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Biomedical subjects

B Pfausler

Publications and source records attributed to B Pfausler.

At least 37 records · Page 2Linked to original sources
PubMed1998

Tolerance and bactericidal action of N-chlorotaurine in a urinary tract infection by an omniresistant Pseudomonas aeruginosa.

N-chlorotaurine, a weak antimicrobial oxidant produced by stimulated human leukocytes, was used to treat cystitis caused by an omniresistant Pseudomonas aeruginosa. A 21-year-old male patient was treated by repeated daily lavages of the urinary bladder with an aqueous solution of 1% N-chlorotaurine for one month. N-chlorotaurine was well tolerated; no local or systemic side effects could be detected. Despite killing of > 10(6) cfu/ml of bacteria within ten minutes in vitro and in vivo, it was not possible to eradicate the Pseudomonas infection obviously caused by inflammation of the upper urinary tract and perpetuated by intravesical concrements. Nevertheless, in actually localized infection, treatment with N-chlorotaurine might be successful because of its sufficient bactericidal action.

Adult↗
PubMed1998

Cerebral blood flow velocity and perfusion in purulent meningitis: a comparative TCD and 99M-TC-HMPAO-SPECT study.

In 15 patients (median age 33 years; range 17-74 years) suffering from acute pneumococcal (10 cases) and meningococcal (five cases) meningitis, cerebral blood flow velocity (CBFV) was measured in the M1 - segment of the middle cerebral artery (MCA) by transcranial Doppler sonography, and cerebral perfusion changes were evaluated by 99m-Tc-hexamethylpropylene amine oxime single photon emission computed tomography (HMPAO SPECT). The objective of the study was to test whether increased CBFV during the acute phase of purulent meningitis reflects hyperemia, and to evaluate focal perfusion abnormalities and their correlation to CBFV changes. In eight patients with marked side-differences in CBFVs during the acute phase of the disease SPECT scans were normal in five. In three patients unilateral perfusion defects correlated with the side of higher CBFV. In seven patients presenting with symmetrically elevated CBFV, SPECT scans were normal in four and revealed focal abnormalities in the remaining three. Follow up SPECT scans were normal in 14/15 patients. The results of our study suggest that elevated CBFV in acute bacterial meningitis does not reflect cerebral hyperemia. Focal cerebral perfusion defects occur independently from functional alterations in the cerebral macrovasculature. A causative pathophysiologic relationship of high CBFV and focal perfusion defects cannot be drawn from these data.

Journal Article↗
PubMed1998

The persistent vegetative state after closed head injury: clinical and magnetic resonance imaging findings in 42 patients.

OBJECT: In this retrospective study, the authors analyzed the frequency, anatomical distribution, and appearance of traumatic brain lesions in 42 patients in a posttraumatic persistent vegetative state. METHODS: Cerebral magnetic resonance (MR) imaging was used to detect the number of lesions, which ranged from as few as five to as many as 19, with a mean of 11 lesions. In all 42 cases there was evidence on MR imaging of diffuse axonal injury, and injury to the corpus callosum was detected in all patients. The second most common area of diffuse axonal injury involved the dorsolateral aspect of the rostral brainstem (74% of patients). In addition, 65% of these patients exhibited white matter injury in the corona radiata and the frontal and temporal lobes. Lesions to the basal ganglia or thalamus were seen in 52% and 40% of patients, respectively. Magnetic resonance imaging showed some evidence of cortical contusion in 48% of patients in this study; the frontal and temporal lobes were most frequently involved. Injury to the parahippocampal gyrus was detected in 45% of patients; in this subgroup there was an 80% incidence of contralateral peduncular lesions in the midbrain. The most common pattern of injury (74% in this series) was the combination of focal lesions of the corpus callosum and the dorsolateral brainstem. In patients with no evidence of diffuse axonal injury in the upper brainstem (26% in this series), callosal lesions were most often associated with basal ganglia lesions. Lesions of the corona radiata and lobar white matter were equally distributed in patients with or without dorsolateral brainstem injury. Moreover, cortical contusions and thalamic, parahippocampal, and cerebral peduncular lesions were also similarly distributed in both groups. CONCLUSIONS: The data indicate that diffuse axonal injury may be the major form of primary brain damage in the posttraumatic persistent vegetative state. In addition, the authors demonstrated in this study that MR imaging, in conjunction with a precise clinical correlation, may provide useful supportive information for the accurate diagnosis of a persistent vegetative state after traumatic brain injury.

Adolescent↗
PubMed1997

Near infrared spectroscopy (NIRS) in patients with severe brain injury and elevated intracranial pressure. A pilot study.

Near infrared spectroscopy (NIRS) was used to asses changes in regional cerebral oxygen saturation (rSO2) in 8 head injured patients with an intracranial pressure (ICP) higher or lower than 25 mmHg (n = 4 for each group). NIRS values in the high ICP group (> 25 mmHg) were significantly lower than in the low ICP group (< 25 mmHg). In contrast, arterial pO2, pCO2, peripheral oxygen saturation and transcranial Doppler sonography (TCD) values were similar in both groups. To further investigate changes in rSO2 to changes in peripheral oxygen saturation and arterial pO2, patients of both groups underwent an artificial hyperoxygenation (50% O2) period of 3 minutes. Both groups revealed similar values in peripheral oxygen saturation, arterial pO2, and TCD velocities at the end of the hyperoxygenation period. However, rSO2 values in patients with an ICP > 25 mmHg were significant lower than in patients with an ICP < 25 mmHg after the hyperoxygenation period. In addition, patients with an ICP < 25 mmHg revealed a significant increase in rSO2 values at the end of the hyperoxygenation period, not detectable in patients with an ICP > 25 mmHg. Our results suggest that NIRS may be an additional diagnostic tool in the non-invasive evaluation of impaired cerebral microcirculation in patients with increased intracranial pressure.

Adult↗
PubMed1997

Cerebrospinal fluid (CSF) pharmacokinetics of intraventricular vancomycin in patients with staphylococcal ventriculitis associated with external CSF drainage.

We studied the efficacy and pharmacokinetics of intraventricularly administered vancomycin in three patients with shunt-associated staphylococcal ventriculitis. We instilled 10 mg of the drug intraventricularly every 24 hours. Cerebrospinal fluid (CSF) levels were measured 1 hour after instillation and then every 2 hours. Peak vancomycin levels reached a mean of 292.9 microg/mL. The mean trough levels, measured immediately before readministration of vancomycin, were 7.6 microg/mL; this level has proved to be sufficient for maintaining the necessary steady-state serum concentration of vancomycin. All three patients were cured clinically and bacteriologically, and CSF parameters returned to normal within 5-13 days. No side effects were observed. Our results suggest that intraventricularly administered vancomycin is a valuable therapeutic strategy for treating shunt-associated staphylococcal ventriculitis. In addition, we provide evidence that 10 mg of vancomycin, administered intraventricularly every 24 hours, allows maintenance of therapeutic drug levels in the CSF for at least 24 hours.

Brain Injuries↗
PubMed1997

Central nervous system pathology in patients with the Guillain-Barré syndrome.

Thirteen autopsy cases of patients with clinical criteria of the Guillain-Barré syndrome were investigated for pathological changes and cellular composition of inflammatory infiltrates in the CNS and PNS. The survival times from the onset of neurological symptoms until death ranged from 1 day to 12 months. In the CNS, degeneration of spinal posterior tracts was seen in three cases. Mononuclear infiltrates consisted of evenly proportioned lymphocytes and macrophages in cases with survival of 1 and 2 days, whereas macrophages predominated in cases with survival of 5 days and longer. Infiltrates presented as nodular clusters around blood vessels and neurons, or were scattered diffusely. They were found within the spinal cord in eight out of 13 cases, within the medulla oblongata in eight out of 12 cases, within the pons in five out of nine cases, and in one out of four midbrains. Activation of microglia, either focal or diffuse, was found in various degrees in 11 out of 13 cases, involving the spinal cord (six out of 13 cases), the medulla oblongata (10 out of 12 cases), the pons (five out of nine cases) or as subependymal rims along the walls of the ventricular system and the central canal of the spinal cord (seven out of 13 cases). In the PNS, myelin loss (12 out of 13 cases), axonal degeneration (six out of 13 cases) and mononuclear cell infiltrates (13 out of 13 cases) were seen in segmental and cranial nerves, spinal ganglia and spinal roots in varying distribution and severity. Mononuclear cell infiltrates were composed of macrophages and T lymphocytes, with even distribution in cases with short survival (1 and 2 days), and predominance of macrophages in cases with protracted clinical course. T lymphocytes were equally composed of OPD4+ and CD8+ cells without obvious differences between cases of short and long duration, or between PNS and CNS infiltrates in 11 out of 12 cases, whilst two cases had a dominant OPD4+ subset. We conclude that CNS pathology is frequent in patients with Guillain-Barré syndrome. It involves axons with secondary myelin impairment, microglial activation and inflammatory infiltration. In this series, primary demyelination is not found in the CNS. Changes such as degeneration of spinal posterior tracts are secondary to pathology in the PNS. Inflammatory cell reactions in the CNS are similar to those in the PNS and to CNS pathology in experimental allergic neuritis. This inflammation might reflect CNS immune activation in the absence of the relevant antigen, in addition to cellular reactions accompanying secondary CNS changes. The presence of distinct pathology in the CNS is in contrast with other recent studies on the pathology of Guillain-Barré syndrome which, unlike this study, may have been influenced by recently introduced treatments.

Adult↗
PubMed1997

Impaired microcirculation and tissue oxygenation in human cerebral malaria: a single photon emission computed tomography and near-infrared spectroscopy study.

Serial single photon emission computed tomography (SPECT), near-infrared spectroscopy (NIRS), and transcranial doppler (TCD) sonography examinations were performed to investigate changes of cerebral perfusion and tissue oxygenation in a patient with complicated cerebral malaria that have been acquired in Nigeria. On admission to the Neurologic Intensive Care Unit in Innsbruck, Austria, SPECT and NIRS revealed focal right hemispheric hypoperfusion and decreased oxygen saturation, respectively, correlating exactly to the patient's right hemispheric localizing signs. In contrast, TCD examinations of the basal cerebral vessels revealed normal flow patterns. The patient showed an initial Plasmodium falciparum parasitemia rate of 30% and was cured by intravenous quinine and oral mefloquine therapy. He was discharged without neurologic symptoms. Follow-up SPECT and NIRS examinations revealed regular cerebral perfusion and oxygenation patterns in both cortical hemispheres. In summary, the presented findings provide first evidence that noninvasive SPECT and NIRS may be important diagnostic tools in the evaluation of impaired cerebral microcirculation in patients with P. falciparum malaria.

Adult↗
PubMed1996

Cerebral Venous Thrombosis - A New Diagnosis in Travel Medicine?

Cerebral venous thrombosis is a syndrome seen in association with a large number of disease processes. The commonest reported causes in adults are oral contraception,1 pregnancy and complications associated with the postpartum period,2 systemic malignancy,3 and infection.4 In approximately 20% of adult cases reported during the past 20 years no etiology was established.5 Cerebral venous thrombosis can be caused by similar mechanisms, such as venous thrombosis, occurring elsewhere in the body, e.g., blood vessel wall alterations attributable to inflammation, infection, or invasion of malignant cells, as well as from changes in blood flow due to dehydration and changes in the coagulability of the blood (e.g., from use of oral contraception). PC Gates and HJM Barnett list 38 causes of cerebral venous thrombosis that were proven by angiography or autopsy. One item on their list was dehydration/ hyperpyrexia.5 Recently thrombosis of the venae saphena or femoralis/iliaca has been reported to occur in long distance air travelers.6 We would like to report on five patients (out of 15) in whom cerebral venous thrombosis was causatively linked with either long distance air travel alone, air travel and diarrhea, or air travel and exposure to tropical heat.

Journal Article↗
PubMed1996

Affinity of anti-GM1 antibodies in Guillain-Barré syndrome patients.

In this study, we investigated the affinity of anti-GM1 IgG antibodies as well as their IgG subclass distribution in a series of 38 patients with Guillain-Barré syndrome. In 7 sera elevated titres of IgG anti-GM1 antibodies could be detected. With respect to affinity there were two distinct groups of anti-GM1 antibodies: one group was of high affinity and did not cross-react with other glycolipids; the other group was of low affinity and cross-reacted with asialo-GM1. IgG1 was the predominant and almost exclusive subclass of high affinity anti-GM1 antibodies. Axonal degeneration occurred significantly more frequently in patients with high affinity anti-GM1 antibodies than in patients without anti-GM1 antibodies or in patients with low affinity anti-GM1 antibodies. The presence of anti-Campylobacter jejuni antibodies was not associated with a specific electrophysiological pattern. The prognosis was not dependent on the detection of any of the antibodies, whereas axonal loss and ventilation were associated with a poor prognosis.

Adult↗
PubMed1996

Molecular epidemiology of Klebsiella pneumoniae producing SHV-5 beta- lactamase: parallel outbreaks due to multiple plasmid transfer.

Over a period of 22 months, 32 patients treated in three independent intensive care units of the Innsbruck University Hospital were infected with extended-spectrum beta-lactamase-producing members of the family Enterobacteriaceae (30 Klebsiella pneumoniae isolates, 1 Klebsiella oxytoca isolate, and 1 Escherichia coli isolate). As confirmed by sequencing of a bla gene PCR fragment, all isolates expressed the SHV-5-type beta-lactamase. Genomic fingerprinting of epidemic strains with XbaI and pulsed-field gel electrophoresis grouped 20 of 21 isolates from ward A into two consecutive clusters which included 1 of 3 ward B isolates. All six K. pneumoniae isolates from ward C formed a third cluster. Stool isolates of asymptomatic patients and environmental isolates belonged to these clusters as well. Additionally, 2,600 routine K. pneumoniae isolates from the surrounding provinces (population, 900,000) were screened for SHV-5 production. Only one of six nonepidemic isolates producing SHV-5 beta-lactamase was matched with the outbreak strains by genomic fingerprinting. Plasmid fingerprinting, however, revealed the epidemic spread of a predominant R-plasmid, with a size of approximately 80 kb, associated with 29 of the 30 K. pneumoniae isolates. This plasmid was also present in the single K. oxytoca and E. coli isolates from ward C and in three nonepidemic isolates producing SHV-5. Our results underline that strain typing exclusively on the genomic level can be misleading in the epidemiological investigation of plasmid-encoded extended-spectrum beta-lactamases. Our evidence for multiple events of R-plasmid transfer between species of the family Enterobacteriaceae in this nosocomial outbreak stresses the need for plasmid typing, especially because SHV-5 beta-lactamase seems to be regionally spread predominantly via plasmid transfer.

Base Sequence↗
PubMed1996

Terson's syndrome in spontaneous subarachnoid hemorrhage: a prospective study in 60 consecutive patients.

Sixty consecutive patients with spontaneous subarachnoid hemorrhage (SAH) were prospectively studied by means of indirect funduscopy to address the question of incidence and prognostic implications of Terson's syndrome (TS) after SAH. Terson's syndrome was diagnosed in 10 (16.7%) of 60 patients and was associated with subarachnoid rebleeding in seven of 10. No correlation was found between anatomical localization of the ruptured aneurysm and TS laterality. Case fatality was nine (90%) of 10 in patients with TS compared to five (10%) of 50 in non-TS patients. It is concluded that TS is not infrequent (16.7%) in spontaneous SAH and has a poor prognosis, often heralding subarachnoid rebleeding.

Adult↗
PubMed1995

A randomised comparison of meropenem with cefotaxime or ceftriaxone for the treatment of bacterial meningitis in adults. Meropenem Meningitis Study Group.

Third-generation cephalosporins are presently the agents of choice for the empirical antimicrobial therapy of bacterial meningitis. However, a number of factors associated with these agents, namely the development of resistance by pneumococci, limited activity against some Enterobacteriaceae and Pseudomonas spp., and the possible adverse effects of their bacteriolytic mode of action, indicate that newer classes of antimicrobial agents be evaluated for the treatment of bacterial meningitis. Meropenem is a carbapenem antibiotic which is highly active against the major bacterial pathogens causing meningitis, and penetrates well into the cerebrospinal fluid. Two prospective randomised studies in 56 adult bacterial meningitis patients have compared meropenem 40 mg/kg 8-hourly, up to a maximum of 6 g/day (n = 28) with cephalosporin treatment, i.e. cefotaxime (n = 17) or ceftriaxone (n = 11). Patients were assessed by neurological examination, Glasgow Coma Score and Herson-Todd score. Clinical cure was observed in all 23 evaluable patients treated with meropenem (100%) and with 17 of the 22 evaluable cephalosporin-treated patients (77%). All pre-treatment isolates were eradicated except one isolate of Staphylococcus aureus in a cefotaxime-treated patient. Neurological sequelae were noted in three meropenem and four cephalosporin-treated patients. No patients in either treatment group experienced seizures after the start of therapy. This was despite the fact that a patient in each group had experienced seizures before therapy, several had underlying CNS disorders, and that doses of 6 g/day of meropenem were given. Hearing impairment was recorded in 11 meropenem and nine cephalosporin treated patients. Three patients in the meropenem group and one in the cephalosporin group died during treatment for reasons unrelated to study therapy. Overall, the results of this study indicate that meropenem is an effective and well-tolerated antibiotic for the treatment of bacterial meningitis in adults.

Adult↗
PubMed1993

Time course of cerebral blood flow velocity in central nervous system infections. A transcranial Doppler sonography study.

In a 3-year period, 110 patients with central nervous system infections of various causes were examined serially by means of transcranial Doppler sonography. In viral-induced infections, no changes of flow velocity in basal cerebral arteries were seen, whereas in bacterial meningitis, a significant increase of blood flow velocity in the middle cerebral artery was recorded. Its extent was mainly associated with the type of the infectious agent, most frequently observed in pneumococcal meningitis (77%). The increase was up to 100% of the baseline values and was reversible in all cases. All patients were offered full-scale neurointensive care, and all subjects with bacterial meningitis were fully heparinized.

Adolescent↗
PubMed1993

[Course and management of tetanus].

Within a span of 18 months 4 patients (2 men, 2 women) were admitted with generalized tetanus to our neurological intensive care unit. The "period of onset" ranged from 2 to 14 days. All patients needed artificial ventilation over 17 to 38 days. The clinical course was complicated by gram-negative pneumonia in 3 of the 4 patients. Time of hospitalization ranged between 35 and 60 days. One patient had never been immunized against tetanus. The other 3 had not received a booster dose for over 10 years. All 4 patients survived, 3 of them without sequelae.

Adult↗