Decompression only versus fusion in octogenarians with spinal epidural abscesses: early complications,clinical and radiological outcome with 2-year follow-up

Despite increased life expectancy due to health care quality improvements globally, pyogenic vertebral osteomyelitis (PVO) treatment with a spinal epidural abscess (SEA) remains challenging in patients older than 80 years. We aimed to assess octogenarians for PVO prevalence with SEA and compare after-surgery clinical outcomes of decompression and decompression and instrumentation. A retrospective review of electronic medical records at a single institution was conducted between September 2005 and December 2020. Patient demographics, surgical characteristics, complications, hospital course, and 90-day mortality were collected. Comorbidities were assessed using the age-adjusted Charlson comorbidity index (CCI). Over 16 years, 35 patients aged ≥80 years with PVO and SEA were identified. Eighteen patients underwent surgical decompression (“decompression group”), and 17 underwent surgical decompression with instrumentation (“instrumentation group”). Both groups had a CCI >6 (mean±SD, 8.9±2.1 vs. 9.6±2.7, respectively; p=0.065). Instrumentation group patients had a significantly longer hospital stay but no ICU stay. In-hospital and 90-days mortality rates were similar in both groups. The mean follow-up was 26.6±12.4 months. No further surgeries were performed. Infection levels and neurological status were improved in both groups at discharge. At the second-stage analysis, significant improvements in the blood infection parameters and the neurological status were detected in the decompression group. Octogenarians with PVO and SEA have a high adverse events risk after surgical procedures. Surgical decompression might contribute to earlier clinical recovery in older patients. Thus, the surgical approach should be discussed with patients and their relatives and be carefully weighed.

     

Intrakranielle Druck-Volumen-Beziehung

Posttraumatic increase of intracranial pressure (ICP) is a strong prognostic factor for the outcome of patients after traumatic brain injury. After exhausting all compensatory mechanisms ICP increases exponentially, where ICP_norm=(CSF production*CSF flow resistance)+venous pressure_{(sinus sagittalis)}=10–15 mmHg. The ICP curve is influenced by the compliance (ΔV/ΔP) and elasticity (ΔP/ΔV) of the brain. Marmarou could demonstrate that the non-linear cranio-spinal pressure-volume relationship describes a logarithmic, mono-exponential, strongly linear relationship between pressure and volume and named this the pressure volume index (PVI=log ICP/ΔV). The pressure volume index describes the volume necessary to increase ICP by a factor of 10. Additionally to PVI the measurement of volume-pressure response (VPR) was introduced. The continuous intracranial compliance could be determined on the principle of pulsatile volume increases as an equivalent of very small intra-cranial volume increases. However, to ascertain functional status of the injured brain a combination of measurements of different parameters, such as tissue oxygen partial pressure (p_tiO₂), cerebral blood flow (CBF), microdialysis and electrocorticography (ECoG) is recommended.     

Effects of lisuride hydrogen maleate on pericontusional tissue metabolism, brain edema formation, and contusion volume development after experimental traumatic brain injury in rats

After traumatic brain injury (TBI), the primary insult is followed by a cascade of secondary events which lead to enlargement of the primary lesion and are potentially amenable to therapeutic intervention. Lisuride is a dopaminergic agonist with additional serotoninergic, adrenergic, and glutamate antagonistic properties. In lack of previous data on lisuride in TBI, and based on well documented changes of dopamine metabolism after TBI, we speculated that lisuride could provide neuroprotection in the acute and post-acute stage of controlled cortical impact (CCI) injury in rats. The effect of varying dosages of lisuride on physiological parameter was investigated. Cerebral microdialysis (CMD) was employed to provide a temporal profile of lactate, pyruvate, glucose and glutamate in the pericontusional brain tissue. Additionally, brain edema formation and the development of contusion volume were assessed. In this study, no effect of treatment was seen on physiological parameters or microdialysis profiling of tissue metabolites. Whereas posttraumatic increase in brain water content and an increase in contusion volume could be observed, there was no significant effect of treatment. Taken together, our results suggest that lisuride does not provide neuroprotection in the CCI model at the acute and subacute stages. Based on the available literature, however, it might be possible that dopamine agonists such as lisuride, respectively, improve outcome in terms of cognitive function in a chronic setting.     

Cerebral metabolism after early decompression craniotomy following controlled cortical impact injury in rats

After traumatic brain injury, a cascade of metabolic changes promotes the development of secondary brain damage. In this study, we examined metabolic changes in rats in the acute stage after trauma. Furthermore, we investigated the effect of a very early decompression craniotomy on intracranial pressure (ICP) and on metabolic parameters. For this study, a moderate controlled cortical impact injury (CCII) on rats was performed. The observation time was 180 minutes after trauma. ICP was measured continuously and microdialysate samples were collected every 30 minutes from the peri-contusional region. As representative metabolic parameters, glutamate, lactate, lactate/pyruvate ratio (L/P ratio), and glucose concentrations were measured. Compared to sham-operated animals, a significant, sustained decrease in glucose concentration and increase in L/P ratio occurred immediately after CCII. Additionally, delayed increase in lactate and glutamate concentrations occurred 60 minutes after trauma. After this initial peak, glutamate concentrations declined continuously via the observation time and reached levels comparable to sham-operated animals. In our model, thus we could detect a very early deterioration of glucose utilization and energy supply after trauma that recovered, due to the moderate intensity of the trauma, within 60 minutes without leading to ischemia in the peri-contusional region. Following decompression craniotomy, the increase of intracranial pressure could be reduced significantly. Any significant beneficial effects on metabolic changes, however, could not be proven in this very early stage after moderate CCII.     

Classification and therapy of craniocerebral injury (CCI)

In spite of great success in research severe traumatic brain injury (TBI) remains the most frequent cause for morbidity and mortality in the age < 45 years. The primary lesion emerges at the moment of trauma. Due to several pathophysiological mechanisms secondary lesions occur that enlarge size of contusions significantly. As a consequence of intracranial bleedings and brain edema intracranial pressure (ICP) increases and threaten the patient. Extent of severity (declared in Glasgow Coma Scale Score [GCS]), expansion and type of bleedings (acute and chronic subdural hemorrhage, epidural bleeding, contusion bleedings and intracerebral hemorrhage) determinate operative and conservative therapy as well as intensive care medicine. A specific feature represents frontobasal lesions that, apart of penetrating injuries, are treated interdisciplinary not before ICP is stable, brain edema declining and coagulation sufficient several days after trauma. A persisting rhinoliquorrhoe cause meningitis up to 85 % within 10 years. Patient with GCS < 8 have to be intubated and controlled ventilated. Basic monitoring does not differ from those of other patients treated at the intensive care ward (sufficient breathing [pO (2), pCO (2)], arterial blood pressure, CBC and coagulation parameters, fluid monitoring and nutrition). Additionally, ICP have to be measured and be treated corresponding to the algorithm of ICP treatment. Complementary, oxygen saturation of brain tissue (ptiO (2)), local cerebral blood flow (r-CBF) and cerebral metabolism (micro dialysis) can be measured. Just the combination of the single monitoring parameters gives evidence of the functional condition of the injured brain and relieved planning and performing of the appropriate therapy.     

Neurochemical Monitoring of Therapeutic Effects in Large Human MCA Infarction

Background and purpose  Cerebral microdialysis is an invasive monitoring tool allowing analysis of various substances derived from the extracellular space in brain tissue such as glutamate, glycerol, lactate, and pyruvate. In order to assess the potential effects of hemicraniectomy, hypothermia and conservative therapy on these substances, we used neurochemical monitoring with microdialysis in large human stroke patients. Methods  This is an open, prospective observational study in 24 patients with large MCA infarction undergoing either hypothermia (33°C), hemicraniectomy, or maximum conservative therapy. Microdialysis probe placement was aimed at the peri-infarct tissue within 24 h after stroke onset. Glutamate, glycerol, pyruvate, and lactate were analyzed every 60 min. Measurements of two consecutive days were pooled for statistical analysis. Results  Average glutamate concentrations in patients treated with hemicraniectomy (5.3 ± 0.5 μmol/l, P < 0.0001; n = 6) and hypothermia (14.5 ± 3.6 μmol/l, P < 0.0001; n = 14) were significantly lower than in conservatively treated patients (68.3 ± 5.2 μmol/l; n = 4). Glycerol concentration was significantly lower in patients treated by hypothermia (111 ± 17 μmol/l; P < 0.0001) and hemicraniectomy (138 ± 8 μmol/l; P < 0.0001) as compared to conservatively treated patients with 612 ± 27 μmol/l. The lactate–pyruvate ratio was significantly lower both in the hypothermia (16.2 ± 3.3) and hemicraniectomy groups (31.3 ± 1.5) than in the conservative treatment group (56 ± 2.9). Conclusion  Microdialysis allows bed-side monitoring of neuroprotective effects of stroke rescue therapies such as hypothermia and hemicraniectomy. Rescue of peri-infarct tissue and/or prevention of secondary ischemic injury could be associated with a lower mortality in invasively treated patients.     

The BrainIT group: concept and core dataset definition

Summary ¶Introduction. An open collaborative international network has been established which aims to improve inter-centre standards for collection of high-resolution, neurointensive care data on patients with traumatic brain injury. The group is also working towards the creation of an open access, detailed and validated database that will be useful for post-hoc hypothesis testing. In Part A, the underlying concept, the group coordination structure, membership guidelines and database access and publication criteria are described. Secondly, in part B, we describe a set of meetings funded by the EEC that allowed us to define a Core Dataset and we present the results of a feasibility exercise for collection of this core dataset. Methods. Four group meetings funded by the EEC have enabled definition of a Core Dataset to be collected from all centres regardless of specific project aim. A paper based pilot collection of data was conducted to determine the feasibility for collection of the core dataset. Specially designed forms to collect the core dataset demographic and clinical information as well as sample the time-series data elements were distributed by both email and standard mail to 22 BrainIT centres. A deadline of two months was set to receive completed forms back from centres. A pilot data collection of minute by minute physiological monitoring data was also performed. Findings. A core-dataset was defined and can be downloaded from the BrainIT web-site (go to Core dataset link at: www.brainit.org). Eighteen centres (82%) returned completed forms by the set deadline. Overall the feasibility for collection of the core data elements was high with only 10 of the 64 questions (16%) showing missing data. Of those 10 fields with missing data, the average number of centres not responding was 12% and the median 6%. An SQL database to hold the data has been designed and is being tested. Software tools for collection of the core dataset have been developed. Ethics approval has been granted for collection of multi-centre data as part of a pilot data collection study. Interpretation. The BrainIT network provides a more standardised and higher resolution data collection mechanism for research groups, organisations and the device industry to conduct multi-centre trials of new health care technology in patients with traumatic brain injury.Published online July 23, 2003     

Anticonvulsive effects of the dopamine agonist lisuride maleate after experimental traumatic brain injury

Traumatic brain injury is a heterogeneous disease, encompassing a wide range of pathologies. The dopamine agonist lisuride is well established in the therapy of Parkinson's disease. Additionally to its dopaminergic effects it decreases prolactine release, reducing the amount of inflammatory mediators such as TNF-α or Il-6. Lisuride has strong binding affinity to serotonergic and histaminergic receptors on neuronal and glial cells leading to scavenging of highly reactive free radicals. Due to its interaction with dopaminergic D2 and D4 receptors as well as 5-HT-1A receptors, NMDA-receptor signaling and glutamate-mediated excitotoxicity can be modulated beneficially. Despite of these promising neuroprotective effects, experimental data scrutinizing the effects of lisuride after acute brain injury are sparse. We therefore investigated the effect of lisuride after controlled cortical impact injury (CCII) in rats. 70 male Sprague–Dawley rats were randomized to lisuride or to placebo treatment by an initial s.c. loading dose (0.3 mg/kg BW) and following continuous application (0.5 mg/kg/d) by s.c. implanted osmotic pumps. In three experimental groups we determined (sub)acute neuro-physiological changes after trauma. Mean arterial blood pressure, intracranial pressure, and electrical brain activity were monitored acutely for up to 3 h after trauma. Brain edema formation was assessed 24 h after CCII. Furthermore, contusion volumes were quantified by magnetic resonance tomography and neurological testing was performed for up to 7 days after injury. Associated with the administration of lisuride there was a significant reduction in duration and number of post-traumatic seizures. Despite of a sustained arterial hypotension following the initial bolus administration in the treatment group, contusion volumes and neurological function tests did not differ significantly in comparison to the control group. Overall, lisuride seems to have significant anticonvulsive effects but seems not to influence secondary brain damage in this experimental model.     

Thirty days complication rate following surgery performed for deep-brain-stimulation.

Serious adverse events (SAEs) during the first 30 postoperative days after stereotactic surgery for Deep-Brain-Stimulation performed in 1,183 patients were retrospectively collected from five German stereotactic centers. The mortality rate was 0.4% and causes for death were pneumonia, pulmonary embolism, hepatopathy, and a case of complicated multiple sclerosis. The permanent surgical morbidity rate was 1%. The most frequently observed SAEs were intracranial hemorrhage (2.2%) and pneumonia (0.6%). Skin infection occurred in 5 of 1,183 patients (0.4%). Surgical complications caused secondary AEs (e.g. pneumonia) preferentially in older patients and in patients treated for Parkinson's disease (PD). Complication rates did not differ among the five centers.