Christof Thees

Pseudohypoxic brain swelling: a newly defined complication after uneventful brain surgery, probably related to suction drainage.

OBJECTIVEThis is the first description of a severe and sometimes fatal complication after uneventful intracranial surgery. The clinical presentation and imaging features mimic those of global cerebral hypoxia. Extensive investigations were performed to discover the pathogenesis. METHODSSeventeen cases of pseudohypoxic brain swelling (PHBS) were collected from our institution and from various other neurosurgical departments and were studied for common features. PHBS can occur in a mild, moderate, or severe degree. It is characterized by a very early postoperative onset of clinical deterioration (clouded or lost consciousness and pupillary abnormalities), in association with typical bilateral computed tomographic or magnetic resonance imaging changes (hypodensities or altered intensities in the basal ganglia and/or thalamus). The following variables were considered: age, primary pathological lesion and intracranial location, previous cranial surgery, anesthetic risk, type of anesthesia, approach and duration of surgery, intraoperative observations, technical monitoring results, and blood gas analyses. The results of postoperative computed tomography and various other imaging studies, intracranial pressure measurements, transcranial Doppler sonography, toxicological analyses, brain and muscle biopsies, and autopsies were also considered in the investigation. Several countermeasures were instituted and evaluated. RESULTSAnoxemic and ischemic hypoxia was excluded as a cause of PHBS. No evidence was found for inhibition of the respiratory chain, mitochondriopathy, poisoning, or adverse effects of drugs. CONCLUSIONIndications of intracranial hypotension, induced by suction drainage, being the main pathomechanism of PHBS are discussed. A serious warning is issued regarding the use of suction drainage after intracranial surgery.

Relationship between Intracranial Pressure and Critical Closing Pressure in Patients with Neurotrauma

Background The driving pressure gradient for cerebral perfusion is the difference between mean arterial pressure (MAP) and critical closing pressure (CCP = zero flow pressure). Therefore, determination of the difference between MAP and CCP should provide an appropriate monitoring of the effective cerebral perfusion pressure (CPPeff). Based on this concept, the authors compared conventional measurements of cerebral perfusion pressure by MAP and intracranial pressure (CPPICP) with CPPeff. Methods Simultaneous synchronized recordings of pressure waveforms of the radial artery and blood flow velocities of the middle cerebral artery were performed in 70 head trauma patients. CCP was calculated from pressure–flow velocity plots by linear extrapolation to zero flow. Results Intracranial pressure measured by intraventricular probes and CCP ranged from 3 to 71 and 4 to 70 mmHg, respectively. Linear correlation between ICP and CCP was r = 0.91. CPPICP was 77 ± 20 mmHg and did not differ from CPPeff; linear correlation was r = 0.92. However, limits of agreement were only ± 16.2 mmHg. Therefore, in 51.4% of the patients, CPPICP overestimated CPPeff by 19.8 mmHg at most. Conclusion Assuming that CPPeff (MAP − CCP) takes into account more determinants of cerebral downstream pressure, in individual cases, the actual gold standard of CPP determination (MAP − ICP) might overestimate the CPPeff of therapeutic significance.

Individual value of brain tissue oxygen pressure, microvascular oxygen saturation, cytochrome redox level, and energy metabolites in detecting critically reduced cerebral energy state during acute changes in global cerebral perfusion.

The authors assessed the diagnostic value of brain tissue oxygen tension (PbrO2), microvascular oxygen saturation (SmvO2), cytochrome oxidase redox level (Cyt a+a3 oxidation), and cerebral energy metabolite concentrations in detecting acute critical impairment of cerebral energy homeostasis. Each single parameter as well as derived multimodal indices (arteriovenous difference in oxygen content [AVDO2], cerebral metabolic rate for oxygen [CMRO2], fractional microvascular oxygen extraction [OEF]) were investigated during controlled variation of global cerebral perfusion using a cisternal infusion technique in 16 rabbits. The objective of this study was to determine whether acute changes between normal, moderately, and critically reduced cerebral perfusion as well as frank ischemia defined by local cortical blood flow (lcoBF), brain electrical activity (BEA), and brain stem vasomotor control can be reliably identified by SmvO2, PbrO2, Cyt a+a3 oxidation, or energy metabolites (glutamate, lactate/pyruvate ratio). PbrO2, SmvO2, and Cyt a+a3 oxidation, but not cerebral perfusion pressure, were closely linked to lcoBF and BEA and allowed discrimination between normal, moderately reduced, and critically reduced cerebral perfusion (P < 0.01). Glutamate concentrations and the lactate/pyruvate ratio varied significantly only between moderately reduced cerebral perfusion and frank ischemia (complete loss of BEA and brain stem vasomotor control). Therefore, PbrO2, SmvO2, and Cyt a+a3 oxidation, but not glutamate and the lactate/pyruvate ratio, reliably predict the transition from moderately to critically reduced cerebral perfusion with impending energy failure.

Influence of fentanyl, alfentanil, and sufentanil on motor evoked potentials.

The effects of the opioids fentanyl, alfentanil, and sufentanil on motor pathways were studied in a total of 30 rabbits. Compound muscle action potentials (CMAP) were recorded from the extensor muscles of the upper extremity as well as evoked spinal cord potentials (ESCP) from the thoracic epidural space in response to electrical stimulation of the motor cortex. After establishing stable baseline values, an equipotent intravenous bolus of one of the three opioids was applied that abolished reflex motor response to noxious stimulation. Motor evoked potentials (MEP) were recorded from the time of bolus administration until recovery of MEP amplitudes and latencies. Afterwards, the opioids were administered continuously with cumulative dosage up to total absence of motor evoked response. Our results show a dose-dependent suppression of the CMAP: When reflex movement to noxious stimulation was extinguished, we found a significant (P < .001) reduction of the amplitudes to 34+/-18% (mean +/- SD) in the fentanyl group, to 43+/-24% in the alfentanil group, and to 53+/-20% of baseline values in the sufentanil group. Increasing opioid plasma levels were associated with complete extinction of the CMAP. We hypothesize that the descending volleys within motor pathways are mainly inhibited at a spinal level, because ESCP, particularly the number of spinal I-waves, are not severely affected even when CMAP are completely suppressed. In conclusion, intraoperative monitoring of descending pathways by means of MEP during anesthesia with opioids is feasible at anesthetic plasma concentrations maintaining a surgical level of analgesia. Even with high opioid plasma levels, a valid MEP monitoring could be performed evaluating neural activity of spinal MEP.

Cerebral haemodynamics and carbon dioxide reactivity during sepsis syndrome

BackgroundMost patients with sepsis develop potentially irreversible cerebral dysfunctions. It is yet not clear whether cerebral haemodynamics are altered in these sepsis patients at all, and to what extent. We hypothesized that cerebral haemodynamics and carbon dioxide reactivity would be impaired in patients with sepsis syndrome and pathological electroencephalogram patterns.MethodsAfter approval of the institutional ethics committee, 10 mechanically ventilated patients with sepsis syndrome and pathological electroencephalogram patterns underwent measurements of cerebral blood flow and jugular venous oxygen saturation before and after reduction of the arterial carbon dioxide partial pressure by 0.93 ± 0.7 kPa iu by ypervent ilation. The cerebral capillary closing pressure was determined from transcranial Doppler measurements of the arterial blood flow of the middle cerebral artery and the arterial pressure curve. A t test for matched pairs was used for statistical analysis (P < 0.05).ResultsDuring stable mean arterial pressure and cardiac index, reduction of the arterial carbon dioxide partial pressure led to a significant increase of the capillary closing pressure from 25 ± 11 mmHg to 39 ± 15 mmHg (P < 0.001), with a consecutive decrease of blood flow velocity in the middle cerebral artery of 21.8 ± 4.8%/kPa (P < 0.001), of cerebral blood flow from 64 ± 29 ml/100 g/min to 39 ± 15 ml/100 g/min (P < 0.001) and of jugular venous oxygen saturation from 75 ± 8% to 67 ± 14% (P < 0.01).ConclusionIn contrast to other experimental and clinical data, we observed no pathological findings in the investigated parameters of cerebral perfusion and oxygenation.

S(+)-ketamine attenuates myogenic motor-evoked potentials at or distal to the spinal α-motoneuron

UNLABELLED We investigated the effect of S(+)-ketamine on spinal cord evoked potentials (ESCPs) and myogenic motor-evoked potentials after electrical stimulation of the motor cortex in a rabbit model. This study was designed to characterize the relationship between ESCP characteristics and corresponding changes in compound muscle action potentials (CMAPs) derived from fore and hind limbs. Direct (D) and indirect (I) corticospinal volleys (ESCP) from the upper and lower thoracic spinal cord, recorded by two bipolar epidural electrodes, were assessed during IV administration of 0.02, 0.05, 0.1, and 0.2 mg. kg(-1) x min(-1) of S(+)-ketamine, each before and after neuromuscular blockade (0.4 mg/kg of cisatracurium), in 16 New Zealand White rabbits after single-pulse bipolar electrical stimulation of the motor cortex at 50 (threshold), 60, and 70 V. CMAP amplitudes at fore and hind limbs were significantly suppressed (P < 0.01) during infusion at 0.1 and 0.2 mL x kg(-1) x min(-1), whereas neither corresponding D- nor I-waves were altered. Similar findings were obtained during variation of stimulus amplitude (50-70 V). Multivariate regression analysis of CMAP amplitudes and various ESCP characteristics demonstrated no apparent interparametric association. These findings indicate that S(+)-ketamine modulates CMAP independent from corticospinal D- and I-wave-mediated facilitation at or distal to the spinal alpha-motoneuron. IMPLICATIONS S(+)-Ketamine combines several anesthetic properties suitable for total IV neuroanesthesia, including minimal effects on neurophysiological monitoring. Recording of neural and myogenic responses after electrical stimulation of the motor cortex indicates that S(+)-ketamine modulates myogenic motor-evoked potentials by a peripheral mechanism at or distal to the spinal alpha-motoneuron.