Transcatheter closure of atrial septal defects without fluoroscopy: feasibility of a new method.

BACKGROUND: In an effort to reduce x-ray exposure, we developed a technique for transcatheter closure of atrial septal defects under echocardiographic guidance without fluoroscopy. To assess the efficiency of this procedure for routine use, we compared our initial results with those for the conventional procedure. METHODS AND RESULTS: Twenty-two randomly selected patients (median age 18 years; range 2 to 66 years) with atrial septal defects (n=13) or patent foramen ovale (n=9) underwent cardiac catheterization for possible interventional defect closure with echocardiography as the only imaging tool. Median stretched diameter was 9 mm (range 6 to 26 mm); median left-to-right shunt over the atrial septal defects was Qp/Qs=1.8 (range 1.5 to 2.6). An Amplatzer septal occluder was successfully implanted in 19 defects without fluoroscopy and in 3 with the help of radiography. After 1 month, complete defect closure was documented in all patients. Compared with the conventional procedure of a control group of 131 patients, procedure times were not significantly different (88 versus 100 minutes; P=0.09). However, the study group received significantly higher doses of propofol for sedation (9.9 versus 5.6 mg/kg body weight; P=0.002) owing to extended transesophageal echocardiography. CONCLUSIONS: In the majority of patients in whom transcatheter closure of interatrial communications with the Amplatzer septal occluder is possible, the procedure can be safely performed under echocardiographic guidance without fluoroscopy.

[Value of dexamethasone therapy in bacterial meningitis]. / Stellenwert der Dexamethasontherapie bei der bakteriellen Meningitis.

Due to growing understanding of pathophysiological mechanisms in acute inflammation new strategies for treatment of bacterial meningitis have been developed. The use of dexamethasone as adjunctive therapy for bacterial meningitis during the first 4 days (0.15 mg per kilogram body weight every six hours 30 min before antibiotic treatment for four days) showed a significantly reduce of neurologic sequelae in four clinical studies. A reduction of case fatality rate in more severe cases down to 50% was observed. In regard of these results the American academy of infectious diseases recommends since 1991 for children from the age of 3 month with Haemophilus influenzae meningitis a therapy regime as above.

[Hearing disorders in children less than 16 months of age after bacterial meningitis with reference to cerebrospinal fluid elastase]. / Hörstörungen bei Kindern unter 16 Monaten nach bakterieller Meningitis unter Berücksichtigung der Liquorelastase.

Hearing impairment as a sequela of acute bacterial meningitis is a well known complication. Dexamethasone therapy in addition to antibiotics is beneficial in the reduction of deafness, implicating that inflammation may be one reason for hearing impairment. The risk of hearing impairment in different types of bacterial meningitis is well studied. In very young children < 1.5 years of life the incidence of hearing loss and the possible correlation of laboratory data with the development of deafness is yet unknown. We therefore examined the brainstem auditory evoked potentials in 25 children between the first month and the 16th month of life who we treated for meningitis during 3 years in our hospital. 11 children were treated with dexamethasone. In 9 children we found abnormal brainstem auditory evoked potentials, which we controlled every 3 months. 7 children had transient conductive hearing impairment with good recovery during the first year after the disease. In 2 cases we found permanent bilateral sensorineural hearing loss. There was a significant relationship between hearing loss and elastase in cerebrospinal fluid. Dexamethasone reduced this relationship. A screening of hearing should be performed as routine control in all patients with acute meningitis. The association of high elastase in cerebrospinal fluid and later hearing impairment indicates a pathophysiological relation between activation of granulocytes and hearing loss.

[Elastase-alpha 1-proteinase inhibitor complex (E alpha 1 PI) and lactoferrin plasma concentrations in viral and bacterial infections]. / Elastase-alpha 1-Proteinaseinhibitorkomplex (E alpha 1 PI) und Lactoferrinplasmakonzentrationen bei viralen und bakteriellen Infektionen.

Typical alterations of the white blood cell count are often missed during the acute course of infectious diseases. Activiation and degranulation of granulocytes are followed by elevation of E alpha 1 PI and lactoferrin plasma concentrations under these conditions. The aim of our study was the evaluation of the diagnostic significance of these granulocyte parameters in relation with the absolute granulocyte count in infected pediatric patients. A total number of 106 patients at the age of 1 day to 16 years were studied. 25 children suffered from viral, 26 from localized and 23 from systemic bacterial infections, 32 children exhibiting no signs of infection served as controls. Results of the study are given as medians and ranges. Total granulocyte count was elevated above controls (4.8; 2.2-12.7/nl) only in patients with localized bacterial infections (13.3; 5.5-36.5/nl). E alpha 1 PI and lactoferrin plasma concentrations correlated well (r = 0.72) and were found to be significantly elevated in patients with localized bacterial infections (856; 363-4820 micrograms/l and 748; 206-2078 micrograms/l) and septicemia respectively (661; 256-2078 micrograms/l and 871; 160-9550 micrograms/l). A clearcut differentiation of septic and locally infected patients was given by the ratio of E alpha 1 PI and total granulocyte counts. Significantly elevated E alpha 1 PI concentrations of patients exhibiting viral infections (295; 86-690 micrograms/l) may suggest effective granulocyte activation under this condition. Finally we conclude that E alpha 1 PI and lactoferin plasma concentration related to total granulocyte counts in infected patients may serve as a helpful indicator of granulocyte activation during the acute course of the disease.

Elastase alpha 1 proteinase inhibitor complex, granulocyte count, ratio of immature to total granulocyte count, and C-reactive protein in neonatal septicaemia.

In a prospective study elastase alpha 1-proteinase inhibitor (E alpha 1PI), polymorphonuclear (PMN) count, the immature to total neutrophil count ratio (I/T ratio), and C-reactive protein (CRP) were analysed in 74 patients (76 cases) with neonatal septicaemia at the time of initial clinical symptoms. At that early stage of the disease, 94% of the patients had abnormal values for E alpha 1PI, 71% for I/T ratio, 61% for PMN count, and only 54% for CRP. PMN count was a poor indicator of septicaemia. Neutropenia, present in 26% of all patients, was related to normal E alpha 1PI in only 4 patients. The combined use of E alpha 1 and I/T ratio was the most sensitive indicator. In all patients irrespective of causative bacteria or disease onset at least one of these parameters was elevated. In early-onset septicaemia (n = 31), normal CRP values occurred significantly more often (63%) than in late-onset sepsis (33%). Even in five of the seven fatal cases, initial CRP measurements were normal. The sensitivity of PMN count and I/T ratio did not differ significantly between early- and late-onset septicaemia. Laboratory changes observed in 18 newborns during the first 3 days of the septic episode show that the rate of pathological values for E alpha 1PI and I/T ratio was highest at the time of initial clinical symptoms and decreased on days 2 and 3. In contrast, CRP reached maximal values as late as day 2 (88% abnormal values), followed by a decrease on day 3. We conclude that the use of E alpha 1PI may improve the laboratory detection of neonatal septicaemia especially if used in combination with I/T ratio.

Proteinase-antiproteinase imbalance in meningitis: determination of alpha 1 proteinase inhibitor (alpha 1PI), elastase-alpha 1PI complex, and elastase inhibition capacity in cerebrospinal fluid.

Mortality and long-term neurologic sequelae are still frequent complications of meningitis despite effective antibiotic treatment. This suggests that pathogen-independent inflammatory mechanisms may play an important role in the course of this illness. Neutrophil granulocytes form the primary immune defense in meningitis. Once activated, these cells release elastase into the cerebrospinal fluid (CSF). Elastase may induce tissue damage if local antiproteinase capacity is low as under normal conditions. To define the relevance of this mechanism we studied 22 patients with meningitis. Concentrations of elastase in complex with the main antiproteinase alpha 1-proteinase inhibitor (elastase-alpha 1 PI), alpha 1-proteinase inhibitor (alpha 1PI), and elastase inhibition capacity (EIC) were measured in CSF of 9 patients with bacterial meningitis (BM), aged 1 month-14 years; 13 patients with non-bacterial meningitis (NBM), aged 1 month-15 years; and 20 patients in whom meningitis was excluded after spinal tap (control group), aged 6 months-15 years. The concentration of elastase-alpha 1PI in the BM group (median 552 micrograms/l) was significantly higher than in either the NBM group (median 30 micrograms/l, p less than 0.01) or the control group (median 30 micrograms/l, p less than 0.01). Similarly, the alpha 1PI-concentration in the BM group was significantly higher (median 113 mg/l) than either the NBM group (median 13.7 mg/l, p less than 0.025) or the control group (median 6.3 mg/l, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

[Long-term substitution in homozygous alpha 1-antitrypsin deficiency. Effect of the proteinase-antiproteinase equilibrium in plasma and sputum]. / Dauersubstitution bei homozygotem alpha 1-Antitrypsin-Mangel. Einfluss auf das Proteinasen-Antiproteinasen-Gleichgewicht in Plasma und Sputum.

Long-term replacement with human alpha 1-antitrypsin (60 mg/kg once a week intravenously) was carried out in seven patients with homozygous alpha 1-antitrypsin deficiency (7 males, mean age 50.8 [40-59] years) and progressive pulmonary emphysema for an average of 16 (13-20) weeks. After at least 12 weeks' therapy the concentrations of alpha 1-antitrypsin, elastase-alpha 1-antitrypsin complex, alpha 2-macroglobulin, lactoferrin and elastase inhibition capacity in plasma and sputum were assayed, these assays being performed before starting the alpha 1-antitrypsin infusion and at various times during the following week. After the infusion the plasma concentration of alpha 1-antitrypsin rose from a depressed initial level (median 1.22 g/l) to a level approximately five times higher (median after 1 hour: 5.96 g/l, P less than 0.001), and then declined exponentially, though it never fell below the threshold of 35% of normal which is regarded as the protective level. Elastase inhibition capacity displayed similar changes (r = 0.85). The sputum concentration of alpha 1-antitrypsin rose more slowly than the plasma concentration; from the initial level (median 8 mg/l) it reached a maximum about four times higher after 24 hours (median 36 mg/l; P less than 0.02). Elastase inhibition capacity rose from 151 mIU/ml (median) before the alpha 1-antitrypsin infusion to 450 mIU/ml at 24 hours. These findings suggest that alpha 1-antitrypsin replacement will have beneficial effects on proteinase-antiproteinase equilibrium. Determination of elastase inhibition capacity in the sputum is suitable for monitoring dosage during replacement therapy.