J. Meixensberger

Decompressive Craniectomy in Patients with Uncontrollable Intracranial Hypertension

There has been controversial discussion about the benefits of decompressive craniectomy in patients with critically raised intracranial pressure (ICP) after severe head injury. The aim of this retrospective study was to analyze the results of secondary decompressive craniectomy in patients with uncontrollable raised ICP after maximum aggressive medical treatment. The data of 28 patients (mean age 22 years, range 8-44 years) with severe head injury and posttraumatic cerebral edema were analyzed retrospectively. Surgery was not indicated in patients with vast primary lesions, hypoxia, ischemic infarction, brainstem injuries and central herniation. The outcome was classified according to the Glascow Outcome Scale (GOS) after one year. The decompressive crainectomy was performed an average of 68 hours after trauma, and ICP (< 25 mm Hg) decreased always while cerebral perfusion pressure (CPP > 75 mm Hg) improved as well as cerebral blood flow and microcirculation to normal values. 15 patients (56%) had a good outcome after one year (GOS 4 + 5). 5 patients (18%) were severely disabled, 4 patients (14%) remained in vegetative state and 3 patients (11%) died. Decompressive craniectomy should be kept in mind as the last therapeutic step, especially in young patients with head injury and raised ICP, which is not controllable with conservative methods.

Brain tissue pO2 in relation to cerebral perfusion pressure, TCD findings and TCD-CO2-reactivity after severe head injury

SummaryAs a reliable continuous monitoring of cerebral blood flow and/or cerebral oxygen metabolism is necessary to prevent secondary ischaemic events after severe head injury (SHI) the authors introduced brain tissue pO2 (ptiO2) monitoring and compared this new parameter with TCD-findings, cerebral perfusion pressure (CPP) and CO2-reactivity over time on 17 patients with a SHI. PtiO2 reflects the balance between the oxygen offered by the cerebral blood flow and the oxygen consumption by the brain tissue. According to TCD-CO2reactivity PtiO2-CO2-reactivity was introduced.After initally (day 0) low mean values (ptiO2 7.7 +/−2.6 mmHg, TCD 60.5 +/−32.0 cm/sec and CPP 64.5 +/−16.0 mmHg/, ptiO2 increased together with an increase in blood flow velocity of the middle cerebral artery and CPP. The relative hyperaemic phase on days 3 and 4 was followed by a decrease of all three parameters. Although TCD-CO2-reactivity was except for day 0 (1.4+/−1.5%), sufficient. ptiO2-CO2-reactivity sometimes showed so-called paradox reactions from day 0 till day 3, meaning an increase of ptiO2 on hyperventilation. Thereafter ptiO2-CO2-reactivity increased, increasing the risk of inducing ischaemia by hyperventilation.The authors concluded that ptiO2-monitoring might become an important tool in our treatment regime for patients requiring haemodynamic monitoring.

Studies of Tissue PO2 in Normal and Pathological Human Brain Cortex

Brain cortex PO2 was measured after craniotomy and opening of the dura mater in 26 patients. We determined the brain tissue PO2 under standard narcotic conditions and after changing arterial PO2 and PCO2. Patients were divided into two groups (normal and pathological), depending on the aspect of their cortex on Ct/MRI and intraoperative appearance of the cortex. No statistical significantly difference was seen between tissue PO2 of the normal and the pathological group. A significant difference was seen only between the normal group and a subgroup with brain swelling (p = 0.0344). In the normal group no correlation was seen between tissue PO2 and arterial PO2 (r = 0.1541, p = 0.3076), whereas in the pathological group and especially in the oedema subgroup there was a highly significant correlation between tissue PO2 and PaO2 (r = 0.754, p = 0.0015 and r = 0.888, p = 0.0007). Breathing 100% oxygen changed tissue PO2 to 137.8 or 352 mmHg in the normal or the pathological group, respectively. Again, there was no correlation between tissue PO2 and PaO2 in the normal group (r = 0.1071, p = 0.392), whereas this correlation was significant in the pathological and the oedema subgroup (r = 0.6291, p = 0.0473 and r = 0.8385, p = 0.0185). This is evidence for regulatory mechanisms of tissue PO2. During hyperventilation no significant difference in tissue PO2 between the normal and the pathological group was seen. Low tissue PO2 values, however, indicate a risk for inducing ischemia.

Influence of body position on tissue-pO2, cerebral perfusion pressure and intracranial pressure in patients with acute brain injury

It is a common practice to position head-injured patients in bed with the head elevated above the level of the heart in order to reduce intracranial pressure (ICP). This practice has been in vivid discussion since some authors argue a horizontal body position will increase the cerebral perfusion pressure (CPP) and therefore improve cerebral blood flow (CBF). However, ICP is generally significantly higher in the horizontal position. The aim of this study was to evaluate changes in regional microcirculation using tissue pO2 (ti-pO2), as well as changes in cerebral perfusion pressure (CPP) and intracranial pressure induced by changes in body position in patients with head injury. The effect of 0 degree and 30 degrees head elevation on ti-pO2. CPP, ICP and arterial blood pressure (MABP) was studied in 22 head injured patients during day 0-12 after trauma. The mean ICP was significantly lower at 30 degrees head elevation than at 0 degree (14.1 + 8.6 vs. 19.9 + 8.3 mmHg). While MABP was unaffected by head elevation, CPP was slightly higher at 30 degrees than at 0 degree (76.5 + 13.5 vs. 71.5 + 13.2 mmHg). However, regional ti-pO2 was unaffected by body position (30 degrees vs. 0 degree: 24.9 + 13.1 vs. 24.7 + 12.9 mmHg). In addition, there was no change in the time course after trauma concerning these findings in the individual patients. The data indicate that a moderate head elevation of 30 degrees reduces ICP without jeopardizing regional cerebral microcirculation as monitored using a polarographic ti-pO2 microcatheter.

Brain tissue pO2 and outcome after severe head injury

Although the use of on-line monitoring of brain ti-pO2 is increasing, so far the critical level of 10 mmHg is derived from animal experiments and clinical analyses: no hard proof on outcome basis has been given until now. The authors present an outcome analysis of 35 patients with severe head injury. Inclusion criteria were: start of ti-pO2 monitoring < or = 40 h post-injury, the probe lying in CT scan normal tissue and the GOS at 6 months being available. The good outcome group (GOS 4 + 5, n = 17) showed a 17.7+/-9.1 h delay from the injury to the monitoring compared to the bad outcome group (GOS 1-3, n = 18) with (14.2+/-9.1 h) (p < 0.05). Age and initial Glasgow Coma Score were not different. In the bad outcome group there were more patients with a diffuse injury type 3 and 4. The distribution of the ti-pO2 values show in all the examined time intervals (day 0-6, 0-72 h, 0-48 h and 0-24 h) a left shift in the bad outcome group with most pronounced difference for ti-pO2 < or = 10 mmHg. For the period from 0-48 h and even more from 0-24 h post-injury, the difference between both groups was significant (p = 0.036 and p = 0.013). In the bad outcome group 35.5% of the values from 0-24 h were < 10mmHg (compared to 10.6% in the good outcome group. ti-pO2 values > or = 50 mmHg were seen more often in the bad outcome group; this occurred mainly after 48-72 h post-injury. The authors concluded that brain ti-pO2 monitoring is able to detect the occurrence of early hypoxic insults. Brain ti-pO2 monitoring is an important parameter in the multimodality monitoring system.

Autocrine growth regulation in neuroectodermal tumors as detected with oligodeoxynucleotide antisense molecules.

The cell lines of three neuroectodermal tumors, two glioblastomas (HTZ-146, HTZ-17) and one melanoma (HTZ-19) were established and screened for the expression of growth factors by northern blotting and immunochemical methods. All three tumors were positive for platelet-derived growth factor- (PDGF-) A-, -B-chain, and basic fibroblast growth factor (bFGF) messenger ribonucleic acids. Cultured cells as well as original tumor material were also positive for PDGF-AA-, PDGF-BB, and bFGF protein, as shown by immunochemistry. To investigate the possible pathophysiological role of PDGF and bFGF, antisense technology was employed with chemically modified nuclease-stable 14-mer phosphorothioate oligodeoxynucleotides. Proliferation of all three tumors was reduced to a different extent with antisense phosphorothioate oligodeoxynucleotides in vitro, targeted against PDGF-A-chain-, -B-chain-, and -bFGF-messenger ribonucleic acid. These data indicate autocrine stimulatory loops for PDGF and bFGF, which may be blocked, may have different relevance in neuroectodermal tumors in vitro, and may have conceivable future therapeutic implications.

Intra-operative colour-duplex-sonography in the surgical management of cerebral AV-malformations.

Summary In this prospective study the role of intra-operative Colour-Duplex-Sonography (=CDS) during surgery of arteriovenous malformations (=AVM) is evaluated. During the last three years 20 consecutive patients with supratentorial AVMs were examined by intra-operative CDS in order to evaluate the potential of CDS to 1) localize the AVM, 2) differentiate between embolized and perfused parts, 3) identify feeding and draining vessels and 4) control the complete excision of the AVM. All AVMs were localized supratentorially, 9 were grade I and II (according to Spetzler and Martin [31]), 8 grade III and 3 grade IV. 11 were partly embolized and 8 associated with an intracerebral bleeding. In all cases the nidus was correctly localized sonographically by its typical bidirectional flow pattern in Colour-mode. CDS guided the surgeon directly to all (11 cases) deep-seated AVMs (2 to 4cm subcortically). The smallest nidus measured 10 mm. 28 of 34 angiographically defined main feeding and 18 of 23 draining vessels were identified. 14 patients were controlled sonographically at the end of the resection regarding the completeness of excision. In 11 patients CDS was negative and was confirmed by either postoperative angiography or MRI in 10 patients. In one case residual AVM tissue was missed by CDS. Positve CDS findings in 3 cases were all confirmed by microscopic re-inspection, angiography and CCT. Our results suggest that CDS is able to localize AVMs intra-operatively with minimal instrumentation. It allows safe navigation to deep-seated malformations with high accuracy. Feeding and draining vessels can be identified and completeness of resection can be controlled.

Brain tissue pO2-monitoring: Catheterstability and complications

The authors report on the stability and complications of 73 LICOX brain ti-pO2-microcatheters in 70 patients. Mean monitoring time was 7.5 +/- 4.0 days. Patients prone to cerebral hypoxia (after severe head injury (GCS < 9) or a subarachnoid hemorrhage) had a ti-pO2-microcatheter inserted next to the ICP-probe in the typical frontal position. After the first 15 insertions, instead of the 3-way-screw (needing a 6 mm burrhole), a 1-way-screw (needing a 2.7 mm burrhole) was used for fixation in the bone; by doing so, the procedure can be performed in the ICU and takes only 15 min. Whenever possible a calibration at room air (to determine the sensitivity-drift) and in oxygen free solution (to determine the zero-drift) was performed after removal of the catheters. Ideally the expected pO2 at room air was around 154 mmHg (temperature dependent) and at zero calibration 0 mmHg. Mean sensitivity-drift for 54 catheters was -8.5 +/- 15.4%. Dividing the catheters into groups, depending on the duration of monitoring (1-4, 5-8 and 9-16 days), revealed that the greatest part of the (negative) sensitivity-drift occurred during day 1-4 after insertion. After 1 week of monitoring sometimes a positive drift occurred (being far less than the negative drift during the first 4 days). Compared to the old catheters (-10.3 +/- 17.3%) (on the first half of the patients) the new ones showed a lower sensitivity-drift (-6.8 +/- 13.4%). The zero-drift of 56 catheters was low with mean drift after 7.5 +/- 4.0 days of 1.5 +/- 1.5 mmHg. Here also the highest drift occurred on day 1-4 after insertion. No infection was seen and 2 times (2.7%) a small hematoma, not needing evacuation occurred. As the ti-pO2-catheter (having a smaller diameter) and the ICP-catheter were inserted at the same time, one cannot distinguish which catheter caused the hematoma. A possible explanation for the occurrence of the two hematomas is the insertion of the catheters too close to the midline. The authors conclude that LICOX ti-pO2-monitoring is a safe and reliable method. Further decrease of the complication rate and increase of the catheter-stability may be expected.

Multimodal Hemodynamic Neuromonitoring — Quality and Consequences for Therapy of Severely Head Injured Patients

Fifty-five head injured patients (GCS < 8) were studied at an average of 7.5 +/- 3.4 days on the ICU to check quality of hemodynamic monitoring and the consequences for therapy. Multimodal neuromonitoring included intracranial pressure (ICP), mean arterial pressure (MAP), cerebral perfusion pressure (CPP), endtidal CO2 (EtCO2) as well as brain tissue--pO2 (p(ti)O2), regional oxygen (rSO2) and jugular venous oxygen saturation (SjO2). Regional p(ti)O2 as well as global SjO2 were sensitive technologies to detect hemodynamic changes. However analyzing reliability and good data quality regional p(ti)O2 (up to 95%) was superior to jugular bulb oximetry (up to 50%). Longterm-measurements of rSO2 using near infrared spectroscopy reached, if possible, a restricted reliability (good data quality up to 70%) and sensitivity in comparison to p(ti)O2. Especially p(ti)O2 enabled detection of critical p(ti)O2 (< 15 mm Hg) in up to 50% frequency during the first days after trauma and a second peak after day 6 to 8 according to evidence of CPP insults. Knowledge of baseline p(ti)O2 and CO2-reactivity allowed minimizing risk of ischemia by induced hyperventilation and improvement on cerebral microcirculation after mannitol administration could be individually recognized.

Maffucci's syndrome with bilateral cartilaginous tumors of the cerebellopontine angle.

Maffuccis syndrome is characterized by the combination of multiple enchondromas (Olliers disease) and hemangiomatosis. These hemangiomas develop in the subcutaneous tissue and form red-blue tumors dispersed over the whole body. Intracranial involvement is rare, making a preoperative radiological diagnosis and differentiation from other tumors rather difficult. The radiological characteristics and successful removal of the intracranial part of a chondrosarcoma of the cerebellopontine angle in a case of Maffuccis syndrome are reported in this paper.