Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with angiodysgenetic necrotizing encephalopathy or diffuse meningocerebral angiomatosis complicated by intraventricular hemorrhage, posthemorrhagic hydrocephalus, and signs of heart failure is reported. The hydrocephalus and cardiomegaly were diagnosed by fetal ultrasonography. Based on these pathologic findings, a vaginal delivery was induced at 36 weeks gestation. The patient was a female infant who died 24 hours after birth.
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PMID:Angiodysgenetic necrotizing encephalopathy or diffuse meningocerebral angiomatosis. 870 30

Here we report the clinical and pathological findings in a 30-year-old drug addict in whom an intravenous injection of heroin led to reversible coma with respiratory depression and heart failure. On regaining consciousness, the patient was found to have rhabdomyolysis with renal failure requiring dialysis and peripheral neuropathy. Three weeks later his neurological condition suddenly deteriorated and delayed encephalopathy developed, leading to death 20 days later. The neuropathological study of the brain disclosed pale, spongy myelin with diffuse reactive astrogliosis and microglial proliferation, without hypoxic necrotic lesions. The cerebral and cerebellar cortices were unchanged. The absence of typical hypoxic lesions and the presence of spongiosis with massive astrocytosis distinguished this case from the previously reported cases of delayed leukoencephalopathy following severe hypoxia. An immunocytochemical study designed to exclude an underlying alteration of the metabolic oxidative pathway detected normal expression of the respiratory chain complexes IV, III and V. Despite the absence of an oxidative chain alteration in our patient, we cannot exclude the possibility that an individual predisposition played a pathogenetic role in this delayed leukoencephalopathy.
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PMID:Delayed spongiform leukoencephalopathy after heroin abuse. 922 35

Recently, spinal cord stimulation (SCS) has been used for the treatment of patients in prolonged coma. However, the results of SCS in unresponsive patients with hypoxic encephalopathy at the chronic stage have not been satisfactory. Considering these circumstances, we began SCS from one month after the onset of hypoxic encephalopathy and evaluated its effect. Twelve patients (5 males and 7 females) with hypoxic encephalopathy, ranging in age from 7 to 72 years, were treated with SCS. The causes of hypoxia were acute cardiac failure in 4, automobile exhaust gas poisoning in 2, and asthma, pneumothorax, anaphylaxis, asphyxia, drowning and hypotension during aortic surgery in one patient each. One month after the onset, an electrode for electrical stimulation was implanted in the epidural space at the C2-C4 level under general anesthesia. The spinal cord was stimulated for 8 hours each day, starting on the day after implantation, and was continued for 3 months. Magnetic resonance imaging (MRI), cerebral blood flow (CBF) measurement using xenon-computed tomography (Xe-CT), and measurement of auditory evoked potential (AEP) and somatosensory evoked potential (SEP) were carried out 3 weeks after the onset for presurgical evaluation. Among the 12 patients, 7 (58%) showed clinical improvement, beginning within two weeks after starting stimulation. They were able to communicate with others and to express their emotion. However, disturbance of writing, picture drawing and calculation were not improved by stimulation. From presurgical evaluation, cases in which SCS therapy was effective had the following features: 1) No hemorrhagic infarction in the basal ganglia was demonstrable by MRI. 2) Mean hemispheric CBF measured by the Xe-CT method exceeded 25 ml/100 g per min. 3) The mean increase in hemispheric CBF 20 min after acetazolamide administration exceeded 5 ml/100 g per min. 4) An N20 peak was evident on the median nerve SEP, SCS appears to be an effective supplementary for unresponsive patients with hypoxic encephalopathy at the subacute stage, in addition to rehabilitation and drug therapy.
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PMID:[Spinal cord stimulation therapy at an early stage for unresponsive patients with hypoxic encephalopathy]. 959 12

Neonatal asphyxia is a major topic of neonatal research. However, no clear-cut physiologic parameters exist which enable an early identification of neonatal infants who are either at risk to develop brain damage or posthypoxic heart failure. Parameters indicating dysfunction of the heart and kidneys as creatinine and creatinine kinase have been evaluated. In our study, 47 asphyxiated infants (umbilical artery pH < 7.18 and either a 1-min Apgar score < 4 or a 5-min Apgar score < 7) were compared to 27 nonasphyxiated controls regarding significant differences in creatinine, creatinine kinase, its MB fraction, and a newly introduced myocardial hypoxia indicator -- troponin T -- to establish the value of these parameters in the retrospective diagnosis of asphyxia. Further we evaluated two subsets of these 47 asphyxiated infants with either subsequent signs of encephalopathy (seizures) or heart failure. Creatinine, creatinine kinase and troponin T were significantly elevated in asphyxiated infants compared with controls; no differences were found in creatinine kinase and its MB fraction. In asphyxiated infants with heart failure, troponin T was significantly higher than in the other asphyxiated infants. However, none of the parameters studied was significantly different in patients with brain damage compared with asphyxiated infants without neurological sequelae. Troponin T has a high positive predictive value in the postnatal diagnosis of asphyxia. The diagnostic power of troponin T equals that of creatinine. However, troponin T is more sensitive in the identification of infants with asphyxia and cardiocirculatory failure than creatinine. Creatinine kinase and its MB fraction have no diagnostic value.
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PMID:Value of myocardial hypoxia markers (creatine kinase and its MB-fraction, troponin-T, QT-intervals) and serum creatinine for the retrospective diagnosis of perinatal asphyxia. 961 54

Early detection of pathophysiological factors associated with permanent brain damage is a major issue in neonatal medicine. The aim of our study was to evaluate the significance of the CO2 reactivity of cerebral blood flow (CBF) in neonates with perinatal risk factors. Fourteen ventilated neonates with perinatal risk factors (pathological cardiotocogramm, low cord pH, postpartal encephalopathy) were enrolled into this prospective study. The study was performed 18-123 h after birth. CBF was measured using the noninvasive intravenous 133Xe method. Two measurements were taken with a minimal PaCO2-difference of 5 mm Hg. From the two CBF values the CO2 reactivity was calculated. Outcome was evaluated 1 year after birth. The CBF values at a lower PaCO2 ranged from 6.6 to 115. 2 ml/100 g brain issue/min (median = 18.2) and at a higher PaCO2 level from 7.1 to 125.7 ml/100 g brain tissue/min (median = 18.75). The calculated CO2 reactivity ranged from -9.6 to 6.6% (median 1.1%) change in CBF/mm Hg change in PaCO2. CO2 reactivity correlated with lowest pH (r2 = 0.35, p = 0.02). Two infants died, one of neonatal sepsis, the other of heart failure. Neurological outcome at the age of 1 year was normal in 11 patients, 1 had severe cerebral palsy. From the 12 surviving patients the patient with severe neurological deficit showed the highest CBF values (125.7 ml/100 g/min). Impaired chemical coupling of cerebral blood flow is compatible with intact neurological outcome in neonates with perinatal risk factors. CO2 reactivity in these newborns correlates with the lowest pH and may reflect the severity of perinatal asphyxia.
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PMID:Impaired chemical coupling of cerebral blood flow is compatible with intact neurological outcome in neonates with perinatal risk factors. 983 79

A 27-year-old female with short stature and mild hearing loss was diagnosed as having focal-segmental glomerulosclerosis by renal biopsy at our hospital. One year later she developed progressive renal dysfunction and cardiac failure and was admitted again to our hospital for evaluation. Though her only neurological disorder was mild hearing loss, her short stature and elevated lactate and pyruvate values in cerebrospinal fluid suggested mitochondrial cytopathy. A muscle biopsy specimen of the left biceps brachii, using modified Gomori trichrome stain, showed a typical image of ragged-red fibers, and an increased number of giant mitochondria with paracrystalline inclusions were visible by electron microscopy. Mitochondrial DNA from the skeletal muscle showed an A-to-G transition at 3243 of transfer RNALeu(UUR), the common point mutation for mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes. These data confirmed the diagnosis of atypical mitochondrial cytopathy with renal and heart involvement. Mitochondrial cytopathies are often associated with hypertrophic cardiomyopathy but rarely with renal disease. Among the few reported cases with associated renal disease, most included renal tubular disorders; few cases with focal glomerular sclerosis are known. The present case of atypical mitochondrial cytopathy was characterized by a unique clinical course and rare complications with focal-segmental glomerulosclerosis.
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PMID:A case of mitochondrial cytopathy with a typical point mutation for MELAS, presenting with severe focal-segmental glomerulosclerosis as main clinical manifestation. 984 35

The most venomous scorpion species are Buthotus tamulus of India, the Leiurus quinquestriatus and Androctonus crassicauda of North Africa and the Middle East, the Tityus serrulatus of Brazil, and the Centruroides suffussus of Mexico. The severity of scorpion envenomation varies with the scorpion's species, age, and size, and is much greater in children. Systemic intoxication reflects the overstimulation of the CNS, the sympathetic and parasympathetic nervous system. Severity ranges from local pain and paresthesia to fatal cardiotoxicity and encephalopathy. Symptoms include: agitation, tachycardia, vomiting, abdominal pain, salivation, diaphoresis, dehydration, muscle rigidity and twitching, tremor, seizures, coma, pupillary changes, hyperthermia, tachyarrythmias and occasionally bradyarrhythmias, hypertension, and less often hypotension, cardiac failure, and priapism in males. Laboratory abnormalities include: hyperglycemia, leucocytosis, transient elevation of cardiac and pancreatic enzymes, ischemic changes in the ECG, and evidence of cardiac dysfunction on echocardiography. The principles of management are: observation, cardiac monitoring, supportive treatment with intravenous fluids and electrolytes, and a meticulous use of cardiovascular agents: vasodilators, adrenergic antagonists, or calcium channel blockers in the hypertensive phase; and inotropic agents in the event of hypotension. Antiarrhythmics such as lidocaine, may be required. There is increasing evidence for the efficacy of specific antivenom. The advance in supportive care and antivenom efficacy has markedly improved the outcome of patients with scorpion envenomation.
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PMID:Clinical manifestations and management of scorpion envenomation. 1044 63

A 56-year-old woman with Werner's syndrome was admitted to our hospital because of intractable foot ulcer and malnutrition. She presented dementia consisting of childish behaviour, loss of intelligence, and severe amnesia. Brain CT revealed diffuse periventricular low density areas, and brain MRI also disclosed periventricular high intensity areas under T2-intensified conditions. These findings gave a diagnosis of progressive subcortical vascular encephalopathy of the Binswanger type, which seemed to be the cause of her dementia. She finally died of heart failure due to acute myocardial infarction. Mild to moderate demyelinization was found in the subcortical area of the autopsied cerebrum, confirming the clinical diagnosis. Generalized atherosclerosis characteristic of Werner's syndrome may have predisposed this patient to Binswanger's encephalopathy.
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PMID:[Werner's syndrome associated with progressive subcortical vascular encephalopathy of the Binswanger type]. 1057 50

Acute liver failure is a rare but potentially fatal disease. Adult definition of fulminant hepatic failure, which includes the development of hepatic necrosis and encephalopathy within 8 weeks of onset of liver disease does not apply to acute liver failure in children particularly if secondary to autoimmune or metabolic liver disease. The etiology of acute liver failure varies with the age of the child. In neonates, infection or an inborn error of metabolism are common, while viral hepatitis and drug induced liver failure are more likely in older children. The clinical presentation of acute liver failure includes jaundice, coagulopathy and encephalopathy. In neonates, encephalopathy may be subclinical. The management of acute liver failure includes assessment of prognosis for liver transplantation; prevention and treatment of complications while awaiting hepatic regeneration or a donor liver and hepatic support. The major complications of acute liver failure are sepsis, gastro-intestinal bleeding, cerebral edema, renal and cardiac failure. Selection for liver transplantation depends on the etiology of the disease, prognostic factors, the presence or absence of multisystem disease and/or reversible brain damage. Prognostic factors for survival are less well established in children than in adults but children with metabolic liver disease, prothrombin time > 50 seconds, rising bilirubin and falling transaminase, grade II or higher grade of hepatic coma indicate poor prognosis. Most children receive a reduced or split liver graft. Living related donations for acute liver failure are also carried out by some centres. Survival post liver transplantation for acute liver failure has improved and most recipients can expect a 70% five year survival.
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PMID:Acute liver failure. 1113 56

Congestive liver disease can be one of the clinical aspects of chronic heart failure. Fulminant hepatic failure can be a consequence of ischemic liver disease secondary to cardiogenic shock. We report a patient with chronic heart failure who was admitted to our hospital presenting general malaise with abnormal liver function tests, prothrombin time and renal failure. The study of viral and autoimmune liver diseases were negative. She did not consume hepatotoxic drugs. She presented encephalopathy without initial evidence of shock. On the fourth day, she presented clinical deterioration compatible with cardiogenic shock. Laboratory abnormalities were similar to those seen in congestive and ischemic liver disease. The patient died 24 hours later. The histology showed congestive and ischemic liver disease. There are several reports of chronic liver diseases without a clear etiology, caused by constrictive pericarditis or restrictive myocardiopathy. In this case, the patient presented fulminant hepatic failure without clear evidence of progressive heart failure. We emphasize the importance of cardiac diseases as possible causes of liver diseases without another clear explanation.
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PMID:[Fulminant hepatic failure. Atypical form of cardiac failure presentation]. 1118 58


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