Axel Piepgras

Management of severe traumatic brain injury by decompressive craniectomy.

OBJECTIVE The beneficial effect of decompressive craniectomy in the treatment of head trauma patients is controversial. The aim of our study was to assess the value of unilateral decompressive craniectomy in patients with severe traumatic brain injury. METHODS We retrospectively investigated 49 patients who underwent decompressive craniectomy. Intracranial pressure, cerebral perfusion pressure, therapy intensity level, and cranial computed tomographic scan features (midline shift, visibility of ventricles, gyral pattern, and mesencephalic cisterns) were evaluated before and after craniectomy. The gain of intracranial space was calculated from cranial computed tomographic scans. Patient outcome was graded using the Glasgow Outcome Scale. RESULTS Thirty-one patients (63.3%) underwent rapid surgical decompression within 4.5 +/- 3.8 hours after trauma; in 18 patients (36.7%), delayed surgical decompression was performed 56.2 +/- 57.0 hours after injury. Patients younger than 50 years or patients who underwent rapid surgical decompression had a significantly better outcome than older patients or patients who underwent delayed surgical decompression. Craniectomy significantly decreased midline shift and improved visibility of the mesencephalic cisterns. The state of the mesencephalic cisterns correlated with the distance of the lower border of the craniectomy to the temporal cranial base. Alterations in intracranial pressure, cerebral perfusion pressure, and therapy intensity level were not significant. The overall mortality of the patients corresponded to the reports of the Traumatic Coma Data Bank (1991). CONCLUSION Although there was a significant decrease in midline shift after craniectomy, this did not translate into decompressive craniectomy demonstrating a beneficial effect on patient outcome.

Rapid active internal core cooling for induction of moderate hypothermia in head injury by use of an extracorporeal heat exchanger.

OBJECTIVE Moderate hypothermia (32 degrees C) may limit postischemic neuronal damage and is increasingly used clinically in head injury and stroke. For the use of hypothermia as a neuroprotective agent in the prevention of ischemic damage, it is necessary to induce it as soon as possible after the insult and to keep it at the lowest safe level. Active core cooling using an extracorporeal heat exchanger may circumvent the rather slow induction speed and temperature drifts experienced with surface cooling techniques. METHODS In eight patients with severe head injuries (Glasgow Coma Scale score, 4-5), a venovenous extracorporeal circulation was established via a percutaneously introduced double-lumen cannula in the femoral vein. A heat exchanger was connected via a pressure-controlled roller pump. In addition to standard parameters, brain white matter temperature was continuously recorded as the target temperature. Cooling was initiated as early as possible with an extracorporeal temperature of 30 degrees C and maintained at a 32 degrees C brain temperature for 48 hours, and then gradual rewarming for 24 hours. RESULTS Cooling was able to be initiated within 6 hours and 48 minutes +/- 3 hours and 47 minutes (mean +/- standard deviation) after trauma. A brain temperature of 32 degrees C was reached within 1 hour and 53 minutes +/- 1 hour and 21 minutes after induction of cooling with a cooling speed of 3.5 degrees C per hour. Brain temperature was able to be controlled within 0.1 degrees C intervals, which was especially helpful in gradual rewarming. No cardiac abnormalities or statistically significant changes in coagulation parameters occurred. Mean platelet count decreased to 89,614+/-42,090 on Day 3 after treatment. No clinical bleeding complications or problems resulting from extracorporeal circulation occurred. Moderate hypothermia was a helpful tool for managing increased intracranial pressure; however, five patients of this series died either of their intracranial abnormalities (n = 4) or of a delayed septic shock after pneumonia (n = 1) at various points in time during therapy. The three survivors experienced either an excellent or a good recovery. CONCLUSION The results of this investigation suggest that the use of an extracorporeal heat exchanger to achieve active core cooling is suitable for fast and accurately controllable induction, maintenance, and reversal of moderate hypothermia in emergency situations with reliable control of temperature. In this small series of highly selected patients with severe head injuries, we did not note a beneficial effect of hypothermic therapy on outcome.

Effect of Moderate Hypothermia on Experimental Severe Subarachnoid Hemorrhage, as Evaluated by Apparent Diffusion Coefficient Changes

OBJECTIVE The aims of this study were to investigate the early changes in the mean apparent diffusion coefficient (ADC) after severe subarachnoid hemorrhage (SAH), as a marker of ischemic damage, and to examine the effects of moderate hypothermia, induced at various time points, on ADC changes. METHODS ADC maps were calculated from diffusion-weighted, blipped-epi, spin echo, magnetic resonance imaging sequences (2.35-T BIOSPEC 24/40 scanner; Bruker Medizin Technik GmbH, Karlsruhe, Germany) for 21 anesthetized (0.45–1% halothane, temperature-adjusted/30% oxygen/69% nitrogen) and ventilated Wistar rats. After baseline scanning, bolus injection of 0.5 ml of autologous arterial blood or artificial cerebrospinal fluid (control group), into the cisterna magna, was performed. Serial scanning was performed for 3 hours after injection, using normothermic or hypothermic (32°C) rats. In an additional series of experiments, hypothermia was initiated either immediately or 60 minutes after normothermic SAH. The water contents of the removed brains were calculated using the wet/dry weight method. RESULTS The ADC values did not change in the control group but decreased to 88.6 ± 5.2% (P < 0.05 versus baseline) after SAH and remained significantly decreased throughout the experiment in normothermia. An injection of blood during hypothermia caused an initial decrease in ADC to 96.1 ± 5.6% (P < 0.05 versus baseline); values continuously increased and reached normal levels within 60 minutes. Delayed hypothermia also normalized ADC values within the observation period. The brain water content in the control group was 80.3 ± 0.1%, that after SAH in normothermia was 81.1 ± 0.7%, and that after SAH in hypothermia was 79.3 ± 0.5%. CONCLUSION This model of severe SAH in rats causes significant ADC changes, which are reversible by application of moderate hypothermia even when it is induced after a 60-minute delay. These findings support the concept of moderate hypothermia exerting a neuroprotective effect in severe SAH.

Characterization of an Anterior Circulation Rat Subarachnoid Hemorrhage Model

BACKGROUND AND PURPOSE Our aim was to demonstrate the feasibility of an angiographically controlled rat model for the study of macrocirculatory and microcirculatory changes of the anterior intracranial circulation after subarachnoid hemorrhage. METHODS Subarachnoid hemorrhage was induced by transorbital injection of 0.3 mL of nonheparinized autologous arterial blood into the chiasmatic cistern. Changes in regional cerebral blood flow were continuously recorded with the use of laser-Doppler flowmetry over the parietal cortex. Angiographic verification of middle cerebral artery diameter was performed by carotid catheterization at baseline and 2 days after injection of blood or artificial cerebrospinal fluid. We monitored intracranial and systemic blood pressure during and after injections. RESULTS Injection of artificial cerebrospinal fluid in the control group did not change the diameter of the middle cerebral artery. Injection of blood caused a significant arterial narrowing of 17.5%, from 0.37 +/- 0.04 mm to 0.31 +/- 0.04 mm after 2 days (P = .0001). In the control group regional cerebral blood flow decreased to 75.9 +/- 16.8% of preinjection control but quickly recovered to 99.7 +/- 19.4%. Intracranial pressure increased for 5 minutes after the injection to a maximum of 27.3 +/- 8.9 mm Hg, accompanied by a 10% decrease in mean arterial pressure. A fall in cerebral blood flow to 53.1 +/- 26.3% in blood-injected animals that recovered to only 80.7 +/- 16.9% of baseline values during the observation period of 30 minutes was noted. A peak intracranial pressure of 45.7 +/- 11.5 mm Hg occurred 2 minutes after injection with a decrease in mean arterial pressure of 13%, resulting in a markedly lower cerebral perfusion pressure than in the control group. CONCLUSIONS An angiographically controlled model of subarachnoid hemorrhage primarily involving the anterior circulation is feasible in the rat. The resulting narrowing of the middle cerebral artery reflects moderate vasospasm and will allow further microcirculatory studies with cranial windows.

Mild and Moderate Hypothermia (α-Stat) Do Not Impair the Coupling Between Local Cerebral Blood Flow and Metabolism in Rats

BACKGROUND AND PURPOSE The effects of hypothermia on global cerebral blood flow (CBF) and glucose utilization (CGU) have been extensively studied, but less information exists on a local cerebral level. We investigated the effects of normothermic and hypothermic anesthesia on local CBF (LCBF) and local CGU (LCGU). METHODS Thirty-six rats were anesthetized with isoflurane (1 MAC) and artificially ventilated to maintain normal PaCO(2) (alpha-stat). Pericranial temperature was maintained normothermic (37.5 degrees C, n=12) or was reduced to 35 degrees C (n=12) or 32 degrees C (n=12). Pericranial temperature was maintained constant for 60 min until LCBF and LCGU were measured with autoradiography. Twelve conscious rats served as normothermic control animals. RESULTS Normothermic anesthesia significantly increased mean CBF compared with conscious control animals (29%, P<0.05). Mean CBF was reduced to control values with mild hypothermia and to 30% below control animals with moderate hypothermia (P<0.05). Normothermic anesthesia reduced mean CGU by 44%. No additional effects were observed during mild hypothermia. Moderate hypothermia resulted in a further reduction in mean CGU (41%, P<0.05). Local analysis showed linear relationships between LCBF and LCGU in normothermic conscious (r=0.93), anesthetized (r=0.92), and both hypothermic groups (35 degrees C r=0. 96, 32 degrees C r=0.96, P<0.05). The LCBF-to-LCGU ratio increased from 1.5 to 2.5 mL/micromol during anesthesia (P<0.05), remained at 2.4 mL/micromol during mild hypothermia, and decreased during moderate hypothermia (2.1 mL/micromol, P<0.05). CONCLUSIONS Anesthesia and hypothermia induce divergent changes in mean CBF and CGU. However, local analysis demonstrates a well-maintained linear relationship between LCBF and LCGU during normothermic and hypothermic anesthesia.

Relationship between local cerebral blood flow and metabolism during mild and moderate hypothermia in rats.

Background: Hypothermia may interfere with the relationship between cerebral blood flow (CBF) and metabolism. Because this conclusion was based on the analysis of global values, the question remains whether hypothermic CBF/metabolism uncoupling exists on a local cerebral level. This study investigated the effects of hypothermic anesthesia on local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU). Methods: Thirty-six rats were anesthetized with isoflurane (1 minimum alveolar concentration) and artificially ventilated to maintain normal arterial carbon dioxide partial pressure (p H-stat). Pericranial temperature was maintained as normothermic (37.5°C, n = 12) or was reduced to 35°C (n = 12) or 32°C (n = 12). Pericranial temperature was maintained constant for 60 min until LCBF or LCGU were measured by autoradiography. Twelve conscious rats served as normothermic controls. Results: Compared with conscious animals, mean CBF remained unchanged during normothermic anesthesia. Mean CBF significantly increased during mild hypothermia but was unchanged during moderate hypothermia. During normothermic anesthesia, mean CGU was 45% lower than in conscious controls (P < 0.05). No further CGU reduction was found during mild hypothermia, whereas CGU further decreased during moderate hypothermia (48%;P < 0.05). Local analysis showed a linear LCBF/LCGU relationship in conscious (r = 0.94) and anesthetized (r = 0.94) normothermic animals, as well as in both hypothermic groups (35°C: r = 0.92; 32°C: r = 0.95;P < 0.05). The LCBF-to-LCGU ratio increased from 1.4 (conscious controls) to 2.4 (normothermic isoflurane) and 3.6 ml/&mgr;mol (mild and moderate hypothermia, P < 0.05). Conclusions: Decrease of mean CGU at unchanged or increased mean CBF during hypothermic anesthesia may not indicate uncoupling. Local analysis shows a maintained linear relationship that is reset to a higher CBF/CGU ratio.

Hypothermia Reduces Acute Vasospasm Following SAH in Rats

Subarachnoid hemorrhage (SAH) due to rupture of an aneurysm results in acute brain injury manifesting itself clinically as an acute neurologic deficit. Depending on the severity of the bleeding, the patients are classified according to clinical grading scales. This classification allows estimation of individual prognosis, as the extent of acute injury constitutes the crucial parameter for outcome following SAH. This statement has only recently been confirmed by Proust et al. [8], who reported a favorable outcome after Hunt and Hess grades IV and V in only 10% of cases.

Assessment of the CAMINO Intracranial Pressure Device in Clinical Practice

The purpose of this study was to investigate reliability, handling characteristics and complication rate of the CAMINO-ICP-monitor-system in clinical routine. In a case controlled study 82 patients with intracranial pathology necessitating ICP-monitoring received either a ventricular or a parenchymal CAMINO-device. Clinical assessment of curve shape and apparent reliability of the measurement was documented. Probe position and presence of hematoma was evaluated in all patients with a CT after probe insertion. Handling complications, i.e. dislocation were recorded. At the end of the measuring period the drift of the probe was checked ex vivo and a two point calibration was performed using a water column. During one year 82 patients received 95 probes (parench, 73. ventric. 22). The average measuring period was 91.3 +/- 70.6 hrs. Catheter position was verified by CCT for 67 (70.5%) probes. 92.5% of the devices were placed correctly. Clinically 88.4% of the measurements were assessed plausible, in 8.2% the displayed ICP-values were judged to be too high, in 2.1% too low. Probe drift after explanation was -0.21 mmHg/24 hrs. The mean value of the recalibrated probes in the water column corresponding to 15.8 mmHg was 14.7 +/- 1.9 mmHg. There was no correlation between neither drift nor function in the water column and the duration of the measurement. Technical complications exclusively related to the construction of the CAMINO-system like kinking of the cable, dislocation (probe pulled out) or dislocated fixation screw were too high (25.3%).