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Matthias Jaeger

Publications and source records attributed to Matthias Jaeger.

5 recordsLinked to original sources

Continuous assessment of cerebrovascular autoregulation after traumatic brain injury using brain tissue oxygen pressure reactivity.

OBJECTIVE: To evaluate whether two newly developed indexes of brain tissue oxygen pressure reactivity (ORx and bPtio2) provide information on the status of cerebrovascular autoregulation after traumatic brain injury. This was accomplished by analyzing the relationship between these indexes and an index of cerebrovascular pressure reactivity (PRx). PRx is an established parameter for estimation of cerebrovascular autoregulation. DESIGN: Retrospective analysis of prospectively collected data. SETTING: Neurosurgical intensive care unit of a university hospital. PATIENTS: Twenty-seven patients suffering from severe traumatic brain injury. INTERVENTIONS: Continuous monitoring of mean arterial blood pressure, intracranial pressure, cerebral perfusion pressure, and partial pressure of brain tissue oxygen (Ptio2) was performed for an average of 6.5 days. ORx was calculated as a moving correlation coefficient between values of cerebral perfusion pressure and Ptio2. The bPtio2 was calculated as a moving value of the slope of the linear regression function between cerebral perfusion pressure and Ptio2. PRx was calculated as a moving correlation coefficient between values for intracranial pressure and mean arterial blood pressure. Outcome was assessed at 6 months after traumatic brain injury (Glasgow Outcome Scale). MEASUREMENTS AND MAIN RESULTS: Both ORx and bPtio2 correlated significantly with PRx (r=.55 for ORx, r=.52 for bPtio2, p<.01). PRx and ORx showed a significantly negative correlation to the monitored Ptio2 values (r=-.42 for PRx, r=-.41 for ORx, p<.05) and outcome (r=-.52 for PRx, r=-.62 for ORx, p<.01), whereas bPtio2 did not. CONCLUSIONS: ORx and, to a lesser extent, bPtio2 correlated with the autoregulatory marker PRx and provide additional information about the status of cerebrovascular autoregulation after traumatic brain injury. The data also suggested that patients with impaired autoregulation are at increased risk for secondary cerebral hypoxia.

Adolescent↗

Online assessment of brain tissue oxygen autoregulation in traumatic brain injury and subarachnoid hemorrhage.

Monitoring of brain tissue oxygenation (ptiO2) enables early diagnosis of secondary cerebral ischemia and may guide a cerebral perfusion pressure (CPP) orientated therapy. The purpose of our study was to explain the concept of ptiO2-autoregulation, defined as the ability of the brain to maintain ptiO2 despite changes in CPP, and to show the different states of ptiO2-autoregulation we found. Microcatheters to assess ptiO2 and intracranial pressure were implanted into cerebral 'tissue at risk' of patients suffering from traumatic brain injury or subarachnoid hemorrhage. By using a multimodal neuromonitoring setup and in-house built software we assessed and displayed online the relationship between ptiO2 and CPP based on a data buffer consisting of 12 h. Depending on the linear regression slope (bptiO2 = delta ptiO2/delta CPP), we defined the state of ptiO2-autoregulation as present (0 < or = bptiO2 < or = 1/6), moderate (1/6 < bptiO2 < or = 1/3), impaired (bptiO2 > 1/3) or inverse (bptiO2 < 0). When ptiO2-autoregulation is present, an elevation in CPP is ineffective to raise ptiO2. In contrast, an increase in CPP elevates ptiO2 more pronounced in impaired than in moderate ptiO2- autoregulation, but decreases ptiO2 in inverse ptiO2-autoregulation. We conclude that online assessment of ptiO2-autoregulation gives valuable information on which patient will benefit from an increase in CPP and which CPP should be achieved to do so.

Adult↗

Monitoring of brain tissue oxygenation following severe subarachnoid hemorrhage.

The purpose of this prospective observational study was to investigate the relation between the frequency of critical neuromonitoring parameters (brain tissue pO2, (PtiO2) < or = 10 mmHg, intracranial pressure (ICP) > 20 mmHg, cerebral perfusion pressure (CPP) < or = 70 mmHg) and outcome after severe aneurysmal subarachnoid hemorrhage (SAH). In a prospective study on 42 patients monitoring of ICP, CPP, and PtiO2 (in the area at risk for vasospasm) was performed. All patients were primarily classified as Hunt and Hess grade 4 or with secondary deterioration to this grade. Relative proportions of PtiO2 < or = 10 mmHg (n = 42), ICP > 20 mmHg (n = 25) and CPP < or = 70 mmHg (n = 23) were derived from multimodal neuromonitoring data sets for different time intervals, i.e. 1. the total monitoring time; 2. the total monitoring time without the last two monitoring days; 3. the second last monitoring day; and 4. the last monitoring day. Patients were divided into nonsurvivors (GOS = 1) and survivors (GOS = 3-5). For the total monitoring time, significant differences in the relative proportion of critical values were found for all neuromonitoring parameters (p < 0.05). The detailed analysis of consecutive time intervals revealed significantly increased proportions of critical values in nonsurvivors for all neuromonitoring parameters during the last day only. Additionally, ICP > 20 mmHg was significantly more frequent during the second last day (p < 0.01). For other time periods no differences were observed. We conclude, that critical neuromonitoring values are not early predictors of nonsurvival in patients suffering from severe SAH.

Adult↗

Neurosurgical emergencies and missing neurosurgical intensive care unit capacity: is "operate-and-return" a sound policy?

Available neurosurgical intensive care beds are rare and are often regarded as a precondition for accepting remote neurosurgical emergencies for operative treatment. From a medical and ethical point of view, the practice of rejecting acute patients as a result of a shortage of intensive care unit beds is questionable, because the primary need is fast treatment, and postoperative intensive care is secondary. We performed a retrospective analysis of outcome of 36 patients, who returned straight from our operating room to the intensive care unit of the referring hospital because no domestic neurosurgical intensive care unit beds were available (group 1). For the two largest cohorts, acute subdural haematoma ( =12) and primary intracerebral haemorrhage ( =15), outcome was compared by matched pair analysis with control patients kept in-house postoperatively (group 2). The mortality rate was higher in group 1 compared with group 2 (acute subdural haematoma 67 versus 58%; intracerebral haemorrhage 47 versus 40%). Despite this tendency, we regard "operate-and-return" treatment as a sound and practicable alternative to offer to hospitals trying to refer patients with neurosurgical emergencies. It is to be preferred to denying treatment, because this results in a delay or cancellation of treatment, with the associated negative effects on outcome. However, postoperative neurosurgical intensive care unit treatment has to be considered the optimum goal, and there needs to be a continuous demand to authorities to increase the number of neurosurgical intensive care unit beds.

Aged↗

Monocyte-derived dendritic cells release neopterin.

Increased neopterin concentrations in body fluids are found in diseases associated with activated, cell-mediated immunity including infections, autoimmune diseases, and certain malignancies. Monocytes/macrophages are known to secrete large amounts of neopterin upon stimulation with interferon-gamma (IFN-gamma). Ontogenetically, the major part of dendritic cells (DC) belongs to the myeloid lineage. Therefore, we investigated whether cultured monocyte-derived DC can elaborate neopterin. Cells were treated with cytokines in the presence or absence of monocyte-conditioned medium as a maturation stimulus. DC secreted an average 3.5 nmol/l neopterin. In response to IFN-gamma, cells significantly increased their output of neopterin. In distinction to monocytes/macrophages, neopterin production in DC was highly sensitive to IFN-alpha and IFN-beta. Further, lipopolysaccharides (LPS) enhanced neopterin synthesis, whereas tumor necrosis factor alpha, interleukin (IL)-1beta, IL-2, IL-10, and IL-18 were ineffective. Simultaneously, tryptophan degradation by induction of indoleamine (2,3)-dioxygenase (IDO) was tested in stimulated cells. Our results showed that IFN-gamma as well as LPS are inducers of IDO in DC.

Cell Culture Techniques↗