) could be implicated. Remaining causes were acute uremia (n = 1), meningioma (n = 1), and unknown (n = 2). All patients were initially treated with anticonvulsants. Median follow-up of 2 years did not reveal seizure recurrence after discontinuation of anticonvulsants. We conclude that the majority of new-onset seizures after OLT are not indicative of a poor prognosis. Immunosuppression neurotoxicity is the most frequent cause. Anticonvulsant therapy is not necessary for favorable long-term outcome.
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PMID:Causes and outcome of seizures in liver transplant recipients. 896 Jul 38

A 31-year-old pregnant woman who was an active cocaine abuser presented to our emergency department five times in 1 week for abdominal pain and vomiting. She continued to use cocaine regularly despite having abdominal pain. Her fifth admission was for seizures. There were no objective signs of peritoneal inflammation and the rectal guiac examination was repeatedly negative. The patient progressed to severe septic shock. Intraabdominal sepsis and/or bowel perforation was suspected. Exploratory laporatomy revealed gangrene and perforation of the small intestine and fecal peritonitis. She rapidly developed multiorgan failure and died. Gastrointestinal complications resulting from cocaine use are uncommon. Our case is unique in that the patient was pregnant, used cocaine by the intranasal route, and lacked objective signs of acute abdomen. Emergency physicians should be aware of the morbidity associated with the use of cocaine.
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PMID:Cocaine-associated intestinal gangrene in a pregnant woman. 927 Mar 93

Neonatal seizures in the neonatal period are symptoms of numerous underlying disorders of the neonate. We present a case in which neonatal seizures due to cerebral infarction led to a diagnosis in the mother. Neonatal convulsions caused by cerebral artery thrombosis is relatively rare in the neonatal period and is often secondary to indwelling intravascular catheters that cause thromboembolism, but may be associated with many conditions.1 Cerebral artery thrombosis in newborns, in which antiphospholipid antibodies (APA) were found in the mother, has been described in three case reports. Two of these premature infants were born with other risk factors for thrombosis. APA could not be identified in any of these three infants. In the two cases reported by Silver et al the diagnosis was made several months after birth. This case is unique in the fact that no other risk factors for thrombosis could be identified to explain the infarction, and that APA were found in the offspring of an apparently healthy mother. Whether the prior fetal death was caused by APA remains unclear. The finding of lupus anticoagulant in her child led to the diagnosis of antiphospholipid antibody syndrome in her. We believe that in case of cerebral artery thrombosis in a neonate, with no trivial cause such as an indwelling catheter or sepsis, both mother and infant should be tested for presence of APA, even when the mother seems healthy.
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PMID:An unusual cause of neonatal seizures in a newborn infant. 931 May 41

The newborn who presents with neurologic symptoms such as seizures or lethargy due to inborn error of metabolism is an important problem. Although each inborn error that presents in this manner is rare, these conditions are not rare as a group, and more than one in 1000 babies is affected with one of the more than 100 different inborn errors that are now known. Many of these conditions present with much the same features seen in sepsis or asphyxia and, when untreated, can lead rapidly to death or permanent neurologic damage. Early diagnosis and management may prevent some or all of this morbidity, and also permits the parents to be informed about the chances of having other affected children. Despite the large number and complexity, most metabolic encephalopathies can be diagnosed by applying a few simple clinical principles and laboratory tests. These principles, and the typical features of some inborn errors that present in the neonate, are detailed in this article.
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PMID:Catastrophic metabolic encephalopathies in the newborn period. Evaluation and management. 939 62

The main manifestations of neuromuscular disease in the newborn period are hypotonia and weakness. Infants with severe hypotonia but only marginal weakness usually do not have a disorder of the lower motor unit. These infants may have genetic conditions, metabolic disturbances, congenital heart disease, hypothyroidism, sepsis, or other systemic disorders. Early on, neonates with central nervous system pathology may present with profound hypotonia, decreased reflexes, and moderate to severe but transient weakness. However, they also tend to have seizures, obtundation, cranial nerve signs, or history of perinatal asphyxia.
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PMID:Neuromuscular disorders in the newborn. 939 65


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